Joanne Weinberg
Affiliate Investigator, BC Children's Hospital
Professor and Distinguished University Scholar, Emerita, Department of Cellular and Physiological Sciences, Faculty of Medicine, Life Sciences Institute, University of British Columbia
Full Member, Djavad Mowafaghian Centre for Brain Health
Prenatal alcohol exposure (PAE) can have adverse consequences for the fetus, resulting in physical, neurobiological, cognitive, adaptive, health, and behavioral alterations that can persist into adulthood. The umbrella term fetal alcohol spectrum disorder (FASD) describes the full range of adverse effects. Recent studies suggest that prevalence of FASD may be as high as 1%-5%, higher than that of other neurodevelopmental disorders such as Autism Spectrum Disorder and Down Syndrome. FASD is thus an international public health, education, economic, and social issue. The consequences of PAE vary depending not only on the amount, timing, and pattern of exposure, but also on environmental, genetic, epigenetic, and other factors that influence development.
Our research focuses on the effects of prenatal alcohol exposure, stress, and neuroendocrine-neuroimmune regulation, with a specific focus on mechanisms underlying prenatal alcohol effects on fetal programming of neurobiological systems. Our studies have demonstrated that alcohol, in addition to its teratogenic effects, is an early life insult that programs developing systems and markedly increases risk for diseases/disorders throughout life, the “Developmental Origins of Health and Disease” (DOHaD) concept. We have developed rodent models to examine brain-behavior relationships from prenatal life through adulthood, utilizing a broad multidisciplinary approach to tackle problems from the molecular to the behavioral level. We have also collaborated actively with clinical researchers to extend our expertise on stress, programming and development to human populations.
Our animal model studies have shown that PAE results in hyperresponsiveness to stressors, and marked changes in central regulation of hypothalamic-pituitary-adrenal (HPA) or stress axis activity under both basal and stress conditions. Utilizing an animal model of adjuvant-induced arthritis, data have demonstrated marked alcohol-exposed offspring exhibit more severe and more prolonged responses to immune challenge, reflecting alterations in neuroimmune function. For the past 10 years, we have been part of the NIH/NIAAA Collaborative Initiative on FASD, providing the opportunity to translate research on animal models of PAE to cohorts of pregnant women and their children. This research is the first to identify a link between maternal alcohol consumption, inflammation, and child outcomes: Unique immune signatures in pregnant women were identified in association with whether or not they consumed alcohol and with the neurodevelopmental outcomes (typically developing/developmentally delayed) of their children. Similarly, immune profiles of the children were shown to reflect both alcohol exposure and neurodevelopmental status. This research is currently testing a “multiple hit” hypothesis that PAE results in a vulnerable organism that may be further impacted by social adversity and lack of resources/coping skills, resulting in immune and endocrine dysregulation that in turn, may be key drivers of early-onset health and neurobehavioral problems over the life course. Our research has been funded over the years by the BC Health Research Foundation, MRC/CIHR, Coast Capital Savings Depression Research Fund, the Canadian Foundation on Fetal Alcohol Research, and since 1988, by NIH/ NIAAA. From 2009-2020, I held a MERIT Award.
