Prenatal stress may mutate child’s DNA, increase risk for disease
Maternal stress during pregnancy may mutate the child’s DNA and thus affect risk for developing disease, according to study results published in Biological Psychiatry.
This risk may be particularly prevalent among Black women, researchers noted.
"There are a lot of conditions that start in childhood that have ties to mitochondrial dysfunction, including asthma, obesity, [ADHD] and autism," Kelly Brunst, PhD, assistant professor of environmental and public health sciences at the University of Cincinnati College of Medicine and lead author of the study, said in a press release. "The fetal and infant period is a vulnerable time for environmental exposure due to heightened development during these periods.”
According to Brunst, programming effects linked to environmentally induced shifts occur over time and likely begin during gestation at the cellular and molecular levels. These shifts affect physiological states that may play a role in an individuals’ likelihood for developing adverse health outcomes, Brunst said.
The investigators sought to assess the link between maternal lifetime stress and placental mitochondrial DNA mutational load among an urban multiethnic cohort. They used the validated Life Stressor Checklist-Revised to assess maternal lifetime exposure to stressful events. Further, they conducted whole mitochondrial DNA sequencing and determined mutations for 365 placenta samples with complete data for exposures and covariates. The researchers modeled maternal lifetime stress in relation to placental mitochondrial DNA mutational load using multivariable regression and examined racial/ethnic differences by cross-product terms and contrast statements. They also conducted gene-wise analyses.
Brunst and colleagues identified 13,189 heteroplasmies. Results showed a higher number of total placental mitochondrial mutations and heteroplasmic mutations, but not homoplasmic mutations, among women who experienced increased psychosocial stress over their lifetime. The researchers observed the strongest associations among Black women and genes that coded for NADH dehydrogenase and cytochrome c oxidase subunits.
“A deeper investigation into the role of mitochondrial function and the intergenerational (and potentially transgenerational) consequences of women’s experiences of cumulative stress and trauma in disparities of childhood and later-life outcomes among offspring is warranted,” Brunst and colleagues wrote.