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?
Fatty liver is now considered to be the liver expression of the metabolic syndrome. This syndrome is a cluster of abnormalities including central obesity (fat around your waist), raised blood glucose, high triglycerides, low HDL-cholesterol and high blood pressure. Usually, not all of these occur in the same person but if you have central obesity and any two of the others then you have the metabolic syndrome. And you are a good candidate for fatty liver too. Not surprisingly, people with type 2 diabetes are twice as likely as the general population to have fatty liver. The association with the metabolic syndrome explains why people with fatty liver are at increased risk for cardiovascular disease.
The critical link between metabolic syndrome and fatty liver is insulin resistance i.e. the cells of the body have become less sensitive to insulin. When insulin resistance is present more free fats flow from the body’s fatty tissue to the liver which then packages them up into triglycerides and pushes them out into the bloodstream. This high flux of fat through the liver may be the driver of fatty liver.
Lifestyle management of fatty liver
In the absence of any evidence-based drug treatment of fatty liver the best option is lifestyle intervention but it has to be said that there is little in the scientific literature to go on. With the general acceptance that insulin resistance is the core of the problem strategies that are known to improve insulin sensitivity, such as increased physical activity and weight loss, are generally supported.
There were encouraging findings from a recent meta-analysis that showed a benefit of exercise on liver fat, even when weight loss was minimal or absent. However, the quality of the available trials included in this study was only fair.
Weight loss of 5% or more lessens fatty liver and weight loss of 7% or more lowers inflammation of the liver, according to a recent meta-analysis by Musso and colleagues. Again, there are only a handful of good studies. The American Association for the Study of Liver Diseases recommends weight loss of 5-10% for overweight people with fatty liver.
There is no established diet for fatty liver and no evidence-based clinical guidelines. There are simply too few published randomised controlled trials to provide the data necessary to create such guidelines.
A review by Conlon and colleagues draws on the American Diabetes Association guidelines for the prevention and management of diabetes and cardiovascular disease for inspiration for the dietary management of fatty liver. A dietary intake pattern that emphasises whole grains, fruits, vegetables, legumes and low-fat dairy is recommended, together with a limit on calories, less saturated fat and less refined carbohydrates. No limit on total carbohydrate is recommended. Glycaemic Index is discussed but there are no firm guidelines. It’s all quite general and all extrapolated from recommendations for other conditions.
Recently, an Australian randomised controlled trial into the effects of a Mediterranean diet on people with insulin resistance and fatty liver was published. Compared to the control low fat/high carbohydrate diet the Mediterranean diet improved insulin sensitivity and reduced liver fat, even though body weight was not affected. Whether the effect was due to the monounsaturated fats in the Mediterranean diet or the carbohydrates they effectively displaced is unclear. The higher polyphenol content of the Mediterranean diet may also be relevant.
It has been hypothesised that fructose intake may affect the risk for fatty liver. To test this hypothesis Chiu and colleagues recently conducted a meta-analysis of controlled feeding trials to determine the effect of fructose on two markers of fatty liver. They considered two types of trials – one where fructose was exchanged for other carbohydrates without affecting calorie intake, and the other where diets were supplemented with fructose thereby increasing the energy intake.
The researchers found that when calorie intake was constant fructose had no effect on markers of fatty liver. But overfeeding with fructose was associated with increases in both markers of fatty liver. They concluded that the adverse effects observed in the latter trials may be due to excess calorie intake rather than fructose per se.
The authors noted that the small number of trials available for inclusion in their meta-analysis was a limitation. They identified a need for larger, longer, high-quality trials of the effect of ‘real-world’ intake patterns of fructose on markers of fatty liver in at-risk populations.
For people with fatty liver, regular physical activity and 5-10% weight loss in those who are overweight are the best ways of managing the problem. Because these lifestyle measures also improve insulin sensitivity they will have beneficial effects on other elements of the metabolic syndrome and lower the risk for cardiovascular disease.