Acne vulgaris is an inflammatory cutaneous condition that disproportionately affects the pediatric population. While there are several risk factors, emerging evidence suggests that ultra-processed foods (UPFs), as part of Western dietary patterns, may contribute to acne pathophysiology through activation of inflammatory pathways, such as mTORC1. This comprehensive review synthesizes current evidence regarding acne pathogenesis in conjunction with diet-associated inflammatory cascades to better illustrate the potential role of diet as an adjunct to clinical management in pediatric patients. The current literature suggests that increased insulin/IGF-1 levels may contribute to alterations in the skin and gut microbiota. Additionally, components commonly found in UPFs have been proposed to activate the mechanistic target of rapamycin complex (mTORC1) through insulin/IGF-1-dependent and -independent mechanisms, perpetuating inflammatory pathways that give rise to acne pathogenesis. However, the majority of available evidence is derived from adult cohorts; pediatric-specific evidence remains limited. While studies have demonstrated clinical significance in acne severity with dietary interventions, future high-quality studies are required. Through understanding the relationship between diet and acne pathogenesis, future therapeutic and preventative strategies may be developed to improve pediatric acne clinical outcomes.

Autoimmune myocarditis is an inflammatory disease of the myocardium driven by immune dysregulation and genetic predisposition. Recent advances in genomics, including genome-wide association studies (GWAS), have revealed key loci and pathways involved in disease susceptibility. This review synthesizes current knowledge on genetic determinants, from classical candidate genes to emerging GWAS findings, and explores their clinical implications for risk stratification and precision medicine.