Nutritional Exposures and Cognitive Impairment in Alcohol Use Disorder: A Structured Narrative Review of Prioritized Human Evidence

Background/Objectives: Cognitive impairment in alcohol use disorder (AUD) may reflect alcohol exposure, withdrawal, nutritional disruption, systemic illness, and social vulnerability. We evaluated prioritized human-adult evidence linking nutritional exposures with objective cognition and examined separately whether AUD severity modifies nutrition–cognition associations and whether nutritional disruption mediates the relationship between alcohol exposure and cognitive outcomes. Methods: This structured narrative review used documented multi-database retrieval, pre-access prioritization, full-text adjudication, evidence appraisal, and qualitative sensitivity scenarios. A targeted vitamin B12 update supplemented the baseline corpus. Results: Thiamine had the broadest and most clinically actionable evidence, but biomarker thresholds, optimal cognitive dosing, and independent treatment effects remained uncertain. Evidence for folate, vitamin B12, niacin outside pellagra, other micronutrients, diet, body mass index, and albumin was sparse, mixed, or nonspecific. The targeted B12 evidence was null or contradictory rather than supportive. Cognitive improvement during detoxification could not be separated from abstinence and bundled care. No included study verified causal mediation by nutrition or a formal nutrition-by-severity interaction. Conclusions: Nutritional assessment and prompt treatment of recognized deficiency remain clinically important, but the prioritized retrieved corpus does not justify nutrient-specific causal claims for typical AUD-related cognitive impairment. Longitudinal studies should align repeated nutrition, alcohol exposure, cognition, and function and prespecify interaction and mediation tests.