Abstract 1: Sleep apnea, sleep deprivation and cardio-metabolic risk

Abstract 1: Sleep apnea, sleep deprivation and cardio-metabolic risk

Professor Virend Kristen Somers is professor of medicine, consultant, and clinical investigator at the department of internal medicine at Mayo Clinic and Mayo Foundation. Also he is the, director of Mayo GCRC Cardiovascular Core Laboratory, and international director of International Clinical Research Center, in Brno, Czech Republic. He is board certified from Canada, United Kingdom, South Africa, and the USA. In addition to his academic teaching and clinical activities, he holds senior positions in many clinical and scientific committees. He serves in the editorial boards for many well-known medical and health journals. Prof. Somers was the recipient of tens of awards by different highly distinguished bodies. He holds seven different registered patents. His research focuses on neural circulatory studies in sleep and sleep apnea, neural metabolic interactions in obesity, and genetic modulation of neural circulatory control. Prof. Somers has published hundreds of original research articles, reviews, book chapters, and books.


Abstract 1: Sleep apnea, sleep deprivation and cardio-metabolic risk

Obese individuals are at increased risk for sleep apnea. However, people with sleep apnea may be at increased risk for weight gain. Thus there is the potential for a vicious cycle of sleep apnea leading to weight gain leading to worsening sleep apnea. Untreated patient with sleep apnea report a significant weight gain in the year prior to diagnosis. Conversely, treatment of obstructive sleep apnea (OSA) with continuous positive airway pressure (CPAP) is associated with a reduction in visceral fat. Visceral fat has been linked to increased cardio-metabolic risk. Therefore, effective treatment of sleep apnea may be an important strategy in treating obese individuals with co-morbid OSA. Sleep apnea induces hypoxemic stress but also leads to impaired sleep quality. Inadequate sleep has been implicated in a broad range of cardio-metabolic abnormalities. Individuals sleeping less than 6 hours a night may be at increased risk for hypertension, glucose intolerance, and myocardial infarction. Sleep deprivation has also been linked to increased levels of systemic inflammation. The advent of electric lighting has resulted in an overall reduction in total sleep duration, especially over the last century. More recently, widespread use of computer screens and portable smart devices has resulted in prolonged exposure to light, which may reduce melatonin levels, thus affecting propensity to sleep. The influence of smart phones and social media on reducing sleep time is especially evident in younger individuals. This widespread reduction in sleep may conceivably have later consequences for cardiovascular and metabolic regulation, with very significant public health consequences when the current teenage and young adult population reaches middle age.

Abstract 2: Beyond BMI – advances in the diagnosis and management of obesity

In order to more comprehensively address the emerging epidemic of obesity, it is important that the problem be clearly defined and that etiologic factors be identified. While BMI is widely used as a surrogate for obesity, this measure takes account of not only fat mass but also muscle mass. Therefore individuals with very large muscle mass may be inappropriately classified as being obese. Conversely individuals with low muscle mass but a high fat mass may have a normal BMI even though they fall into the classification of “normal weight obesity”. Normal weight individuals with a high body fat may be prone to increased cardiac and metabolic risk. The use of BMI as a surrogate for obesity may help explain some of the controversies regarding BMI and adverse events. Furthermore, adverse effects of obesity may not be simply a function of total body fat but rather a reflection of the relative pathophysiologic contributions of visceral versus subcutaneous fat. For example, in healthy lean individuals undergoing increased feeding with a consequent modest increase in body fat (approximately 4 kg), those in whom the excess fat accumulated in the visceral area manifested impairment of endothelial function, which was not evident in those with predominant subcutaneous fat accumulation. Novel behavioral factors such as inadequate sleep, need to be considered in the etiology of obesity. Observational data have linked shortened sleep duration to an increased risk for weight gain. Indeed in experimental studies, healthy normal subjects exposed to a 2-hour reduction in sleep time for 8 consecutive nights manifested a marked increase in caloric intake but no increase in activity levels, hence resulting in a positive calorie balance and thus predisposing to obesity. Therefore it is important that sleep duration and quality be taken into account in weight reduction strategies.