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Researchers have identified a significant genetic link to obesity, anxiety, and postnatal depression through the discovery of the TRPC5 gene. This finding may pave the way for new treatments, including the use of oxytocin to alleviate symptoms, according to studies involving mice.

Postnatal depression affects over 10% of women within a year of childbirth and is associated with heightened suicide risks, contributing to a substantial portion of maternal deaths in high-income nations. Concurrently, global obesity rates have doubled in adults and quadrupled in adolescents since 1990, as reported by the World Health Organization.

According to Neuroscience News, the investigation began with two boys exhibiting severe obesity, anxiety, autism, and sensory sensitivity, prompting researchers from the University of Cambridge, UK, and Baylor College of Medicine, Houston, USA, to identify a common genetic anomaly: the absence of TRPC5 on the X chromosome.

Further study revealed that both boys inherited this gene deletion from their mothers, who also showed signs of obesity and experienced postnatal depression.

To validate their findings, researchers used genetically modified mice with a defective Trpc5 gene. Male mice exhibited similar symptoms to the boys, including weight gain, anxiety, social aversion, and aggression. Female mice displayed comparable behaviors and additionally showed signs of postnatal depression and impaired maternal care.

Dr. Yong Xu, Associate Director for Basic Sciences at Baylor College of Medicine, highlighted the striking parallels between the mice and human behaviors associated with TRPC5 deficiency, emphasizing the gene's role in these conditions.

TRPC5, part of a gene family involved in sensory signal processing, operates within the hypothalamus to regulate appetite and, as discovered by the team, influences oxytocin-producing neurons. Oxytocin, often called the 'love hormone,' regulates emotions and social bonding.

Deleting TRPC5 from oxytocin neurons in mice resulted in increased anxiety, overeating, and impaired sociability, mimicking human behaviors. Restoring TRPC5 reversed these effects, suggesting potential therapeutic avenues.

Professor Sadaf Farooqi from the University of Cambridge noted, "There's a reason why people lacking TRPC5 develop all of these conditions. We've known for a long time that the hypothalamus plays a key role in regulating 'instinctive behaviours' - which enable humans and animals to survive - such as looking for food, social interaction, the flight or fight response, and caring for their infants."

"Our work shows that TRPC5 acts on oxytocin neurons in the hypothalamus to play a critical role in regulating our instincts."

While TRPC5 deficiencies are rare, analysis of DNA from 500,000 individuals in UK Biobank identified 369 carriers of TRPC5 variants linked to higher body mass index, predominantly women.

The findings reported in Cell suggest oxytocin supplementation could benefit individuals with TRPC5 deficiencies and potentially aid in treating postnatal depression.

Professor Farooqi added, "This research reminds us that many behaviours which we assume are entirely under our control have a strong basis in biology, whether that's our eating behaviour, anxiety or postnatal depression. We need to be more understanding and sympathetic towards people who suffer with these conditions."