Bacteria vs. genetic predisposition: the spread of chronic disease in familiesAuthor: Amy Proal
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Sam is a 32-year-old patient who is using the Marshall Protocol to treat CFS and depression (and doing extremely well). But Sam is certainly not he only person in his family suffering from Th1 disease – the name given to inflammatory illness caused by L-form bacteria that reside undetected inside biofilms and the cells of the immune system.
Sam’s mother suffers from
fibromyalgia, accompanied by
insomnia,
fatigue, and
irritable bowel disorder. His father recently had a stroke, and deals with substantial fatigue and
depression. His older brother has debilitating back pain and is hard of hearing. His youngest sister suffers from
alopecia, brain fog, depression, excessive fatigue, and mild
attention deficit disorder. The youngest brother in the family has a severe case of bipolar disorder, as well as irritable bowel syndrome.
It’s obvious that every member of Sam’s immediate family harbors a substantial load of L-form bacteria and that these pathogens have, over time, spread from person to person. Clearly, just like other forms of bacteria,
L-form bacteria can be passed around. Although Th1 diseases are not obviously contagious, they are communicable – meaning that transmission of L-form bacteria requires close contact and is seen often within the family unit. The pathogens can also be transmitted from person to person through bodily fluids released during coughing, sneezing and other intimate contact.
L-form bacteria can survive in sperm cells.People whose parents harbor high loads of L-form bacteria are much more likely to fall ill with a Th1 disease earlier in life. L-form bacteria are able to survive in sperm, so a father can pass these pathogens to his child at the moment of conception. Evidence is also growing that L-form bacteria and other pathogens are able to cross the placental barrier – meaning they can be passed from a pregnant woman to her fetus.
Researchers at Peking University in Beijing recently discovered that the H5N1 bird flu virus can pass through a pregnant woman’s placenta to infect her fetus.[1] Other studies have revealed that other bacterial species such as Borrelia burgdorferi and Mycobacterium tuberculosis are also capable of crossing the placental barrier during pregnancy.[2] If these pathogens can be passed from mother to child during gestation, then why not other forms of bacteria that are capable of transforming into the L-form?
[glow=red,2,300]Successive infection[/glow]
Infants born into families whose members harbor high loads of L-form bacteria are also more likely to pick up these pathogens after birth. As described here, it takes an infant several weeks to develop a fully functional innate immune system, meaning that during the first few weeks of life, infants are particularly vulnerable to bacteria passed around by other members of the family unit. But in order to fully understand what eventually causes an infant to develop a full-fledged Th1 disease, one must understand the concept of successive infection.
Inside every cell in the body are sequences of DNA that make up our genes. Over thousands of years, bacteria, viruses, bacteriophages, and other pathogens have evolved mechanisms that allow them to mutate and alter the expression of the genes inside the cells they infect. Researchers at the Institute of Genetics in China found that when the bacterial species Mycobacterium tuberculosis infects immune cells called macrophages, it causes mutations in about 70 genes and affects the expression of another 366.[3]
The genes affected by pathogens inside a cell are active in regulating the activity of cytokines, coding for receptors on the surface of cells, regulating cell signaling pathways, monitoring cell death (apoptosis), controlling cell mediated immunity, regulating the production of proteins, creating enzymes, and many other essential processes.
Unfortunately, as pathogens gradually gain control over the genes that regulate the above processes, many of the mutations or changes in gene expression they produce can manipulate the host cell in order to aid their survival and reproduction. These changes also create an environment inside the cell that makes it easier for new pathogens to invade and persist. For example, Bukholm and team found that Measles virus infection of cell cultures makes the cells more susceptible to a secondary bacterial invasion.[4] Quite a few species of bacteria have even developed the ability to use the Beta-lactams antibiotics in order to increase the likelihood of DNA sharing as they transform into the L-form.
“When one of the nasty bugs arrives, does it find your DNA intact in the cell it invades, or has the DNA already been altered by a previous pathogen?” asks Marshall. “If it tries to act on an altered gene, then the result will be different from if it acts on a ‘clean’ gene.”
Thus, as each subsequent pathogen that a person encounters proceeds to make even more changes to their cellular DNA, eventually these mutations create a snowball effect where, as a person acquires an increasing number of pathogens, it becomes even easier for them to pick up a diverse array of other infectious agents.
In addition to the genetic changes that accumulate as a person encounters an increasing number of pathogens, some bacteria also alter the activity of the immune system by creating substances that bind and block the
Vitamin D Receptor (VDR) – a fundamental receptor of the body that controls the activity of the innate immune system and the expression of the antimicrobial peptides (AMPs) – proteins that kill bacteria, viruses, and fungi by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell. As a person acquires more and more L-form bacteria, the activity of their innate immune system decreases, and less antimicrobial peptides are produced, making it even easier for these pathogens to survive in the body and continue to alter human cellular DNA.
Inside every cell of the body are sequences of DNA that form genes...................really LONG Article there SAMMY~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
It makes some interesting points. Thanks for finding this!
Here is the LINK to the COMPLETE article:bacteriality.com/2007/10/31/family/researchers have been unable to isolate any specific sequences of DNA that might make a person susceptible to a certain disease. They fail to understand that the predisposition for any Th1 illness is not genetic, it is acquired.
It’s only logical that in the coming years, medicine will move away from the hypothesis of genetic predisposition and towards the concept of successive infection. As this new understanding of chronic disease spreads, the concept of inheritance will no longer refer to parents passing on a defective genes, but will instead be superseded by the notion that bacteria themselves are acquired from the mother during pregnancy, and through a father’s sperm.