ReviewPsychopharmacology2026
Early life adversity, oxytocin system alterations, and addiction vulnerability: a narrative review.
Review in Psychopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prenatal and early-life stress (ELS) reprogram the hypothalamic-pituitary-adrenal (HPA) axis and intersecting neurotransmitter circuits, producing long-lasting alterations in the oxytocin (OXT) system. Accumulating clinical and pre-clinical evidence links these neurobiological changes to increased vulnerability for addiction. This narrative review synthesizes recent (2005-2025) literature on: how ELS disrupts the maturation of OXT neurons and receptors; the consequent cross-talk with glutamatergic, GABAergic and HPA-peptide signaling that biases the mesocorticolimbic reward network toward addiction; and the emerging therapeutic potential of exogenous OXT. Rodent models of maternal separation, limited bedding or gestational restraint reveal OXT-system hypofunction-marked by OXTR hyper-methylation, reduced hypothalamic OXT mRNA and diminished receptor density in the amygdala and nucleus accumbens. Parallel human studies report analogous epigenetic signatures in cord blood and peripheral tissues of stress-exposed offspring. Functionally, OXT curtails presynaptic glutamate release in the ventral tegmental area, augments tonic GABA_A currents in medial prefrontal cortex, and attenuates AVP-driven CRH output, thereby normalizing reward- and stress-circuit activity. These adaptations translate into lower drug intake, reduced cue-induced reinstatement and blunted withdrawal anxiety in animal models. Early clinical trials corroborate these findings; intranasal OXT reduces craving and withdrawal severity, with the largest effect sizes observed in individuals exhibiting low baseline plasma OXT or high OXTR methylation. It can be concluded that prenatal stress is a potent risk factor for later substance use disorders (SUDs), in part via durable disruption of the developing OXT system. Targeted OXT pharmacotherapy-alone or combined with stress-axis modulators-holds promise for a precision-medicine approach to addiction, particularly in ELS-exposed subpopulations.
Indexed as
Identifiers
42126578What 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.