Association between abdominal obesity and cognitive outcomes in middle-aged adults: a systematic review

This systematic review aimed to evaluate the association between abdominal obesity and cognitive outcomes in middle-aged adults and to summarize the underlying biological mechanisms and potential modifying factors, with intervention evidence discussed as a complementary clinical perspective.

We systematically retrieved relevant literature published from January 2000 to May 2026 across PubMed, Embase, Web of Science, Cochrane Library and CNKI databases. Eligible observational and interventional studies focusing on middle-aged adults were included. Two independent researchers strictly completed study selection, data extraction and methodological quality assessment in accordance with the PRISMA 2020 reporting guidelines.

A total of 96 qualified studies were finally included for systematic analysis. Abdominal obesity assessed by waist circumference, waist-to-hip ratio and other central adiposity indicators was consistently associated with poor cognitive performance and elevated risk of cognitive decline in middle-aged populations. Multiple biological mechanisms were involved, including chronic inflammation, oxidative stress, insulin resistance, neuroendocrine dysregulation, mitochondrial dysfunction and gut-brain axis imbalance. Dietary patterns, physical activity and sleep quality effectively modify this association, while genetic susceptibility and long-term chronic stress further increase cognitive impairment vulnerability. Lifestyle interventions exert positive effects on improving metabolic status and cognitive function in short-term trials, whereas high-quality evidence for pharmacological treatment, surgical intervention and traditional Chinese medicine remains relatively limited and requires further investigation.

Current evidence supports a clinically relevant association between greater midlife central adiposity and poorer cognitive outcomes across a spectrum from domain-specific deficits to cognitive decline and dementia-related endpoints. The evidence is biologically coherent but does not establish that abdominal obesity is independently causal in every population or that reducing waist circumference alone will prevent cognitive decline. Future studies should standardize abdominal obesity severity categories and cognitive impairment grades, use repeated exposure and cognitive measurements, and integrate neuroimaging and biomarker data to clarify dose-response, mediation, and temporality.