The mind–body connection in women’s reproductive health: how psychological stress shapes gut and ovarian function - a narrative review
- 1School of Psychological Sciences, CHRIST University, Bengaluru, India
Abstract
Psychological stress plays a critical role in modulating women’s reproductive health through integrated neuroendocrine, immune, and microbiome-mediated pathways. Activation of the hypothalamic–pituitary–adrenal (HPA) axis leads to elevated secretion of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol, which suppress hypothalamic gonadotropin-releasing hormone (GnRH) pulsatility, thereby disrupting the hypothalamic–pituitary–gonadal (HPG) axis. This results in reduced secretion of luteinising hormone (LH) and follicle-stimulating hormone (FSH), impairing folliculogenesis, ovulation, and menstrual cyclicity. Chronic stress further induces oxidative stress, mitochondrial dysfunction, and apoptosis in ovarian cells, thereby reducing oocyte competence and diminishing ovarian reserve. Additionally, stress-induced gut microbiota dysbiosis alters the composition of key microbial taxa, including Lactobacillus, Bifidobacterium, and Clostridium, disrupting the estrobolome and impairing oestrogen metabolism. This dysregulation increases intestinal permeability and promotes systemic inflammation, as evidenced by biomarkers including interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and C-reactive protein (CRP), which adversely affect endometrial receptivity and implantation success. Emerging evidence also indicates that microbial metabolites such as short-chain fatty acids (SCFAs), tryptophan metabolites, and serotonin play a crucial role in modulating neuroendocrine signalling and reproductive outcomes. Despite growing evidence, the lack of standardised biomarkers and well-designed clinical trials limits translation into clinical practice. Future research should focus on integrative, personalised therapeutic approaches combining psychological interventions, lifestyle modifications, and microbiome-targeted therapies to improve reproductive outcomes and overall well-being.
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BibTeX
@article{purushotham2026mindbody,
title = {{The mind–body connection in women’s reproductive health: how psychological stress shapes gut and ovarian function - a narrative review}},
author = {Arpitha Yachanahalli Purushotham and Borehalli Mayegowda Shilpa and Divya Sundaram},
journal = {Frontiers in Gastroenterology},
year = {2026},
month = oct,
doi = {10.3389/fgstr.2026.1854862},
url = {https://doi.org/10.3389/fgstr.2026.1854862},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The mind–body connection in women’s reproductive health: how psychological stress shapes gut and ovarian function - a narrative review
AU - Arpitha Yachanahalli Purushotham
AU - Borehalli Mayegowda Shilpa
AU - Divya Sundaram
PY - 2026
DA - 2026/10/12
JO - Frontiers in Gastroenterology
DO - 10.3389/fgstr.2026.1854862
UR - https://doi.org/10.3389/fgstr.2026.1854862
AB - Psychological stress plays a critical role in modulating women’s reproductive health through integrated neuroendocrine, immune, and microbiome-mediated pathways. Activation of the hypothalamic–pituitary–adrenal (HPA) axis leads to elevated secretion of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol, which suppress hypothalamic gonadotropin-releasing hormone (GnRH) pulsatility, thereby disrupting the hypothalamic–pituitary–gonadal (HPG) axis. This results in reduced secretion of luteinising hormone (LH) and follicle-stimulating hormone (FSH), impairing folliculogenesis, ovulation, and menstrual cyclicity. Chronic stress further induces oxidative stress, mitochondrial dysfunction, and apoptosis in ovarian cells, thereby reducing oocyte competence and diminishing ovarian reserve. Additionally, stress-induced gut microbiota dysbiosis alters the composition of key microbial taxa, including Lactobacillus, Bifidobacterium, and Clostridium, disrupting the estrobolome and impairing oestrogen metabolism. This dysregulation increases intestinal permeability and promotes systemic inflammation, as evidenced by biomarkers including interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and C-reactive protein (CRP), which adversely affect endometrial receptivity and implantation success. Emerging evidence also indicates that microbial metabolites such as short-chain fatty acids (SCFAs), tryptophan metabolites, and serotonin play a crucial role in modulating neuroendocrine signalling and reproductive outcomes. Despite growing evidence, the lack of standardised biomarkers and well-designed clinical trials limits translation into clinical practice. Future research should focus on integrative, personalised therapeutic approaches combining psychological interventions, lifestyle modifications, and microbiome-targeted therapies to improve reproductive outcomes and overall well-being.
SN - 2813-1169
ER -