What your doctor may not know about cholesterol !

Cardiologist Dr. William Davis writes:

"Confusion over cholesterol issues is everywhere and shared by most people, including doctors. Unfortunately, it means that, by seeing your primary care doctor or even cardiologist, you are being advised with information that is superficial and largely ineffective while ignoring the MANY issues that really should be addressed to manage risk for cardiovascular disease. Admittedly, these are somewhat complicated issues and even I have been guilty at times of giving overly simplistic answers. I’ll try to keep this as straightforward as possible, but it is a bit hairy. 

I blame this situation on the statin drug industry, as they have painted a misleading picture that, if you take a statin drug or reduce LDL cholesterol, you are absolved of cardiovascular risk. The exaggerated statistical manipulations used by industry—“Lipitor reduces cardiovascular events by 36%” when the real value is, at best, 1%, not to mention the fact that the majority of statin data was paid for by statin manufacturers, a big no-no in any other industry—persuaded practitioners that statins and cholesterol reduction were virtual cures. They are not, of course, as anyone in healthcare who witnesses all the people admitted to the hospital with heart attacks, angina, and sudden cardiac death taking statin drugs will attest. The statin drug industry has therefore caused doctors to wear blinders, rarely looking beyond statins and cholesterol.

So what exactly don’t they know about cholesterol? Plenty. For example:

Cholesterol does not occur as free molecules in the bloodstream, as they are fats and would separate from the aqueous plasma. Cholesterol is therefore solubilized by being complexed within lipoprotein particles—fat-carrying proteins—and cell walls. Even if you eat something rich in dietary cholesterol, such as an egg yolk, it does not enter the bloodstream as cholesterol but as complex particles such as chylomicrons created in the intestines or VLDL particles manufactured by the liver. 

Lipoproteins—can deliver cholesterol and other components to the walls of arteries such as the coronary or carotid arteries. Whether or not such components contribute to atherosclerosis does not depend on the amount of cholesterol contained within a volume of blood but on the composition of lipoprotein particles, e.g., size, surface conformation, presence of binding proteins, oxidation state, glycation state, electrical charge, etc.

Because up until the mid twentieth century, characterization of the various lipoproteins in the bloodstream was laborious and technically challenging, researchers in the 1950s and 1960s devised a crude workaround: estimate the number of lipoproteins in various fractions of the blood (low-density, very low-density, high-density levels in centrifuged plasma) by measuring a select component. They selected cholesterol, as it was easier to measure. Problem: Using cholesterol as an indirect means of estimating lipoproteins means that you have to assume that everyone shares similar lipoprotein composition, an assumption that is potentially and commonly inaccurate. A crude equation (the Friedewald calculation) was also devised to not measure, but calculate, LDL cholesterol, the focus of most mainstream efforts to reduce cardiovascular risk. LDL cholesterol is calculated from total cholesterol in the entire sample minus the cholesterol in the high-density and very low-density fractions. Once again, assumptions were made to allow this calculation. Cholesterol is therefore a crude marker for the particles that cause atherosclerosis, but that should also not be construed to mean that cholesterol is therefore causal.

When LDL cholesterol, the darling of the pharmaceutical industry and most doctors, is compared to superior measures that actually quantify and characterize lipoproteins (nuclear magnetic resonance, gel electrophoresis, ultracentrifugation), there is a statistical correlation of the two measures in large populations, but poor correlation when applied to an individual. LDL cholesterol, i.e., the cholesterol in the low-density lipoprotein fraction estimated via calculation, also tells you nothing about the number of lipoprotein particles, their size, their surface conformation, their binding characteristics, oxidative state, etc. In other words, LDL cholesterol tells you virtually nothing when applied to a specific individual.

If you cut dietary fat and saturated fat and observe the effects on lipoprotein number and composition, you will witness minor effects, such as a reduction in total LDL particle number but increase in the proportion of small LDL particles, increased VLDL particles, decreased HDL particle number and a shift towards less functional small HDL. Cut grains and sugars and you will witness dramatic transformation of lipoprotein composition and number, effects that handily and dramatically outperform the trivial effects of statin drugs.

Of all the measures on a standard cholesterol or lipid panel, it’s triglycerides that offer the most insight, as triglycerides track the number of very low-density lipoproteins, VLDL, closely. VLDL particles are crucial because they begin the process of transforming large, benign, short-lived LDL particles into small, harmful, oxidation- and glycation-prone, long-lived LDL particles (via a complex process called “heteroexchange” of cholesterol for triglycerides followed by enzymatic “remodelling” of the LDL particle). Where does VLDL come from? Consumption of grains and sugars that fuel liver de novo lipogenesis that converts carbs to triglycerides.

HDL cholesterol, a useful index of overall metabolic health, is reduced by cutting dietary fats, since this increases triglycerides/VLDL that lead to HDL degradation and clearance, and reduced by statins such as Lipitor. HDL is raised, often dramatically, by increasing fat consumption and decreased grain and sugar consumption. 

Detailed lipoprotein analyses have been available commercially for over 20 years but are not commonly used, as it requires (as you can appreciate) a deeper understanding of lipoprotein metabolism and do not point towards statins as the solution—they quickly point towards diet and efforts to correct factors such as inflammation and insulin resistance corrected, for example, by losing visceral fat, supplementing vitamin D, and cultivating healthy bowel flora that also contribute substantially to overall health, i.e., all the strategies we put to you" ...

Picture and words above taken from 'Wheat Belly Blog', more to see and read here

All the best Jan