Gout and the Sleep Apnea Connection
by Burton Abrams
There is a frequently overlooked factor that can cause an acute increase in the concentration of uric acid in the blood as well as increased likelihood of its precipitation as MSU (monosodium urate or uric acid crystals. See, Gout Basics for background). That factor is the reduction of the concentration of oxygen in the blood, which occurs in an individual suffering from sleep apnea.
Sleep apnea is the repeated cessation of breathing for many seconds at a time during sleep, when the muscles lining the airway relax enough to allow it to close, until the brain jolts them to reopen. The resulting reduction of oxygen in the blood causes the cells in the body to undergo a process of disintegration, which leads to their generation of excess uric acid. Once the uric acid is formed, the process is irreversible, even when breathing restarts. With each apneic period, more and more uric acid is fed into the blood, faster than the kidneys can dispose of it. Furthermore, the increased ratio of carbon dioxide to oxygen in the blood makes the blood more acidic, so that its ability to hold uric acid in solution is reduced and MSU is more likely to precipitate. These processes were described in medical journal literature about twenty years ago, and subsequent literature has confirmed that sleep apnea leads to excess uric acid in the blood and in the urine.
Thus, sleep apnea hits gout attacks with a double whammy. It feeds more uric acid into the blood plus it reduces the ability of the blood to hold the uric acid in solution so that MSU precipitates. The result is a gout attack that develops while sleeping.
This dysfunctional blood chemistry begins to resolve after the sleeper awakens, when the apneic periods cease and the kidneys have time to catch up in their removal of uric acid from the blood. Thus, a blood test of uric acid taken several hours after awakening will often measure as normal. The excess uric acid occurs as a flare that the belated blood test never detects.
The factors for increased risk of developing gout – heredity, overweight, alcohol use, middle or elderly age, male gender, female gender past menopause – are all the same increased risk factors for developing sleep apnea. But those who do not fall into these categories can develop either condition. It’s just less likely. I am not overweight, and I never was. Yet I developed both in middle age. Now I have neither.
Where Are The Data?
One would think that in the twenty-year period since these physiologic processes were described, gout researchers would have conducted studies to determine what percentage of gout sufferers also have sleep apnea, and in what percentage of those does resolving the sleep apnea cure their gout. It hasn’t happened. One can only speculate as to why, and some speculated conclusions may have a very cynical view of gout experts. What has been reported recently is a long list of serious diseases that have been found to have a strong association with elevated uric acid, but with no recognition given that all these diseases have previously been shown to be consequences of sleep apnea.
I realized the sleep apnea/gout connection over five years ago when resolving my sleep apnea resulted in the complete cessation of my gout attacks. And I know that I am not the only one who has observed that result. Based on my information, my primary care physician has been screening all his gout patients for sleep apnea. He has found that a large majority of them have sleep apnea, when neither he nor they would have otherwise suspected it.
Why This Is So Important
The results found by my literature search and by my primary care physician have convinced me the sleep apnea is a major cause of gout attacks. I have the view that all gout sufferers should assume they have sleep apnea as the underlying cause of gout until proven otherwise. That means that all gout sufferers should be screened for sleep apnea, not only to cure their gout, but more importantly to prevent the development of much more serious diseases.
Resolving gout is important. Even more important is diagnosing and resolving sleep apnea. Gout is very painful, but by itself it is not life threatening. If left untreated, sleep apnea is known to have numerous consequences that are life threatening – heart attack, heart arrhythmias, heart failure, stroke, diabetes, depression, kidney disease, and many other maladies. It is no wonder that this list matches closely the list of associations with hyperuricemia presented in the Is Gout Dangerous? posting on this website, because hyperuricemia is a direct consequence of sleep apnea. A fourteen-year study in Australia of people with sleep apnea who refused treatment concluded that the life expectancy of these people was 18 years shorter that of the general population, a conclusion that stunned even the study’s researchers.
Unfortunately, palliating your gout by using NSAIDs or prescription drugs does nothing to overcome your sleep apnea. It just masks the warning until one or more of the dire consequences of sleep apnea smacks you. In my case it was a transient ischemic attack (ministroke), atrial fibrillation heart arrhythmia, and diabetes, all of which I have recovered from. I was lucky that my sleep apnea consequences turned out to be reversible, but I have to maintain a strict diet to prevent the return of my diabetes.
There are about 80 times as many people with sleep apnea as there are with gout. Ironically, those of us with gout may be the fortunate ones because we have an early warning of our sleep apnea, but only if we and our doctors know about the connection.
A recent study performed in Australia of the medical records of over 16,000 patients diagnosed with obstructive sleep apnea found that gout was present in about 5% of them. Other sources estimate that the prevalence of gout in Australia is .27% of the population. That means that in Australia the likelihood of gout is 19 times higher in people with sleep apnea vs. the general population. Statistics for other first world countries are probably very similar.
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