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Post by fritolay66 on Mar 23, 2009 0:24:34 GMT -5
Administration,
I have no idea where the appropriate place to post this would be. It is pertinent to Morgellon's, Lyme, Multiple Chemical Sensitivites, Gulf War Syndrome, Gilbert's Syndrome, supplements, the liver detox pathways, et al. I have posted this on other boards, and I really feel a lot of us here would benefit from it being put somewhere. It is long, but it packs a lot of important info. Please, click on the links too as they are just as good.
Fritowww.gilbertssyndrome.com/detoxification.phpThe Detoxification System -------------------------------------------------------------------------------- Contents: Detoxification | Phase I Detoxification Pathways | Phase II Detoxification Pathways | Imbalances Between Phase I and II -------------------------------------------------------------------------------- This is a work in progress and is being updated regularly. Check back regularly, as I will be steadily improving the site and adding more information. Detoxification (The Liver) www.lef.org/protocols/prtcl-143a.shtmlThe detoxification process is an elaborate mechanism conducted chiefly by the liver to eliminate both exogenous and endogenous toxins. The liver participates in the detoxification process, largely by the action of two sequential steps referred to as Phase I and Phase II systems. Phase I reactions involve blood filtration, bile excretion, and the interaction of enzymatic processes acting upon the toxin. Bile excretion is most efficient, in regard to the detoxification process, if adequate amounts of dietary fiber are simultaneously available to escort the toxin from the intestines. Ideally, Phase I and Phase II detoxification mechanisms work synergistically. If Phase I detoxification is highly active and Phase II detoxification is lethargic, the individual is referred to as a "pathological detoxifier," a condition which increases sensitivities to environmental poisons. (I also quoted this below) www.somis.dundee.ac.uk/staffprofiles/d/2000120700/Chemical defence is achieved by detoxification of compounds in the body and is generally considered a two step process; phase I metabolism includes oxidation, reduction, hydration, hydrolysis, isomerization and other specific reactions. In general, the products of phase I reaction are more chemically reactive than the parent compound, and phase I is seen as the creation of a reactive species prior to true detoxification by phase II metabolism. In phase II metabolism the substrate is conjugated to a polar hydrophobic group rendering the aglycone more water soluble and suitable for excretion. tuberose.com/Liver_Detoxification.htmlThe liver is one of the most important organs in the body when it comes to detoxifying or getting rid of foreign substances or toxins. The liver plays a key role in most metabolic processes, especially detoxification. The liver neutralizes a wide range of toxic chemicals, both those produced internally and those coming from the environment. The normal metabolic processes produce a wide range of chemicals and hormones for which the liver has evolved efficient neutralizing mechanisms. However, the level and type of internally produced toxins increases greatly when metabolic processes go awry, typically as a result of nutritional deficiencies. These non-end-product metabolites have become a significant problem in this age of conventionally grown foods and poor diets. Many of the toxic chemicals the liver must detoxify come from the environment: the content of the bowels and the food, water, and air. The polycyclic hydrocarbons (DDT, dioxin, 2,4,5-T, 2,3-D, PCB, and PCP), which are components of various herbicides and pesticides, are on example of chemicals that are now found in virtually all fat tissues measured. Even those eating unprocessed organic foods need an effective detoxification system because all foods contain naturally occurring toxic constituents. The liver plays several roles in detoxification: it filters the blood to remove large toxins, synthesizes and secretes bile full of cholesterol and other fat-soluble toxins, and enzymatically disassembles unwanted chemicals. This enzymatic process usually occurs in two steps referred to as phase I and phase II. Phase I either directly neutralizes a toxin, or modifies the toxic chemical to form activated intermediates which are then neutralized by one of more of the several phase II enzyme systems. Proper functioning of the liver's detoxification systems is especially important for the prevention of cancer. Up to 90% of all cancers are thought to be due to the effects of environmental carcinogens, such as those in cigarette smoke, food, water, and air, combined with deficiencies of the nutrients the body needs for proper functioning of the detoxification and immune systems. The level of exposure to environmental carcinogens varies widely, as does the efficiency of the detoxification enzymes, particularly phase II. High levels of exposure to carcinogens coupled with slow detoxification enzymes significantly increases susceptibility to cancer. Filtering the Blood One of the liver's primary functions is filtering the blood. Almost 2 quarts of blood pass through the liver every minute for detoxification. Filtration of toxins is absolutely critical as the blood from the intestines contains high levels of bacteria, bacterial endotoxins, antigen-antibody complexes, and various other toxic substances. When working properly, the liver clears 99% of the bacteria and other toxins during the first pass. However, when the liver is damaged, such as in alcoholics, the passage of toxins increases by over a factor of 10. Bile Excretion The liver's second detoxification process involves the synthesis and secretion of bile. Each day the liver manufactures approximately 1 quart of bile, which serves as a carrier in which many toxic substances are dumped into the intestines. In the intestines, the bile and its toxic load are absorbed by fiber and excreted. However, a diet low in fiber results in inadequate binding and reabsorption of the toxins. This problem is magnified when bacteria in the intestine modify these toxins to more damaging forms. www.chiro.org/nutrition/ABSTRACTS/Detoxification_Enzyme_Systems.shtmlCurrently, over 10 families of Phase I enzymes have been described, which include at least 35 different genes. Phase II reactions are equally complex, and involve multiple gene families as well. A good picture of the whole system: www.chiro.org/nutrition/FULL/Detoxification_Fig2.jpg-------------------------------------------------------------------------------- Phase I Detoxification Pathways www.lef.org/protocols/prtcl-143a.shtmlPhase I detoxification involves a group of enzymes, referred to as the cytochrome P450 family. Some 50-100 enzymes make up the cytochrome P450 systems, with each enzyme working more efficiently at neutralizing certain classes of chemicals. Phase I enzymes can directly neutralize some chemicals, but most toxins are converted to an intermediate form of the toxin. The intermediate form is considered more toxic than the original and requires the action of Phase II detoxification to complete the cycle. www.liverdoctor.com/03_detoxpathways.aspAn example of the phase one pathway is the Cytochrome P-450 mixed function oxidase enzyme pathway. These enzymes reside on the membrane system of the liver cells (called Hepatocytes). Human liver cells possess the genetic code for many isoenzymes of P-450 whose synthesis can be induced upon exposure to specific chemicals. This provides a mechanism of protection from a wide variety of toxic chemicals. To put it simply, this pathway converts a toxic chemical into a less harmful chemical. This is achieved by various chemical reactions (such as oxidation, reduction and hydrolysis), and during this process free radicals are produced which, if excessive, can damage the liver cells. Antioxidants (such as vitamin C and E and natural carotenoids) reduce the damage caused by these free radicals. If antioxidants are lacking and toxin exposure is high, toxic chemicals become far more dangerous. Some may be converted from relatively harmless substances into potentially carcinogenic substances. Excessive amounts of toxic chemicals such as pesticides can disrupt the P-450 enzyme system by causing over activity or what is called 'induction' of this pathway. This will result in high levels of damaging free radicals being produced. Substances that may cause overactivity (or induction) of the P- 450 enzymes: Caffeine, Alcohol, Dioxin, Saturated fats, Organophosphorus pesticides, Paint fumes, Sulfonamides, Exhaust fumes, Barbiturates The family of P-450 enzyme systems is quite diverse, with specific enzyme systems being inducible by particular drugs, toxins or metabolites. It is this characteristic that has allowed the development of special tests to check the function of the various pathways - see liver tests. The substrate is the substance that is acted upon by the enzyme. Substrates of cytochrome P-450 enzymes: Theophylline, caffeine, phenacetin, acetaminophen, Lidocaine, erythromycin, cyclosporin, ketoconazole, testosterone, estradiol, cortisone, Alprenolol, bopindolol, carvedilol, metoprolol, propranolol , Amitriptyline, clomipramine, desipramine, nortriptyline , Codeine, dextrometh- orphan, ethylmorphine, 4-methoxyamphetamin Family Phenytoin, ibuprofen, naproxen, oxicam drugs, S-warfarin, Diazepam, hexobarbitone, imipramine, omeprazole, alcohol, chlorzoxazone, enflurane. tuberose.com/Liver_Detoxification.htmlThe liver's third role in detoxification involves a two-step enzymatic process for the neutralization of unwanted chemical compounds. These not only include drugs, pesticides, and toxins from the gut, but also normal body chemicals such as hormones and inflammatory chemicals (e.g. histamine) which become toxic if allowed to build up. Phase I enzymes directly neutralize some chemicals, but most are converted to intermediate forms that are then processed by phase II enzymes. These intermediate forms are much more chemically active and therefore more toxic. If the phase II detoxification systems are not working adequately, these intermediates can cause substantial damage, including the initiation of carcinogenic processes. Phase I detoxification of most chemical toxins involves a group of enzymes which, collectively, have been named cytochrome P450. Some 50-100 enzymes make up the cytochrome P450 system. Each enzyme works best in detoxifying certain types of chemicals, but with considerable overlap in activity among the enzymes. The activity of the various cytochrome P450 enzymes varies significantly from one individual to another, based on genetics, the individual's level of exposure to chemical toxins, and his or her nutritional status. Since the activity of cytochrome P450 varies so much, so does an individual's risk for various diseases. This variability of cytochrome P450 enzymes is seen in the variability of people's ability to detoxify the carcinogens found in cigarette smoke and helps to explain why some people can smoke with only modest damage to their lungs, while others develop lung cancer after only a few decades of smoking. Patients with underactive phase I detoxification will experience caffeine intolerance, intolerance to perfumes and other environmental chemicals, and an increased risk for liver disease, while those with an overactive system will be relatively unaffected by caffeine drinks. One way of objectively determining the activity of phase I is to measure how efficiently a person detoxifies caffeine. Using this test, a surprising fivefold difference in the detoxification rates of apparently healthy adult has been discovered. When cytochrome P450 metabolizes a toxin, it chemically transforms it to a less toxic form, makes it water-soluble, or converts it to a more chemically active form. Caffeine is an example of a chemical directly neutralized by phase I. Making a toxin water-soluble allows its excretion by the kidneys. Transforming a toxin to a more chemically reactive form makes it more easily metabolized by the phase II enzymes. A significant side-effect of phase I detoxification is the production of free radicals as the toxins are transformed--for each molecule of toxin metabolized by phase I, one molecule of free radical is generated. Without adequate free radical defenses, every time the liver neutralizes a toxin exposure, it is damaged by the free radicals produced. The most important antioxidant for neutralizing the free radicals produced in phase I is glutathione. In the process of neutralizing free radicals, however, glutathione (GSH) is oxidized to glutathione disulfide (GSSG). Glutathione is required for one of the key phase II detoxification processes. When high levels of toxin exposure produce so many free radicals from phase I detoxification that the glutathione is depleted, the phase II processes dependent upon glutathione stop. Recent research shows that the cytochrome P450 enzyme systems are also found in other parts of the body, especially the brain cells. Inadequate antioxidants and nutrients in the brain result in an increased rate of neuron damage, such as seen in Alzheimer's and Parkinson's disease patients. As with all enzymes, the cytochrome P450s require several nutrients to function, such as copper, magnesium, zinc and vitamin C. A considerable amount of research has found that various substances activate cytochrome P450 while others inhibit it. www.chiro.org/nutrition/ABSTRACTS/Detoxification_Enzyme_Systems.shtmlGood picture of Phase I activities: www.chiro.org/nutrition/FULL/Detoxification_Tab2.jpgGood picture of Phase I enzymes: www.chiro.org/nutrition/FULL/Detoxification_Fig3.jpgInducers of Phase I Detoxification Note: The term "induce" can be misleading as it refers to anything that fires up the system - those that are harmful which need processing, and those which arent harmful and activate processing. tuberose.com/Liver_Detoxification.htmlCytochrome P450 is induced by some toxins and by some foods and nutrients. Obviously, it is beneficial to improve phase I detoxification in order to eliminate toxins as soon as possible. This is best accomplished by providing the needed nutrients and non-toxic stimulants while avoiding those substances that are toxic. However, stimulation of phase I is contraindicated if the patient's phase II systems are underactive. Drugs and environmental toxins activate P450 to combat their destructive effects, and in so doing, not only use up compounds needed for this detoxification system but contribute significantly to free radical formation and oxidative stress. Among foods, the brassica family, i.e. cabbage, broccoli, and Brussels sprouts, contains chemical constituents that stimulate both phase I and phase II detoxification enzymes. One such compound is indole-3-carbinol, which is also a powerful anti-cancer chemical. It is a very active stimulant of detoxifying enzymes in the gut as well as the liver. The net result is significant protection against several toxins, especially carcinogens. This helps to explain why consumption of cabbage family vegetables protects against cancer. Oranges and tangerines (as well as the seeds of caraway and dill) contain limonene, a phytochemical that has been found to prevent and even treat cancer in animal models. Limonene's protective effects are probably due to the fact that it is a strong inducer of both phase I and phase II detoxification enzymes that neutralize carcinogens. Drugs: alcohol; nicotine in cigarette smoke; Phenobarbital; sulfonamides; steroids Foods: cabbage, broccoli, and brussels sprouts; charcoal-broiled meats; high-protein diet; oranges and tangerines (but not grapefruits) Nutrients: niacin; vitamin B1; vitamin C Herbs: caraway and dill seeds Environmental toxins: carbon tetrachloride; exhaust fumes; paint fumes; dioxin; pesticides Inhibitors of Phase I Detoxification Note: In general, inhibition of detoxification is not desired. In the case of Gilbert's Syndrome, there is an exception to Phase 1 inhibitors, as at a certain level it can allow Phase II detox to keep up with it. tuberose.com/Liver_Detoxification.htmlMany substances inhibit cytochrome P450. This situation can cause substantial problems as it makes toxins potentially more damaging because they remain in the body longer before detoxification. For example, grapefruit juice decreases the rate of elimination of drugs from the blood and has been found to substantially alter their clinical activity and toxicity. Eight ounces of grapefruit juice contains enough of the flavonoid naringenin to decrease cytochrome P450 activity by a remarkable 30%. Curcumin, the compound that gives turmeric its yellow color, is interesting because it inhibits phase I while stimulating phase II. This effect can be very useful in preventing certain types of cancer. Curcumin has been found to inhibit carcinogens, such as benzopyrene (found in charcoal-broiled meat), from inducing cancer in several animal models. It appears that the curcumin exerts its anti-carcinogenic activity by lowering the activation of carcinogens while increasing the detoxification of those that are activated. Curcumin has also been shown to directly inhibit the growth of cancer cells. As most of the cancer-inducing chemicals in cigarette smoke are only carcinogenic during the period between activation by phase I and final detoxification by phase II, curcumin in the turmeric can help prevent the cancer-causing effects of tobacco. Those exposed to smoke, aromatic hydrocarbons, and other environmental carcinogens will probably benefit from the frequent use of curry or turmeric. The activity of phase I detoxification enzymes decreases in old age. Aging also decreases blood flow through the liver, further aggravating the problem. Lack of the physical activity necessary for good circulation, combined with the poor nutrition commonly seen in the elderly, add up to a significant impairment of detoxification capacity, which is typically found in aging individuals. This helps to explain why toxic reactions to drugs are seen so commonly in the elderly. Drugs: benzodiazepines; antihistamines; cimetidine and other stomach-acid secretion blocking drugs; ketoconazole; sulfaphenazole Foods: naringenin from grapefruit juice; curcumin from turmeric; capsaicin form chili pepper; eugenol from clove oil; quercetin from onions Botanicals: curcuma longa (curcumin); capsicum frutescens (capsaicin); eugenia caryophyllus (eugenol); calendula officianalis Other: aging; toxins from inappropriate bacteria in the intestine -------------------------------------------------------------------------------- Phase II Detoxification Pathways www.lef.org/protocols/prtcl-143a.shtmlPhase II reactions include sulfation and glucuronidation, which are key to human detoxification, along with glutathione conjugation, methylation, amino acid conjugation, and acetylation. Phase II detoxification typically involves biochemical conjugation, in which various enzymes in the liver attach small chemical moieties to the toxin. The conjugation reaction neutralizes toxins and reactive intermediates left over from Phase I detoxification. Both Phase I and Phase II detoxification require assistance from a healthy supply of enzymes. Enzyme quantity can be influenced by dietary components. Green tea and products found in red wine grapes encourage glucuronidation and glutathione conjugation enzymes, respectively. Glucuronidation, a significant pathway in the Phase II detoxification mechanism, is the combining of glucuronic acid with toxins, a process that requires the enzyme UDP, glucuronyl transferase (UDPGT). Foods rich in limonene, a monoterpene found in citrus peel, dill weed oil, and caraway oil, can increase UDPGT activity and encourage the glucuronidation mechanism. Many commonly used substances--for example, aspirin, menthol, synthetic vanilla, acetaminophen, morphine, diazepam, digitalis, benzoates, and some hormones--are detoxified through the glucuronidation pathway. Beta-glucuronidase, regarded as a dangerous enzyme, interferes with the glucuronidation process, allowing toxic levels of drugs and contaminants to accumulate. Older individuals appear particularly susceptible to increased beta-glucuronidase formation because of long-term exposure to toxic agents. Murray et al. (1998) report that the glucuronidation pathway is also impaired in the 5% of the population with Gilbert's syndrome. Gilbert's syndrome is a benign hereditary condition characterized by hyperbilirubinemia (serum bilirubin level 1.2-3.0 mg/dL) and jaundice. The Gilbert's syndrome patient typically complains of loss of appetite, malaise, and fatigue, symptoms often identifiable with liver dysfunction. www.liverdoctor.com/03_detoxpathways.aspThis is called the conjugation pathway, whereby the liver cells add another substance (eg. cysteine, glycine or a sulphur molecule) to a toxic chemical or drug, to render it less harmful. This makes the toxin or drug water-soluble, so it can then be excreted from the body via watery fluids such as bile or urine. Major Phase II pathways include glutathione, sulfate, glycine, and glucuronide conjugations. Individual xenobiotics and metabolites usually follow one or two distinct pathways. Again, this makes testing of the various pathways possible by challenging with known substances. The conjugation molecules are acted upon by specific enzymes to catalyse the reaction step. Through conjugation, the liver is able to turn drugs, hormones and various toxins into excretable substances. For efficient phase two detoxification, the liver cells require sulphur-containing amino acids such as taurine and cysteine. The nutrients glycine, glutamine, choline and inositol are also required for efficient phase two detoxification. Eggs and cruciferous vegetables (eg. broccoli, cabbage, Brussels sprouts, cauliflower), and raw garlic, onions, leeks and shallots are all good sources of natural sulphur compounds to enhance phase two detoxification. Thus, these foods can be considered to have a cleansing action. The phase two enzyme systems include both UDP-glucuronyl transferase (GT) and glutathione-S-transferase (GSH-T). Glutathione is the most powerful internal antioxidant and liver protector. It can be depleted by large amounts of toxins and/or drugs passing through the liver, as well as starvation or fasting. Phase II reactions may follow Phase I for some molecules or act directly on the toxin or metabolite. www.chiro.org/nutrition/ABSTRACTS/Detoxification_Enzyme_Systems.shtmlGood picture of Phase II conjugation reactions: www.chiro.org/nutrition/FULL/Detoxification_Tab3.jpgtuberose.com/Liver_Detoxification.htmlPhase II detoxification typically involves conjugation in which various enzymes in the liver attach small chemicals to the toxin. This conjugation reaction either neutralizes the toxin or makes the toxin more easily excreted through the urine or bile. Phase II enzymes act on some toxins directly, while others must first be activated by the phase I enzymes. There are essentially six phase II detoxification pathways: · Glutathione conjugation · Amino acid conjugation · Methylation · Sulfation · Acetylation · Glucuronidation In order to work, these enzyme systems need nutrients both for their activation and to provide the small molecules they add to the toxins. In addition, they utilize metabolic energy to function and to synthesize some of the small conjugating molecules. Thus, mitochondrial dysfunction, such as found in chronic fatigue syndrome, a magnesium deficiency or physical inactivity, can cause phase II detoxification to slow down, allowing the build-up of toxic intermediates Nutrients needed by phase II detoxification enzymes Glutathione conjugation: Glutathione, vitamin B6 Amino acid conjugation: Glycine Methylation: S-adenosyl-methionine Sulfation: Cysteine, methionine, molybdenum Acetylation: Acetyl-CoA Glucuronidation: Glucuronic acid Inducers of Phase II Detoxification Enzymes Note: The term "induce" can be misleading as it refers to anything that fires up the system - those that are harmful which need processing, and those which arent harmful and activate processing. tuberose.com/Liver_Detoxification.htmlGlutathione conjugation: Brassica family foods (cabbage, broccoli, Brussels sprouts); limonene-containing foods (citrus peel, dill weed oil, caraway oil) Amino acid conjugation: Glycine Methylation: Lipotropic nutrients (choline, methionine, betaine, folic acid, vitamin B12) Sulfation: Cysteine, methionine, taurine Acetylation: None found Glucuronidation: Fish oils, cigarette smoking, birth control pills, Phenobarbital, limonene-containing foods Inhibitors of Phase II Detoxification Enzymes Note: Inhibition of phase II detoxification is not desired, especially in those with Gilbert's Syndrome, as these enzymes are already inhibited. tuberose.com/Liver_Detoxification.htmlGlutathione conjugation: Selenium deficiency, vitamin B2 deficiency, glutathione deficiency, zinc deficiency Amino acid conjugation: Low protein diet Methylation: Folic acid or vitamin B12 deficiency Sulfation: Non-steroidal anti-inflammatory drugs (e.g. aspirin), tartrazine (yellow food dye), molybdenum deficiency Acetylation: Vitamin B2, B5, or C deficiency Glucuronidation: Aspirin, probenecid Glucuronidation Pathway www.somis.dundee.ac.uk/staffprofiles/d/2000120700/Glucuronidation is a major phase II detoxification pathway in which the sugar moiety of UDP-glucuronic acid is covalently linked to a xenobiotic or endobiotic, facilitating its removal from the body in the urine or bile. The directed excretion of glucuronides from the lumen of the endoplasmic reticulum (ER) to the plasma membrane and the exterior of the cell is an important regulated process. Impaired excretion leads to liver damage. Specific transporters for excretion of glucuronides have been implicated in lever cell function in ER and bile canaliculus. www.liverdoctor.com/03_detoxpathways.aspPolycyclic aromatic hydrocarbons, steroid hormones, some nitrosamines, heterocyclic amines, some fungal toxins, and aromatic amines. It also removes "used" hormones, such as estrogen and T4 (thyroid hormone) that are produced naturally by the body. tuberose.com/Liver_Detoxification.htmlGlucuronidation, the combining of glucuronic acid with toxins, requires the enzyme UDP-glucuronyl transferase (UDPGT). Many of the commonly prescribed drugs are detoxified through this pathway. It also helps to detoxify aspirin, menthol, vanillin (synthetic vanilla), food additives such as benzoates, and some hormones. Glucuronidation appears to work well, except for those with Gilbert's syndrome--a relatively common syndrome characterized by a chronically elevated serum bilirubin level (1.2-3.0 mg/dl). Previously considered rare, this disorder is now known to affect as much as 5% of the general population. The condition is usually without serious symptoms, although some patients do complain about loss of appetite, malaise, and fatigue (typical symptoms of impaired liver function). The main way this condition is recognized is by a slight yellowish tinge to the skin and white of the eye due to inadequate metabolism of bilirubin, a breakdown product of hemoglobin. The activity of UDPGT is increased by foods rich in the monoterpene limonene (citris peel, dill weed oil, and caraway oil). Methionine, administered as SAM, has been shown to be quite beneficial in treating Gilbert's syndrome www.answers.com/main/ntquery;jsessionid=2bawkmhkcb1np?method=4&dsid=2222&dekey=Glucuronidation&curtab=2222_1&sbid=lc05bGlucuronidation is a major inactivating pathway for a huge variety of exogenous and endogenous molecules, including drugs, polluants, bilirubin, androgens, estrogens, mineralocorticoids, glucocorticoids, fatty acid derivatives, retinoids and bile acids. The Glucuronidation Subfamilies carcin.oxfordjournals.org/cgi/content/full/22/7/1087N-Glucuronidation of 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP) and N-hydroxy-PhIP by specific human UDP-glucuronosyltransferases Glucuronidation has been well established as a major conjugation reaction in the biotransformation of many xenobiotics. These conjugation reactions are catalyzed by numerous isoforms of UDP-glucuronosyltransferase (UGT) (1). These enzymes are primarily found in the endoplasmic reticulum of many tissues, with the liver being, quantitatively, the most significant site of glucuronidation. In addition to a wide tissue distribution of UGTs, different isozymes can be preferentially expressed in specific tissues. Furthermore, polymorphic expression of certain UGTs has also been observed (2). Three UGT families have been identified in humans; designated UGT1, UGT2 and UGT8 based on their evolutionary divergence (1). Of these three families UGT1 and UGT2 have been shown to catalyze the glucuronidation of a wide variety of xenobiotic substrates, with UGT1 being more active in the glucuronidation of amines (3,4). Aryl- and alkylamines, sulfonamides, heterocyclic amines and hydroxylated compounds have all been reported to undergo glucuronidation in many animal species and humans. The primary function of UGTs is to eliminate substrates from the body via urine and feces by catalyzing the formation of hydrophilic glucuronide conjugates (5). In Short: UGT detoxifies many xenobiotics. The UGT1 family specializes in processing amines, arylamines and alkylamines, sulfonamides, heterocyclic amines and hydroxylated compounds. SCIENCE: PDF UGT pharmacogenomics: implications for cancer risk and cancer therapeutics UDP-glucuronosyltransferases (UGTs) belong to a superfamily of microsomal enzymes responsible for glucuronidation of numerous endogenous and exogenous compounds including bilirubin, hormones, various drugs as well as environmental carcinogens. Glucuronidation predominantly serves as a pathway for elimination of the different glucuronidated compounds. Seventeen human UGT transcripts have been identified thus far, and the UGT proteins are differentially expressed in a wide-range of human tissues. Most of the UGTs are expressed in the liver as well as other extrahepatic tissues; however, some are exclusively extrahepatic (Table 1). The tissue specific regulation of UGTs ensures a unique complement of UGT proteins to various tissues, and defines the capacity of each tissue's ability to eliminate or inactivate various exogenous and endogenous substrates. Table 1 UGT expression in human tissues UGT isoform Tissue expression References UGT1A1 Biliary tissue, colon, intestine, liver, stomach Reviewed in 1 and 6 UGT1A3 Biliary tissue, colon, liver, stomach Reviewed in 1 UGT1A4 Biliary tissue, colon, intestine, liver Reviewed in 1and 6 UGT1A5 Not detected UGT1A6 Biliary tissue, brain, colon, intestine, kidney, larynx, liver, lung, stomach Reviewed in 1; 53, 54, 55 UGT1A7 Esophagus, orolaryngeal tissue, stomach Reviewed in 1; 54 UGT1A8 Colon, esophagus, intestine, kidney, larynx Reviewed in 1; 54 UGT1A9 Breast, colon, esophagus, liver, kidney, prostate, ovary, skin, testis Reviewed in 1; 54, 56 UGT1A10 Biliary tissue, colon, esophagus, intestine, orolaryngeal tissue, stomach Reviewed in 1 and 6; 54 UGT2A1 Brain, fetal lung, olfactory epithelium 57 UGT2A2 Colon, intestine, liver, stomach 6 UGT2B4 Adipose tissue, adrenals, breast, kidney, liver, lung, ovary, placenta, prostate, skin, testis 42 UGT2B7 Brain, breast, colon, esophagus, intestine, kidney, liver, lung, pancreas 50 UGT2B10 Breast, esophagus, kidney, liver, lung, placenta, prostate, testis 50 UGT2B11 Adipose, adrenal, breast, kidney, liver, lung, prostate, skin 51 UGT2B15 Adipose, breast, esophagus, kidney, liver, lung, ovary, placenta, prostate, skin, testis, uterus 48 UGT2B17 Adrenals, breast, kidney, liver, lung, placenta, skin, ovary, prostate, testis, uterus 52 UGT2B28 Breast, liver 5 Glutathione Conjugation Pathway tuberose.com/Liver_Detoxification.htmlA primary phase II detoxification route is conjugation with glutathione (a tripeptide composed of three amino acids--cysteine, glutamic acid, and glycine). Glutathione conjugation produces water-soluble mercaptates which are excreted via the kidneys. The elimination of fat-soluble compounds, especially heavy metals like mercury and lead, is dependent upon adequate levels of glutathione, which in turn is dependent upon adequate levels of methionine and cysteine. When increased levels of toxic compounds are present, more methionine is utilized for cysteine and glutathione synthesis. Methionine and cysteine have a protective effect on glutathione and prevent depletion during toxic overload. This, in turn, protects the liver from the damaging effects of toxic compounds and promotes their elimination. Glutathione is also an important antioxidant. This combination of detoxification and free radical protection, results in glutathione being one of the most important anticarcinogens and antioxidants in our cells, which means that a deficiency is cause of serious liver dysfunction and damage. Exposure to high levels of toxins depletes glutathione faster than it can be produced or absorbed from the diet. This results in increased susceptibility to toxin-induced diseases, such as cancer, especially if phase I detoxification system is highly active. Disease states due to glutathione deficiency are not uncommon A deficiency can be induced either by diseases that increase the need for glutathione, deficiencies of the nutrients needed for synthesis, or diseases that inhibit its formation. Smoking increases the rate of utilization of glutathione, both in the detoxification of nicotine and in the neutralization of free radicals produced by the toxins in the smoke. Glutathione is available through two routes: diet and synthesis. Dietary glutathione (found in fresh fruits and vegetables, cooked fish, and meat) is absorbed well by the intestines and does not appear to be affected by the digestive processes. Dietary glutathione in foods appears to be efficiently absorbed into the blood. However, the same may not be true for glutathione supplements. In healthy individuals, a daily dosage of 500 mg of vitamin C may be sufficient to elevate and maintain good tissue glutathione levels. In one double-blind study, the average red blood cell glutathione concentration rose nearly 50% with 500 mg/day of vitamin C. Increasing the dosage to 2,000 mg only raised red blood cell (RBC) glutathione levels by another 5%. Vitamin C raises glutathione by increasing its rate of synthesis. In addition, to vitamin C, other compounds which can help increase glutathione synthesis include N-acetylcysteine (NAC), glycine, and methionine. In an effort to increase antioxidant status in individuals with impaired glutathione synthesis, a variety of antioxidants have been used. Of these agents, only Mega H-, vitamin C and NAC have been able to offer some possible benefit. Over the past 5-10 years, the use of NAC and glutathione products as antioxidants has become increasingly popular among nutritionally oriented physicians and the public. While supplementing the diet with high doses of NAC may be beneficial in cases of extreme oxidative stress (e.g. AIDS, cancer patients going through chemotherapy, or drug overdose), it may be an unwise practice in healthy individuals. Genovations - The Great Smokies Diagnostic Laboratory Glutathione-S-transferase detoxifies many water-soluble environmental toxins, including many solvents, herbicides, fungicides, lipid peroxides, and heavy metals (e.g., mercury, cadmium, and lead). The various forms of GST work together to eliminate toxins. Decreased glutathione conjugation capacity may incrase toxic burden and increase oxidative stress. GSTM1 (1p13.3) Health Implications: Glutathione-S-tranferase affords protection against oxidative stress (especially by reducing hydrogen peroxide and by regenerating oxidized vitamins C and E). GST also detoxifies electrophilic compounds including solvents, herbicides, fungicides, polycyclic aromatic hydrocarbons and heavy metals (Mercury, Lead, and Cadmium). Decreased glutathion conjugation capacity may increase toxic burden and increase oxidative stress resulting in a greater risk for various cancers and fatigue syndromes, especially if exposed to toxic compounds. Minimizing Risks: Regardless of genotype, increasing the body's production of glutathione will reduce oxidative stress and afford greater protection against a wide array of toxins. Numerous supplements can help raise glutathione levels including liberal consumption of colorful vegetables and fruits, vitamin C, n-acetylcysteine and milk thistle. Liberally consume bassica vegetables (broccoli, cauliflower, kale, cabbage, bok choi, etc.) and allium vegetables (onions, garlic, shallots, etc.). Vitamin E supplementation may also be helpful. COnsult your healthcare provider to find the supplement regimen that best fits your overall health needs. If you smoke, stop. Avoid exposure to herbicides, fungicides, insect sprays and industrial solvents. Amino acid conjugation Pathway tuberose.com/Liver_Detoxification.htmlSeveral amino acids (glyucine, taurine, glutamine, arginine, and ornithine) are used to combine with and neutralize toxins. Of these, glycine is the most commonly utilized in phase II amino acid detoxification. Patients suffering from hepatitis, alcoholic liver disorders, carcinomas, chronic arthritis, hypothyroidism, toxemia of pregnancy, and excessive chemical exposure are commonly found to have a poorly functioning amino acid conjugation system. For example, using the benzoate clearance test (a measure of the rate at which the body detoxifies benzoate by conjugating it with glycine to form hippuric acid, which is excreted by the kidneys), the rate of clearance in those with liver disease is 50% of that in healthy adults Even in apparently normal adults, a wide variation exists in the activity of the glycine conjugation pathway. This is due no only to genetic variation, but also to the availability of glycine in the liver. Glycine, and the other amino acids used for conjugation, become deficient on a low-protein diet and when chronic exposure to toxins results in depletion. Methylation Pathway tuberose.com/Liver_Detoxification.htmlMethylation involves conjugating methyl groups to toxins. Most of the methyl groups used for detoxification come from S-adenosylmethionine (SAM). SAM is synthesized from the amino acid methionine, a process which requires the nutrients choline, vitamin B12, and folic acid. SAM is able to inactivate estrogens (through methylation), supporting the use of methionine in conditions of estrogen excess, such as PMS. Its effects in preventing estrogen-induced cholestasis (stagnation of bile in the gall bladder) have been demonstrated in pregnant women and those on oral contraceptives. In addition to its role in promoting estrogen excretion, methionine has been shown to increase the membrane fluidity that is typically decreased by estrogens, thereby restoring several factors that promote bile flow. Methionine also promotes the flow of lipids to and from the liver in humans. Methionine is a major source of numerous sulfur-containing compounds, including the amino acids cysteine and taurine. Genovations - The Great Smokies Diagnostic Laboratory Catechol-O-methyl transferase is the enzyme primarily responsible for breaking down the neurotransmitters dopamine, epinephrine, and norepinephrine. COMT (V158M) Health Implications: Catechol-O-methyltransferase inactivates catecholamines, catechol estrogens, and catechol drugs such as L-DOPA. A polymorphism in COMT results in reduced COMT activity, thus decreased degradation of these compounds. Risk may be increased for some neuropsychiatric disorders, imparied estrogen metabolism, increased sensitivity to pain, and late-onset alcoholism. Minimizing Risks: Avoid excessive alcohol consumption; seek help if alcohol consumption is a health issue. Minimize sustained mental and environmental stress (stress hormones require COMT for their degradation, thus can decrease the methylation of estrogen compounds). Ensure adequate intake of B vitamins, magnesium, and protein. Note: Epinephrine is the same as adrenaline, and norepinephrine is the same as noradrenaline. Sulfation Pathway tuberose.com/Liver_Detoxification.htmlSulfation is the conjugation of toxins with sulfur-containing compounds. The sulfation system is important for detoxifying several drugs, food additives, and, especially, toxins from intestinal bacteria and the environment. In addition to environmental toxins, sulfation is also used to detoxify some normal body chemicals and is the main pathway for the elimination of steroid and thyroid hormones. Since sulfation is also the primary route for the elimination of neurotransmitters, dysfunction in this system may contribute to the development of some nervous system disorders. Many factors influence the activity of sulfate conjugation. For example, a diet low in methionine and cysteine has been shown to reduce sulfation. Sulfation is also reduced by excessive levels of molybdenum or vitamin B6 (over about 100 mg/day). In some cases, sulfation can be increased by supplemental sulfate, extra amounts of sulfur-containing foods in the diet, and the amino acids taurine and glutathione. www.liverdoctor.com/03_detoxpathways.aspNeurotransmitters, steroid hormones, certain drugs such as Acetaminophen (also known as paracetamol) ,and many xenobiotic and phenolic compounds. Me: And the polymorphism - the first one - that affects disposal of ephinephrine (adrenaline), norepiniephrine (noradrenaline), and dopamine. That struck true with me. When I get mad I have a hard time calming down. And... wow. My own personal research and experience with dopamine reveals that it deals with the attention-switching threshold. I often find myself obsessing in certain projects or games, and hard to shift out. If my liver cant dispose of those chemicals, that would explain that as well. Good lord that's a match. Acetylation Pathway tuberose.com/Liver_Detoxification.htmlConjugation of toxins with acetyl-CoA is the primary method by which the body eliminates sulfa drugs. This system appears to be especially sensitive to genetic variation, with those having a poor acetylation system being far more susceptible to sulfa drugs and other antibiotics. While not much is known about how to directly improve the activity of this system, it is known that acetylation is dependent on thiamine, pantothenic acid, and vitamin C. Genovations - The Great Smokies Diagnostic Laboratory N-acetyl Transferase detoxifies many environmental toxins, including tobacco smoke and exhaust fumes. Polymorphisms can result in slower than normal or faster than normal addition of an acetyl group to these toxins. Slow acetylators have a build up of toxins in the system and rapid acetylators add acetyl groups so rapidly that they make mistakes in the process. Both slow and rapid acetylators are at increased risk for toxic overload if they are exposed to environmental toxins. If the toxin exposure is reduced, the risk is reduced. NAT2 (I114T & K268R) Health Implications: N-acetyltransferase 1 is found in extra-hepatic tissues, while NAT2 is found predominantly in the liver and the gut. Both are used in the Phase II acetylation of numerous environmental toxins, including heterocyclic aromatic amines. Slow acetyleators do not clear toxins well and the resulting increased total toxic burden can increase the risk of lung, colon, breast, bladder, and head and neck cancers, though results have not been consistent in all studies. Urinary bladder cancer appears to have the most consistent association with low acetyleation. Minimizing Risks: If you smoke, stop. Your risk of lung cancer is substantially higher than someone with normal NAT activity. Even occasional smoking or exposure to second hand smoke is harmful. Liberal consumption of most vegetables and fruits but especially cruciferous vegetables (broccoli, Brussels sprouts, cauliflower, watercress, and cabbage), garlic, onions, soy, grapes and berries will increase Phase II efficienty, including acetylation. Glycination Pathway www.liverdoctor.com/03_detoxpathways.aspSalicylates and benzoate are detoxified primarily through glycination. Benzoate is present in many food substances and is widely used as a food preservative. Many other substances are detoxified as well via the glycine conjugation pathway. Patients suffering from xenobiotic overloads and environmental toxicity may not have sufficient amounts of glycine to cope with the amount of toxins they are carrying. -------------------------------------------------------------------------------- Imbalances in Phases I and II tuberose.com/Liver_Detoxification.htmlAnother potential problem occurs because the toxins transformed into activated intermediates by phase I are substantially more reactive. Unless quickly removed from the body by phase II detoxification mechanisms, they can cause widespread problems, especially carcinogenesis. Therefore, the rate at which phase I produces activated intermediates must be balanced by the rate at which phase II finishes their processing. People with a very active phase I detoxification system coupled with slow or inactive phase II enzymes are termed pathological detoxifiers. These people suffer unusually severe toxic reactions to environmental poisons. An imbalance between phase I and phase II can also occur when a person is exposed to large amounts of toxins or exposed to toxins for a long period of time. In these situations, the critical nutrients needed for phase II detoxification are depleted, which allows the highly toxic activated intermediates to build up. www.lef.org/protocols/prtcl-143a.shtmlIdeally, Phase I and Phase II detoxification mechanisms work synergistically. If Phase I detoxification is highly active and Phase II detoxification is lethargic, the individual is referred to as a "pathological detoxifier," a condition which increases sensitivities to environmental poisons. Toxic Overload www.liverdoctor.com/03_detoxpathways.aspIf the phase one and two detoxification pathways become overloaded, there will be a build up of toxins in the body. Many of these toxins are fat soluble and incorporate themselves into fatty parts of the body where they may stay for years, if not for a lifetime. The brain and the endocrine (hormonal) glands are fatty organs, and are common sites for fat-soluble toxins to accumulate. This may result in symptoms of brain dysfunction and hormonal imbalances, such as infertility, breast pain, menstrual disturbances, adrenal gland exhaustion and early menopause. Many of these chemicals (eg. pesticides, petrochemicals) are carcinogenic and have been implicated in the rising incidence of many cancers.
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Post by fritolay66 on Mar 23, 2009 0:30:06 GMT -5
www.lef.org/protocols/prtcl-143b.shtml#singleGulf War Syndrome Chelation Therapy: A Means of Extracting Heavy Metals Chelation therapy refers to a treatment in which certain synthetic chemicals and body proteins bind metal molecules, extracting them from the system. Literally, chelation therapy is derived from the Greek word chele, which alludes to a claw-like action imposed upon unwanted materials accumulating in the body. Chelation is currently best associated with the clearance of plaque from the arteries, establishing normal blood flow to the vasculature. Historically, chelation therapy has been used for other objectives apart from cardiovascular health. As early as 1941, Providence Hospital in Detroit used chelation, employing intravenously administered ethylenediaminetetraacetic acid (EDTA), a synthetic amino acid, to extract lead. EDTA, a nontoxic chelator, also clears mercury, cadmium, nickel, copper, calcium, and other metals from the body. Even physicians who are not proponents of chelation therapy admit that evidence in regard to extracting heavy metals appears convincing. Chelation therapy has been useful in treating schizophrenia and Lou Gehrig's disease as well. For the 25% of the U.S. population who have varying levels of heavy metal poisoning, the dangers are manifold. Illustrative of this, molecularly, some metals closely resemble the chemical structure of enzymes, with a small amount of the metal chelated into the enzyme's structure (Walker 1990). If an excess of the metals replaces the normal mineral content of the enzyme, the enzyme can become chemically altered and nonfunctional, hindering metabolic activity. Because enzymes ignite detoxification, the process suffers when enzymes are in short supply. The Gulf War veteran who was exposed to unreasonable amounts of environmental metallic poisons could be shutting down enzymatic systems vital to detoxification processes. The signs of heavy metal poisoning closely resemble the complaints of the service personnel of the Gulf War, for example, headache, fatigue, muscle aches and pains, tremors, anemia, mental confusion, mental illness, depression, tingling in the extremities, abnormal nerve reflexes, insomnia and/or drowsiness, dizziness, irritability, disorientation, decreased male fertility, spontaneous abortions in women, and poor circulation. Virtually every organ system responds adversely to heavy metal accumulations, including the respiratory, cardiovascular, muscular, integumentary (skin, hair, nails), nervous, endocrine, skeletal, urinary, and digestive systems. Walker (1990) believes that chelation therapy is 3.5 times safer than taking an aspirin tablet for a headache. LD-50 refers to the pharmaceutical term "lethal dose 50," the dose of a substance that is fatal to 50% of test animals. Aspirin has a LD-50 at only 558 mg per kilogram in humans, while EDTA's LD-50 is 2000 mg/kg. A crucial phase of chelation is re-establishing the beneficial minerals that were extracted, along with the heavy metals. This may be accomplished either orally or intravenously. It would be to the patient's advantage were the physicians using autonomic balancing as the premise for refusion of the minerals. The selection of appropriate minerals to normalize imbalances occurring in the autonomic nervous system appears an integral phase of the success or failure of chelation therapy. An individual wishing to obtain chelation therapy may want to contact a physician who follows the standard chelation protocol of the American College of Advancement in Medicine. The number of sessions required to enact a change cannot be presupposed, but the recommended maximum dosage is currently about 3 grams of EDTA, dosage usually calculated by body weight, given by IV infusion 1-3 times weekly, as a drip for 3-4 hours. Initially, the dosage may be as small as 1/2-1 gram of EDTA. Can What You Eat Make a Difference? According to Dr. Steven Whiting of the Institute of Nutritional Science, supplemental fiber, as well as fibrous food choices, not only protects the digestive system from concentrated toxins, but it also serves as a cleansing factor for many poisons accumulating in the body. Certain foods, such as bran, whole grain wheat, oats, corn, cereals, lentils, beans, peas, peanuts, figs, dates, and apples, are natural chelators. Supplementing with psyllium seed husks, oat, and wheat bran (if not allergic to wheat), and acacia gum, plus emphasizing high-fiber food choices assists in binding noxious materials in the digestive tract and expelling them in fecal material. Other Treatments for GWS Mycoplasma Forecast Dioxychlor A Single Herbal that Appears Helpful Oxygenation Therapy Exercise Intolerance Exercise Conclusion Mycoplasma Forecast Nicolson et al. (1998) have released the heartening news, gathered from their research at the Institute for Molecular Medicine, Huntington Beach, CA, that thousands of soldiers are being helped when mycoplasma infections are identified and killed.
The presence of mycoplasma infections in the blood of fractions of patients with CFIDS, FMS, GWS, or RA enable health care professionals to rule out psychological or psychiatric based illness as a causative factor in the above-mentioned conditions and instead direct their efforts toward correction of medical anomalies. Administering antibiotic therapy is sometimes a chosen treatment modality. Appropriate cyclic treatments with antibiotics or other medications that suppress chronic infections have resulted in improvement and even recovery in most of the individuals treated. If blood infections are diagnosed, patients receive continuous antibiotics for at least 6 months before beginning a 6-week cyclic treatment. The recommended treatments for mycoplasmal blood infections require long-term antibiotic therapy, usually multiple 6-week cycles of doxycycline (200-300 mg a day), ciprofloxacin (Cipro) (1500 mg a day), azithromycin (Zithromax) (500 mg a day), or clarithromycin (Biaxin) (750-1000 mg a day). (Note: Administering some antibiotics produces no favorable clinical response; in fact, penicillin results in patients becoming more symptomatic.)
Multiple antibiotic cycles are required because few patients recover after only a few cycles or even within the first year of therapy if the illness is chronic, possibly because of the intracellular locations of the infections and the slow-growing nature of the microorganisms. As with other treatments used to rid infiltrations of noxious materials or microorganisms, a Herxheimer's reaction usually occurs, meaning the patient feels poorer than before beginning the curative. This reaction occurs as die-off or release of toxic materials from damaged microorganisms is increased. As die-off decreases, stabilization occurs, and the patient slowly moves nearer recovery.
Confounding the treatment, some patients recover only to a certain point and then fail to continue to respond to the antibiotics, suggesting that other problems, such as viral infections, environmental exposures, and other toxic events, are working synergistically with the microorganism to produce a state of ill health.
A 3-year follow-up of antibiotic therapy by the SHASTA CFIDS Association of Northern California reported that a majority (about 80%) of the patients with confirmed mycoplasmal infections who participated in the antibiotic therapy recovered from 50-100% of their preillness health, within the 3 years.
Antibiotics are not without their dark side. Apart from an ugly list of side effects that commonly accompany antibiotic therapy, antibiotics can disrupt the friendly flora that resides symbiotically in the gut. Gut flora represents several pounds of highly sensitive material that is regarded as immune modulating. Disturbance of "friendly flora" can antagonize the immune and inflammatory process. Reinoculation of the gut with cultures of Lactobacillus acidophilus, Lactobacillus rhamnosus, Bifidobacterium longum, and Bifidobacterium breve is vital to recovery. Selection of a probiotic that is touted to be antibiotic resistant is recommended.
To be successful, each patient must comply with a complementary health approach that employs the best of orthodox and natural medicine. Gulf War veterans presenting with mycoplasmas typically display nutritional deficiencies and poor absorption that must be corrected. Mega vitamin/mineral therapy is warranted, and sublingual or liquid supplements should be considered. Vitamin C, which detoxifies most heavy metals (5-15 grams daily, in divided doses), vitamin E (600-1000 IU daily), CoQ10 (50-150 mg daily), bioflavonoids (200 mg 3 times a day), choline (1000 mg daily, in divided doses), inositol (750 mg daily), vitamin B5 (500-1500 mg daily), PABA (500-1000 mg daily), sublingual vitamin B12 (1000 mcg daily dose), and flaxseed or fish oils (1 tbsp daily), along with minerals, such as zinc (50 mg daily), calcium (1000 mg a day), and selenium (up to 300 mcg a day), may be used. Minerals should be taken apart from antibiotics because minerals can affect antibiotic absorption. Garlic (Allium sativum) is a potent detoxifier. Use 2 capsules (300 mg each) 3 times a day with meals. Use 500 mg of L-cysteine, L-tyrosine, L-glutamine, and L-carnitine daily on an empty stomach.
Interest has been keen in regard to patients wishing to be tested for mycoplasmas, though additional volunteers are welcomed into the clinical trials conducted by the VA. The Institute for Molecular Medicine can test patients for evidence of mycoplasmal infections and other infections of the types that worsen human diseases, such as chronic fatigue immune deficiency syndrome, fibromyalgia syndrome, Gulf War syndrome, and rheumatoid arthritis. Blood sample can be sent to:
Prof. Garth L. Nicolson The Institute for Molecular Medicine 15162 Triton Lane Huntington Beach, CA 92649-1401 Tel: 714-903-2900 Fax: 714-379-2082 E-mail:gnicimm@ix.netcom.com Dioxychlor Dr. Robert W. Bradford, president of Bradford Research Institute, states that Dioxychlor is the major oxidant of demonstrated effectiveness, capable of ridding the system of pathogenic organisms. An inorganic compound composed of chlorine and two atoms of nascent oxygen covalently bonded, Dioxychlor is currently being used to treat individuals suffering with GWS, Epstein-Barr virus, and cytomegalovirus. Nicolson (1998) reported the usefulness of this therapy. Broad-spectrum antibiotics bring short-term relief of infections, but the positive effect of antibiotics may be countered by long-term negativity. The Bradford Institute has determined that environmental diseases are typically characterized by systemic Candida, numerous allergies, autoimmune disorders, and compromised antigen kill. Largely, these disorders are iatrogenic in nature, meaning they are caused by either diagnostic or treatment procedures. Chronic or haphazard administering of antibiotics participates in this decadent cascade. Dioxychlor, a homeopathic substance displaying low toxicity, offers an alternative to this quandary. Dioxychlor appears to destroy mycoplasmas while reducing sensitivity reactions and improving the status of gravely ill patients, such as those suffering from ALS. An oral dose of Dioxychlor is 5-20 drops in 2 oz of water (4 tbsp), 1-3 times daily, based on patient tolerance. Should "die off" of foreign materials intensify symptoms, reduce the dosage. Dioxychlor can also be administered by slow drip with the assistance of a qualified physician. A Single Herbal that Appears Helpful in Gulf War Syndrome Complaints Duke (1997), botanist and humanitarian, illustrates that yellow sweet clover (Melilotus officinalis) contains herbal activity that may prove beneficial in regard to symptoms apparent in those stricken with GWS, for example, headache, myalgia, spasms, mycoplasmosis, ischemia, rheumatism, nervousness, sores, and cardiopathy. Yellow sweet clover contains 0.9-2% coumarin, which may be the substance that elicits the benefit. Coumarin should, however, be used cautiously, for high doses can cause symptoms, such as headache, stupor, thinning of blood, and elevated liver enzymes, which appear transient upon discontinuance. Individuals wishing to purchase yellow sweet clover may do so by contacting the following two suppliers: Dragon River Herbals P.O. Box 74 Ojo Caliente, NM 87549 Tel: (800) 813-2118 Mark's Drugs Roselle 384 E. Irving Park Rd. Roselle, Illinois 60172 Tel: (630) 529-3400 Use 1/2 tsp (30 drops), taken 2-3 times a day, for 7-10 days. It is advisable to observe a 3-5-day respite from yellow sweet clover before repeating the herbal therapy. Oxygenation Therapy Oxidative therapy can be useful in suppressing a variety of anaerobic infections when administered at 1.5 ATM for 60 minutes. Hyperbaric oxygen therapy (HBO) refers to a monoplace chamber, in which only one patient is entirely enclosed in a pressure chamber, breathing oxygen at a pressure greater than atmospheric pressure. HBO is regarded as a therapeutic modality because significant physiological mechanisms are activated as a result. HBO delivers 10-15 times the oxygen to tissues as normal breathing. Popularly, HBO is used in the formation of new capillaries around a wound area and to treat anemia, ischemia, and some poisonings. The flooding of the body with oxygen, as in hyperbaric therapy, tends to remove other gases, such as carbon monoxide and acute cyanide poisoning. HBO inhibits the growth of a number of anaerobic, as well as aerobic, organisms by enhancing phagocytic activity. This effect complements the improved action of host disease-fighting factors and is useful in disorders involving immunosuppression. Studies have demonstrated a prolonged postantibiotic effect when hyperbaric oxygen is combined with therapeutic dosages of antibiotics.
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Post by fritolay66 on Mar 23, 2009 0:39:17 GMT -5
Chronic Fatigue Syndrome This is a work in progress and is being updated regularly. Check back regularly, as I will be steadily improving the site and adding more information. Chronic Fatigue Syndrome / ME / Post-Viral Fatigue Syndrome / CFIDS / CEBV www.psychnet-uk.com/dsm_iv/chronic_fatigue_syndrome.htmThe illness is also known as chronic fatigue immune dysfunction syndrome (CFIDS), and outside of the USA is usually known as myalgic encephalomyelitis (ME). In the past the syndrome has been known as Chronic Epstein-Barr virus (CEBV). Chronic Fatigue Syndrome is also mistaken for Fibromyalgia which is a chronic musculoskeletal syndrome. www.cfsresearch.org/cfs/research/treatment/9.htmIn CFS/ME it seems that we should see this as an illness probably caused by enteroviruses, acting on a body that is for many reasons already stressed biologically, with high pre-morbid levels of oxidative stress, resulting in high peroxynitrite levels. Other biological stressors may be the cause or add to this, such as IAG or these may be mechanical, dietary, environmental, physical, infective or psychological. What seems important is that the blood-brain barrier becomes permeable allowing viral entry. Treatments should be aimed at identifying and removing these stressors There also exists a chronically activated immune system, which may result from the initial insult or co-existent microbial, or toxin overload or a combination of the two. It seems that there is over-expression of aberrant RNA, derived initially from an enterovirus, protected by a viral type coat which in the presence of LMWRNase L leads to extreme ATP depletion... Pollution and vaccines have been suggested as a cause for the loss of control of HERV associated mRNA production. Following this hypercoagulability develops, causing problems in both blood and lymph microcirculation's. This hypercoagulability may arise from a combination of hereditary, immune mediated and oxidative stress pathways. We have chronic sympathetic system activation, from many causes. Multiple subtle endocrine changes are also present in the CFSME/FM complex, both quantitatively in terms of hormone levels, and also qualitatively, with loss of circadian rhythmicity. Given the bi-directional flow of information between the nervous, endocrine and immune systems, we are presented with a perfect example of Chaos Biology. This results in a failure of homeostasis and homeodynamics. Simply stated, a body that cannot respond to any form of biological stress, be it environmental, infective, physical or psychological. Medical history is littered with illnesses that were thought to be psychogenic e.g. Tuberculosis, epilepsy and Hypothyroidism. www.cfsresearch.org/cfs/research/treatment/9.htmChronic Fatigue Syndrome/ME and Fibromyalgia plus Associated Syndromes Evidence for their organic basis: A summary of the suggested underlying pathophysiologies and treatment approaches Dr. Andrew John Wright Epidemiology The epidemiology data below is mainly from the pen of Dr. Betty Dowsett, Hon. Consultant Virologist. "The illness usually affects young to middle aged adults. The studies which have been done tend to show that this is mainly a disease of temperate climates, where bowel and respiratory infections are seasonably interrupted. This is in comparison with tropical areas, where solid adult immunity exists, by the reasons of continuous exposure to infection and where lesser standards of hygiene persist. "Of the studies that have been done, the average statistical increase in the incidence of ME between l965 and l990 was between 50 and 70%. It is thought that this is possibly due to an enteroviral infection. The majority of patients, between 60% and 80%, report that a 'flu'-like illness rushes in the onset of ME, which is more common in Summer and Autumn than in Winter and Spring (63% compared with 37% in a study of 225 patients). "Studies show that the commonest age of onset in both sexes actually lies between the third and fourth decade. There is unity of ratio between males and females until puberty and then a 3 to 1 ratio develops between females and males. "In an analysis of 420 patients who presented between ten days and two years of the onset of the illness, 31% were seen to be improving; 20% were still fluctuating between relapse and remission; 25% had achieved a steady level of disability, and 24% had experienced no remission or were deteriorating. This shows CFS/ME is not a short-term illness and improvement does not proceed in a linear fashion. "If it is an enterovirus that initially commonly circulates in local populations, the effects are probably asymptomatic in the majority. However, those people affected through genetic and environmental factors then go on to develop disabling fatigue. This is probably around 6% of those exposed. However, although around 25% to 30% improve, the others develop a more serious multi-system disease involving cardiac, endocrine and immune system abnormalities. Unfortunately, there appears to be a lifetime risk of relapse in all patients." Number Spring Summer Autumn Winter Acute Onset 184 23.4% 18% 29% 29% Chronic Decline 86 29% 18.6% 28% 24.4% Therefore there seems to be a lull in summer. A recent population based study in Chicago, using telephone screening and medical screening for those identified with Chronic Fatigue Syndromes, revealed an incidence of 422/100,000. The highest incidence being in women aged 40-49, amongst ethnic minorities and those with poor education and socio-economic status. A further study sponsored by AfME and the SAMEC Trust also showed a high incidence in ethnic minorities, but also little understanding amongst the population, as it has always been viewed as an illness of white middle classes. This leads to a reduced quality of life, inability to work, and depression. In Short: 60-80% report a flu-like illness begins CFS. The commonest time of onset is age 20-30. CFS is not a short-term illness and fluctuates between periods of being more or less debilitating. There appears to be a lull in symptoms in summer. CFS Symptoms www.geocities.com/ctfutures2001/index.html#contentsChronic fatigue syndrome (CFS) is an emerging illness characterized by debilitating fatigue (experienced as exhaustion and extremely poor stamina), neurological problems, and a variety of flu-like symptoms. The core symptoms include excessive fatigue, general pain, mental fogginess, and often gastro-intestinal problems. Many other symptoms will also be present, however they will typically be different among different patients. These include: fatigue following stressful activities; headaches; sore throat; sleep disorder; abnormal temperature; and others. The degree of severity can differ widely among patients, and will also vary over time for the same patient. Severity can vary between getting unusually fatigued following stressful events, to being totally bedridden and completely disabled. The symptoms will tend to wax and wane over time. This variation, in addition to the fact that the cause of the disease is not yet known, makes this illness difficult to diagnose. For a slight majority of patients, the illness begins suddenly as though one had come down with the flu. Except that this "flu" doesn't seem to completely go away. For many other patients, the onset appears gradually over a long period of time. In many cases, a high-stress event seems to "trigger" the illness. There are many cases in which CFS appears to have begun with a severe head injury, for example. But since such events seem to have no apparent logical connection to the illness that follows, many have speculated that the CFS was latent in people beforehand in these cases, and that the stress of trauma merely triggered the stress-hypersensitivity aspect of the illness. Some have further speculated that other stressful factors in our environment, be they microbes or pollution, may also prompt this illness to bloom. The illness varies greatly in its duration. A few recover after a year or two. More often, those who recover are more likely to do so from 3 to 6 years after onset. Others may recover after a decade or more. Yet for some, the illness seems to simply persist. CFS often occurs in cycles. It can be frustrating to obtain some relief, but then not know whether you have recovered or if you are merely between cycles. Me: Notice that this is an almost exact description of the symptoms of Gilbert's Syndrome, even as far as the cycles of symptoms and the triggers that set it off. Such a high degree of similarity implies a close correspondence between GS and CFS. www.cfsresearch.org/cfs/research/treatment/9.htmChronic Fatigue Syndrome/ME and Fibromyalgia plus Associated Syndromes Evidence for their organic basis: A summary of the suggested underlying pathophysiologies and treatment approaches Dr. Andrew John Wright In a study of 66 CFS/ME patients and 53 healthy controls blood was analysed using reverse transcriptase PCR using primers for nontranslated enteroviral sequences. The blood was analysed for the presence of a prominent 750base pair sequence previously reported in 12 out of 24 Gulf War Veterans. 77% of patients had a prominent 750 base pair sequence compared to 0% of the controls. Interestingly Dr Brooks has shown a specific deficit using this technique. CFS/ME patients have significantly reduced levels of N-acetyl aspartate in the right hippocampus signifying neuronal death. Similar changes have been found in the brain stems of Gulf War Veterans. Poor blood flow to the thalamus has also been reported. These findings help explain problems with cognitive functioning and central processing of information. Although I accept that my observations are open observations, the main abnormalities I found were: Abnormal melatonin rhythms These were sometimes high outputs of melatonin and these were often phase shifted by 6 to 12 hours, giving the sufferer a syndrome, I suppose, similar to severe jet lag. In a review of my first sixty patients, this occurred in 36% of cases. Interestingly there was no melatonin output in 60% of cases, patients therefor losing the main molecular manifestation of darkness. As sleep is in part induced by melatonin triggered elevation of Prostaglandin D2 in the Histamine-Interleukin–Prostaglandin pathway, these problems may explain patient's problems with sleep initiation. This possibly indicates problems with enzymatic conversion of serotonin into melatonin, or internal desynchronisation between the suprachiasmatic nuclei in the hypothalamus Abnormalities in cortisol and DHEA These hormones form a major part of the catabolic / anabolic balance in the body. Cholesterol is converted into pregnenolone by the adrenals. It then goes one way to produce the 'Structural' hormone DHEA from which Oestrogen and Testosterone are made, and the other way to the 'Functional' hormones cortisol and progesterone. As an analogy, when considering their effect on cell structure and organisation, the structural hormones are like house builders and the functional hormones are like interior decorators. Invariably, DHEA levels were low, a point discovered by other workers, but cortisol levels fluctuated. They could be high or low. They could also, over a period of a day, be normal in level, but were not produced rhythmically. Indeed, they often showed flat output curves, which are biologically useless. The body relies on steroid hormones to change concentration in order to be read as a signal, rather like listening to FM radio. It is the velocity of change that is important as well as permissive levels. Levels also changed over time in the same patients, but invariably, the sicker patients had a low output of cortisol and DHEA. Most patients show a catabolic dominance. Recent urinary amino and organic acid studies have shown an increase in protein breakdown, which may result because of an altered Cortisol and DHEA ratio, or Growth hormone / IGF-1 abnormalities. One of the larger studies that has been carried out is that by Dr. Lucinda Scott for her PhD thesis, 'The role of the HPA axis in Chronic Fatigue Syndrome.' Her main findings were: a) Low levels of DHEA and cortisol It would seem that in CFS/ME, there is a specific problem with the CRH receptor, with it being down-regulated, or the V1b receptor, which is the one that Vasopressin acts on, being upregulated. In humans, Vasopressin is not as effective an ACTH releasing agent. Therefore, in CFS/ME, where people are unable to use this as their main hypothalamic pituitary stress-releasing hormone, homeostasis cannot be maintained in the presence of any form of biological stress. Another explanation would be that constant biological stress causes adrenal fatigue, i.e. constant output causes depletion of the functional reserve of the gland. c) Central opioid tone She then went on to look at central opioid tone in Chronic Fatigue Syndrome and found that using Naloxone to induce ACTH and cortisol release produced a blunted response. This would suggest depressed central opioid tone in chronic fatigue syndrome, which may account for some of the pain that these people experience. d) Adrenal gland imaging Finally, she looked at CT and MRI imaging studies of the adrenal gland and found consistently atrophied adrenals in CFS/ME. She performed this study with 8 patients who showed a poor response to the 1 mcg. Synacthen Test. A 50% reduction in adrenal size was seen. Therefore, the principal findings of her study were: 1. There is a reduction in adrenal gland size and secretory reserve. 2. End organ hypofunctioning occurs which is probably due to a deficiency of ACTH. 3. Under activity of this is not explained by increased opioid tone. 4. An increased contribution of Vasopressin to adrenal regulation is probable. Finally, before finishing with the adrenals, it is also postulated that another steroid, 'ouabain-like' steroid, (OLS), is low in CFS/ME. OLS has mainly been researched with regards to hypertension. It is produced, along with aldosterone, by the zona glomerulosa of the adrenal cortex. It may be that the atrophy of the gland also causes reduction in OLS levels. It plays an important role in modulating the Na-K-ATPase pump in cell membranes. This is vital for maintaining the electrical homeostasis of the cell membrane. Failure of this regulatory enzyme has profound effects on cell energetics and may in part also account for many of the symptoms found in this illness. CFS can also begin following after exposure to toxins including Organophosphates and chlorines, which are known to produce abnormal sodium ion channels. Finally, CFS/ME patients have increased resting energy expenditure, a state influenced by abnormal transmembrane ion transport. It may be that down regulation of the adrenals is an attempt by the body to downregulate a system that is constantly receiving stress messages from the brain, because of sympathetic overdrive. The body can take no more and it puts you flat on your back to enforce rest. Alternatively it could be seen as part of a general downregulation secondary to hypothalamic dysfunction. One of the other problems is the effect of the illness on thyroid functioning. It has long been noted that people are often functionally hypothyroid. That is, they produce enough thyroid hormones from the thyroid gland, as measured by levels in the blood, but they appear to be hypothyroid at a cellular level. This tends to occur in adult Fibromyalgia patients. Numerous effects could explain this: 1. The blood test for thyroid function is not a dynamic test, unlike, e.g. HbA1c. It simply represents what is in the blood, and not what is active at a cellular level. It is based on population sampling and would therefore include people with subclinical hypothyroidism. We will have to wait until the development of the nuclear membrane thyroid receptor volume test before we have a dynamic test of thyroid function. In medicine we tend to treat extremes and not subtle alterations in physiology. This means that people at the lower end of ‘normal’ are not treated. They may actually need to be at the upper end of normal, but the test will not tell you that. The body also has the ability, it seems, to keep the blood levels normal despite cellular thyroid problems. This can happen in any chronic illness. 2. In cytokine mediated illness the production of central and locally generated cytokines can affect the de-iodination pathways of thyroid hormones. It seems that high level of rT3, and low levels of T2 may ensue. Reverse T3 is a non-competitive inhibitor of T3 and is raised in stress situations. T2 is thought to be important for the functioning of mitochondria. High levels of rT3 have been found in post-operative patients subsequent to high cortisol output. It is thought to be an adaptive response in order to conserve energy. The situation of poor conversion of serum T4 to cellular T3, for whatever reason, has been called Wilson's Thyroid Syndrome. 3. Other hormones affect thyroid functioning. Cortisol is permissive for hormone uptake into cells and low cortisol levels can therefore have an effect on this. High cortisol can also inhibit functioning through its action on rT3 as mentioned above. 4. There is hypothalamic downregulation of the thyroid axis with altered sensitivity to TRH and TSH at their receptors The treatment studies by Teitelbaum and Ali that I quote later both incorporated low dose thyroid hormone replacement in selected patients. This seems to be of great benefit especially to fibromyalgia patients, particularly borderline hypothyroid patients (T4 in lower 1/3 of reference interval TSH >3) or those with evidence of low T3. In Short: A genetic sequence was found in 77% of CFS sufferers and 0% of controls, which helps explain cognitive problems. Phase-shifted high metatonin output in 36% of cases and no melatonin output in the rest indicates disturbance in conversion of serotonin into melatonin and help explains insomnia. Low DHEA and oddly fluctuating cortisol lead to catabolic dominance. There is also a depressed central opioid tone which accounts for some of the pain. Atrophied adrenal glands were consistently found, 50% of normal size. It is possible that adrenals are downregulated by the brain due to constant stress messages. Another steroid, OLS, is low, leading to poor cell energetics. CFS patience expend more energy when resting. CFS can be triggered by exposure to organiophosphates and chlorines. There is a functional hypothyroidism in CFS. They produce enough hormone but are hypothyroid in a cellular level. This could be a result of cytokine mediated illness or high or low levels of cortisol. www.geocities.com/ctfutures2001/index.html#contentsNotes: Temperature of 97.5 often. Common complaints: fatigue, chest pain on right side, headache, sinus congestion, foggy, light headed, cold sweats, back pain, loose stools Doctor: “On examination your general appearance was healthy. Your blood pressure was normal… In short, you had the typical appearance of patients with chronic fatigue syndrome, which is, you looked entirely normal. Subsequently, you have had symptoms of sinusitis and have taken several antibiotics for this. Sinus symptoms are fairly common in patients with chronic fatigue, and often have no demonstrable bacterial etiology.” “As we discussed, the chronic fatigue syndrome is a mysterious illness that can devastate an individual’s life and ability to work without producing any abnormalities on physical examination or laboratory testing.” Causes www.geocities.com/ctfutures2001/index.html#contentsThe cause of the illness is not yet known. Current theories are looking at the possibilities of neuroendocrine dysfunction, viruses, environmental toxins, genetic predisposition, or a combination of these. For a time it was thought that Epstein-Barr Virus (EBV), the cause of mononucleosis, might cause CFS but recent research has discounted this idea. The illness seems to prompt a chronic immune reaction in the body, however it is not clear that this is in response to any actual infection -- this may only be a dysfunction of the immune system itself. A recent concept promulgated by Prof. Mark Demitrack is that CFS is a generalized condition which may have any of several causes (in the same way that the condition called high blood pressure is not caused by any one single factor). It *is* known that stressors, physical or emotional, seems to make CFS worse. Some current research continues to investigate possible viral causes including HHV-6, other herpes viruses, enteroviruses, and retroviruses. Additionally, co-factors (such as genetic predisposition, stress, environment, gender, age, and prior illness) appear to play an important role in the development and course of the illness. Many medical observers have noted that CFS seems often to be "triggered" by some stressful event, but in all likelihood the condition was latent beforehand. Some people will appear to get CFS following a viral infection, or a head injury, or surgery, excessive use of antibiotics, or some other traumatic event. Yet it's unlikely that these events on their own could be a primary cause. Genetics www.cfsresearch.org/cfs/research/treatment/9.htmChronic Fatigue Syndrome/ME and Fibromyalgia plus Associated Syndromes Evidence for their organic basis: A summary of the suggested underlying pathophysiologies and treatment approaches Dr. Andrew John Wright Immunology and Toxicology Some of the more striking abnormalities are those found in the 2-5 Synthetase/Rnase L anti-viral pathway. These are not specific to CFS/ME though, and abnormalities can occur in other viral illnesses. This pathway works as follows: viruses activate the 2-5-synthetase enzyme. This in turn converts ATP into 2-5 oligoadenylate and activates the RNase L enzyme, which degrades viral and single stranded RNA. Various Protein kinase enzymes also becomes activated and elevated, which again inhibits both viral replication and protein synthesis. It has been suggested that environmental toxins in the presence of heat shock proteins can also activate this pathway. Dr. Robert Suhadolnik, at Temple University, showed as far back as 1989, that activity in this pathway was upregulated in patients with chronic fatigue syndromes. Crucially in 1996 it was also noted that a proportion of patients had an abnormal version of the RNase L enzyme. This low molecular weight form is 37 kDaltons, compared with the normal 80 and 47 kDalton versions. It was thought initially that all chronic fatigue patients had this abnormal form. The most recent figures I could find by Dr. K De Meirleir showed that the low molecular weight version was found in 680 out of 705 patients. The levels quantitatively vary though, and the amounts correlate with the Karnofsky Disability Index. The low molecular weight RNase L enzyme is up to six times more biologically active and resists protein degradation. Therefore when expressed, patients suffer an even greater depletion of ATP reserves and inhibition of protein synthesis. It has been suggested that mycoplasma genus cause the splitting of Rnase L. The overwhelming fatigue with an acute viral illness is due in part to ATP depletion in order to fuel anti-viral pathways. Interestingly studies have shown that those suffering from Fibromyalgia do not express the low molecular weight RNase L. If confirmed by larger studies this would be a major difference between the two illnesses. This upregulated system, either expressing RNase L or low mol wt RNase L can then cause problems to varying degrees with enzymatic detoxification pathways, particularly in the liver. It can monopolise protein synthesis and deplete essential nutrients such as glutathione. Low white cell glutathione is a feature of treatment resistant patients. Some very interesting and important work has come from Professor Vojdani, in California. In 1998 he published a paper which showed that RNase L inhibitor, the controlling enzyme in the 2-5 Synthetase / RNase L pathway, is low in CFS/ME patients. This may be the underlying problem. The reason this occurs is not yet known. Vojdani suggests that measurements of RNase L inhibitor and Protein Kinases can be used to show a viral aetiology and monitor relapses and remissions. Measurements of Protein Kinase 1 are very important in studying the mechanism of interference with signal transduction in lymphocytes. This signal transduction system consists of eleven different isoenzymes, each having different biological actions, and distinct abnormalities can be seen in CFS/ME patients. Also important is measuring NK cell activity, which is often low. [graph shows CFS/ME patients with 569 RNase L inhibitor levels while normal people have 2296] Other evidence on the importance of this upregulation and expression of the abnormal enzymes has come from the use in patients of the agent Ampligen, also called poly (1)-poly (C12U). This is a synthetic, mismatched double-stranded RNA with potent anti-viral and regulatory properties. In a double blind study involving 92 patients, measures of clinical response such as cognitive functioning, exercise ability and less reliance on other medications, improved in 80% of sufferers. Ampligen is best given early in the illness, and in those positive for low molecular weight RNase L. Not only does it have potent anti-viral properties, it is also an immune system modifier, i.e. an allosteric modifier. It can downregulate an activated immune system, as in CFS/ME, and upregulate a depressed immune system, as in AIDS patients. Unfortunately Ampligen is expensive, around £6-8000 per treatment. It also has to be given IV twice a week. Relapses can occur on completing treatment and repeat courses may be necessary. Another interesting study by Vojdani, published in 1999, showed that not only could viruses elevate the above anti viral pathway, but so could environmental pollutants, particularly Methyl Tertiary Butyl Ether, (MTBE), and Benzene, components of petrol fumes. Whilst talking about chemicals, it is interesting to note that about 20-47% of CFS /ME and Fibromyalgia sufferers complain of severe multiple chemical sensitivities. About 4-6% of the general population also has severe chemical intolerance. The levels of chemicals needed to trigger these problems would normally be considered to be non toxic, however, host factors involving sensitisation / amplification of endogenous responses seem to be to blame. Research to date has shown that these sensitised pathways react unfavourably with exposure to volatile organic compounds and pesticides, facilitating behavioural, autonomic, endocrine and immune function dysfunction. This is seen by sensitisability of cardiovascular parameters, resting EEG alpha-wave patterns, beta-endorphin levels and impairment of divided-attention task performance. This fits in well with Professor Behan's work. It shows that people exposed chronically to low dose organophosphates, who also have CFS/ME, exhibit a neuroendocrine profile identical to acutely exposed people. An example would be farm workers with 'sheep dip flu.' Here the results of investigations looking at serotonin, acetylcholine and brain glucocorticoid steroid receptor activity were identical in OP exposed workers and those with CFS/ME. In Short: The RNase L anti-viral enzyme is upregulated in CFS. 680 out of 705 patients had an abnormal low-weight version of the RNase L enzyme. This enzyme is 6x more biologically active. Therefore when expressed, patients suffer an even greater depletion of ATP reserves and inhibition of protein synthesis. The overwhelming fatigue with an acute viral illness is due in part to ATP depletion in order to fuel anti-viral pathways. It has been suggested that mycoplasma genus cause the splitting of Rnase L. It is also found that the RNase L inhibitor is low in patients with CFS (569 as opposed to 2296), which may be the reason for the upregulation. Environmental pollutants can also activate this antiviral pathway. This upregulated system can then cause problems to varying degrees with enzymatic detoxification pathways, particularly in the liver. It can monopolise protein synthesis and deplete essential nutrients such as glutathione. Low white cell glutathione is a feature of treatment resistant patients. 20-47% of CFS sufferers have severe multiple chemical sensitivity. These sensitized pathways respond unfavorably to exposure to volatile organic compounds and pesticides, reacting from low doses similarly to normal people reacting from high levels of exposure. Gilbert's Syndrome www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8096054&dopt=AbstractGilbert's and chronic fatigue syndromes in men Gilbert's syndrome, a symptomless familial hyperbilirubinaemia, has also been described as "benign" and a condition in which "some patients complain of symtoms such as... weakness but these are non-specific and may reflect a coincidental occurrence". We report 7 men with chronic fatigue syndrome and Gilbert's syndrome These patients were from a total of 45 men referred with chronic fatigue syndrome. Therefore 16% of this population had Gilbert's syndrome, which compares with 2% in the general population. All 7 were referred to our fatigue clinic and met the Oxford criteria for chronic fatigue syndrome. The fatigue was severe, had been present for at least 6 months, and was incapacitating. They had no conditions known to produce chronic fatigue. Liver function and gamma-glutamyltransferase concentrations were normal. There was no evidence of haemolysis. Gilbert et al originally described a clinical syndrome associated with hyperbilirubinaemia. They described psychological symptoms that included neurasthenia, the historical equivalent of chronic fatigue syndrome. They also described bleeding disorders, pruritus, urticaria, and anaemia, which imply that not all their patients had a simple unconjugated hyperbilirubinaemia and suggest other hepatic pathologies. Foulk et al reviewed 118 patients said to have a diagnosis of constitutional hepatic dysfunction. 58 were thought to have Gilbert's syndrome. Fatigue was the most common symptom, mentioned by 38. Gastrointestinal symptoms were also common. The investigators thought that the symptoms were secondary to anxiety about being told of chronic hepatic illness. Olsson et al isolated finding of hyperbilirubinaemia, and suggested that "Gilbert's" is merely a label applied to patients whose serum bilirubin is greater than two standard deviations above the mean. We do not think that our observations can be attributed to the patient being told that he had a chronic liver disease because few knew they had Gilbert's syndrome when referred. We reject the modern view that Gilbert's syndrome is symptomless, and think that it is a predisposing or perpetuating factor for the chronic fatigue syndrome, especially in men. Another illness, such as an infection, may precipitate a chronic fatigue syndrome in these predisposed men. Note: The study states that Gilbert's Syndrome occurs in 2% of the general population, and 16% of people with CFS have GS. This would be an 8x greater chance of having CFS, but many figures I've seen say that the percentage of people with GS is 5-10%. This reveals a 2x-3x greater chance of having CFS. Still significant, but I'm curious where the oft-quoted "4x more likely" comes from. www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=8097856&query_hl=9&itool=pubmed_docsumGilbert's syndrome and chronic fatigue syndrome Dr Cleary and Dr White (March 27, p842) describe a high prevalence of Gilbert's syndrome (16%) in men with chronic fatigue syndrome (CFS) and suggest that "Gilbert's syndrome is a predisposing or perpetuating factor for the CFS, especially in men". Since November, 1991, we have been investigating the prevalence of CFS among patients with severe fatigue. Among more than 120 subjects referred to out fatigue clinic, we identified 41 female and 16 male subjects with fatigue persisting for at least six months and several non-specific symptoms (fever, sore throat, myalgia, arthralgia, neuropsychiatric disturbances). 6 subjects (5 female, 1 male) met Centers for Disease Control criteria for CFS diagnosis (group A); 33 (22 female, 11 male) did not fulfill the second major criterion of this definition (absence of any other conditions producing fatigue), and an alterative diagnosis was formulated (group B); and 18 (14 female, 4 male) were classified as probable CFS (two major criteria associated with six or seven minor criteria) (group C). Gilbert's syndrome was diagnosed in 6 (11%) of the 57 patients with lasting debilitating fatigue. Gilbert's syndrome was identified in a female patient with overy CFS (1 of 6, 17%), in 2 men and 1 woman of 18 (17%) with probably CFS and in 2 women in group B (6%) with relapsing polychodritis and hypothyroidism, respectively. As Clearly and White show, 16% of our overt and probable CFS population had Gilbert's syndrome. This prevalence is much higher than the 6% in the group with fatigue associated with causes other than CFS and the 2% in the general population. However, we identified the syndrome in women and therefore we would like to modify slightly their conclusion: GIlbert's syndrome can be regarded as a predisposing or perpetuating factor for CFS in both sexes. In Short: This expands the above to both sexes. PERSONAL: Gilberts Web Forums crismatt The doctor said that as there were no symptoms with GS, these were being caused by ME. We were given a leaflets about ME and told that eventually she would get better. On her next visit another doctor didn't mention ME at all. When I questioned this he said that he didn't like people being labelled with ME (or as he preferred to call it 'Chronic Fatigue Syndrome'). He said that although medical opinion was that there were no symptoms with GS, everyone he saw diagnosed with it suffered similar symptoms. He said although there was no proof they were caused by GS, it seemed likely that GS did have something to do with it. I had a similar experience. I tried to discuss with various Doctors I have seen over the years certain aspects of GS but the moment I mention the possibility of a link with GS there seems to be a perceivable change in attitudes. The whole experience over many years was frustrating in itself. My Doctor eventually diagnosed Fybro Myalgia but I still ended up in the ME clinic all be it after a three and a half year wait just for an appointment. They suggested reading some books regarding approaches to life which all seemed a bit of an anti climax in the context of a desire for some relief when symptoms were at their worst. When I mentioned the wait for the appointment I was just advised "it was a very busy department". Now there's a thought. Dannystalley Its disturbing to see that the majority of GP's are still ignorant to ME & GS. I agree with you that ME/CFS is often wrongly diagnosed as the illness where recent evidence (for me at least) clearly points to GS. p075.ezboard.com/fgilbertswebfrm1.showMessage?topicID=15.topicbyjingo Has anyone had ME or CFS (Chronic Fatigue Syndrome) with Gilberts? I have had CFS off and on since 1985, but Gilberts only started to show up in the past two years. Jeelbear When I first got sick around 1990 the docs all assumed it was CFS because all the symptoms were there. They ran lots of tests for everything including poisoning, and then decided it may be CFS but was probably just exhaustion from overwork and yada-yada. I never really bought that idea. The Gilberts turned up in the tests (they told me as an aside but reassured me it was nothing at all) and they never put it together as the possible root cause but now that I am more informed I believe that is the case. Byjingo There is a set of symptoms that is now recognised as CFS, and I quote below: "Chronic Fatigue Syndrome/Fibromyalgia (CFS) is an emerging illness characterized by debilitating fatigue (experienced as exhaustion and extremely poor stamina), neurological problems, and a variety of flu-like symptoms. The illness is also known as chronic fatigue immune dysfunction syndrome (CFIDS), and outside of the USA is usually known as myalgic encephalomyelitis (ME). In the past the syndrome has been known as Chronic Epstein-Barr virus (CEBV). The core symptoms include excessive fatigue, general pain, mental fogginess, and often gastro-intestinal problems. Many other symptoms will also be present, however they will typically be different among different patients. These include: fatigue following stressful activities; headaches; sore throat; sleep disorder; abnormal temperature; and others. The degree of severity can differ widely among patients, and will also vary over time for the same patient. Severity can vary between getting unusually fatigued following stressful events, to being totally bedridden and completely disabled. The symptoms will tend to wax and wane over time. This variation, in addition to the fact that the cause of the disease is not yet known, makes this illness difficult to diagnose" Like you, I wonder if Gilberts has not been the cause all along. You wonder how 'benign' it is, given that there are a number of us who are identifying the same health problems. For me, I regularly have a sore throat, swollen glands and fatigue, sometimes fever, and fairly frequent headaches. My acupuncturist has identified the liver as a real problem for me (before I knew about Gilberts). Macpgh I got sick in the big wave back in 1985/1986, with CFIDS. About 6 years after that fact & previous blood test results, is when my bilirubin began to exceed the high limits significantly. It has been elevated since then, and at the end of 2001 I had new blood work that showed I was even higher. I have never recovered from CFIDS and I'm having the neuro problems now for the last several years. Martin SNap! I was diagnosed with Post-Viral fatigue syndrome (also knowb as ME or CFS or CFIDS) nearly 10 years ago and my liver tests came up with Gilberts Syndrome, but they said it was nothing to worry about. SO, I had the diagnosis ME! Now I am in a relapse I went to see Dr Hyams who is a harley street specialist of ME/CFS and he is giving me high doses of vit B12 (like 25000% RDA 3 times a day) and I might need some injections of Glutathione...he did say that people with Gilberts are more suceptible to getting ME/CFS.....but then noone know what ME/CFS really is after 50 years of looking and the doctors say that GS doent cause any symptoms. whosGilbert I was diagnosed with GS in 1990. That diagnosis also coincided with a diagnosis of meningitis, twice in one year, and also glandular fever, from which it's suspected that I had/still have CFS. The CFS diagnosis was arrived at by doing a Live Blood Test (in Australia), which means the practitioner can actually see white blood cells as they "swim around" in your blood sample and count them, and also identify which type they are. This gives a clear picture in conjunction with blood tests as to a diagnosis. What was found in my case was that there were many "left over" white cells used in killing Glandular Fever, and that these should have by that time disappeared from the blood stream unless the body had not fully recovered (and now I know that is often the case with GS...it takes us longer to get over viruses) and therefore, along with all my symptoms I still had (and have), a diagnosis of CFS was made. It is now 2002, and I'm still battling this, only now I have alot more information thanks to everyone's feedback here......K. Nosnoborrenoele Wow! What an interesting thread! I have a diagnosis of post viral fatigue syndrome (CFS/ME). I just came across this website yesterday when I was doing a bit of research into my CFS. I have slightly elevated bilirubin levels and wondered what this has to do with the CFS. Well that was how I learnt about GS. I must stress that I have NOT been diagnosed with GS but I'm just beginning to wonder if it might be a possibility PERSONAL: Gilberts Web Forums crismatt At one point my 15 year old daughter was told by one doctor she had Chronic Fatigue Syndrome as well as GS. We think this was the doctors way of saying GS is benign so we need an answer for the symptoms! WE don't think she has CFS at all. www.geocities.com/ctfutures2001/index.html#contentsNote: Carl also has GS. www.cfsresearch.org/cfs/research/treatment/15.htmIs Glutathione Depletion an Important Part of the Pathogenesis of Chronic Fatigue Syndrome? It talks about Gluthathione Depletion with respect to Chronic fatigue. I have absoltuely no medical knowledge but I can see plainly the thread of Gilberts/Gluthathione/phase 2 pathway/endocrine/hormone/fatigue/psychological/etc. It has become obvious. I would like to hear your comments on the site in general. CFS research - there is some very interesting stuff- the links are all there and they just need linking to GS. This is another forum that discusses glutathione a lot in the context of chronic fatigue. health.groups.yahoo.com/group/CFSFMExperimental/p075.ezboard.com/fgilbertswebfrm1.showMessage?topicID=160.topicJuly15 I was supposedly diagnosed with CFIDS among many other things- you name it- Lyme disease, "candida", so on and so forth. I had a doctor (well known) who dealt with what I would consider contraversial maladies who told me that the GS was not the source of my problems. Wrong, wrong. I can tell you some of what has gone on with me. For instance, I have always had fairly low blood pressure (not too low, but low enough to evoke comments from the nurses who took my stats). I had also noticed throughout the years that I got tired fairly easily and that around my menstrual cycle I would have a bout of nausea. I was very intolerant of aspirin and became intolerant of sulfa drugs. Alcohol didn't agree with me at all. In 1988, I had several events that happened all at once and I believe that they were what triggered a major attack that was to last 7 years. I had a flu virus, on top of which I wasn't getting any sleep at night, was taking Pepto Bismol (salicylates are a major NO for GS), had been not eating for long hours at a time (AKA dieting), and was taking a supplement called "Chromium". I got sick all at once and had the following symptoms: nausea, backache, headache, cooking odors were offensive, totally no appetite, depression, intolerance to antibiotics which I had previously been tolerant to, extreme exhaustion, and what to me were "autistic" symptoms- couldn't stand loud noises, etc. p075.ezboard.com/fgilbertswebfrm4.showMessage?topicID=43.topicMauiForce I have GS and I have a short of vit. B12 and my Fe level is very high p075.ezboard.com/fgilbertswebfrm4.showMessage?topicID=37.topicmartin I was diagnosed 10years ago as having Post-Viral Fatigue Syndrome otherwise known as ME or Chronic fatigue syndrome and in the media as Yuppie Flu ou chronic Flu in america. Tests came up with Gilberts Syndrome but they said it was nothing to worry about. The symptoms were sudden... a sudden dizziness, brainfog, fatigue and later on I have had aches and pains after exerting myself..........ie classic ME symptoms. The specialist i saw yesterday said that people with GS have a susceptibility to get ME/CFS. As noone knows what ME really is perhaps it is just GS I dont know. p075.ezboard.com/fgilbertswebfrm2.showMessage?topicID=107.topicmartinlong1978 I actually wonder if many cases of CFS are actually GS. Before I was diagnosed I was wandering the net (after being told it was probably GF), and kept coming up with CFS - and it really seemed to fit the bill. With doctors thinking GS is benign are they not picking up this cronic fatigue as GS, and thinking it is CF p075.ezboard.com/fgilbertswebfrm2.showMessage?topicID=86.topicPinawa Alas, just a few weeks ago I was dismissively told I have GS. Ironically, tests they did about 7 years ago came up with the same results and I was not told - but there they were in my file. As the GP insists there are no symptoms, she is now sending me to a Chronic Fatigue Specialist. PERSONAL: Gilberts Web Forums imgeha The Gilberts is a marker for deeper toxicity issues that the doctors don't understand and / or won't acknowledge. If you have Gilberts Syndrome you are 4 TIMES more likely to get chronic fatigue. If you are still suffering after 2 years of good diet, no alcohol, milk thistle etc etc, then Gilberts is the marker for chronic fatigue. Investigate why you have chronic fatigue. This is a good starting point. www.beatcfsandfms.org/. Yeasts & Mycoplasmas www.cfsresearch.org/cfs/research/treatment/9.htmMycoplasma The question of microbe interaction with hypercoagulable blood has been raised above. After viruses Mycoplasma are the smallest and simplest micro-organisms known. They have no cell wall and this allows them to invade tissue cells and replicate utilising the cells nutrients. When it becomes extra-cellular it takes a piece of the cell membrane with it and this can initiate an autoimmune process e.g. rheumatoid arthritis. According to Nicholson it can invade the Central Nervous System and NK cells. With induction of CD4+ cells Mycoplasma can trigger the release of the cytokines IL-1, IL-6 and TNF-alpha. Mycoplasma species are found in almost all body fluids and bone marrow as well. In a study by Prof. Vojdani the following results were obtained using multiplex PCR tests. CFS(ME) n=100 CONTROLS n=100 Mycoplasma genus 52% 15% Mycoplasma fermentans 32% 8% Mycoplasma hominis 9% 3% Mycoplasma penetrans 6% 2% Prof. Nicholson has found similar results. He has also shown that multiple Mycoplasma infections are commoner in these illnesses. When he examined CFSME/FM patients for the presence of M.fermentans, M pneumoniae, M penetrans, and M hominis, he found multiple infections in over half of patients. I must say though that after testing 70 patients for mycoplasma genus with PCR, I have only found 1 positive result. Why there is variance between different centres is not yet understood. Oxidative Stress Oxidative stress has a central role to play in this illness. In a paper published by Prof. Richards from Newcastle, Australia, it has been shown that oxidative stress, as measured by methaemoglobin, malondialdehyde and 2,3 diphosphoglycerate levels, was significantly raised in CFS/ME patients compared to controls. When comparing 33 patients against controls he found the following: Blood parameter Mean control values Mean CFS (ME) values Malondialdehyde 31.3 47.63 MetHb 0.62 1.45 2,3-DPG 5.07 5.73 Mean Red cell volume(MCV) 87.43 89.73 The amount of elevation correlated significantly with symptom expression in CFS /ME. His team felt that the mechanisms are similar to those found in rheumatoid arthritis. They also feel that bacterial toxins and Nitric Oxide can play a part in the elevated oxidative stress levels. Prof. Pall has postulated that an excess of cytokines could cause a sustained increase in peroxynitrite levels. This is a potent free radical. The mechanism would involve cytokine induction of nitric oxide synthetase. This then causes an increase in nitric oxide levels, which reacts with the free radical superoxide to generate peroxynitrite. As peroxynitrite acts via six known biochemical mechanisms to increase the level of nitric oxide and superoxide, multiple amplification and feedback then occurs. This mechanism may be one reason for the high oxidative stress seen in this illness. Following on from this is the important fact that peroxynitrite inhibits our anti-oxidant enzymes, Superoxide dismutase, Glutathione peroxidase and Catalase, again increasing oxidative stress. It is suggested that this increase in oxidative stress could cause damage to the hypothalamus and account for all the hormone problems. Also, high peroxynitrite and nitric oxide levels could account for the sodium channelopathies seen in this group of syndromes. Finally these high free radical levels would favour uncoupling of Krebs cycle oxidative phosphorylation in mitochondria. This could also lead to the abnormalities in urinary organic and amino acids as seen by McGregor. Prof. Pall himself cites that there are twelve different observations on CFS(ME) and its symptoms that provide support for his theory 1 The level of neopterin, a marker for the induction of the inducible nitric oxide synthetase is elevated in CFS/ME. 2. Mitochondria are reported to be dysfunctional in CFS/ME. Also mitochondria are known to be damaged by peroxynitrite and by nitric oxide. 3. Both cis-aconitate and succinate levels are reported to be elevated in CFS/ME, and the enzymes that metabolise these two compounds are inactivated by peroxynitrite 4. The cytokines that can cause peroxynitrite elevation have been reported as being elevated in ten different studies. 5. These same cytokines have been reported to cause fatigue when injected into humans 6.An animal model(mouse) of CFS/ME has inducible fatigue after being exposed to a bacterial extract that induces both inflammatory cytokines and inducible nitric oxide 7. Polyunsaturated fatty acid pools are reported deleted in CFS/ME and such polyunsaturated fats are known to be oxidised by oxidants such as peroxynitrite 8. Studies and anecdotal evidence has shown / suggested that antioxidants such as co-enzyme Q10, flavinoids and glutathione precursors are / may be useful in CFS /ME. 9. Women are reported to produce more nitric oxide than men do. A similar gender bias is seen in autoimmune diseases such as lupus. 10. Cases of CFS/ME are associated with high levels of deleted mitochondria DNA. 11. Biochemical similarities i.e. depletion of glutamine and cysteine pools have been reported in CFS/ME and several other disease characterised by elevated peroxynitrite. 12. Studies by other authors show high levels of oxidative stress in CFS/ME. Prof. Pall feels that many of the clinical features of this illness can be explained in terms of oxidative stress e.g. infection induces nitric oxide which stimulates receptors that initiate pain perception. Nitric oxide has a central role in learning and memory and may be a partial explanation of the cognitive dysfunction in CFS /ME Elevated Nitric oxide levels can also be linked to related conditions. Exposure to organic solvents and pesticides, has been reported to precede Multiple Chemical Sensitivity and these induce nitric oxide synthesis and inflammatory cytokine production. Neopterin has also been found elevated in MCS as well as CFS /ME. In Fibromyalgia it has been reported that there is an excess of NMDA activity. This is known to increase nitric oxide and peroxynitrite. In Gilbert's syndrome, i.e. unconjugated hyperbilirubinaemia, there is a four fold increased incidence in sufferers. This also independently increases oxidative stress as well as having an impact on cellular uptake of thyroid hormones. Professor Majid Ali from New York is a leading researcher in this field... He calls CFS/ME and Fibromyalgia, 'Oxidative – Dysoxygenative,' disorders. In hypercoagulable states microclots and plaques measuring from 2-3 microns to over 40 microns can be seen. Also evident are many fibrin spicules, which are platelet derived. Embedded in the clots are platelet clumps and bacteria, and yeast like forms. Mycoplasma can also be seen. There is a correlation between the amount of abnormality and disease severity. Red cell shape abnormalities abound. The appearances are, according to Prof. Ali, a direct result of increased oxidative stress. The overall result is an oxidative coagulopathy, where the microcirculation is clogged up producing: 1.Poor oxygen transport to cells 2.Poor oxidation in cells 3.The build up of organic acids causing acidosis I now move on to the controversial topic of yeasts. Yeast- like organisms can clearly be identified through the video microscope. Again, only with phase contrast and magnifications greater than x8000. They appear generally after a few minutes and can be seen to spread across the field of view in yeast-like fashion. Majid Ali has extensively commented on the yeasts, their morphology and associations, with a detailed analysis of their growth patterns. There is a correlation between the amount of yeast – like forms and the rate of proliferation and severity of illness. Incidence of yeast forms in Peripheral Blood of 100 patients with Fibromyalgia and or CFSME and 100 controls seen with High Resolution Phase Contrast Microscopy per 25 high power fields at 15,000x magnification Incidence <3 4-9 10-14 >15 Patients 0% 12% 21% 67% Controls 37% 54% 6% 0% Frequency of Active Proliferation of yeast forms in peripheral blood of 100 patients with Fibromyalgia and/or CFS/ME and 100 controls expressed as a percentage of those germinating per 25 HPFs. Germination rate <1 1-3 4-6 7 or more Patients 6% 13% 28% 53% Controls 7% 91% 2% 0% Obviously, the presence of these yeast forms is not diagnostic. They seem to be another co-factor. Prof. Ali feels they are there as a result of an 'Oxidative regression to a primordial cellular state', an interesting and plausible explanation for the development of chronic ill heath. The growth of the yeasts is a direct result of the anaerobic/glycolytic pathway dominance in these patients. He has also carried out a study that showed treatment with anti-fungals decreased the amount of yeast-like forms and improved symptoms. Symptom score 0 (no symptoms) to 4 (severe symptoms). Symptom Pre-Treatment AfterTreatment Fatigue 3.5 2 Myalgia 3 2 Cognitive difficulties 3.5 0.5 Malaise 3 1 he calls the ecological terrain existing in CFS/ME and Fibromyalgia an ‘Oxidative regression to primordial cellular ecology.’ In this state he feels we favour the overgrowth of latent microbes such as mycoplasma and chlamydia, as well as yeasts. They seem to be associated with erythrocytes. We already know that yeasts like Candida will use haemoglobin as a source of Fe. In summary they are only seen when oxidative stress exists. Prof. Vojdani looked at serum from clinical cases, based on seronegativity or seropositivity for IgG, IgM and IgA autoantibodies against thyroid, adrenal and ovarian tissue. He then tested each sample for the presence of Candida antibodies. Expressed as a percentage expressing Candida antibody overall: Seropositive for autoantibodies - 60% had Candida antibodies Seronegative for autoantibodies -7.5% had Candida antibodies Controls - 10% had Candida antibodies Confirmatory evidence came from the fact that when antibody positive tissue was treated with rabbit anti-Candida antibodies and human positive sera, it produced a reduction in thyroid autoantibody levels. When talking about thyroid antibodies researchers found have those thyroid antibodies can disappear after 3-6 months on a gluten free diet. However, an excess of hsp's can have deleterious effects. Too many inhibit protein folding and increased levels may be seen as dangerous or foreign antigens by the immune system. Studies in the past have shown that because all hsp's are very similar genetically, they can trigger autoimmune states, such as in leprosy, TB and Histoplasmosis by cross reactivity between the infective agent hsp's and human hsp's. Candida produces several hsp's. The important ones in this story are hsp 47, 90 and 70. These Hsp's are involved in hormone action. They are required to fold steroid hormone receptors until the steroid hormone binds to the receptor. But, in candidiasis, an excess of hsp 47 effectively blocks this action. People who survive deep-seated Candidiasis make a lot of antibodies against hsp 47. Also, another very important fact is that peroxynitrite has been shown to be a strong stress to human monocytes, leading to a dose dependent increase in hsp 70. When discussing upregulation of the 2-5 Synthetase/RNase L system you will recall Vojdani showing that this can be induced by MTBE and benzenes in the presence of hsp 70. Is it therefore, the cross reactivity between hsp from the yeasts, and human hsp's with the immune system that is contributing to the clinical picture? The more yeasts seen on microscopy, the sicker you are. It would help to explain not only the upregulation of the RNase L enzymes, be they normal or low molecular weight, but the hypercoagulable state found in patients, and also steroid hormone resistance, which I see a lot of. Bacterial Overgrowth www.geocities.com/ctfutures2001/index.html#contentsMany CFS sufferers, myself included, report an improvement while on antibiotics. While temporarily reducing the pathogen in question, beneficial bacteria populations are also being systematically eliminated, forever perpetuating the vicious cycle. Diagnosed with Chronic Fatigue Syndrome one year ago I am now convinced that most all of my symptoms were a result of an overgrowth of Citrobacter freundii identified by your lab (GSDL) in December 1996. Chronic sinus infections treated with six antibiotics proved ineffective and only sterilized my intestinal tract of friendly bacteria.(Bactrim, Lorabid, Zithromax twice, Biaxin, Augmentin) By the time I took the correct antibiotic Cipro, as suggested by your sensitivity chart, the bacteria was so entrenched that a ten day dose could not eradicate this pathogen. I speak from experience when I say that this bacteria can be devastating to ones health. It feeds on sugar and is capable of leaving the intestinal tract taking up residence in the mucus membranes of the sinus and lungs. A severe respiratory infection could not be treated with yet another antibiotic in February of this year. Fortunately intravenous hydrogen peroxide arrested its progress. Eliminating sugar from the diet similar to the anti-candida diet and taking citrus seed extract has proven to be most effective in controlling the growth of this bacteria. Any cheating whatsoever on the sugar intake proves disastrous. A recent follow-up CSA shows a reduction of the pathogen from previous levels. Adding close to 100 billion Acidophilus and Bifidus bacteria per day for the past two months has increased the levels of healthy bacteria shown on the CSA results. The point I'm trying to relay here is the seriousness of this pathogen and what it is capable of. Which takes me back to the attached file concerning the use of Citrobacter freundii in a probiotic bacterial culture administered to young chicks to competitively inhibit Salmonella bacteria in their intestinal tracts. Why would the USDA approve one pathogen to replace another? I am convinced that it was this bacteria that was responsible for my Chronic Fatigue Syndrome. The bizarre symptoms associated with this illness are a result of the toxins released after the microorganism dies. Q: How strong was the Citrobacter Freundii on your CDSA? (Mine was just 1+.) A: My test results showed Citrobacter freundii was at a level 4+ a
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Post by fritolay66 on Mar 23, 2009 0:44:51 GMT -5
Q: How strong was the Citrobacter Freundii on your CDSA? (Mine was just 1+.) A: My test results showed Citrobacter freundii was at a level 4+ and like yourself, NO lactobacillus! Four months later Citrobacter freundii was still present at 1+ Diagnosing CFS www.healingwell.com/library/cfs/info1.aspIn addition to the official researchers' definition discussed below, patients and experienced clinicians have noticed symptom patterns that seem prominent in CFS. These include the observations that cognitive dysfunction often increases over time (over several years), and that brain scans often show that blood flow to the brain is decreased. CFS is defined somewhat differently by various medical groups in different countries. The 1994 research definition published by the U.S. Centers for Disease Control and Prevention recommends a step-wise approach for identifying CFS cases. The first step is to clinically evaluate the presence of chronic fatigue, i.e. "self-reported persistent or relapsing fatigue lasting 6 or more consecutive months". Conditions that explain chronic fatigue should exclude a diagnosis of CFS. These are: - "any active medical condition that may explain the presence of chronic fatigue ..." - any previous condition which might explain fatigue and which has not documentably come to an end; - "any past or current diagnosis of a major depressive disorder with psychotic or melancholic features; bipolar affective disorders; schizophrenia of any subtype; delusional disorders of any subtype; dementias of any subtype; anorexia nervosa; or bulimia"; - substance abuse within 2 years prior to onset; - severe obesity. The following should not exclude a diagnosis of chronic fatigue: - conditions which cannot be confirmed by lab tests, "including fibromyalgia, anxiety disorders, somatoform disorders, nonpsychotic or nonmelancholic depression, neurasthenia, and multiple chemical sensitivity disorder"; - any condition which might produce chronic fatigue but which is being sufficiently treated; - any condition which might produce chronic fatigue but whose treatment has already been completed; - any finding which on its own is not sufficient to strongly suggest one of the exclusionary conditions. After the above criteria are met, the following core criteria for CFS are applied: "A case of the chronic fatigue syndrome is defined by the presence of the following: 1) clinically evaluated, unexplained persistent or relapsing chronic fatigue that is of new or definite onset (has not been lifelong); is not the result of ongoing exertion; is not substantially alleviated by rest; and results in substantial reduction in previous levels of occupational, educational, social or personal activities; and 2) the concurrent occurrence of four or more of the following symptoms, all of which must have persisted or recurred during 6 or more consecutive months of illness and must not have predated the fatigue: - self-reported impairment in short term memory or concentration severe enough to cause substantial reduction in previous levels of occupational, educational, social or personal activities; - sore throat; - tender cervical or axillary lymph nodes; - muscle pain; - multi-joint pain without joint swelling or redness; - headaches of a new type, pattern or severity; - unrefreshing sleep; - and post exertional malaise lasting more than 24 hours." Treatments Lifestyle www.healingwell.com/library/cfs/info1.aspAvoid stress As odd as it may seem, typically the most beneficial program is for the patient to avoid stress and to get lots of rest. This is usually the most effective regimen, among others that might also be undertaken. Stress does not merely mean unpleasant experiences, but rather any biological stressors, physical or emotional, which prompt a protective reaction in the body and which may alter physiologic equilibrium ("homeostasis"). Failure to avoid stress often leads to short-term and long-term set-backs which may be serious. Many patients believe that if they had done more to avoid stress in the early phases of the illness, they would not have become nearly so disabled later on. The correlation between stress and the progress of this illness appears to be strong. Medications www.healingwell.com/library/cfs/info1.aspMedications Treatments tend to address the symptoms, since the underlying mechanism of the disease is not really understood. Medications which are helpful are often those which have immune-modulating characteristics. CFS patients are unusually sensitive to drugs and they usually must take doses that are 1/4 or less than standard doses. Some drugs will be a big help to some patients and little or no help to others. And drugs that seem to work for a while may stop being effective later. According to studies presented at the October 1994 CFS medical conference, widely used treatments included: SSRIs ("selective serotonin re-uptake inhibitors" such as Zoloft, Paxil and Prozac) used to address fatigue, cognitive dysfunction and depression; low dose TCAs ("tricyclic anti-depressants" such as doxepin and amitriptyline) for sleep disorder, and muscle and joint pain; and NSAIDs ("non-steroidal anti-inflammatory drugs" such as ibuprofen and naproxen) for headache, and muscle and joint pain. Other treatments often prescribed are Klonopin, intra-muscular gamma globulin (IMgG), nutritional supplements (particularly anti-oxidants, B-vitamins generally and B-12 specifically), herbs, and acupuncture. Less often prescribed were chiropractic therapy, intra-muscular gamma globulin (IVgG), kutapressin, antivirals, interferon, and transfer factor. Research from Johns Hopkins University in 1995 indicate that treatment for neurally mediated hypotension may be effective for the many CFS patients who may show positive for that condition. www.cfsresearch.org/cfs/research/treatment/9.htmAnti-fungals* These can help if testing reveals overgrowths. I normally use a combination approach. Nystatin* can help in gastrointestinal Candida, and in cases where a leaky gut is suspected, at a dose of 1 or 2 tablets four times a day for two to six weeks. I use Fluconazole* 50gs once daily for one week with Terbinafine* 250 mgs per day for two weeks initially, although this can be extended. Hormones www.cfsresearch.org/cfs/research/treatment/9.htmHydrocortisone* This is converted into cortisol directly. Dose range is 2.5 mg (Corlan Pellet*) to 15 mg in divided doses, (4mg of hydrocortisone = 1mg of prednisolone). Safety studies have been carried out which indicate that up to 25 mgs does not suppress endogenous ACTH. DHEA* For women use10 mg bd., and in men 25mg bd. Conversion of DHEA to extra oestrogen and testosterone does not occur significantly until > 50 mgs daily. Melatonin Use 0.5mg at 8-9pm. This helps to initiates sleeps via the Histamine-Interleukin-Prostaglandin system. Melatonin is the 'molecular manifestation of darkness'. It may be possible to reset the internal body clock with about 4-6 months treatment. Thyroid replacement* This is useful in clinically hypothyroid patients with low/borderline levels, and especially if autoantibodies are present. Aim to keep T4 and T3 within the reference interval. Exercise www.healingwell.com/library/cfs/info1.aspRole of Exercise CFS patients will need to avoid stressful activities, and each patient's toleration for stress will be different, and can change). It is nonetheless important for patients who can exercise to do so, up to their level of toleration. But this should be done with great care, since crossing the "invisible line" of exercise intolerance for this illness may prompt a serious relapse, and may negatively affect the longer-term future course of the illness. Diet www.geocities.com/ctfutures2001/index.html#contents The typical American diet continues to feed this bacteria which makes it stronger and virtually impossible to eliminate since it is a glucose fermenter. Complex sugars from carbohydrates and starches will allow this pathogen to proliferate, mutate and become even stronger. The only relief to this cycle is to eliminate its food source as I have done. Following the Gottschall diet "Breaking the Vicious Cycle" gave immediate results. Note: The "Specific Carbohydrate Diet" described in Gottschall's book is a variety of low-carb diet. Many different low-carb diets have been beneficial to those with Gilbert's Syndrome. www.cfsresearch.org/cfs/research/treatment/9.htmFood choices are very important. In general, a glycaemic diet should be followed (a protein to carbohydrate ratio of 1:2 by weight or calorie counting as they are calorie equivalent), with good quality proteins and slowly digested carbohydrates. Organic food is preferable, but still expensive. Dairy and gluten avoidance helps some people and research is under way at present on this. www.healingwell.com/library/cfs/info1.aspDietary Changes CFS patients appear to be alcohol intolerant. Other food products often recommended against include caffeine, sugar and nutrasweet. Since in many patients it appears that the immune system is over-active, it may be more important than usual to take nutritional supplements to replenish burnt up reserves. Many patients have or develop food sensitivities, and in these cases relief may be found by avoiding foods that prompt problems. Patients tend to gain weight and they don't have vigorous exercise available as a counterbalance, so diet needs to be monitored with this in mind. Supplements, Minerals & Vitamins www.cfsresearch.org/cfs/research/treatment/9.htmVitamins / Minerals and Nutritional Supplements 1. A good antioxidant /mineral mixture They should contain a balance of both fat and waters soluble vitamins, include selenium, and be taken all the time. Oxidative stress can be measured using blood methaemoglobin, or Vespro's Free Radical Test kit which measures urinary malondialdehyde levels. This is an easy to use kit based on a visual colormetric scale. Supplement levels should be adjusted until normal ranges are achieved. These should be checked periodically at around monthly intervals. It is particularly important to get this right before anti-fungals are taken to prevent die-off reactions. 2. B Vitamins* Poor functional levels of B Vitamins have been reported by Heap et al using AST, glutathione reductase, and transketolase as markers of pyridoxine, riboflavin and thiamine respectively. (P< .001). Compounds with up to 50mgs of each per day can be used. Low levels of B12 are found in the cerebrospinal fluid of patients, reflecting poor neuro-axis levels. High CSF levels of homocysteine are also found. B12 deficiency causes deficient remethylation of homocysteine. Indeed Low brain levels have been associated with many degenerative neurological disorders. It is thought that B12 couples with environmental toxins in an attempt to detoxify the brain... B12 also acts as a nitric oxide scavenger helping deal with excessive oxidative stresss. 3. Magnesium malate* 1000mgs once a day – used in the Teitelbaum study. This is good for muscle physiology. Also, Dr. David Dowson published a double blind study in 1991 showing low red cell magnesium levels in CFS/ME patients which improved with treatment, as did symptoms in patients. 4.Folic acid* 5mg once daily. Some patients need very high doses. Again abnormalities in folic acid metabolism are common. 5. Oral NADH (Enada) Recommended dose is 5-10 mgs / day. The reduced form is absorbable orally. Nicotinamide adenine dinucleotide is used in ATP production. In a double blind crossover study, 26 patients were given oral NADH at a dose of 10 mgs per day. On active treatment 31% responded favourably against 8% on taking placebo. 6. Undenatured whey proteins (Immunocal* Imuplus* Immune Pro *Solgars Whey To Go*) Basically, these are milk-derived products, which are very close biochemically to human breast milk. They have anti-viral, bacterial and possibly fungal action. They contain two cysteine molecules bound together, which is a requirement for absorption. This is an essential precursor for glutathione. Low glutathione levels are seen in patients, particularly in white cells. It has been shown to raise glutathione levels www.geocities.com/ctfutures2001/index.html#contents It wasn’t until I was introduced to Dr. Jack Larmer ND on Nov. 14, 1997 that this constant struggle came to an end. Dr. Larmer’s approach was to change the environment so it is not conducive to the overgrowth of pathogens. His method of treatment spans forty five years of experience. I mix a drink in the morning using apple cider as a base liquid along with the juice of a freshly squeezed large lemon. Included in this drink is a variety of intestinal clensers, concentrated liquid ionic minerals, oxygenating cellular formula, live enzymes, amino-acids, anti-oxidants, essential fatty acids, phytochemical rich herbs, and other natural ingredients. Along with this drink he has included support for the liver, pancreas, thyroid and adrenal glands. -Amylase breaks down starches -Protease breaks down proteins -lipase breaks down fats Probiotics www.cfsresearch.org/cfs/research/treatment/9.htmAnti-microbials Wherever possible I start with natural methods and increasingly use olive leaf extract and a probiotic/real food liquid called ‘Before everything’ followed Prime Directive to heal the gut in every patient. Olive leaf is an immune booster and the probiotics contains 12 species of lactobacilli, 2 saccromyces species, enzymes, whole foods and micronutrients. www.geocities.com/ctfutures2001/index.html#contents Carl: Instead of trying to shoot the bacteria with that magic bullet, why not fight bacteria with bacteria. Not just any bacteria but a specific group designed to devour any pathogen and restore that environment to healthy status. I believe that I am now taking the correct combination of beneficial bacteria in sufficient quantities necessary to reestablish healthy populations. I began taking these capsules (Nature's Biotics 1-800-713-3888) on Saturday Jan. 10Th and within the hour experienced "Herxheimer reaction" (die-off) lasting most of the morning. This die-off has been experienced with natural substances as reported in my previous email. This is the first time a group of beneficial bacteria has produced this effect. My past experience with die-off was an indication that a substance was effective. I will keep you informed of my progress. The following list of symptoms are experienced when the bacteria is no longer kept under control by natural agents: 1. loose stools/ steatorrhea (yellow diarrhea)following meals 2. Lightheaded/shortness of breath 3. Fatigue/weakness 4. Anemia 5. Sinus congestion 6. Lung congestion/mucus 7. Chest pain on right side 8. Stiff neck 9. Sleep disturbance 10.Brain fog/memory loss/loss of words I have experienced “Herxheimer reaction” (die-off) with the following natural agents (Level of die-off): 1. Entrocaps (berberis/grapefruit seed extract) Severe 2. Black walnut extract capsules: Moderate 3. Uva Ursi capsules: Severe 4. Clove raw: Slight Tinctures: 1. Black walnut extract/39-44% grain alcohol *Severe 2. Wormwood extract/70-75% grain alcohol *Severe 3. Ginger extract/72-78% grain alcohol *Severe Liquids: 1. 3% hydrogen peroxide (ingested): Slight 2. Pau D`Arco tea: Slight 3. Liquid grapefruit seed extract: Moderate 4. Colloidal silver: Unknown Here is an explanation of "die-off" Toxins are released when bacteria die. These toxins are absorbed into the blood stream and overwhelm the liver and its filtering capability. Bacteria die every 20 minutes. When bacteria die in large numbers symptoms worsen. A temporary toxic reaction does occur. The technical name for this experience is Herxheimer reaction Drew: My pH is 7.8. Carl Tuttle: 7.8 pH is far too alkaline for aciddophilus to survive. Drew: Interesting ... my CDSA reported Lactobacillus is 0+ (though Bifodobacterium is 4+). Carl Tuttle: Acidophilus means "acid loving" Dr. Larmer prefers a slightly acidic environment. One way to acidify the gut is to squeeze the juice from one large or two small lemons into six ounces of water, heat in the microwave for one minute, add one dropper of ginger extract. I took this twice per day. Bacillus subtilis can eat a lot of harmful bacteria. Taking various natural substances allowed me to keep this pathogen somewhat under control although never eliminating it completely. Over time the bacteria developed resistance to each and every agent (grapefruit seed extract, black walnut extract, uva ursi, ginger extract, wormwood extract). Me: I myself am not convinced of the efficacy of this. The first three days I had yogurt a few months after my course of antibiotics I felt incredibly improved, almost cured. But then it stopped having any effect - in fact for the rest of the month that I was eating yogurt and taking probiotics daily, it caused a food-coma like reaction- fatigue and brain fog. I thought this was a sign of die-off, but that appears to be a tautology of sorts. If it makes you feel better, it's working. If it makes you feel worse, it's working. Under what condition is it not working? For me that was that there was no improvement after a month. It appears in the end that Carl came to a similar conclusion. Although he still recommends probiotics on his web site. Good Sites www.beatcfsandfms.org/The link to this part would be: www.gilbertssyndrome.com/chronicfatigue.php
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Post by fritolay66 on Mar 23, 2009 0:46:17 GMT -5
www.gilbertssyndrome.com/candida.phpCandida This is a work in progress and is being updated regularly. Check back regularly, as I will be steadily improving the site and adding more information. Candida Overgrowth www.candida-society.org.uk/Moderate amounts of candida (and other yeast) live in every one of us without causing any harm, but when given free rein to grow unchecked, e.g. by wiping out the surrounding bacteria with broad-spectrum antibiotics, candida can change into its fungal form and spore through the intestinal wall into the rest of the body. Once through, it rampages around the body producing a multitude of symptoms. www.candidafree.net/pages/1/index.htmAll it needs for Candida to invade your gut is for something to kill off the normal flora; the bacteria that aid digestion and protect the gut from yeast. Once the flora are damaged, yeast will invade. In ideal circumstances, Candida can double in quantity every half hour, so it takes very little time for it to populate a damaged intestine. Hormones, antibiotics, environmental toxins, heavy metals and poor dietary habits can all contribute or cause a yeast infection. Once in the gut, candida creates an environment that prevents the normal flora from repopulating. The lack of flora causes mal-digestion of certain sugars, carbohydrates, minerals and trace nutrients and leaves food to rot in the gut, creating an ideal environment for the Candida. According to the conditions it finds, candida can exist in 3 forms; a budding, multiplying yeast, a hyphae form, which penetrates the gut wall in search of nutrition in the blood and as highly invasive spores, which penetrate the gut wall to be transported in the blood stream to other organs. Once the yeast has overgrown the gut, malnutrition will result, in the form of vitamin and trace nutrient deficiencies. In addition, the constant presence of a pathogen will stimulate the immune system 24 x 7 x 365, eventually causing immune deficiency (as found in CFS) and severe fatigue. Victims will experience a multitude of symptoms caused by malnutition, an impaired immune system, toxins from the yeast's metabolic processes and from the physical presence of the yeast." Yeast make a number of chemical compounds which are then picked up and absorbed into the body. These compounds are quite toxic to the nervous system. These compounds include toxic alcohols and aldehydes, as well as the powerful nervous system poison hydrogen sulfide (editor's note: this is a totally different substance than hyrodgen sulfate). Alcohols depress the nervous system and at least some aldehydes are anesthetic agents, which of course put the brain to sleep. These chemicals slow the brain down so that the brain no longer works correctly. These chemicals should be cleared by the liver so that these chemicals never reach the brain. www.toronto.com/health_fitness/article/000-000-233Candida mainly exists in two forms: a round yeast that remains in the colon and is actively reproducing and the other in its fungal form that 'eats' through the intestinal wall and travels via the blood to any site in the body. Sugar (in many forms) activates candida metabolism and its by-products are neurotoxins (toxins that damage or destroy nerve tissue) such as formaldehyde, and alcohol. The nervous system can become deranged with candida due to specific neurotoxins. Autism is one example of this. Metabolites of candida are found in urine samples of children with autism. Specific bacteria and fungi migrate from the large to small intestines to break down undigested carbohydrates. Candida is also known to impair immune functioning. Approximately 80% of our immune system lies within the intestinal walls. What you do to your intestines directly affects your 'immune' system. The immune system will respond to candida and its by-products along with food molecules that escape into the bloodstream by secreting histamines causing classic symptoms of allergies and intolerances. www.theherbspecialist.com/save/candida.htmlOccasionally, Candida overgrowth occurs throughout the body including the liver and blood. Once in the blood, the fungus can be carried anywhere in the body resulting in a myriad of health problems including frequent urinary tract infections, respiratory problems, gastrointestinal and liver problems, food allergies, decreased immunity, frequent or chronic fungus infections of the skin and nails, and weight gain. This condition is referred to as Systemic Candidiasis (also known as candidosis and moniliasis.) Note: This doesnt match at all, while the other ones do quite well. REFERENCE: Wikipedia - Candidiasis Candidiasis, commonly called yeast infection or thrush, is a fungal infection of any of the Candida species, of which Candida albicans is probably the most common. Yeast organisms are always present in all people, but are usually prevented from "overgrowth" (uncontrolled multiplication resulting in symptoms) by naturally occurring microorganisms... However, when it gets out of balance with the other "normal flora", such as lactobacilli, an overgrowth and symptoms can result. Pregnancy, the use of oral contraceptives and some antibiotics, and diabetes mellitus can lead to an increased incidence in yeast infections. In immunocompromised patients, the Candida infection can become systemic, causing a much more serious condition, fungemia. REFERENCE: Wikipedia - Fungemia Fungemia is the presence of fungi or yeasts in the blood. It is most commonly seen in immunosuppressed or immunocompromised patients with severe neutropenia, oncology patients, or in patients with intravenous catheters. The diagnosis is complicated, as routine blood cultures have poor sensitivity. Treatment involves use of antifungals, eg. fluconazole or amphotericin. The two most important risk factors are: • Use of broad-spectrum antibiotics • Colonization by fungi (see eg. candidiasis) The most common pathogen is Candida albicans, causing roughly 70% of fungemias, followed by Torulopsis glabrata with 10%, and Aspergillus with 1%. However, the frequency of infection by T. glabrata, Candida tropicalis, C. krusei, and C. parapsilosis is increasing, especially when significant use of fluconazole is common. Symptoms of Candida www.candida-society.org.uk/Common symptoms of Candida A minority of suffers have numerous symptoms; the vast majority have thrush + a few others; not every sufferer has thrush. Group 1: The damage to the intestinal wall allows undesirable toxins to permeate into the bloodstream. This condition called ‘leaky gut syndrome' often leads to: • food allergies and intolerances • migraines • foggy brain • muscle aches Group 2: Once through to the rest of the body, candida has the ability to disrupt the endocrine system causing symptoms such as: • thrush • cystitis • PMS • menstrual irregularities • joint pains • asthma • hayfever • sinusitis • fungal infections of the nails/skin e.g. athlete's foot • weight gain or weight loss • ear infections • chronic tiredness • allergies • sensitivity to perfume, tobacco smoke and petrol Group 3: Symptoms in the intestines include: • bloatedness • flatulence • diarrhoea and/or constipation • itchy anus In addition, candida involvement has been implicated in some cases of other illnesses e.g. ME/CFS, Endometriosis. www.askshelley.com/faq.php?cat=38Candida leads to brain fog because having systemic candidiasis means you're constantly drinking alcohol, as yeasts convert sugars into alcohol. This also congests the liver, another major co-factor in brain fog. If the liver, the filter for blood, is congested, it cannot take toxins out of the bloodstream fast enough. These toxins will pass the blood-brain barrier of the brain and deplete the brain of oxygen and glycogen. www.liver-cirrhosis-failure.com/pages/liver-damage-causes.htmlCandida yeast ferments dietary sugars into liver-toxic acetaldehyde in the process of turning sugar into energy. Candida also appears to increase gut and urinary levels of ammonia, another liver toxin. www.pureliquidgold.com/candida-diet.htmCandida overgrowth can produce a large number of symptoms. Among them are headaches, migraines, bad breath and rectal itching. Mood swings, canker sores and persistent heartburn. Muscle and joint pain, numbness and tingling sensations in the face or extremities. Also acne, night sweats, sore throat, nagging cough and clogged sinuses. PMS and thrush; a yeast infection of the mouth causing a burning tongue and white spots on the tongue and in the mouth, also cystitis and fungal infections of the skin and nails. Kidney and bladder infections, arthritis, flatulence (gas) gastritis, diarrhea, and chronic constipation. Colitis and ulcers in the digestive tract, leaky gut syndrome, female disorders; including sterility, fibrosis or pregnancy problems and vaginitis. Plus the Male disorders; prostatitis and impotence. Further symptoms are allergies, hormonal imbalance, heart problems and poor memory / balance. Earaches and ear infections, asthma, sinusitis, fluctuation in blood sugar levels and meningitis. These toxins represent a great strain on the liver. Which can no longer adequately detoxify the body, causing extreme fatigue and a general feeling of discomfort. Depression, hyperactivity and indigestion join the previously mentioned symptoms. These various symptoms can be caused by the fungus candida albicans. Which produces almost 100 different toxins. www.smartbomb.com/readingroom-renew-life-candida.htmlWhat are the Signs and Symptoms of Candida Overgrowth? Gas and Bloating Some symptoms of Candida overgrowth are localized in the digestive system, other symptoms are found in different locations in the body. Just as bread rises from yeast due to carbon dioxide production from fermentation of carbohydrates, Candida also produces carbon dioxide in the intestine. The result is persistent gas and bloating. Brain Fog Another by-product of Candida is acetaldehyde, a poison that is converted into ethanol by the liver. As yeast multiplies and produces more acetaldehyde, the blood alcohol level rises, resulting in symptoms associated with drunkenness, including impaired mental and physical functioning. Infections As yeast moves through the holes in the mucosal barrier and travels throughout the bloodstream, it produces such disorders as chronic ear infections and sinus infections. Physicians commonly prescribe antibiotics for fungal ear infections and sinus infections, which can make the condition worse by further destroying the good bacteria in the body. Candida overgrowth is also responsible for fingernail and toenail fungus and recurrent vaginal yeast infections. Fatigue Excess toxins produced by Candida can leave a person feeling lethargic and fatigued and sometimes with joint and muscle pain. Quite simply, the body must exert energy to cleanse itself, and when Candida is overgrown, the toxic load on the body increases. Sugar and carbohydrate cravings are a common Candida symptom as yeast feeds on sugars. The result can be an increased desire for sugar, which in turn causes a rollercoaster effect in your energy. Candida can cause autoimmune diseases due to the fact that Candida can increase the permeability of your intestinal lining, also known as "leaky gut syndrome." With leaky gut, large undigested food molecules can enter your bloodstream which the body recognizes as a foreign material. When this occurs, the immune system attacks the food. The immune response involves making antibodies, which are the equivalent to the immune system's memory. The next time the same type of food enters the body, the immune system remembers and attacks again. The result is a sudden food allergy or sensitivity to commonly eaten foods. Toxins made by candida also signal an immune response to produce antibodies. An autoimmune disorder occurs when the immune system reacts with a hyperactive response to the digestive process and the toxins within it. The hyperactive immune system begins to attack the body's own tissues. There are about 80 known autoimmune diseases. Among these diseases are: rheumatoid arthritis, fibromyalgia, chronic fatigue syndrome, Chrohn's disease, diabetes, Lupus, and multiple sclerosis. www.toronto.com/health_fitness/article/000-000-233Following are a few classic symptoms of candida overgrowth: Gastrointestinal: indigestion, gas, bloating, inflammatory bowel diseases, diarrhea, constipation, heartburn, bad breath and thrush (coating on tongue). Physical: numbness, burning or tingling; painful, swollen, stiff joints; muscle aches and tension, nasal congestion, chronic headaches, blurred vision, shortness of breath, chest pains, dizziness, sinusitis, and chemical sensitivity. Mental/Emotional: depression, mental confusion, irritability, insomnia, nervousness, anxiety, disorientation, impaired decision making, low energy, fatigue, hyperactivity, chronic ear infections and poor memory. Skin: white fungal skin patches like dandruff, acne, athlete's foot, anal itch, diaper rash, psoriasis, dermatitis, finger and toenail infections, unpleasant body or hair odour, genital touching in infants and young children, skin rashes and behavioural problems. Sexual: vaginitis, discharge, itch, bladder infection, menstrual irregularities, pain, cramps, lowered libido, infertility, impotency, prostate problems. Urinary: frequent urination, burning, fluid retention and edema. www.karinya.com/fungus.htmWeight problems, vaginal yeast, athlete's foot, scalp problems such as dandruff, nail fungus, joint inflammation, poor immune response, headaches, allergies, shingles, oral thrush, canker sores, excessive sneezing, poor memory, brain fog, tooth plaque, hemorrhoids, throat mucous, and skin eruptions like acne, are all connected with Candida overrun… And "Sleep" in the corner of the eye indicates a Candida problem, so does a coated tongue. Most allergies can be eliminated with the elimination of Candida overgrowth. The waste products of Candida flood the lymph system with more toxins than it can handle, and the body develops allergies. Candida overgrowth drastically reduces digestion, allowing undigested food into the blood stream. This undigested food causes an immune response, the making of an allergy. Many reoccurring sinus problems are Candida overgrowth. Toxic bowel from Candida leaks toxins into the sinus cavities. The body rids itself of these toxins with a "runny nose." Headaches, particularly migraine, may be Candida. Bowels overrun with Candida form excess mucous as a protection. This causes a very toxic, dehydrated lymph system. The immune system's response is to build antigens that flood the lymph. Toxic dehydrated lymph will give you a headache. My favorite symptom, bloating and gas, can come from Candida. When high glycemic foods are eaten, the Candida feasts. A by-product of this is gas, just like the making of beer. The bad breath and gas makes for interesting company, probably lets you know who your friends are, too. Candida may cause gum problems by weakening the gum below the tooth line. As stated earlier, most excess plaque is Candida related. Toe fungus is Candida. Losing a toenail to fungus is like losing your teeth to it. www.synergy-health.co.uk/articles/yeast_infections20040628.htmlWhat are the symptoms of Candida Overgrowth? The symtoms are many and are so varied and manifest as so many other problems that you would not believe that they can be caused by the same thing. Some symptons are listed below, if you only have more two or three of these symptoms on a regular basis then you may have a problem with candida overgrowth: * Recurring headaches/ migraines. * Rashes, itching skin. * Thush - oral/vaginal. * Abdominal bloating. Intestinal bloating can also be caused by 'swallowing air' and the simple cure is 'catch yourself doing it and stop it'. * Recurrent indigestion. * Dry mouth or throat, constantly having to clear throat when speaking. * Joint pain. * Brain fog, fuzzy thinking. * Feeling 'blue', mood swings. * Hangover symptoms after bread/cakes. * Sinus problems. * Athletes foot type fungal problems. www.jigsawhealth.com/articles/depression.html12) As touched on above, pioneering researchers believe that depression is another symptom of Candida overgrowth—or more specifically, the 80 plus poisonous toxins and neurotoxins that candida yeast can produce inside the body. It is this toxic waste that they believe to be the primary cause of depression, especially for the chronically ill. These toxins can mimic and interfere with many of the body's hormones. When this happens, feelings of intense depression may be induced.8,9,10 In addition to the toxins put off by the yeast itself, Candida also survives by manufacturing toxic substances from refined carbohydrates and sugars in the digestive system. Hypersensitivity to these Candida yeast toxins, the most harmful of which is acetaldehyde (a by-product of alcohol and the chemical that naturally causes a "hangover"), can lead to anxiety, depression and impaired intellectual functioning. Causes of Candida Overgrowth www.candida-society.org.uk/Contributory factors The popular perception is that candida is the consequence of antibiotics usage.The medical profession dismisses this as fantasy, saying that antibiotics could not have that effect in a healthy individual. But it may be that antibiotics act as the ‘final straw' where health has already been compromised, most probably by one or more of the following: • use of the contraceptive pill or HRT • use of natural progesterone cream • use of other steroids (hydrocortisone, prednisolone etc.) • use of immuno-suppressive drugs • repeated use of broad-spectrum antibiotics e.g. for acne • dental mercury amalgam poisoning • other heavy metal poisoning e.g. lead, cadmium • chemical poisoning from the home, garden, workplace etc. • hormonal changes e.g. puberty, pregnancy, menopause • stress www.toronto.com/health_fitness/article/000-000-233There are many causes of candida growth. It is adversely affected by drugs (prolonged use of antibiotics promote overgrowth), vaccinations, steroids and birth-control pills; chemicals such as mercury and other toxic metals, pesticides, aspartame, MSG and perfumes; diet including sugars and refined carbohydrates, consistent alcohol consumption, nutritional deficiencies, overeating and refined, canned, smoked, preserved and fried foods. Mercury www.earthtym.net/ref-candida-t.htmMercury is an antibacterial, yet, in concentrations lower than fatal to humans, bacteria are often encouraged. Health forms of candida, normally found in the mouth, mutate under the influence of the mercury and the destructive bacteria to become harmful varieties of Candida. Mutated Candida produces at least 79 toxins. Sugar activates candida metabolism and some of its by-products are neurotoxins such as formaldehyde, alcohol and acetlyaldehyde. One's nervous system can become confused during candida infestation due to specific neurotoxins. Candida converts the element mercury to methyl mercury which is 100 times more toxic. Mononucleosis / Glandular Fever p075.ezboard.com/fgilbertswebfrm2.showMessage?topicID=86.topicozzie135 The glandular fever/candida link is often put down to the body's inability to control the bacteria in the gut when the immune system is compromised and under stress. The medical profession dismiss the fact that this can happen with a viral infection such as glandular fever because it is a relatively minor infection. Populations More Susceptible To Candida SCIENCE: National Library of Medicine Comparison of Candida albicans adherence to human corneocytes from various populations. Epidemiological data indicate that patients suffering from diabetes, hypothyroidism, obesity, or following prolonged treatment with antibiotics, corticosteroids or oral contraceptives, have an increased tendency to develop cutaneous candidiasis. Since it is generally believed that attachment of microorganisms to host cells is an initial step in the evolution of infection, the aim of the present study was to investigate whether cells from susceptible individuals have increased capacity to bind the fungus. Corneocytes collected from the forearms of individuals of these susceptible groups were exposed in vitro to Candida albicans and adhesion to the cells was evaluated in comparison with adherence to cells from a non-susceptible population. Adherence in vitro was assayed microscopically and evaluated quantitatively by two parameters: 1) percentage of adherence - number of corneocytes with adhering yeasts on their surface, and 2) the total number of adhered yeasts. Results of the study revealed that the mean percentage of adherence and the mean total number of yeasts adhering to cells from individuals of the susceptible populations was twice as high as values in a healthy population. Statistical analysis of the data by Student's t-test indicated that the difference was significant (p less than 0.001). In Short: Candida adheres twice as much to cells from individuals suffering from diabetes, hypothyroidism, obestiy, or following prolonged treatment with antibiotics, corticosteroids, or oral contraceptives. SCIENCE: National Library of Medicine Chronic mucocutaneous candidosis associated with hypothyroidism: a distinct syndrome? Chronic mucocutaneous candidosis (CMC) is a rare, complex disorder characterized by chronic and recurrent candida infections of the skin, nails and oropharynx. In over 50% of cases there is an associated endocrine disease, the complex being described as the candida endocrinopathy syndrome. Inheritance of familial endocrine associated cases has been thought to follow an autosomal recessive pattern. In addition, autosomal recessive and autosomal dominant forms of CMC not associated with endocrinopathy have been described. We report a new syndrome in which there is vertical transmission of CMC within families associated with primary hypothyroidism. This suggests that the candida endocrinopathy syndrome can be subdivided into at least two types, one associated with hypoparathyroidism and/or hypoadrenalism which is inherited as an autosomal recessive trait, the other associated with hypothyroidism which is an autosomal dominant disease. We emphasize the importance of early and regular monitoring thyroid function in individuals with CMC and a need to provide appropriate genetic counselling to affected members. In Short: 50% of people who develop recurrent candida infections of the skin, nails and oropharynx have endocrine disease, including hypothyroidism. What Candida Feeds On www.nutramed.com/nutrition/carbohydrates.htmThe yeast, Candida Albicans, became the most popular colon microbe in the 1980's and many people still pursue yeast-free diets in an attempt to treat "candida infection" and to solve bowel symptoms. Claims that candida overgrowth in the GIT cause ill-defined illnesses are probably not true. Candida populations are balanced by competitive microbes. Colon candida are fed by milk sugar and starches in the diet which reach the colon undigested, not free sugars in food which tend to be absorbed before reaching the yeast. The presence of other kinds of yeast or fungi in the diet has little or no effect on the growth of candida in the colon. On a food holiday, the food supply to the Candida and all other colon microorganisms is reduced and the population decreases. The use of an elemental nutrient formula, even with high glucose content, is associated with reduction or disappearance of candida in the colon. www.ajcn.org/cgi/content/abstract/69/6/1170Limited effect of refined carbohydrate dietary supplementation on colonization of the gastrointestinal tract of healthy subjects by Candida albicans Infections due to Candida albicans occur readily in situations in which ample glucose is available. In mice, dietary refined carbohydrate supplementation leads to higher rates of Candida growth in the gastrointestinal tract and favors mucosal invasion. No correlation between C. albicans counts in the specimens and the habitual uptake of refined carbohydrates was observed. A high-sugar diet did not increase the frequency of C. albicans–positive samples, the number of subjects positive for C. albicans in the mouth washes, or the concentration of candidal blastoconidia in the samples of the 28 subjects. However, in selected subjects with elevated counts of oral C. albicans, we observed an increase in fecal C. albicans counts in response to the diet. www.pureliquidgold.com/candida-diet.htmCandida thrives on carbohydrates, preserved refined foods and mold. Also foods that contain yeast and gluten, a wheat bread protein... Symptoms often worsen in damp and or moldy places. Also after consumption of food products rich in yeast or carbohydrate (sugars and starches) or after eating any the foods that contain mycotoxins. Estrogens & Candida's Fungal Mode SCIENCE: National Library of Medicine Binding and reactivity of Candida albicans estrogen binding protein with steroid and other substrates. In this report recombinant estrogen binding protein (EBP1), isolated originally from Candida albicans as a result of its high affinity for 17beta-estradiol... It is shown that like OYE, the protein binds a variety of compounds with a phenolic structure, including 17beta-estradiol, and compounds with an alpha, beta-unsaturated keto or aldehyde structure. ec.asm.org/cgi/content/abstract/5/1/180Cellular and Molecular Biology of Candida albicans Estrogen Response Candida albicans is the most common etiological agent of vaginal candidiasis. Elevated host estrogen levels and the incidence of vaginal candidiasis are positively associated. Elevated estrogen levels may affect host and/or fungal cells. This study investigates the effect of 17-ß-estradiol, 17-{alpha}-estradiol, ethynyl estradiol, and estriol on several C. albicans strains at concentrations ranging from 10–5 to 10–10 M. The addition of 17-ß-estradiol or ethynyl estradiol to C. albicans cells caused an increase in the number of cells forming germ tubes and an increase in germ tube length in a dose- and strain-dependent manner. The addition of 17-{alpha}-estradiol or estriol did not have a significant effect on germ tube formation by the cultured cells. Exposure to exogenous estrogens did not significantly change the biomass of any C. albicans culture tested. The transcriptional profile of estrogen-treated C. albicans cells showed increased expression of CDR1 and CDR2 across several strain-estrogen concentration-time point combinations, suggesting that these genes are the most responsive to estrogen exposure. Analysis of strain DSY654, which lacks the CDR1 and CDR2 coding sequences, showed a significantly decreased number of germ tube-forming cells in the presence of 17-ß-estradiol. PDR16 was the most highly up-regulated gene in strain DSY654 under these growth conditions. The cell biology and gene expression data from this study led to a model that proposes how components of the phospholipid and sterol metabolic pathways may interact to affect C. albicans germ tube formation and length. In Short: Candida albicans grows more and longer germ tubes when exposed to 17-ß-estradiol or ethynyl estradiol. SCIENCE: National Library of Medicine The effect of estradiol on Candida albicans growth. The size of colonies growing on Sabouraud's dextrose agar (SDA) supplemented with 1 microM beta estradiol (1,3,5[10]-estratiene-3,17B-diol) was compared to those growing without the estrogen supplement. Data (video pixel counts) were obtained by video capture and image analysis and revealed that yeast strains were not uniformly stimulated by estradiol. One estrogen-responsive strain was evaluated in a chemically defined medium to evaluate growth in the presence of 17-alpha and 17-beta isomers of estradiol. The beta isomer promoted more rapid growth of the test organism and resulted in greater biomass production than the alpha isomer. Understanding of the role of mammalian hormones as growth promoting signals may provide information on this organism's shift from saprophytic to commensal to pathogenic status in vivo. Strain variation in response to estrogen may provide an explanation for differences in virulence. In Short: Some strains of candida albicans respond to beta estradiol, others do not. But importantly, this reveals terminology of the stages - saprophytic, commensal, pathogenic. SCIENCE: National Library of Medicine Genistein effects on growth and cell cycle of Candida albicans. Microbial virulence is generally considered to be multifactorial with infection resulting from the sum of several globally regulated virulence factors. Estrogen may serve as a signal for global virulence induction in Candida albicans. Nonsteroidal estrogens and estrogen receptor antagonists may therefore have interesting effects on yeast and their virulence factors. Growth of C. albicans was monitored by viable plate counts at timed intervals after inoculation into yeast nitrogen broth plus glucose. To determine if increased growth of yeast in the presence of estradiol was due to tyrosine kinase-mediated signaling, we measured growth in the presence of genistein, estradiol or genistein plus estradiol and compared these conditions to controls, which were not supplemented with either compound. Unexpectedly, genistein stimulated growth of C. albicans. In addition, genistein was found to increase the rate of germination (possibly reflecting release from G(0) into G(1) cell cycle phase) and also increased Hsp90 expression, demonstrated by a dot blot technique which employed a commercial primary antibody detected with chemiluminescence with horseradish peroxidase-labeled secondary antibody. These biological effects may be attributable to genistein's activity as a phytoestrogen. In contrast, nafoxidine suppressed growth of Candida and mildly diminished Hsp90 expression. This study raises the possibility of receptor cross-talk between estrogen and isoflavinoid compounds, and antiestrogens which may affect the same signaling system, though separate targets for each compound were not ruled out. In Short: LOOK AT THIS! Genistein stimulates growth of Candida albicans and increases the rate of germination. As a phytoestrogen (isoflavone) it's an activator of candida albicans! And those with Gilbert's have trouble processing estrogens, making an environment that encourages candida albucans growth. Also, investigate nafoxidine as a possible way to regulate this environment.
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Post by fritolay66 on Mar 23, 2009 0:47:49 GMT -5
www.gilbertssyndrome.com/candida.phpTesting for Candida Some sites with tests and questionaires: pages.britishlibrary.net/lobster/candida/test.htmlwww.victorie-inc.us/Threelac_Candida_Free_Test.htmwww.candidasupport.org/candidatests.htmlwww.cfs-recovery.org/research.htmThe biggest problem in proving the existence of Candida Related Complex in non-immune compromised people is that until very recently, there were no good tests for the condition. Everyone has Candida in their system and in small amounts it is harmless. It is only in larger amounts that Candida is harmful. Therefore it is tricky to test for Candida. Simply showing that Candida is present in a person's system is useless. What are needed are tests that show how much is present in the system. The IgA, IgG, and IgM are three tests which are somewhat reliable separately, and together have a good degree of reliability. The candida immune complexes test is even more reliable. SCIENCE: National Library of Medicine Rapid identification of Candida albicans by dot-enzyme immunoassay. A highly sensitive and specific dot-enzyme immunoassay for the rapid identification of Candida albicans was developed using a murine monoclonal antibody (Mab), which adsorbed to cell surface-exposed determinants. This Mab reacted with 28 of the 28 C. albicans strains tested including the serotypes A and B and 2 C. stellatoidea. It did not react with 32 other isolates representing eight other Candida species commonly encountered in human materials. All the test could be performed in four steps in less than an hour. The yeasts were directly spotted on a strip of immunodyne membrane. Then the strip was incubated for 5 min. with the Mab, for 15 min. with a peroxidase-conjugate and for 30 min. with the enzyme substrate and 4-chloro 1 naphthol. This test proved useful for rapid and easy identification of C. albicans. SCIENCE: National Library of Medicine Evaluation of a newly developed down-flow immunoassay for detection of serum mannan antigens in patients with candidaemia. A down-flow immunoassay has been developed to detect serum mannan antigens, and the test was recently marketed as the Unimedi Candida monotest. Using 251 serum samples from 105 patients with candidaemia, a comparison of the Unimedi Candida monotest with the Cand-Tec latex agglutination test and 2 microplate enzyme immunoassay tests (Platelia Candida Ag test and Unimedi Candida) was conducted. One hundred and seventy-five febrile patients without clinical and microbiological evidence of fungal infections and pneumocytosis were examined as controls. The Cand-Tec test had a sensitivity of 38% and a specificity of 82%. The sensitivity and specificity of the Platelia Candida Ag test, the Unimedi Candida and the Unimedi Candida monotest were 53 and 92%, 69 and 89% and 82 and 96%, respectively. The sensitivity of the Unimedi Candida monotest was significantly (P<0.01) higher than that of the Plateria Candida Ag test for diagnosing candidaemia caused by Candida parapsilosis. The beta-D-glucan assay had a high sensitivity of 95%, with a specificity of 84%. Of 74 patients with candidaemia whose sera were available before or on positive blood culture sampling, 29 (39%), 38 (51%) and 48 (65%) patients had antigenemia detected using the Platelia Candida Ag test, the Unimedi Candida and the Unimedi Candida monotest, respectively. The Unimedi Candida monotest seems to be a promising tool for the early diagnosis of invasive candidiasis, because the test was sensitive, simple, rapid (approx. 1 h) and cost-effective. www.rainbowminerals.net/candida_elimination.htm The Candisphere is a blood test that shows the toxic waste that the Candida is releasing into the blood. The toxic wastes detected can only be released by large amounts of harmful Candida and not by small amounts of normal Candida. This test helps us to determine what stage of Candida overgrowth the person is in. This test was determined to be 90% accurate for Candida by the FDA. When combined with the CDSA test it gives us the most accurate view of a patient's level of Candida and the cause of it. As stated above, the CDSA also reveals what needs to be done to eliminate the cause of Candida in the digestive tract. In the natural health field many substances have bean promoted as being able to reduce yeast Infection. I have found that they do create a reduction in symptoms, but cannot destroy a yeast overgrowth in a systemic case. Both undecylenic and caprylic acid are poorly absorbed into the blood stream making them ineffective in systemic cases. They only eliminate OR destroy it in the intestinal tract and will leave behind the colonies that have traveled to other parts of the body. Acidophilus is helpful with some Candida symptoms while it is being used regularly. It is supposed to replace Candida in the intestines. But it cannot regrow and replace Candida until enough Candida has been cleaned out and the intestines are cleaner! Note: This test appears to have been discontinuned www.synergy-health.co.uk/articles/yeast_infections20040628.htmlHome Candida Test. The Candida Saliva Test. First thing in the morning before having anything to eat or drink, get a clear glass and fill with water. Work up some saliva and drop a spittle on top of the water and observe. If in 10 minutes time the spittle is still sitting on top of the water then you most probably do not have a candiadiasis problem. If however the spittle spreads and breaks up or you see streamers going down into the water then you may well have an imbablence. www.fungusfocus.com/html/diagnostic_lab_tests.htmMedical Diagnostic Lab Tests For Fungus, Yeast, Candida, And Parasites GENERAL INFORMATION This page is about medical diagnostic lab tests that will discover "clinical" evidence of a fungus, yeast, Candida, or intestinal parasite infection. The following material is a survey of medical labs having specialty tests or a reputation for executing standard tests to actually find these organisms. Candida and other fungus and yeast infections are notoriously difficult to identify. Yeast infections, and in particular, intestinal Candida yeast infections (and systemic Candidiasis), can lurk for years with few overt symptoms that allow a diagnosis. Consequently, medical diagnostic lab tests that irrefutably identify a yeast infection are vital in order for your doctor to be convinced, and for you to receive proper treatment. TYPES OF TESTS Although this web site is oriented to fungus and yeast infections, this section includes information on diagnostic testing for intestinal parasites since they occur commonly in conjunction with intestinal yeast infections. Available diagnostic tests include tests of blood, stool, urine, saliva , and tissue or bodily fluid samples (for example, cerebrospinal fluid from a spinal tap, fluid irrigated from the lungs, etc.). Blood tests include antibody tests that look for IgG, IgA, and IgM antibodies to a specific fungus or yeast, and PCR (Polymerase Chain Reaction) tests which discover the presence of DNA of the fungus or yeast. (PCR is a method of multiplying an infinitesimally small amount of DNA into a measurable quantity.) Whereas antibodies may be present even after the infection is cured, the existence of DNA is positive indication of a current infection -- the bug is actually there, floating around in your blood stream. PCR may also be used to identify a specific strain of bacteria, fungus, or yeast. In addition, blood may be cultured to discover the presence of bacteria, fungus and yeast infections, although blood cultures are hard to grow, and most turn out negative. "Finding Candida by blood culture is considered the definitive test for systemic yeast infection. However, in one of the most intensive studies done (18), there was a very high incidence of false negatives using blood cultures for Candida. In children who really did have yeast invasion of their organs including brain, liver, or heart that was confirmed by autopsy, only 17% of the children's blood samples tested positive for yeast even though they had been tested repeatedly (an average of ten times) for Candida." (Quote from Dr. Shaw at Great Plains Lab.) Stool tests include microscopic visual examination for parasites and yeast, and culturing for specific pathogenic bacteria and yeasts. Since stool may contain a great many varieties of bacteria, mainstream labs normally only conduct cultures to discover a particular and suspected bacterial pathogen, as requested by the doctor. Similarly, they do not culture for fungus and yeast. However, there are several specialized labs that perform comprehensive analyses of stool, including culturing for bacteria and yeasts. There are widespread opinions expressed on the web that the mainstream commercial and hospital labs are not attuned to the problems of intestinal yeasts and parasites, and consequently these infections may go undetected despite the submission of numerous specimens. Therefore, there appears to be a consensus among alternative medical thinking expressed on the web that patients and doctors attempting to diagnose and identify the cause of suspected intestinal yeast and parasite infections should steer stool analyses to labs that focus on these problems. Several of these labs are identified on this page. Culturing for fungi and yeast is problematic – many are very slow growing (fastidious) – so fungal and yeast cultures usually require 4 weeks before the lab will call it negative. However, only a culture can show the sensitivity of a discovered pathogen to drugs, so unless a culture is performed the selection of the drug is an empirical choice. You can find selection criteria at the excellent DOCTORFUNGUS site. FUNGAL ANTIBODY TESTS FOR BLOOD SERUM A fungal antibody test is a blood test that shows either Positive or Negative, but only for the specific fungi or yeast in the test. Basically, they put a drop of your blood serum, a drop of an antibody for the fungus or yeast being tested, and a drop of a "control" blood serum each into a separate spot in a Petri dish filled with a thin gel. (The antigen is the bad thing; the antibody is the good thing in the immune system that tries to kill the bad thing.) The control blood serum has a known quantity of the antigen (the fungus or yeast) being tested for and is used to ensure that the test was performed correctly – it should always show a positive reaction. The blood components and the antibody slowly diffuse through the gel (hence, it's an "immunodiffusion test"), and will meet in about 30 minutes. If the antigen and antibody are an exact match the antibody latches onto the antigen and precipitates out, forming a visible line. If a line shows up, the test is positive, if not, it is negative. A positive may be reported as an "identity", since it demonstrates that the antigen in your blood serum is identical to the antigen in the control blood serum. The two major diagnostic labs in the U.S. are Quest Diagnostics and Labcorp and both offer a version of the fungal antibody test. The Quest test (single immunodiffusion) is qualitative only – it detects the presence of the fungal antibody but does not indicate the degree of infection; by contrast, the Labcorp test (double immunodiffusion) also indicates the amount of antibody present. You can read more from IMMY (Immuno-Mycologics, Inc.), the manufacturer of the Quest test, at this description of their antibody test. There is a somewhat better description provided for the Candida test. "Immunodiffusion tests are used for the detection of precipitating antibodies (primarily of the IgG and IgA classes) against antigens of C. albicans. The presence of precipitating antibodies indicates active or recent infection." The Quest test number is 4077N, and the Labcorp test number is 091454. Each test suite only covers the most common pathogenic fungi as listed in the table. The Quest test includes Candida; the Labcorp test does not. A doctor does not need to specify the test number since he may not know which lab will be used – the doctor can simply order "fungal antibody test". However, if Candida is suspected, the doctor's order obviously must specify Candida to steer the request to an appropriate lab (e.g. "fungal antibody test with Candida"). Most labs, presumably including Labcorp, will send out to another lab to fulfill a request if they don't provide it themselves. AAL Reference Laboratories provides a Candida-specific antibody test #2323 Candida Antibodies (IgG, IgM & IgA) with Candida Immune Complexes. Immune complexes are other proteins floating in the blood in accompaniment with the antibodies. "The only laboratory test that has been proven by independent clinical studies to be effective for the detection and monitoring of Active Candida Overgrowth is the Candida Immune Complex Assay." Their reported rationale for measuring the Candida immune complexes in addition to the Candida antibodies is as follows: Standard Candida antibody analyses are both sensitive and specific with the following benefits: • Elevated IgM levels suggest active or recent infection. • Elevated IgG levels suggest a past infection. • Elevated IgA levels are seen in patients who have had localized mucosal Candida infections (i.e., vaginal or mouth). Although these tests have applications to the physician for the above reasons, they have the following limitations: • IgM antibodies are transient and therefore, present for only a short period of time. • IgG antibodies persist for many years after the infection has been cured. • Antibodies tests lack the specificity for a conclusive diagnosis of clinical candidiasis (active Candida overgrowth). Why Test for Candida Specific Immune Complexes? For many years, Antibody Assay Laboratories has provided Candida specific immune complex measurements to physicians. They have found it extremely useful in the diagnosis and treatment of patients with active Candida overgrowth (Candidiasis) for these important reasons: • Elevated Candida Specific Immune Complexes establish the presence of Candida overgrowth • Immune Complexes levels drop quickly when the Candida load is reduced • Candida Specific Immune Complexes are useful in monitoring the effectiveness of treatment. (Candida Immune Complexes will be reduced if the patient has responded to treatment). • Elevated Candida Immune Complexes correlates with clinical symptoms of Candidiasis or Candida Overgrowth • Candida Immune Complexes levels decrease with patient improvement Note: For maximum effectiveness, Antibody Assay Laboratories suggests to repeat the Candida Immune Complexes assay after three months of treatment or when symptoms subside. FOR SALIVA Saliva Antibody Test: A laboratory in London, the Institute for Individual Wellbeing, has modified the standard blood serum antibody test to work from a saliva sample. Performing the test is still complex (see Candida Saliva ELISA Test on this link), and requires a professional lab environment, but collecting the sample should be easier than a blood draw with the presumed intent for the patient to collect their own sample and mail to the lab. Saliva Antibody Test: Also see BioHealth Diagnostics Mucosal Barrier Function #304 discussed below. This is a comprehensive test that evaluates a number of conditions. It detects antibodies to yeasts, and aerobic and anaerobic bacteria, among others. The test kit can be sent directly to the patient. URINE TESTS FOR CANDIDIASIS Multiple laboratories perform an "organic acid" test on urine to detect metabolic byproducts of Candida and other pathogens that pass into the blood stream from the intestines and are discarded in the urine. Versions of this test are available from several sources, including Great Plains Labs, Metametrix Lab, the Biamonte Center, and JackTips (all discussed below). (We should point out that the Biamonte Center and JackTips are treatment organizations, not labs, and probably either use purchased lab kits or send the samples out to a qualified lab.) "Organic acid tests can analyze a much broader spectrum of health conditions by examining a large number of different types of metabolites. Intestinal dysbiosis can be a significant factor in many health problems. The Metametrix Dysbiosis Metabolic Marker Profile measures the byproducts of bacterial and yeast metabolism that are excreted in urine. The Dysbiosis Profile is particularly useful in detecting the presence of pathogenic microbial overgrowth and monitoring therapy." See the Metametrix publication and the Great Plains lab test description. Urine Test: A urine test for systemic candidiasis, called the Bio-Screen 'Yeast Cult' test, is available from Advanced Nutrition, Broadway House, Tunbridge Wells, Kent, UK. TN1 1QU (Tel: 01892-542012). The reference for this is from Carol Mason in the UK. This is likely to be an organic acid test as just previously described. OTHER TESTS In addition to the more common tests that have been described, there are a number of other tests to mention. Here is a listing provided by Cerodex Labs, a wholly owned subsidiary of IMMY: Complement Fixation tests for antibody to: • Histoplasma mycelial antigen • Histoplasma yeast antigen • Blastomyces A antigen • Coccidioides antigen • Aspergillus fumigatus antigen Latex Agglutination tests • Antibody detection: • Histoplasma antibody • Coccidioides ('IDTP') antibody • Sporothrix schenckii antibody • Antigen detection: • Cryptococcus neoformans capsular polysaccharide antigen Yeast Agglutination: • Cryptococcus neoformans antibody Due to the esoteric nature of these tests, one would presume (or hope) that the lab would make the determination of when the use of each is appropriate, rather than expecting the requesting physician to know exactly what to ask for. The Candisphere test, once produced by IMMY and available through Cerodex, has been discontinued, presumably replaced by more effective tests (the immunodiffusion antibody tests discussed above). Candisphere was an Enzyme Immunoassay test (EIA) detecting antibody to Candida cytoplasmic antigens. The term Candisphere appears with some frequency on Candida associated web sites. CHROMagar is a diagnostic test developed by French biologist Dr. Alain Rambach which causes specific pathogens to appear in unique colors as they grow in a Petri dish coated with the proprietary agar growth medium. The growth medium product CHROMagar Candida will not only allow the growth and detection of yeasts - like traditional media - but in addition, just by the color of the colony, will instantly differentiate various Candida species. For detection and differentiation of major Candida species by colony color: • Candida albicans- green • Candida tropicalis - steel blue • Candida krusei - rose, fuzzy The growth medium product CHROMagar Orientation, although primarily intended for the detection of urinary tract pathogens, also serves as a general nutrient agar for isolation of various microorganisms. For rapid detection and differentiation of pathogens, including gram negative and gram positive bacteria - pathogens which are identified by unique colors include: • E. Coli - red • Klebsiella - steel blue • Enterococcus - turquoise blue • Proteus - brown halo • Pseudomonas - yellow • Staphylococcus - white Distributors in the U.S. and elsewhere sell the liquid growth medium as well as prepared Petri dishes to diagnostic labs. Some of the labs listed in this report are likely to use CHROMagar as part of their testing suite. INTESTINAL PERMEABILITY AAL Reference Laboratories, Inc. provides a blood serum antibody test to detect intestinal permeability (Intestinal Permeability Evaluation #2330) (also see the above discussion of AAL's Candida blood serum Antibody test): "There appears to be a relationship between intestinal Candida overgrowth and increased intestinal permeability. This occurs particularly in patients that have chronic unresponsive Candida overgrowth with persistently elevated Candida immune complexes, despite prolonged antifungal therapy. These patients may have casein (from milk) and/or gliadin (from wheat) antibodies. Therefore, we recommend that patients with Candida overgrowth should also be evaluated for intestinal permeability by measuring IgA & IgG to casein or gliadin, as well as Candida immune complexes. Conversely, patients with suspected intestinal permeability should have Candida immune complexes measured as well as antibodies to casein and gliadin. "A recent study 11 has also shown that patients with chronic unresponsive Candida overgrowth and increased intestinal permeability, also have a reduction in leucocyte phagocytosis. It is suggested in this study that this reduction is secondary to free radical damage to the neutrophils. It is important to identify these patients with poor leucocyte phagocytosis, because they may benefit from increased antioxidant therapy. "The treatment of these patients should be focused on resolving their bowel dysfunction and should include: antifungal measures, mineral supplements, and antioxidants. Initially, they should have casein and gliadin removed from their diet and then after six months of this regime casein and gliadin can be reintroduced. Retesting for casein and gliadin IgA and IgG antibodies should be performed in the next month to assess the current intestinal permeability status." Other labs performing Intestinal Permeability tests include Great Smokies Lab, and the Do It Yourself Tests from JackTips. Me: I tested myself for estradiol, the most potent form of estrogen in the body, after eating a lot of soy for a day. Normal range for an adult male is 0-53, and mine was 20. I found out later that soy actually diminishes estradiol in the blood by about 25% by taking its place. That means my normal level may have been 28. But still well within range. The test did not measure genistein levels. On the subject of candida - systemic candemia specifically - there was just approved this month a new safer drug for its treatment. It's called Eraxis. Existing drugs were extremely danerous to the liver and kidneys. So my blood test for candida antibodies was negative. However, I've read that this test shows a lot of false negatives, and it wasnt the test they advertised, which gives numerical results - this one gave only positive/negative results. I've read that people have died from systemic candidemia and had nothing show up in this blood test. They also had my blood sitting around for 5 days before they tested it. Treatments for Candida Eraxis - A New, Safer Drug SCIENCE: Quest Diagnostics New Drug for Candida Infections (May, 2006) When we hear “Candida infections” or candidiasis, we don’t normally think fatal but certain forms can be. In the case of blood infections caused by Candida (usually Candida albicans), the mortality rate is about 40 % and there are about 60 thousand cases annually in this country. FDA recently approved the use of a new, novel drug called “anidulafungin” (Eraxis®). This drug can be used to treat all kinds of Candida infections including blood stream infections (candidemia), esophageal infections (candidiasis), abdominal abscesses, peritonitis and other types of infections. The drug, which is administered intravenously, is well tolerated and the only adverse effects noted thus far have been mild diarrhea, headache and slight elevations in liver enzymes. SCIENCE: FDA FDA Approves New Treatment for Fungal Infections The Food and Drug Administration approved Eraxis™ (anidulafungin) to treat certain infections caused by Candida, a yeast-like fungus that can cause serious infections in hospitalized patients or patients with compromised immune systems. "This product offers a new alternative therapy for several types of infections associated with Candida", said Dr. Steven Galson, director of the FDA's Center for Drug Evaluation and Research. "It is a helpful addition to the available antifungal medications that can be used in the treatment of these potentially serious fungal conditions." Eraxis, a new molecular entity that has never been marketed in the United States, is an antifungal drug that is administered intravenously, and is used to treat Candida infections in the esophagus (candidiasis), blood stream (candidemia), and other forms of Candida infections, including abdominal abscesses and peritonitis (inflammation of the lining of the abdominal cavity). The safety and efficacy of Eraxis was evaluated in clinical studies and Eraxis was shown to be safe and effective in the treatment of esophageal candidiasis, candidemia, and other Candida infections including abdominal abscesses and peritonitis. Eraxis was generally well tolerated in clinical studies. The most commonly reported adverse events were mild diarrhea, mild elevations in laboratory tests of liver enzymes, and headache. Some patients experienced infusion-related reactions, most of which were mild. In a few patients with significant underlying medical conditions who were on multiple concomitant medications, there were reports of serious hepatic abnormalities. Drugs (dangerous) REFERENCE: Wikipedia - Amphotericin Amphotericin B (Fungilin®, Fungizone®, Abelcet®, AmBisome®, Fungisome®, Amphocil®, Amphotec®) is a polyene antimycotic drug, used intravenously in systemic fungal infections. Side effects Very often a most serious acute reaction after the infusion (1 to 3 hours later) is noted consisting of fever, shaking chills, hypotension, anorexia, nausea, vomiting, headache, dyspnea, and tachypnea. This reaction sometimes subsides with later applications of the drug and may in part be due to histamine liberation. An increase in prostaglandin-synthesis may also play a role. Often the most difficult decision has to be made, whether the fever is disease- or drug-related. In order to decrease the likelihood and severity of the symptoms, initial doses should be low and increased slowly. The liposomal preperation obviously has a lower incidence of the syndrome. Acetaminophen, pethidine, diphenhydramine and/or hydrocortisone have all be used to treat or prevent the syndrome, but the prophylactic use of these drugs should be limited. Nephrotoxicity (kidney damage) is a major issue and can be severe and/or irreversible. It is much milder when amphotericin B is delivered in liposomes (AmBisome). Electrolyte imbalances (e.g. hypokalemia and hypocalcemia) may also occur. Increased liver enzymes and hepatotoxicity up to acute liver failure, several forms of anemia and other blood dyscrasias (leukopenia, thrombopenia), serious cardiac arrhythmias (including ventricular fibrillation), and cardiac failure have also been reported frequently. Skin reactions, including serious forms, are also possible. From studies it appears that liposomal amphotericin B preparations exhibit fewer side-effects while having similar efficacy. Various preparations have recently been introduced. All of these are more expensive than plain Amphotericin B. AmBisome is a liposomal formulation of amphotericin B for injection, developed by NeXstar Pharmaceuticals (acquired by Gilead Sciences in 1999). It is marketed by Gilead in Europe and licensed to Astellas Pharma (formerly Fujisawa Pharmaceuticals) for marketing in the USA, and Sumitomo Pharmaceuticals in Japan. Fungisome is a liposomal complex of Amphotericin B and being the latest and cheapest addition to the lipid formulations of Amphotericin B has many advantages. It is marketed by Lifecare Innovations of India. Other liposomal formulations include Amphotec® (Intermune) and Abelcet® (Enzon Pharmaceuticals). REFERENCE: Wikipedia - Fluconazole Fluconazole is a synthetic antimycotic drug of the triazole class of compunds. The drug is sold under the brand name Diflucan®. It is used orally and intravenously to treat yeast and other fungal infections. Contraindications and cautions Male rats treated with 5 mg and 10 mg/kg weight respectively showed a higher incidence of hepatocelluar adenomas than expected. No data exists on human carcinogenity. • Known hypersensitivity to fluconazole is an absolute contraindication. • Fluconazole may infrequently cause severe or lethal hepatotoxicity. Liver function studies should be obtained regularly. Patients showing clinical signs of liver damage should be immediately withdrawn from the drug. Patients with preexisting liver disease should be treated with particular care. • Some patients develop severe skin reactions (Steven-Johnson-Syndrome or toxic epidermal necrolysis) under treatment. Patients with HIV-infections are particularly prone. All patients should be carefully watched for development of any skin reaction and should be advised to discontinue the drug immediately if rash or other forms of skin reactions are observed. • Fluconazole may cause rare cases of prolongation of the QT interval, leading to serious arrhythmias. Risk factors are preexisting prolonged QT interval, electrolyte imbalances including hypokalemia, low serum level of magnesium and hypocalemia. These patients should be treated with caution and the electrolyte imbalances should be corrected before therapy is initiated. Side-effects • GI tract: Nausea, dyspepsia, abnormal taste, abdominal pain, vomiting, diarrhea, and flatulence were reported in 5.3% of patients. In female patients receiving a high single dose treatment for vaginal infections, the incidence of these side-effects may be higher. • Skin : Skin rash, diffuse reaction with eosinophilia, and pruritus were encountered in up to 5%. Also alopecia and exfoliative skin reactions (including Stevens-Johnson-Syndrome and Lyell's-Syndrome) were seen. The latter had been fatal in some patients. • Liver, kidney, hematology : Some patients, particular those with AIDS or malignancies, developed increased liver enzymes, bilirubin, AP, BUN, serum creatinine, eosinophilia, anemia, and leukopenia including agranulocytosis as well as thrombopenia. Symptomatic hepatotoxicity (hepatitis, hepatic necrosis, jaundice, cholostatic hepatosis, and fulminant liver failure) including fatalities had been infrequent. • Central nervous system : Frequently headache, less frequently vertigo and convulsions. Some of these side-effects might have been due to the underlying disease (cryptococcal meningitis). An acute psychotic (paranoid) reaction had been noted in one case of overdose. • Heart : QT interval prolongation and torsade de pointes (a serious arrhythmia) may occur. • Different Side-Effects : Anaphylactic reaction (including facial edema, angioedema, and pruritus). Hypokalema, increased triglycerides, and increased cholesterol had also been encountered. www.rainbowminerals.net/candida_elimination.htmAnother drug Nizoral impairs the productions of ergosterol, a vitamin D like substance, which is vital to the integrity of the yeast cell membranes. This drug is difficult for Candidiasis patients to absorb because proper stomach acid is required to absorb it. Most patients are deficient in stomach acid. Yeast infections sometimes produce symptoms that make people believe they have excess acid. www.candidafree.net/pages/1/index.htmTaking yeast medication like Diflucan or Nystatin can temporarily relieve symptoms, but unless measures are taken to repopulate the gut with friendly bacteria and correct whatever caused them to die off in the first place, the yeast will simply grow back, hence reports that while killing the yeast helps alleviate symptoms, the effect is usually only temporary. SCIENCE: National Library of Medicine Candidaemia and antifungal therapy in a French University Hospital: rough trends over a decade and possible links. ABSTRACT: BACKGROUND: Evidence for an increased prevalence of candidaemia and for high associated mortality in the 1990s led to a number of different recommendations concerning the management of at risk patients as well as an increase in the availability and prescription of new antifungal agents. The aim of this study was to parallel in our hospital candidemia incidence with the nature of prescribed antifungal drugs between 1993 and 2003. METHODS: During this 10-year period we reviewed all cases of candidemia, and collected all the data about annual consumption of prescribed antifungal drugs RESULTS: Our centralised clinical mycology laboratory isolates and identifies all yeasts grown from blood cultures obtained from a 3300 bed teaching hospital. Between 1993 and 2003, 430 blood yeast isolates were identified. Examination of the trends in isolation revealed a clear decrease in number of yeast isolates recovered between 1995-2000, whereas the number of positive blood cultures in 2003 rose to 1993 levels. The relative prevalence of Candida albicans and C. glabrata was similar in 1993 and 2003 in contrast to the period 1995-2000 where an increased prevalence of C. glabrata was observed. When these quantitative and qualitative data were compared to the amount and type of antifungal agents prescribed during the same period (annual mean defined daily dose: 2662741; annual mean cost: 615629 ) a single correlation was found between the decrease in number of yeast isolates, the increased prevalence of C. glabrata and the high level of prescription of fluconazole at prophylactic doses between 1995-2000. CONCLUSION: Between 1993 and 2000, the number of cases of candidemia halved, with an increase of C. glabrata prevalence. These findings were probably linked to the use of Fluconazole prophylaxis. Although it is not possible to make any recommendations from this data the information is nevertheless interesting and may have considerable implications with the introduction of new antifungal drugs. Note: It'd be interesting to see the actual numbers of people, maybe in percentages, with candidemia. ThreeLac www.candidafree.net/pages/1/index.htm(about ThreeLac:) About 10% of people tell us they feel better very quickly, within weeks. Another 10% may take 4-6 months to get the overgrowth under control, but the vast majority we have heard from achieve dramatic improvement in about 2 ½ to 4 months. Every person is different, so please be patient with the process. When you feel you are ready to graduate back down in your dosage, go just as slowly (one packet at a time) as you did in the first place. If your symptoms start coming back, you're going down too soon. Anti-Estrogens www.gynecomastia.org/content/letters/01060801.shtml2) An anti-estrogen like Chrysin may lower estrogen levels. Chyrsin is legal but is NOT intended to cure any diseases(*** remember I'm not a doctor ***). Supplements www.thecrystaltarot.com/nutrition-autism-treatment.html• Candida binds with B vitamins, particularly vitamin B6 which interferes with the production of serotonin, melatonin, and other neurotransmitters • Caprylic acid is a natural fatty acid that kills candida (1-2 grams with meals) p075.ezboard.com/fgilbertswebfrm1.showMessage?topicID=571.topicImgeha Molybdenum breaks down the formaldehyde produced by the candida so it is not so harmful to the liver. Anti-Candida Diet www.candidafree.net/pages/1/index.htmA Candida diet without antimicotics will simply cause the Candida to change form and send hyphae through the wall of the gut and into the underlying blood vessels in search of glucose, resulting in leaky gut syndrome. In leaky gut syndrome, food particles are then free to enter the blood circulation and trigger allergic reactions. www.toronto.com/health_fitness/article/000-000-233Candida therapy starts with eliminating its energy foods from the diet, killing the fungus with various remedies, cleaning the intestinal walls, rebuilding the intestines, rebalancing intestinal flora and strengthening the immune system. Strategies for success: 1. Suppress or kill the yeast with anti-fungals. Garlic is one of the most potent antimicrobial agents along with oregano. Pau D'arco is an extract of the bark of a South American tree known to have potent anti-fungal properties. 2. Deprive or starve the yeast by diet modification. A simple approach is to remove refined simple sugars, milk/dairy foods, alcohol, melons, fermented foods and dried fruit. 3. Cleanse and rebuild the walls of the gastrointestinal tract. 4. Rebalance bacteria in the colon with beneficial bacteria. 5. Identify and avoid drugs, chemicals, foods and other allergens such as, insecticides and preservatives that you know trigger candida and its symptoms. p075.ezboard.com/fgilbertswebfrm1.showMessage?topicID=571.topicImgeha The way to deal with this is starve the candida by eliminating all sugar, yeast, gluten, dairy and complex carbs - rice, pasta, potatoes, starchy vegetables - and take a good probiotic (Nature's Biotics)... People with GS tend to have blood sugar issues as well, so eliminating or minimising complex carbs is not a bad thing to do anyway. Estrogen Metabolism cancerres.aacrjournals.org/cgi/content/full/64/3/1202The Functional UGT1A1 Promoter Polymorphism Decreases Endometrial Cancer Risk In humans, more than 18 functional UGTs have been isolated, and several have demonstrated significant reactivity toward estrogens and their metabolites, catecholestrogens (14, 15, 16, 17, 18, 19, 20, 21) . UGT1A1 is thought to play a major role in the metabolism of estradiol (E2) because a Crigler-Najjar patient deficient in UGT1A1 had a 70% decrease in the hepatic glucuronidation of E2 compared with liver microsomes from healthy subjects (18) . UGT1A1 also catalyzes the glucuronidation of hydroxylated metabolites of E2 and estrone (17)... A common variant in the UGT1A1 gene, designated as UGT1A1*28 [A(TA)7TAA], is known to decrease the level of gene expression (30 , 31) . Variability in the expression of the UGT1A1 protein resulting from this polymorphism may lead to important differences in estrogen biotransformation. Interindividual variability in levels of conjugated estrogens, in the form of estrogen glucuronides, have been measured in urine, breast cyst fluid, and follicular fluid, suggesting that UGT enzymes have an effect on the inactivation and elimination of estrogens and their accumulation in target tissues (13 , 32 , 43 , 44) . toxsci.oxfordjournals.org/cgi/content/abstract/45/1/52?ijkey=daf65a1e32346ebf753ee137efc9ba66fb12ea8f&keytype2=tf_ipsecshaGlucuronidation of Catechol Estrogens by Expressed Human UDP-Glucuronosyltransferases (UGTs) 1A1, 1A3, and 2B7 Catechol estrogens are major estrogen metabolites in mammals and are the most potent naturally occurring inhibitors of catechol-amine metabolism. These estrogen compounds have been implicated in carcinogenic activity and the 4/2-hydroxyestradiol concentration has been shown to be elevated in neoplastic human mammary tissue compared to normal human breast tissue. Three human liver UDP-glucuronosyltransferases, UGT2B7, UGT1A1, and UGT1A3, have been shown to catalyze the glucuronidation of catechol estrogens and lead to their enhanced elimination via urine or bile. endo.endojournals.org/cgi/content/abstract/140/7/3292?ijkey=8d97b79fba4a726f61d1897ddb6449b9bc9a4017&keytype2=tf_ipsecshaThe Monkey and Human Uridine Diphosphate-Glucuronosyltransferase UGT1A9, Expressed in Steroid Target Tissues, Are Estrogen-Conjugating Enzymes Of the more than 30 endogenous substrates tested, both proteins show the highest activity on 4-hydroxyestradiol and 4-hydroxyestrone, followed by 2-hydroxyestradiol and estradiol. RT-PCR analysis demonstrate that UGT1A9 transcript is expressed in several tissues, which include the prostate, testis, breast, ovary, and skin of the monkey and humans. The expression of UGT1A9 in extrahepatic estrogen-responsive tissues, and its high activity on estrogens is consistent with this enzyme having a role in estrogen metabolism. jncicancerspectrum.oxfordjournals.org/cgi/content/full/jncimono;2000/27/113Chapter 6: Estrogen Metabolism by Conjugation Conjugation of parent estrogens to sulfate and glucuronide moieties; of catechol estrogens to methyl, sulfate, and glucuronide conjugates; and of catechol estrogen quinones to glutathione conjugates all represent potential "detoxification" reactions that may protect the cell from estrogen-mediated mitogenicity and mutagenesis. Estrogens exert biologic responses in steroid hormone-responsive cells largely via interaction with ERs, members of a superfamily of nuclear hormone receptors that act as ligand-activated transcription factors (5). There are two known ER subtypes, ER{alpha} and ER{beta} , which share similar estrogen affinities but have dissimilar expression patterns and response to antiestrogens (5–7). The two most potent endogenous estrogens, estrone and 17{beta}-estradiol, are both ligands for the ERs, although those receptors have higher affinity for 17{beta}-estradiol than for estrone and it is 17{beta}-estradiol that is believed to be the predominant endogenous activator of ER-mediated cellular processes (5). The most abundant circulating estrogen, however, is the sulfate conjugate of estrone (8,9). Biologic Role of Estrogen Conjugation The endogenous formation of estrogen conjugates has long been recognized as a major route of estrogen metabolism (17). Both endogenous and synthetic exogenous estrogens are extensively biotransformed to estrogen conjugates in humans (Fig. 1Go) (2,18). The most abundant circulating estrogen conjugates are the sulfates, followed by the glucuronides. It is important to note that conjugated estrogens are not appreciable ligands for the ERs; thus, they do not promote ER-mediated activity (2). Intuitively, it was initially assumed that sulfate and glucuronide conjugation of estrogens represented a pathway resulting in less active, more polar, and more readily excreted estrogenic compounds. It is now appreciated, however, that estrogen sulfates actually exhibit a much longer half-life than do the parent estrogens (2,8,11). Estrone sulfate is the most abundant circulating estrogen, at concentrations approximately 10-fold higher than unconjugated estrone (8). That finding, as well as increasing knowledge about the transport and subsequent desulfation of estrogen sulfates, has led to a widely held belief that sulfated steroid hormones serve an important biologic role as steroid hormone precursors, particularly for steroid hormone-responsive tissues (2,9). An increasing body of scientific data supports the hypothesis that sulfation and desulfation of estrogens may well represent an endogenous system important in the regulation of biologically active steroid hormones in target tissues (10,11). Specifically, it is currently hypothesized that inactive estrone sulfate is transported to target tissues via the circulatory system, taken into target cells, most likely by organic anion transporters, enzymatically hydrolyzed to estrone by intracellular membrane-bound steroid sulfatase (arylsulfatase C), and hydroxylated to active 17{beta}-estradiol via catalysis by 17{beta}-hydroxysteroid dehydrogenases (2,11,18,19). 17{beta}-Estradiol activates the ER via ligand binding and initiates a number of downstream ER-mediated events—most notably related to transcriptional activation of those genes that contain DNA sequences that bind and respond to activated ERs (5,18). Enzymes responsible for the glucuronidation and deglucuronidation of estrogens are also expressed in a variety of human tissues, including the breast (24,25). Estrogen glucuronides have received much less attention, however, than have the sulfate conjugates as steroid hormone precursors, most likely because they are less abundant and more readily cleared from the body (2). Biochemistry of Estrogen Conjugation Sulfation. Sulfate conjugation of estrogens is catalyzed by several members of a superfamily of cytosolic sulfotransferase (SULT) enzymes (27,28). SULT enzymes catalyze the transfer of SO3- from 3'-phosphoadenosine-5'-phosphosulfate, the enzymatic cofactor, to, in the case of estrogens, phenolic acceptor groups (28). Cytosolic SULTs are active as homodimers. Sulfation of estrone and 17{beta}-estradiol occurs at the 3-phenolic group of the steroidal A ring (Fig. 1Go). Estrogen SULT activity has been demonstrated in a variety of human tissues, including liver, small intestine, kidney, placenta, uterus, adrenal gland, and breast (29–33). The level of estrogen SULT activity in the human liver is high, and this activity is believed to contribute significantly to the high circulating levels of estrone-3-sulfate (29,30). Although from a quantitative perspective, sulfation of estrogens in the liver is probably the most important overall estrogen-conjugating activity in the body, sulfation of estrogens in steroid target tissues, including the breast, has also been demonstrated and may well be important in affecting the biologic activity of estrogens within those tissues (2,11). Glucuronidation. Estrogen glucuronidation is catalyzed by several members of a superfamily of microsomal UDP-glucuronosyltransferase (UGT) enzymes (25,37). UGTs catalyze the conjugation of UDP-glucuronic acid, the UGT cosubstrate, to a variety of endogenous and exogenous aglycones, including steroid hormones (38). Whereas estrogens are sulfated predominantly at the 3 position, glucuronidation can occur at either the 3 or 17{beta} hydroxyl group of steroidal hormones, with the 17{beta} position being the apparent predominant site of glucuronidation for 17{beta}-estradiol (Fig. 1Go). Glucuronidation of estrogens renders those molecules less lipophilic and more readily excreted in both urine and bile. 17{beta}-Glucuronides of estradiol are known to induce cholestasis, putatively via interaction with hepatocyte canalicular membrane efflux transporters such as MDR1 and MRP2/cMOAT (39,40). Steroid hormone glucuronidation has been observed in human liver, biliary epithelium, kidney, gut, prostate, ovary, and breast (25,26,38). Molecular and Cellular Aspects of Estrogen Conjugation There are a surprising number of SULT and UGT isoforms capable of contributing to the conjugation of estrogens. Those isoforms are often expressed in a tissue-specific manner and are often under specific regulatory control. Furthermore, a number of those conjugative enzymes are encoded by genes known to harbor common genetic polymorphisms. These factors help explain many of the complexities of estrogen conjugation—and this knowledge allows us to probe estrogen conjugation reactions in a systematic fashion. Glucuronidation of estrone and 17{beta}-estradiol appears to be catalyzed by several members of the UGT1 family. Thus far, recombinant human UGTs 1A1, 1A3, 1A4, 1A8, 1A9, and 1A10 have all been shown to catalyze the glucuronidation of estrone and/or 17{beta}-estradiol (Table 1Go) (25,26,56–60). It is interesting to note that, for some human recombinant UGT isoforms, there appears to be selective affinity for estrone or 17{beta}-estradiol as substrate. For example, UGTs 1A1 and 1A4 exhibit activity toward 17{beta}-estradiol but not toward estrone, whereas UGTs 1A9 and 1A10 have been reported to catalyze the glucuronidation of both of these estrogens (25,26,56,58,60). Activity for UGTs 1A8 and 1A3 toward estrone has been reported, but the activity of those isoforms toward 17{beta}-estradiol has apparently not been evaluated (57,59). UGT1A1 is expressed in human liver, colon, and biliary epithelium (gallbladder) but not in stomach (60). UGT1A3 has been reported to be expressed in human colon, biliary epithelium, and liver, but the level of expression in liver varied significantly between individuals and was fivefold to 10-fold less than the level of UGTs 1A1 and 1A4 (57,60). UGT1A4 is expressed in human liver, colon, and biliary epithelium but not in stomach (60). UGT1A8 appears to be expressed specifically in human intestinal tissues (59,60). UGT1A9 is expressed in human prostate, testis, breast, ovary, skin, skeletal muscle, stomach, small intestine, colon, liver, and kidney but not in biliary epithelium or stomach (25,60). UGT1A10 is expressed in colon, biliary epithelium, and stomach but not in liver (60). As previously noted, the capacity for estrogen conjugation and, specifically, glucuronidation is known to vary widely in the human population (51). That observation raises the possibility that genetic variation may exist in the UGT isoforms that contribute significantly to estrogen glucuronidation. A functionally significant common polymorphism in the promoter sequence of the UGT1A1 gene has been described and well characterized (61–63). That polymorphism is a variable length (TA)n TAA repeat in the functional TATA box upstream of exon 1 of the UGT1A1 gene. The wild-type allele is defined as n = 6. Allelic variants identified to date include n = 5, 7, and 8 (63). In vitro studies utilizing reporter constructs driven by allelic variants of the UGT1A1 promoter (63) have shown that promoter activity appears to decrease with increasing n. Furthermore, clinical association of the most common variant (n = 7) with a relatively poor ability to glucuronidate bilirubin (Gilbert's syndrome), as well as the chemotherapeutic agent SN-38, has been observed (61,64). Studies determining the association of UGT1A1 alleles with estrogen metabolism and risk modification of breast cancer have not yet been reported, but they will be of great interest. Note: MAYBE THEY HAVE SINCE 2000! Estrogen Dominance www.womhoo.com/index.asp?PageAction=Custom&ID=3Too much estrogen (estrogen dominance) causes the body to become less sensitive to thyroid hormone. In other words, you will have normal or low thyroid hormone by lab test, but look hypothyroid. Thus, too much estrogen causes hypothyroid even though lab tests are normal. If you are hypothyroid due to estrogen dominance, then you will have fat on the hips and thinning hair. www.diagnose-me.com/cond/C8779.htmlEffects of Estrogen Dominance 1. When estrogen is not balanced by progesterone, it can produce weight gain, headaches, bad temper, chronic fatigue and loss of interest in sex - all of which are part of the clinically recognized premenstrual syndrome. 2. Not only has it been well established that estrogen dominance encourages the development of breast cancer thanks to estrogen's proliferative actions, it also stimulates breast tissue and can trigger fibrocystic breast disease - a condition which wanes when natural progesterone is introduced to balance the estrogen. 3. Excess estrogen implies a progesterone deficiency. This, in turn, leads to a decrease in the rate of new bone formation in a woman's body by the osteoblasts - the cells responsible for doing this job. Although most doctors are not yet aware of it, this is the prime cause of osteoporosis. 4. Estrogen dominance increases the risk of fibroids. One of the interesting facts about fibroids is that, regardless of the size, fibroids commonly atrophy once menopause arrives and a woman's ovaries are no longer making estrogen. Doctors who commonly use progesterone with their patients have discovered that giving a woman natural progesterone may cause fibroids to atrophy. 5. In estrogen-dominant menstruating women where progesterone is not peaking and falling in a normal way each month, the ordered shedding of the womb lining doesn't take place. Menstruation becomes irregular. This condition can usually be corrected by making lifestyle changes and using a natural progesterone product. It is easy to diagnose by having a doctor measure the level of progesterone in the blood at certain times of the month. 6. Endometrial cancer (cancer of the womb) develops only where there is estrogen dominance or unopposed estrogen. This, too, can be prevented by the use of natural progesterone. The use of the synthetic progestins may also help prevent it, which is why a growing number of doctors no longer give non-human estrogens without combining them with progesterone drug during HRT. However, all synthetic progestins have side effects. 7. Water logging of the cells and an increase in intercellular sodium, which predispose a woman to high blood pressure or hypertension, frequently occur with estrogen dominance. These can also be side effects of progestins use. A natural progesterone cream often resolves this problem. 8. The risk of stroke and heart disease is increased dramatically when a woman is estrogen-dominant. ... 2. Many peri- or post-menopausal women with clinical signs of hypothyroidism, such as fatigue, lack of energy, intolerance to cold, are actually suffering from unrecognized estrogen dominance and will benefit from supplementation with natural progesterone. 3. Estrogen and most of the synthetic progestins increase intracellular sodium and water uptake. The effect of this is hypertension. 4. Whereas estrogen impairs homeostatic control of glucose levels, natural progesterone stabilizes them. Thus, natural progesterone can be beneficial to both those with diabetes and those with reactive hypoglycemia. Estrogen should be contraindicated in patients with diabetes. Progesterone increases sensitivity of estrogen receptors, and can therefore redirect estrogen activity and inhibit many of unopposed estrogen's undesirable side-effects, which includes interference with thyroid hormone activity. Cold hands and feet, often caused by low thyroid function, may be a symptom of estrogen excess or low progesterone influencing thyroid function. www.alternativementalhealth.com/articles/estogen.htmList of Estrogen Dominance Symptoms Acceleration of aging Agitation or Anxiety Allergy (asthma, hives, rashes, sinus congestion) Autoimmune disorders Lupus, Thyroiditis (Hashimoto's) Breast cancer (men and women) Breast tenderness with period Cervical dysplasia (abnormal pap smear) Cold hands and feet Copper excess Decreased sex drive Depression with anxiety or agitation Dry eyes Endometriosis Fat gain around abdomen hips and thighs Fatigue Fibrocystic (lumpy breasts) Fibroids Foggy thinking Gall bladder disease Hair loss Headaches Hypoglycemia (low blood sugar esp. 3-4 pm) Increased blood clotting Infertility Irregular menstrual periods Irritability Insomnia Magnesium deficiency Memory loss Mood swings Osteoporosis Ovarian cancer Ovarian cysts PMS/PMT Polycystic ovaries Pre-menopausal bone loss Prostrate cancer (in men) Sluggish metabolism Thyroid dysfunction Uterine cancer Water retention, bloating Zinc deficiency tsangenterprise.com/news75.htmMen produce estrogen (Estradiol) but in much lower amount than women. Men also produce progesterone, but about half the amount from that of females. Progesterone is made in men by the adrenal glands and testes. Progesterone is vital to good health in both women and men. It is the primary precursor of our adrenal cortical hormones and testosterone. The male hormone, testosterone, is an antagonist to estradiol (E2). It is made from progesterone. Men normally continue to produce relatively normal level of testosterone for their age and well into the seventies. Contrary to common perception, testosterone does not cause prostate cancer. Young men have high levels of testosterone and old men low levels. If testosterone were the cause of prostate cancer, young men would be dying of prostate cancer. Studies had shown that men with the highest level of testosterone have the least prostate enlargement. Conversely, men with the highest level of estrogen have enlarged prostates. Declining testosterone from aging, together with increasing level of estrogen, is the most likely reason for prostate enlargement and cancer in men. The prostate is embryologically the same as the uterus in the female. Research Studies (Listed at the end of this newsletter) have shown that when prostate cells are exposed to estrogen, the cells proliferate and become cancerous. When progesterone or testosterone was added, cancer cell dies. lib.store.yahoo.net/lib/gentlepharmacy/Q-A-Men.html6 What are the symptoms of "estrogen dominance"? According to John R. Lee, M.D.*, symptoms of estrogen dominance that men can experience include weight gain, bloating, mood swings, irritability, headaches, fatigue, depression and hypoglycemia. Estrogen dominance is known to contribute to cancer of prostate and the breast. It may seem paradoxical, but men are not immune to breast cancer.
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Post by fritolay66 on Mar 23, 2009 0:50:15 GMT -5
www.gilbertssyndrome.com/allergies.phpAllergies -------------------------------------------------------------------------------- Contents: My Story | What Are Allergies? | Physical Symptoms | Emotional & Behavioral Symptoms | Causes | Allergies & CFS | Testing | Treatments -------------------------------------------------------------------------------- My Story Growing up, I found myself in a near-constant cold. My nose was almost always runny. I remember at one point thinking to myself that it seemed I had had a cold for almost ten years. I had periodic bouts of asthma, and used an inhaler for a few months. Sometime around the age 13-15 someone had the thought to take me in for allergy testing. I got the skin test, and the results were that I was allergic to dust mites and plant mold. Some adjustments were made to our home environment, and I began taking allergy shots. A few years later, they had done their job and I wasnt having allergy problems anymore. Then, at the age of 30, my health began a steady and serious decline. Before long, I had constant terrible headaches for which it took 3-4 Advil/Aleve/Tylenol a day to dim the pain. My sinuses hurt terribly. I found myself constantly fatigued, unable to experience pleasure, foggy-headed, antisocial, depressed, irritable, and physically weak. My memory was terrible, I couldnt concentrate, and it took a great effort to be able to talk with people. I found myself having energy crashes after eating certain foods. My feet and hands were always cold, and my temperature was always around 97.3. There was an inexplicable lump in my throat where food was getting caught and causing constant discomfort. I felt poisoned, toxic. I reacted strongly to any kind of smoke, perfume, varnish, or other environmental irritants. My sense of smell disappeared. I had night sweats where I soaked the sheets, and was sensitive to bright light. I had problems from acid reflux. Normally I am a playful, creative, friendly and affectionate person. Whatever was happening to me submerged that part of me for weeks at a time. The problems were cyclical. There was a baseline malady that would grow intensely worse for weeks at a time, then for a day or two I would emerge from it all, nearly my old self. Then it would come on again, dragging me into these hopeless depths. It seemed I had lost the person I was, and had become consumed by this unknown illness which it seemed I had no hope of recovery. I investigated my health history, and discovered I had Gilbert's Syndrome. I researched this for years, and tried many herbals and medicines, and after a while was able to make some positive progress. The horrible depths diminished slightly, and the periods of returning to normal lasted longer, but then I would crash down again for two weeks and wonder how it could still be happening. One day when talking with my doctor about my headaches, I discovered that it was possible for someone with allergies to relapse and become allergic again. I went and got tested, and was shocked by the results: Animals: dogs, cats, mice, dust mites (major), and cockroaches I have a cat and a dog. Atlanta, where I live, is known by some as the "dust mite capital of the world". Our house occasionally has cockroaches. Trees: Red Oak, Hickory, Red Birch, Red Maple, Red Cedar, Ash, Pecan I have never seen pollen like I have here. We have a "yellow season" where everything turns yellow from the pollen. Grasses: Bahia, Timothy, Fescue Our yard is Fescue. Weeds: both varieties of Ragweed, Cocklebur We have 10 foot tall ragweed plants lining the entire street to our house, as well as all over in the woods Molds: Alternaria, Helminthosporium, Penicillium, Epicoccum, Rhizopus We live in a wet, shady area near a creek, and there are many fallen trees in the woods. Perfect conditions for mold growth. Foods: peanuts, sesame Of the most common allergens they tested, I found out I was allergic to 50% of the trees, 60% of the grasses, 50% of the weeds, 45% of the molds, and 100% of the animals. My immune system had seriously gone into crisis at about age 30 and stayed in crisis ever since. I began taking allergy shots and taking antihistamines. I began watching what I ate and how I reacted more closely, and over a period of months, tracked my reactions, and then went to a total elimination diet. I found more and more foods I was reacting to. The reaction was a 2-3 day descent into sinus pain, headaches, and all the personality changes and symptoms I described above. After months of testing I came to a discovery of perhaps the worst food allergy one can have: citric acid. Foods: citric acid Citric acid is found naturally in: tomatoes, oranges, pineapple, strawberries, limes, lemons, tangerines, raspberries, gooseberries, cranberries, currants, blackberries, elderberries, kumquats, pomegranites. Worse yet, its use as a preservative is nearly ubiquitous. It's found in 99% of canned or bottled sweet or energy drinks. It's used in many canned vegetables. It's used in crackers, breads, and manufactured products of every kind. The only way to be sure something doesnt have citric acid is if it's a raw food not on the above list or by reading the ingredient list. My Allergy Symptoms The symptoms of my allergies this time around are somewhat unusual. I never sneeze. My eyes never itch or water. My nose is almost always clear. I dont have any asthma. My symptoms are horrible PAIN in my sinuses, which become headaches, and the changes to my energy and personality that always happen the same each time. Physical Symptoms Explained From my experiences with different medications and lifestyle changes, I was able to come to understand the source of many, if not all, of my symptoms as being caused by allergies. Sinus Pain: caused by inflammation of the sinuses as a result of histamine. I wonder if the lack of mucus makes the pain worse than usual. Headaches: they are sinus headaches, caused by the above sinus inflammation The Throat Lumps: I finally figured this one out. When I sleep, I sleep most of the time on my right side. The post-nasal drip trickles down the right side of my throat during the night and perhaps the histamines present in it cause that side of my throat to swell. The swelling causes food or mucus to easily get stuck and difficult to get out. Since I've started taking prescription antihistamines, this has almost entirely disappeared. The Symptom Cycles: Another tricky one to understand. They were caused by the coming and going of tree pollen, weed pollen, grass pollen, mold, and dust mite seasons. They were also caused by what I ate. Eating something I'm allergic to causes a 2-3 day tremendous increase in symptoms. If that food made leftovers which I ate over the following week, that descent into a dark state would last a week. By then, I'd have eaten more foods I'm allergic too and started the cycle and layered more pain and symptoms on top. Acid Reflux: This is an effect of high histamine levels. What Are Allergies? Allergies in General www.nlm.nih.gov/medlineplus/ency/article/000812.htmAn allergy is an exaggerated immune response or reaction to substances that are generally not harmful. Allergy is caused by an oversensitive immune system, which leads to a misdirected immune response. The immune system normally protects the body against harmful substances, such as bacteria and viruses. In contrast, an allergic reaction is when the immune system reacts to substances (allergens) that are generally harmless and in most people do not cause an immune response. www.immunesupport.com/92fal004.htmAllergies and asthma are inflammatory conditions usually triggered by air- or food-borne pollens and chemicals called "allergens." After these allergens are absorbed into the blood (through the lungs, skin, or intestines), they cause the B cells (white blood cells) of allergy-sufferers to produce billions of molecules of the allergic antibody IgE. The IgE molecules then travel through the bloodstream until they combine to with mast cells or basophils. Mast cells (which line many blood vessels) and basophils (a type of white blood cell circulating in the bloodstream) are the main storage sites for histamine and serotonin. The IgE allergic antibody then causes the cell membranes of the mast cells/basophils to become "leaky, " allowing their storage load of histamine and serotonin to pour into the surrounding blood and tissues. The IgE-released histamine and serotonin then produce the familiar allergic symptoms of runny, swollen nose; blocked sinuses; itchy eyes; skin blotches; coughing and wheezing; etc. www.medicinenet.com/allergy/page2.htmThe aim of the immune system is to mobilize its forces at the site of invasion and destroy the enemy. One of the ways it does this is to create protective proteins called antibodies that are specifically targeted against particular foreign substances. These antibodies, or immunoglobulins (IgG, IgM, IgA, IgD), are protective and help destroy a foreign particle by attaching to its surface, thereby making it easier for other immune cells to destroy it. The allergic person however, develops a specific type of antibody called immunoglobulin E, or IgE, in response to certain normally harmless foreign substances, such as cat dander. IgE is an antibody that all of us have in small amounts. Allergic persons, however, produce IgE in large quantities. Normally, this antibody is important in protecting us from parasites, but not from cat dander or other allergens. During the sensitization period, cat dander IgE is being overproduced and coats certain potentially explosive cells that contain chemicals. These cells are capable of causing an allergic reaction on subsequent exposures to the dander. This is because the reaction of the cat dander with the dander IgE irritates the cells and leads to the release of various chemicals, including histamine. These chemicals, in turn, cause inflammation and the typical allergic symptoms. This is how the immune system becomes misguided and primed to cause an allergic reaction when stimulated by an allergen. Note: IgE is also used for protection from parasites. www.gdx.net/home/assessments/allergy/index.htmlIgE Mediated Allergies Immediate onset (within minutes) Circulating half life of 1-2 days Permanent allergies Stimulates histamine release Includes foods, inhalants & molds IgG Mediated Allergies Delayed onset (4-72 hours) Circulating half life of 21 days Temporary allergies Stimulates histamine release Includes foods, herbs & spices Food Allergies www.gdx.net/home/assessments/allergy/appguide/index.htmlIn the 1930s, Rinkel first described food sensitivities that differed from the classic immediate anaphylactic reactions. The symptoms he described occurred hours or days subsequent to ingestion and could be masked or unmasked by the offending food. Rinkel's discovery has been borne out by recent research confirming that delayed-type food allergies play a primary role in the immune system's response to ingestants. www.medicinenet.com/food_allergy/article.htmHow do allergic reactions to food work? The allergens in food are those components that are responsible for an allergic reaction. They are proteins that usually resist the heat of cooking, the acid in the stomach, and the intestinal digestive enzymes. As a result, the allergens survive to cross the gastrointestinal lining, enter the bloodstream, and go to target organs, causing allergic reactions throughout the body. The mechanism of food allergy involves the immune system and heredity. www.diagnose-me.com/cond/C39005.htmlFood allergy and sensitivity is an important, complex, and often overlooked cause of symptoms and disease. Chasing down the culprits may require the services of a doctor. The incidence and severity of food allergies has increased dramatically during the last 15 years. Some physicians claim that food allergies are the leading cause of most undiagnosed symptoms. Others maintain that at least 60% of the American population suffers from symptoms associated with food reactions. Theories of why the incidence has increased include: * Increased stresses on the immune system (such as greater chemical pollution in the air, water, and food). * Earlier weaning and earlier introduction of solid foods to infants. * Genetic manipulation of plants resulting in food components which cross-react with normal tissues. Causes & Development Repeated exposure, improper digestion and compromised integrity of the intestinal barrier are all factors in the development and maintenance of food allergy. It has been well documented that partially-digested or undigested dietary protein can cross the intestinal barrier intact and be absorbed into the blood stream. The immune system must decide how to deal with this non-self protein. Is it friend or foe? If viewed as an enemy (something that shouldn't be on the inside of the GI tract), an allergic response can occur. This reaction can be localized, systemic, or at specific distant sites. Allergy Symptoms The symptoms of allergies are the symptoms of high histamine levels. There are four known histamine receptors, and each produces it's own range of symptoms. The Three Known Targets of High Histamines en.wikipedia.org/wiki/HistamineHistamine exerts its actions by combining with specific cellular histamine receptors. The four histamine receptors that have been discovered are designated H1 through H4. H1 histamine receptor - Found on smooth muscle, endothelium, and central nervous system tissue. Causes vasodilation, bronchoconstriction, smooth muscle activation, separation of endothelial cells (responsible for hives), and pain and itching due to insect stings; the primary receptors involved in allergic rhinitis symptoms and motion sickness. H2 histamine receptor - Located on parietal cells. Primarily stimulate gastric acid secretion H3 histamine receptor - Decreased neurotransmitter release: histamine, acetylcholine, norepinephrine, serotonin H4 histamine receptor - Found primarily in the thymus, small intestine, spleen, and colon. It is also found on basophils and in the bone marrow. Unknown physiological role. Physical Symptoms - H1 and H2 Reactions Most allergy literature sticks to the well-known physical reactions from the H1 and H2 histamine receptors. When histamine interacts with H1 receptors, it causes the familiar allergic reaction symptoms: inflammation, asthma, sinus trouble, hives, itchy skin, congestion, watery eyes, and runny nose. Interaction with H2 receptors produce the well-documented but less well-known reaction of increasing stomach acidity producing gastric reflux, irritable bowel syndrome, heartburn and constipation. The descriptions below stick mostly to the symptoms of activation of these two histamine receptors. allergies.about.com/cs/symptoms/a/aa020402a.htmSymptoms: • Absentmindedness • Anaphylaxis • Asthma • Burning eyes • Constipation • Coughing • Dark circles under or around the eyes • Dermititis • Depression • Diarrhea • Difficulty swallowing • Distraction, difficulty with concentration • Dizziness • Eczema • Embarrassment • Fatigue • Flushing • Headaches • Heart palpitations • Hives • Impaired sense of smell • Irritability/behavioral problems • Itchy nose and/or throat • Itchy skin • Joint aches • Muscle pains • Nasal congestion • Nasal polyps • Nausea • Postnasal drainage (postnasal drip) • Rapid pulse • Rhinorrhea (runny nose) • Ringing, popping or fullness in the ears • Shortness of breath • Skin Rashes • Sleep difficulties • Sneezing • Swelling (angioedema) • Throat hoarseness • Tingling nose • Tiredness • Vertigo • Vomiting • Watery, itchy, crusty or red eyes • Wheezing www.diagnose-me.com/cond/C39005.htmlFood Allergies Signs & Symptoms Most food reactions are delayed up to several days and are thus more difficult to identify. To further complicate matters, delayed food reactions can be cyclic or fixed in nature. * Cyclic types account for 80+% of food allergies. A sensitivity may slowly develop by repetitive eating of a food. Avoidance for months may result in tolerance again unless eaten too frequently. Such foods may be tolerated every one to four days. * Fixed allergies are sensitivities that occur whenever a food is eaten regardless of the time span between contacts. Signs, symptoms & indicators of Allergy to Foods * Childhood Allergies as a child * Rapid pulse rate * Abdominal Pain * Epigastric pain - The first part of the body to react to food is often the gastrointestinal tract. Sometimes mast cells are involved in allergic reactions and release chemicals such as histamine. If the affected mast cells are in the gastrointestinal tract, a person may suffer vomiting, abdominal pain or diarrhea. * Allergy * Bloating caused by specific foods * Moderate sneezing or frequent sneezing / attacks * Excess mucus * (Very) frequent stools * Bowel movement changes * Heart racing/palpitations * (High) cigarette smoke sensitivity * Craving specific foods * Craving and eating wheat * General flatulence * Meal-related bloating * (Frequent/regular) unexplained nausea * Anal itching or anal itching at night * Chronic fatigue for over 3 months * Dark areas under eyes * Bags under eyes * A swollen tongue * Allergic rhinitis * Afternoon headaches * Low energy/stamina * Frequent colds/flus * Spacey/unreal feelings * Facial burning/tingling - Tingling in the face has been known to be caused by food allergies. For example, several recent cases include this and other symptoms as an allergy to barley after consuming only a small amount of beer. * Discomfort caused by mold/mustiness * Pain/burning behind breastbone - Wheat has been known to be a cause of esophagitis, as have other hidden food allergens. * Chronic productive cough * History of eczema * (Frequent) difficulty falling asleep * Drowsiness after meals Conditions that suggest Allergy to Foods Allergy * Allergic Tension Fatigue Syndrome * Environmental Illness / Multiple Chemical Sensitivity People with multiple chemical sensitivities often have multiple food allergies as well. While reactions to chemicals in the environment are generally quicker and more easily identified, food allergies are usually delayed, making it harder to pinpoint the offending food. People with MCS are often unaware of hidden food allergies which could be contributing to their overall allergic load. Indoor Allergies * Allergic Rhinitis / Hay Fever The ear, nose, and throat are common target organs for food allergens. Congestion or inflammation of the nose (rhinitis) may be due to airborne irritants and allergens, but food allergy may be an undiagnosed cause of this common problem. Diet * Picky-Eater Tendency Food allergies are sometimes addictive in nature, requiring continued consumption of the allergenic food in order to prevent the appearance of withdrawal symptoms. However, eating the same foods over and over increases the likelihood of eventually becoming allergic to them. Digestion * Constipation * Heartburn / GERD / Acid Reflux * IBS (Irritable Bowel Syndrome) The presence of food allergy is concealed in a variety of diagnoses including irritable bowel syndrome. Immunity * Weakened Immune System Food allergies divert some of the immune system's resources away from preventing and dealing with illness. Thus, continuous consumption of a food which is causing symptoms weakens your immune system. A weakened immune system enables infections and cancerous growths to develop and take hold. Many patients report that they suffer from more than one symptom or illness when reintroducing a known food allergen into their diet after a period of abstinence. Metabolic * Migraine/Tension Headaches * Edema (Water Retention) * Bruxism (Clenching/Grinding Teeth) Hidden food allergies may contribute to the chronic clenching of teeth. Musculo-Skeletal * Muscle Pains (Myalgia) Muscle pain can be due to food allergies. Such pains will disappear after elimination of the offending foods from the diet. Respiratory * Asthma Asthma is one of the three manifestations of a pattern of allergy that is called atopy. The associated disorders are eczema and hay fever. Asthma due to allergy can come from both airborne and food sources. Patients with delayed pattern food allergy have the most severe and persistent inflammatory form of chronic asthma. Skin-Hair-Nails * Hives Foods and drugs are common causes of hives. A reaction that occurs immediately after ingestion of certain foods, producing hives and difficulty breathing is termed anaphalactic and is potentially dangerous. Delayed reactions are less serious but more difficult to pinpoint. Some patients get hives occasionally only when they ingest a specific food or food additive. Others develop hives as a chronic problem that can continue for years. Most studies of chronic hives suggest that only a low percentage are due to food allergy; this is usually because diet revision attempts were inadequate for revealing the hidden food causes. Emotional, Behavioral, & Social Symptoms - H3 Reactions When histamine comes into contact with H3 histamine receptors, it causes emotional, behavioral, and social symptoms by reducing levels of several primary neurotransmitters, including serotonin, noradrenaline, dopamine, GABA, and acetylcholine. These can have a profound effect on the way we think, feel, and interact with the world around us. These are less well known in relation to allergies, but can be seen by the large number of antidepressants being prescribed these days. My own reaction to Tramadol and Dextromethorphan (which raise levels of serotonin and norepinephrine back to normal) have been life-changing. Histamine & Neurotransmitter Inhibition en.wikipedia.org/wiki/Histamine_H3_receptorHistamine H3 receptors are expressed in the central nervous system and, to a lesser extent, the peripheral nervous system, where they act as autoreceptors in presynaptic histaminergic neurons, and control histamine turnover by feedback inhibition of histamine synthesis and release as well. The H3 receptor also been shown to presynaptically inhibit the release of a number of other neurotransmitters (i.e. it acts as an inhibitory heteroreceptor) including, but probably not limited to dopamine, GABA, acetylcholine, noradrenaline, and serotonin. Because of its ability to modulate other neurotransmitters, H3 receptor ligands are being investigated for the treatment of numerous neurological conditions, including obesity (because of the histamine/orexinergic system interaction), movement disorders (because of H3 receptor-modulation of dopamine and GABA in the basal ganglia), schizophrenia and ADHD (again because of dopamine modulation) and research is even underway as to whether H3 receptor ligands could be useful in modulating wakefulness (because of effects on noradrenaline, glutamate and histamine). Note: It seems the higher the histamine levels, the lower are key neurotransmitter levels, including serotonin. Serotonin is a neurotransmitter essential for people to be able to experience happiness and human connection. It raises one's mood, diminished anxiety and anger, and physically warms the body. www.bioportfolio.com/LeadDiscovery/PubMed-120407.htmlProgress has however been made in the development of H3 receptor antagonists, notably by researchers at Abbott. A-304121, A-317920 and A-349821 have demonstrated efficacy in animal models, although species differences in receptor binding, poor blood brain barrier penetration and the potential cardiovascular adverse effects have blocked their progress. A new Abbott molecule, ABT-239, looks to be more promising. Esbenshade et al (2005) have reported that this molecule has high affinity and selectivity for human H3 receptors, good oral bioavailability and excellent blood brain barrier penetration. In a second paper Fox et al (2005) report the activity of ABT-239 in various rodent models. Note: This is very interesting. While the effects of Tramadol and Dextromethorphan do great good to me by increasing serotonin and norephinephrine, a drug such as this would stop histamine from turning down the levels of these neurotransmitters in the first place. THEN AGAIN, an antagonist of H3 would also stop histamine from being quietted down, which is one effect I'm quite glad to have. en.wikipedia.org/wiki/SerotoninIn the central nervous system, serotonin is believed to play an important role as a neurotransmitter, in the regulation of anger, aggression, body temperature, mood, sleep, vomiting, sexuality, and appetite. In addition, serotonin is also a peripheral signal mediator. For instance, serotonin is found extensively in the human gastrointestinal tract (about 90%), and the major storage place is platelets in the blood stream. Recent research suggests that serotonin plays an important role in liver regeneration and acts as a mitogen (induces cell division) throughout the body... Pathology Low levels of serotonin may be associated with several disorders, namely increase in aggressive and angry behaviors, clinical depression, obsessive-compulsive disorder (OCD), migraine, irritable bowel syndrome, tinnitus, fibromyalgia, bipolar disorder and anxiety disorders. Histadelia - High Histamine Levels Because not much is mentioned in allergy circles about the emotional, behavioral, and social symptoms of being in a state of high histamine, many people in alternative medicine have stepped forward to describe this state using the term Histadelia (meaning high histamine). Those sources provides a wealth of information on these effects, which match the effects of low serotonin levels (for one) and they match my own experience very well. As I go into an allergic reaction, these symptoms become worse and worse, and as the reaction fades, so do these symptoms. Antihistamines keep the level of these symptoms lower than they would otherwise be, as do medications which rebalance the neurotransmitters involved. Unlike Histadelia, which is a constant state of high histamine levels, those with allergies have histamine levels that range up and down depending on exposure to allergens. Those with a large number of allergies probably live a lot of the time in a Histadelic state, such that their personality is often associated with these symptoms. You wont find Histadelia mentioned in many of the more scientific sources out there, including MayoClinic.com, WebMD.com, the National Library of Medicine, or even Wikipedia. The scientific community seem to prefer to look at it as schizophrenia caused by very low or very high histamine levels, which is what we'll look at after this section. www.drkaslow.com/html/histadelia.htmlIndividuals with high-histamine levels may be due to a metabolic imbalance that results from under-methylation. As a consequence, these individuals overproduce and retain excessive levels of histamine. Histamine is a substance in the body that has wide ranging effects. There are receptors for histamine in the brain, stomach, skin, lungs, mucus membranes, blood vessels, etc. For some individuals, high levels of blood histamine (called histadelia) have psychological, behavioral, and cognitive symptoms. Many patients with obsessive-compulsive tendencies, "oppositional-defiant disorder," or seasonal depression are under-methylated, which is associated with low serotonin levels. Often with inhalant allergies, frequent headaches, perfectionism, competitiveness and other distinctive symptoms and traits. Tend to be very low in calcium, magnesium, methionine, and vitamin B-6 with excessive levels of folic acid. People with histadelics have a positive effect from SSRIs and other serotonin-enhancing medications (Paxil, Zoloft, Prozac, Celexa, Effexor, etc.) because methylation is a step in the manufacture of mood stabilizing neurotransmitters. Unfortunately, histadelics often have nasty side effects with these medications. Histamine excess can be manifest as asthma, vasomotor rhinitis, allergic skin disorders with pruritis, excess stomach acid production (acts as a gastric hormone to stimulate flow of HCl), saliva, tears, and thin nasal and bronchial secretions, and certain types of vascular headaches. This is the basis of anti-histamine medications. Excessive histamine results because of the inadequate methylation in liver detoxification. Histamine opposes adrenalin in its effects and as expected fatigue occurs just as it occurs in adrenal exhaustion. Note: This says that the low serotonin levels are caused by under-methylation, which also produces high histamine levels. Whether this is true or not I dont know, but we do know that low serotonin levels can be brought about as a result of histamine interacting with H3. www.diagnose-me.com/cond/C447056.htmlHistadelia, more common in males, is characterized by elevated blood levels of histamine. It is estimated that 15-20% of schizophrenics are probably histadelic. This is a disorder, prominent in males, of too much histamine in the blood, as opposed to histapenia in which case there is too little. Signs & Symptoms Symptoms include hyperactivity, compulsions, obsessions, inner tensions, blank mind episodes, phobias, chronic depression, and strong suicidal tendencies. Physical signs can include little tolerance for pain, rapid metabolism, lean build, profuse sweating, seasonal allergies, and frequent colds. Symptoms Info Excess mucus Histamine can cause additional mucus production. Good tolerance of cold Poor tolerance of heat Unexplained nausea Poor pain tolerance Excess / abundant saliva in mouth Hyperactivity Histamine speeds up metabolism producing a tendency towards hyperactivity. Frequent colds / flus Phobias Being highly motivated Those with elevated histamine (histadelics) tend to work compulsively. A hard-driving personality Histadelics tend to work compulsively. Good creativity / imagination Histadelics are often highly creative. Strong sexual desire Joint pain / swelling / stiffness Excess perspiration Warm skin Allergic Rhinitis / Hay Fever Depression Histadelics are often chronically and suicidally depressed. Obsessive-Compulsive Disorder (OCD) Histadelics are often prone to obsessions, compulsions, and addictions. Addictions / Addictive Tendencies Nutritional treatment for drug and alcohol users will depend on the results of a test for blood histamine levels. In one series of such analysis, all users proved to have high histamine levels, leading the scientist to conclude that this abnormality - with its impact on brain function - is a major force in creating addiction. Headaches Insomnia The overarousal seen in histadelia may contribute to insomnia. Muscle Pains (Myalgia) Skeletal Slender fingers / toes Histadelics often have long fingers and toes. www.nutrition4health.org/nohanews/NNSp97NutrientsDepression.htmHistadelic depressives have a particular imbalanced amino-acid cycle, which results in low levels of serotonin and elevated histamine. Histadelics often exhibit obsessive-compulsive tendencies, perfectionism, seasonal allergies, easy tears, high libido, and headaches. They have addictive tendencies with a high incidence of alcoholism, drug abuse, anorexia, and bulimia. They often are diagnosed with seasonal affective disorder which is most serious during Fall and Winter. The decisive chemical test for this condition is whole blood histamine. Note: Another alternate explanation for high histamine, but with the same symptoms. www.nutrition4health.org/NOHAnews/NNS91BiochemTreatment.htmHistadelia represents the chemical antithesis of histapenia in that it involves elevated blood histamine. This condition (involving about 20 percent of schizophrenics) is characterized by delusions, severe depression, obsessive/compulsive behavior, and blank-mindedness, and often results in a diagnosis of schizo-affective disorder. Allergy-Triggered "Simple Schizophrenia" The results of H3 histamine reaction as a result of allergies is still coming into focus. While alternative medicine calls it histadelia, mainstream science calls it, somewhat inaccurately, schizophrenia. First things first - don't be scared off by the term schizophrenia. Schizophrenia is used to describe a surprisingly wide variety of mental states (as you will see), and is often criticized for this very reason. Hollywood often mistakenly portrays schizophrenia with multiple personality disorder, but the two have nothing in common. What we're describing here adds nothing new except a name used in psychiatry, which we can use to find out more information. Schizophrenia was known for a long time before it was new discoveries that showed that about 50% of schizophrenics have very high or low levels of histamine. With treatments that bring histamine levels back to normal, people suffering histamine-based schizophrenia were able to recover from their illness. The schizophrenia related to high histamine levels (or histadelia) is, from what I can tell, known as "simple schizophrenia" - one that lacks the well-known delusional symptoms and focuses on what are called the "negative" symptoms - which are those related to suppression (or negating) of normal traits. From my own experiences, it appears that at periods of high histamine levels, I go into what I would call Allergy-Triggered Simple Schizophrenia which is emotional deadness, flat affect, poverty of speech, inability to feel pleasure, lack of motivation, depression and impairment of social cognition. Low-level obsessive behavior is sometimes a result of these high histamine episodes, too. The symptoms are such a departure from the classic schizophrenia, and completely lacking in any positive symptoms (aside from mild obsessive-compulsive behavior) that it should really be considered something else entirely. Since the literature has yet to come up with a better term, and is full of connections using the old term, I've included some of the information. The following describes the broad definition of schizophrenia. en.wikipedia.org/wiki/SchizophreniaPositive and negative symptoms Schizophrenia is often described in terms of positive (or productive) and negative (or deficit) symptoms. Positive symptoms include delusions, auditory hallucinations , and thought disorder, and are typically regarded as manifestations of psychosis. Negative symptoms are so-named because they are considered to be the loss or absence of normal traits or abilities, and include features such as flat or blunted affect and emotion, poverty of speech (alogia), anhedonia, and lack of motivation (avolition). Despite the appearance of blunted affect, recent studies indicate that there is often a normal or even heightened level of emotionality in Schizophrenia especially in response to stressful or negative events. A third symptom grouping, the disorganization syndrome, is commonly described, and includes chaotic speech, thought, and behaviour. There is evidence for a number of other symptom classifications. Subtypes Historically, schizophrenia in the West was classified into simple, catatonic , hebephrenic (now known as disorganized), and paranoid. The DSM contains five sub-classifications of schizophrenia: * paranoid type: where delusions and hallucinations are present but thought disorder, disorganized behavior, and affective flattening are absent (DSM code 295.3/ICD code F20.0) * disorganized type: named 'hebephrenic schizophrenia' in the ICD. Where thought disorder and flat affect are present together (DSM code 295.1/ICD code F20.1) * catatonic type: prominent psychomotor disturbances are evident. Symptoms can include catatonic stupor and waxy flexibility (DSM code 295.2/ICD code F20.2) * undifferentiated type: psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types have not been met (DSM code 295.9/ICD code F20.3) * residual type: where positive symptoms are present at a low intensity only (DSM code 295.6/ICD code F20.5) The ICD-10 recognises a further two subtypes: * post-schizophrenic depression: a depressive episode arising in the aftermath of a schizophrenic illness where some low-level schizophrenic symptoms may still be present (ICD code F20.4) * simple schizophrenia: insidious but progressive development of prominent negative symptoms with no history of psychotic episodes (ICD code F20.6 ) This following is ALL very good: www.nmrc.ca/schizophrenia.htmHistamine Imbalance What is histamine and why is it so important? Carl Pfeiffer studied more than 20,000 people with schizophrenia and determined that 90% of them fell into three bio-chemical subgroups: high histamine, low histamine, and pyrroluria - hence the term "The Schizophrenia's" (Pfeiffer, 1970; Walsh, 1997b). Histamine is integral in balancing the electrical activity of the nucleus accumbens, which is an area of the brain responsible for behavioral responses, filtering incoming sensory information, and communicating with the hypothalamus, ventral tegmentum, and amygdala (Shoblock & O'Donnell, 2000; Otake & Nakamura, 2000; Chronister et al, 1982). A plethora of research has determined that people with schizophrenia have poor ability to filter incoming sensory information. It has also been reported that 15-20 % of people with schizophrenia have high whole blood histamine levels and another 30-40 % of people with schizophrenia have low whole blood histamine levels (Heleniak, 1999; Pfeiffer, 1988; Heleniak, 1985; Chronister & DeFrance, 1982; Rauscher et al, 1977; Pfeiffer, 1972a). A person with schizophrenia who has high histamine is under-methylated (Walsh, PTC- Ref. B; Heleniak & Frechen, 1989). A person with schizophrenia who has low histamine is over-methylated (Walsh, PTC- Ref.B; Heleniak & Frechen, 1989). Taking detailed patient histories is key (Jackson et al, 1998; Edelman, 1996; Jaffe & Kruesi, 1992; Pfeiffer, 1988; Walsh, PTC- Ref.B). People with high histamine have been found with typical symptoms of high intelligence, thought blanking, low grade hallucinations and thought disorder, perfectionism, competitiveness, obsessions, compulsions, suicidal and seasonal depression, defiance, and phobia. High histamine individuals have low serotonin levels and therefore usually benefit from drugs that increase serotonin such as Zoloft, Prozac, and Paxil (Walsh, PTC- Ref.B). High histamine individuals typically have a history of seasonal allergies. High histamine individuals are inherently high in folic acid. Although folic acid is used along with B-12 in the production of methionine it is also involved in histamine production along with B-12. Consequently B-12 and folic acid are strictly avoided in high histamine patient care. These patients need to avoid multi-vitamins. People with low histamine have been found with typical symptoms of under-achievement, more severe thought disorder and hallucinations, paranoid thoughts with less pronounced obsessions, suicidal depression, cyclic or suicidal depression, and anxiety (Jackson et al, 1998; Edelman, 1996; Jaffe & Kruesi, 1992; Pfeiffer, 1988; Walsh, PTC- Ref.B). Excess copper and zinc deficiency, discussed below under heavy-metal overload, are typical low histamine traits that need to be adressed (Sandstead, 1994; Wallwork, 1987; Pfeiffer & Braverman, 1982; Walsh, PTC- Ref.B).
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Post by fritolay66 on Mar 23, 2009 0:54:32 GMT -5
Abandoning the Term: Schizophrenia en.wikipedia.org/wiki/SchizophreniaDiagnostic issues and controversies Schizophrenia as a diagnostic entity has been criticised as lacking in scientific validity or reliability, part of a larger criticism of the validity of psychiatric diagnoses in general. One alternative suggests that the issues with the diagnosis would be better addressed as individual dimensions along which everyone varies, such that there is a spectrum or continuum rather than a cut-off between normal and ill. This approach appears consistent with research on schizotypy and of a relatively high prevalence of psychotic experiences and often non-distressing delusional beliefs amongst the general public. Another criticism is that the definitions used for criteria lack consistency; this is particularly relevant to the evaluation of delusions and thought disorder. More recently, it has been argued that psychotic symptoms are not a good basis for making a diagnosis of schizophrenia as "psychosis is the 'fever' of mental illness — a serious but nonspecific indicator". Perhaps because of these factors, studies examining the diagnosis of schizophrenia have typically shown relatively low or inconsistent levels of diagnostic reliability. Most famously, David Rosenhan's 1972 study, published as On being sane in insane places, demonstrated that the diagnosis of schizophrenia was (at least at the time) often subjective and unreliable.[26] More recent studies have found agreement between any two psychiatrists when diagnosing schizophrenia tends to reach about 65% at best. This, and the results of earlier studies of diagnostic reliability (which typically reported even lower levels of agreement) have led some critics to argue that the diagnosis of schizophrenia should be abandoned... In 2006, campaigners in the UK, under the banner of Campaign for Abolition of the Schizophrenia Label, argued for a similar rejection of the diagnosis of schizophrenia and a different approach to the treatment and understanding of the symptoms currently associated with it Symptoms of Low Serotonin We can also look directly at the effects of H3 receptor activation, which is the reduction of serotonin, norepinephrine, dopamine, GABA, and acetylcholine. www.enotalone.com/article/4116.htmlSerotonin, first isolated in 1933, is the neurotransmitter that has been identified in multiple psychiatric disorders including depression, obsessive-compulsive disorder, anorexia, bulimia, body dysmorphic disorder (nose doesn't look perfect after ten surgeries), social anxiety, phobias, etc. Serotonin is a major regulator and is involved in bodily processes such as sleep, libido (sexual interest), body temperature, and other areas. When we find ourselves living in a high stress situation for a prolonged period of time, we use more Serotonin than is normally replaced. Imagine a list of your pressures, responsibilities, difficulties and environmental issues (difficult job, bad marriage, poor housing, rough neighborhood, etc.). Prolonged exposure to such a high level of stress gradually lowers our Serotonin level. As we continue to "hang on" we develop symptoms of a severe stress-produced depression. When Serotonin is low, we experience problems with concentration and attention. We become scatterbrained and poorly organized. Routine responsibilities now seem overwhelming. It takes longer to do things because of poor planning. We lose our car keys and put odd things in the refrigerator. We call people and forget why we called or go to the grocery and forget what we needed. We tell people the same thing two or three times. When Serotonin is moderately low, we have the following symptoms and behaviors: · Chronic fatigue. Despite sleeping extra hours and naps, we remain tired. There is a sense of being "worn out" · Sleep disturbance, typically we can't go to sleep at night as our mind/thought is racing. Patients describe this as "My mind won't shut up!" Early-morning awakening is also common, typically at 4:00 am, at which point returning to sleep is difficult, again due to the racing thoughts. · Appetite disturbance is present, usually in two types. We experience a loss of appetite and subsequent weight loss or a craving for sweets and carbohydrates when the brain is trying to make more Serotonin. · Total loss of sexual interest is present. In fact, there is loss of interest in everything, including those activities and interests that have been enjoyed in the past. · Social withdrawal is common – not answering the phone, rarely leaving the house/apartment, we stop calling friends and family, and we withdraw from social events. · Emotional sadness and frequent crying spells are common. · Self-esteem and self-confidence are low. · Body sensations, due to Serotonin's role as a body regulator, include hot flushes and temperature changes, headaches, and stomach distress. · Loss of personality – a sense that our sense of humor has left and our personality has changed. · We begin to take everything very personally. Comments, glances, and situations are viewed personally and negatively. If someone speaks to you, it irritates you. If they don't speak, you become angry and feel ignored. · Your family will have the sense that you have "faded away". You talk less, smile less, and sit for hours without noticing anyone. · Your behavior becomes odd. Family members may find you sitting in the dark in the kitchen at 4:00 am. When Serotonin is severely low, you will experience some if not all of the following: · Thinking speed will increase. You will have difficulty controlling your own thoughts. The brain will focus on torturing memories and you'll find it difficult to stop thinking about these uncomfortable memories or images. · You'll become emotionally numb! You wouldn't know how you feel about your life, marriage, job, family, future, significant other, etc. It's as though all feelings have been turned off. Asked by others how you feel – your response might be "I don't know!" · Outbursts will begin, typically two types. Crying outbursts will surface, suddenly crying without much warning. Behavioral outbursts will also surface. If you break the lead in a pencil, you throw the pencil across the room. Temper tantrums may surface. You may storm out of offices or public places. · Escape fantasies will begin. The most common – Hit the Road! The brain will suggest packing up your personal effects and leaving the family and community. · Memory torture will begin. Your brain, thinking at 100 miles an hour, will search your memories for your most traumatic or unpleasant experiences. You will suddenly become preoccupied with horrible experiences that may have happened ten, twenty, or even thirty years ago. You will relive the death of loved ones, divorce, childhood abuse – whatever the brain can find to torture you with – you'll feel like it happened yesterday. · You'll have Evil Thoughts. New mothers may have thoughts about smothering their infants. Thoughts of harming or killing others may appear. You may be tortured by images/pictures in your memory. It's as though the brain finds your most uncomfortable weak spot, then terrorizes you with it. · With Serotonin a major bodily regulator, when Serotonin is this low your body becomes unregulated. You'll experience changes in body temperature, aches/pains, muscle cramps, bowel/bladder problems, smothering sensations, etc. The "Evil Thoughts" then tell you those symptoms are due to a terminal disease. Depressed folks never have gas – it's colon cancer. A bruise is leukemia. · You'll develop a Need-for-Change Panic. You'll begin thinking a change in lifestyle (Midlife Crisis!), a divorce, an extramarital affair, a new job, or a Corvette will change your mood. About 70 percent of jobs are lost at this time as depressed individuals gradually fade away from their life. Most extramarital affairs occur at this time. · As low Serotonin levels are related to obsessive-compulsive disorders, you may find yourself starting to count things, become preoccupied with germs/disease, excessively worry that appliances are turned off or doors locked, worry that televisions must be turned off on an even-numbered channel, etc. You may develop rituals involving safety and counting. One auto assembly plant worker began believing his work would curse automobiles if their serial number, when each number was added, didn't equal an even number. · Whatever normal personality traits, quirks, or attitudes you have, they will suddenly be increased three-fold. A perfectionist will suddenly become anxiously overwhelmed by the messiness of their environment or distraught over leaves that fall each minute to land on the lawn. Penny-pinchers will suddenly become preoccupied with the electric and water consumption in the home. · A "trigger" event may produce bizarre behavior. Already moderately low in Serotonin, an animal bite or scratch may make you suddenly preoccupied with rabies. A media story about the harmful effects of radiation may make you remember a teenage tour of the local nuclear power plant – suddenly feeling all your symptoms are now the result of exposure to radiation. www.nutritional-healing.com.au/content/articles-content.php?heading=Serotonin%20deficiency Serotonin deficiency signs/symptoms: * Depressed * Nervous/anxious * Worrier * Fears/phobias * Negative/pessimistic * Irritable/impatient/edgy * Obsessive compulsive tendency * Think about the same things over & over again * Self destructive or suicidal thoughts/plans * Low self esteem/confidence * Rage/anger/explosive behavior/assaultive * Sleep problems/light sleeper * Feel worse in & dislike dark weather * Crave sugar/carbohydrates/alcohol/marijuana o Use these substances to improve mood & relax * Chronic pain ( e.g. headaches, backaches, fibromyalgia) * PMS * Antidepressants or 5-HTP improve mood * Family history of depression/anxiety/OCD/eating disorders www.diagnose-me.com/cond/C14113.htmlLow Serotonin Level • Having a CFS diagnosis • Having a fibromyalgia diagnosis • Emotional instability • Being a light sleeper • Migraine/Tension Headaches • Depression - Serotonin levels can dictate if you feel depressed or not. Antidepressant medications like Paxil, Zoloft, St. John's Wort, and Prozac work by preventing serotonin destruction and loss. These antidepressants inhibit serotonin uptake (or reuptake) by the neurons in the brains. Low serotonin levels cause depression. • Serotonin levels are often low among people with anxiety disorders. • Obsessive-Compulsive Disorder (OCD) - Although the exact cause is not known, experts believe that OCD may be caused by low levels of a chemical in the brain called serotonin. • Sugar craving • Bulimic Tendency • Problems Caused By Being Overweight • Restless Leg Syndrome • Inability to recover from alcoholism or being a recovering alcoholic www.doctormurray.com/conditions/Migraine_Headache.aspWhat causes Migraine Headache? Considerable evidence supports an association between migraine headache and instability of blood vessels. The mechanism of migraine can be described as a three-stage process: initiation, prodrome (time between initiation and appearance of headache), and headache. Although a particular stressor may be associated with the onset of a specific attack, it appears that initiation is dependent on the accumulation of several stressors over time. These stressors ultimately affect serotonin metabolism. Once a critical point of susceptibility (or threshold) is reached, a "cascade event" is initiated that sets in process a domino-like effect that ultimately produces a headache. Food allergies, histamine-releasing foods, alcohol (especially red wine), stress, hormonal changes ( e.g., menstruation, ovulation, birth-control pills) and weather changes especially barometric pressure changes are examples of some common triggers of migraines. What dietary factors are important in Migraine Headache? Food allergy or sensitivity plays a primary role in many cases of tension and migraine headaches. Many double-blind, placebo-controlled studies have demonstrated that the detection and removal of allergenic foods will eliminate or greatly reduce headache symptoms in the majority of patients. Food allergy/intolerance induces a migraine attack largely as a result of platelets releasing serotonin and histamine. In addition, foods such as aged cheeses, beer, canned figs, chicken liver, chocolate, food additives, pickled fish, the pods of broad beans, wine, and Brewer's yeast contain histamine, tyramine and/or other compounds that can trigger migraines in sensitive individuals by causing blood vessels to expand. Red wine is much more likely than white wine to cause a headache because it contains higher levels of phenols and 20-to-200 times as much histamine. 5-Hydroxytryptophan (5-HTP) has been shown to be as effective as drug therapy, but may be safer. 5-HTP is the direct building block for serotonin. Because migraine sufferers have low levels of serotonin in their tissues, this led researchers to refer to migraine as a "low-serotonin syndrome." Low serotonin levels are thought to lead to a decrease in the pain threshold in patients with chronic headaches. This contention is strongly supported by over thirty-five years of research, including positive clinical results in double-blind studies with the serotonin precursor 5-hydroxytryptophan (5-HTP). The recommended dosage is 50 to 100 mg daily in adults and 5 mg per 2.2 pounds of body weight in children. Symptoms of Low Norepinephrine www.enotalone.com/article/4117.htmlLow levels of norepinephrine are associated with a loss of alertness, poor memory, and depression. Norepinephrine appears to be the neurotransmitter of "arousal" and for that reason, lower-than-normal levels of this neurotransmitter produce below-average levels of arousal and interest, a symptom found in several psychiatric conditions including depression and ADHD. It is for this reason that medications for depression and ADHD often target both dopamine and norepinephrine in an attempt to restore both to normal level. Note: While I've put a lot of attention into serotonin, norepiniephrine is also a neutransmitter diminished by histamine, and I certainly feel these effects as well. Symptoms of Low Dopamine www.enotalone.com/article/4115.htmlDopamine in the thinking areas of the brain might be considered the neurotransmitter of focus and attending. Low levels impair our ability to focus on our environment or to “lock on” to tasks, activities, or conversations. Low levels of Dopamine make concentration and focus very difficult with low levels also associated with Attention-Deficit Hyperactivity Disorder (ADHD). Symptoms of Low GABA www.enotalone.com/article/4118.htmlLow levels of GABA are associated with Bipolar Disorder, Mania. With GABA levels below average, the brain is too stimulated. We begin talking rapidly, staying up for days at a time, and develop wild and grandiose ideas. In a Manic state, we are so “high” and out of control that social problems are quick to develop, often due to hypersexuality, excessive spending, reckless decisions, risk-taking behavior, and grandiose ideas. We may feel so good that we think we are a heavenly spirit, an intellectual genius, or possessing extraordinary powers. I personally had one patient who locked himself in his mobile home and spent one week rewriting the New Testament in “hillbilly”. Another, with limited education, began purchasing books on the Theory of Relativity by Albert Einstein, sensing he may be able to use the information to invent “warp drive”. Low levels of GABA are also associated with problems of poor impulse control, including clinical conditions such as gambling, temper tantrums, and stealing. When GABA is low in the brain, impulsive behaviors are not inhibited (stopped) by logical or reasonable thinking. Symptoms of Low Acetylcholine I had a hard time finding information on low acetylcholine, except the following, which associates it with muscle weakness and fatigue. en.wikipedia.org/wiki/AcetylcholineAssociated disorders ACh Receptor Agonists are used to treat myasthenia gravis and Alzheimer's disease. Myasthenia gravis The disease myasthenia gravis, characterized by muscle weakness and fatigue.... A New Social Archetype Incidence of allergies in the world have been on the rise for decades, as are symptoms that are likely related to the neurological effects of high histamine levels - depression, ADHD, OCD, and several others. Use of antidepressants is rising, as well, and it is likely much of this is a result of the rising allergy levels and lack of awareness or treatment for the emotional/behavioral H3 receptor reactions that go along with it. These problems are prevalent enough to be shaping society, and have produced a new stereotype. Look again at the symptoms of high histamine levels: excess mucus, excess saliva, excess perspiration, frequent colds, phobias, being highly motivated, compulsive working, perfectionist, good creativity and imagination, strong sexual desire, joint pain, runny nose, depression, headaches, muscle pain, poor pain tolerance, slender fingers and toes, hyperactivity, and social isolation. Are you starting to get the picture? Have you known anyone who fits this description? Physically, this person is thin with bony fingers. He is sniffling, sweaty, often sick, and more often than not male. He is competitive, motivated, hard-working perfectionist, who excels at school. His headaches, allergies, low pain threshhold, and joint pain make him uninterested in sports and physical activity. He is creative and enjoys fantasy such as video games, comics, or role playing games. Yet his fears, depression, hyperactivity, and OCD behavior make him antisocial. He has a high sex drive but is too awkward to form relationships. You probably know several people like this. People with these characteristics are called nerds, dweebs, and geeks in high school. They are awkward, unpopular, and not physically active, but really smart and good at difficult but logical subjects. During my first allergy episode, I went from a fairly popular class clown to someone who had difficulties in social situations. I became obsessed with a video game and played it ceaselessly. After the years of allergy shots I became much more social and outgoing again. And now, in this new, far worse allergic crisis, the same has happened again. In the last few years I have found myself shying from social engagements because it's hard to interact with people, and I am obsessed with a new video game. Allergy Causes Environmental Allergies www.aafa.org/display.cfm?id=9&cont=79Like baldness, height and eye color, the capacity to become allergic is an inherited characteristic. Yet, although you may be born with the genetic capability to become allergic, you are not automatically allergic to specific allergens. Several factors must be present for allergic sensitivity to be developed: • The specific genes acquired from parents. • The exposure to one or more allergens to which you have a genetically programmed response. • The degree and length of exposure. www.personalhealthzone.com/disease/allergies/allergycauses.html• Allergies seem to have some link to heredity. (If both your parents have them, it's more likely you'll develop them.) • There is some belief that babies, who are not breastfed, are more predisposed to developing allergies. • A depressed immune system can encourage the development of allergies. Food Allergies www.healingdaily.com/conditions/allergies.htmFood allergies and 'leaky gut' The most common cause of multiple food allergies, according to many allergies experts, is having a 'leaky gut' - increased intestinal permeability. Small openings can develop in the lining of the intestine, which allow large molecules of undigested or incompletely digested foods to enter the bloodstream. The liver is the main organ inside the human body whose function is to process substances which are "foreign" to our body and to make them "friendly". If the quantity of incompletely digested foods which enters the bloodstream is too great for the liver to 'clear' almost immediately, the immune system then recognizes these molecules as being foreign to the body and produces antibodies against them. When the food is eaten again and again and passes into the bloodstream undigested or only partially digested, the antibodies bind with the food. These antibody-food complexes can travel through the bloodstream to any part of the body where they then cause problems. There are many causes of 'leaky gut'. Babies for example are born with higher intestinal permeability than older children or adults. Therefore, ideally infants should consume only breast milk for the first several months of life and other foods should be introduced cautiously. If breast feeding is not possible, a completely hydrolyzed formula such as "Nutramigen" should be used because it is already broken down into simple sugars, free amino acids, and other very small units. Cow’s milk is highly allergenic and should not be given to babies. Neither should soy formula. Internal factors in a patient's body can cause or contribute to a leaky gut. These include nutritional deficiencies, inflammatory bowel disease, poor digestion, and food allergies. There is a vicious cycle involved with these internal factors since the leaky gut also causes them or contributes to their severity. Finally, unfriendly organisms present in the digestive tract can cause increased intestinal permeability. These infections can involve protozoan parasites, yeasts such as Candida albicans, bacteria which are conventionally considered “pathogens” such as Salmonella or an overgrowth of bacteria usually considered nonpathogenic, such as Klebsiella or Pseudomonas. Hence the importance of maintaining a healthy intestinal flora. Parasitic infestations are on the increase because of changes in our lifestyles which have occurred over the last few decades. International travel is now commonplace. If you are not a traveler, the world and its parasites will come to you, brought in by imported produce from countries where sanitation is sub-standard. A common cause of bacterial or fungal problems in the intestine is often the repeated or long term use of antibiotics. Antibiotics kill both the bacteria you want them to kill AND the 'friendly' bacteria in the intestine. This leaves these areas open to be colonized by unfriendly bacteria, yeast, and parasites. Alcoholic beverages, nonsteroidal anti-inflammatory drugs - NSAIDs - (aspirin, ibuprofen, ketoprofen, naproxen, prescription arthritis medications, etc) cause increased intestinal permeability and can compound the problem of 'leaky gut' and contribute to food allergies.. Note: During the period when my symptoms got really really bad, I was taking 4 Advil or Aleve every day for several months. I am fairly confident this led to enough intestinal permeability, and is likely the cause of my food allergies. Organophosphates & Allergies I include this section because when I was growing up, I probably ingested tons of organophosphates. I lived in a rural area, literally surrounded on all sides by sod fields which were regularly sprayed with organophosphates. Our water source was a well. www.deploymentlink.osd.mil/deploymed/projectDetail.jsp?projectId=903&agency=3The central nervous system (CNS) and the immune system communicate bidirectionally, and cholinergic agents modulate the immune system. Organophosphates, such as the nerve gas sarin, are powerful irreversible inhibitors of cholinesterases (ChEs) and might cause neurotoxicity, seizures, and death. Because of the ease and low cost of production, sarin gas is a tool of mass destruction in the hands of terrorist groups and rogue nations. Even a subclinical dose of sarin causes subtle changes in the brain. Increasing evidence suggests that the major health effects of sarin are primarily through its effects on the central nervous system (CNS). Although unsubstantiated, subclinical exposure of Gulf War veterans to sarin has been implicated in the development of the Gulf War Syndrome (GWS). Interestingly, the symptoms of GWS are similar to diseases that result from impaired immune/inflammatory responses and include muscle fatigue, general malaise, myalgia, impaired cognition, ataxia, headaches, fever, joint pain, skin rash, gastrointestinal and sleep disturbances, and respiratory difficulties. Our preliminary experiments show that repeated exposure to low doses of sarin (0.2-0.4 mg/m 3 ) for 5 days suppressed T cell proliferation to mitogens and antigens and inhibited the T cell antigen receptor (TCR)-induced rise in intracellular Ca 2+ concentration. en.wikipedia.org/wiki/CholinesterasesCholinesterase is an enzyme which catalyzes the hydrolysis of the neurotransmitter acetylcholine into choline and acetic acid, a reaction necessary to allow a cholinergic neuron to return to its resting state after activation. Fungal Infections & Chronic Sinusitis www.sciencedaily.com/releases/1999/09/990910080344.htmMayo Clinic Study Implicates Fungus As Cause Of Chronic Sinusitis Sept. 10, 1999 "We can now begin to treat the cause of the problem instead of the symptoms" ROCHESTER, MINN. -- Mayo Clinic researchers say they have found the cause of most chronic sinus infections -- an immune system response to fungus. They say this discovery opens the door to the first effective treatment for this problem, the most common chronic disease in the United States. An estimated 37 million people in the United States suffer from chronic sinusitis, an inflammation of the membranes of the nose and sinus cavity. Its incidence has been increasing steadily over the last decade. Common symptoms are runny nose, nasal congestion, loss of smell and headaches. Frequently the chronic inflammation leads to polyps, small growths in the nasal passages which hinder breathing. "Up to now, the cause of chronic sinusitis has not been known," say the Mayo researchers: Drs. David Sherris, Eugene Kern and Jens Ponikau , Mayo Clinic ear, nose and throat specialists. Their report appears in the September issue of the journal Mayo Clinic Proceedings. "Fungus allergy was thought to be involved in less than ten percent of cases," says Dr. Sherris. "Our studies indicate that, in fact, fungus is likely the cause of nearly all of these problems. And it is not an allergic reaction, but an immune reaction." The researchers studied 210 patients with chronic sinusitis. Using new methods of collecting and testing mucus from the nose, they discovered fungus in 96 percent of the patients' mucus. They identified a total of 40 different kinds of fungi in these patients, with an average of 2.7 kinds per patient. In a subset of 101 patients who had surgery to remove nasal polyps, the researchers found eosinophils (a type of white blood cell activated by the body's immune system) in the nasal tissue and mucus of 96 percent of the patients. The results, the researchers say, clearly portray a disease process in which, in sensitive individuals, the body's immune system sends eosinophils to attack fungi and the eosinophils irritate the membranes in the nose. As long as fungi remain, so will the irritation. "This a potential breakthrough that offers great hope for the millions of people who suffer from this problem," says Dr. Kern. "We can now begin to treat the cause of the problem instead of the symptoms." More research is underway at Mayo Clinic to confirm that the immune response to the fungus is the cause of the sinus inflammation. The researchers are also working with pharmaceutical companies to set up trials to test medications to control the fungus. They estimate that it will be at least two years before a treatment will be widely available. The researchers distinguish chronic sinusitis -- sinusitis that lasts three months or longer -- from acute sinusitis, which lasts a month or less. They say that the cause of the acute condition is usually a bacterial infection. Antibiotics and over-the-counter decongestants are widely used to treat chronic sinusitis. In most cases, antibiotics are not effective for chronic sinusitis because they target bacteria, not fungi. The over-the-counter drugs may offer some relief of symptoms, but they have no effect on the inflammation. "Medications haven't worked for chronic sinusitis because we didn't know what the cause of the problem was," says Dr. Ponikau. "Finally we are on the trail of a treatment that may actually work." Thousands of kinds of single-cell fungi (molds and yeasts) are found everywhere in the world. Fungal spores (the reproductive part of the organism) become airborne like pollen. Some people develop allergies to fungi. The new evidence from the Mayo study suggests that many people also develop a different kind of immune system response. Note: It seems from what I read that it was found that most people have fungi in their sinuses, which seemed to cast doubt on this as a source of the problem. Allergies & Chronic Fatigue Syndrome en.wikipedia.org/wiki/Chronic_fatigue_syndromeAllergies Similarly to the theory of immune dysfunction, some doctors believe that CFS patients suffer from immune dysfunction caused by exposure to allergens, ranging from food allergies or food intolerances (see below) to pollen and dander allergies. However, this theory fails to explain the many reported and documented cluster outbreaks of CFS, and is therefore not taken seriously by leading researchers in the field. Instead, severe allergies may occasionally cause CFS-like symptoms, or patients with CFS may develop additional problems with allergies or food intolerances, which is common. However, there is no evidence that allergies are at the root of CFS... Allergy identification and treatment In cases where CFS-like symptoms may be caused by allergies, enzyme deficiencies or food intolerance, such as chronic sinusitis , coeliac disease, or irritable bowel syndrome, allergy testing, treatments, or elimination diets may prove beneficial. Since some CFS patients show decreased immune response or symptoms of MLS, pre-existing mild allergies may increase to harmful levels after CFS onset. Some studies suggest that a form of CFS may be triggered by a rare reaction to dental metals. Tests in Sweden showed that 76% of CFS patients who tested positive to metal allergy and swapped metal fillings for ceramic substitute achieved partial or full health improvement. Metal allergy can be detected by a blood test named MELISA... A study found that while exercise worsened symptoms in CFS patients, it also increased allergen challenge response only in the CFS group, regardless of allergy status. www.nationaljewish.org/news/y1998/news118.aspxCFS is defined as six months of fatigue that interferes with daily functioning with no other disease being identified. (Depending on the way CFS is defined, between 13 and 300 people in every 100,000 have the disease.) Symptoms include swollen lymph nodes, sore throat, muscle and joint aches, cognitive problems, headaches and sleep difficulties followed by an increase of symptoms 24 hours after exercise. Researchers have looked at a number of chemical changes in the body as a signal of CFS, but Dr. Jones found that "the only consistent finding is allergy." Seventy-five percent of people with CFS have allergies; 10 to 20 percent of the general population has allergies. www.aafp.org/afp/20020315/1083.htmlGiven the association between CFS and allergies, there is a strong possibility that allergies are essential to the pathology of CFS. Not only do patients with CFS present with positive skin tests to allergens, but they also have elevated levels of circulating eosinophilic cationic proteins compared with healthy subjects. www.gdx.net/home/assessments/finddisease/cfs/allergies.htmlChronic Fatigue Syndrome has been closely tied to immune system dysfunctions that trigger hypersensitivity to food and environmental allergens.[1,2] Because a constant, sensitized immune response can provoke chronic and disabling symptoms of fatigue, CFS patients typically display a much higher prevalence of allergy.[3,4] In fact, studies have found that simply having a history of allergy/asthma significantly increases the likelihood that individual will eventually develop chronic fatigue.[5] References: 1 Dechene L. Chronic fatigue syndrome: influence of histamine, hormones and electrolytes. Med Hypotheses 1993;40(1):55-60. 2 Conti F, Magrini L, Priori R, Valesini G, Bonini S. Allergy 1996;51(2):124-7. 3 Straus SE, Dale JK, Wright R, Metcalfe DD. Allergy and the chronic fatigue syndrome. J Allergy Clin Immunol 1988;81(5 Pt 1):791-5. 4 Matsumoto Y, Ninomiya S. Allergy among Japanese patients with chronic fatigue syndrome. Arerugi 1992;41(12):1722-5. 5 Bell KM, Cookfair D, Bell DS, Reese P, Cooper L. Risk factors associated with chronic fatigue syndrome in a cluster of pediatric cases. Rev Infect Dis 1991;(13 Suppl 1):S32-8. www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9723665&dopt=AbstractThe close association between atopy and CFS led us to speculate that CFS may arise from an abnormal psychologic response to the disordered expression of these proinflammatory and antiinflammatory cytokines. Psychologic variables were predictive of immune status within the CFS sample (65.9% of the variance in immune status; F (3,10) = 6.44, P < .05). Specifically, the absence of a personality disorder but greater endorsement of global psychiatric symptoms was predictive of immune activation. CONCLUSIONS: Most of our subjects with CFS were allergic, and the CFS and allergy cohorts were similar in terms of their immune status. www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8738520&dopt=AbstractChronic fatigue syndrome (CFS) is a syndrome of uncertain etiopathogenesis characterized by disabling fatigue associated with a variable number of somatic and/or neuropsychologic symptoms. In patients with CFS, several immunologic abnormalities can be detected, including a higher prevalance of allergy. The aim of this study was to determine whether CFS patients, well studied for their allergy profile, show signs of eosinophil activation, as detectable by the measurement in serum of eosinophil cationic protein (ECP) levels. In 35 consecutive CFS outpatients (diagnosis based on the Centers for Disease Control case definition), ECP was measured in serum by a competitive enzyme immunoassay (ECP-FEIA kit, Kabi Pharmacia Diagnostics, Uppsala, Sweden). Fourteen disease-free subjects with no history of CFS or allergy were selected as controls. ECP serum levels were significantly higher in CFS patients than in controls (18.0 +/- 11.3 micrograms/l vs 7.3 +/- 2.1 micrograms/l; P < 0.01). In the CFS population, the prevalence of RAST positivity to one or more allergens was 77%, while no control showed positive RAST. Twelve of the 14 CFS patients with increased ECP serum levels were RAST-positive. However, CFS RAST-positive patients had no significantly higher ECP serum levels than CFS RAST-negative patients (19.3 +/- 12.4 micrograms/l vs 13.6 +/- 3.7 micrograms/l; P = 0.4). This is the first report of increased serum levels of ECP in CFS. On the basis of the available data, it is discussed whether eosinophil activation has a pathogenetic role in CFS or is linked to the frequently associated allergic condition, or, finally, whether a common immunologic background may exist for both atopy and CFS. phoenix-cfs.org/The%20SITE/CFSABAVIII.htmONSET, IMMUNE CHANGES AND INFECTIONS. AN INTEGRATED MODEL THAT EXPLAINS THE SYMPTOMS OF CFS Seven different groups of predisposing and onset factors can produce the immune alterations (poor cellular immunity, Th2 dominated immunity) seen in CFS (1) Cellular Stress - A significant number of CFS patients experienced an onset of their symptoms shortly after blood transfusions or pregnancy. Both events (as well as radiation exposure!) can increase cellular stress. (2) Acute Viral Infections can cause immune suppression for long periods of time during which endogenous viruses may reactivate and opportunistic infections can occur. (3) Toxins such as heavy metals, organophosphates, PCP, etc. can cause immune dysfunction. (4) Long Term Physical or Mental Stress negatively impacts both cellular immunity and cytokine balance and causes shifts in the Th1/Th2 balance. Viral reactivation occurs after high cortisol levels (a stress induced hormone) decrease macrophage function. (Since the macrophages are at the heart of any infectious response this would put quite a damper on the immune system.) How to explain high levels of Th1 cytokines (IFN-y, IL-12) but low levels of Th1 activity (NK cells)? The authors suggest that fragmentation of the STAT I signaling protein is preventing NK cells responding to IFN-y. Thus, while the Th1 system appears to be upregulated in CFS in reality it is not. (5) Estrogen. Situations that cause high estrogen levels such as pregnancy and other physiological and pathological situations can shift the Th1/Th2 balance towards Th2. Even in the presence of Th1 cytokines such as IFN-y and IL-12, high estrogen levels can illicit a Th2 response. (6) Infections that are eliminated slowly can shift the Th1/Th2 balance. A Th2 environment that prevails during pregnancy may give intracellular organisms a better chance to invade. (7) Having a Atopic Environment (having a lot of allergies) favors the development of stealth organisms. www.ei-resource.org/cfs-me.aspImmune Dysfunction CFS has long been considered to be an illness of immune dysfunction and there is ample evidence that considerable immune dysfunction is present in patients. Immune activation is a global finding with a range of specific abnormalities present in significant numbers of patients. The most common of these include elevated T lymphocyte numbers and elevated circulating cytokines (immune signaling chemicals). Despite this, immune cell function of CFS patients is poor, with low natural killer cell cytotoxicity (NKCC), poor lymphocyte response to mitogens in culture, and frequent immunoglobulin deficiencies, most often IgG1 and IgG3 (4). Another finding is that the immune system of CFS patients is unbalanced, with T-helper cells of type 2 heavily outnumbering those of type 1 (5). Th1 cells stimulate immunity directed at organisms which invade cells, such as viruses whereas Th2 cells stimulate immunity targeted towards invaders found outside of cells such as bacteria, parasites, toxins and allergens. This finding could certainly explain the fact that CFS sufferers have a higher occurrence of allergies than the healthy population. It also provides a reason why CFS patients may have chronic viral infections as immunity is directed away from protecting against them. Endocrine Dysfunction Much research has centred around the endocrine system of CFS patients. Particular interest has been paid to the hypothalamic-pituitary-adrenal (HPA) axis which is responsible for the stress response. A number of abnormalities have been observed in CFS patients with regards to this including low cortisol and DHEA sulphate levels as well as altered melatonin metabolism (6). Cortisol and DHEA-S work in synergy to control how the body reacts to stress. Low levels affect your ability to deal with stress and can cause fatigue, low blood pressure, hypoglycemia, poor brain function and a number of other problems common to CFS sufferers. Genetic Factors Genetics can be said to be a factor of varying importance in the development of any illness. Consistent with this statement, a number of possible areas of genetic susceptibility have been identified for CFS in various studies. One such study involving twins with CFS and healthy control twins found that the CFS group had much slower reaction times on all speed related cognitive tests. The researchers postulated that this indicated a central information processing deficit in the brain (16). This finding illustrates one theory about the pathogenesis of CFS best described by Dr. J. Goldstein. Dr. Goldstein has treated thousands of CFS patients based on his theory that their brains process sensory information abnormally as a result of certain neurochemical deficiencies. Other research, also centered around brain function, found that CFS patients have differences in genes responsible for serotonin production which leads to lower reservoirs of serotonin, the chemical responsible for maintaining positive moods and also healthy sleep cycles, amongst other functions (17). Finally, a study again using twins, found evidence of immune dysfunction indicating a possible genetic susceptibility (18). There have been two genetic studies recently that have been hailed as major advances in understanding chronic fatigue syndrome: The first hit the headlines in July 2005. It suggests that gene expression, the pattern in which genes are switched on and off' is significantly different for certain genes in those with CFS. Researchers at Imperial College, London, looked at the way genes are activated in immune cells of 25 CFS patients and 25 healthy controls. They initially found 35 genes that showed differences while more precise examination revealed 16 that showed definite and significant abnormalities. The lead researcher, Dr Jonathon Kerr suggests that the results support the theory that the illness is often triggered by a virus, namely those discussed previously on this page. Many of the genes that were identified affect the functioning of the mitochondria, the energy generating plants within cells. As such, the abnormal gene expression could account for symptoms of fatigue and lack of energy. The energy producing mitochondria within patients cells may literally be not producing enough energy. The team behind the research hopes to run a much larger study of 1000 patients in the future and it is hoped the research will lead to reliable diagnostic tests for CFS and to new treatment approaches. The second study, the largest ever to focus on CFS, was completed in 2006 and provided the results that the CFS community has been waiting for. Dr. Julie Gerberding, director of the Centers for Disease Control (CDC) said at a press briefing "It really is the first credible evidence of a biological basis for chronic fatigue syndrome." The study involved 227 CFS patients and was conducted in Wichita, Kansas at a cost of $2 million. The study volunteers spent two days in hospital undergoing detailed clinical evaluations including sleep studies, cognitive functioning measurements, autonomic nervous system evaluations, extensive blood work and genetic testing. The activity levels of 20,000 genes were assessed and it is here where the really groundbreaking findings were discovered. At the press briefing, Dr. Reeves, the lead CFS researcher at the CDC, stated "For the first time ever, we have documented that people with CFS have certain genes that are related to those parts of brain activity that mediate the stress response. And that they have different gene activity levels…that are related to their body's ability to adapt to challenges and stresses that occur throughout life, such as infections, injury, trauma or various adverse events." What this means is that people with chronic fatigue syndrome generally have a lower tolerance to these various stressors. The result of this is that in people predisposed to CFS, their bodies can become overwhelmed by events that other people would be able to shrug off, and this is where dysfunction in various body systems such as the nervous, endocrine and immune systems sets in. The researchers at the CDC went on to say that they identified a number of different subgroups within the patients tested, verifying what many had suspected, that CFS isn't a single easily identifiable disease with a single cause and diagnostic marker, but rather the result of a complex disease process. They also stated that this research proves once and for all that CFS is a very real biological disease and hope that it will lead to better diagnosis and treatment in the near future. www.allergyclinics.co.uk/cfs.htm80% of all people suffering with chronic fatigue have a history of classic allergies (i.e. allergy to dust mites, pollens and so on). This is way above the incidence of immediate allergy in the general population (5-15%). • Thyroid and adrenal function tests and other common laboratory tests – ordinary tests sometimes fail to identify dysfunction of important endocrine glands unless the problem becomes more advanced. • Tests for abnormal intestinal fermentation – in several studies chronic fatigue has been linked with yeast overgrowth (also wrongly referred to as “candida”) • Food reactivities – Type B food allergy is a common cause of chronic fatigue. We use specific dietary changes as a process of Elimination & Challenge to identify reactive from non reactive foods but if one’s circumstances are too restrictive, intracutaneous tests can be used for guidance • Tests for toxicity or sensitivity to mercury, silver and nickel, metals used in dental amalgams; tests for organophosphates and other environmental chemicals (many of these are used in carpets and furniture as fire retardants, adhesives in electrical appliances, TV & computers and many others • Parasitology screen – for protozoan (amoebic) parasites. Many people are unaware they carry these, because they do not cause acute/severe symptoms, however, up to 30% of chronic fatigue sufferers are found to have this type of parasites. Allergy Testing Allergy testing is done primarily through skin testing, in which dozens of common allergens are introduced into the skin. Those that cause an itchy, swelling reaction reveal allergies. There are also blood tests for allergens which are more accurate, but also more expensive. Food allergy testing can be more tricky, as many food allergies dont give results on the skin test. A diet where you start with white rice and introduce something new each day is a good way of determining what you are allergic to. findarticles.com/p/articles/mi_m0ISW/is_246/ai_112728008With regards to IgE testing, the ELISA method offers an excellent confirmatory test for IgE-mediated food allergies when skin prick testing is equivocal or negative, as it is not unusual for a patient to be skin prick test negative and ELISA positive. Generally, the assumption in such a case is that the extracts used for IgE skin prick testing were defective, unstable or non-standardized. Conversely, a false positive skin test may be due to nonspecific enhancement of the hypersensitive reaction through an axon reflex of a neighboring strong wheal-and-flare reaction... Furthermore, the results of skin prick testing do not exhibit a strong correlation to food allergy symptoms. ELISA is reported to be more sensitive than skin prick testing in the identification of IgE-mediated food allergies, and as most food allergies are nonIgE-mediated, skin prick testing is rather obsolete.
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Post by fritolay66 on Mar 23, 2009 0:55:50 GMT -5
Allergy Treatments Treatments for H1 Symptoms Antihistamines - H1 Antagonists Allegra (Fexofenadine) en.wikipedia.org/wiki/FexofenadineFexofenadine hydrochloride (brand names include Allegra and Telfast) is an antihistamine drug used in the treatment of hayfever and similar allergy symptoms. Fexofenadine, like other second and third-generation antihistamines, does not readily enter the brain from the blood, and so causes less drowsiness than first-generation histamine-receptor antagonists. It works by being an antagonist to the H1 receptor. Note: Worked well and stopped the constant sinus headaches. Caused no drowsiness. Astelin (Azelastine) en.wikipedia.org/wiki/AstelinAzelastine is an antihistamine and mast cell stabilizer available as a nasal spray (Astelin®) for hay fever and as eye drops (Optivar®) for allergic conjunctivitis. Note: Astelin brought back my sense of smell, which was wonderful and unexpected. However, it also made me lose interest in everything. I went off it and on it again, and it had that affect each time. Antiimflammatories Singulair (Montelukast) en.wikipedia.org/wiki/SingulairMontelukast is a leukotriene receptor antagonist (LTRA) used for the maintenance treatment of asthma and to relieve symptoms of seasonal allergies. It is usually administered orally. Montelukast blocks the action of leukotriene D4 on the cysteinyl leukotriene receptor CysLT1 in the lungs and bronchial tubes by binding to it. This reduces the bronchoconstriction otherwise caused by the leukotriene, and results in less inflammation. en.wikipedia.org/wiki/Leukotriene_receptor_antagonistA leukotriene antagonist is a hormone antagonist acting upon leukotrienes. It has been demonstrated that leukotrienes are implicated in the inflammatory cascade leading to asthma. Leukotriene modifiers are an important therapeutic advance in managing asthma. Note: Singulair works slightly better for me than Allegra, and I now use it as my main antihistamine. I dont have asthma, but it seems to work by reducing inflammation. Quercetin (flavonoid) en.wikipedia.org/wiki/QuercetinQuercetin is a flavonoid and more specifically a flavonol. Quercetin is found to be the most active of the flavonoids in studies,[citation needed] and many medicinal plants owe much of their activity to their high quercetin content. Quercetin has demonstrated significant anti-inflammatory activity because of direct inhibition of several initial processes of inflammation. For example, it inhibits both the manufacture and release of histamine and other allergic/inflammatory mediators. Recent studies have supported that quercetin can help men with chronic prostatitis, possibly because of its action as a mast cell inhibitor. Quercetin may have positive effects in combating or helping to prevent cancer, prostatitis, heart disease, cataracts, allergies/inflammations, and respiratory diseases such as bronchitis and asthma. Foods rich in quercetin include capers (1800mg/kg), lovage (1700mg/kg), apples (440mg/kg), tea (Camellia sinensis), onions (higher concentrations of quercetin occur in the outermost rings), red grapes, citrus fruits, broccoli and other leafy green vegetables, cherries, and a number of berries including raspberry, bog whortleberry (158 mg/kg, fresh weight), lingonberry (cultivated 74mg/kg, wild 146 mg/kg), cranberry (cultivated 83 mg/kg, wild 121 mg/kg), chokeberry (89 mg/kg), sweet rowan (85 mg/kg), rowanberry (63 mg/kg), sea buckthorn berry (62 mg/kg), crowberry (cultivated 53mg/kg, wild 56 mg/kg), and the fruit of the prickly pear cactus. A recent study found that organically grown tomatoes had 79% more quercetin than conventionally grown. A study by the University of Queensland, Australia, has also indicated the presence of quercetin in varieties of honey, including honey derived from eucalyptus and tea tree flowers. Quercetin is also a potent inhibitor of CYP3A4, an enzyme which breaks down most drugs in the body. www.immunesupport.com/92fal004.htmQuercetin to the rescue! Quercetin has a strong affinity for mast cells and basophils. It tends to stabilize their cell membranes, preventing them from spilling their pro-inflammatory, allergy-symptom-causing load of histamine/serotonin into the surrounding blood and tissue in response to the IgE antibody. And without the release of these potent inflammatory mediators, the familiar misery of allergies simply will not occur, even though you've inhaled the pollen, animal hair, or whatever normally triggers allergy attacks. Unfortunately, quercetin is barely soluble in water, so poor dietary absorption may limit its efficacy. Because of this, Murray, N.D., has suggested that quercetin be taken in combination with bromelain to improve its absorption. Bromelain is a natural, protein-digesting enzyme derived from pineapples. It has been used "to increase absorption of compounds, including antibiotics. Also, bromelain has powerful anti-inflammatory properties that synergize with quercetin. Bromelain inhibits several other common inflammatory mediators, including bradykinin and fibrin. It's widely used in sports medicine to reduce the pain and swelling of bruises, sprains, muscle tears, etc., for this reason. As a clinical nutritionist I have had numerous occasions to use quercetin on allergy and asthma suffers. About 1,000 to 2,000 mg. a day, divided into three to six doses, is sufficient to control most cases of allergy and many cases of asthma. I have remained virtually allergy and asthma free for several years through daily use of quercetin, and finding it much more effective for this purpose than other bioflavonoids. Bromelain (enzyme) en.wikipedia.org/wiki/BromelainBromelain is a mixture of sulfur-containing protein-digesting enzymes—called proteolytic enzymes or proteases—and several other substances in smaller quantities. Bromelain is present in all parts of the pineapple plant (Ananas comosus) but the stem is the most common commercial source, presumably because it is readily available after the fruit has been harvested. Pineapples have had a long tradition as a medicinal plant among the natives of South and Central America. However, just eating pineapple will not give you a great deal of extra bromelain, because it is mostly concentrated in the stem, which is not nearly as tasty (albeit still edible). Bromelain can be used in a vast array of medical conditions. It was first introduced in this area in 1957, and works by blocking some proinflammatory metabolites that accelerate and worsen the inflammatory process. It is an anti-inflammatory agent, and so can be used for sports injury, trauma, arthritis, and other kinds of swelling. Its main uses are athletic injuries, digestive problems, phlebitis, sinusitis, and aiding healing after surgery. Note: I started taking a Quercetin & Bromelain supplement when I was having terrible sinus pain. The day I took it, the pain receded a great deal, and has not returned at the level it was before. I've been taking it ever since. Nasonex (Mometasone Nasal) www.drugs.com/nasonex.htmlMometasone is a steroid. It prevents the release of substances in the body that cause inflammation. Nasonex is used to treat nasal symptoms such as congestion, sneezing, and runny nose caused by seasonal or year-round allergies. Nasonex is also used to treat nasal polyps in adults. Before using Nasonex nasal, tell your doctor and pharmacist if you have a viral, bacterial, or fungal infection of any kind. The absorption of this drug into your system can inhibit your body's ability to fight off infections. You may not be able to use Nasonex nasal if you have an infection. Other, less serious side effects may be more likely to occur. Continue to use Nasonex nasal and talk to your doctor if you experience: * headache * viral infection * sore throat * bleeding nose * coughing * upper respiratory tract infection * painful menstruation * muscle pain * stinging or burning of the nose Note: For me Nasonex causes terrible burning in my sinuses, and once led to a sinus infection. Treatments for H2 Symptoms H2 symptoms are those associated with increased stomach acid. Earlier stomach acid medicines focused on H2 receptor antagonism. But the recent discovery of proton pump inhibitors replaced them because they worked better and had fewer side effects. Proton Pump Inhibitors Prevacid (Lansoprazole) en.wikipedia.org/wiki/PrevacidLansoprazole (lan-SOE-pra-zole, INN) is a proton pump inhibitor which prevents the stomach from producing acid. Note: Prevacid works really well for decreasing my stomach acid symptoms. Treatments for H3 Symptoms A few years ago, during the worst era of my allergic symptoms, I had a bad cold. While taking Dayquil for it, I noticed something interesting. I found that, aside from the relief I had gotten from the cold, something that had been off for years had corrected itself. Withing 30 minutes, my voice deepened and felt more intimate and close in a way hard to describe. An hour and a half in,my headache was gone, I felt more relaxed, and my hands felt warm for the first time in ages. My mood improved, the world around me seemed to soften, and the overall pain I felt diminished. I felt sociable and friendly. In the next week after I got over my cold, I tried the ingredients separately - first Acetaminophen (nothing), and then Dextromethorphan. Bingo. The effect returns. My hands feel warmer, my voice deeper, and I become happily social and outgoing. The world is softer, less painful, less dangerous. My speech flows freely from my thoughts. But why? Dextromethorphan is listed as a cough suppressant. I investigate and learn that it acts as a serotonin, NMDA, and dopamine reuptake inhibitor. I had stumbled across the first treatment for the histamine H3 receptor symptoms associated with my allergies. Dextromethorphan Dextromethorphan is sold as an OTC cough suppressant. Dextromethorphan is non-addictive and has few side affects. en.wikipedia.org/wiki/DextromethorphanDextromethorphan (DXM or DM) is an antitussive (cough-suppressant) drug found in many over-the-counter cold and cough medicines. Dextromethorphan has also found other uses in medicine, ranging from pain relief to psychological applications. Dextromethorphan crosses the blood-brain barrier, and the following pharmacological actions have been reported: • NMDA glutamatergic receptor antagonist • ó1 and ó2 receptor agonist. • á3â4 nicotinic receptor antagonist • Serotonin reuptake inhibitor • Dopamine reuptake inhibitor (disputed) More research revealed that some people take dextromethorphan recreationally as it can bring on euphoria and interesting experiences. The minimum dose used for recreational usage is 12x - 30x the normal dose (equivalent to drinking two whole bottles), and recreational use can run up as high as 75x - 100x the normal dose. My experimentation, and the associated positive effects, are just with the normal dose, and it is actually on the low end - 15mg. That was all it took to counter the effects of H3 receptor activation and the decrease in neurotransmitters it caused. But after taking it a 2-3 times a week for two weeks, it stopped having any effect. If I waited a week or two and tried it again, it would then work for me again. Tramadol I found that Dextromethorphan would sometimes work, and at other times would have no effect. After entering an extended period of severe sinus pain that two Tylenol/Advil/Aleve could not touch, I turned to Hydrocodone, which finally was able to diminish, but not completely releive the pain. Nearing the limits of my supply, I found I was able to obtain Tramadol, which I selected as it seemed to be reviewed better than others at the revealing askapatient.com. It also had a serotonin and norepinephrine boosting effect which, after seeing how helpful Dextromethorphan was in that respect, got my attention. On a particularly painful evening in which two Tylenol was not having much affect on the pain, I decided to give Tramadol a try. The pain releif effects were minor - it helped, but not a huge amount. However, the serotonin / norepinephrine boosting effect did wonders to me. My visual field brightened perceptably. My voice got deeper and felt more natural. I became more loose, talkative, free. My body got warm, and the things that used to bring me pleasure began to do so once again. I became my old self - playful, talkative, passionate. I felt like I had been rebalanced. I didnt feel weird or high in any way. Tramadol was a miracle. I took just one 50mg dose once a day for a few days, then stopped to see if there was a withdrawal effect. I didnt feel any. I went back on, and a few days later, after another break, felt a counter-effect, in which my symptoms were worse. So there does appear to be a counter-swing. Each is supposed to last 4-6 hours. I find that one in the morning and one at 6:00 works well. I feel so much better, so much more balanced, happy, outgoing, and healthy. Acute allergic reactions will roll back the effects as the H3 receptor counters neurotransmitter production, but they're less terrible under the effects of Tramadol. Amazingly, it has fixed the following symptoms and conditions, some of which I had no idea were related: sinus pain, headaches, social withdrawal, loss of sense of smell, low libido, anxiety, lack of motivation, fatigue, irritability, emotional deadness, inability to feel pleasure, cold hands and feet, intestinal paralysis / constipation, shallow breathing, loss of personality, depression, wanting to run away, feelings of panic, and lack of personal connection. en.wikipedia.org/wiki/TramadolTramadol is an atypical opioid which is a centrally acting analgesic, used for treating moderate to severe pain. It is a synthetic agent, as a 4-phenyl-piperidine analogue of codeine, and appears to have actions on the GABAergic, noradrenergic and serotonergic systems... Tramadol is approximately 10% as potent as morphine, when given by the IV/IM route. Oral doses range from 50–400 mg daily, with up to 600 mg daily when given IV/IM... Tramadol is used to treat moderate and severe pain and most types of neuralgia, including trigeminal neuralgia. It has been suggested that tramadol could be effective for alleviating symptoms of depression and anxiety because of its action on GABAergic, noradrenergic and specifically serotonergic systems... Off-label and investigational uses • diabetic neuropathy • postherpetic neuralgia • fibromyalgia • restless legs syndrome • opiate withdrawal management • migraine headache • obsessive-compulsive disorder • premature ejaculation opioids.com/tramadol/prescribe.htmlTramadol causes significantly less respiratory depression than morphine. In contrast to morphine, tramadol has not been shown to cause histamine release. Note: Another reason this is a better treatment for pain than opiates - it doesnt release histamine. I noticed when taking Percaset or Hydrocodone that I'd get very itchy. Tryptophan Tryptophan has a positive modulating effect on Tramadol, but it makes me very sleepy so I take it at night before bed. en.wikipedia.org/wiki/TryptophanTryptophan is one of the 20 standard amino acids, as well as an essential amino acid in the human diet. For many organisms (including humans), tryptophan is an essential amino acid. This means that it cannot be synthesized by the organism and therefore must be part of its diet. The principal function of amino acids including tryptophan are as building blocks in protein biosynthesis. In addition, tryptophan functions as a biochemical precursor for the following compounds (see also figure to the right): * Serotonin (a neurotransmitter), synthesized via tryptophan hydroxylase. Serotonin, in turn, can be converted to melatonin (a neurohormone). * Niacin is synthesized from tryptophan via kynurenine and quinolinic acids as key biosynthetic intermediates. Dietary sources Tryptophan is a routine constituent of most protein-based foods or dietary proteins. It is particularly plentiful in chocolate, oats, bananas, mangoes, dried dates, milk, yogurt, cottage cheese, red meat, eggs, fish, poultry, sesame, chickpeas, sunflower seeds, pumpkin seeds, spirulina, and peanuts. It is also found in turkey at a level typical of poultry in general. Food Tryptophan [g/100 g of food] turkey 0.24 cheese, cheddar 0.32 chicken 0.24 beef 0.23 pork, chop 0.25 salmon 0.22 perch, Atlantic 0.21 milk 0.08 egg 0.17 wheat flour, white 0.13 potatoes, russet 0.02 rice, white 0.08 Use as a dietary supplement For some time, tryptophan was available in health food stores as a dietary supplement, although it is common in dietary protein. Many people found tryptophan to be a safe and reasonably effective sleep aid, probably due to its ability to increase brain levels of serotonin (a calming neurotransmitter when present in moderate levels) and/or melatonin (a sleep-inducing hormone secreted by the pineal gland in response to darkness or low light levels). Clinical research have been tending to confirm tryptophan's effectiveness as a sleep aid and for a growing variety of other conditions typically associated with low serotonin levels or activity in the brain such as premenstrual dysphoric disorder and seasonal affective disorder. In particular, tryptophan have been showing considerable promise as an antidepressant alone, and as an "augmenter" of antidepressant drugs. However others have questioned the reliability of these clinical trials. Other Serotonin Modulators en.wikipedia.org/wiki/SerotoninVarious agents can inhibit 5-HT reuptake including MDMA (ecstasy), amphetamine, cocaine, dextromethorphan (an antitussive), tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs)... Psychedelic modulation There exist many recreational drugs that innately modulate the 5-HT system in such a way to produce alterations in perception, emotional response, and thought process. These include psilocin/psilocybin, DMT, mescaline, LSD, MDMA (ecstasy), MDA, MDEA and ibogaine. Therapeutic modulation Various drugs are used to modulate the 5-HT system including some antidepressants, anxiolytics, antiemetics, and triptans. Many are classified as psychiatric medications, including the monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), atypical antipsychotics, the selective serotonin reuptake inhibitors (SSRIs), and amphetamines. Research by GW Pharma in the UK has shown that cannabis modulates serotonin levels through g-proteins, also resulting in an antiemetic effect. Antidepressants The MAOIs prevent the breakdown of monoamine neurotransmitters (including serotonin), and therefore increase concentrations of the neurotransmitter in the brain. MAOI therapy is associated with many adverse drug reactions, and patients are at risk of hypertensive emergency triggered by foods with high tyramine-content and certain drugs. Some drugs inhibit this re-uptake of serotonin, again making it stay in the synapse longer. The tricyclic antidepressants (TCAs) inhibit the re-uptake of both serotonin and norepinephrine. The newer Selective Serotonin Re-uptake Inhibitors (SSRIs) have fewer (though still numerous) side effects and fewer interactions with other drugs. Treatments for All Symptoms Histamine Clearance Methionine (Essential Amino Acid) www.puttingitright.com.au/aminoacids.htmMethionine Uses: Fluid balance Immune response Atherosclerosis Allergies High histamine schizophrenia Protective - against heavy metals, drugs, chemicals, alcohol Fatty liver, hepatitis, cirrhosis Premature ejaculation Retards cancer growth Skin, hair, nails disorders Food sources: apple, apricot, avocado, banana, cantaloupe, dates, figs, oranges, papaya, peach, pear, persimmon, pineapple, strawberry, tomato.All vegetables Grains, legumes, nuts, seeds, meat, fish, eggs, chicken, cheese Note: Methonine has a bodily effect on me. It's hard to explain, but it removes an irritation or inflammation in my body that I'm so accustomed to I dont realize it's there until its gone. It works sometimes, and sometimes it seems to have no effect. www.nutrition4health.org/nohanews/NNSp97NutrientsDepression.htmWe treat histadelia with a biochemical one-two punch in which (1) calcium is given to release excess histamine from tissues into the bloodstream, and (2) methionine is provided to add a methy group to blood histamine and hasten its exit from the body. With good compliance, improvement is usually noted in 4-8 weeks with about 3-6 months needed to correct this chemical imbalance. www.diagnose-me.com/cond/C447056.htmlMethionine - Methionine supplements lower blood levels of histamine by increasing histamine breakdown. www.nutrition4health.org/nohanews/NNSp97NutrientsDepression.htmWe treat histadelia with a biochemical one-two punch in which (1) calcium is given to release excess histamine from tissues into the bloodstream, and (2) methionine is provided to add a methy group to blood histamine and hasten its exit from the body. Various www.diagnose-me.com/cond/C447056.htmlTreatment Reason Plant-Based Nutrition Nutritionists recommend a low-protein, high complex carbohydrate diet. Histidine, which is more common in animal proteins, should be avoided as it can be converted into histamine. Calcium Copper Copper levels may be low to normal in patients with histadelia. Copper is part of the enzyme histaminase, which is involved in the metabolism of histamine. Magnesium Manganese Vitamin B6 (Pyridoxine) Vitamin C (Ascorbic Acid) Things That Can Increase Histamine Exercise www.mayoclinic.com/health/food-allergy/DS00082/DSECTION=2Exercise-induced food allergy Some people have an allergic reaction to a food that is triggered by exercise. As the body is stimulated by exercise, a person with an exercise-induced food allergy may feel itchy and lightheaded. In severe cases, it can cause reactions such as hives or anaphylaxis. Not eating for a couple of hours before exercising can prevent this problem. Note: On several occasions my allergy symptoms intensified a great deal while out running. My sinus pain would increase to terrible levels and I'd become muddled, antisocial, irritable, and withdrawn. Dehydration www.causeof.org/depression.htm#DehydrationEffectsDeprDehydration: Tryptophan, Serotonin, Melatonin, Histamine The amino acid tryptophan is required by the brain to produce the neurotransmitter serotonin, which subsequently is needed to make melatonin. An adequate amount of water is required for tryptophan to be transported into the brain. Dehydration may limit the amount of tryptophan available to the brain. To complicate matters, the histamine levels may actually stimulate tryptophan's breakdown in the liver. Note: I include this because it might be a good link between high histamine levels and low serotonin levels. Also, if making sure you drink enough water can help, that's good to know. Orgasm en.wikipedia.org/wiki/HistamineSexual response Research has shown that histamine is released as part of the human orgasm from mast cells in the genitals. If this response is lacking this may be a sign of histapenia (histamine deficiency). In such cases, a doctor may prescribe diet supplements with folic acid and niacin (which used in conjunction can increase blood histamine levels and histamine release), or L-histidine. Conversely, men with high histamine levels may suffer from premature ejaculations. Note: I often feel an effect similar to increased allergic activation in these cases, a clear sign of histamine levels increasing. Yet, obviously this is not something you should avoid. Just be aware that it has a histamine-releasing effect. Histamine-Releasing Foods www.drtahira.com/allergies.htmlUltimately, food allergies need to be identified and eliminated, thereby making the appropriate dietary and lifestyle changes. These include avoiding histamine-containing foods (sausage, sauerkraut, tuna, wine, preserves, spinach and tomato), histamine-releasing foods (crustaceans, strawberry, tomato, chocolate, protease-containing fruits like bananas and papayas, and alcohol) and intolerances to foods with vasoactive amines – tyramine (cabbage, cheese, seafood, citrus, and potato) and serotonin (banana). Incorporation of essential fats into the diet, while reducing saturated fats (red meats, dairy and margarine) is vital to enhance the anti-inflammatory pathway. www.factssa.com/foodall.htmFoods that may trigger a Non-Immunological Reaction Many different foods contain the histamine, or serotinin, or other chemicals which are also the mediators normally released by mast cells triggered by an IgE-allergen bridging reaction. These may have direct or indirect effects on the vascular system. Histamine may cause symptoms like headache, diarrhoea, or a rash. Tyramine and phenylethylamine are reported to trigger migraine headaches. Examples of these foods are: Food Substance Alcohol - histamine liberators Aubergine - histamine Avocado - vasoactive amines Banana - serotonin, histamine Beans (unboiled) - lectins, hemagglutins Beer - tyramine, sulphites, histamine Cheese - histamine, tyramine, phenylethylamine, mould toxins Citrus fruit - vasoactive amines, tyramine, chlorogenic acid Cocoa / chocolate - histamine liberators, phenylethylamine Coconut - mould toxins Egg white - histamine liberators Fermented food - vasoactive amines Grains - histamine liberators, mould toxins Herring - histamine Fruit juices - tartrazine Mackerel - histamine Nuts - mould toxins Pork - histamine liberators Salami sausage - histamine, tyramine, sodium nitrate Shellfish - histamine liberators Soy bean - mould toxins Strawberry - histamine, histamine-liberators, aromatic substances Tomato - vasoactive amines Tuna fish - histamine Wine - histamine, sulphur dioxide, chemical additives Tricyclic Antidepressants en.wikipedia.org/wiki/NorepinephrineTricyclic antidepressants (TCAs) increase norepinephrine activity as well. Most of them also increase serotonin activity, but tend to have side effects due to the nonspecific activation of histamine and acetylcholine receptors. Side effects include tiredness, increased hunger, dry mouth, and blurred vision. For this reason, they have largely been replaced by newer selective reuptake drugs such as Prozac. Folic Acid (Vitamin B9) & Vitamin B12 www.patrickholford.com/content.asp?id_Content=1026* Check your histamine status. If high don't take large amounts of folic acid or B12 Histamine imbalances are another biochemical twist in the tale of schizophrenia. We all make histamine, but some more than others. Some people produce excessively large amounts of histamine and are called 'histadelics'. High histamine levels in these people can lead to compulsive and obsessive behaviour and pits of depression... Since Folic acid and B12 stimulate the production of histamine, these supplements... should be avoided by those with a high histamine status. www.diagnose-me.com/cond/C447056.htmlHistadelics should avoid supplemental folic acid as it can produce excess histamine. In fact, anti-folate drugs may be required. Folic acid increases depression in histadelic patients and a trial of folic acid could be used to distinguish between histapenics and histadelics. In extreme cases, folic acid in food or in multivitamins is enough to produce the adverse effects.
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Post by fritolay66 on Mar 23, 2009 0:57:37 GMT -5
www.gilbertssyndrome.com/hypothyroidism.phpHypothyroidism This is a work in progress and is being updated regularly. Check back regularly, as I will be steadily improving the site and adding more information. How The Thyroid System Works REFERENCE: Wikipedia - Thyroid The thyroid is one of the larger endocrine glands in the body. It is located in the neck and produces hormones, principally thyroxine (T4) and triiodothyronine (T3), that regulate the rate of metabolism and affect the growth and rate of function of many other systems in the body. The thyroid is composed of spherical follicles that selectively absorb iodine (as iodide ions, I-) from the blood and for production of thyroid hormones. Twenty-five percent of all the body I- is in the thyroid gland. The follicles are made of a single layer of thyroid epithelial cells, which secrete T3 and T4. Inside the follicles is a colloid which is rich in a protein called thyroglobulin. The colloidal material serves as a reservoir of materials for thyroid hormone production and, to a lesser extent, a reservoir of the hormones themselves. he primary function of the thyroid is production of the hormones thyroxine (T4), triiodothyronine (T3), and calcitonin. Up to 40% of the T4 is converted to T3 by peripheral organs such as the liver, kidney and spleen. T3 is about ten times more active than T4[1]. T3 and T4 Production and Action Thyroxine is synthesised by the follicular cells from the tyrosine residues of the protein called thyroglobulin (TG). Iodine, captured with the "iodine trap" is activated by the enzyme thyroid peroxidase (TPO) and linked to the 3' and 5' sites of the benzene ring of the tyrosine residues on TG. Upon stimulation by TSH (see below), the follicular cells reabsorb TG and proteolytically cleave the iodinated tyrosines from TG, forming T4 and T3 (in T3, one iodine is absent compared to T4), and releasing them into the blood. Thyroid hormone that is secreted from the gland is about 90% T4 and about 10% T3[1]. Cells of the brain are a major target for thyroid hormone. A transport protein (OATP1C1) has been identified that seems to be important for T4 transport across the blood brain barrier[2]. A second transport protein (MCT8) is important for T3 transport across brain cell membranes[2]. In the blood, T4 and T3 are partially bound to thyroxine-binding globulin, transthyretin and albumin. Only a very small fraction of the circulating hormone is free (unbound) - T4 0.03% and T3 0.3%. Only the free fraction has hormonal activity. As with the steroid hormones and retinoic acid, thyroid hormones cross the cell membrane and bind to intracellular receptors (á1, á2, â1 and â2), which act alone, in pairs or together with the retinoid X-receptor as transcription factors to modulate DNA transcription[1]. T3 and T4 Regulation The production of thyroxine is regulated by thyroid-stimulating hormone (TSH), released by the pituitary. The thyroid and thyrotropes form a negative feedback loop: TSH production is suppressed when the T4 levels are high, and vice versa. The TSH production itself is modulated by thyrotropin-releasing hormone, which is produced by the hypothalamus and secreted at an increased rate in situations such as cold (in which an accelerated metabolism would generate more heat). TSH production is blunted by somatostatin (SRIH). Hypothyroidism www.stopthethyroidmadness.com/myxedema-craziness/Scientists now consider thyroid hormone one of the major “players” in brain chemistry disorders. And as with any brain chemical disorder, until treated correctly, thyroid hormone imbalance has serious effects on the patient’s emotions and behavior. Once the important thyroid hormones, T3 and T4, are released into your bloodstream, they enter cells of organs and play an important role in regulating major functions in the body. Adequate amounts of thyroid hormone are also required throughout your life if your brain is to function normally. Most of your cognitive abilities — such as concentration, memory, and attention span — as well as mood and emotions depend on normal thyroid hormone levels. Mounting evidence suggest that T3, the most potent form of thyroid hormone, is a bona fide brain chemical. It is found in the junction of nerve (synapse) cells that allow these cells to communicate with one another. This thyroid hormone also regulates the levels and actions of serotonin, noradrenaline, and GABA (gamma-aminobutyric acid), now accepted as the main chemical transmitters implicated in both depression and some anxiety disorders. Maintaining normal serotonin and noradrenaline levels in the brain depends to a great extent on whether the correct amount of T3 is available. Extensive animal and human research has led scientists to conclude that serotonin levels in the brain decrease if T3 is not delivered in the right amount. Also, a deficit of T3 in the brain is likely to result in noradrenaline’s working inefficiently as a chemical transmitter, and noradrenaline deficiency or inefficiency is, in some people, the chemical reason for depression. “…Thyroid patients, particularly those with hypothyroidism, want peace and quiet. They feel the need to withdraw from activity and noise. They have a low tolerance for sound. In essence, they wish to insulate themselves in a surrealistic world of tranquility.” ”Patients may become withdrawn from friends, and they do not want to talk or go out with people. They may lose all interest in doing things with their partners… Hypothyroid patients want to be left alone. They just want to sleep and withdraw from those around them. In some cases, they realize the people around them are doing the best they can, but they still want to maintain their isolation.” What are some of the behavioral and psychiatric symptoms of a low thyroid condition in the brain? Depression, anxiety, panic attacks, agoraphobia, obsessive compulsive tendencies, ultra-sensitive to the comments of others, social phobia, self-image concerns, unable to concentrate, lack of motivation, mood swings, dementia, phobias, delusions, suicidal ideation, memory loss, alterations in the accuracy of perceptions, visual and other hallucinatory distortions and more. Many low thyroid sufferers may tend to be on the selfish side because they have a pervasive feeling of not having enough resources for themselves, much less enough to make the lives of any other people better. They sometimes tend to be cranky, abusive, stingy, critical, judgmental, and have a whole set of other exceedingly undesirable tendencies. They can suffer from lack of motivation or ambition and find it difficult to accomplish even simple tasks. These folks know their feelings and behavior are quite inappropriate. They often feel frustrated, because in spite of their best efforts, there doesn’t seem to be much they can do to control these feelings, especially when the symptoms worsen during times of stress or just prior to the menstrual cycle. It is often hard for them to find enjoyment in activities. They have a tendency to not feel like doing anything. They frequently can no longer find enjoyment in the things that they used to find quite interesting and enjoyable. For them, molehills frequently seem like mountains. Why aren’t health professionals more informed about behavioral and psychiatric conditions resulting from a low thyroid condition? Thyroid disease in general used to be treated by symptoms prior to the advent of the TSH test in the 1970s. People are now realizing this test does not detect many cases of low thyroid. It wasn’t until this lab test became the “gold standard” test for thyroid function that diseases like chronic fatigue syndrome, fibromyalgia, Irritable Bowel Syndrome and others came into existence. Many have surmised that these new “invisible diseases” are simply low thyroid conditions that are not being detected by the standard TSH test. Therefore it is quite possible that some psychiatric disorders are actually hypothyroid conditions which are not being detected by the TSH tests. So although a health professional may know about the link with behavioral/psychiatric conditions, the unreliable TSH test may cause them to rule out thyroid as an origin of the problems. Additionally, many health professionals think the TSH is the only test that is needed, and do not realize that thyroid antibodies alone can cause problems or that someone could be functionally hypo (low T3, normal TSH and Free T4). Symptoms of Hypothyroidism www.drlam.com/physician_support/hypothyroidism.cfm· Fatigue and low energy, with need for daytime nap. · Depressed, down, or sad. · Skin that becomes dry, scaly, rough, and cold. · Hair becomes coarse, brittle, and grow slow. · Excessive unexplained hair loss. · Sensitivity to cold in a room when others are warm. · Difficulty in sweating despite hot weather. · Constipation that is resistant to magnesium supplementation. · Difficulty in loosing weight. · Unexplained weight gain. · High cholesterol resistant to cholesterol lowering drugs. thyroid.about.com/cs/testsforthyroid/a/selftest.htm____ I am gaining weight inappropriately ____ I'm unable to lose weight with diet/exercise ____ I am constipated, sometimes severely ____ I have hypothermia/low body temperature (I feel cold when others feel hot, I need extra sweaters, etc.) ____ I feel fatigued, exhausted ____ Feeling run down, sluggish, lethargic ____ My hair is coarse and dry, breaking, brittle, falling out ____ My skin is coarse, dry, scaly, and thick ____ I have a hoarse or gravely voice ____ I have puffiness and swelling around the eyes and face ____ I have pains, aches in joints, hands and feet ____ I have developed carpal-tunnel syndrome, or it's getting worse ____ I feel depressed ____ I feel restless ____ My moods change easily ____ I have feelings of worthlessness ____ I have difficulty concentrating ____ I have more feelings of sadness ____ I seem to be losing interest in normal daily activities ____ I'm more forgetful lately ____ I have worsening allergies Related Symptoms: ____ My hair is falling out ____ I can't seem to remember things ____ I have no sex drive ____ I am getting more frequent infections, that last longer ____ I'm snoring more lately ____ I have/may have sleep apnea ____ I feel shortness of breath and tightness in the chest ____ I feel the need to yawn to get oxygen ____ My eyes feel gritty and dry ____ My eyes feel sensitive to light ____ My eyes get jumpy/tics in eyes, which makes me dizzy/vertigo and have headaches ____ I have strange feelings in neck or throat ____ I have tinnitus (ringing in ears) ____ I get recurrent sinus infections ____ I have vertigo ____ I feel some lightheadedness ____ I have severe menstrual cramps Checklist: thyroid.about.com/cs/basics_starthere/a/hypochecklist.htmMe: (collected from various places): The thyroid glad is located just below the adam’s apple. It regulates the energy output and metabolism of the body- low for sleep, medium for waking, high for physical activity. Also calcium levels are regulated by the thyroid (my kidney stone was made of calcium). Hypothyroidism is the swelling of the thyroid. Symptoms are forgetfulness, fatigue, increased aggressive behavior, decreased affiliative behavior, low cognitive test scores, Alzheimer’s, brain aging, increased anxiety and stress, problems with memory and learning, thyroid enlargement, apathy, difficulty swallowing, and dry hair and skin. Hypothyroidism & Body Temperature www.stopthethyroidmadness.com/temperature/Generally, the average temperature of an adult with a healthy thyroid is 98.6 degrees fahrenheit or 37.0 degrees celsius, and that occurs around mid-afternoon. To take your temperature, it’s important to have an accurate thermometer. Some digitals will give you a reading one degree less or more than a Mercury thermometer. So if you have any doubts about your digital thermometer, try an old-fashioned Mercury thermometer, which can be quite accurate if you leave it under your tongue long enough.When you’re hypo–and that includes EVEN being on the lousy T4-only medications, you can have a mid-afternoon temp in the 97’s, and a few I’ve read had their in the 96’s. BRRRR.So when you start on natural desiccated thyroid like Armour, and consistently raise your doses, you will see your temps climb over time, with matching feel-good symptoms to match. But what if you are seeing your temperature all over the map, such as one temp one day, and a temp two degrees lower at the same time the next day?? That could be a sign that you have low-functioning adrenals, which means you aren’t producing enough cortisol. And for some folks, it takes supplementing with low-dose Hydrocortisone or other adrenal products to bring that stability in the temperature back. www.drrind.com/tempgraph.asp#directions· Thermal activity reflects metabolic activity. A low temperature means low metabolism and vice versa. For example, the temperature typically found in someone who is old, frail, pale and weak is low and typically ranges from 95 to 97 degrees if no infection is present. A healthy person will have an average temperature of 98.6 degrees, but may have a 100 degree or higher temperature in a hyperthyroid state or as high as a 104 to 105 degree temperature if there is a fever present these are high metabolic states. · Wide variability in daily temperatures indicates a weak adrenal function since the adrenal glands help the body maintain stability. Good adrenal function produces a stable temperature. As adrenal function improves, the temperature variability decreases and vice versa. As adrenals get stressed (either from emotional stress, excess metabolic stimulation such as excessive thyroid stimulation, or for other reasons), the variability increases. · In a hypothyroid state, the day-to-day averages are low and very stable. In a hypoadrenal state including adrenal exhaustion or adrenal stress, the temperatures are low and unstable -- one day they may average 96 degrees and one to two degrees higher the next day. Causes of Hypothyroidism www.drlam.com/physician_support/hypothyroidism.cfmCauses of Hypothyroidism There are a variety of factors that can contribute to the development of thyroid problems: · Exposure to external radiation such as occurred after the Chernobyl nuclear plant accident. · Over-consumption of isoflavone-intensive soy products such as soy protein or powder. Isoflavones act as potent anti-thyroid agents, and are capable of suppressing thyroid function, and causing or worsening hypothyroidism. · Some anti-thyroid drugs, such as lithium and the heart drug cordarone. · History of radiation treatment to the head and neck area. · Over-consumption of uncooked "goitrogenic" foods, such as broccoli, turnips, radish, cauliflower, and Brussels sprouts. · Radioactive iodine treatment for hyperthyroidism/Graves' Disease. · Post-surgical removal of all or part of the thyroid due to nodules or cancer. · Adrenal insufficiency (commonly caused by chronic stress). · Mercury intoxication (amalgams are 50% mercury). Amalgam fillings have been associated with a variety of problems such as Alzheimer's disease, infertility, neurotransmitter imbalances, and thyroid problems. Associated Disease As many as 10 percent of 98 million Americans with high cholesterol and high LDL ("bad") cholesterol may not know that their cholesterol is high due to undiagnosed thyroid problem. Older women with sub clinical or under-active hypothyroidism was shown to be twice as likely as women without this condition to have heart attacks. Thyroid disease is also intricately tied to adrenal gland and ovarian function. thyroid.about.com/cs/basicinformation/l/aathyroid101_b.htmIn hypothyroidism, the thyroid is not producing enough thyroid hormone. This may be due to autoimmune disease that makes it underactive, radiation or drugs that has partially or fully disabled the thyroid, or surgical removal of all or part of the thyroid. When you are hypothyroid, your thyroid doesn't produce any or enough thyroid hormones, and the missing hormone is replaced by thyroid hormone replacement drugs. Me: Soy can cause hypothyroidism because it has goitrogenic properties. See the section on Soy for more information. I eat probably three times as much soy protein isolate as you do. Not only do I eat it for dinner sometimes, but I have it via soy milk every time I eat cereal, and I have it for most of my lunches via chick patties and other veggie-burger-type things. Connections to Gilbert's Syndrome PERSONAL: Gilberts Web Forums imgeha I have a theory I thought I'd post, and get your reactions. One of the main problems Gilberts sufferers seem to have is that doctors don't believe it causes any problems. I discovered I had Gilberts over 18 months ago, and I am still suffering badly - but not with Gilberts, rather chronic fatigue, or rather hypothyroidism and hypoadrenalism. In standard blood tests, Gilberts shows up, and is often casually dismissed by the doctor as a benign condition. Yet many of us suffer and cannot understand why Gilberts is ignored by the medical profession. I personally am devastated by this - I am a 39 year old female, struggling to bring up 3 small children with severe chronic fatigue, and have been dismissed as just having Gilberts. After much research, I understand Gilberts to be due to an enzyme shortage in the phase 2 pathway, which operates sluggishly. I believe this sluggishness also affects other processes that are performed in the phase 2 pathway, including the conversion of the thryoid hormones T4 to T3. Low thyroid levels will affect the phase 2 pathway efficacy, as well as the adrenals. Anecdotal evidence from these boards leads me to believe that many Gilberts people suffer hypothyroidism, ie, the rate of T4 to T3 conversion is slow, and so we are cold and fatigued, have anxiety, possible hypoadrenalism (don't produce enough cortisol) and hypoglycaemia. Sound familiar to anyone? Heavy metals also burden the phase 2 pathway (got any mercury fillings? they won't help your Gilberts or your thyroid).Some of us may end up on thyroid treatment (Synthroid, Euthyrox etc etc) but this does not solve the problem. As most of us have problems converting T4 to T3, giving us T4 alone will not help us much, and will possibly cause us to become hyper on a low dose. This happened to me at Christmas with a total adrenal crash. I believe a combination of T4 / T3 like Armour or Thyroid S will be much more helpful. I am about to start this treatment myself, and I will be reporting back on progress. My theory is that so-called Gilberts symptoms - cold, fatigue, brain fog, anxiety, digestive problems, feeling lousy in the mornings, better in the evenings, headaches - are actually undiagnosed, and untreated thyroid problems. And we can try all we like to improve our liver function with juicing, milk thistle, liver diet, etc etc, and doubtless these will do no harm, but the real issue here may be hypothyroidism that may not show up on standard blood tests. Low thyroid levels affect the efficacy of the phase 2 pathway of the liver, and thus the bilirubin levels in GS sufferers. PERSONAL: Gilberts Web Forums imgerha If you are still troubled by fatigue, despite good diet, milk thistle etc etc, get your thyroid checked!! No amount of healthy eating will replace the hormones your body needs to function properly. Hypothyroid symptoms are identical to Gilberts syndrome - the yellow skin, digestive problems, fatigue, feeling cold, anxiety.Everything I have read says that the bulk of T4 / T3 conversion happens in the liver, though not specifically the phase 2 pathway. BUT -thyroid levels have an impact on the glucoronidation process which takes place in the phase 2 pathway. (This is from the book Amalgam Illness by Dr Andy Cutler - he suggests increasing thyroid levels in order to increase the glucoronidation process) This glucoronidation process is what breaks down the bilirubin in normal people, and is the process where the enzyme is lacking or less efficient in people with Gilberts. So, what I am saying is that low thyroid levels can hamper the glucoronidation process, and increase the build up of bilirubin. I understand that T4 (thyroid hormone) is converted to T3 by the enzyme 5'-deiodinase, a process that also takes place in the liver. A sluggish liver will have difficulties with thyroid conversion as well. So on a standard blood test, you may get 'normal' TSH / T4 results (which as you have probably read by now are next to useless) and elevated bilirubin, get the diagnosis of Gilberts, and 'there's nothing wrong with you, it's a benign condition', when in fact you are hypothyroid. It is possible that the adrenals will also need to be treated, as the body needs cortisol to drive the T3 and T4 into the cells. If the adrenals aren't producing enough cortisol, the body won't be able to use the thyroid hormone. Hypoadrenalism is common with hypothyroidism - the working of the thyroid impacts the adrenals, and vice versa. If one is underperforming, the other will too. Treating just one, ie the thyroid, will cause stress on the adrenals, and can lead to adrenal collapse (I experienced this at Christmas - not pleasant). You may need to treat the adrenals first, then begin thyroid treatment. PERSONAL: Gilberts Web Forums runagain During those episodes of debilitating fatigue and depression did you happen to take your temperature? Do you know what your average body temps are on a daily basis? If your temps fall below 97.8 consistently you are experiencing hypometabolism and the reason could be associated with that sluggish liver. The liver is responsible for converting T4 thyroid to the active form T3 which is required in every living cell. Conventional thyroid tests fail to identify this condition. Your body temps could still be low while your test results are within normal limits. I too experienced fatigue and depression (I have GS) until supplementing with T3 following Dr Denis Wilson's protocol: wilsonssyndrome.com/ My other symptoms relieved by T3: Reactive Hypoglycemia Sleep disturbances Sleep Starts Inability to get out of bed in the morning Lack of self confidence lack of motivation PERSONAL: Gilberts Web Forums WhosGilbert I've just today had another diagnosis to add to my already hypochondriac-sounding list ........ it seems I'm also hypothyroid, which, after years of swollen thyroid gland makes sense, really. Apparently, this is what has been causing some of my digestive upsets, fatique and nausea, according to the hospital doctor. It went undiagnosed for years, as nothing showed up on blood tests, and the symptoms were milder. (Interestingly, I also have a tender liver today, noticed by the doctor on examination, and yellow eyes. But the bili is normal. Hmmm) On Sunday, I passed out at work, and this morning again, that's why I had this looked into today. I'd been doing much better in general lately, though, after the anti-candida diet, and looking after myself better, etc. p075.ezboard.com/fgilbertswebfrm4.showMessage?topicID=72.topickglittering I have just found out i have Gilberts syndrome after months of frustration of not knowing what was happening to me. I aslo have thyroid problems which i take 100mg of thyroxine. p075.ezboard.com/fgilbertswebfrm2.showMessage?topicID=107.topicWhosGilbert I've noticed that a few of you guys also have the "lump in the throat" thing/thyroid problems (either suspected or diagnosed). I've had this condition for years (suspected, and now they say I HAVE a thyroid condition, but the details on that are fuzzy at the moment), plus GS, CFS, allergies, and digestive disturbances for all that time too. I wonder how many of you have the throat problems, as I've just found out that thyroid problems can cause many digestive problems, fatigue, of course, allergies, shaking/trembling, nausea, dizziness, hair loss, etc. Sound familiar ?!? PERSONAL: Gilberts Web Forums rBuckner I was diagnosed with hypothyroidism a couple of years after the official GS diagnosis. I did have thyroid checked not long before that and it was fine. Once I got on the thyroid meds I felt much better. I bet there's a link somewhere. I did have the amalgam fillings which have all been replaced with gold p075.ezboard.com/fgilbertswebfrm1.showMessage?topicID=224.topicimgeha I have learned a huge amount about hypothyroidism, mercury, the liver pathways, candida and treatments from Andy Cutler's book Amalgam Illness, available from Amazon. Expensive but really worth it for identifying and treating these issues. He states that the efficacy of the glucorinidation pathway (the culprit in Gilberts people) can be increased by raising thyroid hormones, ie that the Gilberts can be exacerbated by hypothyroidism, rather than Gilberts causing hypothyroidism. I was diagnosed with Gilbert's syndrome hypothyroidism in the 1980s and am taking Synthroid. I have symptoms many of you write about--extreme fatigue, brain fogginess, difficulty concentrating, and long-standing memory problems... I suspect that there are a number of conditions that seem to co-occur and reading this forum was the first I realized that there is a good likelihood that Gilbert's and hypothyroidism co-occur at a higher rate than you would suspect and that they may be related. T3 in Illness jcem.endojournals.org/cgi/content/abstract/41/1/27High incidence of decreased serum triiodothyronine concentration in patients with nonthyroidal disease Serum thyroxine (T4) and triiodothyronine (T3) concentration and binding were measured in 34 clinically euthyroid patients hospitalized for a wide variety of nonthyroidal diseases. Despite clinical euthyroidism, serum T3 was in the hypothyroid range (less than 90 ng/100 ml) in 24 of the 34 patients, and the mean serum T3 of this group, 78.4 +/- 38.3 (SD), was significantly decreased from that of control, 134.0 +/- 29.3 ng/200 ml. Mean serum T4 levels were essentially the same in both groups, 7.3 +/- 2.0 for sick patients and 7.2 +/- 1.0 mug/100 ml for the controls. Plasma binding of both T4 and T3 was decreased in the patient group to 69.9 and 78% of control values, respectively. In accord with previous studies, the mean free T4 index, proportional to free T4 concentration, was significantly increased to 10.0 +/- 4.1 in the patient group (control, 7.6 +/- 1.3). However, the mean free T3 index of the patient group, 92.9 +/- 38.4 remained decreased from that of control, 138.9 +/- 34.4. Of the 24 patients with decreased serum T3 (less than 90 ng/100 ml), low T3 levels could be attributed to decreased plasma binding in 8; in 5, serum T3 was within the normal range for their advanced age. Mean TSH was greater in the patient group 2.6 +/- 1.9, than in the controls, 1.9 +/- 1.1 muU/ml. Moreover, the TSH response to administered TRH was moderately exaggerated in 7 patients with low free T3 index compared to 7 patients with normal free T3 index. Although significant statistically, neither the basal nor TRH induced TSH levels were in the range generally found in primary hypothyroidism. The data suggest that the high incidence of low serum T3 (70%) and free T3 index (32%) in nonthyroidal disease may be related to the catabolic state that accompanies illness rather than to specific disease entities. At the present time, the use of serum T3 or free T3 measurements for the diagnosis of hypothyroidism does not appear justified in patients with nonthyroidal disease. In Short: Patients with a wide variety of nonthyroid diseases showed much lower T3 levels (70% were in the hypothyroid range) while T4 levels remained normal. Plasma binding of T4 was 70% that of normal and T3 was 78% of normal. These findings may be due to the catabolic state that accompanies illness. www.cfsresearch.org/cfs/research/treatment/9.htmOne of the other problems is the effect of the illness on thyroid functioning. It has long been noted that people are often functionally hypothyroid. That is, they produce enough thyroid hormones from the thyroid gland, as measured by levels in the blood, but they appear to be hypothyroid at a cellular level. This tends to occur in adult Fibromyalgia patients. Numerous effects could explain this: 1. The blood test for thyroid function is not a dynamic test, unlike, e.g. HbA1c. It simply represents what is in the blood, and not what is active at a cellular level. It is based on population sampling and would therefore include people with subclinical hypothyroidism. We will have to wait until the development of the nuclear membrane thyroid receptor volume test before we have a dynamic test of thyroid function. In medicine we tend to treat extremes and not subtle alterations in physiology. This means that people at the lower end of ‘normal’ are not treated. They may actually need to be at the upper end of normal, but the test will not tell you that. The body also has the ability, it seems, to keep the blood levels normal despite cellular thyroid problems. This can happen in any chronic illness. 2. In cytokine mediated illness the production of central and locally generated cytokines can affect the de-iodination pathways of thyroid hormones. It seems that high level of rT3, and low levels of T2 may ensue. Reverse T3 is a non-competitive inhibitor of T3 and is raised in stress situations. T2 is thought to be important for the functioning of mitochondria. High levels of rT3 have been found in post-operative patients subsequent to high cortisol output. It is thought to be an adaptive response in order to conserve energy. The situation of poor conversion of serum T4 to cellular T3, for whatever reason, has been called Wilson's Thyroid Syndrome. 3. Other hormones affect thyroid functioning. Cortisol is permissive for hormone uptake into cells and low cortisol levels can therefore have an effect on this. High cortisol can also inhibit functioning through its action on rT3 as mentioned above. 4. There is hypothalamic downregulation of the thyroid axis with altered sensitivity to TRH and TSH at their receptors The treatment studies by Teitelbaum and Ali that I quote later both incorporated low dose thyroid hormone replacement in selected patients. This seems to be of great benefit especially to fibromyalgia patients, particularly borderline hypothyroid patients (T4 in lower 1/3 of reference interval TSH >3) or those with evidence of low T3. www.hotthyroidology.com/editorial_144.htmlTHE THYROID IN NON-THYROIDAL ILLNESS Elaine M. Kaptein, MD, FRCP(C), FACP In the absence of hypothalamic, pituitary or thyroid diseases, systemic illnesses have multiple effects on thyroid hormone metabolism and on serum thyroid hormone concentrations (1-3). These changes are primarily related to the severity (2) (Figure ), and perhaps to the chronicity of illnesses (4), rather than to the specific disease states. Changes related to chronicity may be secondary to worsening malnutrition and/or catabolism which result in progressive declines in thyroid binding protein concentrations.
Most frequently, serum levels of total T3 are reduced leading to the term “the low T3 syndrome” or “the low T3 state of nonthyroidal illness”. Less frequently, serum total and free T4 values and TSH concentrations are increased or decreased.
Serum total T3 concentrations are frequently reduced even with mild nonthyroidal disorders such as caloric deprivation, with the highest frequency and lowest values occurring in patients with the most severe illnesses (1, 2). Serum total T3 values return to normal only after complete recovery of the nonthyroidal illness and of the nutritional deficiency.
3) T4 uptake into rapidly equilibrating tissues like liver may be reduced in critically ill patients with NTIS (2). 4) Total T3 content of cerebral cortex, hypothalamus, anterior pituitary, liver, kidney, and lung are reduced in NTIS as is hepatic content of total T4; total hormone content may reflect primarily bound hormone (18). 5) T3 production rates are decreased in all NTIS patients (2)
Controversy exists as to whether the fall in total T4 concentrations during acute NTIS are primarily due to central suppression indicating hypothyroidism, to reduced serum T4 binding to TBG due to protease cleavage, indicating euthyroidism, or a combination of these factors (2, 6, 19). Wadwekar and Kabadi (20) addressed this question in a study of six euthyroid men with primary hypothyroidism maintained on L-T4 replacement therapy during an acute nonthyroidal illness. Prior to the illness, total T4, total T3 and TSH levels were in the reference range for euthyroid subjects. All of these values decreased during the acute illnesses, returning to pre-illness values with recovery (20).
en.wikipedia.org/wiki/CatabolisisCatabolisis is the process of a body breaking down the muscles and other tissues in your body in order to keep your vital processes working. Catabolisis will not begin until there are no usuable sources of energy coming into the body. Catabolisis will break down muscle tissue before it breaks down fat. Anabolism and catabolism are the two forces that make up metabolism. www.bodyandfitness.com/Information/Fitness/catabolism.htmThe many biochemical processes that make up the body's metabolism can be grouped into two general categories - anabolism and catabolism. Anabolism is the building up of complex molecules, while catabolism is their breakdown. To build molecules and sustain life, the body needs energy. It gets this energy from the breakdown of nutrients such as glucose and fatty acids. So, for molecular construction to occur, molecular destruction must go on at the same time to release the energy required to drive the biochemical reactions. When anabolism exceeds catabolism, net growth occurs. When catabolism excesses anabolism net loss occurs. Anabolism includes the chemical reactions that cause different molecules to combine to from larger, more complex ones. The net result of anabolism is the creation of new cellular material, such as enzymes, proteins, cells, cell membranes, and tissues. Anabolism is necessary for growth, maintenance, and tissue repair. Catabolism includes the chemical reactions that break down complex molecules into simpler ones for energy production, for recycling of their molecular components, or for their excretion. If energy is produced, it is stored as glycogen or fat. Recently, the trend in sports nutrition has been to focus on anti-catabolic training methods and nutrients. For example, when the muscles are strenuously trained and the muscle fibers are damaged, cortisol is released at a higher level, speeding up the breakdown of tissues. Nutrients such as L-Glutamine have been shown to reduce the effects of cortisol, resulting in reduced tissue breakdown. Antioxidants and a number of phytochemicals also have anti-catabolic effects, as does high protein and all around good nutrition. By reducing the rate of catabolism, anabolism is increased, resulting in faster recovering, a higher level of performance, and an increased growth rate. Note: Cortisol and exercise are known triggers for Gilbert's Syndrome. Could they be triggering a catabolic state which prevents T3 synthesis or breaks it down? For the first time in weeks, my temperature is down to 97.9 after a strong workout last night. Though it was 98.4 last night. www.indyrad.iupui.edu/public/lectures/HTML/NM/thyroid/THY01.HTMTri-iodothyronine (T3) is produced by the peripheral deiodination of T4. T3 is much more potent than T4. About 99.5% of circulating T3 is bound (0.5% free). Reverse T3 is also produced by the deiodination of T4, but only when there is excess circulating thyroid hormone (hyperthyroid states). Reverse T3 is not physiologically active, so its production helps to prevent excess catabolism. Levels of reverse T3 are also elevated during periods of severe illness.
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Post by fritolay66 on Mar 23, 2009 0:58:32 GMT -5
Bilirubin & Albumin Saturation Me: An interesting thing I've been looking into as well - albumin is the blood serum carries many things, but large among them are bilirubin and thyroid hormones. And different things compete for space in albumin. Meaning that higher bilirubin counts probably prevent the albumin from carrying as much T4 and T3 hormones. REFERENCE: Wikipedia - Serum Albumin Serum albumin, often referred to simply as albumin is the most abundant plasma protein in humans and other mammals. Albumin is essential for maintaining the oncotic pressure needed for proper distribution of body fluids between intravascular compartments and body tissues. Functions of Albumin • Maintains osmotic pressure • Transports thyroid hormones • Transports other hormones, particularly fat soluble ones • Transports fatty acids ("free" fatty acids) • Transports unconjugated bilirubin • Transports many drugs • Competitively binds calcium ions (Ca2+) • Buffers pH www.sydpath.stvincents.com.au/tests/Albumin.htmElevated concentrations of albumin in plasma are caused by a relative loss of water. This occurs in dehydration, or with prolonged use of a tourniquet. There are no pathological conditions other than dehydration associated with a high albumin concentration. Note however that elevated albumin may indicate artefactual elevation of other analytes such as haemoglobin, lipids and calcium. entc.allenpress.com/entconline/?request=get-document&doi=10.1897%2F02-553Concentrations of PFOS required to saturate albumin would be in excess of 50 to 100 mg/L. Based on current environmental concentrations, it is unlikely that PFOS would cause displacement of hormones from serum proteins in wildlife. Note: implies that albumin can be saturated, and that its saturation with one thing prevents it from transporting other things. For example, when saturated with bilirubin, transportation of energy or thyroid hormones may be diminished. www.garfield.library.upenn.edu/classics1979/A1979HZ24000001.pdfThe cytoxicity of bilirubin cannot be accurately assessed from its total concentration in plasma, because bilirubin is bound to albumin. The current studies demonstrate the ability of albumin to bind bilirubin is significantly reduced when other organic anions (e.g. sulfisoxazole, benzoate, and hematin, which also bind to albumin) coexist in the plasma of neonatal infants with hyper-bilirubinemia. The results indicate that the pathogenesis of bilirubin toxicity is more closely related to that fraction of the circulating bilirubin which is dissociated from albumin or indirectly to the relative saturation of the albumin with bilirubin. SCIENCE: National Library of Medicine The influence of fatty acids on the binding of bilirubin to albumin. The influence of free fatty acids (FFA's) on the albumin binding of bilirubin was studied in vitro in the plasma of infants with neonatal hyperbilirubineamia and in solutions employing crystalline albumin to which bilirubin and FFA (oleic acid) were added. The bilirubin saturation index (SI) was utilized to distinguish between that fraction of bilirubin bound at the primary (high-affinity) site of albumin and bilirubin bound at secondary sites from which it is easily dissociated by salicylate. The relative saturation of albumin with bilirubin was also measured by addition of salicylate to whole blood samples where bilirubin was also measured by addition of salicylate to whole blood samples where bilirubin dissociated from the albumin could be sequestered by the red cells. The present studies indicate that FFA's influence the binding of bilirubin in two ways. At molar ratios of FFA to albumin (2:1 to 4:1), the FFA's compete with bilirubin for binding at the high-affinity site so that a significant portion of the bilirubin is transported at secondary sites, making it susceptible to displacement by water-soluble organic anions. At high molar ratios (greater than 5:1) FFA's compete with bilirubin for albumin binding at the secondary sites as well. In contrast to crystalline albumin where the first two molar equivalents of FFA do not influence the binding of bilirubin to albumin, all FFA concentrations in hyperbilirubinemic plasma reduce the affinity of albumin for bilirubin at its high-affinity site even though there is a molar excess of albumin over bilirubin. sunzi1.lib.hku.hk/hkjo/view/20/2000126.pdfOne gram of adult albumin will bind very tightly at its high affinity binding sites approximately 8 mg of bilirubin. Additional bilirubin can bind to secondary sites on albumin; but these latter complexes have a binding constant approximately two orders of magnitude lower than the high affinity binding sites on the albumin (5). www.metrohealth.org/Clinical/NICU/lecture/Kernicterus.ppt+albumin+bilirubin+saturation&hl=en&gl=us&ct=clnk&cd=20&client=firefox-aKernicterus Reasons why bilirubin may enter brain: 1. Excess bilirubin production which overwhelms albumin and other blood buffering capacity. Unconjugated bilirubin> nonpolar, lipophilic, binds to albumin in plasma (and RBC/platelet membranes and b-globulin); free U-bili normally soluble at ~1 mM-->when binding capacity exceeded, free U-bili in plasma rises One molecule of albumin binds 2 molecules bilirubin (1st is more tightly bound); at 1:1 molar ratio, 1 g albumin binds 8.4 mg bilirubin: serum alb max binding capacity (1, 2 sites) 4.0 g/dl 33.6 mg/dl 77.2 mg/dl 3.5 29.4 58.5 3.0 25.2 50.4 2.5 21.0 42.0 Other factors which decrease U-bili binding to albumin: 1. Free fatty acids (sepsis, IV lipid emulsions) 2. Sulfa drugs (e.g., Bactrim) 3. Indomethacin 4. Ampicillin 5. ?pH web.indstate.edu/thcme/mwking/heme-porphyrin.htmlPeripherally arising bilirubin is transported to the liver in association with albumin, where the remaining catabolic reactions take place. www.ias.ac.in/jbiosci/june2000/article_effectofph.pdfUnder physiological conditions, bilirubin remains bound to serum albumin which carries it to the liver for further metabolism. However, when bilirubin-to-albumin molar ratio (B/A) exceeds 1 : 1, free bilirubin binds to many types of cells including brain cells which is the cause of brain toxicity in premature neonates, a condition called kernicterus or bilirubin encephalopathy. In addition, jaundiced neonates with low plasma pH have been reported to be at greater risk of developing bilirubin encephalopathy (Kim et al 1980). Interaction of bilirubin with cells or cell membranes is well documented (Bratlid 1972; Sato et al 1987; Vazquez et al 1988; Hayer et al 1989; Leonard et al 1989; Tayyab and Ali 1995, 1997) and it is commonly accepted that the toxicity of bilirubin depends on its passage across the plasma membrane and its association with membrane lipids (Ali and Zakim 1993; Zucker et al 1994). At a given pH, increase in the B/A from 0.5 to 3.0 led to an increase in the membrane-bound bilirubin (figure 1). This increase was smaller up to a B/A of 1.5 : 1 but became more significant (P < 0.05) at high B/As at all the pH values used in this study. Nearly two-fold (P < 0.05) increase in membrane-bound bilirubin was noticed on increasing the B/A from 1.0 to 2.0... The amount of membrane-bound bilirubin at any B/A in the range of 0.5 to 3.0 was different at different pH values, being negatively correlated with pH of the medium. In other words, lowering the pH from 7.8 to 7.0 resulted in increased binding of bilirubin to erythrocyte membranes at all the B/As tested even if B/A was below 1 : 1. Within the temperature range of 27°C to 37°C, the amount of membrane-bound bilirubin at any given B/A above 1 : 1 was found to be minimum. Increase in temperature on either side led to an increase in bilirubin binding to erythrocyte membranes at all B/As. Sato and Kashiwamata (1983) also reported minimum binding of bilirubin to erythrocyte membranes at 37°C using a B/A of 2.0. A comparison of bilirubin binding patterns of human erythrocyte membranes at different temperatures and B/As shows that at each temperature, the binding was higher at higher B/As. This unusual behaviour of bilirubin binding to erythrocyte membranes at different temperatures may be either due to the effect of temperature on the binding of bilirubin to albumin or due to the change in the physical state of bilirubin binding sites of the erythrocyte membranes. In Short: Albumin carries bilirubin to the liver for metabolism. However, when bilirubin exceeds albumin, it will bring to many types of cells, including brain cells. Lower blood pH causes higher binding of bilirubin to membranes. Temperatures outside the range of 27°C (80.6°F) to 37°C (98.6°F) also increased bilirubin binding to membranes. Drugs That Displace Bilirubin From Albumin www.albany.edu/sph/coned/bfgr99.pdfDrugs Which Displace Bilirubin From Serum Albumin Salicyclic Acid Sulfonamides Furosemide Phenylbutazone www.gilbertssyndrome.org.uk/Gilbert's%20Syndrome%20All%20About%20Bilirubin.html Drugs that decrease bilirubin measurements include barbiturates, caffeine, penicillin and high dose salicylates. Note: Not sure of the action involved in each of these - some may actually help conjugate and excrete bilirubin, while others might simply displace it from albumin and affect the measurement. Note: These two taken together seem to imply that bilirubin is only picked up in tests when bound to albumin. Salicylates REFERENCE: Wikipedia - Salicylates Salicylic acid is a colorless, crystalline organic carboxylic acid. It is usually prepared by Kolbe synthesis (aka Kolbe-Schmitt reaction). Salicylic acid functions as a plant hormone. Also known as Beta Hydroxy Acid (compare to AHA), salicylic acid is the key additive in many skin-care products for the treatment of acne, psoriasis, callouses, corns, keratosis pilaris and warts. It treats acne by causing skin cells to slough off more readily, preventing pores from clogging up. This effect on skin cells also makes salicylic acid an active ingredient in several shampoos meant to treat dandruff. Aspirin (acetylsalicylic acid or ASA) can be prepared by the esterification of the phenolic hydroxyl group of salicylic acid. Subsalicylate in combination with bismuth form the popular stomach relief aid known commonly as Pepto-Bismol. When combined the two key ingredients help control diarrhea, nausea, heartburn, and even gas. It is also very mildly anti-biotic. SCIENCE: National Library of Medicine Salicylates are used to relieve pain and reduce fever. Most salicylates are also used to relieve some symptoms caused by arthritis (rheumatism), such as swelling, stiffness, and joint pain. However, they do not cure arthritis and will help you only as long as you continue to take them. Note: This is a good resource Caffeine www.clinchem.org/cgi/content/abstract/33/4/597 (this is copied from the Thing That Help section on caffeine) By means of gel-filtration of bilirubin/albumin mixtures, it is shown that unconjugated bilirubin remains completely linked to albumin (both human and bovine) in tetraborate buffer (pH 9.3), protein-free bilirubin appearing only when the bilirubin/albumin molar ratio exceeds two. On the other hand, bilirubin is completely set free from its protein link in the caffeine reagent. Additional chromatographic and spectrophotometric evidence is reported indicating the formation of a low-affinity complex between bilirubin and caffeine. These data explain why the spectrophotometric properties of bilirubin/albumin mixtures are matrix-dependent if measured in the tetraborate buffer but are no longer so when measured in the caffeine reagent. In Short: Caffeine separates unconjugated bilirubin from albumin. The bilirubin then weakly binds to the caffeine. This leads to lower (from what I've read elsewere) measurements of bilirubin. But I wonder if this doesnt also free the albumin to be a carrier for thyroid hormones, which increases energy in a completely different way - a way in which those with GS are lacking. Fluroide Poisoning thyroid.about.com/b/a/040397.htm[Fluoride] is an enzyme poison. Enzymes are complex protein compounds that vastly speed up biological chemical reactions while themselves remaining unchanged. As you read this, there is occurring in all of us a vast multitude of these reactions to maintain life and produce the energy to sustain it. The chains of amino acids that make up these complex proteins are linked by simple compounds called amides; and it is with these that fluorine molecules react, splitting and distorting them, thus damaging the enzymes and their activity. Let it be said at once, this effect can occur at extraordinary low concentrations; even lower than the one part per million, which is the dilution proposed for fluoridation in our water supply. Moreover, fluorides are cumulative and build-up steadily with ingestion of fluoride from all sources, which include not just water but the air we breathe and the food we eat. The use of fluoride toothpaste in dental hygiene and the coating of teeth are further sources of substantial levels of fluoride intake. The body can only eliminate half of the total intake, which means that the older you are the more fluoride will have accumulated in your body. What is the result of these toxic effects? First the immune system. The distortion of protein structure causes the immune proteins to fail to recognise body proteins, and so instigate an attack on them, which is Autoimmune Disease. Musculoskeletal damage results further from the enzyme toxic effect; the collagen tissue of which muscles, tendons, ligaments and bones are made, is damaged. What concerns me so deeply is that in concentrations as low as 1ppm, fluorides damage the thyroid system on 4 levels. 1. The enzyme manufacture of thyroid hormones within the thyroid gland itself. The process by which iodine is attached to the amino acid tyrosine and converted to the two significant thyroid hormones, thyroxine (T4) and liothyronine (T3), is slowed. 2. The stimulation of certain of the G proteins whose function is to govern uptake of substances into each of the cells of the body, from the toxic effect of fluoride, has the effect of switching off the uptake into the cell of the active thyroid hormone. 3. The thyroid control mechanism is compromised. The thyroid stimulating hormone output from the pituitary gland is inhibited by fluoride, thus reducing thyroid output of thyroid hormones. 4. Fluoride competes for the receptor sites on the thyroid gland which respond to the thyroid stimulating hormone; so that less of this hormone reaches the thyroid gland and so less thyroid hormone is manufactured. These damaging effects, all of which occur with small concentrations of fluoride, have obvious and easily identifiable effects on thyroid status. The running down of thyroid hormone means a slow slide into hypothyroidism. Already the incidence of hypothyroidism is increasing as a result of other environmental toxins and pollution together with wide spread nutritional deficiencies. GS & The Lump in the Throat There are also several accounts, including my own, of a lump in the throat in the vicinity of the thyroid gland. Take a look in the Symptoms section. Hypothyroidism Tests PERSONAL: Gilberts Web Forums imgeha I have just read a book about a woman who was hypothyroid for 23 years, and it wasn't picked up by the doctors because they go by the TSH blood test only, not the free T3 and T4 levels as well as clinical observation. She was totally debilitated, ended up in a wheelchair for years, and finally got a proper thyroid assessment. After taking Armour for 12 days, her brain fog lifted, and she recovered slowly. She is now completely fine. health.groups.yahoo.com/group/TPA-UK/ www.thyroideducation.comwww.geocities.com/thyroide/docs-UK.htmlwww.thyroiduk.org/The last one in particular will interest you. If you cannot get a doctor to measure Free T3 and T4 levels, you can do it yourself via a 24 hour urine test. The Free T3 and T4 blood tests are in themselves reliable, but they need sensitive interpretation by an informed doctor. I strongly recommend you read the Tears Behind Closed Doors book - this gives a lot of detail about the problems with blood tests. TSH is felt by the medical profession to be the gold standard of measuring thyroid function. Patients and informed doctors deride it as meaningless, as it only measures the level of thyroid stimulating hormone in the blood, not the actual levels of T3 and T4 at cellular level. It is possible to be hypothyroid and still well within range of the TSH blood test. This is why Free T3 and T4 levels need to be tested. But it is possible for these results to be in range, and for the patient to be hypothyroid. This is where an intelligent and sensitive clinical evaluation of symptoms by the doctor comes in. No dismissing the patient's symptoms as depression, or neurotic. But actually LISTENING to what she is saying. My Free T3 and T4 levels are in range, but only just. I have debilitating hypothyroid symptoms. www.lef.org/newshop/items/itemLC304131.htmlThis panel is used to evaluate thyroid function. The combination of the serum T4 and T3 uptake (THBR) as an indirect assessment of thyroxine-binding globulin (TBG). TBG helps to determine whether an abnormal T4 value is due to alterations in serum thyroxine-binding globulin or to changes of thyroid hormone levels. Deviations of both tests in the same direction usually indicate that an abnormal T4 is due to abnormalities in thyroid hormone. Deviations of the two tests in opposite directions provide evidence that an abnormal T4 may relate to alterations in TBG. This panel consists of the following tests:Thyroid-Stimulating Hormone (TSH), Free Tri-iodothyronine (T3) free, Thyroxine (T4) • Thyroid-Stimulating Hormone (TSH) This test is used to identify primary hypothyroidism and to differentiate it from secondary (pituitary) and tertiary (hypothalamus) hypothyroidism. • Triiodothyronine (T3), Free, Serum This test is used to evaluate thyroid function. It is primarily used to diagnose hyperthyroidism. It is also used to assess abnormal binding protein disorders and to monitor thyroid replacement and suppressive therapy • Thyroxine (T4) This test is used to evaluate thyroid function. T4 is decreased in hypothyroidism and in the third stage of subacute thyroiditis. T4 is increased with hyperthyroidism, subacute thyroiditis in its first stage and with thyrotoxicosis due to Hashimoto disease. T4 is also used to diagnose toxicosis. www.webmd.com/hw/womens_conditions/hw27377.aspThe thyroid gland uses iodine from food to make two thyroid hormones, thyroxine (T4) and triiodothyronine (T3). The thyroid gland stores these thyroid hormones and releases them as they are needed. • Thyroxine (T4) is produced by your thyroid gland when the pituitary gland releases thyroid-stimulating hormone. • Only a small amount of triiodothyronine (T3) is produced directly by your thyroid gland. Most T3 is made by other tissues that convert T4 into T3. Thyroid hormone blood tests include: • Free thyroxine index (FTI or FT4). Free thyroxine (T4) can be measured directly (FT4) or calculated (FTI). The FTI is a measure of the amount of T4 in relation to the amount of thyroxine-binding globulin present. The FTI is calculated from the T4 and T3 uptake, or T3U, values. The FTI value can indicate when an abnormal level of T4 is caused by an abnormal level of thyroxin-binding globulin in the blood. • Triiodothyronine (T3). T3 has a greater effect on metabolism than T4, even though T3 is normally present in lower amounts than T4. The total amount of T3 in the blood or the amount of free T3 (FT3) can be measured. Normally, less than 1% of the T3 is free. • Triiodothyronine uptake (T3U). The T3U test is an indirect measurement of the amount of the protein (thyroxine-binding globulin) that can bind to T3 and T4. The results of this test are useful only when evaluated along with other thyroid function tests. • Total Thyroxine (T4). Most of the T4 in blood is attached to a protein (called thyroxine-binding globulin). Less than 1% of the T4 is unattached. A total T4 blood test measures both bound and free thyroxine. Free thyroxine affects tissue function in the body, but bound thyroxine does not. Me: Note: I was not tested for T3. Just T3 uptake. My test results: TSH: 1.907 (0.35-5.5) Thyroxine (T4): 8.9 (4.5-12.0) T3 Uptake: 30 (24-39) Free Thyroxine Index: 2.7 (1.2-4.9) Thyroid Peroxidase (TPO) Ab: <10 (0-34) Thyroid Antithyroglobulin Ab: <20 (0-40) www.drrind.com/thyroidscale.aspTSH: Reflects the blood level of thyroid stimulating hormone.Total T4: Reflects the total amount of T4 present in the blood, i.e., the protein bound (unavailable) T4 and the Free T4. Note that high levels of estrogens (birth control pills or pregnancy) can increase the amount of the protein that binds T4; giving misleading elevated Total T4 values which can look like ‘hyperthyroidism’ when it is not.Total T3: Reflects the total amount of T3 present in the blood, i.e., the protein bound (unavailable) T3 as well as the Free T3. Again, high estrogen levels create the same effect as mentioned in relationship to T4 above.Free T4: Reflects the biologically active (free) form of T4. This T4 can be converted to T3 or RT3. In the presence of elevated estrogen levels, the Free T4 gives a more accurate assessment of thyroid function.Free T3: Reflects the biologically active (free) form of T3 that can generate production of energy (in the form of ATP). In the presence of elevated estrogen levels, the free T3 gives a more accurate assessment of thyroid function. T3 Uptake: This test is mentioned only as a warning not to use it. In fact, it does not measure T3 levels at all -- the name is misleading. It is an old test that was developed before we were able to accurately measure T4 levels. The assumption was that if the patient had a high T4 level, the blood proteins would be saturated with it. Therefore when mixed with T3 (which is easier to measure), the proteins would take up very little T3. Thus a low T3 uptake implies elevated T4 levels and vice versa. Thus the T3 Uptake test is actually an antiquated, inaccurate way to measure T4 levels. www.mercola.com/article/hypothyroid/diagnosis.htmOld Laboratory Tests Unreliable Most all older thyroid function panels include the following: • Total T4 • T3 Uptake and • Free Thyroxine Index (FTI). These tests should be abandoned because they are unreliable as gauges of thyroid function. The most common traditional way to diagnose hypothyroidism is with a TSH that is elevated beyond the normal reference range. For most labs, this is about 4.0 to 4.5. This is thought to reflect the pituitary's sensing of inadequate thyroid hormone levels in the blood which would be consistent with hypothyroidism. There is no question that this will diagnose hypothyroidism, but it is far too insensitive a measure, and the vast majority of patients who have hypothyroidism will be missed. Basal Body Temperature Basal body temperature popularized by the late Broda Barnes, M.D. He found the clinical symptoms and the body temperature to be more reliable than the standard laboratory tests was provided. This is clearly better than using the standard tests. However there are problems with using body temperature. • Sleeping under electric blankets or water beds falsely raise temperature • Sensitive and accurate thermometer required • Inconvenient and many people will not do (poor compliance) New and More Accurate Way To Check for Hypothyroidism This revised method of diagnosing and treating hypothyroidism seems superior to the temperature regulation method promoted by Broda Barnes and many natural medicine physicians. Most patients continue to have classic hypothyroid symptoms because excessive reliance is placed on the TSH. This test is a highly-accurate measure of TSH but not of the height of thyroid hormone levels. New Range for TSH to Diagnose Hypothyroidism The basic problem that traditional medicine has with diagnosing hypothyroidism is the so-called "normal range" of TSH is far too high: Many patients with TSH's of greater than 2.0 (not 4.5) have classic symptoms and signs of hypothyroidism (see below). • So, if your TSH is above 2.0 there is a strong chance your thyroid gland is not working properly. Free Thyroid Hormone Levels One can also use the Free T3 and Free T4 and TSH levels to help one identify how well the thyroid gland is working. Free T3 and Free T4 levels are the only accurate measure of the actual active thyroid hormone levels in the blood. When one uses free hormone levels one will find that it is relatively common to find the Free T4 and Free T3 hormone levels below normal when TSH is in its normal range, even in the low end of its normal range. When patients with these lab values are treated, one typically finds tremendous improvement in the patient, and a reduction of the classic hypothyroid symptoms. Secondary or Tertiary Hypothyroidism There are a significant number of individuals who have a TSH even below the new 1.5 reference range mentioned above, but their Free T3 (and possibly the Free T4 as well) will be below normal. These are cases of secondary or tertiary hypothyroidism, so, TSH alone is not an accurate test of all forms of hypothyroidism, only primary hypothyroidism. www.circlepoint.org/health0103.htmlUNDERARM TEMPERATURE TEST FOR HYPOTHYROIDISMINSTRUCTIONS: 1. Use any mercury thermometer. Shake it down the night before to 96 degrees or less and put it by your bedside. 2. In the morning, as soon as you wake up, put the thermometer deep in your armpit for ten minutes and record the temperature. Do this before you get out of bed, have anything to eat or drink, or engage in any activity. This will measure your lowest temperature of the day, which correlates with thyroid gland function. The normal axillary temperature is 97.8-98.2 degrees F. we frequently recommend treatment if the temperature averages 97.4 or less. The temperature should be taken for five days. However, if the temperature is 97.0 or less for three consecutive days, you do not need to take the last two temperatures. The axillary (underarm) temperature is used because oral (mouth) temperature does not correlate closely with thyroid function. 3. For women, the temperature should be taken starting the second day of menstruation. That is because a temperature rise occurs around the time of ovulation which may lead to incorrect interpretation of the test. If you miss a day, that is OK, but be sure to finish the testing before ovulation. For men, and for women who are menopausal, it makes no difference when the temperatures are taken. However, do not do the test when you have an infection or any other condition that would raise your temperature. RATIONALE: There is considerable evidence that blood tests often fail to detect hypothyroidism (underactive thyroid). It appears that many individuals have "tissue resistance" to thyroid hormone. Therefore, your body may need more thyroid hormone, even though the amount in your blood is normal. A low axillary temperature suggests (but does not prove) hypothyroidism. We frequently recommend a therapeutic trial with a natural thyroid medication for individuals who have typical hypothyroid signs and symptoms and a low body temperature. This approach to thyroid therapy is controversial and is currently outside of the medical mainstream. However, we have found this method to be safe when properly administered, and in some cases it is the most effective or the only effective treatment for certain chronic problems. SIGNS AND SYMPTOMS ASSOCIATED WITH HYPOTHYROIDISM: Fatigue, depression, difficulty concentrating, difficulty getting up in the morning, cold hands and feet or intolerance to cold, constipation, loss of hair, fluid retention, dry skin, poor resistance to infection, high cholesterol, psoriasis, eczema, acne, premenstrual syndrome, loss of menstrual periods, painful or irregular menstrual periods, excessive menstrual bleeding, infertility (male or female), fibrocystic breast disease, and ovarian cysts. POSSIBLE SIDE EFFECTS: We consider thyroid hormone to be safe when administered properly. Occasionally, people taking thyroid hormone experience nervousness, rapid pulse, insomnia, and (on rare occasions chest pain. If any of these side effects occur, reduce the dose and call the office. www.stopthethyroidmadness.com/recent-new-diseases/Since the 1970’s several new health issues and diseases have been “discovered”. In 1980, Chronic Fatigue Syndrome and Fibromyalgia were first noted. High cholesterol wasn’t considered a widespread health problem until the 1970’s, and Depression has become an epidemic. In 1982, Osteoporosis also became a health issue. In fact, all these health issues have become closely related to undiagnosed or undertreated hypothyroidism.The TSH (thyroid stimulating hormone) test was created in 1973. It is used to diagnose thyroid problems, but it measures a hormone from the pituitary gland, not the thyroid. A feedback loop exists in your body where the pituitary gland produces more or less thyroid stimulating hormone in response to the level of thyroid hormones in the bloodstream, and the thyroid produces more or less hormone based on the level of TSH. The normal range for the TSH test has been lowered several times, (the AACE, American Association of Clinical Endocrinologists, now recommends a range from 0.3 to 3.0), yet patients are not diagnosed until the TSH is much higher than the 3.3. In the case of autoimmune thyroid problems, the TSH can be within the normal range, yet antibodies are attacking the thyroid. Even the AACE estimates that as many as 1 in 5 Americans suffers from hypothyroidism. A human thyroid produces T4, T3, T2, T1 and calcitonin. For nearly 100 years, hypothyroid patients were given desiccated porcine thyroid (dried thyroid gland from pigs), and doses were increased until all symptoms were gone. Synthroid became the treatment of choice for hypothyroidism by the 1970s. This new drug contains only the storage thyroid hormone known as T4, leaving patients undertreated. PERSONAL: Gilberts Web Forums imgeha Get a blood test from the doctor to measure TSH, T4, T3, cortisol and DHEA levels. Something may show up there - but blood tests are very unreliable in showing up problems - you may have all the correct levels of hormones circulating in your blood, but they may not be doing their job where they should. You may have high levels of Reverse T3 which is preventing the T3 from doing its job. Burned out adrenals from continued stress will produce only low levels of cortisol, and can give you all sorts of problems, including fatigue, and hypoglycaemia. Treatments for Hypothyroidism thyroid.about.com/cs/hashimotos/a/tedfriedman_2.htmA study published in the New England Journal of Medicine in 1999 (see article now) suggested that brain T4 to T3 conversion may be impaired in some patients and that a select group of patients should be treated with both T4 and T3. Other studies published in the Journal of Clinical Endocrinology and Metabolism in 2003 (see article now) suggested that addition of T3 to T4 treatment is not needed for most patients with primary hypothyroidism. I recommend that most patients be started on a T4 preparation, which improves symptoms in the large majority of the patients. I have found that most patients prefer Levoxyl or Unithroid to Synthroid, but this varies with each patient. After initial treatment with T4, I adjust their T4 dose until their TSH is between 0.5 and 2 mU/mL. If they remain symptomatic despite an optimized TSH, then low doses of T3 given two or three times a day can be added cautiously to T4. If patients start with a low blood free T3 level, then I am more inclined to treat them with T4 plus T3. On T4 plus T3 therapy, I use blood tests to make sure the free T4 and free T3 are in the upper-normal range. The TSH value is usually suppressed on combination treatment. PERSONAL: Gilberts Web Forums imgeha How to treat hypothyroidism is a whole other medical controversy. Your standard GP will look at your TSH, and if it is over 4, prescribe give you synthetic T4 medications. Firstly,the TSH is meaningless - you need to get your free T3 and T4 levels checked - and even if these are within range but at the low end, it is likely that you will benefit from T3/T4 combo treatment ie Armour or Thyroid S. I am now also taking a T3 T4 combination thyroid medication, and the difference is amazing. From being totally debilitated just a few weeks ago, I am now much brighter and able to do much more without becoming exhausted. I feel almost normal. I still have a long haul ahead - I am half way through removing my amalgams - and I then have chelation to consider - but taking proper thyroid meds has given me my life back. I am so grateful. PERSONAL: Gilberts Web Forums kdhsgf Well, there seems to be a connection with hypothyroidism and GS. When I when for a bloodtest to have my thyroid checked out, the TSH levels were around 7. And followed another test a month later to have the reading just over 3. Apparently when doctors treat you for this their main goal is to get you in between 1 - 2. Since my last reading sat below 4 (reference is 0.32 - 4). I asked the doc if I could have a third test just to make sure, and he said no. So I have had to take measures into my own hands and take iodized (iodine) sea salt (still continueing with a good diet). I have felt much better than I have felt since I had this problem. I hardly get fatigued, and I haven't had an irregular heart-beat for some time now. I am actually starting to work now. I feel motivated enough to do so. So I would recommend getting iodine into your diet, as it gets converted into the required hormones in the bloodstream. Imgeha you need to be careful with iodine. It is not always the best thing for hypothyroidism, especially if you have Hashimotos. p075.ezboard.com/fgilbertswebfrm1.showMessage?topicID=224.topicimgeha health.groups.yahoo.com/group/NaturalThyroidHormones/ Here you will be told how to monitor your own symptoms, take your temperature and slowly and responsibly treat yourself. You can post your blood test results and get a view from very knowlegeable hypothyroid sufferers whether you would benefit from thyroid hormone. You can buy generic Armour online if you cannot get a doctor's prescription. Email me on nicola@the-boltons.com if you want the address. But you must research this issue thoroughly, know the pitfalls, go slowly and what to expect. Body temperature is a dead giveaway - optimum body metabolism is 98.6 - if you are consistently below that you are likely to be hypothyroid. Treatments Thyrolar and Armour include T3 and T4 hormones. Levoxyl and Synthroid have T4 only. Hypothyroidism Links www.stopthethyroidmadness.comwww.thyroidtears.co.uk/introduction.htmlwww.riverhillwellness.com/thyroid.htmthyroid.about.com/cs/basicinformation/l/aathyroid101_b.htm health.groups.yahoo.com/group/NaturalThyroidHormones/ Connections - Wilson's Syndrome wilsonssyndrome.com/Note: This seems scammy, but interested in T3 We have found that a low body temperature is a strong indication that there is something wrong that can be fixed, particularly with the WT3 protocol and/or WTSmed Supplements. Just like a fever (high body temperature) is a good indicator that "something's wrong" and can cause people to feel terrible, so can a low body temperature. In fact, a low body temperature is more than enough to explain almost all of the health problems listed to the left. (below) Fatigue Headaches & Migraines PMS Easy Weight Gain Depression Irritability Fluid Retention Anxiety & Panic Attacks Hair Loss Poor Memory Poor Concentration Low Sex Drive Unhealthy Nails Dry Skin & Hair Cold Intolerance / Heat Intolerance Low Motivation Low Ambition Insomnia Allergies Acne Carpal Tunnel Syndrome Asthma Hives When I began taking the liothyronine [T3 compound], I literally felt better immediately and within a few days felt better than I had ever felt in my life. The fatigue was gone, the headaches were gone, and the depression was gone. Perhaps even more phenomenal, was that days prior to my first menstrual cycle after beginning the medication, I, for the first time in as long as I could remember, experienced no discomfort whatsoever- no mood swings, no cravings, no depression, no irrational behavior, and no cramping. Needless to say I was ecstatic and was almost non-believing that I could feel so generally good. -- Suzanne G. Wilsons Doctors Listings: www.wilsonsthyroidsyndrome.com/DoctorsListing/Doctor.cfmwww.thyroid.org/professionals/publications/statements/99_11_16_wilsons.htmlSome of these symptoms can, in fact, be due to true hypothyroidism... The "Wilson's syndrome" website states that Dr. Wilson named this concept after himself "because it had not been previously described." In fact, for more than a century, the same set of symptoms has been given different names and attributed to a variety of causes by others, including the syndromes of neurasthenia, chronic fatigue, fibromyalgia, multiple chemical sensitivity, chronic Ebstein Barr disease, and chronic candidiasis. Note: This apparently acknowledges the similarity between the symptoms of CFS, neurasthenia, fibromyalgia, multiple chemicle sensitivity, and candidiasis. The site argues against the existence of Wilson's Syndrome, but the argument is weak.
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Post by ibzahp on Mar 23, 2009 1:21:39 GMT -5
Thanks for that-good info
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Post by fritolay66 on Mar 23, 2009 9:03:29 GMT -5
I, Thank you! I was really worried because there is just so much information here. Even though it was originally intended for Gilbert's Syndrome, the information can apply across the board in many disease processes. I am not a fan of following links, so I went ahead and posted so it would be easier for us to find the info again. I couldn't digest it all in one read and it actually took me a couple of weeks. Did you get to the part about mycoplasmas? Frito
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Post by toni on Mar 23, 2009 9:31:13 GMT -5
Thank you Frito, lots to read, but lots of GREAT info.
I noticed "peroxide" was there too. (I'd remembered some were taking peroxide internally) and I know this is a debatable issue...but "if anyone wants to read about peroxide"...it causes CELL death, internally and externally, and I can't help myself from reiterating that.
Internally, peroxide causes (oxidization) which is not what a person wants (IMHO) and I say that from much reading on that issue - because what the name of the game is... is to PRESERVE cells, not destroy or oxidize them, because then FREE RADICALS/toxins in the body attach and proliferate the cells with whatever is roaming inside the body.
So protect those cells - with antioxidants.
(some may say peroxide sprayed externally is fine, which yes, that's true. But consistent use of peroxide on an OPEN wound WILL cause atrophy...sinking in of the skin.
Why? Because the cells cannot regenerate and make new collagen (part of the matrix of what builds tissue back).
So, killing of "cells" that need to regenerate, it can't with consistent use of peroxide, because that causes "cell lysis/death of those cells".
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