Phosphatidylcholine and Your Health

Methylation: The Link Between Phosphatidylcholine, Disease, and Overall Health

Methylation is a metabolic process which occurs in each one of our 75 trillion cells in our bodies, more than 3 billion times per second. It is critical to life. Phosphatidylcholine (PC), often formed from the metabolism of lecithin (which also contains linoleic and linolenic acids) and is an integral component of this methylation process.

What is Phosphatidylcholine and why is it so important?

PC is a major component of cellular membranes and is the most abundant phospholipid in the body. The highest concentrations of PC are found within the liver and the brain. PC plays a role in membrane-mediated cell signaling and activates a binding protein (PCTP), that helps transfer PC between cells and activates other enzymes.

Insufficient levels of phosphatidylcholine (PC) is one of the causal factors of non-alcoholic fatty liver disease (NAFLD), due to its impact on methylation cycle dysfunction. NAFLD is a progressive liver disease strongly associated with metabolic issues such as obesity, insulin resistance, and dyslipidemia. Dyslipidemia can be described as an increased level of plasma cholesterol and triglycerides (TGs) or a low level of high-density lipoprotein. Dyslipidemia contributes to atherosclerosis or the hardening/narrowing of the arteries which in turn can lead to heart attacks, strokes, and even death. NAFLD has also been shown to result in a more serious liver problem termed non-alcoholic steatohepatitis (NASH) and increases the risk of cirrhosis and liver cancer.

Choline deficiency affects VLDL production in the liver, leading to a build-up of triglycerides (steatosis) in the liver given that PC helps transport triglycerides out of the liver. The accumulation of fats in the liver has been demonstrated to inhibit mitochondrial function (energy-producing factories of the cell), reducing fat burning and increasing the production of free radicals (ROS) that trigger lipid peroxidation (oxidation of fats), DNA damage, and apoptosis (cell death).

Phosphatidylcholine (PC) is also the most studied nutrient in breast cancer. The phosphatidylethanolamine methyltransferase (PEMT) enzyme, which makes PC in the methylation cycle, has been shown to inactivate the BRCA gene. The BRCA gene, a hot topic of discussion, has been linked to breast cancer. BRCA gene has been shown to inactivate the PEMT gene impacting choline metabolism. Many women with the BRCA gene mutation opt for radical mastectomies to mitigate the risk of breast cancer.

Who should supplement with Phosphatidylcholine?

Phosphatidylcholine is critical for fetal development, and pregnant women who are choline deficient may be advised to increase their consumption of PC-rich foods or take supplements. Expectant mothers can also suffer additional adverse impacts such as morning sickness and gestational diabetes which may be alleviated through supplementation. Postmenopausal women may also wish to investigate supplementing with phosphatidylcholine (PC), as menopause reduces the production of estrogen, the co-factor for PEMT enzyme, which is necessary for PC production.

Elite athletes are also good candidates for PC supplementation as phosphatidylcholine is depleted during extreme exercise. Vegans are also particularly at risk for choline deficiency (as eggs and organ meats are the best sources of dietary choline), although choline is also present in whole grains, legumes, and cruciferous vegetables. A large part of the population, however, is also likely choline deficient.

Individuals who have problems digesting fats or who have gallbladder issues should take PC with bile salts and taurine, and as PC supplementation may cause gas and bloating, it should preferably be taken in the morning with food. PC should be used in place of lecithin for those with a low active functioning PEMT gene, as lecithin metabolism requires the PEMT enzyme to make PC.

The broader impact of Phosphatidylcholine (PC) on Methylation processes

PC supplementation lowers homocysteine (HCY) levels in the blood, increases S-adenosylmethionine (SAMe), and the SAMe/S-Adenosyl-L-homocysteine (SAH) ratio by decreasing SAMe demand that is required to make PC. This lowering of homocysteine and elevation of SAMe is a critical function in the methylation cycle. Homocysteine is a significant indicator for increased risks of heart disease, heart attack, stroke, and even Alzheimer’s Disease.

PC partners with docosahexaenoic acid (DHA) by adding it to cell membranes, supporting the cell membrane structure and integrity. PC deficiency weakens the cell structure and enables leakage of vital folate from the cells. PEMT enzyme (with the aid of co-factor SAMe) converts phosphatidylethanolamine (PE) into PC. A deficiency in PEMT may also result in increased lipid oxidation and may lead to high levels of homocysteine. Also, the PEMT enzyme, which uses SAMe and creates SAH to produce PC, is inhibited when PC levels are adequate, resulting in more SAMe being available elsewhere in the body such as in the production of essential neurotransmitters such as serotonin and norepinephrine and other important parts of the methylation cycle.