Low peak bone mass is a risk factor for the development of postmenopausal osteoporosis in women. Conceivably, the increased calcium demands of pregnancy and lactation could adversely affect peak bone mass. Studies of changes in bone mass during human pregnancy and lactation have shown no permanent deleterious effect, but most of the subjects have been mature women. Thus, the question remains whether or not bone mineral would recover if the demands of reproduction were imposed during adolescence when deposition of bone is accelerated. As the opportunity to study reproductive teenagers is severely restricted, we used macaques as a model. We followed through first pregnancy and lactation 125 young female macaques and 13 nonreproductive controls to examine the effects of early reproduction on bone mass. The average age was 4.0 years (human equivalent age = 12 years); the animals were sexually mature but had not yet completed growth. Using several methods (DEXA, histolog y an d biochemical assays), we identied and measured the bone lost and gained during reproduction. The animals gained total bone mineral during pregnancy, but during the first 3 months of lactation they lost somewhat over 3%, similar to bone loss reported for lactating women. The bone loss occurred in both compact and cancellous bone, including that of the vertebrae, which is a prime site for osteoporosis in postmenopausal women. However, the bone lost during reproduction had been restored by 3 months after weaning (6 months postpartum). Thus, the females slowed their rates of growth during reproduction, but experienced """"""""catch-up"""""""" growth after weaning. We were therefore unable to document any permanent loss of bone mineral in the adolescent reproductive macaque. The possible effects of multiple, closely spaced reproductive events at young ages were not studied. FUNDING NIH grants RR00166 and AR40813.
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