The Vicious Cycle of Sleep Apnea and Weight Gain

Snoring might be the sound you notice, but the real danger of obstructive sleep apnea is what you don’t hear: your brain repeatedly yanking you out of deep sleep to keep you breathing, over and over, all night long. Dr. Mitchell Rothstein, a board-certified pulmonary and sleep medicine physician, joins us to give a clear update on what modern sleep medicine understands about sleep apnea and why it has become so widespread as BMI rises in the community. 


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Transcript

Who Gets Sleep Apnea

Dr. Mitchell Rothstein 0:00

Hi, I'm Mitchell Rothstein. I'm the phase one medical director at the Jacksonville Center for Clinical Research, where I've worked for the last eight years. For 30 years prior to that, I was a community physician practicing sleep medicine and pulmonary disorders for 30 years, and I'm board certified in both pulmonary medicine and sleep disorders. And today I wanted to kind of break down and give you the update and the skinny on sleep medicine and some of the new things that we've learned about it. And so welcome relief to many people that suffer in the community, and something that we've seen as a more and more prevalent problem in today's community. We know that about 20% of all adults suffer from sleep apnea, and of those, only about half are diagnosed. We also know that it's a problem of continuing pressure on the community. As our community is getting larger and larger in terms of BMI, this is becoming a more and more prominent feature of what we're seeing as a primary problem and as problems associated with it, comorbidities. So the common comorbidities that we see with sleep apnea are things like cardiovascular disease, hypertension, strokes, arrhythmias, heart attack, and heart failure. In fact, if you look at patients with heart failure, 50% of patients with both preserved ejection fraction heart failure and reduced ejection heart failure suffer from forms of sleep apnea. We're going to be primarily concerned on obstructive sleep apnea with this talk. And that's the snoring kind of sleep apnea that is intolerant to bed partners, that often awakens them from sleep. And it's characterized by periods of either complete or partial upper airway obstruction. So to get to that point, let me talk a little bit about sleep physiology, just some simple basics which will tie this all together a little bit better. When we talk about sleep, we recognize sleep by two different activities. One is a change in brainwave activity. Our brain activity during wakefulness is characterized by something we call a low voltage mixed frequency pattern. And that looks something like this. You can see that the waves are relatively small in terms of their amplitude, how far they go up and down, and there's some very fast portions and some somewhat slower portions. As we transition to sleep, light stage sleep, or stage one, the activity remains at a relatively low voltage, but the frequency slows down a little bit. Stage two sleep is characterized by these theta waves or spindles, which represent a blockade of external stimuli getting to your brain. And in deep sleep, delta sleep, we see these large synchronized delta waves. When people are woken up from deep sleep, we refer to that as sleep drunkenness. And I'm sure that's happened to many of you. You don't know where you are, you don't know where what room you're in, what day it is, and it takes a little while for your brain to kind of reorganize to this low voltage mixed frequency pattern. Now, interestingly, when you enter dreaming sleep, your brain also has a low voltage mixed frequency pattern, not quite as prominent as wakefulness, but so very, very similar. And it's kind of like you're awake during sleep and you're having when you remember your dreams, these conscious thoughts, along with this change in brainwave pattern, also occurs a change in muscle tone. So during wakefulness, we have resting, wakeful motor tone. As we fall asleep, that tone goes down. In deeper sleep, it goes down even more. And in dreaming you sleep, your brain actively paralyzes your muscles so you don't act out your dreams. So you can imagine if you're dreaming, you're running down the street and you launch off the bed and go running, you can hurt yourself. And in fact, that's a condition called REM behavior disorder that we treat and is very serious for people. And this change in muscle tone affects some muscles very important in maintaining respiration. Those muscles are the muscles of your upper airway and tongue. So your tongue is one big muscle, and that sits forward in your mouth, attached to your lower jaw, and then the back of your throat is a muscular tube, which is held in a U-shaped pattern away from the back of your throat. As these muscles relax, your tongue moves backward, the back of your throat moves forward, and airflow goes from being open to being obstructed. So I'll demonstrate, but I don't, since I'm a professional, I don't recommend you do this at home. But what happens to people during sleep is they go from having a normal open airway in breathing, as their airway relaxes, their soft palate starts to flutter, and you hear [snoring noise] snoring. And as that muscle softens even more and their tongue falls back even further, often what will happen is [snooring noise]. And then at that point, your brain has to make a decision. Either you stay at that deeper level of sleep and you suffocate, which your brain isn't going to let you do, or you wake up, maybe not to full consciousness, but enough to [snoring noise] get enough airway tone back to open up your throat so you can breathe again. And that can happen over and over during the course of the night, causing numerous episodes of these arousals which stimulate your autonomic nervous system. You can imagine if you're sleeping and I stand next to you, and every minute or so I lean over and choke you, not to the point that you wake up consciously, but just enough to compromise your airway, your nervous system gets activated. You have that fight or flight response. And that goes on repetitively during the night. In fact, during normal sleep, people's blood pressure actually goes down, and we have what's called morning dipping. Your blood pressure is actually the lowest it is all day in the early morning hours when you're in your deepest states of sleep. People that have sleep apnea don't have that normal dipping. In fact, their blood pressure actually can rise during the night. So that can lead to autonomic activation. That autonomic activation leads to stress on your entire body. That stress on your entire body leads to things like hypertension. It leads to what do people do when they're stressed in terms of their appetite? They get hungry, they eat more, they gain weight, which leads to fatty tissue developing not just in their hips and thighs, but also in the back of their throat, narrowing that airway even further and causing more and more of these episodes to occur, activating the autonomic nervous system more and more into a vicious cycle, and people have a difficult time getting out of it. We've known from the first recognition of sleep apnea as a condition that if people are overweight and have sleep apnea, if they lose 20% of their body weight, 80% or more of the time sleep apnea goes away. So we've known that for years. The problem is we have difficulty achieving weight loss, and that's been an ongoing problem since we've recognized it. And we've been through trials of bariatric surgery, which have been good for temporary weight loss, but we know over time in the majority of patients who undergo bariatric surgery, they'll gain the weight back again. And this kind of combination of autonomic activation and weight gain is the cause of the majority of patients that have sleep apnea. So knowing that there's an association between sleep apnea and people who are overweight, we know about some other associations too that define that even further. We know that people have fatty liver, now called MASH, metabolic associated steatohepatitis, 40 to 50% of patients with MASH have sleep apnea. And we also know that people who have a BMI over 35, 40% of those patients also will have sleep apnea. We know in patients that have atrial fibrillation, 50% of those patients have sleep apnea. And we know in patients that have atrial fibrillation, if they have associated sleep apnea and the sleep apnea is untreated, their risk of having recurrent episodes of atrial fibrillation is elevated to about 75%. If the sleep apnea is treated, that risk goes down to about 20%. And that's largely due because once we treat sleep apnea effectively and we reduce that autonomic activation that's always in that fight or flight mode, the risk of those reactivation re-entry rhythms becomes markedly reduced. So when we have identified people with sleep apnea, and then we treat them, what are our options for treatment? Well, when I was in practice, the majority is still now is the first line of therapy we know always works for sleep apnea is CPAP therapy. And it can go by the name of CPAP, BIPAP, APAP. There are a number of different delivery systems that go by different initials as well as different masks. And we know they're virtually 100% effective. The problem is that they're only about 50% tolerated by the patients. So it's very difficult to have a therapy that patients don't tolerate and have the patients follow up with that kind of therapy. So, with that in mind, we've looked at other alternatives. So people looked at surgical approaches to sleep apnea. So the primary initial surgical approach was called a uvulopalatopharyngoplasty or UP3, where the surgeon, usually an ENT surgeon, would snip off the bottom part of the soft palate and cut off the part of the back part of the tongue, trying to open that airspace. Since they couldn't really reduce the entire back of the tongue, we turned loud apnecs that had a fluttering soft palate and made that snoring noise into patients we called silent apnecs. So they still had obstructive events and they would [snoring noise] initially choke because the back of their tongue was still falling backwards and the back of their throat was still coming forward, but they just didn't make the noise to go along with it. And when a surgeon says they have a successful treatment for sleep apnea, that means they've reduced the apnea hypopnea index, the number of events, by 50%. So if you have someone who has 60 events per hour and you reduce that to 30 events per hour, by our criterion, they still have severe sleep apnea, but they're considered a surgical success. So it's also a very difficult surgery to recover from. And with a success rate that a lot of medical sleep specialists don't recognize as being significant, it's not something that we wanted to actively pursue. Something that will work for patients that have a significant underbite is something called a maxillomandibular advancement. Since the tongue is attached to the mandible, if we move the entire jaw forward, we can move the tongue away from the back of the throat. And that'll work, but not many people want to have their jaw broken in two places, have their jaw moved forward because it has a big effect on how you look as well as your bite and your dentition. We also tried things like tongue-retaining devices, which is kind of like an anti-pacifier. If you think about a pacifier that has a hole in it and you stick your tongue in it and then fall asleep with it, and your tongue is trapped in this plastic device around your lips, that'll work, but often isn't well tolerated either. So getting back to what we knew initially was that as people gained weight, their risk of sleep apnea increased, and then they entered this vicious cycle of autonomic activation leading to increased weight, leading to more autonomic activation, worsening sleep apnea, increased weight, more autonomic activation, that vicious cycle. And we knew that a 20% body weight loss would essentially cure a lot of these patients. There was a study in the last year using terzeptide, which is a GLP1/ GIP therapy. So it's a glucagon-like polypeptide associated with a gastric inhibitory polypeptide in a one-year study looking at patients with a BMI of 30 or more and moderate to severe sleep apnea, and whether they received, they stayed on their CPAP therapy and they received the medication, and over the course of the year they lost about 20% of their body weight, and with that, their AHI dropped about 20 per hour as well. So that means the vast majority of these patients that had moderate to severe sleep apnea, defined as an AHI of 15 or greater, had their AHI fall into a mild to high normal range, mean they probably don't need CPAP therapy anymore. So the skinny on sleep apnea new treatments that we know are effective and clinically or FDA approved for treatment is the use of terzeptide for patients with obesity and sleep apnea. And of course, to be followed up to make sure at the end of that trial, once you've lost your 20% of body weight, you still have sleep apnea and no longer and hopefully no longer may need CPAP therapy.

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