I once counseled a man who had something approaching an addiction for hot dogs. He would eat Hebrew Nationals with scrambled eggs for breakfast, Nathan’s with a dab of coleslaw (for the vitamins) for lunch, and Ball Park Franks, the kind that balloon to twice their size when you boil them, for a hearty dinner. He ate hot dogs for snacks and hot dogs for desserts. If he ate lunch with a friend or dined at a banquet, he would have hot dogs when he came home.
An inspection of my client’s refrigerator revealed no fewer than fifteen brands of hot dogs. This hot dog connoisseur—a president of a national scientific organization, a full professor at a major university, and the author of twenty books—only gave up hot dogs when he realized they were causing him gout.
Gout was once considered a rich man’s disease. In the twenty-first century, gout is more of a poor person’s disease. It's hard to imagine, but the high-protein, high-fat foods we now consider cheap, such as Spam and hot dogs, were once luxury items. The fresh foods that help sufferers avoid new attacks take a little more effort to obtain and cost a little more at the checkout counter, but they are still much less expensive than medication.
Gout is a form of arthritis resulting from the accumulation of the metabolic byproducts of uric acid in joints. It causes sudden attacks of pain and tenderness in joints, usually the metarsophalangeal joint of the big toe, but sometimes in other joints, such as the ankles, hands, knees, and wrists. The first attack usually occurs at night. Joints rapidly become warm, red, and tender, and the skin over them often appears as if it had been infected. Untreated, pain and swelling usually continue for 3 to 10 days.
Gout pain is triggered by the accumulation of needle-sharp crystals of a salt of uric acid known as monosodiumurate. These crystals build up in a joint and find their way into surrounding tissues during an acute attack. So much monosodiumurate can accumulate in the synovial fluid in the joint that it takes on a chalky color. The immune system fills the joint with neutrophils to break up injured tissue. The massive inflow of neutrophils makes pain and swelling worse. Over time, this misguided immune process can destroy a joint.
The body makes uric acid by breaking down purines, one of the two types of components of DNA, RNA, and ATP. How purines are recycled depends on xanthine oxidase, an enzyme that generates a potent free radical known as superoxide. Over consumption of foods that are rich in purines can generate more uric acid than the xanthine oxidase system can process. Excessive alcohol consumption, surgery or serious illness, or withdrawal from ACTH, steroid medications, or even gong off the medications prescribed for the treatment of gout can disable the xanthine oxidase system. When this happens, xanthine oxidase cannot process even the normal levels of purines generated by the digestion of food. Byproducts accumulate and precipitate an attack.
Gout is most commonly a disease of men over the age of 50. Women only represent 5 to 17 percent of all cases of gout, and the condition is almost never seen in women before menopause except in women with a strong family history of the condition.
The standard medical intervention for acute attacks of gout is colchicine. This potent anti-inflammatory drug was originally isolated from the autumn crocus. It is extremely effective at controlling inflammation. There's no doubt colchicine works. Up to 75 percent of patients show major improvement in symptoms within the first 8-12 hours of taking the drug.
Unfortunately, colchicine has serious side effects. It can cause bone marrow dysfunction, depression, hair loss, liver damage, respiratory problems, and seizures. Even worse, taking a dose of colchicine low enough to avoid these side effects doubles risk of death from heart failure attack, and the way to avoid increased risk of death from heart failure is to increase the dose of colchicine, increasing the risk of non-fatal side effects. Moreover, colchicine is only an anti-inflammatory. It does nothing to prevent future attacks of gout.
A natural approach to treating gout aims to keep uric acid within normal levels. Considerable personal discipline is required to overcome the condition, but the combination of dietary changes and nutritional supplementation usually prevents further attacks.
Step number one in controlling uric acid is lowering your intake of foods that contain purines. These are the foods that increase uric acid production. You must also avoid alcohol, since alcohol accelerates the breakdown of purines into forms that become uric acid and impairs kidney function. You need to reduce consumption of sugary refined carbohydrates and also of saturated fats. These foods likewise trigger uric acid retention. And you can't go on an Atkins or South Beach style high-protein diet, since the amino acids high protein diets provide displace uric acid in the cleansing apparatus of the kidneys. When the kidneys cannot clear purines, they go back into the bloodstream where it eventually circulates to the joint.
The next step in controlling uric acid is reducing insulin resistance, the inability of muscle cells to accept sugars. The simplest ways of reducing insulin resistance are vigorous exercise and weight loss. Vigorous exercise is not recommended for sufferers of gout since it may precipitate uric acid crystals in the kidneys. In some cases, a deficiency of the enzyme HGPRTase may cause excessive release of hypoxanthine in muscles being exercised.
Limitations on exercise leave diet as the principal means of reducing insulin resistance in gout. A clinical study at the University of Witwatersrand in South Africa enrolling 13 men with gout found that following a calorie-restricted diet for four months normalized uric acid levels in a majority of participants in the trial.
The diet consisted of 1600 calories a day, 40 percent derived from carbohydrate, 30 percent from protein, and 30 percent from fat, simple sugars replaced with complex carbohydrates and saturated fats replaced with polyunsaturated fats. Participants lost an average of 15 pounds (7.7 kilos), and the frequency of attacks was reduced from average of two per month to one attack every other month.
Very nearly the only food gout sufferers can eat as much as they want is cherries. Consuming one-half pound (250 grams) of cherries, fresh or canned, every day is widely recognized as lowering uric acid levels and preventing attacks of gout. Cherries, along with blueberries, and other dark and red-blue berries are rich sources of joint-healthy flavonoids.
These natural healing agents have the ability to cross-link the proteins in collagen, reinforcing the collagen matrix of cartilage and tendons. They also prevent the formation and release of the compounds that cause the intense pain of gout, namely, prostaglandins, leukotrienes, and histamine.
Another way to control the symptoms of gout is to eat more vegetables. Japanese scientists looking into question of what is gout and what causes it reported in 2010 that eating vegetables, which alkalizes the urine, makes it easier for the kidneys to flush away uric acid in the urine stream. Eating your veggies won't break down gout-inducing uric acid crystals the way eating cherries and berries may, but it may help prevent future attacks.