# Cognitive Functioning in Abstinent Patients with Alcohol Use Disorder: Exploring Evidence for Premature Aging

**Authors:** Jeroen Staudt, Yvonne C. M. Rensen, Hein A. De Haan, Jos I. M. Egger, Boukje A. G. Dijkstra

PMC · DOI: 10.3390/brainsci16030320 · 2026-03-17

## TL;DR

This study finds that abstinent alcohol use disorder patients show age-related cognitive changes, but the evidence for premature aging is weak.

## Contribution

The study explores cognitive recovery patterns in abstinent AUD patients and challenges the accelerated aging hypothesis.

## Key findings

- Age-related deviations were observed in perceptual reasoning, verbal comprehension, and short-term memory after six weeks of abstinence.
- Each additional year of age reduced the odds of cognitive recovery and absence of impairment in abstinent AUD patients.
- Findings do not support the accelerated aging hypothesis or the vulnerability hypothesis strongly.

## Abstract

What are the main findings?
Cognitive aging in abstinent patients with AUD may be domain-specific.Perceptual reasoning and recovery may be affected by increasing age.

Cognitive aging in abstinent patients with AUD may be domain-specific.

Perceptual reasoning and recovery may be affected by increasing age.

What are the implications of the main findings?
The findings are not considered strong enough to evidence the vulnerability hypothesis and do not support accelerated aging at all.Replication of the findings is needed with larger sample size and the inclusion of older adults (>60 year).

The findings are not considered strong enough to evidence the vulnerability hypothesis and do not support accelerated aging at all.

Replication of the findings is needed with larger sample size and the inclusion of older adults (>60 year).

Background/Objectives: Chronic alcohol use accelerates biological and cognitive aging, yet it remains unclear how cognitive aging progresses during abstinence in alcohol use disorder (AUD). It is also unknown to what extent this follows models such as accelerated aging or the age-related decline as proposed by the vulnerability hypothesis. This study examined age-related changes and cognitive recovery during abstinence in patients with AUD. Methods: A total of 197 clinically admitted patients, referred for detoxification and extensive neuropsychological examination, were included. Neuropsychological testing was administered in the second and sixth week of admission using well-normed instruments. Using both multi-assessment and cross-sectional data, relationships between age and normed cognitive outcome scores were examined. Results: After six weeks of abstinence, age-related deviations were observed for perceptual reasoning (PRI), verbal comprehension (VCI), and short-term memory (SMI) but not for ten other cognitive indices. During admission, age significantly influenced the change in belonging to a specific recovery category. Each additional year of age reduced the odds of showing no cognitive impairment by 5% and reduced the odds of cognitive recovery by approximately 4%, compared to non-improvers. Conclusions: Age-related influences appear limited to specific cognitive functions and do not follow a uniform or easily interpretable pattern. Perceptual reasoning seems negatively affected after age 60 for participants with six weeks of abstinence. Older participants showed a reduced likelihood of cognitive recovery and a reduced likelihood of having no cognitive problems at all. The findings do not support accelerated aging and are still too weak to be considered evidence for the vulnerability hypothesis. Implications for future research are discussed.

## Full-text entities

- **Diseases:** lupus (MESH:D008180), neurological injury (MESH:D020196), WMS (MESH:D018980), neurological disorders (MESH:D009461), Alzheimer's disease (MESH:D000544), seizures (MESH:D012640), tobacco use disorder (MESH:D014029), suicidal ideation (MESH:D001072), WAIS-IV (MESH:D006011), schizophrenia (MESH:D012559), VCI (MESH:D001308), cerebrovascular accidents (MESH:D020521), decline (MESH:D060825), injury to (MESH:D014947), neuropsychological dysfunction (MESH:D006331), brain injury (MESH:D001930), congenital epilepsy (MESH:D004827), nutritional deficiencies (MESH:D044342), AUD (MESH:D000437), psychosis (MESH:D011618), Addiction (MESH:D019966), psychiatric disorders (MESH:D001523), neurotoxic (MESH:D020258), cognitive disturbances (MESH:D003072), neurodegenerative disorders (MESH:D019636)
- **Chemicals:** MDMA (MESH:D018817), polysubstance (-), amphetamines (MESH:D000662), Alcohol (MESH:D000438), cocaine (MESH:D003042)
- **Species:** Homo sapiens (human, species) [taxon 9606], Nicotiana tabacum (American tobacco, species) [taxon 4097]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC13025035/full.md

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Source: https://tomesphere.com/paper/PMC13025035