Hypermetabolism linked to early-life adversity can be harmful in long term: Study

Mitochondria, responsible for producing energy in a cell, may have an increased respiratory capacity in adults who experienced adversities in early childhood but the ‘hypermetabolism’ can be harmful in the long term, according to a study.

Findings published in the journal Biological Psychiatry suggest that while mitochondria might be better able to respond to cellular stress by producing more energy, the heightened response can be maladaptive in the long term.

Researchers said that early childhood adversity is linked with poorer physical and mental health across a person’s lifespan, but the biological processes translating the lived effects of poverty and trauma into physical functions are starting to come to light.

“This study is the first to examine early life adversity and mitochondrial bioenergetics in a diverse sample of adult men and women, and the first to examine distinct dimensions of threat and deprivation in relation to mitochondrial function,” first author Shiloh Cleveland, a doctoral student at the University of California, Los Angeles, the US, said.

“Elucidating how adversity in childhood and adolescence relates to mitochondrial function could inform targeted intervention efforts earlier in the lifespan to promote positive health outcomes before the onset of age-related diseases,” Cleveland said.

More than 140 participants responded to a questionnaire on early-life adversity and submitted a blood sample.

A ‘stress test’ of live cells from blood samples revealed that cumulative experiences of early-life adversity were associated with an increased respiratory capacity.

Mitochondria from the participants who had experienced early-life adversity were found to have a greater capacity to produce energy while under cellular stress, suggesting that cells respond to stress by producing more energy.

However, the ‘hypermetabolism’ can be harmful to cells in the long term, the researchers said.

Exploring the nature of adversities that the participants experienced revealed that a ‘threat’ adversity was associated with a lower production of cell energy, while also being prepared to meet the demands of potential future cell stressors.

However, ‘deprivation’ was associated with increased inefficient energy production, which researchers said may indicate greater cellular dysfunction.

“Under chronic stress, mitochondria may adapt in ways that supply cells with the energy needed to respond quickly to adversity, which can be useful in the short-term when they actually need to respond to these challenging experiences,” senior author Jennifer Sumner, a psychologist at the University of California, Los Angeles, said.

“But, over time, if the mitochondria are always working as if they’re under stress even when they’re not, it might wear them out more quickly and lead to adverse downstream effects on the cell. In the long run, performance could decrease to less than optimal levels, which can affect health in harmful ways,” Sumner said.

The results show that effects of adversity are not solely cumulative and the type of adversity experienced may be uniquely related to mitochondrial function, the researchers said.

The authors wrote, “Greater cumulative ELA (early life adversity) was associated with lower proton leak and ATP (adenosine triphosphate) production rate from glycolysis and greater maximal respiration and reserve capacity. Dimensional analyses revealed unique and nuanced associations between threat- and deprivation-related ELA and mitochondrial parameters.”