Abstract
Evaluate cardiometabolic risk as a potential sequel to a mass terrorist attack using October 7th, 2023 as a focus. Narrative review surveying PubMed, PsycNet, UN and Council on Foreign Relations websites on. 1. PTSD following terrorism, rocket attacks and conflict related sexual violence. 2. The relationship between cardiometabolic illness and PTSD. 3. Humoral, genetic and epigenetic mechanisms relating cardiometabolic risk, inflammation and PTSD. 4. Treatments for PTSD and associated cardiometabolic risk factors and their effectiveness. Cardiometabolic sequelae occur after trauma. This is most pronounced when trauma, sexual or violence related, occurs during childhood. The risk of cardiometabolic sequelae increases with PTSD diagnosis in adults. Inflammation as well as genes related to inflammatory function (e.g. FKBP5, AHRR, NR3C1) impact vulnerability to PTSD, response to treatment and cardiometabolic outcomes. Treatments for PTSD appear somewhat more effective at lowering cardiometabolic risk in civilian, rather than military populations. There is little published research on directly treating cardiometabolic sequelae of PTSD. Israelis, particularly those with exposure to the terror events of October 7, 2023 should be screened for psychological and metabolic sequelae. This should occur in a primary care setting and be part of observational research to help understand relationships between trauma, metabolic outcomes and their treatment.
Published Version
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