Type 2 diabetes in the young: the evolving epidemic: the international diabetes federation consensus...

Type 2 Diabetes in the Young: TheEvolving EpidemicThe International Diabetes Federation Consensus Workshop

GEORGE ALBERTI, FRCP, PHD

PAUL ZIMMET, FRACP, PHD

JONATHAN SHAW, FRACP, MD

ZACHARY BLOOMGARDEN, MD

FRANCINE KAUFMAN, MD

MARTIN SILINK, FRACP, MD

FOR THE CONSENSUS WORKSHOP GROUP

EXECUTIVE SUMMARY

1. The aims of the consensus meetingwere to review the epidemiology,pathophysiology, management, andimplications of the rising prevalence oftype 2 diabetes in young people and tosuggest means by which the continu-ing rise in incidence and prevalencemight be prevented.

2. The overall global prevalence of type 2diabetes is rising steadily. Previously,type 2 diabetes was predominantly adisease of middle-aged and older peo-ple. In recent decades, the age of onsethas decreased and type 2 diabetes hasbeen reported in adolescents and chil-dren worldwide, particularly in high-prevalence populations. Japan hasseen an approximate fourfold rise inthe incidence of type 2 diabetes in 6- to15-year-olds, and between 8 and 45%of newly presenting children and ado-lescents in the U.S. have type 2 diabe-tes. The problem is particularlynoticeable in indigenous peoples.Population-based data, however, are

sparse and indeed absent in mostcountries.

3. Additional cardiovascular risk factorsare often associated with type 2 diabe-tes in the young, and microangiopathyis as common or commoner in thosedeveloping type 2 diabetes at a youngage as in those with type 1 diabetes.This has profound societal implica-tions.

4. Diagnostic separation of type 2 fromother types of diabetes in young peo-ple can be difficult, and sophisticatedtesting may be necessary.

5. Data on the pathophysiology in theyoung are sparse, but there is no evi-dence to suggest differences fromadults. The incidence of type 2 in theyoung is rising in parallel with the in-cidence of overweight and obesity,suggesting a possible causal relation-ship, particularly when the obesity iscentral and in relation to decreasedphysical activity. Other factors includefamily history, gestational diabetes inthe mother, and low birth weight. Allof these are associated with insulin re-

sistance, although decreased insulinsecretion is also required.

6. Mass screening for type 2 diabetes inthe young has been carried out in cer-tain countries (Taiwan and Japan) butis probably appropriate only for indi-viduals at very high risk. The bestscreening test for young people is notknown.

7. Treatment should be aimed at physicaland psychological well-being andavoidance of long-term complications.Lifestyle modification must accom-pany other forms of therapy. In certaincountries, metformin is available fortreatment of children, but efficacy re-mains unproven. Newer oral agentshave not been tested systematically inchildren or adolescents. Insulin re-mains the most frequently used treat-ment. Hypertension and dyslipidemiaare also common and require activeintervention.

8. Prevention must be the main strategyfor the future. School-based programshave been shown to be effective in theU.S. and Singapore. Major govern-mental actions that focus on lifestylewill be required.

9. Recommendations for action aremade.

RECOMMENDATIONS

1. Population-based prevalence studiesare urgently needed, particularly in“at-risk” populations. These should befollowed by outcome studies.

2. Study methods need to be standard-ized with regard to classification, diag-nostic methods, and diagnosticcriteria.

3. Data on the natural history of type 2diabetes in the young, particularly oncomplications, are required.

4. Further research is required to deter-mine the role of the oral glucose toler-ance test (OGTT) in screeningasymptomatic young people, as well asthe appropriate glucose load and tim-

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The International Diabetes Federation Consensus Workshop, “Type 2 Diabetes in the Young: The EvolvingEpidemic,” took place in Santa Monica, California, on 7–9 February 2003. A complete list of workshopparticipants and their respective affiliations is listed in the APPENDIX.

Address correspondence and reprint requests to Dr. Jonathan Shaw, MD, MRCP(UK), FRACP, Director ofResearch, International Diabetes Institute, 250 Kooyong Rd., Caulfield, Victoria 3162, Australia. E-mail:[email protected].

Received and accepted for publication on 13 April 2004.F.K. has been a member of an advisory panel, a standing committee, or the board of directors for Eli Lilly,

Novo Nordisk, Aventis, Medtronic MiniMed, Insulet, Clinical Products, LifeScan, and Amylin; has receivedgrant and research support from Medtronic MiniMed, Novo Nordisk, BMS, and Merck; and holds stock inClinical Products.

Abbreviations: ADA, American Diabetes Association; CVD, cardiovascular disease; DKA, diabetic keto-acidosis; IDF, International Diabetes Federation; HNF, hepatocyte nuclear factor; IFG, impaired fastingglucose; IGT, impaired glucose tolerance; MODY, maturity-onset diabetes of youth; OGTT, oral glucosetolerance test; PCOS, polycystic ovary syndrome.

A table elsewhere in this issue shows conventional and Systeme International (SI) units and conversionfactors for many substances.

© 2004 by the American Diabetes Association.

R e v i e w s / C o m m e n t a r i e s / P o s i t i o n S t a t e m e n t sC O N S E N S U S S T A T E M E N T

1798 DIABETES CARE, VOLUME 27, NUMBER 7, JULY 2004

ing of blood sampling to be used in theOGTT.

5. The costs and psychosocial impact ofscreening in young people need to beexamined.

6. The safety and efficacy of oral hypogly-cemic drugs in children need to be de-termined.

7. The role of insulin therapy for childrenwith type 2 diabetes needs to be deter-mined in multicenter randomizedcontrolled trials. These should exam-ine the optimum type, timing, inten-sity, and duration of insulin therapy.

8. Existing registers for type 1 diabetes inchildren should be expanded to in-clude those with type 2 diabetes.

9. Innovative ways of working with chil-dren with diabetes and their families toinstitute long-standing and sustain-able lifestyle change need to be sought.

10. Strategies for the prevention of type 2diabetes in children need to involvegovernment and societal, as well asindividual, change. Programs shouldfocus on the prevention of obesitythrough increasing physical activityand promoting healthy eating, thepromotion of breast feeding, andachieving excellent pregnancy out-comes with regard to avoiding lowbirth weight and treating gestationaldiabetes.

AIM AND OBJECTIVES OFTHE WORKSHOP — The Consen-sus Workshop on “Type 2 Diabetes in theYoung: The Evolving Epidemic” was con-vened by the International Diabetes Fed-eration (IDF) in response to the manyreports of the occurrence of type 2 diabe-tes in children and adolescents. The ob-jective of this document is to review thecurrent information on type 2 diabetes inyouth and to reach a consensus on whatactions need to be taken to slow or reversethis trend. The topic has become a clini-cal, research, and health economic prior-ity, with important implications for thehealth status of future generationsthroughout the world.

The workshop sought to:

● Assess current information on type 2diabetes in the pediatric population interms of epidemiology and publichealth implications

● Review the classification and diagnosisof type 2 diabetes in children and ado-lescents

● Discuss the pathogenesis of type 2 dia-betes in youth

● Evaluate screening recommendations● Assess the burden of complications● Make recommendations on therapeutic

options● Assess the opportunities for prevention

in order to reach a consensus on whatactions need to be taken to slow or re-verse the epidemic.

INTRODUCTION ANDBACKGROUND — Until recently,type 2 diabetes was typically regarded as adisease of the middle-aged and elderly.While it still is true that this age-groupmaintains a higher risk than youngeradults, evidence is accumulating that on-set in those aged under 30 years is increas-ingly common. Even children andadolescents are now becoming caught upin the diabetes epidemic. Although type 1diabetes remains the main form of the dis-ease in children worldwide, it is likely thattype 2 diabetes will be the predominantform within 10 years in many ethnicgroups. Type 2 diabetes has already beenreported in children in a number of coun-tries, including Japan, the U.S., India,Australia, and the U.K. (1–5).

This new phenomenon brings a seri-ous new aspect to the global diabetes ep-idemic and heralds an emerging publichealth problem of major proportions.Among children in Japan, type 2 diabetesis already more common than type 1 andaccounts for 80% of childhood diabetes.The rising prevalence of obesity and type2 diabetes in children is yet anothersymptom of the effects of sedentary life-styles as part of globalization and indus-trialization affecting all societies (1).

This fall in the age of onset of type 2diabetes is an important factor influenc-ing the future burden of the disease andwas part of the stimulus for the IDF toorganize the workshop. Onset of diabetesin childhood or adolescence heraldsmany years of disease and an increasedrisk that the full range of both micro- andmacrovascular complications will occurwhen affected individuals are still rela-tively young. Thus, future generationsmay be burdened with morbidity andmortality at the height of their productiv-ity, potentially affecting the workforceand health care systems of countriesacross the world.

EPIDEMIOLOGY — The g loba lburden of type 2 diabetes is both signifi-cant and rising, with most of the increaseregistered in the last two decades (6).From 2003 to 2025, the worldwide prev-alence of diabetes in adults is expected toincrease from 5.0 to 6.2%, or 328 million(7). The largest proportional and absoluteincrease will occur in developing coun-tries, where the prevalence will rise from4.2 to 5.6%. In India and China, the adultdiabetic population is expected to doubleby 2025 to about 73 million and 46 mil-lion, respectively.

While most of the rise in the preva-lence of type 2 diabetes has been seen inthe middle-aged and elderly, there is nowstrong evidence of a rise among youngeradults. In Australia, 1.7 and 1.4% of per-sons aged 35–44 and 45–54 years haddiabetes in 1981 (8), and these prevalencerates increased to 2.4 and 6.2%, respec-tively, in 2000 (9). Chinese data showthat the prevalence of diabetes among 35-to 44-year-olds rose from 1.7% in 1994 to3.2% in 2000 (10). These data confirm atrend to an earlier age of onset of diabetes.

There are ever increasing reports oftype 2 diabetes in children worldwide,with some as young as 8 years old beingaffected (11). These are mostly in ethnicgroups with a high susceptibility to type 2diabetes. However, there are now also re-ports of type 2 diabetes occurring amongEuropid (white Caucasoid) teenagers (4).In Japan, the prevalence of type 2 diabetesamong junior high school children hasdoubled from 7.3 per 100,000 between1976 and 1980 to 13.9 per 100,000 in1991–1995, with type 2 diabetes nowoutnumbering type 1 diabetes in thatcountry (1). Recent studies from the U.S.indicate that between 8 and 45% of re-cently diagnosed diabetes in the young isdue to type 2 diabetes (12). Despite thelarge increase, the prevalence is still, for-tunately, much lower than in the adultpopulation.

Inadequate data at presentThe available information on type 2 dia-betes incidence and prevalence in child-hood and adolescence is sparse comparedwith that for adults. Most surveys areclinic based or case series, with a paucityof population-based surveys, particularlyoutside North America (13) and Japan(1). Information on the natural historyand etiology of type 2 diabetes in the pe-diatric age range is also sparse. There is

Report of the IDF Consensus Workshop

DIABETES CARE, VOLUME 27, NUMBER 7, JULY 2004 1799

also a lack of uniformity in case definition(resulting in misclassification so thatsome children are being misdiagnosedand treated as type 1 diabetes), data col-lection, and follow-up (14).

The studies in the literature may bedivided into population- and clinic-basedstudies.

Population-based studiesThe largest study reported is from Japan(1), with �7 million youth studied be-tween 1976 and 1997. The initial screen-ing step of the study was a urine glucosetest, with blood testing reserved only forthose with glycosuria; thus, the figures areprobably an underestimate. Over the 20-year period, type 2 diabetes incidence in-creased 10-fold in children aged 6–12years: 0.2 per 100,000 per year from1976 to 1980 vs. 2.0 per 100,000 per yearfrom 1991 to 1995. Similarly, over thesame time period, type 2 diabetes inci-dence doubled among 13- to 15-year-olds: 7.3 vs. 13.9 per 100,000 per year.

A screening program in which fastingblood glucose was measured in those withpersistent glycosuria carried out in 3 mil-lion students (aged 6–18 years) in Taiwan(15) found the prevalence of undiagnoseddiabetes to be 9.0 and 15.3 per 100,000boys and girls, respectively. The preva-lence of undiagnosed diabetes was 62%higher in girls than boys, after adjustmentfor other factors, and the cases were mostcommonly identified between the ages of12 and 14 years. A 3-year follow-up ofthese cases showed that 54% had type 2diabetes, 10% had type 1 diabetes, 9%had secondary diabetes, 20% were nondi-abetic, and 8% had no definite diagnosis.The cases identified as having type 2 dia-betes had a higher mean BMI, cholesterol,and blood pressure than those with a nor-mal fasting glucose, suggesting that evenat this young age, cardiovascular risk wasstarting to rise.

In Pima Indians aged 15–19 years, theprevalence of type 2 diabetes markedlyincreased from 2.4% in males and 2.7% infemales in 1967–1976 to 3.8% in malesand 5.3% in females in 1987–1996 (14).In the U.S., among Navajo Indians, diabe-tes or impaired glucose tolerance (IGT)was found in 3 and 13%, respectively, ofgirls and boys aged 12–19 years (16). InCanada, among the Cree-Ojibway ab-originals, diabetes and impaired fastingglucose (IFG) were found in 1 and 3% ofchildren aged 4–19 years (17), and IGT

was found in 10% of those aged 10–19years (18). A 4% prevalence of diabetesamong adolescent girls in native popula-tions in Canada has been reported fromseveral surveys (19). A cohort of indige-nous Australian children aged 7–18 yearswas surveyed in 1989 and again in 1994.Over the 5 years, the prevalence of type 2diabetes almost doubled to 1.3%, whilethat for IGT increased almost sevenfold to8.1% (20). At the follow-up, 18% of thepopulation was overweight or obese, andone-third had elevated cholesterol levels.

National U.S. data from 1988 to 1994(21) show that of �3,000 persons aged12–19 years, the prevalence of IFG was1.8% and the prevalence of elevatedHbA1c (�6%) was 0.4%, while diabetesof all types (9 of the 13 diagnosed withdiabetes were on insulin) was diagnosedin 0.4%, suggesting some glycemic ab-normality in �600,000 adolescents in theU.S.

Clinic studiesClinic and register-based studies make upthe largest group of studies. They revealtype 2 diabetes occurring in children asyoung as 8 years old (11). In addition,they have demonstrated a female prepon-derance (22–24), a strong family historyof diabetes (22,25,26), and associationswith obesity (11,22,25–27), acanthosisnigricans (11,26,27), and polycysticovary syndrome (PCOS) (28).

A number of clinic-based studies haveestimated incidence rates. In Cincinnati,Ohio, the annual incidence of type 2 dia-betes in 10- to 19-year-olds increasedfrom 0.7 per 100,000 in 1982 to 7.2 per100,000 in 1994 (26). Among African-American and Latino children (aged 0–17years) in Chicago, Illinois, the incidenceof type 2 diabetes rose by 9% per yearfrom 1985, reaching 3.8 per 100,000per year (29) by 1994. This studyshowed higher rates in girls and in Afri-can Americans.

The prevalence of diagnosed diabetesamong American Indians aged 15–19years, as reported right across the IndianHealth Service, increased from 0.32 to0.54% from 1990 to 1998 (30). Althoughthe prevalence of type 2 diabetes washigher among females, the relative in-crease over this time period was greateramong males (0.23 to 0.41% for males vs.0.42 to 0.68% for females). Over the sametime period, the prevalence among those

younger than 15 years was unchanged at0.12%.

Some studies that analyzed referralsto diabetes clinics have reported the per-centage of diabetes cases labeled as type 2.From 1994 to 1998, the proportion ofnew cases of pediatric diabetes in Floridathat were labeled as having type 2 in-creased from 9.4 to 20% (31). In Cincin-nati in 1994, type 2 diabetes accountedfor 16% of all new cases of diabetes inchildren aged up to 19 years and ac-counted for 33% of new cases among the10- to 19-year-old age-group (26). InMexican-American youth aged 0 –17years, a California clinic reported that31% of the diabetic children had type 2diabetes (32). Among newly diagnoseddiabetic children and adolescents inBangkok, type 2 diabetes increased from5% of all cases during 1986 –1995 to17.9% during 1996–1999 (27). In con-trast, among European populations,which have lower overall prevalences oftype 2 diabetes, two very large studieshave reported that only 0.5% of childrenand adolescents with diabetes have beenclassified as having type 2 diabetes(33,34).

Complications—morbidity andmortalityAs with adults, it can be expected thatyouth with type 2 diabetes will also de-velop diabetes-related micro- and macro-vascular complications, and there isalready evidence available of microvascu-lar complications. In a study from Can-ada, subjects who developed type 2diabetes as children were resurveyed asyoung adults aged between 18 and 33years. Of the 51 subjects, 9% had died,6% were on dialysis, 1 had a toe amputa-tion, and 1 was blind (35). Another fol-low-up study from Japan compared thosewith type 1 and type 2 diabetes diagnosedat �30 years of age for development ofnephropathy (36). After 30 years of dia-betes, 44% of those with type 2 and20.2% of those with type 1 had nephrop-athy. Krakoff et al. (37) looked at inci-dence of retinopathy and nephropathyamong Pima Indians diagnosed with type2 diabetes at �20 years of age (youth),20–39 years of age (young adults), and40–59 years of age (older). Nephropathywas equally common in all age-groupsand was not related to age of diabetes on-set (at �5 years’ duration of type 2 diabe-tes, nephropathy incidence per 1,000

Consensus Statement


person-years was 13/1,000 youth,8/1,000 young adults, and 7/1,000older). However, unlike those with adult-onset diabetes, in whom retinopathy wasapparent at even this short duration, ret-inopathy did not appear among youth-onset cases until at least 5 years’ duration.Retinopathy was less common in youth-onset than in adult-onset groups at all du-rations of diabetes.

Although it is not known if the com-plication rate is similar for other ethnicgroups, these studies have important im-plications in that they highlight the risk ofcomplications occurring at a young age andsoon after diagnosis. This will place a signif-icant burden on health budgets as well as onsociety as a whole, especially as these peoplewould be entering their peak working andearning capacity at the time when compli-cations begin to occur. Early detection andintervention are therefore essential to re-duce the risk of future complications.

CLASSIFICATION ANDDIAGNOSIS — The appearance oftype 2 diabetes in children and adoles-cents has exacerbated the existing issuesin the classification of diabetes. There isnow a problem in clinically distinguish-ing the etiology of diabetes in childrenand adolescents, often necessitating labo-ratory studies to differentiate type 1 fromtype 2 diabetes (Table 1). This requirestests that are not always available in theprimary care environment or in many de-veloping countries.

The presence of diabetic ketoacidosis(DKA) is a classic manifestation of type 1diabetes. However, DKA may occur at

presentation in subjects who are eventu-ally found to have type 2 diabetes (38);that is, they have elevated C-peptide andan absence of antibodies to islet cells(ICA) or glutamic acid decarboxylase (an-ti-GAD), and after the initial period of se-vere metabolic disturbance, they do notrequire insulin (13). Initial reports wereamong African-American adults, and anautosomal dominant inheritance was sug-gested (38,39). Subsequent studies haveconfirmed that type 2 diabetes often pre-sents with ketosis or DKA and occurs in�40% of African-American children(40,41) with type 2 diabetes, 4% of chil-dren with Canadian aboriginal back-grounds (42), and 30% of children withMexican-American backgrounds (32). Astrong family history of type 2 diabetes iscommon, but an autosomal dominant in-heritance has not been confirmed. It hasvariously been called Flatbush diabetes,atypical diabetes (ADM), and phasic insu-lin dependence.

At the root of the classification prob-lem is the incomplete understanding ofthe pathogenesis of the two major types ofdiabetes, as knowledge of causation is theoptimal basis for classification. The asso-ciation of autoimmune serologic reactionsand particular HLA alleles in type 1 dia-betes strongly implicates autoimmunityin the pathogenesis, and these tests can beused to help with classification. However,classification is complicated because au-toimmunity (at least as determined bycurrent antibody assays) does not con-tribute to type 1 diabetes as substantiallyin non-Europid as in Europid popula-tions (43,44).

Further differential diagnoses are ma-turity-onset diabetes of youth (MODY),which is attributable to mutations of theglucokinase genes and hepatocyte nuclearfactor (HNF)-1� and -4� genes (45), anddiabetes due to mutations of mitochon-drial DNA (46).

The increasing recognition of difficul-ties with diagnosis and the potentiallymajor influence of diagnosis on therapy(particularly the decision to institute life-long insulin treatment) suggest the needto consider laboratory investigations,even in apparently typical cases. There-fore, in ideal circumstances it is recom-mended that apparently typical cases oftype 1 diabetes are confirmed with a mea-surement of autoantibodies, and typicalcases of type 2 diabetes are confirmedwith an assessment of insulin resistance(e.g., fasting C-peptide). It is recognizedthat in many settings worldwide such anapproach is not affordable and that pre-cise cutoffs for some of the diagnostic tests(especially for insulin resistance) have notbeen established. When diagnostic testsdo not confirm the clinical diagnostic la-bel, further investigations are indicated.In such cases, particularly when there is aparental history of diabetes, genetic test-ing will often be required. Diagnostic mo-lecular testing is now available (fordetails, visit www.diabetesgenes.org) andwhen used appropriately provides valu-able clinical information on diagnosis,prognosis, and treatment since most pa-tients with MODY respond best to sulfo-nylureas (47). It is relevant to note thatamong non-Hispanic Europid popula-tions, the prevalence of monogenic diabe-tes in children is similar to or higher thanthat of type 2 diabetes and is not excludedby the presence of obesity (48).

PATHOGENESIS — There is sparseinformation on the pathophysiology oftype 2 diabetes in the young; therefore,extrapolation from adults is necessary.Type 2 diabetes is characterized by disor-ders of insulin action and insulin secre-tion, either of which may be thepredominant feature (49). Both are usu-ally present at the time that type 2 diabe-tes clinically manifests. Persons with type2 diabetes usually have plasma insulinconcentrations that appear normal or ele-vated but insulin secretion, particularlyfirst phase, is defective and insufficient tocompensate for the insulin resistance(49). The specific reasons for the develop-

Table 1—Features to differentiate type 1 and 2 diabetes in young people

Type 1 diabetes Type 2 diabetes

Onset Acute—symptomatic Slow—often asymptomaticClinical picture ● Weight loss ● Obese

● Polyuria ● Strong family history type 2 diabetes● Polydipsia ● Ethnicity—high-prevalence populations

● Acanthosis nigricans● PCOS

Ketosis Almost always present Usually absentInsulin ● C-peptide negative ● C-peptide positiveAntibodies ● ICA positive ● ICA negative

● Anti-GAD positive ● Anti-GAD negative● ICA 512 positive ● ICA 512 negative

Therapy Insulin invariably Oral hypoglycemic agentsAssociated autoimmune

diseasesYes No



ment of these abnormalities are not yetknown, but it is of heterogeneous etiologywith behavioral and environmental riskfactors unmasking the effects of geneticsusceptibility (50).

The key factors involved in the devel-opment of type 2 diabetes are as follows:

GeneticDue to complex inheritance patterns andinteraction with the environment, identi-fying the genes involved in the commonforms of type 2 diabetes has proved diffi-cult. Only a small percentage of cases canbe explained by the single gene defectssuch as those known to cause MODY. Thegenetic component of type 2 diabetes inchildren and adolescents has yet to be ex-plored, but it is reasonable to assume thatit is similar to that in adults, and indeed astrong family history of type 2 diabetes isoften seen among adolescents with thedisease (see “Other factors” below). Anumber of major predisposing genes havebeen found on chromosomes 1q, 12q,20q, and 17q (51). Minor genes that havebeen defined by a candidate approach in-clude the Pro12Ala polymorphisms inperoxisome proliferator–activated recep-tor (PPAR)-� (52) and the Kir 6.2 E23Kvariant (53). In Ojibwa-Cree indigenousCanadians, a private mutation (G319SHNF1�) present in 20% of the popula-tion predisposes to diabetes (phenotypi-cally like type 2 diabetes), with a relativerisk of 2 when a single copy is inherited

and a relative risk of 4 when two copiesare inherited (54). This may yet prove tobe another form of MODY. Sellers et al.showed an inverse relationship betweennumber of copies of the mutation andmarkers of insulin resistance, suggestingthat the gene is related to secretory defects(55). The data on the genetic componentin adult type 2 diabetes are extensivelyreviewed elsewhere (51).

ObesityOn a global basis, the rise in type 2 diabe-tes rates mirrors the growth in urbaniza-tion and economic development (6,56).Obesity appears to be the key link, andthis is exemplified by the situation in Ja-pan, where a parallel rise in type 2 diabe-tes incidence in children and levels ofobesity occurred from 1975 to 1995 (1)(Fig. 1). Overweight and obesity are be-

coming major problems in adolescentsaround the world (Table 2).

The prevalence of overweight (de-fined as at or above the 95th percentile ofthe sex-specific BMI for age growthcharts) among children in the U.S. in-creased from 7% in 1988 to 10% in 1999among those aged 2–5 years and from 5%in 1976 to 11% in 1988 and to 15% in1999 among those aged 6–19 years (57).The rise in the prevalence has been muchmore pronounced among African-American and Hispanic children thanamong non-Hispanic whites (120% risevs. 50% rise in 12 years) (58). Behavioraldifferences have been observed, whichmay explain some of these differences.While African-American and Europidyouth may consume the same amount ofcalories, African-American children tendto get a greater percentage of their caloriesfrom fat, in addition to increased intake ofsweetened drinks (59). Moreover, Afri-can-American adolescents do not per-ceive themselves to be heavy and actuallyexpress a desire to be heavier (60).

Secular increases in the prevalence ofobesity in children have also been re-corded in China (62), Hong Kong (63),the U.K. (64), and Australia (65). In Aus-tralia (using age- and sex-specific BMIcutoffs designed to be the equivalent per-centiles to a BMI of 25 and 30 kg/m2 in18-year-olds), �5% of children are cur-rently obese and an additional 16% areoverweight (66). These prevalences dou-bled over the past decade after beingnearly stable at around 10% from 1969 to1985 (65). In India, a recent study foundthat the age-adjusted prevalence of beingoverweight (using the same cutoffs as theAustralian study) among 13- to 18-year-olds was 18% in boys and 16% in girls(67). Prevalence rates increased with age,decreasing physical activity, and higher

Figure 1—Annual incidence of type 2 diabetes and prevalence of obesity among Japanese schoolchildren. Adapted from Kitagawa et al. (1), with permission.

Table 2—Prevalence of overweight and obesity in six countries at age 18 years (61)

Overweight and obesity(BMI �25 kg/m2) Obesity (BMI �30 kg/m2)

Males Females Males Females

Brazil 4.7 15.2 0.1 2.0Great Britain 9.6 11.7 0.9 1.2Hong Kong 11.7 9.8 3.1 1.8Netherlands 5.5 6.5 0.3 0.3Singapore 10.5 7.0 1.7 1.0United States 18.1 16.5 3.3 4.0

Data are percent.

Consensus Statement


socioeconomic status (67). In the Cana-dian Ojibwa-Cree community, 48–51%of children aged 4–19 years were foundto have a weight �90th percentile (17).Changes in traditional lifestyles amongindigenous communities, such as a reduc-tion in hunting and gathering and theadoption of a more sedentary life with awesternized diet, are thought to contrib-ute to rising obesity levels (68).

Physical inactivityInactivity is one of the major contributorsto overweight and obesity. A recent lon-gitudinal study of girls in the U.S. showeda marked decline in physical activity over10 years, such that by the age of 16–17years, 56% of black and 31% of white girlsreported no habitual leisure-time physicalactivity (69). Pregnancy, cigarette smok-ing, higher BMI, and lower parental edu-cation at baseline were all associated witha subsequent decline in physical activity.Participation in physical education in U.S.schools fell from 41.6% in 1991 to 24.5%in 1995 (70). Another study found thatwhite students in the U.S. have higherphysical activity levels than other ethnicgroups, with boys usually more activethan girls, regardless of race (71).

Television-viewing time has beenlinked with childhood obesity (72),which may be related to the associatedconsumption of high-energy foods (73).On average, children’s programming inthe U.S. includes 10 food advertisementshourly (74), more than twice that in adultviewing (75).

Insulin resistancePublished studies linking insulin resis-tance directly with type 2 diabetes in ad-olescents and children are very limited.However, observations about the typicalage of onset of diabetes, evidence of insu-lin resistance in normoglycemic childrenfrom high-risk ethnic groups, and the vastliterature on insulin resistance in adultsmake a compelling case. Most observa-tions in youth with type 2 diabetes wouldsuggest that insulin resistance is an earlyfeature in these children. Initially, insulinresistance manifests itself in compensa-tory hyperinsulinemia. Over time there is�-cell failure, resulting in the clinical ex-pression of type 2 diabetes (76) (77).

In a cross-sectional study of 14 ado-lescents with IGT matched with 14 con-trol subjects of similar age, BMI, body fat,and leptin, the children with IGT were

found to have greater insulin resistance.Furthermore, they had higher visceraland lower subcutaneous abdominal fatand decreased first-phase insulin secre-tion and glucose disposition index (78).Intramyocellular fat content (as measuredby nuclear magnetic resonance spectro-scopy) showed a strong positive correla-tion with insulin resistance and with 2-hpostload plasma glucose (78), suggestingthat it may be important in pathogenesis.Further evidence of the importance of in-sulin resistance can be drawn from theobservation that the onset of type 2 dia-betes frequently occurs around the timeof puberty, when insulin sensitivity de-clines (79–81). Even in healthy, prepu-bertal African-American children, afamily history of diabetes is associatedwith an �20% reduction in insulin sensi-tivity (82). The hyperinsulinemia and re-duced insulin sensitivity observed inHispanic and black children has been as-sociated with both increased insulin se-cretion and reduced insulin clearance(83,84).

In a variety of ethnic groups, obesityis associated with evidence of insulin re-sistance and impaired insulin secretionamong children, as in adults (85,86).Central obesity is of particular impor-tance as a determinant of hyperinsulin-emia (87). Compared with white childrenwith obesity and similar insulin sensitiv-ity levels, black children have lower he-patic glucose output, lower total and LDLcholesterol, and lower triglyceride levels,with considerably lower visceral fat levels.Visceral adiposity was associated withlower insulin sensitivity in both groups.This was compensated by higher insulinsecretion in whites, but not in blacks (88).These findings suggest a greater diabeto-genic risk of obesity among African Amer-icans but greater atherogenic risk amongwhites. The dietary fat-to-carbohydrateratio correlates significantly with insulinresistance and may partly explain themetabolic differences seen between blackand white children (83). Indeed, a num-ber of studies have shown that African-American children have higher total fatand cholesterol intake, prefer greatersweetness in liquids, are physically lessactive, and spend more time watchingtelevision (59,89).

It is possible to ameliorate insulin re-sistance by increasing the level of physicalactivity. This has been demonstrated inobese children and more recently in non-

diabetic, normal weight children (90),where more active subjects had lowerfasting insulin values and greater insulinsensitivity, as measured by a glucoseclamp.

Acanthosis nigricans and PCOSAcanthosis nigricans is a well-establishedphysical marker of insulin resistance andis reported to occur in up to 60–90% ofyoung people with type 2 diabetes(91,92). This seems to be especially truefor African Americans, Mexican Ameri-cans, and some Native Americans, but notin other populations, such as in Japan.PCOS is associated with a state of insulinresistance and compensatory hyperinsu-linemia (83). Obese adolescents withPCOS have a 50% reduction in peripheraltissue insulin sensitivity and evidence ofhepatic insulin resistance and compensa-tory hyperinsulinemia (93). Approxi-mately 30% of adolescent girls with PCOShave been found to have IGT, with 4%having type 2 diabetes (28). In these ad-olescents, glucose intolerance is associ-ated with decreased first-phase insulinsecretion, decreased glucose dispositionindex, and increased hepatic glucose pro-duction (94).

Intrauterine environmentTwo aspects relating to the intrauterineenvironment—birth weight and maternalhyperglycemia—may possibly affect thedevelopment of type 2 diabetes amongthe young. There is now abundant evi-dence that low birth weight predicts type2 diabetes in middle age (95). Recent datafrom Taiwan confirm this in children(96). A study of 6- to 18-year-oldsshowed a U-shaped relationship, inwhich the risk of type 2 diabetes was low-est in those with a birth weight of 3–3.5kg, and was significantly increased inthose children who had either low (�2.5kg) or high (�4.0 kg) birth weight, de-spite adjustment for other factors, includ-ing gestational diabetes, family history ofdiabetes, and socioeconomic status (96).Recent evidence seems to indicate that thegreatest risk for obesity and glucose intol-erance in adulthood is in those with lowbirth weight who gain weight rapidly inchildhood (97,98). The risk in this groupis higher than in those who are over-weight from birth.

Gestational diabetes mellitus (GDM)also seems to increase the risk of diabetesdeveloping in offspring (99). A prospec-



tive study (100) found that the prevalenceof IGT in the children of mothers with adiabetic pregnancy increased with timefrom 1.2% at �5 years of age to 19.3% at10–16 years of age. This was comparedwith 2.5% at 10–16 years of age in con-trol subjects. Higher levels of amnioticfluid insulin at 33–38 weeks of gestationwas a strong predictor of later IGT (100).The specific environmental role of mater-nal hyperglycemia, as separate from ma-ternal genetics, has been demonstrated inPima Indians, in whom offspring born af-ter the mother developed diabetes weremore obese as children and more likely tohave diabetes in their twenties than theirsiblings born before their mothers devel-oped diabetes (14). No such differenceswere seen before and after fathers devel-oped diabetes. Age at diagnosis inHNF-1� mutation carriers was �10 yearsyounger when the mother was diagnosedbefore pregnancy compared with whenthe mother was diagnosed after preg-nancy (101). The father’s age at diagnosisdid not, however, influence the off-spring’s age at diagnosis.

Other factorsFamily history. Many studies show astrong family history among affectedyouth, with 45–80% having at least oneparent with diabetes and 74–100% hav-ing a first- or second-degree relative withtype 2 diabetes (12,102). Children withdiabetes are also more likely to have afamily history of cardiovascular disease(CVD), with one study showing that up to28% have a positive family history of CVD(103). In a study among Pima Indians, itwas shown that the cumulative incidenceof type 2 diabetes was highest in offspringif both parents had diabetes (104). Japa-nese children with type 2 diabetes showfamilial clustering, with siblings having a

175- to 250- fold increase in diabetes overthe frequency in the general population,and parents have a 48–60% likelihood ofhaving type 2 diabetes (105,106). A life-style predisposing to obesity and type 2diabetes seems to characterize familieswith adolescents who have type 2 diabe-tes (26). Specifically, members of suchfamilies tend to be overweight and inac-tive and have a tendency to high-fat intakeand even binge eating (107).Sex. Girls are 1.7 times more likely thanboys to develop type 2 diabetes in an anal-ysis of a large set of studies (108). Thereason for this is not clear, and it appearsto be a special feature of type 2 diabetes inyouth, as sex differences in diabetes prev-alence are only a very minor feature inadults.Socioeconomic status. Socioeconomicstatus has been associated with type 2 di-abetes and obesity in adults. In developedcountries, the risk of diabetes is highest inthose with lower socioeconomic status(109,110); however, the opposite appearsto apply in developing countries, wherehigher socioeconomic status is associatedwith an increased risk of diabetes (111).Physical inactivity probably explainsthese findings in both settings. In chil-dren, no data on diabetes are yet available,but a recent large study of 3-year-olds inthe U.K. found that those in the most de-prived group were 30% more likely to beobese than those in the least deprivedgroup (112).

SCREENINGA major consequence of the appearance oftype 2 diabetes in the younger age-groupis that subjects with diabetes will have alonger duration of the disease that in-creases medical costs and increases therisk that both microvascular and macro-vascular complications will develop at an

earlier age. This makes the issue of screen-ing in the young a very relevant and, in-deed, urgent issue. However, certaincriteria need to be met before screeningcan be considered in the public healtharena. These are summarized below.

● The disease is common among the gen-eral population or among easily identi-fiable high-risk subgroups

● The disease is serious in terms of mor-bidity and mortality

● The disease has a prolonged latencywithout symptoms

● The screening test is adequately sensi-tive and specific

● Intervention is available to prevent ordelay disease onset or treat at an earlystage.

Type 2 diabetes in children appears tomeet a number of these criteria, suggest-ing that it may be an appropriate target forscreening. However, even when consider-ing the screening of adults for diabetes,there remains heated debate, as it hasbeen suggested that evidence is not yetavailable to demonstrate that it fulfills thecriteria for population-based massscreening (113). The IDF consensusgroup noted the recommendations of the2000 American Diabetes Association(ADA) report on type 2 diabetes in chil-dren and adolescents (12), as outlined inTable 3. Consistent with those recom-mendations, only children at substantialrisk for the presence or the developmentof type 2 diabetes should be consideredfor screening.

The Third National Health and Nutri-tion Examination Survey (NHANES III)data suggest that the ADA risk criteriawould lead to testing of 10% of youths inthe U.S., for a total of �2.5 million ado-lescents between 12 and 19 years of age,of whom 5% might be expected to haveIFG (fasting plasma glucose 6.1– 6.9mmol/l) or undiagnosed diabetes, while1.8% of those not tested under such rec-ommendations would be expected tohave IFG (114). It should be noted thatthe ADA has recently recommended low-ering the criteria for IFG to 5.7– 6.9mmol/l (115).

The question of what tests to use forthe initial screening for type 2 diabetes isdifficult. Evidence from adult popula-tions clearly shows that �30% of all thosewith undiagnosed diabetes have a nondi-abetic fasting glucose (116) but are nev-

Table 3—ADA recommendations for testing for type 2 diabetes in children (12)

Criteria for considering screening for diabetes*Overweight (BMI 85th percentile for age and sex, weight for height 85th percentile, or

weight 120% of ideal for height)Plus any two of the following risk factors:● Family history of type 2 diabetes in first- or second-degree relative● Race/ethnicity (American Indian, African American, Hispanic, Asian/Pacific Islander)● Signs of insulin resistance or conditions associated with insulin resistance (acanthosis

nigricans, hypertension, dyslipidemia, PCOS)Age of initiation: age 10 years or at onset of puberty if puberty occurs at a younger ageFrequency: every 2 yearsTest: fasting plasma glucose preferred

*Clinical judgment should be used to test for diabetes in high-risk subjects who do not meet these criteria.

Consensus Statement


ertheless at high cardiovascular risk(117), suggesting that the OGTT shouldbe part of the screening process. Others(118) have questioned this assertion, butthe World Health Organization (WHO)and many national diabetes organizationscontinue to recommend its use for adults,particularly in those with a high but non-diabetic fasting glucose. It should benoted that it is currently unknownwhether the diagnostic cut points used foradults are applicable to children. Further-more, the evidence base for the standard1.75-g/kg (to a maximum of 75 g) dose ofglucose used in the OGTT is not strong,and the evidence needs to be further ex-amined in order to review its validity.

Estimates from the Japan and Taiwanscreening programs of the unselectedgeneral school population show a cost ofapproximately $10,000 (U.S.) per casefound, indicating the need to focus onhigh-risk groups. Cost-effectiveness anal-ysis suggests that the optimal approachfor screening adults is to use “opportunis-tic screening” for undiagnosed diabetes atroutine medical system contacts (119).Such an approach may not work withchildren who generally have less frequentcontact with health care systems.

The psychosocial impact of diagnos-ing an asymptomatic disease throughscreening warrants consideration. Thepotential for distress to occur when anasymptomatic individual is diagnosedwith a lifelong disease is considerable,particularly when the diagnosis occursduring adolescence and when it carrieswith it implications about an individual’sor family’s lifestyle habits. Evidencewould suggest that in adults there is not asignificant detrimental effect of identify-ing diabetes through screening (120), butthere are no such data available for chil-dren and adolescents, and it would beparticularly dangerous to extrapolatesuch findings.

TREATMENT — The appearance oftype 2 diabetes in a younger age-groupraises new issues in management of diabetesapart from the difficulty in classification.What therapies are safe in this age-group?Most pharmacologic therapies for diabetesand its associated conditions (apart from in-sulin) are not approved for use in children,and the same applies for those for bloodpressure and dyslipidemia.

The goals of treatment for type 2 dia-

betes in children and adolescents are toachieve:

● Physical well-being● Long-term glycemic control● Prevention of microvascular complica-

tions of diabetes● Prevention of macrovascular disease● Psychological well-being.

Physical well-beingThe attainment of physical well-being hasshort-term and long-term goals. Short-term goals include treatment of acutemetabolic decompensation if present (ke-toacidosis), the elimination of symptomsassociated with hyperglycemia (polyuria,polydipsia), treatment of acute andchronic infections (vaginal candidiasis isfrequent at presentation), and treatmentof medical problems associated with obe-sity (e.g., sleep apnea, steatosis).

The long-term goals for physical well-being include achieving normal growthfor the younger adolescent with diabetes,achieving and maintaining a reasonablebody weight, maintaining a reasonablelevel of fitness by a regular physical activ-ity program, avoidance of smoking, andpreventing the complications of diabetes.

Glycemic controlThe theoretical glycemic goal is to achieveand maintain normoglycemia; however, amore pragmatic target is to maintainHbA1c �7%. Lifestyle intervention (diet,exercise, and weight control) is the cor-nerstone of management and if successfulis likely to benefit blood pressure and lip-ids as well as glycemia. If diabetes is diag-nosed early, lifestyle intervention maysuffice, although this only appears to beapplicable to �10% of patients in clinicalpractice (121).

In principle, there is no reason to sup-pose that pharmacological treatment ofhyperglycemia should be any different inadults and children. What does pose aproblem is our lack of knowledge aboutthe long-term implications of drug treat-ment of diabetes in this age-group.

A proposed therapeutic algorithm forasymptomatic children with type 2 diabe-tes is to start with lifestyle interventionapproaches; then add monotherapy, par-ticularly emphasizing the use of met-fo rmin ; and subsequent l y usecombinations of two oral medicationsand, if adequate control is not achieved,the addition of insulin. For symptomatic

children, with blood glucose persistentlyexceeding 17 mmol/l or when DKA ispresent, insulin therapy is indicated, withsubsequent efforts to taper this phenom-enon and substitute metformin mono-therapy once blood glucose levels arenormal (108,121). Many youth maintainnear-normal blood glucose levels formonths to years after one course of insulinat diagnosis (122).

In clinical practice in the U.S., ap-proximately one-half of young patientswith type 2 diabetes receive insulin andone-half receive oral agents, most com-monly metformin (108,121). In anotheranalysis of treatment regimens for type 2diabetes in young persons, 28% begantherapy with metformin, with the remain-der using insulin alone or the two in com-bination (123).

Pharmaceutical agentsInsulin. The apparent “overuse” of insu-lin therapy in adolescent type 2 diabetes isprobably multifactorial. It is possible thatsignificant insulin deficiency may be com-mon among the symptomatic adolescentswith type 2 diabetes presenting to diabe-tes centers. Insulin is very familiar to pe-diatricians and is necessary for treatingacute metabolic decompensation. At pre-sentation, there is often uncertainty aboutwhether the patient has type 1 or type 2diabetes. Experience with oral agents inchildren is limited and safety data arescant. Formal approval by the Food andDrug Administration (FDA) (and othernational therapeutic goods agencies) fortheir use in childhood and adolescence islimited. Insulin may in addition convey amessage of more serious illness, perhapsimproving compliance.

The optimum schedule and type ofinsulin need to be determined in this age-group. It is a priority to study the opti-mum type of insulin, timing, intensity,duration, and follow-up in multicenterrandom controlled trials.Metformin. This is approved in the U.S.for pediatric use. It is recommended asinitial pharmacologic treatment in the ab-sence of severe hyperglycemia. Data onmetformin in children are limited, but a16-week study (124,125) showed it to besafe and effective in 10- to 16-year-oldswith type 2 diabetes. Long-term outcomestudies are needed, as analysis of efficacyof metformin in a small group of Cree innorthern Manitoba, Canada, showed littleeffect of metformin on HbA1c or body



weight after 1 year among adolescentswith type 2 diabetes (17). Gastrointestinalside effects were common with treatment.Poor adherence to oral therapy among rel-atively asymptomatic young persons withtype 2 diabetes may be a major barrier toimprovement in outcome.Sulfonylureas. This class is well studiedin adults; they are effective, safe, and in-expensive, although sulfonylureas havethe potential to cause weight gain and hy-poglycemia. They are the treatment ofchoice in patients with mutations inHNF1� and HNF4�, but only very lowdoses may be required (47).Thiazolidinediones. This newer class ofdrugs is not yet approved for use in child-hood and adolescence. Clinical studies forpediatric use are in progress, and al-though associated with weight gain, theirreduction of visceral fat suggests overallbenefit if long-term safety concerns can beaddressed. Their safety profile with re-gard to edema and weight gain may bemore favorable in children than adults,although this needs to be determined.�-Glucosidase inhibitors. They havebeen used infrequently but are safeagents, although, like metformin, theirgastrointestinal side effects may decreaseacceptance among young persons.

Lipid-lowering therapyThe ADA has recently published consen-sus-based guidelines for the managementof dyslipidemia in children (126). Therecommendations for type 2 diabetes arethat lipids should be measured every 2years; optimal levels are as follows: LDL�2.6 mmol/l, HDL �0.9 mmol/l, andtriglycerides �1.7 mmol/l. When optimallevels are not present, dietary adviceshould be provided and blood glucoseshould be treated aggressively. If after 6months, LDL is �4.1 mmol/l, medicationshould be started (resins should be con-sidered and if not accepted or tolerated,statins can be used). If LDL is 3.4–4.1mmol/l after 6 months of diet and bloodglucose management, medication shouldbe considered in those with additionalcardiovascular risk factors (includingblood pressure, family history, and smok-ing status). Medication is not advised forthe specific treatment of triglycerides (un-less �11.2 mmol/l) or HDL.

HypertensionHypertension is a comorbidity of type 2diabetes in youth and is a major risk factor

for nephropathy and atherosclerosis. Hy-pertension is defined in pediatric patientsas an average systolic or diastolic bloodpressure �95th percentile for age, sex,and height, taken on three occasions.Blood pressure measurement should beobtained in all children with type 2 dia-betes during diabetes health care visits. Ifhypertension does not respond to lifestylechanges, first-line pharmacological ther-apy for hypertension is an angiotensin-converting enzyme inhibitor, withangiotensin II receptor antagonists beingreserved as second-line therapy due to lit-tle primary data in pediatric subjects.

HypercoagulabilityThe risk of Reye’s syndrome, which is ex-tremely rare after puberty, has led theADA to recommend against the use of as-pirin in those �20 years of age.

Barriers to treatmentAttainment of treatment goals poses chal-lenges, especially for the adolescent age-group when the developmental stage ofmoving toward independence is fre-quently marked by risk-taking behavior,lack of long-term planning, noncompli-ance, and resistance to lifestyle changes.Additional problems affecting the treat-ment of type 2 diabetes include familyand/or psychosocial dysfunction and eth-nic influences. Depression due to the highfamily burden of illness, poverty and iso-lation, and substance abuse are also notuncommon in lower socioeconomicgroups and in many indigenous popula-tions, leading to difficulties in the treat-ment of type 2 diabetes.

For young individuals, the importantrole of the family in diabetes managementcannot be overestimated, as involvementof the family has been shown to lowerHbA1c (127).

PREVENTION — There is now veryclear evidence supporting both lifestyleintervention and pharmaceutical agentsin the prevention of type 2 diabetes inadults (128). However, the only evidenceon diabetes prevention in children relatesto breast-feeding, which may minimizeexcessive energy intake and perhaps im-prove insulin sensitivity by its higherpolyunsaturated fat content. Studies ofPima Indians (129) and Native Canadianchildren (68) have shown a lower preva-lence of type 2 diabetes among childrenand adolescents who were breast-fed dur-

ing infancy. Compared with formulafeeding, breast-feeding has been associ-ated with a lower weight for length andsmaller skinfold thickness up to the age of2 years (130) and with a lower plasmaglucose in infants undergoing electivesurgery (131).

Further relevant findings can befound in studies of overweight and obesechildren. In a 20-week study of 50 obeseadolescents, those randomized to aweight loss program had, at the end of thestudy, lower serum insulin levels andblood pressure than those in the controlgroup (132). In a similar study of 29obese, hyperinsulinemic adolescents witha positive family history of type 2 diabetesrandomized to metformin or placebo,BMI and fasting insulin improved mod-estly with metformin, but no changecould be demonstrated in insulin sensitiv-ity, HbA1c, lipids, or glucose disposal(133).

In a trial of 192 children in two Cali-fornia schools, television and videotapeviewing and video game use was reducedfrom 12 to 8 h/week in the interventiongroup, with no change in the controlgroup. Those in the intervention grouphad a 0.45-kg/m2 lesser increase in BMIand a 2.3-cm lesser increase in waist cir-cumference during the 6-month study(134).

The “Trim and Fit” program in Singa-pore integrated nutrition education intothe school curriculum, controlled theschool canteens, encouraged water drink-ing by providing water coolers, targetedobese children for additional assistance,and rewarded schools achieving goodhealth outcomes. Over 8 years of the pro-gram, from 1992 to 2000, the prevalenceof obesity fell from 16.6 to 14.6% in 11-to 12-year-olds and from 15.5 to 13.1%in 15- to 16-year olds (135). An exerciseintervention in Japan decreased the prev-alence of overweight from 40 to 37%among boys and to 32% among girls be-tween the ages of 10 and 13 years, with nochange in a control group (136).

A school-based program among Mex-ican-American children has shown theimportance of creating a network of socialsupport in the classroom, the home, theschool cafeteria, and among friends andclassmates. In comparison to children in acontrol setting, those in the program haveshown improved physical fitness, re-duced numbers with fasting plasma glu-

Consensus Statement


cose �6.1 mmol/l, and reduced body fat(137,138).

Beyond individual and community-based interventions, to successfully pre-vent lifestyle diseases such as diabetes,changes in government policies and leg-islation are essential. Government inter-vention can include mandating a greateremphasis on more exercise and dietaryeducation in schools, banning the adver-tising of unhealthy products, and subsi-dizing healthy food at the expense of lesshealthy food.

CONCLUSIONS — Until recently,type 2 diabetes has been viewed as a dis-ease of older adults. With increasing ratesof obesity, it is clear that the age of diseaseonset is falling in all ethnic groups andthat type 2 diabetes is occurring in child-hood (39). While much of the informa-tion is currently based on case reports andclinic-based series, and any generaliza-tions should therefore be very guarded,the underlying problem of childhoodobesity is, unfortunately, well docu-mented. It would indeed be surprising iftype 2 diabetes does not follow in itswake. The challenge to epidemiologists isto define its extent.

The pathophysiology of type 2 diabe-tes in children and adolescents appears tobe very similar to that of adults. Insulinresistance (often exacerbated by puberty)is initially compensated by increased in-sulin secretion, but over time, �-cell func-tion declines and hyperglycemia ensues.The pancreatic islet �-cell failure may oc-cur very rapidly but the reasons for thisare unclear.

The management of type 2 diabetes inthe younger age-groups presents severalmajor challenges. First, differentiationfrom type 1 diabetes can be difficult, no-tably when those presenting with DKAsubsequently manifest many features typ-ical of type 2 diabetes. Agreement on clas-sification is required, and the frameworkneeds to be useful in the clinical (both atthe time of presentation and later on) andresearch settings. Successful treatmentwill require intensive efforts to alter life-style, which will need to focus on familiesas well as the individual. There do notappear to be any reasons why pharmaco-logical treatment should differ from thatused in adults, but more evidence isneeded is about long-term safety and effi-cacy in relation to currently available oralhypoglycemic agents.

Prevention must remain a high prior-ity and is only likely to be successful ifgovernments and communities providethe environment within which individu-als can make lifestyle changes that willprevent and, when necessary, reverseobesity. The school systems provide anideal setting for prevention of obesity anddiabetes, because the whole target popu-lation is available and both diet and phys-ical activity can be influenced. In an idealworld, it would be possible to implementthe proposed wide-reaching recommen-dations. In reality, this may be difficultgiven the socioeconomic contraints andthe already tight health budgets of manygovernments. In addition, achieving goodpregnancy outcomes with regard toavoiding low birth weight and treatinggestational diabetes also provides an im-portant prevention opportunity.

A consequence of urbanization is theparallel emergence of CVD, obesity, andtype 2 diabetes, which until recently wasmainly a problem of the developed world.Therefore, governments are going to beforced to deal with the problem of type 2diabetes in children. As such, it would bebetter to address the problem as a publichealth issue under the heading of primarycare and prevention instead of dealingwith the consequences of an entrenchedcondition and its complications in ayoung population.

APPENDIX: WORKSHOPPARTICIPANTS

Organizing Group● Co-chairperson: Sir George Alberti,

FRCP (UK), Imperial College School ofMedicine, Department of Diabetes, TheMedicalSchool.E-mail:[email protected]

● Co-chairperson: Paul Zimmet, AO(Australia), International Diabetes In-stitute. E-mail: [email protected]

● Francine Kaufman, MD (USA), Chil-dren’s Hospital Los Angeles. E-mail:[email protected]

● Martin Silink, MD (Australia), Ray Wil-liams Institute for Pediatric Endocri-nology, Royal Alexandra Hospital forChildren. E-mail: [email protected]

Participants● Stephanie Amiel, MD (UK), Guy’s,

King’s and St. Thomas School of Medi-cine, Kings College. E-mail: [email protected]

● Silva Arslanian, MD (USA), Children’sHospital University of Pittsburgh. E-mail: [email protected]

● Peter Bennett, MD (USA), National In-stitute of Diabetes and Digestive KidneyDiseases. E-mail: [email protected]

● Zachary Bloomgarden, MD (USA), Mt.Sinai Medical Center. E-mail: [email protected]

● Sonia Caprio, MD (USA), Yale Univer-sity School of Medicine. E-mail:[email protected]

● Juliana Chan, MD (China), The Chi-nese University of Hong Kong, Divisionof Clinical Pharmacology, Departmentof Medicine and Therapeutics, Prince ofWales Hospital. E-mail: [email protected]

● Lee-Ming Chuang, MD (Taiwan), Na-tional Taiwan University Hospital. E-mail: [email protected]

● Dan Cooper, MD (USA), University ofCalifornia, Irvine. E-mail: [email protected]

● Paul Czernichow, MD (France), Uni-versity of Paris, Hospital Robert Debre.E-mail: [email protected]_hop_paris.fr

● Heather Dean, MD (Canada), Univer-sity of Manitoba. E-mail: [email protected]

● Phillipe Halban, PhD (Switzerland),Univer s i ty o f Geneva . E-mai l :[email protected]

● Andrew Hattersley, MD (UK), Diabetes& Vascular Medicine, Peninsula Medi-cal School. E-mail: [email protected]

● Kenneth Lee Jones, MD (USA), Univer-sity of California, San Diego, Depart-ment of Pediatrics. E-mail: [email protected]

● Richard Kahn, PhD (USA), AmericanDiabetes Association. E-mail: [email protected]

● Kaichi Kida, MD, PhD (Japan), Depart-ment of Pediatrics, Ehime University,School of Medicine. E-mail: [email protected]

● Pierre Lefebvre, MD, PhD (Belgium),Department of Medicine, University ofLiege. E-mail: [email protected]

● Dinky Levitt, MD (South Africa), Uni-versity of Cape Town. E-mail: [email protected]

● Sir Michael Marmot, MD (UK), De-partment of Epidemiology and PublicHealth, University College London.



E-mail: [email protected] [email protected]

● Abdullah Nakhi, MD (Kuwait), KuwaitDiabetes Society. E-mail: [email protected]

● Kerin O’Dea, PhD (Australia), MenziesSchool of Health Research, Royal Dar-win Hospital. E-mail: [email protected]

● Stefan Rossner, MD (Sweden), ObesityUnit, Huddinge University Hospital. E-mail: [email protected]

● Jonathan Shaw, MD (Australia), Inter-national Diabetes Institute. E-mail:[email protected]

● Jay Skyler, MD (USA), Diabetes Re-search Institute. E-mail: [email protected]

● Allen Spiegel, MD (USA), National In-stitute of Diabetes and Digestive andKidney Diseases. E-mail: [email protected]

● Robert Trevino, MD (USA), Social andHealth Research Center. E-mail:[email protected]

● Frank Vinicor, MD (USA), Centers forDisease Control and Prevention. E-mail: [email protected]

● Rhys Williams, MD, PhD (UK),TheClinical School, University of Wales,Swansea. E-mail: [email protected]

● Chittaragnan Yajnik, MD (India), KingEdward Memorial Hospital. E-mail:[email protected]

Acknowledgments— The Expert Workshopwas supported by an educational grant fromJohnson & Johnson.

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Consensus Statement


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Consensus Statement


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Type 2 diabetes in the young: the evolving epidemic: the international diabetes federation consensus...

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