Abstract: Obesity is a known risk factor for the development of non-alcoholic fatty liver disease (NAFLD); however, it has been suggested that dietary fat, both amount and composition, may play a pivotal role in its development, independent of body fatness. Studies that have investigated the role of dietary fat on liver fat accumulation are reasonably sparse. We review here the available work that has investigated the impact of dietary fat: amount, composition and frequency, on liver fat accumulation in human observational and intervention studies. Overall, it would seem that total calorie consumption, rather than dietary fat composition, is an important factor in the development of fatty liver disease in humans.
Alex’s Notes: In the last two weeks we learned that a high-fat, low fructose diet does not worsen liver fat accumulation in obese persons with and without nonalcoholic fatty liver disease (NAFLD), but that a low-fat, moderate fructose diet actually reduces liver fat. Moreover, a single high-fat and high-carbohydrate meal was shown to elevate liver fat by 20-30% and keep it there for at least the next five hours. However, neither of these studies controlled for the type of dietary fat.
A handful of epidemiological studies have attempted to find a connection between certain foods and liver fat. One such found that intake of “other fats” and cheese from a food frequency questionnaire (FFQ) was not associated with liver fat while meat and alcohol were. Another in adolescents found that those with NAFLD consumed more than 35% of their total energy intake from fat and also consumed more fried foods. Finally, a study of obese men found that a single high-fat assault had no correlations to liver fat while habitual fat intake (average 31% energy intake) did.
What does all this mean? No idea and that is why I don’t like observational studies for drawing conclusions.
Fortunately, we have intervention studies that investigate the effect of acute and chronic changes in the amount and composition of dietary fat on liver fat accumulation. In general, under isocaloric conditions, consumption of a low fat diet (total fat <25% TE) appears to lead to a decrease in liver fat compared to consumption of a high fat diet (total fat <40% TE). But if you remember our study from last week, we already knew this. When looking at the type of fat, consumption of a diet containing 27% MUFA lowered liver fat to a greater degree than consumption of a diet containing 16% MUFA, and consumption of a diet enriched with n-6 PUFA (vegetable oil) for 10 weeks notably decreased liver fat compared to the SFA enriched diet (from butter).
Things become worse when we begin to overeat. One study of healthy males found that consuming 130% of maintenance calories with the 30% coming from saturated fat increased liver fat by 86% in just seven days. Additionally, doubling habitual calorie intake for 3 days with the added calories coming from cream (fat was 69% total energy intake) resulted in a 112% increase in liver fat in healthy 25 year old males. And again, looking to the type of fat, studies demonstrate that seven weeks of overfeeding with saturated fat leads to greater liver fat accumulation than overfeeding on n-6 PUFA.
So what about the n-3 PUFAs? Four grams of n-3 supplementation reduced liver fat in obese women with polycystic ovary syndrome (PCOS) over eight weeks. It appears that the reductions in liver fat are linearly associated with increased enrichment of red blood cells with DHA.
But dieting may be a better solution. The authors of the current review cite four studies that demonstrate hypocaloric diets to reduce liver fat independently of the total amount or composition of the fat consumed. Moreover, the effects appear to be more pronounced during low-carbohydrate hypocaloric diets.
Why liver fat starts to accumulate when individuals are metabolically healthy may be due to the composition of their diet. For example, with isocaloric feeding, having a diet rich in fat, notably saturated fat, caused liver fat accumulation, whereas diets rich in MUFA or PUFA tended to do the opposite. This could possibly be to the potentially lipotoxic effects of SFAs, including ER stress, oxidative stress, and mitochondrial dysfunction. Conversely, MUFA and n-6 PUFA are preferentially partitioned toward oxidation pathways compared to SFAs, and PUFAs suppress the expression of lipogenic genes.
Now before you go bashing me as a fat hater, I’m just reporting on the literature. This review provides some great insight. For starters, dieting is the most important determinant for reducing liver fat, and this will aid in other metabolic outcomes as well assuming that it was obesity and comorbidities that led to NAFLD. However, it also suggests that consumption of an isocaloric diet rich in SFA may be an important determinant of liver fat accumulation, while a diet rich in PUFA (n-6 or n-3) appears to have the opposite effect. MUFA is another seemingly “good” fat in this regard.
So if weight maintenance or weight gain is the goal, which would require eating an isocaloric or hypercaloric diet, then it seems prudent to limit saturated fat intake in preference of unsaturated varieties. Clearly there are other problems linked with high PUFA intake, so with that in mind, a focus should be on MUFA intake. No problem right? I mean, who doesn’t love avocados, macadamia nuts, and olives.