Boron deprivation experiments with humans have yielded some persuasive
findings for the hypothesis that boron is an essential nutrient. in t
he first nutritional study with humans involving boron, 12 postmenopau
sal women first were fed a diet that provided 0.25 mg boron/2000 kcal
for 119 days. and then were fed the same diet with a boron supplement
of 3 mg boron/day for 48 days. The boron supplementation reduced the t
otal plasma concentration of calcium and the urinary excretions of cal
cium and magnesium, and elevated the serum concentrations of 17 beta-e
stradiol and testosterone. This study was followed by one in which fiv
e men over the age of 45, four postmenopausal women, and five postmeno
pausal women on estrogen therapy were fed a boron-low diet (0.23 mg/20
00 kcal) for 63 days, then fed the same diet supplemented with 3 mg bo
ron/day for 49 days. The diet was low in magnesium (115 mg/2000 kcal)
and marginally adequate in copper (1.6 mg/2000 kcal) throughout the st
udy. This experiment found higher erythrocyte superoxide dismutase, se
rum enzymatic ceruloplasmin, and plasma copper during boron repletion
than boron depletion. The design of the most recent experiment was the
same as the second study, except this time the diet was adequate in m
agnesium and copper. Estrogen therapy increased plasma copper and seru
m 17 beta-estradiol concentrations; the increases were depressed by bo
ron deprivation. Estrogen ingestion also increased serum immunoreactiv
e ceruloplasmin and erythrocyte superoxide dismutase; these variables
also were higher during boron repletion than depletion for all subject
s, not just those ingesting estrogen. Dietary boron had no effect on t
hose variables in the men and women not ingesting estrogen. These find
ings suggest that boron can both enhance and mimic some effects of est
rogen ingestion. The findings from ail three studies are consistent wi
th the hypothesis that boron has an essential function that affects ma
cromineral and cellular metabolism at the membrane level.