Cancer is the second leading cause of death from non-communicable diseases in the world. In 2015, there were 17·5 million new cases of cancer and 8·7 million cancer-related deaths, with 208·3 million disability-adjusted life-years. Cancer incidence is expected to continue to increase, partly due to changes in the prevalence of risk factors such as obesity, diabetes, and other lifestyle factors. Obesity, defined as body-mass index (BMI) of 30 kg/m2 or more, has become increasingly common in all age groups and every country over the past few decades, irrespective of the country’s sociodemographic status or region. Many countries have experienced a rapid change in their populations’ BMIs from underweight to overweight and obesity, which has coincided with an increase in the prevalence of diabetes. In 2016, 125 million children and adolescents aged 5–19 years were obese and an additional 213 million were overweight worldwide, while among adults, 671 million were obese and 1·3 billion were overweight.
A sizeable body of evidence supports causal links between obesity and diabetes and many types of cancer, suggesting that many cancer cases might be due to obesity and diabetes. On this basis, Jonathan Pearson-Stuttard and colleagues assessed the impact of the prevalence of high BMI—overweight and obese defined as a BMI greater than or equal to 25 kg/m2—and diabetes on the number of new cancer cases 2012, assuming a 10-year lag for cancer development. Overall, 5·6% of all cancer in 2012 was attributable to high BMI and diabetes in 2002. When the estimation was restricted to 12 obesity-related cancers and six diabetes-related cancers, 15·0% of cancer cases in men and 13·3% of cases in women were due to the combined effect of high BMI and diabetes. However, there was substantial variation in a proportion of cancer due to high BMI and diabetes by cancer sites—for example, 23·3% of liver cancer, 18·0% of pancreatic cancer, and 8·6% of colorectal cancer cases in men were attributable to the combined effect of high BMI and diabetes. Pearson-Stuttard and colleagues suggest that 26·1% of diabetes-related cancers and 31·9% of cancers related to high BMI in 2012 were due to increases in the prevalence of these risk factors from 1980 to 2002. The burden of cancer due to diabetes and high BMI is projected to continue to increase in the future: in 2035, more than a third of liver cancer cases in men and half of endometrial cancer cases in women will be attributable to a combination of diabetes and high BMI.
Pearson-Stuttard and colleagues’ data highlight the substantial burden of cancer due to diabetes and high BMI at global, regional, and national levels. However, the study might have underestimated the burden of cancer because the time lag between exposure and cancer was limited to 10 years. Although the 10-year lag takes into account the process of carcinogenesis and cumulative exposure over time, it understates the importance of early life exposure, especially from high BMI, on cancer. Emerging evidence suggests that high BMI in late adolescence and young adulthood is directly related to risk of cancer in old age. Results from a pooled analyses of individual participant data from prospective cohort studies showed that each five unit increase in BMI in young adulthood was associated with an increased risk of pancreatic cancer (relative risk [RR] 1·18, 95% CI 1·11–1·25), thyroid cancer (RR 1·13, 1·02–1·25), and myeloma (RR 1·22, 1·09–1·35). A meta-analysis of studies in colorectal cancer noted an RR of 1·13 (1·08–1·19) for the risk of colorectal cancer per five unit increase in BMI during young adulthood. Adolescent obesity was also associated with an increased risk of non-cardia gastric cancer in mid-life (median age 47 years; RR 1·78, 1·12–2·83) compared with normal weight. The lag between high BMI in adolescence and young adulthood and development of cancer far exceeds the 10 years used in this study and is consistent with the longer carcinogenesis process reported in cancer development models. A focus on adiposity in midlife or later and insufficient consideration of lifetime adiposity could lead to substantial underestimation of the contribution of high BMI to the global burden of cancers, especially given the rapidly increasing prevalence of childhood and adolescent adiposity. Future projections that include the changing global patterns of obesity in childhood and adult populations might better account for the impact of lifetime adiposity.
For their assessment of diabetes-related cancers, Pearson-Stuttard and colleagues selected colorectal, gallbladder, pancreatic, liver, breast, and endometrial cancer, on the basis of the results of an umbrella review of meta-analyses of diabetes and cancer studies. Although the review comprehensively summarised the associations between diabetes and cancer, the use of stringent statistical criteria excluded several cancer types and sites—including bladder, kidney, and oesophageal cancer and myeloma—that might also be associated with diabetes. Given the methodological limitations of the umbrella review and accumulating evidence of the role of diabetes in these cancers, it is likely that Pearson-Stuttard and colleagues’ study underestimated the burden of cancer due to diabetes.
As predicted in this study, the global burden of cancer due to high BMI and diabetes will continue to increase unless the prevalences of these conditions fall. Both obesity and diabetes are preventable causes of cancer for which intervention is possible at multiple levels—in individuals, communities, health-care systems, and policy. More prompt actions are needed to help people maintain a healthy body weight throughout the life course, starting at an early age.