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Hypothalamic-pituitary-gonadal axis in major depressive disorders
F Undén1, J G Ljunggren, J Beck-Friis
1Department of Psychiatry, Karolinska Institute, Stockholm, Sweden.
Acta Psychiatrica Scandinavica
|August 1, 1988
Summary
Depressed males with abnormal dexamethasone suppression tests (DST) showed altered follicle-stimulating hormone (FSH) levels and testosterone changes during acute major depressive disorder compared to remission. These findings suggest complex HPG axis interactions in depression.
Area of Science:
- Neuroendocrinology
- Psychiatry
- Reproductive Endocrinology
Background:
- Major depressive disorder (MDD) is associated with neuroendocrine dysregulation.
- The hypothalamic-pituitary-gonadal (HPG) axis and hypothalamic-pituitary-adrenal (HPA) axis may interact in the pathophysiology of depression.
Purpose of the Study:
- To investigate baseline and stimulated luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone levels in patients with acute major depressive disorder.
- To compare hormonal profiles between depressed patients and healthy controls, and between acute depression and remission states.
- To explore the relationship between HPA axis activation (via DST) and HPG axis function in depression.
Main Methods:
- Assessed baseline LH, FSH, and testosterone levels in 28 patients with acute MDD and 20 healthy controls.
- Administered TRH-LHRH to measure LH and FSH response (delta LH, delta FSH).
- Reinvestigated 22 patients in remission and performed cross-sectional and longitudinal comparisons, stratified by sex and menopausal status.
Main Results:
- Depressed males with abnormal dexamethasone suppression test (DST) response exhibited significantly higher delta FSH during acute depression compared to controls (P < 0.03).
- Longitudinally, these males showed decreased testosterone levels and increased delta FSH in the acute state versus remission.
- No correlation was found between HPG axis hormones and melatonin, prolactin (PRL), or thyrotropin-releasing hormone (TRH)/LHRH-stimulated thyroid-stimulating hormone (TSH) response.
Conclusions:
- The results do not support a hypothesis of stimulus-induced downregulation of pituitary LHRH receptors in depressed patients.
- The mechanisms linking HPA axis activation to HPG axis alterations in depression require further investigation.