A large-scale systematic review and meta-analysis published in Nature Metabolism has significantly expanded our understanding of the relationship between body mass index (BMI) and cancer risk.

The study combined data from more than 1.5 million documented cancer cases and found that elevated BMI is associated with at least 19 different types of cancer, rather than the 13 previously recognized.

Researchers analyzed 226 peer-reviewed studies from 23 countries, covering 25 cancer types. This extensive dataset enabled a standardized comparison of how BMI influences cancer risk across different populations and malignancies.

The results confirmed a strong positive association between excess body weight and several cancers. The most pronounced links were observed for endometrial cancer, where the risk increased by 58% for every 5-unit rise in BMI, and esophageal adenocarcinoma, where the risk rose by 47%.

The analysis also identified statistically significant associations that have received less attention in the past, including links between higher BMI and leukemia, non-Hodgkin lymphoma, bladder cancer, and glioma. Although the increases in risk were more modest, they remained consistent across studies.

At the same time, the researchers observed several inverse associations. Among premenopausal women and people who had never smoked, higher BMI was linked to a lower risk of certain forms of lung cancer and esophageal squamous cell carcinoma. These findings highlight the complex biological mechanisms connecting body weight and cancer development.

The study also revealed notable geographic and sex-related differences. For example, the obesity-associated risk of postmenopausal breast cancer was approximately twice as high in East Asian populations as in European populations.

For colorectal cancer, the association with obesity was substantially stronger in men, whereas for gallbladder cancer the relationship was more pronounced in women.

The authors additionally compared BMI with waist circumference as predictors of cancer risk. Overall, both measures demonstrated similar predictive value, although differences emerged for specific cancer types, suggesting that various patterns of fat distribution may influence cancer risk through distinct biological pathways.

To strengthen evidence for a causal relationship, the researchers employed Mendelian randomization, a method that uses genetic variants associated with body weight to assess causality. These analyses generally supported the observational findings, although the strength of evidence varied among different cancers.

In their conclusion, the authors emphasize that obesity remains one of the most important modifiable risk factors for cancer. However, they note that current models do not adequately account for regional differences. In particular, there is a shortage of data from Africa, South Asia, and Central America, limiting the global applicability of existing conclusions.