Our findings suggest that impaired grip strength is associated with the individual features, as well as with the overall summary definitions, of the metabolic syndrome. The potential for grip strength to be used in the clinical setting needs to be explored.

Although excessive glucocorticoids are a well-recognized cause of osteoporosis, little is known about the role of endogenous glucocorticoids in determining skeletal mass. We have performed a detailed study of the hypothalamic-pituitary-adrenal (HPA) axis to explore the relationships between cortisol secretion and adult bone mass in 151 healthy men and 96 healthy women aged 61 to 73 years. At baseline and 4-year follow-up, bone mineral density (BMD) was measured by dual energy X-ray absorptiometry (DXA) at the lumbar spine and proximal femur; a lifestyle questionnaire was completed; and height, weight, and waist and hip circumferences were measured. At follow-up subjects underwent a very low-dose (0.25 mg) dexamethasone suppression test, a low-dose (1 microg) short synacthen test, and a 24-hour urine collection for measurement of cortisol and its metabolites. In men, elevated peak plasma cortisol was associated with accelerated loss of mineral density in the lumbar spine (r = 0.16, P = 0.05). This relationship remained significant after adjustment for testosterone, estradiol, 25-hydroxyvitamin D, and parathyroid hormone levels (r = 0.22, P = 0.01) and after additional adjustment for age, (BM), activity, cigarette and alcohol consumption, and Kellgren/Lawrence score (r = 0.19, P = 0.03). In contrast in women, elevated peak plasma cortisol was associated with lower baseline BMD at the femoral neck (r = -0.23, P = 0.03) and greater femoral neck loss rate (r = 0.24, P = 0.02). There was no association between plasma cortisol concentrations after dexamethasone or urinary total cortisol metabolite excretion and bone density or bone loss rate at any site. These data provide evidence that circulating endogenous glucocorticoids influence the rate of involutional bone loss in healthy individuals.

Background: The renin angiotensin system is important in the regulation of vascular tone and fluid and electrolyte balance. The angiotensin converting enzyme gene (ACE) genotype has been shown to affect exercise response and glucose load response dependent on birth weight. Angiotensin II type I receptor (AGTR1) A1166C has previously been associated with the development of hypertension and coronary disease, but its metabolic effects have not been investigated. Method: AGTR1 A1166C was genotyped by allele specific PCR in 378 individuals from Hertfordshire, UK, who had been characterised for metabolic syndrome traits. Results: Genotype counts were: AA, 183; AC, 170; CC, 25, consistent with Hardy-Weinberg equilibrium. The CC genotype was associated with significantly lower body mass index (by 1.7 units) in men (p = 0.03), and the same magnitude effect in women with significant lower weight in both genders (p = 0.01), also lower waist circumference and waist-hip ratio (p = 0.01) in men, with a trend for lower waist circumference in women also. Additionally, the CC genotype and/or C allele was associated with lower fasting glucose and insulin, and 30 and 120 min glucose in men (respectively, p = 0.08, 0.04, 0.01, 0.06). Lower means of systolic blood pressure, pulse pressure, cholesterol, and fasting triglyceride were also observed for the CC genotype in both genders though these were not statistically significant. Conclusions: The AGTR1 1166 CC genotype appears to predispose to favourable anthropometric and metabolic traits, relative to cardiovascular risk.

A short food-based questionnaire provides useful information about the diet quality of older adults. This simple tool does not require nutrient analysis, and has the potential to be of value to non-specialist researchers.

These findings suggest dietary TAC may have important protective effects on glucose tolerance, especially in older obese women.

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Background: Reduced physical performance and physical activity have serious health consequences, but adult determinants do not fully explain variation in older people. Objective: Our objective was to investigate the relationship between early growth, physical performance and physical activity in older people. Methods: We studied 349 men and 280 women born 1931–1939 with known birth weight and weight at 1 year who were taking part in the Hertfordshire Cohort Study, UK. Physical performance was measured (3-m walk, chair rises and standing balance) and physical activity was assessed by questionnaire and converted to estimated energy expenditure. Results: Poor balance was associated with lower birth weight (odds ratio [OR] for poor balance per standard deviation [SD] increase in birth weight = 0.68, p = 0.01) and weight at 1 year (OR for poor balance per SD increase in weight at 1 year = 0.67, p = 0.03) after adjustment for age and current size in men, but not in women. There were no significant positive relationships between early size and growth and the other measures of physical performance or physical activity in men or women. Conclusion: Current lifestyle factors, particularly those affecting adult weight, may be more important than developmental influences on most measures of physical performance and physical activity in older people.

Lifetime cumulative occupational activity was not associated with hip BMD at retirement age. Our findings suggest that, if sedentary work conveys an increased risk of hip fracture, it is unlikely that the mechanism is through reductions in BMD at the hip and may relate to other physical effects, such as falls risk. Further studies will be needed to test this hypothesis.