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Substance Related Disorders / Diffusion Magnetic Resonance Imaging · Journal article
Dialogues in Clinical Neuroscience · August 25, 2026
Early or partial results. Treat as a signal, not a conclusion.
This longitudinal study found that substance use involvement moderated the relationship between childhood cortisol response and white-matter microstructure in the cingulum, such that elevated cortisol associated with greater secondary-fibre anisotropy only at higher levels of substance involvement. The finding is hypothesis-generating and based on a small neuroimaging sample; replication and clarification of the clinical significance of anisotropy changes are needed.
Longitudinal prospective observational cohort study. Participants from a larger longitudinal study on substance use disorder aetiology, enrolled at ages 10–12 years; follow-up diffusion MRI conducted after age 18 years.. Intervention: No intervention; observational measurement of cortisol response at baseline and substance use involvement over time.. Compared with: Moderation by substance use involvement; no active control group.. n = 69. Not stated in the source text provided..
Cortisol response levels were related to secondary- and tertiary-fibre anisotropy in the cingulum Substance use involvement moderated the association between cortisol response and right cingulum secondary-fibre anisotropy At heightened substance use involvement levels, cortisol response was associated with greater anisotropy
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This preliminary finding suggests substance use involvement may alter stress–brain relationships in youth, but lacks direct clinical endpoints (e.g., SUD diagnosis, cognitive outcomes). Clinicians should not yet adjust practice; the result is descriptive and requires replication with larger samples and defined clinical outcomes.
A single-centre longitudinal observational study with a small sample (n=69) examining a moderation effect on a surrogate neuroimaging endpoint; results require replication and lack hard clinical outcomes.
As stated by the source record.
Quoted from the source exactly as published.
This preliminary finding suggests substance use involvement may alter stress–brain relationships in youth, but lacks direct clinical endpoints (e.g., SUD diagnosis, cognitive outcomes). Clinicians should not yet adjust practice; the result is descriptive and requires replication with larger samples and defined clinical outcomes.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Introduction. Stress contributes to substance use (SU) involvement (SUI) and differences in brain white matter (WM). However, longitudinal relationships involving SUI, stress hormones, and WM are not well understood. This study examined the moderating role of SUI on the prospective association between cortisol response (CR) and WM microstructure.Methods. Data were drawn from a larger longitudinal study on SU disorder (SUD) aetiology. Participants were enrolled at ages 10-12 years when salivary cortisol was assayed. The Drug Use Chart assessed cumulative involvement with 10 substance categories by age 18 years. Diffusion-weighted data were acquired from sixty-nine participants after reaching age 18 years and were used to compute crossing-fibre measures. Analyses were conducted in a priori regions of interest linked to SU and stress.Results. CR levels were related to secondary- and tertiary-fibre anisotropy in the cingulum. SUI moderated associations between CR and right cingulum secondary-fibre anisotropy wherein CR levels associated with greater anisotropy at heightened SUI levels.Conclusions. This study identified stress-linked differences in distinct cingulum WM fibres among individuals with greater SUI. Involvement with SU overall, may modulate stress effects and enhance WM anisotropy in region- and fibre-specific manners. Potential biomarkers associated with SUI in WM among vulnerable stress-exposed youth require further investigation with respect to SUD aetiology.
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