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Groundbreaking research from the Brenhouse Lab at Northeastern University has unveiled how early life adversity can trigger premature puberty and lead to anxiety in later life. This discovery, published in Hormones and Behavior, offers new insights and potential pathways for medical interventions to address these issues.

For decades, the average onset of puberty in girls has been decreasing. In the United States, girls typically reach puberty between 8.8 and 10.3 years old, an early start associated with numerous health risks. Chronic stress in children has been identified as a key trigger for this premature development.

The Northeastern study is the first to identify the specific brain mechanism affected by early life stress that leads to early puberty. Researchers found that chronic stress disrupts a receptor in the hypothalamus, a brain region crucial for hormone regulation, thereby accelerating the onset of puberty.

“Early puberty is very important because it seems to be associated with later life psychopathologies like anxiety-related disorders,” said Heather Brenhouse, a psychology professor at Northeastern University. “Physiological medical conditions also seem to be potentially linked to early puberty.”

Children experiencing early puberty are at a higher risk of developing reproductive cancers, metabolic syndromes like diabetes, cardiovascular disease, and emotional and social problems in adulthood. The findings of this research could lead to significant advancements in medical interventions aimed at mitigating these risks.

The research was led by Lauren Granata, a Northeastern graduate with a doctoral degree in psychology. She explored how early life stress affects puberty in animal models, specifically focusing on maternal separation as a form of adversity. The results indicated that stress hormones typically act as brakes on puberty by activating the CRH-R1 receptor in the hypothalamus. However, chronic stress can impair this receptor, leading to an early release of puberty-related hormones.

Granata noted the counterintuitive nature of these findings: “It’s pretty well understood nowadays that stress is dampening reproduction. I thought there was a lot of opportunity to find out something new.”

Their study confirmed that early childhood adversity, such as disrupted maternal care, triggers early puberty in female rats. These rats exhibited higher levels of anxiety in adolescence, as demonstrated by their response to acoustic startle tests.

“We found that brain cells start expressing and releasing proteins associated with puberty earlier in female rats exposed to maternal separation,” Granata explained. The CRH-R1 receptor, which normally suppresses premature puberty, becomes less responsive to stress hormones under chronic stress, allowing puberty to commence prematurely.

Interestingly, the researchers did not observe accelerated puberty in male rats exposed to the same stress conditions, suggesting a gender-specific response to early life adversity.

The implications of this research extend beyond animal models. Brenhouse and her team hope these findings will lead to new interventions and treatments for girls at higher risk of anxiety and depression due to early puberty.

As research continues, the potential to develop therapeutic strategies to delay puberty in stressed children could provide a significant breakthrough in reducing the associated health risks and improving long-term mental health outcomes.

More information: Lauren Granata et al., “Early life adversity accelerates hypothalamic drive of pubertal timing in female rats with associated enhanced acoustic startle,” Hormones and Behavior (2024).

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