A 2013 study by published in the New England Journal of Medicine (NEJM) has proposed a new link between eggs and coronary heart disease (CHD) that doesn’t involve cholesterol. A team of researchers, led by Dr. Stanley Hazen, showed that dietary choline—a nutrient found largely in eggs, beef liver, and other animal foods—is metabolized by bacteria in our gut and then converted by the liver into TMAO.
They demonstrated this with a “choline challenge:” feeding volunteers two large hard-boiled eggs (with approximately 250 mg of choline each) along with 250 mg of supplemental choline that was tagged with a heavy isotope. The isotope acts like a chemical “label” that allowed the researchers to track what happened to the choline after it was ingested. Their data did indeed show an increase in both labeled TMAO and total TMAO (in urine and blood) in the volunteers after they consumed the eggs and supplemental choline.
In a second study, Dr. Hazen’s group showed that increased levels of TMAO in the blood are associated with cardiovascular disease (CVD). The researchers followed roughly 4,000 adults for three years. At the end of the study period, those with the highest levels of TMAO had a 2.5-fold increased risk of heart attack, stroke and death.
On the surface this sounds like very bad news for omnivores. But let’s take a closer look at the studies to see if it’s really time to swap your morning eggs for a tofu scramble.
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Do Choline-Rich Foods Increase TMAO Levels?
Dr. Hazen’s team did show a temporary increase in total TMAO after eating eggs. However, as Dr. Chris Masterjohn pointed out to me in an email dialog, the researchers’ own data show that there’s no way that the “choline challenge” could have contributed to this increase in total TMAO. If it had, we would expect to see an initial increase in labeled TMAO followed by an increase in labeled TMAO. This would indicate that the labeled choline supplement (that participants ate with the eggs) had been metabolized by the gut bacteria and then converted into TMAO in the liver.
But that’s not what happened. I re-created Figure 1C and 1D from the study. Figure 1C (below) shows an increase in total serum TMAO at one hour after the choline challenge. But by hour four, total TMAO is back to baseline and by hour 8 it’s even below baseline (i.e. the participants had lower TMAO at 8 hours than they did before they ate the eggs/choline).
However, Figure 1D (below) shows that labeled TMAO did not increase at all until hour four, and it didn’t increase significantly until hour six! This shows that the eggs and supplemental choline the participants ate had nothing to do with the increase in total TMAO that occurred one hour after the challenge.
What’s more, the researchers didn’t mention that other commonly eaten foods have a much more significant impact on TMAO than eggs. A 1999 study tested the effects of 46 different foods on the urinary excretion of TMAO in 6 human volunteers. (1) Eggs had no effect on TMAO excretion compared to a light control breakfast, yet 19 out of 21 types of seafood tested did. In fact, halibut generated over 53 times as much TMAO as eggs! This is not surprising, because although all species of seafood contain lower amounts of choline than eggs, they do contain trimethylamine and TMAO. Dr. Hazen’s team was aware of this study, because they referenced it briefly in the discussion section of the NEJM paper. They acknowledged that “TMAO has been identified in fish” and “the ingestion of fish raises urinary TMAO levels.” But remarkably, they did not explain how much greater fish’s impact on TMAO was when compared to eggs.
They said: “the high correlation between urine and plasma levels of TMAO argues for effective urinary clearance of TMAO.” In other words, even if eating food does increase total TMAO levels, most people are able to quickly and efficiently clear that TMAO from their blood by excreting it in the urine. This makes it doubtful that dietary factors alone explain chronic elevations in TMAO.
Instead, there are several other factors that are more likely to explain such an increase, including:
- Impaired urinary clearance of TMAO due to impaired kidney function: This is at least partially supported by data in the NEJM paper. Those with the highest levels of TMAO had an average glomerular filtration rate (GFR) of 69 mL/min. According to National Kidney Foundation guidelines, a GFR between 60–89 ml/min is indicative of a reduced capacity to filter blood through the kidneys. (2)
- Differences in the gut microbiota that predispose toward increase TMAO production: Previous work by Dr. Hazen’s group has shown that people with higher levels of Prevotella bacteria in their gut produce higher levels of TMAO. (3) (Interestingly enough, other research has shown that consumption of whole grains—not animal products—is associated with higher levels of Prevotella bacteria.) (4)
- Enhanced conversion of trimethylamine to TMAO in the liver: An enzyme called Fmo3 carries out this conversion, and its activity is affected by genetic factors, iron or salt overload, and a number of common pharmaceutical drugs used to treat arthritis, GERD, and infections. (5)
- Diabetes and metabolic syndrome: Fmo3 activity is upregulated in cases of insulin resistance and insulin deficiency. (6)
If food really did make a significant contribution to TMAO levels, and high TMAO levels cause heart disease, then we’d expect to see much higher rates of CHD among people who eat more fish—since fish has a much greater effect on TMAO than eggs. Yet this is the opposite of what studies indicate: Eating more fish (especially cold-water, fatty fish) has consistently been shown in both observational and randomized controlled trials to reduce the risk of death from heart disease. (7, 8)
Do Choline-Rich Food Cause Heart Disease?
At the end of their paper, Dr. Hazen’s group cautions against “excessive consumption of dietary phosphatidylcholine and choline” and recommends a high-fiber, vegetarian diet as a means of protecting your heart health.
Yet as I’ve argued above, they failed to present convincing evidence that eating eggs significantly increases TMAO over time—especially when compared to other foods like fish. Moreover, if eating choline-rich foods did increase the risk of heart disease (via TMAO or any other mechanism), we’d expect to see higher rates of CHD in those that eat more eggs. Yet numerous studies have failed to find any such association. For example, a meta-analysis of prospective studies involving a total of 474,000 participants followed from 8 to 22 years published in the British Medical Journal found no association between higher egg consumption (up to one per day) and CHD or stroke. (9) An analysis of data from the National Health and Nutrition Examination Study found an inverse association between egg consumption and stroke, and a cohort study from Japan found that consumption of animal products including eggs was associated with reduced risk of death from stroke. (10, 11) The lack of association—or inverse association—between egg consumption and CHD is even more impressive when you consider that those who eat more eggs are also more likely to smoke and be physically inactive. (12)
This same study found that egg consumers had diets higher in nutrients that have been shown to reduce the risk of cardiovascular disease compared to non consumers, including vitamins E, B12, and folate.
Finally, as I pointed out above, some research suggests that consuming large amounts of whole grain increase Prevotella bacteria in the gut, which were associated with the highest levels of TMAO in Dr. Hazen’s previous study on TMAO. If this is the case, consuming large amounts of fiber from whole grains may actually increase the risk of heart disease.
The hypothesis that increased serum TMAO is associated with heart disease is interesting and should be investigated further. But the data presented by Dr. Hazen’s group doesn’t support the conclusion that dietary choline is a major cause of increased TMAO, nor does it support their advice to avoid choline-rich foods like eggs, liver, beef, and pork.
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Anecdotal to say the least, but my hens have provided me with (more than) three eggs a day for decades. I seem, at 67, to be physically capable than most (or may I say, nearly all) of people my age. I just rode a 20km challenging mountain bike track with a dozen of my outdoor ed students. Three of us waited patiently at trail intersections for the other 16 year olds. Boom.
Are there any known nutraceuticals or probiotics that combat or reverse the accumulation of TMAO?
Trimethylamine-N-oxide (TMAO): a compound produced by bacteria in the stomach that appears to correlate with risk of heart disease, according to preliminary studies. TMAO is produced in the body from egg yolks and red meat. Researchers believe that it affects the body’s metabolism of cholesterol, leading to enhanced development of plaque on blood vessel walls, and can increase risk of heart disease. Studies showed that people with high TMAO levels had higher risk for heart attack, heart disease, and stroke. Consumption of a heart-healthy diet has been shown to reduce TMAO levels.
So it is ok to eat hard boil eggs and thank you for the recent article and is it worth it to get this blood test. Thank you
The TMAO from 46 different food , done in 1999 was TMAO + trimethylamine. Chris Kresser did not say this above, he lumped the two together. The graph in the reference is TMAO + TMA ( trimethylamine) . Fish is high in the combination. It does not have the data on TMAO alone . Does the TMA you injest all convert to TMAO or is it excreted before it has the chance for this to happen. I think Chris has done a poor analysis. Make sure you read all of his references.
New Study Published regarding TMAO on Jan 11, 2017. Here is the conclusion from the paper:
“Conclusions: Elevated plasma TMAO levels, a pro‐atherogenic metabolite formed by gut microbiota metabolism of the choline group of PC, portend stronger incident risk of major adverse cardiovascular events and all‐cause death in patients with PAD, independent of traditional risk factors.”
Here is the announcement on this research from Physicians Committee for Responsible Medicine:
Animal Products Increase Risk for Heart Attack and Stroke
Trimethylamine N-oxide (TMAO), a molecule produced during digestion of red meat, eggs, and dairy products, increases the risk for a fatal heart attack or stroke, according a study published in European Heart Journal. Researchers monitored TMAO levels for 530 participants and tracked the number of cardiac events. Those with elevated TMAO levels increased their risk for heart attacks or strokes and increased their risk of death from these events. Researchers suggest dietary interventions may mitigate these risks by reducing TMAO levels.
Li XS, Obeid S, Klingenberg R, et al. Gutmicrobiota-dependent trimethylamine N-oxide in acute coronary syndromes: a prognostic marker for incident cardiovascular events beyond traditional risk factors. Eur Heart J. Published online January 11, 2017.
You can read the research for yourself here at PubMed where all government research is published:
The research itself was conducted at The Cleveland Clinic, one of the premier heart disease research and treatment hospitals in the world. People come from all over the world to be treated at The Cleveland Clinic in Cleveland, Ohio.
I still was not convinced that I should give up my meat or eggs. Dr. Hyman interviewed Dr. Kozen and the two amicably disagreed. Dr. Kozen is a vegetarian and Dr. Hyman is not. Both pretty smart guys. I think Dr. Kozen’s recommendation was not to eat meat or eggs more than once per week. I stand with Dr. Hyman on this one until more is reasearched on this.
IMO Dr. Hyman leans to whatever diet is most popular. Look at his published books for the proof.
I would suggest that people read this very comprehensive study for themselves and not take Mr. Kresser’s interpretation at face value:
For instance, his comment on gut bacteria of grain eaters vs meat eaters was a huge leap (african vs european children) and the bacteria was of the same genus as the one identified in the study but, as the study pointed out, different species of bacteria have different abilities to create TMAO from choline and carnitine.
The difference between vegan TMAO levels and meat eater levels is striking.
The study you cited claims not to know which variety of bacteria are more prone to producing TMAO but this is no longer the case.
Hi-so I have a question about a medication I take, and eggs and also NSAIDS. (yeah, sounds a little convoluted)
So I have been taking Nexium for GERD for the past few years. Recently I have had to buy generic Nexium online because I lost my health care and can’ t afford the name brand version anymore.
My question is this, can I take generic Nexium and NSAIDS? I know I could take NSAIDS with name brand Nexium, but I dont know the difference. Especially because the place I have been ordering from has a picture of regular Nexium but says its generic. I’m really confused about this. Also, are eggs something I can eat with Nexium? I find sometimes it makes me queasy after taking the medicine if Ive eaten eggs. This is where I buy the meds: http://canadapharmacyrx.com/generic-nexium.html
This article is very effective. Choline obtainment alone is not associated with anything other than benefit to biophysiology, as is phosphatidylcholine. Numerous studies linking it to oncology invert mistakenly the association, misplace the association for survey of levels of these factors in nutrition before diagnoses, and often show post diagnosis benefit of choline in controlled studies sometimes within these same populations.
The distinction is what is good vs not so good microbes. The literature is all over the place on that one. However, a broad spectrum antibiotic is the invariable answer. Microbes which do not produce trimethylamine would then be next, however, prebiotic and probiotic therapy are widely regarded as remediative. Particularly, studies have shown the solid carnitine, choline and phosphatidylcholine can induce increases in TMAO levels about 4 to 8 hours after ingestion. The levels degrade, although the second most useful indicator of susceptibility to sudden demise is TMAO, showing how important ph and vasoconstriction are at circumvention biophsyiological mechanisms to induce sudden demise. Asymmetrical dimethylarginine, trimethylamine-n-oxide, symmetrical dimethylargine, methylglyoxyl, impaired insuling management, c-reactive protein, D or L lacatate and NAD+/NADH imbalance, are principle cause of these, and are pervasively the cause of ‘natural causes’ of demise. If populations are provided choline, trimethylglyciine, L-arginine, phosphatidylcholine, niacin, other b vitamins, folate, glutathione, superoxide dismutase, and prebiotic and probiotic daily, these would pervasively be prevented. These could be supplemental, or provided by intraveneous methods or subcutaneously in therapeutic settings, although prebiotics and probiotics are ingested regardless of the setting. A broad spectrum antibiotic can supplant the prebiotic and probiotics therapeutically,
Importantly, studies have shown the habitual ingesting of meat, pork, chicken, eggs of fish, particularly meat and pork, can product exhibition of remnants for many months if not years in digestive pathways. Thus, regular flushes of digestive pathways can be essential although care to not induce dependency is required. It is known that TMAO is exhibited in a slow wave function similar to how digestive pathway peristalsis functions. The more one ingests meats, pork and chicken, the more TMAO levels are upon each ingestion. Peristalsis works by having having neurotransmitters activating post synaptic neurons to induce a less than complete polarization change, such that the action potential threshold is not met. The induced polarization change, however, is not allowed to reset to its base at rest level which is something like 0.4 Ionic difference between intracellular and extracellular environment. The next neurotransmitter activation occurs before the resting level is reached, and these continue until the threshold level of is met, producing an action such as an opening of large combination of Ion channels within cellular entities in an area that causes a muscle contraction. There are more details to this, this is a high level perspective. The similar circumstances seems to occur with TMAO levels and ingestion of meat, chicken eggs or fish. There are some indications that choline is not involved, because trimethylamine is exhibited within phosphatidylcholine and potentially within l-carnitine. Microbes, however, are the cause of this phonomenon. Ingesting fish increases TMA and TMAO both because TMAO is exhibited in fish, although the other factors in fish such as omega fatty acids assist in reducing ancillary inflammation exhibited with TMAO. Again TMAO, like homocystine, asymmetrical dimethylarginine, symmetrical dimethylarginine, c-reactive protein, methylglyoxal, insulin cycles, D or L lactate, NAD+/NADH, general redox oxidation/reduction balances, and systemic ph, can induce all manner of detriment and are best characterized as imparting detriment through inflammation, tissue degradation, inhibition of nitric oxide, induction of vasconstriction, changing thrombosis/fibrin/fibronectin/fibrinolysis and changing ph, thereby converging as the principle causes of demise. These are all at the behavioral and metabolic nexus of choline and phospholipid pathway inadequacy which constitutes the principle progressive influence in the emergence and progression of pathology of any nature, as well as the principle culminating circumstance in any instance of demise. As this article is accurate in the way it handles choline being associated with detrimental outcomes, you are all accurate in affording this your attention and priority.
An excellent analysis!
Apparently Dr. Hazen et al appear to be cherry picking the association between TMAO and the “heart disease”.
Thank you (Researcher).
If you look at Dr. Hazen’s webcast on the Cleveland Clinic Web site,he has provided ample evidence of a direct relationship between TMAO and CAD in humans and animals with CV risk rising with higher TMAO levels and he was able to induce CAD in mice with ingestion of TMA and precursors.
Importantly, Nitrogen cycles may be essential factors in these circumstances. Nitrogen is a component of amino acids, Geneome and proteins. Nitrogen is the component which ADMA, TMAO and Homocysteine, Methylglyoxyl, diabetes, and other factors deprive from circulatory pathways to induce vasoconstriction. Nitrogen is affixed into the nutritional pyramid/continuum pervasively through bacteriological or microbial methane metabolism in root plant nutritional factors or other plants. B12 methylcobalamin provides Nitrogen, carbon, methyl groups, phosphorus, cobalt and oxygen. Choline and phosphatidylcholine provide more factors including adipose acids which are the principal components of cellular membranes. B12 methylcobalamin is required by kingdom animalia to produce methione through the only pathway of methionine synthesis which does not exhibit homocysteine as a byproduct. Plants have a b12 independent methionine synthase in such regard. b12, folate and Methyltetrahydrafolate pervasively only provide marginal benefit, although trimethylglycine provides more substantial benefit with similar limitation, because Choline is required to supply the Choline and phospholipid pathways. b12 supported MTHF and folate associated synthesis of methionine requires homocysteine obtained from choline metabolism or obtained from catabolism of cellular membranes by phospholipases during choline deficiency. The empirical causality of these are a choline deficiency, dependency upon external sources of choline and phosphatidychloline resultant of genetic impairment, as well as the affects of adma, tma, tmao, diabetes, and other factors which may all be cyclically exhibited as result of the progressive adaptations or pathology produced by a choline deficiency. Empirical causality is the standard for these analysis. Pervasively, impairment of adaptations to deficiency or pathology resultant of such deficiency that has become to be observed as typical biological function, may be the loci of analyses and therapeutics. Illustratively, Choline deficiency introduces P53, which induces G1 phase cellular cycle pause, and then either senescence, apoptosis, hypertrophy, segmentation of the pentose phosphate pathway, accumulation of glycogen in such segmented phase, impaired ability of glycine to deplete glucose, which changes pervasive cellular entities toward degradative outcomes. P53 impaired cellular material is then able to flourish, without the essential protecting, repairing and managing influence of P53 and without adequate material to produce additional membranes, DNA, extracellular factors, transcription products, neurotransmitters and other factors. 96+ percent of oncology exhibits impaired P53.
The incipient Egg resultant influx of Choline and phosphatidycholine provides several circumstances. TMA is a constituent molecule within Choline and phosphatidylcholine. The influence of Choline and phosphatidylcholine could have enabled availability of methyl groups which were transfered to homocysteine or other factors to produce choline, methionine or other factors. Fish exhibit substantial amounts of TMAO which is utilized to stabilize quaternary molecular structure at depths within aquatic environment. Adequate amounts of choline induces a phenomenon in which the lipid within biological fluid becomes transformed into minuscle droplets which are easily metabolized and unable to adhese to vasculature. TMAO is produced by FMO1 and FMO3 within the hepatic tissues once TMA is produced and moves through the digestive membranes into circulatory pathways. molecules, however, typically do not traverse between cellular entities in such membranes, they may typically move through cellular membranes to move from digestive to circulatory pathways. Inflammation from homocysteine, resultant of choline and phospholipid deficiency, typically produces catabolism of cellular membranes to obtain choline factors, producing inflamation, as well as exhibition of TNF ‘alpha’. These impair tight junction proteins, loosening the adhesion between cellular entities, enabling increased permeability of TMA into circulatory pathways and enabling TMAO to move from circulatory pathways to digestive pathways. The delay in observing increases in TMAO after ingesting meat, chicken, eggs or fish, is resultant of L-carnitine, Choline, Phosphatidylcholine or other factors ingested, to also exhibit or be comingled with oxygen. Some research suggests that the anaerobic transition of digestive microflora represents the pathology transition, and the emergence of the cycle of of TMA to TMAO produciong in liver, followed by TMAO movement into digestive pathway may either sustain aerobic aspects of such cycles or provide TMAO as substrate for anaerobic metabolism. TMAO is Trimethylamine-N-Oxide, and the nitrogen can become the sustaining factor instead of oxygen. Specifically, however, TMA to TMAO transitions, deplets Nitrogen from circulatory pathways and inhibits nitric oxide synthase. It also is degradative factor of tissues and membranes, including vasculature. It also participates in interactions which change thrombin, fibrin and fibronectin characteristics, thereby changing inflammation cascade, potentially inducing thrombosis, coagulation, deposition of fibronectin and changing thresholds for activation of these biophysiologically essential capabilities. Homocysteine, from choline deficiency or impaired metabolism of choline associated factors, as well as asymmetric dimethylarginine impart similar influence. Methylglyoxyl and Trimethylamine may also impair Nitric oxide synthase. Together, these are the most indicztive factors of susceptibility to adverse health events, less optimal prognoses, susceptibility to accompanying conditions and complications, inability of therapeutics to accomplish required outcomes, as well as potential for emergence of any human pathology. The issue is a choline deficiency or impairment of genes encoding enzymes within Choline or phospholipid pathways, which comprise more than 90% of cellular membranes, included in 99.5 of biosynthesis products, more than 60 percent of extracellular matrix, and all but a few neurotransmitters. These are also influences to pervasive aspects of genetic material, and the detrimental factors exhibited here, along with deficiency, have been implicated in pervasive aspects of genetic anomalies. If one determines the molecular circumstances underlying any pathology, it is ubiquitously possible to arrive within one or two iterations of causality to the multiplicity of effects resultant of a choline deficiency or choline dependency.
A Prebiotic and probiotic supplement, particular if ingesting choline, phospholipids, carnitine, meat, chicken, eggs or fish is typical manner of remediating TMAO associated susceptibility. A diverse spectrum antibiotic also provides benefit. For asymmetric dimethylarginine, l-arginine, citrulline, ornithine, water and other factors are beneficial, as well as trimethylglycine.
For homocysteine, choline (chl), phospholipids, folate only with with chl, B12 methylcobolamin only with chl , or trimethylgliycine with choline, can be beneficial.
The oncology association with choline is not precise, though correlative. Surveys of oncology study participants pervasively show a positive association, which disappears during therapeutics, and is thus very suggestive. Relevantly, ingesting of factors which exhibit choline can induce TMA which induces a principal systemic inflammation factor associated with oncology, TMAO. Asymmetric dimethylarginine, homocysteine, methylglyoxyl, and impaired insulin management, all which may be detrimental principally resultant of a choline deficiency, each induce such susceptibility.
Thanks A Researcher for this thorough comment. I know this post is old, but if you happen to see this response, I have a few questions. While I’ve taken some biochemistry, I don’t have nearly the understanding of the subject that you seem to have. So what is your overall takeaway here? Is it that choline deficiency if the greater evil? Or perhaps if the individual has a well established gut microbiome, they may be able to stave off the negative effects of TMAO? Basically, put this into layman’s terms for me. 🙂 Also, my family has a history of ADHD. I believe we would be more likely to have genetic susceptibility to choline deficiency. I guess I’m just trying to understand how to look at this information and what relevancy it should have in how my family eats. Thanks for any info you’re able to provide. I also apologize if I totally butchered my interpretation of what you were saying. As you can see, I am not “a researcher”. 🙂
An additional answer is that the choline pathways seem to not be optimal through ingestion, at least not with the microflora that has now emerged to be exhibited in the typical digestive pathway. Nutritional regimens, however, as well as environment determine much of digestive microflora characteristics, suggesting why prebiotics and probiotics are useful. The best way to obtain choline, phosphatidylcholine, trimethylglycine, folate, complete B vitamins with Niacine and methylcobalamin as well as B6 in particular, L arginine, ornithine, citrulline, methylcobalamin, glutathione, small amounts of cystathionine, is through intravenous application for several weeks of therapy at least once each year. Ingesting these as foods or supplements should be assured to be as easily digestible as possible, as granular or oil based, as well as having these either emulsified or within extended release protected capsules. Choline and phospholipid inadequacy is most probably the incipient causal factor in every biophysiologically or behaviorally detrimental outcome. Autism is pervasively a fluid, energy balance, progressive aspect of choline deficiency, including autoimmunological, disorder. However, the spatial aspects of the syndrome are that the same imbalances which cause ADHD, improved interactivity with others, environment and the universe, are the same idiosyncrasies that produce the most artistic, musical, explorative, athletic, expository, expressive or other outcomes. Humans interact at less than conscious, conscious, and peripheral levels, with the universe and one another. Consider a butterfly which is hypersensitive to weather, solar cycles, changes in large aquatic environment, lunar cycles or electromagnetic and communications fields. In large group of other butterflies, it would seem very disruptive. Someone who grows up on a farm, would find an urban context very inundating with influences, particularly because their biophysiology has become accustomed to decoding the patterns in such influence instead of finding a narrow range of influences in which to focus consciously directed focus. The human physiology is interactive within fields of influence that span the universes, and go backwards and forward in time. If biophysiology has become entangled with much more of these than is typical, then that is more normal than being able to focus on a narrow range of such influence. However, to assimilated, its probably best to add the factors suggested above 1 by 1, including a probiotic and prebioitic, until the condition becomes manageable. It might be useful to be sure that all information systems in which those experiencing ADHD are listed or included, have as little information as is possible, including location or immediate contact info. Pervasive contexts of information, reference and consideration exist in civilization, and information permeates, interacts with, affects, and is reimparted by biophysiology. It is possible to purchase a electromagnetic frequency protector that can be attached to any communications device, utilized alone, or plugged into a location in which the ADHD affect individual may be. Try these, and share the results with your health professionals, as well as acquaintances. There could be many amazing changes in health status among humanity emerging somewhat immediately. It is important that these be achieved together, in community among one another.
Here’s a recent news story describing the role of TMAO in fish: