Fat and lipid abnormalities are the major risk factors for cardiovascular disease. The use of the pharmaceutical statin drugs has been shown to reduce the risk factors for cardiovascular disease by reducing LDL cholesterol. Statins are believed to have reduced the incidence of coronary events, such as heart attacks, but atherosclerotic disease continues to be the primary cause of death in industrialized nations.
Now, the search is on to find agents that raise low levels of HDL cholesterol to further reduce the risk factors and HDL cholesterol has protective effects. HDL levels are strongly genetic and involve liver enzyme and lipoprotein genes. Studies have shown the potential for reducing cardiovascular disease by raising HDL cholesterol though there is not definite proof.
The uptake of excessive LDL cholesterol by arterial wall cells leads to “foam cells” with excessive fat. HDL cholesterol directs the exit of the fat from foam cells. People with Tangier’s disease have almost no HDL cholesterol because of very rapid metabolism and have very rapid development of atherosclerosis. The foam cells eventually die and leave their cholesterol to become the dead core of an atherosclerotic lesion.
HDL cholesterol has the ability to take up particles of cholesterol from foam cells to reduce the build up of excessive foam cells in arterial walls. The HDL cholesterol returns the particles to the liver to be excreted as bile. HDL cholesterol can inhibit the effects of tumor necrosis factor and is important for the health of the inner lining of arteries by activating nitric oxide synthetase enzyme (eNOS).
The metabolic syndrome, with its high risk factors for cardiovascular disease, has become more common worldwide. Low HDL cholesterol is one of the diagnostic features of the metabolic syndrome.
Statin drugs are able to raise HDL levels by 5 to 10%. Fibrates and nicotinic acid (niacin, vitamin B-3) are able to increase HDL levels. Niacin is good at reducing triglycerides and increasing HDL cholesterol has bothersome side effects, which include flushing, impaired glucose tolerance and increased uric acid levels due to prostaglandin release. Extended release niacin has the problem of liver toxicity. Attempts are being made by pharmaceutical companies to develop drugs which will duplicate the beneficial effects of niacin without the side effects.
CONCLUSION: The current strategy to attempt to reduce cardiovascular episodes and atherosclerosis by finding ways to increase blood levels of HDL cholesterol. Besides statin and fibrate pharmaceuticals, niacin can be used to reduce triglyceride and increase HDL cholesterol levels. Extended release niacin has fewer side effects but has considerable liver toxicity that plain niacin does not have.
NOTE: Read about the effects of olive oil on cardiovascular risk factors.
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