Wait, I'm confused, regarding the cold showers/ice baths, you (Synth) are saying that they are in the realm of pseudoscience. You're talking in the context of stress relief, and not reducing inflammation, right? If cold water therapy doesnt decrease inflammation (initially), then my mind is blown.
A side note... Cold showers make me irritable and mean.
"Inflammation" is one of those words that has been co-opted by pseudoscience to justify all sorts of bogus claims.
Sometimes, inflammation is good. Sometimes it's bad. The important question is not "what does cold water do for inflammation?" The question is "what does cold water do to treat this particular condition?"
https://www.ncbi.nlm.nih.gov/pubmed/18212134https://www.ncbi.nlm.nih.gov/pubmed/26888646https://www.ncbi.nlm.nih.gov/pubmed/27294485Anyway, it looks like the jury is still out on whether CWI has any particular effect, but as with the breathing shenanigans, the downside is "generally harmless," unless you go off the deep-end and give yourself frostbite or something.
Also, since I can't help but beat a dead horse:
This is the study used by Innerfire/Wim Hof to justify the purported immunomodulatory effects of the breathing method.
The physiological breakdown is simple: the breathing method increases adrenergic drive (measured here by plasma epinephrine concentration), epinephrine up-regulates IL-10, IL-10 down-regulates TNF-alpha and other pro-inflammatory cytokines. Okay, that sounds legit at first.
1. The fact that voluntarily-induced respiratory alkalosis produces a larger epinephrine response might be a novel finding, so that's interesting. However, if you look at the charts in the study, the absolute increase is modest, although there does seem to be a marked increase in onset-of-maximal-epinephrine response. Furthermore, 3 hours into doing the breathing method, epinephrine response is more or less tracking with the control group, and after cessation, there's no significant difference. So if the breathing does anything, it only does it while you're intentionally hyperventilating. I suppose that could have some clinical implications, but I have serious doubts about the practicality of sitting there hyperventilating for hours at a time on a regular basis.
2. We already knew that epinephrine down-regulates IL-10, especially in the context of bacterial endotoxin, as far back as
1996.
So essentially, this is on the level of a science trick: you have something that works in a known way, and you initiate the sequence of events in a novel/unexpected manner that has questionable practical applications. I'd like to see the study repeated with a different treatment group that is exposed to a known epinephrine-inducer (like, say...exercise) for 30 minutes prior to endotoxin administration. I'd also like to see the study repeated measuring IL-10 reduction for those 2 treatment groups compared to another treatment group that receives some commonplace NSAID like ibuprofen, acetaminophen, or naproxen, because previous studies have shown that COX-2 products can induce/enhance IL-10 production.