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Phosphatidylcholine: Can it raise HDL?
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Note: The question of phosphatidylcholine (PC) and related supplements has arisen repeatedly in Track Your Plaque Forum discussions, as well as from our face-to-face experiences in the Track Your Plaque program. To date, phosphatidylcholine has not been an ingredient in our experience. However, interest is so great, and some of the anecdotal results so positive, that we decided to investigate further. Here is a discussion of the potential merits of this supplement, phosphatidylcholine, as a means of raising HDL cholesterol, possibly shifting its subclass distribution, as well as other lipid effects. 


What is high-density lipoprotein, or HDL?

HDL is a family of blood particles that share several features. They all contain a crucial protein, Apoprotein A-I (ApoA-I), some contain another protein called Apoprotein A-II of uncertain significance, and the phospholipid, phosphatidylcholine.

One of HDL’s essential roles is to bind cholesterol in various cells, such as macrophage inflammatory blood cells that accumulate in artery walls and create atherosclerotic plaque. HDL particles thereby accumulate cholesterol, the first step for disposal of cholesterol, or “reverse cholesterol transport.”

After release from the liver, immature HDL particles interact with other particles via enzyme-driven reactions that modify HDL structure. For instance, one crucial reaction occurs between HDL particles and an enzyme called lecithin-cholesterol acyl transferase (LCAT) which modifies cholesterol molecule to become cholesteryl esters within HDL.

If triglyceride-rich particles are present in the blood, such as excess very low-density lipoproteins (VLDL) or intermediate-density lipoproteins (IDL), then HDL reacts with the enzyme cholesteryl ester transfer protein (CETP), which exchanges the cholesteryl ester on HDL for a triglyceride from the VLDL or IDL. This results in triglyceride-rich HDL particles.

HDL particles rich in triglycerides are abnormal. They are susceptible to an undesirable reaction with another enzyme, hepatic lipase, which degrades the HDL and removes triglycerides. This results in small, ineffective HDL particles that are also more readily permanently degraded, yielding a drop in total HDL on your cholesterol panel. Interestingly, hepatic lipase activity is increased by excessive insulin levels (as in metabolic syndrome) and reduced by omega-3 fatty acids from fish oil, saturated fats, and, perhaps, niacin and statin drugs (Perret B et al 2002; Zambon A et al 1999).

You can readily see that one strategy to obtain higher HDL levels and encouraging larger HDL particles is to keep triglycerides and triglyceride-rich lipoproteins like VLDL and IDL at a low level. This is why we advocate keeping triglycerides ≤60 mg/dl in the Track Your Plaque program, as well as eliminating IDL. (Keeping triglycerides at this level predictably also keeps VLDL at low levels without need for specific target values.)

Another approach to keeping HDL cholesterol high and large is to block the enzyme, cholesteryl-ester transfer protein, or CETP. This is the basis for the drugs torcetrapib and anacetrapib, both of which are potent CETP inhibitors and cause HDL to skyrocket. However, thus far, this line of drug development has resulted in catastrophe, as witnessed in the Pfizer-sponsored ILLUMINATE Trial of torcetrapib, in which excess heart attacks, hospitalizations, and deaths occurred in participants taking the drug. The initial report on Merck’s agent, anacetrapib, was favorable, but given torcetrapib’s crash and burn, longer-term data will clearly be necessary to assure everyone of safety.

More about phosphatidylcholine

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