Abstract
OBJECTIVE To examine childhood BMI, fasting glucose, and insulin in relation to incident adult type 2 diabetes mellitus (T2DM). RESEARCH DESIGN AND METHODS We used data from the International Childhood Cardiovascular Cohort (i3C) Consortium. Data included childhood (age 3–19 years) measurements obtained during the 1970s– 1990s; a health questionnaire, including self-report of adult T2DM (occurrence age, medication use) obtained at mean age 40 years; and a medical diagnosis registry (Finland). RESULTS The sample included 6,738 participants. Of these, 436 (6.5%) reported onset of T2DM between ages 20 and 59 (mean 40.8) years, and 86% of them reported use of a confirmed antidiabetic medication. BMI and glucose (age and sex standardized) were associated with incident T2DM after adjustment for cohort, country, sex, race, age, and calendar year of measurement. Increasing levels of childhood BMI and glucose were related to an incrementally increased risk of T2DM beginning at age 30 years, beginning at cut points <95th percentile for BMI and <100 mg/dL for glucose. Insulin was positively associated with adult T2DM after adjustment for BMI and glucose and added to T2DM discrimination. CONCLUSIONS Childhood BMI and glucose are predictors of adult T2DM at levels previously considered to be within the normal range. These easy-to-apply measurements are appealing from a clinical perspective. Fasting insulin has the potential to be an additional predictor.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2821-2829 |
| Number of pages | 9 |
| Journal | Diabetes care |
| Volume | 43 |
| Issue number | 11 |
| DOIs | |
| State | Published - Nov 2020 |
Bibliographical note
Funding Information:Funding. This work was supported by National Heart, Lung, and Blood Institute (grant R01-HL-121230). Harmonization and other data work before obtaining National Institutes of Health funding was supported by the Australian National Health and Medical Research Council Project (grants APP1098369 and APP211316); the Academy of Finland (grants 126925, 121584, 124282, 129378, 117787, and 41071); the Social Insurance Institution of Finland; Kuopio, Tampere, andTurkuUniversityHospitalMedicalFunds;Juho Vainio Foundation; Paavo Nurmi Foundation; Finnish Foundation of Cardiovascular Research; Finnish Cultural Foundation; Sigrid Juselius Foundation; and Yrjö Jahnsson Foundation. Duality of Interest. No potential conflicts of interest relevant to this article were reported. Author Contributions. T.H. wrote the manuscript and analyzed data. D.R.J. provided oversight for data analysis. A.R.S. contributed to the discussion and reviewed/edited the manuscript. L.A.B., T.L.B., S.R.D., T.D., N.H.-K., M.J., K.A.M., R.J.P., O.T.R., E.M.U., A.V., and J.G.W. contributed to the study design and data collection and reviewed/ edited the manuscript. J.S. contributed to study design and data collection and designed, reviewed, and edited the manuscript. J.S. is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and accuracy of the data analysis. Prior Presentation. Parts of this article were presented in abstract form at the American Heart Association EPI|Lifestyle 2020 Scientific Sessions, Phoenix, AZ, 3–6 March 2020.
Funding Information:
This work was supported by National Heart, Lung, and Blood Institute (grant R01-HL-121230). Harmonization and other data work before obtaining National Institutes of Health funding was supported by the Australian National Health and Medical Research Council Project (grants APP1098369 and APP211316); the Academy of Finland (grants 126925, 121584, 124282, 129378, 117787, and 41071); the Social Insurance Institution of Finland; Kuopio, Tampere, and Turku University Hospital Medical Funds; Juho Vainio Foundation; Paavo Nurmi Foundation; Finnish Foundation of Cardiovascular Research; Finnish Cultural Foundation; Sigrid Juselius Foun-dation; and Yrjö Jahnsson Foundation.
Publisher Copyright:
© 2020 by the American Diabetes Association.
