The NY Times provokes a mini reader revolt with their 'Everything Old Is New Again' report that eggs will give you heart disease:
Eggs, Too, May Provoke Bacteria to Raise Heart Risk
By GINA KOLATA
For the second time in a matter of weeks, a group of researchers reported a link between the food people eat and bacteria in the intestines that can increase the risk of heart attacks.
Two weeks ago, the investigators reported that carnitine, a compound found in red meat, can increase heart disease risk because of the actions of intestinal bacteria. This time they reported that the same thing happens with lecithin, which is abundant in egg yolks.
Lecithin is used for treating memory disorders such as dementia and Alzheimer’s disease. It is also used for treating gallbladder disease, liver disease, certain types of depression, high cholesterol, anxiety, and a skin disease called eczema.
Save my heart but lose my brain, liver and skin? Hmm, we make these tough calls every day...
And did I say there was something fishy about this? Here is the mechanism the authors identify for the perils of eggs:
In the case of eggs, the chain of events starts when the body digests lecithin, breaking it into its constituent parts, including the chemical choline. Intestinal bacteria metabolize choline and release a substance that the liver converts to a chemical known as TMAO, for trimethylamine N-oxide. High levels of TMAO in the blood are linked to increased risk of heart attack and stroke.
So choline and TMAO are in play. We will come back to choline, but if TMAO is the culprit then the researchers should have tested fish, a famous source of the TMAO precursors - so famous, in fact, that researchers have pondered the "fish odor syndrome". Since you asked:
Trimethylaminuria is a disorder in which the volatile, fish-smelling compound, trimethylamine (TMA) accumulates and is excreted in the urine, but is also found in the sweat and breath of these patients. Because many patients have associated body odours or halitosis, trimethylaminuria sufferers can meet serious difficulties in a social context, leading to other problems such as isolation and depression. TMA is formed by bacteria in the mammalian gut from reduction of compounds such as trimethylamine-N-oxide (TMAO) and choline. Primary trimethylaminuria sufferers have an inherited enzyme deficiency where TMA is not efficiently converted to the non-odorous TMAO in the liver.
And how might one deal with this?
Intriguingly, many individuals have learned by trial and error how best to manage the disorder, including avoiding marine fish in their diet...
If you don't want to smell like fish, don't eat... eggs. We are so much smarter now.
An interesting clue as to where researchers might seek answers is tossed out here:
Given that even on the same dose of substrate precursor in loading tests there is a big variation in the amount of TMAO and TMA excretion, it is possible that the nature of the gut microflora may play a significant role in the generation of symptoms in some individuals.
So maybe the problem with eggs isn't the precursors (such as lecithin) but the way the gut flora process those precursors. So instead of telling people that eggs are the problem, maybe they we should be told that eggs will be a problem for people with an unhealthy mix of gut flora. One last aside as to why the smell of fish might bother us:
Marine fish contain large amounts of the N-oxide TMAO which plays a major role in osmoregulation, allowing marine fish to colonise a profoundly saline environment. Bacterial activity in rotting fish reduces the TMAO to TMA, imparting the characteristic odour, and the human ability to detect this odour so readily has led some to suppose that this may have a role in preventing humans from ingesting rotten fish.
I find that interesting. Of course, the rotten egg smell is also notable, but different.
But back to choline. The major building block of lecithin is choline, and the authors cited that as a problem. So where do we find choline in our diet?
The largest dietary source of choline is egg yolk. Choline can also be found in high amounts in liver, peanuts, fish, milk, brewer's yeast, wheat germ, soy beans, bottle gourd fruit, fenugreek leaves, shepherd's purse herb, Brazil nuts, dandelion flowers, poppy seeds, mung beans and other beans, and a variety of meats and vegetables, including cabbage and cauliflower.
I don't think vegetarians will be running from wheat germ, soy products, beans, cabbage or cauliflower. Yet somehow choline from eggs is dangerous, because it leads to TMAO. Of course, eating fish leads to TMAO and no one claims fish to be heart-unhealthy; quite the contrary. Which means we have a study with a lot more questions than answers.
The absolute collapse of critical thinking at the Times on certain health-related topics is both alarming and comical. I can think of several of their columnists who would happily cite any study denouncing red meat, even if the causal mechanism invoked extra-terrestials angered by the slaughter of their brethren. And eggs manage to linger in that "Flyover Country Only, Not Fit For The Upper West Side" niche, although the Times busts the mold ocassionally. Here is Mark Bittman trying to keep a foot in each camp:
Let’s cut to the chase: The diet that seems so valuable is our old friend the “Mediterranean” diet (not that many Mediterraneans actually eat this way). It’s as straightforward as it is un-American: low in red meat, low in sugar and hyperprocessed carbs, low in junk. High in just about everything else — healthful fat (especially olive oil), vegetables, fruits, legumes and what the people who designed the diet determined to be beneficial, or at least less-harmful, animal products; in this case fish, eggs and low-fat dairy.
Let me press on a bit more. Science jockeys will want to peruse "Does Dietary Choline Contribute to Heart Disease?" by Chris Masterjohn. He pounds the table for fish and adds this:
There’s just one major problem with this [TMAO] hypothesis. Studies in humans have shown that neither phosphatidylcholine nor choline-rich foods produce detectable increases in trimethylamine.
In fact, these authors even fed 46 different foods to humans and looked at the subsequent excretion of trimethylamine and TMAO. Choline-rich foods like liver and eggs did not produce any increase in urinary trimethylamine or TMAO over control levels. In fact, even carnitine-rich meats failed to increase excretion of these compounds. The only foods that increased excretion of TMAO were seafoods, which naturally contain some trimethylamine, giving them their “fishy” smell.
In normal, healthy people our liver and kidneys deal with this stuff. However...
Blood levels of choline are currently considered an emerging marker for destabilization of coronary plaques or ischemia in acute coronary syndrome, as reviewed here. During the process of blood clotting, inflammatory enzymes release choline from membrane phospholipids in order to also generate phosphatidic acid, which is used as an important signaling molecule. Elevated blood levels of choline, then, and perhaps its metabolite betaine, could simply reflect an inflammatory or pro-clotting environment.
So elevated choline may be a symptom rather than a cause of heart disease.