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Does lowering Homocysteine lower CVD Risk?

Alzheimer's, cardiovascular, and other chronic diseases; biomarkers, lifestyle, supplements, drugs, and health care.
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Does lowering Homocysteine lower CVD Risk?

Postby giftsplash » Wed Sep 07, 2016 3:37 pm

It is known that lower homocysteine levels correlates with lower CVD events. And it is also known that vitamins such as B12 can lower homocystiene levels.
But has there been any studies showing that lowering homocysteine levels via vitamins actually lowers CVD risk?
I have not been able to find any studies on Pubmed to support this.

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Re: Does lowering Homocysteine lower CVD Risk?

Postby Stavia » Wed Sep 07, 2016 4:00 pm

Giftsplash, very good question.
The mainstream medical view is that lowering homocysteine does not reduce coronary events. This view is held by mainstream but not necessarily by functional practitioners, for whom I do not speak.
Here is the Cochrane review

http://www.cochrane.org/CD006612/VASC_h ... lar-events
We found no evidence that homocysteine-lowering interventions, in the form of supplements of vitamins B6, B9 or B12 given alone or in combination, at any dosage compared with placebo or standard care, prevent myocardial infarction or stroke, or reduce total mortality in participants at risk of or with established cardiovascular disease. Homocysteine-lowering interventions compared with placebo did not significantly affect serious adverse events (cancer).

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Re: Does lowering Homocysteine lower CVD Risk?

Postby cdamaden » Wed Sep 07, 2016 10:17 pm

Dr. Ruscio discusses his research in this podcast, http://drruscio.com/homocysteine-heart-episode-54/, with a variety of studies. Then he interviews Dr Gordon here, http://drruscio.com/homocysteine-follow ... pisode-60/, where she said that "currently the optimal level for homocysteine to reverse dementia is a much lower level than is accepted as normal in the standard clinical trials. So they might try and lower it to 15 or 13. But for cognitive benefits you have to lower it to between 5 and 8. So maybe those cardiovascular trials didn’t take it low enough." And "And this is sort of because I believe that lowering homocysteine wisely reduces actually cardiovascular risk…And there is that one study which I sent to you, the Swiss Study, where they really took the homocysteine down farther and then lower cardiovascular risk. It lowers stroke risk. And it’s part of Bredesen’s protocol. And there’s good research behind it for addressing dementia."

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Re: Does lowering Homocysteine lower CVD Risk?

Postby Silverlining » Thu Sep 08, 2016 2:13 am

This is timely for me. I stopped taking b vitamins a couple of years ago and did not realize the very real elevated homocysteine effect. My dr pulled a lab in January and I was at 15. I began retaking vitamin b spectrum and yesterday received new lab results and my level is now 7.6. I did wonder yesterday if this means anything for me as I don't think I'm much of a cvd risk; now I believe addressing homocysteine does matter. Thanks for the info.

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Re: Does lowering Homocysteine lower CVD Risk?

Postby SusanJ » Thu Sep 08, 2016 7:15 am

There are other diseases where high homocysteine is found at the scene of the crime. It's still not clear if its just piling on during some other disease process or implicated as cause. Many studies look at homocysteine as a biomarker but others, like those above, see direct effects so my guess it's some type of signaling molecule (try putting homocysteine in PubMed - almost 22000 articles). Someday, I'll go down that rabbit hole.

High homocysteine is implicated in inflammation (brought about by high insulin and blood glucose levels) and increasing IL-6.
The other example is the hypomethylation in CpG islands within the IL-6 promoter gene in monocytes. IL-6 is a pro-inflammatory cytokine that participates in B cell response. When this promoter is hypermethylated, there is an overexpression of IL-6 that will cause an overexpression of pro-inflammatory cytokines at the same time. This will be associated with a local hyperactive of the inflammation circuit. But there is evidence that we can also find a hypermethylation mechanism in monocytes such as in the case of the CpG islands with the promoter of death receptor 3 (DR-3). DR-3 is a protein that cause apoptosis and activation of transcription factor NF-kappa-M. However, when there is a downregulation of tis protein because of the hypermethylation of its promoter, the RA synovial cell will be resistant to apoptosis.

Glucose and insulin levels are determinants of methylation. They alter homocysteine metabolism by increasing cell homocysteine production through its inhibition of trans-sulfuration. When there is an increase in the levels of homocysteine, methionine in cells will be catalyzed by DMNTs in S-adenosylmethionine. This will enhance DNMT activity that will subsequently lead to increased global DNA methylation.


High homocysteine is implicated in osteoporosis.
Our analyses of data from three cohorts of subjects in two independent studies show a strong association between increased homocysteine levels and the risk of osteoporotic fracture. The age- and sex-adjusted risk of fracture increased by 30 percent for each increase of 1 SD in the homocysteine level. A serum homocysteine level in the highest quartile doubled the risk of fracture. The magnitude of this effect is similar to that previously observed for the increase in the risk of cardiovascular disease and dementia according to homocysteine level.12-14,28

According to a long-standing hypothesis, the mechanism underlying the association between the homocysteine level and the risk of fracture may involve interference by homocysteine in collagen cross-linking.7

Besides B vitamins, look at D:

Serum vitamin D was a significant positive explanatory variable for HDLC (partial R (2) = 1.4%, P < 0.0001), and a significant inverse explanatory variable for homocysteine (partial R (2) = 6.0-12.6%).


Since my family history includes CVD and AD, and I am now in the osteopenia camp, I watch mine closely.

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