The Homocysteine Debate

dr_duane_graveline_m.d._134By Duane Graveline, MD, MPH

As one who has researched the role of homocysteine in cardiovascular disease, I thought, when I wrote my book, Statin Drugs Side Effects, and reviewed Kilmer McCully's brilliant 30-year research thriller on this, The Homocysteine Revolution, that homocysteine's role in atherosclerosis was firmly established.

Inflammation, not cholesterol, he determined, was the cause of atherosclerosis and increased cardiovascular risk and that homocysteine was the direct cause of this vascular inflammatory process in at least 40% of cases.

McCully, through a lifetime of medical detective work, had single-handedly and methodically not only discredited the role of cholesterol and the entire low fat, low cholesterol diet debacle, but introduced the inflammatory concept of atherosclerosis, now accepted by many, and placed homocysteine firmly in the center of it.

Finally, the glaring deficiencies of the cholesterol concept were laid to rest by an atherosclerotic mechanism that made sense. More importantly McCully presented overwhelming evidence that the B complex vitamins, B6, B12 and folic acid played major roles in controlling homocysteine levels in the human body, placing the condition of elevated homocysteine in the category of our common deficiency diseases, controllable by dietary and supplemental intake of these simple and economical vitamins.

Led by Brigit and David Wilcken's series of papers on homocysteine's role in atherosclerosis, the numbers of published papers supporting McCully's research soon became a flood and the list of studies vindicating McCully's departure from established research pathways now goes on and on.

The decision of his Harvard "masters" not to renew the research contract of this intractable loner back then, during his dark days, will forever remain a black spot on their judgment and capacity to lead.

Finally, after all these years, two research teams published back to back studies on the inability of B6, B12 and folic acid supplementation and the lowering of homocysteine levels to help reduce cardiovascular disease in their secondary prevention trials.

Ordinarily such reports would not make it to the mass media without confirmation, for our media has an obligation for balanced news. How then did these alarming and for the general public, terribly confusing stories originate?

If the science writers themselves, in their attempts to sensationalize information, however inconsequential, did not observe the rules of balance, what of their editors? Whose responsibility is it to assure their millions of readers that reasonable people are making reasonable efforts to present news reasonably?

Should we insist that all technical and scientific reports be withheld from the media for a year to give greater opportunity for scientific scrutiny and rebuttal? Frankly I do not know the answer but we all know a problem exists.

In 2006, I saw a BMJ publication by Wald DS and others, titled Folic Acid, Homocysteine and Cardiovascular Disease (1). In this comprehensive meta-analysis of cohort studies, genetic polymorphism studies and randomized trials of homocysteine effect, the only explanation that can account for all the observations is that homocysteine is a cause of cardiovascular disease.

These were Kilmer McCully's words summarizing his 30 years of work when he wrote the Homocysteine Revolution

Ref: (1) Wald DS and others. Folic Acid, Homocysteine and Cardiovascular disease. BMJ 333:1114-7, 2006

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

Updated March 2016

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