Back in my raver days, when this was still doable, one of my boys started driving to Mexico and buying K there and bringing it back in cheap water bottles to get by the border DEA.
One day he shows up at the club and says, "hey, check out my car trunk" and was like "uhhh ok that's kinda weird" but I went out and presto, there was 4 one-liter water bottles full of ketamine.
Thats a shitload of K, considering a vial is 50ml and costs around $100. So I started selling it for him, and man did it go fast. Almost everyone loved it, including myself. Oddly enough, even people who did too much the first time and had a really wack k-hole experience would try it again.
It was rather miraculous to me, and surely did some sort of transformative rearranging of my brain while I was dosing it. I think what I remember best was that it became my self-described "drug of choice", which, honestly, was a pretty huge achievement in my life.
I liked it because it removed my desire to do other, much darker and destructive drugs somehow, and it wasn't just a matter of typical substitution, but something much more fundamental, so studies like this are very unsurprising to me, and I really hope these researchers keep at it.
I'm glad to hear you're alright. As I'm sure you know, dissociatives can be terribly addictive. I've watched friends with similar supplies (nowadays it comes in bulk powder from India) turn into the walking dead. That's not even to mention the permanent damage and having to urinate every 10 minutes.
In a rather elegant experiment, the authors deuterated ketamine at the methylene next to its carbonyl group, and showed that this compound (as expected) displayed the same NMDA activity as the parent compound – but that it was far slower at producing the metabolite, and had no activity in the antidepressant screens.
The "antidepressant screens" referred to here are in mice, not humans. The Nature paper is an amazing set of experiments that provide very compelling evidence that (2R,6R)-HNK is responsible for the antidepressant effects of ketamine in mouse models of depression, but Neuroskeptic is right that it's not clear that (2R,6R)-HNK is also responsible for the antidepressant effects of ketamine in humans. We know that mouse models of depression are not necessarily great; SSRIs seem to be more effective in mouse models than they are in humans.
Has there been any increase in illegal use of ketamine since research on its use as a depression treatment first started being published?
Having dealt with those issues for many years, and recovered, I can see a real danger in those who suffer from depression saying "K will fix this? I'll try anything". I would have.
I'm a firm believer in drug law reform and decriminalization of drug use but from what I've seen of it Ketamine isn't something you want people taking out of desperation, with little knowledge of how crazy it just might get. Or worse, developing a dependency on. It's pretty serious stuff.
I've used ketamine to self-medicate depression. I decided to out of desperation. It was extremely effective for me.
Several provisos for potential users:
- Read the papers. If you can't read the papers on K as a depression treatment and come up with your own dosing protocol, you probably shouldn't try K.
- Probably don't try it if you have an addictive personality.
- Make sure you're aware of potential side effects such as memory and urinary issues. That said, doses used in treatment protocols shouldn't come anywhere near that.
I waited forever to just get some goddamn K and treat myself, because everybody on the internet is like "don't do it, you'll fuck yourself up". I'm smart and do my homework, and I regret not trusting myself and suffering for longer than needed.
The blog says that HNK (the purported antidepressant) is a known metabolite of ketamine, but then claims:
> However, getting regulatory approval for such a study, which would technically (as far as I know) be a first-in-man trial of HNK, might take a long time.
I don't understand this. We already know that when we give ketamine to patients they are exposed to HNK. Is there a real risk that it is more dangerous in isolation?
Even if caution is required in the first patients, why do we accept as normal that developing treatments like this should involve years of waiting for bureaucratic approval?
Disassociatives have been used for a while in the treatment of opiate addiction, including the usage of higher doses of dextromethorphan to treat heroin addicts. To me it comes with little surprise that this could also be an effective treatment for depression, despite the fact that depression isn't necessarily something that can just be treated away. I've personally done more than my fair share of recreational ketamine and it seemed to aid my coping with some major life issues I've had, though I suppose this could also be placebo. Regardless, I'm glad these types of studies are being done and hope to see some more concrete evidence of positive effect.
Ketamine is still far too drastic and probably only really necessary when the depression is acute and prolonged. I would rather advise a non-SSRI like tianeptine. At least that is currently O.C. without an Rx required.
Edit: looks like HN has been down this very same road before[0] when Ketamine was brought up; and I'm smiling to see that I'm not the only one to think of Tianeptine in contrast to the drastic use of Ketamine. Psychopharmacology is the tried and true drug pusher of our times.
Well, afaik antidepressant doses of ketamine seem to be lower than 100 mg - which is quite a bit less than the most drastic of recreational doses - I don't know (but would love to see research conducted on) whether that's actually that risky.
Tianeptine is a mu-opioid receptor agonist, so it has abuse & addiction potential above therapeutic doses. It's also rx-only in many countries, according to Wikipedia.
Additionally, ketamine works for a week whereas it's not uncommon for people who use tianeptine to split their daily regimen into something like 3 separate doses throughout the course of the day.
At least neither require several weeks to reach efficacy while initially potentially increasing the severity of depression...
So this is what Nature has come to? Following up on a study where people took Ketamine once and felt good for a while? Nobody was doubting that people could get high on Ketamine. Isolating the most intoxicating metabolite is a bit useful, but it really bothered me that "studies" looking at a single dose of Ketamine and labeling the rather short effect "sustained" get so much press.
The Nature paper was about isolating a metabolite of ketamine that is not responsible for the intoxicating aspects, but is responsible for the antidepressant activities (at least in mice).
Yes, but these newer therapeutic uses have much lower dosing than recreational use. Recreational users take doses of about a gram or more. These thereutic doses tend to be on the order of 5 mg per kg of body weight.
(If you have any information about problems caused by long term low dosing I'd be really interested to read it).
It would be interesting to see how the various research chemicals out there - deschloroketamine, ephenidine, and others - would fare. There are anecdotal reports of varying levels of the antidepressant effect and they shouldn't be left unacknowledged.
Depression, like obesity, is acquired, habitual change due to environmental factors. Non fraudulent CBT (active traveling in a unfamilar environment as a simplest example) is enough to introduce persistent changes (that is why there are so many stories about profound changes people undergo after visiting the East - radical behavioral change will lead, through conditioning, to change in biochemistry - body is a dynamic, adaptive system).
There is, of course, no way to change one's physical or mental conditions without introducing changes to habits, daily routines and environment.
This is, of course, bullshit. I know two friends who acquired their depression genetically from their parents, and it manifested itself in them, and their siblings as well. At times they were extremely suicidal, and they described it as waking up and wanting to kill themselves every day, and not killing themselves was the biggest struggle they ever faced.
This may very well be true, however, some people may still need help in the form of drugs to get them to a point where they can actually begin to make those changes.
[+] [-] cubano|10 years ago|reply
One day he shows up at the club and says, "hey, check out my car trunk" and was like "uhhh ok that's kinda weird" but I went out and presto, there was 4 one-liter water bottles full of ketamine.
Thats a shitload of K, considering a vial is 50ml and costs around $100. So I started selling it for him, and man did it go fast. Almost everyone loved it, including myself. Oddly enough, even people who did too much the first time and had a really wack k-hole experience would try it again.
It was rather miraculous to me, and surely did some sort of transformative rearranging of my brain while I was dosing it. I think what I remember best was that it became my self-described "drug of choice", which, honestly, was a pretty huge achievement in my life.
I liked it because it removed my desire to do other, much darker and destructive drugs somehow, and it wasn't just a matter of typical substitution, but something much more fundamental, so studies like this are very unsurprising to me, and I really hope these researchers keep at it.
[+] [-] brbsix|10 years ago|reply
[+] [-] DanBC|10 years ago|reply
The studies I've seen for medical psychiatric use were about 5 mg per kg of body weight.
[+] [-] tshtf|10 years ago|reply
In a rather elegant experiment, the authors deuterated ketamine at the methylene next to its carbonyl group, and showed that this compound (as expected) displayed the same NMDA activity as the parent compound – but that it was far slower at producing the metabolite, and had no activity in the antidepressant screens.
[+] [-] simonster|10 years ago|reply
[+] [-] mabbo|10 years ago|reply
Having dealt with those issues for many years, and recovered, I can see a real danger in those who suffer from depression saying "K will fix this? I'll try anything". I would have.
I'm a firm believer in drug law reform and decriminalization of drug use but from what I've seen of it Ketamine isn't something you want people taking out of desperation, with little knowledge of how crazy it just might get. Or worse, developing a dependency on. It's pretty serious stuff.
[+] [-] lumpypua|10 years ago|reply
Several provisos for potential users:
- Read the papers. If you can't read the papers on K as a depression treatment and come up with your own dosing protocol, you probably shouldn't try K.
- Probably don't try it if you have an addictive personality.
- Make sure you're aware of potential side effects such as memory and urinary issues. That said, doses used in treatment protocols shouldn't come anywhere near that.
I waited forever to just get some goddamn K and treat myself, because everybody on the internet is like "don't do it, you'll fuck yourself up". I'm smart and do my homework, and I regret not trusting myself and suffering for longer than needed.
[+] [-] tominous|10 years ago|reply
> However, getting regulatory approval for such a study, which would technically (as far as I know) be a first-in-man trial of HNK, might take a long time.
I don't understand this. We already know that when we give ketamine to patients they are exposed to HNK. Is there a real risk that it is more dangerous in isolation?
Even if caution is required in the first patients, why do we accept as normal that developing treatments like this should involve years of waiting for bureaucratic approval?
[+] [-] YngwieMalware|10 years ago|reply
[+] [-] superobserver|10 years ago|reply
Edit: looks like HN has been down this very same road before[0] when Ketamine was brought up; and I'm smiling to see that I'm not the only one to think of Tianeptine in contrast to the drastic use of Ketamine. Psychopharmacology is the tried and true drug pusher of our times.
[0]: https://news.ycombinator.com/item?id=4615750
[+] [-] pizza|10 years ago|reply
Tianeptine is a mu-opioid receptor agonist, so it has abuse & addiction potential above therapeutic doses. It's also rx-only in many countries, according to Wikipedia.
Additionally, ketamine works for a week whereas it's not uncommon for people who use tianeptine to split their daily regimen into something like 3 separate doses throughout the course of the day.
At least neither require several weeks to reach efficacy while initially potentially increasing the severity of depression...
[+] [-] daodedickinson|10 years ago|reply
[+] [-] simonster|10 years ago|reply
[+] [-] alfonsoperez|10 years ago|reply
http://jneuroinflammation.biomedcentral.com/articles/10.1186...
[+] [-] KaiserPro|10 years ago|reply
[+] [-] DanBC|10 years ago|reply
(If you have any information about problems caused by long term low dosing I'd be really interested to read it).
[+] [-] droithomme|10 years ago|reply
[+] [-] mookerific|10 years ago|reply
[+] [-] dschiptsov|10 years ago|reply
There is, of course, no way to change one's physical or mental conditions without introducing changes to habits, daily routines and environment.
[+] [-] pfarnsworth|10 years ago|reply
[+] [-] nefitty|10 years ago|reply
http://www.theguardian.com/lifeandstyle/2015/jul/03/why-cbt-...
[+] [-] s_m_t|10 years ago|reply
[+] [-] a2m|10 years ago|reply