Associations of age at menopause with postmenopausal bone mineral density and fracture risk in women

Author(s):  
Albert Shieh ◽  
Kristine M Ruppert ◽  
Gail A Greendale ◽  
Yinjuan Lian ◽  
Jane A Cauley ◽  
...  

Abstract Context Menopause before age 45 is a risk factor for fractures, but menopause occurs at age 45 or later in ~90% of women. Objective To determine, in women with menopause at age 45 or later, whether: 1) years since the FMP is more strongly associated with postmenopausal bone mineral density (BMD) than chronological age; and 2) lower age at FMP is related to more fractures. Design and Setting The Study of Women’s Health Across the Nation, a longitudinal cohort study of the menopause transition (MT). Participants A diverse cohort of ambulatory women (pre- or early perimenopausal at baseline, with 15 near-annual follow-up assessments). Main Outcome Measures 1) Postmenopausal lumbar spine (LS) or femoral neck (FN) BMD (N=1,038); 2) Time to fracture (N=1,554). Results Adjusted for age, BMI, cigarette use, alcohol intake, baseline LS or FN BMD, baseline MT stage, and study site using multivariable linear regression, each additional year after the FMP was associated with 0.006 (p<0.0001) and 0.004 (p<0.0001) g/cm 2 lower postmenopausal LS and FN BMD, respectively. Age was not related to FN BMD independent of years since FMP. In Cox proportional hazards regression, accounting for race/ethnicity, BMI, cigarette use, alcohol intake, prior fracture, diabetes status, exposure to bone-modifying medications/supplements, and study site, the hazard for incident fracture was 5% greater for each one-year decrement in age at FMP (p=0.02). Conclusions Years since the FMP is more strongly associated with postmenopausal BMD than chronological age, and earlier menopause is associated with more fractures.

Author(s):  
Albert Shieh ◽  
Arun S Karlamangla ◽  
Mei-Hua Huang ◽  
Weijuan Han ◽  
Gail A Greendale

Abstract Context Bone mineral density (BMD) decreases rapidly during the menopause transition (MT), and continues to decline in postmenopause. Objective To examine whether faster BMD loss during the combined MT and early postmenopause is associated with incident fracture, independent of starting BMD, before the MT. Design and Setting The Study of Women’s Health Across the Nation (SWAN), a longitudinal cohort study. Patients or Participants 451 women, initially pre- or early perimenopausal, and transitioned to postmenopause. Main outcome measures Time to first fracture after early postmenopause. Results In Cox proportional hazards regression, adjusted for age, body mass index, race/ethnicity, study site, use of vitamin D and calcium supplements, and use of bone--detrimental or beneficial medications, each SD decrement in lumbar spine (LS) BMD before the MT was associated with a 78% increment in fracture hazard (p=0.007). Each 1% per year faster decline in LS BMD was related to a 56% greater fracture hazard (p=0.04). Rate of LS BMD decline predicted future fracture, independent of starting BMD. Women with a starting LS BMD below the sample median, and a LS BMD decline rate faster than the sample median had a 2.7-fold greater fracture hazard (p=0.03). At the FN, neither starting BMD nor rate of BMD decline was associated with fracture. Conclusions At the LS, starting BMD before the MT and rate of decline during the combined MT and early postmenopause are independent risk factors for fracture. Women with below-median starting LS BMD and faster-than-median LS BMD decline have the greatest fracture risk.


1996 ◽  
Vol 82 (1) ◽  
pp. 65-67 ◽  
Author(s):  
Sandro Barni ◽  
Paolo Lissoni ◽  
Gabriele Tancini ◽  
Antonio Ardizzoia ◽  
Marina Cazzaniga

In this study, the authors have analyzed the possible effects of one-year adjuvant treatment with tamoxifen on bone mineral density in postmenopausal breast cancer women. Bone mineral content was studied by photon absorptiometry (I-125), whereas bone balance was analyzed indirectly by serum PTH, osteocalcin, calcitonin, calcium and alkaline phosphatase levels. Bone mineral content and serum bone-related substances were measured before starting treatment and after one year. Results were analyzed using Student's t test for paired data. No difference was found between the two measurements for bone mineral content, PTH, calcitonin, calcium and alkaline phosphatase levels. Measurements at entry and after one year of treatment showed a statistically significant difference ( P < 0.001) only for osteocalcin. In accordance with other authors, we can conclude that treatment with tamoxifen does not cause an increase in menopausal bone resorption. The finding that osteocalcin levels decreased after one year of therapy with tamoxifen is interesting, but further studies are necessary to clarify the role of such levels in predicting a turnover of bone balance towards osteoblastic activity.


2018 ◽  
Vol 3 (4) ◽  
pp. 62
Author(s):  
Jose Antonio ◽  
Anya Ellerbroek ◽  
Cassandra Carson

The effects of long-term high-protein consumption (i.e., >2.2 g/kg/day) are unclear as it relates to bone mineral content. Thus, the primary endpoint of this investigation was to determine if consuming a high-protein diet for one year affected various parameters of body composition in exercise-trained women. This investigation is a follow-up to a prior 6-month study. Subjects were instructed to consume a high-protein diet (>2.2 g/kg/day) for one year. Body composition was assessed via dual-energy X-ray absorptiometry (DXA). Subjects were instructed to keep a food diary (i.e., log their food ~three days per week for a year) via the mobile app MyFitnessPal®. Furthermore, a subset of subjects had their blood analyzed (i.e., basic metabolic panel). Subjects consumed a high-protein diet for one year (mean ± SD: 2.3 ± 1.1 grams per kilogram body weight daily [g/kg/day]). There were no significant changes for any measure of body composition over the course of the year (i.e., body weight, fat mass, lean body mass, percent fat, whole body bone mineral content, whole body T-score, whole body bone mineral density, lumbar bone mineral content, lumbar bone mineral density and lumbar T-score). In addition, we found no adverse effects on kidney function. Based on this 1-year within-subjects investigation, it is evident that a diet high in protein has no adverse effects on bone mineral density or kidney function.


2009 ◽  
Vol 127 (5) ◽  
pp. 278-282 ◽  
Author(s):  
Maria Eugênia Farias Almeida Motta ◽  
Maria Eduarda Nóbrega de Faria ◽  
Gisélia Alves Pontes da Silva

CONTEXT AND OBJECTIVE: Low bone mineral density may be a finding among children and adolescents with celiac disease, including those undergoing treatment with a gluten-free diet, but the data are contradictory. The aim of this study was to determine the frequency of bone mineral density abnormalities in patients on a gluten-free diet, considering age at diagnosis and duration of dietary treatment. DESIGN AND SETTING: Cross-sectional prevalence study at the Pediatric Gastroenterology Outpatient Clinic of Instituto Materno Infantil Professor Fernando Figueira. METHODS: Thirty-one patients over five years of age with celiac disease and on a gluten-free diet were enrolled. Bone mineral density (in g/cm²) was measured in the lumbar spine and whole body using bone densitometry and categorized using the criteria of the International Society for Clinical Densitometry, i.e. low bone mineral density for chronological age < -2.0 Z-scores. Age at diagnosis and duration of dietary treatment were confirmed according to the date of starting the gluten-free diet. RESULTS: Low bone density for chronological age was present in 3/31 patients in the lumbar spine and 1/31 in the whole body (also with lumbar spine abnormality). At diagnosis, three patients with low bone mineral density for the chronological age were more than 7.6 years old. These patients had been on a gluten-free diet for six and seven months and 3.4 years. CONCLUSION: Pediatric patients with celiac disease on long-term treatment are at risk of low bone mineral density. Early diagnosis and long periods of gluten-free diet are directly implicated in bone density normalization.


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