^ Very true about ketamine riding the psychedelic PR wave. I've surely said it before too, in fact I made a thread a while back arguing that the very grouping of dissociatives and psychedelics into one forum was sending the wrong message and not in line with BL's harm reduction ethos, although it got somewhat mixed responses and I guess I understand the administrative overhead involved with creating a whole new forum.
I'll admit, I was always kinda doubtful if this really made any difference. However I did a little reading about oral and nasal bio-availability and it seems there might be something to this.
Nasal bioavailability is generally reported to be around 25-50%, with
one study from 2003 recent study putting this figure at 45% - it's worth noting that this was with a nasal spray, so when snorting dry powder, as most people do, this figure is surely on the lower end, and will not remain constant over a session (generally tending downwards as the nasal passages get more and more clogged) and I have seen even low figures reported although I can't be bothered to go digging up the links right now and I don't think it will matter for this broscience analysis.
Oral bioavailability
seems to be around 59% - I've seen a lot lower figures reported also but this study also takes into account the contribution of norketamine, which evidently was not always included in other measurements. But the important factor anyway is that the greater the relative difference between oral and nasal bioavailabilities, the greater the relative impact of not swallowing the un-absorbed residue.
It we assume a (possibly optimistic) figure of 40% nasal bioavailability, and take the oral figure at face value, then spitting out the drip should yield almost a 50% reduction in the amount of ketamine you're consuming (
Percentage extra absorbed when swallowing drip = 100*(1-Nb)*Ob / Nb where
Nb = Nasal Bioavailability and
Ob = Oral bioavailability). Playing with the absorption values can move this figure up and down but it's still not an insignificant amount.
Obviously also there is the norketamine issue, I've never seen any studies directly looking at the difference between ketamine and norketamine toxicities - although there is evidence that ketamine itself does have some direct toxicities in vitro - but oral administration does seem to yield significantly higher quantities of norketamine compared to other methods of administration... and again, I'm not sure if it's ever been studied but there seems to be a general perception that intranasal administration is more likely to result in undesirable pathologies than IM.
Kind of veering even beyond broscience now into pure speculation, but relative to ketamine, norketamine has a 6-7 fold higher affinity for the α7-nicotinic acetylcholine receptor, and activity at this receptor is one of the methods by which nicotine increases atherosclerosis (arterial hardening) and
proliferation of certain types of cancer - again involving the epithelial-mesenchymal transition, that same biological mechanism that is theorised to be involved in ketamine-induced bladder damage in a few of the studies I linked previously. So perhaps there is something to the idea that norketamine is more toxic and thus oral ingestion and first pass metabolism should sensibly be avoided...
Disclaimer, obviously none of this speculation is a substitute for actual data. But, in the absence of any such data, maybe it's better than nothing. Personally I'm going to try not to do any more ketamine but if I do end up doing it again I'm definitely going to be spitting out the drip... just in case.
Besides that, don't have too much to say about this right now but thought it was an interesting look at some of the possible mechanisms by which ketamine causes organ damage, as well as a few different approaches to prevention and treatment:
Possible pathophysiology of ketamine‐related cystitis and associated treatment strategies
I can't remember where I read it now but I did read a report about one person who was successfully treated over the course of a year with oral chondroitin sulphate, which is used in treatment of non-ketamine associated cystitis as well, although typically only to relieve some of the symptoms - in this case supposedly they experienced a complete reversal of both symptoms and measurable damage, although I don't have any information to hand about exactly how far gone they were. If this is repeatable, obviously it's a slightly more convenient method of treatment than the hyaluronic acid route as it can be administered orally.
