Long-Term Exposure to Adversity May Dampen Dopamine Production
Chronic psychosocial stress disrupts dopaminergic functions, a new study finds.
Posted Nov 13, 2019
The UK-based researchers found that chronic stress in childhood and adulthood was associated with dampened dopamine production and exaggerated threat perceptions during short-term situations that induced acute stress.
According to the authors, these findings help to explain why a lifetime of chronic stress and psychological trauma may disrupt automatic physiological responses designed to help people cope with stressful circumstances in day-to-day life.
Previous research has shown that high levels of exposure to adverse childhood experiences (ACEs) and chronic psychosocial adversity increases the risk of mental illness, substance abuse, and addiction.
"We already know that chronic psychosocial adversity can induce vulnerability to mental illnesses such as schizophrenia and depression," lead author Michael Bloomfield of the Translational Psychiatry Research Group at University College London said in a news release. "This study can't prove that chronic psychosocial stress causes mental illness or substance abuse later in life by lowering dopamine levels, but we have provided a plausible mechanism for how chronic stress may increase the risk of mental illnesses by altering the brain's dopamine system."
For this study, Bloomfield and colleagues recruited 34 volunteers to undertake the Montreal Imaging Stress Task, which triggers acute stress by subjecting study participants to criticism while they're trying to calculate complicated mental arithmetic. Half of the study participants (n = 17) had a known history of "high" lifetime exposure to stress; the other half (n = 17) had "low" levels of long-term exposure to chronic psychosocial stress.
Two hours after performing the stress task, each participant was injected with a tracer that allowed the researchers to observe the brain's dopamine production using a neuroimaging technology called positron emission tomography (PET) scans.
As mentioned, the PET scans revealed that participants with low exposure to chronic adversity across their lifespan displayed robust dopamine production that matched the degree of threat the person felt while being criticized.
However, on average, those with high exposure to chronic psychosocial adversity in childhood and adulthood experienced a double whammy of exaggerated threat perceptions during the Montreal Imaging Stress Task combined with dampened dopamine production.
"Our findings of heightened stress-induced threat are consistent with the threat-anticipation model of delusion formation (Freeman, 2007) and evidence that elevated sensitivity to socio-environmental stress via enhanced threat anticipation in daily life may be important psychological processes underlying the association between childhood adversity and psychosis (Reininghaus et al., 2016)," the authors write.
Given their findings of decreased dopamine production in association with high psychosocial stressors, the authors speculate, "[It] remains possible that repeated psychosocial stressors in childhood increase the risk of psychotic symptoms by hypodopaminergic or non-dopaminergic processes."
That said, the authors acknowledge that their study has significant limitations: "Future studies of individual risk factors are needed to examine what type of risks may be driving our findings. Finally, as our study is cross-sectional, we cannot rule out reverse causality and a longitudinal design is required to distinguish between the interpretations discussed above."
"Further work is now needed to better understand how changes in the dopamine system caused by adversity can lead to vulnerability towards mental illnesses and addiction," senior author Oliver Howes, Professor of Molecular Psychiatry at MRC London Institute of Medical Sciences and King's College London, concluded.
Michael A.P. Bloomfield, Robert A. McCutcheon, Matthew Kempton, Tom P. Freeman, Oliver Howes. "The Effects of Psychosocial Stress on Dopaminergic Function and the Acute Stress Response." eLife (First published: November 12, 2019) DOI: 10.7554/eLife.46797