PutSleepApneatoBed

Yes, Sierra, I’ve seen the same claims. the manufacturers have always recommended against using the O3 sanitizers. In fact, using them will void the warranty.

Ozone is highly reactive.

From what I’ve heard from someone on the ASAP Board who used to manage a sleep lab, the foam IS, in the first instance, in a separate compartment. However, over time, or in the case of damage to the machine’s integrity, the seams in the machines can open up or gap, giving humidity (and in the case of the O3 sanitizers, ozone) access to the foam. That’s how the degradation can occur. And, yes, it was also apparently a poor choice of foam material. I’m not sure what kind of seals were used in the Respironics machines….

Good question Huffnpuffing…..you’re quite correct. It’s either a design defect or a manufacturing defect….

Those aren’t really different types of Sleep Apnea.

They are just obstructive apneas occurring in people of different ages or physical attributes.
Some have other names though. Infant OSA can lead to SIDS, sadly.

In each instance there is no obstructive apnea unless the breathing is shut down by an obstruction/throat muscle collapse. Once the throat muscles shut down, in order to open the airway for the next breath, the sleeper must either awake, or get up to the first level sleep. Until then, the throat muscles will remain in lockdown, which is one reason why no one with an unknown sleep status (Or known OSA) should take sleeping pills. The only thing that is keeping them alive, is that they DO wake up to breathe.

This isn’t a solution but a possible line of inquiry. At that hour, you are likely to be experiencing REM Sleep during which you may need much higher pressures.

Check your sleep study. If done in a lab, that number may be broken out separately. (My overall AHI was 19, but during REM it was 83.)

If you are experiencing apneas during REM due to the higher pressure needs, what would happen to the nasal pillows? Could the vacuum effect of an apnea make them collapse? I use a nasal mask, personally, and not the pillows, because they always felt too claustrophobic, but people who use them may have some other ideas….

BTW, I am the author of the “How to Get your Brain Back” blog on this site.

A few months after starting completely adherent and successful treatment, when my blackouts and seizures didn't immediately abate, I sought help from a neurologist and went through three days of neurological testing with a neuropsychologist.

I KNEW what was wrong (Sleep Apnea), but I wanted help in “getting my brain back.” Well, I was barking up the wrong tree. Despite my telling them at great length about my SA diagnosis and treatment , the neurologist and neuropsych apparently thought I had EOAD. Without my knowledge or consent, the neurologist did the genetic testing for that. (In fourteen states that is illegal, and in the other thirty-six, it is merely completely unethical- Why? Because it could make your entire family uninsurable.) and then stonewalled me about giving me the results.

Net/net I got NO help whatsoever with getting my brain back, and once I figured out what had happened had to fight to get the test results which I eventually did, of course, because EVERYTHING leaves a financial trail (the lessons of Iran-Contra—follow the money) And as I knew it would be, it was negative for the genetic bases for EOAD. (Had it been positive, there would have evidence of that in the family tree, and that, Thank God, didn't exist.)

But the point is, that by their mid fifties. long term untreated SA looks pretty much like EOAD from the standpoint of neuropsych testing. And it wouldn’t be the only time that someone with long term untreated SA had been mistaken for someone with EOAD.

Or maybe, as a neurologist/sleep doc turned SA patient once told me: the people with AD are the SA patients who survive long enough. The rest die of CVD causes earlier on-hence the gender differential in AD.

It’s based on my experience. And logic. What causes sleep apnea is a narrow and/or collapsable airway.

I have a female friend, 5’7” and 400#. Her doctor was CERTAIN she would have DM2 or at least be pre-diabetic. To the doctor’s shock, She didn’t, and wasn’t.

Why?

My friend additionally reported “sleeping like a bear”. (She also didn't have sleep apnea.) But her dentist had an interesting finding. The interior of her throat was so wide, he was afraid of losing his instruments down her throat.

The first order, root cause of sleep apnea is a narrow or collapsable airway, which either anatomically of functionally collapses during sleep.

So, let’s take it to the next step: what are the second order causes of A narrow airway or collapsable airway?

The second order causes are several, among them:

1) a narrow face and/or high arched palate will result in a narrow airway in the left to right dimension;

2) a square jaw and/or receding chin will result in a narrow airway, top to bottom.

Add the loss of muscle tone that occurs during REM and you have an airway that will occlude.

Take thirty or forty years of undiagnosed (and hence untreated sleep apnea) and even the the most stalwart and self-disciplined will be hard put to avoid weight gain. And, of course, that will often further narrow the airway, making the SA worse.

The heritable anatomical causes are the reason SA runs in families.

Medicine has no idea how many people had the sleep apnea before the weight gain, because they aren't looking for it.

Besides, it is easier to blame the victim-than to deal with the costs and implementation strategies for societal-wide mass screening and testing for a condition for which many patients will not accept the gold standard treatment, PAP, anyway.

But the rich who have SA are routinely testing and treating their children, because they are on to this. The first line of treatment in children is to remove the tonsils and adenoids, followed by palate expansion and orthodonture, if necessary. Those measures alone sometimes result in “a cure”, although it may not be life long.

But even if the “cure” doesn't hold, it will moderate the AHI, allowing PAP treatment in patients who might otherwise require higher pressures than an ordinary APAP can provide. If you have SA, have your family members tested young, and then retested throughout life.

Can obesity, alone, cause SA? At the margin, certainly. Fatty deposits can narrow the airway. But the fundamental problem is the airway dimension and patency. (There are also neurological causes of loss of muscle tone in the airway.)

But I had severe SA at a very young age with a BMI of 19 and I know a lot of other people with the same experience. It’s just next to impossible to get diagnosed if you are some combination of young, thin, and female.

PAP treatment will cure SOME problems caused by SA but not some of the most serious, which is why we need to be diagnosing and treating people MUCH earlier.

Treating SA “cured” my seizures, blackouts and irregular heartbeat/premature bigeminy, ADHD, cognitive/memory issues, perpetual exhaustion and loss of sense of direction. Treatment significantly increased my HDL level. It went from 35 to 55 within two months of starting treatment.

Treatment can also cure gout and AFIB, where those are caused by SA. I’ve seen it in others.

Treatment could NOT cure my prediabetes, which shortly became overt diabetes, HBP, NAFLD. The metabolic damage at the level of the mitochondria is probably not reversible, nor is most of the other metabolic damage, hence the general inability to lose weight, even with treatment. (Although some people do.) Usually, a lot of attention to diet and exercise will be required.

Net/net, some damage is reversible— and some is not. Pretty much what you might expect.

Sierra; it is NOT true that the cause of SA is obesity. That is a terrible stereotype, and it is killing people.
SA causes the obesity, where it exists, because it decreases leptin the hormone of satiety, and increases gherlin, the hormone of appetite.

Sleep Apnea is pervasive on both sides of my family. Almost everyone has it. A few ARE overweight, but most are not. And most die relatively young, undiagnosed. But the symptoms/comorbidities are obvious—HBP, DM2, CVD

My 94 y.o. Mom was the exception. She escaped, because at the age of three, her tonsils and adenoids were removed, expanding her airway.

I had SA so severe, that I couldn't maintain REM sleep from puberty on. Many years later it was determined that I obstructed 83 times an hour in REM, when I could get into REM, which wasn’t often.

But I stopped dreaming at puberty, followed by a lot of other symptoms and comorbidities, all of which were misdiagnosed-probably because I was young, thin and female.

When I finally self-diagnosed in my 50s, the doctors told me that the reason for my SA was the combination of a narrow airway and a square jaw. (They couldn’t blame obesity, because I wasn’t.)

And yes, apnea DOES cause diabetes. Even one night of poor sleep causes insulin resistance. What do you think a lifetime of it does? But more to the point, SA causes obesity and if you desaturate badly, the hypoxia kills beta cells. (The pancreas is very sensitive to low O2 levels.)

Nor am I. It is really quite effective. Improvements at this point are likely to be only at the margin. `