Premature graying, balding, and low bone mineral density in older women and men: the Rancho Bernardo study.

OBJECTIVE: The authors report the association of balding or graying with BMD in older adults. METHOD: BMD was measured at the spine, hip, and total body in 1,207 participants. Of these, 508 women and 380 men responded to a 1986 survey about balding patterns; in 1994, all participants answered questions about graying. RESULTS: Among men, 10.7% reported graying, and 51.1%, balding; 9.9% of women reported graying, and 9.5%, balding. Models were adjusted for age, body mass index, alcohol consumption, smoking, exercise, calcium supplements, diuretics, glucocorticoids, thyroid hormone, and estrogen. CONCLUSION: Graying was not significantly associated with BMD in either group. Balding men averaged 5% lower total body BMD (p

Differences in association of bone mineral density with coronary artery calcification in men and women: the Rancho Bernardo Study.

OBJECTIVE: Whether osteoporosis and calcification of atherosclerotic plaque are two independent, age-related processes or linked by similar mechanisms of bone mineralization and plaque calcification is unknown. This study examines the sex-specific association between bone mineral density (BMD) and coronary artery calcification with a particular focus on hormone therapy (HT). DESIGN: Participants were 180 men (aged 47-86 years) and 186 women (aged 58-81 years) without a history of heart disease who had hip and spine BMD assessed by dual-energy x-ray absorptiometry and coronary artery calcium score (CACS) measured by electron-beam computed tomography. Calcium scores were categorized into none/minimal (or=400). Ordinal and binary logistic regressions examined the associations between site-specific BMD and CACS. RESULTS: In men and women not using HT, there was no age-independent association between BMD at any site and CACS. In contrast, among current HT users an inverse association of BMD with coronary artery calcification was observed at the total hip (odds ratio [OR] = 0.56, 95% CI, 0.33-0.95), trochanter (OR = 0.55, 95% CI, 0.32-0.93), and intertrochanter area (OR = 0.60, 95% CI, 0.41-0.86) after adjustment for age and other risk factors. Other skeletal sites showed similar, but not statistically significant, associations (P < 0.1). CONCLUSION: Lack of association between BMD and CACS in men and women not using HT and the inverse association in women on HT suggest that the association between coronary and bone calcium might be mediated by estrogen.

Randomized trial of effect of alendronate continuation versus discontinuation in women with low BMD: results from the Fracture Intervention Trial long-term extension.

UNLABELLED: To determine the effects of continuation versus discontinuation of alendronate on BMD and markers of bone turnover, we conducted an extension trial in which 1099 older women who received alendronate in the FIT were re-randomized to alendronate or placebo. Compared with women who stopped alendronate, those continuing alendronate for 3 years maintained a higher BMD and greater reduction of bone turnover, showing benefit of continued treatment. However, among women who discontinued alendronate and took placebo in the extension, BMD remained higher, and reduction in bone turnover was greater than values at FIT baseline, showing persistence of alendronate's effects on bone. INTRODUCTION: Prior trials including the Fracture Intervention Trial (FIT) have found that therapy with alendronate increases BMD and decreases fracture risk for up to 4 years in postmenopausal women with low BMD. However, it is uncertain whether further therapy with alendronate results in preservation or further gains in BMD and if skeletal effects of alendronate continue after treatment is stopped. MATERIALS AND METHODS: We conducted a follow-up placebo-controlled extension trial to FIT (FIT long-term extension [FLEX]) in which 1099 women 60-86 years of age who were assigned to alendronate in FIT with an average duration of use of 5 years were re-randomized for an additional 5 years to alendronate or placebo. The results of a preplanned interim analysis at 3 years are reported herein. Participants were re-randomized to alendronate 10 mg/day (30%), alendronate 5 mg/day (30%), or placebo (40%). All participants were encouraged to take a calcium (500 mg/day) and vitamin D (250 IU/day) supplement. The primary outcome was change in total hip BMD. Secondary endpoints included change in lumbar spine BMD and change in markers of bone turnover (bone-specific alkaline phosphatase and urinary type I collagen cross-linked N-telopeptide). RESULTS: Among the women who had prior alendronate therapy in FIT, further therapy with alendronate (5 and 10 mg groups combined) for 3 years compared with placebo maintained BMD at the hip (2.0% difference; 95% CI, 1.6-2.5%) and further increased BMD at the spine (2.5% difference; 95% CI, 1.9-3. 1%). Markers of bone turnover increased among women discontinuing alendronate, whereas they remained stable in women continuing alendronate. Cumulative increases in BMD at the hip and spine and reductions in bone turnover from 8.6 years earlier at FIT baseline were greater for women continuing alendronate compared with those discontinuing alendronate. However, among women discontinuing alendronate and taking placebo in the extension, BMD remained higher and reduction in bone turnover was greater than values at FIT baseline. CONCLUSIONS: Compared with women who stopped alendronate after an average of 5 years, those continuing alendronate maintained a higher BMD and greater reduction of bone turnover, showing benefit of continued alendronate treatment on BMD and bone turnover. On discontinuation of alendronate therapy, rates of change in BMD at the hip and spine resumed at the background rate, but discontinuation did not result in either accelerated bone loss or a marked increase in bone turnover, showing persistence of alendronate's effects on bone. Data on the effect of continuation versus discontinuation on fracture risk are needed before making definitive recommendations regarding the optimal length of alendronate treatment.

Elevated depression symptoms, antidepressant medicine use, and risk of developing diabetes during the diabetes prevention program.

OBJECTIVE: To assess the association between elevated depression symptoms or antidepressant medicine use on entry to the Diabetes Prevention Program (DPP) and during the study and the risk of developing diabetes during the study. RESEARCH DESIGN AND METHODS: DPP participants (n = 3,187) in three treatment arms (intensive lifestyle [ILS], metformin [MET], and placebo [PLB]) completed the Beck Depression Inventory (BDI) and reported their use of antidepressant medication at randomization and throughout the study (average duration in study 3.2 years). RESULTS: When other factors associated with the risk of developing diabetes were controlled, elevated BDI scores at baseline or during the study were not associated with diabetes risk in any arm. Baseline antidepressant use was associated with diabetes risk in the PLB (hazard ratio 2.25 [95% CI 1.38-3.66]) and ILS (3.48 [1.93-6.28]) arms. Continuous antidepressant use during the study (compared with no use) was also associated with diabetes risk in the same arms (PLB 2.60 [1.37-4.94]; ILS 3.39 [1.61-7.13]), as was intermittent antidepressant use during the study in the ILS arm (2.07 [1.18-3.62]). Among MET arm participants, antidepressant use was not associated with developing diabetes. CONCLUSIONS: A strong and statistically significant association between antidepressant use and diabetes risk in the PLB and ILS arms was not accounted for by measured confounders or mediators. If future research finds that antidepressant use independently predicts diabetes risk, efforts to minimize the negative effects of antidepressant agents on glycemic control should be pursued.