Dietary calcium intake and rates of bone loss in women.

We measured bone mineral density (BMD) at the midradius and lumbar spine in 106 normal women, ages 23-84 yr (61 were postmenopausal). Three to nine measurements (median, four) were made over 2.6 to 6.6 yr (mean, 4.1 yr). The correlation between calcium intake (range, 260-2,035 mg/d) and rate of change in BMD was not significant at the midradius (r = 0.06) or lumbar spine (r = 0.08), even after adjusting for age, menopausal status, and serum estrogen levels by multiple regression analysis. Women in the lower (mean, 501 mg/d) and in the upper (mean, 1,397 mg/d) quartiles of dietary intake had similar rates of change in BMD (%/yr [mean +/- SE], at midradius, -0.78 +/- 0.24 and -0.91 +/- 0.17 for lower and upper quartiles, respectively; at lumbar spine, -1.06 +/- 0.24 and 0.98 +/- 0.24). These data do not support the hypothesis that insufficient dietary calcium is a major cause of bone loss in women.

Rates of bone loss in the appendicular and axial skeletons of women. Evidence of substantial vertebral bone loss before menopause.

We made longitudinal measurements of bone mineral density (BMD) in 139 normal women (ages 20-88 yr) at midradius (99% cortical bone) and lumbar spine (approximately 70% trabecular bone) by single- and dual-photon absorptiometry. BMD was measured 2-6 (median, 3) times over an interval of 0.8-3.4 yr (median, 2.1 yr). For midradius, BMD did not change (+0.48%/yr, NS) before menopause but decreased (-1.01%/yr, P less than 0.001) after menopause. For lumbar spine, there was significant bone loss both before (-1.32%/yr, P less than 0.001) and after (-0.97%/yr, P = 0.006) menopause; these rates did not differ significantly from each other. Our data show that before menopause little, if any, bone is lost from the appendicular skeleton but substantial amounts are lost from the axial skeleton. Thus, factors in addition to estrogen deficiency must contribute to pathogenesis of involutional osteoporosis in women because about half of overall vertebral bone loss occurs premenopausally.

Ascertainment of risk factors for osteoporosis: comparison of interview data with medical record review.

To determine the accuracy of self-reported risk factors for osteoporosis, an age-stratified random sample of Rochester, MN, women was studied. Results from a structured face-to-face interview were compared with information documented in contemporary inpatient and outpatient health care records in the community. Using the kappa statistic to evaluate concordance of these two data sources, we found substantial agreement for a history of proximal femoral and distal forearm fractures, peptic ulcer disease, estrogen replacement therapy and oral contraceptive use, and cigarette and alcohol exposure. Moderate agreement was seen for histories of other age-related fractures, hysterectomy or oophorectomy, thyroidectomy, and use of thyroid supplements. Poor agreement was found for prior thyroid disease, gastrectomy, and corticosteroid or anticonvulsant use. This study demonstrates a need for greater attention to the quality of self-reported risk factor data in studies of bone loss and fractures.

Relative contributions of aging and estrogen deficiency to postmenopausal bone loss.

Debate continues on whether aging or estrogen deficiency is the more important determinant of postmenopausal bone loss. We compared 14 women who had undergone oophorectomy during young adulthood, 14 normal perimenopausal women, and 14 normal postmenopausal women (mean ages, 54, 52, and 73 years, respectively; mean duration of estrogen deficiency, 22, 0.3, and 22 years, respectively). Bone mineral density was assessed by single-photon and dual-photon absorptiometry. As compared with the perimenopausal group, the other two groups had significantly lower bone mineral density at the midradius, femoral neck, femoral intertrochanteric area, and lumbar spine (-15 per cent, -25 per cent, -16 per cent, and -23 per cent, respectively, in the oophorectomized group and -18 per cent, -28 per cent, -26 per cent, and -23 per cent, respectively, in the postmenopausal group). Because bone loss in the oophorectomized group (differing from the perimenopausal group in menopausal status but not in age) was almost as great as in the postmenopausal group (differing in both characteristics), we suggest that estrogen deficiency, and not aging, may be the predominant cause of bone loss occurring during the first two decades after natural menopause.

Osteoporosis and the risk of hip fracture.

The incidence of cervical and intertrochanteric proximal femur fractures at various levels of cervical and intertrochanteric bone mineral density, respectively, was estimated by using population-based data from ongoing studies of osteoporosis and fractures among women residing in Rochester, Minnesota. Hip fractures were uncommon among women with femoral bone density greater than or equal to 1.0 g/cm2, but their frequency increased as bone density declined below that point at both femoral sites. The incidence of cervical femur fractures was estimated at 8.3 per 1,000 person-years among women with cervical bone density less than 0.6 g/cm2, while the estimated incidence of intertrochanteric femur fractures reached 16.6 per 1,000 person-years among those with intertrochanteric bone density less than 0.6 g/cm2. This new approach to the assessment of fracture risk from bone mineral density measurements indicates that osteoporosis is an important underlying cause of hip fractures.