Those of you following these Wheat Belly and Undoctored Blog posts know that it is no secret that Big Pharma is a predatory, manipulative, cutthroat industry that employs underhanded and unethical tactics as routine business. Part of their huge economic success is that they are so effective in getting my colleagues, mainstream physicians, to drink their Kool-Aid and do a lot of the dirty work for them. Just witness what happened in the opioid crisis—it couldn’t have happened without the willing participation of physicians.
It’s no different with “treating” cholesterol, total and LDL, with statin drugs. If you read the Wheat Belly Total Health or Undoctored books, you know that cholesterol testing is a woefully outdated method to gauge cardiovascular risk, a remnant of old research from the 1950s and 1960. If you spin blood down in a high-speed centrifuge, the various lipoproteins (fat and proteins) separate out by density: high-density lipoproteins at the bottom, low-density above, very low-density at the top, each layer comprised of huge numbers of lipoproteins. Quantifying lipoproteins at each density level in 1960 was not easy, so an indirect method was developed: choose one marker that could be used to crudely estimate the number of lipoproteins in each density fraction. They could have chosen triglycerides or various proteins, but they chose cholesterol, as it was present in all density layers. They found specifically that if the cholesterol content of the entire tube was measured and that in the high-density layer also measured, then the cholesterol estimated in the very low-density measure by a minor calculation, they could then calculate how much cholesterol was in the low-density fraction. Problem: The equation they derived to calculate LDL cholesterol was weak, subject to all sorts of influences that would make it inaccurate or invalid. Yet that same equation is still in use today despite being wildly inaccurate with any change in diet or blood levels of triglycerides, for instance.
But the LDL cholesterol calculation was interpreted to mean that cholesterol was not just a crude marker for lipoprotein quantification, but it also came to be viewed as the actual cause of heart disease, which it is not. The biggest tragedy of the cholesterol debacle is not the imprecision nor misinterpretation of the value of cholesterol values; the biggest problem is that the REAL causes of heart disease are ignored even though they are easily addressed.
If the layer of lipoproteins in the low-density layer of the centrifuged blood specimen were broken down into subcomponents, you would see that LDL particles—not cholesterol as an indirect gauge of LDL particles, but actually examining the LDL particles—are a hodgepodge of various sizes, shapes, and composition. Just trying to characterize this heterogenous mixture by measuring the cholesterol in the low-density fraction is foolish and simpleminded, but nonetheless the basis for a multi-billion dollar industry.
But look closely at this low-density lipoprotein layer of particles and you would see two dominant forms: large LDL particles and small LDL particles. Large LDL particles result mostly from fat consumption, while small LDL particles result from consumption of grains and sugars. But the differences go far beyond just size. Small LDL particles, for instance:
- Persist much longer in the bloodstream–typically lasting 5 or more days, rather than the 24-48 hours of large LDL particles. This is because the liver that clears LDL particles does not recognize the altered conformation of small LDL particles, slowing their clearance. Eating grains and sugars with some regularity therefore causes massive accumulation of small LDL particles.
- More prone to glycation and oxidation–Glycoxidized, i..e, both glycated and oxidized, small LDL particles are the dominant lipoprotein cause of heart disease. Small LDL particles are many times more prone to these alterations.
- The reduced size alters the particles’ surface configuration, making them much more likely to adhere to the arterial wall and contribute to accumulation of atherosclerotic plaque (the material that leads to heart attack, angina, stroke, etc.)
- Once it gains entry into the wall of arteries, it is more likely to trigger an inflammatory response of the sort that can grow atherosclerotic plaque and trigger plaque rupture, the event that leads to heart attack.
As an aside, if fat consumption increases large LDL particle number but grains and sugars cause formation of small LDL particles, a diet that combines fats + grains + sugars is a particularly lethal combination, as it causes an explosion of a mixture of LDL particles, including plenty of small.
Small LDL particles are therefore a far superior predictor of heart attack, peripheral arterial disease, and cardiovascular death, far superior to the nearly useless LDL cholesterol. In the Women’s Health Study of 27,000 women, for example, small LDL—but not LDL cholesterol—was a strong predictor of peripheral arterial disease (e.g., carotid), a finding corroborated many times in other studies.
Let’s say we conduct a lipoprotein assessment of someone using the NMR (nuclear magnetic resonance) method that I have used for 20 years. Starting values include a total LDL particle number of 2400 nmol/L (number of particles per volume), of which 1800 nmol/L are the abnormal small LDL particles—a very high level strongly associated with cardiovascular disease risk. This person then eliminates grains and sugars, as well as engages in the other components of our programs such as fish oil, vitamin D, and cultivation of bowel flora. Follow-up values (after weight loss plateaus, remember): total LDL particle number 600 mol/L, of which zero—ZERO—small LDL particles remain.
Let’s subject the same starting values of total LDL particle number of 2400 nmol/L and 1800 nmol/L to a statin drug such as Lipitor 40 mg. Follow-up values: 1680 mol/L total LDL particle number, 1260 nmol/L—about a 30% across-the-board reduction in LDL particles of all sizes but leaving a substantial proportion of small LDL particles. This is because statin drugs are dumb and cannot discriminate between bad particles like small LDL and less harmful or harmless particles like large LDL. Yet your doctor insists that you take a statin drug that 1) has only a minor and incomplete impact on abnormal lipoprotein distortions, 2) reduces cardiovascular risk minimally (though with benefits wildly exaggerated by statistical shenanigans), while 3) telling you to follow a diet low in saturated fat and rich in “healthy whole grains” that causes an explosion of small LDL particles, as well as weight gain, type 2 diabetes, fatty liver, and other conditions.
And those are just the issues surrounding LDL cholesterol and LDL particle number. There are other issues that are ignored in conventional healthcare but worsened with blundering modern dietary advice. For example, a diet low in fat and filled with grains causes a huge surge in liver de novo lipogenesis, i.e., liver conversion of carbohydrates (grains and sugars) into triglycerides. This raises blood levels of triglycerides and causes accumulation of triglycerides in the liver, i.e., fatty liver. Triglycerides in the blood are mostly in the form of very low-density lipoproteins, or VLDL. Modern dietary advice is therefore associated with a huge increase in postprandial (after-meal) VLDL particles that contribute to heart disease. VLDL particles interact with large LDL particles and begin a cascade of events that causes small LDL particles to result.
Do you begin to grasp the enormity of the bungling that goes on in modern conventional healthcare? Can you also begin to appreciate that examining lipoproteins and understanding their behavior makes statin drugs look absurd, nearly useless, because the entire constellation of abnormalities that lead to heart disease is magnificently corrected by choosing the right diet?