Associations of maternal folic acid supplementation and folate concentrations during pregnancy with foetal and child head growth: the Generation R Study

Purpose Folic acid supplementation during pregnancy \nhas been associated with a reduced risk of common neurodevelopmental delays in the offspring. However, it is \nunclear whether low folate status has effects on the \ndeveloping brain. We evaluated the associations of \nmaternal folic acid supplementation and folate concentrations during pregnancy with repeatedly measured prenatal \nand postnatal head circumference in the offspring. \nMethods Within a population-based prospective cohort, \nwe measured maternal plasma folate concentrations at \napproximately 13 weeks of gestation (90 % range \n10.5\xe2\x80\x9317.2) and assessed folic acid supplementation by \nquestionnaire (2001\xe2\x80\x932005). Up to 11 repeated measures of \nhead circumference were obtained during foetal life (20 \nand 30 weeks of gestation) and childhood (between birth \nand age 6 years) in 5866 children (2002\xe2\x80\x932012). \nResults In unadjusted models, foetal head growth was \n0.006 SD (95 % CI 0.003; 0.009, P\\0.001) faster per \nweek per 1-SD higher maternal folate concentration. After \nadjustment for confounders, this association was attenuated \nto 0.004 SD per week (95 % CI 0.000; 0.007, P = 0.02; \nestimated absolute difference at birth of 2.7 mm). The \nassociation was independent of overall foetal growth. No \nassociations were found between maternal folate concentrations and child postnatal head growth. Preconceptional \nstart of folic acid supplementation was associated with \nlarger prenatal head size, but not with prenatal or postnatal \nhead growth. \nConclusions Our results suggest an independent, modest \nassociation between maternal folate concentrations in early \npregnancy and foetal head growth. More research is needed \nto identify whether specific brain regions are affected and \nwhether effects of folate on foetal head growth influence \nchildren\xe2\x80\x99s long-term functioning

Dietary patterns and changes in frailty status: the Rotterdam study

Purpose: To determine the associations between a priori and a posteriori derived dietary patterns and a general state of health, measured as the accumulation of deficits in a frailty index. Methods: Cross-sectional and longitudinal analysis embedded in the population-based Rotterdam Study (n = 2632) aged 45 years. Diet was assessed at baseline (year 2006) using food frequency questionnaires. Dietary patterns were defined a priori using an existing index reflecting adherence to national dietary guidelines and a posteriori using principal component analysis. A frailty index was composed of 38 health deficits and measured at baseline and follow-up (4 years later). Linear regression analyses were performed using adherence to each of the dietary patterns as exposure and the frailty index as outcome (all in Z-scores). Results: Adherence to the national dietary guidelines was associated with lower frailty at baseline (β −0.05, 95% CI −0.08, −0.02). Additionally, high adherence was associated with lower frailty scores over time (β −0.08, 95% CI −0.12, −0.04). The PCA revealed three dietary patterns that we named a “Traditional” pattern, high in legumes, eggs and savory snacks; a “Carnivore” pattern, high in meat and poultry; and a “Health Conscious” pattern, high in whole grain products, vegetables and fruit. In the cross-sectional analyses adherence to these patterns was not associated with frailty. However, adherence to the “Traditional” pattern was associated with less frailty over time (β −0.09, 95% CI −0.14, −0.05). Conclusion: No associations were found for adherence to a “healthy” pattern or “Carnivore” pattern. However, Even in a population that is relatively young and healthy, adherence to dietary guidelines or adherence to the Traditional pattern could help to prevent, delay or reverse frailty levels

Dietary patterns and changes in frailty status: the Rotterdam study

Prevention, Population and Disease management (PrePoD)Public Health and primary car

The contribution of environmental exposure to the etiology of autism spectrum disorder

Autism spectrum disorder (ASD) is a neurodevelopmental condition of heterogeneous etiology. While it is widely recognized that genetic and environmental factors and their interactions contribute to autism phenotypes, their precise causal mechanisms remain poorly understood. This article reviews our current understanding of environmental risk factors of ASD and their presumed adverse physiological mechanisms. It comprehensively maps the significance of parental age, teratogenic compounds, perinatal risks, medication, smoking and alcohol use, nutrition, vaccination, toxic exposures, as well as the role of extreme psychosocial factors. Further, we consider the role of potential protective factors such as folate and fatty acid intake. Evidence indicates an increased offspring vulnerability to ASD through advanced maternal and paternal age, valproate intake, toxic chemical exposure, maternal diabetes, enhanced steroidogenic activity, immune activation, and possibly altered zinc-copper cycles and treatment with selective serotonin reuptake inhibitors. Epidemiological studies demonstrate no evidence for vaccination posing an autism risk. It is concluded that future research needs to consider categorical autism, broader autism phenotypes, as well as autistic traits, and examine more homogenous autism variants by subgroup stratification. Our understanding of autism etiology could be advanced by research aimed at disentangling the causal and non-causal environmental effects, both founding and moderating, and gene-environment interplay using twin studies, longitudinal and experimental designs. The specificity of many environmental risks for ASD remains unknown and control of multiple confounders has been limited. Further understanding of the critical windows of neurodevelopmental vulnerability and investigating the fit of multiple hit and cumulative risk models are likely promising approaches in enhancing the understanding of role of environmental factors in the etiology of ASD.peerReviewe