A study from the University of Cincinnati suggests that stressful psychosocial factors such as lack of social support, loneliness, marital status, or bereavement can cause mutations in a child's mitochondrial DNA and may be a precursor to a range of diseases.
A recent study published in Biological Psychiatry explored the impact of maternal stress during pregnancy on the development of diseases in children. This study examined the relationship between maternal lifetime stress and placental mitochondrial DNA mutational load in a multi-ethnic urban cohort. Assessments were conducted using a validated Life Stress Checklist. Whole-mitochondrial DNA sequencing and mutation detection were performed on 365 placental samples using complete exposure and covariate data. Multivariate regression methods were used to model the relationship between maternal lifetime stress and placental mitochondrial DNA mutational load.
Dr. Kelly Brunst, an assistant professor of environmental and public health sciences at the University of California School of Medicine and the study’s lead author, said, “Many diseases that begin in childhood are associated with mitochondrial dysfunction, including asthma, obesity, attention deficit hyperactivity disorder, and autism.”
“The fetal and infant periods are vulnerable times for exposure to the environment because development accelerates during these periods,” Dr. Brunst said. “We don’t wake up one day with asthma or ADHD. The programming effects of environment-induced changes occur over time and can begin at the molecular and cellular levels during pregnancy. ”
Researchers performed mitochondrial genome sequencing on 365 placental samples from Boston and New York City between 2013 and 2018, identifying mutations. They identified 13,189 heterogeneous mutations (Phred score >10,000, minor allele frequency <0.5, mutation read >1). Women experiencing increased psychosocial stress throughout their lives showed a higher number of total placental mitochondrial mutations (β = .23, 95% confidence interval = .03 to .42) and heterogeneous mutations (β = .18, 95% confidence interval = .05 to .31), but no homogeneous mutations (β = .008, 95% confidence interval = .03 to .01). The strongest associations were observed in Black women and in genes encoding NADH dehydrogenase and cytochrome c oxidase subunits.
“The idea behind this work is to understand our environment, and in this case, how maternal stress and trauma affect mitochondrial function and ultimately neurobehavioral development,” Brunst said. “The aim of this study is to understand why certain children are susceptible to a complex set of conditions linked to long-term exposure to environmental factors such as chronic stress or air pollution. Black women are more prone to certain conditions, such as obesity, diabetes, and certain cancers, so they may be more susceptible to stress and subsequently develop these stress-related conditions.”
What's interesting about this study is that Hispanic individuals exposed to stress had fewer mitochondrial DNA mutations in their placenta. One explanation might be what the researchers call the "Hispanic Paradox." This is an epidemiological phenomenon that suggests Hispanics, despite higher risk and lower socioeconomic status, have better health and lower mortality rates. Despite exposure to more stress and trauma, Hispanic-specific sociocultural dynamics might mitigate the stressful experience, which in turn has downstream effects on psychophysiological mechanisms and leads to better outcomes—of course, this is only one possible explanation.
In summary, cumulative maternal lifelong stress is associated with a greater mitochondrial mutational load, particularly in Black women. The racial/ethnic differences in gene mutational load on placental function, directly impacting offspring development and/or contributing to differences in chronic diseases, warrants further investigation.
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