Andrew Siegel, M.D. Blog # 58
Why is a blog on gout relevant to “promiscuous eating”? Simply because gout can often be precipitated by dietary indiscretion (promiscuous eating), although it is often multi-factorial, with the most common underlying factor being an impairment of the kidneys’ ability to excrete uric acid. This subject touches both health/wellness and urology, subjects that are dear to my heart.
I once had a “wicked” gout attack, which pretty much ruined my wilderness medicine meeting/vacation in beautiful Big Sky, Montana. I never imagined that gout was in the cards for me, assuming naively that gout was a problem of portly and sedentary Dickens-like characters that enjoyed their Porterhouse steaks, red wine and cigars. However, the day my family arrived in Big Sky I became aware of throbbing in my left big toe. It progressed dramatically and when I examined myself, I noticed that the toe was red, swollen and painful. A few days before, I had stubbed it walking up the stairs in my home, so my immediate assumption was that I had unknowingly broken it. The situation rapidly progressed to the point where the entire foot became extremely swollen, red, hot-to-the-touch, and literally grotesque; I had trouble bearing weight on the foot and it was so tender that even the contact of a bed sheet on the foot caused severe pain. I phoned my buddy Frank Alberta, a sports orthopedist, to ask some advice for management of a broken toe. When I explained the scenario to him, he replied that I was having a classic case of gout and I would need to obtain some anti-inflammatory medication and ride it out. I suffered through that week, limping meekly through Yellowstone Park with the support of my daughter on one side and my wife on the other. Eventually it resolved, but left me with some limitation of mobility of that toe. After the resolution of the acute attack, I had my uric acid levels checked and they were found to be elevated. Subsequently, I went on Allopurinol, which has knocked my uric acid down to an acceptable level. Between the Allopurinol and being attentive to my diet, I have never had another attack.
In retrospect, I believe that a number of factors triggered my attack. There was the injury factor—not a broken toe, but certainly an injured one. Then, what I later found to be my high serum uric acid levels, likely inherited as my grandfather suffered with gout. There was the dehydration factor from several vigorous and lengthy tennis matches played a few days prior in the heat of August. Finally, my dinner at home before leaving for Montana can be described as very gout inducing—crab cakes, sushi, asparagus and beer—all items high in purines, those chemicals that are broken down into uric acid.
Uric acid is the end product of the breakdown of proteins known as purines. If there is too much uric acid production or not enough excretion, the result is high levels of uric acid in the blood. Gout occurs almost exclusively in those with elevated uric acid, although only a minority of those with elevated uric acid levels actually develops gout.
Gout is a chronic inflammatory arthritis most often caused by a deficit in the kidneys’ ability to excrete uric acid, resulting in elevated levels of uric acid in the blood. When uric crystals get deposited in joints and tendons, there is an inflammatory response resulting in intense pain, redness and swelling of the affected area. It most often involves the big toe, but can affect any joint.
Tophi—deposits of crystalline uric acid at the surface of joints or in skin or cartilage—can be a feature of gout. Risk factors for gout are genetics, a diet high in purines, aging, declining estrogen levels in women and obesity. High levels of uric acid are correlated with chronic kidney disease, high blood pressure, heart failure, diabetes, and high cholesterol.
If the uric acid crystals precipitate in the joints, a gout attack occurs; if the uric acid crystals precipitate in the kidney, kidney stones occur. Increased uric acid levels are associated with red meats and poultry; organ meats (liver and kidney); many forms of seafood including anchovies, mussels, scallops, crab, shrimp, lobster, oysters and a variety of fish; certain vegetables including asparagus, spinach, mushrooms, lima beans, kidney beans, and lentils; fructose-sweetened beverages; and alcohol, particularly beer.
The good news is that gout is very treatable—in fact, it is the only form of chronic arthritis that is indeed curable. When uric acid levels are reduced over the long-term, uric acid crystals in joints, soft tissues, and tophi dissolve, and acute attacks diminish. Proper management of gout is aimed at treating the elevated blood levels of uric acid. Uric acid levels of < 6.0 mg/dL are desirable.
Acute flares of gout are typically managed with non-steroidal anti-inflammatory medications to treat the pain and inflammation. At times, alternatives such as colchicine or corticosteroids need to be employed for an acute attack. Long-term management usually begins with allopurinol to reduce uric acid levels. An alternative is febuxostat. Sometimes probenecid, a medication to increase the kidneys’ excretion of uric acid is used. For refractory gout, an intravenous medication known as pegloticase is sometimes called for—it is relatively new and can literally dissolve tophi.
Andrew Siegel, M.D.
Author of Promiscuous Eating: Understanding and Ending Our Self-Destructive Relationship with Food
Now available on Amazon Kindle