Got gout? Try milk -- or cherries

In 1842, the English writer Sydney Smith wrote, "Gout is the only enemy that I do not wish to have at my feet."

Anyone who has suffered a painful attack of gouty arthritis would probably agree.

Gout is the result of an imbalance between the production and excretion of urate, the metabolic end product of dietary purines that are found in abundance in animal proteins.

If blood levels of urate rise high enough, the chemical can settle as crystallized deposits in joints. Most frequently, the big toe is affected -- becoming so swollen and sensitive that even the weight of a sheet or blanket on the area can cause excruciating pain.

Gout has a long history. It's often called "the disease of kings and the king of diseases," because in the past only the wealthy could afford to overindulge on purine-rich organ meats, gravies and seafood.

Most mammals have low blood levels of urate due to the activity of an enzyme, uricase, which converts urate into the more soluble chemical, allantoin. We humans are different. Millions of years ago, our hominoid ancestors experienced several mutations in the gene responsible for uricase, rendering it nonfunctional. Lacking the active enzyme, humans and great apes have higher urate levels than other mammals.

A research group at Baylor College of Medicine suggests that this genetic mutation may have helped ancient humans survive. Elevated urate levels increase salt sensitivity, helping to maintain blood pressure when the sodium content of the diet is low. And although we may be swimming in salt today, it's been estimated that the fruit- and leaf-based diet of our ancestors a million years ago supplied a paltry 225 milligrams to 700 milligrams of sodium per day.

But a chronically high urate level is a disadvantage to the average American today, who consumes a whopping 4,000 milligrams of sodium daily. It contributes to hypertension, which is often seen in association with gout.

Not surprisingly, diets rich in animal protein increase the risk of gout, which strikes seven to nine times more males than females. So does high alcohol intake and obesity. In parallel with rising obesity rates, the prevalence of the disease has doubled over the last twenty years.

Because of this strong relationship, the primary emphasis of dietary treatment for gout is placed on weight reduction and less on drastically slashing purine intake. Low purine diets are quite limiting (animal proteins, many vegetables, whole grains and beans are restricted) and thus can be hard to follow. They're also only moderately effective in lowering blood urate levels because most gout sufferers are poor urate excreters.