Diurnal cortisol and obesity in adolescents with and without Down syndrome.
Cortisol does not drive obesity in teens with Down syndrome, so look past stress hormones when planning weight care.
01Research in Context
What this study did
The team measured saliva cortisol three times a day in teens with Down syndrome and in typical peers.
They also checked body fat to see if higher weight went with higher stress hormone.
All kids were part of the same Spanish UP&DOWN project.
What they found
Cortisol waking curve looked the same in both groups.
Heavier teens did not have steeper or flatter slopes.
In plain words: stress hormone did not explain extra weight in DS.
How this fits with other research
Bertapelli et al. (2016) already showed that up to seven in ten youths with DS carry extra weight, so the null cortisol link is notable.
Mulder et al. (2020) used the same teen sample and found higher fat mass did pair with worse inflammatory markers — cortisol is simply not the pathway here.
McQuaid et al. (2024) muddied the water: in adults with DS, obesity hardly hurt metabolism except for leptin. The teen cortisol data now join that pattern — adiposity acts differently in DS at every age.
Esparza Ocampo et al. (2025) push the idea further: even normal-weight DS kids show poor lipids. Together these papers tell us to stop hunting single biomarkers and screen broadly.
Why it matters
You can stop blaming "high stress hormone" for weight gain in teens with Down syndrome. Focus your energy on food choice, activity, and sleep instead. Track waist-to-height ratio and lipids early, because cortisol won’t flag risk.
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02At a glance
03Original abstract
BACKGROUND: The prevalence of obesity in adolescents with Down syndrome (DS) far exceeds that in the general population. Cortisol, an adrenal hormone, can be obesogenic when dysregulated. However, the diurnal patterns of this hormone have not been examined among individuals with DS. Variations in adiposity may also mediate cortisol regulation. This study sought to examine diurnal cortisol patterns in adolescents with DS as well as associations between cortisol function and obesity. METHOD: A total of 32 adolescents, including 16 with DS and 16 controls with typical development (TD) of similar sex, age and Tanner pubertal stage (P > 0.05), participated in this preliminary study. Participants completed a dual-energy X-ray absorptiometry scan to measure body composition and collected saliva samples for cortisol measurements in the morning, afternoon and night. Linear mixed models with random intercepts and repeated measures were used to examine the daily trajectory of log-transformed cortisol concentrations between adolescents with and without DS. A second model examined the interaction between DS and presence of elevated body fatness. RESULTS: Adolescents with DS had higher morning cortisol concentrations (intercept = 0.37 μg/dL), but this was not significantly different than in TD (0.35 μg/dL, P = 0.16). Cortisol significantly declined across hours (b = -0.026 μg/dL/h, P < 0.001), but this decline also did not differ from that observed in TD (b = -0.024 μg/dL/h, P = 0.43). While cortisol levels were slightly higher among adolescents with elevated body fatness, this difference was not statistically significant (P > 0.05; d = 0.30). CONCLUSIONS: This study is the first to examine diurnal cortisol in DS but is limited in sample size. These preliminary findings suggest that diurnal cortisol patterns are not significantly different between adolescents with DS and TD and that cortisol levels are not associated with adiposity in this population. Despite these non-significant differences, youth with DS continue to be an 'at-risk' population for paediatric obesity in need of clinical intervention.
Journal of intellectual disability research : JIDR, 2019 · doi:10.1111/jir.12682