Identification of the andrological variables most sensitive to zinc depletion would expedite the diagnosis of male reproductive pathology induced by zinc deficiency. Eleven volunteers living on a metabolic ward were fed a diet composed of a mixture of a semisynthetic formula and conventional foods supplemented with ZnSO4 to supply a total of 1.4, 2.5, 3.4, 4.4, or 10.4 mg Zn/d. After an equilibration period of 28 d (10.4 mg Zn/d), all treatments were presented for 35 d each, the first four in random order and the fifth last. Compared with when they were consuming 10.4 mg Zn/d, volunteers consuming 1.4 mg Zn/d exhibited decreased semen volumes (3.30 vs 2.24 mL) and serum testosterone concentrations (26.9 vs 21.9 nmol/L), and no change in seminal zinc concentrations. Compared with 10.4 mg Zn/d, treatments of 1.4, 2.5, and 3.4 mg Zn/d decreased the total semen zinc loss per ejaculate (6.29 vs 3.81, 4.68, and 5.03 mumols/ejaculate). Seminal loss accounted for 9% of total body zinc loss when 1.4 mg Zn/d was consumed. Seminal phosphorus concentrations were elevated during all four phases of zinc depletion (28.4 vs 32.9, 31.0, 34.2, and 33.6 mmol/L). The findings suggest that serum testosterone concentrations, seminal volume, and total seminal zinc loss per ejaculate are sensitive to short-term zinc depletion in young men.

Findings from animal studies indicate that dietary boron affects several aspects of mineral metabolism, especially when animals are subjected to nutritional stressors. Eleven postmenopausal volunteers living on a metabolic ward for 167 d (one 23-d equilibration period and six 24-d treatment periods) were fed a conventional basal diet that supplied a daily average intake of 0.36 mg B, 109 mg Mg, and < 0.10 mg A1/8400 kJ. They were given supplements of 0 (BB) or 3 mg B (SB, last two periods only), 0 (BMg) or 200 mg Mg (SMg) (with magnesium supplements held constant during the last two periods), or 0 (BAl) or 1000 mg A1 (SAl)/d. The SB treatment, compared with the BB treatment, provided a 9.0-fold increase in dietary boron but yielded only a 1.5-fold increase in plasma boron concentrations. Regardless of boron dietary treatment, fecal plus urinary excretion of boron accounted for nearly 100% of dietary boron intake with no evidence of boron accumulation over time. Lack of boron accumulation and relatively small changes in blood boron values during a substantial increase in dietary boron support the concept of boron homeostasis. In subjects fed BMg, SB decreased the percentage of dietary calcium lost in the urine but increased that percentage in volunteers fed SMg, a relation that may be important in understanding metabolic mineral disorders that perturb calcium balance. Reduced calcium absorption during SAl suggests that aluminum supplementation should be limited or at least monitored in postmenopausal women prone to excessive calcium loss. Decreased total urinary oxalate during SB in BMg subjects indicates a possible role for boron in the control of urolithiasis during low-magnesium nutriture.