Debate continues on the limitations of using body mass index (BMI) to assign youth overweight/obesity status. Calculated as weight in kilograms divided by height in meters squared, BMI might not be applicable in youth during periods of rapid growth. Although recent evidence has indicated that triponderal mass index (TMI, calculated as weight in kilograms divided by height in meters cubed) might have better accuracy in estimating youth body fat levels than BMI,1 its clinical importance in estimating adulthood outcomes has not been examined. Therefore, we assessed whether youth TMI and its combination with BMI or subscapular skinfold thickness (SST), compared with BMI alone, have better utility in estimating adult obesity-related outcomes.
From September 15 to December 5, 1980, a total of 3596 participants aged 3 to 18 years were randomly selected from the national register in the Cardiovascular Risk in Young Finns Study,2 which found an association between youth risk factors and adult cardiometabolic outcomes. Participants were followed up in 2001 (October 1, 2001, to January 21, 2002), 2007 (January 2, 2007, to February 13, 2008), and 2011 (January 10, 2011, to March 27, 2012). Excluded participants had type 1 diabetes (n = 20) or were pregnant at follow-up (n = 91). Our analyses, performed from April 1 to June 30, 2018, included 2626 participants who had weight, height, and SST measurements from baseline and obesity-related outcomes from follow-up. Participants or their parents gave written informed consent, and the study was approved by the Joint Commission on Ethics of the Turku University and the Turku University Central Hospital.
Type 2 diabetes (T2D) was confirmed if participants had a fasting plasma glucose level of 126 mg/dL or higher (to convert to millimoles per liter, multiply by 0.0555), had conditions diagnosed by a physician, had a hemoglobin A1c level of 6.5% or greater (to convert to proportion of total hemoglobin, multiply by 0.01) at the 2011 follow-up, used glucose-lowering medication at the 2007 and 2011 follow-up visits (including metformin, pioglitazone, glyburide, vildagliptin, and sitagliptin), or had T2D confirmed by the National Social Insurance Institution Drug Reimbursement Registry. Other adulthood outcomes were obesity (BMI, ≥30), hypertension, abnormal low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and high carotid intima-media thickness as previously defined.3 Mean SST was obtained from 3 measures using Harpenden skinfold calipers. To estimate and compare the association of youth BMI, TMI, SST, or their combinations with adult outcomes, logistic regression was used to estimate the odds ratio (OR) and area under the receiver operating characteristic curve values. The category-free net reclassification index was used to quantify the improvement in the association when a new marker (TMI or SST) was added to the model.
Youth TMI, BMI, and SST were significantly associated with adult T2D (TMI: OR, 1.22; 95% CI, 1.03-1.44; BMI: OR, 1.78; 95% CI, 1.54-2.07; and SST: OR, 1.52; 95% CI, 1.34 -1.72), obesity (TMI: OR, 1.61; 95% CI, 1.46-1.77; BMI: OR, 2.09; 95% CI, 1.89-2.32; and SST: OR, 1.80; 95% CI, 1.64-1.98), high carotid intima-media thickness (TMI: OR, 1.18; 95% CI, 1.06-1.33; BMI: OR, 1.19; 95% CI, 1.06-1.34; and SST: OR, 1.17; 95% CI, 1.06-1.31), and high low-density lipoprotein cholesterol level (TMI: OR, 0.85; 95% CI, 0.76-0.95; BMI: OR, 1.32; 95% CI, 1.20-1.46; and SST: OR, 1.11; 95% CI, 1.01-1.23) (Table). Other significant associations included BMI (OR, 1.64; 95% CI, 1.49-1.80) and SST (OR, 1.41; 95% CI, 1.29-1.53) with hypertension. Youth BMI had the best or an equal association with adult outcomes compared with TMI and SST (Table). The combination of TMI or SST with BMI did not improve or marginally improved the association compared with BMI alone. These findings remained similar after including age in the model.
Although superior to BMI in estimating body fat in adolescents,1 TMI or its combination with BMI or SST did not outperform BMI alone in estimating adult obesity-related outcomes in our study. This study had long-term follow-up, which allowed the examination between child obesity measures and clinically important outcomes in adulthood. An inherent issue for longitudinal studies, loss to follow-up, in this cohort was not differential from the original representative sample.3 One explanation for the study findings is that TMI does not account for fat distribution,4 which has been associated with the risk of developing T2D.5 The SST alone or in combination with TMI had comparable utility with BMI, suggesting that fat distribution might be more important than body fat percentage in determining T2D. In addition, TMI does not distinguish fat mass from muscle mass, although low muscle mass has been associated with an increased risk of incident T2D, independent of general obesity.6 Future studies should determine whether youth muscle mass is associated with adult obesity-related outcomes.
Accepted for Publication: July 6, 2018.
Published Online: October 15, 2018. doi:10.1001/jamapediatrics.2018.3034
Correction: This article was corrected on February 18, 2019, to add an affiliation for Dr Magussen.
Corresponding Author: Costan G. Magnussen, PhD, Menzies Institute for Medical Research, University of Tasmania, 17 Liverpool St, Hobart, Australia 7000 (firstname.lastname@example.org).
Author Contributions: Drs Raitakari and Magnussen contributed equally to the work. Dr Magnussen had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Concept and design: Wu, Hutri-Kähönen, Magnussen.
Acquisition, analysis, or interpretation of data: Wu, Buscot, Juonala, Viikari, Raitakari, Magnussen.
Drafting of the manuscript: Wu.
Critical revision of the manuscript for important intellectual content: Buscot, Juonala, Hutri-Kähönen, Viikari, Raitakari, Magnussen.
Statistical analysis: Wu, Buscot.
Obtained funding: Juonala, Raitakari.
Administrative, technical, or material support: Hutri-Kähönen, Viikari, Raitakari.
Supervision: Raitakari, Magnussen.
Conflict of Interest Disclosures: None reported.
Funding/Support: The Young Finns Study has been financially supported by grants 286284, 134309, 126925, 121584, 124282, 129378, 117787, and 41071 from the Academy of Finland; the Social Insurance Institution of Finland; grant X51001 from the Competitive State Research Financing of the Expert Responsibility area of Kuopio, Tampere, and Turku University Hospitals; Juho Vainio Foundation; Paavo Nurmi Foundation; Finnish Foundation for Cardiovascular Research; Finnish Cultural Foundation; The Sigrid Juselius Foundation; Tampere Tuberculosis Foundation; Emil Aaltonen Foundation; Yrjö Jahnsson Foundation; Signe and Ane Gyllenberg Foundation; Diabetes Research Foundation of Finnish Diabetes Association; and grant 755320 for TAXINOMISIS (A Multidisciplinary Approach for the Stratification of Patients With Carotid Artery Disease) from EU Horizon 2020; and grant 742927 for the MULTIEPIGEN (Ancestral Environmental Exposures and Offspring Health–A Multigenerational Epidemiologic Cohort Study Across 3 Generations) project from European Research Council; and the Tampere University Hospital Supporting Foundation. This study was supported by grant APP1098369 from the National Health and Medical Research Council Project. Dr Magnussen was supported by a grant 100849 from the National Heart Foundation of Australia Future Leader Fellowship. Dr Wu is supported by an Arthritis Foundation Australia–Australian Rheumatology Association Heald Fellowship, funded by the Australian Rheumatology Association and Vincent Fairfax Family Foundation.
Role of the Funder/Sponsor: The funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
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