The answer to that foolish question is certainly going to be “both.” But the finger pointing at the guilty party has wobbled around a good deal in the past few years, and just before Christmas, the American Heart Association came out with a set of dietary recommendations once again apparently putting at least some blame for heart disease on dietary cholesterol. This is a pretty big switch. In the past decade, the recommendations have bounced around a good bit; for example, as late as the 2018 cholesterol management guidelines from the American College of Cardiology and the American Heart Association shifted the emphasis on cholesterol management away from dietary cholesterol.
What, we may ask, is going on? Here’s how the American Heart Association science advisory puts it:
“Historically, nutrition guidelines for reducing cardiovascular disease (CVD) risk and achieving optimal plasma lipoprotein profiles have included recommendations to limit dietary cholesterol. However, contemporary guidelines for CVD risk reduction from the American Heart Association (AHA) and American College of Cardiology (ACC) and the “2015–2020 Dietary Guidelines for Americans” have not issued explicit guidance for dietary cholesterol. Because of the inconsistencies in the evidence base and the inherent difficulty in conducting and interpreting studies to isolate the independent effect of dietary cholesterol on CVD risk, controversy has ensued about whether dietary cholesterol should be a target for CVD prevention and management. (Carson et al “Dietary Cholesterol and Cardiovascular Risk” Circulation. 2019;140:00–00)
From where Doc Gumshoe sits, the AHA is being more than a bit weasely. To answer my previous question, what has been going on is that for several decades, the official positions of the major medical associations emphatically advised limiting the consumption of foods that were high in cholesterol, which specifically included red meat, eggs, and full-fat dairy products. But in the past five years or so, they have effectively backed away from those recommendations, without explaining why they did so. And then, in this past year, the AHA perhaps realized that they may have backed away a bit too far.
What do we know about cholesterol that got us to this point?
More than a century ago, it was determined firmly and clearly, and without “inconsistencies in the evidence base,” that cholesterol was the substance deposited in the walls of human arteries and was the main component in arterial plaque.
It was understood that cholesterol is a simple molecule, solid at body temperature, and not water soluble. It is present in virtually all our tissues, providing structure, and is absolutely essential for life. But, since cholesterol is not water soluble, in order to be transported in our bloodstream, it has to hitch a ride with substances that can be carried around in blood. These are lipoproteins – little particles containing both proteins and lipids, not in any fixed chemical combination, but bundles of varying sizes. Cholesterol attaches to the lipid part of these bundles, and the protein part permits them to be transported in blood.
These particles range in size and density. The low-density, loosely packed bundles, called low-density lipoprotein cholesterol, or LDL-cholesterol, are the ones nicknamed “bad” cholesterol, because they are the ones that are apt to shed the cholesterol molecules themselves, which can attach to the walls of the arteries and even penetrate those walls. But, we have to remember, the LDL-C is absolutely essential to our lives, because those particles are the ones that convey cholesterol to where it’s needed, which is pretty nearly everywhere in our bodies.
The smaller, denser bundles, called high-density lipoprotein cholesterol, or HDL-cholesterol, carries cholesterol back to the liver, where it is taken up by the bile and carried in the bile duct to the colon for excretion in the feces. Therefore, HDL-C is dubbed “good cholesterol.”
It’s worth just mentioning that only about 15% to 20% of the total cholesterol in our bodies enters our digestive systems as cholesterol. The rest we synthesize daily. Some of the foods we eat are more easily transformed into cholesterol, such as solid fats, especially partially hydrogenated fats (transfats). But no matter what we eat or don’t eat, we’ll go on synthesizing cholesterol, because we need it.
The balance between LDL-C and HDL-C is a homeostatic mechanism. Those two types of particles have properties beyond their role as cholesterol delivery systems. LDL-C appears to be highly susceptible to oxidative damage, and may also inhibit the synthesis of nitric oxide, which is thought to be one of the body’s natural mechanisms to combat atherosclerosis. And HDL-C has the opposite effect. Its principal lipoprotein, apo A-1, plays a part in preventing particles involved in atherosclerosis from adhering to arterial walls.
So, not only do LDL-C and HDL-C play different roles in cholesterol transport, they do the same with regard to arterial damage. We could say that the nicknames “bad” and “good” cholesterol are fully justified.
Maintaining good levels of HDL-C in the circulation is highly important to cardiac health. Some activities, such as exercise, have a beneficial effect on HDL-C levels. >It’s the view of many cardiologists that the ratio of total cholesterol to HDL-C is more indicative of overall cardiac risk than the total cholesterol value by itself, so, while a TC value of more than 200 is thought to be higher than the optimal range, this can be offset by an HDL-C value higher than 50.
However, despite the necessity of cholesterol in our bodies, for most of the 20th century it was taken for granted that cholesterol was the cause of atherosclerosis and a principal cause of heart attacks (myocardial infarctions, or MIs).
Efforts to reduce the risk of MIs by cutting back on foods rich in cholesterol failed to lead to reliably clinically effective results. In other words, people who significantly reduced their intake of eggs, butter, and beefsteak, did not have fewer MIs – at least, statistically.
It wasn’t until the mid-1990s that a drug, simvastatin, was clearly and definitively demonstrated both to lower cholesterol in the blood and to reduce the incidence of heart attacks. Initially, this beneficial effect was demonstrated only in individuals thought already to be at an elevated risk for heart attacks.
Statins target the formation of cholesterol, termed cholesterol biosynthesis, which takes place mostly in the liver. They inhibit an enzyme labeled HMG-CoA reductase, which is active in cholesterol biosynthesis. However, statins have no effect on cholesterol that enters our bodies as cholesterol – only on the process of cho