Just Read: The role of diet and nutritional intervention for the management of patients with non-alcoholic fatty liver disease (NAFLD)

Continuing a little pre-reading before #LCB18. This is a paper referenced from the European Guidelines I posted about previously, it is also from a pre-historic era (2014), so it’s posted here just as baseline.

It seems to me to add to the confusion about non-alcoholic fatty liver disease and what should be done about it.

Reminder of the significant impact of NAFLD

estimated prevalence of 20% to 30% in affluent nations. This prev- alence increases to 50% in patients with diabetes and 70% in obese individuals.

In comparison, that’s in the range of high blood pressure prevalence. And unlike high blood pressure, there is no valid drug treatment for this condition.

It may become the #1 reason for liver transplantation.

And yet, there are statements as recently as 2018 in my own medical specialty journal like this:

Nonalcoholic fatty liver is generally benign and treated successfully with lifestyle modificationOh RC, Hustead TR, Memorial Health H, Syed Ali KM, Pantsari MW. Mildly Elevated Liver Transaminase Levels: Causes and Evaluation. 2017 [cited 2018 Feb 19];96(11). Available from: www.aafp.org/afp

Are we sure about that?

On the other hand, it should also be remembered that NAFLD is independently associated with an increased risk of dia- betes mellitus (T2DM) (2-fold increase) and cardiovascular disease (CVD) (1.4- to 2.0- fold increase)

The focus on weight loss, confusion about the method

There is a discussion of carbohydrate restriction vs fat restriction as the method, and what I would call a non-recommendation for low carbohdrate diets over low-fat ones.

And yet:

Regarding NAFLD, in a recent epidemiologic cross-sectional study (n 5 19,479), aminotransferase levels (a surrogate measure of NAFLD at a population level) increased in direct relation to CHO intake after adjusting for age, BMI, and energy intake. Higher aminotransferases were particularly observed in patients in whom the CHO intake was greater than 60% of the total calories.

Thus, although moderate CHO restriction seems to have no additional effect on liver steatosis in
patients with significant weight loss (!7%), its impact on liver inflammation and fibrosis and its utility in patients without significant weight loss remains to be elucidated.

SAD is really BAD

Regardless of weight loss strategy, there’s general agreement that the Standard American Diet (SAD) comes together in a very unhealthy way for the liver and ultimately the entire body:

The typical Western diet pattern abundant in red meat, trans FA, high-fructose- containing soft drinks, and high-GI CHO and low in PUFA, MUFA, vegetable- derived proteins, and fiber provides an ominous mixture of nutrients for the liver and for metabolic processes.

I have questions about the implication of (a) red meat and (b) saturated fat in these statements that I’d like to follow-up on via newer research. The challenge of saturated fat implication is that most saturated fat in the SAD is eaten in processed foods.

Low carb, low fat, DIETFITS

Also noting that in the DIETFITS study just published, the apparent equal amount of weight loss from both approaches using real food, also showed a lipid disturbance in the low fat group that travels with NAFLD.

Just Read: DIETFITS and Effect of Low-Fat vs Low-Carbohydrate Diet, real food is better, is the low fat diet worse for metabolic health?

I’ll post on a few more papers. See you (whoever that is) at #LCB18 🙂

Citation: Barrera F, George J. The role of diet and nutritional intervention for the management of patients with NAFLD. Clin Liver Dis [Internet]. Elsevier Inc; 2014;18(1):91–112. Available from: http://dx.doi.org/10.1016/j.cld.2013.09.009

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