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Background: Physical activity (PA) is associated with reduced mortality. However, whether there is an added benefit of long‐term endurance training is unclear. Thus, we aimed to examine 10‐year mortality in older male endurance athletes compared with an older male general population. Method: Male athletes (n = 503) participating in an annual long‐distance ski race (median years of participation: 14, range: 1–53) from the Norwegian Birkebeiner Aging study (BiAS), and non‐athletic men (n = 1867) attending the sixth Tromsø Study (Tromsø6) aged ≥65 years were included. Associations with endurance sport practice and joint exposures of endurance sport practice and self‐reported leisure‐time PA with all‐cause mortality were examined. We analyzed the data with Cox proportional hazard models and regression standardization. Results: After 10 years (median: 10.4, range: 0.5–11.1) the mortality rate was lower in athletes (hazard ratio (HR) 0.34, 95% confidence interval (CI): 0.24–0.49) compared with non‐athletes, corresponding to a 15% (95% CI: 12–19%) absolute risk reduction associated with endurance sport practice. In joint analyses categorized according to PA and endurance sport practice, we observed an inverse dose–response relationship with mortality (p < 0.001). Compared to inactive non‐athletes, PA was associated with lower mortality in both active non‐athletes and athletes. However, the observed benefit among participants reporting moderate‐to‐vigorous PA was larger in athletes (HR: 0.21, 95% CI: 0.14–0.32) than non‐athletes (HR: 0.43, 95% CI: 0.31–0.59) (p < 0.01). Conclusion: Endurance sport practice was associated with reduced 10‐year mortality, beyond the effect of PA in older men. This study suggests that long‐term endurance sport practice maintained into older adulthood promotes longevity. [ABSTRACT FROM AUTHOR]

Introduction: Central ghrelin signaling is required for the rewarding effects of alcohol in mice. Because ghrelin is implied in other addictive behaviors such as eating disorders and smoking, and because there is co-morbidity between these disorders and alcohol dependence, the ghrelin signaling system could be involved in mediating reward in general. Furthermore, in humans, single nucleotide polymorphisms (SNPs) and haplotypes of the pro-ghrelin gene (GHRL) and the ghrelin receptor gene ( GHSR) have previously been associated with increased alcohol consumption and increased body weight. Known gender differences in plasma ghrelin levels prompted us to investigate genetic variation of the ghrelin signaling system in females with severe alcohol dependence ( n = 113) and in a selected control sample of female low-consumers of alcohol from a large cohort study in southwest Sweden ( n = 212). Methods: Six tag SNPs in the GHRL (rs696217, rs3491141, rs4684677, rs35680, rs42451, and rs26802) and four tag SNPs in the GHSR (rs495225, rs2232165, rs572169, and rs2948694) were genotyped in all individuals. Results: We found that one GHRL haplotype was associated with reports of paternal alcohol dependence as well as with reports of withdrawal symptoms in the female alcohol-dependent group. Associations with 2 GHSR haplotypes and smoking were also shown. One of these haplotypes was also negatively associated with BMI in controls, while another haplotype was associated with having the early-onset, more heredity-driven, type 2 form of alcohol dependence in the patient group. Conclusion: Taken together, the genes encoding the ghrelin signaling system cannot be regarded as major susceptibility genes for female alcohol dependence, but is, however, involved in paternal heritability and may affect other reward- and energy-related factors such as smoking and BMI. [ABSTRACT FROM AUTHOR]

OBJECTIVES: To examine whether total serum homocysteine (tHcy) in a population-based sample of middle-aged women is an independent risk factor for presence of lacunar infarcts (LIs) 24 years later. DESIGN: Prospective population study, follow-up time 24 years. SETTING: Gothenburg, an urban area in western Sweden. PARTICIPANTS: Five hundred twenty-six women, 89.6% of the original study sample of the Population Study of Women in Gothenburg, aged 46 to 60 at baseline in 1968/69 and re-examined at age 70 to 84. MEASUREMENTS: After 24 years of follow-up, all subjects underwent a psychiatric examination, and 277 computerized tomography (CT) scans of the brain were performed. Two radiologists assessed LIs and white matter lesions (WMLs). Baseline serum tHcy was analyzed from frozen stored serum samples. Logistic regression analyses were performed controlling for potential confounders such as age and selected cardiovascular risk factors. RESULTS: Thirty-four subjects had LIs in 1992 (12.3%). In the full multivariate-adjusted stepwise model, LIs were associated with elevated tHcy (odds ratio (OR)=1.09, 95% confidence interval (CI)=1.01–1.17 per μmol/L of tHcy increment). Women with tHcy values in the highest tertile were almost three times as likely to have LIs (OR=2.82, 95% CI=1.34–5.93) as were those in the lowest tertile. tHcy was not related to WMLs. Subjects who did not undergo a CT scan did not differ from those who did regarding tHcy or any of the covariates studied. CONCLUSION: tHcy in middle-aged women is an independent risk factor for LIs, but not WMLs, as observed using CT later in life. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Mid-Pregnancy Androgen Levels Are Negatively Associated With Breastfeeding," by S. M. Carlsen et al that was published in a 2010 issue.

A letter to the editor is presented in response to the article "Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study" by H. Petursson and colleagues in the February 2012 issue.

Alzheimer's disease (AD) and age-related macular degeneration (AMD) share several epidemiological and biochemical features. The present study aimed to assess the possible influence of the AMD-associated complement factor H (CFH) Y402H (1277T > C) polymorphism on the risk of AD. Caucasian subjects (n = 800) meeting the criteria for probable (n = 717) or definite (n = 83) AD and Caucasian non-demented controls (n = 1265) were included in this multi-center case-control study, in which genotype and allele frequencies of the CFH 1277T > C polymorphism were determined and related to diagnosis, APOE genotype, Mini-Mental State Examination score (MMSE) and the cerebrospinal fluid (CSF) biomarkers total-tau (T-tau), phospho-tau(181) (P-tau(181)), and beta-amyloid(1-42) (Abeta(1-42)). The AMD-associated CFH genotypes (1277CC and 1277TC) were overrepresented in subjects with AD as compared to control individuals (P = 0.029). Positive C carrier status was associated with an odds ratio (OR) for AD of 1.24 (95% confidence interval [CI] 1.02-1.50). When APOE epsilon4 carrier status was included in the regression model, this association was even stronger (OR 1.34, 95% CI: 1.08-1.65, P = 0.007). Subgroup analysis showed that the association between CFH C allele positivity and AD was only evident for individuals carrying the APOE epsilon4 allele. Positive C carrier status was also associated with lower levels of CSF Abeta(1-42) selectively in the control group in an APOE epsilon4-independent manner (P = 0.003). In conclusion, the CFH 1277T > C polymorphism seems to influence the risk of AD and there appears to be an interaction between CFH 1277C and APOE epsilon4 alleles. The CFH 1277C allele may predispose patients for co-morbidity in AD and AMD., (2007 Wiley-Liss, Inc.)