This presentation draws on ethnographic research with a group of epigenetics and neuroscience researchers in Montreal, Canada whose work asks: why, in response to negative life events and shared psychiatric diagnoses, do some people die of suicide while others do not?
The response their research proposes is that the experience of early life adversity establishes durable neurobiological profiles that put people at elevated suicide risk. In particular, this neurobiological risk is thought to set people on pathological trajectories, characterized by susceptibility to mental illness and a variety of unhealthy behaviours whose extreme end point is suicide.
In this presentation, we argue that a highly specific understanding of the nature of trauma, and of how our past experiences invade our present, had to be stabilized in order for environmental epigenetics models of suicide risk to be posited. Through an examination of these narratives of risk, we consider how early trauma came to be understood as playing an etiologically significant role in the development of suicide risk. Suicide, in these models, has come to be seen as a behaviour that has no significant precipitating event, but rather an exceptional precipitating neurochemical state, whose origins are identified in experiences of early traumatic events. We suggest that this is a part of a broader move within contemporary neurosciences and biopsychiatry to see life as post: seeing life as specific form of post-traumatic subjectivity.
A critical consideration of these at-risk models speaks directly to debates about to whether we might envision life as epigenetically programmed or conditioned, with implications for how we understand personal life trajectories.