Autoimmune Illness, Infections, and Genetic Risk for Anorexia Nervosa
Despite its prevalence and high mortality, norexia nervosa treatment is a poorly studied condition, with no effective treatments and no medication targeting the core biology of the illness; the recovery process takes, on average, seven years. Dr. Zerwas proposed to study whether the combination of autoimmune illness and repeated infection exposure will work together to increase risk for anorexia. Her goal is to improve both prevention and early detection of anorexia by understanding how genetic predispositions and medical history interact to increase risk for the disorder.
Stephanie Zerwas, Ph.D.
Need/Problem: We don’t know enough about why some people develop anorexia nervosa and others do not. Our recent studies have suggested that autoimmune illness may increase risk for anorexia nervosa. This study will examine whether the combination of autoimmune illness, bacterial infections, and genetics work together to increase risk for anorexia nervosa.
Grant Summary: By drawing on the wealth of genetic medical data available from the Danish register, we will be able to examine the joint risk of autoimmune illness, infection load and genetic risk for the development of anorexia nervosa.
Goals & Projected Outcomes: Our ultimate goal is to improve both prevention and early detection of anorexia nervosa by understanding how genetic predispositions and medical history interact to increase risk for the disorder.
Grant Details: Anorexia nervosa (AN) is a serious and perplexing psychiatric disorder. Around 30% of AN patients develop a chronic, relapsing course. In those who do recover, the recovery process is long (7 years on average).8 The AN treatment is weak with no efficacious treatments and no medications targeting the core biology of the illness. Thus, AN ranks among the ten leading causes of disability in young women and has the highest mortality rate of any psychiatric illness. Funding for AN research is limited. In a white paper published by the National Institute of Mental Health (NIMH), director Dr. Thomas Insel wrote, “eating disorders …receive less funding than they ‘should’ based on” estimates of the life lost to illness. Funding for innovative research on AN etiology and biology is desperately needed to help us a) prevent AN and b) treat AN. Translating these findings back to prevention efforts, clinical care, and future pharmacotherapy, has potential to reduce the unacceptably high societal and personal burden on patients with AN and their families.
In previous studies, autoimmune illness has been associated with anorexia nervosa risk. We hypothesize that the combination of autoimmune illness and repeated infection exposure will work together to increase risk for anorexia nervosa. We also hypothesize a dose-response relationship—as infection exposure increases, the risk for anorexia nervosa increases. Because previous studies have found that risk variants for psychiatric illness are related to neuro-immunity, we will include the anorexia nervosa genetic risk as a predictor of both autoimmune illness and anorexia nervosa. We also hypothesize that autoimmune illness and infections will interact. When individuals have few genetic variants that predispose them to risk for anorexia nervosa (i.e., a less anorexia nervosa genetic risk), we anticipate that autoimmune illnesses and infections will have a larger effect for AN risk. We propose examining maternal autoimmune and illness exposure during the critical prenatal period. In previous studies, exposure to infections during pregnancy increased risk for anorexia nervosa in offspring. We hypothesize that anorexia nervosa genetic risk, exposure to maternal autoimmune illness, and infection exposure in utero will work together to increase the risk for AN.