Richard Bruno

Vitamin E and Oxidative Stress

An Interview with Richard Bruno, Ph.D.
LPI Research Associate

Q: What have you been investigating?

A: The project I have been working on for the last couple of years has been the relationship between oxidative stress, in the form of cigarette smoking, on vitamin E utilization in smokers. For all of our studies, we recruited otherwise healthy smokers and nonsmokers and supplemented them with deuterium-labeled vitamin E.

Q: What’s deuterium?

A: Deuterium is an isotope of hydrogen, but it is not radioactive. Our deuterium-labeled vitamin E functions identically to the vitamin E you can buy in any health-food store, but because of the isotope it serves as a tracer of vitamin E in the circulation, so we can distinguish it in the blood from vitamin E you get in the diet. We supplemented these individuals with deuterated vitamin E and measured how quickly it disappeared from the blood. What we found was very exciting. For the first time ever in humans, we showed that oxidative stress—cigarette smoking in this case—causes vitamin E to disappear more quickly from the blood. So this means that smokers have higher requirements for vitamin E than nonsmokers. We also found that vitamin E in smokers disappeared even faster when vitamin C was low in the blood. So it is not only important that smokers get enough vitamin E, but they should also be conscious of the amount of vitamin C they consume!

Q: Is the faster disappearance of vitamin E in the smokers due to their increased oxidative stress?

A: Yes. We know this because we found increased oxidized fat. We also measured the amount of vitamin E that was metabolized and excreted in the urine. We found that it was lower in smokers compared to nonsmokers. So this means that vitamin E was disappearing by oxidation, not by metabolism.

Q: Vitamin E supplementation in smokers decreases their oxidative stress, but would vitamin E overcome the huge health risk caused by smoking?

A: Our studies weren’t designed to make healthier smokers, but rather to understand the impact of oxidative stress on vitamin E utilization. Cigarette smoking provides a good model to study this. Despite the recommendation to smokers to quit smoking, the prevalence of smoking in the United States in the last decade has not declined substantially.

Q: Qualitatively, is there any difference between the oxidative stress that runners might experience and that produced by smoking cigarettes?

A: One of the markers of oxidative stress that we analyzed in plasma was F2-isoprostanes, which are formed by the free radical oxidation of arachidonic acid, a fatty acid used in the biosynthesis of prostaglandins. We noticed that the levels of F2-isoprostanes in smokers were similar to those seen in ultramarathon runners who run 30-mile races. The difference is that increases in F2-isoprostanes in runners are transient, whereas smokers’ levels are chronically elevated. Also, runners may be healthier because their bodies learn how to cope with oxidative stress and remove damaged molecules. In contrast, smokers continuously expose themselves to high levels of radicals and have weakened defense mechanisms.

Q: Would long-term oxidative stress be expected to result in DNA damage or other harmful effects related to specific diseases?

A: Absolutely. Smoking is a huge risk factor for cancer and heart disease. We recently demonstrated, through a collaboration with Dr. Emily Ho, that smokers have a greater number of micronuclei in their red blood cells. Micronuclei are markers of damage that may serve as a mutagenic risk factor.

Q: Was DNA damage observed in marathon runners as well?

A: Dr. Angela Mastaloudis of LPI found that DNA damage in ultramarathon runners was also elevated, but disappeared by two hours after the race. Again, damage didn’t remain elevated chronically.

Q: What do you want to investigate next?

A: Our next experiment is an expansion of our earlier work on the interaction between vitamin C and vitamin E. We’re going to supplement smokers and nonsmokers with vitamin C for a few weeks to increase their vitamin C levels and then repeat the earlier study and see if vitamin C, because of its antioxidant properties, can slow the disappearance of vitamin E.

Q: When do you expect to complete that study?

A: Any day now!

Vitamin E and the Common Cold?

A recent study published in the Journal of the American Medical Association found that daily supplementation with vitamin E significantly decreased the number of colds among elderly residents of nursing homes. Researchers at Tufts University, Boston University, and the University of Sydney reported that daily supplementation with 200 IU of synthetic vitamin E resulted in about a 20% decrease in the incidence of colds compared to the incidence in subjects taking a placebo. In the randomized, double-blind, placebo-controlled trial, 451 residents at least 65-years old in 33 long-term care facilities in the Boston area were followed for about one year. Vitamin E supplements had no effect on the incidence of lower respiratory tract infections. Other human studies on vitamin E and infections have had mixed results, although studies in old mice have found some protection by vitamin E against viral but not bacterial infections. It will be interesting to see if additional positive studies are reported in the future.

In his 1970 book, Vitamin C and the Common Cold, Linus Pauling proposed that vitamin C has value against the cold. A meta-analysis by a Finnish investigator of the 21 placebo-controlled studies on the common cold and vitamin C between 1971 and 1994 that used at least 1 gram per day found that vitamin C supplements shortened the duration of colds by about 25% and ameliorated symptoms, although there was no consistent effect on incidence. Perhaps the consumption of both vitamin E and vitamin C supplements may be the most effective strategy.

Last updated November 2004


Micronutrient Research for Optimum Health

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