A: Before I answer that question, why bother to increase HDL cholesterol at all? Many studies have found that people with low levels of HDL are at increased risk for heart attacks, strokes, and other complications of arteries diseased by atherosclerosis: that's why we call HDL the "good" cholesterol. Given that, you'd think that raising HDL levels would reduce a person's risk for atherosclerosis. Unfortunately, despite a lot of research, we don't yet know if that's true, nor how best to raise HDL levels.
So far, these studies have been disappointing, to say the least. The first major trial (concluded in 2006) with the first CETP inhibitor drug, torcetrapib (from Pfizer), not only failed to show a reduction in risk when HDL was increased but actually showed an increase in cardiovascular risk. Another study with another CETP inhibitor - dalcetrapib (from Roche) - was halted in May 2012 for lack of effectiveness. Both of these related drugs significantly increased HDL levels, but doing so did not result in any clinical benefit.
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Black beans, kidney beans, lentils, oh my! All are rich in soluble fiber, which binds to cholesterol in the blood and moves it out of the body. Recent studies show eating 4.5 ounces of beans a day can reduce LDL levels by 5 percent. Try black bean burritos, or dip some veggies in hummus, which is made with chickpeas, for an afternoon snack. Or try this Caramelized Onion and White Bean Flatbread -- beans are so versatile, the possibilities are endless.
The good news is that changing your cholesterol levels is well within your control as some of the smallest lifestyle tweaks can yield a profound impact. A fast track to boosting HDL includes quitting smoking and increasing physical activity. The American Heart Association recommends 30 minutes of moderate physical activity at least 5 times per week with two sessions of resistance training. Your choices at mealtimes, however, may prove to be an easier more attainable way to make lasting change. Here are the foods that raise HDL cholesterol.
There are two types of dietary fiber: soluble (viscous) and insoluble. To receive the greatest health benefit, eat a wide variety of all high-fiber foods. Refined foods, like white bread, white pasta and enriched cereals are low in fiber. The refining process strips the outer coat (bran) from the grain, which reduces the amount of fiber that's left.
When your body has too much LDL cholesterol, the LDL cholesterol can build up on the walls of your blood vessels. This buildup is called “plaque.” As your blood vessels build up plaque over time, the insides of the vessels narrow. This narrowing blocks blood flow to and from your heart and other organs. When blood flow to the heart is blocked, it can cause angina (chest pain) or a heart attack.
Berberine – this is a plant-based natural supplement to raise HDL. It’s ideal for promoting healthy cholesterol and blood sugar levels. It may very well be the single most powerful supplement we carry. Due to soil depletion and modern farming practices, it’s nearly impossible to get the nutrition you need from food alone. Use Berberine as the supplement of choice to boost HDL.
Foods high in monounsaturated fats (such as olive oil, nuts, and the oils in many salad dressings) seem to boost HDL best; it’s likely that foods high in omega-3 fatty acids (such as cold-water fish) do so as well. Saturated fats, the kind in meat and dairy foods, are likely to drive up harmful LDL, so take this opportunity to cut way back. Worst of all are trans-fatty acids, the hardened oils often found in margarine, crackers and other snack foods-a substance Harvard Medical School nutrition expert Walter C. Willett, M.D., author of Eat, Drink, and Be Healthy, calls “uniquely bad.” These foods can do exactly the opposite of what you want, lowering HDL while raising LDL.
A desirable level of LDL (“bad”) cholesterol is less than 100 mg/dL – the lower your LDL, the better in terms of heart disease risk. Levels between 139 and 150 mg/dL are borderline high and those between 160 to 189 mg/dL are considered high, while LDL levels above 190 mg/dL are classed as very high. According to the American Heart Association, the mean level of LDL cholesterol for American adults age 20 and older is 115.0 mg/dL.
In humans, diets high in saturated fat and cholesterol raise HDL-cholesterol (HDL-C) levels. To explore the mechanism, we have devised a mouse model that mimics the human situation. In this model, HuAITg and control mice were studied on low fat (9% cal)-low cholesterol (57 mg/1,000 kcal) (chow) and high fat (41% cal)-high cholesterol (437 mg/1,000 kcal) (milk-fat based) diets. The mice responded to increased dietary fat by increasing both HDL-C and apo A-I levels, with a greater increase in HDL-C levels. This was compatible with an increase in HDL size observed by nondenaturing gradient gel electrophoresis. Turnover studies with doubly labeled HDL showed that dietary fat both increase the transport rate (TR) and decreased the fractional catabolic rate of HDL cholesterol ester (CE) and apo A-I, with the largest effect on HDL CE TR. The latter suggested that dietary fat increases reverse cholesterol transport through the HDL pathway, perhaps as an adaptation to the metabolic load of a high fat diet. The increase in apo A-I TR by dietary fat was confirmed by experiments showing increased apo A-I secretion from primary hepatocytes isolated from animals on the high fat diet. The increased apo A-I production was not associated with any increase in hepatic or intestinal apo A-I mRNA, suggesting that the mechanism of the dietary fat effect was posttranscriptional, involving either increased translatability of the apo A-I mRNA or less intracellular apo A-I degradation. The dietary fat-induced decrease in HDL CE and apo A-I fractional catabolic rate may have been caused by the increase in HDL particle size, as was suggested by our previous studies in humans. In summary, a mouse model has been developed and experiments performed to better understand the paradoxical HDL-raising effect of a high fat diet.
Substantial evidence now shows that a low-fat diet often reduces — rather than increases — HDL levels. This result is not specifically caused by “not enough fat,” but rather, is caused by consuming too many carbohydrates. The American Heart Association and the American College of Cardiology have quietly stopped recommending low-fat diets for heart disease prevention. Indeed, it is low-carb diets — and not low-fat diets — which are associated with higher HDL levels.
Population studies have shown that low levels of HDL cholesterol—less than 40 mg/dL for men and less than 50 mg/dL for women—increase the overall risk of coronary artery disease (CAD) and heart attacks. A person whose HDL level is lower than 35 mg/dL has eight times the risk of CAD as someone with an HDL level of 65 mg/dL. Experts have long thought that boosting HDL levels promotes heart health. But while low HDL is a strong and well-established risk factor for heart disease, the evidence for raising HDL remains uncertain. But experts agree that taking these heart healthy steps are still worthwhile.
Nuts are high in polyunsaturated fatty acids, so almonds, walnuts, or pistachios can help reduce your LDL levels. Try sprinkling them on your salad, or eat them right out of hand as a snack. Just be sure to choose the low-salt option, and keep it to about 1.5 ounces a day -- nuts are also high in calories. For almonds, that’s about 30 almonds or 1/3 cup.
HDL serves as a chemical shuttle that transports excess cholesterol from peripheral tissues to the liver. This pathway is called the RCT system. In this system, plasma HDL takes up cholesterol from the peripheral tissues, such as fibroblasts and macrophages. (A study by El Khoury et al indicated that in persons with HALP, macrophages have an increased plasma cholesterol efflux capacity.  ) This may occur by passive diffusion or may be mediated by the adenosine triphosphate (ATP)–binding cassette transporter 1. The latter interacts directly with free apo A-I, generating nascent, or so-called discoidal, HDL. Cholesterol undergoes esterification by lecithin-cholesterol acyltransferase (LCAT) to produce cholesteryl ester, which results in the production of the mature spherical HDL. Cholesterol is also taken up from triglyceride-rich lipoproteins in a process mediated by a phospholipid transfer protein (ie, CETP). [19, 20, 21, 22]