The stress of a pregnant woman could affect her baby’s chances of developing a disease – perhaps even during the child’s life, UC researchers have found.
Psychosocial stressors – such as lack of social support, loneliness, marital status, or bereavement – can mutate their child’s mitochondrial DNA, and could be the precursor, according to a University of Cincinnati study. from a multitude of diseases.
“There are a lot of conditions that start in childhood and have links to mitochondrial dysfunction, including asthma, obesity, attention deficit hyperactivity disorder, and autism,” says Kelly. Brunst, PhD, Assistant Professor of Environmental Sciences and Public Health at UC College of Medicine. and lead author of the study.
âThe fetal and infantile period is a period vulnerable to environmental exposure due to the increased development during these periods,â explains Brunst. “We don’t just wake up one day and have asthma or attention deficit hyperactivity disorder. The programming effects resulting from environment-induced changes occur over time and likely begin during the day. gestation at the molecular and cellular level. These changes alter physiological states that likely play a role in who will continue and develop negative health outcomes. “
As part of the study, researchers sequenced the mitochondrial genome and identified mutations in 365 placenta samples from birth mothers in Boston and New York City from 2013 to 2018. A multivariable regression model was used to examine the maternal lifelong stress in relation to the number of genetic mutations in the mitochondrial genome of the placenta.
Women experiencing increased psychosocial stress – which can range from sexual assault, domestic violence, or serious injury to incarceration, physical or mental illness, and family difficulties – during their lifetimes experienced higher numbers. elevated placental mitochondrial mutations. The strongest associations were seen in black women. Higher stress-related DNA mutations in the placenta have been seen in black and white women, but not in Hispanic women.
The results of the study were published in the scholarly journal Biological Psychiatry.
âThe idea behind this work is to understand how our environment, in this case maternal stress and trauma, impacts mitochondrial function and, ultimately, neurobehavioral development,â explains Brunst. “The hope is to understand why some children are vulnerable to developing a range of complex conditions previously linked to environmental exposures such as chronic stress or air pollution.”
âWe’re asking about events that might have happened before their pregnancy, even during the mother’s own childhood as part of our study,â says Brunst. “So what this tells us is that the stress a woman went through before she was even pregnant could impact the fetal mitochondrial genome.”
Brunst said that there are certain diseases that black women are more at risk for – obesity, diabetes and certain cancers – so they could be more affected by stress and subsequently develop these diseases which have also been linked. to stress. “
âWhat was interesting about the study was that Hispanics exposed to stress had fewer placental mitochondrial DNA mutations,â says Brunst.
She says one explanation could be what researchers call the “Hispanic Paradox.” This is the epidemiological phenomenon documenting better health and lower mortality compared to non-Hispanic whites despite a higher risk and lower socioeconomic status for Hispanics. “
âDespite exposure to more stress and trauma, sociocultural dynamics specific to Hispanics may alleviate stressful experiences which in turn have downstream effects on psychophysiological mechanisms and better outcomes,â explains Brunst. “This is only one possible explanation.”
The other co-authors of this study are Xiang Zhang, PhD, and Li Zhang, PhD, both associate professors at UC College of Medicine, as well as Andrea Baccarelli, MD, PhD, and Tessa Bloomquist, both of the Columbia University, Mailman School of Public Health, and Rosalind Wright, MD, Icahn School of Medicine at Mount Sinai, New York.
The study was funded by the National Heart, Lung, and Blood Institute under grants R01HL095606 and R01HL114396; the National Institute of Environmental Health Sciences under grants R00ES024116, P30ES006096 and P30ES023515.
Brunst led a previous research study that examined the correlation between exposure to traffic-related air pollution and anxiety in children, examining altered neurochemistry in pre-teens. She also received a recent five-year, $ 2.9 million grant from the National Institutes of Health for the “Epigenetics, Air Pollution, and Children’s Mental Health” research project.