In the last post, I promised to blog on the role dietary fat and cholesterol play in endotoxemia and heart disease. However, before I do, I feel a need to clarify exactly what part of the digestive tract these toxins are most likely coming from. Where these endotoxins cross the gut wall helps give us some idea about what dietary factors are most likely contributing to the problem.
Just as any open sore on the skin can allow bacteria, viruses or other harmful foreign substances access to the bloodstream, so do open sores in the mouth or gums. For this reason periodontal disease is a potential source of infection that may contribute to the development of cardiovascular disease. As mentioned in the last post, oral pathogens are commonly found in arterial plaque.
However, while I do believe oral dysbiosis is a source of pathogens, I doubt direct translocation from the mouth accounts for more than a small fraction under normal circumstances. Intense immune responses and the pain they generate at the site of gum and tooth infections are usually agonizing enough to cause the person experiencing them to do anything to alleviate the problem, even if that means yanking out one or more teeth with or without professional assistance. Moreover, the surface area of the mouth is not very large so potential pathogen exposure to the bloodstream is somewhat limited in comparison to the intestines.
Yes, chronic dental infections afflict millions around the world who are malnourished, cannot afford dental care or do not have access to it, including here in the United States. So I don’t want to downplay the problem. It’s just that oral pathogens are also swallowed in saliva. Combine this with impaired gastric barrier function and it’s easy to see how these bacteria can also colonize the intestines.
I suspect that oral pathogens translocating from the small intestine are of bigger concern because of the liver dysfunction that is a common feature in those diseases we group under metabolic syndrome: diabetes, cardiovascular disease, obesity and fatty liver. Bacteria that crosses the gut wall and is not encased in a lipid carrier or chylomicron makes its way to the liver first, and it is here that early manifestations of metabolic diseases are usually detected.
Weston A. Price, an early 20th century dentist, traveled across the globe in search of healthy populations. What he found was that dental health mirrored overall health and documented these findings in his ground-breaking book, Nutrition and Physical Degeneration. None of the healthy communities Weston A. Price visited had dentists or regularly brushed their teeth. Their dental health was a sign of their excellent nutritional status and the absence of dietary factors that would otherwise negatively impact oral microbiota and impair nutrient absorption via disordered gut flora.
To have small gut dysbiosis means being unable to digest food properly and produce the necessary gut hormones that regulate a whole host of processes not least of which is digestion itself. This is why nutritional deficiencies are common in those with small intestinal bacterial overgrowth. This malnutrition, even in the presence of overeating, itself a symptom of malnutrition, will impact all systems of the body, including the teeth and gums. So I believe that oral dysbiosis, like chronically elevated cortisol levels or glucose dysfunction or fatty liver, is a symptom of small gut dysbiosis and the nutritional deficiencies that result from this.
Gut dysbiosis can initiate oral dysbiosis or conversely, oral dysbiosis in the presence of compromised gastric barrier function, can cause gut dysbiosis; once either develops the one fuels the other in an endless positive feedback loop. Whether the oral or gut dysbiosis comes first is open to debate. However, since most of the same dietary factors are involved in both processes our concern should be focused on eliminating those agents and resolving the disordered flora.
The colon contains the most bacteria of any area in the body. If the colon is perforated for whatever reason, sepsis can set in threatening life itself. At this point it’s somewhat moot whether the bacteria flooding the bloodstream are commensals or pathogens because they all represent a potential threat to survival.
Ironically, many people who undergo a colonoscopy risk precisely this outcome. An estimated 70,000 people are killed or injured yearly when undergoing these procedures. (1) My spouse was one such statistic who developed intestinal bleeding, but luckily no serious infection less than a week after having a polyp removed. Four days of hospitalization, eight transfusions of blood and exhaustive upper and lower GI exams ensued. All tests came back negative so the colonoscopy seems the most likely reason for this frightening experience.
Apart from perforation, colonic dysbiosis that results in an inflammatory bowel disease causing gut wall inflammation is another potential source of endotoxemia. As I detailed in my SIBO series, what happens in the small intestine, or to be more precise, what doesn’t happen in the small intestine, often has knock-on effects further down the gastrointestinal tract. The entry of improperly digested protein, carbohydrate and fat due to small gut dysbiosis can initiate large intestinal dysbiosis by encouraging the growth of certain pathogenic bacteria or yeast that ferment these foods thus favoring their growth. Other dietary factors like binge drinking of alcohol can also cause or exacerbate colon dysbiosis.
Nevertheless, when we’re talking about how diet impacts endotoxemia we’re mainly talking about how it affects the small intestine, the major site of food digestion. The colon or large intestine is not a site of much absorption apart from water, sodium and some fat-soluble vitamins.
In comparison to the small intestine (the word “small” is a true misnomer for this part of the digestive tract), the large intestine has a relatively small surface area for the absorption of endotoxins. Because of the presence of numerous folds and finger-like structures or villi, the surface area of the small bowel is far greater than the colon so the potential for exposure and absorption of pathogens is therefore higher, hence the reason for the extensive small intestinal immune network. (2)
Fun fact of the day kids: the typical human “small” intestine when unfurled would cover the size of a tennis court!
Gastric Bypass Surgery
I’m sure you’re wondering what the hell gastric bypass surgery has to do with the topic at hand. Well, I want to clue you in on a miraculous thing that tends to happen as a side effect of these surgeries. Almost immediately after the procedure is completed, but well before any weight loss, many of these patients experience amazing normalization of glucose control and a complete cure of their type 2 diabetes. Not only that, their cholesterol and blood pressure also normalizes and sleep apnea disappears. (3)
What happens during these operations? Well first, a small pouch is formed to serve as a new stomach. This smaller stomach fills up rapidly after eating causing the person to feel full sooner thus curtailing their appetite.
Secondly, the small intestine is cut at a certain distance from where the stomach empties into the first part of the small intestine or duodenum. The severed bottom half of the small intestine is then reattached to the newly formed stomach pouch. The intestinal segment that is still attached to the stomach is then reattached to the small intestine forming a “Y” configuration. This allows digestive enzymes and bile access to the part of the small intestine that has food still traveling through it. To see a short animation of what I just described, see this. I promise it won’t gross you out.
In my post Insulin Resistance, Diabetes and Endotoxemia, I wrote how endotoxins are the most likely explanation for the development of type 2 diabetes. So my guess is that bypassing the diseased part of the small intestine, a portion rife with gut pathogens and made leaky by these same organisms, the liver is no longer under constant inflammatory assault. For the first time in years or decades, it’s able to finally do the many things it’s designed to do: help regulate blood glucose, take part in blood pressure regulation, export fat, excrete toxins in bile, etc. In other words, cut out the dysbiosis and the liver heals. Imagine that!
As I also covered here, curtailing this low-grade inflammation will stop impacting the hypothalamic-pituitary-adrenal axis. I suspect that the inflammation noted in the brain centers of weight regulation are mediated by these mechanisms.
Another result often seen in those undergoing these types of procedures are increases in gut hormone production. Two such hormones are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). (4)
GIP is responsible for inducing post-meal insulin release. Obviously, this gut hormone is important for proper glucose control. GLP-1 also affects glucose metabolism but in addition to that, it delays gastric emptying contributing to a feeling of fullness which reduces appetite. Other gut hormones that increase after bypass surgery are PYY and oxyntomodulin, both of which are satiety hormones.
Bacterial populations also seem to undergo changes for the better after these operations:
“Because RYGB [Roux-En-Y Gastric Bypass] may affect how nutrients are absorbed in different portions of the intestine, a new study conducted by researchers at the University of Zurich measured the bacterial composition and the amounts of different peptides that affect food intake along different intestinal segments after RYGB in rats. They found that 14 weeks after surgery, Bifidobacteria spp, and Bacteroides-Prevotella spp content were significantly increased in several portions of the intestine in RYGB rats compared to control animals. In fact, the changes in gut microbe populations after RGYB resembled those seen after treatment with prebiotics. Gut microbiota changes were also associated with altered production of gastrointestinal hormones known to control energy balance.”
The lead author on this study, Melania Osto, Ph.D. said:
“Our findings show that RYGB surgery leads to changes in gut microbiota that resemble those seen after treatment with prebiotics. The results of this study suggest that postsurgical gut microbiota modulations may influence gut peptide release and significantly contribute to the beneficial metabolic effects of RYGB surgery.” (5)
Now, if you ask me, I would think it far better and more cost-effective to correct the dysbiosis that is causing the problem than undergo a radical operation with post-surgical complications stemming from a newly shortened small bowel. However, far be it from me to deny all these surgeons and the wealthy shareholders of major hospital, pharmaceutical and insurance corporations their profits.
Can you imagine how horrifically tragic it would be to their bottom line if the solution were as simple as identifying those dietary factors that promote small gut dysbiosis, curing this bacterial and yeast overgrowth, and preventing a recurrence through probiotic and prebiotic supplementation? It makes me tear up just thinking about it. Perish the thought dear reader, perish the thought!
OK, now that I’ve got that out of the way, I promise, really I do, to discuss how dietary fat impacts endotoxemia in the next post.
Erridge C. (2011). Diet, commensals and the intestine as sources of pathogen-associated molecular patterns in atherosclerosis, type 2 diabetes and non-alcoholic fatty liver disease. Atherosclerosis, 216: 1-6.