The effect of two structured exercise programmes on the bone mass of 48 healthy postmenopausal white women aged 50-62 was studied after one year. Volunteers were randomised to group 1 (control), group 2 (aerobic exercise), or group 3 (aerobic and strengthening exercises). Before and after the training programme each subject had evaluations of bone mass (determined by neutron activation analysis and expressed as calcium bone index) and maximum oxygen uptake attained on a multistage exercise treadmill test.After one year both exercise groups had higher levels of fitness and greater bone mass than controls. Mean values (2 SEM) for changes in the calcium bone index were -0.011 (0.037), 0-039 (0.035), and 0-066 (0.036) for groups 1, 2, and 3, respectively. Analysis of variance on the observed data and analysis of covariance adjusting changes to the initial mean value for the whole group showed significant differences between each exercise group and the controls but no difference between the exercise groups themselves. Both exercise groups showed a significant improvement in maximum oxygen uptake.This study suggests that exercise may modify bone loss in healthy postmenopausal women.

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To determine the effect of suppressive doses of thyroxine (T4) on bone mass, we studied 50 women on suppressive doses of T4 for 3-27 years (mean of 11 years). Twenty-five had nontoxic goiter and 25 had well-differentiated thyroid carcinoma. Fifty controls were matched for age, menopausal status, and body mass index. Bone mineral density (BMD) was measured in the lumbar spine (LS), femoral neck (FN), trunk (TK), and extremities (EXT) by dual-energy X-ray absorptiometry (DXA). In addition, the trunk area was measured by neutron activation analysis and recorded as a calcium bone index (CaBI). Twenty-one patients were restudied with DXA measurements at a mean of 1.5 +/- 0.5 (1 SD) years. The total population of 50 patients showed no difference in bone mass from controls. In patients with nontoxic goiter, there was no evidence of any loss in bone mass. Cancer patients showed insignificant reductions of 2-5% in BMD of LS, FN, and TK and a significant 5% reduction in BMD of EXT, compared to controls, and a 12% reduction in CaBI compared to goiter patients. Cancer patients had a slightly higher (p < 0.001) mean daily dose of T4 than goiter patients (0.23 vs 0.15 mg/day) but had a similar degree of TSH suppression. BMD and CaBI values did not correlate with free T4 index) with the daily T4 dose, accumulative dose, or with duration of T4 therapy. There were no significant changes in bone mass in either goiter or cancer patients restudied after a mean of 1.5 years.(ABSTRACT TRUNCATED AT 250 WORDS)

We have prospectively investigated calcium and bone metabolism in 16 patients receiving total parenteral nutrition for periods ranging from 7 to 89 months. In 12 patients, bone biopsies at 6 to 73 months after the start of parenteral nutrition showed osteomalacia. Plasma 25-hydroxyvitamin D levels were normal in all patients. Seven persons developed hypercalcemia, and 10 had hypercalciuria with a negative calcium balance. Serum phosphorus was normal and plasma parathyroid hormone level, normal or decreased. Three patients with the severest form of the disease had vitamin D withdrawn from their solutions. Subsequently, urinary calcium decreased, and serum calcium became normal; two persons reverted to a positive calcium balance. Thus, patients receiving total parenteral nutrition may develop metabolic bone disease characterized by osteomalacia, hypercalcemia, hypercalciuria, and a negative calcium balance. This may be caused by both defective mineralization and increased bone resorption induced by vitamin D, its metabolites, or another unrecognized factor.