Effect of zinc supplementation on serum testosterone level in adult male sickle cell anemia subjects

Prasad, Ananda S.; Abbasi, Ali; Rabbani, Parviz; DuMouchelle, Elizabeth

doi:10.1002/ajh.2830100203

Cited by 81 publications

(28 citation statements)

References 13 publications

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“…In contrast to the present study, previous trials which reported an increase of testosterone levels after zinc supplementation were conducted with zinc-deficient subjects: in pathological conditions, in which the zinc status is often poor, such as uraemia/haemodialysis (Antoniou et al, 1977;Mahajan et al, 1982), growth retardation (GhavamiMaibodi et al, 1983), sickle-cell anaemia (Prasad et al, 1981) or infertility (Netter et al, 1981;Favier, 1992), it was shown that administration of the trace element caused a reversal of previously lowered testosterone concentrations. Kilic et al (2006) reported that supplementation of zinc reversed reduced serum testosterone levels caused by exhaustion exercise.…”

Section: Discussioncontrasting

confidence: 94%

Serum testosterone and urinary excretion of steroid hormone metabolites after administration of a high-dose zinc supplement

et al. 2007

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Objectives: To investigate whether the administration of the zinc-containing nutritional supplement ZMA causes an increase of serum testosterone levels, which is an often claimed effect in advertising for such products; to monitor the urinary excretion of testosterone and selected steroid hormone metabolites to detect potential changes in the excretion patterns of ZMA users. Subjects: Fourteen healthy, regularly exercising men aged 22-33 years with a baseline zinc intake between 11.9 and 23.2 mg day À1 prior to the study. Results: Supplementation of ZMA significantly increased serum zinc (P ¼ 0.031) and urinary zinc excretion (P ¼ 0.035). Urinary pH (P ¼ 0.011) and urine flow (P ¼ 0.045) were also elevated in the subjects using ZMA. No significant changes in serum total and serum free testosterone were observed in response to ZMA use. Also, the urinary excretion pattern of testosterone metabolites was not significantly altered in ZMA users. Conclusions: The present data suggest that the use of ZMA has no significant effects regarding serum testosterone levels and the metabolism of testosterone in subjects who consume a zinc-sufficient diet.

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Section: Discussioncontrasting

confidence: 94%

Serum testosterone and urinary excretion of steroid hormone metabolites after administration of a high-dose zinc supplement

et al. 2007

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“…Hyperzincuria was noted in both Hb H dis ease and /Hha!assemia/Hb E disease. This is similar to that in sickle cell anemia [4,10,13). The hyperzincuria leading to zinc defi ciency in such cases seems to occur from chronic hemolysis.…”

Section: Discussionsupporting

confidence: 58%

Zinc and Copper Status in Hemoglobin H Disease and β-Thalassemia/Hemoglobin E Disease

S¹,

Pringsulka²,

Kritalugsana³

et al. 1982

Acta Haematol

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The plasma zinc and copper and urinary zinc levels were determined by an atomic absorption spectrophotometer technic in 14 patients with hemoglobin (Hb) H disease, 34 patients with β-thalassemia/Hb E disease and 30 control subjects. Plasma zinc levels were lower and the plasma copper levels were higher in the patients than in controls. The plasma Cu:Zn ratios, a more valuable indicator of body zinc status, increased in the diseased subjects, indicating zinc deficiency. Higher urinary zinc levels in the both Hb H disease and β-thalassemia/Hb E disease suggest that chronic hemolysis is responsible for hyperzin-curia leading to zinc deficiency. The thalassemic patients with undergrowth had higher plasma Cu:Zn ratios than the patients with normal development, indicating a more severe zinc deficiency in the former.

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“…Normal plasma [114,115] and erythrocyte [(lOO, 111,114)] zinc levels in sickle cell disease have also been described, but these results are questionable because of the likelihood of spuriously high plasma zinc levels secondary to hemolysis. More recently, Prasad and co-workers have advocated the use of neutrophil zinc, a measurement that they report as being more accurate than plasma zinc, and more sensitive to recent changes in body stores than erythrocyte zinc [ 102,106,108].…”

Section: Mineralsmentioning

confidence: 99%

Nutrition and sickle cell disease

1987

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The role of protein and calorie deficiency in sickle cell disease remains poorly defined. While such features as growth retardation, impaired immune function, and delayed menarche do suggest a relationship between sickle cell disease and undernutrition, measurement of more direct nutritional parameters in these patients have yielded mixed results. Anthropometric measurements such as skinfold thickness are subnormal in many but not all reports. Serum protein levels are normal, but low values for serum lipids have been reported. Finally, one small study shows an improvement in both growth parameters and clinical course following caloric supplementation. A variety of micronutrient deficiencies have been suggested in sickle cell disease. Numerous case reports describing an exacerbation of the chronic anemia that was reversed by folic acid therapy led to routine folate supplementation. More recent studies have shown, however, that clinically significant folic acid deficiency occurs only in a small minority of sickle cell patients. Clearly, more work is necessary to define the cost/benefit ratio of routine folic acid supplementation. Pharmacological amounts of vitamin B6 and certain of its derivatives possess in vitro antisickling activities. Nevertheless, a small clinical trial failed to demonstrate any consistent hematologic effects of B6 supplementation. Several reports indicate that vitamin E levels are low in sickle erythrocytes. Since these abnormal red cells both generate excessive oxidation products and are more sensitive to oxidant stress, and because oxidants appear to play a role in ISC formation, vitamin E deficiency could well be linked to ISC formation and hemolysis. Small clinical trials, however, have again failed to produce a clear hematological response in sickle cell anemia. The role of zinc in sickle cell disease has received considerable attention. Though studies are generally small, most do support a relationship between sickle cell disease and zinc deficiency. Etiologic associations between zinc deficiency and such complications of sickle cell disease as poor ulcer healing, growth retardation, delays in sexual development, immune deficiencies, and high ISC counts have all been suggested. Most of these studies need further corroboration. Iron deficiency is now known to be a relatively common occurrence in sickle cell anemia, especially in children and pregnant women. The theoretical benefits of concomitant iron deficiency and sickle cell anemia remain to be proven in a controlled clinical trial.(ABSTRACT TRUNCATED AT 400 WORDS)

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Effect of zinc supplementation on serum testosterone level in adult male sickle cell anemia subjects

Cited by 81 publications

References 13 publications

Serum testosterone and urinary excretion of steroid hormone metabolites after administration of a high-dose zinc supplement

Serum testosterone and urinary excretion of steroid hormone metabolites after administration of a high-dose zinc supplement

Zinc and Copper Status in Hemoglobin H Disease and β-Thalassemia/Hemoglobin E Disease

Nutrition and sickle cell disease

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