A deficiency of zinc fosters the development of cancer of the upper digestive tract in rats.
A lack of zinc increases inflammation and the release of the COX-2 enzyme. Zinc is needed for
healthy DNA activity, the creation of new healthy cells, and for the removal of damaged cells.
Researchers at Thomas Jefferson University in Philadelphia examined the effect of zinc on cancer
be cause zinc deficiency is widespread throughout the world and a lack of zinc contributes to
cancers of the digestive tract in humans.
Rats were placed on a zinc deficient diet or they were given supplemental zinc to replete their
zinc levels. Zinc deficiency lead to hyperplasia lesions and the release of the inflammation
causing COX-2 enzyme (hyperplasia lesion is an excessive growth of cells causing an injury or
wound). The COX-2 enzyme causes cell damage that leads to many cancers. This damage was 14.7
fold higher in the esophagus and tongue than in control rats. Giving zinc to the d3eficient rats
led to decreased cell proliferation (restored control of cell growth) within hours, and reduced
the level of the COX-2 enzyme to normal within 48 hours. Treatment with Celebrex or indomethacin
also reduced COX-2 over expression but not as well as zinc.
When zinc deficient rats were treated with a cancer causing chemical it caused lingual cancer
(cancer near or on the tongue) in 74% of these animals versus in only 22% of the animals with
normal zinc. 39% of the zinc deficient animals developed esophageal cancer, and a whopping 61%
of zinc deficient animals developed cancer of the fore stomach. The cancers were connected to
the COX-2 enzyme induced damage. None of the control animals developed either esophageal or fore
stomach cancer. According to the researchers zinc supplementation along with low doses of
carotenoids and COX-2 inhibitors may help prevent these cancers in high risk people and may be
of use in reversing oral leukoplakia (precancerous sores in the mouth). The study is published
in the January 5th edition of the Journal of the National Cancer Institute.
Restless Legs Syndrome in Kids Connected to Family Genes and a Lack of Iron
Restless legs syndrome (RLS) is a neurological condition where a person suffers unpleasant
sensations in then legs with an irresistible urge to move the limbs to relieve the discomfort.
The condition is especially evident at night leading to a poor nights sleep and daytime fatigue.
Researchers at the Mayo Clinic in Rochester, Minnesota, studied 32 children with RLS (6% of the
children examined in this study). 72% of these children had a parent with RLS (usually the mother).
87% of these children had trouble falling or staying asleep. These children tended to have low but
normal levels of iron. Iron is needed for the synthesis of dopamine in the brain, and dopamine is
needed for the control of movement. Dopamine deficiency due to a problem with iron may be the
cause of RLS. The researchers note that some children with ADHD have RLS. The study is published
in the December 2004 issue of the journal Annals of Neurology.
Commentary by Jerry Hickey, R.Ph.
On December 16th we report on a study from the journal Archives of Pediatrics and Adolescent
Medicine that 84% of the children with ADHD enrolled in this study had low iron levels. Additionally,
the lower the level of iron in these children, the worse were the symptoms of ADHD.
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