It would be a gross understatement to say that opinions and beliefs in medicine can change. Numerous examples can be found throughout the annals of history. How about the idea that you get a cold from being outdoors or leaving a window open? Another, a personal favorite, is that cuts heal faster if exposed to the air. Long disproven, this continues to be espoused by the lay public and health care providers alike.

One of my favorites, a more recent casualty, is the notion that a gout attack is the result of a rich meal, accompanied by a good wine, perhaps with a rich shellfish dish and a side of beef. This belief remains prevalent, even by those who should know better. But the tide has turned and this notion is no longer offered up as the explanation for an attack.

Before we can examine this common misbelief, a brief explanation of gout and hyperuricemia is necessary. This requires a discussion of purine metabolism and uric acid levels. Purines are a substance found in many diverse food types, with seafood and red meat containing especially high amounts, although some purine is found in a great many food sources. For example, beer is high in purines while dairy products are low.

Uric acid, a waste product found in blood, is the final product of the breakdown of purines (although some of the uric acid in our blood is a result of cell turnover by the body).

Most uric acid is dissolved in the blood, passes through the kidneys and leaves the body in urine. Uric acid becomes dangerous when levels of uric acid in our blood rise above certain levels.

This is what constitutes the diagnosis of hyperuricemia: the increase of this naturally-occurring substance in the bloodstream. This can be the result of many different factors, with diet being a minor one. Diet alone generally is not sufficient to cause hyperuricemia.

Very important is the amount excreted in the urine by our kidneys. Many individuals have poor kidney function when it comes to uric acid levels and do not filter out enough. Predictably, this results in rising levels in the blood and, hence, the diagnosis of hyperuricemia.

Great controversy surrounds this topic, of whether to treat these high levels in the blood if someone does not have gout attacks? But the evidence is becoming clear that we should. If untreated, high uric acid levels can eventually cause permanent bone, joint and tissue damage with repeated gout attacks. This is well-recognized and accepted. Yet, further research has clearly demonstrated the long term consequences to other organs as well.

Hyperuricemia appears to frequently lead to kidney disease and heart disease. Recent studies have demonstrated a correlation with an increased risk of stroke. Research has also shown a link between high uric acid levels and type 2 diabetes, high blood pressure, and fatty liver disease. Three-fourths of those suffering from gout will have metabolic syndrome, a constellation of conditions including abdominal obesity, high blood pressure, insulin resistance (a primary component of diabetes), and high lipid levels in the blood.

I believe a prior statement bears repeating: diet alone does not cause a gout attack. It can worsen already high uric acid levels in the blood and, consequently, initiate a gout attack, but genetics seems to be a common and very important component. Obesity is also associated with a propensity for hyperuricemia and recurrent gout attacks.

But what exactly occurs in this infamous condition? To illustrate the process leading to this painful joint, I would draw your attention to a simple glass of warm water into which some salt has been added. The salt disappears upon entering the water; the salt has gone into solution. As the water cools, the salt appears at the bottom of the glass, having come out of solution.

Like salt, uric acid in or around a joint is in a crystalline form. I liken it to having tiny shards of glass collecting inside this sensitive structure. Doesn’t sound very comfortable, does it? Gout is a form of inflammatory arthritis, resulting from chronically high levels of uric acid.

Gout is characterized by these recurrent attacks producing a red, tender, hot, and swollen joint. Pain typically comes on rapidly, often over-night. The joint at the base of the big toe is affected in about half of the cases, but can afflict various joints, including the other toes, the ankle, even the knee.

Chronically high uric acids, in which the concentration is high enough to lead to deposition of urates into soft tissues, will often result in the development of strange lumps and bumps. These masses are called tophi (a single one is a tophus) and not only are disfiguring, but destructive as well. Although not often considered, these deposits can occur in other organs like the kidneys and in blood vessels. Both can be harmful. The deposition of uric acid crystals into tissues will activate the immune system, causing chronic inflammation.

In modern culture, high uric acid levels are one of the most common disturbances in metabolism. Studies tell us one out of every four men, and every tenth woman, suffer from hyperuricemia, be it asymptomatic or symptomatic (in which there are gout attacks and/or tophi). Malnutrition or excessive consumption are considered important but secondary factors.

A genetically determined problem with the secretion of uric acid is considered the leading factor for elevated blood levels of uric acid. The clinical image of gout varies widely. It may manifest as acute or chronic arthritis, tophi on the skin, subcutaneous tissue and the skeletal system as well as leading to kidney disease.

The major goal of treatment is to reduce blood uric acid levels below the threshold for saturation. This can result in the dissolution of previously formed crystals, meaning the longstanding lumps can disappear. But if the reduced levels are not maintained, the concentration in the blood will likely rise, especially without a significant change in diet.

Currently, no uric acid‐lowering therapy is recommended in asymptomatic hyperuricemia, despite the fact we now know of many complications associated with high blood levels of uric acid, including kidney disease, cardiovascular diseases including hypertension, coronary heart disease, peripheral vascular disease, and stroke.

Clearly, non-pharmacological treatment, especially dietary changes, should be instituted in all patients with hyperuricemia. But many in health care believe it is time to evaluate those with hyperuricemia more carefully. Controversial is what therapies should be prescribed in the absence of any specific uric acid-related symptomatic disease, ie gout attacks.

When it comes to the prescribing of medications to lower blood levels, many feel we need to be more aggressive, quicker to treat hyperuricemia, and so reduce the many complications of high blood levels of uric acid. A gout attack is certainly a painful experience, but kidneys and a functioning cardiovascular system are essential for life.

Editor’s note: Dr. Conway McLean is a physician practicing foot and ankle medicine in the Upper Peninsula, with a move of his Marquette office to the downtown area. McLean has lectured internationally on wound care and surgery, being double board certified in surgery, and also in wound care. He has a sub-specialty in foot-ankle orthotics. Dr. McLean welcomes questions or comments atdrcmclean@outlook.com.