Zinc deficiency in humans was first reported in 1963 with symptoms of dwarfism, hypogonadism and anorexia(loss of appetite). Decreased appetite is said to be the first sign of zinc deficiency. Zinc supplementation rapidly restores the intake of zinc deficient mice to normal.
In one study half of all anorexia nervosa patients were found to be zinc deficient and zinc supplementation improved their weight gain. In another study supplementation with 14 mg. of zinc gluconate doubled the rate of increase in body weight of patients as compared to people who did not receive zinc supplementation.
Thiamine deficiency produces a specific and intense loss of appetite in animals.
Dietary levels of tyrosine and tryptophan can change the amounts of norepinephrine and serotonin in the central nervous system and change the state of hunger of a person. This may be because of an effect in the hypothalamus. Norepinephrine has a strong stimulating effect on food intake.
Leptin is a protein produced by the fatty tissue. Leptin regulates appetite and weight control through the hypothalamus. Leptin blood levels are reduced during zinc deficiency in humans.
CONCLUSION: In this article the authors carefully review the research previously done on the relationship between low zinc blood levels and loss of appetite. They conclude that zinc is intimately involved with anorexia (loss of appetite) in humans. In some cases supplementation with zinc stimulates the appetite.
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