Genetic factors underlying insomnia and ovarian insufficiency

Premature ovarian insufficiency (POI) is characterized by a loss of regular hormone production and egg release in women below the age of 40 years, which often leads to infertility, vaginal dryness and dysfunctional sleep. Acknowledging the common co-occurrence of insomnia and POI, we tested the overlap between POI and insomnia-associated genes, which were implicated in previous large-scale populational genetics efforts. Among the 27 overlapping genes, three pathways were found as enriched: DNA replication, homologous recombination and Fanconi anemia. We then describe biological mechanisms, which link these pathways to a dysfunctional regulation and response to oxidative stress. We propose that oxidative stress may correspond to one of the convergent cellular processes between ovarian malfunction and insomnia pathogenic etiology. This overlap might also be driven by cortisol release associated with dysregulated DNA repair mechanisms. Benefiting from the enormous advances in populational genetics studies, this study provides a novel outlook on the relationship between insomnia and POI. The shared genetic factors and critical biological nodes between these two comorbidities may lead to identification of putative pharmacological and therapeutical targets, which can leverage novel approaches to treat or alleviate their symptoms.

Automated summary

Premature ovarian insufficiency (POI) is a condition where women below the age of 40 experience a loss of regular hormone production and egg release, leading to infertility, vaginal dryness, and dysfunctional sleep. A study found overlapping genes between POI and insomnia, particularly in pathways related to DNA replication, homologous recombination, and Fanconi anemia. The overlap may be due to oxidative stress and dysregulated DNA repair mechanisms, which could be potential targets for treatment. This study provides a new understanding of the relationship between insomnia and POI.