Biological sex and menstrual cycle phase modulation of cortisol levels and psychiatric symptoms in a non-clinical sample of young adults
Prior research examined the complex, bidirectional interplay of the hypothalamic–pituitary–adrenal (HPA) and hypothalamic–pituitary–gonadal axes and their roles in (clinical) cognitive/behavioral functions. Less well understood are contemporaneous relationships in non-clinical samples. This pilot st...
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Published in | Psychiatry research Vol. 197; no. 3; pp. 314 - 321 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Kidlington
Elsevier Ireland Ltd
30.05.2012
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Prior research examined the complex, bidirectional interplay of the hypothalamic–pituitary–adrenal (HPA) and hypothalamic–pituitary–gonadal axes and their roles in (clinical) cognitive/behavioral functions. Less well understood are contemporaneous relationships in non-clinical samples. This pilot study explored cortisol in relation to psychiatric symptoms/personality as a function of self-reported menstrual cycle phase and sex differences in a non-clinical, young adult sample. Consistent with literature and hypotheses, cortisol levels were lowest during early-follicular, intermediary during late-follicular, and highest during mid-luteal phases (not significant), and greater among males than early-follicular females. An acute stressor uniformly affected cortisol across phases and sex, though magnitude and time course differed. Psychiatric symptoms were greater among early-follicular/late-follicular females versus males, and early-follicular and/or late-follicular versus mid-luteal. Contrary to hypotheses, positive psychotic-like symptoms were greater among males than (mid-luteal) females. Cortisol inversely related to early-follicular symptoms, and directly related to late-follicular/mid-luteal symptoms. Results suggest menstrual cycle phase modulates non-clinical psychiatric symptomatology and HPA activity. Findings tentatively bolster a dimensional/continuum model of psychopathology with implications for understanding neurobiological underpinnings and risk/protective factors for mental/physical health conditions, particularly those marked by sex differences and neuroendocrine dysfunction (depression/schizophrenia/Alzheimer's/multiple sclerosis). We speculate a dose–response cortisol effect on symptoms, modulated by endogenous gonadal hormones via gene expression. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0165-1781 1872-7123 |
DOI: | 10.1016/j.psychres.2011.09.009 |