Obesity as disruptor of the female fertility.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms and clinical associations without systematic methodology.
PubMed 29523133 · doi:10.1186/s12958-018-0336-z
What was done
This narrative review synthesized literature on how overweight and obesity disrupt female reproductive health. It examined endocrine perturbations along the hypothalamic-pituitary-ovarian axis, adipokine secretome signaling, and reproductive outcomes including ovulation, conception, assisted reproductive technology success, and miscarriage.
What was found
The abstract reports no numerical data, odds ratios, or statistical results. It outlines mechanistic and clinical pathways wherein adipocytes act as endocrine organs releasing adipokines that interact with insulin resistance, inflammation, and oocyte maturation. It qualitative notes that obesity correlates with menstrual dysfunction, anovulation, delayed conception, and higher miscarriage rates, while lifestyle-induced weight loss can restore cyclicity and ovulation.
Why it matters
It consolidates mechanistic pathways linking adipose tissue biology directly to female reproductive dysfunction and reinforces lifestyle-driven weight management as a foundational intervention for subfertility in obese women.
Limits
As a narrative review, it lacks systematic search methodology, formal quality assessment, and meta-analytic pooling. The abstract provides no primary data, sample sizes, or quantitative risk estimates.
Cited by
- supports Fat cells synthesize estrogen, alter ovulation, and generate inflammatory signals.