Brett McAllister-Byrne was in his early 30s when he first noticed a sharp ache in his ankle and big toe. “I felt it the night after playing football, and I thought I must have had a knock or something,” he says. “But then it just got worse and worse.” The next morning McAllister-Byrne, an urban planner, was in too much pain to go to work. When he described the episode to his family, they suggested it might be gout.“I was like, really?” he says. “Can you get that in your 30s?”Gout has been with us for as long as we know: in 1910 a case was diagnosed in a mummy found near a temple in Upper Egypt.
It is the most common form of inflammatory arthritis – and, it is often said, the only curable one – resulting from raised levels of uric acid in the blood. Uric acid is produced when your metabolism breaks down molecules called purines, which are found in your body’s own cells and in certain foods you eat.
Excess uric acid is normally processed by the kidneys and passed through urine, but persistently high urate levels can eventually lead to sharp crystals forming in the joints. The presence of these crystals can in turn trigger a profound immune response: inflammation, redness and pain.
Eventually, hardened lumps of urate crystals called tophi can form under the skin.High urate levels can have many causes, but they are not, in themselves, the sole cause of gout. “Virtually all people with gout will have a raised urate level,” says consultant rheumatologist Prof Edward Roddy. “But most people with a raised urate level don’t get gout.”The majority of gout sufferers experience the first attack in their big toe. Photograph: jittawit.21/Getty ImagesThe pain of a gout attack is so debilitating that it can be hard to describe: the 19th-century writer and clergyman Sydney Smith said it felt “like walking on my eyeballs”. “Sometimes people think they’ve broken a bone – that’s quite a common thing,” says Roddy. “There is some qualitative research showing that people compare the intensity of the pain to having a heart attack or a kidney stone, and that women with gout compare the intensity of the pain to childbirth.”It can also arrive, in the first instance, with little or no warning. “Often it comes on overnight,” says Roddy. “So somebody goes to bed pain-free, then they wake up and can’t put their foot to the floor.”In the UK, Europe and the US, gout afflicts 2%-4% of the population.
In the UK that equates to about 1.6 million people. “That is an awful lot more people in this country, for example, than have rheumatoid arthritis,” says Lucy Donaldson, director of research at Arthritis UK. She thinks persistent misunderstandings about gout can be a barrier to effective treatment. “There’s a lack of recognition about how common it is, and therefore people think it’s more isolated,” she says. “And, there’s a very judgmental attitude.”Most sufferers will experience their first attack in the big toe, but if left untreated gout can spread to other joints in the foot and ankle, or the knee, or even hands, wrists and elbows. “You start to recruit different joints, and the flares become more common,” says Roddy. “Trying to avoid that happening is one of the important justifications for earlier treatment.”An 18th-century illustration of gout, by the artist Charles Meryon.
Photograph: Heritage Images/Heritage Art/Getty ImagesAcross the world gout affects about three times as many men as women (it is especially rare in pre-menopausal women). Certain ethnic groups, including Maori people, have a high susceptibility. “Some people may have gene variants that predispose them to having less tight control over urate levels in blood,” says Donaldson.
But the genetic predisposition to gout is not perfectly understood. “Most of the focus has been on the genetics of uric acid levels,” says Roddy, “but we know less about the genetics determining crystal formation and inflammatory processes.”Global incidence of gout is predicted to increase by 70% from 2020 to 2050; this is largely due to population growth and ageing. It’s more common among older people, but it’s also possible to suffer a first attack in one’s 20s. “There are reports coming in suggesting that the age of people developing gout is coming down,” says Donaldson.If we still don’t hear too much about younger people getting gout, it could be because they often don’t seek treatment for the first flare.
Painful as it is, gout tends to subside quickly.“I just waited and eventually, a couple of days later, it went away,” says McAllister-Byrne, who is now 40. “A year or two after that, it would come back, and I’d wait for it to go. It’s only in the last two or three years that I went to the doctor.”Historically, gout was understood as an affliction of leisure, of indulgence, even of quality.
The Georgians thought it “a disease of the better sort, a superiority tax, a celebrity complaint,” according to the book Gout: The Patrician Malady. “Gout is the distemper of a gentleman,” Lord Chesterfield said, “whereas rheumatism is the distemper of a hackney coachman.” Gout was a hereditary trait that ran in good families; a badge of honour; a mark of distinction.To some extent, those beliefs still colour our view of gout as a comical malady brought on by excess and idleness. “We’ve got the history of seeing pictures of people with a bandaged big toe in a bath chair,” says Donaldson. “And it often looks to be somebody who’s quite well off and clearly has quite a rich diet.”A 15th-century engraving showing a doctor prescribing a tonic to a gout sufferer. Photograph: Bettmann/Bettmann Archive“It definitely isn’t treated very seriously by other people,” says McAllister-Byrne, who says he had to endure unflattering comparisons to Henry VIII. “That’s what everyone always says, insinuating that it’s self-inflicted, from drinking lots of red wine and eating red meat.” He is in fact mostly vegetarian, and doesn’t drink regularly.
McAllister-Byrne’s gout was probably part of his inheritance, however. “That’s what I think, because my dad has it.”The National Institute for Heath and Care Excellence (Nice) guidelines for gout treatment call for patients with persistent flare-ups to be given urate-lowering therapy on a treat-to-target basis: that is, to establish a level of medication that will work and adjust the dose as required. Allopurinol is the most common prescription; febuxostat is another that will keep blood uric acid levels below a prescribed target of 360 micromoles per litre.
Under that level, new crystals are prevented from forming and existing crystals in the joints should eventually dissolve. The risk of further gout attacks can be effectively eliminated.That’s the theory, but it’s not always common practice in primary care. “Changing practice is like stopping a juggernaut sometimes,” says Roddy, who was instrumental in establishing the Nice guidelines in 2022.“Not everybody’s treating to target,” says Donaldson. “They’re just giving a dose that they think is appropriate, but not then testing to see if it’s having the right effect.
People were getting about 50% of what the effective dose should be in many cases.”Very often the patients themselves do not follow up their initial treatment once the symptoms have abated, at least not until they’ve had several more painful flare-ups. As Roddy puts it: “The episodic nature of the condition contributes to suboptimal management.”Then, of course, the stigma associated with gout can inhibit people from seeking treatment.
It’s still regarded as a lifestyle disease, a consequence of a rich diet and too much drink. And while there are certain dietary risk factors – alcohol and foods rich in purine such as red meat and seafood can increase urate levels – the whole picture is much more complicated.“Moderate wine consumption doesn’t really increase your risk,” says Roddy. “The risk is greatest with beer, and the reason for that is that beer is very rich in a compound called guanosine that the body breaks down to make urates.” But ultimately dietary precautions will not, on their own, alleviate gout. “There’s no good evidence that dietary modification makes much difference to urate levels,” says Roddy.A high level of uric acid raises the risk of gout.
Photograph: MarioGuti/Getty ImagesApart from treatment, McAllister-Byrne hasn’t made any changes to his lifestyle. “When I was desperate during last year, I looked into it and I was like: I’m pretty much doing most of that,” he says.The true causes of gout are a complex interplay of genetics, ethnicity, diet and related conditions including obesity, heart disease and poor kidney function. But the stigma associated with the historical disease persists.
Could that be because, centuries on, we still call it gout?We don’t diagnose people with apoplexy or dropsy any more, but we still have no better name for gout than gout, with all its ancient associations, misunderstandings and prejudices. A 2018 study found that when members of the public completed a questionnaire about gout, they were likely to believe it was caused by the patient’s own behaviour, but when it was called “urate crystal arthritis” (UCA), they were more likely to attribute it to ageing.
Participants also considered UCA a more serious condition requiring medication, while gout was seen as more socially embarrassing.Since starting treatment with allopurinol at the beginning of the year, McAllister-Byrne has had no further flare-ups of the disease. He is, however, reluctant to consider himself cured. “It’s managed, but it’s a sort of niggle in the back of my mind – if there were ever any issues, climate change or whatever, that stopped supply chains,” he says. “It’s made me think: should I stockpile some?
Because quite quickly, I would be hobbling around.”