Background: High fructose intake has been suggested to be a key factor that induces nonalcoholic fatty liver disease (NAFLD), but the evidence from large epidemiologic studies is lacking.
Objective: We examined the cross-sectional association between fructose intake and NAFLD by using the Fatty Liver Index (FLI) and the NAFLD liver fat score.
Design: The Helsinki Birth Cohort Study investigated 2003 Finnish men and women born in 1943–1944 in Helsinki who participated in a clinical health examination in the years 2001–2004. Trained study nurses measured weight, height, and waist circumference, and BMI was calculated. Laboratory staff drew fasting blood for measurements of triglycerides and γ-glutamyl-transferase. The FLI and the NAFLD liver fat score were calculated on the basis of these measurements. Habitual fructose and other dietary intake over the past year were assessed by using validated and standardized 131-item food-frequency questionnaires. Data were analyzed in a cross-sectional manner by using logistic regression modeling with statistical software.
Results: In a model adjusted for age, sex, and energy intake, participants in the highest fructose intake quartile (range: 29.2–88.0 g/d) had lower risk of NAFLD assessed by using the FLI (OR 0.56; 95% CI: 0.42, 0.75; P-trend < 0.001) and NAFLD liver fat score (OR: 0.72; 95% CI: 0.53, 0.99; P-trend < 0.001) than that of the lowest intake quartile (range: 2.2–15.2 g/d). This association remained after adjustment for educational attainment, smoking, physical activity, and other dietary variables only for the FLI (OR: 0.68; 95% CI: 0.47, 0.84; P-trend < 0.05).
Conclusion: Our cross-sectional results did not support the current hypothesis that high intake of fructose is associated with a higher prevalence of NAFLD as assessed by using the FLI and NAFLD liver fat score.
Alex’s Notes: The main claim made by fructose-bashers is that it leads to non-alcoholic fatty liver disease (NALFD). While many studies do indeed show that this occurs, the amounts of fructose used to achieve these effects are unrealistic. Yet fructose consumption is a normal part of a standard diet, so it is interesting to look at the associations between its intake and the occurrence of NAFLD. The study at hand did just that in 1611 Finnish adults. Anyone who drank more than 20g of alcohol daily or who was on medications associated with fatty liver were excluded from analysis.
I will say upfront that the limitations of epidemiology hit us hard from the beginning. How do you assess NAFLD in people who you don’t even meet face-to-face? The authors used two methods: The Fatty Liver Index (FLI) and the NAFLD liver fat score. Unfortunately, the FLI is based on BMI, waist circumference, fasting triglycerides, and fasting GGT, while the NAFLD liver fat score is based on the presence of type-2 diabetes and metabolic syndrome, fasting insulin, AST, and the AST:aminotransferase ratio. Both these methods provide a good estimation, but they are not an ultrasound. To make matters worse, diets were assessed with a 128-item food frequency questionnaire, but I digress.
The people who at the most fructose tended to be women, have more years of education, non-smokers, and are more physically active than those who ate the least fructose. Moreover, waist circumference decreased as fructose intake increased, and fiber intake was greater in the fructose eaters. After adjustment for age, sex, and energy intake, those with the greatest fructose intake (38 grams per day) were 28-44% less likely to have NAFLD than those with the lowest intake (11 grams per day) depending on the FLI or NAFLD liver fat score. After remaining adjustments for leisure-time physical activity, smoking, and nutrient intake, the likelihood of having NAFLD was 32% less in the highest fructose intake group with the FLI, and there was no association for the NAFLD liver fat score.
So at best a 32% reduced risk, and at worst no association whatsoever.
Now, there are some interesting tidbits that must be mentioned. For example, the average fructose intake across all subjects was about 20 grams per day, with only 45 (2.8%) exceeding 60 grams daily. Moreover, the authors note that whereas the proportion of fructose from fruit was 54-80%, the contribution from soft drinks was 0-8%. Thus, this lack of an association between fructose intake and NAFLD could likely be a result of the relatively normal fructose intakes, and the sources of that fructose. It is highly likely that the greater fructose quartile consumed more fruits, which could have counteracted any negative effects the fructose would have had on the liver. Regardless of the method, it is clear that this study supports the notion that fruit intake needn’t be a concern provided it is in “normal” amounts (i.e. not 10 bananas per day).