|« Deep Vein Thrombosis, Factor V Leiden and Blood Groups||Osteoporosis and Blood Type »|
The consequences of severe human zinc deficiency have been known since the 1960s, but only more recently have the effects of milder degrees of zinc deficiency, which are highly prevalent, been recognized. Trials have shown that zinc supplementation results in improved growth in children, lower rates of diarrhoea, malaria, and pneumonia, and reduced child mortality. In total about 800 000 child deaths per year are attributable to zinc deficiency (1).
It has been shown that in people with zinc deficiency, activity of serum thymulin (a thymus specific hormone involved in T cell function) is decreased, an imbalance between T helper cell (Th1) and Th2 function develops, and lytic activity of natural killer cells (destructive action on enemy cells) is decreased (2).
Zinc has been used effectively to treat Wilson's disease, hepatic encephalopathy, sickle cell disease, and the common cold. Zinc is an essential part of metalloproteins and transcription factors involved in gene expression of various proteins. Zinc activates nuclear factor-kappa B in T helper cells and in zinc deficiency binding of nuclear factor-kappa B to DNA is decreased, leading to decreased gene expression of interleukin 2 and its production (2).
Zinc deficiency commonly coexists with other micronutrient deficiencies including iron, making single supplements inappropriate. Authors of a paper in the British Medical Journal now suggest: "Until the results of trials of multiple micronutrient interventions are available, zinc supplements should be given to children with infections" (3).
As zinc is essential in the activation of the enzyme intestinal alkaline phosphatase (IAP) as demonstrated in the IAP of calves (4), it is particularly important for ABH salivary non-secretors to maintain adequate zinc levels due to their lower levels of IAP (5).
If taken in doses greater than 15 mg per day, zinc supplementation should be supervised by a physician.
1. BLACK, R.
Micronutrient deficiency: an underlying cause of morbidity and mortality.
Bull World Health Organ. [online]. 2003, vol.81, no.2, p.79-79.
Available from: . ISSN 0042-9686.
2. Prasad AS.
BMJ. 2003 Feb 22;326(7386):409-10.
3. Shrimpton R, Gross R, Darnton-Hill I, Young M
Zinc deficiency: what are the most appropriate interventions?
BMJ, Feb 2005; 330: 347 - 349.
4. Yan S, Liu Y, Tian X, Zhang Y, Zhou H.
Effect of extraneous zinc on calf intestinal alkaline phosphatase.
Protein Chem. 2003 May;22(4):371-5.
5. Matsushita M, Irino T, Stigbrand T, Nakajima T, Komoda T.
Changes in intestinal alkaline phosphatase isoforms in healthy subjects bearing the blood group secretor and non-secretor.
Clin Chim Acta. 1998 Sep 14;277(1):13-24.
No feedback yet
Comments are not allowed from anonymous visitors.