NathanK
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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.
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.
