Gout is a form of arthritis. Specifically, it’s an inflammatory arthritis caused by the buildup of uric acid crystals inside a joint. It affects roughly 56 million people worldwide, and it’s more than three times as common in men as in women. While it shares the joint pain and swelling that define all types of arthritis, gout has a distinct cause, a distinct pattern of flare-ups, and its own treatment approach.
What Makes Gout Different From Other Arthritis
Arthritis is a broad term covering more than 100 conditions that cause joint pain and inflammation. Gout falls into the inflammatory arthritis category, alongside rheumatoid arthritis and psoriatic arthritis. But where rheumatoid arthritis involves the immune system attacking joint tissue for reasons that aren’t fully understood, gout has a very specific, identifiable trigger: needle-shaped crystals of uric acid that form inside a joint.
Uric acid is a normal waste product your body creates when it breaks down substances called purines, found in certain foods and in your own cells. Normally, uric acid dissolves in your blood, passes through your kidneys, and leaves your body in urine. When levels get too high (above about 6.8 mg/dL in the blood), the uric acid can crystallize and settle into joints. Those crystals provoke a fierce inflammatory reaction. Your immune cells recognize them as foreign invaders, flooding the area with inflammatory signals that cause the intense pain, redness, and swelling of a gout flare.
There’s also a condition called pseudogout, which mimics gout but involves a different type of crystal (calcium-based rather than uric acid). Pseudogout tends to affect larger joints like the knee, often causes longer episodes lasting weeks to months, and is more common in older adults with certain metabolic conditions. The only way to tell the two apart definitively is by examining fluid drawn from the joint under a microscope.
What a Gout Flare Feels Like
Gout flares are sudden and severe. Many people experience their first attack in the big toe, though gout can strike the ankle, knee, wrist, or other joints. Flares often begin at night. You might go to bed feeling fine and wake up with a joint so painful that even the weight of a bedsheet is unbearable. The joint typically looks red, feels hot, and swells noticeably.
A flare usually peaks within the first 24 hours, then gradually improves over one to two weeks. Between flares, most people have no symptoms at all. Some people go years between episodes. But without treatment, flares tend to become more frequent, last longer, and affect additional joints over time.
What Causes Uric Acid to Build Up
High uric acid results from either producing too much of it or not excreting enough of it, and often both. Several factors push levels higher:
- Diet. Foods rich in purines raise uric acid. Organ meats like liver and kidney have the highest purine content of any food. Veal, chicken with skin, and lamb are also high. Among seafood, anchovies, sardines, herring, mackerel, trout, and shellfish are notable contributors. Red meat contains moderate purine levels but is eaten in large enough quantities to matter.
- Sugary drinks. High-fructose corn syrup drives uric acid production through a separate pathway, by accelerating the breakdown of energy molecules in cells. People who drink two or more sweetened beverages per day have a 62% higher rate of developing gout compared to those who drink less than one per day.
- Alcohol. Beer is particularly problematic because it contains purines and also impairs the kidneys’ ability to clear uric acid. Liquor raises risk to a lesser degree. Wine appears to have a smaller effect.
- Medications. Low-dose aspirin, certain blood pressure medications (particularly diuretics and some beta blockers), and the immunosuppressant cyclosporine can all reduce the kidneys’ ability to eliminate uric acid.
- Genetics and kidney function. Some people simply produce more uric acid or excrete less of it due to inherited traits. Kidney disease of any kind reduces uric acid clearance.
How Gout Is Diagnosed
The gold standard for diagnosing gout is finding uric acid crystals in fluid drawn from a swollen joint. When that’s confirmed, no further testing is needed. In practice, doctors often diagnose gout based on a combination of symptoms, blood uric acid levels, and imaging. Ultrasound can reveal a characteristic “double contour” sign where urate crystals coat the surface of cartilage. Specialized CT scans can detect urate deposits directly. Standard X-rays may show a distinctive type of bone erosion in people with longer-standing disease.
Blood uric acid levels are always part of the evaluation, but a single reading can be misleading. Uric acid sometimes drops during an acute flare, so a normal level during an attack doesn’t rule out gout.
What Happens if Gout Goes Untreated
Left unmanaged, chronic high uric acid leads to urate crystal deposits called tophi. These are chalky, sometimes visible lumps that form under the skin, around joints, in tendons, and on bony prominences. Tophi develop in roughly 12% to 35% of gout patients and signal years of poorly controlled disease. They restrict joint movement, deform joints, and can break through the skin to create chronic wounds that are slow to heal and prone to infection. Joint destruction from tophi is permanent.
Beyond the joints, persistently high uric acid is linked to kidney stones and may contribute to cardiovascular risk, making long-term management important even between flares.
How Gout Is Managed
Gout treatment works on two timelines: stopping the pain of an active flare and lowering uric acid over the long term to prevent future attacks.
For acute flares, anti-inflammatory medications reduce pain and swelling, usually within a few days. Ice and rest help. Most flares resolve within one to two weeks with treatment.
Long-term management focuses on bringing uric acid below 6 mg/dL, the threshold at which existing crystals begin to dissolve and new ones stop forming. The American College of Rheumatology recommends urate-lowering therapy for anyone with tophi, joint damage from gout, or frequent flares. The preferred approach starts at a low dose and gradually increases, with regular blood tests to track uric acid levels and adjust as needed. This “treat-to-target” strategy is more effective than a fixed-dose approach because people vary widely in how much medication they need to reach that 6 mg/dL goal.
Dietary changes alone rarely bring uric acid low enough to prevent flares in people with established gout, but they help. Reducing organ meats, shellfish, sugary drinks, and alcohol (especially beer) lowers the purine load your body has to process. Staying well hydrated supports kidney function. These changes work best alongside medication, not as a replacement for it.
Gout Compared to Other Common Arthritis Types
Osteoarthritis, the most common form of arthritis, results from gradual cartilage breakdown and tends to cause a dull, aching pain that worsens with use. It develops slowly over years. Rheumatoid arthritis is an autoimmune condition that typically affects joints symmetrically (both hands, both wrists) and causes persistent daily stiffness and fatigue.
Gout is none of these things. It hits one joint at a time, arrives explosively, and disappears completely between episodes, at least early on. That intermittent, dramatic pattern is one of its most recognizable features. But like all forms of arthritis, it causes real joint damage when left untreated, and managing it effectively can prevent that damage entirely.