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Sorry...you were the OP.
Your first post was an elaborate "science" presentation.
When challenged for evidence, you adopt a defensive pose suggesting that we're being unreasonable asking for published backup. Obvious that you've never published before. What a load of codswallop.
Your first post was an elaborate "science" presentation.
When challenged for evidence, you adopt a defensive pose suggesting that we're being unreasonable asking for published backup. Obvious that you've never published before. What a load of codswallop.
Balderdash. You tried to answer @Diver0001 with a meaningless quote. It's all in the thread. If you had no intention of substantiating your OP (and responding to him). why did you do that? Hoisted by your own petard.
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
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
This is great. Just great.
Michael Guerrero
Contributor
My suspicion is that it was due to their approach. They did their bubble scoring 30 minutes after the dive. Big bubble differences show up usually an hour or two after a dive in the studies I've seen--and deep stop and bubble model profiles always cause more and bigger bubbles. They took their blood samples 90 minutes after the dive, which is when you would expect to start getting the bubble showers through your bloodstream. It seems very plausible to me that had they done their bubble scores when they took the blood (at 90 minutes), they would have seen a correlation between bubbles and inflammation.
That said, I like this study because it is exactly what people dissatisfied with the dive profiles in the NEDU study asked for. Real profiles using real gases. And it showed that profiles that emphasize deep stops cause more inflammation even than a dissolved gas model that has been modified to create deeper stops.
Dan_P
Contributor
Hi Simon,
I apologize in advance for this interjection.
I don't mean to deflect from the branch of discussion on the aptness of the Spisni-study in supporting that (over-)emphasis on deep stops can be problematic, nor underplay the contribution of that study - this is purely to touch on the branch of discussion on whether O2-exposure can be correlated to inflammation;
This is relevant to all divers regardless what level of deep stop emphasis - and method - they employ, as it touches also on the generally applicable exposure to high ppO2s of any generally employed decompression schedule.
While we're still talking in hypothetical terms, it's well established that there is a correlation across even mild and aclinical hypoxia, and inflammation, but of course the question here is whether there is also a relation across hyperoxia and inflammation.
I would argue that it's not an unreasonable hypothesis.
Looking at studies in mice[1], it is in fact documented that hypoxia does produce an inflammatory response, but of course we can't thereby prove a relation to CCL2 and, particularly, CCL5, nor that this all even has significance in humans or diving.
But I'd argue that the hypothesis is reasonable enough to give serious consideration.
[1] "Time course of inflammation, oxidative stress and tissue damage induced by hyperoxia in mouse lungs", Int J Exp Pathol. 2012 Aug; 93(4): 269–278, Akinori C Nagato,* Frank S Bezerra,† Manuella Lanzetti,* Alan A Lopes,* Marco Aurélio S Silva,* Luís Cristóvão Porto,*and Samuel S Valença.
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Intuitively, one might expect a greater oxygen exposure to induce greater inflammation levels, due to oxidative stress. This study, however, suggests the opposite and fails to support what Ross is suggesting.
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