From: judgebean23x@gmail.com   
      
   BJPsych    
   The British Journal of Psychiatry   
   EDITORIALS   
      
   Alcohol-related dementia: a 21st-century silent epidemic?   
      
   Susham Gupta, James Warner   
   The British Journal of Psychiatry Oct 2008, 193 (5) 351-353; DOI:   
   10.1192/bjp.bp.108.051425   
   ArticleFigures & DataInfo & MetricseLetters PDF   
   Abstract   
      
   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.   
      
   Many adverse consequences of excessive drinking have been highlighted in both   
   the medical and popular press, but one that remains relatively obscure and   
   poorly addressed is that of alcohol-related dementia. The `Alcohol Harm   
   Reduction Strategy for    
   England'1 fails to mention the possibility of dementia as a consequence of   
   excessive drinking and does not address the problems of older drinkers or   
   potential challenges posed by alcohol-related dementia on the health and   
   social services. Various    
   definitions have been used to describe excessive drinking in medical   
   literature. The Department of Health's `sensible drinking' document recommends   
   no more than 3–4 units of alcohol daily for men and 2–3 units for women.   
   Some evidence suggests    
   limited drinking in earlier adult life may be protective against incident   
   dementia later. Long-term alcohol consumption above these limits is generally   
   considered harmful. The concurrent increase in use of recreational drugs may   
   contribute to later-onset    
   cognitive problems.   
      
   Changes in alcohol consumption   
      
   Attitudes towards alcohol and its use have undergone significant changes in   
   this country over the past few decades. These started in the baby-boomer years   
   with liberalisation of social values and greater individual freedom. Alcohol   
   has become cheaper in    
   relative terms and more widely available. There is a close link between   
   affordability and consumption. The price of alcohol relative to the average UK   
   income has halved since the 1960s, while per capita consumption of total   
   alcohol has nearly doubled    
   from under 6 l/year in the early 1960s to over 11.5 l/year by 2000.2 This is   
   still increasing in all age groups. Alcohol misuse in the elderly is also   
   underestimated and under-diagnosed. If the present trend of alcohol   
   consumption continues, within a    
   decade the UK will rise from the middle range to the top among European   
   countries.   
      
   Alcohol and its effects on the brain   
      
   Harper3 has reported a statistically significant loss of brain tissue in   
   chronic alcoholics compared with controls.3 This loss appears to be primarily   
   from the white matter with reduction in the number of cortical neurons in the   
   superior frontal cortex,    
   hypothalamus and cerebellum; but not in basal ganglia, nucleus basalis, or   
   serotonergic raphe nuclei. This seems to occur independently of Wernicke's   
   encephalopathy but nutritional deficits may make the situation worse. Chronic   
   alcoholism inhibits N-   
   methyl-d-aspartate (NMDA) causing upregulation of the NMDA subtype of   
   glutamate receptors in the frontal cortex, probably reflecting alcohol-induced   
   chronic neurotoxicity with increased intracellular calcium (mediating   
   oxidative stress) along with loss    
   of cholinergic muscarinic receptors. This may be related to the clinical   
   symptoms of alcohol withdrawal and alter seizure activity in the brain.   
      
   A review on the effect of alcohol on the frontal lobe noted that   
   neuroradiological findings support the occurrence of morphological   
   abnormalities in brains of chronic heavy drinkers, suggesting cerebral   
   atrophy.4 Structural imaging using computed    
   tomography scans of male alcoholics showed larger ventricles and wider   
   cerebral sulci and fissures compared with controls.5 Functional imaging   
   studies have reported decreased frontal lobe glucose utilisation and reduced   
   cerebral blood flow. Women are    
   probably more vulnerable to the effects of alcohol, exhibiting earlier changes   
   but also faster recovery on abstinence.6   
      
   Various mechanisms have been attributed to the effects of alcohol on the brain   
   including a direct neurotoxic effect of alcohol, oxidative stress,   
   excitotoxicity, mitochondrial damage and apoptosis. Repeated withdrawal may be   
   associated with greater    
   cognitive impairment due to neuronal damage and may have a bearing on the   
   dementing process. Those having two or more detoxifications showed a greater   
   degree of cognitive impairment compared with those with one or none.7 Repeated   
   withdrawals may be    
   associated with `kindling-effect' of worsening of withdrawal symptoms and   
   associated brain damage. A study found structural brain changes in   
   treatment-naïve alcoholics to be less severe than those of clinical samples   
   of alcoholics.8 However, difference    
   in severity, concomitant psychopathology and the age at drinking onset may   
   confound the effect of repeated detoxification.   
      
   Adverse effect of heavy drinking   
      
   The protective effect of light-to-moderate drinking is considered to be via a   
   number of mechanisms, both direct and indirect. These include increased serum   
   concentration of high-density lipoprotein, lowering of cholesterol, beneficial   
   effects on platelet    
   function, clotting and fibrinolysis, and improved insulin sensitivity. The   
   non-alcoholic components may have antioxidant, anti-inflammatory and   
   vasorelaxant properties.   
      
      
   [continued in next message]   
      
   --- SoupGate-Win32 v1.05   
    * Origin: you cannot sedate... all the things you hate (1:229/2)