Gout: The Complete Guide to Attacks, Diet, Medicines and Prevention

Gout is the most common form of inflammatory arthritis in the world. It affects tens of millions of people, and its numbers have risen steadily over the past three decades, driven by ageing populations, obesity, high blood pressure, kidney disease and changes in diet. A gout attack is one of the most painful experiences a person can have. Yet gout is also one of the few forms of arthritis that can effectively be cured, in the sense that attacks can be stopped completely with the right long-term treatment.

Despite this, most people with gout are not treated properly. Many are told to “watch what they eat” and take painkillers when it flares. Attacks become more frequent, joints become damaged, and lumps of crystals called tophi form under the skin. This complete guide explains what gout really is, why diet alone is rarely enough, how to stop an attack quickly, how urate-lowering treatment works, what to eat and drink, and how to protect your heart and kidneys, which are closely linked to gout.

What is gout?

Gout is a type of arthritis caused by crystals of monosodium urate forming in and around joints. These crystals form when the level of uric acid in the blood (called serum urate) stays too high for too long. When crystals build up and are then released into the joint, the immune system reacts strongly, causing sudden, severe inflammation. This is a gout attack, also called a gout flare.

Uric acid is a normal waste product made when the body breaks down substances called purines. Purines are found in the body’s own cells and in many foods. Most uric acid is removed by the kidneys into the urine, and some through the gut. When the body makes too much uric acid or, much more commonly, the kidneys do not remove enough, levels rise. This is called hyperuricaemia.

Not everyone with high uric acid develops gout. But the higher the level and the longer it stays high, the more likely crystals are to form. Crystals can be present in joints for years before the first attack.

Who gets gout?

Gout is more common in:

• Men, particularly from middle age. Oestrogen helps the kidneys remove uric acid, so women are relatively protected until after menopause, when their risk rises.
• Older adults.
• People living with overweight or obesity.
• People with high blood pressure, heart disease, type 2 diabetes, high cholesterol and kidney disease.
• People taking certain medicines, especially diuretics (“water tablets”) such as furosemide and hydrochlorothiazide, low-dose aspirin, ciclosporin and some tuberculosis medicines.
• People with a family history of gout. Genetics strongly influence how the kidneys handle uric acid.
• People who drink a lot of alcohol, especially beer and spirits, or sugary drinks sweetened with fructose.
• Certain populations, including Pacific Islander, Māori and some other groups, have particularly high rates of gout because of genetic differences in uric acid handling.

Gout is sometimes seen as a disease of overindulgence. This stereotype is unfair and unhelpful. Genetics and kidney function are often the biggest factors, and many people with gout eat healthily. The stigma stops people seeking proper care.

Symptoms of a gout attack

A typical gout attack:

• Starts suddenly, often at night or early in the morning.
• Reaches its peak within 24 hours.
• Causes severe pain, swelling, warmth and redness in one joint.
• Makes the joint extremely tender to touch.
• Often affects the joint at the base of the big toe. This is the first joint affected in about half of people. Other common sites include the top of the foot, ankle, knee, wrist, fingers and elbow.
• Settles over one to two weeks, even without treatment, though treatment speeds recovery.

Some people also have a mild fever and feel generally unwell during an attack. The skin over the joint may peel as the attack settles.

Common triggers for attacks include:

• A large meal rich in meat or seafood.
• Drinking alcohol, especially binge drinking.
• Dehydration, for example in hot weather, after intense exercise or during illness.
• Injury to a joint.
• Surgery or acute illness.
• Starting or changing doses of diuretics.
• Starting urate-lowering treatment without protection against flares (explained below).
• Sudden changes in uric acid levels, including crash dieting or fasting.

How gout progresses without treatment

Gout tends to follow a pattern if uric acid is not lowered:

1. High uric acid without symptoms (asymptomatic hyperuricaemia).
2. Acute attacks with long gaps of no symptoms in between. Over time, attacks usually become more frequent, longer and affect more joints.
3. Chronic gout, with persistent pain and stiffness, joint damage visible on X-ray, and tophi.

Tophi are firm, chalky lumps of urate crystals that form under the skin, often on the ears, fingers, elbows, toes and around the Achilles tendon. They can discharge a white, toothpaste-like material and can damage bones and joints. They are a sign that the body has a large load of crystals, but they can shrink and disappear when uric acid is lowered effectively over time.

Gout can also cause kidney stones made of uric acid, and long-term high uric acid is linked to kidney damage.

Diagnosing gout

Gout is often diagnosed from the typical pattern of attacks and examination. Helpful tests include:

• Joint fluid analysis: the gold standard. A small amount of fluid is drawn from the swollen joint with a needle and examined under a special microscope. Needle-shaped urate crystals confirm gout. This also helps rule out infection.
• Serum urate blood test: measures uric acid in the blood. Importantly, uric acid can be normal or even low during an attack, so a normal result at that time does not rule out gout. The test is best repeated a few weeks after the attack has settled.
• Other blood tests: kidney function, blood sugar, cholesterol and a full blood count, because gout is linked to these conditions.
• Imaging: ultrasound can show urate deposits on joint cartilage. Dual-energy CT scanning, where available, can detect urate crystals. X-rays show damage in long-standing gout.

Gout or infection?

A hot, swollen, painful joint can also be caused by septic arthritis, a bacterial infection of the joint that is a medical emergency because it can destroy the joint within days. Seek urgent medical care if you have a hot swollen joint with a high fever, feel very unwell, have had recent joint surgery or a joint replacement, have a weakened immune system, or if this is your first attack and the diagnosis is not clear. Gout and infection can occasionally occur together.

Treating a gout attack

The aim is to reduce pain and inflammation as quickly as possible. Treatment works best when started early, ideally within 12 to 24 hours of the attack starting. If you have had gout before, agree a “flare plan” with your healthcare provider so you can start treatment immediately.

Self-care during an attack

• Rest the joint and keep it raised.
• Apply an ice pack wrapped in a cloth for up to 20 minutes at a time, several times a day. Cold reduces inflammation and pain.
• Keep bedclothes off the joint; a bed cradle or a box at the foot of the bed can help.
• Drink plenty of water.
• Avoid alcohol.
• Do not stop urate-lowering medicine such as allopurinol if you are already taking it. Stopping it during an attack can make things worse.

Medicines for gout attacks

The three main options work equally well when used correctly. The choice depends on your other health conditions and medicines:

• Non-steroidal anti-inflammatory drugs (NSAIDs) such as naproxen, ibuprofen, diclofenac or etoricoxib, taken at full anti-inflammatory dose for a few days. They are not suitable for people with significant kidney disease, heart failure, a history of stomach ulcers or bleeding, or for those taking blood thinners. A stomach-protecting medicine is often given at the same time.
• Colchicine, an old medicine that reduces the inflammatory response to crystals. Modern guidelines recommend low doses, because high doses commonly cause diarrhoea, nausea and vomiting without working better. Colchicine interacts with several medicines, including some antibiotics, antifungals and statins, and needs dose adjustment in kidney disease. Never take more than the dose prescribed.
• Corticosteroids (steroids), given as a short course of tablets such as prednisolone, or as an injection into the joint or a muscle. They are a good option for people who cannot take NSAIDs or colchicine. They may raise blood sugar in people with diabetes.

For people with frequent, difficult-to-treat attacks who cannot use these medicines, specialist treatments that block a key inflammatory messenger called interleukin-1 may be used in some countries.

Simple painkillers such as paracetamol can be added for extra pain relief, but they do not treat the inflammation.

Long-term treatment: lowering uric acid

This is the most important and most under-used part of gout care. Treating attacks one at a time does nothing to dissolve the crystals that cause them. Only lowering uric acid below the level at which crystals form, and keeping it there, dissolves existing crystals and stops new ones forming. Over months to years, attacks become less frequent and then stop, and tophi shrink.

Who should have urate-lowering therapy?

International guidelines increasingly recommend offering urate-lowering therapy to most people with gout, and strongly recommend it for anyone with:

• Two or more attacks a year.
• Tophi.
• Joint damage visible on imaging.
• Chronic kidney disease.
• Kidney stones.
• Gout starting at a young age (for example, under 40).
• Very high uric acid levels.
• Heart disease, high blood pressure or diabetes alongside gout.

Many experts now suggest discussing urate-lowering therapy after the first attack, because gout tends to progress.

The target

The usual target is to keep serum urate below 360 micromoles per litre (6 milligrams per decilitre). For people with tophi, frequent attacks or chronic gout, a lower target of below 300 micromoles per litre (5 milligrams per decilitre) is often recommended, at least until tophi have gone. Urate is checked with blood tests, every few weeks while the dose is being adjusted and then at least once a year.

This “treat to target” approach is the key to success. Many people are put on a standard dose of allopurinol and never have their urate rechecked, so their dose remains too low to work.

Allopurinol

Allopurinol is the first-choice urate-lowering medicine in most countries. It reduces the amount of uric acid the body makes. Important points:

• It is started at a low dose and increased gradually, usually every few weeks, until the target urate level is reached. Many people need doses higher than the starting dose.
• It is a long-term, usually lifelong, treatment. Stopping it allows uric acid to rise and crystals to return.
• It is safe for most people, including those with kidney disease, when doses are adjusted carefully.
• A rare but serious side effect is a severe skin reaction, which is more common in the first few months, in people with kidney disease, and in people of certain genetic backgrounds, notably some Han Chinese, Thai and Korean populations who carry a gene called HLA-B*5801. In some countries, genetic testing is offered before starting allopurinol in these groups. Stop the medicine and seek urgent medical advice if you develop a rash, especially with fever, blisters, sore mouth or eyes, or feeling unwell.

Febuxostat

Febuxostat also reduces uric acid production. It is usually used when allopurinol is not tolerated or does not reach target. Some regulators have issued cautions about its use in people with established heart disease, so the choice should be discussed with a healthcare provider.

Other urate-lowering medicines

• Uricosurics, such as probenecid, benzbromarone (in some countries) and lesinurad (no longer widely marketed), help the kidneys remove more uric acid. They are less suitable for people with kidney stones or poor kidney function.
• Pegloticase, an intravenous enzyme treatment that breaks down uric acid rapidly, is used in specialist centres for severe, tophaceous gout that has not responded to other treatments.

Preventing flares when starting treatment

One of the most common reasons people stop allopurinol is that they get an attack soon after starting it. This happens because as uric acid falls, crystals begin to dissolve and loosen, which can trigger inflammation. It is a sign that the treatment is working, not failing.

To prevent this, guidelines recommend taking a low dose of colchicine, or a low-dose NSAID or steroid if colchicine is unsuitable, for the first three to six months of urate-lowering therapy. Starting at a low dose and increasing gradually also reduces the risk. Make sure you understand this before you start, so you are not discouraged by an early flare.

Diet and gout: what really matters

Diet does affect uric acid levels, but for most people diet changes alone lower uric acid only modestly, typically by around 10 to 15 percent. That is rarely enough to reach target in someone with established gout. Diet is an important partner to medicines, not a replacement for them. A healthy diet also protects the heart and kidneys, which matters greatly for people with gout.

Foods and drinks to limit

• Organ meats such as liver, kidneys and sweetbreads, which are very high in purines.
• Some seafood, including anchovies, sardines, mussels, scallops, herring, mackerel and shellfish, especially in large amounts.
• Large portions of red meat such as beef, lamb, pork and goat, and game meats.
• Meat extracts and gravies, and yeast extracts.
• Beer, including low-alcohol beer, which contains purines from yeast, and spirits.
• Sugary drinks and foods high in fructose, such as sweetened soft drinks, energy drinks and many fruit juices, as fructose increases uric acid production.

Foods that may help

• Low-fat dairy products such as milk and yoghurt, which are associated with lower uric acid and fewer attacks.
• Vegetables, including those once thought to be problematic, such as spinach, mushrooms, peas and cauliflower. Research shows purine-rich vegetables do not increase gout risk the way meat and seafood do.
• Legumes such as beans and lentils, which are good sources of protein.
• Wholegrains.
• Coffee, in moderation, has been linked with lower uric acid in some studies.
• Cherries have been associated with fewer attacks in some studies, although the evidence is not strong enough to recommend them as a treatment.
• Vitamin C may modestly lower uric acid.

Water

Drinking enough water helps the kidneys remove uric acid and reduces the risk of kidney stones. Aim for pale yellow urine, and drink more in hot weather, during exercise and during illness.

Weight

Gradual weight loss lowers uric acid and reduces attack frequency. Crash diets, fasting and very-low-carbohydrate diets that produce ketones can temporarily raise uric acid and trigger attacks, so slow, steady weight loss is best. Our complete guide to weight management explains safe approaches.

Alcohol and gout

Alcohol increases uric acid production and reduces how much the kidneys excrete. Beer is the worst for gout, followed by spirits. Wine appears to have a smaller effect in moderate amounts, though large amounts of any alcohol can trigger attacks. Binge drinking is a particularly common trigger. If you have gout, keep alcohol low, have several alcohol-free days each week, and avoid binge drinking completely.

Gout, the heart and the kidneys

Gout rarely exists on its own. People with gout are much more likely to have high blood pressure, heart disease, heart failure, stroke, type 2 diabetes, fatty liver and chronic kidney disease. Some of this is because these conditions share risk factors, and some may be because high uric acid and chronic inflammation affect blood vessels and organs.

This means a diagnosis of gout is a good reason to have a full check of your cardiovascular and kidney health, including blood pressure, cholesterol, blood sugar and kidney function. Managing these conditions also helps gout: for example, some blood pressure medicines, such as losartan, and some diabetes medicines, such as SGLT2 inhibitors, have a mild urate-lowering effect, whereas diuretics raise urate. Your healthcare provider may review your medicines with this in mind.

Gout in women

Gout is less common in women before menopause but increases afterwards. Women with gout are more likely to be older, to take diuretics and to have kidney disease, high blood pressure and obesity. Gout in women is sometimes missed because it is not expected, and it may affect the fingers or other joints rather than the big toe. Treatment principles are the same.

Living with gout: practical tips

• Have a flare plan: keep your prescribed attack medicine at home and when travelling so you can start it immediately.
• Take urate-lowering medicine every day, including when you feel well. Gout is “silent” between attacks, but crystals are still there.
• Know your urate number and your target, just as people with diabetes know their blood sugar.
• Stay hydrated, especially in hot climates, during exercise and when unwell.
• Wear comfortable, supportive shoes and protect your joints from injury.
• Tell any healthcare provider who treats you that you have gout, especially before surgery, if you are admitted to hospital, or if you are prescribed new medicines.
• Be patient: it can take six months to a year or more of good urate control for attacks to stop completely and for tophi to shrink. Stick with it.

A note for nurses and healthcare workers

Nurses have a central role in improving gout care. Studies of nurse-led gout clinics, in which nurses educated patients, checked urate levels and increased allopurinol doses according to a protocol, found that most patients reached their urate target and had far fewer flares than those receiving usual care. Simple steps such as explaining why urate-lowering medicine is lifelong, preparing patients for possible early flares, checking urate regularly and making sure doses are increased can transform outcomes. In hospital, nurses can help prevent attacks by keeping patients well hydrated, continuing their allopurinol unless told otherwise, and recognising and reporting new hot, swollen joints promptly.

Common myths about gout

• “Gout is caused by eating too much rich food.” Diet plays a part, but genetics and kidney function are often more important.
• “If I change my diet, I won’t need medicine.” Diet alone rarely lowers urate enough in established gout.
• “Allopurinol should be stopped during an attack.” Keep taking it. Stopping can make things worse.
• “Allopurinol caused my attack, so it doesn’t suit me.” Early flares are common when uric acid starts falling. Preventive treatment helps, and the attacks reduce over time.
• “My uric acid was normal during the attack, so it’s not gout.” Urate can fall during an attack. Repeat the test when the attack has settled.
• “Gout only affects the big toe.” Gout can affect almost any joint.

Gout around the world

Gout was once described as the “disease of kings” because it was associated with wealthy people who ate rich food and drank heavily. Today it affects people of every income level in every region. Global studies show the number of people living with gout has more than doubled since 1990. The highest rates are found among Indigenous peoples of the Pacific, including Māori in New Zealand and many Pacific Island communities, where genetic variants affecting how the kidneys handle uric acid are common. Rates are also high and rising in North America, Europe, Australia, the Middle East and parts of Asia, and gout is increasingly diagnosed in Africa and South Asia as diets change, obesity and diabetes rise, and life expectancy increases.

In many health systems, gout care remains poor. Studies in several countries have found that fewer than half of people with gout are prescribed urate-lowering therapy, and of those who are, many never reach their urate target. Access to urate tests, cost of medicines, and the belief that gout is a self-inflicted lifestyle problem all contribute. Better education for patients and health workers, and nurse-led or pharmacist-led treat-to-target programmes, are among the most effective ways to close this gap.

High uric acid without gout

Many people find out they have a high uric acid level from a routine blood test, without ever having had gout. This is called asymptomatic hyperuricaemia. Most people with high uric acid never develop gout. Current guidelines in most countries do not recommend starting urate-lowering medicines for high uric acid alone, without gout or uric acid kidney stones, because the benefits are not proven and medicines have side effects. Some countries, particularly in parts of Asia, take a different approach for very high levels.

If you have high uric acid without gout, it is worth looking at the reasons: weight, alcohol, sugary drinks, kidney function, blood pressure and medicines such as diuretics. Addressing these improves overall health. If you develop joint pain and swelling, mention your high uric acid to the healthcare provider who assesses you.

Uric acid kidney stones

High uric acid in the urine, especially when the urine is concentrated and acidic, can form uric acid kidney stones. These cause severe pain in the side or back that may spread to the groin, often with blood in the urine, nausea and vomiting. People with gout are at higher risk of kidney stones of several types. Prevention includes drinking plenty of fluid to produce at least two litres of urine a day, reducing animal protein and sugary drinks, and sometimes taking medicines that make the urine less acidic. Urate-lowering therapy also reduces stone risk. Seek urgent care for severe pain with fever, inability to pass urine, or if you have only one working kidney.

Gout or pseudogout?

A condition called calcium pyrophosphate deposition disease, often known as pseudogout, also causes sudden hot, swollen joints, but it is caused by a different type of crystal. It most often affects the knee and wrist, and is more common in older adults. Under the microscope, its crystals look different from urate crystals. Pseudogout attacks are treated in a similar way to gout attacks, with anti-inflammatory medicines, colchicine or steroids, but urate-lowering medicines like allopurinol do not help. This is one reason why joint fluid testing is valuable when the diagnosis is uncertain.

Gout in hospital and around surgery

Hospital admissions and operations are common triggers for gout attacks, because of dehydration, fasting, changes in medicines, stress and illness. If you have gout:

• Tell the team caring for you that you have gout and which medicines you take for it.
• Ask that your allopurinol or other urate-lowering medicine is continued unless there is a specific reason to pause it.
• Keep well hydrated if you are allowed to drink, and ask about intravenous fluids if you cannot.
• Report any new joint pain or swelling early, so it can be treated quickly and checked for infection.

A sample gout-friendly day of eating

There is no single “gout diet”, but a pattern similar to the Mediterranean or DASH diet (designed to reduce blood pressure) suits most people with gout and protects the heart. A typical day might include:

• Breakfast: porridge or wholegrain cereal with low-fat milk or yoghurt and fruit such as berries or a banana, with water, tea or coffee.
• Lunch: a bean, lentil or chickpea stew with vegetables and brown rice, or a wholegrain wrap with eggs, salad and a small amount of chicken.
• Snack: a handful of unsalted nuts, a piece of fruit or a pot of low-fat yoghurt.
• Dinner: a palm-sized portion of chicken or a modest portion of fish, with plenty of vegetables and potatoes, yam, sweet potato or wholegrains.
• Drinks through the day: water, with tea or coffee in moderation; avoid sugary soft drinks and limit fruit juice and alcohol.

Festive meals, weddings and celebrations do not have to be avoided. Eat moderate portions, fill half your plate with vegetables and grains, drink water between any alcoholic drinks, and keep your flare plan to hand.

Questions to ask your healthcare provider

• Is my diagnosis confirmed, and has infection been ruled out?
• What is my uric acid level now, and what is my target?
• Should I start urate-lowering therapy, and how will the dose be increased?
• What should I take to prevent flares while starting treatment, and for how long?
• What is my flare plan, and which medicine should I keep at home?
• Do any of my current medicines raise my uric acid, and are there alternatives?
• Should my blood pressure, cholesterol, blood sugar and kidney function be checked?
• How often will my uric acid be checked from now on?

Monitoring and follow-up

Once you start urate-lowering treatment, regular follow-up is essential. Blood tests are usually done every two to five weeks while the dose is being increased, then every six to twelve months once the target is reached. Kidney and liver function are checked at the same time. Keep a simple record of your urate results, doses and any flares, either in a notebook or on your phone. Seeing your urate number fall below target is motivating, and it helps you and your healthcare team decide when the dose is right. If your kidney function changes, you start new medicines, or you have a flare after a long time without one, ask for your urate to be rechecked.

The emotional side of gout

Gout is often joked about, and that can make it harder to talk about. People with frequent attacks describe missing work, cancelling family events, being unable to walk or drive, and feeling embarrassed by the assumptions others make about their lifestyle. Repeated severe pain and poor sleep during attacks can lead to low mood, irritability and anxiety about when the next attack will strike. Some people start avoiding social occasions, travel or exercise because they fear triggering a flare.

These feelings are understandable, and they usually improve dramatically once gout is properly controlled. If you are struggling, talk to your healthcare provider. Effective treatment of gout itself is often the best treatment for the worry it causes, and support for low mood or anxiety is available if you need it. Sharing accurate information with family and colleagues, including the fact that gout is strongly linked to genetics and kidney function and is very treatable, can also help reduce stigma.

Gout and work

For people in physical jobs, including nursing, construction, farming, hospitality and manufacturing, a gout attack can make work impossible for days. If you have frequent attacks, discuss a return-to-work plan and temporary adjustments with your employer or occupational health service, such as seated duties during recovery. More importantly, use these absences as a sign that your long-term treatment needs to be reviewed, because effective urate lowering is the best way to protect your ability to work.

What success looks like

When gout is treated properly, the change can be remarkable. In the first few months after starting urate-lowering therapy, attacks may continue or even increase slightly as crystals begin to dissolve, which is why flare prevention matters. Once urate has been at target for six to twelve months, most people find attacks become rare. After a year or two, many have no attacks at all. Tophi gradually soften and shrink, and some disappear completely. Joints that were constantly sore often become comfortable again, though any damage that has already occurred to bone and cartilage may not fully reverse. The earlier treatment starts, the more joint function is protected. Success is not just fewer painful nights: it is being able to plan your life again without fearing the next attack.

Frequently asked questions

Can gout be cured?

Gout cannot be cured in the sense that the tendency to high uric acid is usually lifelong. But with urate-lowering medicine taken consistently to target, crystals dissolve, attacks stop and tophi disappear. For practical purposes, many people become free of gout.

How long does a gout attack last?

Without treatment, an attack usually settles within one to two weeks. With prompt treatment, it can settle within a few days.

Do I have to take allopurinol for life?

For most people, yes. Stopping allopurinol usually leads to uric acid rising again and attacks returning, though this may take months or years.

Is it safe to exercise with gout?

Yes. Regular exercise is good for weight, heart health and joints. Rest the affected joint during an attack, and stay well hydrated during exercise.

Can women get gout?

Yes, particularly after menopause and in women with kidney disease or taking diuretics.

Are tomatoes bad for gout?

Some people report tomatoes trigger their attacks, but the evidence is limited. If you notice a clear pattern, reduce them, but there is no need for everyone with gout to avoid them.

But what if I keep having attacks even though I take allopurinol?

This is very common and usually has a simple explanation: the dose is too low to reach the urate target, the urate level has not been checked, the medicine is not being taken every day, or flare prevention was not given when starting. Ask your healthcare provider for a urate blood test and a plan to increase the dose step by step until you reach target. If allopurinol is not tolerated or does not work at the maximum suitable dose, other medicines and specialist referral are available. Persistent attacks are a sign the treatment needs adjusting, not that gout cannot be controlled.

Related: Gout symptoms and foods to avoid · Chronic kidney disease: the complete guide

Sources: European Alliance of Associations for Rheumatology (EULAR) gout recommendations, American College of Rheumatology gout guideline, British Society for Rheumatology gout guideline, Global Burden of Disease Study (gout estimates), Doherty et al. nurse-led gout care trial (The Lancet), National Institute for Health and Care Excellence (NICE) gout guideline.