Q J Med 2009; 102:221–222 doi:10.1093/qjmed/hcn176 Advance Access publication 7 January 2009
Commentary Alcohol—it’s more than the liver S.H. SONG From the Diabetes Centre, Northern General Hospital, Sheffield, UK
increased production of ketogenic substrate, a harbinger for alcoholic ketoacidosis (AKA), even in controlled study environment. Clinical implication from this study is that significant ketoacidosis may supervene in less favourable condition of excessive alcohol consumption and poor diabetes control. As AKA is not without significant morbidity, the authors’ suggestion of raising the awareness of this condition in patient education is appropriate. AKA is a metabolic complication of alcohol abuse (particularly binge drinking) and starvation on glucose metabolism resulting in high production of ketone bodies (ß-hydroxybutyrate and acetoacetate) and metabolic acidosis without significant hyperglycaemia. AKA and diabetic ketoacidosis (DKA) share some common pathophysiological grounds in which the ketoacidotic state is the consequence of absolute or relative insulin deficiency and increase in counter-regulatory hormones.4 Diagnosing and differentiating AKA from DKA can be challenging. Clinical presentation can be similar in both conditions. Plasma glucose is usually not elevated in AKA but this can also occur in euglycaemic DKA.5 If hyperglycaemia ensues which has been reported in AKA,6 both conditions can be indistinguishable and may co-exist. Plasma alcohol level may be absent or low due to anorexia, decreased drinking and delayed clinical presentation. Conditions that predispose to AKA may also precipitate DKA. Excessive alcohol intake and binge drinking are often associated with poor adherence to diabetes self care behaviour including compliance with treatment such as insulin.7 A recent survey showed worrying trend in the pattern of alcohol consumption in young people.8 In both sexes, up to 30% of those aged between
Address correspondence to Dr Soon H. Song, Diabetes Centre, Northern General Hospital, Herries Road, Sheffield S5 7AU, UK. email:
[email protected] ! The Author 2009. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email:
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In the last year, excessive alcohol consumption and its associated medical and social consequences have emerged as one of the major health concerns in the UK. In 2007, the Alcohol Health Alliances UK, a coalition of 24 organizations consisting of medical bodies, patient representatives and alcohol health campaigners, was formed with the objectives of highlighting the magnitude of this problem and to propose evidence-based solutions to overcome it through engagement with key decision-makers. The statistics for alcohol-related harm are worrying. Over the last decade, the number of hospital admissions attributed to alcohol has doubled with alcoholic liver disease admissions increasing at the fastest rate.1 The financial cost is staggering. The Alcohol Harm Reduction Strategy Unit estimated the cost to the National Health Service (NHS) of England and Wales of treating alcohol-related conditions to be up to £1.7 billion per annum.2 This statistical data focused on alcohol-specific disease conditions, namely, mental and behavioural disorders, liver disease and toxic effects of alcohol. Publication by Kerr et al.3 in this issue adds another dimension to this growing problem by highlighting the potential detrimental health effects of alcohol in diabetes, a condition not included in the statistical analysis of alcohol-related harm. This study assessed the metabolic consequences of binge drinking, defined by consuming at least 8 or 6 units of alcohol by men and women, respectively, on at least 1 day in the week, in type 1 diabetes. Ingestion of liberal amount of alcohol led to the rise in ß-hydroxybutyrate and lactate levels without increment in lipolysis and counter-regulatory hormones indicating that consuming alcohol in quantities that exceed the recommended threshold can result in
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S.H. Song susceptibility to problem drinking, responsible drinking must be promoted to all segments of the society through effective public health measures.
References 1. Hospital Episode Statistics (HES). The NHS Information Centre, 2008. 2. Alcohol Harm Reduction Strategy for England. Cabinet Office, 2004. 3. Kerr D, Penfold S, Zouwail S, Thomas P, Begley J. The influence of liberal alcohol consumption on glucose metabolism in patients with type 1 diabetes: a pilot study. QJM 2009; 102:169–174. 4. Umpierrez GE, DiGirolamo M, Tuvlin JA, Isaacs SD, Bhoola SM, Kokko JP. Differences in metabolic and hormonal milieu in diabetic- and alcoholic-induced ketoacidosis. J Crit Care 2000; 15:52–9. 5. Munro JF, Campbell IW, McCuish AC, Duncan LJ. Euglycaemic diabetic ketoacidosis. Br Med J 1973; 2:578–80. 6. Wrenn KD, Slovis CM, Minion GE, Rutkowski R. The syndrome of alcoholic ketoacidosis. Am J Med 1991; 91:119–28. 7. Ahmed AT, Karter AJ, Liu J. Alcohol consumption is inversely associated with adherence to diabetes self-care behaviours. Diabet Med 2006; 23:795–802. 8. General Household Survey 2006. Office for National Statistics. 9. Laing SP, Swerdlow AJ, Slater SD, Botha JL, Burden AC, Waugh NR, et al. The British diabetic association cohort study II: cause-specific mortality in patients with insulintreated diabetes mellitus. Diabet Med 1999; 16:466–71. 10. O’Keefe JH, Bybee KA, Lavie CJ. Alcohol and cardiovascular health. J Am Coll Cardiol 2007; 50:1009–14. 11. Beulens JWJ, Kruidhof JS, Grobbee DE, Chaturvedi N, Fuller JH, Soedamah-Muthu SS. Alcohol consumption and risk of microvascular complications in type 1 diabetes patients: the EURODIAB prospective complications study. Diabetologia 2008; 51:1631–8. 12. Koppes LLJ, Deker JM, Hendriks HFJ, Bouter LM, Heine RJ. Moderate alcohol consumption lowers the risk of type 2 diabetes. Diabetes Care 2005; 28:719–25. 13. Fan AZ, Russell M, Naimi T, Li Y, Liao Y, Jiles R, et al. Patterns of alcohol consumption and the metabolic syndrome. J Clin Endocrinol Metab 2008; 93:3833–8. 14. McKee M, Briton A. The positive relationship between alcohol and heart disease in Eastern Europe: potential physiological mechanisms. J R Soc Med 1998; 91:402–7. 15. Naimi TS, Brown DW, Brewer RD, Giles WH, Mensah G, Serdula MK, et al. Cardiovascular risk factors and confounders among nondrinking and moderate-drinking US adults. Am J Prev Med 2005; 28:369–73.
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16 and 44 years engage in binge drinking. Young people are more likely to be admitted with acute intoxication and those who are current drinkers are consuming more. Furthermore, binge drinking can result in hypoglycaemia, the treatment of which can be delayed due to hypoglycaemia unawareness and mistaken for intoxication by third party. As the major cause of mortality in subjects with type 1 diabetes aged below 30 years is acute metabolic decompensation such as DKA and hypoglycaemia,9 this observation paints a clinical picture of concern. The consequences of adverse pattern of alcohol consumption also pervades into the realms of chronic diabetes complications and the risk of developing type 2 diabetes. Current evidence indicates a U or J-shaped relationship between alcohol consumption and risk of cardiovascular disease,10 microvascular complications11 and risk for type 2 diabetes.12 Light to moderate drinkers have a lower risk of these complications than abstainers and heavy drinkers. The cardio-protective benefits of alcohol are thought to be due to enhancement of insulin sensitivity, positive modulation of inflammatory activity and central obesity and possibly elevation of HDL cholesterol.10 However, excessive consumption and binge drinking are associated with higher incidence of metabolic syndrome, adverse cardiovascular risk and type 2 diabetes.13 Binge drinking has been linked with increased cardiovascular events and sudden cardiac death even among light to moderate drinkers possibly through elevation of atherogenic low density lipoprotein, increased risk of thrombosis, reduced threshold for ventricular fibrillation and acute or sustained rise in blood pressure.14 As Abraham Lincoln once said ‘It has long been recognized that the problems with alcohol relate not to the use of a bad thing but to the abuse of a good thing’ seems pertinent even today. Having a drink is very much part of our lives and national culture. Whilst it is enjoyable with some evidence for health benefits, light to moderate drinking cannot be universally recommended to the general public. It is not possible to predict in which individual alcohol abuse will become a problem. There is no randomized controlled trial evidence to definitively prove the health benefits of alcohol and unmeasured confounding factors could play a role in the benefits associated with light to moderate drinking in observational studies.15 Until we have firm evidence for positive health outcomes and tools to predict
