Sleep is tightly regulated by thermoregulatory processes that include core body temperature (CBT) modulation, the distal–proximal temperature gradient (DPG), and melatonin rhythms. In this review, we examine how these factors intersect with sleep physiology and contribute to the pathophysiology of common sleep disorders such as ADHD, insomnia, narcolepsy, Obstructive Sleep Apnea (OSA), depression, and Restless Legs Syndrome (RLS). We discuss evidence showing that delayed or disrupted CBT minima, impaired DPG, and altered melatonin secretion can prolong sleep latency, fragment rest, and lead to daytime symptoms. In addition, we explore temperature-based interventions, including foot baths, passive body heating, whole-body hyperthermia, and adjustments in room temperature, which have demonstrated potential to mitigate symptoms and enhance sleep quality. Collectively, these findings emphasize the need for personalized interventions to address thermoregulatory disruptions, presenting a noninvasive avenue for more effective sleep disorder management.

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.

Obstructive sleep apnea (OSA) is associated with increased cardiovascular, respiratory, and all-cause mortality, yet the long-term survival impact of continuous positive airway pressure (CPAP) remains contested, and treatment is usually analysed as a binary exposure rather than by the quality of the response achieved. In a single-centre cohort of 4368 adults referred for polysomnography and followed for 8–20 years (prespecified subgroup with apnea–hypopnea index [AHI] ≥ 15, n = 2304), we applied cause-specific Cox and Fine–Gray competing-risks models, together with machine-learning classifiers, to characterise all-cause, cardiovascular, and pulmonary mortality. CPAP was associated with reduced all-cause (hazard ratio [HR] 0.75), cardiovascular (HR 0.75), and pulmonary mortality (HR 0.54), with the benefit confined to severe OSA (HR 0.66) and absent in moderate disease (HR 0.95). Good responders showed a significant 34% reduction in all-cause mortality (HR 0.66), whereas poor responders showed no significant reduction. Nocturnal desaturation (time with oxygen saturation < 90%) was the dominant independent predictor of pulmonary mortality, and baseline features predicted response category only moderately (macro-averaged AUC 0.76). Long-term CPAP confers a severity- and response-dependent survival benefit; nocturnal hypoxaemia is a key, modifiable driver of respiratory death.