Background The risk of type 2 diabetes mellitus is increasedin people who have low birth weights and who subsequently becomeobese as adults. Whether their obesity originates in childhoodand, if so, at what age are unknown. Understanding the originof obesity may be especially important in developing countries,where type 2 diabetes is rapidly increasing yet public healthmessages still focus on reducing childhood "undernutrition."
Methods We evaluated glucose tolerance and plasma insulin concentrationsin 1492 men and women 26 to 32 years of age who had been measuredat birth and at intervals of three to six months throughoutinfancy, childhood, and adolescence in a prospective, population-basedstudy.
Results The prevalence of impaired glucose tolerance was 10.8percent, and that of diabetes was 4.4 percent. Subjects withimpaired glucose tolerance or diabetes typically had a low body-massindex up to the age of two years, followed by an early adiposityrebound (the age after infancy when body mass starts to rise)and an accelerated increase in body-mass index until adulthood.However, despite an increase in body-mass index between theages of 2 and 12 years, none of these subjects were obese atthe age of 12 years. The odds ratio for disease associated withan increase in the body-mass index of 1 SD from 2 to 12 yearsof age was 1.36 (95 percent confidence interval, 1.18 to 1.57;P<0.001).
Conclusions There is an association between thinness in infancyand the presence of impaired glucose tolerance or diabetes inyoung adulthood. Crossing into higher categories of body-massindex after the age of two years is also associated with thesedisorders.
This study of pregnancy outcomes and childhood growth was begunin 1969 in a defined area of 12 km2 in South Delhi, India.10All families living there between December 1, 1969, and November30, 1972, were identified. Among a population of 119,799, therewere 20,755 married women of reproductive age who were assessedevery other month (±3 days) in order to record menstrualdates. Women who became pregnant were seen by a health visitorevery 2 months (±3 days) initially and on alternate daysfrom the 37th week of gestation. There were 9169 pregnancies,resulting in 8181 live births (8030 singletons and 151 twins),202 stillbirths, and 867 abortions. Trained personnel recordedthe weight and the length or height of the babies within 72hours after birth; at the ages of 3, 6, 9, and 12 months (±7days); and at 6-month intervals (±15 days) thereafter.There were several phases in this cohort study (Figure 1). Morethan 30 percent of the cohort (2414 subjects) was lost to follow-upbetween the end of phase 1 and the beginning of phase 2, a timewhen unauthorized housing was demolished in South Delhi.
Figure 1. Summary of the Various Phases of the Cohort Study in Relation to the Age of Subjects and the Number Available for Study.
In Phase 4, recruitment was restricted to the subjects who would have reached 20 years of age during this period. The mean, minimal, and maximal ages of the subjects at each year of follow-up are shown by the diagonal rows of symbols. Numbers of subjects remaining in follow-up at the beginning and end of phases 1 through 4 are shown.
At the time of recruitment, 59.9 percent of families had anincome above 50 rupees per month (national average, 28.4). Only14.9 percent of parents were illiterate (national average, 66.3).Nevertheless, 43.0 percent of families lived in only one room.Hindus were the majority religious group (84.3 percent), followedby Sikhs (11.6 percent), Christians (2.1 percent), Muslims (1.1percent), and Jains (0.7 percent).
Current Phase of Study
From August 1998 to August 2002, we located 2584 (31.6 percent)of the initial cohort. A social worker performed home visitsand recorded each subject's occupation and level of education,physical activity, and alcohol and tobacco consumption. Thesubjects were asked to attend a clinic after an overnight fastfor further investigations. Of the 1583 subjects (61.3 percent)who agreed to participate, 57 were excluded (24 were pregnant,2 withdrew, and 31 were unreliably linked to earlier data),leaving 1526. In comparison with the original cohort, this cohorthad 7 percent more male subjects, the rate of maternal literacywas 6 percent higher, the mean birth weight was 32 g higher,and the mean birth length was 2 mm longer. The height, weight,and body-mass index (the weight in kilograms divided by thesquare of the height in meters) in childhood and adolescencewere approximately 0.1 SD lower than in the original cohort.
The subjects' blood pressure, weight, height, waist and hipcircumferences, and skinfold thicknesses (triceps and subscapular)were measured according to standardized techniques. Subjectswere categorized as obese if their body-mass index was 30 ormore.11 Two definitions of overweight were used, the standardWorld Health Organization11 cutoff value of a body-mass indexof 25 and that recommended for Asians12 of 23.
A standard glucose-tolerance test with an oral 75-g anhydrousglucose load was administered.13 Plasma glucose concentrationsin samples obtained after an overnight fast and 30 and 120 minutesafter the ingestion of glucose (fasting, 30-minute, and 120-minutevalues) were analyzed by means of a glucose oxidase method (GOD-PAP,Randox) with a Beckman autoanalyzer. Aliquots of plasma werestored at –70°C for up to eight months, and insulinconcentrations were measured by radioimmunoassay (Coat-a-Countinsulin kit, Diagnostic Products). The intraassay and interassaycoefficients of variation were less than 5 percent and lessthan 7.5 percent, respectively. Insulin resistance was calculatedaccording to the homeostasis-model assessment.14
The 30-minute increment in insulin — calculated as the(30-minute insulin concentration – the fasting insulinconcentration) ÷ the 30-minute glucose concentration— was used as a measure of first-phase insulin secretion.15Impaired glucose tolerance was defined as a fasting plasma glucoseconcentration of less than 126 mg per deciliter (7.0 mmol perliter) and a 120-minute value of at least 141 mg per deciliter(7.8 mmol per liter); diabetes was defined as a fasting glucoseconcentration of at least 126 mg per deciliter or a 120-minuteconcentration of at least 200 mg per deciliter (11.1 mmol perliter).13
The All India Institute of Medical Sciences approved the study.Informed consent was obtained from each subject.
Statistical Analysis
Using all recorded data, not just those for subjects recruitedfor the current studies, we generated height, weight, and body-massindex standards so as to derive internal sex-specific SD scores(the SD score is the number of standard deviations by whichan observation differs from the mean for the cohort). Recruitedsubjects had an average (±SD) of 23±5.5 observationsbetween birth and the age of 21 years. We modeled the progressof the median, spread, and skewness of the measurements as ageincreased. For each subject we interpolated values linearlybetween successive SD scores to estimate SD scores at 6 monthsand at birthdays from 1 to 21 years of age.16 The interpolatedvalues were used if a measurement had been made within 6 months(up to 1 year), 1 year (age of 2 years), 1.5 years (age of 3years), and 2 years (all ages after 3 years). Back transformationprovided estimates of the measurements at all these ages. Theponderal index at birth was calculated as 1000 times the weightin grams divided by the cube of the height (or the crown–heellength) in centimeters.
Table 1 shows the characteristics of the 886 men and 640 womenin the current sample. Most were married, college graduates(with a bachelor's degree or above), and not in manual employment.Few women drank alcohol or smoked tobacco. Almost half the subjectswere overweight according to the conventional definition,11and nearly two thirds were overweight when the Asian cutoffvalue was used.12
Eight of the 1526 subjects who attended the clinic had not fasted,and a further 26 declined to provide a blood sample. Fifty subjectsdid not complete the glucose-tolerance test and therefore couldnot be classified as having normal or impaired glucose toleranceor diabetes. Of the remaining 1442 subjects, 156 (10.8 percent)had impaired glucose tolerance and 63 (4.4 percent) had diabetes.
As compared with subjects with normal glucose tolerance, thosewith impaired glucose tolerance or diabetes had higher meanvalues for body-mass index, waist:hip ratio, fasting and 120-minuteplasma insulin concentrations, and insulin resistance (Table 2).The 30-minute insulin-increment values, however, were significantlylower in the subjects with diabetes or impaired glucose tolerancethan in the subjects with normal glucose tolerance and werelowest in those with diabetes. The presence of impaired glucosetolerance and diabetes was unrelated to a subject's level ofeducation or employment status, alcohol consumption, smokingstatus, or level of physical activity. A history of diabetesin a first-degree relative (present in 36.7 percent of subjects)was associated with an increased risk of impaired glucose toleranceor diabetes (P=0.004), but this relation was no longer statisticallysignificant (P=0.08) after adjustment for adult body-mass indexand the waist:hip ratio. In further analyses of the predictorsof impaired glucose tolerance and diabetes, we adjusted forage, sex, adult body-mass index, and the waist:hip ratio unlessotherwise stated.
Table 2. Mean Plasma Glucose and Insulin Concentrations, Values for Body-Mass Index, and Waist:Hip Ratios According to Glucose-Tolerance Status.
Size at Birth and during Infancy
Across the range of birth weights, 120-minute plasma glucoseconcentrations in the young adult subjects fell from 113 mgper deciliter (6.28 mmol per liter) in subjects with a birthweight of 2.25 kg or less to 105 mg per deciliter (5.85 mmolper liter) in those with a birth weight of more than 3.5 kg(P=0.02). This relationship was not changed by further adjustmentfor the length of gestation. There were similar trends in fastinginsulin concentrations (P=0.02), 120-minute insulin concentrations(P=0.008), and insulin resistance (P=0.009). These variableswere also inversely related to the ponderal index at birth (P=0.04,P=0.01, and P=0.03, respectively). Although the developmentof impaired glucose tolerance and diabetes was not related tobirth weight, in combination the prevalence of these conditionswas inversely related to weight and body-mass index at one yearof age (P=0.04 and P=0.03, respectively; odds ratio, 1.6; 95percent confidence interval, 1.0 to 2.5) for those in the lowestquartile of body-mass index as compared with those in the highestquartile of body-mass index at one year.
Childhood Growth and Obesity
Figure 2 shows the growth of boys and girls in whom impairedglucose tolerance or diabetes subsequently developed. The SDscore for the cohort is set at zero. A child maintaining a steadyposition as large or small in relation to other children wouldfollow a horizontal path on the figure. The SD scores for body-massindex fell between birth and two years of age among childrenin whom impaired glucose tolerance or diabetes later developed,although this decrease was not statistically significant (P=0.29).From two years of age onward they had an accelerated increasein body-mass index, while SD scores for height remained relativelyconstant.
Figure 2. Mean Sex-Specific Unadjusted SD Scores for Height (Panel A) and Body-Mass Index (Panel B), According to Age, for Subjects in Whom Impaired Glucose Tolerance or Diabetes Developed.
The mean SD scores (solid lines) are obtained by linear interpolation of yearly means, with one additional observation at six months. The dotted lines represent 95 percent confidence intervals. The dashed portions of lines indicate years in which there was no follow-up. The SD score for the cohort is set at zero (solid horizontal lines).
As shown in Table 3, the highest prevalence of impaired glucosetolerance and diabetes was among subjects who were in the lowestthird of the group with respect to body-mass index at the ageof 2 years and the highest at the age of 12 years. In a simultaneousregression, the opposing effects of body-mass index at 2 yearsand at 12 years were both statistically significant (P=0.002for body-mass index at 2 years and P<0.001 for body-massindex at 12 years, adjusted for age and sex). An increase of1 SD in body-mass index between the ages of 2 and 12 years wasassociated with an odds ratio of impaired glucose toleranceor diabetes of 1.36 (95 percent confidence interval, 1.18 to1.57; P<0.001). This finding was similar after further adjustmentfor current body-mass index and the waist:hip ratio (odds ratio,1.26; 95 percent confidence interval, 1.08 to 1.48; P=0.004).An increase of 1 SD in body-mass index between 2 years of ageand adulthood was associated with only a slightly higher oddsratio than that for such an increase between 2 and 12 yearsof age (odds ratio, 1.46; 95 percent confidence interval, 1.28to 1.66; P<0.001, adjusted for age and sex).
Table 3. Prevalence of and Odds Ratios for Impaired Glucose Tolerance or Diabetes, According to the Body-Mass Index (BMI) at 2 Years and 12 Years of Age and 2 Years of Age and Currently.
Using the definitions of the International Obesity Task Force,17we found that only 3.3 percent of the children in whom impairedglucose tolerance or diabetes subsequently developed were overweightat the age of 12 years, and none were obese at this age. Thesefigures had increased by the age of 16 years to 11.4 percentand 0.5 percent, respectively. A 1-unit increase in the body-massindex at the age of 12 years was associated with a correspondingincrease of 1.4 units (95 percent confidence interval, 1.3 to1.5) at the age of 30 years (correlation coefficient, 0.61).
Adiposity Rebound
The mean body-mass index at the time of adiposity rebound wassimilar in subjects in whom impaired glucose tolerance or diabetesdeveloped and subjects whose glucose tolerance remained normal(13.8 and 13.9, respectively), but the mean age was younger(6.3 years, as compared with 6.7 years; P=0.007). Children withthe earliest adiposity rebound (five years of age or younger)had the highest body-mass index in later childhood, and thisdifference persisted into adulthood (Table 4). However, theyhad the lowest ponderal index at birth, the lowest body-massindex at two years, and a small increase in body-mass indexfrom birth to two years of age (P=0.004). The prevalence ofimpaired glucose tolerance and diabetes fell with increasingage at the time of adiposity rebound.
Table 4. Ponderal Index at Birth; Body-Mass Index at the Age of 2 Years, 12 Years, and Currently; and Prevalence of Impaired Glucose Tolerance or Diabetes, According to the Age at the Time of Adiposity Rebound.
The study subjects came from a population of neonates representingall live births within a defined area. Since only 18.7 percentof the original cohort participated in the present study, thesubjects may well be unrepresentative of the cohort as a whole.However, the differences in their mean size at birth and inchildhood, though statistically significant, were trivial. Ouranalysis was based on internal comparisons within the studysample and would be biased only if the association between earlygrowth and current glucose or insulin status differed betweenthose who were included in the current study and those who werenot. Some of these young adults with diabetes may not have hadtype 2 diabetes; however, since only one required insulin, thenumber with type 1 diabetes is likely to be small.
Our study had several strengths. It was population-based; gestationalage was assessed prospectively; trained personnel collectedanthropometric data at frequent intervals; and the relativelyyoung age of subjects ensured minimal modification as a resultof complications of disease or medications. The cohort is unique,in that it represents an urban population of people who grewup during a period of rapid nutritional transition in a developingcountry and who are now having a rapid loss of glucose homeostasisrelatively young in adult life.
The mean insulin concentrations in our cohort would be consideredhigh in whites with similar values for body-mass index in Westerncountries, but such values have been well described in SouthAsians.18,19 As in earlier reports,4,8,20 we also found thata small size at birth, defined by a low birth weight or ponderalindex, was associated with increased plasma glucose and insulinconcentrations and insulin resistance during adulthood. It wasnot, however, associated with the occurrence of impaired glucosetolerance or diabetes in our study. Given the association betweenbirth weight and both fasting and 120-minute glucose concentrations,the lack of a significant association with disease may be dueto a loss of sensitivity resulting in the change from a continuousto a dichotomous variable. Consistent with studies in Hertfordshire,United Kingdom,4 and Helsinki, Finland,21 we found that lowweight and thinness at one to two years of age were associatedwith impaired glucose tolerance and diabetes in adulthood. Childrenwho are thin at two years of age tend to have been thin at birth,though postnatal influences such as infection and feeding practicesalso contribute.
The children in whom impaired glucose tolerance or diabetes later developed were not overweight or obese in childhood.Theyremained below the cohort average for body-mass index untilthe age of 10 years. At the age of 12 years, only 3.3 percentwere overweight according to the current definitions, and nonewere obese. Instead, they were characterized by their high rateof gain in body mass after the age of two years. We proposethat an upward trajectory of body-mass index, starting in earlychildhood, underlies the current epidemic of diabetes in India.
Our findings are remarkably similar to those in the only Westernpopulation with comparable data.21 Among 8760 boys and girlswho grew up in Helsinki, Finland, during the Second World War,childhood obesity was uncommon, affecting only 0.4 percent atthe age of 12 years, according to International Obesity TaskForce definitions.17 The 290 children in that study in whomtype 2 diabetes developed in adult life had below-average bodysize at birth and low weight at one year of age. Thereafter,they had an early adiposity rebound and an accelerated gainin weight and body-mass index, but not height. Their mean body-massindex did not exceed the average for the cohort until aroundfive years of age. Early adiposity rebound was associated withlow weight and body-mass index at one year of age. The prevalenceof type 2 diabetes fell progressively from 8.6 percent in peoplewhose adiposity rebound occurred before the age of five yearsto 1.8 percent in those in whom it occurred after seven years.
In conclusion, the young adults in our study who had impairedglucose tolerance or diabetes were, as a group, overweight.They were not, however, overweight as young children but, rather,became overweight as a result of an accelerated gain in bodymass starting in early childhood, having been thin in infancy.The ability of children to have an accelerated increase in bodymass may be a recent phenomenon in India, a consequence of nutritionaltransition. Our data do not allow us to distinguish betweenthe events that lead to increasing body-mass index and the expressionof the diabetic phenotype. However, assuming that the changein body-mass index is causal rather than the result of a simpleassociation, we speculate that the primary prevention of theepidemic of diabetes in India may require measures to preventchildren from crossing into higher categories of body-mass indexafter the age of two years. Individual children will need tohave serial measurements of body-mass index for such a growthtrajectory to be identified.
Supported by a grant (RG 98001) from the British Heart Foundation.The original cohort studies were supported by the National Centerfor Health Statistics and the Indian Council of Medical Research.
We are indebted to the men and women and their families whotook part in the study, as well as to the field and laboratorystaff for their contribution.
Source Information
From the Department of Pediatrics, Sunder Lal Jain Hospital, Delhi, India (S.K.B.); the Department of Pediatrics, Maulana Azad Medical College (H.S.S., S.R.), the Department of Cardiology, All India Institute of Medical Sciences (R.L., D.P., K.S.R.), and the Indian Council of Medical Research (S.K.D.B.) — all in New Delhi, India; and the Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, United Kingdom (C.H.D.F., C.O., D.J.P.B.).
Address reprint requests to Prof. Sachdev at E-6/12 Vasant Vihar, New Delhi 110 057, India, or at hpssachdev{at}hotmail.com.
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