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Folic acid, B vitamins not linked to reduced risk of cardiovascular events in high-risk women
Women at high-risk of cardiovascular disease who took a daily supplement of folic acid and vitamin B6 and B12 for seven years did not have an overall reduced rate of cardiovascular events, despite a significant lowering of homocysteine levels, according to a study in the May 7 issue of JAMA.
“Homocysteine [an amino acid produced by the body] levels have been directly associated with cardiovascular risk in observational studies; and daily supplementation with folic acid, vitamin B6, vitamin B12, or a combination have been shown to reduce homocysteine levels to varying degrees in intervention studies,” the authors write.
Observational data suggest cardiovascular benefits from B-vitamin supplementation may be greater among women, yet women have been underrepresented in published randomized trials. “Given the paucity of data on women and the known influences of estrogen on homocysteine levels, adequately powered randomized trials of homocysteine lowering in women are still needed.”
Christine M. Albert, M.D., M.P.H., of Brigham and Women’s Hospital and Harvard Medical School, Boston, and colleagues tested whether a combination of folic acid, vitamin B6 and vitamin B12 would reduce total cardiovascular events among women at high risk for the development of cardiovascular disease (CVD) over 7 years of follow-up. Within an ongoing randomized trial of antioxidant vitamins, 5,442 women who were U.S. health professionals age 42 years or older, with either a history of CVD or three or more coronary risk factors, were enrolled in a randomized trial to receive a combination pill containing folic acid (2.5 mg), vitamin B6 (50 mg), and vitamin B12 (1 mg) or a matching placebo.
During the 7.3 years of follow-up, 796 participants (14.6 percent) experienced a confirmed CVD event included in the primary end point (heart attack, stroke, coronary revascularization, or CVD death), with some individuals experiencing more than one event. There was no difference in the cumulative incidence of the primary combined end point in the active vs. placebo treatment groups at any time during study follow-up. A total of 406 women (14.9 percent) in the active treatment group and 390 (14.3 percent) in the placebo group experienced at least one cardiovascular event included in the primary end point.
When analyzed separately, there were no significant differences for each of the components of the primary outcome including heart attack, stroke, and CVD death, between the active treatment and placebo groups. Also, the risk of death from any cause was similar between the active and placebo treatment groups.
The researchers also found that the average plasma homocysteine level was 18.5 percent lower in the active group than that observed in the placebo group.
“Our results are consistent with prior randomized trials performed primarily among men with established vascular disease and do not support the use of folic acid and B vitamin supplements as preventive interventions for CVD in these high-risk fortified populations,” the authors write.
Citation: JAMA. 2008;299[17]:2027-2036.
Source: JAMA and Archives Journals
Observational data suggest cardiovascular benefits from B-vitamin supplementation may be greater among women, yet women have been underrepresented in published randomized trials. “Given the paucity of data on women and the known influences of estrogen on homocysteine levels, adequately powered randomized trials of homocysteine lowering in women are still needed.”
Christine M. Albert, M.D., M.P.H., of Brigham and Women’s Hospital and Harvard Medical School, Boston, and colleagues tested whether a combination of folic acid, vitamin B6 and vitamin B12 would reduce total cardiovascular events among women at high risk for the development of cardiovascular disease (CVD) over 7 years of follow-up. Within an ongoing randomized trial of antioxidant vitamins, 5,442 women who were U.S. health professionals age 42 years or older, with either a history of CVD or three or more coronary risk factors, were enrolled in a randomized trial to receive a combination pill containing folic acid (2.5 mg), vitamin B6 (50 mg), and vitamin B12 (1 mg) or a matching placebo.
During the 7.3 years of follow-up, 796 participants (14.6 percent) experienced a confirmed CVD event included in the primary end point (heart attack, stroke, coronary revascularization, or CVD death), with some individuals experiencing more than one event. There was no difference in the cumulative incidence of the primary combined end point in the active vs. placebo treatment groups at any time during study follow-up. A total of 406 women (14.9 percent) in the active treatment group and 390 (14.3 percent) in the placebo group experienced at least one cardiovascular event included in the primary end point.
The researchers also found that the average plasma homocysteine level was 18.5 percent lower in the active group than that observed in the placebo group.
“Our results are consistent with prior randomized trials performed primarily among men with established vascular disease and do not support the use of folic acid and B vitamin supplements as preventive interventions for CVD in these high-risk fortified populations,” the authors write.
Citation: JAMA. 2008;299[17]:2027-2036.
Source: JAMA and Archives Journals
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So when you feed a test cohort B6, B-12 or folic acid, you have a problem:
Insufficient methylation pool for conversion of these el cheapo synthetic vitamins to their active METHYLATED form. Folate, for instance, requires not one, but four methyl groups to form the active coenzyme necessary to function in the transmethylation pathway.
This problem of cardiovascular disease is, at it's core, a problem of insufficient gluthathione biosythesis. And that is what you want the transmethylation pathway to do: supply reducing equivalents to drive cellular redox offset of respiratory oxidation byproducts (ROS).
You saw the article on TSH (thyrothrophin) correlation to CVD in women? That, too, is linked to insufficient methylation activity and homocysteine activity in the hypothalamus.
Ultimately, they loop back to a fundamental issue in selenium that is largely missing in American diets, due to poor dietary habits (low vegetable and whole grain intake) AND to decades of gungho agricultural practices that have stripped soils of zinc, copper and selenium - all necessary to drive reductive equivalent biosythesis (mostly in liver, CNS, lungs and muscle tissue that bear the brunt of oxidative energy metabolism).
To utilize selenium in diet, you need to methylate it. You also need to recycle its form back from the oxidized state, in selenoproteins. For that to occur, you need adequate intake of other antioxidants.
The medical research world is MORE than happy to shoot down the use of dietary supplements to offset dietary insufficiency that results in much of our chronic and infectious disease issues of modern society.
After all, they stand to profit handsomely. So they design these simplistic two-bit studies that are bound to show negative results because they ignore the larger interaction of biosythetic pathways). Only a very few homocysteine reduction studies have bothered to employ properly methylated B-vitamins/folate to assess overall effect on homocycteine reduction and CVD effects.
Lastly, these idiot studies ignore a very, very solid basis of study that show the connection between muscle, liver, and CNS signaling. If you don't exercise and get off your fat kester, all the supplements in the world will not upregulate an aging antioxidant recycling system in cells.
The bottom line is this: prudent dietary choices, daily exercise, and good sleep hygiene are the ultimate prescription to health and reduced healthcare costs.