By Duane Graveline, MD, MPH
I learned about sleep apnea in the Andes mountains. The study of high altitude effects and ways of modifying them was the reason we traveled three consecutive years to the Camp of the Condors.
There for a week at 18,000 feet our thirty-man team tested each other and our guides and porters with every medical test we could conceive.
It was my first night of our first trip that I suddenly awoke with the terrifying sensation of suffocation — as if I had been suddenly placed deep underwater with no air. In the Andes this is known as sleep terrors (for good reason) but it is nothing more than old-fashioned sleep apnea, with a few extra physiological twists due to the altitude.
At 18,000 feet, hypoxia dulls the sensitivity of the body's respiratory center to carbon dioxide (CO2). So your next breath takes longer and longer after the previous breath and finally apnea occurs — you stop breathing, sometimes for several minutes.
Finally either your CO2 gets critically high or your blood oxygen level gets critically low and you waken with a desperate need to breathe, to get out of the confines of your constricting sleeping bag and even your tent — you must breathe freely.
Like a madman you fight with your sleeping bag and tent flap's frozen zippers in your haste to stand erect and bring in huge quantities of icy cold air. It feels so good when finally it is over. Your blood CO2 and oxygen (O2) levels have by then returned to normal and you are satisfied for the moment, dreading only your return to sleep. You have passed your first night terror and for most, what is your first episode of sleep apnea.
There are some differences between altitude sleep apnea and normal, sea level sleep apnea in that the individual with sea level sleep apnea is rarely aware of having difficulty breathing upon awakening. They are not afraid to sleep. Sleep apnea generally is recognized as a problem by others witnessing the individual during episodes when they have observed cessation of breathing for prolonged periods of time.
This condition may go on for years or even decades without change. Reports of apnea for 30-45 seconds are not unusual. Respirations return with a loud grunt or gasp, only to revert again to apnea after varying time periods. Loud snoring is often associated with sleep apnea.
Sleep studies have documented both rises in CO2 levels and falls in blood O2 levels during these episodes. Some authorities have reported an association of sleep apnea with nocturnal angina and myocardial infarctions on the basis of these transient arterial blood oxygen reductions.
An individual with sleep apnea may or may not present with a history of tiredness and chronic fatrigue. Only after such a person is permitted to sleep with some form of breathing assistance do they realize how much better they feel after normal sleep for the end result is sleep deprivation.
Many statin users have reported sleep apnea. Some report that the effect is somewhat more likely with the lipophilic statins such as Lipitor, Mevacor, Vytorin or Zocor but some reports have been associated with use of Pravachol and Crestor. This should not be a surprise since the effects of all statins are primarily those of mevalonate blockade.
The use of statins results in reducing natural values of cholesterol, CoQ10 and dolichols to unnaturally low levels with the opportunities for dramatic physiologic consequences since all three of these substances have been shown to play strong roles in cellular function and information transfer.
Cholesterol has a critical role in the formation of the lipid rafts so important in cell communication. Similarly, dolichols are vital for glycoprotein synthesis and glycoproteins of one type or another are necessary for so many different cellular functions from cell identification to cell communication and far more. CoQ10 energizes every cell including those of the respiratory center presenting yet another opportunity for respiratory effect.
Then there is the vital importance of cholesterol to myelin fiber maintenance. A major role of respiratory control comes from pulmonary stretch receptors and their myelinated fibers that give input to our respiratory centers supplementing that from CO2, O2, pH (measure of the acidity or basicity of a solution) and neurohormonal factors.
Which of these possibilities are involved with statin use have not as yet been explained, but simply on the basis of their inevitable mevalonate blockade many possibilities come to mind.
As to treatment we have advocates of many different approaches. Plastic devices worn on the nose or in the mouth to prevent collapse of weak anatomical structures may help some. Control of obesity has helped many cases. Where alcohol and drugs exert their adverse effect by sedating the respiratory center — similar to the effect of low oxygen — most people will respond to appropriate counsel.
But the consistently most effective treatment is the use of the continuous positive airway pressure (CPAP) device. For those without obvious predisposing factors, this should be the first treatment option investigated.
In the Andes, the only thing that works is Diamox. Once I discovered the magic of carbonic anhydrase inhbition, I was never without it.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
Updated February 2016