CENTER ON BEHAVIORAL MEDICINE
BODY- MIND CONNECTION
Essential Nutrients-Behavior: Related Paper
graciously given by the author to reproduce this paper
Zinc Deficiency and Behavioral
William J. Walsh
Most Americans receive all the zinc they need if they have a reasonably well-balanced diet involving the major food groups. However, many persons are born with a metal-metabolism disorder which results in zinc depletion regardless of diet.
Zinc is a component of more than 80 enzymes. High concentrations have been found in brain hippocampus, and many medical researchers believe that zinc is a neurotransmitter. Low zinc levels at these sites could reduce the inhibition of neuron activity, thus leading to abnormal behavior. The discovery of zinc "finger proteins" in the past decade has led to a vastly improved understanding of how cells replicate and divide. There role in behavior is not yet clear, but could be involved in the transport or availability of zinc. Recent research has shown zinc to be far more important than previously believed and low levels of zinc are associated with behavior disorders.
Many of the patients of the Carl Pfeiffer Treatment Center suffer from behavior disorders. The most common ones are attention deficit hyperactive disorder (ADHD), oppositional defiant disorder (ODD), obsessive compulsive disorder (OCD), and conduct disorder (CD). These patients typically have a history of extensive counseling and multiple medications and many have experienced residential care. They represent a narrow and rather uncharacteristic segment of the general population.
A high percentage of behavior
persons exhibit abnormal levels of copper, zinc, lead, cadmium,
magnesium and manganese in blood, urine, and tissues, based on chemical
analysis results from thousands of patients. With regard to zinc, this
condition appears to involve a malfunction of the metal-binding protein
metallothionein. Most of these patients have symptoms of zinc
along with depressed levels of zinc in their blood plasma.
The two principal factors which lead our Center's physicians to a diagnosis of zinc deficiency are: 1) depressed plasma zinc, and 2) presence of clinical symptoms of zinc depletion which are alleviated by zinc supplementation2, 3, 4, 5, 6, and 7. Since zinc tolerance tests show plasma levels to be affected for 6 hours following zinc supplementation8 and 9, zinc supplements are avoided for 24 hours prior to sampling of plasma.
The clinical symptoms associated with zinc deficiency or depletion include the following:
* Eczema, acne, and/or
12, 13, and 14,
A "working diagnosis" of zinc deficiency can be made if clinical symptoms of zinc deficiency are clearly evident from the initial physical examination and medical history. Usually more than one or the above symptoms are present in zinc deficiency. This initial diagnosis is later supported or negated by laboratory analysis for plasma zinc along with observed response (or non-response) to zinc supplementation.
The Carl Pfeiffer Treatment
retests plasma zinc and evaluates symptoms after 4-6 months of
to determine if dosages need adjustment.
Zinc depletion is corrected by
with zinc (picolinate or gluconate) along with augmenting nutrients
L-cysteine, pyridoxine, ascorbic acid, and vitamin E. Manganese is also
useful in promoting proper metallothionein function. If copper levels
elevated, effective treatment must also enhance the release of copper
tissues and copper excretion. L-cysteine helps mobilize and excrete
while enhancing zinc absorption. Correction of zinc deficiency is best
accomplished under the care of a physician or nutritionist who is
in metal metabolism disorders. Indiscriminant dosages of zinc to
who do not need it can cause anemia and imbalanced trace metals.
The Center involves the collaboration of biochemists and medical doctors. We believe that this coupling of disciplines provides an ideal capability for biochemical evaluation and medical treatment.
1. Walsh, W.J., Isaacson, H.R., Rahman, F., Hall, A., and Young, I.J., "Elevated blood copper:zinc ratios in assaultive young males", Neuroscience Annual Meeting, Abstract of Papers, Miami Beach, 1994 (In Print).
2. Cunnane, S.C., Zinc: Clinical and Biochemical Significance, CRC Press, Inc., Boca Raton, FL (1988).
3. Prasad, A.S., "Deficiency of
man and its toxicity", in Trace Elements in Human Health and Disease,
1, Academic Press, New York, 1976.
5. Smith, J.C., Holbrook, J.T., and Danford, D.E., "Analysis and evaluation of zinc and copper in human plasma and serum", J. Amer. College of Nutr., 4:627-638 (1985).
6. Kleimola, V., et al, "The zinc, copper, and iron status in children with chronic diseases", in Trace Element Analytical Chemistry in Medicine and Biology, Walter de Gruyter, New York (1983).
7. Reding, P., DuChateau, J., and Bataille, C., "Oral zinc supplementation improves hepatic encephalopathy", Lancet, ii, 493 (1984).
8. Pohit, J., Saha, K.C., and Pal, B., "A zinc tolerance test", Clin. Chim. Acta, 114: 279 (1981).
9. Pecoud, A., Donzel, P., and Schelling, J.L., "Effects of foodstuffs on the absorption of zinc sulphate", Clin. Pharmacol. Ther., 17, 469 (1975).
10. Molokhia, M.M. and Portnoy, B., "Zinc and copper in dermatology", in Zinc and Copper in Medicine, Charles C. Thomas, Springfield, IL (1980).
11. Schmidt, K., et.al., "Determination of trace element concentrations in psoriatic and non-psoriatic scales with special attention to zinc", in Trace Element Analytical Chemistry in Medicine and Biology, Vol. 1, Walter de Gruyter, New York (1980).
12. McMillan, E.M., and Rowe, D., "Plasma zinc in psoriasis. Relation to surface area involvement", Br. J. Dermatol., 108, 301 (1983).
13. Ecker, R.J. and Schroeder, A.L., "Acrodermatitis and acquired zinc deficiency", Arch. Dermatol., 114: 937 (1978).
14. Withers, A.F., Baker, H., and Musa, M, "Plasma zinc in psoriasis", Lancet, ii: 278 (1968).
15. Van Rij, A.M., "Zinc supplements in surgery", in Zinc and Copper in Medicine, Charles C. Thomas, Springfield, IL (1982).
16. Henzel, J.H., et al., "Zinc concentrations within healing wounds: significance of post-operative zincuria on availability and requirements during tissue repair", Arch. Surg., 349: 357 (1970).
17. Weismann, K., "Lines of Beau: Possible markers of zinc deficiency", Acta Dermatol. Venereol., 57: 88 (1977).
18. Collipp, P.J., et al., "Zinc deficiency: Improvement in growth and growth hormone levels with oral zinc therapy", Ann. Nutr. Metab., 26: 287 (1982).
19. Hambridge, K.M., and Walravens, P.A., "Zinc deficiency in infants and preadolescent children", in Trace Elements in Human Health and Disease, Vol. 1, Prasad, A.S. and Oberleas, D., Eds., Academic Press, New York (1976).
20. Golden, B.E. and Golden, M.H.N., "Effect of zinc supplementation on the dietary intake, rate of weight gain and energy cost of tissue deposition in children recovering from severe malnutrition", Am. J. Clin. Nutr., 34: 900 (1981).
21. Laditan, A.O. and Ette, S.I., "Plasma zinc and copper during the acute phase of protein-energy malnutrition (PEM) and after recovery", Trop. Geogr. Med., 34: 77 (1982).
22. Sandstead, H.H., Prasad, A.S., et al., "Human zinc deficiency, endocrine manifestations, and response to treatment", Amer. J. Clin. Nutr., 20:422 (1967).
23. Heinkin, R.I., and Bradley, D.F., "Hypogeusia corrected by nickel and zinc", Life Sci., 9: 701 (1970).24. Sprenger, K.B.G. et al., "Improvement of uremic neuropathy and hypogeusia by dialysate zinc supplementation: a double-blind study", Kidney Int., Suppl. 16: 5315 (1983).
25. Cunningham-Rundles, C., et al., "Zinc deficiency, depressed thymic hormones and T-lymphocyte dysfunction in patients with hypogammaglobulinemia", Clin. Immunol. Immunopathol., 21: 387 (1981).
26. Good, R.A., et al., "Zinc and
in Clinical, Biochemical, and Nutritional Aspects of Trace Elements,
A.S. Ed., Alan R. Liss, New York (1982).