Interview with James Coffman: Early Life Stress in Adult Illness

Q Can you give me an idea of the type of work you have been doing to date?

I am a developmental biologist. Research in my laboratory is focused on understanding how exposure to environmental stressors during early development can affect adult anatomy and physiology. The work has two prongs. The first looks at how networks of transcriptional regulatory genes and their protein products control gene expression to direct the course of development. This is something I have been studying for over 25 years, beginning as a postdoctoral associate of the late Eric Davidson at the California Institute of Technology (CA, USA). The second prong examines how environmental variables and stressors influence the activities of transcriptional regulatory proteins that play important developmental roles, thus altering the course of development. So the work is centered on the problem of developmental plasticity.

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.

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? It is a problem of development and epigenetics.