Spisni study

[Dan_P]

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.

No - I'm all on board with a lower deep stop emphasis than was employed on the RD-side of the Spisni-study, mainly because of the results of the Spisni-study. I'll reiterate that I acknowledge it's findings.
I'm simply not content with a lowest-echelon learning that "deep stops, bad, shallow good" when there may well be much more to it and much more to be learnt from this study and others.

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.

Agreed, but isn't inflammation at the very core of the Spisni-study?
I would have expected a greater emphasis on bubbles measuments in the trial if that weren't the case, at least.
As the Spisni-study goes, inflammation is the main argument against (too) high emphasis on deep stops.

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!

I'll ask a question here, and present my point with that question after the next quote.

If RD is 'unfavourable by evidence in human trials for showing the results it did here, doesn't it stand to reason that the Rec-dive group showing similar-ish results, would be too?

Looking at the Rec-dive group, they had a pretty heavy emphasis on shallow stops: "The maximum depth was reached after 2 min, and divers remained at 30 msw up to 25 min of dive time. The ascent was at 10m min up to a safety stop at 3 msw for 3 min and then they surfaced at an ascend rate of 3m/min."

My point is this:

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?

I see your logic, I understand what you're saying and I agree with that - but in turn, can you not see that the inflammation level could be high on one dive (Rec group) due to the decompression stress you mention, and on another (RD group) due to increased O2-related stress?
That's why I'm making such a fuss about it not being isolated, not because I don't understand what you're saying.

That's not to be misinterpreted as me saying the study's findings haven't appropriateness in a diver's appraisal of which deep stop emphasis to employ.
I would argue that it does.

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?

If you dive a computer with whichever GF you prefer, and I dive RD, and we come out actually diving the same deep stop emphasis, would you find that problematic?

I'm not relentless in picking apart evidence from human experiments, but I don't mind picking at overconfident conclusions based on that evidence, such as this example (albeit from a neighbouring thread):

"Advocating for a "strategy" that moves deco time around in a profile, rather than emphasizing more time in shallower stops on higher O2 concentrations flies in the face of the science we have. Purporting that divers are "engaging" in their deco diving because they are arbitrarily moving stops around in ways unsubstantiated by science is simply endorsing voodoo. I think it is irresponsible and a shame."

That's based on a question about what to do if subjected to hypothermia.
Just incontextual assumptions about RD being coupled with overconfidence in what one or two studies mean or even themselves claim to mean - most commonly, NEDU and Spisni.

 

[Storker]

All you have given us so far: your interpretation which is based on the philosophical "Occam's Razor" principle.... but of what?

Just FTR, Occam's razor isn't philosophy, it's sound scientific thinking. The MDs have a saying which basically is Occam's razor in different words: when you hear hoofbeats, think horses, not zebras.

 

[Dr Simon Mitchell]

Looking at the Rec-dive group, they had a pretty heavy emphasis on shallow stops: "The maximum depth was reached after 2 min, and divers remained at 30 msw up to 25 min of dive time. The ascent was at 10m min up to a safety stop at 3 msw for 3 min and then they surfaced at an ascend rate of 3m/min."

Dan, this is a reductio ad absurdum argument along the lines of claiming that coming straight to the surface and getting bent proves that getting shallow more quickly doesn't work. Nobody is saying you don't need stops and obviously, therefore, there will be a deepest one at some optimal depth. That rec diving profile could probably do with a few more stops! The point the current evidence is making is that bubble models and UTD-RD make those stops too deep for optimal decompression. That's all.

I see your logic, I understand what you're saying and I agree with that - but in turn, can you not see that the inflammation level could be high on one dive (Rec group) due to the decompression stress you mention, and on another (RD group) due to increased O2-related stress?

Exactly the same pattern in exactly the same cytokines caused by two completely different stresses? Yes, there could be fairies at the bottom of the garden too and I admit I can't prove there aren't. Occams Razor. The most obvious explanation is probably the correct one.

This is the problem with discussing these imperfect studies with you (and all diving studies are imperfect because no one can circumvent the costs and ethical constraints to perform the perfect one). You will always pick on some small chink in the methodology and milk it for all its worth. I'm sorry, but you have been doing this to such an extent now that I do not trust your intentions. Yes, I agree, some commentators are making statements / drawing conclusions that are too strong and I do agree that it is fair to point that out. But while you have insisted that is your primary motivation I have formed the view that it is more than that.

And again, you have not provided the evidence that supports the approach to decompression that you advocate so strongly for.

Caveat: written in a plane so a bit hypoxic!

Simon M

 

[Dr Simon Mitchell]

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.

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Ross,

You came onto this thread with a confident conclusion that the outcome of the Spisni study was explained by hyperoxic stress despite the fact that this was something that the authors do not agree with you on, and despite the fact that the peer reviewers accepted their version of events. As I have pointed out, the finding of exactly the same pattern of inflammatory activation in the low oxygen air dive (but with moderate decompression stress) as the high oxygen UTD-RD dive, while a moderate oxygen GF profile did not produce any inflammatory activation makes it very hard to understand your confident conclusion. I would like you to explain it to me.

As far as your graphs are concerned, you have been told in the past by multiple commentators that the way you compare supersaturation in dives is flawed. You have been told that the correct approach to this sort of evaluation is to compare supersaturation and time across all tissues (integral supersaturation); an analysis which correctly predicted the outcome of the NEDU study. Parenthetically, in an earlier post in this thread it was ironic to see you cite the world's leading decompression modeller stating that supersaturation is important as justification for your graphs, because it was him (amongst others) who told you that integration of supersaturation and time (integral supersaturation) is the only valid approach to this sort of analysis, but you labelled this a "junk science measure" and persist with your uninterpretable version. If you undertake a valid analysis you might find a different answer.

But why don't you answer the oxygen question first? You said you were working on it.

Simon M

 

[Dan_P]

Dan, this is a reductio ad absurdum argument along the lines of claiming that coming straight to the surface and getting bent proves that getting shallow more quickly doesn't work. Nobody is saying you don't need stops and obviously, therefore, there will be a deepest one at some optimal depth. That rec diving profile could probably do with a few more stops! The point the current evidence is making is that bubble models and UTD-RD make those stops too deep for optimal decompression. That's all.

It might well do a better job on the Rec-side of the study, but that'll have to be a sidenote.

Look, I don't really disagree with you on this - I think it's clear enough from the Spisni-study that the deep stop emphasis on the RD-side was too great. I don't have a conflict with that.

This is the problem with discussing these imperfect studies with you (and all diving studies are imperfect because no one can circumvent the costs and ethical constraints to perform the perfect one). You will always pick on some small chink in the methodology and milk it for all its worth. I'm sorry, but you have been doing this to such an extent now that I do not trust your intentions. Yes, I agree, some commentators are making statements / drawing conclusions that are too strong and I do agree that it is fair to point that out. But while you have insisted that is your primary motivation I have formed the view that it is more than that.

I offer you my utter silence when in turn I see you correct such too strong statements in disfavor of RD with the same vigor that you do any in favor of it.

And again, you have not provided the evidence that supports the approach to decompression that you advocate so strongly for.

Again, if you dive a computer with whichever GF-setting you prefer, and I dive RD with whichever deep stop emphasis I prefer, and we both end up on the same deep stop emphasis, would you find that problematic?

I trust you acknowledge the paradox it would be to say that I can't adjust when using RD, while at the same time applying GFs to, say, ZH-L-16 to achieve exactly the same.

If you do, then the question is not about deep stop emphasis - rather, whether one is using a computer or RD.

 

[rossh]

Ross,

You came onto this thread with a confident conclusion that the outcome of the Spisni study was explained by hyperoxic stress despite the fact that this was something that the authors do not agree with you on, and despite the fact that the peer reviewers accepted their version of events. As I have pointed out, the finding of exactly the same pattern of inflammatory activation in the low oxygen air dive (but with moderate decompression stress) as the high oxygen UTD-RD dive, while a moderate oxygen GF profile did not produce any inflammatory activation makes it very hard to understand your confident conclusion. I would like you to explain it to me.

As far as your graphs are concerned, you have been told in the past by multiple commentators that the way you compare supersaturation in dives is flawed. You have been told that the correct approach to this sort of evaluation is to compare supersaturation and time across all tissues (integral supersaturation); an analysis which correctly predicted the outcome of the NEDU study. Parenthetically, in an earlier post in this thread it was ironic to see you cite the world's leading decompression modeller stating that supersaturation is important as justification for your graphs, because it was him (amongst others) who told you that integration of supersaturation and time (integral supersaturation) is the only valid approach to this sort of analysis, but you labelled this a "junk science measure" and persist with your uninterpretable version. If you undertake a valid analysis you might find a different answer.

But why don't you answer the oxygen question first? You said you were working on it.

Simon M

So in summary,

• For the bio-marker changes, you cannot demonstrate or show any relevance to supersaturation whatsoever?
• You have nothing to show or demonstrate the bio-markers have any connection to the 3 minutes of stops in the 36 to 24m regions.
• No math or graph to show whatsoever.
• Your argument is that your interpretation, assumption or implied association is based on an (unproven,un-calibrated, baseless) ISS measure, that you have not actually performed.

Like I said before... where is the science and valid connection to prove your argument its exclusively in the deeper stops Simon?

.

 

[The Chairman]

@Dan_P Dr Mitchel has asked for your studies that justify RD. You've yet to provide any. Do they even exist? If not, why are you so surprised that many of us lend it the same credence as we do Santa Claus or the Tooth Fairy?

 

[rossh]

@Dan_P Dr Mitchel has asked for your studies that justify RD. You've yet to provide any. Do they even exist? If not, why are you so surprised that many of us lend it the same credence as we do Santa Claus or the Tooth Fairy?

Pete,

FYI...... I'm not here to justify RD... It's not my invention. I'm here to help investigate what might have been at the root cause of the bio-marker changes. At the same time we can check any existing assumptions that have been made so far.

You do want to get to the real answer of this Pete?

.

 

[Dr Simon Mitchell]

So in summary,

• For the bio-marker changes, you cannot demonstrate or show any relevance to supersaturation whatsoever?
• You have nothing to show or demonstrate the bio-markers have any connection to the 3 minutes of stops in the 36 to 24m regions.
• No math or graph to show whatsoever.
• Your argument is that your interpretation, assumption or implied association is based on an (unproven,un-calibrated, baseless) ISS measure, that you have not actually performed.

Like I said before... where is the science and valid connection to prove your argument its exclusively in the deeper stops Simon?

.

Ross, you seem to be trying to avoid answering the question.....

You came onto this thread with a confident conclusion that the outcome of the Spisni study was explained by hyperoxic stress despite the fact that this was something that the authors do not agree with you on, and despite the fact that the peer reviewers accepted their version of events. As I have pointed out, the finding of exactly the same pattern of inflammatory activation in the low oxygen air dive (but with moderate decompression stress) as the high oxygen UTD-RD dive, while a moderate oxygen GF profile did not produce any inflammatory activation makes it very hard to understand your confident conclusion. I would like you to explain it to me.

I asked you this first. When you answer it, I will address your question about supersaturation, and if I use any graphs they will be interpretable.

Also, just a quick memory check. Do you remember how the last time you called integral supersaturation an "unproven, un-calibrated, baseless measure" (amongst other things) it was pointed out to you (by multiple scientists) that the integral of supersaturation and time is at the central core of the mathematics of VPM? I can put the relevant formula up again if you really need reminding. It can be linked to here. Do you also remember how the NEDU decompression research team used integral supersaturation to analyse and interpret the results of the NEDU study? Finally, do you remember being told by the world's leading decompression modeller that integral supersaturation is the core measure of decompression stress in several US Navy decompression algorithms?

Simon M

 

[rossh]

Ross, you seem to be trying to avoid answering the question.....

You came onto this thread with a confident conclusion that the outcome of the Spisni study was explained by hyperoxic stress despite the fact that this was something that the authors do not agree with you on, and despite the fact that the peer reviewers accepted their version of events. As I have pointed out, the finding of exactly the same pattern of inflammatory activation in the low oxygen air dive (but with moderate decompression stress) as the high oxygen UTD-RD dive, while a moderate oxygen GF profile did not produce any inflammatory activation makes it very hard to understand your confident conclusion. I would like you to explain it to me.

I asked you this first. When you answer it, I will address your question about supersaturation, and if I use any graphs they will be interpretable. Also, just a quick memory check. Do you remember how the last time you called integral supersaturation an "unproven, un-calibrated, baseless measure" it was pointed out to you (by multiple scientists) that the integral of supersaturation and time is at the central core of the mathematics of VPM? I can put the relevant formula up again if you really need reminding.

Simon M

No... your version of ISS and the VPM formula are not related..... your version of ISS is one giant number .... goes against the rules and concepts of parallel mono-exponential models, duplicates data, has no concept of relative stress, un-calibrated, not verified... etc, etc. But hey.... its looks good with pretty colors added..

*****

I don't have any information on O2 bio-markers causes and bio-physics interactions.... not my job. That is your field of work, but you have not given any information to back up your deep stop theory.

I don't think the authors looked hard enough at the ppO2 exposures. I think they overlooked the differences at 1.55 and 1.4, because when this is considered, the difference elevated ppO2 exposure is doubled. There are also other differences between the NDL profiles and deco (CDM\RDS) profiles, which we will look at too.

*****

Your argument Simon, seems to be is that a 2 to 3 min difference at 36 to 24m, is what caused this. Take a look:

Can you seriously suggest that the bio-marker change was from the difference of average 2 to 3 mins @ 27m? A 2 minute difference????

And what happens to the divers who do a 27 min dive, and no deeper stops (like you advocate). They will have the same amount on gassing.... will they have higher bio-markers too?

.