Smoking out the links between nutrition and oral cancer (press

release)
Friday, October 06, 2006 by: NaturalNews, citizen journalist

Every year, nearly 300,000 people worldwide are diagnosed with oral cancer. This type
of cancer has the highest incidence in people who use tobacco, including cigarettes, but
the means by which tobacco promotes the development of oral cancer is unknown.
Researchers at the Jean Mayer USDA Human Nutrition Research Center on Aging
(USDA HNRCA) at Tufts University are investigating whether nutritional factors may be
involved. A causal link has not been established, but their results provide early insights
into the complex relationships among oral cancer, smoking, and two groups of nutrients:
folates and select antioxidants.

Folate levels are different in smokers and non-smokers, according to Joel Mason, MD,
director of the USDA HNRCA's Vitamins and Carcinogenesis Laboratory and assistant
professor at the Friedman School of Nutrition Science and Policy at Tufts. Mason and
colleagues, who reported their results in the American Journal of Clinical Nutrition,
analyzed the diets and studied blood and cheek cells of 56 men and women between 30
and 80 years of age. Approximately half of these were chronic smokers, defined by a
history of smoking at least 10 cigarettes daily for at least the past year.

"Regardless of dietary intake, smokers had lower levels of folate in both blood and cheek
cells, compared with non-smokers," says Mason. These findings confirm those of
previous studies. Also consistent with previous research results, cheek cells of smokers
had significantly more genetic aberrations called micronuclei, which indicate increased
risk of oral cancer.

Mason notes that these observations raise the question, "does cigarette smoke promote
cancer by depleting cells of folate?" Folate is a B vitamin found in leafy green vegetables
and fortified foods that not only helps create and preserve cells, but is also critical for
synthesis of DNA; the latter serves as a universal set of blueprints for cells and which, if
sufficiently altered, often leads to cancer. "It's possible that diminishing folate in cells
may cause the cellular milieu to change, inducing the formation of cancerous cells," says
Mason.

"However, based on our findings," Mason says, "it does not appear that folate depletion
induced by smoking is a major avenue for the formation of the genetic aberrations
(micronuclei) that increase risk of oral cancer." He explains, "Oral micronuclei and low
oral folate are each linked with smoking, but they were not related to each other in this
study." Mason notes there are other possibly relevant pathways involving folate,
however, which were not examined in this study.

In addition to measuring total levels of folate, Mason and colleagues took their analysis a
step further. "Folate exists in several different forms, so we also measured the levels of
each form present in the cheek cells," corresponding author Jimmy Crott, PhD, scientist
in the Vitamins and Carcinogenesis Laboratory at the USDA HNRCA explains.
Compared to cheek cells of non-smokers, those of smokers had higher levels of some
forms and lower levels of others. Crott stresses that it is not known if the altered
distribution of various forms of folate contribute to carcinogenesis. "However," he
continues, "it is thought that imbalances in different forms of folate may partly explain
why low folate availability enhances cancer risk."

Overall, Mason says, "our observations do not support a mechanistic role for folate in
development of oral cancer. However, they do not exclude a potential protective role of
adequate folate intake or supplementation." He says that "additional studies are clearly
needed to elucidate mechanisms responsible for the observed shifts in folate form
distribution due to smoking."

In a study using the same participants, Elizabeth Johnson, PhD, scientist in the
Carotenoids and Health Laboratory at the USDA HNRCA and an assistant professor at
the Friedman School, and colleagues, conducted similar analyses looking at nutrients
such as carotenoids and vitamin E. Carotenoids, plant pigments found in fruits and
vegetables, and vitamin E, a fat-soluble vitamin found in nuts, seeds, and vegetable oils,
are both antioxidants, which protect cells from damage. Compared to non-smokers,
chronic cigarette smokers had lower levels of carotenoids, such as beta-carotene, in blood
and cheek cells.

As in the folate study, however, a direct nutrient-cancer link could not be established
because the carotenoid levels in the mouth did not correspond with the number of
micronuclei, or genetic aberrations, that indicate increased risk of cancer.

Johnson and colleagues also found that, in non-smokers, blood and cheek cell levels of
carotenoids were correlated. If levels were high in blood, they were also high in oral
tissue. This correlation was not found in smokers. Johnson points out that this difference
suggests that tobacco may alter the distribution of some nutrients. Further evidence is the
finding that smokers tended to have higher levels of a form of vitamin E common in
food, called gamma-tocopherol, compared with non-smokers. Levels of alpha-tocopherol,
the more easily absorbed form of vitamin E in the body, however, were lower in smokers
than in non-smokers. "We can only speculate," Johnson says, "but perhaps this is a
protective mechanism in which one form of the antioxidant vitamin goes up when
another goes down."

The authors note that epidemiologic observations show that smokers tend to eat diets
lower in fruits and vegetables than do non-smokers. However, in both the folate study
and the antioxidant study, differences detected in nutrient levels between smokers and
non-smokers were not attributable entirely to diet. "So," Johnson concludes, "although
our results do not support a direct role for these nutrients in oral carcinogenesis, we
uncovered some interesting relationships between smoking and nutrient distribution that
deserve further exploration."
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Finding a summary in article

There are some researchers to research into the complex relationship

among oral cancer, smoking, and two groups of nutrients (folates and select
antioxidants). Folate levels are different in smokers and non-smokers, and if
regardless of dietary intake, smokers had lower levels of folate in both blood
and cheek cells, compared with non-smokers. cheek cells of smokers had
significantly more genetic aberrations called micronuclei, which indicate
increased risk of oral cancer, compared to cheek cells of non-smokers, those
of smokers had higher levels of some forms and lower levels of others.
Folate is a B vitamin found in leafy green vegetables and fortified foods that
not only helps create and preserve cells, but is also critical for synthesis of
DNA; the latter serves as a universal set of blueprints for cells and which, if
sufficiently altered, often leads to cancer. It’s possible that diminishing
folate in cells may cause the cellular milieu to change, inducing the
formation of cancerous cells. Oral micronuclei and low oral folate are each
linked with smoking, but they were not related to each other, there are other
possibly relevant pathways involving folate. Folate exist in several different
forms. An imbalance in different forms of folate enhances cancer risk.
That epidemiologic observations show that smokers tend to eat diets
lowers in fruits and vegetables than do non-smokers. However, in both the
folate study and the antioxidant study, differences detected in nutrient levels
between smokers and non-smokers were not attributable entirely to diet. And
although our results do not support a direct role for these nutrients in oral
carcinogenesis.