*This content has been reviewed by Dr. Donna Vine (Agriculture, Food and Nutritional Sciences, University of Alberta)
Non-alcoholic fatty liver disease (NAFLD) is an umbrella term for a spectrum of progressive liver diseases.
- NAFLD Diagnosis. NAFLD is diagnosed using blood tests, imaging tests, or in some cases by taking a liver biopsy. Individuals are also asked several questions about their diet-lifestyle factors, to determine if they are at risk for alcoholic fatty liver disease.
- Risk Factors. Obesity, in particular central or abdominal obesity, is the most common risk factor for NAFLD.
- Treatment and Prevention. The primary treatment and preventative recommendations for NAFLD is body weight reduction if individuals have overweight or obesity, in addition to sustained healthy dietary habits and increased physical activity.
- Sugars and NAFLD. Current research states there is insufficient evidence to determine the role of excess dietary sugar(s) or fructose in the development of NAFLD, and that consumption of excess calories, not sugar(s) or fructose specifically, influences NAFLD risk. To understand the role of sugars in the development of NAFLD, high-quality randomized clinical trials that include energy-balanced diets are needed.
NAFLD can be diagnosed with blood tests, imaging tests, or with a liver biopsy (1). The doctor would assess relevant medical, family history, and lifestyle-diet related criteria. Following this, blood could be analyzed for the detection of liver enzymes. For example, when the cells in the liver are damaged, some of the enzymes normally found within the liver may leak into the blood. The two most common enzymes to measure from the blood are alanine aminotransferase, and aspartate amino transferase. If the blood work is not conclusive, imaging of the liver (ultrasound, computed tomography (CT) scan, or magnetic resonance imaging (MRI), may take place.
Alcohol-related fatty liver disease is diagnosed when the fat volume of the liver is 5% or greater, and alcohol consumption is above recommended levels.
NAFLD encompasses several different liver diseases and stages of liver disease, ranging from fat accumulation, inflammation, damage to the liver tissues, and scarring of the liver, such as in non-alcoholic steatohepatitis (1). The disease usually progresses in stages over decades and there are many possible factors that affect the progression of NAFLD, including genetic and environmental factors.
Risk Factors for Developing NAFLD
The development of NAFLD depends on a variety of factors. Some of these factors can be modified by lifestyle, while others cannot. The table below summarizes risk factors associated with NAFLD (1, 2). Obesity is the most common risk factor for NAFLD, but not all individuals who have NAFLD have obesity (1, 2).
|Unmodifiable Risk Factors||Modifiable Risk Factors|
Polycystic ovary syndrome
Type 2 Diabetes
Rapid weight loss
Treatment and Prevention of NAFLD
There are currently no approved medications to treat NAFLD. Instead, the primary treatment strategy focuses on sustained diet and lifestyle modification to reduce the amount of fat in the liver, and achieve body-weight loss if necessary (2). Lifestyle modification includes general healthy dietary habits and increased physical activity. A healthy lifestyle is similarly recommended for the prevention of NAFLD.
According to the Canadian Liver Foundation (1), dietary recommendations may include:
- Increasing fiber consumption
- Limiting saturated fats
- Limiting sugars consumption
- Limiting fried foods
- Avoiding alcohol
Current research suggests that sustained weight loss and calorie restriction are more important than the macronutrient composition of the diet (2).
Sugars and NAFLD
Some research proposes that dietary sugars, specifically fructose, may play a unique role in the development and progression of NAFLD. Fructose is thought to increase an individual’s risk of NAFLD due to the difference in the way it is metabolized by the body compared to glucose. Fructose can contribute to metabolic pathways that could result in an increased amount of fat being made (synthesized) in the liver. Fructose may also trigger inflammation in the liver, resulting in fat accumulation and liver injury (3).
However, it is unclear if these processes occur due to the specific consumption of fructose from foods in the diet, independent of excessive dietary energy intake. An excessive intake of calories may lead to increased risk for overweight, in particular central or abdominal obesity.
When evaluating scientific research, it is important to consider the hierarchy of scientific evidence. Well conducted clinical trials examining liver health can help determine the effect of fructose in the development or progression of NAFLD, and these studies usually measure liver enzyme levels and liver fat content as indicators of NAFLD.
Several recent systematic reviews and meta-analyses evaluating the totality of available research have analyzed the available literature and have reported the following:
- Dietary interventions with sugars reported that individuals who consumed extra Calories from sugars added to the diet had an increase in liver fat when compared to individuals who were in a state of energy balance (4). There were no significant differences in trials with different added sugars (ie. glucose, fructose, sucrose, or high fructose corn syrup), but this data was limited.
- Dietary interventions with fructose reported that individuals who consumed extra Calories from fructose added to the diet at a high dose, had an increase in liver fat and liver enzymes (5). When fructose was substituted for other sources of carbohydrates (glucose, sucrose, or starch), providing the same amount of total calories in the diet, there was no independent effect of fructose. This suggests that the effect of fructose is not different from an excess of Calories from other carbohydrates in the diet (5).
- Another systematic review and meta-analysis concluded there was insufficient evidence to determine the effect of fructose, high fructose corn syrup, and/or sucrose in the development of NAFLD (6).
Currently, there is no conclusive evidence to suggest that sugar(s) or fructose specifically contribute to the risk of developing NAFLD. The results to date suggest that it is the consumption of excess Calories, not fructose specifically, that influences NAFLD risk. Sugar(s) and fructose may be found in higher calorie foods, which may be linked to increased risk of obesity, which is linked to an increased risk of developing NAFLD.
These scientific reviews acknowledged that high-quality studies in the field are sparse due to limitations such as study design and dietary intervention including controlling energy intake, high risk of bias, measurement of NAFLD biomarkers, and short study duration (4-6). It is also acknowledged that signaling out single nutrients like sugar(s), glucose or fructose, to have a causal effect in the development of a health condition is extremely difficult. Researchers suggest that more high-quality trials with energy-balanced interventions are needed.
For more information, additional resources include:
“Fatty Liver Disease” by Canadian Liver Foundation
- Carbohydrate News – The Not So Toxic Truth About Sugar
- Canadian Liver Foundation. Fatty Liver Disease.
- Chalasani N et al. The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018;67(1):328-357.
- Jegatheesan P et al. Fructose and NAFLD: The Multifaceted Aspects of Fructose Metabolism. Nutrients. 2017;9(3):10.3390/nu9030230.
- Ma J et al. Potential link between excess added sugar intake and ectopic fat: a systematic review of randomized controlled trials. Nutr Rev. 2016;74(1)18-32.
- Chiu S et al. Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials. Eur J Clin Nutr. 2014;68(4):416-423.
- Chung M et al. Fructose, high-fructose corn syrup, sucrose, and nonalcoholic fatty liver disease or indexes of liver health: a systematic review and meta-analysis. Am J Clin Nutr. 2014;100(3):833-849.