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Risk factors for cardiovascular disease and type 2 diabetes retained from childhood to adulthood predict adult outcomes: the Princeton LRC Follow-up Study

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      Abstract

      Background

      Pediatric risk factors predict adult cardiovascular disease (CVD) and type 2 diabetes (T2DM), but whether they predict events independently of adult risk factors is not fully known.

      Objective

      Assess whether risk factors for CVD and T2DM retained from childhood to adulthood predict CVD and T2DM in young adulthood.

      Study design

      770 schoolchildren, ages 5–20 (mean age 12), 26-yr prospective follow-up. We categorized childhood and adult risk factors and 26-year changes (triglycerides [TG], LDL cholesterol, BMI, blood pressure [BP] and glucose ≥, and HDL cholesterol < pediatric and young adult cutoffs). These risk factors and race, cigarette smoking, and family history of CVD and T2DM were assessed as predictors of CVD and T2DM at mean age 38.

      Results

      Children who had high TG and retained high TG as adults had increased CVD events as adults ( p = .0005). Children who had normal BMI and retained normal BMI as adults had reduced CVD events as adults ( p = .02). Children who had high BP or high TG and retained these as adults had increased T2DM as adults ( p = .0006, p = .003).

      Conclusions

      Risk factors for CVD and T2DM retained from childhood to adulthood predict CVD and T2DM in young adulthood and support universal childhood screening.

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      Most cited references 47

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      Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women.

      Elevated nonfasting triglycerides indicate the presence of remnant lipoproteins, which may promote atherosclerosis. To test the hypothesis that very high levels of nonfasting triglycerides predict myocardial infarction (MI), ischemic heart disease (IHD), and death. A prospective cohort study of 7587 women and 6394 men from the general population of Copenhagen, Denmark, aged 20 to 93 years, followed up from baseline (1976-1978) until 2004. Hazard ratios (HRs) for incident MI, IHD, and total death according to baseline nonfasting triglyceride level categories of 1 to 1.99 mmol/L (88.5-176.1 mg/dL), 2 to 2.99 mmol/L (177.0-264.6 mg/dL), 3 to 3.99 mmol/L (265.5-353.0 mg/dL), 4 to 4.99 mmol/L (354.0-441.6 mg/dL), and 5 mmol/L or more (> or =442.5 mg/dL) vs triglyceride levels of less than 1 mmol/L (<88.5 mg/dL). With increasing levels of nonfasting triglycerides, levels of remnant lipoprotein cholesterol increased. During a mean follow-up of 26 years, 1793 participants (691 women and 1102 men) developed MI, 3479 (1567 women and 1912 men) developed IHD, and 7818 (3731 women and 4087 men) died. For MI, among women, the age-adjusted HRs and multifactorially adjusted HRs (aHRs) for each respective category per 1-mmol/L increase in nonfasting triglyceride levels were 2.2 (aHR, 1.7), 4.4 (aHR, 2.5), 3.9 (aHR, 2.1), 5.1 (aHR, 2.4), and 16.8 (aHR, 5.4); for both, P for trend < .001. For MI, among men, the values were 1.6 (aHR, 1.4), 2.3 (aHR, 1.6), 3.6 (aHR, 2.3), 3.3 (aHR, 1.9), and 4.6 (aHR, 2.4); for both, P for trend < .001. For IHD, among women, the values were 1.7 (aHR, 1.4), 2.8 (aHR, 1.8), 3.0 (aHR, 1.8), 2.1 (aHR, 1.2), and 5.9 (aHR, 2.6); for both, P for trend < .001. For IHD, among men, the values were 1.3 (aHR, 1.1), 1.7 (aHR, 1.3), 2.1 (aHR, 1.3), 2.0 (aHR, 1.2), and 2.9 (aHR, 1.5); P for trend < .001 for age-adjusted and P for trend = .03 for multifactorially adjusted. For total death, among women, the values were 1.3 (aHR, 1.3), 1.7 (aHR, 1.6), 2.2 (aHR, 2.2), 2.2 (aHR, 1.9), and 4.3 (aHR, 3.3); for both, P for trend < .001. For total death, among men, the values were 1.3 (aHR, 1.2), 1.4 (aHR, 1.4), 1.7 (aHR, 1.5), 1.8 (aHR, 1.6), and 2.0 (aHR, 1.8); for both, P for trend < .001. In this general population cohort, elevated nonfasting triglyceride levels were associated with increased risk of MI, IHD, and death in men and women.
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        Childhood adiposity, adult adiposity, and cardiovascular risk factors.

        Obesity in childhood is associated with increased cardiovascular risk. It is uncertain whether this risk is attenuated in persons who are overweight or obese as children but not obese as adults. We analyzed data from four prospective cohort studies that measured childhood and adult body-mass index (BMI, the weight in kilograms divided by the square of the height in meters). The mean length of follow-up was 23 years. To define high adiposity status, international age-specific and sex-specific BMI cutoff points for overweight and obesity were used for children, and a BMI cutoff point of 30 was used for adults. Data were available for 6328 subjects. Subjects with consistently high adiposity status from childhood to adulthood, as compared with persons who had a normal BMI as children and were nonobese as adults, had an increased risk of type 2 diabetes (relative risk, 5.4; 95% confidence interval [CI], 3.4 to 8.5), hypertension (relative risk, 2.7; 95% CI, 2.2 to 3.3), elevated low-density lipoprotein cholesterol levels (relative risk, 1.8; 95% CI, 1.4 to 2.3), reduced high-density lipoprotein cholesterol levels (relative risk, 2.1; 95% CI, 1.8 to 2.5), elevated triglyceride levels (relative risk, 3.0; 95% CI, 2.4 to 3.8), and carotid-artery atherosclerosis (increased intima-media thickness of the carotid artery) (relative risk, 1.7; 95% CI, 1.4 to 2.2) (P ≤ 0.002 for all comparisons). Persons who were overweight or obese during childhood but were nonobese as adults had risks of the outcomes that were similar to those of persons who had a normal BMI consistently from childhood to adulthood (P>0.20 for all comparisons). Overweight or obese children who were obese as adults had increased risks of type 2 diabetes, hypertension, dyslipidemia, and carotid-artery atherosclerosis. The risks of these outcomes among overweight or obese children who became nonobese by adulthood were similar to those among persons who were never obese. (Funded by the Academy of Finland and others.).
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          Prevalence of a metabolic syndrome phenotype in adolescents: findings from the third National Health and Nutrition Examination Survey, 1988-1994.

          In adults the metabolic syndrome imposes a substantial risk for type 2 diabetes mellitus and premature coronary heart disease. Even so, no national estimate is currently available of the prevalence of this syndrome in adolescents. To estimate the prevalence and distribution of a metabolic syndrome among adolescents in the United States. Analyses of cross-sectional data obtained from the Third National Health and Nutrition Examination Survey (1988-1994), which was administered to a representative sample of the noninstitutionalized civilian population of the United States. Male and female respondents aged 12 to 19 years (n = 2430). The prevalence and distribution of a metabolic syndrome among US adolescents, using the National Cholesterol Education Program (Adult Treatment Panel III) definition modified for age. The overall prevalence of the metabolic syndrome among adolescents aged 12 to 19 years was 4.2%; 6.1% of males and 2.1% of females were affected (P=.01). The syndrome was present in 28.7% of overweight adolescents (body mass index [BMI], >/=95th percentile) compared with 6.8% of at-risk adolescents (BMI, 85th to <95th percentile) and 0.1% of those with a BMI below the 85th percentile (P<.001). Based on population-weighted estimates, approximately 910 000 US adolescents have the metabolic syndrome. Perhaps 4% of adolescents and nearly 30% of overweight adolescents in the United States meet these criteria for a metabolic syndrome, a constellation of metabolic derangements associated with obesity. These findings may have significant implications for both public health and clinical interventions directed at this high-risk group of mostly overweight young people.
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            Author and article information

            Affiliations
            [1 ]From the Division of Cardiology, Children’s Hospital of Cincinnati, 3333 Burnet Avenue, 45229, Cincinnati, USA
            [2 ]From the Cholesterol and Metabolism Center, Jewish Hospital of Cincinnati, Cincinnati, USA
            [3 ]Cholesterol Center, UC Health Business Center, 3200 Burnet Avenue, Cincinnati, OH 45229, USA
            Contributors
            Journal
            Int J Pediatr Endocrinol
            Int J Pediatr Endocrinol
            International Journal of Pediatric Endocrinology
            BioMed Central
            1687-9848
            1687-9856
            2012
            16 April 2012
            : 2012
            : 1
            : 6
            3466140
            1687-9856-2012-6
            22507454
            10.1186/1687-9856-2012-6
            Copyright ©2012 Morrison et al.; licensee BioMed Central Ltd.

            This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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