Obesity as a Neuroendocrine Disorder.

Obesity is one of the most prevalent diseases in the world. Based on hundreds of clinical and basic investigations, its etiopathogenesis goes beyond the simple imbalance between energy intake and expenditure. The center of the regulation of appetite and satiety lies in the nuclei of the hypothalamus where peripheral signals derived from adipose tissue (e.g., leptin), the gastrointestinal tract, the pancreas, and other brain structures, arrive. These signals are part of the homeostatic control system (eating to survive). Additionally, a hedonic or reward system (eating for pleasure) is integrated into the regulation of appetite. This reward system consists of a dopaminergic circuit that affects eating-related behaviors influencing food preferences, food desires, gratification when eating, and impulse control to avoid compulsions. These systems are not separate. Indeed, many of the hormones that participate in the homeostatic system also participate in the regulation of the hedonic system. In addition, factors such as genetic and epigenetic changes, certain environmental and sociocultural elements, the microbiota, and neuronal proinflammatory effects of high-energy diets also contribute to the development of obesity. Therefore, obesity can be considered a complex neuroendocrine disease, and all of the aforementioned components should be considered for the management of obesity.

Risk Factors Associated with Mortality among Patients with COVID-19: Analysis of a Cohort of 1213 Patients in a Tertiary Healthcare Center.

The presence of cardio-metabolic and respiratory comorbidities, immunosuppression, and chronic kidney disease have been associated with an increase in mortality from COVID-19. The objective of this study is to establish the risk factors associated with 30-day mortality in a cohort of hospitalized patients with COVID-19. This paper conducts a retrospective and analytical study of patients hospitalized for COVID-19 in a tertiary care center. A Cox proportional hazard analysis was performed to estimate the association of comorbidities with 30-day mortality. A total of 1215 patients with a median age of 59 years were included. In the adjusted Cox proportional hazards regression model, hypothyroidism, D-dimer ≥ 0.8 µg/mL, LHD ≥ 430 IU/L, CRP ≥ 4.83 ng/mL, and triglycerides ≥ 214 mg/dL were associated with an increased risk of death. The presence of a history of hypothyroidism and biomarkers (D-dimer, lactic dehydrogenase, CRP, and triglycerides) were associated with an increase in mortality in the studied cohort.