Cardiovascular and metabolic influences of fetal smoke exposure

Many epidemiological studies showed associations of low birth weight with cardiovascular disease, type 2 diabetes and obesity. The associations seem to be consistent and stronger among subjects with a postnatal catch up growth. It has been suggested that developmental changes in response to adverse fetal exposures might lead to changes in the fetal anatomy and physiology. These adaptations may be beneficial for short term, but may lead to common diseases in adulthood. Maternal smoking during pregnancy is one of the most important adverse fetal exposures in Western countries, and is known to be associated with a 150–200 g lower birth weight. An accumulating body of evidence suggests that maternal smoking during pregnancy might be involved in pathways leading to both low birth weight and common diseases, including cardiovascular disease, type 2 diabetes and obesity, in adulthood. In this review, we discuss epidemiological studies focused on the associations of maternal smoking with fetal growth and development and cardiovascular and metabolic disease in later life. We also discuss potential biological mechanisms, and challenges for future epidemiological studies

Early influences on cardiovascular and renal development

The hypothesis that a developmental component plays a role in subsequent disease initially arose from epidemiological studies relating birth size to both risk factors for cardiovascular disease and actual cardiovascular disease prevalence in later life. The findings that small size at birth is associated with an increased risk of cardiovascular disease have led to concerns about the effect size and the causality of the associations. However, recent studies have overcome most methodological flaws and suggested small effect sizes for these associations for the individual, but an potential important effect size on a population level. Various mechanisms underlying these associations have been hypothesized, including fetal undernutrition, genetic susceptibility and postnatal accelerated growth. The specific adverse exposures in fetal and early postnatal life leading to cardiovascular disease in adult life are not yet fully understood. Current studies suggest that both environmental and genetic factors in various periods of life may underlie the complex associations of fetal growth retardation and low birth weight with cardiovascular disease in later life. To estimate the population effect size and to identify the underlying mechanisms, well-designed epidemiological studies are needed. This review is focused on specific adverse fetal exposures, cardiovascular adaptations and perspectives for new studies. Copyrigh

Persistence of butterfly populations in fragmented habitats along urban density gradients: motility helps

In a simulation study of genotypes conducted over 100 generations for more than 1600 butterfly’s individuals, we evaluate how the increase of anthropogenic fragmentation and reduction of habitat size along urbanisation gradients (from 7% to 59% of impervious land cover) influences genetic diversity and population persistence in butterfly species. We show that in areas characterised by a high urbanisation rate (> 56% impervious land cover), a large decrease of both genetic diversity (loss of 60-80% of initial observed heterozygosity) and population size (loss of 70-90% of individuals) is observed over time. This is confirmed by empirical data available for the mobile butterfly species Pieris rapae in a sub-part of the study area. Comparing simulated data for P. rapae with its normal dispersal ability and with a reduced dispersal ability, we also show that a higher dispersal ability can be an advantage to survive in an urban or highly fragmented environment. The results obtained here suggest that it is of high importance to account for population persistence, and confirm that it is crucial to maintain habitat size and connectivity in the context of land-use planning