Intrauterine life is a phase of rapid growth and maturation that is highly sensitive to environmental insults.  When adverse intrauterine conditions provoke adaptations in developmental trajectories, this can have a lasting impact on organ function that increases the risk for adult-onset chronic disease. Understanding these developmental underpinnings of later-life chronic disease is the overall goal of our laboratory. 

Our lab is focused on two of the most salient environmental challenges facing pregnant women and children. First, in today's obesogenic environment, metabolic disorders such as maternal obesity and gestational diabetes, have burgeoned into the most common pregnancy conditions. Human studies reveal that babies born from mothers who were obese or diabetic during pregnancy are more likely to develop cardiovascular risk factors in childhood, adolescence and adulthood. Given the high prevalence of maternal obesity in countries like Canada and the US, the intrauterine environment is a significant driver of cardiovascular risk factors in the pediatric population, which have now reached epidemic proportions. We are working to identify the developmental perturbations at the cellular, organ and organ system level that underlie phenotypic programming that render offspring vulnerable to later-life disease. This insight is critical to design strategies effective in optimizing long-term outcomes in babies born at risk.   

Second, chemical intensification of our environment is a significant, yet underappreciated, contributor to chronic diseases such as obesity and other cardiometabolic disorders. Developmental windows during fetal life are particularly susceptible to adverse effects of environmental toxicants, many which have endocrine disrupting properties. Currently, we are investigating substitutes used to replace bisphenol A (BPA), a plasticizer used to manufacture many household products. A growing body of evidence reveals BPA substitutes as another example of 'regrettable substitutions' where industry replace toxic chemicals with equally toxic substitutes. Our work aims to determine if BPA substitutes impact development of the adipose tissue and microvasculature.

We believe that a complete understanding of the current epidemic of cardiometabolic disease is incumbent upon determining how environmental and lifestyle factors act through the intrauterine environment to shape cardiovascular health in the offspring and in succeeding generations. 

New Research:

High maternal adiposity during pregnancy programs an imbalance in the lipidome and predisposes to diet-induced hepatosteatosis in the offspring. 

Prenatal exposure to a low dose of BPS causes sex-dependent alterations to vascular endothelial function in adult offspring. 

Exploring oxidative stress and endothelial dysfunction as a mechanism linking bisphenol S exposure to vascular disease in human umbilical vein endothelial cells and a mouse model of postnatal exposure. Published in Environmental International. 

Potentiation of adipogenesis by reactive oxygen species is a unifying mechanism in the pro-adipogenic properties of bisphenol A and its new structural analogues. * Just accepted to Antioxidants and Redox 

Accelerated developmental adipogenesis programs adipose tissue dysfunction and cardiometabolic risk in offspring born to dams with metabolic dysfunction.

Plasticizers and cardiovascular health: role of adipose tissue dysfunction