Neurobiological mechanisms of eating disorders
Anorexia nervosa is a debilitating and sometimes life-threatening eating disorder with a higher mortality rate than most other psychiatric disorders. Its onset often occurs in adolescence, a stage in which the human brain is still developing. Neurobiological risk factors and consequences of the disorder are still poorly understood. In ongoing research, we are studying molecular and brain processes in anorexia nervosa. With this research, we hope to better understand underlying neurodevelopmental processes in eating disorders.
Early risk factors for eating disorders
Childhood is a key stage in human development and there is increasing evidence indicating that eating disorders are rooted in this sensitive period. Specific eating behaviors, along with psychosocial stressors can be observed during childhood and might increase the risk for disordered eating symptoms later in life. In ongoing work, we are studying community samples to learn whether or not eating behaviors in childhood along with other risk factors in early life are predictive of eating disorder symptoms in adolescence. Findings could guide preventive strategies for early identification of at-risk individuals thus allowing for timely intervention, before the onset of an eating disorder.
Emotional-cognitive processes of eating disorder risk
Our work on eating disorders in community samples focuses on investigating the role of emotional-cognitive processes on eating-disorder risk.
Early life stress and brain development
The impact of in-utero environment on the developing brain of infants: an MRI study of genetically identical twins
This project involves a sample of identical twins followed since birth. The study of resemblance between monozygotic twins (a.k.a., PDIMOZY) is based in the CHU Sainte-Justine Research Centre and involves the collection of DNA samples in the first years of life, as well as questionnaire data at critical developmental milestones. The twin pairs also undergo MRI scans in early childhood so that we can examine differences in brain anatomy. With these data we hope to gain insight on how the environment affects brain development.
In utero exposure to environmental contaminants and child development. Exposure to contaminants
Environmental contaminants such as PBDEs and BPA are present in everyday objects such as plastics, textiles, foams, vehicles and food. We are all exposed to them at varying levels. Some of them can accumulate in the body and have been associated with negative effects. This investigation is a collaboration with researchers across Canada who are part of the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, involving a Canada-wide longitudinal cohort. Our aim is to examine the role of specific contaminants on child development. To do so, we are comparing data from children with high and low levels of exposure to certain contaminants and how these differences are associated with key developmental characteristics.
Effects of histone methylation in individuals with and without a history of childhood adversity.
Epigenetic changes refer to chemical processes that occur at the DNA level which can alter gene activity. One type of epigenetic change occurs when a methyl group binds to the histone proteins at the core of a DNA helix. This process is called histone methylation and it can interfere with gene expression. Positron Emission (PET) imaging technology allows us to tag brain areas and to investigate how the activity of certain histone acetylase enzymes are associated with specific behaviours and brain morphology. In this study, we study individuals with various levels of childhood adversity and investigate whether individuals with high and low childhood adversity differ in the activity of histone deacetylase in brain regions that play a role in emotion regulation.