Vitamin B supplements offer no protection from heart disease

November 07, 2017

In a study by Norwegian scientists it has been revealed that supplements of vitamin B did not reduce the rates of heart attacks or strokes in patients with coronary artery disease.

Earlier research appeared to suggest that folic acid, either alone or combined with vitamins B12 and B6, reduced levels in the blood of homocysteine, an amino acid linked to a higher risk of heart attack.

This latest research appears to dispute these claims and is yet the another example of science questioning the benefits of supplementary vitamins.

The research involved more than 3,000 patients in two Norwegian hospitals between 1999 and 2006 who were given folic acid plus vitamin B12 and vitamin B6, or folic acid plus B12, B6 alone, or a placebo.

The researchers found that while homocysteine levels did fall by 30 per cent after a year of treatment with folic acid and B12, there was no corresponding fall in heart attacks or strokes and in the group given folic acid, there was a decline in strokes, but an increase in cancer, though neither was considered significant.

The research team led by Dr. Marta Ebbing, from Haukeland University Hospital in Bergen, say their findings do not support the use of B vitamins as secondary prevention in patients with coronary artery disease.

The study is published in the Journal of the American Medical Association.

One of the candidates for a hypothetical molecule that should convert physical force into biochemical messages was a protein called platelet endothelial cell adhesion on molecule-1 (PECAM-1). When researchers stretched the model, PECAM-1 was indeed phosphorylated at two key points in its amino acid chain. Phosphorylation, the attachment of a phosphate group to a protein chain, is used by cells to switch on biochemical signals. In the study, PECAM-1 phoshorylation occurred in a lifeless model purely as a result of mechanical stretching force, which presumably pushed PECAM-1 and a nearby, built-in enzyme close enough to each other for phosphorylation to occur.

In addition, the team, via a series of clever eliminations, also identified from a library of 244 candidates the single enzyme, called Fyn, which phosphorylates PECAM-1 in response to force. Only when production of Fyn was greatly reduced, removing it from the stretch model, did PECAM-1 phosphorylation no longer respond to stretching force. When Fyn expression was silenced in live endothelial cells in a related study, PECAM-1 phosphorylation no longer responded to shear stress either.

The medical relevance of the study comes from a hypothesis that the phoshorylation of PECAM-1 enables it to activate, via signaling partners, the extracellular signal-regulated kinase (ERK) pathway. Past Aab CVRI studies suggest that ERK activation inhibits the expression of pro-inflammatory genes in endothelial cells. Experts once believed that atherosclerosis developed when too much cholesterol clogged arteries with fatty deposits in vessel walls called plaques. Today most agree that the reaction of the body's immune system to fatty build-up, as much as the build-up itself, creates risk for heart attack (complete blockage of an artery). Immune cells traveling with the blood mistake fatty deposits for intruders, akin to bacteria, and attack. Resultant inflammation makes plaques more likely to cut off flow.

The work was supported in part by grants from the National Institutes of Health and the American Heart Association.

"Obviously, we should all be exercising to get our hearts pumping fast, which increases blood flow force through our vessels," said Fujiwara. "Beyond that, genetic engineers may in the future design gene therapy that delivers genes only into cells at blood vessel branch points to increase PECAM-1 signaling. Alternatively, drug designers might create super-active Fyn, amplifying the signaling effects of PECAM-1 phosphorylation to protect vulnerable areas of blood vessels from inflammation."


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