The B Vitamins

Dr Kilmer McCully pointed out that homocysteine in the blood rises when folic acid is low.  Interestingly, folic acid is powerfully protective against Alzheimer’s disease.  At or above the RDA (meaning supplements are necessary for most people), the risk of Alzheimer’s disease is more than halved.

 

Homocysteine is directly toxic to the endothelial cells which line the arteries, so homocysteine is emerging as a risk factor for heart disease.  Since the level of enrichment of folate in refined cereal grains was increased in 1998, the rate of fall in the incidence of heart disease has increased from 1% to 4.5% per year.  It’s clear that B6 and B12 are also involved.

 

Vitamin B6 is involved in the metabolism of homocysteine, and studies show that B6 deficiencies are an independent contributor to the heart problem.  Dr John Ellis of North Carolina maintained a large patient population on 50-300mg of vitamin B6 per day for many years, and a retrospective study by Ellis and Kilmer McCully found 73% fewer heart attacks among them compared to other residents of the area.

 

One reason may be that low B6 interferes with collagen formation because B6 is the co-enzyme of lysyl oxidase so the cross-linking step in the process of collagen formation cannot be completed.  Researchers Rinehart and Moon found the initial lesion of atherosclerosis of B6-deficient monkeys was the deposit of mucin in the blood vessel walls.  Only then was cholesterol deposited in this mucoid formation.  This is entirely consistent with, and adds to, Linus Pauling’s idea of heart disease. (Rinehart JF and Moon HD, Circulation, 1952)  

 

When Dr Walter Willett of Harvard studied the Nurses Health Study data, he found the risk of heart attack for those who had the highest folate and B6 levels to be less than half of those who had the lowest. He concluded in a masterly piece of understatement that “intake of folate and vitamin B6 above the current recommended dietary allowance may be important in the primary prevention of CHD among women.”

 

Vitamin B6 must be converted in the body into the active form, P5P, before we can make use of it.  The conversion is performed by a magnesium-dependent enzyme, so a magnesium deficiency affects vitamin B6 utilization.  Since some 85% of the population fails to achieve the RDA for magnesium in their diet, this must contribute a functional B6 deficiency.

 

A 2004 case-control study found low P5P to almost doubled CHD risk, and that the low-P5P state was associated with high C-Reactive Protein, the inflammatory risk factor for heart disease.

 

When vitamin B6 was given to mature men who were deficient in it, their cholesterol levels and their LDL cholesterol levels fell.