The latest attempt to show us that red meat is a problem comes from the interaction between a nutrient in red meat and your gut bacteria.
So let’s talk about this interesting, but far from conclusive study. First let me say openly, I have not had access to the full article (anyone with access that’d like to shoot me a copy, I’d love to look at it), so that means it’s possible I’ve completely missed something and my conclusions could be wrong.
That aside, here are the main points of the study:
Carnitine (a nutrient found exclusively in animal foods) can be converted to TMAO by gut bacteria
Specific bacteria have been associated with increased levels of TMAO
TMAO has been shown to increase plaque formation in the arteries (atherosclerosis) by upregulating cholesterol accumulation in macrophages (a type of immune cell) and forming foam cells and also by reducing reverse cholesterol transport (removing cholesterol from the arteries)
Ominvores show greater levels of TMAO than vegetarians or vegans following administration of carnitine (unclear whether this was via a carnitine supplement – assuming this was so – or via administration of meat), assumedly because of their different gut bacteria.
Levels of L-carnitine in the blood predicted increased risk for cardiovascular disease and heart attack, stroke and death in patients who had high TMAO levels (so high carnitine + high TMAO = increased risk)
In mice given carnitine supplementation their gut flora changed and their levels of TMAO increased
So, case closed right?
Meat + gut bacteria = TMAO = increased risk of heart disease. Maybe, but let’s examine a few more points.
Carnitine is not meat. We have to be careful of reductionistic science/nutrition-ism here. In the same way that beta-carotene does not equal carrots, and iodine does not equal seaweed, meat is a lot more than just carnitine. Is it possible other components of meat may offset or negate the effects noted in this study?
Mice are not meat-eaters. They are (to the best of my knowledge) seed-eaters and insectivores. Are the levels of carnitine used in this study, and therefore the subsequent amounts of TMAO generated within the genetic norm for mice? That is, are we creating a situation where TMAO far exceeds what mouse physiology normally deals with, therefore leading to “abnormal” atherosclerosis? Would we see the same thing in dietarily realistic meat consumption for opportunistic omnivores like humans?
If this truly is a risk factor, how much of a risk is it really? Another study I looked at on TMAO in mice suggested “Analysis of natural genetic variation among inbred strains of mice indicates…TMAO levels explain 11% of the variation in atherosclerosis.”(2) An 11% variation is real, but far from a death sentence. Clearly, for these mice the lions share of atherosclerosis is caused by other factors.
Humans with normal kidney function seem to rapidly clear TMAO. This study suggested that when given a big dose of TMA (precursor to TMAO) 96% of it was cleared within 24 hours. And normal humans (assumedly omnivores) seem to have “low” amounts of TMAO. Are these “normal” levels really a risk?
There have a number of primarily meat eating cultures in human history with relatively low levels of atherosclerosis, such as the Inuit. If this meat-TMAO-atherosclerosis connection were a very serious issue for humans, these cultures with their correspondingly high levels of carnitine should show very high levels of atherosclerosis. But, maybe their gut flora is different from what we were seeing in this study’s omnivores and mice. So we wonder about…
Gut flora – are the gut flora seen in the humans in this study healthy for humans or are they dysbiotic (abnormal – “bad”)? Are the changes seen in the gut flora of the mice normal changes in a healthy flora or are they changes occurring in a dysbiotic flora? Would this happen in a “healthy” human? Is a bad gut flora the main problem here, not carnitine?
A couple of other points:
This study calls out “red” meat, but fish has much higher, naturally occurring levels of TMA (precursor to TMAO) which can be absorbed without needing bacterial conversion. If TMAO levels are a risk factor, then fish consumption, with or without “troublesome” gut bacteria should much more of a risk factor than red meat. I have not seen any studies bearing this out.
A side note: Paleo is not an all-meat diet. This is a straw man argument I saw trotted out a lot against Paleo. While there are many shades of Paleo diets and people adopt their own variations that work best for them, the Paleo template calls for the abundant consumption of vegetables and fruits (as tolerated). Many people who adopt a Paleo diet joke, truthfully, that they consume more vegetables than most vegetarians.
And most importantly:
Evaluating risk factors – at the end of the day, we really have to evaluate the balance of risk factors. If someone adopts a Paleo-style diet, increases their meat consumption and increases their TMAO which turns out to really be a risk factor, accounting for let’s say 10% of the risk of developing atherosclerosis, but by avoiding reactive foods they decrease their systemic inflammation. By losing weight and reducing excessive carbohydrate consumption they stabilize and normalize their blood sugars and increase their HDL levels. And by increasing their nutrient density they decrease their homocysteine. What does their risk equation look like? One risk factor increased, four risk factors decreased. I’m comfortable with that, and I’d call that a win.
This is an interesting study, but, in my opinion, nothing to get worked up over. It may be true that meat + bacteria are a real and significant risk factor necessitating that we modify our eating patterns. But this study is far from proof that this is true. We’re left with far more questions than answers at this point. My recommendation is, if you’re current diet, meat or no-meat is working well for you, stick with it.
The bigger take-away for me, is that the future of nutrient + gut bacteria interactions are going to yield us fascinating discoveries. It’s possible that in the future, a stool sample will allow us to tailor your diet much more precisely to you.
I look forward to what we have to learn!
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