Dr. Sofiya Milman is an Associate Professor of Medicine in the Divisions of Endocrinology and Geriatrics and is the Director of Human Longevity Studies at Einstein’s Institute for Aging Research . Dr. Milman’s research focuses on a unique population of centenarians and their families who are generally free of age-related diseases. Healthy longevity runs in most of these families, suggesting a heritable basis for this phenomenon. Dr. Milman's team conducts translational research focused on the discovery of genomic mechanisms that regulate endocrine and metabolic pathways that protect against common age-related diseases, like diabetes, cardiovascular disease and Alzheimer's.
Many of the discovered longevity genes and phenotypes are related to hormonal pathways. Changes in most hormones are observed throughout the human lifespan, but it remains unknown whether the observed changes cause aging, are associated with age but are not the cause of aging, or are protective for the aging body. Identification of protective endocrine parameters will inform our understanding of the mechanisms of healthy aging and lead to the discovery of interventions that protect from age-related diseases.
A biological pathway that has been repeatedly implicated in aging is the somatotropic axis that involves signaling via growth hormone and insulin-like growth factor-I (IGF-I). Substantial evidence exists that diminished signaling via this pathway delays aging, resulting in longer lifespan and health-span, not only in animal models, but also in humans. In fact, Dr. Milman's research demonstrated that lower IGF-I levels were associated with longer survival and better cognition in humans with exceptional longevity and provided evidence against supplementing older adults with growth hormone in an attempt to delay aging. Dr. Milman's team uses computational approaches to integrade genetic information, such as whole-exome sequencing, with rich phenotype data in families with inherited longevity to understand the genetic and molecular mechanisms that lead to protective effects of low IGF-I.