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Letter
Animal protein intake and hepatic steatosis in the elderly
  1. George Yizhou Tang1,
  2. Jake Peter Mann2
  1. 1 School of Clinical Medicine, University of Cambridge, Cambridge, UK
  2. 2 Department of Paediatrics, University of Cambridge, Cambridge, UK
  1. Correspondence to George Yizhou Tang, School of Clinical Medicine, University of Cambridge, Addenbrooke’s Hospital, Cambridge CB2 0SP, UK; george.tang{at}doctors.org.uk

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We read with interest the work by Alferink et al,1 which reports that intake of animal protein, but not that of monosaccharides and disaccharides, was found to be independently associated with non-alcoholic fatty liver disease (NAFLD). This is a surprising finding from a well-conducted cohort study that facilitated adjustment for metabolic covariates, in addition to sociodemographics and other lifestyle factors. However, we have reservations about the generalisability of these findings to patients with NAFLD or non-alcoholic steatohepatitis (NASH).

The studied population had an average age of 70 years, which is unusual for a first presentation of NAFLD. A large retrospective study identified 52.8 years as the average age of NASH-cirrhosis.2 Given the estimated rate of disease progression in NAFLD and NASH, most patients with clinically significant NAFLD are likely to have presented before the age of 70 years.3

Table 1 of the trial shows that the average caloric intake was 1996 for participants with NAFLD and 2052 for those without, despite those with NAFLD having a higher BMI (29.3 vs 25.8). This is unusual and not typical of most patients with obesity, NAFLD and the metabolic syndrome. This intake is roughly in line with most national guidelines. Other studies have found a significantly higher caloric intake for patients with NAFLD compared with controls, for example, 2739 kcal vs 2173 kcal per day.4

The study suggests that haem iron found in animal protein may be responsible for oxidative stress. However, the imaging modality used was abdominal ultrasound, which is able to detect steatosis, but has a low sensitivity for detecting NASH.5 These data would be more persuasive if animal protein intake was shown to correlate with advanced fibrosis.6 It may be possible to calculate non-invasive fibrosis scores (such as FIB-4 or NAFLD Fibrosis Score) in this cohort; however, age is a major factor in these calculations and the scores have a low specificity in an elderly population such as the one in this study.7

While there is other evidence to support a detrimental effect of animal protein, a rigorous clinical study on patients with diabetes found isocaloric animal and plant protein diets to reduce liver fat and aminotransferases.8

This study has interesting findings linking dietary animal protein to hepatic steatosis, and focuses on a healthy, elderly population. We feel these data suggest that development of steatosis in the elderly is influenced by different processes than seen in younger adults and these findings may not be generalisable to patients with clinically significant NASH.

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Footnotes

  • Contributors GYT and JPM made substantial contributions to the conception of the work, drafting and revising it, gave final approval to the version submitted for publication and agreed to be accountable for all aspects of the work.

  • Competing interests None declared.

  • Patient consent Not required.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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