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Home»Weight loss»The Human GI Tract: A Vitamin-Producing Powerhouse
Weight loss

The Human GI Tract: A Vitamin-Producing Powerhouse

By fitsavers-January 25, 2022No Comments5 Mins Read
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People supplement B vitamins for a variety of reasons: to prevent vitamin B12 deficiency, prevent birth defects (B9 or folate), encourage hair growth (B7 or biotin), reduce blood levels of homocysteine (B6, B9, B12, sometimes B2), among other effects. And there is no question that addition of B vitamins can indeed achieve specific health benefits. Supplementation of vitamin B9 (folate, folic acid) by pregnant females, for instance, reduces the incidence of spina bifida in newborns, while supplementation of nicotinamide (a form of vitamin B3) reduces the incidence of basal and squamous cell skin carcinomas, and supplementation of B7 or biotin restores hair growth for some people.

But it is becoming clearer and clearer that microbes in the human intestinal microbiome have the potential for production of substantial quantities of B vitamins that include B1, B2, B3, B5, B6, B7, B9, and B12. Akkermansia and many species of Bacteroidetes, for instance, are vigorous producers of multiple B vitamins. Yogurts fermented with Streptococcus thermophilus produce substantial quantities of folate (though even more would be produced if prolonged fermentation was used, not the meager 4 hour fermentation used by commercial yogurt manufacturers), as can Bifidobacterium longum and some strains of L. reuteri.

Here’s my question: If intestinal microbes are able to produce the full panel of B vitamins, are the apparent benefits of B vitamin supplementation really just compensating for a disrupted microbiome that lacks B vitamin-producing species? Overweight and obese people, for instance, lack Akkermansia and species of Bacteroidetes and have over-proliferation of Firmicutes, tipping the balance towards less B vitamin production. Does restoration of a healthy intestinal microbiome provide sufficient B vitamins that makes supplementation unnecessary?

While the evidence remains preliminary, I do believe that we are heading in that direction. In other words, the human body and microbiome have adapted to generating their own nutrients and the apparent need for exogenous nutrients is a modern phenomenon, a product of the microbiome that we have disrupted due to antibiotics, glyphosate, herbicides and pesticides in food, obesity, stomach acid-suppressing drugs and the myriad other factors that disrupt the microbes living in our GI tracts.

It means that many health questions need to be reconsidered in light of the contribution of the intestinal microbiome. You can begin to appreciate, for example, that concerns over high homocysteine levels that have been blamed on lack of vitamins B6, folate, B12 and sometimes B2 (riboflavin) may have been misplaced, as these nutrients are all bacterial products. In other words, while higher levels of homocysteine, especially levels of 14 micromol/L or greater have been confidently associated with increased risk for cardiovascular death, depression, dementia, and various cancers, eight randomized placebo-controlled clinical trials have demonstrated that B vitamin supplementation that reduces blood levels of homocysteine do not reduce risk. In other words, there is a disconnect between blood levels of homocysteine and risk for these conditions, and supplementing B vitamins has no impact on the incidence of disease.

What if higher homocysteine levels are instead viewed as the failure of the intestinal microbiome to produce B vitamins? Supplementing B vitamins would then, of course, have no effect on disease incidence because a disrupted intestinal microbiome and its accompanying endotoxemia would be the explanation for increased cardiovascular risk, depression, dementia, and cancer. Trillions of microbes, living and dying every hour of every day, release their breakdown products into the bloodstream (“endotoxemia”) that inflames arteries, causes atherosclerotic plaque rupture, raises blood pressure, triggers depression, activates inflammation in various organs including the brain, causes or worsens insulin resistance. The solution would therefore not be supplementation of B vitamins, but to address the disrupted intestinal microbiome that involves a shift away from species that produce B vitamins. Taking B vitamins without addressing the disrupted microbiome responsible for reduced B vitamin levels then achieves nothing. It also suggests that higher blood levels of homocysteine can serve as markers for dysbiosis and small intestinal bacterial overgrowth, SIBO, and does not suggest a need for B vitamin supplementation.

Are you beginning to appreciate that insights into the intestinal microbiome should cause us to reconsider ALL common chronic diseases that afflict modern people? “Treat” depression with SSRI antidepressant drugs while ignoring the dysbiosis/SIBO and endotoxemia and you have only managed to Band-Aid some of the emotional turmoil of depression but leaves you susceptible to developing fibromyalgia, irritable bowel syndrome, ulcerative colitis, type 2 diabetes, obesity, hypertension, atrial fibrillation, diverticular disease, etc. “Treating” psoriatic arthritis with a biologic, prednisone, and naproxen that block inflammatory pathways while ignoring dysbiosis/SIBO and endotoxemia likewise leaves you susceptible to a long list of chronic diseases.

It means that every doctor should be an expert in the microbiome and how to assess it, help you manage and reconstruct it, just as they should all be experts in nutrition and health.  But you know that is not the case, since talk of nutrition and the microbiome does not yield revenues like performing a colonoscopy, carotid endarterectomy. or injections for macular degeneration do. That’s why efforts to reconstruct a healthy intestinal microbiome are up to YOU. This is why I wrote my new book, Super Gut: A 4-Week Plan to Reprogram Your Microbiome, Restore Health and Lose Weight  that provides readers with a step-by-step path to not just “treat” health conditions, but address the actual cause.

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