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http://onlinelibrary.wiley.com/doi/10.1 ... 411.x/fullTo find out, Mazmanian and his colleagues tried to induce MS in animals that were completely devoid of the microbes that normally inhabit the digestive system. "Lo and behold, these sterile animals did not get sick," he says.
Then the researchers decided to see what would happen if bacteria were reintroduced to the germ-free mice. But not just any bacteria. They inoculated mice with one specific organism, an unculturable bug from a group known as segmented filamentous bacteria. In prior studies, these bacteria had been shown to lead to intestinal inflammation and, more intriguingly, to induce in the gut the appearance of a particular immune-system cell known as Th17. Th17 cells are a type of T helper cell—cells that help activate and direct other immune system cells. Furthermore, Th17 cells induce the inflammatory cascade that leads to multiple sclerosis in animals.
"The question was, if this organism is inducing Th17 cells in the gut, will it be able to do so in the brain and central nervous system?" Mazmanian says. "Furthermore, with that one organism, can we restore to sterile animals the entire inflammatory response normally seen in animals with hundreds of species of gut bacteria?"
The answer? Yes on all counts. Giving the formerly germ-free mice a dose of one species of segmented filamentous bacteria induced Th17 not only in the gut but in the central nervous system and brain—and caused the formerly healthy mice to become ill with MS-like symptoms.
http://www.pulsus.com/cddw2012/abs/279.htmSegmented filamentous bacteria (SFB) are present in the gastrointestinal tract of mice from weaning until the maturation of the immune system. Probiotic bacteria also have an effect on host immunity. To study the relationships established between these bacteria, samples from a mouse model fed with Lactobacillus plantarum under different immunological conditions were analysed. SFB populations were measured by a newly designed group-specific quantitative PCR assay. The results confirmed the presence of the probiotic in the intestine and an expansion of SFB in the ileum of immunocompromised mice, which was abolished upon administration of L. plantarum, an effect not described to date.
Importantly, Segmented Filamentous Bacteria(SFB), Clostrium coccoides sp. deemed to be important in modulated Th17 and regulatory T cells respectively, were significantly decreased in mice fed fish oil supplemented diets.
Blurg! Well why haven't you?! Lol. (I haven't had mine tested either). I want a magic Polaroid instalab so I can get answers to all my questions within moments. You haven't seen one anywhere, have you?jimmylegs wrote:I haven't personally, but I definitely helped a close family member kick chronic ebv infection using antiviral nutrition science
Quantitative PCR analysis of 16S rRNA showed that exposure of C57BL6 mice to side-stream cigarette smoking increased the amount of Clostridium clostridiforme and mouse intestinal bacteria (MIB) in the cecal microflora, while decreasing the content of Lactoccoci, Ruminococcus albus, Enterobacteriaceae and segmented filamentous bacteria (SFB) compared with those of control mice (Figure 1).
Regarding lipoic acid, You might be interested in this thread, Lipoic Acid: R vs. S.grandsons4 wrote:Briefly then: inosine to eat peroxynitrite; ketogenic/Terry Wahls diet; low dose naltexone (LDN); alpha-lipoic acid (ALA); N-acetylcysteine (NAC); and several other supplements. No DMD’s.
One of the criteria used in any decision was “risk vs. reward.” ANY THOUGHTS?
Hi grandsons4,grandsons4 wrote:After what I consider to be ample research, I have formulated what I believe to be a prudent, present course of action for my son, who was recently diagnosed with MS. I will attempt to explain how I came to this formulation. Although I will write as though what I say is fact, it is just my opinion. I will not be too specific.
Firstly, Multiple Sclerosis is more of a syndrome then a disease in the classical sense, and diagnosis is by definition. Nevertheless, the definitive hallmark of the disease is the breakdown of the blood-brain barrier (BBB) and/or the blood-spinal cord barrier (BSCB), which allows a cascade of pathologies to arise, ultimately resulting in the death of oligodendrocytes and the subsequent loss of myelin. The cause of this breakdown is mediated by a combination of environmental (pathogens, toxins, poor diet), genetic (inability to metabolize certain substances, missing genes, abnormal gene expression), and lifestyle (daily stresses, lack of exercise, no sun) factors. It is my belief that the effects of these factors can be mitigated (if not eliminated), thus restoring the BBB and repairing the damage done (even to the myelin).
Since changing my son’s genetic predispositions is unlikely to happen, addressing the environmental and lifestyle factors remains. Likely pathogenic triggers for MS are the Epstein-Barre virus (EBV) , Borrelia burgdorferi (Bb), Chlamydia pneumoniae (Cpn), and human herpesvirus 6 (HHV-6).
As for EBV. EBV is persistent; resveratrol compromises survival and proliferation of EBV. Th17 cells enhance viral persistence and inhibit beneficial T cell cytotoxicity; zinc suppresses TH17 development. EBV-specific CD8+ T cells are involved in the immunopathogenesis of MS; vitamin D has a direct immunomodulatory effect on CD8+ T cells of patients with early multiple sclerosis. So, supplement with resveratrol, vitamin D3, and zinc.
Bb and Cpn are both intially treated with minocyline, which is shown to have increased the efficacy of Copaxone (if Copaxone, indeed, had any), and which also has been shown to inhibit poly(ADP-ribose) polymerase (PARP), proteins implicated in the death of oligodendrocytes. So, treat for either Lyme (which my son tends to believe he has) or Cpn: or, which seems quite feasible, an aggregate of both protocols.
Wow, has this become wordier than I anticipated. Briefly then: inosine to eat peroxynitrite; ketogenic/Terry Wahls diet; low dose naltexone (LDN); alpha-lipoic acid (ALA); N-acetylcysteine (NAC); and several other supplements. No DMD’s.
One of the criteria used in any decision was “risk vs. reward.” ANY THOUGHTS?
GS4,grandsons4 wrote:Anonymoose, thanks. I too agree that antibiotics are not without risks, with actions and consequences beyond the depletion of the microbiome, a very serious, if not catastrophic, matter on its own. May I ask, considering your poor reaction to the protocol, did you attempt to counter the die off of you gut flora with probiotics? Anecdote, as I believe you're aware, ultimately had very positive results. While realizing that people are different, I'm trying to glean from the different personal experiences posted on these forums (one of the reasons this site is great) any variations in regimens that might account for the wide discrepancies in experiences. Knowledge is power! Thanks again.