While diet and exercise should be your two main options for fighting off LDL cholesterol, you can also look into the various dietary supplements that are on the market today. Consider omega-3 fish oils, artichoke extract, and green tea extract. Keep in mind that these natural products have not been fully proven to reduce your level of LDL cholesterol, but they may be able to help along the way.
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.
Dr. Pacold notes that exercise has a greater effect on raising HDL cholesterol, which protects you from heart disease, than on lowering the LDL cholesterol that puts you at risk. It's good to know that even if you don’t see the numbers changing right away, regular exercise strengthens your heart and protects you from heart disease. If you’re not a big fan of exercise and not in great shape to begin with, remember that all you need to do to start reaping the heart-healthy benefits of exercise is 30 minutes of walking at a moderate pace every day. If you have a heart condition, talk with your doctor first about how much exertion is right for you when you begin, and then work your way up to your fitness goals for heart health.

Foods naturally rich in soluble fiber have proven particularly good at lowering cholesterol. Excellent sources include oats, oat bran, barley, peas, yams, sweet potatoes and other potatoes, as well as legumes or beans, such as pinto beans, black beans, garbanzo beans, and peas. Vegetables rich in soluble fiber include carrots, Brussels sprouts, beets, okra, and eggplant. Good fruit sources are berries, passion fruit, oranges, pears, apricots, nectarines, and apples.
A study of over 1 million US veterans showed a U-shaped relationship between HDL and total mortality, with 50mg/dL as the level associated with the lowest mortality. [7, 2] In addition, an analysis of the Framingham study demonstrated that LDL and triglyceride levels modify HDL’s predictive value; CHD risk was found to be higher when low HDL was combined with high LDL and/or triglycerides as compared with the presence of low HDL levels alone. [8, 2]  The relationship between HDL and CHD risk is also confounded by the presence of pro-atherogenic and inflammatory markers. [2]
Plain and simple, exercise raises HDL levels. “We looked at doctors and others who ran the Boston Marathon,” notes Castelli. “While the average male HDL is 45, men who ran the marathon ranged around 55.” One Georgetown University study found increased HDL in those who ran seven miles a week or took part in four moderate 30-minute sessions of any aerobic activity.

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. [18] ) 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]