At Hampton Court, one of King Henry VIII’s sixteenth century palaces outside London, tour guides regale visitors with tales of Henry’s obesity and the miseries he suffered during flare-ups of gout – exquisitely painful episodes of arthritis that come from the buildup of uric acid crystals in joints. Gout was known as “the king’s disease,” because it afflicted wealthy people who could afford the meats and sea foods that trigger uric acid crystal formation. The guides also point out the “confectionary,” a corner room near the kitchen wing, and describe the sugar-rotted royal teeth produced by the then scarce sweetener. The guides do not link Henry’s gout to the royal sweets, but perhaps they should. Sugar is composed of equal parts glucose and fructose, and scientists are now beginning to link increased fructose intake not only to obesity and type II diabetes, but also to increased uric acid in the blood – a risk factor for gout.
What is uric acid
Some uric acid in the blood is normal, because every cell in the body makes uric acid out of purines, chemical compounds that come from the regular breakdown of DNA and RNA as cells recycle themselves. Purines also come from many foods, but are particularly concentrated in red meat, organ meats like liver, many fish and shellfish, and yeasty beverages like beer and red wine. Uric acid in the blood is not bad – it serves as a powerful antioxidant. However, in some genetically susceptible people, uric acid levels become too high because they make too much, or because their kidneys don’t excrete enough into the urine.
When uric acid crystallizes
Abnormally high uric acid levels in the blood, a condition called hyperuricemia, can be present for 10-20 years without any symptoms. But just as minerals crystallize out of water in caves and form stalagmites and stalactites, uric acid can crystallize out of fluids in the body, forming microscopic deposits in tissues, especially kidneys, joints, tendon sheaths and skin. The painful part comes with the inflammation that ensues when the body attempts to eliminate the crystals. The classic case of gout, also known as podagra, begins suddenly with exquisitely painful, bright red swelling in the joint space between the foot and the big toe. Symptoms last from days to weeks.
The swelling comes from inflammatory fluid in the joint space. Diagnosis of gout depends on withdrawing some of this fluid through a needle and examining it under a microscope, where the uric acid crystals show up as pointy spicules which bend light waves in an identifiable way. Fluid withdrawal can also relieve some of the pain, but the mainstays of treatment during acute attacks are anti-inflammatory drugs such as Indocin, ice and or heat, and plenty of water. Prevention of attacks depends on efforts to lower uric acid levels, by diet, weight loss and use of medications that block uric acid production or increase its elimination in the urine.
Fructose is a building block for uric acid
For centuries, dietary advice about gout has revolved around foods high in protein. But as numbers of gout cases climbed steadily over the last forty years and average uric acid levels in people without gout also increased, a correlation with increased sugar consumption began to emerge. Scientists are now studying the relationship of sugar intake to uric acid and gout and also attempting to tie uric acid to hypertension, obesity and heart disease.
Sugar consumption was once rare to non-existent. Table sugar, a mixture of the two simple sugars sucrose and fructose, came only from sugar cane, which originally grew only tropical regions. Sugar’s spread around the world followed trade routes, and accelerated markedly after the discovery of the beet as a sugar source in the 18th C. But the most dramatic rise in sugar consumption followed the invention of high fructose corn syrup (HFCS) in the 1970s. From work done so far, it appears that sugar’s fructose is a bigger culprit than its glucose in aggravating the metabolic syndrome (obesity, high blood pressure, heart disease and diabetes). And the metabolism of fructose actually produces uric acid.
When the glucose/fructose mix of sugar enters the body, glucose is transported directly into cells for use, but fructose requires processing. This requires energy, provided by ATP (adenosine triphosphate), and ATP breakdown produces uric acid. Eating fructose regularly also makes fructose easier to metabolize because it “induces,” or makes the body produce specific enzymes required to break it down. For someone prone to overproducing uric acid, or someone whose kidneys excrete it inefficiently, a diet chronically high in fructose may not only provide the building blocks for uric acid, but also speed its production.
Cutting fructose may help – and will do no harm
Cutting purine-rich foods down in a diet helps many susceptible people remain gout free. There is no data yet on the effectiveness of limiting fructose intake on gout or hyperuricemia, but such a diet can do no harm. Limiting fructose sources to whole fruits would dramatically lower total fructose intake for most people. Fructose is the major sugar in fruits, but it is combined with fiber and vital nutrients and present in much lesser quantities than in sugar-sweetened beverages, soft drinks, baked goods and many processed foods. Even ketchup contains HFCS.
When dietary modification is not enough to keep people gout free, drugs that block uric acid production or increase its elimination help. Ideally, uric acid levels should be in the range of 3-6 mg/dl. Diet is important not only for those who have suffered acute gout attacks, but also for those who have high uric acid levels without any symptoms. Hyperuricemia warrants a good look at the amount of dietary fructose.
Henry VIII’s confectionary was a clue to the relationship of girth to gout. As uric acid research progresses, blood tests for uric acid will probably become routine, because high levels often precede the development of high blood pressure and Type II diabetes, even in people not susceptible to gout.
Other Gout Facts
Many diuretics in common use raise uric acid levels and can trigger gout, especially the thiazide group.
Gout attacks commonly follow trauma or surgery because tissue breakdown produces purines.
Cancer treatments may also raise uric acid levels as tumor cells break down.
Uric acid levels increase in women after menopause and women rarely suffer from gout before then.
Uric acid levels in men rise at the time of puberty.