Snoredog wrote: You damn right that is my reply, like I said you like to argue with yourself. Why don't YOU SHOW US some real data on your "collapsing" airway theory?
The only reason it looks like I'm arguing with myself is because you have no evidence (from your own work or from others) to dismiss the evidence presented by other groups. Why is that? Your are convinced about the tongue yet can argue against other evidence. Pretty much a cop out.
Here's a copy of my abstract for my abdominal compression study:
Introduction: Abdominal obesity evident in obese males may reduce tension on the upper airway (UA) (thus, increasing UA collapsibility) due to cranial displacement of the diaphragm and intrathoracic structures.
Objective: To examine the effects of experimental abdominal compression on UA collapsibility during sleep.
Methods: Fifteen obese (body mass index: 34.5±1.1kg∙m-2) male obstructive sleep apnoea patients (Apnoea-hypopnea index: 58.1±6.8events∙hr-1) aged 50±2.6years participated. Changes in gastric pressure (Pga), transdiaphragmatic pressure (Pdi), UA closing pressure (UACP), UA airflow resistance (RUA) and abdominal and thoracic compartmental volume were calculated during stable stage II sleep with and without abdominal compression via inflation of a pneumatic cuff. UACP was assessed during brief mask occlusions. Linear regressions were also undertaken to evaluate the relationships between Pga, Pdi and UACP.
Results: Abdominal compression significantly increased Pga (10.8±0.7 versus 16.2±0.8cmH2O, p<0.001), Pdi (7.6±1.2 versus 11.7±0.9cmH2O, p<0.001) and UACP (0.9±0.9 to 1.4±0.8cmH2O, p=0.04) but not RUA (6.9±1.4 versus inflated; 6.5±1.4cmH2O∙l-1∙s, p=0.58). Pga and Pdi significantly correlated with UACP without abdominal compression (r2=0.61, p=0.001 and Pdi; r2=0.67, p<0.001) but not following abdominal compression (Pga; r2=0.24, P=0.08 and Pdi; p2=0.13, P=0.21).
Conclusion: These data suggest that increased abdominal pressure impacts upon UA function
Snoredog wrote: I bet it is because you don't have any.
Task completed above
Snoredog wrote: I don't need you to explain it away with links to unrelated studies done by others, PROVE your point, like my dad used to say either sh*t or get off the pot.
Where is YOUR own data? You ridicule me for presenting data from other studies yet that's all you do. I have PROVEN my point. I have provided evidence that other factors (other than the tongue flopping back) which are likely to cause airway collapse. Researchers don't have to always repeat studies if there is already ample evidence to support the hypothesis. These weren't studies which looked at relationships. These studies were studies which looked at 'cause and effect,' just like the MRI imaging studies. The evidence is there in black and white yet you can't provide any coherent discussion to disprove any of it.
Snoredog wrote: You are the one NOT showing any evidence here of what you claim yet we are all supposed to throw out all the current knowledge on the subject and ACCEPT your theory based upon your crayon drawings
The evidence I presented is PART of the common knowledge. Just because you have the blinkers on doesn't mean the evidence isn't there. I'm not asking anyone to throw out all common knowledge OR accept my ideas. I said I'm aware of the tongue flopping back. But there is loads of evidence to stuggest that this isn't the only reason the airway collapses. Why don't YOU provide evidence which suggests that the data I provided is fable.
Snoredog wrote:Others say it is Paradoxical vocal-cord dysfunction (PVCD) from effects of GERD, which makes a whole more sense to me than your theory, but I haven't seen any evidence of that being the case either, so just like yours, it is only theory.
The lung volume stuff isn't theory. It's FACT.
Snoredog wrote: Maybe you can explain to us WHY is it when a patient uses an extreme alternate treatment such as GA or MMA they are cured OSA?
Why should I answer that? You don't answer my questions. Why don't you provide YOUR own data? A quick search in the literature shows that MMA does improve AHI, but not necessarily cure OSA in all cases (if AHI <5 is considered cured). Any type of surgery isn't 100% effective.
Snoredog wrote:What do they do during those procedures that eliminates your collapsing "airway" theory?
Where's your OWN data to back all this up?
Snoredog wrote: Wouldn't you still have a collapsing airway after those procedures? My guess is YES so why are those procedures shown effective at addressing OSA?
You are obviously getting confused. I never said that the 'beer belly'
causes OSA. I have always said it may
contribute to it. However, upper airway surgery is likely to tighten i.e. stretch the airway. As I said before, cranial ascent of the diaphragm may reduce the tension in the upper airway. Perhaps surgery couteracts this effect.
Snoredog wrote:Take it a step farther, there is a new procedure being tested right now in the Chicago area basically referred to as the tongue tether, it keeps your tongue from falling into the back of the throat thereby reducing AHI.
It may do so, but I bet there will be non-responders.
Snoredog wrote:There is currently over 100 tongue retaining devices on the market not including dental devices. Most have been shown to reduce AHI when used, but they all have one inherent problem, that is discomfort associated with use so most fail as an accepted treatment option.
Next, dental devices like TAP have been clinically proven to work in addressing mild-moderate OSA, they work by repositioning the mandible down and out. Not only does that movement open up the airway at the back of the throat it moves the tongue forward during the same process. Only problem is if you have severe OSA and a overly large tongue it may NOT move it enough, so you are left with residual AHI. You can only move your mandible so far.
Many of those dental devices also perform another function, that is physically prevent the tongue from falling into the back of the throat, so you remove that obsticle and you widen the airway at the same time. But it doesn't work for everyone.
So WHERE is your collapsing airway theory here? Why do those patients show improvement using those devices?
Yes, many show improvement (not necessarily cured) but many do not. Again, I provided evidence which shows that the tongue flopping back isn't the only cause. You continue to ignore it. You should be able to disprove this evidence.
Snoredog wrote: You medical guys are all the same, you want patients to all believe their airway is collapsing like a flattened fire hose laying on the asphalt under no water pressure, but you never can prove that theory.
If you don't belive it, why don't YOU do some experiments yourself?
Snoredog wrote:Collapsing airway: Define that for us will you? Show us exactly where it collapses as you say it does?
I never denied that the collapse occurs behind the back of the throat. It's HOW it collapses which is important.
Snoredog wrote: Come on now, we are not back in the 1930's or 1940's there are plenty of imaging techniques today to prove your theory including endoscopy. So what's the hang up here in providing that?
I'm not trying to show where the airway collapses. It's been done before. I'm more interested in what happens to airway tension. Experiements looking at airway tension can be conducted in animals but it would be unethical in humans. The only indirect evidence I have is studies which look at the change in distance between the carina and an endotracheal tube following CO2 insufflation into the abdomen.
Anaesthesia. 1996 Sep;51(9):823-6.Links
Comment in:
Anaesthesia. 1997 Feb;52(2):189.
Changes in tracheal tube position during laparoscopic cholecystectomy.Inada T, Uesugi F, Kawachi S, Takubo K.
Department of Anaesthesia, Matsue Red Cross Hospital, Shimane, Japan.
The distance from the carina to the tip of the tracheal tube was measured with a fibreoptic bronchoscope in 21 consecutive patients undergoing elective laparoscopic cholecystectomy. After placement of an Eschmann tracheal tube with a printed intubation guide mark at the vocal cords, the distance was 28 (15) [5-54] mm (mean (SD) [range]). The tube was then repositioned so that the distance was 34 (3) [30-40] mm from tip of the tube to the carina. After creation of pneumoperitoneum, the distance was significantly decreased to 26 (5) [17-35] mm (p < 0.005), which was not significantly altered by subsequent moving of the patient to the reverse Trendelenburg and left lateral tilt position. The maximum distance of tube migration was 8 (4) [0-15] mm. Four out of 21 patients would have been at risk of bronchial intubation after pneumoperitoneum if the tube had not been repositioned. Placement of the tube according to the guide mark is not recommended for laparoscopic cholecystectomy.
This shows that the carina moves up following an increase in pressure inside the abdomen. This upwards movement may decrease theamount of tension in the upper airway. A similar event may have happened in my study.
Snoredog wrote: As for the other theories abound such as effects of GERD and PVCD? there was some more information revealed on that the other day by Rooster a few weeks back where they were able to to trigger the UES into closure and a corresponding arousal seen on the EEG, I would be more inclined in believing that theory over yours. They explained it to where even I could understand it, they didn't throw up a bunch of smoke and mirrors and refer us to someone else.
You obviously don't know a lot about the scientific method. When deciding on a study you don't simply come up with a hypothesis out of thin air. You read the literature and try to identify flaws in previous work or find gaps in the literature. It's not that you don't understand my idea, but more the fact you are chose to ignore other possibilities other than the tongue. There's no smoke and mirrors in my study. I have fully explained the reasons behind it. I have provided ample evidence to support the possibility that increased pressure inside the abdomen may result in airway collapse via a reduction in tension in the upper airway.
Snoredog wrote:But if you cannot show me either real life MRI/CT imaging of your collapsing airway theory as you describe it, then it is all smoke and mirrors to me.
Like they say, without pictures it don't exist.
Lol...so only pictures prove stuff? That's a new one.
