ABSTRACT
Background: This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) provides an overview of the mechanisms and treatment of obesity and hypertension. Methods: The scientific support for this CPS is based upon published citations, clinical perspectives of OMA authors, and peer review by the Obesity Medicine Association leadership. Results: Mechanisms contributing to obesity-related hypertension include unhealthful nutrition, physical inactivity, insulin resistance, increased sympathetic nervous system activity, renal dysfunction, vascular dysfunction, heart dysfunction, increased pancreatic insulin secretion, sleep apnea, and psychosocial stress. Adiposopathic factors that may contribute to hypertension include increased release of free fatty acids, increased leptin, decreased adiponectin, increased renin-angiotensin-aldosterone system activation, increased 11 beta-hydroxysteroid dehydrogenase type 1, reduced nitric oxide activity, and increased inflammation. Conclusions: Increase in body fat is the most common cause of hypertension. Among patients with obesity and hypertension, weight reduction via healthful nutrition, physical activity, behavior modification, bariatric surgery, and anti-obesity medications mostly decrease blood pressure, with the greatest degree of weight reduction generally correlated with the greatest degree of blood pressure reduction.
ABSTRACT
Background: This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) is intended to provide clinicians an overview of type 2 diabetes mellitus (T2DM), an obesity-related cardiometabolic risk factor. Methods: The scientific support for this CPS is based upon published citations and clinical perspectives of OMA authors. Results: Topics include T2DM and obesity as cardiometabolic risk factors, definitions of obesity and adiposopathy, and mechanisms for how obesity causes insulin resistance and beta cell dysfunction. Adipose tissue is an active immune and endocrine organ, whose adiposopathic obesity-mediated dysfunction contributes to metabolic abnormalities often encountered in clinical practice, including hyperglycemia (e.g., pre-diabetes mellitus and T2DM). The determination as to whether adiposopathy ultimately leads to clinical metabolic disease depends on crosstalk interactions and biometabolic responses of non-adipose tissue organs such as liver, muscle, pancreas, kidney, and brain. Conclusions: This review is intended to assist clinicians in the care of patients with the disease of obesity and T2DM. This CPS provides a simplified overview of how obesity may cause insulin resistance, pre-diabetes, and T2DM. It also provides an algorithmic approach towards treatment of a patient with obesity and T2DM, with "treat obesity first" as a priority. Finally, treatment of obesity and T2DM might best focus upon therapies that not only improve the weight of patients, but also improve the health outcomes of patients (e.g., cardiovascular disease and cancer).
ABSTRACT
We show that an individuals immune status to Covid-19 can be monitored through quantitative antibody measurements using a method based on centrifugal microfluidics, specifically designed for speed to result (20 min), high throughput (8 samples simultaneously) and accuracy from a finger-prick blood sample. Anti-Receptor Binding Domain (RBD) IgG concentration showed a log-normal distribution with mean decreasing with time following the second vaccination with mRNA BNT162b2 (Pfizer). Using a model for an individuals antibody concentration-dependent vaccine efficacy allowed comparison with literature data on changing vaccine efficacy against symptomatic disease across a population. Even though the trial was small (n = 100) the computed population vaccine efficacy was in reasonable agreement with that obtained from a large population survey. The derived parameters for the vaccine efficacy model were in good agreement with those expected from previous studies and from a simple theoretical model. The results and modelling show that the major proportion of breakthrough infections are for people whose antibody concentration is in the tail of the distribution. The results provide strong support for personalized booster programmes that, by targeting people in the tail of the distribution, should be more effective at diminishing breakthrough infection and optimising booster dose supply than a program that simply mandates a booster at a specific post-vaccination time point.
