Dr. Yung received his medical degree from the University of Liverpool, England. He completed an internal medicine residency at Sinai Hospital in Detroit, and fellowship training in rheumatology (1994) and geriatric medicine (1996) at the University of Michigan. He is board-certified in Internal Medicine, Geriatric Medicine, and Rheumatology. Dr. Yung’s clinical interests include the management of arthritis in older adults. He is the editor of two textbooks, including Geriatric Rheumatology A Comprehensive Approach. He is a recipient of the NIH Individual National Research Service Award (1994-1996) and Clinical Investigator Award (1997-2002), and the Paul Beeson Physical Faculty Scholars in Aging Research Award (1998-2001). In addition, he has received the American College of Rheumatology Senior Rheumatology Scholar Award (1994). He has been continuously funded by the NIH since 1994. He is the principal investigator of the Michigan Claude D. Pepper Older Americans Independence Center P30 award. His research interest focuses on the gene-environment interaction in chronic inflammation in aging. He is currently funded by the NIH in his research effort on the effects of aging on the gut microbiome. Dr. Yung was chief of the Division of Geriatric and Palliative Medicine (2011-2022), and is director of the Institute of Gerontology, and director of the Geriatrics Center at the University of Michigan. He held the interim chair of the Department of Internal Medicine (2023-2024) and is also currently the Executive Vice Chair of Internal Medicine.

Dr. Yung's research focuses on understanding both the origins and the effects of low level chronic inflammation in the onset and progression of age-related diseases and conditions. Aging represents a state of chronic low grade inflammation. Throughout his career, Dr. Yung has been interested in the relationship between “epigenetic drift”, autoimmunity and age-related inflammation (“inflamm-aging”). The chemokine system is critical to initiating and sustaining inflammation. Dr. Yung was the first to report that T cell DNA hypomethylation in aging is associated with increased T cell pro-inflammatory chemokine and simultaneously impaired T cell homeostatic chemokine responses. These observations help explained the observed low level chronic inflammation in aging. Epigenetics is the key that links genes and environment. He believes the origin of late-life inflammation diseases is in part determined by early-life environmental factors that act on the immune system through epigenetic mechanisms, consistent with the “Developmental Origins of Adult Disease (Barker) Hypothesis. His research group recently reported that pre-natal supplementation with key “methyl-donors” can ameliorate the pro-inflammatory T cell chemokine response in aging, which in turn reduces the burden of late-life cardiovascular disease.