Fatty liver is reaching epidemic proportions in western countries. What causes it and what diet and lifestyle measures can be used to manage it?
About 30% of adult Australians are thought to have non-alcoholic fatty liver disease – fatty liver for short – and its prevalence is increasing. In its early stages fatty liver is of minor concern and there are no symptoms. But it can progress to a stage called NASH where liver cells begin to be damaged and this is associated with inflammation. At the next stage the risk of cirrhosis of the liver increases which may lead to liver failure and even cancer of the liver. Together, fatty liver and NASH are now the number one cause of liver disease in Western countries. However, the major cause of death in people with fatty liver is cardiovascular disease.
What causes fatty liver?
Fatty liver develops when the liver’s normal processes of delivery and removal of fats go awry. Although the exact cause is not known several things could be going wrong:
• Perhaps too much fat is being delivered to the liver
• The liver may have a problem ‘burning’ fats for energy
• Fat (triglyceride) production by the liver may be increased
• The movement of triglycerides from the liver into the bloodstream may be impeded.
But what is the underlying cause?
Addressing the obesity epidemic by taxing sugary soft drinks sounds good in theory but it appears to fall down in practice. How could a taxation strategy be made to work?
Obesity is proving to be an intractable public health problem demanding innovative solutions and one idea that is attracting attention is the taxation of sugar-sweetened beverages. The theory is simple enough. Basic economics tells us that if the price of sugary soft drinks were to rise, their consumption would fall; lower intake should mean lower calorie intake which would lead to lower body weights. But would it work in practice?
The Ohio experience
A recent research study conducted in the United States provided some interesting insights. Taxing soft drinks has a long history in the US and occurs in many states today, though historically the rates have been low and the purpose has been to raise revenue. But there was an interesting exception. In 1992, the state of Ohio introduced high taxation of sugary soft drinks which was then repealed at the end of 1994. This provided an opportunity to test the effect of taxation of soft drinks on body weights over a period of two years. The researchers compared changes in body weights in Ohio over this period to (1) all other states that had no increased taxation and (2) a bundle of states with the same mean BMI as Ohio. The researchers found:
… very little evidence that the large tax imposed in Ohio had any detectable effect on population weight … our results cast serious doubt on the assumptions that proponents of large soda taxes make on its likely impacts on population weight.
How come? Why didn’t quite high taxation of sugary soft drinks affect body weights?
Public health advocates have consistently failed to get substantial Government support for their initiatives to tackle the obesity epidemic. And they only have themselves to blame.
Last week on ABC radio’s AM current affairs program the former chair of the National Preventative Health Taskforce lamented that the Government had failed to address obesity. In 2009, the Taskforce released a report titled Obesity in Australia: a need for urgent action which was supposed to be the springboard for Government action on the issue. Instead, the report was tossed onto a large pile of obesity reports and recommendations that have been ignored by our politicians.
What went wrong? Why did the then Government, which was favourably disposed to public health and disease prevention, fail to act? My guess is that it was the appalling quality of the report.
Surely lowering body weight and maintaining it for 11 years will prevent heart disease and strokes in overweight people with diabetes. Apparently not, according to the findings of a much anticipated trial.
The Look AHEAD Study
People with type 2 diabetes have increased risk for cardiovascular disease. As overweight is often associated with cardiovascular risk factors it has always been assumed that excess body weight contributes to the burden of cardiovascular disease and that weight loss would lower it.
The Look AHEAD Study was conceived to test this hypothesis. This large, multi-centre, randomised controlled trial began 11 years ago in the United States. Over 5000 overweight men and women with type 2 diabetes were recruited – half received active weight loss intervention and the control group received a general program of support and education. The intervention group successfully lost weight. After one year they had lost nearly nine per cent of their initial body weight and at 11 years their average weight was still about five per cent less than baseline.
Over the years the good news started to flow from the Look AHEAD Study. A string of papers showed that weight loss in the intervention group was linked to improvements in fitness, mobility, blood glucose, sleep apnea, urinary incontinence, symptoms of depression, blood clotting and body image. And use of medications was reduced. All very positive, but the real test was yet to come: would weight loss lower rates of cardiovascular disease?
As concern about the health implications of the obesity epidemic has increased one frequently mentioned claim is that the current generation will be the first to live shorter lives than their parents. The assumption is that the effects of obesity on the risk for chronic disease are so significant that life expectancy will inevitably fall. But new evidence suggests that this assumption may be wrong.
A new meta-analysis of the effects of overweight and obesity on all-cause mortality was published this month in the Journal of the American Medical Association. The analysis included data from 97 studies from around the world, providing a combined sample size of more than 2.88 million subjects and more than 270,000 deaths.
The risk of death of all obese subjects (BMI>30) was substantially and significantly higher (18%) than that of subjects of normal weight (BMI 18.5-25) – the sort of finding that we have come to expect. However, the results told a different and perplexing story when narrower weight categories were considered. For example, those who were overweight (BMI 25-30) experienced 6 per cent lower risk of mortality than subjects of normal weight. Subjects with grade 1 obesity (BMI 30-35) had the same mortality risk as subjects of normal weight. Consequently, the mortality risk associated with obesity appeared to be due entirely to higher grades of obesity – BMI greater than 35, which was associated with a 29% increase in risk.