Prof. Eric Fombonne

Professor at Oregon Health & Science University
Director of Autism Research at the Institute for Developmental Disabilities

Dr. Eric Fombonne trained in child and adolescent psychiatry in France. He held appointments as clinical scientist at the National Institute of Health and Medical Research  (INSERM, France), as Senior Lecturer and Reader at the Institute of Psychiatry and Maudsley Hospital, King’s College London, UK (1993-2001), as tenured Professor of Psychiatry at McGill University (Canada), Head of the Division of Child Psychiatry and Canada Research Chair in Child Psychiatry (2001-2012).  In September 2012, he joined the Department of Psychiatry at Oregon Health & Science University in Portland, Oregon (USA), and is now Director of Autism Research at the Institute for Developmental Disabilities. He has a long experience of clinical work with children with autism and their families, over the lifespan, and has been also directing clinical services for teenagers with depression. His research activities on developmental disorders and child and adolescent psychiatric disorders encompass clinical/longitudinal and population-based epidemiological studies, clinical trials, and genetic studies. He has published over 300 articles in peer-reviewed journals, 40 chapters in books. He is past Associate Editor of the Journal of Autism and Developmental Disorders (JADD; 1994-2004); he is currently Joint Editor of Journal of Child Psychology and Psychiatry (JCPP) and is on the editorial board of several other journals in the field of autism and child psychiatry.



Short Description of the Lectures:

1. Keynote Lecture – Epidemiology of ASD: Rates, Trends and Environmental Risk
Recent epidemiological findings on autism spectrum disorders (ASD) worldwide will be reviewed. There is no standardized methodology to conduct epidemiological surveys, and each survey has unique design features that need to be taken into account when comparing results across studies. Overall, many surveys converge towards estimates of 1% to 1.5% at school age.  The meaning of the historical increase in prevalence over time will be discussed. Few environmental risk factors have been reliably identified today (paternal age, prenatal valproate exposure) that explain a small proportion of population risk. Many other findings should be considered as preliminary. In evaluating published findings, readers should be aware of common methodological problems (confounding by indication, residual confounding, multiple testing, ecological fallacy) that limit causal inference.

2. Childhood Vaccines and Autism: Facts and Fictions
In the late 1990s, claims that childhood vaccines increased the risk of autism were widely publicized despite weak empirical evidence to support them. They entailed 2 purported separate mechanisms. The first one incriminated the measles component of the triple MMR vaccine, the second implicated the cumulative dose of thimerosal (ethylmercury) received through other childhood vaccines up to age 2. Observational studies showed that underlying trends in rates of autism were uncorrelated to trends in MMR coverage or to use of the preservative thimerosal in vaccine preparations. Case-control and cohort studies equally failed to show that risk of ASD was increase by exposure to MMR or thimerosal-containing vaccines. Claims that the risk could be confined to a small, vulnerable, subgroup were not substantiated by careful research. The convergence of negative findings across studies has been impressive. Yet, residual beliefs on a link between immunizations and autism risk recently led to a dangerous drop in vaccine uptake in several countries, leading to resurgence of epidemics and children deaths due to infectious diseases that could be totally prevented.

3. Reflection Session: Panel Discussion