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Childhood obesity is predictive of excess mortality in several divergent settings, indicating that obesity itself is causally related to either death or other commonly related factors. Even if preventing childhood obesity does not affect the risk of death, increased physical activity and modification of diet are likely to have long-term benefits. The lack of specific data on such factors is a limitation of this study.
Childhood Obesity, Other Cardiovascular Risk Factors, …
It is possible that the relationship between childhood BMI and mortality is confounded by unmeasured lifestyle factors. Nevertheless, obesity can be both the cause and the consequence of adverse lifestyle factors such as physical inactivity, excessive caloric intake, and specific nutrient preferences. Thus, such factors may be important components of the causal pathway between obesity and death. It is also possible that genetic factors have pleiotropic effects on BMI and mortality.
Although there was no significant association between childhood hypercholesterolemia and death before 55 years of age in this young cohort, an elevated cholesterol level in childhood may emerge as a significant risk factor and other causes of death may predominate if the cohort is followed to older ages. Cholesterol levels, however, are lower in American Indians than they are in most other ethnic groups, a finding that may partially explain the absence of association for this trait. The relationship between BMI and high-density lipoprotein (HDL) cholesterol is relatively strong in Pima children (r=−0.3 to −0.6), but the relationship between BMI and total cholesterol is weaker (r=0.1). The effect of BMI on premature death might be attributable in part to low HDL-cholesterol concentrations, which were not measured in most of the study participants. Nevertheless, we speculate that low HDL-cholesterol levels are likely to mediate rather than confound this relationship.
ADHD in Childhood May Raise Risk for Obesity in …
The absence of an association between premature death and cholesterol levels may be due partly to the low proportion of deaths due to cardiovascular disease in this cohort (13.3%). Treatment for any of the predictor traits during childhood or during adulthood did not appear to explain the pattern of association (data not shown). No childhood risk factor that was examined significantly predicted rates of premature death from external causes.
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It is well known that obesity, glucose intolerance, hypertension, and hypercholesterolemia in adulthood increase mortality rates. We conducted the present study to determine whether the presence of these risk factors in childhood predicts premature death. The rate of death from endogenous causes in the highest quartile of childhood BMI was more than double that in the lowest quartile, and the rate in the highest quartile of childhood two-hour plasma glucose levels during a 75-g oral glucose-tolerance test was 73% higher than that in the lowest quartile. Although neither blood pressure nor cholesterol level in childhood, when included as a continuous variable, significantly predicted premature death, childhood hypertension increased the risk of premature death from endogenous causes by 57%.
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Most deaths occurred in study participants who were not known to have diabetes. Of the 559 participants in whom diabetes developed, 79 died: 40 from endogenous causes and 39 from external causes. Adjusting the BMI prediction models for incident diabetes did not significantly alter the risk estimates (incidence-rate ratio for the highest BMI quartile vs. the lowest quartile, 2.70; 95% CI, 1.70 to 4.31). In contrast, inclusion of diabetes in the 2-hour glucose model reduced the risk estimate for the highest quartile of 2-hour glucose levels, and the association between the highest and lowest quartiles was not significant (incidence-rate ratio, 1.10; 95% CI, 0.72 to 1.68). In Cox proportional-hazards models that included 2672 participants, there were no significant associations between childhood BMI and alcohol dependency in adulthood (incidence-rate ratio per unit of BMI z score, 1.01; 95% CI, 0.96 to 1.07).
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The 2-hour plasma glucose level during a 75-g oral glucose-tolerance test, expressed in age-standardized and sex-standardized units, was not associated with premature death from either endogenous or external causes. However, children in the highest quartile of glucose level had a 73% higher risk of premature death from endogenous causes than children in the lowest quartile (). Adjustment for childhood BMI reduced the magnitude of the association (incidence-rate ratio, 1.24; 95% CI, 0.79 to 1.96).