Why Young Adults Hold the Key to Assessing the Obesity Epidemic in Children FREE

Type 2 diabetes mellitus is a chronic disease associated with long-term microvascular complications, such as neuropathy, retinopathy, and end-stage renal disease, and macrovascular complications, including cardiovascular disease and stroke.^{1 - 2} Because of its devastating complications and reported increases in prevalence,^{3 - 7} type 2 diabetes has been described as one of the “major threats to human health” for the 21st century.³

Obesity is the hypothesized critical factor contributing to an increased risk for type 2 diabetes,^{8 - 10} and rates of obesity in the United States have increased significantly. In adults, the prevalence of obesity (body mass index [BMI] [calculated as weight in kilograms divided by height in meters squared] ≥30) has increased more than 2-fold since the 1960s,^{11 - 12} with 32.2% of adults classified as obese by 2004. Given the relation between obesity and diabetes, increases in type 2 diabetes among adults would be expected to parallel the increases in obesity and, in fact, that pattern is seen. Figure 1 shows sharp increases in obesity prevalence among US adults between 1976 and 2000, and Figure 2 shows increases in type 2 diabetes prevalence among US adults during the same period.¹³

Rates of obesity among US children (BMI ≥95th percentile for age and sex) have increased even more dramatically, with a 3-fold increase since 1976 (Figure 3).^{11 ,14 - 15} Presumably because of childhood obesity trends, reports surfaced in the mid-1990s regarding increasing numbers of children with type 2 diabetes. Initial studies from tertiary care clinics documented 10-fold increases in type 2 diabetes incidence between 1982 (0.7 per 100 000 population) and 1994 (7.2 per 100 000 population),¹⁶ with type 2 diabetes accounting for 8% to 45% of new-onset diabetes cases.¹⁷

Further evidence of increases in childhood type 2 diabetes was based on studies in high-risk populations. The prevalence of type 2 diabetes doubled among Pima Indian adolescents between 1977-1986 and 1987-1996,¹⁸ and type 2 diabetes incidence rates among Pima Indian children were 5.7 times higher in 1991-2003 compared with 1965-1977.¹⁹ The Chicago Childhood Diabetes Registry also reported increases in the proportion of children with type 2 diabetes among a subset of urban black and Latino children between 1985 and 2001.²⁰

Prompted by these assessments of type 2 diabetes in high-risk groups, epidemiologic rates of childhood diabetes have been assessed more recently through larger population-based studies. Figure 4 shows population-based rates of type 2 diabetes among adolescents aged 12 to 19 years between 1988 and 2000 based on National Health and Nutrition Examination Survey (NHANES) data.^{21 - 22} Rates of type 2 diabetes among adolescents remained relatively stable, despite the notable increase in obesity prevalence among children seen during a similar period in Figure 3, in contrast to the pattern seen in adults (Figure 1 and Figure 2). Admittedly, the number of children with type 2 diabetes in these studies was low, with possible underestimation of type 2 diabetes prevalence because of treatment-based classification. However, these children were drawn from large representative population samples of 2867²¹ and 4370 adolescents²² that oversampled for racial/ethnic minorities.

The results of additional population-based studies in children appear to be consistent with NHANES data. The Table presents a comparison of diabetes prevalence estimates from population-based studies between 1988 and 2004.^{21 - 25} Although slight differences in type 2 diabetes prevalence exist because of sampling variability and classification methods (treatment based^{21 - 22} vs pathogenesis based^{23 - 24} ), similar rates were reported in a racially and socioeconomically diverse cohort of adolescents within an urban-suburban school district (0.12%).²³ Furthermore, the SEARCH for Diabetes in Youth Study,²⁴ a multicenter population-based study that used gold standard classification methods, reported an even lower type 2 diabetes prevalence among adolescents aged 10 to 19 years (0.04%) and children aged 0 to 19 years (0.02%).²⁴ Except for high-risk groups (ie, Pima Indians and urban minority children), no population-based data on type 2 diabetes prevalence are available before 1988, so significant increases in type 2 diabetes rates among the population of US adolescents before 1988 cannot be ruled out.

It may seem difficult to reconcile the documented increases in type 2 diabetes seen in population-based studies of high-risk groups with the lack of increases in type 2 diabetes measured in broader samples, but these findings are consistent with those of the SEARCH study, which found higher incidence rates of type 2 diabetes compared with type 1 diabetes mellitus among African American, Asian American, Hispanic, and American Indian adolescents, although among US children as a whole, the incidence of type 1 diabetes was still higher than the incidence of type 2 diabetes.²⁶ Therefore, increases in type 2 diabetes among high-risk minority groups may not yet be reflective of trends in the overall population. The lack of recent increases in type 2 diabetes rates among children compared with adults at the population level, despite significant increases in obesity, demonstrates that the overall burden of type 2 diabetes is still concentrated mostly among adults.

The absence of concurrent increases in childhood obesity and type 2 diabetes at the population level may be largely attributable to a latency period between obesity and type 2 diabetes. Figure 5 shows the hypothesized physiologic pathway leading to development of type 2 diabetes.^{27 - 29} Obesity is a risk factor for development of insulin resistance, with pancreatic β cells compensating for insulin resistance by augmenting insulin secretion. The failure of the β cells to maintain adequate insulin secretion is believed to cause prediabetes, eventually leading to type 2 diabetes. Consistent with this model, studies in Pima Indians have shown that the latency period between onset of obesity and type 2 diabetes can last 10 years or longer.³⁰ Because of this latency period, childhood obesity trends likely have a delayed effect on rates of type 2 diabetes, reflected in significant increases in type 2 diabetes among young adults who were obese as children.

Both degree and duration of obesity likely influence the length of the latency period. A number of studies^{10 ,31} have shown that the higher the BMI, the higher the risk of incident type 2 diabetes, with a recent study³² finding an inverse linear relation between age of diagnosis of type 2 diabetes and BMI. For example, mean BMI at diagnosis was 38.3 for individuals younger than 30 years, 35.9 for individuals 46 to 50 years old, and 31.1 for individuals 66 to 70 years old, suggesting that degree of obesity will influence the timing of incident type 2 diabetes. Studies^{30 ,33} have also shown that a longer duration of obesity is associated with a higher type 2 diabetes incidence after controlling for age, sex, and current BMI. The degree and duration of obesity extending from childhood through young adulthood may confer a cumulative risk of type 2 diabetes analogous to the relation between pack-years of smoking and lung cancer³³ ; this risk is accumulating at an unprecedented rate given recent childhood obesity trends.

In addition to absolute increases in obesity prevalence, the degree of obesity among US children has increased, resulting in shifts in the overall weight distribution.^{15 ,34} Jolliffe³⁴ calculated the extent of obesity for US children, defined as the average amount by which each child's BMI exceeded his or her age- and sex-specific obesity threshold. Although the prevalence of obesity increased by 182% between 1971 and 2000, the extent of obesity increased by 247% during the same period.³⁴ Children are also increasingly becoming obese at younger ages (6 months to 5 years).¹⁴ Because more US children are becoming heavier at earlier ages, younger cohorts may experience a greater degree and longer duration of obesity during their lifetime, which could lead to a shortening of the latency period and onset of type 2 diabetes in young adulthood.

Consistent with this hypothesis, recent studies^{6 ,35} suggest possible increases in rates of diabetes among US young adults. We recently assessed trends in hospitalizations associated with a diagnosis of diabetes for individuals from birth to the age of 29 years, using a nationally representative sample of hospital discharges between 1993 and 2004. During the 12-year period, we found significant increases among young adults aged 20 to 29 years (185.2 per 100 000 population in 1993 to 275.0 per 100 000 population in 2004, representing a 48% increase) but not among children 19 years or younger.³⁵

This study could not distinguish between diabetes type. Furthermore, individuals with diabetes may not require inpatient hospitalization. However, type 2 diabetes accounts for 90% to 95% of adult diabetes,⁷ and according to the Centers for Disease Control and Prevention (CDC),³⁶ hospitalizations among individuals with diabetes have decreased since 1980. Therefore, increases in population-adjusted hospitalization rates for young adults are likely an indication of increasing type 2 diabetes prevalence in the young adult population.³⁶ Increases in particular were seen after 2000 among a generation of young adults who grew up in the midst of the childhood obesity epidemic during the late 1970s and early 1980s. The birth cohort effects of large increases in childhood obesity may be presenting just now as the first indication of significant increases in type 2 diabetes among young adults.

An epidemiologic shift to younger ages at onset of type 2 diabetes may have profound intergenerational consequences. The onset of type 2 diabetes among young women during the child-bearing years may lead to a possible “vicious cycle” of type 2 diabetes in subsequent generations because studies have shown a higher risk of obesity and type 2 diabetes among offspring with intrauterine exposure to maternal diabetes.³⁷

Furthermore, studies suggest that early-onset type 2 diabetes may represent a more aggressive disease with regard to cardiovascular outcomes, rates of end-stage complications, and overall mortality. One recent study³⁸ described the rates of diabetes complications for individuals with early-onset (aged 18-44 years) compared with late-onset (aged ≥45 years) type 2 diabetes after initial diagnosis. Early-onset type 2 diabetes was associated with a 14-fold higher hazard of developing a myocardial infarction compared with age- and sex-adjusted controls without diabetes, a far stronger association than found in the late-onset type 2 diabetes group, who had a 4-fold higher hazard for late-onset type 2 diabetes compared with controls.³⁸

Because end-stage complications develop as a function of duration of disease,³⁹ young adults with type 2 diabetes will likely face greater morbidity and mortality during their lifetime compared with individuals whose diabetes is diagnosed at older ages. One Pima Indian study⁴⁰ documented higher incidence rates of end-stage renal disease and mortality among individuals with youth-onset type 2 diabetes compared with adult-onset type 2 diabetes, with a longer duration of diabetes largely accounting for these differences.

Finally, a number of studies^{41 - 42} have shown that the relative risk of death attributable to type 2 diabetes in adults is highest in the youngest age groups and declines with increasing age. Accordingly, demographers are predicting that recent childhood obesity trends will result in a shorter life expectancy for future generations as a result of diseases including type 2 diabetes.⁴³

A life course approach to chronic disease risk suggests that risk factors and experiences early in life impact long-term health and disease outcomes,^{44 - 45} and interventions to attenuate early risk factors in childhood may lead to prevention of disease in adulthood.⁴⁶ The childhood obesity epidemic has important implications for type 2 diabetes risk during the life course because of possible increases in type 2 diabetes during young adulthood. If cumulative exposure to obesity in childhood is associated with early onset of type 2 diabetes, then health care investments or policy interventions to prevent or treat childhood obesity to reduce this exposure will have important effects on the overall health of the population, although improved health and related health economic outcomes may not be noted for several years.

Given the possible link between trends in childhood obesity and trends in type 2 diabetes among young adults, health care policy and financing may need to shift focus to disease prevention interventions earlier in the life course.

First, investment in and incentives for screening and treatment of childhood obesity in the clinical setting are likely needed, as studies have shown greater reversibility of obesity at younger ages.⁴⁷ Unfortunately, obesity prevention and treatment-related services for children are not usually covered by third-party payers.⁴⁸ In contrast, programs for managing adult chronic diseases (type 2 diabetes, hypertension, and cardiovascular disease) have increased in number and scope.^{49 - 50} This imbalance is reflected in overall health care spending for the population, which is substantially lower in US children compared with US adults on a per capita basis, with proportional decreases in spending during the past decade for children accompanied by proportional increases in spending among adults.⁵¹

Second, schools represent a critical arena for obesity prevention among children.⁵² School-based interventions that promote decreased television and video viewing time,⁵³ increased physical activity and healthy eating,⁵⁴ and elimination of sugar-sweetened beverage intake⁵⁵ have been shown to be effective in lowering BMI and decreasing the prevalence of obesity, suggesting the need for increased funding for conducting and monitoring the effects of school-based obesity prevention initiatives.

Third, although controversial, the importance of monitoring population trends in obesity by school-based BMI measurement^{56 - 57} is critical for assessing the effectiveness of innovative school-based policy interventions.^{58 - 59} For example, Arkansas passed legislation in 2003 that included a variety of measures to combat childhood obesity. Through school-based BMI assessment, they were able to document that multimodal interventions have apparently halted the progression of childhood obesity within 2 years of implementation.⁵⁷

The CDC estimates that approximately  48.3 million individuals in the United States will have diagnosed diabetes by 2050.⁶⁰ Because childhood obesity trends have not been accounted for, their projections may substantially underestimate future cases of type 2 diabetes. Therefore, further studies are needed to model the impact of the dynamics of childhood obesity on future rates and age at onset of type 2 diabetes and to assess both the effectiveness and cost-effectiveness of interventions for preventing type 2 diabetes over the life course.

Modeling the link between childhood obesity and type 2 diabetes risk over the life course will be critical for estimating the changing rates of microvascular and macrovascular complications and changes in life expectancy owing to trends in childhood obesity. Information from the model will be highly relevant for understanding the impact of potential increases in incident type 2 diabetes in the clinical setting, in terms of access to and provision of services for those affected, and the potential future financial burden on Medicare, the primary payer for end-stage renal disease. It will also be essential for assessing the effectiveness of interventions across the life course for preventing type 2 diabetes and its complications. Using a life-time simulation, Herman et al⁶¹ showed that both lifestyle modification and metformin were cost-effective interventions for delaying or preventing the onset of type 2 diabetes among high-risk adults, concluding that diabetes prevention interventions among high-risk adults represent a worthwhile investment for policy makers. Information regarding the cost-effectiveness of obesity prevention and treatment interventions earlier in the life course is needed for comparison, which will guide future health policy to evaluate which high-risk demographic groups should be targeted for interventions and to determine at what ages across the life course interventions should be introduced to achieve maximal benefit.

One recent study¹⁹ in the Pima Indians showed that between 1965 and 2003 the greatest increases in type 2 diabetes incidence occurred among children aged 5 to 14 years and, in fact, decreases in type 2 diabetes incidence occurred among individuals aged 25 to 34 years. This epidemiologic shift to an even earlier onset of type 2 diabetes, reaching into childhood and adolescence, may be a scenario faced by the entire US population if the childhood obesity epidemic continues unabated. Given that the current US health care system is not designed to promote disease prevention over the life course, the traditional models of “pediatric” and “adult” health care will need to be challenged, leading to development of new models of care that address long-term chronic disease risk originating in childhood and extending into adulthood. There are several diseases to which such a new life-course model could be applied, but perhaps no condition more prevalent among children than obesity and no consequence more clinically severe than type 2 diabetes for which a life-course model will be a crucial platform for success.

Correspondence: Joyce M. Lee, MD, MPH, Division of Pediatric Endocrinology, Child Health Evaluation and Research Unit, University of Michigan, 300 NIB, Room 6E08, Campus Box 5456, Ann Arbor, MI 48109-5456 (joyclee@umich.edu).

Accepted for Publication: January 4, 2008.

Financial Disclosure: None reported.

Funding/Support: Dr Lee was supported by the Clinical Sciences Scholars Program at the University of Michigan. This study used the Modeling Core of the Michigan Diabetes Research and Training Center, funded by National Institutes of Health grant 5P60 DK20572 from the National Institute of Diabetes and Digestive and Kidney Diseases.

Additional Contributions: Matthew Davis, MD, MAPP, Gary Freed, MD, MPH, James Gurney, PhD, Beth Tarini, MD, MS, and Sandeep Vijan, MD, provided helpful comments during the preparation of the manuscript.