Childhood trauma and addiction share a common biological pathway
Researchers have identified how childhood maltreatment and substance abuse disorders activate the same stress-response system in the body, potentially explaining why trauma survivors face higher addiction risk. The finding could help companies developing mental health treatments and inform public health policies targeting vulnerable populations.
Originaltitel: Individual and additive effects of childhood maltreatment and substance use disorder histories on baseline and stress-induced changes in peripheral stress biomarkers
<p>BackgroundExposure to childhood maltreatment (CM) has serious consequences on the health of affected individuals, potentially elevating vulnerability to various psychopathologies, including substance use disorders (SUDs). Recent investigations have implicated several biological signaling systems in vulnerability to SUD development following CM, including the kynurenine (KYN) pathway and endocannabinoid (eCB) system. Potential crosstalk between these systems has scarcely been explored.MethodsThe present exploratory analysis investigated the relationship between baseline and stress-induced changes in eCBs, KYN metabolites, inflammatory biomarkers, and cortisol across CM and SUD status (CM + SUD, CM only, SUD only, and healthy controls) using a factor analysis. Participants (N = 101) completed an acute laboratory stressor and blood samples were collected at five-timepoints throughout the task.ResultsFactor analysis revealed that KYN metabolites explained the majority of total variance in the dataset. The pro-inflammatory marker CRP was associated with neurotoxic KYN metabolites. Subsequent group-level analyses revealed that CM status significantly impacted a pro-inflammatory factor (baseline and stress-induced changes in CRP and IL-6). Additionally, CM and SUD status exhibited an interaction effect on a factor primarily comprised of 2-AG at baseline and throughout stress, such that in absence of CM, SUD was associated with significantly reduced levels of 2-AG.ConclusionsExposure to CM is associated with pro-inflammatory states at baseline and across stress exposure. Additionally, 2-AG may be a marker of SUD pathology in the absence of CM. However, no effect of CM or SUD status was found on KYN pathway metabolites. The mechanisms underlying elevated susceptibility to SUD following CM-exposure require further investigation.</p>