MDI Biological Laboratory

Q&A with James A. Coffman, Ph.D.: Early-Life Stress in Adult Illness

  • January 27, 2017

In this Q&A excerpt from Future Neurology, MDI Biological Laboratory scientist James A. Coffman, Ph.D., speaks about his research on the mechanisms by which chronic early-life stress increases adult disease risk. He uses zebrafish as a model organism to ask how such stress affects immune system development and regulation. Read the full Q&A here. 

Q What first drew you toward investigating early-life stress & its association with adult illness?

A few years ago I became interested in the problem of how chronic stress promotes human aging; and more specifically, the role that glucocorticoid stress signaling plays in that process. As I delved into the literature, I became intrigued by the ‘fetal origins of disease’ hypothesis and the idea that chronic early-life exposure to elevated stress signaling can program development of phenotypes that are more prone to immune dysfunction and inflammatory disease. The mechanisms for this remain poorly understood and as a developmental biologist, I was naturally attracted to the problem.

Q What are the major issues associated with chronic exposure to psychosocial stress early in life?

It is known that chronic psychosocial stress early in life increases disease risk later in life and possibly even in subsequent generations. A common denominator of the diseases that are predisposed to develop – ranging from asthma and rheumatoid arthritis all the way to mental health problems such as depression and anxiety – is chronic inflammation and immune dysregulation. So a major question is: how does chronic psychosocial stress early in life lead to chronic inflammation and immune dysregulation later in life?

Q How do you think this early preclinical work might be translated to benefit humans in the future and what needs to be done to achieve this?

Ultimately, if we can elucidate the epigenetic mechanisms that mediate the effects we have observed, then we will be able to design therapies that target those mechanisms or their effects, for example, small molecules designed to reverse the adverse effects caused by specific epigenetic modifications. Beyond that, our work adds weight to the growing consensus that chronic early life stress, or even just prenatal exposure to such stress, is a major public health issue, which should motivate public policy toward mitigating those factors that contribute psychosocial adversity – for example, economic inequality, social injustice and loss of social safety nets.
James A. Coffman, Ph.D.