Elsevier

Journal of Hepatology

Volume 67, Issue 4, October 2017, Pages 829-846
Journal of Hepatology

Review
Treatment of NAFLD with diet, physical activity and exercise

https://doi.org/10.1016/j.jhep.2017.05.016Get rights and content

Summary

Lifestyle intervention can be effective when treating non-alcoholic fatty liver diseases (NAFLD) patients. Weight loss decreases cardiovascular and diabetes risk and can also regress liver disease. Weight reductions of ⩾10% can induce a near universal non-alcoholic steatohepatitis resolution and fibrosis improvement by at least one stage. However, modest weight loss (>5%) can also produce important benefits on the components of the NAFLD activity score (NAS). Additionally, we need to explore the role of total calories and type of weight loss diet, micro- and macronutrients, evidence-based benefits of physical activity and exercise and finally support these modifications through established behavioural change models and techniques for long-term maintenance of lifestyle modifications.

Following a Mediterranean diet can reduce liver fat even without weight loss and is the most recommended dietary pattern for NAFLD. The Mediterranean diet is characterised by reduced carbohydrate intake, especially sugars and refined carbohydrates (40% of the calories vs. 50–60% in a typical low fat diet), and increased monounsaturated and omega-3 fatty acid intake (40% of the calories as fat vs. up-to 30% in a typical low fat diet). Both TV sitting (a reliable marker of overall sedentary behaviour) and physical activity are associated with cardio-metabolic health, NAFLD and overall mortality. A ‘triple hit behavioural phenotype’ of: i) sedentary behaviour, ii) low physical activity, and iii) poor diet have been defined. Clinical evidence strongly supports the role of lifestyle modification as a primary therapy for the management of NAFLD and NASH. This should be accompanied by the implementation of strategies to avoid relapse and weight regain.

Introduction

Non-alcoholic fatty liver disease (NAFLD) is a major health problem because of its high prevalence and the associated risk of progression to liver cirrhosis, liver cancer and also, increased cardiovascular and solid neoplasm risk. NAFLD comprises a wide pathological spectrum ranging from simple steatosis to steatohepatitis (NASH) with variable degrees of fibrosis and cirrhosis.1 The strongest predictor of fibrosis progression in NAFLD is the presence of steatohepatitis.2 The risk of detrimental outcomes is increased in patients with significant fibrosis, or steatohepatitis, whilst it is lower in patients with simple steatosis. Liver biopsy remains the gold standard for histological evaluation of the disease. Non-invasive methods combining imaging and biochemical tests are warranted to pre-empt the need for liver biopsies.

The prevalence of NAFLD varies largely from 20% to 30% and increases with age,3 with an annual incidence of around two new cases/100 patients/year. Since NASH is becoming one of the most frequent causes of cirrhosis and liver transplantation worldwide,[4], [5] it is crucial to identify patients at risk of NAFLD progression in order to implement therapeutic interventions that can lead to prevention or reversal of the deleterious consequences of advanced NASH.

Patients with NAFLD are frequently obese and/or have diabetes, and insulin resistance is a key pathogenic trigger. Four phenotypes of patients with NAFLD have been defined: i) obese, ii) type 2 diabetes, iii) metabolic syndrome and iv) lean patients. PNPLA3 is the genetic hallmark of NAFLD. Patients bearing genotype GG were at three times greater risk of NAFLD. This increased risk is more evident in patients without metabolic syndrome.6 Indeed, TM6SF2 mutation has an additive effect on NAFLD risk.7

Section snippets

Role of energy restriction

Excess caloric consumption leading to obesity and related comorbidities is a leading risk factor for NAFLD.8 Furthermore, weight gain by itself, even only a modest 3–5 kg, predicts the development of NAFLD, regardless of baseline body mass index (BMI).9 Interestingly, not only excess caloric consumption, but also the way food consumption is distributed throughout the day, affects liver fat accumulation. In a 6-week randomised controlled trial (RCT), high fat high sugar, or high sugar

Weight loss as the first endpoint treating NASH

Losing weight decreases cardiovascular and diabetes risk and also regresses liver disease.

The primary approach to treat NAFLD focuses on the control of the underlying risk factors like diabetes, hyperlipidaemia, obesity and other comorbidities. Lifestyle changes through diet and physical activity modifications are well-established therapeutic strategies for conditions such as diabetes and cardiovascular disease.[138], [139] To date, only a few studies have evaluated the impact of lifestyle

Behavioural aspects of lifestyle modification

There is no doubt that lifestyle modification and weight loss pose a great challenge to both the patients and caregivers. NAFLD patients may have a low level of readiness for change and motivation to adopt a healthier lifestyle.159 Furthermore, NAFLD diagnosis is not necessarily associated with lower general health perception nor is it associated with higher health care utilisation.160 It has been repeatedly demonstrated that weight loss achieved by diet is highest at 6-months follow-up and

Summary & conclusions

Lifestyle change, including dietary habits and physical activity, are and should be the first line of treatment in NAFLD and NASH. Weight reduction is the most established treatment for both NAFLD and NASH, with a clear dose-response association. Generally, any form of healthy diet (low fat or low carbohydrates or Mediterranean diet), which will lead to caloric reduction and is acceptable by the patient, should be encouraged. For those who find caloric restriction difficult, changing dietary

Conflict of interest

The authors who have taken part in this study declared that they do not have anything to disclose regarding funding or conflict of interest with respect to this manuscript.

Authors’ contribution

All three authors contributed equally in the elaboration of the manuscript.

Acknowledgement

PI 16/ 01842 Instituto de Salud Carlos III, MINECO, Spain.

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