While your doctor prattles on about saturated fat, LDL cholesterol, and statin cholesterol drugs, the healthcare system has had almost no impact on the incidence of cardiovascular disease. More than 80 million Americans, for instance, take a statin cholesterol drug, yet hospitals are still every bit as busy dealing with just as many heart attacks, unstable angina, heart catheterizations, bypass surgeries, and implantable defibrillators as they were 30 years ago. Heart disease remains the number one revenue-generating category of health problems. It also means that your doctor or cardiologist has had virtually no impact on your future risk for heart-related events, including sudden cardiac death. Obviously, if reducing cholesterol values yields only minor reduction in risk for cardiovascular disease, more of the same is not the answer. (See this discussion on how the cholesterol paradigm has recently been taken to its extreme, yet yields almost no additional reduction in risk). It means that, if you are truly interested in reducing, or even eliminating, risk for the several forms of heart disease, the answers are to be found elsewhere. Problem: the nearly exclusive focus by your doctor on cholesterol and saturated fat has blinded him/her to all the other causes of heart disease, the majority of which are readily identifiable and easily correctable.

Recall that the conversation I generated with wheat, grain, and sugar elimination via the Wheat Belly conversations originated with efforts to eliminate small LDL and VLDL particles that are superior predictors for heart disease risk, many times better predictors than cholesterol values. The amylopectin A carbohydrate of wheat and grains, as well as sugars in various forms, are flagrant triggers for these heart disease-causing particles. The Wheat Belly lifestyle also managed to substantially reverse insulin resistance and inflammation, two additional drivers of cardiovascular disease. The Wheat Belly lifestyle essentially causes you to revert back to the way of eating that sustained humans and is programmed into our genetic code from the first three million years our species has walked this planet before we made recent dietary blunders, such as incorporating seeds of grasses (“grains”) into diet. And it is a lifestyle that yields substantial reductions in the factors that lead to heart disease, not to mention reductions in tooth decay, tooth misalignment, osteoarthritis, constipation, irritable bowel syndrome, autoimmune diseases, and numerous other modern conditions.

But how about the contribution of the gastrointestinal (GI) microbiome to cardiovascular disease? The latest insights show us that disruptions of the GI microbiome is a major factor in causing cardiovascular disease, thereby telling us that purposeful and informed restoration to something closer to its ancestral human form could reduce its contribution to cardiovascular risk. After all, indigenous humans in the Brazilian rainforest, Tanzanian savannah, or jungles of New Guinea have virtually no coronary disease.

How might a disrupted GI microbiome contribute to risk for heart disease? There is a surprisingly long list of ways that the trillions of microbes colonizing your GI tract could contribute to heart disease in its various forms. The greatest risk develops if dysbiotic microbial species in the colon ascend to colonize the 24-feet of small intestine, i.e., small intestinal bacterial overgrowth, or SIBO, a situation that applies, by my estimation, to 50% of the U.S. population. Because the small intestine has a more permeable single-layer mucus barrier, more readily breached than the two-layer mucus barrier of the colon, endotoxin generated by the death of microbes is more readily able to enter the bloodstream, “endotoxemia,” a more potent risk for cardiovascular disease than something as silly and outdated as cholesterol values.

The GI microbiome leads to cardiovascular disease mostly via endotoxemia:

  • Generating insulin resistance and inflammation—Recall that fecal microbes that proliferate and ascend to colonize the 24-feet of duodenum, jejunum, and ileum live and die over just a few hours. showering the bloodstream (initially the portal vein system draining to the liver) with bacterial breakdown products, especially endotoxin, yielding “endotoxemia,” a flood of endotoxin into the bloodstream. This fuels insulin resistance and inflammation body-wide.
  • Endotoxemia inflames the liver, adding to risk for non-alcoholic steatohepatitis, NASH, on top of fatty liver, situations also associated with increased production of triglycerides by the liver (de novo lipogenesis), released into the bloodstream as VLDL particles that are both a direct cause for coronary disease, as well as modifying LDL particles to make them the dangerous and heart disease-causing small LDL particles. (Note that vegan and vegetarian diets worsen these phenomena–no, they do not stop or reverse coronary disease. This is the misinterpretation, a result of poor methods, and misrepresentation of the low-fat community, as championed by people such as Drs. Dean Ornish and Caldwell Esselstyn, who committed medical student-level errors in their clinical and case studies, a tale for another day.) People with SIBO and endotoxemia have greater insulin resistance, higher levels of C-reactive protein, IL-1 beta, IL-6, TNF-alpha and other markers for inflammation. In fact, it is uncommon to have coronary disease in the absence of increased insulin resistance and inflammation. Management of these situations are therefore key to management of cardiovascular risk. Cholesterol? Don’t make me laugh.
  • Endotoxemia increases the number of small LDL particles—by the above mechanism. Recall that small LDL particles persist longer in the bloodstream (5-7 days, compared to one day for normal large LDL particles), are more adherent to the structural tissues of artery walls, are more prone to oxidation and glycation, and more likely to initiate an inflammatory response in the walls of arteries. Small LDL particles occur alongside other metabolic disruptions such as low HDL, small non-protective HDL particles, increased VLDL and triglycerides, higher HbA1c, higher fasting blood glucose and insulin, higher markers of inflammation, higher levels of coagulation proteins such as fibrinogen and factor VII. (LDL cholesterol, by the way, does not co-occur with any other abnormal markers—because it is, after all, a fictitious value.)
  • Endotoxemia disrupts the protective arterial glycocalyx—that regulates entry of various factors into the walls of arteries. In other words, disruption of the protective glycocalyx permits entry of lipoproteins such as small LDL and VLDL into the artery wall and initiate the cascade that leads to atherosclerosis. It also leads to endothelial dysfunction, loss of the normal capacity for arterial relaxation, generating abnormal constriction that further adds to development of atherosclerosis.
  • Endotoxemia worsens congestive heart failure—It is clear that people with endotoxemia have worse outcomes (e.g., hospitalization, need for implantable defibrillators, sudden cardiac death, increased water retention) in the setting of heart failure.
  • Endotoxemia increases risk for atrial fibrillation–A. fib is a common (about 15% of people over age 65) heart rhythm disorder. Ask anyone with A. fib. how this changes your life—frightening recurrences with heart rates of 180-220 beats per minute, repeated hospitalizations, numerous medications to slow the heart rate, anticoagulants to thin the blood, toxic anti-arrhythmic medications to encourage return to normal heart rhythm, cardioversions (passing an electrical current through your chest to reset rhythm, similar to the defibrillation you see on TV in people with cardiac arrest). and the imperfect world of ablations in the electrophysiology laboratory.

Attention to colonic dysbiosis, SIBO, and endotoxemia are going to prove to be far more important than this silly notion of cholesterol. Management of cardiovascular risk must therefore involve attention to the GI microbiome, intestinal mucus barrier, and other ways to reduce endotoxemia.

Low HDL, small LDL, increased triglycerides and VLDL, increased insulin resistance, increased inflammation, greater insulin resistance and higher blood sugars, higher blood pressure, disruption of the endothelial glycocalyx, and perhaps bacterial translocation (migration of microbes into the walls of arteries)—are you coming to understand how silly and overly-simplistic it is believe that we can reduce cardiovascular risk by reducing fat and taking statin cholesterol drugs? The cholesterol and statin drug paradigm will go down in history as one of the biggest, costliest, and most mindless blunders of 21st century healthcare—but it makes a lot of money for healthcare insiders.

The solution? Attention to all things involving the GI microbiome. If you are new to this conversation, start with my Super Gut book and/or join the vigorous discussions we have on my DrDavisInfiniteHealth.com website, including our weekly two-way Zoom conversations. It will NOT involve advice to reduce saturated fat, reduce LDL cholesterol, or take statin drugs. It will provide advice to naturally, safely, and inexpensively address the real causes of cardiovascular disease. We begin by eliminating the foods (wheat, grains, sugars) that trigger liver de novo lipogenesis that creates VLDL and small LDL particles; restoring nutrients lacking in modern lifestyles (vitamin D, omega-3 fatty acids, iodine, magnesium) that synergize to reduce insulin resistance and inflammation, strengthen the intestinal immune response, and ensure normal transit; and we address the disrupted microbiomes, including strategies such as SIBO Yogurt to eradicate SIBO and thereby endotoxemia.