Monday, May 9, 2011

How does childhood adversity get “under the skin” to increase susceptibility to disease years or even decades later?  

Please join the Department of Psychology and Social Behavior and the Program in Public Health for talks by two distinguished speakers whose groundbreaking research addresses this question.

Monday, May 9th in SBSG 1517

12:00-1:30 pm
Socioeconomic Disparities in Childhood Asthma:  Understanding Psychobiological Pathways


Edith Chen, Ph.D.
Professor & Canada Research Chair in Health & Society
Department of Psychology
University of British Columbia

 

3:30-5:00 pm
The Behavioral and Biological Residue of Childhood Adversity

Greg Miller

Department of Psychology
University of British Columbia



For abstracts, click "read more" below.

 Socioeconomic Disparities in Childhood Asthma:  Understanding Psychobiological Pathways
Edith Chen, Ph.D.
 
Low socioeconomic status (SES) is one of the most robust risk factors for a variety of diseases throughout the lifespan across both countries with and without universal health care. For example, asthma is the most common chronic illness in childhood, and children who are lower in SES are at greater risk for more severe exacerbations of asthma. Despite this widely acknowledged epidemiological phenomenon, the psychobiological mechanisms underlying this relationship have been less well understood. This talk will provide an overview of our laboratory’s approach to testing the biological pathways that link the larger social environment to physical health outcomes in childhood, using asthma as one example.  It will also discuss psychosocial pathways at the individual, family, and neighborhood levels that we have explored in an effort to understand how broad social environments affect individuals and their health.
 
The Behavioral and Biological Residue of Childhood Adversity
Gregory Miller, Ph.D.
 
Children who are exposed to social and economic adversity in the early years of life show increased susceptibility to the chronic diseases of aging when they reach their 50's and 60's. These findings raise a difficult mechanistic question: How does early adversity “get under the skin” in a manner that is sufficiently persistent to affect vulnerability to diseases that arise many decades later? In this lecture I will discuss findings from our ongoing research, which suggest that early adversity is programmed into cells of the immune system at the level of the genome, resulting in a pro-inflammatory phenotype that probably contributes to the chronic diseases of aging. I also will discuss newer findings which identify the family context as a powerful moderator of these effects, such that high levels of maternal warmth in early life can offset the pro-inflammatory residue of childhood adversity.