RESILIENCE MARKERS IN FAMILIES OF STRESSED PATIENTS: ReMaFaSt STUDY

Background ReMaFaSt study is the first Argentinean study aimed to evaluate the biochemical markers of resilience. Resilience is the capacity and dynamic process of adaptively overcoming stress and adversity while maintaining normal psychological and physical functioning. Stressful life events, trauma, and chronic adversity can have a substantial impact on brain function and structure, and can result in the development of Post-Traumatic Stress Disorder (PTSD), depression and other psychiatric disorders. However, most individuals do not develop such illnesses after experiencing stressful life events, and are thus thought to be resilient. The risk of mental illness is defined by the relationship between genetic predisposition and environmental factors after a life stress. Early stress factors are a key for “turning on” diseases. Several resilience or vulnerability (features and state) markers have been identified in patients. Often the patient´s relatives share the traumatic experience. Our patients develop depression or PTSD but often their families do not, despite enduring the same traumatic experience. So why do not relatives develop illness? The aim of the study is to look at missing markers of resilience (genetic and PINE markers) as well as lower environmental vulnerability. Methods Adult first degree healthy relatives of patients were invited to participate in the ReMaFaSt study. All participants gave written informed consent before the procedures and the aim of the study were explained completely. A total of 25 first degree patients relatives. First degree relatives were defined as father, mother, brothers, sisters and children. Inclusion criteria: first degree relatives psychiatrically healthy, aged between 21–70 y/o have undergone the same traumatic experience as our patients with depression or PTSD (DSM V). Exclusion criteria: psychopathic features, severe organic diseases or psychiatric disease. Beck, HAM D, CAPS-5, neurocognitive testing, Trail Mb were used to evaluate the psychiatric condition of the participants. Thus, our aim was to determine genetic variants of 5-HTTLPR among other biochemical tests; metabolic testing (BMI, Glycosylated, hemoglobin, lipids profile, Waist-hip ratio), and PNIE testing –periferical- (cortisol rhythm, FUC, DHEA, Thyroid profile, NK cells, CD4/CD8 ratio). Results The preliminary results show an increase in l/l variant of 5-HTTLPR among (at least one l allele has been found) first degree relatives of depressive and PTSD patients compared to affected patients. Immunological response, rhythm of cortisol secretion and metabolic determination trend were normal in our sample. Discussion This is an ongoing study with a very small sample. However, the normal clinical test and the l/l genotype suggest a protective factor for PTSD and MDD.