Post-traumatic stress disorder (PTSD) is a condition characterized by the development of symptoms after exposure to a traumatic event in the form of relapsing and intrusive memories of a traumatic event. It has a particularly negative impact on quality of life, and the severity of symptoms correlates with the intensity and duration of trauma. In this paper, I will review etiological models of PTSD development with an emphasis on the biological model, comparison of diagnostic criteria from DSM and ICD, current therapeutic methods, the most common psychiatric comorbidities of PTSD, and analysis of up to date studies on somatic comorbidities caused by PTSD. Specifically, PTSD symptoms over-activate stress-related neurobiological pathways. The molecular changes resulting from this hyperactivation accelerate aging of the epigenoma, cellular aging, increase inflammatory processes and, consequently, impaire immune system activity. Through a systematic analysis of the pathophysiological processes crucial in the occurrence of somatic comorbidities, the aim of this paper is to point out the need for additional research into altered biological mechanisms that influence premature and accelerated aging of the diseased organism and to apply their results to the advancement of therapeutic methods. Finally, I will refer to epidemiological data on the health status of Croatian veterans as representatives of a directly endangered, vulnerable group of people with a high risk of PTSD and all associated comorbidities.