Background: Vitamin D modulates innate and adaptive immunity and has been investigated for preventing pediatric respiratory infections. Objective: To assess the effects of vitamin D supplementation on respiratory tract infections (RTIs), including upper RTIs, lower RTIs/recurrent pneumonia, and hospitalization/clinical severity in children and adolescents. Methods: Systematic review and random-effects meta-analysis of 16 publications, of which 13 contributed to quantitative synthesis. Twenty-four effect estimates were pooled, eight per outcome. The odds ratio (OR) was analyzed on its natural logarithmic scale (logOR), using restricted maximum likelihood (REML) estimation and Knapp-Hartung (KH) adjusted inference. Where necessary, risk ratios (RRs), hazard ratios (HRs), and incidence rate ratios (IRRs) were approximated on the logOR scale. Results: For respiratory infection/upper RTI, pooled logOR was −0.284 (KH-adjusted 95% confidence interval [CI]: −0.678 to 0.110; OR 0.753; p = 0.132; I ² = 97.2%). For lower RTI/recurrent pneumonia, logOR was −0.445 (95% CI: −0.987 to 0.097; OR 0.641; p = 0.093; I ² = 89.5%). For hospitalization/clinical severity, logOR was −0.609 (95% CI: −1.134 to −0.083; OR 0.544; p = 0.029; I ² = 78.3%). Conclusions: Pooled estimates favored supplementation in direction for all three groups, although confidence intervals included the null for the first two. Heterogeneity was substantial, and the results are limited by approximations among effect measures, clinically diverse endpoints, and potentially correlated effects from individual studies.

Introduction: Obesity and metabolic syndrome are conditions associated with chronic low-grade inflammation, characterized by elevated markers such as high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). Intermittent fasting and ketogenic diets have independently demonstrated anti-inflammatory effects, yet a quantitative synthesis on the combined effect of these strategies is lacking. Objective: To synthesize the available evidence on the effects of intermittent fasting combined with a ketogenic or carnivore diet on hs-CRP, IL-6, and TNF-α levels in adults with overweight, obesity, or metabolic syndrome. Methods: A meta-analysis was conducted in accordance with PRISMA guidelines, with searches performed in PubMed/MEDLINE, ScienceDirect, and Google Scholar. Studies including adults (≥18 years) with overweight, obesity, or metabolic syndrome undergoing intermittent fasting combined with a ketogenic or carnivore diet and reporting hs-CRP, IL-6, or TNF-α outcomes were included. Inflammatory markers were dichotomized based on clinical cutoff points. A random-effects model was used, with Odds Ratio (OR) as the effect measure. Heterogeneity was assessed using the Q test and I² index. Results: Seven studies comprising 301 participants were included. A significant reduction was observed across all three markers: hs-CRP (OR 0.21; 95% CI: 0.07–0.68; p=0.017), IL-6 (OR 0.27; 95% CI: 0.08–0.87; p=0.032), and TNF-α (OR 0.43; 95% CI: 0.21–0.90; p=0.026). Substantial heterogeneity was detected for hs-CRP (I²=73.3%) and IL-6 (I²=72.3%), while TNF-α showed moderate heterogeneity (I²=35.9%). The most pronounced effects were found in studies combining fasting with a ketogenic diet. Conclusion: The combination of intermittent fasting with a ketogenic diet significantly reduces hs-CRP, IL-6, and TNF-α levels in adults with overweight, obesity, or metabolic syndrome, representing a promising non-pharmacological strategy for modulating chronic inflammation in this population. The observed heterogeneity warrants caution in generalizing these findings.

Background: Vitamin B12 is essential for one-carbon metabolism, deoxyribonucleic acid (DNA) synthesis, and myelination, and inadequate maternal status during pregnancy may influence fetal growth and child neurodevelopment. Objective: To evaluate the association between maternal vitamin B12 status and perinatal and child neurodevelopmental outcomes. Methods: We conducted a systematic review and meta-analysis of observational studies and randomized clinical trials. The main outcomes were preterm birth, low birth weight, small for gestational age (SGA), and cognitive/global development. For binary outcomes, the natural logarithm of the relative risk (logRR) was the primary analytical effect measure; for neurodevelopment, Hedges g was used. Random-effects models were fitted, between-study variance was estimated by restricted maximum likelihood (REML), and inference used Knapp-Hartung (KH) adjustment. Results: For preterm birth, nine estimates yielded a pooled logRR of 0.190 (95% confidence interval [95% CI] KH: –0.046 to 0.427; p = 0.101; I2 = 19.2%). For low birth weight, nine estimates yielded a pooled logRR of 0.136 (95% CI KH: –0.013 to 0.286; p = 0.069; I2 = 4.8%). For SGA, six estimates yielded a pooled logRR of 0.047 (95% CI KH: –0.083 to 0.177; p = 0.397; I2 = 0%). Cognitive/global development, assessed in five independent studies, showed a pooled Hedges g of 0.266 (95% CI KH: 0.034 to 0.499; p = 0.034; I2 = 55.7%). Conclusions: logRR estimates for preterm birth and low birth weight were directionally compatible with higher risk among mothers with lower vitamin B12 availability, but their 95% CIs included the null. No consistent association was observed for SGA. Higher maternal vitamin B12 availability or supplementation was associated with a small favorable effect on cognitive/global development, with moderate heterogeneity.

Introduction: Growth hormone (GH) plays a key role in metabolic adaptation to fasting by stimulating lipolysis and preserving lean mass. However, there is no consensus on the magnitude of the GH response to short-term fasting in healthy adults. Objective: To systematically review the literature on the effect of 24-48 hour fasting on GH levels in healthy adults. Methods: A search was conducted in PubMed, Google Scholar, and Science Direct (2000-2025). Original studies with healthy adults undergoing 24-48h fasting and measuring GH as an outcome were included. A narrative synthesis was performed due to study heterogeneity. Results: Six studies (n=119 participants) were included. Twenty-four-hour fasting increased GH by 3-5 fold, without IGF-1 elevation (hepatic resistance). Prolonged fasting (≥36h) intensified the response, increasing GH pulse frequency and amplitude. The GH increase was associated with decreased insulin and leptin, stimulating lipolysis. Individuals with low basal GH showed greater relative increases. Discussion: Twenty-four to forty-eight-hour fasting significantly increases GH secretion in healthy adults, with a more pronounced response during prolonged fasting and in individuals with low basal GH. The GH-IGF-1 dissociation suggests adaptive hepatic resistance.

Introduction: Iron deficiency during pregnancy and early childhood may affect myelination, neurotransmission, and neural network maturation, with potential consequences for motor, cognitive, and language development. Objective: To quantitatively synthesize the effects of iron supplementation on motor, cognitive/global, and language development by integrating the original dataset with a complementary search for original studies. Methods: Systematic review with random-effects quantitative synthesis. The expanded review included 11 publications. Continuous outcomes and adjusted estimates were harmonized to log odds ratios (logOR), with positive values indicating better performance with greater iron exposure. Between-study variance was estimated by restricted maximum likelihood (REML). Ten motor, 11 cognitive/global, and 7 language effect estimates were pooled. Results: For motor development, the pooled effect was logOR 0.31 (95% CI 0.14 to 0.48; OR 1.36; p < 0.001; τ² = 0.044; I² = 69.3%). For cognitive/global development, the pooled effect was logOR 0.11 (95% CI -0.10 to 0.33; OR 1.12; p = 0.307; τ² = 0.088; I² = 74.8%). For language, the pooled effect was logOR -0.02 (95% CI -0.26 to 0.21; OR 0.98; p = 0.851; τ² = 0.048; I² = 50.7%). Conclusion: The expanded synthesis yielded a positive pooled estimate for motor development, whereas pooled cognitive/global and language estimates remained close to the null. Effect magnitude and direction varied across populations, timing and dose of supplementation, baseline iron status, and age at assessment.

Background: Intermittent fasting and carbohydrate-restricted dietary strategies have been investigated for improving insulin resistance and glycemic control, but interventions and study populations differ substantially. Objective: To summarize reported effects on fasting insulin, HOMAIR, fasting glucose, HbA1c, and the GH/IGF-1 axis in adults with excess weight or metabolic disorders. Methods: A systematic review of controlled dietary interventions was described using searches of PubMed, ScienceDirect, and Google Scholar for reports published from January 2016 to March 2026. Random-effects standardized mean differences (SMDs) were transcribed from the corresponding supplementary forest plots. Results: The available plots include eight estimates for insulin (SMD -0.79; 95% CI -1.03 to -0.56; I² 22.17%), seven for HOMA-IR (-0.84; -1.10 to -0.58; I² 26.21%), 13 for fasting glucose (-0.60; -0.84 to -0.35; I² 62.66%), and seven for HbA1c (-0.81; -1.17 to -0.44; I² 64.15%). Only one study supplied GH/IGF-1 findings. The source PRISMA diagram and descriptive study table disagree on the number of included entries, preventing confirmation of a unique participant total from the supplied documents. Conclusions: The reported summaries favor lower markers of insulin resistance and glycemic exposure during the evaluated dietary interventions. Their clinical interpretation is limited by mixed protocols, incomplete outcome reporting, uncertainty about the precise within-study contrasts, and the absence of a documented study-level risk-of-bias evaluation.