The Sweet Pain of Gout

Gout is commonly associated with obesity and the over-indulgence of foods and alcohol. Indeed, gout was common in Europe between the 17th and 19th centuries where it affected primarily royalty and the wealthy, and the affliction of gout was often the subject of satire.
sweet pain of gout

A great example was the 1818 lithograph by George Cruikshank of a painting by Captain Simon Hehl of a wealthy nobleman who was about to be “introduced to gout”1. The man, who is quite overweight, is seated at a table, drinking his port wine and eating a variety of fruits. As a premonition for what is about to happen, one can see a painting of Mount Vesuvius erupting in a painting behind him. And emerging from a fireplace with smoke behind him, a little devil is about to drop a red-hot coal on the man’s foot to inflict the pain of gout.

What might strike you from looking at the painting is that the absence of the usual gout-provoking meal, such as duck steeped in gravy served with a pint of ale. Indeed, the classical teaching from physicians is that gout is primarily driven by the ingestion of purines, which are nitrogen-containing substances used to make nucleic acids. These nucleic acids are the building blocks for RNA (which direct the production of proteins) and DNA (which make up our genes). When one ingests excessive amounts of purines, these purines are broken down to uric acid. This is why physicians classically tell their patients that if they have gout, they should reduce their intake of purines. Indeed, studies have linked purine-rich foods, such as meats (especially red meats), seafood (especially shellfish), and alcohol (especially beer) with gout2.

Sugar, Fructose, and Gout

While it is commonly recognized that high intake of purine-rich meat and beer can increase uric acid levels and the risk for gout, many people with gout have noted that attacks can be precipitated by sugar. This association was recognized by physicians in the past, but seems to have been forgotten until relatively recently. When sugar was first being imported into Holland in the 16th century, the physician Steven Blankaart noted that those who were eating a lot of sugar were developing obesity, gout and dental caries. Sir William Osler, the father of modern medicine, also noted in his “Principles and Practice of Medicine” (Appleton Inc, New York, 1893) that to prevent recurrent attacks of gout “the sugar should be reduced to a minimum. The sweeter fruits should (also) not be taken.” Indeed, the nobleman in the Cruikshank lithograph, appears to be holding a peach on his fork with a plate of pineapple and other fruits on his table.

sugar fructose and gout

Today, sugary beverages are well recognized to increase the risk for gout. Indeed, in retrospect, one reason for the epidemic of gout among the wealthy in the 1700s and 1800s was that alcohol often had substantial amount of sugar added to it. In fact, one of the more common drinks was “sack and sugar,” in which spirits from sugarcane and sugar beets were added to wine3. Another common drink was “hippocras,” in which sugar, nutmeg and cinnamon were added to wine. Indeed, Sir John Falstaff, who was a character in several of Shakespeare’s plays, liked sack and sugar so much that it became his nickname, and he developed gout in the bard’s “Henry IV”. Shown is a depiction of Falstaff from an 1867 painting by Adolf Schrodter4.

Why Does Sugar Increase the Risk for Gout?

The reason sugar increases the risk for gout is that sugar contains a substance known as fructose. Fructose is the type of sugar that makes fruits and honey taste sweet. Table sugar contains sucrose, which is made by binding two sugars (glucose and fructose) together. When one eats table sugar, the sucrose rapidly breaks down in the gut, allowing the fructose and glucose to be absorbed. Fructose is distinct from glucose in that it generates uric acid when it is broken down. Indeed, when one eats fructose, uric acid is generated very rapidly, and increases in the blood just minutes after ingestion, peaking one or two hours later. Another common sweetener is high fructose corn syrup, or HFCS, and—just like it sounds—it can contain a lot of fructose and can also raise uric acid.
Today sugar and HFCS make up almost 15 percent of all of the calories we eat, so these two sugars are the major source of fructose in our diet. Interestingly, there is increasing evidence that these two sweeteners are not just driving gout, but also increasing our risk for obesity and diabetes. Thus, there is a very strong argument to reduce our intake of these two sweeteners. This may be also a reason to use other sweeteners. However, agave is not a good choice as it almost entirely consists of fructose. Some artificial sweeteners, such as sorbitol, can also be converted to fructose in the body.

What about Fruit and Uric Acid?

As mentioned, the sweeter fruits can also be a risk factor for gout, and one should be careful especially with sweet apples, pears, plums, watermelon, pineapple and bananas. More tart fruits, and fruits with low sugar content, can be ingested, such as lemons, limes, and kiwi, while oranges also seem relatively fine. Small servings are also likely to be tolerated, as the amount of fructose in fruits is relatively low, and about 4 or 5 grams of fructose is safely inactivated in the intestine. Fruits also contain a lot of fiber, vitamin C and potassium that are beneficial. Nevertheless, drinking juice or eating dried fruits rich in fructose should be avoided if you are at risk for an attack of gout5.

What about Other Carbohydrates?

There is some recent evidence that some starchy foods may also increase the risk for gout, including potatoes and white bread6. Not surprisingly, the astute Sir William Osler noted this nearly 130 years ago when he wrote that “hot rolls and cakes of all sorts, hominy, grits and the more starchy forms of prepared foods are not suitable. (However), fats are easily digestible and may be taken freely.”
The observation that potatoes, and especially salty, fried potatoes can be associated with gout may be surprising, as starch is broken down to glucose which does not produce uric acid when it is metabolized. However, recently it was shown that some of the glucose ingested in starchy foods is converted to fructose, where it can increase the risk for obesity and diabetes7. Indeed, there is increasing evidence that it is not just the fructose we eat that increases our risk for obesity and gout, but that it may include the fructose we make.

What is the Role of Diet Versus Genetics?

Certain foods increase our risk for gout, but genetics are the most important factor in determining whether or not someone may develop gout. Indeed, while serum uric acid and our risk for gout has increased markedly in the last century in association with western diet and increasing intake of sugar, there is also evidence that the role of genetics is also very important. Nevertheless, reducing sugary and starchy foods will likely be of benefit to everyone.

And if you or a family member has gout, keep in mind that gout is not simply driven by diets high in meats, seafoods and alcohol. Rather, sugar HFCS, sweet fruits and starchy foods, may also contribute to the “sweet pain” of gout.

Richard J Johnson MD is a physician and researcher who has studied uric acid for over 25 years and is a board member of the Gout Education Society. He is also author of “Nature Wants Us to Be Fat” (Benbella books, 2022) that discusses the role of fructose and uric acid in the epidemics of obesity and diabetes. Check out his website:


  1. Cruikshank, G., 1818. A self-indulgent man afflicted with gout: The pain is represented by a demon burning his foot. [image] Available at: [Accessed 4 August 2022].
  2. Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004 Mar 11;350(11):1093-103. doi: 10.1056/NEJMoa035700. PMID: 15014182.
  3. Rivard C, Thomas J, Lanaspa MA, Johnson RJ. Sack and sugar, and the aetiology of gout in England between 1650 and 1900. Rheumatology (Oxford). 2013 Mar;52(3):421-6. doi: 10.1093/rheumatology/kes297. Epub 2012 Nov 21. PMID: 23175570.
  4. Schrodter, A., 1867. Falstaff und sein Page. [image] Available at: [Accessed 4 August 2022].
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  6. Major TJ, Topless RK, Dalbeth N, Merriman TR. Evaluation of the diet wide contribution to serum urate levels: meta-analysis of population based cohorts. BMJ. 2018 Oct 10;363:k3951. doi: 10.1136/bmj.k3951. PMID: 30305269; PMCID: PMC6174725.
  7. Lanaspa MA, Ishimoto T, Li N, Cicerchi C, Orlicky DJ, Ruzycki P, Rivard C, Inaba S, Roncal-Jimenez CA, Bales ES, Diggle CP, Asipu A, Petrash JM, Kosugi T, Maruyama S, Sanchez-Lozada LG, McManaman JL, Bonthron DT, Sautin YY, Johnson RJ. Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome. Nat Commun. 2013;4:2434. doi: 10.1038/ncomms3434. Erratum in: Nat Commun. 2013;4:2929. Ruzicky, Philip [corrected to Ruzycki, Philip]. PMID: 24022321; PMCID: PMC3833672.