Probiotics are dietary supplements of live bacteria or yeasts thought by many to be healthy for the host organism. Autoimmunity Research Foundation has no official recommendation on if a patient should or should not take probiotics. However, patients who take probiotics may want to think twice before consuming probiotics, and for several reasons.
First, the introduction of additional bacteria increases the workload of the innate immune system, thereby diverting resources from fighting the infection of intracellular pathogens. Also, consumption of probiotics increases the likelihood of horizontal gene transfer between pathogenic forms of bacteria and their “friendlier” cousins.
Probiotics have a number of seeming benefits including the lowering of cholesterol, reduction of blood pressure, decrease of certain kinds of diarrhea, reduction of inflammation, etc. Many researchers are convinced that probiotics exert these positive effects by overwhelming the bad bacteria. Perhaps the “beneficial” bacteria found in yogurt and supplements exert some positive effect – lowering the pH in the human gut, for example. That said, it remains unclear how exactly probiotics improve health outcomes.
The goal of the Marshall Protocol is to eradicate the pathogens which cause inflammatory diseases. The bacterial die-off reaction is known as immunopathology, and it is a necessary part of recovery. Epidemiological evidence has shown that substances which interfere with immunopathology decrease symptoms in the near term and increase disease over the long term. Drugs or substances which interfere with immunopathology – whether they be prescription medications such as TNF-alpha inhibitors, corticosteroids, interferon, or a vitamin D supplement – are limiting progress.
When bacteria enter the body – whether described as “friendly” or pathogenic – the innate immune system mounts a response to that presence. Even commensal bacteria can activate innate immune responses.1 2 One research team found that treatment with probiotics doubles levels of the inflammatory cytokine Interferon-gamma,3 confirming that the bacteria do generate a Th1 inflammatory reaction upon their entry into the gut.
It is likely that probiotics' seeming effectiveness is that patients taking them are overloading their immune response and reducing the amount of bacteria killed, a process which itself leads to diminished immunopathology and relative symptom improvement.
One 2011 study which administered fermented milk to mice concluded that the effects of probiotics on gut bacteria may be subtle.4 “Cocktails of classic probiotics, which people have been trying for years, may have some benefit but the effect seems to be quite small,” according to David Relman.
Supporting the above hypothesis is one study which showed that patients with acute pancreatitis (inflammation of the pancreas) that were given probiotics were more than twice as likely to die as compared to those who received placebos.5
One compelling explanation for this unexpected result is that the patients who were given probiotics effectively diverted their immune system from fighting infection at the site of the pancreatitis to the bowel. Perhaps the additional bacteria load was enough to increase the burden on the immune response to the point where a significant number of additional patients was no longer able to effectively muster a response to the acute pancreatitis, a condition which itself is caused by the Th1 pathogens.
Developing gum disease may require not only bad bacteria but also a benign background microbiota, researchers reported in Cell Host and Microbe.8 When the gingivitis-associated Porphyromonas gingivalis was introduced at low levels into the mouths of normal mice, it triggered a substantial growth in the healthy bacteria already there, and the ensuing periodontal disease led to bone loss.
But no such thing happened when the gingivitis bacteria were introduced to mice with sterile mouths that harbored no normal bacteria. It seems that a single species, even at low levels, can disrupt the stability of the bacterial ecosystem in the mouth, the researchers noted.
Blaney: “Prebiotics article may explain negative effects of probiotics that contain FOS etc.” http://www.biomedcentral.com/1471-2180/9/245
BMC Microbiol. 2009 Nov 30;9:245. Some putative prebiotics increase the severity of Salmonella enterica serovar Typhimurium infection in mice. Petersen A, Heegaard PM, Pedersen AL, Andersen JB, Sørensen RB, Frøkiaer H, Lahtinen SJ, Ouwehand AC, Poulsen M, Licht TR. The National Food Institute, Department of Microbiology and Risk Assessment, Technical University of Denmark, Moerkhoej Bygade 19, DK-2860 Soeborg, Denmark. email@example.com Abstract BACKGROUND: Prebiotics are non-digestible food ingredients believed to beneficially affect host health by selectively stimulating the growth of the beneficial bacteria residing in the gut. Such beneficial bacteria have been reported to protect against pathogenic infections. However, contradicting results on prevention of Salmonella infections with prebiotics have been published. The aim of the present study was to examine whether S. Typhimurium SL1344 infection in mice could be prevented by administration of dietary carbohydrates with different structures and digestibility profiles. BALB/c mice were fed a diet containing 10% of either of the following carbohydrates: inulin, fructo-oligosaccharide, xylo-oligosaccharide, galacto-oligosaccharide, apple pectin, polydextrose or beta-glucan for three weeks prior to oral Salmonella challenge (107 CFU) and compared to mice fed a cornstarch-based control diet. RESULTS: The mice fed with diets containing fructo-oligosaccharide (FOS) or xylo-oligosaccharide (XOS) had significantly higher (P < 0.01 and P < 0.05) numbers of S. Typhimurium SL1344 in liver, spleen and mesenteric lymph nodes when compared to the mice fed with the cornstarch-based control diet. Significantly increased amounts (P < 0.01) of Salmonella were detected in ileal and fecal contents of mice fed with diets supplemented with apple pectin, however these mice did not show significantly higher numbers of S. Typhimyrium in liver, spleen and lymph nodes than animals from the control group (P < 0.20).The acute-phase protein haptoglobin was a good marker for translocation of S. Typhimurium in mice. In accordance with the increased counts of Salmonella in the organs, serum concentrations of haptoglobin were significantly increased in the mice fed with FOS or XOS (P < 0.001). Caecum weight was increased in the mice fed with FOS (P < 0.01), XOS (P < 0.01), or polydextrose (P < 0.001), and caecal pH was reduced in the mice fed with polydextrose (P < 0.001). In vitro fermentation in monocultures revealed that S. Typhimurium SL1344 is capable of fermenting FOS, beta-glucan and GOS with a corresponding decline in pH. CONCLUSION: Supplementing a cornstarch-based rodent diet with 10% FOS or XOS was found to increase the translocation of S. Typhimurium SL1344 to internal organs in mice, while 10% apple pectin was found to increase the numbers of S. Typhimurium in intestinal content and feces. PMID: 19948011
Nat Med. 2009 Sep;15(9):1016-22. Epub 2009 Aug 23. A human colonic commensal promotes colon tumorigenesis via activation of T helper type 17 T cell responses. Wu S, Rhee KJ, Albesiano E, Rabizadeh S, Wu X, Yen HR, Huso DL, Brancati FL, Wick E, McAllister F, Housseau F, Pardoll DM, Sears CL. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Comment in: Gastroenterology. 2010 Jul;139(1):353-5. Abstract The intestinal flora may promote colon tumor formation. Here we explore immunologic mechanisms of colonic carcinogenesis by a human colonic bacterium, enterotoxigenic Bacteroides fragilis (ETBF). ETBF that secretes B. fragilis toxin (BFT) causes human inflammatory diarrhea but also asymptomatically colonizes a proportion of the human population. Our results indicate that whereas both ETBF and nontoxigenic B. fragilis (NTBF) chronically colonize mice, only ETBF triggers colitis and strongly induces colonic tumors in multiple intestinal neoplasia (Min) mice. ETBF induces robust, selective colonic signal transducer and activator of transcription-3 (Stat3) activation with colitis characterized by a selective T helper type 17 (T(H)17) response distributed between CD4+ T cell receptor-alphabeta (TCRalphabeta)+ and CD4-8-TCRgammadelta+ T cells. Antibody-mediated blockade of interleukin-17 (IL-17) as well as the receptor for IL-23, a key cytokine amplifying T(H)17 responses, inhibits ETBF-induced colitis, colonic hyperplasia and tumor formation. These results show a Stat3- and T(H)17-dependent pathway for inflammation-induced cancer by a common human commensal bacterium, providing new mechanistic insight into human colon carcinogenesis. PMID: 19701202
Is Yogurt Good for You?
Probiotics and “Science by Product Release”
Friendly Gut Bacteria May Trigger MS
In an astonishing new study published in Nature today, researchers at the Max Planck Institute of Neurobiology in Martinsried in Munich, Germany say they have found evidence that suggests multiple sclerosis (MS) is triggered by natural intestinal flora, the so-called friendly bacteria that reside in the gut. They found genetically engineered mice with normal gut bacteria developed brain inflammation similar to MS in humans. They say the bacteria first activated the immune T-cells, then the B-cells, which resulted in an attack on the myelin layer in the brain. The same could happen in humans with a corresponding genetic predisposition, they say.
Nature. 2011 Oct 26. doi: 10.1038/nature10554. [Epub ahead of print] Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination. Berer K, Mues M, Koutrolos M, Rasbi ZA, Boziki M, Johner C, Wekerle H, Krishnamoorthy G. Source Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany. Abstract Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. These pathogenic immune cells derive from progenitors that are normal, innocuous components of the healthy immune repertoire but become autoaggressive upon pathological activation. The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis, here we show that the commensal gut flora-in the absence of pathogenic agents-is essential in triggering immune processes, leading to a relapsing-remitting autoimmune disease driven by myelin-specific CD4(+) T cells. We show further that recruitment and activation of autoantibody-producing B cells from the endogenous immune repertoire depends on availability of the target autoantigen, myelin oligodendrocyte glycoprotein (MOG), and commensal microbiota. Our observations identify a sequence of events triggering organ-specific autoimmune disease and these processes may offer novel therapeutic targets. PMID: 22031325
The first description of the possible involvement of bacterial flora in the pathology of arthritis came in the late 1970s when rats raised under germ-free conditions developed severe joint inflammation with 100% penetrance in an adjuvant-induced arthritis model, while conventionally raised controls showed only mild disease at a very low incidence.67 This finding suggests that, although a microbiota is not necessary for the development of arthritis, its presence has a potential suppressive effect through modulation of the immune response. The mechanism behind this suppressive effect remains unclear. The humoral immune system is not a prerequisite for arthritis, as germ-free rats do not produce specific autoantibodies to heat-shock protein (hsp) 65 and yet do develop clinical disease. This observation seems to indicate that immunity to hsp65 in experimental arthritis is unrelated to disease and may instead be regarded as an epiphenomenon dependent on the presence of gut flora.68