About 80 percent of calories in nuts come from fat, but it's healthy unsaturated fat, not the artery-clogging kind. Nuts also are high in plant sterols, substances that block the absorption of cholesterol. Given these advantages, nuts are a natural for a heart-healthy diet. About an ounce and a half to two ounces a day should do it. Walnuts, almonds, hazelnuts, pecans and pistachios all confer benefits. So do peanuts, although they're technically a legume and not a nut.
Ground-breaking research published in the Journal of the American Medical Association (JAMA) studied nearly 9,000 European patients. All had previously suffered heart attacks. The trial found that those who reduced their LDL levels to an average 81 with high-dose statins significantly reduced their risk of major coronary events like heart attacks and strokes at the 4.8 year follow-up compared to patients who reduced their LDL to 104 on usual-dose statin therapy.
Foods like oatmeal, apples, prunes, and beans are high in soluble fiber, which keeps your body from absorbing cholesterol. Research shows that people who ate 5 to 10 more grams of it each day saw a drop in their LDL. Eating more fiber also makes you feel full, so you won’t crave snacks as much. But beware: Too much fiber at one time can cause abdominal cramps or bloating. Increase your intake slowly.
Where HDL is concerned, “you can’t be too thin,” Castelli says. One report found about a 1 percent rise in HDL for every pound of fat lost. This doesn’t mean you have to turn yourself into a toothpick, but that you should work on getting rid of excess flab as you add muscle. (Use a body-fat monitor rather than a scale to chart your progress.) Fortunately, fat loss is likely to go hand in hand with the exercise and dietary modifications that also raise HDL levels.
Besides putting your heart health at risk, sugar is also known to be one of the most significant contributors to metabolic syndrome. In fact, the recent 2015 Dietary Guidelines labeled sugar as a “nutrient of concern” and voiced recommendations for added sugars to not exceed greater than 10% of total daily calories. So, if your goal is to nip sugar in the bud and increase your HDL cholesterol levels, start by evaluating your libations.
Because increasing HDL levels is thought to be such a beneficial thing, and because there is no easy or reliable way to do so, developing drugs that substantially raise HDL levels has become a major goal for several pharmaceutical companies. And indeed, several of these drugs have been developed, and have led to clinical trials to demonstrate their safety and efficacy.
So if there is a cholesterol that is actually good for us, how can we naturally increase its levels? The short answer is lifestyle. Your lifestyle actually has the single greatest impact on your HDL cholesterol level. So making changes to daily and completely controllable habits like diet and exercise can equate to healthier HDL cholesterol levels, which can lower your risk for life-threatening health issues.
The small HDL particles consist of the lipoprotein ApoA-1, without much cholesterol. Thus, the small HDL particles can be thought of as “empty” lipoproteins, that are on their way to scavenge excess cholesterol from the tissues. In contrast, the large HDL particles contain a lot of cholesterol. These particles have already done their scavenging work, and are just waiting to be taken back up by the liver.
Could one of your current prescriptions be a cause of your low HDL levels? Possibly! Medications such as anabolic steroids, beta blockers, benzodiazepines and progestins can depress HDL levels. If you take any of these medications, I suggest talking to your doctor and considering if there is anything you can do that could take the place of your current prescription.
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society
Salmon is rich in omega-3 fatty acids, which are healthy fats that can help reduce blood pressure. Eating salmon can improve your "good" HDL cholesterol, but it won't lower your "bad" LDL cholesterol. HDL cholesterol helps sweep cholesterol off your artery walls, preventing dangerous plaque from forming. The American Heart Association recommends eating fatty fish like salmon at least twice per week for heart-healthy benefits. Other fish that contain omega-3s, such as mackerel, tuna and sardines, can also help.
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.