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

 Corresponding author: Ashraf T. Soliman Copyright © 2025 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution License 4.0. Dietary Composition and Endocrine Programming in Childhood and Adolescence: Implications for Growth and Pubertal Development Ashraf T. Soliman 1, *, Fawzia Alyafei 1, Shayma Ahmed 1, Noora AlHumaidi 1, Noor Hamed 1, Ahmed Elawwa 1, Nada Alaaraj 1, Sohair Seddig 1 and Nada Soliman 2 1 Department of Pediatrics, Division of Endocrinology, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar. 2 Primary Health Care Corporation & Ministry of Health, Alexandria, Egypt. World Journal of Advanced Research and Reviews, 2025, 28(02), 688-701 Publication history: Received on 27 September 2025; revised on 05 November 2025; accepted on 08 November 2025 Article DOI: https://doi.org/10.30574/wjarr.2025.28.2.3747 Abstract 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 animalversus 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, plantprotein/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 lowquality/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 World Journal of Advanced Research and Reviews, 2025, 28(02), 688-701 689 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. Energydense/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. Keywords: Pediatric Nutrition; Puberty Timing; GH–IGF-1 Axis; Ultra-Processed Foods; Protein Quality; Micronutrients 1. Introduction Nutrition profoundly modulates endocrine maturation, growth, and puberty in childhood and adolescence. Macronutrient profile influences insulin, leptin, GH–IGF-1 signaling, thyroid hormones, and adrenal steroids, collectively determining height velocity, bone age advancement, and pubertal tempo (1). Both undernutrition and caloric excess disrupt these axes and shift pubertal timing (2). High caloric intake, particularly from diets rich in refined carbohydrates and saturated fats, accelerates puberty through enhanced leptin–insulin signaling and stimulation of hypothalamic kisspeptin pathways (3). However, this association is not universal; some cohorts report inconsistent effects of adiposity on male puberty and ethnic differences in sensitivity to adiposity-driven pubertal advancement (4,5). Protein intake is a central nutritional regulator of growth and puberty. High animal-protein exposure in early childhood stimulates IGF-1 and adrenal androgen production, advancing puberty and increasing BMI (6). Yet recent pediatric epidemiologic data reveal paradoxical associations between very high total protein intake and increased stunting risk in some populations, raising debate on protein quality versus socioeconomic confounding (7). Vegetable protein has been associated with milder endocrine stimulation and delayed puberty, partly attributed to phytoestrogen–IGF-1 interactions (8). However, systematic reviews argue that isoflavones exert minimal endocrine disruption in well-nourished children (9), and several cohorts show normal or accelerated growth among soy consumers, challenging historical concerns (10). Undernutrition provides the opposite endocrine profile. Severe caloric deficiency suppresses GH–IGF-1, reduces gonadotropins, lowers thyroid hormones, and delays puberty (11). However, mild caloric restriction within balanced diets (e.g., Mediterranean models) may enhance metabolic resilience without impairing growth, introducing controversy over energy-restriction thresholds (12). Fruits and vegetables exert endocrine effects through antioxidants, polyphenols, and micronutrients; vitamin-C-rich produce supports adrenal steroidogenesis, while flax and soy modulate estrogen metabolism (16). Nevertheless, the clinical magnitude of these effects remains modest in iodineand nutrient-replete individuals (17). Micronutrients including zinc, iodine, vitamin D, and omega-3 fatty acids modulate endocrine glands, yet effects vary. Zinc deficiency correlates with delayed pubertal onset and impaired linear growth (13), but interventional data show mixed benefit from supplementation (14). Similarly, cruciferous vegetables possess goitrogens, yet clinically relevant thyroid suppression occurs mainly in iodine-deficient children (15). Ultra-processed foods and sugar-sweetened beverages independently predict earlier puberty and higher adiposity, but intervention trials show variable reversibility, implying critical developmental windows and potential epigenetic imprinting (18). This aligns with observations that childhood stress, circadian disruption, and endocrine-disrupting chemicals also influence puberty onset, complicating attributes to diet alone (19). This review synthesizes 25 years of mechanistic and clinical evidence on dietary composition and endocrine physiology in children, integrating points of consensus and debate regarding nutrition-driven endocrine programming (20). World Journal of Advanced Research and Reviews, 2025, 28(02), 688-701 690 Objectives • To assess how different dietary patterns influence endocrine function, growth, and pubertal development in children and adolescents. • To compare the effects of animal-based vs plant-based proteins, high-calorie diets, and undernutrition on hormonal and growth outcomes. • To explore the biological mechanisms linking diet composition to endocrine changes and pubertal timing. 2. Methods 2.1. Search Strategy A structured literature search was performed to identify studies evaluating the impact of dietary composition on endocrine function, growth, and pubertal development in children and adolescents. Searches were conducted in PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar (the latter used for secondary verification and citation chaining) covering the period from January 2000 to January 2025. A combination of Medical Subject Headings (MeSH) and keywords was used, including terms such as child, adolescent, diet, nutrition, macronutrients, animal protein, plant protein, energy intake, micronutrients, puberty, pubertal timing, growth, IGF-1, thyroid, adrenal, endocrine function, leptin, insulin, obesity, malnutrition, stunting, phytoestrogens, goitrogens, Mediterranean diet, and ultra-processed food. In addition, the reference lists of relevant articles and pediatric endocrine and nutrition guidelines were manually screened to capture any additional eligible studies. 2.2. Inclusion Criteria Studies were eligible for inclusion if they involved human participants aged 1–18 years and evaluated dietary exposures such as caloric intake, dietary patterns, animal versus plant protein sources, micronutrient intake, fruit and vegetable consumption, malnutrition, or ultra-processed food intake. Eligible study designs included randomized controlled trials, cohort and case–control studies, longitudinal observational studies, and systematic reviews or meta-analyses published in English between 2000 and 2025. Studies were required to report endocrine outcomes, including IGF-1, insulin, leptin, thyroid and adrenal hormone levels—alongside growth measures and pubertal development indicators such as height velocity, BMI, Tanner staging, or age at menarche. Only human research was included. 2.3. Exclusion Criteria Studies were excluded if they focused exclusively on adult populations, were conducted in animals or in vitro, or lacked clear nutritional exposure data or endocrine-related outcomes. Articles were also excluded if they consisted solely of narrative commentary or non-systematic reviews, examined pharmacologic supplementation in the absence of habitual dietary context, or addressed endocrine disorders unrelated to nutrition—such as congenital endocrine syndromes— without assessing dietary influence. 2.4. Data Extraction Two reviewers independently extracted relevant data from each eligible study, including study design, sample size, country, and participant age range. Extracted information also covered the nature of dietary exposures—such as highcalorie intake, animal versus plant protein, micronutrient status, fruit and vegetable consumption, and undernutrition— as well as reported endocrine outcomes, including IGF-1, sex steroids, thyroid and adrenal hormones, insulin, and leptin levels. Growth and pubertal parameters were recorded when available, such as height velocity, BMI, Tanner staging, and age at menarche. Mechanistic or biochemical pathways proposed by the studies to explain diet–endocrine interactions were also documented to support synthesis and mechanistic interpretation. 2.5. Quality Assessment Methodological quality of included studies was assessed using the NIH Quality Assessment Tool for observational studies, the Cochrane Risk of Bias tool for randomized trials, and AMSTAR-2 for systematic reviews. Evaluation criteria included study design and sampling methods, validity of dietary assessment instruments (such as food-frequency questionnaires and dietary recalls), accuracy and standardization of hormonal assays, adequacy of adjustment for confounders—including BMI and socioeconomic status—and completeness of follow-up. Studies with substantial methodological limitations or high risk of bias were excluded from primary synthesis. Given the considerable heterogeneity in dietary exposures, endocrine outcomes, and methodological approaches, a narrative synthesis was used. Where available, effect sizes, odds ratios or risk ratios, confidence intervals, and trends in World Journal of Advanced Research and Reviews, 2025, 28(02), 688-701 691 endocrine markers and pubertal outcomes were extracted to inform interpretation. A formal meta-analysis was not performed due to variability in study design, exposure definitions, and outcome measurements. This review adhered to PRISMA principles for structured evidence synthesis. Ethical approval was not required, as no new human data was collected. Figure 1 PRISMA Flow Diagram for Study Selection The PRISMA flow diagram summarizes the screening process, starting with 180 identified records. After removing duplicates and screening titles and abstracts, 38 full-text articles were reviewed. Sixteen were excluded for reasons including irrelevance to dietary exposures, lack of endocrine or growth outcomes, insufficient data, or methodological limitations. Ultimately, 22 studies met the inclusion criteria and were analyzed, demonstrating a rigorous and transparent study-selection process. World Journal of Advanced Research and Reviews, 2025, 28(02), 688-701 692 3. Results Table 1 Acute and chronic endocrine effects of diet on growth and pubertal outcomes in children and adolescents (2000–2025) Dietary exposure (ref no.) Acute endocrine effects Chronic growth & pubertal outcomes Key mechanistic notes High-calorie / high– glycemic-load diets (3,4) ↑ insulin, ↑ leptin, ↑ kisspeptin signaling Earlier puberty, ↑ BMI/adiposity (girls>boys) Adiposity stimulates hypothalamic–gonadal axis High animal-protein intake (6,8) ↑ IGF-1, ↑ adrenal androgens, ↑ mTOR Earlier menarche & PHV, ↑ BMI Protein-IGF-sex steroids pathway activation Higher plant protein (soy/legumes) (8,9,10) Mild IGF-1 ↑; phytoestrogen modulation of ER/IGF-1 Neutral or slightly delayed puberty; leaner phenotype Phytoestrogens increase SHBG, modulate ER signaling Very high total protein, low diet quality (7) Variable insulin/IGF-1 rise Paradoxical ↑ stunting risk (contextual SES effect) May reflect dietary imbalance, micronutrient deficiency Low protein / chronic undernutrition (11) ↓ IGF-1; GH resistance; ↓ T3 & gonadotropins Delayed puberty, ↓ height velocity & BMI Energy/protein deficiency suppresses GH-IGF axis High saturated fat / refined carbs (3) ↑ insulin/leptin; ↑ inflammation ↑ adiposity, faster pubertal tempo Overlaps with hypercaloric Westernized pattern High unsaturated fat / omega-3 rich patterns (21) ↓ inflammation; ↑ adiponectin Normal puberty; favorable metabolic profile Modulates inflammatory and insulin pathways Fiber-rich whole-food diets (21) Improved leptin/insulin sensitivity ↓ obesity risk; neutral to healthy puberty timing Supports gutbrain/endocrine axis Ultra-processed foods / sugar-sweetened beverages (18) Rapid glycemic spikes; ↑ leptin Earlier puberty, ↑ adiposity Independent predictor of early thelarche High fructose intake (22) ↑ hepatic lipogenesis; ↑ insulin resistance ↑ adiposity; potential puberty advancement Fructose amplifies metabolic inflammation Dairy (adequate intake) (23) Post-prandial IGF-1 ↑ Normal growth; unclear effect on puberty timing Effect size < total animalprotein effect Mediterranean diet (12) Improved insulin sensitivity; antioxidant effects Optimal growth; no pubertal delay when energy adequate Balanced anti-inflammatory nutritional pattern Adequate iodine + crucifers cooked (15) Euthyroid stability Normal growth/puberty Goitrogen risk clinically negligible with iodine sufficiency High raw crucifers + low iodine (15) ↓ thyroid hormone production Hypothyroid-mediated delayed growth/puberty Goitrogens inhibit thyroid peroxidase/iodine uptake Phytoestrogen-rich foods (soy/flax) with iodine replete status (9,10) Mild estrogenic/antiestrogenic balance Neutral to slight pubertal delay; lean phenotype ER modulation + SHBG ↑ Vitamin-C rich fruits & adrenal cofactors (16) Supports adrenal steroidogenesis Maintains stress physiology; no pubertal acceleration Vitamin-C cofactor for adrenal enzymes Abbreviations: IGF-1 = Insulin-like growth factor-1; GH = Growth hormone; PHV = Peak height velocity; BMI = Body mass index; ER = Estrogen receptor; SHBG = Sex hormone–binding globulin; T3 = Triiodothyronine; UPF = Ultra-processed foods; ω-3 = Omega-3 fatty acids; SES = Socioeconomic status. World Journal of Advanced Research and Reviews, 2025, 28(02), 688-701 693 Table 1 summarizes the acute hormonal shifts and long-term growth-pubertal consequences associated with major dietary patterns in children and adolescents. Diets rich in calories, saturated fats, and rapidly absorbed carbohydrates consistently produce rapid rises in insulin and leptin, activating hypothalamic kisspeptin pathways and advancing pubertal timing, particularly in girls, whereas ultra-processed food intake enhances metabolic load and adiposity with similar pubertal acceleration. Animal-protein–dominant diets strongly stimulate IGF-1 and adrenal androgen secretion, aligning with earlier pubertal onset and increased BMI, while high plant-protein and fiber-rich patterns show milder endocrine stimulation and may modestly delay puberty when overall nutrition remains adequate. Conversely, insufficient protein or chronic malnutrition suppresses the IGF-1 secretion and thyroid-gonadal signaling, delaying puberty and impairing growth. Important considerations include the finding that very high-protein diets of poor quality in disadvantaged settings may still be associated with stunting, that cruciferous vegetables and soy have little impact on thyroid function when iodine intake is sufficient, and that dairy is generally neutral for pubertal timing when overall energy and protein intake are adequate. Collectively, the evidence indicates that diet quality, macronutrient pattern, and micronutrient sufficiency—not merely energy quantity—shape endocrine programming, growth tempo, and pubertal progression across youth. Table 2 Long-term endocrine, growth, and pubertal outcomes by dietary pattern, with endocrine axis and mechanisms (children/adolescents, 2000–2025) Dietary pattern (ref no.) Long-term growth & pubertal outcome Predominant endocrine axis Mechanistic pathways Key evidence / clinical notes High-calorie / highglycemic-load (3,4) Earlier pubertal onset/tempo; ↑ BMI/adiposity (girls>boys) HPG; insulin– leptin Hyperinsulinemia/leptin → hypothalamic kisspeptin activation; adipose signaling to GnRH Consistent association in girls; variable in boys (3,4) Animal-protein dominant (6,8) Earlier menarche/PHV; ↑ BMI GH–IGF-1; adrenal androgens; HPG ↑ IGF-1, ↑ adrenal androgen output; mTOR activation → growth and earlier puberty Robust across cohorts (6,8) Plant-protein predominant (soy/legumes/mixed) (8,9,10) Neutral to slightly delayed puberty; leaner phenotype GH–IGF-1; HPG (modest) Phytoestrogens modulate ER & SHBG; milder IGF-1 stimulation vs animal protein Minimal endocrine disruption in iodine-replete settings (9,10) Very high total protein with low diet quality (7) Context-linked ↑ stunting risk; mixed BMI effects GH–IGF-1 (dysregulated) Protein excess without micronutrients → growth constraint; SES confounding Paradox noted in population data (7) Low protein / chronic undernutrition (11) Delayed puberty; ↓ height velocity; ↓ BMI GH–IGF-1; HPG; thyroid GH resistance, ↓ IGF-1; hypothalamic suppression; ↓ T3 Classic suppression profile (11) Ultra-processed foods / SSBs (18,22) Earlier puberty; ↑ adiposity trajectory Insulin–leptin; HPG Rapid glycemic excursions → hyperinsulinemia/leptin; adiposity-driven GnRH activation Independent predictor of early timing (18); fructose risks (22) High fructose load (22) ↑ Adiposity; possible advancement of puberty Insulin–leptin; hepatic– metabolic Hepatic DNL, insulin resistance, low-grade inflammation Pediatric metabolic risk signal (22) Dairy-inclusive balanced diet (23) Normal growth; no consistent shift in puberty timing GH–IGF-1 (modest) Small IGF-1 rise without robust HPG acceleration Generally neutral for puberty when diet is balanced (23) World Journal of Advanced Research and Reviews, 2025, 28(02), 688-701 694 Mediterranean-style (12) Healthy growth/weight; physiologic puberty timing Insulin–leptin; antiinflammatory milieu Improved insulin sensitivity; antioxidant/antiinflammatory effects Protective, balanced pattern (12) Omega-3 / fiber-rich whole-foods (21) Favorable metabolic profile; neutral timing Insulin–leptin; adrenal stress modulation Anti-inflammatory actions; adiponectin ↑; gut–brain axis support Benefits on metabolic risk, not accelerating puberty (21) Crucifers/soy with adequate iodine (15,9,10) Normal growth/thyroid; neutral puberty Thyroid; HPG (soy modest) Goitrogen risk negligible when iodine-replete; phytoestrogen effects mild Safety hinges on iodine sufficiency (15); minimal impact (9,10) High raw crucifers + low iodine (15) Risk of hypothyroidmediated growth delay Thyroid Goitrogens inhibit iodine uptake/TPO; ↓ T4/T3 Contextdependent risk (15) Abbreviations: HPG = hypothalamic–pituitary–gonadal; GH = growth hormone; IGF-1 = insulin-like growth factor-1; PHV = peak height velocity; BMI = body mass index; ER = estrogen receptor; SHBG = sex hormone–binding globulin; SSBs = sugar-sweetened beverages; DNL = de novo lipogenesis; TPO = thyroid peroxidase. Table 2 shows that across long-term outcomes, energy surplus and animal-protein–dominant diets consistently align with earlier puberty and higher adiposity via insulin–leptin–kisspeptin and IGF-1–adrenal androgen pathways, while plant-protein–predominant, Mediterranean, and omega-3/fiber-rich patterns support normal pubertal timing and healthier metabolic trajectories. Undernutrition predictably delays puberty through GH–IGF-1 and thyroid suppression, and UPF/SSB and fructose-heavy patterns track with adiposity and earlier timing. Thyroid effects from crucifers/soy are clinically minimal when iodine intake is adequate, with risk emerging primarily under iodine deficiency. Dairy’s impact on puberty is generally neutral when overall energy and protein are balanced. Table 3 Growth/development domains: associated diets, long-term findings, mechanisms, and evidence strength (children/adolescents, 2000–2025) Growth / Development Domain Diets Associated (ref no.) Long-Term Findings Mechanistic Contribution Evidence Strength* Height velocity & final height Animal-protein dominant (6,8); Low protein/undernutrition (11); Dairy within balanced diet (23) Animal protein associated with greater height gains and earlier PHV; undernutrition → reduced height velocity and shorter adult stature; dairy neutral– supportive when energy/protein adequate IGF-1 upregulation (animal protein); GH resistance with energy/protein deficit; modest IGF-1 rise with dairy High (6,8,11,23) BMI trajectory / adiposity High-calorie/high-GL & refined carbs (3,4); Ultra-processed foods/SSBs (18); High fructose (22); Mediterranean/wholeObesogenic patterns → higher BMI trajectory; UPF/SSBs and fructose predict adiposity; Mediterranean/ω Hyperinsulinemia/lept in signaling; hepatic DNL & insulin resistance; antiinflammatory/adipone ctin effects with ω3/fiber High for obesogenic & UPF/SSBs (3,4,18,22); Moderate protective signal (12,21) World Journal of Advanced Research and Reviews, 2025, 28(02), 688-701 695 food ω-3/fiber patterns (12,21) -3/fiber patterns associated with healthier BMI Bone maturation & skeletal health Adequate dairy/protein within balanced diet (23); Undernutrition/low protein (11); Mediterranean pattern (12) Adequate dairy/protein supports bone accrual; undernutrition linked to reduced bone mass; Mediterranean diet compatible with normal skeletal development IGF-1-mediated bone formation; nutrient sufficiency (calcium, protein); antiinflammatory milieu Moderate–High (11,12,23) Puberty onset & tempo High-calorie/high-GL (3,4); Animal protein (6,8); Plant protein/soy (8,9,10); Mediterranean pattern (12); UPF/SSBs & fructose (18,22) Energy surplus and animal protein → earlier puberty; plantprotein patterns neutral to slight delay; Mediterranean pattern neutral/physiolog ic; UPF/SSBs and fructose linked to earlier timing Insulin–leptin– kisspeptin stimulation; IGF-1/adrenal androgen increases; phytoestrogen modulation of ER/SHBG (mild); improved insulin sensitivity with Mediterranean High for earlier puberty with energy surplus/animal protein (3,4,6,8,18,22); Moderate for plantprotein/Mediterran ean neutrality (9,10,12) Metabolic/endocr ine programming Highcalorie/UPF/SSBs/fruct ose (3,18,22); Plantprotein/whole-food ω3/fiber (9,12,21); Iodine-adequate crucifers/soy (15,9,10) Obesogenic/fruct ose patterns program insulin resistance and adverse adipokine profiles; plantprotein/ω-3/fiber patterns support healthier metabolic and endocrine profiles; crucifers/soy neutral for thyroid when iodine is sufficient Insulin/leptin resistance vs. antiinflammatory signaling; gut–brain axis; thyroid homeostasis with iodine sufficiency High for adverse programming with UPF/fructose (3,18,22); Moderate for protective patterns; High for thyroid neutrality with adequate iodine (15) Abbreviations: PHV = peak height velocity; GL = glycemic load; IGF-1 = insulin-like growth factor-1; GH = growth hormone; SSBs = sugar-sweetened beverages; ω-3 = omega-3 fatty acids; ER = estrogen receptor; SHBG = sex hormone–binding globulin; DNL = de novo lipogenesis. Table 3 reveals that across domains, energy surplus and ultra-processed/fructose-rich patterns consistently drive higher BMI, earlier puberty, and adverse metabolic programming via insulin–leptin–kisspeptin and hepatic insulinresistance pathways (3,4,18,22). Animal-protein–dominant diets elevate IGF-1/adrenal androgens and are linked to earlier pubertal tempo and greater height velocity around PHV (6,8), while plant-protein and Mediterranean/ω-3/fiberrich patterns support physiologic pubertal timing and healthier BMI with anti-inflammatory and insulin-sensitizing effects (9,12,21). Undernutrition predictably suppresses the GH–IGF-1 axis and bone accrual, delaying puberty and impairing growth (11), and crucifers/soy remain thyroid-neutral when iodine intake is adequate (15,9,10). World Journal of Advanced Research and Reviews, 2025, 28(02), 688-701 696 Table 4 Comparative Impact of Major Dietary Patterns on Growth Velocity and Pubertal Timing in Children and Adolescents Diet Pattern Growth Height Velocity Pubertal Timing Evidence Strength Animal-protein dominant ↑ Earlier Strong High-calorie / UPF / fructose Neutral or ↑ (BMI effect dominant) Earlier Strong Plant-protein / legume dominant Normal Neutral → Slight delay Moderate Mediterranean / ω-3 / fiber Normal Physiologic Strong Low protein / undernutrition ↓ Delayed Strong Balanced dairy patterns Normal Neutral Moderate Crucifers/soy + adequate iodine Normal Neutral → Slight delay Moderate Conceptual impact of dietary patterns on growth and pubertal timing in children/adolescents (2000–2025). Animalprotein and high-calorie/UPF/fructose patterns trend toward earlier puberty (via IGF-1, insulin–leptin–kisspeptin), plant-protein and Mediterranean/ω-3/fiber are neutral to protective, and undernutrition delays growth and puberty through GH–IGF-1 and thyroid suppression. Effects of dairy and crucifers/soy are generally neutral when overall energy/protein and iodine are adequate (3–12, 15, 18, 21–23). Table 5 Cochrane Risk-of-Bias Assessment for Included Evidence Study (Reference) Design D1 Randomization D2 Deviations D3 Missing Data D4 Outcome Measures D5 Reporting Overall RoB Brix 2020 (24) Prospective cohort — Low Low Low Low Low Cheng 2010 (25) Prospective cohort — Low Low Low Low Low Remer 2010 (26) Prospective cohort — Low Low Some concerns Low Some concerns Günther 2010 (27) Prospective cohort — Low Low Some concerns Low Some concerns Biro 2013 (28) Prospective cohort — Low Low Low Low Low Wang 2002 (29) Crosssectional — Some concerns Low Some concerns Some concerns Some concerns Soliman et al. (PEM) (30) Clinical cohort — Low Low Some concerns Some concerns Some concerns Imdad 2017 (31) RCT metaanalysis Low Low Low Low Low Low Brown 2009 (32) Metaanalysis Low Low Low Low Low Low Messina 2022 (33) Narrative + cohort review — Some concerns Low Low Some concerns Some concerns Low risk = robust design/adjustment, Some concerns = observational or confounding risk, High risk = substantial bias concerns