Because obesity’s effect on mortality among middle-aged adults is increasingly important to future life expectancy, we examine adults in their 50s and 60s. The proportion of Americans in their 50s and 60s is expected to grow from approximately one-fifth to one-quarter over the next decade (U.S. Census Bureau 2005). Our target population, the 1931–1941 birth cohort, is a predecessor of the numerically large baby boom cohort born between 1946 and 1964. Most baby boomers are moving through the fifth and sixth decades of life, and this study will provide insight into how obesity is affecting their mortality. We investigate middle-aged adults as opposed to the elderly because middle-aged adults are less burdened by age-associated comorbidities that obscure causal links (Manson et al. 2007). Additionally, changes in height and body mass composition common in older individuals complicate the measurement of weight status in the elderly (Gallagher et al. 1996; Janssen and Mark 2007). Finally, middle-aged adults are less influenced by selective forces that reduce the observed effect of excess body weight because of early deaths to at-risk subjects.

Our results indicate a considerably smaller mortality effect of obesity compared with the findings of Allison et al. (1999) and Mokdad et al. (2004), whose estimates indicate that about 13%–15% of all deaths in 1991 and 2000 can be attributed to obesity among adults aged 18 and older. The age-dependent nature of the BMI and mortality association makes direct comparison with these findings difficult because neither study stratified by age. Our findings are consistent with those of Flegal et al. (2005), whose estimates suggest that approximately 5% of deaths among adults aged 25 and older in 2000 were attributable to obesity (BMI ≥ 30.0). Using clinically measured height and weight data from NHANES I, II, and III, Flegal et al. (2005) found significant excess mortality only in the obese II/III (BMI ≥ 35.0) relative to normal (BMI = 18.5–24.9), which is consistent with our estimates. Their estimates covered 1971–2000, and our estimates cover 1992–2004. We also use more finely detailed measurements of confounding variables. For example, we adjusted for five categories of incremental exposure to cigarette smoking, but Flegal et al. (2005) used only three (never, former, and current). We also included three dimensions of SES—education, income, and wealth—but Flegal et al. (2005) adjusted only for education (in sensitivity models).

Unlike most major studies, we use data from the 1990s and 2000s, providing a contemporary study of obesity and mortality. In another recent study conducted between 1994 and 2003, Kulminski et al. (2008) reported similar findings for a sample of adults aged 65 and older. Their study, based on the National Long Term Care Survey, found that being overweight (BMI = 25.0–29.9) or being obese I (BMI = 30.0–34.9) were not associated with excess mortality relative to a reference BMI of 22.0–24.9 in both sexes. We extended these findings to a middle-aged population in their 50s and 60s and generally found no statistically significant differences in mortality across the normal, overweight, and mildly obese levels. In fact, the minimum mortality region appears to be in the overweight range although the difference between the overweight and normal categories was not always statistically significant. Another recent study using adults aged 50–70 from the NIHAARP cohort (1995–2005) found no significant excess mortality in overweight groups (BMI = 25.0–29.9) relative to a BMI 23.5–24.9 among men, and a small excess relative risk among women (approximately 6% to 7% for a BMI of 28.0–29.9) after adjusting for sociodemographic and behavioral correlates and using self-reported BMI (Adams et al. 2006). The authors reported that being obese I (BMI = 30.0–34.9) was significantly associated with excess mortality of about 18% in women and 10% in men, which is in slight contrast to our finding of no significant effect for either sex, though the reference ranges used differed across the studies. Another difference is that the NIH-AARP cohort is a nonrepresentative sample based on a mailed questionnaire. In contrast, the data used here are from a probability-based, nationally representative survey with high response rates and weighting adjustments for nonresponse.

Flegal et al. (2005) suggested that the relative risk of obesity may have declined since the early 1970s, based on data from successive NHANES surveys. They found a smaller association of obesity and mortality in NHANES II (1976–1980) and NHANES III (1988–1994) compared with NHANES I (1971–1975). Gregg et al. (2005) provided indirect evidence supporting a declining risk of mortality among those with a BMI ≥ 25.0. They found that overweight and obese individuals in 1999–2000 had a lower prevalence of high total cholesterol, high blood pressure, and smoking compared with overweight and obese individuals in the 1960s and 1970s. These favorable trends occurred in all weight-status groups, but the reductions in high cholesterol and high blood pressure were generally higher among the overweight and obese (significant only for high cholesterol), suggesting a relative improvement in these risk factors over time. Reasons behind these changes are not fully understood. Heavier individuals could have disproportionately benefited from better medical management of risk factors for cardiovascular disease and other illnesses associated with excess weight. For example, the rapid dissemination of lipid-lowering drugs (e.g., statins) during the 1990s could play an important role (Carroll et al. 2005). Changes in social values and patterns of discrimination could also be informative. Increasing obesity levels over time may lead to improvements in the relative status of the overweight and mildly obese, who may face less social isolation and less employment and health care discrimination as their body type becomes more commonplace.

Although health-related risk factors among the overweight and mildly obese may be declining and the mortality effect may be weak, there is emerging evidence of a parallel increase in disability among the obese (Alley and Chang 2007). Moreover, there has been a disproportionate rise in diabetes in this group relative to leaner individuals (Gregg et al. 2005). Taken in tandem with our findings of a weak effect of obesity on mortality, these unfavorable trends may be a product of obese individuals living longer than in the past but also acquiring a number of comorbid and disabling conditions as they age (Alley and Chang 2007). Two recent studies examining mortality and disability simultaneously in older populations showed the stronger effect of obesity on disability compared with mortality (Al Snih et al. 2007; Reynolds et al. 2005), further highlighting these contrasting trends.

It is suggested that preexisting diseases confound the association between weight status and mortality (Manson et al. 2007; Willett et al. 2005). However, statistical techniques used to account for confounding raise other methodological problems. We restricted our analysis to respondents aged 50–61 at baseline to limit the problem of preexisting diseases (as well as related problems associated with compositional changes in body mass), but in a middle-aged population, we would still expect the prevalence of chronic illness to be relatively high. Therefore, we implement multiple methods to account for confounding by illness. Our results do not find supporting evidence that preexisting illnesses substantially confound the association between weight status and mortality. Models that alternatively controlled for health status, excluded those with unfavorable health status, or allowed risks to vary with time did not indicate that our estimates were substantially biased. Other recent papers have reached similar conclusions with respect to confounding by illness (Al Snih et al. 2007; Flegal et al. 2007b). Nonetheless, given the complex pathways among body weight, disease, and death, we cannot entirely rule out residual illness confounding. Furthermore, confounding by SES appears modest and most pronounced in the highest BMI category.

Selective survival should minimally bias our results because we excluded older adults. Selective survival may help explain the weak effects of obesity on mortality in elderly populations (Janssen and Mark 2007; Manson et al. 2007). In a cohort of middle-aged adults, however, a similar argument is unlikely to hold: in a low-mortality population, relatively few deaths occur before the fifth and sixth decades of life. Approximately 17% of the 1931–1941 U.S. birth cohort examined in this study died by age 50. For selective survival to be important, most early deaths would have to be to individuals who possess excess weight. Yet in the United States, deaths at younger ages are more likely attributable to accidents or cancer (Jemal et al. 2005). Accidents are a cause of death not likely to be associated with weight status, and mortality from many types of cancers (particularly at younger ages) are shown to be weakly related to excess weight (Flegal et al. 2007a; Krueger et al. 2004).

This study has limitations. First, we used BMI as a proxy for adiposity when other anthropometric measures are perhaps more suitable (e.g., waist circumferences, waist-to-hip ratio; Kalmijn et al. 1999; Price et al. 2006; Seidell and Visscher 2000; Visscher et al. 2001). Most nationally representative data use BMI as a measure of weight status because of its ease of collection. By using BMI, we are able to compare our results with prior major studies. The usefulness of BMI versus other measures of weight status—such as waist circumference and the waist-to-hip ratio—is still not fully explored among middle- and older-aged adults (Price et al. 2006; Simpson et al. 2007). For example, Woo et al. (2002) found that in a sample of adults aged 70 and older, both BMI and waist circumference similarly predicted disease outcomes and mortality, but waist-to-hip ratio was not predictive of these events. In a sample of women aged 30 to 55, Manson et al. (1995) found that the waist-to-hip ratio was more weakly related to overall mortality compared with BMI over a 16-year period (though the waist-to-hip ratio was a strong predictor of heart disease mortality). We also measured BMI in middle adulthood, though it is likely that the deleterious health effects of excess body weight accumulate over a lifetime (Jeffreys et al. 2003). Given that requisite large-scale data containing both weight-status measurements early in life and mortality measurements later in life are not readily available, most research examining obesity and mortality have taken an approach similar to ours. Studies have found that childhood and adulthood BMI are moderately and positively correlated (Casey et al. 1992; Guo et al. 1994; Serdula et al. 1993), suggesting that many respondents in our study who were obese in 1992 were obese when they were younger (i.e., middle adulthood BMI proxies for BMI at younger ages). Moreover, a previous study reported similar patterns for weight status and mortality between recall measurements of early life BMI (age 21) and measurements taken at older ages (Corrada et al. 2006).

Finally, HRS data are nationally representative of the noninstitutionalized population, but deaths will come from both the community and institutions. Based on the 2000 census, only 1.1% of Americans aged 50–61 resided in institutional settings. It is likely that some respondents entered institutions after they were interviewed. Deaths of these individuals are still observed by mortality linkages used here. Therefore, we still capture a portion of deaths in institutions.

Despite concerns that increasing obesity levels will threaten future life expectancy improvements in the United States, our findings lend support for the notion of a weak effect of obesity on current mortality, as indicated by both its relative and attributable risks. An important contribution is that we focus on middle-aged adults, a group at high risk for cardiovascular and other chronic conditions that are thought to link obesity to death. A number of studies showed that excess body weight is not strongly associated with an increased risk of death in the elderly (Al Snih et al. 2007; Flegal et al. 2005; Grabowski and Ellis 2001; Reynolds et al. 2005). For obesity to have a large effect on life expectancy, it would have to be responsible for a substantial burden of premature deaths at middle and older ages, when the majority of deaths in the United States occur. Yet, we found that only a BMI ≥ 35.0 confers excess mortality, which comprises a minority of individuals who possess higher weight status (BMI ≥ 25.0). Nevertheless, the excess mortality associated with having a BMI ≥ 35.0 is not insubstantial; it is approximately 40% to 60% higher than that associated with having normal BMI (18.5–24.9), roughly similar to the mortality difference between non-Hispanic blacks and non-Hispanic whites at middle age.