Higher Fructose Intake Is Inversely Associated With Risk Of Nonalcoholic Fatty Liver Disease In Olde

Mufasa

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Hi all, my first post here. I would love to talk with you guys more about health and metabolism. I have learned so much from posts here, especially @haidut.

I found this great study about fructose, which states it is is NOT associated with NAFLD:
Higher fructose intake is inversely associated with risk of nonalcoholic fatty liver disease in older Finnish adults. - PubMed - NCBI
Higher fructose intake is inversely associated with risk of nonalcoholic fatty liver disease in older Finnish adults

To our knowledge, this study is among the first large-scale studies to report a cross-sectional association between fructose intake and NAFLD assessed by using the FLI and the NAFLD liver fat score. Participants with higher fructose intake were significantly less likely to have a positive FLI score independently of the participants’ age, sex, lifestyle, and various nutrients. When NAFLD was assessed by using the NAFLD liver fat score, no association between intake of fructose and NAFLD emerged.

Much of the evidence on the association of fructose intake and NAFLD has been based on animal studies
that showed that high fructose intake increased lipogenesis and triglyceride concentration, lowered HDL cholesterol concentrations, and lead to NAFLD (29). However, the few human trials and small-scale (n < 500) observational studies have provided inconsistent results (12, 14). A meta-analysis of 16 trials did not find any effect on HDL cholesterol when other carbohydrates were exchanged for fructose (13), and higher intake of fructose did not change triglycerides concentrations in healthy individuals (13, 14). In contrast, higher fructose intake has been associated with a lower prevalence of steatosis and a higher fibrosis grade in older subjects (12). Our findings in a cohort of 1611 adult Finns supports the evidence that higher intake of fructose is not associated with a higher prevalence of NAFLD.

The conflicting results between animal studies, experimental human trials, and our findings may have stemmed from the different levels of exposure. Animal and human feeding studies have been criticized for providing supraphysiologic doses of fructose that have varied typically between intake of 60–220 g/d. In our cohort, eg, the median fructose intake was 20 g/d, and only 45 participants had fructose intake ≥60 g/d. Because fructose is approximately one-half of the intake of sucrose, these numbers are in line with the sucrose intake in the general Finnish population, which is 54 g/d for men and 43 g/d for women (30). When sugars were compared with other macronutrients, an isocaloric high-fat diet increased liver fat and insulin concentrations more than did an isocaloric high-carbohydrate diet (31). Furthermore, in healthy individuals, overfeeding with fructose increased liver fat less than did overfeeding with fat (32). Overall, it seems that adverse changes related to fructose intake have been more due to excess caloric intake rather than sugar composition (33). This finding has been consistent in clinical trials conducted thus far (34). Our results, which adjusted fructose intake for the intake of energy, also suggest that, in an energy-controlled situation, fructose does not associate with an increased prevalence of NAFLD.
 

haidut

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Thanks for the nice words and the study! Excellent way to introduce yourself, so welcome and enjoy!
 

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