Worldsleep07

Just got back from this conference which was held in Cairns, Australia. Some nice work which was presented over the four days. Here's some of the work which I thought was interesting:

1) Sleep deprivation or sleep deprivation + cocaine was found to lead to erectile dysfunction (in rats). Presenter stated that erectile dysfunction is common in male OSA patients (perhaps due to sleep deprivation?) Three weeks of CPAP was not enough to cure erectile dysfunction.

2) MRI of the brain and neurocognitive function --> OSA patients were no different compared to controls in terms of cognitive function BUT had increased neuronal activation in the brain during these tasks --> perhaps increased activation was some sort of compensatory action due to 'damaged' regions of the brain? This increased activation occurs with aging. What about OSA + aging? Older OSA subjects had decreased brain performance and decreased neuronal activation --> perhaps brain just can't compensate?

3) Insomnia patients --> brain scanning showing increased metabolic processes/activity happening during wake and sleep --> i.e. brain is 'overactive' which perhaps prevents initiation of sleep or maintainence of sleep.

4) Absence or reduction in slow wave sleep may lead to obesity. Slow wave sleep results in secretion of growth hormone. Growth hormone plays a role in fat metabolism --> therefore, decrease in slow wave sleep -> less growth hormone produced --> less fat metabolism --> increased fat storage

5) Slow wave sleep also associated with increased insulin secretion and also increased glucose sensitivity. Slow wave sleep may help prevent diabetes.

6) There was a poster which showed that the upper airway collapsed differently in a group of OSA patients during sleep. There were several patients in which the posterior movement of the soft palate (AND NOT THE TONGUE) resulted in airway collapse. This agrees with previous work indicating that airway collapse occurs differently in OSA patients.

7) Increasing lung volume during anaesthesia (to eliminate upper airway muscle activity) reduced flow limitation i.e. prevented snoring. This indicates that airway collapsibility is simply not only the result of the tongue flopping back in the throat. This clearly shows that other factors are important when looking at how the airway collapses.
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split_city wrote:6) There was a poster which showed that the upper airway collapsed differently in a group of OSA patients during sleep. There were several patients in which the posterior movement of the soft palate (AND NOT THE TONGUE) resulted in airway collapse. This agrees with previous work indicating that airway collapse occurs differently in OSA patients.

Perhaps you should post a picture? I know some people here really like their pictures...

blarg wrote:

split_city wrote:6) There was a poster which showed that the upper airway collapsed differently in a group of OSA patients during sleep. There were several patients in which the posterior movement of the soft palate (AND NOT THE TONGUE) resulted in airway collapse. This agrees with previous work indicating that airway collapse occurs differently in OSA patients.

Perhaps you should post a picture? I know some people here really like their pictures...

I would love to post a picture, but I the ones I took didn't turn out very well as I was using a camera phone and the pics on the poster weren't that big

same picture works for that theory too, soft palate is clearly shown lower right at the end of the hard palate, but from what I can tell it still includes the tongue in the blockage even with that theory:



So with that theory, if I was an ENT surgeon you just remove the soft palate and Uvula, you don't need that extra tissue anyway. Explains why UPPP has such a poor outcome. Only problem is it is pretty hard to put that tissue back once it has been removed.

Interesting stuff. Thanks for sharing!

split_city wrote: ... 3) Insomnia patients --> brain scanning showing increased metabolic processes/activity happening during wake and sleep --> i.e. brain is 'overactive' which perhaps prevents initiation of sleep or maintainence of sleep.

That overactive, busy brain thing has been a big problem for me. Like the darn thing just won't turn off and relax so I can get to sleep. I go in spurts w/that problem. With or w/o CPAP. I'll have problems for a month or two, and then I'll do all right for a couple of months. We haven't been able to tie it to stress or medications or come up w/any other explanation for why this occurs.

split_city wrote:Just got back from this conference which was held in Cairns, Australia. Some nice work which was presented over the four days. Here's some of the work which I thought was interesting:

1) Sleep deprivation or sleep deprivation + cocaine was found to lead to erectile dysfunction (in rats). Presenter stated that erectile dysfunction is common in male OSA patients (perhaps due to sleep deprivation?) Three weeks of CPAP was not enough to cure erectile dysfunction.

If I was Lindsay Lohan, this could possibly impact me.

split_city wrote:
2) MRI of the brain and neurocognitive function --> OSA patients were no different compared to controls in terms of cognitive function BUT had increased neuronal activation in the brain during these tasks --> perhaps increased activation was some sort of compensatory action due to 'damaged' regions of the brain? This increased activation occurs with aging. What about OSA + aging? Older OSA subjects had decreased brain performance and decreased neuronal activation --> perhaps brain just can't compensate?

change in white matter? Plaques? the link between OSA and cardiovascular disease is growing stronger with every study. CV is systemic, so if you have clogged arteries say of the heart you most likely have similar effects on the cerebral arteries of the brain.

split_city wrote:

3) Insomnia patients --> brain scanning showing increased metabolic processes/activity happening during wake and sleep --> i.e. brain is 'overactive' which perhaps prevents initiation of sleep or maintainence of sleep.

wonder how that compares to SPECT Imaging,
http://www.brainplace.com/bp/atlas/

split_city wrote: 4) Absence or reduction in slow wave sleep may lead to obesity.
Slow wave sleep results in secretion of growth hormone. Growth hormone plays a role in fat metabolism --> therefore, decrease in slow wave sleep -> less growth hormone produced --> less fat metabolism --> increased fat storage

First simple explanation I've seen other than "OSA causes obesity" with no explanation. You would think here in the USA with our obesity epidemic, some drug company would come out with a HGH pill you could take to increase the growth hormone and lose weight.

We know from our own PSG's with untreated OSA we many times lack Slow Wave Sleep and REM.

Who was here that said "we don't need SWS" think it was RG if not mistaken, oh wait she is skinny.

split_city wrote: 5) Slow wave sleep also associated with increased insulin secretion and also increased glucose sensitivity. Slow wave sleep may help prevent diabetes.

6) There was a poster which showed that the upper airway collapsed differently in a group of OSA patients during sleep. There were several patients in which the posterior movement of the soft palate (AND NOT THE TONGUE) resulted in airway collapse. This agrees with previous work indicating that airway collapse occurs differently in OSA patients.

Wonder who that was, but that is a pretty broad statement with no real facts to support it.

All I ever asked was SHOW us those other ways the airway collapses?

We live in a day and age with more scanning techniques available than ever before including soft tissue imaging. I've showed you the way the tongue becomes the obstruction and collapse of the airway,

now you show us HOW our airway collapses when it does NOT involve the tongue as you suggest. Just saying it collapses doesn't tell us anything.

Get out your Crayons and show us exactly where that airway COLLAPSES in one of those other theories?

split_city wrote: 7) Increasing lung volume during anaesthesia (to eliminate upper airway muscle activity) reduced flow limitation i.e. prevented snoring. This indicates that airway collapsibility is simply not only the result of the tongue flopping back in the throat. This clearly shows that other factors are important when looking at how the airway collapses.

Can you show us where that airway collapse takes place? use any color you want but no pink (same color as tissue).

You are a Ph.D student, you should be able to do that pretty easy.

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CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP

Snoredog wrote:

split_city wrote: 4) Absence or reduction in slow wave sleep may lead to obesity.
Slow wave sleep results in secretion of growth hormone. Growth hormone plays a role in fat metabolism --> therefore, decrease in slow wave sleep -> less growth hormone produced --> less fat metabolism --> increased fat storage

First simple explanation I've seen other than "OSA causes obesity" with no explanation. You would think here in the USA with our obesity epidemic, some drug company would come out with a HGH pill you could take to increase the growth hormone and lose weight.

We know from our own PSG's with untreated OSA we many times lack Slow Wave Sleep and REM.

Who was here that said "we don't need SWS" think it was RG if not mistaken, oh wait she is skinny.

My goal here was to provide a brief summary of what was said in some of the sessions. Not to go into extensive details. I was providing some points of discussion. While I tend to disagree with you most of the time, I agree about the "we don't need SWS" comment. There is work being conducted saying that SWS is potentially very important for our health and well being.

The presenter didn't actually talk about a HGH pill but other drugs which promote SWS. Gaboxadol was one of the drugs mentioned. They only mentioned that this drug increased SWS and didn't talk about the effects of the drug on GH or weight,

Snoredog wrote:

split_city wrote: 6) There was a poster which showed that the upper airway collapsed differently in a group of OSA patients during sleep. There were several patients in which the posterior movement of the soft palate (AND NOT THE TONGUE) resulted in airway collapse. This agrees with previous work indicating that airway collapse occurs differently in OSA patients.

Wonder who that was, but that is a pretty broad statement with no real facts to support it.

Yeah I wonder which who said this? Anyways, I took a photo of their MRI images showing that airway obstruction was not the result of the tongue flopping back. However, the pics were too small and the area of the room too dark so I cannot post them on here. I'm sure you will be one of the first to read their work when it's published. I will like to hear your thoughts about them as they would be "smoke and mirrors" to you.

There is a new technique being developed in Australia which uses a nasal catheter with a rotating optical beam to visualise static and dynamic movement of the upper airway. This group has been able to successfully use this catheter to visualise upper airway collapse during sleep. They plan to run a study using this catheter.

Snoredog wrote:All I ever asked was SHOW us those other ways the airway collapses?

See above.

Snoredog wrote:We live in a day and age with more scanning techniques available than ever before including soft tissue imaging. I've showed you the way the tongue becomes the obstruction and collapse of the airway,

There have been many scans in OSA patients during wakefulness. Unfortunately, trying to image the airway with these scanning techniques during sleep is extremely difficult without prior sleep deprivation and/or sedatives (both which can impact upon airway structure and function). This is why there is little direct visual observations of the airway during sleep. I've said this before, perhaps you will catch up...eventually.

You showed me 1-2 pictures of the a collapsed airway during sleep or anaesthesia(?) which was the result of the tongue flopping back. Do you think that 1-2 pics infers what happens in ALL OSA patients? I thought you were smarter than that.

Snoredog wrote:now you show us HOW our airway collapses when it does NOT involve the tongue as you suggest. Just saying it collapses doesn't tell us anything.

While I stated the reasons why I cannot post a picture, this was on the poster in reference to soft palate collapse:

"Palatal obstruction during sleep. Obstruction during sleep was caused by posterior movement of the soft palate without tongue movement."

Again, I'll highlight this point. Perhaps you will make a comment about it for once. Why can the airway collapse when an individual sleep on their side of even in the prone position? How does the tongue come into it in these postures, particularly when a patient is in the prone posture? The tongue would have to be working (flopping back) against gravity. Pretty hard to do given that the tone of the tongue decreases during sleep...

I don't expect an answer from you about this as you have never done so previously.

Snoredog wrote:Get out your Crayons and show us exactly where that airway COLLAPSES in one of those other theories?

Crayons will not be needed when the study is published. Perhaps YOU will use the crayons to edit the picture to make it look like the tongue had collapsed back.

Snoredog wrote:

split_city wrote: 7) Increasing lung volume during anaesthesia (to eliminate upper airway muscle activity) reduced flow limitation i.e. prevented snoring. This indicates that airway collapsibility is simply not only the result of the tongue flopping back in the throat. This clearly shows that other factors are important when looking at how the airway collapses.

Can you show us where that airway collapse takes place? use any color you want but no pink (same color as tissue).

You are a Ph.D student, you should be able to do that pretty easy.

I've asked questions about this before but you continue to ignore it. I would raise these points again but you would continue to deflect away from them.

You go on about the tongue flopping back and that it should be easy to cure the problem. If it's so easy, why haven't you come up and conducted studies to test this cure of yours? Ever heard of the saying "all talk and no action." This pretty much sums up you in a nutshell.

Anyways, back to the lung volume stuff. The data I presented to you in the past directly shows that changes in lung volume affects upper airway collapsibility, independently of the tongue muscle status. You can do a search for this data as I am getting sick of repeating myself. This is commonly accompanied by a lack of response from you (as you have nothing to counter argue with it). This is followed by your tiresom and stubborn tongue flopping back argument a few days or weeks later.

I'd rather listen and take on board discussions by well respected Professors, doctors and researchers in regards to the various causes of OSA than some naive internet warrior such as yourself.

Snoredog wrote:same picture works for that theory too, soft palate is clearly shown lower right at the end of the hard palate, but from what I can tell it still includes the tongue in the blockage even with that theory:



So with that theory, if I was an ENT surgeon you just remove the soft palate and Uvula, you don't need that extra tissue anyway. Explains why UPPP has such a poor outcome. Only problem is it is pretty hard to put that tissue back once it has been removed.

Lol...so giving me cartoon pictures proves your case? Oh, please....

The MRI pictures I saw showed that in a number of patients, airway collapse was ONLY due to posterior movement of the soft palate. The tongue remained a fair distance away from the posterior wall of the upper airway.

There goes your theory...