Childhood maltreatment is associated with changes in mitochondrial bioenergetics in maternal, but not in neonatal immune cells

Abstract

Childhood maltreatment (CM) comprises experiences of abuse and neglect during childhood. CM causes psychological as well as biological alterations in affected individuals. In humans, it is hardly explored whether these CM consequences can be transmitted directly on a biological level to the next generation. Here, we investigated the associations between maternal CM and mitochondrial bioenergetics (mitochondrial respiration and intracellular mitochondrial density) in immune cells of mothers and compared them with those of their newborns. In n = 102 healthy mother-newborn dyads, maternal peripheral blood mononuclear cells and neonatal umbilical cord blood mononuclear cells were collected and cryopreserved shortly after parturition to measure mitochondrial respiration and intracellular mitochondrial density with high-resolution respirometry and spectrophotometric analyses, respectively. Maternal CM was assessed with the Childhood Trauma Questionnaire. Maternal and neonatal mitochondrial bioenergetics were quantitatively comparable and positively correlated. Female newborns showed higher mitochondrial respiration compared to male newborns. Maternal CM load was significantly and positively associated with mitochondrial respiration and density in mothers, but not with mitochondrial respiration in newborns. Although maternal and neonatal mitochondrial bioenergetics were positively correlated, maternal CM only had a small effect on mitochondrial density in newborns, which was not significant in this study after adjustment for multiple comparisons. The biological relevance of our finding and its consequences for child development need further investigation in future larger studies. This study reports data on mitochondrial bioenergetics of healthy mother-newborn dyads with varying degrees of CM.

Expression of DNA-repair genes and its relevance for DNA repair in peripheral immune cells of patients with posttraumatic stress disorder

“…This energy-metabolic shift possibly serves to ensure NAD + availability while at the same time decreasing additional oxidative stress-related DNA damage. In line with this, we and others have previously demonstrated alterations in the mitochondrial bioenergetics in traumatic stress and related mental disorders [44][45][46] .…”

Stress and circulating cell-free mitochondrial DNA: A systematic review of human studies, physiological considerations, and technical recommendations

“…Evidence that mitochondria are a downstream target of stress is derived from studies showing that chronic stress influences mitochondrial structure and function (e.g., ( Cai et al, 2015 ), see ( Picard and McEwen, 2018 ) for a systematic review). In humans, positive mood has also been found to predict higher leukocyte mitochondrial energy production capacity within days ( Picard et al, 2018 ), and early life adversity is associated with alterations in mitochondrial respiratory capacity ( Boeck et al, 2018 , 2016 ; Gumpp et al, 2020 ), indicating that mitochondria are likely targets of psychological states.…”

The link between mitochondria, psychopathology, and intelligence: A bioenergetic model of cerebral function

“…The behavioural risk factors include physical inactivity 57,58 and a Western pro-inflammatory diet 59 . The stress-related risk factors of p 3,60 and g 61 that affect MB includes a high trauma load and childhood maltreatment 62,63 . Childhood maltreatment was related to increased mitochondrial respiration and density 62 , lower cognitive performance 61 , and higher general psychopathology 3 .…”

“…The stress-related risk factors of p 3,60 and g 61 that affect MB includes a high trauma load and childhood maltreatment 62,63 . Childhood maltreatment was related to increased mitochondrial respiration and density 62 , lower cognitive performance 61 , and higher general psychopathology 3 . In addition, the biological risk factors of g and p are linked with MB, which includes low-grade inflammation 64,65 , oxidative stress 66,67 , carnitine 68 , lack of micronutrients such as Coenzyme Q10 69,70 , folic acid, vitamin deficiencies 42,71 , hyperhomocysteinemia, low polunsaturated fatty acids 71 and impaired cardiac autonomic nervous system [72][73][74] .…”