Objective To describe new onset and persistence of self reported post-traumatic stress disorder symptoms in a large population based military cohort, many of whom were deployed in support of the wars in Iraq and Afghanistan.
OBJECTIVE -Accumulating research suggests low-circulating vitamin D concentrations, i.e., 25-hydroxyvitamin-D [25(OH)D], may be associated with an increased prevalence of metabolic syndrome; however, previous studies have not accounted for parathyroid hormone (PTH) levels. We examined the association of 25(OH)D and PTH with the prevalence of metabolic syndrome in a community-based cohort of older adults. RESULTS -In men, there was a significant trend (P ϭ 0.03) of increasing adjusted odds for metabolic syndrome with increasing PTH concentrations, primarily due to an odds ratio of 2.02 (95% CI 0.96 -4.24) in men in the top quintile (Ն63 ng/l) of PTH concentration. This association remained unchanged after taking into account 25(OH)D levels and excluding men with diabetes or impaired renal function; it was attenuated after adjustment for the homeostasis model assessment of insulin resistance. Neither PTH in women nor 25(OH)D levels in either sex was related to the metabolic syndrome.
RESEARCH DESIGN AND METHODSCONCLUSIONS -These findings suggest an increased risk of metabolic syndrome with elevated PTH levels in older men and no effect of 25(OH)D concentrations in either sex. The reason for the sex difference in the PTH-metabolic syndrome association is unknown. Prospective studies are necessary to better determine the roles of 25(OH)D and PTH in the etiology of metabolic syndrome.
Diabetes Care 30:1549-1555, 2007D ecreased vitamin D and elevated parathyroid hormone (PTH) levels may play a role in the etiology of metabolic syndrome, either through an association with individual components of metabolic syndrome or via insulin resistance (1,2). Vitamin D levels have been shown to be inversely related both with fasting glucose concentrations (3-5) and adiposity (6 -10) and have been suspected to be involved in the regulation of blood pressure, based on blood pressure reduction with vitamin D 3 supplementation in patients with essential hypertension (11,12). Other evidence suggests a role for vitamin D in maintaining normal insulin synthesis and secretion (13,14). Vitamin D and PTH are both responsible for maintaining extracellular calcium homeostasis (19). Vitamin D increases the efficiency of intestinal calcium absorption, and PTH is secreted in response to low-circulating calcium concentrations. Elevated PTH secondary to low vitamin D increases calcium resorption from the skeleton at the expense of an increased risk of fracture (20). Secondary hyperparathyroidism may also increase the risk of developing components of metabolic syndrome, including hypertension (21-26), obesity (6,9,10,27-29), and diabetes (30 -32). However, we are unaware of previous research investigating whether PTH levels are also associated with the metabolic syndrome.Previous studies linking low 25(OH)D with an increased prevalence of metabolic syndrome (1,18) were limited by their inability to simultaneously account for PTH, since both vitamin D and PTH operate within a tightly controlled feedback system to maintain extracellular calcium conce...
The IGF system has been implicated in cardiovascular disease (CVD) development. The prospective association of serum IGF-I and IGF-binding protein-1 (IGFBP-1) with all cause, ischemic heart disease (IHD), and non-IHD CVD mortality was examined in 633 men and 552 nonestrogen-using postmenopausal women, aged 51-98 yr (mean, 74 yr) in 1988-1992, who were followed through July 2001 (96% follow-up). During the 9- to 13-yr follow-up, there were 522 deaths; 224 were attributed to CVD, and 105 were caused by IHD. IGF-I and IGFBP-1 were independently and jointly related to risk of IHD mortality. In a proportional hazards model including both IGF-I and IGFBP-1 and adjusting for CVD risk factors, the relative risk of IHD mortality was 38% higher for every 40 ng/ml (1 SD) decrease in IGF-I (95% confidence interval, 1.09-1.76; P = 0.005) and 3.11 times greater for those in the lowest quintile of IGFBP-1 (95% confidence interval, 1.74-5.56; P < 0.001) compared with those with higher IGFBP-1 levels. IGF-I and IGFBP-1 (alone or in combination) were not related to risk of all cause or non-IHD CVD mortality. We conclude that low baseline levels of IGF-I and IGFBP-1 increase the risk of fatal IHD among elderly men and women independent of prevalent IHD and CVD risk factors.
This study examined cross-sectional and prospective associations of exercise with depressed mood in a community-based sample of older men and women (aged 50--89 years in 1984--1987) in southern California. Regular strenuous exercise and exercise > or =3 times per week were reported; depressed mood was assessed by using the Beck Depression Inventory (BDI). After exclusion of persons with categorical depression and those rating themselves largely or extremely physically limited during the previous month, data on 932 men and 1,097 women were available for cross-sectional analysis. Exercise and depressed mood were reassessed for 404 men and 540 women in 1992--1995; these data were the focus of prospective analyses. In 1984--1987, exercise rates were high (>80%), and average BDI scores were low. Cross-sectional analyses indicated that before and after adjustment for covariates, exercise was significantly associated with less depressed mood. However, prospective analyses of the 944 persons who attended both clinic visits indicated no association between baseline exercise and either follow-up BDI score (p > 0.10) or change in BDI score between baseline and follow-up (p > 0.10). Results confirm that exercisers have less depressed mood. However, exercise does not protect against future depressed mood for those not clinically depressed at baseline.
These results suggest that isoflavone supplementation has a favorable effect on cognitive function, particularly verbal memory, in postmenopausal women.
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