ArticlePsychopharmacology2026
Individual and additive effects of childhood maltreatment and substance use disorder histories on baseline and stress-induced changes in peripheral stress biomarkers.
Article in Psychopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- EBPS2023 special issue: Stress, trauma and cannabinoids.Psychopharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.