Dr. Harvey Levy is senior physician in Medicine/Division of Genetics and Genomics at Boston Children’s Hospital and professor of pediatrics at Harvard Medical School. Over his long and storied career, he has made multiple seminal contributions to the diagnosis, treatment, and scientific understanding of metabolic disorders. Following his graduation from the Medical College of Georgia in 1960, Dr. Levy trained in pediatrics at Boston City Hospital, Columbia-Presbyterian Medical Center, and Johns Hopkins Hospital. After his pediatrics training, he briefly rejoined the Boston City Hospital as chief resident of pediatrics before taking a position at Massachusetts General Hospital (MGH) as a research fellow in metabolism and pediatric neurology research under Dr. Mary Efron, a pioneer in metabolism and metabolic disease. After completing this fellowship, Dr. Levy joined the faculty of the MGH and Harvard and also served as a consultant in metabolism to the Massachusetts newborn screening program. In 1978, Dr. Levy moved to Boston Children’s Hospital to found and serve as the first director of the metabolic program.
Dr. Levy’s work has been mainly focused on homocystinuria and sulfur metabolism. During his fellowship period, he identified the first case of homocystinuria diagnosed from a newborn screening. Shortly after, he helped co-discover the first example of increased homocysteine due to a non-homocystinuric disorder, a condition that is now referred to as cobalamin C defect. This was also the first example of a human disorder of vitamin B12 metabolism. He has authored over 400 medical articles and book chapters on metabolic disorders, including the various homocystinemias, and has received numerous national and international awards for his body of work. Currently, Dr. Levy and Boston Children's are one of the three U.S. sites that is participating in the Natural History Study of Cystathionine Beta-synthase Deficiency Homocystinuria (National Clinical Trial number NCT02998710), which will help improve our understanding of the disease course and clinical outcomes of homocystinuria and aid in the development of better treatments for this devastating disease.