Oxysterols: The True Cardiovascular Culprits

By Ian MacArthur

Cholesterol has long been vilified by health professionals as a primary contributor to heart disease. Now, after over sixty years of research, Fred Kummerow of the University of Illinois is challenging this view. Decades of probing the biochemistry of heart disease has led Kummerow to identify oxidized cholesterols and other oxidized lipids as the molecules responsible for the calcification of arteries and lessened blood flow of patients suffering from heart ailments. Oxidized cholesterols, referred to as oxysterols, share a common carbon structure with cholesterol but contain various additional oxygen-containing functional groups.

The research process that led Kummerow to reach his conclusion about oxysterols began with a finding that the arteries of patients with heart disease contained elevated levels of sphingomyelin, a phospholipid component of the cell membrane. Comparing the arterial compositions of newborn babies with patients that had undergone bypass surgery, Kummerow found that while newborn arteries contained 10% sphingomyelin and 50% phosphatidylcholine, another phospholipid membrane component, the arteries of bypass patients contained up to 40% sphingomyelin and 27% phosphatidylcholine. Years of additional research then led to the finding that elevated cellular oxysterol levels contribute to the conversion of phosphatidylcholine to sphingomyelin.

Arterial calcification in action – when the buildup of calcium from sphingomyelin and calcium ions blocks the flow of blood in blood vessels.

Sphingomyelin has since been implicated as a major player in the calcification of arteries. When the phospholipid interacts with ions in blood, it develops a negative charge. Positively charged calcium ions are then drawn towards the negatively charged arterial walls where they amass and constrict blood flow. Oxysterols, then, can be said to facilitate arterial calcification by elevating sphingomyelin levels.

Aiding in arterial calcium buildup is not the only way that oxidized lipids contribute to heart disease, Kummerow claims. Additionally, oxidized low density lipoprotein (LDL), erroneously stigmatized as the unhealthy variety of cholesterol, has been linked to the production of thromboxane, a lipid involved in the aggregation of platelets to form blood clots. Further, oxidized LDL may interact with arterial walls to form hazardous lesions. The combined effect that oxidized fats have on calcification and blood clot formation make them one of the most important groups of compounds involved in heart disease.

What, then, is the biological significance of cholesterol? Far from causing heart disease, cholesterol has been demonstrated to function as an antioxidant, a substance that inhibits oxidation. In fact, it is believed that cholesterol plays a role in preventing the oxidation of LDL, thereby halting the production of thromboxane and the formation of blood clots. Furthermore, cholesterol is involved in the maintenance of cell membranes, intercellular transport, membrane permeability, and hormone production.

While some cholesterol is naturally oxidized enzymatically by the body, the process of frying food produces enough oxysterol to have a deleterious effect on cardiovascular health. Exposure of cholesterol to light, oxygen, and high heat during the frying process gives rise to a host of oxysterols and other oxidized fats that may cause great harm when ingested. Therefore, eating foods high in cholesterol is not necessarily damaging to heart health. However, careful attention to the preparation of such foods should be paid by cardiovascular conscious individuals so as to avoid the ravages of oxysterols, the true culprits behind heart disease.

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