In a MASLD diet trial, weight and processed-food cuts beat diet type
A six-month randomised trial found liver-fat improvement tracked weight loss and lower ultra-processed food intake, not whether people were assigned a Mediterranean or low-carbohydrate pattern.
Diet is the first thing patients with metabolic dysfunction-associated steatotic liver disease (MASLD) are told to change, but the specific pattern that gets prescribed varies by clinic and by fashion. A six-month randomised trial from a group in Turin set out to test whether the pattern itself matters, or whether it is the weight loss and the improvement in diet quality that come with any structured advice [s1]. The answer landed on the second option.
What the trial did
The study enrolled patients who had MASLD together with overweight or obesity and who had never had structured nutritional counselling before [s1]. It was a three-arm, parallel-group design: participants were randomised to a Mediterranean diet, a low-carbohydrate, high-protein diet, or standard nutritional recommendations, and followed for six months [s1]. Liver fat was measured by controlled attenuation parameter (CAP), an ultrasound-based estimate, with body composition, metabolic markers and ultra-processed food (UPF) intake tracked as secondary outcomes [s1].
Of 173 participants enrolled, 148 (85.5%) completed the study [s1]. The trial was funded by the Italian Ministry of University and Research, not by a food or drug company [s1].
The numbers
CAP fell significantly within the low-carbohydrate arm, with a change of −19.5 (−48.8 to 8.0; p = 0.004), and within the standard-care control arm, at −11.0 (−32.0 to 12.0; p < 0.001) [s1]. The result that matters, though, is what happened between the arms: there were no significant between-group differences in the change in liver fat [s1]. Every arm improved on body weight, BMI, adiposity measures, metabolic profile and dietary quality, including reductions in ultra-processed food intake [s1].
To work out what was actually driving the liver-fat change, the authors used structural equation modelling. It found no direct or total effect of the assigned dietary pattern on CAP [s1]. Instead, two things independently and significantly predicted the improvement: the reduction in BMI, with a coefficient of β = 14.34 (95% CI 10.55–18.13), and the reduction in ultra-processed food consumption, β = 0.64 (95% CI 0.25–1.03) [s1].
In plain terms: how much weight someone lost, and how much they cut back on ultra-processed food, explained the liver-fat improvement — the label on the diet did not. The two predictors are on different scales in the model, so the coefficients are not directly comparable in magnitude, but both cleared statistical significance and both pointed the same way [s1].
Why this is not a surprise, and where it is limited
A trial that shows "no difference between diets" is easy to misread. It does not mean the diets are useless; every arm improved. It means the trial could not attribute the benefit to one pattern over another, and that the mechanism it could identify was weight loss plus better food quality — factors any of the three approaches delivered.
The caveats are real. CAP is an estimate of liver fat, not the biopsy or MRI-based fat fraction used as a gold standard, so it carries measurement noise. Six months is short for a disease that plays out over years, and the trial reports no liver histology. It was a single-centre study, and the between-arm null could partly reflect limited power to detect modest differences rather than their true absence. None of that is resolved here.
The ultra-processed food signal is the more novel piece, and it fits a wider, still-unsettled literature. A 2026 systematic review and meta-analysis of randomised trials found that ultra-processed diets tended to raise energy intake and produced significantly greater weight gain than less-processed diets (standardised mean difference 0.65), but also concluded that the effect may be explained by the higher energy density of the ultra-processed foods used in trials, and that the overall certainty of evidence is low [s2]. When trial diets were matched so that the ultra-processed arm was not more energy-dense, the effect on energy intake nearly vanished (standardised mean difference 0.02 versus 0.71 when it was denser) [s2].
Read together, the two papers point the same way: what a diet is made of — its energy density, its processing, the weight change it produces — appears to matter more than the branded pattern it is sold under.
What to watch
The Turin trial is a case for a flexible, patient-centred approach to MASLD rather than a rigid prescription, but it is one modest study using a surrogate liver-fat measure [s1]. The questions it leaves open are the ones dietary trials in this field keep leaving open: whether the same holds over years rather than months, whether it shows up on histology, and whether cutting ultra-processed food adds anything once weight loss is accounted for, or is simply how the weight loss happens. Larger trials with harder endpoints will have to settle that.
This article is informational and does not constitute medical advice.
Sources
- [s1] Impact of weight loss and reduction of ultra-processed foods on liver fat content in MASLD: A randomized controlled trial. JHEP Reports, 22 June 2026. https://doi.org/10.1016/j.jhepr.2026.101929
- [s2] A systematic review and meta-analysis of randomized controlled trials examining the effect of ultra-processed food on energy intake and weight gain. Critical Reviews in Food Science and Nutrition, 16 September 2026. https://doi.org/10.1080/10408398.2026.2731838
Sources
- Impact of weight loss and reduction of ultra-processed foods on liver fat content in MASLD: A randomized controlled trial — JHEP Reports , June 22, 2026
- A systematic review and meta-analysis of randomized controlled trials examining the effect of ultra-processed food on energy intake and weight gain — Critical Reviews in Food Science and Nutrition , September 16, 2026
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