The GP, guy that runs the practice, who is assigned as my personal GP, he is fully supporting it. Although its an off-license indication, and the only licensed indication for memantine is moderate to severe alzheimer's disease.
The reason I'd be using it is multi-fold. I find it both levels me out in a way very hard to explain or put into words, I can't really say how, but it does. The main aim is that it improves my executive functioning, it also nearly negates the issues I have with memory, and as additional benefits, as an NMDA antagonist with its unusual particular profile (although many other NMDA receptor antagonists also work for this purpose) its excellent for neuropathic pain in a way that opioids just aren't suited for, opiates being pretty poor for nerve pain.
Also it STAMPS on opiate tolerance with an iron-shod boot. Both tolerance that already exists, is driven down, and hard, fast, and it also helps a great deal in both dramatically lessening the development of tolerance yet to be, in degree, as well as in speed of that development.
I'd like to try pairing it with ultra-low-dose naltrexone too. Typically naltrexone, like the emergency opioid OD antidote naloxone (main differences are, naloxone lasts for maybe 10-15 minutes so I read, whilst naltrexone lasts for a day at least, maybe longer), acts to kick opiates off their receptors, and taken by anyone who is taking opioids longterm would immediately throw them into an incredibly extreme, severe and brutal precipitated withdrawal.
But when taken in, rather than doses around between the 25 and 50-100mg doses often used for opioid addicts who have physically detoxed and want to essentially opioid-proof themselves so that a relapse would result in the drug taken having no effect, it can also be used in doses of between maybe, when first starting, 500 nanograms to 1 microgram, building up to a few micrograms over time, and slowly, very, very slowly in tiny incremental stages, sometimes even higher than a few micrograms, it has a quite different effect profile. Rather than blocking opioid activity it enhances it, the mechanisms of action are thought to be preventing recruitment of beta-arrestin 2 to opioid receptors when they are stimulated by an opioid agonist (beta-arrestin 2 is a molecule recruited to receptors typically when activated by agonists to tag the receptor for internalization and recycling), also when activated, Mu-opioid receptors can it seems undergo a switch from being coupled to Gi/o type G-proteins that they couple to in their native state, which when activated, produce the inhibitory type responses that take place upon administration of a typical opioid (there also exists some biased agonists which are splice-variant selective, etc. or which don't induce, or else induce much less beta-arrestin 2 recruitment than most and less tolerance as a result, an example being herkinorin, a semisynthetic derivative of the compound salvinorin A, found in the mexican diviner's sage, Salvia divinorum, which is an extremely potent and highly selective kappa-opioid receptor agonist, which possesses very rapid onset, pretty short duration but intense hallucinogenic-dissociative effects as well as a propensity to do really weird things to sensory propioception, such as feeling for example that one's arms were swapped over, left to right and vice versa, and being turned elbow inwards [just imagine trying to light a pipe containing Salvia divinorum extract with THAT happening whilst the entire universe begins to be perceived in a multi-dimensional way completely alien to normal baseline perception, in five or six dimensions at least, potentially more in ways that would require complex math way beyond my ability even to draw, when all the while the room, or rather, the environment perceived that replaces the room whilst salvinorin acts, is sprouting vines, all over and through the walls while a little old lady stands outside, with no walls in a Mazatec shaman lady's herb garden, whilst living a thousand lifetimes as a plant which is grown exclusively from clones, as Salvia divinorum is, and has been for a long, long long time by the indigenous people who grow it, pushing up through her garden's soil and growing leaves, sprouting and growing leaves and vigorously thirsting for the sun, and the water sprinkled on one by your little old lady shamaness taking care of you)
Herkinorin is a Mu-opioid agonist as well, and a biased one that doesn't much induce recruitment that doesn't produce as much beta-arrestin 2 recruitment induced tolerance.
MOR agonists (typical opioids) apparently undergo the aforementioned switch between Gi/o type inhibitory G-protein coupling to GalphaS and other excitatory second messanger intracellular signalling cascades which results, with continual opioid use, it seems, in a subpopulation of MORs with an excitatory profile, which produces the opposite effects upon activation than one would expect, and ultra-low-dose naltrexone can suppress this, as well as an additional and powerful interaction with a regulatory region of the protein filamin-A, which, although I haven't read up on the deep molecular mechanics of the regulation process blocked, causes a very, very strong antitolerance effect on opioids.
I've even read of someone using ULD-naltrexone alone to reduce their tolerance from injecting 60-something milligrams of hydromorphone (dilaudid) every couple of hours to tapering off using CODEINE to take the worst of the edge off in just weeks. Thats fucking impressive. And together the combination of ULD naltrexone and memantine ought to be nearly unstoppable.
Memantine alone, I've tried, and it both nearly nullifies psychologically addictive properties of opioids when administered simultaneously, making a psychological addict who isn't physically dependent simply indifferent to cravings. It even enhances the euphoria-inducing properties of opiates whilst squashing compulsivity towards use.
Being that there are a great many benefits here for me, and even more if I can get my doc to pair it with ULD-naltrexone (he's aware of the concept too, and probably won't be averse to it), but all these things are atypical, extremely unusual uses of memantine, that I brought to the table and explained to my GP myself, along with bringing him both some printouts of supplementary journal research articles, as well as anecdotes about for example that hydromorphone IV addict and the way he killed his tolerance so fast and so powerfully, which normally, would have been at his dose a MASSIVE habit, a typical starting dose being just 4mg, and that being bloody powerful, although short-lived, it took years of trying but now he realizes that I've a lot of experience with the drug (memantine), that I know exactly what I'm doing with it, and how much suits me best how often, he is fully backing me.
But he needs formal approval from a specialist consultant, which he is pushing through as best he can, he thinks we might be close, and that it will be a matter of getting forms signed etc., dotting I's, crossing T's, but that it will be done, and he's prepared to fight for it on my behalf.
And once approval is gained from a specialist, etc. then I should think that he (my doc) will more or less defer to my knowledge of how my body interacts with memantine, and experience with dosages, cycling, and other such things. He's a decent guy, and as well, he isn't one of those high-and-mighty prick types, who take a patient with a superior knowledge of medicine in any area as apersonally offensive shit on their competence and reputation. Indeed he's told me before that when it comes to pharmacology/psychopharmacology and biochemistry that he knows full well that I am far, far, far ahead of his level of knowledge and competence, that much he just volunteered during several appointments. Wasn't mocking him or anything, but he realizes that in this case, I know best, safety-wise, with respect to my own reactions to it, what it can do, what I'm doing with the stuff etc. Should trust me once he can get the authority to write the prescriptions.
And besides, he doubtless realizes that I'll either find a suitable russian online pharmacy, or if I really, really must, I'll go all out and construct the entire 5,7-diethyladamantane skeleton itself, as a derivative with suitable leaving group at the 1-position and convert that to the final amino derivative myself, even if it means weeks or even months of preparation and work, and churn out a few kg at a time, so as to last me ages, after say, working on several individual 10s then 100s of gram batches to work out the details, fine tune everything, scale it all up and then make it amenable to large scale synthesis, to let me just do the job infequently, and make it in big batches to give me a large supply that'll last years.
He isn't daft, and I know he wants what is best for my health, so the logical conclusion from his point of view is to abandon any initial resistance, given I've been trying to get the ball rolling for years and only now is it beginning to move, albeit painfully slowly. And he'd probably rather I pick it up from a pharmacy rather than pop up to the lab and fire up the stills and vacuum line etc. then get to work making my own, on some sort of general doctor-principle.
And hey, a patient in need shouldn't HAVE to resort to making their own medication. I shouldn't have the need to do so, although if it doesn't get done soon enough then I'll get myself a small supply from an online pharmacy to help facilitate my working on making myself a good sized batch.
No, not for selling to people or anything, but just to last me a good long time without having to repeat the process regularly, larger batches should allow for higher yields, less wastage of precursors and reagents etc. And I'd sooner have enough to last me, that way I can always start the next batch before I even get low, and thus never run out, or get short.
"Is she gone yet?"