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WBB: Leprechauns, nymphs, high cholesterol, and other fanciful notions

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Posted: 9/17/2015 12:00:00 PM
Edited: 5/29/2022 4:51:24 PM (1)
 

Originally posted by Dr. Davis on 2015-09-17
on the Wheat Belly Blog, sourced from and currently found at: Infinite Health Blog.
PCM forum Index of WB Blog articles.


Leprechauns, nymphs, high cholesterol, and other fanciful notions

Little Red Riding Hood and the wolf in grandma’s bed

Because the campaign of misinformation surrounding cholesterol and heart disease risk is so widespread, I thought I’d share an excerpt from chapter 10 of Wheat Belly Total Health, the chapter entitled Grainless Metabolic Mastery: Regain Control Over Blood Sugar, Cholesterol, Bone Health, and Inflammation. I recount how and why we find ourselves with such silly and misleading notions such as high cholesterol, limiting saturated fats, and statin drugs that dominate most conversations about heart disease risk. Recall that the Wheat Belly concepts got their start with efforts to develop better tools to deal with heart disease risk.

If you are wondering whether the Wheat Belly lifestyle of no wheat, no grains, and unlimited healthy fat will impact heart disease risk, read this (admittedly lengthy) discussion and you will understand. As with every other widespread campaign of misinformation, you will once again smell the hidden profit motive that drives conventional notions of heart health. By ignoring advice to eat more “healthy whole grains,” limit total fat, saturated fat, and cholesterol, as advised by the American Heart Association, you discover that notions such as “high cholesterol causes heart disease” and “everyone must take a statin drug to reduce cholesterol” resemble the truth about as much as kissing frogs creates handsome princes.

Leprechauns, nymphs, high cholesterol, and other fanciful notions: An excerpt from Wheat Belly Total Health
People often start their grain-free journey with concerns about losing the purported health benefits of grains while upping their intake of fats, including saturated fats. They are worried that such a dietary change will “increase cholesterol” and thereby increase risk for heart disease.

Let’s get this straight right from the start: Cholesterol in the diet does not cause heart disease, any more than fat, saturated fat, or a voodoo doll pricked with pins by your worst enemy causes heart disease. Just because cholesterol is found in both particles in the bloodstream as well as in atherosclerotic plaque does not necessarily mean that one caused the other. Cholesterol, after all, comprises 25% of the fat content of all cells of the body. Cholesterol in the bloodstream does not cause heart disease, but is a convenience of measurement. Just as you would not blame the dipstick in the crankcase of your car for the engine failing to start, we should not blame this “dipstick” for the particles in the blood, cholesterol, for causing heart disease. Then why this astounding focus on something as blameless as cholesterol, billions of marketing dollars spent on urgings to reduce it, armies of drug representatives and physicians dispensing drugs to treat it, media reports endlessly warning us of its dangers?

To understand this situation, we have to review how and why we got here, as well as what really goes on in the body that raises risk for heart disease. It may be a bit painful, but I believe that the world of cholesterol will become crystal clear once you grasp these concepts.

A quick history lesson in cholesterol testing: Back in the early 1960s, Dr. William Friedewald and other research scientists at the National Institutes of Health (NIH), conducting sophisticated studies on the various components of the blood, came to understand that fat-carrying proteins in the bloodstream, “lipoproteins,” appeared to gain access to the walls of arteries, such as those of the heart, thereby leading to accumulations of atherosclerosis and, eventually, heart attacks. They reasoned that quantifying lipoproteins in the bloodstream might offer a way to gauge long-term potential for coronary atherosclerosis. The NIH team also knew that, when blood was spun (centrifuged) at high-speed, it would separate lipoproteins in test tubes into various fractions: a high-density fraction at the bottom, followed by a low-density and very low-density fractions towards the top. In particular, the particles found in the low-density fraction appeared to be the most cholesterol-rich, cholesterol being one of the compounds retrieved from arteries bearing atherosclerosis.

Each lipoprotein particle, regardless of which density fraction it came from, shares various components, such as phospholipids, proteins, triglycerides, and cholesterol. Dr. Friedewald and colleagues reasoned that, by choosing one component and measuring it, they could compare this one component from one individual and compare it to other individuals. Measuring one component in each density fraction thereby indirectly quantified the amount of lipoproteins in each density fraction: higher levels of a component in one fraction correlated, albeit crudely, with greater numbers of lipoproteins in that fraction—a virtual dipstick of lipoproteins. They chose cholesterol as their indirect measure, since it was an important component of atherosclerotic plaque, was present in every density fraction and could be easily measured using 1960s technology. So they measured the cholesterol in the unseparated blood, “total cholesterol,” then in each density fraction: a high-density lipoprotein (HDL) fraction, then low- (LDL), and very low-density (VLDL) fractions. The amount of cholesterol in each fraction was used to compare the amount of cholesterol in one person versus that of another and thereby indirectly compare the number of lipoproteins in each density fraction.

Cholesterol was therefore a convenience of measurement. They could have chosen phospholipids, triglycerides, or others, but they chose cholesterol. Cholesterol was not measured because it was the cause of atherosclerosis; it was simply a component of atherosclerotic plaque that could be also measured in the bloodstream, then used as an indirect means of comparing its quantity among various people and populations as an indirect assessment of lipoproteins. Dr. Friedewald and colleagues went a step further: Because the low-density fraction, in particular, was cumbersome to measure in high-volume laboratory practice, they devised a simple equation that allowed laboratories to measure the cholesterol in the total blood sample, the high-density and very low-density fractions, then estimate the fraction in the low-density fraction through a crude calculation. This calculation was successful in calculating a value that approximated the true measured value when many measures were collected from a population—provided diet composition was maintained within a “standard” range of fat and carbohydrate intake and provided high- and very low-density cholesterol fractions stayed within a relatively narrow range. Despite its admitted shortcomings, this was the birth of the conventional lipid panel in which three measures are made—total cholesterol, HDL cholesterol, VLDL cholesterol (now estimated by measuring triglycerides)—then used to calculate LDL cholesterol:

LDL cholesterol = total cholesterol – HDL cholesterol – triglycerides/5

(Triglycerides divided by 5 is an estimate of VLDL cholesterol.)

Such simple testing became widely adopted to gauge risk for coronary disease and heart attack, despite Dr. Friedewald and colleagues misgivings about its limitations, including the inaccuracies introduced when the high-density and very low-density values strayed from the assumed range. Accordingly, as lipid panels, including LDL cholesterol values obtained using the “Friedewald equation,” expanded in clinical use, numerous objections have been raised over the years that such testing was crude, imprecise, and outdated (Barter 2006).

Beyond the crude, indirect nature of this assessment, combined with its faulty built-in assumptions, it also suffered from several other deficiencies. Because, for instance, it relied mostly on measuring or calculating the amount of cholesterol in the various density fractions of blood, it made no effort to decipher the actual shape, conformation, density, surface characteristics, duration of persistence, or other crucial aspects of lipoprotein behavior. Instead, it assumed that every lipoprotein particle within, say, the low-density fraction, was the same in every person regardless of age, sex, diet, weight, insulin or blood sugar status, diabetic or non-diabetic, etc. because it was viewed only from the perspective of cholesterol content.

Fast forward to the 1980s and 1990s, and a very clever way to enterprise on this widely adopted, though flawed, method of testing was devised: the birth of “statin” drugs that inhibit the liver synthesis of lipoproteins by blocking the HMG-CoA reductase enzyme. These drugs were billed as “cholesterol reducing” drugs because, by reducing liver production of cholesterol, lipoprotein production was also restricted.

Even though the dietary contribution to cholesterol synthesis from cholesterol content of foods, such as egg yolks and animal fats, is small to negligible compared to the body’s capacity to manufacture cholesterol, such foods got labeled as unhealthy, while foods low in cholesterol, such as foods from grains, vegetables, and sugars, got labeled as healthy. Largely ignored was the contribution carbohydrates make to increasing cholesterol production by the liver (by providing acetyl CoA, an early step in cholesterol production) (Fears 1981). Even worse, the potential for carbohydrates, especially amylopectin A from grains, to provoke formation of excessive quantities of VLDL that cause dramatic shifts in the size, density, and composition of other particles, such as convert LDL particle size from large to small, was never acknowledged, since that the standard cholesterol panel does not reflect these phenomena.

Focusing on the crude values, especially calculated LDL cholesterol, yielded by cholesterol testing also prompted national advice to reduce total fat, saturated fat, and cholesterol intake, advice followed by many people and resulting in reduced intake. Despite this, the campaign has failed to reduce total or LDL cholesterol in the U.S. (Ford 2013). Nationwide reductions in total and LDL cholesterol are only attributable to use of statin drugs, not diet. (Yes: advise people to follow the wrong diet, then come to their “rescue” with prescription drugs.) We focus on only one component of lipoproteins, cholesterol, ignore the varied ways in which lipoproteins behave, then equate cholesterol in lipoproteins with cholesterol in atherosclerotic plaque: This is where we find ourselves in the early 21st century, having blundered our way here with hundreds of millions of people worldwide being treated for “high cholesterol.”


D.D. Infinite Health icon

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