
Now this is some serious stuff! Most of you medicos will understand that vitamins are antioxidants which help the cell fight against cancer. They do this by donating ions to free radicals to curb the production of reactive oxygen species and thus reducing oxidative stress. What this means is that they help us fight cancer in the body.Thats what we know, but this research is proving that they infact cause more harm than the good we have always associated them with...
Read and drop your comments... Many people take vitamins such
as A, E, and C thinking that their antioxidant properties will ward off
cancer. But some clinical trials have suggested that such antioxidants,
which sop up DNA-damaging molecules called free radicals, have the
opposite effect and raise cancer risk in certain people. Now, in a
provocative study that raises unsettling questions about the widespread
use of vitamin supplements, Swedish researchers have showed that
moderate doses of two widely used antioxidants spur the growth of early
lung tumors in mice.
Some cancer specialists caution against basing public health advice on the study,
published online this week in Science Translational Medicine.
“You can’t extrapolate from this study to make a recommendation to
people,” says Barry Kramer, director of the Division of Cancer
Prevention at the National Cancer Institute in Bethesda, Maryland. He
notes that the science of antioxidants is complicated and that the
results of mice studies often don’t apply to humans. Still, Kramer and
others say the new findings demand further exploration.
The observation decades ago that people who consumed lots of fruits
and vegetables had less cancer suggested that the antioxidants in these
foods might be protecting them. But in the 1980s, researchers launched
two large clinical trials to test whether the antioxidants β carotene (a
vitamin A precursor), vitamin A, and vitamin E protect smokers from
lung cancer—and found more cases of lung cancer in volunteers taking β
carotene, leading one trial to end early. A more recent trial testing
vitamin E and selenium to prevent prostate cancer was stopped when
prostate cancer turned out to be more common in the vitamin E group.
The Swedish researchers, led by Per Lindahl and Martin Bergö of the
University of Gothenburg, studied two antioxidants: n-acetylcysteine
(NAC), a water-soluble drug used to thin mucus in people with lung
disease, and fat-soluble vitamin E. They gave mice genetically
engineered to develop lung tumors a dose of NAC comparable to what a
patient would receive or chow containing about 10 times more vitamin E
than is in ordinary mouse food. “A lot of vitamin pills contain a lot
more than that. It’s a conservative dose,” Bergö says.
Compared with mice on a normal diet, the mice consuming the
antioxidants developed more lung tumors, their tumors were more
aggressive, and they lived only half as long. Follow-up studies
suggested that by reducing reactive oxidative species and DNA damage in
the cell, the antioxidants turn down a gene,
p53, that is key to keeping cell growth in check and is often inactivated in cancer. For example,
p53’s
protein stops the cell cycle so enzymes can repair damaged DNA and
triggers apoptosis, or self-destruction, in severely damaged cells. In
cancer cells in which
p53 had been turned off, Lindahl and Bergö found, the antioxidants had no effect on cell proliferation.
The implication, Bergö suggests, is that people at high risk of
cancer—such as smokers—and others who have incipient tumors should avoid
taking extra antioxidants. “In a normal cell an antioxidant might be
very good. But if you have a small tumor that might become a cancer, it
will reduce
p53 and the tumor will grow,” Bergö says.
A clinical researcher involved with the aborted trials that tested
antioxidants to prevent lung and prostate cancersays he is “thrilled” by
the study. “It’s the first paper I’ve seen that goes into some of the
molecular biology to explain what we saw,” says medical oncologist Gary
Goodman of the Swedish Cancer Institute in Seattle, Washington. “This
really shows that high doses of vitamins can be harmful.”
Others are more restrained. “It’s a provocative study,” says cancer
biologist David Tuveson of Cold Spring Harbor Laboratory in New York.
“Perhaps we should look more carefully at what’s available over the
counter.” But he would like to see a more detailed explanation of how
the cell’s sensing of reactive species controls
p53 activity.
Lung disease researcher Shyam Biswal of Johns Hopkins University in
Baltimore, Maryland, wonders if the results would be the same in mice
with cancer sparked by a carcinogen, rather than an existing mutation.
“The model is great, but it’s a very aggressive model,” Biswal says.
Another huge caveat, Kramer adds, is that in the earlier lung cancer
prevention trials, only the participants taking β carotene had a higher
risk of lung cancer, not those on vitamin E alone. “It’s not likely that
all antioxidants are exactly the same,” he says. He and others also
emphasize that the study does not suggest that people should eat less
fruit and vegetables, which provide smaller doses of antioxidants and
likely have other benefits.
Bergö and Lindahl now plan to extend their mouse studies to tests of β
carotene and vitamin C and to other cancer types. They also plan to
comb through medical records in Sweden to see if lung disease patients
receiving NAC are at higher risk for lung cancer.