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Why Reading Mainstream Magazines Can be Detrimental to Your Health

December 2010

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.

2. SEARCH Collaborative Group, Armitage JM, Bowman L, et al. Effects of homocysteine-lowering with folic acid plus vitamin B12 vs placebo on mortality and major morbidity in myocardial infarction survivors: a randomized trial. JAMA. 2010 Jun 23;303(24):2486-94.

3. Geisel J, Jodden V, Obeid R, Knapp JP, Bodis M, Herrmann W. Stimulatory effect of homocysteine on interleukin-8 expression in human endothelial cells. Clin Chem Lab Med. 2003 Aug;41(8):1045-8.

4. Poddar R, Sivasubramanian N, DiBello PM, Robinson K, Jacobsen DW. Homocysteine induces expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human aortic endothelial cells: implications for vascular disease. Circulation. 2001 Jun 5;103(22):2717-23.

5. Su SJ, Huang LW, Pai LS, Liu HW, Chang KL. Homocysteine at pathophysiologic concentrations activates human monocyte and induces cytokine expression and inhibits macrophage migration inhibitory factor expression. Nutrition. 2005 Oct;21(10):994-1002.

6. Nygard O, Nordrehaug JE, Refsum H, Ueland PM, Farstad M, Vollset SE. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med. 1997 Jul 24;337(4):230-6.

7. Bonaa KH, Njolstad I, Ueland PM, et al. Homocysteine lowering and cardiovascular events after acute myocardial infarction. N Engl J Med. 2006 Apr 13;354(15):1578-88.

8. Lonn E, Yusuf S, Arnold MJ, et al. Homocysteine lowering with folic acid and B vitamins in vascular disease. N Engl J Med. 2006 Apr 13;354(15):1567-77.

9. Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA. 1995 Oct 4;274(13):1049-57.

10. Iso H, Moriyama Y, Sato S, et al. Serum total homocysteine concentrations and risk of stroke and its subtypes in Japanese. Circulation. 2004 Jun 8;109(22):2766-72.

11. A lethal misconception. Life Extension Magazine®. 1999 Mar;5(3).

12. Baron P. A comprehensive guide to complete blood testing. Life Extension Magazine®. 2004 May;10(5):51-71.

13. Faloon W. Startling findings about homocysteine. Life Extension Magazine®. 2003 Nov;9(11):11-6.

14. Bazzano LA, Reynolds K, Holder KN, He J. Effect of folic acid supplementation on risk of cardiovascular diseases: a meta-analysis of randomized controlled trials. JAMA. 2006 Dec 13;296(22):2720-6.

15. McCully KS. Chemical pathology of homocysteine. IV. Excitotoxicity, oxidative stress, endothelial dysfunction, and inflammation. Ann Clin Lab Sci. 2009 Summer;39(3):219-32.

16. Vizzardi E, Bonadei I, Zanini G, Fiorina C, Raddino R, Dei Cas L. Homocysteine: a casual link with heart failure? Minerva Med. 2009 Oct;100(5):421-7.

17. Park CS, Ihm SH, Yoo KD, et al. Relation between C-reactive protein, homocysteine levels, fibrinogen, and lipoprotein levels and leukocyte and platelet counts, and 10-year risk for cardiovascular disease among healthy adults in the USA. Am J Cardiol. 2010 May 1;105(9):1284-8.

18. Haynes WG. Hyperhomocysteinemia, vascular function and atherosclerosis: effects of vitamins. Cardiovasc Drugs Ther. 2002 Sep;16(5):391-9.

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.

24. Bellamy MF, McDowell IF, Ramsey MW, Brownlee M, Newcombe RG, Lewis MJ. Oral folate enhances endothelial function in hyperhomocysteinaemic subjects. Eur J Clin Invest. 1999 Aug;29(8):659-62.

25. Chambers JC, Obeid OA, Kooner JS. Physiological increments in plasma homocysteine induce vascular endothelial dysfunction in normal human subjects. Arterioscler Thromb Vasc Biol. 1999 Dec;19(12):2922-7.

26. Clarke R, Armitage J. Vitamin supplements and cardiovascular risk: review of the randomized trials of homocysteine-lowering vitamin supplements. Semin Thromb Hemost. 2000;26(3):341-8.

27. Krishnaswamy K, Lakshmi AV. Role of nutritional supplementation in reducing the levels of homocysteine. J Assoc Physicians India. 2002 May;50 Suppl:36-42.

28. Schwammenthal Y, Tanne D. Homocysteine, B-vitamin supplementation, and stroke prevention: from observational to interventional trials. Lancet Neurol. 2004 Aug;3(8):493-5.

29. Hirsch S, Pia De la Maza M, Yanez P, et al. Hyperhomocysteinemia and endothelial function in young subjects: effects of vitamin supplementation. Clin Cardiol. 2002 Nov;25(11):495-501.

30. Flicker L, Vasikaran SD, Thomas J, et al. Efficacy of B vitamins in lowering homocysteine in older men: maximal effects for those with B12 deficiency and hyperhomocysteinemia. Stroke. 2006 Feb;37(2):547-9.

31. Lim HS, Heo YR. Plasma total homocysteine, folate, and vitamin B12 status in Korean adults. J Nutr Sci Vitaminol (Tokyo). 2002 Aug;48(4):290-7.

32. Yajnik CS, Lubree HG, Thuse NV, et al. Oral vitamin B12 supplementation reduces plasma total homocysteine concentration in women in India. Asia Pac J Clin Nutr. 2007;16(1):103-9.

33. Chiu YW, Chang JM, Hwang SJ, Tsai JC, Chen HC. Pharmacological dose of vitamin B12 is as effective as low-dose folinic acid in correcting hyperhomocysteinemia of hemodialysis patients. Ren Fail. 2009;31(4):278-83.

34. Azadibakhsh N, Hosseini RS, Atabak S, Nateghiyan N, Golestan B, Rad AH. Efficacy of folate and vitamin B12 in lowering homocysteine concentrations in hemodialysis patients. Saudi J Kidney Dis Transpl. 2009 Sep;20(5):779-88.