Among 109,172 women followed for >16 years, somatotypes at ages 5 and 10 years were positively associated with the risk of incident type 2 diabetes after adjustment for major risk factors. However, women who were overweight at age 10 but were lean in adulthood did not have an increased risk of diabetes associated with childhood overweight, underscoring the importance of continued efforts to control adiposity among overweight children.
Limited studies have investigated the long-term consequences of childhood overweight and the risk of type 2 diabetes in adulthood, with inferences hindered by small numbers of case subjects and/or lack of differentiation of diabetes type (2
). In addition, some studies included case subjects with young age at onset (<30 years old) (3
). One study using data based on records (185 cases) showed that the cumulative incidence of diabetes was doubled (from 4.2 to 8.4%) among women in the largest BMI group at age 11 years (>17.4 kg/m2
) compared with those in the smallest BMI group (≤15.3 kg/m2
). We found a similar increase in risk using recalled somatotypes. In contrast, a study of older French women using recalled body shape, found an association between childhood thinness and diabetes risk (8
). However, this birth cohort vastly differed from the NHSII as demonstrated by >60% of their case subjects having reported extreme leanness (somatotype 1) at age 8 years, possibly due to their nutritional status having been affected by World War II (8
). Thus, our findings among a more recent birth cohort may be more relevant.
In addition to absolute size, longitudinal changes through different ages are also relevant to the risk of diabetes (17
). Under normal development, infants lose weight after 6 months of age and continue doing so until ~5 years of age when their adiposity rebounds (18
). Although we were unable to assess age at adiposity rebound, earlier rebound has been associated with increased risk of type 2 diabetes (17
), and there is some suggestion that age at rebound matters more than the absolute size of the child at any point in time because it corresponds to weight gain. Our findings of increased risk associated with increases in somatotype and weight gain support the importance of change in size in addition to absolute size. These findings offer support for continued weight reduction efforts across the life span.
Moreover, in analyses of the cumulative effect of overweight through childhood, adolescence, and adulthood, the risk for type 2 diabetes was greatest among women reporting overweight by all three measures, even though the difference was marginal when compared with adolescent overweight. However, women who became lean in adulthood did not have an increased risk of diabetes associated with childhood overweight. Similar observations have been made from other studies of youth overweight and type 2 diabetes or related traits, with findings becoming nonsignificant after accounting for adult BMI (6
). Tracking of metabolic risk factors (e.g., HDL and triglycerides) has also been observed after 21 years of follow-up from childhood (21
), supporting the fact that cumulative overweight is linked with prolonged exposure to metabolic irregularities, putting children on the path to β-cell dysfunction earlier. It should be noted that although there is tracking of overweight to obesity from childhood to adulthood, the trajectory is not fixed from youth (18
). It has been shown that ~10–30% of overweight children do not go on to be overweight as adults with conflicting evidence as to whether there is greater tracking in girls than in boys (22
). Conversely, the majority of adults who are overweight were not in childhood (22
) as confirmed here with only 12–20% of the overweight women reporting childhood overweight.
Our study had some limitations. Although experts have recommended BMI for the measurement of childhood size (18
), we used recalled somatotype. Misclassification of childhood size is inevitable. However, two previous studies have shown that the accuracy of recall between childhood somatotypes and recorded childhood BMI did not differ by adult BMI (10
). The misclassification of childhood size is thus more likely to be nondifferential, which cannot explain the observed positive association between childhood size and type 2 diabetes risk. In addition, our findings were in agreement with those of other studies that used childhood measures of weight and height (4
). The generalizability of our findings may be limited to white women who comprised >95% of our study population. More research is needed in minority populations who have higher rates of overweight and diabetes (1
). Last, we cannot rule out the possibility of residual confounding by unmeasured confounders because of the observational nature of the study.
As for strengths, the NHSII included a large number of women (>3,000 case subjects) and adjusted for many risk factors. Follow-up for previous studies required recontacting participants in adulthood with low to moderate success rates (20–60%) (5
), whereas we evaluated somatotypes at baseline and >90% of the women remained for follow-up.
In summary, our findings demonstrate that the importance of childhood overweight stems largely from adult overweight. Women who do not continue to be overweight in adulthood do not have increased risks. It remains important then to promote lifestyle changes from youth so that the adverse trajectory could be avoided. Multiple interventions to address childhood overweight have been suggested (23
), but these remain to be fully tested.