Birth cohort effects on abdominal obesity in the United States: the Silent Generation, Baby Boomers, and Generation X

INTRODUCTION

Age-period-cohort analyses can help evaluate causes of past population-level health trends, predict future health trends, and illuminate causes of individual-level susceptibility to health outcomes. All previous age-period-cohort analysis of obesity examined obesity assessed by body mass index (BMI). This measure of overall obesity is associated with risk of many chronic diseases. However, alternate measures of obesity bear a more direct relationship to chronic disease risk.

In particular, high waist circumference, which we refer to as “abdominal obesity,” predicts chronic diseases, such as type 2 diabetes and cardiovascular disease, better than obesity assessed by BMI.^{1, 2} Abdominal obesity is highly correlated with total body fat.³ Further, abdominal obesity may more specifically indicate increased amounts of intra-abdominal visceral fat and subcutaneous abdominal fat, which affect hepatic metabolism of insulin and inflammatory markers.⁴ Moreover, in the U.S., abdominal obesity increased continuously in the 1990s and 2000s and is now present in more than half of U.S. adults.²

This analysis evaluated whether there were cohort effects for abdominal obesity for the Silent Generation (born 1925-1945), children of the Great Depression; Baby Boomers (born 1946-1964); or Generation X (born 1965-1980).⁵ These particular birth cohorts were examined because it is unclear whether cohort effects increased monotonically throughout the 20^th century.

If cohort effects did increase monotonically, increasing prosperity and technology are implicated as major causes of cohort-specific risk.^{6, 7} One alternative theory draws upon the growing field of developmental origins of health and disease (DOHaD). DOHaD implicates stress, poverty, and poor intrauterine conditions as influences on lifelong cohort specific risk of obesity.⁸ These factors did not necessarily increase monotonically throughout the 20^th century, nor did they affect women and men similarly. Therefore, this analysis will estimate cohort-specific risks for abdominal obesity among 20^th-century cohorts of men and women.

METHODS

RESULTS

CONCLUSIONS

This work presents a novel finding: evidence of birth cohort effects in prevalence of abdominal obesity in the U.S. The birth cohorts of the post-World War II Baby Boom appeared to have uniquely low cohort-specific risk for abdominal obesity. The birth cohorts preceding the Baby Boom, especially the cohort born in the first years of the Great Depression, appeared to show cohort-specific risks of increased prevalence of abdominal obesity. The birth cohorts immediately succeeding the Baby Boom also showed evidence of birth cohort effects that increased prevalence of abdominal obesity. These generational differences were more pronounced in women than in men.

There are several different ways of conceptualizing the underlying meaning of a cohort effect.²⁵ This paper’s conceptualization is rooted in the potential outcomes counterfactual framework. ^27-29 To understand this conceptualization heuristically, imagine a scenario in which a 16-year-old Baby Boom adolescent (born in 1962) travels in time from 1978 to 1993.²⁹ If the adolescent stayed in her 1993 “future,” then over time, as she aged into her 20s, 30s, 40s, etc., she would be less likely to become obese than other people her age who were born in 1977.²⁹ Thus, this hypothetical counterfactual intervention can be interpreted to mean that the Baby Boomer who traveled in time from 1978 was less sensitive to the obesogenic environment of the 1990s, 2000s, etc., than the same-age Generation X counterparts she was living with in the “future.” The negative cohort effect that we estimated for the Baby Boom, suggests that, in alternative environments, Baby Boomers might be less susceptible to the obesogenic environment due to factors intrinsic to being a member of the Baby Boom cohort that are independent of age and widespread environmental exposures that act the same on all age groups.

No previous studies have examined cohort effects on abdominal obesity. Examining cohort effects for abdominal obesity is important because large waist circumference is a better predictor of obesity-related diseases such as diabetes, metabolic syndrome, and cardiovascular disease than high BMI.^{1, 4, 30} Understanding cohort effects on abdominal obesity serves three important purposes. First, cohort effects help predict trends in metabolic health.^{12, 26, 31} These results indicate that, holding the secular environment constant, as members of Generation X age, they will be more sensitive to abdominal obesity, and therefore, metabolic diseases, than the Baby Boomers.

Second, estimating cohort effects on abdominal obesity aids evaluating hypotheses about the causes of population-level obesity trends.⁶ Komlos et al. have argued that monotonically increasing cohort effects would provide evidence that a root cause of the U.S. obesity epidemic is ever-expanding access to labor-saving technology, including radios and home refrigeration.⁶ In contrast, we find that the cohorts born during the economic and consumerist expansion of the post-World-War II era may have been uniquely protected from abdominal obesity, especially among women. This finding indicates that the generational increases in abdominal obesity could be caused by factors beyond technological innovation, expansion of access to technology, and economic growth.

Third, estimating cohort effects can illuminate the causes of individual-level susceptibility to abdominal obesity. In our analysis, period effects were consistently positive and strong. These period effects could be caused by many dynamic environmental features, including increases in use of some antibiotics, growing use of plastic bottles and ingestion of the chemical contained in them, and even secular trends in sleep deprivation. ³² However, environmental factors can also cause cohort effects through distinct mechanisms. In particular, characteristics of the early-life environment that affect obesity in an age-specific manner may have protected the Baby Boomers against obesogenic influences that they encountered later in life. For instance, hypotheses about the developmental origins of adult obesity posit that in utero and early-childhood exposures to obesogenic environments have latent biological or behavioral consequences that increase susceptibility to excess weight gain throughout adulthood.^{8, 33-35}

While no previous analyses have examined cohort effects on abdominal obesity, three analyses of overall obesity in population-based datasets have also found lower cohort effects for Baby Boomers than the preceding or subsequent generations.^{26, 36, 37} In studies of French and Australian populations, cohort risk was lowest for those born between the mid-1940s and mid-1960s.^{36, 38} In the U.S., analysis of the National Health Interview Survey estimated that cohort effects were lowest for cohorts of the mid-1950s before rising sharply in the cohorts of the 1960s and early 1970s.³⁷

One possible mechanism for cohort differences is early-life psychosocial and socioeconomic stress mechanisms, which may promote abdominal obesity.^{39, 40} The growing prosperity of the post-World-War II may have exposed the Baby Boom generation to lower levels of psychosocial and socioeconomic stress than previous or subsequent generations.⁴¹ Diouf et al. hypothesized that the cohort trends in the French post-World War II generation may be related to “the 30 glorious” years, a period from 1945 to 1973, in which there was a “marked improvement of living conditions that accompanied the economic boom in France.”³⁶ They hypothesized that the improvement in living conditions caused the increase in obesity for cohorts born after 1965. An alternative interpretation is that the specific living conditions associated with a trajectory of increasing prosperity from 1945 to 1965 protected cohorts born after the war. In contrast, the nutritional deprivation and stress experienced by those born during the Great Depression may have predisposed these cohorts to obesity risk, while obesogenic social and economic trends in the mid-1960s and 1970s increased cohort risk.

There are other possible explanations for the observed cohort effects, especially the greater cohort-specific obesity prevalence in Generation X versus the Baby Boomers.³² For instance, cohort differences in sleep patterns could explain greater obesity in Generation X. Another possible mechanism for increased cohort effects for Generation X is endocrine disrupters, which may exert long-standing effects in infancy and childhood. Also, demographic changes could be associated with cohort trends in obesity. In our 2001-2004 sample of U.S.-born non-immigrants, the percentage of the population who were non-Hispanic Black or non-Hispanic White, groups that tend to have higher obesity prevalence than non-Hispanic Whites, increased across the birth cohorts. For instance, the weighted proportion of the sample who were non-Hispanic Black ranged from 7.0% for the 1929-1933 cohort to 16.1% for the 1979-1983 cohort. The share of the population who were non-Hispanic White population decreased from 85.7% for the 1929-1933 cohort to 70.4% for the 1979-1983 cohort.

Stratified analyses indicated more pronounced cohort differences among women than men. This sex difference was also seen in the age-period-cohort analyses of overall obesity described above.^{26, 36, 37} In Europe and the U.S., social conditions for women have changed dramatically throughout the 20^th century. Patterns of fertility, work outside the home, physical activity, and economic autonomy have varied more dramatically for women than men in the cohorts examined.⁴² For instance, the U.S. Title IX law increased girls’ sports participation by 600% between 1972 and 1978, years when Baby Boomers were entering secondary school and college.⁴³ Therefore, cohort effects that are caused or mediated by behavioral or social exposures would be expected to vary more in women than men.

Physiologically, stress mechanisms may also act in a sex-specific manner to influence abdominal obesity.^{39, 44} Previous studies have found evidence linking in utero maternal stress and malnutrition to sex-specific obesity risk, such as interference with sex hormone signaling; alteration of methylation patterns of genes, including insulin-like growth factor-2; and sex-specific effects on appetite and weight regulation.^45-47 Maternal nutritional and psychological stress may be an especially important mechanism for understanding the higher cohort effects for the children of the Great Depression.

Despite its strengths and novelty, this analysis has limitations. The unit of analysis was the prevalence estimate, which was estimated from survey data with error that was not incorporated into our final confidence intervals. Therefore, the confidence intervals may overestimate the precision of the effect estimates. Additionally, these results only apply to non-institutionalized, U.S.-born Americans and not to immigrants, the imprisoned, or those in long-term care facilities.^{48, 49} Finally, the analyses did not assess data collected before the late 1980s. Additional analyses of obesity assessed by BMI indicated that extending the time period would not dramatically affect findings in women but might reveal more evidence of cohort effects in men. Perhaps results in men differed after including earlier data because obesity-related selective mortality obscured cohort effects in men in the more limited dataset. If obese men have higher rates of mortality or old-age institutionalization, then obese men from early birth cohorts would be underrepresented in our dataset. Further, excluding incarcerated men from the data may have caused overestimation of obesity prevalence for men of Generation X.⁴⁹

In conclusion, controlling for age and secular influences on obesity prevalence, Baby Boomers appeared to experience lower cohort-specific risk of abdominal obesity than other birth cohorts. While secular forces in the 20^th century may have introduced technological and cultural changes that increased obesity in the population, cohort-specific influences somewhat protected the Baby Boomers from these secular influences. Broad economic expansion does not necessarily lead to increased cohort-specific risk of abdominal obesity for those born during periods of economic growth. We hope that this work will spur further research into differences between the cohorts of the late 1950s and early 1960s versus other birth cohorts. By identifying factors associated with the Baby Boomers’ low cohort-specific sensitivity to the obesogenic environment, the obesity prevention community can identify early-life factors that can protect future generations from excess weight gain.