Gout and high uric acid: flares, diet and prevention

Gout is inflammatory arthritis caused by urate crystals, usually after uric acid has been high enough for long enough to crystallise in joints or soft tissue. A flare is the painful alarm, but the underlying problem is crystal burden, which is why repeated painkillers without a urate-lowering plan often fails. The practical UK approach is to confirm the diagnosis, treat flares quickly, check serum urate after the flare, and use a treat-to-target plan when gout is recurrent or high risk.¹²

What gout is

Uric acid is produced when the body breaks down purines, substances found in human cells and many foods. Most uric acid leaves through the kidneys. If production is high or excretion is low, blood urate rises. Above a certain level, monosodium urate crystals can form. The immune system can then attack those crystals, causing the sudden inflammation people recognise as gout.

The old image of gout as a punishment for rich food is outdated and unfair. Diet and alcohol can trigger flares, but genetics, kidney function, body weight, blood pressure, diabetes, menopause, diuretics and other medicines often matter more. NHS guidance notes that gout can run in families and is more common in men, after menopause, with excess weight, alcohol use, diuretics, high blood pressure, kidney problems, high cholesterol, osteoarthritis and diabetes.¹

High uric acid is not exactly the same as gout. Some people have high urate and never develop crystal disease. Others have classic gout despite a blood result that looks normal during the flare. The diagnosis is the pattern plus evidence, not a single number in isolation.

Diagnosis and uric acid testing

NICE says to suspect gout when someone has rapid onset, often overnight, of severe pain with redness and swelling in one or both first metatarsophalangeal joints, the big-toe joints, or when tophi are present. Gout should also be considered in other joints such as the midfoot, ankle, knee, hand, wrist or elbow.²

The big diagnostic trap is assuming every hot swollen joint is gout. NICE says clinicians should assess for septic arthritis, calcium pyrophosphate crystal deposition and inflammatory arthritis in people with a painful, red, swollen joint, and refer immediately if septic arthritis is suspected.² Infection inside a joint can destroy cartilage quickly and can be life-threatening.

Serum urate testing is useful, but timing matters. NICE recommends measuring serum urate in people with symptoms and signs of gout to confirm the clinical diagnosis, using 360 micromol/L, or 6 mg/dL, as the threshold. If serum urate is below that during a flare and gout is strongly suspected, repeat the test at least 2 weeks after the flare has settled.²

If the diagnosis remains uncertain, NICE says to consider joint aspiration and microscopy of synovial fluid. If aspiration cannot be done or the diagnosis is still uncertain, imaging such as X-ray, ultrasound or dual-energy CT can be considered.² Crystal confirmation is especially useful when the pattern is unusual, several joints are involved, infection is a possibility, or long-term urate-lowering treatment is being considered.

What to do during a flare

A gout flare should be treated early. NHS advice is to take prescribed medicine as soon as possible, rest and raise the limb, keep the joint cool with an ice pack wrapped in a towel, drink water unless told not to, and avoid pressure on the joint.¹ Do not wait for heroic dietary changes to calm a joint that is already inflamed.

NICE recommends an NSAID, colchicine or a short course of oral corticosteroid for first-line treatment of a gout flare, taking account of comorbidities, co-prescriptions and preference.² That individualisation matters. NSAIDs may be unsuitable with kidney disease, stomach ulcer risk, heart failure, anticoagulants or some blood pressure medicines. Colchicine can cause diarrhoea and has important medicine interactions. Steroids can affect glucose, mood, sleep and infection risk.

If the pain is getting worse, you feel hot, cold or shivery, have a very high temperature, feel sick or cannot eat, NHS says to ask for an urgent GP appointment or get help from NHS 111 because these symptoms could mean infection inside the joint.¹ This is the point where "I always get gout" can become dangerous. Familiar symptoms can still hide a new infection.

Long-term prevention

Long-term prevention is where gout is often under-treated. Painkillers treat the inflammation of a flare. They do not dissolve the crystal burden. NICE says gout progresses without intervention because high urate leads to new urate crystals, and explains that long-term urate-lowering therapy can eliminate urate crystals, prevent flares, shrink tophi and prevent joint damage.²

NICE recommends offering urate-lowering therapy, using a treat-to-target strategy, to people with gout who have multiple or troublesome flares, CKD stages 3 to 5, diuretic therapy, tophi or chronic gouty arthritis. It also says to discuss urate-lowering therapy with people after a first or later flare even if they are not in those groups.²

Allopurinol and febuxostat are the main first-line urate-lowering medicines in NICE guidance. NICE says to start with a low dose and use monthly serum urate levels to guide dose increases until the target is reached.² NHS allopurinol guidance says allopurinol lowers uric acid, but during the first few months it can trigger more gout attacks, so a doctor may prescribe an NSAID or colchicine to help prevent this.⁵

The target is important. NICE says to aim below 360 micromol/L, and to consider below 300 micromol/L for people with tophi, chronic gouty arthritis or ongoing frequent flares despite being below 360.² In practice, a fixed low dose that never reaches target is not a treatment plan. It is a half-plan.

Diet and lifestyle levers

Lifestyle helps, but it is rarely enough for established recurrent gout on its own. NICE explicitly says there is not enough evidence to show that any specific diet prevents flares or lowers serum urate levels, and advises a healthy balanced diet. It also says excess body weight, obesity and excessive alcohol may exacerbate flares and symptoms.²

That does not mean food is irrelevant. In the Health Professionals Follow-up Study, Choi and colleagues followed 47,150 men without gout at baseline for 12 years. Higher meat and seafood intake were associated with higher incident gout risk, while higher dairy intake was associated with lower risk; purine-rich vegetables were not associated with increased risk.³ That is why "avoid all purines" is too blunt. Lentils and mushrooms are not the same as large portions of organ meat or frequent shellfish.

Sugary drinks are a clearer target. Choi and Curhan's BMJ cohort study found sugar-sweetened soft drinks and fructose intake were strongly associated with incident gout in men, while diet soft drinks were not.⁴ For most people, reducing sugary drinks, fruit juice, heavy alcohol, beer, spirits, very large meals and dehydration is more useful than memorising every purine table.

Alcohol deserves separate honesty. Beer and spirits are common flare triggers, and alcohol can worsen dehydration and urate handling. NHS prevention advice includes alcohol-free days, not drinking more than 14 units per week, drinking plenty of fluids, losing weight if overweight while avoiding crash diets, exercising regularly without overloading painful joints, and avoiding lots of sugary drinks and snacks.¹

Crash dieting, fasting and dehydration can trigger flares. So can illness, injury and certain medicines. If gout sits alongside high blood pressure, kidney disease, diabetes, kidney stones or high cholesterol, the plan should not be a one-food ban. It should be a metabolic risk review with medication review, kidney function, blood pressure, HbA1c, lipids and serum urate interpreted together.

A practical plan

First, separate the flare from the disease. During the flare, treat pain and inflammation early, rule out infection if the pattern is worrying, and avoid pressure on the joint. After it settles, measure serum urate, review triggers and ask whether the pattern meets NICE criteria for urate-lowering therapy.

Second, insist on a target if long-term medicine is started. The goal is not "take allopurinol forever and hope". It is to lower serum urate below the agreed threshold, prevent flares while the dose is being adjusted, and monitor yearly once stable. If you still flare despite treatment, the first question is whether the urate target has actually been reached and maintained.

Third, connect gout to the wider risk picture. Gout can overlap with kidney stones, chronic kidney disease, high blood pressure, insulin resistance and cardiovascular risk. Use the health library to map the overlap, the start here guide to prepare for GP review, and insights to avoid diet myths that make gout feel like a moral failure. If you are combining painkillers, colchicine, allopurinol, supplements or alkalinising products, check the plan in the stack builder before adding more.

This article is educational and does not constitute medical advice, diagnosis, or a treatment recommendation. Medication uses described as “off-label” are not licensed for that purpose in the UK and should only be considered under qualified clinical supervision. Always speak to your GP, pharmacist, or a registered specialist before starting, stopping, or changing any treatment. If you have severe or alarm symptoms - unintentional weight loss, blood in your stool, difficulty swallowing, persistent vomiting, a fever, or severe pain - seek urgent medical care.