Spisni study

[Dr Simon Mitchell]

Dan,

There are many things that can incite inflammation and the relationship between oxygen exposure and inflammation is complex.

But you seem to have missed the point. The study group that completed a moderately provocative air dive (30m 25 min) with very low oxygen exposure exhibited the same pattern of inflammatory activation as the UTD-RD group. The gradient factor (GF) decompression group was the only group that did not exhibit these activations, yet the GF group divers had a much greater oxygen exposure than the air dive group. This casts almost overwhelming doubt on the hypothesis that oxygen exposure is what provoked the pattern of greater inflammatory activation seen in the UTD-RD group compared to the GF group.

Your crusade to find fault with these valuable and illuminating studies consistently fails to acknowledge that there are no data supporting the approach you appear to be defending. I would suggest that Diver0001's question to Ross is also pertinent to you. Where is the evidence that UTD-RD was ever a good idea? Where is Georgitsis's evidence base that justifies the approach to decompression he prescribed and taught to you? You behave as though you are defending an established proven methodology against sketchy studies; whereas, in fact, you are perpetrating an arbitrary and idiosyncratic methodology concocted by someone with no relevant training in the face of mounting evidence that it is not the optimal approach.

Simon M

 

[Dan_P]

@RyanT can I trouble you for the citation, please?

 

[Dan_P]

Hi Simon,

I believe my intentions haven't come across as intended, in spite of my efforts to that end.
Let me be clear:

I embrace that the Spisni-study supports a shallower emphasis than that which was tested.
I utilize in my dives a shallower emphasis than was used on the RD side in the trial.
UTD even officially shifted shallower (RD2.0) after it.

I think the O2-and-inflammation question has a wider relevance.

Dan,

There are many things that can incite inflammation and the relationship between oxygen exposure and inflammation is complex.

But you seem to have missed the point. The study group that completed a moderately provocative air dive (30m 25 min) with very low oxygen exposure exhibited the same pattern of inflammatory activation as the UTD-RD group. The gradient factor (GF) decompression group was the only group that did not exhibit these activations, yet the GF group divers had a much greater oxygen exposure than the air dive group. This casts almost overwhelming doubt on the hypothesis that oxygen exposure is what provoked the pattern of greater inflammatory activation seen in the UTD-RD group compared to the GF group.

So a decompression dive to 50m using GFs is less stressful than a rec dive?

To my knowledge - and I do invite to show me wrong in the following - I don't think we can state any high-ppO2 induced inflammation to be a separated factor in the trial. That's not the same as saying the end results are invalid.
I don't believe them to be.

But I will stand by that it's an interesting avenue, and one deserving of more than this:

Your crusade to find fault with these valuable and illuminating studies consistently fails to acknowledge that there are no data supporting the approach you appear to be defending. I would suggest that Diver0001's question to Ross is also pertinent to you. Where is the evidence that UTD-RD was ever a good idea? Where is Georgitsis's evidence base that justifies the approach to decompression he prescribed and taught to you? You behave as though you are defending an established proven methodology against sketchy studies; whereas, in fact, you are perpetrating an arbitrary and idiosyncratic methodology concocted by someone with no relevant training in the face of mounting evidence that it is not the optimal approach.

Simon M

 

[Storker]

good experiment design wants two equal time profiles, but you can't have it when comparing two independent diving models. You need to come up with a better experiment design.

Um, varying two parameters (in this case, time spent in deco and stop profile) goes against every tenet in Experimental Design 101. Long story short: If you vary two parameters at the same time, there's no way to determine which of the two parameters were responsible for the difference in outcome. You. Just. Can't Know.

 

[rossh]

Ross,

You have expended a lot of energy trying to deflect the findings of the Spisni study away from deep stops. Your central unsubstantiated thesis appears to be that the increase in inflammatory markers in the RD (deep stops) profile was caused by greater oxygen exposure.

If oxygen exposure was the explanation for the elevation of inflammatory markers in the RD group, how do you explain the fact that the air dive group (no oxygen deco and much lower total oxygen exposure than either of the other two groups) also exhibited a significant elevation in the same markers? The only group that didn't exhibit this increase was the compartmental decompression group (GF group).

If you can answer that question, it might be worth continuing the discussion of the other things you have gotten wrong in your analysis.

Simon M

I'm working on a post addressing the question on the tests inflammatory markers and O2. But while I'm working on this...

You have expended a lot of energy trying to deflect the findings of the Spisni study away from deep stops.

Perhaps you can tell us.. what is the proven / valid / scientific connection that links the Spisni test result difference to be attributed to the small difference in deep stops, to the exclusion of all other variable factors? The test report leaves the question open, so why do feel the answer is the deep stop difference?

.

 

[RyanT]

@Dan_P, it should be available if you follow the link I put in my last post. Let me know if it's not working.

 

[Dr Simon Mitchell]

Hello Dan,

I think the O2-and-inflammation question has a wider relevance.

Perhaps, but you bring it up here I suspect to sow a little more doubt about the Spisni study. It is a recurring pattern, hence my comments.

As I said, the oxygen / inflammation thing is complex. Hyperbaric oxygen is actually anti-inflammatory in several contexts, but I don't want to take the thread off topic. It can be discussed somewhere else if necessary.

So a decompression dive to 50m using GFs is less stressful than a rec dive?

Yes, absolutely, when it is a deepish "rec dive" right up to the US Navy no-decompression limit and 10 minutes in excess of the DCIEM no decompression limit!

To my knowledge - and I do invite to show me wrong in the following - I don't think we can state any high-ppO2 induced inflammation to be a separated factor in the trial.

Well, it was actually, though not perfectly so. I believe that was part of the reason for inclusion of the rec air dive group. Can you not see that the occurrence of a virtually identical pattern of inflammatory activation in the low oxygen air dive as the high oxygen UTD-RD dive makes it extremely unlikely that oxygen was the explanation for the inflammatory activation in the UTD-RD dive; especially since a third group with "highish" oxygen exposure (the GF dive) exhibited no inflammatory activation?

But I will stand by that it's an interesting avenue, and one deserving of more than this:

And in saying this, you completely ignore the question. You are relentless in picking apart the evidence from human experiments that do not favour UTD-RD. Why not present the evidence from human experiments that supports it?

Simon M

 

[Michael Guerrero]

Lol, this thread has just turned into crazy talk. Both technical profiles used the same bottom mix and deco gasses. The RD one did more deco time on high O2 mixes and resulted in more inflammatory response (this is where the O2-induced inflammation hypothesis is coming from). However, the recreational profile used regular air (21% O2) and also had a markedly raised inflammatory response. The Buhlmann technical profile did not have an inflammatory response and used the same high O2 mixes as the RD profile.

When I run the recreational dive to 100ft for 25 min through my free dive planning software and log program Subsurface (GF 30/85) I get the following schedule:

depth duration runtime
➘ 100ft 2min 2min
➙ 100ft 23min 25min
➚ 30ft 3min 28min
- 30ft 1min 29min
➚ 20ft 0min 29min
- 20ft 2min 31min
➚ 10ft 1min 32min
- 10ft 4min 36min
➚ 0ft 1min 37min

The "recreational" dive was actually a deco dive on air with about 7 min of deco. And the recreational divers didn't used accelerated decompression with Nitrox or O2. So yes, I would expect them to be bubbling quite a bit, and to see an inflammatory response as a result. Plenty of studies have shown that you bubble after every recreational dive, not just technical dives. That means it is not outlandish to say that the "recreational" dive was more provocative than the Buhlmann profile, because the Buhlmann profile had the benefit of high O2 to washout the inert gas efficiently. The "recreational" dive, which was really an air deco dive, did not have the same benefit.

All this seems pretty clear. The more emphasis placed on deep stops the more inflammatory response, most likely due to bubbles. The researchers didn't find the correlation, but in my view they looked for bubbles too early (30 minutes after the dive), and so they invalidate their "non-finding." If you think you might find a correlation between bubbles and inflammation, why wouldn't you do your doppler tests at the same time you're drawing blood? Particularly when previous studies have shown that bubbling increases a couple hours after a dive before leveling off and eventually diminishing. To look for bubbles at 30 minutes and then look for inflammation response at 90 minutes nonsensical. If you want to know what's happening in the bloodstream, with regard to bubbles, at the time you are drawing blood, in the hopes of identifying a correlation...then you should look at the bloodstream at the time you are drawing the blood (i.e., at the 90 minute mark in this study).

But hey, why not find red herrings to chase instead?

 

[Dr Simon Mitchell]

I'm working on a post addressing the question on the tests inflammatory markers and O2.

Great, but please focus on the key question:

You have to explain how you conclude that high oxygen was culprit in the face of a virtually identical pattern of inflammatory activation in the low oxygen air dive as the high oxygen UTD-RD dive, and why a third group with "highish" oxygen exposure (the GF dive) exhibited no inflammatory activation.

Perhaps you can tell us.. what is the proven / valid / scientific connection that links the Spisni test result difference to be attributed to the small difference in deep stops to the exclusion of all other variable factors? The test report leaves the question open, so why do feel the answer is the deep stop difference?

"leaving the question open" is a fairly liberal interpretation of what the authors concluded. After consideration of all their results, this is what they concluded:

This increased secretion of pro-inflammatory chemokines seems related to the decompression system rather than to the longer exposure to high partial pressures of oxygen that RDS divers undergo. Tech RDS and Rec Divers showed very similar inflammatory profiles after the dives. Overall, our findings contradict the idea that adding longer and/or deeper stops is useful to achieve a more effective decompression.

But to your specific question, its Occam's Razor. It's highly unlikely to be oxygen, so we are left with the stopping profile as the authors concluded. The supersaturation evaluation with which you opened the thread drew erroneous conclusions (not for the first time) but we can get to that when you answer the oxygen question.

Simon

 

[rossh]

But to your specific question, its Occam's Razor. It's highly unlikely to be oxygen, so we are left with the stopping profile as the authors concluded. The supersaturation evaluation with which you opened the thread drew erroneous conclusions (not for the first time) but we can get to that when you answer the oxygen question.

Simon

You have not shown or described anything substantial here. No points about tissue pressures, or supersaturation or localized stress. All you have given us so far: your interpretation which is based on the philosophical "Occam's Razor" principle.... but of what? Where is the science Simon?

If you wish to debate this on simply the "plain obvious", then on those grounds, take another look at the stress pictures.... The obvious difference in the great big hole in the middle, where the "S" curve stuff happens. That is the Occam's Razor principle derived answer.