Symposium
Session Room: M1
Session Room: M1
Sunday, June 28, 02:40 PM – 03:55 PM
SCNP-Selected Symposium 16:
Early life stress, inflammation, and metabolic dysregulation: converging pathways to suicide risk and targets for new treatment options
Early life stress, inflammation, and metabolic dysregulation: converging pathways to suicide risk and targets for new treatment options
Lejla Colic will discuss possible mechanisms of the effects of early life adversity on the stress axis markers and emotion brain circuitry. She will present results from a study that investigated chronic stress markers measured in hair, cortisol and dehydroepiandrosterone in relation with clinical factors in a group of individuals with recent attempt (each group n=25). Her talk will include results of association between early life adversity and clinical risk factors, with a specific focus on self-oriented emotion-dysregulation in persons with suicide ideation and attempts (n=150). Lastly, she will present association among severity of early life adversity, emotion dysregulation, structural brain measures from 3 Tesla and risks for suicide attempts in an adult mood disorders cohort (n=150).
Xenia Gonda will discuss on the role of inflammation in suicide. Several chronic inflammatory disorders have been associated with increased risk of suicide; an association that is now recognized as not merely psychological, but also as a consequence of overlapping neurobiological mechanisms between inflammation and suicide. Environmental factors, including early life adversity and recent stress, further contribute to both chronic low-grade inflammation and elevated suicide risk. In individuals genetically predisposed to heightened inflammatory responses, early trauma may amplify this vulnerability. Thus, Investigating the genetic overlap between suicide and somatic conditions, particularly in the context of early and recent stress, offers critical insight into the biological consequences of childhood adversity and identifies targets for preventive intervention. In light of this, the presentation will share results from genome-wide association and environment interaction studies (GWAS/GWEIS) in a well phenotyped sample of different suicide risk phenotypes, highlighting the role of inflammatory variants and the moderating effects of early life stress exposure. Finally, interventions targeting immunological/inflammatory mechanisms with potential for suicide treatment from lifestyle interventions through psycho- and pharmacotherapies will also be summarised.
Metabolic and psychiatric disorders frequently co-occur, and there is an increased risk of suicide in this population. Large population and genomic studies reveal shared alterations in insulin signalling, lipid metabolism, and immune–inflammatory activity, mechanisms that are also involved in stress regulation and suicidal behaviour. The increased risk of suicide in individuals with metabolic disorders underscore the need to address metabolic health in suicide prevention. Amid this shared biology, GLP-1 receptor agonists (GLP-1RAs), widely used for diabetes and obesity, came under regulatory review for a possible increase in suicidality. Yet, comprehensive analyses, including a 2025 meta-analysis of 144 randomised trials and large observational studies, found no causal link and extremely low event rates. Nonetheless, psychiatric populations remain scarcely represented, warranting vigilance. Emerging preclinical and clinical evidence indicates that GLP-1RAs may exert beneficial effects on mood, cognition, and stress regulation, opening repurposing prospects across depression, binge-eating, and addiction. Giuseppe Fanelli, in his presentation, will bridge metabolic–psychiatric comorbidity, latest genomic findings, and psychopharmacological innovation, highlighting how GLP-1 modulation could represent one of the most promising therapeutic advances of recent years.
Xenia Gonda will discuss on the role of inflammation in suicide. Several chronic inflammatory disorders have been associated with increased risk of suicide; an association that is now recognized as not merely psychological, but also as a consequence of overlapping neurobiological mechanisms between inflammation and suicide. Environmental factors, including early life adversity and recent stress, further contribute to both chronic low-grade inflammation and elevated suicide risk. In individuals genetically predisposed to heightened inflammatory responses, early trauma may amplify this vulnerability. Thus, Investigating the genetic overlap between suicide and somatic conditions, particularly in the context of early and recent stress, offers critical insight into the biological consequences of childhood adversity and identifies targets for preventive intervention. In light of this, the presentation will share results from genome-wide association and environment interaction studies (GWAS/GWEIS) in a well phenotyped sample of different suicide risk phenotypes, highlighting the role of inflammatory variants and the moderating effects of early life stress exposure. Finally, interventions targeting immunological/inflammatory mechanisms with potential for suicide treatment from lifestyle interventions through psycho- and pharmacotherapies will also be summarised.
Metabolic and psychiatric disorders frequently co-occur, and there is an increased risk of suicide in this population. Large population and genomic studies reveal shared alterations in insulin signalling, lipid metabolism, and immune–inflammatory activity, mechanisms that are also involved in stress regulation and suicidal behaviour. The increased risk of suicide in individuals with metabolic disorders underscore the need to address metabolic health in suicide prevention. Amid this shared biology, GLP-1 receptor agonists (GLP-1RAs), widely used for diabetes and obesity, came under regulatory review for a possible increase in suicidality. Yet, comprehensive analyses, including a 2025 meta-analysis of 144 randomised trials and large observational studies, found no causal link and extremely low event rates. Nonetheless, psychiatric populations remain scarcely represented, warranting vigilance. Emerging preclinical and clinical evidence indicates that GLP-1RAs may exert beneficial effects on mood, cognition, and stress regulation, opening repurposing prospects across depression, binge-eating, and addiction. Giuseppe Fanelli, in his presentation, will bridge metabolic–psychiatric comorbidity, latest genomic findings, and psychopharmacological innovation, highlighting how GLP-1 modulation could represent one of the most promising therapeutic advances of recent years.