Be Consistent: Unpredictability Increases Your Child’s Risk of Developing Mental Illness

Developmental disruption makes people more susceptible to mental illness and drug dependence.

University of California, Irvine researchers are conducting ground-breaking research into the idea that unpredictable parental behaviors, coupled with an unpredictable environment, such as a lack of routines and frequent disasters, disrupt children’s ability to develop their emotional brain circuits to their full potential, making them more susceptible to mental illness and substance abuse.

Dr. Tallie Z. Baram, corresponding author and distinguished professor in the Departments of Anatomy & Neurobiology, Pediatrics, Neurology, and Physiology & Biophysics at the University of California, Irvine, and Matthew T. Birnie, first author, a postdoctoral researcher at the University of California, Irvine, discuss the principles of emotional brain circuit formation learned from animal studies and their effects on children’s cognitive development and mental health in a study that was recently published in the journal Science.

“This perspective starts from basic principles of how the brain’s sensory – audio and visual – and motor circuits are established and refined, and we apply those to emotional circuits that govern reward-, stress- and fear-related behaviors. It’s not only positive or negative parental signals but also the patterns of these behaviors and especially their predictability or unpredictability, that are linked to adverse outcomes such as poor emotional control in later life. The latter are indicators of higher risks for mental illness, post-traumatic stress disorder, and substance abuse,” said Baram.

The creation of sensory brain circuits begins with a series of genetically and molecularly driven activities, including neuronal migration and synaptic formation. Complex emotional and cognitive human behavior requires many decisions and acts, which are also carried out by brain circuits. The interactions of the prefrontal cortical areas, thalamic nuclei, hippocampus, amygdala, hypothalamic nuclei, and subcortical brain regions are some examples of these higher-order circuits.

They receive numerous streams of information which promote activity of the neurons in the circuits. This activity is required for maturation of the components and refinement of the integrative connections. In early life, as these emotional circuits are developing, parents are the proximate primary environment: They are the source of information that influences the child’s brain maturation.

Studies of mice reared by dams displaying unpredictable behavior sequences (but the same total amount of care) during the early postnatal period show that maternal behaviors influence synaptic connectivity in key brain nodes, including those that contribute to stress. Research involving infants and children suggests that unpredictable patterns of maternal behaviors are associated with later deficits in emotional control and behaviors. These effects persist even after correction for other early-life variables such as maternal sensitivity to the infant’s needs, socioeconomic status, and maternal depressive symptoms.

“What’s significant about this research is that it identifies new targets for intervention and helps us think of measures we can put in place to best support the development of mentally and cognitively healthy children,” Baram said. “Unpredictability is actionable because we can aim to inform and educate parents, caregivers, and others about the importance of predictable signals and environments to infants’ and children’s brain maturation.”

Baram and her team are continuing to build on their research at the UCI Conte Center. “We are conducting mechanistic studies in experimental rodents and monitoring infants, children, and adolescents in the center. We are now ready to test our discoveries in large-scale, ‘real-world’ research,” she said.

Reference: “Principles of emotional brain circuit maturation” by Matthew T. Birnie and Tallie Z. Baram, 2 June 2022, Science.
DOI: 10.1126/science.abn4016

This research was supported by the National Institutes of Health under grants P50 MH096889, MH73136, and NS108296; the Donald L. Bren Foundation; and the Hewitt Foundation for Biomedical Research.