Childhood obesity is an urgent global concern. Growing evidence suggests its roots often extend back to prenatal development. This review examines how maternal nutrition influences the risk of childhood obesity through fetal metabolic programming. A literature search (October–December 2025) was conducted using PubMed, Scopus, Web of Science, and Google Scholar. It identified peer-reviewed studies on maternal diet, metabolic pathways, and long-term offspring health. Maternal macronutrient imbalances, such as excessive energy intake, high glycemic load, high saturated fat intake, or inadequate protein, were associated with altered fetal hormonal regulation. They also led to changes in placental nutrient transfer and epigenetic modifications. These changes affect insulin sensitivity and adipose tissue development. Micronutrient deficiencies, especially vitamin D, folate, and B12, were linked to disrupted metabolic signaling. They were also linked to adverse growth patterns. Maternal conditions, including obesity and gestational diabetes, further increased fetal susceptibility to obesity. This occurs by promoting hyperinsulinemia and adiposity before birth. Other factors, such as maternal genetics, gut microbiota, and early postnatal feeding, also interact with prenatal nutrition to shape long-term outcomes. The evidence highlights pregnancy as a key window for prevention. More longitudinal studies and biomarker-based dietary assessment are needed to support tailored nutritional guidance.

Background/Objectives: Familial hyperaldosteronism type IV (FH-IV) is an extremely rare, clinically heterogeneous condition representing the least characterized familial subtype of primary aldosteronism (PA) caused by germline gain-of-function CACNA1H mutations. Despite growing molecular insights, optimal diagnostic and therapeutic strategies remain poorly defined. This systematic review aims to synthesize available evidence regarding the clinical, biochemical, and genetic characteristics of FH-IV, and to evaluate the efficacy of current pharmacological and surgical treatments. Methods: A systematic review was conducted in accordance with PRISMA guidelines and preregistered in PROSPERO (CRD420261324945). A comprehensive search of MEDLINE, Embase, and Web of Science identified studies reporting genetically confirmed FH-IV patients. Data concerning clinical phenotypes, diagnostic evaluations, treatment outcomes, and genetic backgrounds were extracted and analyzed. Results: The primary cohort included 31 fully characterized symptomatic patients, alongside 8 mutation-positive relatives (4 asymptomatic carriers and 4 symptomatic individuals). The genetic landscape was remarkably heterogeneous, encompassing 17 distinct CACNA1H mutations. Clinically, diagnosis was frequently delayed, often complicated by atypical normokalaemic presentations and misleading adrenal imaging. Surgical treatment was generally ineffective, frequently resulting in persistent or recurrent hypertension and biochemical dysregulation. Pharmacologically, patients often required multiple antihypertensive drugs, most frequently a combination of mineralocorticoid receptor antagonists (MRAs) and calcium channel blockers (CCBs). Conclusions: FH-IV is best conceptualized as a systemic adrenal channelopathy. While standard screening parameters are usually elevated, atypical biochemical profiles and misleading structural imaging can complicate the diagnostic process. Optimal management relies on multigene Next-Generation Sequencing (NGS) panels for definitive diagnosis and cascade screening of relatives. Finally, while the combination of MRAs and CCBs is commonly used in PA, it represents a valuable therapy for FH-IV, with dual L-/T-type CCBs emerging as a potential disease-specific option.