By Stephen T. Sinatra, M.D., F.A.C.C., F.A.C.N., C.N.S., C.B.T.
Myth: Megadoses of vitamin E are good for your heart.
Fact: Megadoses of vitamin E are risky.
My Recommendation: Less vitamin E is better than more, best taken as part of a mixed tocopherol combination that includes gamma.
During the 1990s, vitamin E was widely recognized as important for heart health. The recognition even extended to mainstream medicine, and the American Heart Association, not exactly vitamin-loving domains. In 1996, for instance, Vitamin E was celebrated in a well-publicized study for significantly reducing cardiovascular events over the course of one year among some 2,000 patients with documented heart disease.
The successes and reputation of vitamin E prompted many in the nutritional world to embrace the idea that if a little vitamin E was good than more would be even better. However, critical studies that followed began demonstrating that daily doses of vitamin E − 400 IUs and above − didn’t necessarily generate beneficial results, and, in fact, might be slightly on the detrimental side.
As early as 2003, I wrote in my Heart, Health and Nutrition newsletter about my reluctance to back high-dose vitamin E because of possible pro-oxidant effects emerging from the research. I received a lot of flack about that from readers who believed that more was better. I argued that vitamin E is a low-energy supplement (meaning it lacks the powerful electron-donor capabilities that nutrients such as CoQ10 offer), so more was not necessarily better.
One major statistical analysis from John Hopkins School of Medicine in 2005 concluded that the effects of vitamin E dosage of 400 IUs and over were suspect after a review of about ten earlier studies involving adults with chronic diseases. Such dosage, the researchers said, may actually increase all-cause mortality and should be avoided.
The negative findings were initially puzzling to nutritionally-minded clinicians like me who had been weaned on positive vitamin E news. To be sure, we believed that problems could come from using the synthetic form of vitamin E (designated dl-alpha tocopherol) instead of the natural form (designated d-alpha tocopherol). But a pro-oxidant effect from natural vitamin E? How could that be?
With time, clues began emerging. Major trials with vitamin E were using natural vitamin E alone. The negative results appeared related to using higher dosages and leaving out gamma tocopherol, a member of the vitamin E family of compounds naturally present in dietary vitamin E foods such as sunflower seeds, almonds, wheat germ, dried apricots, and olives. Gamma is not included though in the standard alpha tocopherol supplements.
The research was pointing to the gamma component as the reason for the major antioxidant benefit, such as neutralization of the peroxynitrite free radical that can damage cell membranes. Thus, people taking high-dose alpha tocopherol alone and not getting enough gamma in the diet or in supplement form, could run the risk of a pro-oxidant effect from vitamin E. Moreover, large doses of alpha tocopherol could also deplete the existing gamma in your system. This was why 800-1200 IUs of alpha alone might hurt rather than help.
The Vitamin E-HDL Connection
In 2011, a new study came along that shed more light on the vitamin E conundrum. In laboratory experiments, researchers in Belfast found that vitamin E (alpha and gamma tocopherol) protects very low-density lipoprotein (VLDL) and LDL cholesterol against oxidation. However, they found a “surprising” pro-oxidant effect on high-density lipoprotein (HDL), the cholesterol particle that acts like a garbage truck, picking up harmful oxidized LDL and transporting it back to the liver for removal. Low HDL is a serious risk factor for clogging the arteries. It’s also an unheralded agent in the body’s immune system. Anything that can hinder HDL is of real concern.
The new study provided a sharper image of the two faces of vitamin E: one showing a protective effect on VLDL and LDL and the other a negative effect on HDL.
Of additional interest, the researchers noted a previous study in which adding a small amount of vitamin C at the same time you take alpha tocopherol can help prevent the pro-oxidation effect of vitamin E on HDL. I already knew that CoQ10 protects vitamin E in the body and helps recycle it back to an active form after it is oxidized in biochemical reactions. So here’s another option, with vitamin C.
The Sinatra Solution
I’m a big fan of synergism, of nutrients working together, so my updated recommendation on vitamin E is this:
No vitamin E mega-dosing. No more than 100-200 IUs of alpha tocopherol for women and 200 for men, but best taken as part of a mixed tocopherol combination that includes gamma.
Even better is to take a broad spectrum vitamin E supplement, with the full family of tocopherols and powerful antioxidant tocotrienols, a vitamin E cousin of the tocopherols. That’s like a nature vitamin
In addition, make it a routine to include vitamin C (1,000 mg daily) and CoQ10 (at least 100 mg) into your supplement regimen. Those additions will protect the vitamin E you take and provide major benefits for you as well.
I’m a nutritional-oriented doctor who emphasizes eating smart and supplementing smart, and in the process I’m always evolving and learning. Taking supplements has to involve not just the right supplements to take but the right dosages as well. Too much of anything, no matter how good it is, can wind up being harmful. And that includes vitamins. If I learn that a certain supplement or a dosage of a supplement is either not beneficial or even harmful, I’m going to sound off about it. I regard that as my duty. I’m not a nutritional supplement ideologue.
- Nadeem N, Woodside AV, et al. The two faces of α- and γ-tocopherols: an in vitro and ex vivo investigation into VLDL, LDL and HDL oxidation. J Nutr Biochem, 2011; published online ahead of print. [Abstract.]
- Miller ER 3rd, Pastor Barriuso R, et al. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med. 2005;142(1):37-46. [Abstract.]
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