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Alcohol-related dementia: a 21st-century silent epidemic?

  • Susham Gupta (a1) and James Warner (a1)
Summary

Evidence suggests a J-shaped relationship between alcohol consumption and cognitive impairment and other health indicators, with low levels of consumption having better outcomes than abstention or moderate to heavy drinking. Most research to date has focused on the protective effects of drinking small amounts of alcohol. As alcohol consumption is escalating rapidly in many countries, the current cohort of young and middle-aged people may face an upsurge of alcohol-related dementia. The dangers of heavy drinking and its effect on cognition require further attention.

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Corresponding author
Susham Gupta, Nightingale Unit, St Charles Hospital, Exmoor Street, London W10 6DZ, UK. Email: sushamgupta@yahoo.com
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Declaration of interest

None.

Footnotes
References
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Alcohol-related dementia: a 21st-century silent epidemic?

  • Susham Gupta (a1) and James Warner (a1)
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eLetters

Inclusion of alcohol-related treatable dementia in alcohol-related dementia nosology

Krishna Meena, Lecturer
19 February 2009

The Editorial by Gupta & Warner (2008)(1) on ‘Alcohol – related dementia : a 21st century silent epidemic?’ has significant impact on this neglected area of treatable dementia. This article will create further debate on the effect of wine in elderly population and further sensitize this vulnerable population.

To add to this editorial, the authors probably miss out the point that alcohol plays an important role for nutritional deficiencies include folate and vitamin B12 that can further results in treatable dementias. Inone of the clinic based study (2), conducted in tertiary care centre of developing country, alcohol-related dementia was diagnosed in 10.5%, whilemalnutrition (Vitamin B12 deficiency) related dementia was detected 7.2% of the clinical sample.

Hence, it is worthwhile to include this issue of alcohol related treatable dementia to further strengthen the case for alcohol related dementia.

Reference:1. Gupta S, Warner J. Alcohol – related dementia: a 21st – century silent epidemic? British Journal of Psychiatry 2008; 193 : 351-353. 2. Jha S, Patel R. Some observations on the spectrum of dementia. Neurol India. 2004 ;52(2):213-4.
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Conflict of interest: None Declared

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Alcohol- related cognitive impairment amongst the "Poor"

Prof K.A.L.A. Kuruppuarachchi MD,FRCPsych(UK), Professor of Psychiatry
24 January 2009

The Editorial on Alcohol – related dementia : a 21st century silent epidemic? by Gupta & Warner (2008) has been read with much interest asit has a global relevance.Even though there are problems in the “nosology” of the alcohol related cognitive impairment, this is a very important area in psychiatric practice.Old age population has been increasing globally and particularly in developing countries over the last few decades , hence we are going to encounter more and more old age clinical conditions such as dementia. Consumption of alcohol will add to the cognitive impairment.Another important factor note worthy is an extensive use of illicit alcohol in many developing countries. For example in Sri Lanka most frequently consumed form of alcoholic beverage is “Kasippu”which is a illicitly brewed and sold brand of liquor (WHO, 2004). According to the available data about one fourth to one third of males across South Asian Countries drink alcohol whereas the percentage among the women is very lowas 4-9% . Illicit liquor may be contaminated with other substances which can be neurotoxic such as traces of heavy metals. The percentage of alcohol in the illicit liquor is variable and most of the time it containsa higher percentage. The other contributory factors for cognitive impairment are poor nutrition and deficiency states. Concomitant use of other street drugs such as cannabis can contribute to cognitive impairment. On the other hand as a result of genetic variation metabolism and elimination of alcohol may be different in Asians and which may be having a protective effect against heavy alcohol drinking and alcoholism (Pi & Zhu, 2007). Also the genetic vulnerability to alcohol related cognitive impairment may be different in our part of the world.Many patients with alcohol misuse may not be receiving an adequate amount of thiamine supplements. Studies have demonstrated the need for clear guidelines and education of the therapists involved in the management on all aspects of vitamin deficiency in this vulnerable group (Hope et al.,1999). Research have shown that there is a greater sensitivity to alcohol neurotoxicity among women (Hommer et al., 2001). Fortunately the prevalence of alcohol consumption among women is less in South Asian countries.Relatives may misperceive behavioural disturbances associated with frontallobe damage due to chronic alcohol misuse as “disinhibited behaviour due to alcohol intoxication” or “naughty behaviour” following alcohol abuse and may not seek appropriate medical help.Cognitive impairment including dementia in alcohol misuse seems to be underestimated globally and the clinicians and policy makers should be aware of this important area to minimize the adverse outcomes. Also we need to do more research work in this area.

Gupta S, Warner J. Alcohol – related dementia: a 21st – century silent epidemic? British Journal of Psychiatry 2008; 193 : 351-353.

WHO Global Status Report on Alcohol 2004. World Health Organization 2004.

Pi EH, Zhu W. New research advances in ethno-psychopharmacology : an Asian perspective. International Psychiatry 2007 ; 4 , 57-58.

Hope LC, Cook CCH, Thomson AD. A SURVEY OF THE CURRENT CLINICAL PRACTICE OF PSYCHIATRISTS AND ACCIDENT AND EMERGENCY SPECIALISTS IN THE UNITED KINGDOM CONCERNING VITAMIN SUPPLEMENTATION FOR CHRONIC ALCOHOL MISUSERS. Alcohol and Alcoholism 1999; 34 , 862-867.

Hommer DW, Momenan R, Kaiser E, et al. Evidence for a Gender – Related Effect of Alcoholism on Brain Volumes. American Journal of Psychiatry 2001; 158 , 198-204.
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Drugs of misuse,ilict or street drugs

AK Al-Sheikhli, Consultant Psychiatrist
10 December 2008

Dear Editor

I read with interest Gupta and Warner editorial ,Alcohol-related dementia: a 21st-century silent epidemic?( Journal 2008; 193: 351-353),I was surprised they use the term recreational drugs such as ecstasy? rather than street,illicit,or drugs ofmisuse.

Conflict of interest: None Declared

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Authors' response

James Warner, Consultant Psychiatrist
10 December 2008

We thank Sameer Jauhar and Iain D Smith for their comments which serve to highlight the lack of consistent approach to alcohol-related dementia.

Among clinicians there is generally good awareness of Korsakoff’s syndrome as a sub-acute sequel to prolonged heavy drinking and nutritionaldeficiency (among other causes). We agree there may be a continuum betweenpure Korsakoff’s and dementia. However our article was intended to raise awareness of the less well recognised, broader dementia category at the other end of this spectrum.

Getting tied up in nosological arguments (Alcohol-Related Brain Damage (ARBD) or alcohol related dementia) is unlikely to help get across the health message. We believe ignoring the word "dementia" may reduce the impact of the message and conflate several neurological sequelae of alcohol misuse. The increase in general hospital admissions in Scotland reported by Jauhar and Smith serve to reinforce our message.

We agree there is no definitive neuropathological link between alcohol consumption and dementia although epidemiological studies do suggest an association. There is simply insufficient research on this point. To conjecture that absence of evidence equates to evidence of absence is hazardous.

We are overwhelmed by the level of positive national and international media and scientific interest in our article. Hopefully thiswill result in our twin aims; increasing awareness and stimulating research in this area.

Susham Gupta and James Warner

Declaration of interest: none
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Alcohol Related Brain Damage, not a silent epidemic.

Sameer Jauhar, Specialty Registrar in General Adult Psychiatry
27 November 2008

Dear Editor,

We read with interest the Editorial by Gupta and Warner (1), in whichthey postulated a possible “silent epidemic of alcohol-related dementia”. We welcome the call for increased awareness, but would make the following points;

1) 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(ARBD/I)”, 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 whatthe authors conceptualise as alcohol-related dementia.

2) In Scotland ARBD has been incorporated into health policy and promotion, statistics produced by ISD (Information and Statistics Divisionof the Scottish Health Service) being available since 1997, showing rates of general hospital admissions for ARBD increasing over the last 8 years (155 patients identified under age 65, 99 over 65 in 1996/7, compared to 287 and 185 in 2004/5) (4). There is acknowledgement in Scotland of ARBD’seffects on both those under and over 65, with provision of specific services, distinct from dementia services, acknowledging the differing needs of this group.

3) Whilst 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 this being 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 (eg Alzheimer’s disease and vascular dementia), in keeping with current thinking (3). This would be seen as a separate process from the spectrum of primary ARBD.

4) The quoted epidemiological studies do not provide clear evidence to suggest “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, there being equivalent evidence for moderate drinking having an association with better cognitivefunction (5).

In conclusion our view would be that the effects of alcohol excess oncognition are heterogeneous in terms of clinical syndrome, and multi-factorial 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 United Kingdom.

Declaration of Interest; None

References;

1) Gupta S, Warner J. Alcohol-related dementia; a 21st century silentepidemic? British Journal of Psychiatry 2008; 193;351-353.

2) A Fuller Life; Report of the Expert Group on Alcohol Related BrainDamage, Scottish Executive, 2004.(http://www.alcoholinformation.isdscotland.org/alcohol_misuse/files/ARBD_afullerlife.pdf)

3) Lishman WA. Organic Psychiatry: the psychological consequences of cerebral disorder. Blackwell Science, Oxford, 1998.

4) ISD-personal communication.

5) Rodgers B, Windsor TD, Anstey KJ, Dear KBG, Jorm AF, Christensen H.Non-linear relationships between cognitive function and alcohol consumption in young, middle-aged and older adults: the PATH Through Life Project. Addiction, 2005;100;1280-1290.
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