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Life Extension Magazine December 2010

Why Reading Mainstream Magazines Can be Detrimental to Your Health

By William Faloon

Asking Too Much and Doing Too Little

Fundamentally, these clinical studies were asking too much and doing too little. They produced only moderate reductions in homocysteine levels in people already gravely ill with cardiovascular disease. They add nothing to what we already know about the role of homocysteine in otherwise healthy people—people who still have a chance to make important changes in all of the known cardiovascular risk factors. It’s vital to make those changes early, before damage accumulates, and to make them in as many risk areas as possible. Homocysteine reduction is one such area, and we have solid evidence that an early start aimed at reducing levels substantially can make a big difference.

Traditional wisdom holds that endothelial dysfunction only begins to occur in otherwise healthy people when their homocysteine levels get above the upper limit of “normal,” 15 μmol/L.24 But we’ve known for more than a decade that even small increments in homocysteine levels—within the “normal” range—produce immediate and dangerous disruptions of endothelial function.

In a remarkable study in 1999, British researchers fed healthy young adults several different diets, two of which contained amino acid precursors of homocysteine, and one that was free of such molecules.25 At baseline, volunteers had mean homocysteine levels of 9.5 μmol/L. Both the homocysteine precursor-containing diets induced an immediate rise in plasma homocysteine, but only to the 11-12 μmol/L range. Nonetheless, there was an immediate decrease in flow-mediated dilation, a sensitive measure of endothelial function. The control diet had no effect. It’s hard to ask for more direct proof that small homocysteine elevations produce meaningful reductions in endothelial function and lay the foundation for atherosclerosis.

Vitamin B12’s Effects on Homocysteine
Vitamin B12’s Effects on Homocysteine

Epidemiological studies show a strong association between elevated blood homocysteine levels and higher risks of cardiovascular disease in humans.26,27 The human metabolism requires ample amounts of B vitamins to keep dangerous homocysteine levels under control.28 Folate, vitamin B6, and especially vitamin B12 are vital cofactors required by a number of enzyme systems that detoxify homocysteine by converting it into harmless amino acids. A growing number of experts now regard vitamin B12 as one of the most essential nutrients for lowering homocysteine levels.

A large study combining the results of small earlier studies demonstrated that in typical populations, daily supplementation with both 500 to 5,000 mcg of folic acid and 500 mcg of vitamin B12 would be expected to lower homocysteine levels by one quarter to one third.26 That prediction has been borne out in more recent work, in some cases by studies showing that B12 is more closely related to homocysteine reduction than is folate.29 In general, the higher the baseline homocysteine level, and the lower the B12 level, the greater the effect of B12 supplementation.26 That was recently shown to be especially true in older men living at home, which is doubly important because of the exaggerated effect of homocysteine elevations on cardiovascular risk in some male populations.30,31

Both oral and intravenous forms of B12 supplementation have been shown to reduce total homocysteine concentrations.32,33 High-risk populations, particularly people with end-stage renal disease on dialysis, stand to benefit even more from B12 supplementation.33,34 There’s simply no question that, in the words of international expert Dr. Yvonne Schwammenthal of the Stroke Unit at Sheba Medical Center in Tel Aviv, “Homocysteine-lowering treatment that is cheap and well-tolerated should be considered a rational approach in patients at high risk of stroke and high concentrations of homocysteine.”28

Doomed from the Outset

Armed with a realistic understanding of how homocysteine levels relate to cardiovascular risk, it is easy to see why the recent JAMA study failed to show any impact of minor homocysteine lowering on people with major heart disease. Reducing homocysteine by a few points, at the lower end of the scale, in people with pre-existing severe arterial damage (severe enough to have already had a heart attack), could not possibly be expected to have an impact.

The approach taken by mainstream physicians in studies like the JAMA report are tragically typical of their general strategy. That can be summed up as, “Find a single problem, focus on it and it alone, and judge success or failure by whether changing just the one factor makes a difference.” That’s a great way to sell drugs, of course—one drug per problem adds up to tremendous revenue. But it is a poor way to manage the complexities of cardiovascular disease, for which we can identify no fewer than 17 deadly risk factors (and perhaps many more).

Male and Female Blood Test Panels

The Bottom Line

It’s naive to claim that a single therapy can have an impact on a complex, multifaceted problem like cardiovascular disease. Homocysteine-lowering, by itself, will not prevent a heart attack. By the same token, however, throwing out several decades of solid evidence that homocysteine-lowering can substantially reduce the risk of cardiovascular disease is worse than naive—it’s downright dangerous.

Studies like the JAMA report will no doubt continue to appear, and will continue to be misrepresented as “evidence” that close attention to homocysteine levels is unnecessary. It is in the financial interests of mainstream cardiology to deceive the public into believing the only way of treating heart disease is with bypass surgery, stents, and drugs.

17 Daggers Arterial Disease
17 Daggers Arterial Disease

A plethora of published data, however, reveals that aging humans can successfully circumvent the lethal atherosclerotic process and in many cases reverse it. It all starts with comprehensive blood testing.

The medical establishment charges around $1,000 for the wide-ranging blood tests needed to assess coronary risk markers. As a Life Extension member, you can obtain the same tests for only $269.

When you place your blood test order, we send you a requisition form along with a listing of blood-drawing stations in your area. You can normally walk in during regular business hours for a convenient blood draw.

The sidebar below describes the comprehensive Male and/or Female Blood Test Panels that all health conscious individuals should have done at least once a year. They can be ordered by calling 1-800-208-3444 (24 hours a day).

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.

Male and Female Blood Test Panels

Unlike commercial blood tests that evaluate only a narrow range of risk factors, Life Extension’s Male and Female Blood Test Panels measure a wide range of blood markers that predispose people to common age-related diseases. Just look at the huge numbers of parameters included in the Male and Female Blood Test Panels:

Click here to view
Click here to view

Non-member retail price: $400 • Everyday member price: $269 To obtain these comprehensive Male or Female Panels at these low prices, call 1-800-208-3444 to order your requisition forms.
Then—at your convenience—you can visit one of the blood-drawing facilities provided by LabCorp in your area.

*If you plan to use the results of these blood tests to assist in a medically supervised weight loss program, consider ordering the Male or Female Weight Loss Panels for a member price of $299.  Although a TSH (thyroid-stimulating hormone) test is now included in the comprehensive Male and Female Panels, those with weight problems should know their precise levels of free T3, free T4 and insulin.


1. Available at: Accessed September 7, 2010.

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19. Grassi D, Desideri G, Ferri L, Aggio A, Tiberti S, Ferri C. Oxidative stress and endothelial dysfunction: Say no to cigarette smoking! Curr Pharm Des. 2010 Jun 15.

20. Puntmann VO, Taylor PC, Mayr M. Coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: Systemic inflammation and aging - a mini-review. Gerontology. 2010 Jun 11.

21. Sucharda P. Obesity and atherosclerosis--what’s the link? Vnitr Lek. 2010 Apr;56(4):289-91.

22. Urso C, Hopps E, Caimi G. Adhesion molecules and diabetes mellitus. Clin Ter. 2010 Jan-Feb;161(1):e17-24.

23. Wang M, Monticone RE, Lakatta EG. Arterial aging: a journey into subclinical arterial disease. Curr Opin Nephrol Hypertens. 2010 Mar;19(2):201-7.

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