For years medical students have been trying to remember the good cholesterol is HDL and the bad cholesterol is LDL and they remember H is for “happy” and L is for “lousy.” This was based on studies that showed people who had naturally occurring higher levels of HDL had lower risk of heart disease.
Because of those early studies the next goal for drug therapy was to raise the HDL, with the consequence of reducing heart disease. Two major efforts – one from using niacin, the other from using fish oils- both shown to raise HDL in subjects were universally prescribed in order to diminish heart disease. Any patient with risk factors was put on one or both of those over-the-counter medications.
But as large studies looked at both niacin and fish oil a surprising result came: while they raised HDL they did not appear to protect from heart disease. For those patients who had known heart disease niacin and fish oil appeared to have no effect on the progression of the disease.
This last week the medical journal Lancet examined genetics and discovered that the holy grain of HDL was not protective. In contrast LDL (Low Density Lipoprotein) is still highly predictive of heart disease.
While this appears to be news to the “medical journalists” for those who have been following the story of HDL, and lipo-proteins in general – for those in the field, it has been felt that it was the lipoproteins themselves that caused the damage to the endothelial lining of the arteries of the body. For a simple way of looking at it see our earlier video above. Essentially the lipoproteins, no matter what type, cause the damage to the arteries. Some cause more damage (LDL) – but if you increase the lipoproteins you will have increased damage.
Triglycerides are the focus of much work these days- as processed flours, sugars, rapidly raise triglycerides – increasing the carriers (lipoproteins) which increase risk of heart disease. Simplistic, but thus far it is the hypothesis of choice.
Until then, drugs that lower LDL, statins, clearly decrease incidence of both heart disease, and even cause regression of plaque.
REFERENCES:
Omega-3 Fatty Acids and Secondary Prevention of Cardiovascular Disease—Is It Just a Fish Tale?
Comment on “Efficacy of Omega-3 Fatty Acid Supplements (Eicosapentaenoic Acid and Docosahexaenoic Acid) in the Secondary Prevention of Cardiovascular Disease” Frank B. Hu, MD, PhD; JoAnn E. Manson, MD, DrPH <- they concluded “To date, there is no conclusive evidence to recommend fish oil supplementation for primary or secondary prevention of CVD. However, a diet high in fatty fish (≥2 servings of marine fish per week) should continue to be recommended for the general population and for patients with existing CVD because fish not only provides omega-3 fatty acids but also may replace less healthy protein sources, such as red meat. Individuals who are unable or unwilling to eat fish or related products should consider increasing their consumption of plant-derived omega-3 fatty acid (α-linolenic acid). For primary or secondary prevention, omega-3 supplementation cannot supersede an overall healthy diet, but a cardioprotective diet needs to be rich in omega-3 fatty acids.”
The Lancet, Early Online Publication, 17 May 2012
doi:10.1016/S0140-6736(12)60312-2Cite or Link Using DOI
Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study.