Childhood onset and duration of obesity are significant risk factors for type 2 diabetes in mid-adulthood
- Rhode Island Hospital and Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA
- Correspondence to Charlotte M Boney
593 Eddy Street, Rhode Island Hospital and Warren Alpert Medical School of Brown University, Providence, RI 02903, USA;
Implications for practice and research
■ The increased risk of type 2 diabetes mellitus (T2DM) in obese children and adults is well-established, but it is not clear if the age of onset or the duration of obesity is an independent risk factor for T2DM in adults.
■ Adults with obesity since childhood or young adulthood had the highest body mass index (BMIs) and the greatest risk of T2DM.
■ Non-obese adults who were obese children had an increased risk of elevated HbA1c, suggesting that childhood obesity may be an independent risk factor for T2DM in adulthood.
Obesity has become the most common health problem of children and adults in the developed world. Obesity rates in the USA have levelled off as of 2008, with a prevalence of 32.2% among men, 35.5% among women,1 and 31.7% (>85th percentile BMI for age) among children and adolescents of 2–19 years.2 Numerous studies have demonstrated significant associations between childhood obesity and adult morbidities, including metabolic syndrome, T2DM and cardiovascular disease (CVD). However, it remains to be determined if these associations of childhood obesity and adult disease (T2DM, CVD) reflect duration of obesity since childhood or an independent level of risk from childhood obesity. A recent systematic review of 11 studies found little evidence that childhood obesity is an independent risk factor for T2DM.3
BMI, T2DM prevalence and HbA1c levels were measured in the 45-year-old participants (n=7855) enrolled in the 1958 British birth cohort. BMI was calculated at age 7, 11, 16, 23, 33 and 45 years and waist circumference and HbA1c measured. Analyses examined associations between BMI and HbA1c using linear and logistic regression for HbA1c either as a continuous variable (numeric HbA1c level) or a dichotomous variable (either >7% or T2DM present). Models were adjusted for sex, socioeconomic class, family history of diabetes and ethnicity.
There were three major findings. The first was that obesity at any age is associated with elevated HbA1c at age 45 years, and this association strengthened with age. The second was that duration of obesity matters: childhood obesity was associated with a 24-fold risk of HbA1c >7% versus a 16-fold risk for obesity onset in young adulthood versus a threefold risk for obesity onset during mid-adulthood. Finally, childhood obesity may be an independent risk factor for T2DM in adulthood. In a small number of subjects (n=62) who were obese as children but not as adults, they still had a fivefold risk of HbA1c >7%. However, the subjects who were overweight or obese as children (n=163) but not as adults did not have an increased risk of T2DM.
This study makes some important observations about obesity status from childhood to mid-adulthood and subsequent risk of HbA1c>7%, now an accepted diagnostic marker of T2DM.4 The study's strengths include the longitudinal follow-up of >7000 subjects from birth to 45 years and the finding that childhood obesity may be an independent risk factor for adult T2DM. This observation is unique and is not described in a recent similar study of subjects (n=6328) from four cohorts with a mean follow-up of 23 years.5 This study found that adults with obesity since childhood had increased risks of both T2DM and CVD, but subjects who were overweight or obese as children but not as adults (n=274) had similar risks to non-obese adults. However, Juonala and colleagues did not analyse childhood obesity separately from overweight and obese on T2DM risk as in the present study. These findings suggest that some degree of increased adiposity during childhood may not irreversibly increase the risk of T2DM and CVD if overweight status is not present in adulthood.
The findings in the present study support the ever-enlarging body of evidence that the greatest risk of childhood obesity is adult obesity. T2DM and CVD are major drivers of healthcare consumption, and these diseases, once confined to adults, are now prevalent in children. This study has some good news: if we reverse childhood obesity, then we prevent obesity in adulthood and reduce T2DM risk. We must prevent and treat childhood obesity if we are going to reduce these diseases in our population.