Editorial
Are Children the Future of Type 2 Diabetes Prevention?
N Engl J Med 2010; 362:548-550February 11, 2010
- Article
The lifetime risk of type 2 diabetes is now more than one in three in the general U.S. population, and one in six adolescents is now obese, suggesting that prevention should start in childhood.1,2 Many consider diabetes and obesity to be “common-source” epidemics that are rooted in our culture, as evidenced by national trends toward larger portion sizes and more meals built around calorically dense fast food, sugar-sweetened drinks, and sedentary behavior.3,4 Fighting such a powerful wave with purely clinical and adult-based approaches to prevention may seem like pasting a small bandage on a gaping wound. Rather than focusing on adults who may be set in their ways, we should perhaps target our youth, who may represent a better hope for changing the norms, habits, attitudes, and preferences that define our culture's collective energy balance.
At the same time, we should not naively assume that approaches targeted to youth will result in effective policy for the prevention of type 2 diabetes. Despite the devastating effects of type 2 diabetes, the prevalence among youths (about 1 case per 2400 U.S. youths 10 to 19 years of age) is low enough that even highly effective interventions would need to be applied to thousands of youths to prevent just a few cases.5 Therefore, efforts to prevent diabetes that target youths would require substantial payback in adulthood through reduced levels of diabetes and other illnesses. Bridging the wide gap between risk factors in youth and the prevention of illness in adults needs not only evidence that risk factors track strongly from childhood to adulthood, but also efficient interventions with sustainable effects across life stages.
The article by Franks et al. in this issue of the Journal 6 shows that among Pima Indian youths 5 to 19 years of age, obesity and 2-hour glucose levels below the threshold for impaired glucose tolerance, but above normal levels, were associated with a rate of death in young adulthood and middle age that was about twice that of peers without diabetes. The Pima Indians are sometimes considered to be unrepresentative of the U.S. population because they have an especially high risk of diabetes. However, the prevalence of impaired glucose tolerance among persons in the current study (4%) is similar to the current prevalence in the general population of U.S. adolescents (3%) and is far less than the prevalence among obese adolescents in the United States (9.5%).7 Since the trends with respect to obesity and diabetes among the Pima Indians have been a reliable harbinger for trends in the rest of the U.S. population during recent decades, the present study should intensify the debate about whether interventions that are initiated during childhood and young adulthood can affect our broader diabetes epidemic.
Several aspects of the findings of Franks et al. should inspire new investigations. First, childhood cholesterol and blood-pressure levels were not predictive of death, perhaps indicating that they do not track into adulthood as persistently as obesity and impaired glucose tolerance do. Alternatively, these risks may follow patients into adulthood, but primary care clinicians can then detect and manage elevated blood pressure and lipid levels with drugs, whereas they are ill equipped to manage obesity and impaired glucose tolerance (“prediabetes”). Second, associations related to impaired glucose tolerance should not necessarily be generalized to impaired fasting glucose, as it is defined by the American Diabetes Association. Impaired fasting glucose in adults is associated with the development of diabetes and with death, but whether this association holds true in the case of youths is not clear. In addition, a recent study showed that among adolescents, elevated glucose levels were no more predictive of later diabetes than either body-mass index or systolic blood pressure — reminding us that the best predictors of imminent diabetes among adults may be different from the best predictors of long-term risk of diabetes among youths.8 Third, since most of the deaths from endogenous causes among the population studied in the article occurred before the participants were 45 years of age, this study examined only premature death. The mortality rates were more than twice those of the general U.S. population and were inordinately affected by deaths from liver disease, a finding that merits further study.9 We should not assume that follow-up into the seventh and eighth decades of life, when most people die of more typical causes, would yield similar associations between impaired glucose tolerance and death. Finally, these and other authors suggest that the life spans of future generations may be affected by the epidemics of obesity and diabetes; this might not be so, given the improvements in care and in the treatment of risk factors — improvements that continue to push life spans to record highs and that have ironically contributed to the growing prevalence of type 2 diabetes.10,11 The more pressing question raised by this study, however, is whether increased rates of central obesity, elevated insulin levels, and impaired glucose tolerance among youths will result in increased cases of type 2 diabetes, illness, and disability in future generations.
It will be important to convert these results into effective prevention policies. Impaired glucose tolerance, impaired fasting glucose, and elevated glycated hemoglobin levels are practical targets among adults not only because they indicate a high risk of diabetes but also because structured lifestyle interventions can be highly effective.12 Segregated interventions may not work as well among youths because the long incubation period from risk factor to disease and unclear positive-predictive value for the development of diabetes and its complications make for inefficient risk stratification and allocation of intervention resources.8
The dilemma raised by epidemiologic data — that interventions that are targeted to youths need to be extraordinarily sustainable to pay off later in life — requires us to revisit the common sources of the epidemics of obesity and diabetes. Fortunately, there is active discussion about what the most promising interventions are. Schools, families, and social groups are all potential targets. The HEALTHY study (ClinicalTrials.gov number, NCT00458029), a 3-year cluster-randomized intervention trial involving more than 6000 sixth graders from 42 schools, will provide a unique, rigorous test of a model intervention to reduce glucose levels and other risk factors that incorporates thoroughly integrated nutritional, physical-activity, behavioral, and social-marketing components.13 Other experts suggest that we must reach far outside the schoolhouse to find out whether focusing policies on culturally embedded risk factors — sugar-sweetened beverages, calorically dense foods, excessive television and video watching, the high price and limited availability of healthy foods, and community designs that discourage physical activity — can be as fruitful as targeting tobacco, saturated fat, and trans fats has been for the prevention of cardiovascular disease.3 Targeting food policies to prevent type 2 diabetes has proved to be difficult, however, because the quantity of what we eat may be as damaging as its quality. Finally, we should be mindful that the wellspring of most chronic diseases is not captured by single physiological risk factors or specific exposures. Because variation in the rates of illness and death among persons in specific places, social classes, and communities in the United States and elsewhere in the world is as great as the difference between persons with and persons without impaired glucose tolerance, our search for ways to alter the common source must continue.14
The views expressed here are those of the author and do not necessarily represent the official positions of the Centers for Disease Control and Prevention.
Financial and other disclosures provided by the author are available with the full text of this article at NEJM.org.
I thank Valerie Roback Gregg and Elizabeth Lee Greene for their valuable editorial assistance and insightful suggestions.
Source Information
From the Division of Diabetes Translation, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta.
- References
References
1
Narayan KM ,Boyle JP ,Thompson TJ ,Gregg EW ,Williamson DF . Effect of BMI on lifetime risk for diabetes in the U.S. Diabetes Care 2007;30:1562-1566
CrossRef | Web of Science | Medline2
Ogden CL ,Carroll MD ,Curtin LR , et al. Prevalence of high body mass index in US children and adolescents, 2007-2008. JAMA 2010;303:242-249
CrossRef | Web of Science | Medline3
Ebbeling CB ,Pawlak DB ,Ludwig DS . Childhood obesity: public-health crisis, common sense cure. Lancet 2002;360:473-482
CrossRef | Web of Science | Medline4
Wells HF, Buzby JC. Dietary assessment of major trends in U.S. food consumption, 1970-2005. Washington, DC: Department of Agriculture, 2008. (Economic information bulletin no. EIB-33.)
5
Liese AD ,D'Agostino RB Jr ,Hamman RF , et al. The burden of diabetes mellitus among US youth: prevalence estimates from the SEARCH for Diabetes in Youth Study. Pediatrics 2006;118:1510-1518
CrossRef | Web of Science | Medline6
Franks PW ,Hanson RL ,Knowler WC ,Sievers ML ,Bennett PH ,Looker HC . Childhood obesity, other cardiovascular risk factors, and premature death. N Engl J Med 2010;362:485-493
Full Text | Web of Science | Medline7
Li C ,Ford ES ,Zhao G ,Mokdad AH . Prevalence of pre-diabetes and its association with clustering of cardiometabolic risk factors and hyperinsulinemia among U.S. adolescents: National Health and Nutrition Examination Survey 2005-2006. Diabetes Care 2009;32:342-347
CrossRef | Web of Science | Medline8
Morrison JA ,Glueck CJ ,Horn PS ,Wang P . Childhood predictors of adult type 2 diabetes at 9- and 26-year follow-ups. Arch Pediatr Adolesc Med 2010;164:53-60
CrossRef | Web of Science | Medline9
Minino AM ,Arias E ,Kochanek KD ,Murphy SL ,Smith BL . Deaths: final data for 2000. Natl Vital Stat Rep 2002;50:1-119
Medline10
Gregg EW ,Cheng YJ ,Cadwell BL , et al. Secular trends in cardiovascular disease risk factors according to body mass index in US adults. JAMA 2005;293:1868-1874
CrossRef | Web of Science | Medline11
Lipscombe LL ,Hux JE . Trends in diabetes prevalence, incidence, and mortality in Ontario, Canada 1995-2005: a population-based study. Lancet 2007;369:750-756
CrossRef | Web of Science | Medline12
Gerstein HC ,Santaguida P ,Raina P , et al. Annual incidence and relative risk of diabetes in people with various categories of dysglycemia: a systematic overview and meta-analysis of prospective studies. Diabetes Res Clin Pract 2007;78:305-312
CrossRef | Web of Science | Medline13
Hirst K ,Baranowski T ,DeBar L , et al. HEALTHY study rationale, design and methods: moderating risk of type 2 diabetes in multi-ethnic middle school students. Int J Obes (Lond) 2009;33:Suppl 4:S4-S20
Web of Science | Medline14
Murray CJ ,Kulkarni SC ,Michaud C , et al. Eight Americas: investigating mortality disparities across races, counties, and race-counties in the United States. PLoS Med 2006;3:e260-e260
CrossRef | Web of Science | Medline
- Citing Articles (4)
Citing Articles
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S. Santiago, M. Cuervo, I. Zazpe, A. Ortega, A. García-Perea, J.A. Martínez. (2011) Situación ponderal, hábitos alimentarios y deportivos en población castellano-manchega de 6 a 12 años. Anales de Pediatría
CrossRef2
Hala Tfayli, So Jung Lee, Fida Bacha, Silva Arslanian. (2011) One-hour plasma glucose concentration during the OGTT: what does it tell about β-cell function relative to insulin sensitivity in overweight/obese children?. Pediatric Diabetesno-no
CrossRef3
Jia-Yu Wu, Xiao-Yan Duan, Lui Li, Fei Dai, Yan-Yun Li, Xing-Jian Li, Jian-Gao Fan. (2010) Dyslipidemia in Shanghai, China. Preventive Medicine 51:5, 412-415
CrossRef4
(2010) Childhood Obesity, Other Cardiovascular Risk Factors, and Premature Death. New England Journal of Medicine 362:19, 1840-1842
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