What is gout?
Gout is one of the most common forms of inflammatory arthritis (1, 2).
It is characterized by episodes of severe joint swelling and pain caused by the accumulation of urate crystals in various tissues throughout the body (1, 2).
How common is gout?
In the United States, the prevalence of gout is estimated to be around 4% and is more common in men (3-6%) than in women (1-2%) (2, 3).
What are the signs and symptoms?
Gout begins with sudden, severe joint pain and swelling (referred to as a flare-up or gout attack) (1).
The affected joint may also appear red, feel warm to touch, and be difficult to move (2).
Although any joints may be affected, the first metatarsophalangeal joint (AKA, the big toe) is the most common (2).
A flare-up may also be accompanied by other symptoms, such as fever, fatigue, and malaise (general discomfort) (2).
If left untreated, symptoms typically resolve within a few days to 2 weeks (4).
The skin around the affected joint may begin to itch and peel when the pain and swelling subside (5).
After several years, these flare-ups may become more frequent and longer in duration, and can eventually progress to chronic gout (1).
In chronic gout, joints remain slightly inflamed all of the time and can eventually become disfigured and difficult to move (5).
What causes gout?
The following may contribute to the development of gout:
Having high levels of uric acid in the blood (known as hyperuricemia) is the leading cause of gout (2).
Uric acid is a waste product formed from the breakdown of purines through a process that requires the enzyme xanthine oxidase (found mainly in the liver) (6).
Purines are a type of compound used to make DNA (genetic material), ATP (energy), and other important molecules (6).
Most uric acid (500-600 mg/day) comes from sources within the body, while a smaller portion (100-200 mg/day) is the result of consuming purine-containing foods (6).
Humans lack the enzyme (uricase) needed to break down uric acid, so it builds up in the blood until it can be excreted in the urine or feces (7).
Hyperuricemia occurs when serum uric acid levels exceed 6.8 mg/dL, as this significantly increases the likelihood that uric acid will crystalize and form deposits in the body (6).
It can result from either overproduction (10% of cases) or underexcretion (90% of cases) of uric acid (1).
Interestingly, only about 1/3 of patients with hyperuricemia actually develop symptoms of gout (6).
When uric acid crystals are deposited in the body, this triggers immune cells to migrate to the area (8).
This process begins with macrophages, which engulf the crystals and stimulate the release of lysosomal enzymes (to break down the crystals) and inflammatory mediators (2).
Symptoms of gout are the result of this inflammatory process, which causes swelling and pain in the affected joint (2).
After the crystals have been degraded, macrophages signal the immune system to stop releasing inflammatory mediators, and symptoms subside (8).
What are the risk factors?
The following are risk factors for developing gout:
1. Being male
Men are 2-4 times more likely to develop gout than premenopausal (but not postmenopausal) women (3, 9).
This is thought to be due to the effects of estrogen, which promotes excretion of uric acid in females (6, 10).
2. Older Age
The prevalence of gout is highest (9-13%) among those aged 80 years or older and lowest in those aged 20-39 years (0.4-0.7%) (3, 9).
It’s unclear exactly why the elderly are more likely to be affected, but certain behaviors and health conditions during middle age, such as drinking beer, eating a lot of protein, smoking, using diuretics, having hypertension, obesity, or poor kidney function are all linked with increased risk (11, 12).
It has been estimated that 40-70% of all gout cases are caused by genetic variations (known as single nucleotide polymorphisms, or SNPs) (13, 14).
At least 28 SNPs have been linked with gout, but those affecting the following genes seem to have the strongest effect (13, 14):
- The ABCG2 gene codes for the ATP-binding cassette transporter, a protein found in the intestines and kidney that regulates urate excretion (15, 16).
- The SLC2A9 gene is responsible for making the glucose transporter 9 (GLUT9), which is found in the kidneys and helps the body reabsorb or excrete urate (17)
4. Certain health conditions
- Obesity is linked with increased gout risk, possibly due to increased uric acid production by fat cells and decreased excretion in the urine (18, 19).
- Diabetes is linked with increased production and decreased excretion of uric acid, but this may be due to comorbid conditions (8, 20, 21).
- Hypertension can reduce kidney function, leading to decreased excretion of uric acid in the urine (8).
- Kidney disease increases the risk for gout due to impaired kidney function, which lowers the excretion of uric acid (22, 23).
Any of the following medications may decrease the excretion of uric acid or increase its production (24):
- Aspirin (low-dose)
- Diuretics (loop and thiazide)
- Immunosuppressants (cyclosporine, tacrolimus)
- Nicotinic acid
6. Alcohol use
Alcohol promotes the production of uric acid and inhibits its excretion in the urine (5).
Moderate alcohol consumption (up to 2 drinks/day for men and 1 drink/day for women) is associated with a 41% increased risk of recurrent gout attacks (25).
Consuming large amounts of high-purine foods (red meat, seafood, etc.) has been linked with an increased risk of gout (26).
However, diet likely plays a much smaller role (<0.3%) in the development of gout than previously thought (27).
What are some potential complications of gout?
The following complications are associated with gout:
Over time, uric acid crystals can grow into larger stone-like deposits, called tophi, found in soft tissues, joints, and even bones (28).
Tophi typically don’t cause any pain, but they can become swollen and stretch the skin, which may be uncomfortable (28).
Very large tophi may need to be removed surgically, but most are dissolved after a few months of treatment with medications (28).
If left untreated, tophi can burst open through the skin and release a chalky, white substance made of uric acid crystals (28).
2. Joint damage
The accumulation of tophi can cause joints to appear disfigured and may limit movement due to swelling (8, 29).
Eventually, this leads to the destruction of joint tissue and may require surgery to repair (30).
3. Bone loss
The erosion of bone tissue may occur as tophi grow larger and closer to various bones throughout the body (8, 31).
It is thought that chronic inflammation and the activation of osteoclasts (cells that break down bone tissue) are responsible for this bone loss (32).
4. Kidney stones
Uric acid crystals can accumulate in the kidneys, forming kidney stones that cause severe pain when they move from the kidney through the ureter (33).
In patients with gout, the risk of developing kidney stones is increased by 60% compared to the general population (34).
5. Kidney disease
Some studies suggest that patients with gout are 3 times more likely to develop chronic kidney disease (35).
More research is needed to determine the mechanism, but some experts believe that chronic inflammation in gout contributes to kidney damage over time (36).
6. Eye problems
Uric acid crystals are sometimes deposited in the eyes, where they can cause irritation, inflammation, and conditions such as dry eye syndrome (37).
How is gout diagnosed?
Doctors use a combination of the following methods to diagnose gout:
1. Physical exam
First, doctors will conduct a physical exam to check for joint inflammation (swelling, redness, etc.) and other signs of gout (2).
2. Blood tests
A blood test may be ordered to check for hyperuricemia, although many patients with gout have normal serum uric acid levels (2, 8).
Markers of inflammation, such as C-reactive protein, may also be elevated during a gout flare-up (2).
3. Urine test
Sometimes, urine is collected over a 24-hour period to evaluate the amount of uric acid being excreted by the body (2).
If uric acid levels are higher than 800 mg per day, this may indicate gout but must be confirmed with other tests (8)
4. Synovial fluid analysis
The gold standard for diagnosing gout is synovial (joint) fluid analysis (2).
To perform this test, a needle is inserted into the spaces between two bones, and a sample of fluid is collected (38).
In the laboratory, the fluid is analyzed under a microscope, which helps determine whether uric acid crystals are present (2).
In more advanced stages of gout, uric acid crystals, tophi, and bone deformities may be detected with various types of imaging (x-rays, ultrasound, MRI) (8).
How do doctors typically treat gout?
During an acute flare-up, the goal of treatment is to reduce inflammation and symptoms as quickly as possible (2).
The long-term goal is to reduce serum urate levels in order to suppress flare-ups and inhibit (or resolve) tophi (2).
Doctors typically prescribe the following treatments to achieve these goals.
1. Ice and rest
During flare-ups, patients are instructed to rest and apply ice packs to the affected joint(s) in order to reduce pain and swelling (39).
2. Anti-inflammatory drugs
During acute gout flare-ups, any of the following anti-inflammatory drugs may be prescribed to reduce swelling and pain (39):
- Non-steroidal anti-inflammatory drugs (NSAIDs) work by inhibiting the production of inflammatory cytokines (40). Examples include ibuprofen and naproxen.
- Corticosteroids are synthetic hormones that work by inhibiting suppressing the immune system to prevent the secretion of inflammatory mediators (41). Examples include prednisone and prednisolone.
- Colchicine is a plant-derived hormone that works by preventing immune cells from migrating to the affected joint (42, 43).
- Interleukin-1 (IL-1) inhibitors work by blocking IL-1, an inflammatory cytokine produced by immune cells (44). Examples include anakinra and canakinumab.
These medications are typically prescribed for only short periods of time, until symptoms are resolved (39).
3. Urate-lowering therapy
Patients with more frequent (at least 2 flare-ups/year) and/or severe (evidence of tophi or tissue damage) gout may be considered for urate-lowering therapy (ULT) (39).
The goal of ULT is to achieve and maintain a serum uric acid level of <6 mg/dL using one or more of the following medications (2, 39):
- Xanthine oxidase inhibitors (XOI) work by blocking the conversion of purines to uric acid. Examples include allopurinol and febuxostat.
- Uricosuric agents work by increasing the excretion of uric acid in the urine. Examples include probenecid and lesinurad.
These medications are typically prescribed indefinitely, as long as they are well-tolerated by the patient (39).
4. Diet & lifestyle changes
According to the most recent ACR (American College of Rheumatology) guidelines, the following diet and lifestyle changes are recommended for all patients with gout (39):
- Limit alcohol intake.
- Limit purine intake.
- Limit high-fructose corn syrup intake.
- Use a weight loss program.
These are discussed in greater detail in the sections below.
What diets are recommended for gout?
Doctors and dietitians may recommend the following diets for gout:
1. Low-purine diet
Reducing dietary intake of purines, which are converted to uric acid, may help reduce gout flare-ups (39).
A 2012 study with 633 participants showed that intake of high-purine foods (especially those of animal origin) increased the risk of recurrent gout attacks by almost fivefold (45).
Although purines occur naturally in most foods, they are found in the highest concentrations in animal sources (46).
Some animal foods contain over 400 mg of purines per 100 grams, while most plant foods (fruits, vegetables, etc.) contain less than 70 mg (46).
High- and moderate-purine foods to limit or avoid include (47, 48):
- Wild game
- Red meat
- Organ meats
- Fish and other seafood
A limit of 400 mg per day is sometimes recommended, which would allow for one small serving (4 ounces) of a moderate-purine food (beef, chicken, pork, lamb, salmon) (47).
Interestingly, high-purine vegetables are actually associated with a REDUCED risk of developing gout (26).
2. Low-fructose diet?
Fructose has been shown to increase uric acid levels, because it depletes ATP and increases purine synthesis (49, 50).
A recent meta-analysis found that higher fructose consumption (>11.9% of calories from fructose) was associated with a 62% increase in gout risk (51).
In particular, beverages containing high-fructose corn syrup are associated with hyperuricemia and should be avoided by patients with gout (39, 52).
High-fructose fruits (apples, oranges, raisins, etc.) have also been linked with gout, but more research is needed to determine whether these foods should be avoided (51).
3. Mediterranean diet?
A 2013 pilot study showed a 20% reduction in serum uric acid in subjects with asymptomatic hyperuricemia who followed a Mediterranean diet for 6 months (53).
Unfortunately, no studies have been completed in people with gout.
4. DASH diet?
A 2017 trial in adults with high blood pressure found that the DASH diet significantly reduced serum uric acid within 30 days (54).
More research is needed in patients with gout.
5. Low-glycemic diet?
A 2016 study found that adults with overweight or obesity who consumed only low-glycemic foods (GI</=45) had significantly reduced serum uric acid (55).
However, more research is needed to find out whether low-glycemic diets actually reduce the number of flare-ups in people with gout.
Foods that are good for gout
The following foods may help reduce the risk of gout flares:
A 2016 meta-analysis demonstrated that coffee intake significantly lowered serum uric acid (56).
Women actually needed to drink more coffee (4-6 cups/day) to achieve the same effects as men (1-3 cups), suggesting there are gender differences in the way coffee impacts uric acid (57).
The study also showed people who drank at least 1 cup of coffee per day had a significantly lower risk of gout than those who didn’t drink any coffee, regardless of gender (56).
More research is needed to understand the underlying mechanism, but it might be related to caffeine’s ability to inhibit xanthine oxidase (57).
Gout patients who regularly consume cherries (or cherry juice) report fewer flare-ups (58).
In one study, cherry intake over a 2-day period was associated with a 35% lower risk of gout attacks compared to those with no cherry intake (59).
Cherries may work by lowering serum uric acid and reducing inflammation, but more research is needed (60, 61).
So far, there haven’t been any clinical trials to assess whether cherry consumption actually lowers the risk of gout attacks, although one is currently in the works (62).
3. Dairy products?
Consumption of dairy products has been linked with lower serum uric acid levels in healthy individuals (63, 64, 65).
Certain components of dairy (glycomacropeptide and G600 milk fat extract) may lower inflammation and help reduce gout flare-ups (64, 66).
A 2012 trial found a significant reduction in the frequency of gout flares in participants who received skim milk powder enriched with glycomacropeptide and G600 milk fat extract for 3 months (66).
Are any other lifestyle changes recommended?
The following is also important for reducing gout risk:
1. Ensure adequate hydration
Some evidence suggests dehydration increases serum uric acid due to decreased urinary excretion (67).
According to a 2009 study presented at a conference (but not published in a peer-reviewed journal), patients who consumed more than 8 glasses of water each day had a 46% reduced risk for recurrent gout attacks (68).
What supplements are beneficial for gout?
Research is lacking on the use of supplements for gout. However, the following may have some promise:
1. Vitamin C?
In vitro and animal studies have shown that vitamin C increases excretion and inhibits production of uric acid (70).
A 2011 meta-analysis of 13 trials showed a significant reduction in serum uric acid in participants who received vitamin C supplements (500 mg/day for at least 30 days) (70).
However, a 2013 trial in patients with gout failed to show a significant effect of vitamin C on uric acid levels (71).
More research is needed, and the American College of Rheumatology (ACR) currently recommends against the use of vitamin C supplements for patients with gout (39).
Long-chain fatty acids (especially omega-3s) inhibit the urate transporter 1 (URAT1), which helps reabsorb uric acid in the kidneys (72, 73).
A 2019 study showed that consumption of fish rich in omega-3 fatty acids (salmon, sardines, etc.) was associated with a lower risk of recurrent gout flares (74).
However, omega-3 supplementation alone (via fish oil) had no effect on gout risk.
It is thought that curcumin (the active component of turmeric) might prevent or reduce gout flare-ups by inhibiting inflammation (75).
A 2016 trial in subjects with nonalcoholic fatty liver disease (NAFLD) found that curcuming supplementation (500 mg twice daily for 8 weeks) significantly reduced uric acid levels (76).
However, a recent trial that included participants with hyperuricemia failed to replicate these results (77).
4. Celery seed extract?
Animal studies suggest that celery seed extract may reduce uric acid levels and improve gout symptoms by inhibiting xanthine oxidase activity and lowering inflammation (78, 79).
Human studies are needed to confirm these results and determine dosing.
Animal studies suggest that 6-shogaol (a polyphenol found in ginger) may lower uric acid by inhibiting xanthine oxidase activity (80, 81).
Research in humans is needed.
The following supplements are sometimes also used, but we didn’t find any studies evaluating their effectiveness in patients with gout:
- Apple cider vinegar
Amy is a registered dietitian nutritionist and experienced nutrition editor. She received her Masters in Nutrition Diagnostics from Cox College and her Bachelors in Dietetics from Missouri State University. She currently works as a nutrition editor for Healthline and Greatist. Her passion is finding ways to communicate nutrition research in an interesting and easy-to-understand way.