Lipoprotein(a), or lp(a), is the number one most aggressive cause for heart disease and coronary plaque known.
Lp(a) can account for heart attacks in men in their 40s, women in their 50s. Whenever you hear about families in which heart attacks occur in people in their 40s and 50s, always think Lp(a) until proven otherwise. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners (and often explains the media’s occasional misinterpretation of heart disease in athletes: “Does extreme exercise cause heart disease?”). It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people.
There should be absolutely no remaining doubt that increased levels of Lp(a) are associated with substantially increased risk for heart disease. There are now hundreds of studies that have confirmed this association.
But how is Lp(a) treated? This is where conventional wisdom fails miserably. Niacin (vitamin B3) at higher doses is the conventional number one treatment for Lp(a). Sadly, most doctors are afraid of niacin due to its tendency to trigger an annoying hot “flush.” Lp(a)â”€even if identified in the first placeâ”€nearly always goes untreated, despite its enormous implications.
So here’s a list of little known facts about Lp(a) that can help you educate your doctor about this important pattern:
Niacin is the number one treatment for Lp(a). The key to tolerating niacin is to take with a large meal, such as dinner, and to hydrate vigorously. I advise my patients to drink two 8-12 oz glasses of water to put out the flush; this works for 90% of people. (I tell patients to ignore the idiotic advice advocated by the manufacturer of the prescription form of niacin to “take with a low-fat snack.” This worsens Lp(a), along with small LDL.) Niacin should be taken with the supervision of your doctor and I advocate never taking more than once per day for any long-acting preparation, twice per day for immediate release.
Carbohydrates increase Lp(a), fats reduce it. Thus, a low-fat diet is the worst possible diet for Lp(a). I tell my patients to add healthy oils to every meal.
You know what fraction of fat is most effective for reducing Lp(a)? Saturated fat Peculiar, isn’t it? However, it doesn’t mean you people with this pattern should eat unlimited saturated fat sources. I tell my patients to eat saturated fat sources selectively, such as real cheeses, lean meats, and eggs (but not cured meats, fried foods, and processed foods made with saturated fats).
Hormones have a profound influence over Lp(a). Women can reduce Lp(a) with estrogen (preferably human, not horse) and DHEA. Men can reduce Lp(a) with testosterone and DHEA.
Thyroid has a profound influence over Lp(a). If thyroid function is low (hypothyroidism)â”€surprisingly commonâ”€Lp(a) can skyrocket. Thus, people with Lp(a) may be more susceptible than usual to the undesirable effects of hypothyroidism.
Alcohol reduces Lp(a), in addition to raising HDL.
Vegetarians have higher Lp(a) than meat- and fish-eating people.
Lp(a) can be a cause for substantial high blood pressureâ”€especially in women over 55 years old.
Anyway, that’s just a sampling of the peculiar rules that govern Lp(a). In fact, in many ways, you might view Lp(a) as a genetic factor that reverses many of the conventional rules of heart health.
If you have reason to believe that Lp(a) is part of your risk profile for heart disease (family with history of heart disease, high blood pressure in a slender person, cholesterol poorly responsive to cholesterol-reducing drugs are among the “red flags” for Lp(a)), then you should insist that Lp(a) be tested by your doctor. If he/she refuses, time to go doctor shopping.