Determinants Of Peak Bone Mass Research Articles

Dynamic loads are determinants of peak bone mass

This study investigated the association between non-invasive measurements of bone mass and markers of dynamic and static hip joint loads in subjects expected to be at peak bone mass. The bone mineral density (BMD) and bone mineral content (BMC) of three proximal femoral sites (neck, greater trochanter, and total) were measured by dual energy X-ray absorptiometry, and the peak external joint moments at the hip during walking and jogging were calculated from gait analyses of 31 normal human subjects ranging in age from 30 to 49 years (18 females, 13 males). Various multiple regression analyses were performed to determine how much of the variance in BMD and BMC was explained by height, body mass, and the peak hip joint moments. In total, the models explained up to 40% of the variance in BMD and 58% of the variance in BMC. Inclusion of height or body mass did not increase the explanatory power of the models for BMD and explained no more than 8% of the total variance in BMC once the joint moments from walking were allowed to enter the models. These data support the hypothesis that variance in peak bone mass is associated with variance in dynamic hip loads largely independent of the effect of static factors such as height and body mass.

Genetic and environmental determinants of peak bone mass in young men and women.

Peak bone mass is an important risk factor for the development of osteoporosis in later life. Previous work has suggested that genetic, intrauterine, and environmental factors all contribute to the regulation of bone mass, but the ways in which they interact with each other to do so remain poorly understood. In this study, we investigated the relationship between peak bone mass and polymorphisms of the vitamin D receptor (VDR), estrogen receptor (ER) a, and collagen type Ialpha1 (COLIA1) genes in relation to other factors such as birth weight, lifestyle diet, and exercise in a population-based cohort of 216 women and 244 men in their early 20s. Stepwise multiple regression analysis showed that body weight was the strongest predictor of bone mineral density (BMD) in women, accounting for 16.4% of the variance in spine BMD and 8.4% of the variance in femoral neck BMD. Other significant predictors were VDR genotype (3.8%) and carbohydrate intake (1.6%) at the spine and vitamin D intake (3.4%) and ER genotype (3.4%) at the femoral neck. Physical activity was the strongest predictor of BMD in men, accounting for 6.7% of the variance at the spine and 5.1% at the hip. Other significant predictors were body weight (5%) and ER PvuII genotype (2.8%) at the spine and weight (3.4%) and alcohol intake (2%) at the femoral neck. Birth weight was not a significant predictor of BMD at either site but COLIA1 genotype significantly predicted birth weight in women, accounting for 4.3% of the variance. We conclude that peak bone mass is regulated by an overlapping but distinct set of environmental and genetic influences that differ in men and women. However, much of the variance in BMD was unexplained by the variables studied here, which suggests that either most of the genes that regulate BMD remain to be discovered or major environmental influences on BMD exist that have not yet been identified.

Strategies for skeletal health in the elderly.

Osteoporosis is a common disease in the elderly, and the fractures that result from this disorder affect 40 % of women and 14 % of men over the age of 50 years. The risk of fracture relates to bone mineral density and the risk of falling, among other factors. Low bone mineral density in the elderly can result from either low peak bone mass or accelerated bone loss, or a combination of the two. Nutritional factors play a role in both the attainment of peak bone mass and in the rate of age-related bone loss. The main determinants of peak bone mass are genetic factors, early-life nutrition, diet and exercise. Of the nutritional factors Ca, and particularly milk, are the most important contributors to peak bone mass. Some of these factors may interact; for example, a low dietary Ca in addition to an unfavourable vitamin D receptor gene polymorphism may result in low peak bone mass. The age-related changes in bone mass may also have a genetic basis, but deficiency of oestrogen is a major contributor. In addition, undernutrition is common in the elderly, and lack of dietary protein contributes both to impaired bone mineral conservation and increased propensity to fall. There is a decreased ability of the intestine to adapt to a low-Ca diet with increasing age. Other dietary factors include vitamin K, Zn and fruit and vegetables. Adequate nutritional status, particularly of Ca and vitamin D, is essential for the successful pharmaceutical treatment of osteoporosis. Thus, strategies for enhancing skeletal health in the elderly must begin in early childhood, and continue throughout life.

Puberty and bone development.

Puberty has a key role for bone development. Skeletal mass approximately doubles at the end of adolescence. The main determinants of pubertal gain of bone mass are the sex steroids, growth hormone and insulin-like growth factors (by their effects on bone and muscle mass), 1,25-dihydroxyvitamin D (by stimulating calcium absorption and retention) and muscle mass (by regulating modelling/remodelling thresholds). Calcium intake is an additional factor influencing bone formation. The interactions among these factors are undefined. The accrual of bone mass during puberty is a major determinant of peak bone mass and, thereby, of the risk of osteoporotic fractures during advanced age.

The Osteoporosis Primer.

Janet E. Henderson and David Goltzman, editors. Cambridge, United Kingdom: Cambridge University Press; 2000. 388 pages. $64.95. Although this book is called a primer and has been published as a paperback, it is a very thorough text with outstanding references for each chapter. The chapters are written by scientists and clinicians who are well known in their fields. The book is divided into four parts. The first three parts are devoted to the molecular and cellular environment of bone, the determinants of peak bone mass, and the pathophysiology of the aging skeleton. These sections explore the basic science of …

Bone Mineral Density Testing and Osteoporosis Education Improve Lifestyle Behaviors in Premenopausal Women: A Prospective Study

One way to decrease the risk of osteoporosis is to maximize peak bone mass. Peak bone mass may be moderately influenced by lifestyle behaviors: increasing calcium and exercise, decreasing alcohol intake and smoking may increase peak bone mass. We examined the effects of osteoporosis education and bone mineral density (BMD) testing on self-reported lifestyle behaviors in 669 premenopausal women enrolled in a prospective study to assess determinants of peak bone mass. Study participants completed a questionnaire that assessed lifestyle behaviors, received pamphlets about osteoporosis, and had BMD testing. One year later, the women completed a similar questionnaire. After education about osteoporosis and BMD testing, women reported that they were less likely to smoke (odds ratio [OR] = 0.55; 95% confidence interval [95% CI]: 0.28-1.0), consume alcohol (OR = 0.13; 95% CI: 0.04-0.34), and caffeinated beverages (OR = 0. 43; 95% CI: 0.27-0.68). Women were more likely to use calcium supplements (OR = 4.3; 95% CI: 3.04-6.2), vitamin D supplements (OR = 12.6; 95% CI: 7.4-22.9), and drink at least one glass of milk a day (OR = 13.3; 95% CI: 7.8-23.9). Further, women with low bone mass were more likely to use calcium supplements (OR = 1.7; 95% CI: 1.2-2.3) and vitamin D supplements (OR = 1.6; 95% CI:1.1-2.2) compared with women who had normal bone mass. Thus, our intervention improved self-reported lifestyle behaviors in premenopausal women. Such behaviors may ultimately increase peak bone mass and decrease the risk of developing osteoporosis.

Determinants of peak bone mass: clinical and genetic analyses in a young female Canadian cohort.

Peak bone mass has been shown to be a significant predictor of risk for osteoporosis. Previous studies have demonstrated that skeletal mass accumulation is under strong genetic control, and efforts have been made to identify candidate loci. Determinants of peak bone mass also include diet, physical activity, hormonal status, and other clinical factors. The overall contribution of these factors, genetic and nongenetic, and their interaction in determining peak bone density status have not been delineated. Six hundred and seventy-seven healthy unrelated Caucasian women ages 18-35 years were assessed. A detailed, standardized interview was conducted to evaluate lifestyle factors, menstrual and reproductive history, medical conditions, medication use, and family history of osteoporosis. Bone mineral density (BMD) was measured at the lumbar spine (L2-L4) and the femoral neck (hip) using dual-energy X-ray absorptiometry. Genotyping of the vitamin D receptor (VDR) locus at three polymorphic sites (BsmI, ApaI, and TaqI) was performed. In bivariate analyses, BMD at the lumbar spine and hip was positively correlated with weight, height, body mass index (BMI), and level of physical activity, both now and during adolescence, but negatively correlated with a family history of osteoporosis. Hip, but not spine BMD, correlated positively with dietary intake of calcium, and negatively with amenorrhea of more than 3 months, with caffeine intake, and with age. Spine, but not hip BMD, correlated positively with age and with number of pregnancies. VDR haplotype demonstrated significant associations with BMD at the hip, level of physical activity currently, and BMI. In multivariate analysis, independent predictors of greater BMD (at the hip or spine) were: age (younger for the hip, older for the spine), greater body weight, greater height (hip only), higher level of physical activity now and during adolescence, no family history of osteoporosis, and VDR genotype (hip only). Weight, age, level of physical activity, and family history are independent predictors of peak BMD. Of these factors, weight accounts for over half the explained variability in BMD. VDR alleles are significant independent predictors of peak femoral neck, but not lumbar spine BMD, even after adjusting for family history of osteoporosis, weight, age, and exercise. However, the overall contribution of this genetic determinant is modest. Taken together, these factors explained approximately 17% and 21% of the variability in peak spine and hip BMD, respectively, in our cohort. Future research should be aimed at further evaluation of genetic determinants of BMD. Most importantly, understanding the critical interactive nature between genes and the environment will facilitate development of targeted strategies directed at modifying lifestyle factors as well as earlier intervention in the most susceptible individuals.

Determinants of peak bone mass and mechanisms of bone loss.

Peak bone mass (PBM) is defined as the amount of bony tissue present at the end of skeletal maturation [1]. Bone strength is mainly determined by volumetric density, i.e., the amount of bony tissue per unit of volume, by outer bone dimensions, by intraosseous microarchitecture, and by intrinsic bone quality [2]. The contribution of bone size to strength is illustrated by the recent observation that for matched vertebral height and volumetric density, patients with vertebral fracture have smaller crosssectional vertebral body area than nonfractured subjects [3]. Before puberty, no consistent gender difference in bone mass of axial or appendicular skeleton has been reported [4–6]. Furthermore, there is no evidence for a gender difference in bone mass at birth. Likewise, the volumetric bone mineral density (BMD) appears to be similar among female and male newborns [7]. This absence of gender difference in bone mass is maintained until the onset of pubertal maturation [8–10]. During puberty, bone mineral mass more than doubles in skeletal sites such as the lumbar spine [6,11]. This increase occurs approximately 2 years later in males than females. Then, a gender difference in bone mass is expressed. In addition to a possible late prepubertal increased value due to the 2-year delay in the onset of pubertal maturation in males, this difference appears to result essentially from a more prolonged bone growth period in males than females, with a larger increase in bone size and in cortical thickness [12]. During puberty, the accumulation rate in areal BMD at both the lumbar spine and femoral neck levels increases over a 3or 4year period in females and males, respectively [11]. The change in bone mass accumulation rate is less marked in the long bone diaphyses. Puberty affects bone size much more than volumetric BMD (Fig. 1). There is no significant gender difference in the volumetric trabecular density at the end of pubertal maturation [8,9,13,14]. However, blacks have greater volumetric density than whites [10,14]: trabecular number is similar, but the trabeculae appear to be thicker [15]. In cortical peripheral bone, there is no gender difference in the cross-sectional area of midfemoral shaft after adjustment for height and weight [13]. However, it is greater in blacks than whites for an identical cortical thickness [14]. Thus, despite the same cortical thickness, larger bones result in a greater bone mineral content. Bony tissue situated more distantly from the bone’s central axis confers a greater resistance to bending [2,16]. There is an asynchrony between the gain in statural height and bone mass growth [6,11,17]. Indeed, the peak of statural growth velocity precedes the peak of maximal bone mineral gain. In males, the greatest difference occurs in the 13–14 year age group and is more pronounced for lumbar spine and femoral neck than for midfemoral shaft [11]. In females, the largest difference occurs in the 11–12 year age group, corresponding in both genders to pubertal stages P2– P3. This phenomenon may be responsible for the occurrence of a transient relative increase in bone fragility that may account for the pattern of fracture Osteoporos Int (1999) Suppl. 2:S17–S23 s 1999 International Osteoporosis Foundation and National Osteoporosis Foundation Osteoporosis International

Nutrition, exercise, and bone status in youth.

The maximal amount of bone mass gained during growth (peak bone mass) is an important determinant of bone mass in later life and thereby an important determinant of fracture risk. Although genetic factors appear to be primary determinants of peak bone mass, environmental factors such as physical activity and nutrition also contribute. In this article, bone growth and maintenance are reviewed, and mechanisms are described whereby physical activity can affect bone mass. Studies addressing the effects of physical activity on bone status in youth are reviewed: Although conclusive data are not yet available, considerable evidence supports the importance of activity, especially activity initiated before puberty. The critical role of energy in bone growth is outlined, and studies assessing the impact of calcium intake during childhood and adolescence are reviewed. Although results of intervention trials are equivocal, other evidence supports a role for calcium intake during growth. Recommendations for physical activity and nutrition, directed to children and adolescents, are presented.

Determinants of peak bone mass in Chinese women aged 21-40 years. III. Physical activity and bone mineral density.

Previous studies on the relation between moderate physical activity and bone mass have observed conflicting results. Many of these studies have not dissociated the role of physical activity by age groups and in relation to the period of peak bone mass formation. Our cross-sectional analysis of the baseline data of a longitudinal study of 273 women aged 21-40 attempted to evaluate the role of moderate physical activity on bone mass around the period of peak bone mass attainment. The analyses were carried out separately for the two age groups--21-30 and 31-40--and had also taken into account the effects of age, dietary calcium intake, and lean body mass on bone mineral density (BMD). The total metabolic equivalent values (MET) of leisure time physical activity was based on the MET values for each activity and the reported time spent on each activity in the past year. The results indicated that among the younger group of women, high level of leisure time physical activity was associated with higher bone mass at both the spine and the hip. Additive effects of physical activity and dietary calcium intake on the spine and the hip BMD were observed. Together with age and lean body mass, physical activity and dietary calcium intake accounted for 19% of the variances of bone mineral at the spine and 9-11% at the hip. Among women aged 31-40, presumably after the peak bone mass formation, lean body mass as well as fat mass have independent strong association with BMD. Physical activity was not associated with bone mass in this age group.

Sex steroids and the acquisition of bone mass.

Bone mineralization increases with age, height and weight through childhood, with a significant gain during pubertal development. Approximately 37% of bone mass is accumulated between pubertal stages 2-5. The factors driving the pubertal increase of bone mass is not fully known, but a crucial role is played by the sex steroids. Patients with central precocious puberty show an increased bone mineral density (BMD) for their chronological age, but appropriate for their bone age and pubertal stage. In girls and boys with hypogonadism, as well as in constitutional delay of puberty, the 'tempo' of puberty seems to be another important determinant of peak bone mass. Hypogonadal patients increase their BMD when treated in adulthood with sex steroid substitutive therapy, but normal adult BMD values are not reached. If these patients start sex steroid therapy at the appropriate age for the onset of pubertal development, however, a greater increase in BMD occurs. Both oestrogen and androgen receptors have been demonstrated in bone cells. Patients with oestrogen resistance or aromatase deficiency had a severely undermineralized skeleton. Reduced area and volume BMD are also present in patients with complete androgen resistant syndrome compared to normal. The pubertal increase of BMD may be the result of the coordinated activation of oestrogen and androgen receptors at the bone level in both sexes. In conclusion, the gonadal secretion of sex steroids, the tempo of puberty, and the normal function of both oestrogen and androgen receptors seem to be important factors in the acquisition of bone mass.

Pathogenesis of osteoporosis.

Fractures, the clinical outcome associated with osteoporosis, have a complex pathogenesis involving, in most cases, both trauma to the bone and increased skeletal fragility. Recent evidence also suggests that the geometry of the bone is important in determining fracture risk, and geometric properties are in part genetically determined. Skeletal fragility is largely determined by bone mass and the microstructure of bone. Loss of trabeculae and their connections has been well documented and undoubtedly contributes to risk of some fractures. Microdamage has also been shown to occur within the skeleton and could contribute to fragility. Peak bone mass is a major factor in determination of subsequent fracture risk and it has both genetic and environmental determinants. Twin studies have suggested a major genetic contribution and that a few genes may be responsible, but these genes have not been clearly identified. Nutrition, especially calcium intake, and exercise also contribute to the determination of peak bone mass and are especially important during the major period of bone acquisition up to the age of 18. Bone loss among women begins in the perimenopausal period, although loss from the hip begins earlier. The loss is associated with both estrogen and androgen concentrations. Later in life other factors such as the development of secondary hyperparathyroidism may contribute to the continued loss of bone. Males lose bone at about half the rate of females, but the underlying contributing factors are not well documented. The pathogenesis of osteoporotic fractures is complex, but this allows for the development of multiple interventions, which may reduce the frequency of such fractures.

Urinary calcium, sodium, and bone mass of young females

Calcium is an important determinant of peak bone mass in young adults because of its influence on skeletal development during growth. Attainment of maximum peak bone mass requires optimal positive balance between calcium intake and obligatory losses of calcium, primarily in urine and feces. Urinary excretion is an important determinant of calcium retention in the body. Accordingly, the purpose of this study was to evaluate the influence of various nutrients on urinary calcium excretion, and to assess their impact on bone mass of young females, aged 8-13 y, during early puberty. The study was conducted in 381 healthy white females in pubertal stage 2. From each participant we collected basic anthropometric measurements, a 3-d food record, blood, a 24-h urine sample, and bone mass measurements of the total body and forearm by dual X-ray absorptiometry. Urinary sodium was found to be one of the most important determinants of urinary calcium excretion: [urinary calcium (mmol/d) = 0.01154 x urinary sodium (mmol/d) + 0.823], whereas calcium intake had relatively little impact: [urinary calcium (mmol/d) = 0.02252 x calcium intake (mmol/d) + 1.5261]. Urinary calcium was much higher at a calcium intake of approximately 37.5 mmol/d (1500 mg/d), supporting the notion that calcium is a threshold nutrient. Calcium intake had a significant positive influence on the bone mineral content and density of the whole body and radius shaft whereas urinary calcium had a negative influence, presumably by reducing calcium accretion into the skeleton.(ABSTRACT TRUNCATED AT 250 WORDS)

Childhood growth, physical activity, and peak bone mass in women.

Peak bone mass is an important determinant of the risk of osteoporotic fracture, and preventive strategies against osteoporosis require a clear understanding of the factors influencing bone gain in early life. We report a longitudinal study aiming to identify the relationships between childhood growth, lifestyle, and peak bone mass in women. One hundred and fifty-three women born in a British city during 1968-1969 were traced and studied in 1990. Data on their growth in childhood was obtained from linked birth and school health records; current bone mineral measurements were made by dual X-ray absorptiometry. There were statistically significant associations between weight at 1 year and BMC (but not BMD) at the lumbar spine (r = 0.32, p < 0.01) and femoral neck (r = 0.26, p < 0.01). These remained significant after adjusting for current weight. There were also strong relationships between childhood height measurements and adult BMC at the two skeletal sites. Physical activity was the major lifestyle determinant of BMD after allowing for body build. We conclude that infant growth and physical activity in childhood are important determinants of peak bone mass in women. Growth primarily determines the size of the skeletal envelope, and its trajectory is established by age 1 year. Activity, in contrast, modulates the mineral density within the skeletal envelope and may contribute to the consolidation of bone following the end of linear growth.

Le pic de masse osseuse: réalités et incertitudes

Peak bone mass, which can be defined as the amount of bony tissue present at the end of the skeletal maturation, is an important determinant of osteoporotic fracture risk in adulthood. The techniques of single or dual energy absorptiometry measure the so-called “areal” or “surface” bone mineral density (BMD), a variable which has been shown to be directly related to bone strength. During puberty the gender difference in bone mass becomes expressed. This difference appears to be essentially due to a more prolonged bone maturation period in males than in females, with a larger increase in bone size and cortical thickness, as there is no significant sex difference in the volumetric trabecular density at the end of pubertal maturation. At the beginning of the 3rd decade, there is a large variability in the normal values of areal BMD in axial and appendicular skeleton. This large variance, which is observed at sites particularly susceptible to osteoporotic fractures in adulthood, such as lumbar spine and femoral neck, is barely reduced after correction for statural height, and does not appear to substantially increase during adult life. It is generally accepted that peak bone mass at any skeletal site is attained in both sexes during the mid-thirties. However, recent studies indicate that in healthy caucasian females, bone mass accumulation can virtually be completed before the end of the second decade, for both lumbar spine and femoral neck. Several variables are supposed to influence bone mass accumulation during growth: heredity, sex, diet components, endocrine factors, mechanical forces, and exposure to risk factors. Quantitatively, the most prominent factor appears to be the genetic determinant, as estimated by studies comparing monozygotic and dizygotic twins. That heredity is not the only determinant of peak bone mass is of practical interest, since environmental factors can be modified. With respect to nutrition, the quantitative importance of calcium intake in bone mass accumulation during growth, particularly at sites prone to osteoporotic fractures, still remains to be clearly determined. The same can be said for the impact of physical activity. Finally, the crucial years when external factors will be particularly effective on bone mass accumulation remain to be determined by longitudinal prospective studies in order to produce credible and well-targeted recommendations for the setting up of osteoporosis prevention programs aims at maximizing peak bone mass.

Exercise, smoking, and calcium intake during adolescence and early adulthood as determinants of peak bone mass

To evaluate the contribution to peak bone mass of exercise, smoking, and calcium intake in adolescents and young adults. Prospective cohort study with end point measurement (bone mineral density) after 11 years' follow up for lifestyle. Five university hospital clinics. 264 (153 females, 111 males) subjects aged 9 to 18 years at the beginning of the follow up and 20 to 29 years at the time of measurement of bone mineral density. Bone mineral density of lumbar spine and femoral neck by dual energy x ray absorptiometry; measures of physical activity and smoking and estimates of calcium intake repeated three times during follow up. In the groups with the lowest and highest levels of exercise the femoral bone mineral densities (adjusted for age and weight) were 0.918 and 0.988 g/cm2 for women (P = 0.015, analysis of covariance) and 0.943 and 1.042 g/cm2 for men (P = 0.005), respectively; at the lumbar spine the respective values were 1.045 and 1.131 (P = 0.005) for men. In men the femoral bone mineral densities (adjusted for age, weight, and exercise) were 1.022 and 0.923 g/cm2 for the groups with the lowest and highest values of smoking index (P = 0.054, analysis of covariance). In women the adjusted femoral bone mineral density increased by 4.7% together with increasing calcium intake (P = 0.089, analysis of covariance). In multiple regression analysis on bone mineral density of the femoral neck, weight, exercise, age, and smoking were independent predictors for men; with weight, exercise, and age for women. These predictors together explained 38% of the variance in bone mineral density in women and 46% in men. At the lumbar spine, weight, smoking, and exercise were predictors for men; and only weight for women. Regular exercise and not smoking is important in achieving maximal peak bone mass in adolescents and young adults.

Determinants of total-body and regional bone mineral content and density in postpubertal normal women

Some investigators consider body fat the main determinat of bone mass in women, and others, weight. Although genetics may be the primary determinant of peak bone mass, modifiable secondary factors such as nutrition and hormone exposure may significantly affect bone mass accretion during the second decade of life. To determine the principal determinants of bone mass, we analyzed total and regional bone mass (by dual-energy x-ray absorptiometry), weight, height, percentage body fat, and lean body mass in a group of 50 young women ranging in age from 14 to 18 years. Total-body bone mineral content, total-body bone mineral density, and total-body bone mineral density corrected for height, analyzed by multiple correlation, were not related to percentage body fat, although percentage body fat did correlate with the regional bone mineral content of the trunk ( P < .001), legs ( P < .01), and pelvis ( P < .001). Lean body mass correlated with total-body bone mineral content and density, total-body bone mineral density corrected for height ( P < .001), and regional bone mineral content of the trunk ( P < .05), arms ( P < .01), and legs ( P < .001), but not with regional bone mineral content of the pelvis and head. Weight correlated significantly ( P < .001) with all bone mass measurements except regional bone mineral content of the head, where the significance was P less than .05. Similar results were obtained by multiple regression analysis. These results indicate that weight, not body fat, is the main determinant of bone mass in postpubertal women.

Genetics of osteoporosis.

Identification of the major contribution of genetic factors in determination of peak bone mass at skeletal maturity and possibly on subsequent age-related bone loss has led to efforts to identify possible mechanisms. Recent evidence suggests one mechanism relates to genetic effects on bone turnover mediated via the vitamin D system. This field of research has potential for reducing osteoporotic fracture risk by allowing interventions at different stages in life to reduce this increasing problem of ageing societies.

Determinants of peak bone mass in young adult women: a review.

In concluding this review on the prevention on bone mass throughout the life, it must be emphasized that we need to learn much more about improving the development, maintenance and efficiency of the musculoskeletal system of women during all stages of the life cycle, but especially during adolescence and early adulthood when the greatest gains can be obtained. Even during the adult and postmenopausal years of life, interventions can be effectively tailored to yield significant, but small, improvements in bone mass and reductions in fracture rates. Both dietary and exercise/strength modalities need to be explored, separately and in combination, to accomplish these potentially achievable goals of improved bone mass and reduced fracture rates. Dietary calcium intakes need to be around 800–1000 mg/day (or possibly more) from early adolescence to late life, and such intake levels greatly exceed the WHO recommendation of 400–500 mg/day. In addition, vitamin D intakes need to be adequate so that calcium absorption can be optimized by postmenopausal women. Finally, excessive intakes of animal protein and phosphorus by adult women may adversely affect calcium retention by the skeleton.

Body composition and bone mass in post-menopausal women.

We aimed to assess total body composition and to study the interrelationships between fat and lean tissue mass with total and regional bone mass in healthy British post-menopausal women. Total body composition and regional bone mass were measured in 97 healthy post-menopausal women recruited from the general community. The mean age was 57.9 years, range 49-65. Total body composition (fat, lean tissue and bone mineral) and regional bone density in the lumbar spine and femur were measured by dual energy X-ray absorptiometry on a Lunar DPX. Significant negative correlations with age were found for total body bone mineral density (r = -0.200, P = 0.049), and lumbar spine bone mineral density (r = -0.28, P = 0.006); the calculated rate of bone loss from these two sites was 0.33 and 0.7% per annum respectively. Fat tissue mass showed a positive correlation with age (r = 0.22, P = 0.03). High correlations were observed between total body and regional bone mineral density (r = 0.755-0.829, P < 0.001). After adjustment for age and lean mass, statistically significant correlations were seen between fat tissue mass and all bone mass measurements (P < 0.01-0.001), the strongest correlations being found for total body bone mineral content and density (r = 0.477 and 0.488 respectively). Lean tissue mass showed a strong correlation with total body bone mineral content (r = 0.580, P < 0.001), after adjustment for age and fat mass; it was less strongly correlated with other bone mass measurements than fat mass, showing only weak correlations with total body, trochanteric and lumbar spine bone mineral density (r = 0.228-0.246, P < 0.05). Age-adjusted body weight showed stronger correlations with total and regional bone mass than did either body mass index or height. Both fat and lean tissue mass are related to total and regional bone mass in post-menopausal women, the relationship being strongest for fat mass. Body weight shows stronger correlations with bone mass than either height or body mass index. In view of the direction and magnitude of changes in fat, lean tissue and bone mineral after the menopause, adiposity and muscularity are more likely to be determinants of peak bone mass than of the rate of post-menopausal bone loss.