Serum alarin in relation to depression and anxiety in women with polycystic ovary syndrome
Hend Abd Elhamed, Olfat Fawzy, Doaa Sayed, Shaimaa Younes Abd Elaziz, Hager Abdelgawad, Emad Gamil KhidrAbstract
Objectives
Polycystic ovary syndrome (PCOS) is a common endocrine disorder associated with metabolic, reproductive, and psychological disturbances. Alarin, a neuropeptide of the galanin family, has been implicated in energy metabolism and insulin resistance, and experimental studies suggest a role in mood regulation. However, its association with psychiatric features in PCOS remains unclear. This study aimed to evaluate circulating alarin levels in women with PCOS and their relationship with depression, anxiety, and metabolic-hormonal parameters.
Methods
This case-control study included 180 women divided into four groups: PCOS with depression, PCOS without depression, depression without PCOS, and healthy controls (45 participants each). Clinical, biochemical, and hormonal assessments were performed, including measurement of serum alarin levels. Depression and anxiety were assessed using validated Hamilton rating scales.
Results
Serum alarin levels were significantly higher in women with PCOS, irrespective of comorbid depression, compared with healthy controls and women with depression without PCOS. Women with depression alone showed alarin levels comparable to controls. Factorial analysis showed significant effects of PCOS status and depression status, with no significant PCOS × depression interaction (p=0.37). Serum alarin correlated positively with fasting insulin, HOMA-IR, and luteinizing hormone, but not with depression or anxiety severity. Multivariate analysis identified luteinizing hormone and PCOS status as independent predictors of serum alarin levels. Receiver operating characteristic analysis demonstrated excellent discriminative performance for PCOS.
Conclusions
Circulating alarin is closely associated with the metabolic and reproductive features of PCOS rather than psychiatric symptom severity, indicating a stronger link to endocrine-metabolic dysregulation.