Taurine Blocks Methionine Absorption

and lowers homocysteine and therefore atherosclerosis

Sounds like it might be worth taking if eating out along with your vitamin E and tryptophan transport blockers

Taurine and Homocysteine Reduction
Taurine can protect against coronary artery disease by favorably modulating blood levels of homocysteine. Research suggests that taurine can block methionine absorption from the diet, thereby reducing available substrate for homocysteine synthesis (Zulli A 2009). One animal study found that taurine normalized hyperhomocysteinemia and reduced atherosclerosis by 64% over control animals and reduced endothelial cell apoptosis by 30% (Zulli 2009). Study investigators also observed that taurine supplementation reduced left main coronary artery wall pathology due to a favorable effect on plasma total homocysteine and apoptosis.

A study of 22 healthy middle-aged women (33 to 54 years) found that after taurine supplementation (3g per day for 4 weeks), plasma homocysteine levels exhibited a significant decline, from 8.5 µmol/L to 7.6 µmol/L. The investigators concluded that sufficient taurine supplementation might effectively prevent cardiovascular disease (Ahn 2009).

http://hyper.ahajournals.org/content/53/6/1017.full

DISCUSSION
This is the first comprehensive study examining the effect of high dietary taurine supplementation on the left main coronary artery. The major findings of this investigation are as follows: (1) taurine supplementation inhibited the development of hyperhomocysteinemia and hypermethioninemia and temporal effects of diet on plasma tHcy and methionine levels; (2) taurine supplementation inhibited endothelial cell apoptosis possibly by reduction in ER stress; (3) taurine supplementation reduced left main coronary artery atherosclerosis; and (4) taurine supplementation did not significantly affect the endothelial level of proteins associated with the NOS, RAS, or oxidative stress systems.

The reduction in tHcy by dietary taurine presented in this study was not attributed to increased metabolism of homocysteine to cysteine or other sulfur-containing amino acids, nor the reduced formation of homocysteine from methionine. Indeed, we observed that high dietary taurine significantly impaired the increase in plasma methionine compared with the untreated group, indicating that other possible routes of methionine metabolism are upregulated by taurine or that taurine can impair the absorption of methionine. Indeed, this latter hypothesis is supported by a recent study in cultured CaCo-2 cells, whereby methionine transport across the apical membrane of Caco-2 cells was affected by extracellular pH and taurine.14 Thus, it appears that taurine can impair the absorption of methionine and, thus, provide a novel way to reduce plasma tHcy. These results might have implications in nutrition. As the popularity of processed fast foods high in methionine is increasing and has been linked to increased tHcy,42 the addition of taurine to the diet might help stem the increase in tHcy and, thus, reduce cardiovascular disease risk. Further research to determine whether these results hold true in humans is warranted.

Furthermore, impaired methionine transport across the intestinal epithelia because of other factors could be causing the temporal effect on tHcy and methionine after the first dietary week. Indeed, we first eluded to this temporal effect in a similar study in rabbits on a 3-month dietary protocol.10 It is unclear why this phenomenon occurs; however, it is possible that both gut Na+-dependent and Na+-independent mechanisms14 are involved. As well, these results suggest that, if these effects hold true in humans, plasma methionine or tHcy might not be a reflection of dietary methionine intake.

In the study presented here, taurine inhibited apoptotic coronary endothelial cells even on a background of a worse lipid profile. Apoptosis could be inhibited by a reduction in ER stress, as measured by a normalization of CHOP protein. In vitro research suggests that homocysteine causes ER stress, and this stimulates CHOP mRNA in human umbilical vein endothelial cells43 and apoptosis in cultured endothelial cells.44,45 Our study confirms this theory, because CHOP protein was significantly increased in the atherogenic group, which also had higher plasma tHcy levels, and, thus, a reduction in tHcy would impair apoptosis.

Furthermore, novel insights into the mechanisms involved in homocysteine-induced cellular damage include homocysteinylation of proteins. Both HDL46 and the intracellular atheroprotective enzyme metallothionein47,48 can become dysfunctional via homocysteinylation. For example, Barbato et al47 found that homocysteinylation of metallothionein impairs its zinc binding function, thus impairing its superoxide scavenging properties and possibly amplifying oxidative stress in endothelial cells. Thus, targeting a reduction in both tHcy and cellular homocysteine to reduce protein homocysteinylation could be a novel avenue for the treatment of homocysteine-induced vascular damage.

The decreased intimal thickening and reduced atherosclerosis in the left main coronary artery of this model during taurine treatment could be attributed to the impaired increase in tHcy. Although clinical trials involving the reduction of tHcy by vitamin supplementation have failed to significantly reduce myocardial events,11 our studies in rabbits9,10 and others in mice49,50 show that hyperhomocysteinemia on a hyperlipidemic background does enhance the development of atherosclerotic plaque burden in animal models. The human studies only managed small reductions (eg, 2.4 μmol/L) in plasma tHcy, using an intervention that would reduce tHcy by increasing methionine, which might not be the most advantageous way of reducing tHcy. In addition, it is possible that the role of hyperhomocysteinemia might be more important in the earlier development of atherosclerotic plaque rather than in reducing events in patients with existing plaque.

It is unclear whether increased triglyceride can directly induce apoptosis or is affected by dietary taurine. In this study, we showed that plasma triglyceride is not affected by dietary taurine and that the prevention of endothelial apoptosis can occur regardless of the triglyceride level. This finding is supported by in vitro experiments, whereby Nyblom et al51 showed reduced β-cell apoptosis, although the triglyceride level did not change. Taken together, these results suggest that triglyceride might not be an important determinant of cellular apoptosis, at least in endothelial or β cells.

Taurine supplementation did not significantly affect the endothelial level of proteins associated with the NOS, RAS, or oxidative stress systems. For this discussion, please see the data supplement.

In conclusion, we show that the addition of 2.5% taurine to an atherogenic diet reduces left main coronary artery wall pathology on a background of a worse lipid profile. As well, taurine also significantly reduces endothelial ER stress, hyperhomocysteinemia, and hypermethioninemia and impairs left main coronary artery endothelial cell apoptosis without detectable effects on the NOS, RAS, or oxidative stress systems.

 

I am wondering why methionine is included in master amino pattern formula

 

Good question. I wonder if excess methionine in the diet is recognized, beyond the Peat world, as a widespread problem in medical science at all.

 

Don't you need a minimal amount of methionine (or cysteine) in your diet? For example to make glutathione.

 

For sure. Just like tryptophan. I think the main issue here is that we consume excess of these substances in a typical modern diet. Unless we were vegetarians, then I think it would be hard to ever become methionine deficient. Of course, I wouldnt personally aim to limit any of these without proper testing to see if we have related downstream problems.

 

That is pretty interesting. I have baseline homocysteine test numbers and have been supplementing taurine pretty regularly. I'll redo the test and see if it made a difference.

 

Let me know what you find out. I just got my homocysteine test back and they were around 10, which id like to bring down with some b6 as well.

 

Methionine is officially labelled as an essential amino acid. So, most vendors will include it in their formula if they intend to market it as a protein replacement supplement. Also, you'd be surprised how biochemically blind some medical companies are. They just follow protocol and if it says to add methionine they'll do it regardless of the evidence of harm. Most MDs I have talked to are completely unaware of the lifespan extension through methionine restriction. They know even less about the mechanism through which methionine restriction could achieve this effect.
There is usually plenty of methionine, tyrptophan and histidine in your body so no need to ingest these aminos daily. You may need no more than 200mg methionine in your daily diet and most people get 3g+ daily. Without tryptophan there can be no infection and without histidine no inflammatory/allergic response. Both tryptophan and histidine are disputed as to whether they are really essential. Here is one about histidine.
http://www.ncbi.nlm.nih.gov/pubmed/12421848
If you ingest sufficient niacin, you probably don't need any tryptophan. My version of the MAP pattern with added beta alanine and glycine, ensures depletion of tryptophan, methionine and histidine when ingested chronically. I'd venture a guess that it would be very helpful for weight loss given how much metabolism increases in methionine and tryptophan depleted states.

 

Your adjusted MAP recipe post was extremely helpful. It was what I had been trying to figure out. I knew BCAAs weren't enough for MPS and wasn't sure which I needed to add. Thank you, again.

One challenge I've encountered is creating the time to mix all of these individual aminos (I have ideas of using old pill bottles to make travel mixes, but that would still be cumbersome). It reminded me of when I was in training in the 90's and I would take a tablespoon of liquid aminos (and creatine) every morning before those long grueling days. It worked extremely well without having to make shakes. If feasible, I think this would make an amazing product. The ease of getting more readily digestible protein is better than not getting enough

 

Lol, I guess if there is enough interest I can release a product with it. By my version, I meant my suggestion to omit the 3 "bad" amino acids from whatever mix people end up concocting.

 

Tara, I don't think there is any way to keep bulk dry powder mixed evenly; just mixing two powders evenly can be ambiguous if they are the same color. As NathanK says, making individual dry packages is an alternative.

NathanK, when I first made caps of B vits with the ratios I wanted, it was like a minor PITA, something I had to do. As time went on my attitude changed and it became a ritual of nourishment, and I got into doing it.

I thought about leftover pill bottles, too. But there is an art of making things with paper, I can't remember the name, it'd be cool to whip up a little container for the powder from a sheet of paper, wouldn't it?

BD

 

Origami?

 

Pills are excellent. I once spent a whole weekend making some with all of my powders for various supps. It was really tedious. I just don't have the time or desire to do that again. I don't even bother with my powdered B's anymore except on occasion like to get some B's that aren't in a formulations like Energin. One way old pill bottles may work with aminos is because the dosage is so much higher and wouldn't fit into a pill anyhow. With all the Peaty aminos in one dose could easily reach 20g. One small pill bottle could be good for a whole day. Of course, if Haidut was able to manufacture a liquid amino supp like he did with B vitamins then that would be the easiest way to get it. The current liquid AA out there are filled with junk and that's not counting tryptophan, methionine, or histidine.

 

That's it! Any origami experts out there to make like 1.5 X 1.5 X 1.5 inch pouches? Would that be big enough for a 10g AA dose?

 

I haven't finished reading this study, but it feels almost like a follow up to the first study i posted. Interesting for anyone currently trying to untangle the methylation puzzle (like the researchers in this study are attempting). Off hand, the results here were a little surprising... and telling. Taurine and choline likely play equally important parts in methionine and homocysteine metabolism and in keeping the liver lean.

Taurine supplementation does not decrease homocysteine levels and liver injury induced by a choline-deficient diet
Researchers fed rats a choline deficient diet (CDD) and looked to see if supplemental taurine would offset any liver or cardiovascular damage from the elevated Hcy. Not only did it not work, but I found this interesting and worth looking further into,"...taurine added to CDD caused decreased expression of PEMT,CHKa, and CHKb, key genes involved in phosphatidylcholine (PC) synthesis and liver fat accumulation."