And according to some powerful experiments by software engineer-turned-biohacker Dave Feldman, you can actually increase and decrease your cholesterol at will. It all depends on how much fat you eat — and, directly against mainstream dietary knowledge, the correlation is inverted. In other words, eating more fat will actually lower your cholesterol.
Get Moving – Want healthy HDL levels? It’s time to lace up those sneakers and start exercising! Being physically active is essential for a healthy heart. Many types of exercise will help raise your HDL cholesterol, including high-intensity exercise, aerobic exercise, and strength training. Shoot to exercise most days out of the week for at least 30 minutes each session to experience the benefits.
One drawback of going on a low-fat diet for some people is that it lowers HDL levels. If raising your HDL cholesterol is a primary concern, you should replace carbohydrates in your diet with fats, preferably mono- and polyunsaturated fats. But avoid trans fat, which can lower HDL levels. These steps can lower both total cholesterol and LDL and maintain HDL or boost it slightly, improving the ratio of total cholesterol to HDL.
Hyperalphalipoproteinemia (HALP) may be familial, including primary (without CETP deficiency) and otherwise (with CETP deficiency), or secondary.  Familial HALP (aside from the primary form) is a well-documented genetic form of hypercholesterolemia characterized by a deficiency of CETP, a key protein in the reverse cholesterol transport (RCT) system that facilitates the transfer of cholesteryl esters from high-density lipoprotein (HDL) to beta lipoproteins. Primary HALP is a term used for familial elevated HDL cholesterol levels that are not due to CETP deficiency and for which the cause is unknown. Secondary HALP is due to environmental factors or medications.
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]