In a recent study published in Clinical gastroenterology and hepatologyResearchers have determined the harmful effects of fast food consumption on fatty liver disease.
Fast food consumption in the United States is widespread and associated with an increased risk of cardiovascular disease and diabetes. However, more research is needed regarding the effect of fast food intake on nonalcoholic subjects fatty liver disease (NAFLD) or if the effect of fast food on the incidence of steatosis differs between individuals with metabolic risk factors, such as diabetes and obesity. It has been hypothesized that dietary intake is among the most influential factors for non-alcoholic fatty liver disease. However, there are significant gaps in the evidence linking food consumption to steatosis, especially among people at high risk. Extensive research can help advance public health efforts related to nutritional prevention as well as develop risk mitigation methods to reduce the incidence of NAFLD.
In this study, researchers used vibration-controlled transient elastography (VCTE) to quantify the quantitative effects of fast food intake on the risk of developing steatosis of the liver.
The study involved 20-year-old individuals with reliable assessments of steatosis, who did not report pregnancy in the study period, and who provided food recall data for one or two days. Fatty degeneration was quantified with a controlled attenuation parameter (CAP) measured in decibels/meter (dB/m). Items described as restaurant fast food or pizza were considered fast food and were categorized as having less than 20% or 20% and more of their daily calories.
The team estimated the relationships between hepatic steatosis and fast food intake using multivariate linear and logistic regression. In light of the recognized association between fast food, diabetes, and obesity, possible interactions between diabetes, obesity, and fast food consumption were evaluated. Age, sex, race and ethnicity, body mass index (BMI), consumption of coffee or sugar-sweetened beverages, diabetes mellitus, alcohol use, and physical activity were integrated into the models. To determine how much fast food could influence the occurrence of NAFLD in people at high risk, a population attributable risk (PAR%) associated with a CAP of 263 dB/m or greater was calculated separately for subjects with obesity and diabetes.
Almost 2037 (52%) out of 3954 people consumed fast food. Of the approximately 1147 (29%), those who got 20% or more of their daily calories from eating fast food had a higher chance of being male, younger, obese, and consuming sugar-sweetened beverages, but were less likely to be consuming coffee. After multivariate adjustment, fast food consumption of 20% or greater was significantly associated with higher steatosis, as a continuous estimate, as well as with respect to a CAP cutoff of 263 dB/m or higher. The association between fast food consumption of 20% or greater and a CAP of 285 dBm or greater was not statistically significant. To reduce the possible effects of alcohol use, the team also performed a sensitivity analysis that excluded heavy drinkers and noted that the relationships between fast food consumption and steatosis did not change significantly.
In multivariate models, the team also discovered significant associations between fast food consumption of 20% or higher and obesity and between fast food consumption of 20% and above and diabetes. In addition, fast food intake of 20% or greater was also associated with an adjusted CAP that was 11 units higher in obese individuals, compared to a CAP that was 2 units lower in non-obese individuals. Also, fast food intake of 20% or greater was associated with a 16-unit increase in adjusted CAP among diabetics and a three-unit increase among non-diabetics. Moreover, the PAR% of CAP of 263 dB/m or greater for fast food was 17% among obese individuals and 17% among diabetic patients.
The results of the study showed that eating fast food was associated with fatty degeneration in the liver, regardless of sociodemographic factors, metabolic comorbidities, and other healthy behaviors. Although the extent of the association is moderate in the general population, the team found a significantly higher incidence of steatosis among diabetic and obese individuals who ate fast food compared to non-diabetic and non-obese subjects.
Our data indicate that the effect of fast food consumption on liver fat is significantly worse among individuals with metabolic comorbidities. These findings underscore the need for specialized dietary guidelines for populations at risk, such as diabetics and obese individuals. Ultimately, public health measures are needed to reduce the use of nutrient-poor and high-calorie diets in the United States and to provide access to healthier and more nutritious food alternatives.