Elizabeth A. Reid, MD Girth and Gout: A Sweet Relationship? A


T Hampton Court Pal- ace, one of King Henry VIII’s sixteenth-century residences located outside Lon- don, tour guides regale visitors with tales of Henry’s obesity and the miseries he suffered during his frequent flare-ups of gout— exquisitely painful episodes of ar- thritis that come from the buildup of uric acid crystals in joints. Gout was long known as “the king’s disease” because it primarily af- flicted wealthy people who could afford the meats, seafood, and alcohol that can trigger uric acid crystal formation.


The tour guides also point out


to visitors the king’s confection- ary, a corner room near the wing of the palace containing the royal residence’s kitchen, and describe the sugar-rotted royal teeth pro- duced by the then-scarce sweet- ener. The guides do not link Henry’s gout to the royal sweets, but perhaps they should. Sugar is composed of equal parts glu- cose and fructose, and scientists are now beginning to link in- creased fructose intake not only to obesity, hypertension, and type II diabetes but also to increased uric acid levels in the blood—a risk factor for gout.


Why Gout Occurs


Some uric acid in the blood is normal because every cell in the body makes uric acid out of natu- rally occurring substances called


T H E E L K S M A G A Z I N E Other Gout Facts


• Many diuretics in common use, especially those in the thiazide group, raise uric acid levels and can trigger attacks of gout.


• Gout attacks commonly follow trauma or surgery because tissue breakdown produces naturally occurring substances called purines, which are part of proteins.


• 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.


purines—chemical compounds that are part of proteins and re- sult from the regular breakdown of DNA and RNA as cells recycle themselves. Purines are also present in many foods but are particularly concentrated in red meat, organ meats, as well as many fish and shellfish, and yeasty beverages, like beer and red wine. Uric acid in the blood usually serves as an antioxidant, but in some genetically suscep- tible people, levels of the acid become too high because their bodies make too much or their kidneys don’t excrete enough through urination. Abnormally high uric acid lev- els in the blood, a condition called hyperuricemia, can be present for ten to twenty years without pro- ducing any symptoms. But just as minerals crystallize out of wa-


ter in caves and form stalagmites and stalactites, uric acid can crys- tallize out of fluids in the body and form microscopic deposits in tissues, especially in the kidneys, joints, tendon sheaths, and skin. The painful part of this crystalli- zation process is a result of the inflammation that ensues when the body attempts to eliminate the crystals.


The classic case of gout, also


known as podagra, begins sud- denly 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 results from an accumulation of inflam- matory fluid in the joint space. A diagnosis of gout depends on withdrawing some of this fluid through a needle and examining it under a microscope to look for


the uric acid crystals, which show up as pointy spicules that bend light waves in an identifiable way. Withdrawal of fluid can also re- lieve some of the pain, but the mainstays of treatment during acute attacks of gout are anti- inflammatory drugs such as in- domethacin or colchicine, ice and/ or heat, and plenty of water. Pre- vention of attacks depends on efforts to lower uric acid levels by way of diet, weight loss, and use of medications that block uric acid production or increase its elimination from the body through the urine.


The Sugar Connection For centuries, foods high in protein were considered the main culprits in triggering gout attacks. But as the number of gout cases climbed steadily over the last forty years and average uric acid lev- els in people without gout also increased, a correlation between gout and increased sugar con- sumption began to emerge. Sci- entists are now studying the ef- fect of sugar intake on uric acid levels and the development of gout. They are also beginning to tie uric acid levels to hyperten- sion, obesity, and heart disease. Sugar consumption was once rare to nonexistent. Table sugar, a mixture of the two simple sug- ars glucose and fructose, came only from sugar cane, which grew (Continued on page 60)


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