Sleep Apnea, Obesity, and Diabetes - an Intertwined Trio.

PURPOSE OF REVIEW: To synthesize the existing literature regarding the complex interplay between sleep disturbance, obesity, and diabetes. The review emphasizes the three pillars of health being diet, exercise, and sleep, with the notion that if one is ignored, then the other two could suffer. RECENT FINDINGS: Sleep deprivation is associated with incident obesity, perhaps mediated by dysregulation in leptin and ghrelin - hormones important in regulation of appetite. Sleep apnea is very common particularly among obese people with type 2 diabetes mellitus. Treatment of sleep apnea has clear symptomatic benefits although its impact on long-term cardiometabolic health is less clear. Sleep disturbance may be an important modifiable risk for patients at risk of cardiometabolic disease. An assessment of sleep health may be an important component of the comprehensive care of patients with obesity and diabetes mellitus.

Potential Therapeutic Targets in Obesity, Sleep Apnea, Diabetes, and Fatty Liver Disease.

Obesity and metabolic syndrome affect the majority of the US population. Patients with obesity are at increased risk of developing type 2 diabetes (T2DM), obstructive sleep apnea (OSA), and metabolic dysfunction-associated steatotic liver disease (MASLD), each of which carry the risk of further complications if left untreated and lead to adverse outcomes. The rising prevalence of obesity and its comorbidities has led to increased mortality, decreased quality of life, and rising healthcare expenditures. This phenomenon has resulted in the intensive investigation of exciting therapies for obesity over the past decade, including more treatments that are still in the pipeline. In our present report, we aim to solidify the relationships among obesity, T2DM, OSA, and MASLD through a comprehensive review of current research. We also provide an overview of the surgical and pharmacologic treatment classes that target these relationships, namely bariatric surgery, the glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and glucagon receptor agonists.

Short Disease Duration Is Associated With Increased Risk of Treatment Failure in Biologic-Treated Patients With Ulcerative Colitis.

BACKGROUND: Longer disease duration is associated with inferior response to biologic therapy in Crohn's disease. However, the effect of disease duration on response to biologic therapy in ulcerative colitis (UC) has not been well studied. METHODS: In a single-center retrospective cohort study of outpatients with UC starting a biologic agent, we evaluated treatment response by disease duration. The primary outcome was treatment failure (composite outcome of inflammatory bowel disease [IBD]-related surgery/hospitalization or treatment modification including dose escalation, treatment discontinuation, or addition of corticosteroids); secondary outcomes were risk of IBD-related surgery/hospitalization and endoscopic remission. We conducted multivariate Cox proportional hazard analyses to evaluate the independent impact of disease duration on clinical outcomes. RESULTS: We included 160 biologic-treated UC patients (73% biologic-naïve) with a median age (interquartile range) of 36 (26-52) years and disease duration (range) of 4.5 (1-9) years. After adjusting for immunosuppressive medications, albumin, and body mass index, each 1-year increase in disease duration was associated with a 5% lower risk of treatment failure (adjusted hazard ratio, 0.95; 95% confidence interval [CI], 0.91-0.99) and a 9% higher risk of achieving endoscopic remission (adjusted odds ratio, 1.09; 95% CI, 1.01-1.18). This association of short disease duration with treatment failure was observed only in biologic-naïve patients, but not biologic-experienced patients. No significant association was seen between disease duration and risk of surgery or hospitalization. CONCLUSION: Shorter disease duration is independently associated with increased risk of treatment failure in biologic-treated patients with UC. Requirement of biologic therapy early in the course of disease may be a negative prognostic marker in patients with UC.