If all we do is reshuffle the deck of the Standard American Diet and pick out new winners and losers every year, if we never commit to getting off the processed food grid; if we continuously mangle our microbes with antibiotics and food emulsifiers and continuously hate our health outcomes, well, I don't think we can blame that all on eggs or any other whole food. Do you?
How Dietary Research Generates Conflict: A Case Study in Demonizing Whole Food.
So Dean Ornish recently demonized eggs again, by citing an interesting study entitled: Intestinal Microbial Metabolism of Phosphatidylcholine and Cardiovascular Risk.
Since it’s Easter and eggs are squarely on the menu for most of us, I decided to purchase this study and read the whole thing for myself. Something we might all want to do from time to time.
Are Eggs the New Bad (Again)?
Alright. Here's what I found.
This study shows that some people's microbiome (the collection of good and bad bugs in our gut) transforms phosphatidylcholine (A.K.A. lecithin) into a nasty substance called trimethylamine N-oxide, or TMAO, which accelerates heart disease and early death.
Eggs happen to be a rich source of phosphatidylcholine (which under any other circumstance is thought to be a GOOD thing. Remember choline is brain fuel).
So, are eggs are the new Bad...again?
Not exactly. This is a fascinating study. I can see why a bumper-sticker rendering of it could tempt some people to throw eggs into the dustbin of dietary history and proclaim a brave new world for vegans only.
But upon closer inspection, I don't think this study can actually give us any pat answers (no offense Dean).
Turns out, fish also raises TMAO levels and yet fish is known to be cardioprotective—it’s downright good for your heart.
And then there are a number of plant foods high in phosphatidylcholine that we don't think are bad, like legumes (where do you think all that soy lecithin comes from that is now in everything from chocolate to cheese to pizza dough?).
Even bok choy and broccoli are considered "rich sources" of phosphatidylcholine.
So what gives? Why are we singling out eggs, when it's really lecithin that is under scrutiny here—and lecithin is EVERYWHERE and in EVERYTHING.
Well, like nearly all studies done on food and nutrients, this one suffers from a kind of reductionism that works well for drug trials but not so well for the complexity of human diets. (To say nothing of the complexity of the human microbiome).
A Nutrient Is Not a Meal Is Not a Diet.
This study does not even attempt to evaluate potential confounders in dietary patterns between people with high TMAO levels and people with low levels. Instead it relies purely on classic laboratory findings and demographics to sort people out. It eschews dietary pattern analysis, in favor of looking at things that are, frankly, just easier to measure--like labs and a single nutrient: phosphatidylcholine.
This low-hanging-fruit approach to measuring things is common. But it’s also a little bit like losing your keys in the parking lot and then choosing to look for them only under the street lamps, "because it’s easier".
But what if the answer you’re looking for is in a darker place?
That's not a rhetorical question. Because there are more problems with this study.
The study infers from a small interventional trial (40 people) that eggs must be bad because they appear to temporarily raise TMAO levels in test subjects who were fed two hard-boiled eggs plus 250mg of purified lecithin—and then nothing else.
That’s right, test subjects were given no other foods that might be protective or synergistic, or represent any sort of real-world balanced meal, PLUS enough purified lecithin to increase the phosphatidylcholine load by 100%.
Hmmm. Okay. But who actually eats that way? Imagine yourself sidling up to the breakfast bar and ordering “two eggs and a spoonful of pharmaceutical grade lecithin, please”. “Oh, and by the way, nothing else please. I want to make sure my phosphytidalcholine loading dose is off the charts and distilled, thank you.”
So that's one problem. Two actually:
- Biochemical Reductionism that makes no distinction between an egg (a complex whole food) and purified lecithin.
- Food Reductionism that fails to consider the buffering effect of whole dietary patterns and food synergies.
The Problem of Baseline.
And then there's the problem of baseline. Where are we starting from and what are we trying to say with that?
The forty individuals who volunteered for this study were considered "healthy", even though they were all presumably eating the Standard American Diet (nobody checked)--a diet we know isn't healthy, especially from a gut microbiome perspective.
Why would this be important?
Because the Standard American Diet is at least partially responsible for the decline and fall of the gut microbiome to begin with—which puts a gordian knot into what the researchers are actually trying to study here: microbiome dependent conversion of lecithin into TMAO and it’s implications for giving eggs a passing grade, or not, in healthy people.
But you can't see whether eggs are unconditionally bad for humans or not, if the gut microbiome you're studying is already messed up. That's the point. You'd have to find someone who has taken better care of their gut microbiome and test them to see if eggs or lecithin really are categorically bad for humans. You'd have to find someone eating a traditional ethnic diet for example, full of fiber and fermented foods.
So by this point in the study, all we could really say is:
- The Standard American Diet sucks (not news).
- The Standard American Diet appears to promote a bad microbiome as defined by TMAO production (news).
The Innocent Bystander Effect.
Okay. Let’s follow the study as it enters phase II:
After the preliminary findings were recorded, the researchers extrapolated their results to a larger cohort study, in which they observed 4007 people over a 3-year period to see who dropped dead or stroked out based on TMAO levels. But mind you, this larger cohort consisted of people whose doctors were already concerned about their cardiac status—concerned enough to set them up for elective cardiac catheterizations no less—and again, these were people whose eating habits presumably differed little from the Standard America Diet, which again, is notoriously low in fiber, fermented foods, and omega 3's and fails to support microbial diversity in the gut.
Are you getting this? Almost? Stay with me.
What we are actually looking at here is the possible effect of a wholesome traditional food (an egg) on people who have been eating an unwholesome non-traditional diet and whose microbiome has probably been compromised by that diet (a diet low in fiber, fermented foods, omega 3's, and high in antibiotics, chlorine, pesticides, and emulsifiers) and who already have some pre-existing vascular disease. All clear?
So what did the researches find?
Indeed, they found that TMAO levels did correlate with accelerated heart disease and bad outcomes. And yeah, that sucks.
But here's the point. Was it the eggs? Or was it all the other sources of refined lecithin in the Standard American Diet? Or just forget that. Was it the total dietary pattern of the Western Diet and it's effect on the microbiome? Could lecithin and eggs be innocent bystanders in a much darker public health crisis: the loss of biodiversity in our guts?
Do you see how quickly we can go from demonizing eggs to seeing the devil in the details? And can you see how that opens up a much bigger picture? Doesn’t the current state of the human microbiome worry you more than an egg yolk? It does me.
I fully agree that eggs may be an issue in the absence of other wholesome dietary patterns (which were not evaluated in this study), factors that would support a healthy microbiome for instance, like fiber. It’s entirely possible that, had the researchers chosen to study a group of omnivores with a diet high in fiber, full of omega 3’s, devoid of food additives and emulsifiers (and a group whose doctors weren’t concerned enough to send them to the cath-lab already) would have produced an entirely different conclusion. We don't know. That question was not studied. That question was not even asked.
Ask a Better Question; Get a Better Answer.
Let me put it to you starkly: This study makes no attempt to look at the effect of eggs on a savvy flexitarian who eats more veggies than a vegetarian, (and who probably consumes fewer processed foods as well).
Which by the way, is a whole-food, plant-based diet already!
Yet, the reflexive Newtonian response to this study can be disappointingly black & white, especially among media outlets or among friends: “Eggs are bad for you, I knew it! You should be vegan, like me!” (For the record, Dean Ornish is not vegan. He allows some animal foods and recommends fish oil, according to wikipedia).
Keep in mind that responses like these are well-meaning. But they are responses without all the facts (because all the facts have not been studied) and they come with none of the curiosity you might expect from someone interested enough in the spirit of science to wave around a scientific paper.
In this case, it’s a response that fails to be curious enough (or at least nuanced enough) about the findings and contradictions in the study itself, like fish. And it does not explain numerous meta-analyses showing virtually no connection between eggs and cardiovascular disease except in cases of diabetes. And wow, what about the studies showing that supplemental choline lowers homocysteine, a separate and independent risk factor for heart disease?
Just Be Well: Eat. Real. Food.
Real food is complex. It has a lot of moving parts.
What’s even more complex are the whole dietary patterns, food synergies, lifestyle practices and environmental exposures of real human eaters in the real world.
If we take a nutrient out of the context of the food (choline in this case), and a food out of the context of the meal (eggs in this case), and a meal out of the context of the diet (not even a meal, just a “loading dose” in this case), and a diet out of the context of the culture and lifestyle, then we can certainly get some interesting research questions, but I don't think we can get a slam-dunk indictment of an individual whole food, like eggs, which are themselves a complex food and can vary widely in quality—from pastoral to pathetic.
My fear is that 20 years from now, we will still be arguing about this, unless we change our research models to be more concerned with whole dietary patterns and food quality than with fractured snapshots of individual nutrients and marooned and lonely foods.
If all we do is reshuffle the deck of the Standard American Diet and pick out new winners and losers every year, if we never commit to getting off the processed food grid altogether; if we continuously mangle our microbes with antibiotics and food emulsifiers and continuously hate our health outcomes, well, I don't think we can blame that all on eggs or any other whole food, be it grass-fed beef or barnacles. Do you?
Until we can actually study complexity with more granularity and more gestalt than we do, the jury is out.
I'll keep an eye on this issue for you. If it turns out that indeed, eggs are bedeviled (after 20,000 years of sustaining human populations from every race, tribe, kindred, tongue, and people), I'll let you know.
Yours in Health and Resilience,
Marc Wagner MD, MPH.
Tang, W. H. et al. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk. N. Engl. J. Med. 368, 1575–84 (2013).
Rong, Y. et al. Egg consumption and risk of coronary heart disease and stroke: dose-response meta-analysis of prospective cohort studies. BMJ 346, e8539 (2013)
Shin, J. Y., Xun, P., Nakamura, Y. & He, K. Egg consumption in relation to risk of cardiovascular disease and diabetes: a systematic review and meta-analysis. Am. J. Clin. Nutr. 98, 146–59 (2013).
Andersen, C. J. et al. Egg consumption modulates HDL lipid composition and increases the cholesterol-accepting capacity of serum in metabolic syndrome. Lipids 48, 557–67 (2013).
Olthof, M. R., Brink, E. J., Katan, M. B. & Verhoef, P. Choline supplemented as phosphatidylcholine decreases fasting and postmethionine-loading plasma homocysteine concentrations in healthy men. Am. J. Clin. Nutr. 82, 111–7 (2005).
Cover Photo Credit: "Cake Fight" by David Lee on Flikr