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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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@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.
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.
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.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.
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.
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....?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.
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.
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.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.
I am trying to evaluate the potential benefit or detriment of trying Ketamine.
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.
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.