Lecithin supplements have been heavily promoted as a panacea for:
- Cardiovascular health
- Liver and cell function
- Fat transport and fat metabolism
- Reproduction and child development
- Physical performance and muscle function
- Cell communication
- Improvement in memory, learning, and reaction time
- Relief of arthritis
- Healthy hair and skin
- Treatment for gallstones
I have always been suspicious of promotions that promise to cure all human ailments. But recently, I came across a paper that prompted me to examine the evidence behind those claims. I’ll save you an excruciatingly detailed account—none of the claims have any credible evidence to back it up. There is one possible exception. Lecithin is a natural emulsifier, so claims that it dissolves gallstones may be credible, except that I haven’t come across a good study documenting it. WebMD gives lecithin treatment of gallstones an unenthusiastic “recommendation” of possibly ineffective.
What is lecithin?
Chemically, lecithin is called phosphatidylcholine. It is found in egg yolk, meats, soy, and vegetables. Most commercial lecithin is made from soy. So, you’d assume that when you take lecithin supplements, you get phosphatidylcholine. In fact, as is the case with many nutritional supplements, commercial preparations vary widely (between 20% to 90%) in the amount the substance is actually in their product.
Why such variability? Because the suppliers of supplements were exempted by Congress from adhering to any standards of manufacture, purity, or claims of benefits. How this came about is emblematic of our broken political system, but don’t get me going on this.
Anyway, if only a fraction of commercial lecithin is made up of the real thing—phosphatidylcholine—then what makes up the rest? The answer: fatty acids! Not exactly the stuff to help in weight reduction, cardiovascular health, or liver function. In fact, it may work against all those potentially wonderful benefits.
What’s the downside of lecithin supplements?
If they don’t cause any harm, why not give it the benefit of the doubt? A future study may prove its benefit.
In a paper in Nature, Wang et al. of the Cleveland Clinic studied the metabolic fate of lecithin. But first, by way of explanation, let me introduce a new term. We are all familiar with the concept of genomics, meaning the study of the genome, or the total genetic content and its effect on health and disease. Similarly, the total of chemicals, substrates, and metabolites in the body is called the metabolome, and the study of those substances in health and disease is called metabolomics. The advantage of such an all-inclusive approach is that it is unbiased.
The classical scientific approach is to study a specific gene or molecule, essentially ignoring everything else. This is akin to peeping through a keyhole; you see only what the hole allows you to see. On the other hand, studying the whole genome or the whole metabolome gives a complete picture of everything that is involved in the process being studied.
For instance, for many years, type 2 diabetes was thought to involve only one or two genes. Why? Because these were the only genes that “made sense” as targets for study. The advent of whole-genome studies demonstrated the involvement of dozens of genes in the disease, which was a complete surprise.
Back to the paper. Wang and his collaborators used the metabolomic approach to look for circulating small molecules associated with coronary heart disease. They screened blood from patients who had experienced a heart attack or stroke and compared the results with those from the blood of people who had not. They found major differences in choline, betaine, and trimethylamine (TMA). It turns out that these metabolites are produced from lecithin by gut bacteria and converted to trimethylamine-N-oxide (TMAO). This terminal metabolite, TMAO, is a known atherogenic (involved in atherosclerotic plaque formation).
Indeed, when the gut flora was wiped out with an antibiotic, none of the metabolites appeared in the blood. Could it be that the gut flora in people with cardiovascular disease is different in some way from that of healthy people? We don’t know, but we do know that the physiological state of a person can determine the gut flora. For instance, the gut flora of obese people is markedly different from that of the non-obese.
Based on this study alone, we still can’t tell if these lecithin metabolites are causative factors, or whether they are just markers of the disease. Correlative studies can show only correlations, not cause and effect.
Wait, wait, there’s more
Is lecithin the only culprit that produces TMAO? Red meat contains another triethylamine, similar to choline and lecithin, called L-Carnitine, which should be metabolized by the gut flora into MAO and then converted to TMAO in the circulation. So the same Cleveland Clinic group examined the production of TMAO by omnivores, vegans, and vegetarians following ingestion of L-carnitine. Indeed, the omnivorous humans had higher levels of circulating TMAO. The reason? Meat eaters have gut bacterial flora different than vegetarians and vegans. It contains species that feast on triethylamines: choline, lecithin, and carnitine.
Now let’s look at an interesting study published in the prestigious New England Journal of Medicine by Tang and colleague. It was conducted in two phases. In the first phase, the investigators gave healthy participants a phosphatidylcholine challenge using a stable isotope–labeled form of the phospholipid. They then used mass spectrometry to monitor choline metabolites before and after the suppression of gut microbiota with broad-spectrum antibiotics.
They found that the phosphatidylcholine challenge increased all choline metabolites but that antibiotics suppressed the generation of TMAO, which reappeared when antibiotics were withdrawn. In the second phase, they examined the relationship between fasting plasma TMAO levels and incident cardiovascular events over a 3-year period in more than 4,000 participants undergoing elective coronary angiography. They found an independent, dose-dependent relationship between the metabolite and the risk of a cardiovascular event on the basis of the TMAO quartile: The highest quartile had 2.54 times the risk over the lowest quartile.
The bottom line
Here is what we know about lecithin:
- The phospholipid phosphatidylcholine (lecithin) is the major dietary source of choline, a semi-essential nutrient that is part of the B-complex vitamin family. Choline has various metabolic roles, ranging from its essential involvement in lipid metabolism and cell-membrane structure to its role as a precursor for the synthesis of the neurotransmitter acetylcholine.
- Red meat, processed meat, pork, and egg yolk contain high levels of lecithin.
- Phosphatidylcholine (lecithin) is metabolized by gut flora into three metabolites that show up at high concentrations in people who have had a heart attack or a stroke. We metabolize those bacterial metabolites into TMAO, a known atherogenic.
- A large 4,000-patient study over 3 years showed a significant correlation between TMAO levels and cardiac events and stroke.
Still, although highly suggestive, none of these studies have demonstrated a direct effect of lecithin, or its metabolite TMAO, as a cause of atherosclerosis.
So, how does one make a decision whether to take lecithin supplements?
Since the lecithin metabolite, TMAO, is a known atherogenic, I believe that until we better understand whether it actually causes atherosclerosis, the prudent approach would call for moderation and limiting your intake of these foodstuffs with high levels of lecithin. Further, since there is no credible evidence supporting claims of health benefits, there is no reason to take high doses of lecithin in the form of nutritional supplements. If you do choose to take them, you could be increasing your risk of a heart attack or stroke in exchange for no known benefit.
This post was initially published on 01/25/2012. It has been updated to include findings from the latest scientific studies.