Green, leafy vegetables, esp. kale, collards, swiss chard are a few vegetables which help. Fiber in apples (pectin) may reduce LDL levels. It is VERY important to eliminate all forms of sugar for a few weeks, reintroduce (ONLY one for a month or so) a slightly sweet food, and switch different types of sweet foods to see which sweet food is more tolerable.
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.
A study published in January 2016 in the journal Nutrients found that an antioxidant-rich diet raises HDL cholesterol levels in relation to triglycerides, and might be associated with a reduced risk of stroke, heart failure, and inflammatory biomarkers. Antioxidant-rich foods include dark chocolate, berries, avocado, nuts, kale, beets, and spinach.
Catapano AL, et al. 2016 ESC/EAS guidelines for the management of dyslipidaemias: The task for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitaiton (EACPR). Atherosclerosis. 2016;253:281.
Rich in omega-3 fatty acids and all-around delicious, walnuts have also been shown to improve the HDL-to-total cholesterol ratio, according to a study published in the American Diabetes Association’s peer-reviewed journal, Diabetes Care. This ratio is used by physicians to assess overall cardiovascular risk and can provide more information than just one value alone. A desirable ratio is anything below 5:1, but a ratio of 3.5:1 indicates very minimal cardiovascular risk.
As a result of all this, doctors don’t just want you to lower your total cholesterol count; they want you to change the ratio as well, so you have more HDL and less LDL. “When we looked at the data, we found that the higher your HDL went, the lower your risk of heart attack,” says cardiologist William Castelli, M.D., former director of the Framingham Heart Study in Massachusetts. An HDL level of 75 or more seems to convey extra longevity for many people, while a count of 100 or more is so beneficial that it was dubbed the “Methuselah syndrome” by one researcher. HDL less than 35 or so, meanwhile, can carry significant risk of heart disease. Genetics plays a large role in HDL. A few guys have naturally low levels and need to keep their LDL low as well to make up for it. (As Castelli puts it, you don’t need a substance that removes cholesterol from your blood if you don’t have much to begin with.) But there’s plenty that everyone else can do to pump up their HDL. Never one to shirk from a task that doesn’t involve housecleaning, I managed to find two handfuls of ways to turn my “good” numbers into great numbers.
Paying close attention to what you eat can help you reduce your risk of developing atherosclerosis. Atherosclerosis is the narrowing of arteries caused by plaque build-up inside the arteries. As the arteries narrow, blood can't flow properly through the arteries. Theis can lead to a heart attack or stroke. If the artery-clogging process has already begun, you may be able to slow it down by making changes in your lifestyle, including your diet.
This healthy recipe pairs well with just about anything -- salmon, chicken, or game meat like bison and venison. It's also a superb go-to for quick-fix lunches or snacks. Ladle some into whole-wheat tortillas stuffed with crunchy veggies. Pour a cup or two into some chicken or vegetable stock for an easy soup. Or blend a big scoop of your beans and rice with a big bowl of lettuce greens and sliced tomatoes for a filling lunch salad.
Lentils are pulses, a.k.a. the dry edible seeds of certain crops (like beans, chickpeas, and peas). Pulses are just everywhere these days because they’re packed with plant-based protein and fiber, not to mention antioxidants, minerals, and B vitamins. All of those compounds help protect you from plaque buildup while optimizing blood flow and assisting your body in efficiently using the nutrients you consume.
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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
Cholesterol is then returned to the liver by multiple routes. In the first route, cholesterol esters may be transferred from HDL to the apo B–containing lipoproteins, such as very–low-density lipoprotein (VLDL) or intermediate-density lipoprotein (IDL), by CETP. These lipoproteins undergo metabolism and subsequent uptake by the liver, primarily by a process mediated by the B,E receptor. In the second route, HDL particles may be taken up directly by the liver. In the third, free cholesterol may be taken up directly by the liver. Finally, HDL cholesterol esters may be selectively taken up via the scavenger receptor SR-B1.
A study published in February 2016 in the journal PLoS One concluded as much. For nearly 11,000 adults, researchers found that low to moderate alcohol consumption (20 or fewer drinks a week for a man, 10 or fewer for a woman) led to higher levels of HDL cholesterol. It also helped get them to healthier overall cholesterol levels, decreasing triglycerides (blood fats in blood) and lowering LDL cholesterol.
There's no magical food to keep your heart healthy, but there are a lot of foods that can help—including these foods that help lower your cholesterol. In addition to cutting back on foods that can raise total cholesterol and getting enough exercise, make sure to eat more of these foods that improve your cholesterol profile by raising "good" HDL and/or lowering "bad" LDL cholesterol. These foods include some old standbys, such as oatmeal and fruit, plus a few surprising foods that can help lower cholesterol to reduce your risk of heart attack and stroke.
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]