Lecithin as a dietary supplement has 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
If you believe any of that, please let me know—I happen to have a bridge to sell you. I have always been suspect 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 has any credible evidence to back it up.
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 (the supplement), you get phosphatidylcholine. In fact, commercial preparations contain between 20% and 90% of the stuff.
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 small 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, or cardiovascular health, or liver function. In fact, it may work against all those wonderful benefits.
What’s the downside?
If it doesn’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. 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.
Likewise, the total of chemicals, substrates, and metabolites 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 approach was 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. Studying the whole genome or the whole metabolome gives a complete picture of everything 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 blood of people who had not. They found major differences in choline, betaine and trimethylamine N-oxide (TMAO)—all metabolites of phosphatidylcholine.
Turns out that these metabolites are produced from lecithin by gut bacteria. We still don’t know if these lecithin metabolites are involved in some way as causative factors, or whether they are just markers of the disease; correlative studies can show only correlations, not cause and effect.
To find the source of these compounds, the researchers fed mice isotopically-labelled phosphatidylcholine and demonstrated the appearance of the metabolites in the circulation. The implication was that the gut flora metabolized the lecithin.
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.
The bottom line
Here is the state of what we do know: 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 still don’t know if these compounds play a causative role in those events.
So how does one make a decision whether to take lecithin as a dietary supplement? Consider the fact that none of the myriad claims of benefits have any credible evidence to support it. On the other hand, careful science is showing a correlation of lecithin metabolites with heart attacks and strokes. You decide.