Posted on November 10, 2013 by Dr. Davis
Much of the $23 billion spent each and every year on statin drugs is really targeting the treatment of “high cholesterol” created by consuming grains.

It doesn’t initially seem this way, as people (including most of my colleagues) focus on fat consumption, especially saturated fat, as the cause for high cholesterol. So let me try and clear up this somewhat confusing issue.

Here is a typical panel of someone who consumes grains:

Triglycerides 170 mg/dl
LDL cholesterol (calculated) 150 mg/dl
HDL cholesterol 40 mg/dl
Total cholesterol 224 mg/dl

In other words, HDL cholesterol is lowish, triglycerides high, LDL cholesterol and total cholesterol high. What does this mean? Let’s take each, one by one:

Triglycerides are the byproduct of two digestive processes: 1) De novo lipogenesis or the liver’s conversion of the amylopectin of grains into triglyceride-rich VLDL particles that enter the bloodstream, and 2) absorption of dietary fats (which are triglycerides themselves). De novo lipogenesis dominates triglyceride levels in the bloodstream, far outstripping consumption of fat as a determinant of triglyceride levels. This simple fact was only identified recently, as the rise in triglycerides that occurs after consuming fats and oils develops within 2-4 hours, but the much larger rise in triglycerides from carbohydrate-to-triglyceride conversion starts 6-8 hours later, a fact not uncovered in older studies that failed to track this phenomenon this far out in time. (And, in certain genetic types, such as apo E2, the rise from carbohydrates in grains and sugars can last for days to weeks.)

LDL cholesterol is calculated, not measured. The Friedewald calculation, developed in the early 1960s to provide an easy but crude means of estimating the quantity of cholesterol in the low-density lipoprotein fraction of the blood appled several basic assumptions: 1) that everyone consumes an average diet of average macronutrient composition, and 2) that the triglyceride content of all lipoproteins remained constant from person to person (which is not true, but wildly variable, and 3) that all LDL particles are the same size (also not true, as LDL particles vary in size within a wide range of diameters).

Grain consumption, thanks to the process of de novo lipogenesis, increases blood levels of triglycerides and VLDL particles. VLDL particles interact with LDL particles, enriching LDL particle triglyceride content and reducing cholesterol content. This leads to a process of LDL particle “remodeling” that creates small LDL particles–glycation-prone, oxidazable, adherent to inflammatory blood cells, and persistent in the bloodstream for 7 days, rather than the 24 hours of more benign large LDL particles. Grains thereby trigger the process creating small LDL particles; fats trigger the process that does not.

When we cut out grains, the Friedewald calculation is therefore no longer valid, as the assumptions–weak to begin with–are completely disrupted. LDL cholesterol, this crude, surrogate effort to indirectly quantify LDL particles, is therefore completely useless. This has not, unfortunately, dampened enthusiasm among my colleagues nor the drug industry for trying to treat this number with statin drugs.

Better ways to quantify LDL particles: NMR LDL particle number (which includes quantification of small and large LDL particles) or an apoprotein B. (Each LDL particle contains one apo B, which thereby provides a virtual count of LDL particles, but no breakdown into small vs. large.)

HDL cholesterol is, unlike LDL cholesterol, a measured and reliable value. Ironically, it is among the most ignored. Grain-consuming humans tend to have low HDL because the high triglyceride/VLDL particles interact in the bloodstream with HDL particles, enriching HDL particles in triglycerides and reducing cholesterol content. This leads to a reduction in HDL size and HDL quantity, thus the lowish or low HDL cholesterol values. The lower the HDL, the higher the cardiovascular risk, a relationship that has held up many times over the years.

Total cholesterol is the sum of all three values: LDL cholesterol + HDL cholesterol + triglycerides/5. (More accurately, LDL cholesterol is the calculated value: LDL = total chol – HDL – trg/5.)

Given the mix of values, total cholesterol is therefore essentially useless. A large increase in HDL, for instance–a GOOD thing–will raise total cholesterol; a large reduction in HDL–a BAD thing–will reduce total cholesterol: the opposite of what you would think. Total cholesterol can indeed yield useful prognostic information when applied to a population, though it is crude and the relationship weak. But it is useless when applied to an individual.

If we reject the silly and simpleminded notions of cholesterol panels, and apply the greater insights provided by advanced lipoprotein analysis, several nutritional observations can be made:

–Saturated fat increases HDL, shifts HDL to larger particles, and triggers formation of large LDL particles.
–The amylopectin carbohydrates of grains trigger higher triglycerides, thereby providing more VLDL particles to interact with HDL and LDL particles, the process that leads to triglyceride enrichment and smaller ineffective HDL and smaller atherogenic LDL (heart disease causing).
–Given the unusual persistence time of small (7 days) vs large (1 day) LDL particles, grain consumption is FAR worse than fat consumption.

You can begin to appreciate how overly simplistic this notion of “reducing LDL cholesterol” using statin drugs is–$23 billion per year of overly simplistic. You can also appreciate that the real situation is a bit complicated and beyond the reach of most busy primary care physicians, while being outside the interests of most cardiologists, obsessed as they are with revenue producing activities like heart catheterizations, stent and defibrillator implantation.

But don’t fall for it: The common distortions of cholesterol panels can be easily explained by the chain of events that emits from a diet rich in “healthy whole grains.”