Obesity, body adiposity, and intracranial aneurysms: A narrative review of clinical evidence beyond body mass index

Intracranial aneurysms are a prevalent cerebrovascular condition and a leading cause of aneurysmal subarachnoid hemorrhage (aSAH). Beyond established risk factors, increasing attention has been focused on metabolic conditions that may modulate vascular inflammation and endothelial function. In this context, obesity has been proposed as potential modifiers of intracranial aneurysm vulnerability. However, clinical evidence remains inconsistent and, in some cases, counterintuitive. Most studies rely on body mass index (BMI) as a proxy for adiposity. Across population-based cohorts and clinical series, BMI has not consistently emerged as an independent risk factor for aneurysm formation or rupture after adjustment for major confounders. Conversely, several studies have reported inverse associations between higher BMI and the risk of aSAH or post-hemorrhagic mortality, findings that have contributed to the concept of an “obesity paradox.” Nevertheless, these associations vary widely by study design, population characteristics, and clinical endpoints, and do not show a consistent linear response pattern. Interpretation of these findings is limited by substantial methodological constraints. BMI does not reflect body composition, fat distribution, or the biological activity of adipose tissue, and may instead capture overall health status or nutritional reserve. Overall, current clinical evidence does not support a consistent or independent role of BMI-defined obesity in intracranial aneurysm risk or prognosis. Reported inverse associations should be interpreted with caution, as they may reflect methodological constraints rather than true biological effects. Future research should incorporate direct and biologically meaningful measures of adiposity to better clarify the relationship between metabolic factors and aneurysm disease.