Does fatty liver cause gout? This question reflects growing awareness of the connection between these two increasingly common metabolic conditions. Whilst fatty liver disease does not directly cause gout in a simple cause-and-effect manner, research demonstrates a significant association between them. Non-alcoholic fatty liver disease (NAFLD) affects approximately 25–30% of the UK population, whilst gout impacts around 2.5% of UK adults. People with NAFLD are 1.5 to 2 times more likely to develop gout compared to those without liver disease. The link stems from shared metabolic dysfunction—particularly insulin resistance, obesity, and metabolic syndrome—rather than one condition directly causing the other. Understanding this relationship is clinically important for comprehensive management and prevention strategies.

Understanding the Link Between Fatty Liver and Gout

Fatty liver disease and gout are increasingly recognised as interconnected metabolic conditions, though the relationship is complex rather than directly causal. Non-alcoholic fatty liver disease (NAFLD) affects approximately 25–30% of the UK population and occurs when excess fat accumulates in liver cells in people who drink little or no alcohol. Gout, meanwhile, is an inflammatory arthritis caused by elevated uric acid levels forming crystals in joints, affecting around 2.5% of UK adults.

Research demonstrates a significant association between these conditions. Studies show that individuals with NAFLD have substantially higher rates of hyperuricaemia (elevated blood uric acid) and gout compared to those without liver disease. Systematic reviews have found that people with NAFLD are approximately 1.5 to 2 times more likely to develop gout. However, it is important to understand that fatty liver does not directly cause gout in a simple cause-and-effect manner.

The connection stems from shared underlying metabolic dysfunction. Both conditions are strongly linked to metabolic syndrome—a cluster of abnormalities including central obesity, insulin resistance, hypertension, and dyslipidaemia. The liver plays a crucial role in producing uric acid as the end product of purine metabolism. When affected by fatty infiltration and associated inflammation, hepatic metabolic processes may be altered, whilst the inflammatory state can influence how the kidneys handle uric acid excretion.

Understanding this relationship is clinically important. If you have NAFLD detected through abnormal liver function tests or imaging, your GP may assess your uric acid levels and cardiovascular risk factors. Similarly, people with gout often benefit from assessment for NAFLD and other metabolic conditions. The presence of both NAFLD and gout often signals more severe metabolic disturbance and may require comprehensive management strategies addressing the underlying metabolic dysfunction rather than treating each condition in isolation.

References: NICE NG49 (Non-alcoholic fatty liver disease: assessment and management); NICE NG219 (Gout: diagnosis and management); NHS NAFLD and Gout pages.

How Fatty Liver Disease Affects Uric Acid Levels

The mechanisms linking fatty liver disease to elevated uric acid levels involve complex metabolic pathways. In NAFLD, the liver's normal metabolic functions become disrupted by excessive fat accumulation and associated inflammation. This hepatic dysfunction can influence uric acid metabolism through several interconnected mechanisms, though uric acid is primarily excreted by the kidneys (approximately two-thirds) and intestines (approximately one-third), not the liver.

Insulin resistance, a hallmark feature of NAFLD, plays a central role in this relationship. When cells become resistant to insulin, the body compensates by producing more insulin (hyperinsulinaemia). Elevated insulin levels reduce the kidney's ability to excrete uric acid effectively by affecting the function of urate transporters in the kidney tubules, leading to uric acid retention and hyperuricaemia. Studies have demonstrated that the degree of insulin resistance correlates with both the severity of NAFLD and serum uric acid concentrations.

The liver itself is responsible for producing uric acid as the end product of purine metabolism. In NAFLD, particularly when progressing to non-alcoholic steatohepatitis (NASH), altered hepatic metabolism may increase uric acid production. Additionally, increased de novo lipogenesis—the process by which the liver synthesises new fatty acids—generates metabolic byproducts that can elevate uric acid levels.

Furthermore, the inflammatory state associated with fatty liver disease contributes to metabolic disturbances. Pro-inflammatory cytokines released during hepatic inflammation can affect both uric acid production and renal excretion. The oxidative stress present in NAFLD may also influence purine metabolism pathways. It is worth noting that elevated uric acid itself may contribute to liver damage; however, this bidirectional relationship is based largely on observational data and remains an area of ongoing research, with human causal evidence still limited.

Shared Risk Factors for Fatty Liver and Gout

Fatty liver disease and gout share numerous common risk factors, which explains why they frequently coexist in the same individuals. Recognising these shared risk factors is essential for prevention and early intervention strategies.

Obesity, particularly central or visceral adiposity, represents the most significant shared risk factor. Excess body weight, especially around the abdomen, promotes insulin resistance, increases hepatic fat accumulation, and elevates uric acid production. The risk of both conditions rises substantially with increasing body mass index (BMI). Data from UK populations show that individuals with a BMI over 30 kg/m² have markedly higher rates of both NAFLD and gout.

Dietary factors play a crucial role in both conditions. Diets high in:

• Fructose and sugar-sweetened beverages – fructose metabolism in the liver generates uric acid as a byproduct and promotes hepatic fat accumulation

• Refined carbohydrates – contribute to insulin resistance and weight gain

• Saturated fats – promote hepatic steatosis

• Purine-rich foods (red meat, organ meats, certain seafood) – increase uric acid production

• Excessive alcohol consumption – directly causes alcoholic fatty liver disease (distinct from NAFLD, which by definition occurs in people drinking within or below UK Chief Medical Officers' low-risk guidelines of 14 units weekly) and elevates uric acid levels

Type 2 diabetes mellitus is strongly associated with both conditions and significantly increases the risk of gout. The insulin resistance characteristic of type 2 diabetes underlies much of this association.

Other shared risk factors include:

• Hypertension – commonly coexists with both gout and NAFLD

• Dyslipidaemia – particularly elevated triglycerides and low HDL cholesterol

• Physical inactivity – contributes to weight gain and metabolic dysfunction

• Male sex – both conditions are more prevalent in men, though post-menopausal women see increased risk

• Genetic predisposition – family history increases susceptibility to both conditions

Certain medications may also contribute to hyperuricaemia and gout risk, including:

• Diuretics (thiazides, loop diuretics) – reduce renal uric acid excretion

• Low-dose aspirin – can raise uric acid levels

• Ciclosporin and tacrolimus – immunosuppressants that increase urate

• Niacin – used for dyslipidaemia

• Pyrazinamide and ethambutol – anti-tuberculosis medicines

If you are taking any of these medicines and develop gout, discuss this with your GP; do not stop prescribed medication without medical advice.

References: NICE NG49; NICE NG219; UK Chief Medical Officers' Low Risk Drinking Guidelines.

Managing Both Conditions: Treatment and Lifestyle Changes

Management of coexisting fatty liver disease and gout requires a comprehensive approach addressing shared metabolic dysfunction whilst treating each condition appropriately. NICE guidance emphasises lifestyle modification as the cornerstone of NAFLD management, which fortunately also benefits gout control.

Weight loss represents the most effective intervention for both conditions. For NAFLD, evidence shows that losing 7–10% of body weight can significantly reduce liver fat, inflammation, and even fibrosis. For gout, weight reduction lowers uric acid levels and reduces flare frequency. A gradual, sustained approach is recommended—rapid weight loss can paradoxically trigger gout attacks due to sudden metabolic changes. Aim for 0.5–1 kg weight loss per week through combined dietary modification and increased physical activity.

Dietary modifications should focus on:

• Mediterranean-style diet – rich in vegetables, fruits, whole grains, legumes, nuts, and olive oil; moderate in fish; limited in red meat

• Reducing fructose intake – limiting sugar-sweetened beverages, fruit juices, and foods with added sugars

• Limiting purine-rich foods during active gout, though overall metabolic health is more important than strict purine restriction

• Reducing alcohol consumption – for NAFLD, stay within UK Chief Medical Officers' low-risk drinking guidelines (14 units weekly spread over 3+ days, with several alcohol-free days); for gout, minimise alcohol, especially beer and spirits

• Adequate hydration – particularly important for gout management

Physical activity benefits both conditions through multiple mechanisms: improving insulin sensitivity, promoting weight loss, reducing inflammation, and lowering uric acid levels. NICE recommends at least 150 minutes of moderate-intensity activity weekly.

Pharmacological management requires careful consideration:

For gout:

• Acute flares: NSAIDs (avoid in advanced liver disease or cirrhosis; use with caution and gastroprotection), colchicine, or corticosteroids

• Urate-lowering therapy (ULT): Offered to people with recurrent flares (≥2 per year), tophi, chronic kidney disease stage 3 or worse, or those on diuretics. Allopurinol is first-line; start at a low dose (e.g., 100 mg daily; lower in chronic kidney disease) and titrate gradually every few weeks to achieve a serum uric acid target of below 360 micromol/L (below 300 micromol/L if tophi present). Febuxostat is reserved for people who cannot tolerate or have contraindications to allopurinol; it carries an MHRA warning regarding cardiovascular risk in people with established cardiovascular disease and requires liver function monitoring.

• Flare prophylaxis: When starting or adjusting ULT, offer prophylaxis with colchicine (500 micrograms once or twice daily) or a low-dose NSAID (with proton pump inhibitor) for up to 6 months to prevent flares during the initial treatment period.

For NAFLD:

• No licensed pharmacological treatments currently exist specifically for NAFLD in the UK

• Management of associated conditions (diabetes, hypertension, dyslipidaemia) is essential

• In selected people with type 2 diabetes and NAFLD/NASH, pioglitazone or GLP-1 receptor agonists may be considered under specialist guidance; these are off-label for liver disease

• Statins should not be withheld when indicated for cardiovascular risk reduction; they are safe and beneficial even in people with NAFLD

Medication review is important. If you experience side effects from any medicine, report them via the MHRA Yellow Card scheme (yellowcard.mhra.gov.uk or the Yellow Card app).

References: NICE NG219; NICE NG49; MHRA Drug Safety Update (2019) – Febuxostat; BNF; Allopurinol and Febuxostat SmPCs (emc).

When to Seek Medical Advice for Fatty Liver and Gout

Recognising when to seek medical attention is crucial for preventing complications from both fatty liver disease and gout. Many individuals with NAFLD remain asymptomatic until advanced stages, making risk-based assessment important for at-risk populations.

Seek urgent same-day medical assessment if you experience:

• Severe joint pain with fever and feeling systemically unwell – this may indicate septic arthritis (joint infection), a medical emergency requiring urgent assessment to distinguish from gout

• Abdominal pain with jaundice (yellowing of skin or eyes) – may indicate advanced liver disease or acute liver injury

• Confusion, drowsiness, or altered mental state – potential signs of hepatic encephalopathy in advanced liver disease

• Vomiting blood or black, tarry stools – suggesting gastrointestinal bleeding, a complication of advanced liver disease

Arrange a routine GP appointment if:

• You experience sudden, severe joint pain (especially affecting the big toe, ankle, or knee) without fever or systemic symptoms – this may be a gout flare and warrants prompt GP review

• You have risk factors for NAFLD (obesity, type 2 diabetes, metabolic syndrome) and abnormal liver function tests are detected – your GP can arrange further assessment, including calculation of fibrosis risk scores (FIB-4 or NAFLD Fibrosis Score) and, if indicated, an Enhanced Liver Fibrosis (ELF) blood test or referral to hepatology. Note that liver enzyme levels (ALT) may be normal in NAFLD.

• You experience recurrent gout attacks (two or more per year) – indicating need for urate-lowering therapy

• You have persistent joint pain or swelling between gout attacks, or develop lumps (tophi) around joints

• You are diagnosed with one condition and have risk factors for the other

Regular monitoring is recommended for:

• Individuals with confirmed NAFLD – your GP will use fibrosis risk scores (FIB-4 or NAFLD Fibrosis Score) and, if needed, the ELF blood test to assess fibrosis risk. People at increased risk of advanced fibrosis are referred to hepatology for specialist assessment. Liver ultrasound detects fat but does not assess fibrosis.

• Those on urate-lowering therapy – serum uric acid monitoring to ensure target levels (below 360 micromol/L, or below 300 micromol/L with tophi) are achieved and maintained

• Patients with metabolic syndrome components – regular cardiovascular risk assessment

Your GP may refer you to specialist services including hepatology (for NAFLD with suspected advanced fibrosis) or rheumatology (for complex or refractory gout). Early intervention and regular monitoring can prevent progression to cirrhosis or chronic gouty arthropathy, emphasising the importance of not delaying medical consultation when concerns arise.

References: NICE NG49; NICE NG219; NHS NAFLD and Gout pages.

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