Dietary Composition and Endocrine Programming in Childhood and Adolescence: Implications for Growth and Pubertal Development

Background: Diet quality and composition modulate pediatric endocrine axes—GH–IGF-1, hypothalamic–pituitary–gonadal, thyroid, and adrenal—thereby shaping height velocity, bone maturation, adiposity, and pubertal timing. Evidence from the last 25 years suggests energy surplus, macronutrient balance, and micronutrient sufficiency differentially influence growth and maturation, but controversies remain (e.g., animal vs plant protein, ultra-processed foods, and soy/phytoestrogens).

Objectives: (1) Synthesize evidence on how dietary patterns affect endocrine function, growth, and puberty in children/adolescents; (2) compare animal- versus plant-protein, high-calorie/UPF/fructose, mediterranean/wholefood, and undernutrition patterns; (3) explain biological mechanisms linking diet with endocrine outcomes.

Methods: We searched PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar (January 2000–January 2025) for RCTs, cohorts, case–control, longitudinal observational studies, and systematic reviews in humans aged 1–18 years, in English, reporting dietary exposures and endocrine/growth/puberty outcomes. Two reviewers performed screening and extraction; quality was appraised using NIH tools (observational), Cochrane RoB (trials), and AMSTAR-2 (reviews). Given heterogeneity, we conducted narrative synthesis (effect sizes, OR/RR, CIs when available). PRISMA flow: 180 records → 22 included studies.

Results: Across 22 studies, consistent patterns emerged. High-calorie and high glycemic-load diets, ultra-processed foods (UPF), and high-fructose intake were linked to earlier puberty and higher adiposity; cohorts quantifying timing showed mean advancement of pubertal milestones by ~3–6 months in overweight/obesity, with dose-response gradients. Mechanistically, insulin/leptin elevation reduces SHBG, stimulates hypothalamic kisspeptin and GnRH pulsatility, and advances LH/FSH and sex-steroid output; hepatic lipogenesis and leptin resistance with fructose/UPF reinforce these effects. Animal-protein-dominant diets increased IGF-1 and adrenal androgens, aligning with earlier menarche/APHV and higher BMI; mTOR signaling and IGF-1 mediation predominated. By contrast, plant-protein/legume-rich patterns (with adequate energy) were neutral or modestly delaying for puberty and associated with leaner phenotype, plausibly via higher SHBG, milder IGF-1 stimulation, improved insulin sensitivity, and benign phytoestrogen effects. Mediterranean/wholefood, ω-3/fiber-rich patterns supported physiologic pubertal tempo and normal growth, with anti-inflammatory and insulin-sensitizing mechanisms. Chronic undernutrition and low-quality/low-protein diets suppressed IGF-1 (GH resistance), lowered gonadotropins and T3, and delayed pubertal onset with reduced height velocity. Thyroid outcomes were context-dependent: crucifers/soy were largely thyroid-neutral in iodine-replete settings; risk of hypothyroid-mediated growth delay emerged primarily with low iodine. Dairy within balanced diets modestly raised post-prandial IGF-1 but showed no consistent shift in pubertal timing. Heterogeneity reflected population, diet quality, iodine/micronutrient status, and ethnicity.

Conclusions: Diet composition meaningfully programs pediatric endocrine function and maturation. Energy-dense/UPF/fructose and animal-protein-dominant patterns tend to accelerate puberty; Mediterranean/plant-forward patterns maintain physiological tempo; undernutrition delays growth and puberty. Clinical focus should prioritize nutrient-dense, whole-food patterns, ensure protein and micronutrient adequacy (zinc, vitamin D, iodine), and limit UPF and sugary beverages during critical developmental windows.