We should be fortifying beer to target the people who develop this disorder
MJA 1998; 168: 534-535
Wernicke's encephalopathy (WE) usually occurs in people who have been drinking alcohol heavily and not eating, but can also occur after persistent vomiting or during hunger strikes. It is characterised by an acute global confusional-apathetic state with ophthalmoplegia or nystagmus. The ophthalmoplegia and confusion respond to thiamine treatment. Korsakoff's amnesic psychosis is associated with WE. Typically, it is recognised when the confusion clears in response to treatment with thiamine. While Korsakoff's psychosis (KP) sometimes responds slowly to thiamine, it is often persistent. Wernicke's encephalopathy is not easy to differentiate from other impairments of mental function in alcohol abusers. There is no rapid confirmatory special investigation. A patient with WE can die before being brought to hospital, and, in hospital, if the condition is not quickly recognised it is likely to lead to permanent memory damage in the form of Korsakoff's psychosis.1 Australia appears to have had both a higher incidence of WE than other comparable countries, and more people requiring long term care because of KP.2 In the 1980s, our national incidences of acute WE and of KP were estimated at about 6.5 cases/100 000 adults per year,3 and 22 cases/100 000 adults per year, respectively. As WE is not easily differentiated (as mentioned above) and as KP does not usually respond to thiamine treatment, this is evidently a disease complex more suitable for prevention than treatment. Public health measures have been under active discussion by Commonwealth health authorities since the problem was set out in a 1979 conference.4 In 1987, the National Health and Medical Research Council (NHMRC) recommended addition of thiamine to beer and flagon wine.5 However, nutrification of alcoholic beverages was unprecedented and was opposed by both brewers and anti-alcohol groups. After more discussion the NHMRC adopted the compromise suggested by its Nutrition Committee, that thiamine be added to bread flour as a first measure.6 Thiamine fortification of white bread is common in other industrial countries, introduced to restore losses of this vitamin from wheat by the refining process. Addition of thiamine to bread flour (at 6.4 mg/kg) was made mandatory in Australia on 1 January 1991. The Federal Government did not set up a system to monitor the effect of bread fortification, but information is accumulating that there has been some effect. A retrospective survey of records from the 17 major public health hospitals in greater Sydney for cases of Wernicke-Korsakoff syndrome (WKS) over the 10 years to 1993 showed that numbers of acute cases of WE or KP were lower in 1992 and 1993 than for any of the years preceding fortification.7 In this issue of the Journal, Harper and colleagues report on neuropathological postmortem examination of over 2000 brains at the NSW Institute of Forensic Medicine in 1996 and 1997.8 WKS can be identified by its effects on the mammillary bodies and walls of the third ventricle, and needs to be distinguished from changes caused by Alzheimer's disease, infarction, hypoxia and head injury. With the use of standardised techniques and special stains, 25 cases of WKS were identified, giving a prevalence of 1.1%. This is less than half the rate of 2.8% that Harper found in 4677 people (1783 postmortem brain examinations and 2894 hospital patients) in Western Australia between 1973 and 1978.1 Only two of the 25 NSW cases reported in this issue had been diagnosed at autopsy as acute WKS; six were diagnosed as acute-on-chronic and 17 as chronic. No note of ophthalmoplegia or nystagmus was found in hospital records for the 18 cases for which these were available.8 The neuropathology survey is thus showing a different end of the Wernicke-Korsakoff spectrum than the hospital record survey,7 which specifically sought new, acute cases. Both report from the Sydney area. A third look at WKS trends across Australia is afforded by comparing national mortality data obtainable from the Australian Bureau of Statistics for 1984 and 1989 (before fortification) with data for 1993 and 1996 (after fortification). Deaths from "other thiamine deficiency", "Korsakov's alcoholic psychosis" and "alcoholic cardiomyopathy" (some of which were presumably the result of thiamine deficiency) declined 22% from a combined two-year total of 329 to 255. By contrast, combined deaths from "other alcoholic dementia", "alcohol dependence syndrome" and "non dependent use of alcohol" increased somewhat from 452 to 493. A continuation of the survey of inpatient records in Sydney's 17 public general hospitals7 now includes data to 1996.9 Disregarding 1991, as it was the transition year, the average incidence of acute cases of WE or KP in the five years since fortification (1992-1996) was 40% lower than in the five years before fortification (1986-1990). This difference was statistically significant (P < 0.002),9 but the downward trend is not continuing -- the average of 41 acute cases per year for 1995 and 1996 was no lower than the 40 cases per year in 1992 and 1993.9 Increased thiamine intake from bread seems the most likely explanation for the apparent reductions of Wernicke-Korsakoff syndrome in Australia in the 1990s. Clinical diagnosis is subject to error, and postmortem diagnosis is based on morphological, and not chemical, characteristics. However, the decline, determined by different methods in three different studies,7-9 appears to be consistent over several years. Although the occurrence of Wernicke-Korsakoff syndrome in Australia appears to have been reduced by thiamine fortification of bread, it has not been eliminated. As nearly all cases occur in heavy alcohol drinkers, beer is probably a more appropriate vehicle for thiamine nutrification than bread. Prominent psychiatrist Eric Dax first suggested this 30 years ago.2 Beer is the preferred beverage of patients presenting with Wernicke's encephalopathy;7,10 the taste of thiamine hydrochloride can merge with the flavour of beer11 (but not with that of table wine); and it has been estimated that addition of thiamine to beer would be much more cost-effective than adding it to bread.12 It is clearly time for Commonwealth and State health authorities, the brewers and the NHMRC to seriously reconsider trialling the addition of thiamine to Australian beers -- to make them nutritionally the best in the world. Leslie R Drew A Stewart Truswell
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