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Red wine,  olive oil, balsamic vinegar, and grape seed oil  against  TMAO?   It's a stretch,  but:
 

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Atherosclerosis, commonly known as hardening of the arteries, has been linked to the consumption of high amounts of nutrients such as choline and carnitine, which are abundant in foods such as meat, egg yolks, and high-fat dairy products. Gut microbes convert these nutrients into a compound called trimethylamine (TMA), which in turn is converted by host enzymes into a metabolite called trimethylamine N-oxide (TMAO), which accelerates atherosclerosis in animal models and is associated with an increased risk for heart disease in humans.

Until now, efforts to target this pathway for therapeutic benefit have focused on inhibiting the host enzymes that convert TMA into TMAO. However, this approach causes liver damage as well as an unhealthy build-up of TMA. Hazen and his team figured that a more promising approach would be to directly target gut microbes to prevent the formation of TMA in the first place.

Toward this goal, Hazen and first author Zeneng Wang of the Cleveland Clinic screened for inhibitors of microbial TMA production from choline. They identified a compound called 3,3-dimethyl-1-butanol (DMB), which is naturally abundant in some cold-pressed extra virgin olive oils, [in red wines], balsamic vinegars, and grape seed oils. In mice that were on a choline-rich diet and genetically predisposed to atherosclerosis, DMB treatment substantially lowered TMAO levels and inhibited the formation of arterial plaques without producing toxic effect.

https://www.eurekalert.org/pub_releases/2015-12/cp-dtm121015.php

 

Non-lethal Inhibition of Gut Microbial Trimethylamine Production for the Treatment of Atherosclerosis (2015)

https://www.cell.com/fulltext/S0092-8674(15)01574-3

 

Edited by Sibiriak

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Another anti-TMAO possibility:  foods rich in flavonoids quercetin and rutin.   It's just another rodent study, though.

Protective effects of tartary buckwheat flavonoids on high TMAO diet-induced vascular dysfunction and liver injury in mice (2015)

https://pubs.rsc.org/de/content/articlelanding/2015/fo/c5fo00581g#!divAbstract

https://pubs.rsc.org/de/content/getauthorversionpdf/C5FO00581G

 

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Abstract

This study was performed to investigate the liver and vascular changes in high trimethylamine-N-oxide (TMAO) diet-fed mice, and the possible vasoprotective and hepatoprotective effects of purified tartary buckwheat flavonoid fraction (TBF). HPLC analysis revealed that the content of rutin and quercetin presented in TBF was 53.6% and 37.2%, respectively, accounting for 90.8% of TBF. Mice fed 1.5% TMAO in drinking water for 8 weeks significantly displayed vascular dysfunction and liver damage (p < 0.01). The administration of TBF at 400 and 800 mg per kg bw significantly elevated plasma NO and eNOS concentrations, and serum HDL-C and PGI2 levels, and lowered serum TC, TG, LDL-C, ET-1 and TX-A2 levels of TMAO-fed mice. TBF also reduced serum AST and ALT activities, and hepatic NEFA and MDA levels, and increased the hepatic GSH-Px and SOD activities in TMAO-fed mice, which were consistent with the observations of the histological alterations of the liver. This report firstly showed that dietary TMAO might cause liver damage and TBF prevented TMAO-induced vascular dysfunction and hepatic injury.

Edited by Sibiriak

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Finally,

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Gordo (2017)I had been planning to research more and do a write up on Jiaogulan (Gynostemma pentaphyllum). I think it's quite promising, and is actually called "The Immortality herb" by the locals that first cultivated and drank its green tea (a population that supposedly has a high proportion of centenarians). There are quite a lot of published studies about it, and I believe it is a BAT activator, and is noted for glucose lowering effect. I do take it occasionally and might increase my frequency. I ordered seeds to grow it myself, but they would not germinate unfortunately. I'll probably try again some time.

https://www.crsociety.org/topic/12476-adaptogens/?tab=comments#comment-22171

It's possible that some of Gynostemma's beneficial effects derive from an ability to decrease TMAO levels.   One more rat study!  (TomB loves these.)

 

Metabonomics Study of the Therapeutic Mechanism of Gynostemma pentaphyllum and Atorvastatin for Hyperlipidemia in Rats (2013)

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0078731

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Abstract

Gynostemma pentaphyllum (GP) is widely used for the treatment of diseases such as hyperlipidemia, fatty liver and obesity in China, and atorvastatin is broadly used as an anti-hyperlipidemia drug. This research focuses on the plasma and liver metabolites in the following four groups of rats: control, a hyperlipidemia model, a hyperlipidemia model treated with GP and a hyperlipidemia model treated with atorvastatin. Using 1H-NMR-based metabonomics, we elucidated the therapeutic mechanisms of GP and atorvastatin. Orthogonal Partial Least Squares-Discriminant analysis (OPLS-DA) plotting of the metabolic state and analysis of potential biomarkers in the plasma and liver correlated well with the results of biochemical assays. GP can effectively affect lipid metabolism, and it exerts its anti-hyperlipidemia effect by elevating the level of phosphatidylcholine and decreasing the level of trimethylamine N-oxide (TMAO). In contrast, atorvastatin affects hyperlipidemia mainly during lipid metabolism and protein metabolism in vivo.

 

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[...]In summary, GP acts by affecting lipid metabolism. After hyperlipidemia model rats were treated with GP, cholesterol and low density lipoprotein levels in the plasma decreased and ketone body metabolites returned to normal, but only a weak effect was observed on protein and glucose metabolism.

In contrast to the mechanism of atorvastatin, GP was able to return phosphatidylcholine and TMAO levels to normal. Phosphatidylcholine consists of hydrophobic nonpolar groups and hydrophilic polar groups that have strong surface activity and emulsification. Phosphatidylcholine can improve the absorption and utilization of lipids, decrease the retention of lipids in vessels, remove cholesterol deposits in blood vessel walls, promote diffusion of atherosclerotic spots and reduce high cholesterol. The unsaturated fatty acid of molecules can prevent the absorption of cholesterol in the intestinum tenue and promote cholesterol excretion [36]. Meanwhile, TMAO is closely related to phosphatidylcholine metabolism. The ability of GP to decrease in TMAO suggests that GP has an inhibitory effect on the pathway of phosphatidylcholine to TMAO.

Edited by Sibiriak

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Studies in animals are always iffy when it comes to extrapolating to humans, but these are nice finds anyway. I find the whole topic of choline/TMAO quite confusing, so I appreciate any light thrown by any studies, even in animals. GP looks interesting, though of course I worry about rat physiology being different enough from human that it may not be applicable. I hope we can keep this thread alive, as choline is important enough and TMAO results are robust enough that we really must address it.  

 

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I find it pretty confusing, but well, choline is choline, phosphatidylcholines is speculated to be a better way of consuming it, but the sources matter at least insofar as whatever else it is that travels with it, so if you are getting it from meat you are getting not just choline but the rest of the meat which may not be optimal compared to a vegetarian source. In that case it's not about the choline itself as what else comes with it. The issue is not the choline itself but what happens with it inside of your body. And so, if you are a vegetarian/vegan, your gut mircobiota may not promote TMAO formation, so again it's not just choline and not just what the choline comes with, but what environment it lands in - your gut, it being omnivorous vs vegan. But it's all very confusing because on the one hand high serum TMAO has been definitely linked to negative impact on CV health and all cause mortality, but on the other hand, dumping already pre-formed animal TMAO directly seems to possibly be less or not deletrious at all - yet there it is in the serum; of course I'm talking about fish which is sky high in TMAO, but fish consumption appears to be CV health protective and possibly have good effects on all-cause mortality, if we the stats are to be believed about vegan/vegetrian vs pescetarian outcomes.

Like I said, I don't feel confident at all that I understand the whole choline/TMAO nexus, so I'm trying to get educated, but it's tough going, what with all the studies going this way and that way. The thing that makes this so nettlesome is that choline is an essential nutrient, so you can't just bypass the whole controversy by not consuming any choline. Unfortunatly, you do have to take in choline, and that's where the trouble starts - in what form, under what conditions etc. 

Ultimately, the intake and metabolizing of choline is dependent on multiple factors - the form, the source, the gut microbiota and other nutrients that accompany the direct source of choline as well as the rest of the diet you consume with it. And that's where all of this might be impacted by things like brassica vegetables, red wine, GP and so on.

Bottom line, I don't feel like I have a handle on this at all - so I try to follow this thread in hopes of further elucidation. 

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http://www.clevelandheartlab.com/blog/what-your-gut-says-about-your-heart/

 

for now I am simply going to follow the above advice of the Cleveland clinic. The whole plant thing advantage seems to be based on gut microbes and this some other substances. As for choline one egg a day should be fine and at 150 mg of choline will push me above 500 mg. I will eat eggs from a woman I know personally who sells them and considers them pets and treats them accordingly. They don’t mention it in the above for some reason but elsewhere they recommend balsamic vinegar, grape oil, red wine and EVOO. I will continue with 8 oz of wine with evening meal and add some balsamic vinegar for the 3,3-Dimethyl-1-butanol

Edited by mikeccolella

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15 hours ago, TomBAvoider said:

The thing that makes this so nettlesome is that choline is an essential nutrient, so you can't just bypass the whole controversy by not consuming any choline.

Is there any good evidence that a whole food plant-only diet with sufficient calories can and does lead to choline deficiency?

Based on Michael's crazy supplement regime, he seems to think some form of choline supplementation is necessary or at least prudent for vegans, but I see very little evidence to support this assertion. Per Jack Norris' reading of the literature (here) the DRI for choline was set based on a single study which found people developed signs of choline deficiency (i.e. markers of fatty liver / liver dysfunction) when placed on a diet for six weeks that had less than 50mg of choline per day. Their deficiency was corrected by a diet with ~500mg of daily choline, so they set the DRI at ~500mg. But that begs the question of how much choline is actually needed to avoid deficiency. In fact, one very small study (n=4) Jack cites showed that 138mg/day in 70kg men reversed their markers of choline deficiency in only 10 days. So the true daily requirement may be much less than 500mg.

I've been eating a healthy vegan diet without any choline supplementation for 15 years and my liver shows no sign of fattiness, and my liver enzymes (ALT/AST) are well within the normal range. 

The 2008 USDA update to their nutrition database included data on the choline content of many common foods. Here is an interesting graph from that update (from this pdf) :

Screenshot_20190811-112425_Foxit PDF.jpg

Missing from the graph are Nuts and Seeds, which from the data in the report look to come in around 50mg choline per 100g.

Per this graph, a diet with a mere 3lbs (1350g) of fruits and veggies, 3.5oz (100g) of nuts and seeds, and 3.5oz (100g) of whole grains would contain ~525mg of choline, right around the (dubious and likely inflated) DRI.

So unless I'm missing something, the USDA database and my own personal experience as a vegan suggests that a healthy plant-only diet should easily provide all the choline we need, without requiring choline supplements or animal product consumption, thereby alleviating the worry about TMAO formation.

So am I missing something?

--Dean

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I agree with you Dean; however I’ve found it challenging to eat a vegan diet and to get 550 mg. Which MR says is likely insufficient! Not sure what he’s basing that on. You didn’t mention legumes? How come? I’m eating 4 oz of broccoli, ounce of nuts, cabbage, collards, cup of lentils and cup of chickpeas, mushrooms, whole grains like wheat bran, oats etc and I still only get 388 mg. The egg pushes me up over 500. Me thinks your on to something Dean. This 550 mg. Of Choline just does not ring true. 

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Well, there's the MFTHR issue. For example, I'm pretty extreme insofar as I'm homozygous for C677T. The odd thing is, that I show no symptoms of this supposedly dire condition whilst taking no particular care with my diet to account for my C677T status. None of my bloodwork shows anything dire either - f.ex. my homocysteine is nice and low. 

Be that as it may, apparently one of the best ways to compensate for the inefficient methylation due to C677T is by taking in a lot more choline - in the 1 gram per day territory (which I personally don't hit routinely, if ever). The point being, is that as one may surmise with a lot of nutrients, your individual needs will be specific to you. One person may get by with very little choline, another may need a lot more. 

As always, it's personalized medicine - no one size fits all. 

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23 minutes ago, mikeccolella said:

You didn’t mention legumes? How come?

Oversight. From the USDA table cited above, legumes on average appear to have on average around ~35mg choline / 100g, with soy beans and other soy products somewhat higher.

--Dean

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FWIW,  the authors of  Becoming Vegan: Comprehensive Edition: The Complete Reference to Plant-Base Nutrition  see no problem meeting choline requirements with a reasonable vegan diet:
 

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An RDA hasn’t been set for choline due to insufficient data; however, the AI is set at 425 mg per day for women and 500 mg per day for men. It may be beneficial for women who want to become pregnant to take a choline supplement to prevent infant neural tube defects. 2,4 When The Vegan Plate (page 434) is used as a guide, a diet can easily meet the AIs.

 

image.png.d90c40f83fcfe6d43dd99aa7faf1dcf2.png

 

Because it’s a part of all cells, choline is widely distributed in plant foods, though data regarding exact amounts is limited. Soy foods, quinoa, and broccoli are particularly rich sources. 184 Other good sources are amaranth, artichokes, Brussels sprouts, buckwheat, corn, mushrooms, oats, wheat germ, and whole wheat products.

 

 

Edited by Sibiriak

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16 minutes ago, TomBAvoider said:

None of my bloodwork shows anything dire either - f.ex. my homocysteine is nice and low. 

Then it seems unnecesssary to worry about it.

16 minutes ago, TomBAvoider said:

The point being, is that as one may surmise with a lot of nutrients, your individual needs will be specific to you.

That may be the case. But if there is little to no evidence you are choline deficient, and pretty reasonable evidence that extra dietary or supplementary choline may be deleterious (via TMAO), then do you really believe the best strategy to mitigate risk is striving to add more choline to your diet, particularly since heart disease is one of your primary personal concerns?

--Dean

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Indeed, Dean, you are quite right. However, I feel like I need to keep tabs on this whole choline/TMAO issue, because unfortunately, we are dynamic systems and not in long term stasis. Thus, even if so far there appear to be no deleterious effects of my MFTHR variant that can be discerned, I am aging. As people age, their responses to nutrients, and their physiological needs change. One example is the speculated need for more protein in advanced old age. So, I am not at all confident that while today my MFTHR status is no problem, it will remain so tomorrow. Now, I'm not changing my diet or supplement regimen until I have a lot more clarity on the whole issue - as always, I want to be clear on dosing/protocol with everything. All I'm saying at the moment is that I feel very poorly informed on this issue and so eagerly look forward to what you and others come up with - the more eyes on this, there more (hopefully) clarity can be had down the road. 

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.Plasma trimethylamine-N-oxide following supplementation with vitamin D or D plus B vitamins (2017)
Obeid R1,2, et al.

https://www.ncbi.nlm.nih.gov/pubmed/27569255/

 

 

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Abstract

SCOPE:

We compared the effect of supplementation with vitamin D + B or vitamin D on plasma trimethylamine N-oxide (TMAO) and choline metabolites.

METHODS AND RESULTS:

This is a randomized single-blinded nonplacebo-controlled study. Twenty-seven participants received 1200 IU vitamin D3 and 800 mg calcium, and 25 participants received additionally 0.5 mg folic acid, 50 mg B6, and 0.5 mg B12 for 1 year. Plasma homocysteine (Hcy), TMAO, and choline metabolites were measured at baseline and 12 months later.

TMAO declined in the vitamin D arm by 0.5 versus 2.8 μmol/L in the D + B arm (p = 0.005). Hcy decreased and betaine increased in the D + B compared to the D arm. Within-subject levels of plasma choline and dimethylglycine and urine betaine increased in both arms and changes did not differ between the arms. TMAO reduction was predicted by higher baseline TMAO and lowering Hcy in stepwise regression analysis. The test-retest variations of TMAO were greater in the D + B arm compared to vitamin D arm.

CONCLUSION:

B vitamins plus vitamin D lowered plasma fasting TMAO compared to vitamin D. Vitamin D caused alterations in choline metabolism, which may reflect the metabolic flexibility of C1-metabolism. The molecular mechanisms and health implications of these changes are currently unknown.

 

 

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Soluble Dietary Fiber Reduces Trimethylamine Metabolism via Gut Microbiota and Co-Regulates Host AMPK Pathways (2017)

Li Q1,  et al.

 

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Abstract

SCOPE:

Evidence from animal experiments and clinical medicine suggests that high dietary fiber intake, followed by gut microbiota-mediated fermentation, decreases trimethylamine (TMA) metabolism, the mechanism of which, however, remains unclear. The objective of this analysis was to evaluate, using mice fed with red meat, the effects of soluble dietary fiber (SDF) intervention on TMA metabolism.

METHODS AND RESULTS:

Low- or high-dose soluble dietary fiber (SDF) from natural wheat bran (LN and HN, low- and high-dose natural SDF), fermented wheat bran (LF and HF, low- and high-dose fermented SDF), and steam-exploded wheat bran (LE and HE, low- and high-dose exploded SDF groups) were used to examine whether SDF interventions in mice fed with red meat can alter TMA and trimethylamine N-oxide (TMAO) metabolism by gut microbial communities in a diet-specific manner.

Results demonstrated that SDF-diets could reduce TMA and trimethylamine N-oxide (TMAO) metabolism by 40.6 and 62.6%, respectively. DF feeding, particularly fermented SDF, reshaped gut microbial ecology and promoted the growth of certain beneficial microflora species.

SDF-diet decreased energy intake, weight gain, intestinal pH values, and serum lipid and cholesterol levels. SDF-diet also enhanced the production of short chain fatty acids with activation of the intestinal epithelial adenosine monophosphate-activated protein kinase (AMPK).

CONCLUSION:

These findings suggest a central mechanism via which SDF-diet may control TMA metabolism by gut microflora and co-regulate the AMPK pathways of the host.

 

 

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5 hours ago, Sibiriak said:

soluble dietary fiber (SDF) from natural wheat bran

Hmmm....

I believe that wheat bran is high in INSOLUBLE fiber, and not very high in SDF -- vegetable fiber is much higher in SDF.

While I believe the conclusions of the study -- this (if I'm correct) raises some doubts about the value of the study.

  --  Saul

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Anti-TMAO effects of low-dose aspirin have already been cited in another thread https://www.crsociety.org/topic/16821-basic-blood-tests/?page=2&amp;tab=comments#comment-29329   but I thought I'd bring up the topic here as well.

Gut Microbe-Generated TMAO from Dietary Choline Is Prothrombotic in Subjects (2018)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5460631/

 

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We next tested whether platelet hyper-responsiveness associated with choline supplementation and elevated TMAO was observed in the presence of aspirin. Omnivores previously examined in the absence of aspirin had a choline supplement-free washout period of at least 1 month and then were started on aspirin (81 mg each evening) for 1 month prior to a baseline evaluation, followed by 2 months of choline supplementation. Compared to baseline, choline again increased both fasting plasma TMAO levels and ADP-dependent platelet aggregation responses at 1 and 2 months of supplementation; however, both the degree of TMAO elevation and platelet hyperresponsiveness were attenuated by aspirin therapy (Figure 1C).

These studies show for the first time a direct pro-thrombotic effect of dietary choline and elevated levels of the gut microbial metabolite TMAO in humans. They also suggest the platelet hyperresponsiveness mediated by elevated TMAO can be attenuated by low dose of aspirin. Importantly, they suggest that elevated levels of the gut microbe-generated metabolite TMAO may overcome the anti-platelet effects of low-dose aspirin – a hypothesis that warrants further investigation, particularly in subjects at high cardiovascular risk.

An unanticipated finding was that low dose aspirin partially reduced choline supplement-dependent rise in TMAO.[ Aspirin lowered TMAO by about 40%.] While the mechanism for this is unknown, aspirin has been reported to alter the composition of the gut microbial community5. Finally, aspirin use in primary prevention subjects has recently been debated. The present studies, coupled with published studies linking heightened TMAO levels with thrombotic event risk4, suggest studies are warranted to explore if low dose aspirin is beneficial amongst subjects with elevated TMAO and no clear contraindications to aspirin.

 

 

Edited by Sibiriak

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But long term use of aspirin is associated with bleeding in the stomach and elsewhere in the gastrointestinal tract.

Best is a good diet, and careful monitoring of bloodwork. 

  --  Saul

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Best is a good diet, and careful monitoring of bloodwork. 

I agree. I  wasn't  recommending low--dose aspirin,  just adding to the TMAO-related info.  (It might be useful for someone already taking low-dose aspirin for other reasons.)

(I have deeply researched the  low-dose aspirin gastrointestinal bleeding issue,  though,  and I believe the risk (especially absolute  risk) is very low for those who are are  at low risk to begin with --there are many factors that increase GI bleeding risk--and who include gastroprotective elements in their diet as well.   But  I don't want to get into that discussion here;  there are already other threads on aspirin.)

Personally,  I'm not at all concerned about TMAO.   I follow a  low-calorie, low-protein, moderate-fat,  plant-based  diet,  with about 100g fish/wk,  no meat, no eggs, (close to Valter Longo's suggestions)--  and I don't take choline or l-carnitine  supplements.   Furthermore, I'm not at any particular risk for CV disease.  So I just don't see TMAO as an actionable issue for me.

I do find the topic very interesting though-- it's fascinatingly complex in many ways, and rather paradigmatic of the complexities associated with a number of other controversial health "biomarkers."
 

 

 

 

Edited by Sibiriak

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TomBAvoider: All I'm saying at the moment is that I feel very poorly informed on this issue and so eagerly look forward to what you and others come up with...

 

I found the following to be a good, up-to-date, fairly comprehensive review of the TMAO issue  (covering neurodegenerative as well as cardiovascular disease):

Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target
Nutrients 2018, 10(10), 1398; https://www.mdpi.com/2072-6643/10/10/1398/htm
 
 
I think you might find this interesting as well:
 

How TMAO Fooled Us

https://lesslikely.com/nutrition/tmao-mendelian-randomization/

It takes a skeptical albeit narrowly-focused look at TMAO as a causal factor in cardiovascular disease,  delving into a lot of general methodological issues (eg. confounding) while focusing on a very recent mendelian randomization study:

 

Assessment of Causal Direction Between Gut Microbiota-Dependent Metabolites and Cardiometabolic Health: A bi-Directional Mendelian Randomisation Analysis (2019)

https://diabetes.diabetesjournals.org/content/early/2019/06/05/db19-0153

 

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Abstract

We examined the causal direction between gut microbiota-dependent metabolite trimethylamine-N-oxide (TMAO) or its predecessors and cardiometabolic diseases such as risk of type 2 diabetes mellitus (T2DM), coronary artery disease (CAD), myocardial infarction (MI), stroke, atrial fibrillation (AF), and chronic kidney disease (CKD). We used genetic variants as instruments to test the causal associations.

Genetically predicted higher TMAO and carnitine were not associated with higher odds of T2DM, AF, CAD, MI, stroke, and CKD after Bonferroni correction (P≤0.0005). However, we observed that genetically increased choline showed a suggestive association with higher risk of T2DM (odds ratio: 1.84, 95% confidence interval: 1.00 to 3.42 per 10 units, P=0.05).

In contrast, genetically predicted higher betaine (0.68, 0.48 to 0.95 per 10 units, P=0.023) was suggestively associated with a lower risk of T2DM. We observed a suggestive association of genetically increased choline with a lower level of body fat % (beta: -0.28, SE: 0.11, P=0.013), but a higher level of estimated glomerular filtration rate (0.10±0.05, P=0.034).

We further found that T2DM (beta: 0.130, SE: 0. 0.036, P<0.0001) and CKD (0.483±0.168, P=0.004) were causally associated with higher TMAO levels.

Our MR findings support that T2DM and kidney disease increase TMAO levels and observational evidence for cardiovascular diseases may be due to confounding or reverse causality.

Edited by Sibiriak

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1 hour ago, Sibiriak said:

(I have deeply researched the  low-dose aspirin gastrointestinal bleeding issue,  though,  and I believe the risk (especially absolute  risk) is very low for those who are are  at low risk to begin with --there are many factors that increase GI bleeding risk--and who include gastroprotective elements in their diet as well.   But  I don't want to get into that discussion here;  there are already other threads on aspirin.)

Hi Sibiriak!

My wife is an NP specializing is gastroenterology, and deals routinely with patients that fall into this category.  She has done more than research the problem -- she's dealt with it profusely.  She is quite clear that COX inhibitors -- definitely including aspirin -- should be taken for limited periods only, and not continually, even in low doses -- no matter how good the patients' overall health.

In particular, she includes me (not that I have any reason, need or desire for such stuff).

Unlimited low dose aspirin, sooner or later, will result in gastrointestinal bleeding -- starting in the stomach.

Best to stay off all COX inhibitors.  COX 1 inhibitors are both more powerful and with more side effects than COX 2 inhibitors (not that COX 2 inhibitors are benign).

Aspirin is a COX 1 inhibitor. 

  --  Saul

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Aspirin is in some ways more dangerous than other COX inhibitors -- for historical reasons.  That's because it was the first one used; the popular opinion was a "miracle analgesic".  Many still believe that it's possibly the safest analgesic.

Of course, that's false.  The safest analgesic is low dose Tylenol (which became available much later).

I avoid that too; I don't need it.

  --  Saul

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