In our systematic evaluation of the health effects of high BMI, we found that excess body weight accounted for about 4 million deaths and 120 million disability-adjusted life-years worldwide in 2015. Nearly 70% of the deaths that were related to high BMI were due to cardiovascular disease, and more than 60% of those deaths occurred among obese persons. The prevalence of obesity has increased during the past three decades and at a faster pace than the related disease burden. However, both the trend and magnitude of the BMI-related disease burden vary widely across countries.

Among the leading health risks that were assessed in the Global Burden of Disease 2015 study, high BMI continues to have one of the highest rates of increase. Across levels of development, the prevalence of obesity has increased over recent decades, which indicates that the problem is not simply a function of income or wealth.13 Changes in the food environment and food systems are probably major drivers.18 Increased availability, accessibility, and affordability of energy-dense foods, along with intense marketing of such foods, could explain excess energy intake and weight gain among different populations.18 The reduced opportunities for physical activity that have followed urbanization and other changes in the built environment have also been considered as potential drivers; however, these changes generally preceded the global increase in obesity and are less likely to be major contributors.18

During the past decade, researchers have proposed a range of interventions to reduce obesity.19 Among such interventions are restricting the advertisement of unhealthy foods to children, improving school meals, using taxation to reduce consumption of unhealthy foods and providing subsidies to increase intake of healthy foods, and using supply-chain incentives to increase the production of healthy foods.19 However, the effectiveness, feasibility of widespread implementation, and sustainability of such interventions need to be evaluated in various settings. In recent years, some countries have started to implement some of these policies,1 but no major population success has yet been shown. Many of the countries with the highest increases in the prevalence of obesity are those that have a low or middle SDI and simultaneously have high rates of other forms of malnutrition. These countries generally have limited financial resources for nutrition programs and mostly rely on external donors whose programs often preferentially target undernutrition; consequently, food security frequently takes precedence over obesity in these countries.20 In 2013, the World Health Organization (WHO) called for zero increase in the prevalence of overweight among children and in the prevalence of obesity among adults.21 However, given the current pace of increase and the existing challenges in implementing food policies, achieving this goal appears unlikely in the near future.

Our study showed a greater increase in the rate of exposure to high BMI than in the rate of the related disease burden. This difference was driven mainly by the decline in risk-deleted mortality, particularly for cardiovascular disease; factors such as improved treatment or changes in other risks have resulted in decreases in the rate of cardiovascular disease despite increases in BMI. Existing evidence-based policies, even if fully implemented, are unlikely to rapidly reduce the prevalence of obesity. Clinical interventions, however, have proved to be effective in controlling high levels of systolic blood pressure, cholesterol, and fasting plasma glucose — the major risk factors for cardiovascular disease.22 The expanded use of such interventions among overweight and obese persons could effectively reduce the disease burden related to high BMI. A recent pooled cohort analysis involving 1.8 million participants showed that nearly half the excess risk for ischemic heart disease and more than 75% of the excess risk for stroke that was related to high BMI were mediated through a combination of raised levels of blood pressure, total serum cholesterol, and fasting plasma glucose.23 Together, these findings suggest that clinical interventions to reduce the underlying rate of cardiovascular disease could substantially reduce the burden of disease related to high BMI, although maintaining a normal body weight remains necessary to achieve full benefit.

Globally, 39% of deaths and 37% of disability-adjusted life-years that were related to high BMI occurred among nonobese persons. Although some studies have suggested that overweight is associated with a lower risk of death from any cause than is a normal range of BMI (18 to 25),2,10 recent evidence from a meta-analysis14 and pooled analysis9 of prospective observational studies showed a continuous increase in the risk of death associated with a BMI of more than 25. These studies are particularly notable since they addressed major sources of bias in previous studies (i.e., residual confounding due to smoking and reverse causation due to preexisting chronic disease) by restricting the analysis to persons who had never smoked and who did not have chronic diseases. In addition, the pooled-cohort analysis controlled for the same set of covariates, provided cause-specific relative risks, and evaluated the relationship between BMI and mortality across different regions. The balance of evidence thus supports our minimum risk level of 20 to 25 for BMI. At the same time, to date, there remains insufficient evidence to support the argument that the most beneficial level of BMI should vary according to geographic location or ethnic group9 because of differences in the relationship between BMI and body-fat distribution.

We found that 5% of the disability-adjusted life-years that were related to high BMI were from musculoskeletal disorders. Although high BMI is a major risk factor contributing to years lived with disability globally, and the economic costs associated with treatment are substantial,24 these nonfatal but debilitating health outcomes have received comparatively little policy attention. Weight loss is beneficial in the prevention and treatment of musculoskeletal pain.25 A combination of modest weight loss and moderate exercise provides better overall improvement in musculoskeletal pain than either intervention alone26; however, surgical interventions may be most effective for the morbidly obese.27

Our systematic evaluation of prospective observational studies showed sufficient evidence supporting a causal relationship between high BMI and cancers of the esophagus, colon and rectum, liver, gallbladder and biliary tract, pancreas, breast, uterus, ovary, kidney, and thyroid, along with leukemia. A recent review by the International Agency for Research on Cancer (IARC)4 comes to largely similar conclusions, except with respect to leukemia. (We included leukemia on the basis of a systematic review and meta-analysis of 21 prospective cohort studies.28) In addition, even though the IARC report acknowledged consistent inverse associations between BMI and the risk of premenopausal breast cancer, inconsistent findings from studies that evaluated the effect of waist circumference or body-weight gain resulted in the exclusion of premenopausal breast cancer from its list. However, since high BMI was the exposure of interest in our analysis, we included the protective effect of high BMI on breast cancer in premenopausal women. We did not evaluate the effect of high BMI on gastric cancer (cardia) and meningioma because of a lack of sufficient data to separately estimate the incidence and mortality of these cancers at the population level.

Our study has several important strengths. We have addressed the major limitations of previous studies by including more data sources and quantifying the prevalence of obesity among children. We also systematically evaluated the strength of evidence for the causal relationship between high BMI and health outcomes and included all BMI–outcome pairs for which sufficient evidence with respect to causal relationship was available. We used a beta distribution to characterize the distribution of BMI at the population level, a method that captures the proportion of the population with high BMI more accurately than other distributions.12 We used the best available evidence to determine the lowest-risk BMI. We quantified the trends in high BMI and the associated disease burden across levels of development and estimated the contribution of demographic transition and epidemiologic transition to changes in BMI-related burden.

The potential limitations of our study should also be considered. We used both self-reported and measured data with respect to height and weight and corrected the bias in self-reported data using measured data at each age, sex, and geographic region. To apply a consistent definition for childhood overweight and obesity across sources, we used the definition of the International Obesity Task Force and excluded studies that used the WHO definition. We did not propagate the uncertainty in the age pattern and sex pattern that were used to split the aggregated data. We did not incorporate the uncertainty of the BMI regression coefficients in our analysis. Data were sparse for some locations, particularly in earlier years, and estimates in these locations were based on country-level covariates and regional data. We did not identify a consistent pattern in the relationship between nationally representative data and data representing only urban or rural areas and were not able to correct those data for potential bias. We did not evaluate the trends in other measures of adiposity that may better relate to specific health outcomes, including waist circumference and waist-to-hip ratio. Since we obtained the effect size of BMI on health outcomes from prospective observational studies, the possibility of confounding by lifestyle habits cannot be excluded. Our estimation of relative risks did not capture possible differences owing to ethnic group and did not account for the possibility of geographic variation in relative-risk curves or the lowest-risk BMI. In addition, these studies generally excluded people with prevalent chronic diseases from the analysis of relative-risk estimation. Thus, our estimates represent the effect of BMI among persons without underlying diseases. This issue might be particularly important for older age groups, in which the prevalence of chronic disease increases. Finally, other probable complications or forms of BMI-related burden (e.g., disease burden in children) were not included.

In conclusion, our study provides a comprehensive assessment of the trends in high BMI and the associated disease burden. Our results show that both the prevalence and disease burden of high BMI are increasing globally. These findings highlight the need for implementation of multicomponent interventions to reduce the prevalence and disease burden of high BMI.