OSA and Inflammation
David Gozal, MD, MBA, PhD

Dr. Gozal is currently the Marie M. and Harry L. Smith Endowed Chair and the Chairman of the Department of Child Health at the University of Missouri, as well as Physician-in-Chief of the University of Missouri Health Children’s Hospital. He received his M.D. from the Hebrew University of Jerusalem, and completed MBA degrees from Georgetown University and ESADE, a pediatric residency at the Haifa Medical Center in Israel, and then spent 2 years in Cameroon, West Africa, developing rural healthcare networks, for which he received the title of “Knight of the Order of Merit”. He then completed his pediatric pulmonology and sleep medicine training at Childrens Hospital Los Angeles in 1993, and joined the faculty at the University of Southern California and UCLA. In 1994, he moved to Tulane University, and was appointed tenured Professor and Constance Kaufman Endowed Chair in Pediatric Pulmonology Research. From 1999 till 2009, Dr. Gozal was at the University of Louisville as the Children’s Hospital Foundation Chair for Pediatric Research, Distinguished University Scholar, Director of the Kosair Children’s Research Institute, and Chief of the Division of Pediatric Sleep Medicine and the Sleep Medicine Fellowship Program, both of which were recognized as programs of distinction by the American Academy of Sleep Medicine. From 2009 till 2014, Dr. Gozal served as Chairman of the Department of Pediatrics and Physician-in-Chief and CEO of Comer Children’s Hospital at the University of Chicago, and then assumed the position of Herbert T. Abelson Professor at the University of Chicago, where he also held the title of Pritzker Scholar. Dr Gozal’s research interests include projects such as gene and cellular regulation in hypoxia  and sleep disruption, murine models of sleep disorders, and genomic and proteomic approaches to clinical and epidemiological aspects of sleep apnea in both adults and children. In addition, he has pioneered biomarker discovery and machine learning approaches for the diagnosis of sleep apnea across the lifespan. More recently, he has begun exploration of the role of the gut microbiome and circulating exosomes in sleep disorders and associated morbidities.  

He is Past President of the American Thoracic Society, was a member of the Board of Directors of the Sleep Research Society 2014-2016, and is an editor for the journals Sleep, ERJ, and Frontiers in Neurology. He has been the recipient of the ATS Amberson Lecture in 2002, and was awarded the William C. Dement Academic Achievement Award by the American Academy of Sleep Medicine in 2013 and the 2016 Lifetime Achievement Award of the National Sleep Foundation, the 2019 Kendig Award from the American Academy of Pediatrics, and Doctor Honoris Causa from the Universities of Lleida and Barcelona in Spain.  His research work is supported by grants from the NIH, he has published over 650 peer-reviewed original articles carrying a H index of 109 and >50,000 citations, along with  more than 150 book chapters and reviews, edited 4 books, presented more than 1,000 scientific abstracts, and has extensively lectured all over the world.

 

 
  Lecture Description: OSA and Inflammation  
  Obstructive sleep apnea syndrome (OSA) is a markedly prevalent condition across the lifespan, particularly in overweight and obese individuals, which has been associated with an independent risk for neurocognitive, behavioral, and mood problems as well as cardiovascular and metabolic morbidities, ultimately fostering increases in overall mortality rates. In adult patients, excessive daytime sleepiness (EDS) is the most frequent symptom leading to clinical referral for evaluation and treatment, but classic EDS features are less likely to be reported in children, particularly among those with normal body-mass index. The cumulative evidence collected over the last two decades supports a conceptual framework, whereby sleep-disordered breathing in general and more particularly OSA should be viewed as a low-grade chronic inflammatory disease. Accordingly, it is assumed that a proportion of the morbid phenotypic signature in OSA is causally explained by underlying inflammatory processes inducing end-organ dysfunction. In this lecture, I will describe the cumulative evidence in both murine models and human studies linking OSA to inflammation and to downstream end-organ dysfunction.
 


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