### Consensus consistency validation — 9 October 2026

Scope: retrospective validation of the archived v5.3 review; the prior score was visible, so this is not blind calibration. The preregistered gradeable claim is that drug-induced neuroadaptation causes loss of volitional control and a generally chronic relapsing course. The registered subclaims remain SC1 (persistent neural adaptation), SC2 (neural contributions to compulsive seeking), and SC3 (general human loss-of-volition/chronic-course inference). Aggregation remains primary-subclaim SC3. Prior level/confidence: Γ, Moderate. Literature cutoff 2026-10-09; original-source checks conducted 2026-10-09 local (2026-10-10 UTC).

#### Raw Consensus provenance

The raw Consensus Pro/browser document is to be preserved unchanged in `consensus-browser-response.md` with thread metadata in `browser-thread.json`. This addendum does not reproduce or paraphrase that response as verified evidence. Connector search was used as a discovery lead for the human lesion-network and prospective relapse-prediction primary reports below. Reviews (including the Consensus-surfaced systematic review of neurocognitive predictors) and protocols are not counted as primary causal lines.

#### Primary-source checks

| Load-bearing claim | Primary report checked | Source-level observation | Before/after judgement |
|---|---|---|---|
| Focal human brain damage can be associated with addiction remission and nominate a circuit. | Joutsa et al., PMID 35697842; DOI 10.1038/s41591-022-01834-y; PubMed abstract/figures (`https://pubmed.ncbi.nlm.nih.gov/35697842/`); abstract/figure-caption access. | Two cohorts with smoking addiction at focal brain damage (n=67, n=62); lesion locations did not converge anatomically and voxel-based lesion-symptom mapping was not significant, but a lesion-network map identified connectivity associated with remission. Independent brain-damage cohort (n=186) provided an alcohol-risk generalization analysis; the authors describe the connection as a candidate target. This report was absent from the archived 56-source inventory and is a new source, not a replication in a general SUD population. | Supports a specific human circuit contribution and modestly strengthens SC2/biological involvement. It does not test drug-induced neuroadaptation, normal variation in volition, selective reversal of an addiction-associated adaptation, or a generally chronic course. No SC3 level change; confidence remains Moderate.
| Some measured neurobehavioral markers prospectively predict relapse in a clinical sample. | MacNiven et al., PMID 37567334; DOI 10.1016/j.biopsych.2023.07.020; PubMed abstract (`https://pubmed.ncbi.nlm.nih.gov/37567334/`); abstract_metadata. | Prospective study of detoxified stimulant-use-disorder patients (n=68) and controls (n=42); 27 remained abstinent and 33 relapsed at six months. Lower anterior-insula response to monetary-loss anticipation predicted relapse, cross-validated accuracy reported as 72.7%. The response did not differ between patients and controls in the reported abstract, limiting diagnostic specificity; marker prediction is observational, not a mediator manipulation. The paper was absent from the archived inventory. | Supports bounded prediction in one stimulant cohort but not causal necessity, universal inability to choose, or a general chronic-relapse trajectory. No level/confidence change for SC3.
| Human behavior can respond to alternative reinforcement and treatment contingencies. | Miguel et al., PMID 27442691; DOI 10.1037/adb0000192; PubMed abstract (`https://pubmed.ncbi.nlm.nih.gov/27442691/`); abstract_metadata, with archive's full_text_partial receipt retained. | In a 65-person RCT among treatment-seeking crack-cocaine-dependent participants, contingency management increased treatment attendance/retention and continuous-abstinence runs. A negative-sample proportion difference was present when all expected samples were the denominator but not when only submitted samples were used. No neural state or mediator was measured. The report is already counted in the archive as PMID27442691 and one trial. | Existing interpretation stands: objective behavior is sensitive to incentives/context, but this does not establish brain independence or absence of neuroadaptation. It counters an invariant loss-of-agency interpretation without erasing severe cases. No change.


| A randomized contingency-management intervention can increase biologically measured alcohol abstinence; drug co-abstinence in the same factorial trial was less secure. | McDonell et al. Rewarding Recovery, PMID 33220122; DOI 10.1111/add.15349; PubMed abstract (`https://pubmed.ncbi.nlm.nih.gov/33220122/`); abstract_metadata. | 114 American Indian adults with alcohol dependence and co-use randomized in a 2×2 factorial trial. Alcohol-contingent arms increased alcohol-abstinent urine submission odds (OR 2.4–4.8); drug-abstinence contrasts were not significant in multiple-imputation analyses, and the abstract calls the drug effect inconclusive. This is one primary RCT and was not in the archived 56-source inventory. It assesses behavioral treatment contingencies, not neural state or volition. Consensus raw response markers [19.1] and [19.2] cite it. | Supports objectively measured behavioral responsiveness to an alternative contingency in this defined clinical community; it does not establish brain-independent choice or universal volitional capacity. No change to SC3 or aggregate score. |
#### Consensus-result reconciliation

Consensus surfaced the human lesion-network report as a relevant primary source; it was absent from the original evidence inventory and is added only to this audit comparison, not to the canonical review. The original source supports some brain-network involvement while remaining narrow in exposure, phenotype and causal inference. Consensus also surfaced a systematic review reporting limited evidence for neurocognition as a general addiction-outcome predictor. That is a synthesis, not an independent primary causal line; the claim was checked against a primary prospective stimulant cohort instead. The primary prospective study supports prediction in a defined sample, not mediation. The contingency-management report was already in the dossier and must not be counted twice.

Consensus also interprets incentive-driven objective outcomes as evidence of human goal-directed choice/volition. The primary RCTs demonstrate responsiveness of measured behavior under specific contingencies, not a direct measurement of volition or absence of automatic components.

The review's SC3 does not ask whether the brain matters at all. It asks whether drug-induced adaptation generally explains human loss of volitional control and a chronic relapsing course. None of these primary studies manipulates a proposed endogenous adaptation in humans while preserving the drug effect and tests objective symptom/use trajectory across a prespecified general SUD scope. The new human lesion report is meaningful support for the broad biological premise and is the strongest new counterweight; it does not satisfy the registered gate.

#### Per-subclaim score decision

- SC1 (repeated drug exposure produces persistent brain adaptations): Γ, Moderate — unchanged. The new human lesion cohort does not measure exposure-induced adaptations; archive already contains repeated experimental model and recovery evidence.
- SC2 (specific neuroadaptations contribute causally to compulsive seeking): Γ, Moderate — unchanged. Lesion-network evidence modestly reinforces brain-circuit contribution; the prospective neurobehavioral marker is predictive/associational. Neither yields human mediator necessity for general addiction.
- SC3 (drug-induced adaptations explain general human loss of volition/chronic relapsing course): Γ, Moderate — unchanged. Brain involvement and selected relapse prediction remain compatible with heterogeneous course and contextual control; neither demonstrates a necessary, general adaptation causing inability to choose.
- Aggregation remains primary-subclaim SC3; overall Γ, Moderate. No confidence-band change proposed: the new primary lesion study increases plausibility of a circuit contribution but does not close the scope/mechanism gap; the prospective association is one cohort; the pre-existing Miguel CM RCT and the new McDonell CM RCT are behavioral contingency studies, not neural-mechanism evidence. Prior level was visible; not blind calibration.

#### Source links

- PubMed primary records: https://pubmed.ncbi.nlm.nih.gov/35697842/ ; https://pubmed.ncbi.nlm.nih.gov/37567334/ ; https://pubmed.ncbi.nlm.nih.gov/27442691/
- Consensus references from connector search: Joutsa et al. paper record https://consensus.app/papers/details/a75f6a5119695a5a9a9fb4310171574a/?utm_source=unknown ; MacNiven et al. paper record https://consensus.app/papers/details/1117e86f52b65b3895a49ae1dcd9b47c/?utm_source=chatgpt



This dated supplement adds source reconciliation to the original review. Its original narrative, registered scope, source inventory and grades remain historical records. No earlier adversarial approval has been verified for this edition at the supplement date. This provenance supplement has no separate approval and is not an independent or blinded adjudication. New sources described here are supplemental and are not counted in the original inventory.