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Is not only geese whose livers may show fatty degenerative changes, and later cirrhosis, if they eat too much. Overweight people who are genetically vulnerable to the metabolic syndrome may also develop cirrhosis — without drinking a drop of alcohol or catching hepatitis B or C.
The incidence of liver failure has been increasing steadily over the years. There has been a 24 per cent rise in the number of deaths from cirrhosis since 1997. It is unfair to assume that all deaths from cirrhosis are related to over-indulgence in alcohol. Although excess alcohol is the principal culprit, hepatitis C and B are also responsible for many cases, and the damage they wreak if not diagnosed early and treated is now better known.
Roger Williams, Professor of Hepatology and the director of the Instititute of Hepatology at University College London, gave warning 18 months ago about the increase in non-alcoholic fatty liver disease (NAFLD), a condition that may lead to cirrhosis in humans and to livers not dissimilar to those of Périgord and Languedoc geese.
The survival rate for patients, once cirrhosis has developed, is similar whatever its cause. The metabolic syndrome associated with obesity and NAFLD is characterised by an excess of midline fat, over-generous waist bands and pot bellies — whether they are beer bellies or caused by too much calorie-dense convenience food.
Metabolic syndrome is also associated with insulin resistance that will sooner or later lead to pre-diabetes or diabetes, raised blood fats such as low-density lipoprotein cholesterol and triglycerides or high blood pressure.
Paediatricians from the University of California, San Diego, recently issued a similar warning to that given by Professor Williams. Dr Jeffrey Schwimmer, the study leader and an associate professor of paediatrics at the Rady Children’s Hospital, said that fatty liver disease in young people was a problem that had gone largely unnoticed, although it had enormous implications for their future health.
Statistics derived from individuals under 19 who had suffered sudden death in California suggested that, if the figures were extrapolated to the rest of the US, 6.5 million American children would already have the first signs of fatty liver disease and therefore of future cirrhosis: 81 per cent of these young peoples’ livers were overweight, boys had a higher incidence than girls and there were racial differences. Hispanic-American children had the highest rate of fatty liver disease (11.8 per cent), Asians 10.2 per cent, whites 8.6 per cent and blacks 1.5 per cent.
Professor Williams’s figures for adults showed that 10 per cent of people with the metabolic syndrome also develop NAFLD, 90 per cent of these had central obesity, 60 per cent were women and 50 per cent had diabetes or pre-diabetes; 75 per cent had raised cholesterol level, and a similar number had high blood pressure. Professor Williams said that doctors in this country are also seeing grossly overweight adolescents with incipient cirrhosis; he has recently treated two boys under 15 with NAFLD.
Professor Williams is to combine his role at the Institute of Hepatology with a new role as the clinical director of a private, but charitable, liver centre at the London Clinic.
The London Clinic’s liver centre has gathered together a formidable team to work with Roger Williams. They will have an enviable collection of ground-breaking gadgetry to use in the modern techniques that are now available to treat livers.
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