Anyone tried ketamine?

Messages
679
Likes
1,190
Location
Israel
@redrachel76 I know we discussed this privately but I am yet to be able to try the lidocaine/ketamine infusions here in Toronto because every damn clinic does the infusion in 30-60 minutes and not by Goldstein's preference of 2-3 hours. I guess when you saw Goldstein he only tried the ketamine solution on you and not the IV?

I'm still unsure what to do. I really want to try this treatment but don't want to risk a further deterioration of my condition, which unfortunately continues to deteriorate. I'm tempted to do the 30-60 min infusion but also reluctant considering how many times in BBTB and TTB he warns against this.
The oral ketamine sounds wonderful. If you can do that, then try that instead. How I wish I could get ketamine here to try for pain.

Also if the doses are 1/2 of what Goldstein gave, yes it would be conceiveable to cut the time in half.

I only tried the ketamine nose spray, not the IV.
Don't listen to what everyone says here about it having to be longer, of course it would be better on Goldstein's protocol but we can't have it so try whatever they give... don't waste time.. It is still far better than nothing.

I get lidocaine infusion here in Sheba hospital Israel for pain. It is over 1.5-2 hours, probably nothing like Goldstein's protocol dosage and it is fine. It just makes me dizzy and improves the pain a little. Take whatever you can get and be glad you can try it.
 
Last edited:

Thomas

Senior Member
Messages
325
Likes
438
Location
Canada
Thanks for those details. I notice the page you got them from appears to be available to read here on Google books. Dr Goldstein does not seem to give the actual mg ketamine doses used on that page, but just the concentration of the liquid ketamine solution (concentrations of 1:10 or 1:1).

Although nasal sprays are typically metered around 0.1 ml for each spray, so it should be possible to work out the mg dosage of ketamine in each 0.1 ml spray.


Looking that page, Goldstein appears to be using ketamine there as an agent that acts locally on the trigeminal nerve (a nerve which is found in the eyes, nose and mouth), rather than an agent that has a systemic effect. So he may be using lower doses of ketamine for this local purpose.
I looked up in " Tuning the Brain" p349.
It says he used Ketamine nasal spray 1:10 or 1:1 and oral swirl 1:1
Whatever that means. It is a shame I don't have the original bottle it came in.

I took it for pain and exhaustion, not anhedonia.
In Tuning the Brain, simply using the index to find the correct page for information you are looking for simply isn't enough. In classic Goldstein style, he will start talking about one drug and then by the end of that paragraph he will be on a completely different drug and totally different tangent.

Anyways, with respect to the dosage he used for nasal sprays and eye drops, on page 60 of Tuning the Brain he mentions that he Rx's ketamine for these delivery methods at 50 mg/ml diluted 1:10. He doesn't state the type of ketamine or what the percentage it is (not sure that's important). But with this information, is it enough to be able to correctly ask a doctor to Rx? Regardless, hope this helps.

As for ketamine gel I've seen Goldstein use anywhere from 80mg/Gm - 240 mg/Gm.
 
Messages
1
Likes
0
To me the research into ketamine is fascinating since the only things to ever touch my anxiety/depression have been gaba related. Although not approved by the FDA there are plenty of ketamine clinics across the country treating individuals for pain/depression via IV infusion.

When I first suspected glutamate/gaba imbalance I started a ketogenic diet as its theorized to lower levels of brain glutamate. I've had to play around with the diet but once I got it right I'd say 75% of my issues went away. The other 25% was taken care of by supplements that are known to be nmda antagonists: zinc, magnesium, taurine, cats claw.

Right now I'm good but if depression/anxiety comes back I'm heading straight to a ketamine clinc....or taking one of the new ADS that mimic ketamine without the supposed side effects
 

redaxe

Senior Member
Messages
230
Likes
302
Hi. If you have depression that you suspect is related to glutatmate (and thus excitotoxicity and oxidative stress) you should consider N-Acetyl Cysteine.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3967529/
There is an expanding field of research investigating the benefits of medicines with multiple mechanisms of action across neurological disorders. N-acetylcysteine (NAC), widely known as an antidote to acetaminophen overdose, is now emerging as treatment of vascular and nonvascular neurological disorders. NAC as a precursor to the antioxidant glutathione modulates glutamatergic, neurotrophic, and inflammatory pathways.

I've had considerable success with this supplement but I haven't yet tried the sustained release form but I plan to next time I top up my supply. One challenge with NAC is that as I understand it, it doesn't have a particularly long half life in the body hence the sustained release may be a better option - even if it costs a bit more.

- http://au.iherb.com/product-reviews...cetyl-L-Cysteine-600-mg-100-Tablets/135/?p=17
 

Sushi

Moderation Resource Albuquerque
Messages
19,681
Likes
34,192
Location
Albuquerque
Has anyone tried ketamine recently? If so, what was your experience. I am asking because a doctor yesterday suggested a low dose ketamine IV for me to reduce brain/nervous system excitotoxicity. @Hip have you come across anything new on this?
 

Sushi

Moderation Resource Albuquerque
Messages
19,681
Likes
34,192
Location
Albuquerque
@Sushi Did you see @Hip's post about hydroxynorketamine (HNK), the active metabolite of ketamine?
Thanks, yes, I saw it. But the question for me would be whether it is NMDA receptor antagonist aspect of ketamine that reduces excitotoxicity or some other aspect. HNK is not an NMDA receptor antagonist and does affect depression, but I am not seeking the antidepressant qualities of ketamine.
 

nandixon

Senior Member
Messages
1,092
Likes
3,152
@Sushi, I figured you weren't looking for the antidepressant quality, but I think HNK is likely where the energy invoking aspect of ketamine is coming from (via activation of the mTOR pathway for purposes of improving the PDH complex's production of acetyl-CoA, not for improving depression). And I bet that's where the benefit was coming from for Dr Goldstein's ME/CFS patients.
 

Sushi

Moderation Resource Albuquerque
Messages
19,681
Likes
34,192
Location
Albuquerque
I think HNK is likely where the energy invoking aspect of ketamine is coming from (via activation of the mTOR pathway for purposes of improving the PDH complex's production of acetyl-CoA, not for improving depression). And I bet that's where the benefit was coming from for Dr Goldstein's ME/CFS patients.
So, as I understand it HNK is in the investigative stage whereas ketamine is used clinically. I'm wondering about the downsides of trying ketamine? Obviously dosing, timing of doses and rates of infusion would be important, but if the doc could get that right....?
 

Hip

Senior Member
Messages
16,440
Likes
35,454
But the question for me would be whether it is NMDA receptor antagonist aspect of ketamine that reduces excitotoxicity or some other aspect. HNK is not an NMDA receptor antagonist and does affect depression, but I am not seeking the antidepressant qualities of ketamine.
It was originally assumed the NMDA blocking effect of ketamine was the likely mechanism of its antidepressant effect, but I understand in the light of this new HNK finding, it is now known that ketamine's metabolite HNK is primarily responsible for the antidepressant action.

Whether HNK might also play a role in ketamine's benefits for ME/CFS that Dr Goldstein found, I am not sure; perhaps for ME/CFS, it may a combination of ketamine's effects, including NMDA blocking, that provides the benefits.

Apart from that, I have not come across anything new about ketamine for ME/CFS.

Did you see the thread: Five Ways To Reduce Your ME/CFS "Wired But Tired" Hyperaroused Brain State ?

That thread focuses on five ways to reduce elevated brain glutamate.
 

Sushi

Moderation Resource Albuquerque
Messages
19,681
Likes
34,192
Location
Albuquerque
Did you see the thread: Five Ways To Reduce Your ME/CFS "Wired But Tired" Hyperaroused Brain State ?

That thread focuses on five ways to reduce elevated brain glutamate.
Yes, I read that thread. The question came up for me since a doctor suggested giving me IV low dose Ketamine. I do not feel the usual wired but tired symptoms but I may just be conditioned to them. I already follow a lot of the recommendations in that thread, so I am trying to evaluate the potential benefit or detriment of trying Ketamine.
 

nandixon

Senior Member
Messages
1,092
Likes
3,152
@Sushi, Forgot to mention that by activating the mTOR (mTORC1) pathway, that also decreases SIRT4 repression of the glutamate dehydrogenase enzyme. This increases the conversion of glutamate to alpha-ketoglutarate.

Thus you reduce glutamate before it has a chance to be a problem with respect to the NMDA receptors. So there's no need (in theory) for the NMDA antagonist aspect of ketamine because you've already taken care of the problem upstream by increasing mTOR (and energy) with HNK.

As far as actually trying ketamine itself, I hope you can figure out what's best.
 

Hip

Senior Member
Messages
16,440
Likes
35,454
I am trying to evaluate the potential benefit or detriment of trying Ketamine.
I don't actually know very much about ketamine treatment, Sushi. I have not tried it myself, but just read a few posts on this forum by people who have tried it.

I just did a quick forum search and found that: @redrachel76 said for pain, it stopped working for her. @Misfit Toy also found that it was working well, and then suddenly lost a lot of its effects. @Thomas got negative effects from ketamine.

Let's say it did provide you some benefits; would that then require you to undertake ketamine IVs several times a week to maintain the benefits? I guess that would be OK if you have a conveniently local clinic or doctor.

Of course, you can also take ketamine power intranasally by spray; that's how it was administered in several studies examining the antidepressant of ketamine.

If you look at Dr Goldstein's book, he administered ketamine orally, intranasally and even in the eyes (conjunctivally), and he talks about its effects on the trigeminal nerve (which runs to the face, mouth, teeth nasal and sinus cavities). I am not sure if Goldstein also performed ketamine IVs, but I am guessing these might work in a different way to when ketamine is used more locally to target the trigeminal nerve.
 

Tunguska

Senior Member
Messages
516
Likes
513
One thing of interest with ketamine is that oral or intranasal administration of ketamine hydrochloride (ketamine HCl) has been shown to work just as well for depression as IV ketamine (although a study found that with oral or intranasal administration, it took a little longer for the antidepressant effects to kick in, compared to IV).
[...]
Note: this post was updated on 19 Jan 2017.
Ah there we go, nice post (never saw your original one). The NMDA antagonism always seemed like a bit of a red herring so I discarded it. That and the fact the antagonists lower my IQ consistently.

But the AMPA agonism angle gives them new life, I figured it's like "channeling" the glutamate (down the BDNF/mTor river). I want to try Agmatine since reading it fits this profile: https://www.ncbi.nlm.nih.gov/pubmed/27061850 (2016). Nice to see some people tried it, a few good reports on other forums too. I wonder how much of the benefits of Arginine can be attributed to it (metabolite). Anyhow I doubt it'll substitute for Ketamine alone so I want to try it in concert with others and high protein in particular (won't be for awhile, post office sent my packages to china or something).

Thus you reduce glutamate before it has a chance to be a problem with respect to the NMDA receptors. So there's no need (in theory) for the NMDA antagonist aspect of ketamine because you've already taken care of the problem upstream by increasing mTOR (and energy) with HNK.
I imagine this is hard to quantify, but in the context of high protein diets together with illness* I think you want all the help you can get. The recommendation going around is whey protein (as usual), and it's one of the most quickly absorbed, and practically all protein have more glutamic acid than any other amino (even gelatin is high), so unless you take only free aminos, you'll get quite a bit. Then you're going to add glutamine... Protein is highly desirable but also quite a burden. (Similarly I valued TUDCA most in context of high protein for its likely help in metabolizing) (*where high protein is relative based on illness and they can become interchangeable terms... I'm probably not communicating this properly)

(Thanks for bumping this thread)
 
Last edited: