Post by fritolay66 on Sept 21, 2009 13:29:06 GMT -5
Cat’s Claw or Uncaria Tomentosa
Named after a vine in which the thorns on the bark, look like jaguar’s claws. You can purchase this herb in many forms, but for my own purposes I tend to purchase powders by the pounds or raw herbs in which I can powder myself. From the powder or herb form, I can make tinctures, concoctions, infusions, soaps, salves, linaments, teas, capsules, etc. I feel I save a ton of money and it allows me many options in which to use my particular herb.
Immunomodulator and Adaptogenic
The definition of each heading follows each throughout this text.
An inmmunomodulator is a substance in which has an affect on the immune system. The reference I am using withtin this text is not the specific immunostimulants, but the non-specific in which act seperately or augment the immune system by the stimulation of certain components within the immune system.
An adaptogenic always has antioxidants within its constuitents, is considered non-toxic and has a normalizing effect on the immune system. if the immune system is hyper active, then it will normalize it by downregulating, and if the immune system is hypofunctional, it will upregulate it. An adaptogenic has a non specific response, but an overall systemic response.
Anti-Tumor by Inhibiting NFk-beta and relation to DNA
NFk-beta in short is an imflammatory switch in which cells undergo the effects to cancer cell production. It is a protein in which controls the transcription of DNA. NF-kappaB is widely used by eukaryotic cells as a regulator of genes that control cell proliferation and cell survival. Many different types of human tumors have misregulated NF-kappaB. Active NF-kappaB turns on the expression of genes that keep the cell proliferating and protect the cell from conditions that would otherwise cause it to die via apoptosis!!! You will also notice that some eukaryotes are parasitic to us humans, and so I am wondering if the same be true for them as well.
Part of NF-kappaB's importance in regulating cellular responses is that it belongs to the category of "rapid-acting" primary transcription factors, i.e., transcription factors that are present in cells in an inactive state and do not require new protein synthesis to be activated. This allows NF-kappaB to act as a "first responder" to harmful cellular stimuli. Stimulation of a wide variety of cell-surface receptors, leads directly to NF-kappaB activation and fairly rapid changes in gene expression.
Many bacterial products can activate NF-kappaB. The identification of Toll-like receptors, (TLRs) as specific pattern recognition molecules and the finding that stimulation of TLRs leads to activation of NF-kappaB. Studies have identified TLR4 as the receptor for the LPS component of Gram-Negative bacteria. (Yet another tie as to why I feel Cat’s Claw has benefited me). TLRs are key regulators of both innate and adaptive immune responses.
Antioxidant
Cats Claw is associated with a decrease in peroxyl and superoxide radicals. Something Dr. Hildy has written about in the past, so there for I do take note of it seriously.
Anti-Microbial
Anti-Viral
Potent Anti-Inflammatory
IL-1 and IL-6
Interleukin 1, is a cytokine and is composed of two proteins.
IL-1 alpha and IL-1 beta, and are produced by macrophages, monocytes, and dendritic cells. They form an important part of the inflammatory response of the body to an infection.
These cytokines increase the expression of substances in which cease cell movement on endothelialia (a thin lining of cells within our blood vessels) to enable the ability of the leukocytes to cross and go to active sites of infection.
They also function to reset the hypothalmus thermoregulatory center which leads to an increased body temperature, otherwise known as a fever.
IL-6 is also a cytokine and has two biggie functions. One as a pro-inflammatory. From the cumulative test results of Morgellons patients posted on the MDR web site, I am assuming that the increased levels of IL-6 are of the pro-inflammatory nature. They do not specify further concerning the iL-6, or I haven’t found documentation saying otherwise. Inflammation as being one of the biggest symptoms I have had all along.
I also want to add that a body in constant inflammation is your biggest sign something is not going right. In other words, it is not normal, it is not due because it is what you have always experienced so to be expected for you type of thing. It is a signal and should initiate further investigation by you as to the cause. Yes, aspirin helps, but it only helps the symptoms and not the cause. Before I digress further, lets get back on point.
The other function of IL-6 is as a potent anti-inflammatory. Cats Claw increases this type of IL-6. IL-6's role as an anti-inflammatory cytokine is mediated through its inhibitory effects on TNF-alpha and IL-1, and activation of IL-1ra and IL-10. The IL-1ra is a molecule that competes for receptor binding with IL-1 alpha and IL-1 beta, by blocking their role in immune activation. In order to make sense to me, I believe that Cats Claw would then initiate and increase in the levels of IL-1ra and perhaps IL-1 as well.
Cats Claw also has the ability to regulate IL beta and TNF Alpha. More on the latter in a moment. IL-1 beta, is an important mediator of the inflammatory response, and is involved in multiple cell activities including cell proliferation, differentiation, and apoptosis. Parts of IL-1 are also associated with induction of cyclooxygenase-2 (COX2) in the CNS and are found to contribute to inflammatory pain hypersensitivity. I think I understand Cat’s Claw to decrease prostaglandin E2, an inflammatory mediator and increases the joint protective, insulin-like growth factor-1 and there for decreases pain sensitivity.
Inhibits the production of TNF-alpha
TNF is known as Tumor Necrosis Factor and is also a cytokine. TNF is involved in the acute response of the immune system. In the results I referred to earlier, it does not state whether the TNF- alpha is a chronic occurrence, or that the TNF-alpha levels are found to be continally increased in Morgellon’s patients. If that be the case, then this cytokine gets my attention very quickly. Also, for further clarification, TNF-alpha is a fromer term and the current term is now TNF. So TNF and TNF-alpha denote the same thing.
TNF can be activated by three pathways. These processes are very confusing, so in short, it is important to know that these pathways are conflicting in their elicited responses. What I believe to be important here is that TNF and the concurrent stimulation of other cytokines, or the amount of reactive oxygen species, (ROS), can cause a variation and elicit a response in the balance in favor of one pathway or another. This complicated signaling tell us that, whenever TNF is released, various cells with vastly diverse functions and conditions can all respond to inflammation according to the pathway.
Again, TNF is produced in macrophages although there are a diverse set of cells that can also produce it. What concerns me here is that elevated levels of TNF are associated with the outer membranes of gram-negative bacteria, other bacterial byproducts, and IL-1 (the response to infection).
TNF has a number of actions on various organ systems, generally together with IL-1 and IL-6:
TNF stimulates the hypothalmic-pituitary-adrenal axis by the release of corticotropin releasing hormone-1, (CRH), a hormonal neurotransmitter whose response is to stress and is produced by T cells.
TNF is capable of inducing fever.
In the liver, TNF can stimulate the acute phase response, leading to an increase in C-reactive protein (another elevated inflammatory marker found in the lab report on MDR) and a number of other mediators. It also can induce insulin resistance by promoting serine-phosphorylation of insulin receptor substrate-1 (IRS-1), which impairs insulin signaling. Interestingly enough, one of the liver pathways in which I encounter in my studies of Morgellons is the phosphorylation cycle. In another post perhaps.
TNF’s effects on macrophages by stimulating phagocytosis, and production of IL-1 oxidants and the inflammatory lipid prostaglandin E2 PGE2.
A local increase in concentration of TNF will cause the cardinal signs of Inflammation to occur: heat, swelling, redness, and pain.
Increased concentrations of TNF induce shock-like symptoms and if combined with elevated levels of IL-1 and IL-6 and then the anti-inflammatory IL-1ra and IL-10, is associated with what is called a cytokine storm. Something of which I feel I suffered and barely made it through. I wonder what they would call a low level elevation of these, as I seem to associate them with the Morgellons condition. And hence a warning of sorts. I do not believe that one product, whether in herbal medicine or western, allopathic medicine will resolve our infection. And the vastness of the response system, is such that tinkiering with any one component, such as trying to raise specific levels, could very well be disastrous but wise to know despite. And here, I believe immunomodulation to be the key. Systemic and not specific, by supporting the entire body and its functions.
Lastly,
Intestinal balance, Leaky Gut Syndrome
Cats Claw has been claimed to be the only substance in which is capable of breaking through severe intestinal derrangments and thus a profound ability to get rid of deep-seated infections lodged within the bowel. Sources even indicate that perhaps this may also extend into the mesentary and its associated organs. Said another way, it has the ability to correct and balance by helping to normalize the beneficial microbes and reversing conditons of intestinal dysbiosis. This is huge.
Everything we consume goes through our intestines. Point, if half of Robert Smiths research work is connected to cows or the environment, then chances are exposure has taken place through our gut. Additionally, you look at just about any parasitic disease, be it an offical bug or cell or fungi, and the main place of multiplication of the species takes place within the intestinal walls.
Frito
Named after a vine in which the thorns on the bark, look like jaguar’s claws. You can purchase this herb in many forms, but for my own purposes I tend to purchase powders by the pounds or raw herbs in which I can powder myself. From the powder or herb form, I can make tinctures, concoctions, infusions, soaps, salves, linaments, teas, capsules, etc. I feel I save a ton of money and it allows me many options in which to use my particular herb.
Immunomodulator and Adaptogenic
The definition of each heading follows each throughout this text.
An inmmunomodulator is a substance in which has an affect on the immune system. The reference I am using withtin this text is not the specific immunostimulants, but the non-specific in which act seperately or augment the immune system by the stimulation of certain components within the immune system.
An adaptogenic always has antioxidants within its constuitents, is considered non-toxic and has a normalizing effect on the immune system. if the immune system is hyper active, then it will normalize it by downregulating, and if the immune system is hypofunctional, it will upregulate it. An adaptogenic has a non specific response, but an overall systemic response.
Anti-Tumor by Inhibiting NFk-beta and relation to DNA
NFk-beta in short is an imflammatory switch in which cells undergo the effects to cancer cell production. It is a protein in which controls the transcription of DNA. NF-kappaB is widely used by eukaryotic cells as a regulator of genes that control cell proliferation and cell survival. Many different types of human tumors have misregulated NF-kappaB. Active NF-kappaB turns on the expression of genes that keep the cell proliferating and protect the cell from conditions that would otherwise cause it to die via apoptosis!!! You will also notice that some eukaryotes are parasitic to us humans, and so I am wondering if the same be true for them as well.
Part of NF-kappaB's importance in regulating cellular responses is that it belongs to the category of "rapid-acting" primary transcription factors, i.e., transcription factors that are present in cells in an inactive state and do not require new protein synthesis to be activated. This allows NF-kappaB to act as a "first responder" to harmful cellular stimuli. Stimulation of a wide variety of cell-surface receptors, leads directly to NF-kappaB activation and fairly rapid changes in gene expression.
Many bacterial products can activate NF-kappaB. The identification of Toll-like receptors, (TLRs) as specific pattern recognition molecules and the finding that stimulation of TLRs leads to activation of NF-kappaB. Studies have identified TLR4 as the receptor for the LPS component of Gram-Negative bacteria. (Yet another tie as to why I feel Cat’s Claw has benefited me). TLRs are key regulators of both innate and adaptive immune responses.
Antioxidant
Cats Claw is associated with a decrease in peroxyl and superoxide radicals. Something Dr. Hildy has written about in the past, so there for I do take note of it seriously.
Anti-Microbial
Anti-Viral
Potent Anti-Inflammatory
IL-1 and IL-6
Interleukin 1, is a cytokine and is composed of two proteins.
IL-1 alpha and IL-1 beta, and are produced by macrophages, monocytes, and dendritic cells. They form an important part of the inflammatory response of the body to an infection.
These cytokines increase the expression of substances in which cease cell movement on endothelialia (a thin lining of cells within our blood vessels) to enable the ability of the leukocytes to cross and go to active sites of infection.
They also function to reset the hypothalmus thermoregulatory center which leads to an increased body temperature, otherwise known as a fever.
IL-6 is also a cytokine and has two biggie functions. One as a pro-inflammatory. From the cumulative test results of Morgellons patients posted on the MDR web site, I am assuming that the increased levels of IL-6 are of the pro-inflammatory nature. They do not specify further concerning the iL-6, or I haven’t found documentation saying otherwise. Inflammation as being one of the biggest symptoms I have had all along.
I also want to add that a body in constant inflammation is your biggest sign something is not going right. In other words, it is not normal, it is not due because it is what you have always experienced so to be expected for you type of thing. It is a signal and should initiate further investigation by you as to the cause. Yes, aspirin helps, but it only helps the symptoms and not the cause. Before I digress further, lets get back on point.
The other function of IL-6 is as a potent anti-inflammatory. Cats Claw increases this type of IL-6. IL-6's role as an anti-inflammatory cytokine is mediated through its inhibitory effects on TNF-alpha and IL-1, and activation of IL-1ra and IL-10. The IL-1ra is a molecule that competes for receptor binding with IL-1 alpha and IL-1 beta, by blocking their role in immune activation. In order to make sense to me, I believe that Cats Claw would then initiate and increase in the levels of IL-1ra and perhaps IL-1 as well.
Cats Claw also has the ability to regulate IL beta and TNF Alpha. More on the latter in a moment. IL-1 beta, is an important mediator of the inflammatory response, and is involved in multiple cell activities including cell proliferation, differentiation, and apoptosis. Parts of IL-1 are also associated with induction of cyclooxygenase-2 (COX2) in the CNS and are found to contribute to inflammatory pain hypersensitivity. I think I understand Cat’s Claw to decrease prostaglandin E2, an inflammatory mediator and increases the joint protective, insulin-like growth factor-1 and there for decreases pain sensitivity.
Inhibits the production of TNF-alpha
TNF is known as Tumor Necrosis Factor and is also a cytokine. TNF is involved in the acute response of the immune system. In the results I referred to earlier, it does not state whether the TNF- alpha is a chronic occurrence, or that the TNF-alpha levels are found to be continally increased in Morgellon’s patients. If that be the case, then this cytokine gets my attention very quickly. Also, for further clarification, TNF-alpha is a fromer term and the current term is now TNF. So TNF and TNF-alpha denote the same thing.
TNF can be activated by three pathways. These processes are very confusing, so in short, it is important to know that these pathways are conflicting in their elicited responses. What I believe to be important here is that TNF and the concurrent stimulation of other cytokines, or the amount of reactive oxygen species, (ROS), can cause a variation and elicit a response in the balance in favor of one pathway or another. This complicated signaling tell us that, whenever TNF is released, various cells with vastly diverse functions and conditions can all respond to inflammation according to the pathway.
Again, TNF is produced in macrophages although there are a diverse set of cells that can also produce it. What concerns me here is that elevated levels of TNF are associated with the outer membranes of gram-negative bacteria, other bacterial byproducts, and IL-1 (the response to infection).
TNF has a number of actions on various organ systems, generally together with IL-1 and IL-6:
TNF stimulates the hypothalmic-pituitary-adrenal axis by the release of corticotropin releasing hormone-1, (CRH), a hormonal neurotransmitter whose response is to stress and is produced by T cells.
TNF is capable of inducing fever.
In the liver, TNF can stimulate the acute phase response, leading to an increase in C-reactive protein (another elevated inflammatory marker found in the lab report on MDR) and a number of other mediators. It also can induce insulin resistance by promoting serine-phosphorylation of insulin receptor substrate-1 (IRS-1), which impairs insulin signaling. Interestingly enough, one of the liver pathways in which I encounter in my studies of Morgellons is the phosphorylation cycle. In another post perhaps.
TNF’s effects on macrophages by stimulating phagocytosis, and production of IL-1 oxidants and the inflammatory lipid prostaglandin E2 PGE2.
A local increase in concentration of TNF will cause the cardinal signs of Inflammation to occur: heat, swelling, redness, and pain.
Increased concentrations of TNF induce shock-like symptoms and if combined with elevated levels of IL-1 and IL-6 and then the anti-inflammatory IL-1ra and IL-10, is associated with what is called a cytokine storm. Something of which I feel I suffered and barely made it through. I wonder what they would call a low level elevation of these, as I seem to associate them with the Morgellons condition. And hence a warning of sorts. I do not believe that one product, whether in herbal medicine or western, allopathic medicine will resolve our infection. And the vastness of the response system, is such that tinkiering with any one component, such as trying to raise specific levels, could very well be disastrous but wise to know despite. And here, I believe immunomodulation to be the key. Systemic and not specific, by supporting the entire body and its functions.
Lastly,
Intestinal balance, Leaky Gut Syndrome
Cats Claw has been claimed to be the only substance in which is capable of breaking through severe intestinal derrangments and thus a profound ability to get rid of deep-seated infections lodged within the bowel. Sources even indicate that perhaps this may also extend into the mesentary and its associated organs. Said another way, it has the ability to correct and balance by helping to normalize the beneficial microbes and reversing conditons of intestinal dysbiosis. This is huge.
Everything we consume goes through our intestines. Point, if half of Robert Smiths research work is connected to cows or the environment, then chances are exposure has taken place through our gut. Additionally, you look at just about any parasitic disease, be it an offical bug or cell or fungi, and the main place of multiplication of the species takes place within the intestinal walls.
Frito