Early puberty among men drives type 2 diabetes risk
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Early puberty is associated with increased risk for type 2 diabetes among men, independent of prepubertal BMI, according to findings published in Diabetologia.
“Early puberty might be a novel risk factor for type 2 diabetes, and height and weight monitoring during adolescence is important to identify individuals at increased risk,” Jenny Kindblom, MD, PhD, associate professor at the Institute of Medicine at the Sahlgrenska Academy at University of Gothenburg, Sweden, and medical director at the Pediatric Clinical Research Center at the Sahlgrenska University Hospital, told Healio. “This study does not reveal the mechanisms for this association. Mechanistic studies are needed to understand how early puberty confers the increased risk.”
Kindblom and colleagues analyzed BMI data at age 8 and 20 years from 30,697 men participating in the BMI Epidemiology Study Gothenburg, a cohort of men born between 1945 and 1961 followed until December 2016 (mean follow-up, 30.7 years). Researchers used a modified infancy-childhood-puberty model to calculate age at peak height velocity — an assessment of pubertal timing in men — and determined type 2 diabetes status by linking data with the Swedish National Patient Register. Researchers used Cox proportional hazard regression analyses to estimate the association between pubertal timing and development of type 2 diabetes.
“We observed violations of the assumption of proportional hazards for the association between age at peak height velocity and the risk of type 2 diabetes and, therefore, split the follow-up period at the median age of type 2 diabetes diagnosis (57.2 years) to define early ( 57.2 years) and late (> 57.2 years) type 2 diabetes diagnosis,” the researchers wrote.
Within the cohort, 1,851 men developed type 2 diabetes. Mean age at peak height velocity was 14 years.
The researchers found that age at peak height velocity was inversely associated with early type 2 diabetes. For each 1-year earlier age at peak height velocity, risk for development of early type 2 diabetes was 28% higher (HR = 1.28 per year decrease; 95% CI, 1.21-1.36), whereas risk for development of late type 2 diabetes was 13% greater (HR = 1.13 per year decrease; 95% CI, 1.06-1.19).
Risk for developing early type 2 diabetes nearly doubles among men in the earliest age at peak height velocity quartile. The HR for men with an age at peak height velocity between 9.3 and 13.4 years, the highest quartile, was 1.97 compared with men with an age at peak height velocity between 14.8 and 17.9 years (95% CI, 1.63-2.38). HRs were 1.5 for men in quartile 2 (aged 13.4-14.1 years; 95% CI, 1.23-1.83) and 1.26 for men in quartile 3 (aged 14.1-14.8 years; 95% CI, 1.02-1.54) compared with men in quartile 1.
Associations between age at peak height velocity and risk for developing early and late type 2 diabetes were more similar after researchers adjusted models for BMI, with HRs of 1.24 for early type 2 diabetes (95% CI, 1.17-1.31) and 1.11 for late type 2 diabetes (95% CI, 1.05-1.17); however, results persisted after adjusting for birth weight and education levels.
Researchers also found that early age at peak height velocity predicted the likelihood of receiving insulin therapy for type 2 diabetes (n = 787), with an OR of 1.25 per year decrease in age at peak height velocity (95% CI, 1.17-1.33).
Researchers noted that, assuming a higher risk among those with an age at peak height velocity below the median, the population attributable factor indicates that 15% fewer men diagnosed with type 2 diabetes would have developed the disease had they not reached puberty early.
“These findings strengthen the concept that early puberty is part of an adverse trajectory during childhood and adolescence, and that a high BMI both before and after puberty contributes,” Kindblom said in a press release. “A continuous monitoring of height and weight development during not only childhood but also adolescence is of importance and might help identify individuals with increased risk.” – by Regina Schaffer
For more information:
Jenny Kindblom, MD, PhD, can be reached at the Centre for Bone and Arthritis Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Klinfarmlab, 45 Gothenburg, Sweden; email: jenny.kindblom@gu.se.
Disclosures: The authors report no relevant financial disclosures.
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