The prevalence of obstructive sleep apnea (OSA) increases during pregnancy and is associated with gestational diabetes mellitus (GDM), although its clinical impact on birth outcomes remains unclear. We aimed to assess the effect of several OSA criteria and intermittent hypoxia in the third trimester on perinatal outcomes in women with GDM. In this prospective study, polysomnography was performed on 89 women with GDM. Insulin resistance indices (HOMA-IR/QUICKI) were calculated, and biomarkers (insulin-like growth factor-1 (IGF-1), resistin, soluble endoglobulin, galectin-3, and free fatty acids) were analysed from women and some cord blood samples using enzyme-linked immunosorbent assay. Whereas OSA did not significantly affect overall perinatal outcomes, specific OSA features-including REM-OSA, supine-position OSA, and an oxygen desaturation index (ODI) ≥ 1 h-1-were linked to adverse effects on neonatal birthweight and length. Moreover, apnea duration was an independent predictor of birthweight, while insulin resistance was more impaired in women with OSA and showed an inverse relationship with sleep and REM time, respectively. IGF-1 was elevated and demonstrated a significant predictive value for OSA, as indicated by the AUC-ROC curve. In summary, although OSA did not adversely affect overall perinatal outcomes in women with GDM, specific OSA characteristics were associated with adverse neonatal growth metrics. Insulin resistance was higher in women with OSA, and IGF-1 may serve as a potential biomarker for OSA in this population. Further prospective studies with attention to REM-stage, supine-position OSA, apnea duration, and hypoxic burden are needed to elucidate the complex interactions between OSA, GDM, and fetal outcomes.

Obstructive sleep apnea increases recurrent cardiovascular event risk in younger but not older patients with acute coronary syndrome: a prospective cohort study.

High prevalence of obstructive sleep apnea in patients with Long-COVID.

Understanding gut microbiota dysbiosis as a plausible link between obstructive sleep apnea (OSA), viral infections, and lifestyle diseases.

Could Glucagon-Like Peptide-1 (GLP-1) receptor antagonists be used to treat obstructive sleep apnoea in children and adolescents with obesity?

Beyond the apnea-hypopnea index: The predictive value of oxygen desaturation parameters for metabolic syndrome in OSA.

Dementia risk associated with comorbid obstructive sleep apnea and anxiety/depression: A nationwide retrospective cohort study in Taiwan.

Meta-analyses have demonstrated that physical exercise is associated with a reduction in the severity of obstructive sleep apnea (OSA). However, whether resistance training (RT) has an impact on OSA severity remains less well established. In addition, the potential underlying mechanisms associated with improvements in OSA after resistance training also remain poorly understood. The primary objective of this study was to evaluate the impact of an eight-week RT program on OSA severity. A secondary aim was to investigate potential mechanisms underlying improvements in OSA following RT. Randomized controlled trial involving 25 adults with moderate to severe OSA [male: 52%; age: 55.4±8.3 years; BMI: 36.3±7.3kg/m2; apnea-hypopnea index (AHI): 50.5±25.5 events/hour], allocated to a RT group (RT; 3 weekly sessions for 8 weeks) or a control group (CG; stretching exercises). Nocturnal polysomnography, respiratory muscle strength, rostral fluid shift, and body composition assessments were performed before and after the intervention. Significant group×time interactions were found for AHI (RT: Δ -21.0±6.1 vs. CG: 3.5±3.8 e/h; p=0.015), NREM-AHI (RT: Δ -20.5±6.2 vs. CG: 3.9±3.9 e/h; p=0.022), and arousals (RT: Δ -7.9±4.8 vs. CG: 7.4±5.1; p=0.028). In RT group, a correlation was verified between changes in AHI and waist circumference (r=0.643, p=0.018). An eight-week RT reduces OSA severity and the number of micro-arousals. A reduction in waist circumference was associated with an improvement in OSA severity.

Ocular conditions associated with obstructive sleep apnea: Mechanisms and clinical implications.

Early experience with hypoglossal nerve stimulation in Japanese patients: Trends in operative time and treatment outcomes.

Active strategies for children with obstructive sleep-disordered breathing: a systematic review and meta-analysis.

Excessive daytime sleepiness (EDS) substantially impairs health-related quality of life and cognitive function in obstructive sleep apnea (OSA) patients. However, the underlying neuropathological mechanisms remain poorly understood. To investigate the associations between EDS, cognitive deficits, and brain alterations in OSA patients. Prospective. One hundred two OSA patients (16 female, median age (IQR) 33.00 [28.00-41.00]) and 86 healthy controls (HCs) (16 female, median age (IQR) 33.00 [25.00-50.25]) were prospectively recruited. 3 T, 3D spoiled gradient-echo, diffusion-weighted spin-echo, blood oxygen level-dependent gradient-echo planar. The Epworth Sleepiness Scale, multiparameter MRI, and a series of neuropsychological tests (the number connection tests A and B, digit symbol test, line tracing test, serial dotting test, and Stroop Color/Word test) were performed to evaluate EDS, brain alterations, and cognitive performances. Mann-Whitney U test, independent samples t-test, chi-square test, Spearman's correlation, and mediation analyses were used. Significance level: p < 0.05. OSA patients exhibited statistically poorer cognitive performance (effect size = 0.23-0.37), lower diffusion tensor imaging along the perivascular space (DTI-ALPS) index (effect size = 0.25), and abnormal network topology (effect size = -0.80 to 0.57) compared with HCs. EDS significantly correlated with poorer cognitive performance (r = -0.173 to 0.258), lower DTI-ALPS index (r = -0.199), and abnormal network topology (r = -0.364 to 0.279) in all participants. Furthermore, aberrant degree centrality and nodal efficiency in the bilateral middle frontal gyrus (MFG) and left inferior parietal lobule (IPL) may mediate the relationship between EDS and cognitive deficits (indirect effect = -0.13 to 0.36). These results demonstrate that cognition, DTI-ALPS index, and network topology were all compromised in OSA. Furthermore, abnormal network topology in the bilateral MFG and left IPL may mediate the relationship between EDS and cognitive deficits. Level 2. Stage 2.

Simultaneous hypoxemia and hypercapnia frequently occur in conditions such as obstructive sleep apnea, which may cause peripheral and cerebral vascular dysfunction. However, how hypoxemia and hypercapnia interact in regulating peripheral and cerebral vascular responses remains incompletely understood. Eleven healthy young adults (4 females) completed three resting gas-inhalation trials (5-6 min) under different arterial O2 and CO2 conditions: 1) hypoxemic normocapnia (percutaneous arterial oxygen saturation ∼85%; Hypoxemia), 2) normoxic hypercapnia (end-tidal CO2 partial pressure ∼55 mmHg; Hypercapnia), and 3) hypoxemic hypercapnia (Combined). Femoral artery blood flow and middle cerebral artery mean blood velocity were continuously assessed using Doppler ultrasound and transcranial Doppler ultrasonography, respectively. These values were divided by mean arterial pressure measured by finger photoplethysmography to calculate leg vascular conductance and cerebrovascular conductance index (CVCi). Total vascular conductance was calculated as cardiac output (model-flow method) divided by mean arterial pressure. Relative to before gas inhalation, leg vascular conductance remained unchanged in all trials, whereas total vascular conductance increased during Hypoxemia. CVCi increased during Hypercapnia and Combined. When comparing the summed isolated responses (Hypoxemia + Hypercapnia) with the Combined, changes from baseline (Δ values) of leg vascular conductance tended to be lower (P = 0.054), and total vascular conductance was lower (P = 0.031) in Combined. By contrast, Δ CVCi did not differ between the summed isolated vs. Combined (P = 1.000). We show that hypoxemia and hypercapnia interact to augment systemic vasoconstriction, whereas hypercapnia-induced cerebral vasodilation is well preserved when combined with hypoxemia.NEW & NOTEWORTHY Combined hypoxemia and hypercapnia, which occurs in obstructive sleep apnea, tended to produce greater reductions in leg vascular conductance and a significantly greater reduction in total vascular conductance compared with the sum of the isolated effects. Cerebral vascular conductance index increased to a similar extent during the combined compared with the summed conditions. We show that hypoxemia and hypercapnia interact to augment systemic vasoconstriction, whereas hypercapnia-induced cerebral vasodilation is maintained when combined with hypoxemia.

Effects of a Time-Restricted Eating Intervention on Sleep and Body Composition in Adults with Obstructive Sleep Apnea: A Randomized Cross-over Clinical Trial.

A Physiology-Informed Prediction Model for Postoperative Respiratory Complications in Obese Patients With Obstructive Sleep Apnea.

Oxidative stress alleviated DL-3-n-Butylphthalide against chronic intermittent hypoxia-induced cognitive deficit by regulating Nrf-2/HO-1 Pathway.

Splenic enlargement as a physiologic adaptation to obstructive sleep apnea and nocturnal hypoxemia: A retrospective cohort study.

Effectiveness of non-surgical weight loss interventions on obstructive sleep apnoea severity and cardiometabolic outcomes: A systematic review and meta-analysis.

Gout is a chronic inflammatory disease characterized by the deposition of monosodium urate crystals in the joints. However, growing research suggests a more complex pathophysiology involving genetic susceptibility, metabolic stress, and environmental factors. Among emerging contributors, hypoxia-inducible factor 1 alpha (HIF-1α) has been proposed as a potential regulator that links these processes, though its role in gout remains underexplored. This review examines the emerging evidence supporting HIF-1α's role in both urate production and inflammation, to offer a unifying framework connecting these contributors to gout pathogenesis. Systemically, HIF-1α has been shown to promote a metabolic shift towards glycolysis and purine metabolism, providing a plausible mechanism for hyperuricemia. Locally, metabolic priming helps sustain immune responses, particularly through the release of interleukin-1 beta. Environmental stressors, including hypoxia and pseudohypoxia (e.g., obstructive sleep apnea), can further stabilize HIF-1α and amplify inflammatory signaling. This framework supports a model in which HIF-1α links metabolic stress, immune activation, and environmental exposures, reframing gout as a disorder of metabolic maladaptation and suggesting HIF-1α as a potential therapeutic target.

Mandibular advancement devices and treatment-emergent central sleep apnea (TECSA): Coincidental or critical finding?