Alcohol-related brain damage: not a silent epidemic
Sameer Jauhar, Iain D. Smith

We read with interest the Editorial by Gupta & Warner,1 in which they postulated a possible `silent epidemic of alcohol-related dementia'. We welcome the call for increased awareness, but would make the following points.

First, nosology. The term `alcohol-related dementia' (alcohol-induced persisting dementia in DSM–IV) has generally been superseded in clinical practice by the (more accurate) term `alcohol-related brain damage/injury', incorporated nationally in many countries, including Scotland.2 We were particularly concerned about the authors' exclusion of Korsakoff's syndrome from the aetiology of this entity. The prevailing best synthesis of the evidence on aetiology is the Lishman hypothesis,3 namely that the alcohol amnestic (Korsakoff's) syndrome exists on a spectrum with other forms of alcohol-related brain injury, thiamine depletion injury interacting with alcohol neurotoxicity, resulting in what the authors conceptualise as alcohol-related dementia.

Second, in Scotland, alcohol-related brain damage has been incorporated into health policy and promotion, with statistics – produced by the Information and Statistics Division (ISD) of the Scottish Health Service (available since 1997) – showing increased rates of general hospital admissions over the past 8 years (155 patients identified under age 65 and 99 patients over 65 in 1996–1997 compared with 287 and 185 respectively in 2004–2005) (ISD, personal communication, 2006). There is acknowledgement in Scotland of the effects on both those under and over 65 years, with provision of specific services, distinct from dementia services, recognising the differing needs of this group.

Third, although we accept there is no conclusive evidence on effects of hazardous alcohol use over the life-course in terms of the emergence of a dementia syndrome in old age, we would urge caution in claiming a `silent epidemic'. To date there has been no definitive neuropathological evidence of alcohol being a primary aetiological factor in a dementia syndrome of old age. We would suggest, from clinical experience, that the effects of significant alcohol use in the elderly are better conceptualised as short-term contributory effects on more significant causes of cognitive impairment (e.g. Alzheimer's disease, vascular dementia), in keeping with current thinking.3 This would be seen as a separate process from the spectrum of primary alcohol-related brain damage.

Fourth, the quoted epidemiological studies do not provide clear evidence to suggest that `alcohol-related dementia' will increase at a population level, other than in cohorts with sustained alcohol dependence and poor nutrition. These findings, for those without dependency, are equivocal at best, and do not demonstrate population effects of hazardous drinking on increasing dementia rates. These results illustrate the heterogeneity of alcohol's effects on differing populations, with there being equivalent evidence for moderate drinking having an association with better cognitive function.4

In conclusion, our view would be that the effects of alcohol excess on cognition are heterogeneous in terms of clinical syndrome, and multifactorial in terms of aetiology (including individual susceptibility factors, yet to be determined). The more relevant concept is that of alcohol-related brain damage, where undoubtedly presentations have increased in recent decades, in parallel with rates of alcohol dependency in the UK.