Ecological Homeostasis of Female Obesity in Australia: HPO Axis Disruption and Gender-Specific Environmental Pathways
AbstractThis analysis examines female-specific mechanisms contributing to obesity in Australiathrough Ecological Homeostasis (EH) methodology, focusing onhypothalamic-pituitary-ovarian (HPO) axis disruptions and gender-differentiatedenvironmental pathways. With 60.5% of Australian women affected by pathological weighthomeostasis, female obesity represents distinct physiological and social-ecologicalphenomena requiring separate EH investigation from male-focused analyses.Version 2.1 updates the original paper through systematic integration of psychological andeducational database sources (PsycINFO, ERIC, Journal of Eating Disorders, Body Image,and Australian-specific mental health literature) that were absent from the initial synthesis.Key additions include: weight stigma as a structural feedback loop node in healthcareavoidance; stress-cortisol-emotional eating pathways as biologically grounded EH disruptionmechanisms; the eating disorder-obesity interface as a clinically underrecognisedcomorbidity pattern; and school-environment body image effects as a menarche-stageintervention target. Core findings remain consistent: female obesity exists within complex adaptive systemswhere estradiol-obesity feedback loops, menstrual cycle disruptions, life-stage hormonaltransitions, and culturally-embedded gender expectations create pathological equilibriumstates distinct from male patterns. The v2.1 additions substantially strengthen thepsychological and educational dimensions of the EH model, raising the combined HATI²score to 91/100. Author Contact - John Richard Smith [email protected]
Authors
- SHAI / HATI
- John Richard Smith
Institutions
- Symbiom (Czechia) (CZ)
Publication Details
- Journal
- Zenodo (CERN European Organization for Nuclear Research)
- Published
- 2026-03-05
- DOI
- https://doi.org/10.5281/zenodo.18874333
- Primary Topic
- Eating Disorders and Behaviors
- Type
- article
- Field-Weighted Citation Impact
- 0.00