Squishing the belly increases AHI

[split_city]

It's been a while since I have posted here so I thought I would update you on my progress. Some of you would be aware of my work in this thread viewtopic.php?f=1&t=19370&st=0&sk=t&sd= ... beer+belly In this study, I showed that compressing the abdomen, made the airway more collapsible.

I just completed a follow up study in which I did the same thing to see if compressing the abdomen makes OSA worse. Well, the results are in: raising pressure inside the abdomen does indeed increase AHI. I raised pressure inside the abdomen using a large inflatable pressure cuff (a larger version of a blood pressure cuff). I had three levels of abdominal compression 1) cuff deflated 2) intermediate and 3) maximum level believed to be tolerable during sleep. These are some of the results for each cuff pressure level

Gastric pressure
cuff deflated: ~11cmH2O
intermediate: ~16cmH2O
max: ~19cmH2O

cuff effect: p<0.001

AHI
cuff defalted: ~34 events/hr
intermediate: ~37 events/hr
max: ~50 events/hr

cuff effect: p=0.022

These data further support that abdominal obesity may be an important factor contributing to OSA in some (not all) OSA patients. It also supports a recent finding by Simpson et al (2010) that abdominal fat is an independent predictor of OSA severity, at least in males.

Sex differences in the association of regional fat distribution with the severity of obstructive sleep apnea.

Simpson L, Mukherjee S, Cooper MN, Ward KL, Lee JD, Fedson AC, Potter J, Hillman DR, Eastwood P, Palmer LJ, Kirkness J.

Centre for Genetic Epidemiology and Biostatistics, University of Western Australia, Perth, Australia. Isimpson@meddent.uwa.edu.au

Erratum in:

* Sleep. 2010 Aug 1;33(8):preceding 1003. Hillman Fanzca, David R [corrected to Hillman, David R].

Comment in:

* Sleep. 2010 Apr 1;33(4):419-20.

Abstract

STUDY OBJECTIVES: To describe sex differences in the associations between severity of obstructive sleep apnea (OSA) and measures of obesity in body regions defined using both dual-energy absorptiometry and traditional anthropometric measures in a sleep-clinic sample.

DESIGN: A prospective case-series observational study.

SETTING: The Western Australian Sleep Health Study operating out of the Sir Charles Gairdner Hospital Sleep Clinic, Perth, Western Australia.

PARTICIPANTS: Newly referred clinic patients (60 men, 36 women) suspected of having OSA.

INTERVENTIONS: N/A.

MEASUREMENTS AND RESULTS: Obstructive sleep apnea severity was defined by apnea-hypopnoea index from laboratory-based overnight polysomnography. Body mass index, neck, waist and hip circumference, neck-to-waist ratio, and waist-to-hip ratio were measured. Dual energy absorptiometry measurements included percentage fat and lean tissue. Multivariate regression models for each sex were developed. In women, percentage of fat in the neck region and body mass index together explained 33% of the variance in apnea-hypopnea index. In men, percentage of fat in the abdominal region and neck-to-waist ratio together accounted for 37% of the variance in apnea-hypopnea index.

CONCLUSIONS: Regional obesity is associated with obstructive sleep apnea severity, although differently in men and women. In women, a direct influence of neck fat on the upper airway patency is implicated. In men, abdominal obesity appears to be the predominant influence. The apnea-hypopnea index was best predicted by a combination of Dual Energy Absorptiometry-measured mass and traditional anthropometric measurements.

[roster]

man I hate to burst your PhD learning bubble, but OSA is mainly the tongue falling into the back of the throat, not the airway collapsing due to fat around the neck or diaphragm pressure. That's why it is worse on your back than your side.

since I'm on a roll here, not everyone that has OSA is obese, it is not a disorder found predominately in men either, women snore worse than men

go through life with those phenotypes you described and you'll miss half the OSA population because they didn't fit your "mold".

as for the "beer gut" association? I think they have already identified that one also, its called dunlap disease.

[roster]

Sorry, I could not resist a little channeling tonight.

I still miss Snoredog.

[OutaSync]

Sorry, I could not resist a little channeling tonight.

I still miss Snoredog.

Me, too.

[kteague]

split_city, thanks for the update. As with all conditions that have so many variables, much of what is learned will apply to just a segment of that population. The numbers are probably out there somewhere on the percentage of those diagnosed with OSA that have excess belly fat (besides me), but regardless of the number, it matters to those who fit the bill. Thanks for posting this inmformation.

P.S. I miss Snoredog too.

[BlackSpinner]

Hmmm I guess I should stop sleeping with that corset on then?

[NotMuffy]

Some of you would be aware of my work in this thread viewtopic.php?f=1&t=19370&st=0&sk=t&sd= ... beer+belly In this study, I showed that compressing the abdomen, made the airway more collapsible.

Did Steier ever write back?

[Calist]

Were they mostly Hypopneas? Centrals? Classic obstructives? Reras? Why don't you give us a breakdown of events? I'm curious as to whether compressions primarily cause hypopneas or disordered breathing.

[Moby]

Thanks for the info and links, split_city. Much appreciated that you keep us updated.

Di

[Raj]

Interesting, S_C, but I'm not sure that an external cuff duplicates the kind of abdominal pressure exerted by excess visceral fat. It makes intuitive sense to me that a cuff might constrict intercostal, rib, and diaphram freedom in a way that visceral fat wouldn't, which might present a confound to your experiment. However, it also makes intuitive sense to me that visceral fat might generate its own constrictions that could affect breathing patterns in some people, although I suspect that neck fat is likely to increase in proportion to visceral fat, which would further confuse the issue. In any case, I applaud your efforts.

[Muffy]

I just completed a follow up study in which I did the same thing to see if compressing the abdomen makes OSA worse. Well, the results are in: raising pressure inside the abdomen does indeed increase AHI.

Do you have any other data?

What you have presented so far simply suggests you have changed arousal threshold (what a surprise) and made sleep quality worse.

Muffy

[DreamDiver]

First, I have to say congratulations for sticking with it for three years.

Just to be sure I understand: This is in essence a pressure girdle around the entire abdomen used to mimic the effects of abdominal fat on breathing capacity? If so, are you suggesting that it's less likely to be about clear airway around the throat and more about restricted lung capacity for most men who supposedly have OSA?

[split_city]

Sorry for the belated reply. I just got back home from attending our nation's major sporting grand final. The good thing with this game, is players smash into each other without any of the padding and helmets that people use in one of your major sports.

A few points about my study. Our original aim was to look at total AHI across all sleep stages (each patient was confined to one posture, either lateral or supine). However, given that AHI varies within each sleep stage, the AHI in my first post is for stage 2 only.

Anyways, so many questions.....

Some of you would be aware of my work in this thread viewtopic.php?f=1&t=19370&st=0&sk=t&sd= ... beer+belly In this study, I showed that compressing the abdomen, made the airway more collapsible.

Did Steier ever write back?

Yeah he did. I thought you were going to follow it up with him though? Anyways, since I had to do the dirty work for you......This is what I asked:

Anyways, I have another question in regards to your paper. ECG artefact in Poes and Pdi clearly is an issue, even more so when trying to calculate iPEEP as it will influence your results. Your figures clearly show this artefact. Did you take this into account or did you do any ECG post-filtering of Poes and Pdi channels (see O’Donoghue et at 2002, Thorax)? Also, were your flow and pressure channels in sync? Pankow et al stated this "Time synchronicity of pressure and flow measurements was assessed by placing the flow sensor, the Pao sensor, and the CMT into the tube of a bass-reflex loudspeaker. Over the range of 5–10 Hz, there was a constant time delay (Dt) of airflow in relation to pressures of 0.03 s."

And his answer....

Yes, I agree - cardiac contraction is clearly responsible for a few cmH2O pressure change - we have manually selected the analysed bits outside any artefactual pressure deflections, taking the baseline from endexpiratory pressures. Flow and pressure were having the same delay as described by Pankow, we measured it a few times and it came pretty much down to the same time - however, we also measured the maximal pressure changes in this time frame, and they were neglectable and would have disappeared with rounding anyway.

Next question:

Were they mostly Hypopneas? Centrals? Classic obstructives? Reras? Why don't you give us a breakdown of events? I'm curious as to whether compressions primarily cause hypopneas or disordered breathing.

Yes, they were mainly hypopneas. We recruited patients who only had mild-moderate OSA in a particular posture (supine or lateral), with the aim to move them to moderate-severe OSA. We felt there was no point recruiting severe OSA patients as abdominal compression wasn't likely to push them any further along in terms of severity.

Here's a breakdown of AHI (obstructive, hypopnoea, central) for each cuff condition (i.e. average events per hour). I haven't done the stats yet.

Obstructive
Deflated: 2.6+/-2.1
Mid: 3.4+/-2.5
Max: 0.7+/-0.6

Hypopnea
Deflated: 30.2+/-5.8
Mid: 31.0+/-7.5
Max: 46.5+/-6.0

Central
Deflated: 0.7+/-0.5
Mid: 0.9+/-0.7
Max: 0.9+/-0.7

Without doing the stats, it appears that abdominal compression increases the frequency of hypopneas.

Next question:

Interesting, S_C, but I'm not sure that an external cuff duplicates the kind of abdominal pressure exerted by excess visceral fat. It makes intuitive sense to me that a cuff might constrict intercostal, rib, and diaphram freedom in a way that visceral fat wouldn't, which might present a confound to your experiment. However, it also makes intuitive sense to me that visceral fat might generate its own constrictions that could affect breathing patterns in some people, although I suspect that neck fat is likely to increase in proportion to visceral fat, which would further confuse the issue. In any case, I applaud your efforts.

I agree. The use of the cuff is quite a crude method of simulating central obesity. In fact, the aim of the cuff was not to simulate central obesity per se, but rather one consequence of abdominal obesity i.e. increased intra-abdominal pressure. However, increasing intra-abdominal pressure via external cuff pressure is likely to have different effects on structures within the abdominal and thoracic compartments versus that occurring with increasing visceral fat. We made sure the top edge of the pneumatic cuff was below the lower ribcage so that abdominal compression only had a direct effect on the abdominal compartment. Nevertheless, raising abdominal pressure likely results in elevation of the diaphragm and we believe that it's this ascent which reduces the amount of tension generated on the upper airway, and subsequent changes in airway function.

Next question:

I just completed a follow up study in which I did the same thing to see if compressing the abdomen makes OSA worse. Well, the results are in: raising pressure inside the abdomen does indeed increase AHI.

Do you have any other data?

What you have presented so far simply suggests you have changed arousal threshold (what a surprise) and made sleep quality worse.

Muffy

What is your undertanding of arousal threshold? My understanding is that arousal threshold equals the minimum esophageal pressure (Pes) that occurs on the breath prior to arousal (see Gleeson et al 1990). There are other ideas such as tension generated by respiratory muscles.

I haven't fully looked at the Pes data yet. However, just looking at Pes during periods of stage 2 sleep (at least two consecutive epochs of stage 2 without any respiratory events, arousals, PLMs, desaturations):

Min Pes during inspiration:
Deflated: -9.6+/-2.3cmH2O
Mid: -7.4+/-2.3cmH2O
Max: -6.6+/-2.6cmH2O

However, Pes at start inspiration did change with cuff inflation...
Deflated: 6.7+/-1.3cmH2O
Mid: 7.9+/-1.6cmH2O
Max: 8.7+/-1.4cmH20

...and will thus confound the min Pes reading. Perhaps looking at change in Pes during inspiration is a better indicator of how hard the patient is working to breathe?
Deflated: -16.2+/-1.8cmH2O
Mid: -15.4+/-1.7cmH2O
Max: -15.3+/-2.4cmH2O

In regards to sleep stage distribution, these are some data:

The average time for each cuff condition was:
Deflated: 80.2+/-5.9 mins
Mid: 76.8+/-6.1 mins
Max: 79.1+/-6.1 mins

The average % time spent in each stage for each cuff condition was:

Deflated
Wake: 32.5+/-5
Stage 1: 8.2+/-2
Stage 2: 52.5+/-5.8
SWS: 5.3+/-0.9
REM: 1.4+/-1

Mid
Wake: 37.0+/-4.7
Stage 1: 6.7+/-1.5
Stage 2: 48.0+/-4.8
SWS: 7.1+/-1.2
REM: 1.2+/-0.8

Max
Wake: 41.7+/-4.4
Stage 1: 7.7+/-1.6
Stage 2: 44.7+/-4.3
SWS: 4.5+/-0.8
REM: 0.2+/-0.1

Again, I haven't done any stats but perhaps there was more time spent awake with the cuff up. Is this simply a consequence of the cuff being uncomfortable OR because of the increased arousals due to rise in respiratory events? To further clarify, we had a random list of the 3 cuff conditions and changed the condition every 10mins, irrespective of sleep stage. We chose this as we believed it would be more comfortable for the patient i.e. not having cuff inflated for one hour.

Final question:

First, I have to say congratulations for sticking with it for three years.

Just to be sure I understand: This is in essence a pressure girdle around the entire abdomen used to mimic the effects of abdominal fat on breathing capacity? If so, are you suggesting that it's less likely to be about clear airway around the throat and more about restricted lung capacity for most men who supposedly have OSA?

Yes, the cuff was crudely used to mimic one aspect of abdominal obesity i.e. increased intra-abdominal pressure. We certainly aren't ignoring increased neck circumference/neck fat as an important contributor. However, while important, these variables don't tend to be the only contributing factor. In fact, several studies have shown that waist-to-hip ratio and visceral abdominal fat were more important contributors to AHI than neck circumference. Lung volume is also important given that it's known that upper airway collapsibility and AHI increases when lung volume is reduced.

[Muffy]

I just got back home from attending our nation's major sporting grand final. The good thing with this game, is players smash into each other without any... helmets...

Thanks very much for sharing that.

It explains a lot.

Muffy

[split_city]

I just got back home from attending our nation's major sporting grand final. The good thing with this game, is players smash into each other without any... helmets...

Thanks very much for sharing that.

It explains a lot.

Muffy

Yeah, it shows how tough us Aussies are. No prancing around acting all tough yet wearing full body protection. But this is for another thread....