Joel Finkelstein, M.D.
Physician Investigator (Cl)
Endocrine Division, Research Institute
Professor of Medicine
Harvard Medical School
Endocrine Division, Massachusetts General Hospital
|MD Washington University School of Medicine in St. Louis 1980|
Joel S. Finkelstein, professor of medicine at Massachusetts General Hospital and Harvard Medical School, is the recipient of the Endocrine Society’s 2017 Clinical Investigator Award.
Dr. Finkelstein’s work has generated new concepts in endocrine physiology while providing new information that has directly changed patient care. His early work describing osteoporosis in young men with GnRH deficiency led to the discovery that peak bone mass is compromised in men with histories of delayed puberty. With Dr. Matthew Smith, he demonstrated that antiresorptive agents can prevent GnRH agonist-induced bone loss in men with prostate cancer.
He supervised a group of medical residents at MGH who found that over half of medical inpatients were vitamin D deficient, a finding that raised awareness of the public heath importance of vitamin D. He led the first randomized controlled trial demonstrating that daily teriparatide administration exerts an anabolic effect on bone in humans and later reported that bisphosphonates surprisingly attenuated teriparatide’s anabolic effect.
As an investigator with the Study of Women’s Health Across the Nation (SWAN) for nearly 25 years, he and his colleagues have characterized many of the physiologic and psychosocial changes that women experience across the menopause transition, including a comprehensive natural history of transmenopausal bone loss and the gradual decline in Anti-Mullerian Hormone levels that allows for accurate and precise predictions of the timing of the final menstrual period.His group’s recent work has established the levels of testosterone at which the key features of male hypogonadism begin to develop, thereby providing a physiologically based definition of male hypogonadism. Additionally, his group found many of the key features of male hypogonadism are due to estrogen deficiency rather than androgen deficiency.