A proposed psychometabolic endotype of polyendocrine metabolic ovarian syndrome: bidirectional interplay between psychological distress, eating dysfunction, sleep disruption, chronic stress, and metabolic deterioration.
4 affiliations
- 1South China Research Center for Acupuncture and Moxibustion, School of Acupuncture-Moxibustion and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, China.
- 2The Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, China.
- 3Tianjin University of Traditional Chinese Medicine, Tianjin, China.
- 4School of Nursing, Guangzhou University of Chinese Medicine, Guangzhou, China.
Abstract
Background
Polycystic ovary syndrome was renamed polyendocrine metabolic ovarian syndrome (PMOS) in 2026 to better represent its multisystem biology. Psychological distress, eating dysregulation, sleep disturbance, and metabolic dysfunction frequently coexist, yet clinical care and research commonly treat them as parallel comorbidities.Objective
To define the proposed psychometabolic construct operationally; position it relative to conventional phenotypes and data-driven clusters; and grade evidence for association, temporal prediction, causation, and treatment response across psychological, behavioral, sleep-stress, neuroendocrine, and metabolic pathways.Methods
We conducted a targeted narrative review of PubMed/MEDLINE from inception through 15 September 2026. Seven structured topic blocks returned 1,278 records, 1,009 unique identifiers after PubMed identifier (PMID)-based deduplication, and 1,008 retrievable article records for title/abstract screening. Guidelines, systematic reviews, longitudinal or causal studies, trials, and informative human mechanistic studies were prioritized; general-population and preclinical evidence was used only when its indirectness was explicit.Evidence synthesis
Depression and anxiety, body-image concerns, binge- and bulimia-spectrum symptoms, poor sleep, and obstructive sleep apnea are reported more often in PMOS than in comparison populations, but most estimates are cross-sectional and heterogeneous. One tertiary cohort found that baseline depression and/or anxiety history predicted incident metabolic syndrome over a median seven years (adjusted hazard ratio 1.45, 95% confidence interval 1.02-2.06); this supports prognostic enrichment, not causality. General-population longitudinal and genetic studies support reciprocal depression-metabolic relationships, whereas PMOS-specific causal evidence is inconsistent. Plausible links include insulin-androgen-adipose interactions, neuroactive steroid signaling, ovarian sympathetic input, sleep fragmentation, stress and autonomic regulation, reward-related eating, treatment exposure, stigma, and social context. None validates a discrete endotype.Conclusions
We define a candidate psychometabolic endotype as a cross-cutting, mechanistically coupled pattern that may occur within any conventional PMOS phenotype. Clinical co-occurrence is only an entry profile; endotype status requires replicated longitudinal coupling, incremental prognostic value, interpretable transitions, and preferably treatment-effect heterogeneity. Four overlapping prototypes are working formulations rather than subtypes. A six-step clinical pathway centers shared formulation and nests care-intensity tiers within treatment selection.
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BibTeX
@article{li2026proposed,
title = {{A proposed psychometabolic endotype of polyendocrine metabolic ovarian syndrome: bidirectional interplay between psychological distress, eating dysfunction, sleep disruption, chronic stress, and metabolic deterioration.}},
author = {Hongtao Li and Tong Yin and Yichen Wang and Yixuan Wang and Nenggui Xu and Wei Yi and Han Yang},
journal = {Frontiers in endocrinology},
year = {2026},
month = oct,
doi = {10.3389/fendo.2026.1978249},
url = {https://europepmc.org/article/MED/42909207},
note = {CC BY},
}
RIS
TY - JOUR
TI - A proposed psychometabolic endotype of polyendocrine metabolic ovarian syndrome: bidirectional interplay between psychological distress, eating dysfunction, sleep disruption, chronic stress, and metabolic deterioration.
AU - Hongtao Li
AU - Tong Yin
AU - Yichen Wang
AU - Yixuan Wang
AU - Nenggui Xu
AU - Wei Yi
AU - Han Yang
PY - 2026
DA - 2026/10/07
JO - Frontiers in endocrinology
DO - 10.3389/fendo.2026.1978249
UR - https://europepmc.org/article/MED/42909207
AB - Background Polycystic ovary syndrome was renamed polyendocrine metabolic ovarian syndrome (PMOS) in 2026 to better represent its multisystem biology. Psychological distress, eating dysregulation, sleep disturbance, and metabolic dysfunction frequently coexist, yet clinical care and research commonly treat them as parallel comorbidities.Objective To define the proposed psychometabolic construct operationally; position it relative to conventional phenotypes and data-driven clusters; and grade evidence for association, temporal prediction, causation, and treatment response across psychological, behavioral, sleep-stress, neuroendocrine, and metabolic pathways.Methods We conducted a targeted narrative review of PubMed/MEDLINE from inception through 15 September 2026. Seven structured topic blocks returned 1,278 records, 1,009 unique identifiers after PubMed identifier (PMID)-based deduplication, and 1,008 retrievable article records for title/abstract screening. Guidelines, systematic reviews, longitudinal or causal studies, trials, and informative human mechanistic studies were prioritized; general-population and preclinical evidence was used only when its indirectness was explicit.Evidence synthesis Depression and anxiety, body-image concerns, binge- and bulimia-spectrum symptoms, poor sleep, and obstructive sleep apnea are reported more often in PMOS than in comparison populations, but most estimates are cross-sectional and heterogeneous. One tertiary cohort found that baseline depression and/or anxiety history predicted incident metabolic syndrome over a median seven years (adjusted hazard ratio 1.45, 95% confidence interval 1.02-2.06); this supports prognostic enrichment, not causality. General-population longitudinal and genetic studies support reciprocal depression-metabolic relationships, whereas PMOS-specific causal evidence is inconsistent. Plausible links include insulin-androgen-adipose interactions, neuroactive steroid signaling, ovarian sympathetic input, sleep fragmentation, stress and autonomic regulation, reward-related eating, treatment exposure, stigma, and social context. None validates a discrete endotype.Conclusions We define a candidate psychometabolic endotype as a cross-cutting, mechanistically coupled pattern that may occur within any conventional PMOS phenotype. Clinical co-occurrence is only an entry profile; endotype status requires replicated longitudinal coupling, incremental prognostic value, interpretable transitions, and preferably treatment-effect heterogeneity. Four overlapping prototypes are working formulations rather than subtypes. A six-step clinical pathway centers shared formulation and nests care-intensity tiers within treatment selection.
SN - 1664-2392
ER -