Bone mineral density and chronic lung disease mortality: the Rotterdam study

Context: Low bone mineral density (BMD) has been associated with increased all-cause mortality. Cause-specific mortality studies have been controversial. Objective: The aim of the study was to investigate associations between BMD and all-cause mortality and in-depth cause-specific mortality. Design and Setting: We studied two cohorts from the prospective Rotterdam Study (RS), initiated in 1990 (RS-I) and 2000 (RS-II) with average follow-up of 17.1 (RS-I) and 10.2 (RS-II) years until January 2011. Baseline femoral neck BMD was analyzed in SD values. Deaths were classified according to International Classification of Diseases into seven groups: cardiovascular diseases, cancer, infections, external, dementia, chronic lung diseases, and other causes. Gender-stratified Cox and competing-risks models were adjusted for age, body mass index, and smoking. Participants: The study included 5779 subjects from RS-I and 2055 from RS-II. Main Outcome Measurements: We measured all-cause and cause-specific mortality. Results: A significant inverse association between BMD and all-cause mortality was found in males [expressed as hazard ratio (95% confidence interval)]: RS-I, 1.07 (1.01-1.13), P = .020; RS-II, 1.31 (1.12-1.55), P = .001); but it was not found in females: RS-I, 1.05 (0.99-1.11), P = .098; RS-II, 0.91 (0.74-1.12), P = .362. An inverse association with chronic lung disease mortality was found in males [RS-I, 1.75 (1.34-2.29), P < .001; RS-II, 2.15 (1.05-4.42), P = .037] and in RS-I in females [1.72 (1.16-2.57); P = .008], persisting after multiple adjustments and excluding prevalent chronic obstructive pulmonary disease. A positive association between BMD and cancer mortality was detected in females in RS-I [0.89 (0.80-0.99); P = .043]. No association was found with cardiovascular mortality. Conclusions: BMD is inversely associated with mortality. The strong association of BMD with chronic lung disease mortality is a novel finding that needs further analysis to clarify underlying mechanisms

Early childhood aggressive behaviour: Negative interactions with paternal antisocial behaviour and maternal postpartum depressive symptoms across two international cohorts.

BACKGROUND: Early childhood aggressive behaviour is a predictor of future violence. Therefore, identifying risk factors for children's aggressive behaviour is important in understanding underlying mechanisms. Maternal postpartum depression is a known risk factor. However, little research has focused on the influence of paternal behaviour on early childhood aggression and its interaction with maternal postpartum depression. METHODS: This study was performed in two cohorts: the Fathers Project, in the United Kingdom (n = 143) and the Generation R Study, in The Netherlands (n = 549). In both cohorts, we related paternal antisocial personality (ASP) traits and maternal postpartum depressive (PPD) symptoms to childhood aggressive behaviour at age two (Fathers Project) and age three (Generation R Study). We additionally tested whether the presence of paternal ASP traits increased the association between maternal PPD-symptoms and early childhood aggression. RESULTS: The association between paternal ASP traits and early childhood aggressive behaviour, corrected for maternal PPD-symptoms, was similar in magnitude between the cohorts (Fathers Project: standardized β = 0.12, p = 0.146; Generation R: β = 0.14, p = 0.001), although the association was not statistically significant in the Fathers Project. Strikingly, and in contrast to our expectations, there was evidence of a negative interaction between paternal ASP traits and maternal PPD-symptoms on childhood aggressive behaviour (Fathers Project: β = -0.20, p = 0.020; Generation R: β = -0.09, p = 0.043) in both studies. This meant that with higher levels of paternal ASP traits the association between maternal PPD-symptoms and childhood aggressive behaviour was less and vice versa. CONCLUSIONS: Our findings stress the importance of including both maternal and paternal psychopathology in future studies and interventions focusing on early childhood aggressive behaviour.Wellcome Trus

Predicting hair cortisol levels with hair pigmentation genes

Cortisol concentrations in hair are used to create hormone profiles spanning months. This method allows assessment of chronic cortisol exposure, but might be biased by hair pigmentation: dark hair was previously related to higher concentrations. It is unclear whether this association arises from local effects, such as increased hormone extractability, or whether the association represents systemic differences arising from population stratification. We tested the hypothesis that hair pigmentation gene variants are associated with varying cortisol levels independent of genetic ancestry. Hormone concentrations and genotype were measured in 1674 children from the Generation R cohort at age 6. We computed a polygenic score of hair color based on 9 single nucleotide polymorphisms. This score was used to predict hair cortisol concentrations, adjusted for genetic ancestry, sex, age and corticosteroid use. A 1-standard deviation (SD) higher polygenic score (darker hair) was associated with 0.08 SD higher cortisol levels (SE = 0.03, p = 0.002). This suggests that variation in hair cortisol concentrations is partly explained by local hair effects. In multi-ancestry studies this hair pigmentation bias can reduce power and confound results. Researchers should therefore consider adjusting analyses by reported hair color, by polygenic scores, or by both

Bullying and Victimization Among Young Elementary School Children: The Role of Child Ethnicity and Ethnic School Composition

School-aged children with an ethnic minority background are relatively often involved in bullying and victimization, but the role of ethnic composition of schools in this context remains unclear. This study examined the relation between ethnic minority background, ethnic school composition, and bullying behaviour around primary school entry in the Netherlands. The study was based on a 2008/2009 school survey in Rotterdam, a Dutch city where about 50 % of children have a non-Dutch background. For 8523 children, teacher reports of bullying behaviour at age 5–6 years were available. Children with a non-Dutch background had higher odds of being a victim (adjusted OR 1.41, 95 % CI 1.11, 1.80), bully (OR 1.38, 95 % CI 1.20, 1.58) or bully-victim (OR 1.38, 95 % CI 1.19, 1.62) than children of Dutch national origin. Ethnic diversity in schools increased children’s risk of bullying behaviour (e.g. ORvictim per 0.1 increase in 0–1 diversity range = 1.06, 95 % CI 1.00, 1.13), with children of both Dutch and non-Dutch national origin relatively more often involved in bullying in ethnically diverse schools. The proportion of same-ethnic peers in school reduced the risk of bullying among children of Dutch national origin (e.g. ORvictim per 10 % more same-ethnic children = 0.90, 95 % CI 0.83, 0.98), but not among non-Dutch children. In conclusion, ethnic minority background and ethnic diversity within schools are risk factors for bullying among 5–6 year olds. Plausibly, reductions in absolute numbers of bullying events may be obtained with tailor-made interventions in ethnically diverse schools. Such interventions should preferably be offered early in the school curriculum

The Rotterdam Study: objectives and design update

The Rotterdam Study is a prospective cohort study ongoing since 1990 in the city of Rotterdam in the Netherlands. The study targets cardiovascular, neurological, ophthalmological and endocrine diseases. As of 2008 about 15,000 subjects aged 45 years or over comprise the Rotterdam Study cohort. The findings of the Rotterdam Study have been presented in some 600 research articles and reports (see http://www.epib.nl/rotterdamstudy). This article gives the reasons for the study and its design. It also presents a summary of the major findings and an update of the objectives and methods

Insufficient Sun Exposure Has Become a Real Public Health Problem.

This article aims to alert the medical community and public health authorities to accumulating evidence on health benefits from sun exposure, which suggests that insufficient sun exposure is a significant public health problem. Studies in the past decade indicate that insufficient sun exposure may be responsible for 340,000 deaths in the United States and 480,000 deaths in Europe per year, and an increased incidence of breast cancer, colorectal cancer, hypertension, cardiovascular disease, metabolic syndrome, multiple sclerosis, Alzheimer's disease, autism, asthma, type 1 diabetes and myopia. Vitamin D has long been considered the principal mediator of beneficial effects of sun exposure. However, oral vitamin D supplementation has not been convincingly shown to prevent the above conditions; thus, serum 25(OH)D as an indicator of vitamin D status may be a proxy for and not a mediator of beneficial effects of sun exposure. New candidate mechanisms include the release of nitric oxide from the skin and direct effects of ultraviolet radiation (UVR) on peripheral blood cells. Collectively, this evidence indicates it would be wise for people living outside the tropics to ensure they expose their skin sufficiently to the sun. To minimize the harms of excessive sun exposure, great care must be taken to avoid sunburn, and sun exposure during high ambient UVR seasons should be obtained incrementally at not more than 5-30 min a day (depending on skin type and UV index), in season-appropriate clothing and with eyes closed or protected by sunglasses that filter UVR

Maternal psychological distress and fetal growth trajectories: the Generation R Study

Abstract BACKGROUND: Previous research suggests, though not consistently, that maternal psychological distress during pregnancy leads to adverse birth outcomes. We investigated whether maternal psychological distress affects fetal growth during the period of mid-pregnancy until birth. METHOD: Pregnant women (n=6313) reported levels of psychological distress using the Brief Symptom Inventory (anxious and depressive symptoms) and the Family Assessment Device (family stress) at 20.6 weeks pregnancy and had fetal ultrasound measurements in mid- and late pregnancy. Estimated fetal weight was calculated using head circumference, abdominal circumference and femur length. RESULTS: In mid-pregnancy, maternal distress was not linked to fetal size. In late pregnancy, however, anxious symptoms were related to fetal size after controlling for potential confounders. Anxious symptoms were also associated with a 37.73 g [95% confidence interval (CI) -69.22 to -6.25, p=0.019] lower birth weight. Wh

Air pollution exposure during pregnancy and childhood autistic traits in four European population-based cohort studies : the ESCAPE project

Background: Prenatal exposure to air pollutants has been suggested as a possible etiologic factor for the occurrence of autism spectrum disorder. Objectives: We aimed to assess whether prenatal air pollution exposure is associated with childhood autistic traits in the general population. Methods: Ours was a collaborative study of four European population-based birth/child cohorts— CATSS (Sweden), Generation R (the Netherlands), GASPII (Italy), and INMA (Spain). Nitrogen oxides (NO2, NOx) and particulate matter (PM) with diameters of ≤ 2.5 μm (PM2.5), ≤ 10 μm (PM10), and between 2.5 and 10 μm (PMcoarse), and PM2.5 absorbance were estimated for birth addresses by land-use regression models based on monitoring campaigns performed between 2008 and 2011. Levels were extrapolated back in time to exact pregnancy periods. We quantitatively assessed autistic traits when the child was between 4 and 10 years of age. Children were classified with autistic traits within the borderline/clinical range and within the clinical range using validated cut-offs. Adjusted cohort-specific effect estimates were combined using random-effects meta-analysis. Results: A total of 8,079 children were included. Prenatal air pollution exposure was not associated with autistic traits within the borderline/clinical range (odds ratio = 0.94; 95% CI: 0.81, 1.10 per each 10‑μg/m3 increase in NO2 pregnancy levels). Similar results were observed in the different cohorts, for the other pollutants, and in assessments of children with autistic traits within the clinical range or children with autistic traits as a quantitative score. Conclusions: Prenatal exposure to NO2 and PM was not associated with autistic traits in children from 4 to 10 years of age in four European population-based birth/child cohort studies.NonePublishe