Those of you following my discussions know that I view LDL cholesterol as nonsense, a trumped-up fictitious value that should have been discarded as a measure of cardiovascular risk decades ago. It is, at best, a poor predictor of cardiovascular events—no surprise, as it is an outdated way to guesstimate the particles that actually cause heart disease. But the misguided notion of reducing LDL cholesterol makes billions of dollars for the pharmaceutical industry, so this misbegotten value remains the focus of nearly all practicing physicians, complete with free dinners and all-expense-paid trips to Orlando or Maui.
Most do, however, recognize that reducing LDL cholesterol with statin drugs does not eliminate risk for cardiovascular disease, reducing risk by only a trivial amount (though wildly exaggerated due to statistical mis-reporting). This explains why more than 80 million Americans take a statin cholesterol drug, but there has been no meaningful reduction in heart disease events. Hospitals and cardiologists continue to do a brisk business in heart catheterizations, angioplasty, stent implantations, bypass operations and related procedures. Heart disease remains the number one source of revenue for hospitals and there is, therefore, little incentive to address the real causes of heart disease that could turn off this prodigious source of revenue.
Reduce cardiovascular risk to a trivial degree with statin cholesterol drugs and there is therefore substantial “residual risk,” i.e., risk not addressed by reducing LDL cholesterol. Much of that risk is evidenced by low HDL cholesterol and high triglyceride levels obtainable through a standard cholesterol panel. Unfortunately, while a low HDL value presents a ton of useful information, rarely do conventional physicians address this issue. If they do, they resort to prescribing fibrate drugs such as gemfibrozil, niacin (that does not reduce risk, likely due to effects such as provoking higher blood sugars, insulin resistance, and higher uric acid levels), or relying on statin cholesterol drugs for the minor increase in HDL they provide (although atorvastatin, or Lipitor, reduces HDL).
It is useful to view HDL cholesterol as an index of metabolic health. Low HDL (that I would define as <60 mg/dl, not the absurd 40 mg/dl for men or 50 mg/dl for women often quoted as ideal) is an indicator of poor health: insulin resistance, inflammation, excessive intra-abdominal fat, higher blood sugars, higher blood pressures, more small LDL particles, more VLDL particles. In other words, HDL is a composite reflection of multiple health phenomena. Higher levels of HDL (>60 mg/dl) are therefore an indication of better metabolic health. HDL levels are a useful gauge that you can track as an indicator of overall metabolic health.
Doctors will typically tell you that raising HDL values is difficult or impossible. Or they will provide useless advice such as increasing exercise and drinking wine will raise HDL (to a minor degree). My personal HDL journey began with a value of 27 mg/dl, a value so low that it is often labeled “hypoalphalipoproteinemia,” i.e., a genetically-programmed lack of the apoprotein A1 protein that is a component of HDL particles. Thirty years ago, I made the mistake of adopting a low-fat vegetarian lifestyle. Despite long-distance jogging, biking, and playing tennis, I became a type-2 diabetic with fasting blood glucoses of >160 mg/dl, triglycerides of 390 mg/dl, hypertensive blood pressures, plenty of small LDL particles, and low HDL. Once I recognized how harmful such a low-fat vegetarian lifestyle was, I stopped this and zig-zagged my way back, now no longer diabetic with fasting glucoses in the 80s, triglycerides of 47 mg/dl, blood pressures of around 105/70, and HDL of 94 mg/dl—a nearly four-fold increase. Such an increase in HDL is widely believed to be impossible. Beyond my own personal experience, I’ve witnessed such extravagant rises in HDL many, many times.
What are we doing that could cause such incredible rises in HDL? And can this be accomplished without statins, fibrate drugs, or niacin? Absolutely. To optimize metabolic health, reflected by a significant rise in HDL, we:
- Avoid foods that fuel liver de novo lipogenesis, i.e., the liver’s conversion of carbohydrates to triglycerides. We therefore banish all wheat, grains, and sugars from our diets, foods that cause triglyceride levels to skyrocket. This increases HDL because excessive triglyceride levels cause degradation of HDL particles: lower triglycerides mean that HDL is not metabolized and degraded.
- We do not limit fat intake—Fats are not only satiating, they also increase HDL levels. And, of course, fat intake, including saturated fat, has nothing to do with heart disease.
- We reverse or minimize insulin resistance—In addition to the dietary changes, we address common nutrient deficiencies that, when corrected, reduce insulin resistance: vitamin D, magnesium, omega-3 fatty acids, iodine.
- We minimize inflammation—We reduce measures such as C-reactive protein, IL-6, and IL-1β with diet and the above nutrients.
- We address dysbiosis, SIBO, and endotoxemia—The dominance of unhealthy microbial species in the gastrointestinal (GI) tract yields toxins upon microbial death, toxins that enter the bloodstream and amplify insulin resistance, inflammation, and thereby contribute to reduced HDL.
- We favorably alter body composition—We minimize intra-abdominal fat and restore lost muscle mass. Intra-abdominal fat is not just a source of blood triglycerides, but it amplifies insulin resistance and inflammation that further increase triglycerides that thereby reduce HDL. We improve body composition by restoring the microbe lost by nearly everyone, Lactobacillus reuteri, while also restoring body composition-modifying dietary components lacking in most modern people as part of misguided low-fat dietary advice: collagen and hyaluronic acid.
No, drugs are not necessary at all to enjoy spectacular increases in HDL values. Triglyceride values, by the way, will also plummet with the above formula. It is not uncommon for a HDL value of 37 mg/dl to climb to >90 mg/dl and triglyceride values of 200, 300, or 700 mg/dl to drop to 50 mg/dl or less.
Accordingly, very high levels of HDL of >100 mg/dl are predictors of extreme longevity, of people who live to 100 years of age or older. Ignore conversations about how very high HDL levels are predictors of heart disease—this is true with rare genetic variants, but not with HDL you increase by improving your lifestyle.