There has been some debate in recent months in the liver community about the nomenclature of non-alcoholic fatty liver disease (NAFLD). Understandably, there is some concern that the name is confusing, focussed on what it is not rather than what it is. ‘Metabolic Associated Liver Disease’ (MAFLD) has been proposed as an alternative, but the large elephant in the expert consensus room is that this is (except for a few exceptions) a disease of obesity- ‘obesity-related liver disease.’

For years obesity has come to fore as the most important public health issue in our country, and as our clinics and transplant waiting lists increasingly fill up with advanced cirrhosis secondary to NAFLD, hepatologists and gastroenterologists are waking up to the fact that this is also very much our problem. Certainly, a pre-covid trip into the General Session of a major hepatology conference (remember those?) would see the stage occupied, not by the saviours of Hepatitis C, but by the PIs of major international trials of interventions for non-alcoholic steatohepatitis (NASH). But it is right to regularly step back and take stock to assess whether the direction of travel is right.

The first question to ask is how much progress we have made in addressing the root cause of NAFLD, obesity. A study by Katie Lane and colleagues in Liverpool,¹ published in Frontline, evaluated their lifestyle intervention programme and came to a depressingly familiar conclusion: helping people to lose weight is hard. From 167 patients approached in clinic, only 16 completed the programme on offer, including personalised dietary and exercise advised from a lifestyle trainer in a local community setting. Although this intervention resulted in a significantly greater weight reduction than those who did not complete the intervention, this was still only a mean 2.78kg (~2%), some way off the 10% reduction needed to improve hepatic fibrosis. Even in arguably the most important study demonstrating the benefit of weight loss on the histological features of NASH only 10% achieved a target weight loss of at least 10%.²

In light of these difficulties, it is tempting to become fatalistic- ‘it cannot be done.’ As doctors this line of thinking can lead us into the domain of intensive medical and surgical interventions in which we tend to feel most comfortable. There will of course be important benefits from the innovations in pharmacological interventions on the horizon, and there is no doubt bariatric surgery can produce major metabolic improvements to some groups of patients with morbid obesity; yet one cannot but be concerned about a drift to park expensive ambulances and hospitals at the bottom of the cliff rather than put a fence at the top. This is particularly so with new drugs, which will be expensive, long term, and without clear stopping indications that were licensed on histological endpoints that cannot be replicated for mass longitudinal monitoring.

Ultimately a public health problem needs public health interventions, and as a community of hepatologists and gastroenterologists we must be at the forefront in placing liver disease within the public conversation on obesity. Investment in lifestyle interventions will help, but we need to be vocal on discussions about sugar tax, cycling campaigns and food labelling much as we have been in lobbying for better alcohol policy. We live in an obesigenic society, and it is only though widescale changes to the environment in which we live that we can produce meaningful change.

Placing this into an even broader context, there are also critical environmental issues to consider in our approach to healthcare problems such as obesity. A group of us have recently tried to start a national conversation about ‘Green Endoscopy,’³ and we should also be considering the impact on our planet on all of our medical interventions; the carbon footprint of lifestyle changes will certainly be a fraction of drugs and surgery. Furthermore, local management over secondary care cuts down on travel miles and resource- intensive hospitals. In another paper by Stuart McPherson’s group in Newcastle,⁴ they tried to standardise the management of patients with NAFLD in secondary care. As part of the initial audit, they found only 16% of patients referred had non-invasive screening for fibrosis in primary care. We know that only patients with fibrosis (a minority) are at increased risk of adverse liver-related outcomes in NAFLD, and widespread use of simple tests like FIB-4 could dramatically cut down on unnecessary secondary care referrals with subsequence savings of resources. This is happening across the country and is a positive application of innovations in non-invasive markers of fibrosis.⁵

So how do we solve a problem like obesity-related liver disease? When I see a prominent hepatologist joining a politician and the president of the RCGP on Good Morning TV to discuss the ‘obesity epidemic,’ I will know we’re making progress.

1. Patanwala, I., Molnar, L. E., Akerboom, K. & Lane, K. E. Direct access lifestyle training improves liver biochemistry and causes weight loss but uptake is suboptimal in patients with non-alcoholic fatty liver disease. Frontline Gastroenterol. flgastro-2020-101669 (2020). doi:10.1136/flgastro-2020-101669
2. Vilar-Gomez, E. et al. Weight Loss Through Lifestyle Modification Significantly Reduces Features of Nonalcoholic Steatohepatitis. Gastroenterology 149, 367-378.e5 (2015).
3. Maurice, J. B. et al. Green endoscopy: a call for sustainability in the midst of COVID-19. The Lancet Gastroenterology and Hepatology 5, 636–638 (2020).
4. Neilson, L. J. et al. Implementation of a care bundle improves the management of patients with non-alcoholic fatty liver disease. Frontline Gastroenterol. 1–8 (2021). doi:10.1136/flgastro-2020-101480
5. Srivastava, A. et al. Prospective evaluation of a primary care referral pathway for patients with non-alcoholic fatty liver disease. J. Hepatol. 71, 371–378 (2019).