Non-alcoholic fatty liver disease: From evidence to everyday practice

This webinar focuses on understanding and managing metabolic dysfunction-associated steatotic liver disease (MASLD) from both clinical and naturopathic/functional medicine perspectives. It gives nutrition, health and natural medicine practitioners actionable tools to:

1. Assess risk
2. Identify the mechanisms driving liver fat
3. Put dietary, lifestyle and supplement-based interventions in place

Hosted by Ella Kaur (Practitioner Lead, Registered Nutritionist and Nutritional Therapy Practitioner) with guest speaker Mark Killick, Senior Lecturer at CNM & Registered Functional Nutritionist, mANP.

Key Points Discussed

Why the terminology matters (MASLD vs NAFLD)

The older label 'non-alcoholic fatty liver disease' caused confusion, leaving patients who didn't drink without a clear driver. The new name reframes the condition as metabolic. This helps practitioners explain to clients that the liver problem is driven by metabolic dysfunction (especially insulin and carbohydrate metabolism), not by 'moral failing'.

Burden and risk groups

Fatty liver disease affects a large global population, and prevalence is rising alongside obesity and type 2 diabetes. Rates are higher in people with type 2 diabetes and those who meet the criteria for metabolic syndrome.

Core pathophysiology

Insulin resistance and adipose overflow: Fat cells become unable to store more fat and spill fatty acids into circulation.

De novo lipogenesis: The liver synthesises new fat in response to metabolic signals.

The gut-liver axis: Dietary patterns can shift the microbiome, increase intestinal permeability and promote inflammatory signalling (including via LPS and downstream pathways). This worsens liver inflammation and scarring.

Disease progression ('metabolic spectrum')

A continuum runs from simple steatosis (reversible), to MASH/NASH (inflammation and injury), to fibrosis (F1–F3), to cirrhosis (F4, higher risk and less reversible). The earlier the intervention, the better.

What drives hepatic fat (the 'insulin enabling signal')

A central mechanistic message is that the liver cannot store or export fat appropriately without elevated insulin. Controlling insulin is presented as the most powerful intervention.

Targets beyond conventional advice

• Carbohydrates drive insulin, which drives liver fat. Dietary fat contributes a smaller portion than fat produced internally.
• Fructose and alcohol are additional hepatotoxic drivers. They can damage the liver through pathways that don't rely on the same insulin route.
• Fasting/ketogenesis and carbohydrate restriction reduce insulin signalling and support fat clearance.

Key Takeaways

1. Reframe the conversation: MASLD is fundamentally metabolic. Link counselling to insulin and carbohydrate metabolism rather than stigma.
2. Act early: Interventions are most powerful in simple steatosis (the F0–F2 range). Progression increases fibrosis risk and reduces reversibility.
3. Prioritise insulin reduction: Carbohydrate restriction, ketogenic support and fasting can reduce liver fat by lowering insulin-driven mechanisms. Fructose and alcohol add harm.
4. Use risk stratification tools: Routine blood markers (ALT/AST, fasting insulin) and fibrosis tools (e.g., FIB-4, staging considerations) help determine urgency and the need for referral.

Conclusion

This webinar delivers a clinically oriented, naturopathically actionable framework for MASLD:

1. Understand the metabolic and gut-liver mechanisms.
2. Assess risk early, especially via fasting insulin and fibrosis screening.
3. Implement an insulin-lowering protocol using targeted dietary strategy, fasting, exercise, sleep and stress optimisation, and supportive supplementation.
4. Know when advanced markers require referral.

This webinar is fully approved by BANT^® and accredited for CPD hours.