Phosphatidylcholine appears to be the second most important phospholipid endogenously in the human body (second to sphingolipids) and is generally seen as ubiquitous.
In cell membranes, most phospholipids are based off of phosphatidylcholine with phosphatidylserine contributing a significant portion.
Phosphatidylcholine (PC) is a phospholipid with two fatty acids (these can vary within the molecule and it is still referred to as PC) bound to a glycerol backbone, with the final binding slot occupied by a phosphatic acid and then a choline molecule; demethylation of all methyl groups on the choline results in phosphatidylethanolamine (both phospholipids being common in the diet and sourced in soy lecithin).
If phosphatidylcholine loses both of its fatty acids and retains its choline group, it is referred to as Alpha-GPC.
34g of phosphatidylcholine (conferring 2,600mg of choline) failed to significantly influence the cholesterol profile of otherwise healthy aged men over the course of two weeks.
Supplementation of 2.6g choline via 34g phosphatidylcholine (soybean) over the course of two weeks in otherwise healthy men (aged 50-71) appears to be able to increase circulating triglycerides (8%) relative to placebo (the fatty acid profile of the lecithin replicated, but without PC).
Phosphatidylcholine (PC) injections (usually as 70% PC with deoxycholate at 4.2% as solvent and benzyl alcohol at 3% as preservative) appear to be used for inducing lipolysis (or alternatively, lipid dissolution) with all three agents (but mostly deoxycholate) able to induce adipocyte bursting followed by an increase in triglyceride-rich lipoproteins. It appears to be associated with low rates of significant side-effects when used under the guidance of medical professionals although adverse effects have been reported in case studies.
Injections of PC have been used in models of lipodystrophy (a redistibution of adipose tissue in an abnormal manner, commonly seen in HIV patients), where excised cells from lipodystrophic AIDS patients treated with 20mcg/mL of the above injection mixture lysed within 4-5 hours. In a trial on persons with gynoid lipodystrophy, injections of phosphatidylcholine/deoxycholate (4 injections over 8 weeks) appears to reduce localized fat although the a similar level of efficacy as deoxycholate alone.
Two pilot studies have assess orbital fat pads (under the eye) has noted that 0.4-0.5mL of PC have noted mixed effects, with benefit and null results. Benefit has been noted in a small trial on jaw fat, although there was no control group used (benefits noted relative to baseline).
One study has been conducted assessing visceral adipose (a hardened faty surrounding internal organs), and in this animal model (dogs) there was an apparent lipolytic effect following injections. Animal models have also noted lipolytic effects in rat inguinal fat pads as well.
Adipose tissue necrosis can be induced in vitro with such an infusion of PC that may affect other cell types; necrosis of adipose is sometimes observed in animal models although not all the time. Long term cost-benefit analyses of safety regarding PC/deoxycholate injections have not yet been undertaken.
Injections of a mixture of deoxychlorate and phosphatidylcholine appear to be commonly used for localized fat loss, most commonly studied for lipodystrophies. Phosphatidylcholine may play a role here, but the trial sizes are relatively small and those used in more hedonistic models (aesthetic fat loss rather than lipodystrophy) are less than optimally structured although theoretically it should apply to all fat deposits. A clear cost-benefit analysis has not yet been conducted
Oral phosphatidylcholine is unlikely to possess such effects as those noted with injections
750mg of phosphatdylcholine to pregnant mothers from 18 weeks gestation to 90 days postpartum (in addition to around 360mg of choline in the diet) has failed to enhance the brain function of the offspring, suggesting that the dietary choline intake was sufficient.