The individual age at menopause — An appropriate indicator of postmenopausal body composition?

The interaction between age at menopause and postmenopausal body composition development was tested with in 178 Viennese women aged 47 to 68 years (x=55.4 yr). Postmenopausal body composition was described using dual energy x-ray absorptiometry by absolute fat and lean mass and bone mineral content of the whole body, the arms, legs, the trunk and the head. Upper and lower amount of body fat, the fat percentages of the individual body compartments and the fat distribution index were calculated. Postmenopausal body fat and lean soft tissue mass and postmenopausal bone mineral content were significantly associated with the age at menopause. Women whose menopause occurred late showed the highest amount of body fat (31.2+/−7.7kg) and lean body mass (41.2+/−4.4 kg) postmenopausally, while women with an early menopause exhibited the lowest amount of body fat (27.5+/−8.9kg) and lean body mass (38.4+/−5.4 kg) during the postreproductive phase of life (p<0.05). Women whose menopause occurred later than 51 had a significant higher postmenopausal bone mass (2.26+/−0.9kg versus 2.09+/−0.3 kg; p<0.05). A late menopause was associated with a significantly higher value in fat mass, lean body mass and in bone mineral content. Therefore age at menopause may be assumed as an indicator for body fat and bone mineral content during postmenopause and postmenopausal fat distribution patterns.     

Influence of vitamin D receptor genotype on bone mineral density in postmenopausal women: a twin study in Britain.

OBJECTIVES--To investigate the possible association between vitamin D receptor genotype and bone mineral density in a large group of postmenopausal twins. DESIGN--Cross sectional twin study. SETTING--Twin population based in Britain. SUBJECTS--95 dizygotic (non-identical) pairs of twins and 87 monozygotic (identical) pairs of twins aged 50-69 years, postmenopausal, and free of diseases affecting bone, recruited from a national register of twins and with a media campaign. MAIN OUTCOME MEASURES--Bone mineral density measured at the hip, lumbar spine, forearm, and for the whole body by dual energy x ray absorptiometry in relation to differences in the vitamin D receptor genotype. RESULTS--At all sites the values of bone density among dizygotic twins were more similar in those of the same vitamin D receptor genotype than in those of differing genotype, and the values in the former were closer to the correlations seen in monozygotic twins. Women with the genotype that made them at risk of osteoporotic fracture had an adjusted bone mineral density that was significantly lower by SD 0.5 to 0.6 at the hip, lumbar spine, and for the whole body. The results could not be explained by differences in age, weight, years since menopause, or use of hormone replacement therapy. CONCLUSIONS--The findings that in postmenopausal women in Britain bone density-particularly at the hip and spine-is genetically linked and specifically associated with the vitamin D receptor genotypes should lead to novel approaches to the prevention and treatment of osteoporosis.     

北京地区汉族妇女雌激素受体基因XbaI多态性与骨密度和体重指数的关系

为探讨北京地区汉族妇女雌激素受体（ER）基因XbaI多态性与骨密度的关系,采用双能X线吸收仪检测腰椎、股骨及前臂骨密度;采用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）法,对179例北京地区汉族妇女ER基因XbaI多态性进行分析。北京地区汉族妇女ER基因XX、Xx和xx基因型频率分布为0.302、0.464和0.234,绝经前与绝经后妇女XbaI型基因频率分布有明显差异,绝经后妇女腰椎骨密度（0.836±0.18）g/cm²明显低于绝经前妇女（1.038±0.14);绝经后妇女骨质疏松症的发病率为54%。ER基因XbaI基因型频率分布有明显的种族差异并受绝经影响,ER基因XbaI基因型与骨密度无明显相关性。与体重和BMI有明显相关性。     

Risk Factors of Bone Mass Loss at the Lumbar Spine: A Longitudinal Study in Healthy Korean Pre- and Perimenopausal Women Older than 40 Years

Longitudinal studies on bone mass decline for healthy women are sparse. We performed a retrospective longitudinal study to evaluate the factor associated with bone mass changes at the lumbar spine in healthy Korean pre- and perimenopausal women over the age of 40. We examined the relation of blood tests including thyroid function tests at baseline and follow-up to the annual percentage changes in average BMD of L2-L4 (A%ΔLSBMD). Four hundred and forty-three subjects without diseases or medications pertaining to bone metabolism were analyzed. The mean A%ΔLSBMD in these subjects was -0.45%/year. Though a significant correlation was observed between the A%ΔLSBMD and age, serum thyroid-stimulating hormone (TSH) level, total cholesterol (TC) level, low-density lipoprotein cholesterol (LDL-C) level, and estimated glomerular filtration rate (eGFR) at baseline and follow-up, there was a weak correlation between A%ΔLSBMD and these variables. From multiple linear regression analyses, the percent body fat, age, serum TSH level, serum uric acid level, and the menopause at follow-up were showed to have a significant association with the A%ΔLSBMD. Unlike age, percent body fat, and menopause at follow-up, which had a negative association with the A%ΔLSBMD, serum TSH level and serum uric acid level, had a positive association with the A%ΔLSBMD. The results from our study showed that the notable risk factors of BMD loss at the lumbar spine in population of our study were advancing age, menopause, higher percent body fat, lower normal TSH, and lower serum uric acid levels.     

The prevention and treatment of osteoporosis: a review

Osteoporosis is a disorder characterized by reduced bone strength, diminished bone density, and altered macrogeometry and microscopic architecture. Adult bone mass is the integral measurement of the bone mass level achieved at the peak minus the rate and duration of subsequent bone loss. There is clearly a genetic predisposition to attained peak bone mass, which occurs by a person's mid-20s. Bone loss with age and menopause are universal, but rates vary among individuals. Both peak bone mass and subsequent bone loss can be modified by environmental factors, such as nutrition, physical activity, and concomitant diseases and medications. Osteoporosis prevention requires adequate calcium and vitamin D intake, regular physical activity, and avoiding smoking and excessive alcohol ingestion. Risk of fracture determines whether medication is also warranted. A previous vertebral or hip fracture is the most important predictor of fracture risk. Bone density is the best predictor of fracture risk for those without prior adult fractures. Age, weight, certain medications, and family history also help establish a person's risk for osteoporotic fractures. All women should have a bone density test by the age of 65 or younger (at the time of menopause) if risk factors are present. Guidelines for men are currently in development. Medications include both antiresorptive and anabolic types. Antiresorptive medications--estrogens, selective estrogen receptor modulators (raloxifene), bisphosphonates (alendronate, risedronate, and ibandronate) and calcitonins--work by reducing rates of bone remodeling. Teriparatide (parathyroid hormone) is the only anabolic agent currently approved for osteoporosis in the United States. It stimulates new bone formation, repairing architectural defects and improving bone density. All persons who have had osteoporotic vertebral or hip fractures and those with a bone mineral density diagnostic of osteoporosis should receive treatment. In those with a bone mineral density above the osteoporosis range, treatment may be indicated depending on the number and severity of other risk factors.     

The pathophysiological implications of circulating androgens on bone mineral density in a normal female population

In this cross-sectional study performed on 147 healthy or osteoporotic, but otherwise normal premenopausal (n = 26 and n = 13, respectively) or postmenopausal (n = 40 and n = 68, respectively) women aged 40.1+/-9.9 and 61.9+/-8.9 years, respectively (range 20-82 years), serum ovarian and adrenal sex steroids and their relationship to bone mineral density (BMD) were evaluated. The levels of dehydroepiandrosterone sulfate (DHEAS), dehydroepiandrosterone (DHEA), androstenedione (AD), and estradiol correlated positively with BMD at the hip and spine as did serum testosterone with BMD at the spine. An inverse relationship was found between sex hormone binding globulin (SHBG) levels and BMD at the spine and hip. After adjustment for age, body mass, and sex steroid confounders, the bioavailable testosterone value (but not the DHEAS, DHEA, AD, or SHBG) values was demonstrated to be an independent determinant of BMD at the spine (beta 0.18, P<0.02) and hip (beta 0.24, P<0.02). Similarly, estradiol was found to be an independent determinant of BMD at the spine (beta 0.25, P<0.007). However, only SHBG levels (but not other steroid parameters) correlated positively with indices of bone remodeling, namely, serum osteocalcin and cross-linked telopeptide of type I collagen (ICTP). The present study suggests that a major decline in index of free testosterone (testosterone/SHBG) may influence the development of female osteoporosis. The clinical significance of circulating SHBG levels in the assessement of bone metabolic turnover remains to be established.     

Cadmium, osteoporosis and calcium metabolism

Occupational exposure to cadmium has for long been associated with renal tubular cell dysfunction, osteomalacia with osteoporosis, hypercalciuria and renal stone formation. High environmental exposure in Japan resulting from a stable diet of cadmium contaminated rice caused itai-itai disease, fractures occurring mainly in elderly multiparous women, with a form of osteomalacia, osteoporosis and renal dysfunction. More recently a population based study in Europe, in the vicinity of zinc smelters has shown that low to moderate exposure to cadmium, with a mean urinary excretion of cadmium of the order of 1 microg/g creatinine has been associated with a decrease in bone density, an increased risk of bone fractures in women and of height loss in men. In a population-based study of residents near a cadmium smelter in China, forearm bone density was shown to decrease linearly with age and urinary cadmium in both sexes, suggesting a dose effect relationship between cadmium dose and bone mineral density. A marked increase in the prevalence of fractures was shown in the cadmium-polluted area in both sexes. Concentrations of cadmium in blood and urine were taken as exposure biomarkers, and beta2-microglobulin, retinol binding protein and albumin as biomarkers of effect. A marked dose response relationship between these indicators of exposure and effect was shown. Hypercalciuria, which may progress to osteoporosis, has been taken as a sensitive renal-tubular biomarker of a low level of cadmium exposure. Cadmium may also act directly on bone. Animal studies have shown cadmium to stimulate the formation and activity of osteoclasts, breaking down the collagen matrix in bone. Osteoporosis is the main cause of fracures in post-menopausal women, a common occurrence worldwide, giving rise to disability and a high cost to health services. The identification of cadmium, an environmental pollutant, as one causal factor is highly significant in helping to control the incidence of this complex condition.     

Osteoporosis after Oophorectomy for Non-malignant Disease in Premenopausal Women

The role of oophorectomy in the development of osteoporosis was assessed retrospectively in 258 women who had been hysterectomized premenopausally for non-malignant disease. Bone density was assessed using the radiographic density of the third metacarpal. Oophorectomy before the age of 45 years was found to be associated with a significantly increased prevalence of osteoporosis within three to six years of operation. The bone density of women oophorectomized after the age of 45 years was indistinguishable three to six years after operation from that found in healthy women with intact ovaries. These findings confirm the major part played by loss of ovarian function in the development of postmenopausal osteoporosis.     

Hormone replacement therapy,calcium and vitamin D<Subscript>3</Subscript> versus calcium and vitamin D<Subscript>3</Subscript>alone decreases markers of cartilage and bone metabolism in rheumatoid arthritis: a randomized controlled trial [ISRCTN46523456]

This study aimed to evaluate the effects of hormone replacement therapy (HRT), known to prevent osteoporosis and fractures, on markers of bone and cartilage metabolism. Furthermore, we assessed whether changes in these markers corresponded to alterations in bone mineral density and radiographic joint destructions in postmenopausal women with rheumatoid arthritis. Eighty-eight women were randomized to receive HRT, calcium, and vitamin D3, or calcium and vitamin D3 alone, for 2 years. Bone turnover was studied by analyzing serum levels of C-terminal telopeptide fragments of type I collagen (CTX-I), C-terminal telopeptide of type I collagen (ICTP), bone sialoprotein, and C-terminal propeptide of type I procollagen (PICP) and cartilage turnover by urinary levels of collagen type II C-telopeptide degradation fragments (CTX-II) and cartilage oligomeric matrix protein (COMP) in serum. Treatment with HRT resulted in decrease in CTX-I (P < 0.001), ICTP (P < 0.001), PICP (P < 0.05), COMP (P < 0.01), and CTX-II (P < 0.05) at 2 years. Reductions in CTX-I, ICTP, and PICP were associated with improved bone mineral density. Of the markers tested, CTX-I reflected bone turnover most sensitively; it was reduced by 53 +/- 6% in the patients receiving HRT. Baseline ICTP (P < 0.001), CTX-II (P < 0.01), and COMP (P < 0.05) correlated with the Larsen score. We suggest that biochemical markers of bone and cartilage turnover may provide a useful tool for assessing novel treatment modalities in arthritis, concerning both joint protection and prevention of osteoporosis.     

Role of peak bone mass and bone loss in postmenopausal osteoporosis: 12 year study.

OBJECTIVE--To examine the role of peak bone mass and subsequent postmenopausal bone loss in the development of osteoporosis and the reliability of identifying women at risk from one bone mass measurement and one biochemical assessment of the future bone loss. DESIGN--Population based study. SETTING--Outpatient clinic for research into osteoporosis. SUBJECTS--178 healthy early postmenopausal women who had participated in a two year study in 1977. 154 of the women underwent follow up examination in 1989, of whom 33 were excluded because of diseases or taking drugs known to affect calcium metabolism. MAIN OUTCOME MEASURES--Bone mineral content of the forearm and values of biochemical markers of bone turnover. RESULTS--The average reduction in bone mineral content during 1977-89 was 20%, but the fast losers had lost 10.0% more than had the slow loser group (mean loss 26.6% in fast losers and 16.6% in slow losers; p less than 0.001). Prediction of future bone mineral content using baseline bone mineral content and estimated rate of loss gave results almost identical with the actual bone mineral content measured in 1989. Seven women had had a Colles'' fracture and 20 a spinal compression fracture. The group with Colles'' fracture had low baseline bone mineral content (34.7 (95% confidence interval 31.3 to 38.1) units v 39.4 (38.1 to 40.8) units in women with no fracture) whereas the group with spinal fracture had a normal baseline bone mineral content (38.1 (35.0 to 41.1) units) but an increased rate of loss (-2.4 (-3.5 to -1.3)%/year v -1.8 (-2.1 to -1.5)%/year in women with no fracture). CONCLUSIONS--One baseline measurement of bone mass combined with a single estimation of the rate of bone loss can reliably identify the women at menopause who are at highest risk of developing osteoporosis later in life. The rate of loss may have an independent role in likelihood of vertebral fracture.     

Osteoprotegerin--does it play a protective role in the pathogenesis of bone loss in obese perimenopausal women?

INTRODUCTION: Assessment of serum osteoprotegerin (OPG) concentrations in obese patients in comparison to healthy controls and evaluation of a possible correlation between OPG and other markers of bone turnover or calcitropic hormones. MATERIAL AND METHODS: 50 obese perimenopausal women without concomitant diseases (BMI 36.7 +/- 4.1 kg/m(2), mean age 50.4 +/- 4.9 yrs). The control group consisted of 19 healthy women (BMI 24.2 +/- 2.1 kg/m(2); mean age 53.8 +/- 5.1 yrs). In all patients serum concentration of OPG, C telopeptide of type I collagen containing the crosslinking site (CTX), osteocalcin, parathormone (PTH) and vitamin D (25-OH-D(3)) was assessed. Dual energy x-ray absorptiometry (the DXA method) of the lumbar spine and femoral neck was performed using a Lunar DPXL to measure bone marrow density (BMD). RESULTS: In obese perimenopausal women serum OPG, osteocalcin and 25-OH-D(3) levels were significantly lower, and the serum PTH level was significantly higher in comparison to healthy controls. A significantly positive correlation was found between serum OPG level and age in both obese and control subjects. CONCLUSION: The serum OPG level in obese perimenopausal women is significantly lower in comparison to healthy controls and does not correlate significantly with biochemical markers of bone turnover, calcitropic hormones and BMD. It probably cannot play a protective role in the pathogenesis of bone loss in obese perimenopausal women.     

The Implications of Body Fat Mass and Fat Distribution for Cognitive Function in Elderly Women

Objective: To investigate how body fat mass, an established source of endogenous estrogen after menopause, influences cognitive impairment in elderly women. Research Methods and Procedures: Study participants were 5607 generally healthy postmenopausal women with mean age of 63.8 years at baseline followed for an average of 7.3 years. Cognitive function assessed at follow‐up using the short Blessed test was related to baseline body weight, the yearly change in weight, and follow‐up measures of body fat depots assessed by DXA. Cognitive function was also related to various surrogates of lifetime estrogen exposure. Results: Women with the worst cognitive performance (score ≥ 9) at follow‐up were the ones who lost the most body weight and revealed the lowest central fat mass (CFM). The association of weight loss with worse cognitive performance was apparent across all age groups except for those more than 80 years old. In the multivariate logistic model, the risk of cognitive impairment was 18% lower in women in the second quartile of CFM (p = 0.14), 32% lower in the third (p = 0.01), and 48% lower in the fourth (p < 0.001) compared with those in the first quartile. CFM showed significant correlation with the simultaneously measured serum estradiol (r = 0.25; p < 0.001). Cognitive score showed an inverse linear relationship with the duration of reproductive period and bone mineral density assessed at follow‐up. Discussion: These findings argue for a protective association of body fat mass with cognitive impairment in elderly women. This association seems to involve a more prominent exposure to endogenous estrogens.     

Association of interleukin 10 haplotype with low bone mineral density in Korean postmenopausal women

Osteoporosis is a disease characterized by exaggerated loss of bone mass, with as much as 50 to 85% of the variation in bone mineral density (BMD) commonly accepted as being genetically determined. Although intensive studies have attempted to elucidate the genetic effects of polymorphisms on BMD and/or osteoporosis in several genes, the genes involved are still largely unknown. The possible associations of genetic variants in five-candidate genes (IL10, CCR3, MCP1, MCP2 and GC) with spinal BMD were investigated in Korean postmenopausal women (n = 370). Fourteen SNPs in five candidate genes were genotyped, and the haplotypes of each gene constructed. The associations of adjusted spinal BMD by age, year since menopause (YSM) and body mass index (BMI), with genetic polymorphisms, were analyzed using multiple regression models. Genetic association analysis of Korean postmenopausal women revealed that IL10 -592A > C and/or IL10 ht2 were associated with decreased bone mass, whereas no significant associations were observed with all polymorphisms in other genes. The levels of spinal BMD in individuals bearing the IL10 -592CC genotype were lower (0.78 +/- 0.16) than those in others (0.85 +/- 0.17) (P = 0.02), and the BMD of IL10 ht2 bearing individuals were also lower (0.82 +/- 0.15) than those in others (0.85 +/- 0.17) (P = 0.04). Our results suggest that variants of IL10 might play a role in the decreased BMD, although additional study might need to be followed-up in a more powerful cohort.     

Evaluation of the relative rates of bone mineral content loss in postmenopause due to both estrogen deficiency and ageing

To evaluate the relative rates of bone mineral content loss in postmenopause due to both estrogen deficiency and ageing, three groups of women were studied by computerized bone densitometry at the radius mid-point and at the distal point, modified according to the Abwrey technique. All women were in apparent good health and never had estrogen therapy. In the first group there were 64 women aged between 30 and 50 who were ovariectomized between 25 and 35 years of age. The second group was made up of 309 women between 50 and 55 years. In the third group there were 136 women aged 30-50 with normal ovaric function. The ordinary functions of linear polynomial regression were used to describe the variations in density with age. The percentage of postmenopausal bone loss was determined by calculating the BMC value at the start of the menopause and again twenty years later, according to the linear regression equation of postmenopausal period of each group of women in the study. The women who had natural menopause showed an average bone loss per year of 1.63% at the mid radius and 1.0% at the distal point. The ovariectomized women had an average loss of 0.85% at the mid point and 0.66% at the distal point. No significant decrease of bone mass was found before menopause. From a comparison between the two groups of women with analogous periods of menopause, it comes out that, during the first 20 years of natural menopause, estrogen deficiency is responsible for 52.5%-66.4% of the bone mineral loss, the remaining amount being attributable to other causes, connected with ageing. Estrogen deficiency is therefore, the principal factor causing bone mineral loss in natural menopause.     

Adiponectin is associated with bone mineral density in perimenopausal women.

The aim of the current investigation was to investigate any potential effect of fasting plasma adiponectin concentration on bone tissue, and to find possible relationships of fasting plasma adiponectin level with different body composition, insulin sensitivity and physical performance parameters in a group of healthy perimenopausal women. Twenty-one premenopausal and 17 early postmenopausal women participated in this study. The women were matched for body mass index (BMI) and level of mean daily energy expenditure. Women had similar adiponectin (8.4 +/- 3.9 vs. 9.9 +/- 5.4 microg/ml) and leptin values (12.0 +/- 7.7 vs. 14.0 +/- 8.2 ng/ml) before and after menopause. Significant relationships were observed between plasma adiponectin and bone mineral content, total bone mineral density (BMD) and lumbar spine BMD values (r > - 0.36; p < 0.05). Furthermore, adiponectin had a significant negative association with total BMD (beta = - 1.228; p = 0.004) and lumbar spine BMD (beta = - 0.312; p = 0.005) independent of the influence that other measured body compositional, hormonal or physical performance factors may exert on BMD. Adiponectin was also significantly related to waist-to-hip ratio (WHR) (beta = - 2.300; p = 0.002) and fasting insulin resistance index (FIRI) (beta = - 0.006; p = 0.007) in separate regression models. No relationship was observed between leptin and measured bone, physical performance and insulin resistance values. Leptin significantly correlated to BMI (beta = 0.018; p = 0.034), lean body mass (beta = 0.025; p = 0.024) and fat mass (beta = 0.019; p = 0.001) in separate regression models. In conclusion, the results of present study show that circulating adiponectin appears to exert an independent effect on BMD in perimenopausal women and may represent a link between adipose tissue and bone mineral density.     

Effects of physical training on bone mineral density and bone metabolism

The purpose of this study was to examine the influences of long-term walking training and walking and jumping training on bone mineral density (BMD) and bone metabolism. Data from 28 healthy premenopausal women was assessed. The subjects were divided into the walking group (WG; 17 women mean+/-SE age 35+/-2 years), and the walking and jumping group (WJG; 11 women mean+/-SE age 39+/-1 years). BMD was measured in the lumbar spine and proximal femur using dual energy X-ray absorptiometry (DXA). As markers of bone metabolism, this study was to measure bone formation markers, bone-alkaline phosphatase (B-ALP: measured by enzyme immunoassay/EIA) and osteocalcin (BGP: by radioimmunoassay/RI) as well as bone resorption markers, parathyroid hormone (PTH: measured by/RI) and type I collagen cross-linked N-telopeptides (NTx: by EIA). Despite the significant decrease in body weight (p<0.05), no corresponding decrease in BMD was observed. Moreover, no significant difference in bone markers BGP, PTH, and NTx was observed. B-ALP was significantly increased (p<0.05) after one year, and the rate of this increase was greater in the WJG than in the WG. It is thus concluded that walking training for one year is beneficial for the promotion of bone formation, and that jumping stimulus maintain BMD effectively.     

Influence of the menopause and aging on spinal density in French women

Dual photon absorptiometry (DPA) was used to measure the bone mineral density (BMD) of the lumbar spine in 510 normal women from the south of France. Long-term precision was 2.2%. BMD was stable in young adults and again in women over 70 years of age. Perimenopausal women at an average age of 51 years already evidenced a slight bone diminution (5%) compared to young adults and women within 2 years of the menopause already had a 10% diminution. The average rate of apparent bone loss in this cross-sectional study was 1% per year from age 45 to 65 years, but about 75% of this decrease occurred in the first decade after the menopause. Spinal BMD in our normal French population appears to be 5–10% lower than US values.     

Environmental cadmium exposure and forearm bone density

Environmental exposure to cadmium may give rise to osteomalacia combined with renal dysfunction, so called 'Itai-Itai disease', which was endemic in the heavily polluted area in Japan. The main focus of this study was to investigate whether environmental exposure to cadmium is associated with low bone mass in a population living near a smelter. A total of 790 persons (302 males and 488 females), who were all over 35 years old and resided in areas near a lead, zinc and cadmium smelter and in a control area in southeast China, completed a questionnaire, and bone mineral density was measured by SPA-4 single photon absorptiometry at the radius and ulna. Cadmium content of urine was determined by graphite-furnace atomic absorption spectrophotometry as a measure of dose. The present study shows that forearm bone densities were negatively correlated with urinary cadmium excretion (p < 0.001) and forearm bone density decreased linearly with age (p < 0.001) and urinary cadmium (p < 0.01), suggesting a dose-effect relationship between cadmium dose and bone mineral density. Based on the World Health Organization criteria, (bone mineral density < -2.5 SDs below the normal young adult), the prevalence of osteoporosis in women increased from 34.0% in the control area to 51.9% in the heavily polluted area (p < 0.01) among subjects over 50 years old, and the odds ratio value was 2.09 (95% CI: 1.08-4.03) for the highly polluted area compared with the control area. A striking observation in the study was a marked increase of the prevalence of fracture in the cadmium-polluted area in both sexes. It was concluded that environmental exposure to cadmium is associated with an increased loss of bone mineral density in both gender, leading to osteoporosis and increased risk of fractures, especially in the elderly and in females.     

Relation between body size and bone mineral density with special reference to sex hormones and calcium regulating hormones in elderly females.

We studied the relation between body size and bone mineral density in elderly females. The study included a total of 93 ambulatory females aged over 60 years. They were divided into 3 groups according to their body mass index (BMI; kg/m2): slender group with BMI less than 20 (n = 28), normal group with BMI of 20 to 24.9 (n = 43) and obese group with BMI greater than or equal to 25 (n = 22). Fracture incidence, bone mineral density, calcium regulating hormones and steroid hormones were studied in an intergroup comparative manner. The incidence of vertebral fracture was found to be negatively correlated with BMI (the incidences of vertebral fracture in slender, normal and obese were 78.6, 48.8 and 22.7%, respectively) and bone mineral density was also BMI-related (0.390 +/- 0.016, 0.456 +/- 0.015 and 0.493 +/- 0.018 g/cm2, respectively: p less than 0.01 in ANOVA; mean +/- SE). The number of years after menopause was shorter in patients with a higher BMI. There was no intergroup difference in serum levels of PTH, vitamin D and estrogens. On the other hand, serum levels of calcitonin, DHEA, DHEAS, delta-4 androstenedione and testosterone were found to be higher in subjects with a higher BMI. From the present results, it seems that bone mineral density is supported not only by weight-bearing stress upon bone, but also by serum levels of calcitonin and androgens in obese females.     

绝经期女性血脂及血压水平与糖尿病骨质疏松的关系

目的：探讨绝经期女性血脂及血压与糖尿病骨质疏松发生的关系。方法：选取2014 年3 月-2015 年5 月在我院接受治疗的 绝经期女性糖尿病患者100 例作为研究对象,根据骨密度不同将患者分为骨质疏松组和非骨质疏松组。检测并比较两组研究对 象的血脂及血压水平,分析其与骨质疏松发生的关系。结果：骨质疏松组患者总胆固醇（TC）、三酰甘油（TG）、高密度脂蛋白胆固 醇（HDL-C）及低密度脂蛋白胆固醇（LDL-C）水平均高于非骨质疏松组,差异具有统计学意义（P<0.05）;与非骨质疏松组比较,骨 质疏松组患者舒张压（DBP）升高,而收缩压（SBP）降低,差异具有统计学意义（P<0.05）;Pearson相关性分析结果显示,年龄、总胆 固醇（TC）及低密度脂蛋白胆固醇（LDL-C）与双股骨骨密度呈正相关关系（P＜0.05）,与腰椎骨密度呈负相关关系（P＜0.05）;Logistic 回归分析结果显示,年龄、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）及收缩压（SBP）是糖尿病骨质疏松发生的危险因素 （P<0.05）。结论：绝经期女性糖尿病患者的年龄、总胆固醇、LDL-C 及收缩压与骨质疏松密切相关,临床应给予重视并采取有效措 施进行预防。