Stress in early childhood due to negative experiences — such as illness or divorce of parents — may lead to faster maturation of certain brain regions,during adolescence, a new study suggests.
The study found that these experiences cause faster maturation of the prefrontal cortex and amygdala — that also play a role in the control of emotions, in adolescence.
“From an evolutionary perspective, it is useful to mature faster if you grow up in a stressful environment. However, it also prevents the brain from adjusting to the current environment in a flexible way,” said Anna Tyborowska from the Radboud University in the Netherlands.
In contrast, stress experienced later in life such as low peer esteem at school, is connected to a slower maturation of the brain area hippocampus and another part of the prefrontal cortex in teenage years, the researchers said.
“What makes this interesting is that a stronger effect of stress on the brain also increases the risk of developing antisocial personality traits,” Tyborowska said.
For the study, published in the journal Scientific Reports, the researchers examined a group — which then comprised 129 one-year-olds and their parents — in 1998.
Over the past 20 years, researchers studied, inter alia, their play sessions and interactions with parents, friends and classmates. The children were also subjected to MRI scans.
The team investigated two types of stressors — negative life events and negative influences from the social environment — in two life stages of their subjects: early childhood (0-5 years) and adolescence (14-17 years).
They related these stress levels to the maturation of the prefrontal cortex, amygdala and hippocampus. These brain regions play an important role in functioning in social and emotional situations and are known to be sensitive to stress.
The researchers were surprised to find, however, that social stress later in life seems to lead to slower maturation during adolescence.
“Unfortunately, in this study, we can’t say with certainty that stress causes these effects. However, based on animal studies, we can hypothesise that these mechanisms are indeed causal,” Tyborowska said.
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