Paradoxical as it may seem, people with an extremely high level of “good” cholesterol are significantly more at risk of early death from all causes than those whose cholesterol level is considered to be within the normal range. The European Heart Journal reports this conundrum, citing a recently completed study conducted by scientists at the University of Copenhagen, Denmark.
By “good” cholesterol, health professionals mean high-density lipoprotein cholesterol (HDL-C); “bad” cholesterol is low-density lipoprotein cholesterol (LDL-C). Scientists also refer to “bad” cholesterol as “non-HDL cholesterol” to include other types of cholesterol besides LDL-C.
As for “bad” cholesterol, it is generally understood that high levels of LDL-C result in atherosclerosis—also called arteriosclerosis or hardening of the arteries—by forming deposits, or plaques, in the interior walls of the arteries, causing inflammation, narrowing the blood vessels, and decreasing their elasticity. Plaques in coronary arteries increase the risk of ischemic heart disease, angina, and heart attack. In their article about atherosclerosis and coronary artery disease (CAD), WebMD.com says that atherosclerosis kills half a million Americans a year from CAD alone. Moreover, atherosclerosis can also interfere with circulation to other organs, and high levels of LDL-C in the blood are associated with impaired kidney function, fatty liver, erectile dysfunction, and Alzheimer"s disease.
Nevertheless, despite its being “bad,” we need some LDLC; it provides structural integrity to cell membranes, protects nerve fibers, facilitates digestion, and plays a positive role in metabolism and immune function. Additionally, along with HDL-C, it is a component of steroid hormones, including adrenalin, testosterone, estrogen, and progesterone. In its article, “Cholesterol level: Can it be too low?” the Mayo Clinic says that very low levels of LDL-C—less than 40 milligrams per deciliter of blood—put us at increased risk of cancer and stroke, among other illnesses.
The risks of heart disease related to low levels of HDL-C are well known. Among other beneficial actions, good cholesterol removes cholesterol and fat, or lipids, from cells and transports them to the liver, where they are converted to bile acids that are excreted with bile into the intestine. It is especially important to note that HDL-C also removes cholesterol and fat from atherosclerotic plaques, which has the potential to actually reverse atherosclerosis. HDL-C also helps safeguard heart muscle against damage caused by the hypoxia of ischemic events. Thus, doctors can congratulate their patients on having a high level of good cholesterol—but not too high, if the results of the aforementioned Danish study are confirmed. To observe whether there was an association between extremely high levels of HDL-C and death from all causes, Doctors Madsen, Varbo, and Nordestgaard of the University of Copenhagen analyzed data from over 116,500 people being followed in the Copenhagen General Population Study and the Copenhagen City Heart Study. They established that mortality from all causes was lowest among men with an HDL-C of 73 mg/dL and women with 93 mg/dL. Mortality was 106% higher among men with the most extremely high levels of HDL-C—116 mg/dL—and 68% higher among women with 135 mg/dL—than for people with the optimal HDL-C levels. Moreover, mortality among men with very high levels—between 97 and 115 mg/dL—was 36% higher than for those with the lowest risk, and 10% higher for women with levels between 116 and 134 mg/dL. At the same time, it was confirmed that low levels of HDL-C— lower than 39 mg/dL—were also associated with serious risks to health and greater mortality.
Statistics indicate that people who are overweight, men over forty, and women after menopause are particularly at risk if they have high levels of non-HDL-C and/or low HDL-C. They are urged to monitor cholesterol levels regularly and to strive through diet and, if necessary, with medication, for a total-cholesterol-to-HDLC ratio of 3.5 to 1.
Various theories about what causes atherosclerosis include one that sugar is the villain rather than fat. Some studies find no correlation between fat intake and heart disease. One well-based scientific opinion is that development of atherosclerosis is connected to a low level of lipid transport proteins that help move cholesterol to the liver for excretion in the bile. It is also known that inherited genetic abnormalities cause malfunctions in LDL receptors on the surface of cells and in the liver, resulting in very high levels of LDL-C. This familial hypercholesterolemia is not rare—it may affect as many as 1 in 200 people—but most are never diagnosed with the disorder. Whatever the process, excessive levels of circulating LDL-C result in atherosclerosis, and treatment accordingly is focused on removing the excess. Given that all the cholesterol we need is made in the liver, how much additional cholesterol we can take in through diet without negative consequences is a question. A definitive answer remains elusive. And while it’s clear that there is a direct relationship between LDL-C and atherosclerosis, we don’t yet completely understand the mechanisms involved.