We conducted this study to assess the prevalence of vitamin D insufficiency in a population of normal perimenopausal women, to examine the influence of sun exposure and vitamin D intake on the concentration of 25-hydroxyvitamin D (25OHD) and to examine the association between parathyroid hormone (PTH) and 25OHD. A total of 2016 healthy women aged 45±58, who had recently undergone a natural menopause, were enrolled over a 2´5-year period in the Danish Osteoporosis Prevention Study. A marked seasonal fluctuation of 25OHD was seen, with an abrupt rise in June and high values until October. The fluctuation could be related to number of hours of sunshine per month with a two months time lag. Dietary vitamin D intake, vitamin supplementation, sunlight exposure, and use of sun-bed were all significantly related to 25OHD concentrations. Sun exposure seemed to contribute the most. The overall prevalence of vitamin D deficiency (defined as serum 25OHD , 25 nmolal) was 7 %. However, in the subgroup avoiding direct sunshine and abstaining from vitamin D supplementation 32´8 % were vitamin D deficient in the winter±spring period. Although mean PTH was increased in the group with low serum 25OHD, PTH was not a sensitive marker of hypovitaminosis D in the individual, as only 16 % of those with vitamin D deficiency had PTH levels above normal range. Thus, we have shown, that healthy middle-aged Danish women are prone to vitamin D insufficiency in the winter±spring period, if they avoid sun exposure in the summer period and abstain from vitamin D supplementation.
1. The influence of pregnancy, lactation and weaning on bone mineral density in healthy women was investigated during a 2 year prospective study of 59 pregnant and lactating women from the 18th week of gestation. 2. Bone mineral density was measured by dual energy X-ray absorptiometry at the non-dominant radius ultra distally and more proximally in the 18th and 37th weeks of gestation, and 0, 3, 6, 12 and 18 months after delivery. Measurements of bone mineral density of the lumbar spine, the proximal femur and the whole body were performed at all dates after delivery. 3. Reappearance of menstruation after delivery averaged 6.1 months; mean lactating period was 8.7 months. During pregnancy and lactation bone mineral density tended to decrease, but different measuring sites showed different patterns of bone mineral density changes. The reduction in the ultra distal radius during pregnancy amounted to 2%, and no further changes were observed here during lactation. After delivery, reduction in mean bone mineral density was most pronounced in the spine (5.2% in 3 months), but the fall in bone mass tended to revert after resumption of menstruation. Bone mineral density was still reduced by 3.3% after 12 months in women with menstruation resumption later than 8 months after delivery. No significant reduction was observed 18 months after delivery. No association with calcium intake, weight changes or initial bone mineral density was observed. High calcium intake did not protect against bone mineral loss in the spine and the femur. 4. Thus it can be concluded that bone loss during pregnancy and lactation took place mainly from the trabecular skeleton. Resumption of menstruation tended to result in a regain of bone mass towards baseline.
The aim of this study was to study the influence of hormone replacement therapy (HRT) on weight changes, body composition, and bone mass in early postmenopausal women in a partly randomized comprehensive cohort study design. A total of 2016 women ages 45-58 years from 3 months to 2 years past last menstrual bleeding were included. One thousand were randomly assigned to HRT or no HRT in an open trial, whereas the others were allocated according to their preferences. All were followed for 5 years for body weight, bone mass, and body composition measurements. Body weight increased less over the 5 years in women randomized to HRT (1.94 ؎ 4.86 kg) than in women randomized to no HRT (2.57 ؎ 4.63, p ؍ 0.046). A similar pattern was seen in the group receiving HRT or not by their own choice. The smaller weight gain in women on HRT was almost entirely caused by a lesser gain in fat. The main determinant of the weight gain was a decline in physical fitness. Women opting for HRT had a significantly lower body weight at inclusion than the other participants, but the results in the self-selected part of the study followed the pattern found in the randomized part. The change in fat mass was the strongest predictor of bone changes in untreated women, whereas the change in lean body mass was the strongest predictor when HRT was given. Body weight increases after the menopause. The gain in weight is related to a decrease in working capacity. HRT is associated with a smaller increase in fat mass after menopause. Fat gain protects against bone loss in untreated women but not in HRT-treated women. The data suggest that women's attitudes to HRT are more positive if they have low body weight, but there is no evidence that the conclusions in this study are skewed by selection bias. (J Bone Miner Res 2003;18:333-342)
beta2-Adrenergic receptors have been identified on human osteoblastic and osteoclastic cells, raising the question of a sympathetic regulation of bone metabolism. We investigated effects of treatment with beta-adrenergic receptor antagonists (beta-blockers) on bone turnover, bone mineral density (BMD), and fracture risk. Within the Danish Osteoporosis Prevention Study (DOPS) a population based, comprehensive cohort study of 2016 perimenopausal women, associations between treatment with beta-blockers and bone turnover and BMD were assessed in a cross-sectional design at the start of study. Moreover, in a nested case-control design, fracture risk during the subsequent 5 years was assessed in relation to treatment with beta-blockers at baseline. Multiple regression- and logistic regression-analyses were performed. Treatment with beta-blockers was associated with a threefold increased fracture risk (OR(adj) 3.3; 95% CI: 1.1-9.4). Analyses on duration of treatment showed that women who had been treated for more than 8 years had a higher fracture risk (OR(adj) 5.3; 95% CI: 1.1-26.3) than those treated for less than 8 years (OR(adj) 2.4; 95% CI: 0.6-9.5). In addition, cross-sectional data showed 20% lower serum osteocalcin levels (an osteoblastic marker of bone formation) in women treated with beta-blockers compared to untreated women (P < 0.001), whereas BMD at the lumbar spine and femoral neck did not differ between groups. beta-Blockers may decrease the activity of bone-forming cells and thereby increase fracture risk. However, confirmative studies and studies exploring mechanisms of action are needed.
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