Body mass index across development and adolescent hair cortisol: the role of persistence, variability, and timing of exposure: Pediatrics

• Published in: International Journal of Obesity 2025, Vol.49 (1), p.125-132
• Main Authors: Cantave, Christina Y., Ruttle, Paula L., Coté, Sylvana M., Lupien, Sonia J., Geoffroy, Marie-Claude, Vitaro, Frank, Brendgen, Mara, Tremblay, Richard, Boivin, Michel, Ouellet-Morin, Isabelle
• Format: Article
• Language: English
• Subjects: 13/51; 692/163; 692/499; Epidemiology; Health Promotion and Disease Prevention; Internal Medicine; Medicine; Medicine & Public Health; Metabolic Diseases; Public Health
• ISSN: 0307-0565; 1476-5497
• DOI: 10.1038/s41366-024-01640-1

Background Research suggests a putative role of the glucocorticoid stress hormone cortisol in the accumulation of adiposity. However, obesity and weight fluctuations may also wear and tear physiological systems promoting adaptation, affecting cortisol secretion. This possibility remains scarcely investigated in longitudinal research. This study tests whether trajectories of body mass index (BMI) across the first 15 years of life are associated with hair cortisol concentration (HCC) measured two years later and whether variability in BMI and timing matter. Methods BMI (kg/m 2 ) was prospectively measured at twelve occasions between age 5 months and 15 years. Hair was sampled at age 17 in 565 participants. Sex, family socioeconomic status, and BMI measured concurrently to HCC were considered as control variables. Results Latent class analyses identified three BMI trajectories: “low-stable” (59.2%, n  = 946), “moderate” (32.6%, n  = 507), and “high-rising” (8.2%, n = 128). BMI variability was computed by dividing the standard deviation of an individual’s BMI measurements by the mean of these measurements. Findings revealed linear effects, such that higher HCC was noted for participants with moderate BMI trajectories in comparison to low-stable youth ( β  = 0.10, p  = 0.03, 95% confidence interval (CI) = [0.02–0.40]); however, this association was not detected in the high-rising BMI youth ( β  = −0.02, p  = 0.71, 95% CI = [−0.47–0.32]). Higher BMI variability across development predicted higher cortisol ( β  = 0.17, p  = 0.003, 95% CI = [0.10–4.91]), additively to the contribution of BMI trajectories. BMI variability in childhood was responsible for that finding, possibly suggesting a timing effect. Conclusions This study strengthens empirical support for BMI-HCC association and suggests that more attention should be devoted to BMI fluctuations in addition to persistent trajectories of BMI.