Phosphatidylcholin

Phosphatidylcholine (PC) supplementation has been shown to have a positive effect in many hard to resolve conditions such as Alzheimer's, Parkinson's, senility, neuro-muscular disorders, synaptic dysfunction, elevated blood fats, fatty liver, gall bladder symptoms, gall stones, migraine headaches, and adrenal hypo-function. Known also as triple strength lecithin, phosphatidylcholine contains 3 times the amount of choline as regular lecithin. Choline is necessary for liver and brain function, and helps the body utilize fats and cholesterol properly (lipotropic factor). Choline prevents the deposition of fats in the liver. The liver and kidneys accumulate choline and convert much of it to betaine, also a lipotropic factor. Chronic ingestion of a diet deficient in choline has major consequences that include hepatic, renal, memory, and growth disturbances.  

Phosphatidylcholine (PC) is a prominent phospholipid, a part of all biologic membranes, especially in the outer layer of cell plasma membranes. It is an important source of methyl groups. As the precursor to the neurotransmitter acetylcholine, dietary PC is an important contributor to both blood and brain choline concentrations, which codetermine the rate of acetylcholine biosynthesis, especially during rapid firing of cholinergic neurons. Oral PC is more efficient in raising blood choline levels than equal amounts of free choline. This may explain why it is considered to have therapeutic implications in those diseases such as Alzheimer's pre-senile dementia, tardive dyskinesia and other conditions probably caused by a failing cholinergic activity.

Phosphatidylcholine helps regulate cholesterol and triglycerides, by helping to keep them in solution in the blood stream, preventing them from being deposited in arterial walls. Also, PC is a major phospholipid component of the lipoproteins. High-density-lipoproteins (HDLs) especially have a high content of PC.  In the current understanding of lipoproteins, it is generally agreed that an important function of HDLs is to facilitate cholesterol efflux from tissues. After esterification by the enzyme LCAT and redistribution among the lipoproteins, the cholesterol esters are transported to the liver, where the cholesterol is excreted in the bile and some of it is converted to bile acids.  The mechanism of transporting tissue cholesterol to the liver is known as "reverse cholesterol transport," and it is the only known mechanism by which the body gets rid of excess cholesterol. PC may increase the PC content of HDLs, and HDLs enriched with PC may function more effectively in facilitating cholesterol efflux, thus enhancing the reverse cholesterol transport mechanism. PC is also needed to export triglycerides.

It is well known that increased cholesterol efflux leads to up-regulation of low-density-lipoprotein (LDL) receptor activity, thereby lowering LDL and serum cholesterol. . PC is also mainly responsible for the hydrophilic properties of the surface coat of chylomicrons and very-low-density-lipoprotein (VLDL). Humans that have induced choline deficiency, develop liver dysfunction such as a fatty liver, as is also seen in choline deficient animals. The fatty liver occurs in choline deficiency because PC synthesis is needed for the production of VLDL secretion.

The accumulation of lipids in the liver may be the reason why choline deficient rats develop hepatocarcinoma.  There is evidence which suggests that liver cancer may develop secondarily to abnormalities in protein kinase C-mediated signal transduction during choline deficiency, which is associated with an accumulation of an activator of protein kinase 1,2-diacylglycerol. In choline deficiency, hypomethylation of DNA, abnormalities in DNA repair, and DNA damage caused by lipid peroxides could contribute to the events leading to liver carcinogenesis. 

Supporting Clinical Studies:

·         "Reduction of Hyperlipidemia With 3-sn-Polyenyl-Phosphatidylcholine in Dialysis Patients," Kirsten, R., et al, International Journal of Clinical Pharmacology, Therapy and Toxicology, 1989;27(3):129-134. Twenty patients in 2 different groups took a total dose of 2.7 grams of phosphatidylcholine daily in 6 capsules or placebo. The phosphatidylcholine caused a 37.8 mg/dl decrease in total cholesterol, a 32 mg/dl reduction in LDL cholesterol and triglycerides at 6 weeks by 43.3 mg/dl.

·         "An Investigation Into The Therapeutic Effects of Phosphatidylcholine in Diabetics With Dyslipidemia," Arsenio, L., et al, La Clinica Therapeutica, July 31, 1985;114(2):117-127.  Diabetic patients were given phosphatidylcholine at a dose of 1,200 mg a day which led to a 15.1% reduction in blood cholesterol at 90 days, a rise in HDL of 13% at 90 days and a significant fall in LDL of 20% from 60 days onwards.

·         "Reduction of Hyperlipidemia With 3-sn-Polyenyl-Phosphatidylcholine in Dialysis Patients," Kirsten, R., et al, International Journal of Clinical Pharmacology, Therapy and Toxicology, 1989;27(3):129-134. Twenty patients in 2 different groups received either three 450 mg tablets of 3-sn-polyenyl-phosphatidylcholine (PPC), morning and evening, for a total dose of 2.7 grams daily in 6 capsules or placebo in a double-blind, randomized trial.  The phosphatidylcholine caused a 37.8 mg/dl decrease in total cholesterol 2 weeks after beginning the treatment.  This remained constant throughout the treatment. There was a 32 mg/dl reduction in LDL cholesterol as compared to the placebo.  Triglycerides were reduced by phosphatidylcholine at 4 weeks by 58.2 mg/dl and at 6 weeks by 43.3 mg/dl.  Side effects were similar to placebo. 

·         "An Investigation Into The Therapeutic Effects of Phosphatidylcholine in Diabetics With Dyslipidemia," Arsenio, L., et al, La Clinica Therapeutica, July 31, 1985;114(2):117-127. Twenty-nine diabetic patients were divided into 2 groups. Phosphatidylcholine was given at a dose of 1,200 mg a day in the form of three 200 mg capsules with 2 main meals.  Treatment with phosphatidylcholine led to a rapid fall in blood cholesterol which was evident at 30 days and statistically significant at 90 days with a 15.1% reduction.  There was a rise in HDL of 13% at 90 days and a significant fall in LDL of 20% from 60 days onwards. Polyunsaturated phosphatidylcholine should be considered an important supportive therapy for the treatment of lipid disorders.

·         "Choline:  An Important Nutrient in Brain Development, Liver Function, and Carcinogenesis", Zeisel, Steven H., M.D., Ph.D., Journal of the American College of Nutrition, 1992;11(5):473-481

·         "Low Serum Docosahexaenoic Acid Is a Significant Risk Factor for Alzheimer's Dementia," Kyle DJ, et al, Lipids, 1999;34:S245. Low levels of circulating phosphatidylcholine-DHA may be a significant risk factor for low scores on the Mini-mental State Exam and in the development of Alzheimer's disease in the elderly. Alzheimer's is characterized by the loss of acetylcholine neurons in the brain.

·         Phosphatidylcholine has shown to be beneficial in dealing with chronic active hepatitis (Liver 2:77-81, 1982) and in muscular dystrophy (J Theor Biol 116(1):56-88, 1985 & Proc Soc Exp Biol Med 58:40-1, 1945).


With elevated cholesterol and triglycerides, consider Phosphatidylcholine, Glucobalance and TriChol, each at 2 TID.

Foods rich in phosphatidylcholine include eggs, liver, soybeans, peanuts, oatmeal, cauliflower, etc.