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Tag: Prevotella

  • Might Meat Trigger Parkinson’s Disease?  | NutritionFacts.org

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    What does the gut have to do with developing Parkinson’s disease?

    Parkinson’s disease is an ever-worsening neurodegenerative disorder that results in death and affects about 1 in 50 people as they get older. A small minority of cases are genetic, running in families, but 85% to 90% of cases are sporadic, meaning they seem to pop up out of nowhere. Parkinson’s is caused by the death of a certain kind of nerve cell in the brain. Once about 70% of them are gone, the symptoms start. What kills off those cells? It still isn’t completely clear, but the abnormal clumping of a protein called alpha-synuclein or α-synuclein is thought to be involved. Why? Researchers injected blended Parkinson’s brains into the heads of rats and monkeys, and Parkinson’s pathology and symptoms were induced. It can even happen when injecting just the pure, clumped α-synuclein strands themselves. How, though, do these clumps naturally end up in the brain?

    As I discuss in my video The Role Meat May Play in Triggering Parkinson’s Disease, it all seems to start in the gut. The part of the brain where the pathology often first appears is directly connected to the gut, and we have direct evidence of the spread of Parkinson’s pathology from the gastrointestinal (GI) tract to the brain: α-synuclein from brains of Parkinson’s patients is taken up in the gut wall and creeps up the vagal nerves from the gut into the brain—at least that was the case in rats. If only we could go back and look at people’s colons before they got Parkinson’s. Indeed, we can. Old colon biopsies from people who would later develop Parkinson’s were dredged up, and, years before symptoms arose, you could see the α-synuclein in their gut.

    Research supported by the Michael J. Fox Foundation has found that you can reliably distinguish the colons of patients from controls by the presence of this Parkinson’s protein lodged in the gut wall. But how did it get there in the first place? Are “vertebrate food products…a potential source of prion-like α-synuclein”? Indeed, nearly all the animals with backbones that we consume—cows, chickens, pigs, and fish—express the protein α-synuclein. So, when we eat common meat products, when we eat skeletal muscle, we’re eating nerves, blood cells, and the muscle cells themselves. Every pound of meat contains, on average, half a teaspoon of blood, and that alone could be an α-synuclein source to potentially trigger a clumping cascade of our own α-synuclein in the gut. Though “it may seem intuitive that dietary α-synuclein could seed aggregation in the gut,” this kind of buildup, what evidence do we have that it’s actually happening?

    We have some pretty interesting data. There’s a surgical procedure called a vagotomy, in which the big nerve that goes from our gut to our brain—the vagus nerve—is cut as an old-timey treatment for stomach ulcers. Would cutting communication between the gut and the brain reduce Parkinson’s risk? Apparently so, suggesting that the gut to brain’s vagal nerve may be critically involved in the development of Parkinson’s disease.

    Of course, “many people regularly consume meat and dairy products, but only a small fraction of the general population will develop PD,” Parkinson’s disease. So, there must be other factors at play that “may provide an opportunity for unwanted dietary α-synuclein to enter the host, and initiate disease.” For example, our gut becomes leakier as we age, so might that play a role? What else makes our gut leaky? “Dietary fiber deprivation has also been shown to degrade the intestinal barrier and enhance pathogen entry.” So, this raises “possibilities for food-based therapies.”

    Parkinson’s patients have significantly less Prevotella in their gut, a friendly fiber-eating flora that bolsters our intestinal barrier function. So, low levels of Prevotella are linked to a leaky gut, which has been linked to intestinal α-synuclein deposition, but fiber-rich foods may bring Prevotella levels back up. “Therefore, it is possible that by adopting a plant-based diet, in addition to the beneficial effects of phytonutrients, increasing overall fiber intake may modify gut microbiota and gut permeability [leakiness] in beneficial ways for people with PD.”

    So, does a vegan diet—one with lots of fiber and no meat—reduce risk for Parkinson’s? Parkinson’s “appears to be rare in quasi-vegan cultures,” with rates that are about five times lower in rural sub-Saharan Africa, for instance. All this time, we were thinking the benefits seen for Parkinson’s from plant-based diets were due to the antioxidants and anti-inflammatory nature of the animal-free diets, but maybe it’s also due to the increased intestinal exposure to fiber and decreased intestinal exposure to ingested nerves, muscles, and blood.

    Wasn’t that fascinating? For more on Parkinson’s, see the related posts below.

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    Michael Greger M.D. FACLM

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  • Fiber or Low FODMAP for SIBO?  | NutritionFacts.org

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    It may not be the number of bacteria growing in our small intestine, but the type of bacteria, which can be corrected with diet.

    When researchers tested more than a thousand patients suffering for longer than six months from symptoms typical with irritable bowel syndrome (IBS), such as excess gas, bloating, diarrhea, and abdominal pain, but who do not appear to have anything more serious going on, like inflammatory bowel disease, a significant percentage were found to be suffering from lactose intolerance—intolerance to the milk sugar lactose. In infancy, we have an enzyme called lactase in our small intestine that digests milk sugar, but, understandably, most of us lose it after weaning. “Although genetic mutation has led to persistence of lactase in adults, about 75% of the world’s population malabsorbs lactose after age 30” and have lactose intolerance. However, a third of the patients were diagnosed with small intestinal bacterial overgrowth (SIBO).

    “The evidence for SIBO and IBS is shrouded in controversy, predominantly because of the fact that the [breath] tests used in clinical practice to diagnose SIBO are not valid,” as I’ve explored before. As well, the implications of having more versus fewer bacteria growing in the small intestine are unclear since the number doesn’t seem to correlate with the symptoms. It turns out it isn’t the number of bugs growing in the small intestine, but the type of bugs. So, it’s “small intestinal microbial dysbiosis”—not overgrowth in general, but the wrong kind of growth—that appears to underlie symptoms associated with functional gastrointestinal disorders, like IBS.

    How can we prevent this from happening? The symptoms appear to be correlated with a significant drop in the number of Prevotella. Remember them? Prevotella are healthy fiber feeders, “suggestive of a higher fiber intake in healthy individuals,” while the bugs found more in symptomatic patients ate sugar, which “may reflect a higher dietary intake of simple sugars.” However, correlation doesn’t mean causation. To prove cause and effect, we have to put it to the test, which is exactly what researchers did.

    “Switching a group of healthy individuals who habitually ate a high­-fibre diet (>11g per 1,000 calories) to a low­-fibre diet (<10g per day) containing a high concentration of simple sugars for 7 days produced striking results. First, 80% developed de novo [new] gastrointestinal symptoms such as bloating and abdominal pain that resolved on resumption of their habitual high-fibre diet. Second, diet­-related changes in the small intestinal microbiome were predictive of symptoms (such as bloating and abdominal discomfort) and linked to an alteration in duodenal [intestinal] permeability.” In other words, they developed a leaky gut within seven days. And, while some went from SIBO positive to SIBO negative and others from SIBO negative to SIBO positive, it didn’t matter because the number of bacteria growing didn’t correlate with symptoms. It was the type of bacteria growing, as you can see below, and at 3:12 in my video Fiber vs. Low FODMAP for SIBO Symptoms.

    No wonder their guts got leaky. Levels of short-chain fatty acids plummeted. Those are the magical by-products our good gut bugs make from fiber, which “play an important role in epithelial [intestinal] barrier integrity,” meaning they keep our gut from getting leaky.

    So, while we don’t have sound data to suggest that something like a low FODMAP diet has any benefit for patients with SIBO symptoms, there have been more than a dozen randomized controlled trials that have put fiber to the test. Overall, researchers found there was a significant improvement in symptoms among those randomized to increase their fiber intake. That may help explain why “high-fiber, plant-based diets can prevent many diseases common in industrialized societies.” Such diets have this effect “on the composition and metabolic activity of the colonic microbiota.” Our good gut bugs take plant residues like fiber and produce “health-promoting and cancer-suppressing metabolites” like short-chain fatty acids, which have profound anti-inflammatory properties. “All the evidence points to a physiological need for ~50 g fiber per day, which is the amount contained in the traditional African diet and associated with the prevention of westernized diseases.” That is approximately twice the typical recommendation and three times more than what most people get on a daily basis. Perhaps it should be no surprise that we need so much. Even though we split from chimpanzees millions of years ago, “there is still broad congruency” in the composition of our respective microbiomes to this day. While they’re still eating their 98 to 99 percent plant-based diets to feed their friendly flora with fiber, we’ve largely removed fiber-rich foods from our food supply. 

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    Michael Greger M.D. FACLM

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