Opioids Advice for lowering tolerance?

[SaosinEngaged]

This is tricky. I'm a long term chronic pain patient. A few weeks back, I did a fast sub taper to try and get off everything and see if I could survive without painkillers. I couldn't. Screw the pain of WD, it's fiddlesticks compared to the pain of my shattered back (was hit by a drunk driver, blew apart my car and my spine, literally. I've had a Dr. describe my spine as if someone set off a cherry bomb under my skin next to my spinal column). The pain from my injury is so significant, it's life altering without something to damper it. So I'm back in pain management with a new doctor who, based on my history, will only prescribe me 90mg of Oxy/day with the possibility of getting on Opana in a few weeks (+ a boatload of other mostly useless meds, Tram, Lyrica (only good for WD for me), Celebrex...etc). The problem is, from the way I've acquired tolerance and through a bit (not a ton, but a bit) of misuse, I need AT LEAST 160-180mg of Oxy/day to get any real analgesia that I can deal with.

Obviously, given my prescribed dose and needed dose, this model just isn't sustainable. My question is, what can I do without abstaining from opiates (just not possible at this time), if anything, to lower my tolerance. If I forced myself down, and held at 90mg/day, would my tolerance lower? Or does it not work like that? The aspect of opiate use I know the LEAST about is how tolerance ebbs and flows.

Any advice for me? Without something I can't drive my car, let alone function at work. So I'm kind of in a predicament here.

Honestly, I know there's probably nothing that will really solve this problem, I'm just wondering if any of you geniuses have devised any tricks that may help with just what I'm asking. Thanks!

I've heard something about DXM, but have never tried it before and am a little leery, plus I have no idea how much to take, for how long, and what it does...etc.

 

[tricomb]

NMDA antagonists, like DXM.

Is MXE an NMDA antagonist? Ketamine is, although not as strong of an NMDA antagonist as DXM.

 

[SaosinEngaged]

Yup, that's what I've heard. How does that work?

And how much would I have to take for how long? Is it safe? I've never done DXM even once in my life and know nothing about its effects.

 

[tricomb]

I really don't know about that last bit, I've never done DXM either. Only taken a little bit when sick. I'm also looking into starting DXM for my tolerance.

Where's Toothpastedog, I feel like he knows a lot more about NMDA antagonists than I do.

 

[Tripman]

Aberrant nerve activity manifests as persistent hyperalgesia, allodynia, spontaneous pain, and expansion of painful fields as illustrated in the case. At the molecular level, activation of NMDA receptors initiates intracellular processes that cause enduring increases in neuronal excitability.4 EAA ligands such as glutamate bind to NMDA and initiate the opening of gated calcium channels, which leads to the hydrolysis of phospholipids mediated by guanosine triphosphate–binding proteins. Products such as and inositol 1,4,5-triphosphate increase the concentration of calcium.5 Diacylglycerol mediates activation of an important intracellular messenger called protein kinase C (PKC),6 which produces nitrous oxide that diffuses presynaptically to release more EAA.7 This EAA influx further activates NMDA receptors, creating a positive feedback loop. Activated PKC also binds to neuronal membranes, and this binding correlates with both hyperalgesia and opioid tolerance. Blocking the effects of PKC reverses morphine tolerance.8

Experimentally9 and as reported by Davis et al, NMDA antagonists such as ketamine prevent or reduce opioid-induced hyperalgesia. The critical question concerns how exogenous opioid administration activates NMDA receptors, and thus, might be involved in the production of pain.

Experimental evidence suggests that opioids potentiate the inward membrane current (depolarization) induced by EAA such as glutamate.10 Opioid receptor binding (eg, by morphine) also initiates second-messenger G-protein–mediated PKC translocation and activation.11 This opioid-mediated PKC activation removes magnesium blockade of NMDA receptors, which in effect “activates” the receptors. The resulting activation of NMDA receptors stimulates additional PKC translocation and activation, giving rise, yet again, to a positive feedback loop that can result in hyperalgesia and opioid tolerance. Clearly, the best initial management currently available for opioid-induced pain is NMDA receptor antagonists, because dose reduction or detoxification is not practical for patients experiencing severe pain.

Source

 

[tricomb]

I really need to go buy a bottle of Delsym.

 

[oxymoron310]

Drink 3 bottles of Delsym a day for a month straight and you might see some change... LOL

 

[Jabberwocky]

Obviously the only real way to lower your tolerance is to abstain from opioids, but as that is not possible for you OP, you have certain options.

1. Switch to a more powerful opioid
   
2. Switch to a more effective ROA
   
3. Start potentiating your opioids (since you're a chronic pain patient your doctors can help prescribe you things like hydrazine for this; I find ppi's like Tagamet to work amazingly well for potentiating opioids, especially when paired with an antihistamine)
   
4. Begin an NDMA receptor antagonist regime

Okay, here's the trick about NDMA antagonists like DXM (one of the most potent readily available ones): NDMA antagonists do not reduce tolerance (unless you take them while you're abstaining from opioids that is, but then of course what is primarily reducing your tolerance is the fact you're not taking any opioids!). What they do is inhibit further tolerance from developing. But this means you will have to take your NMDA antagonist with every dose of opioids you take. This is possible to do with doses of 30-90mg of DXM, especially once you develop a tolerance to it's dissociative effects (tolerance upon long term use of DXM dose not seem to form in terms of its NDMA antagonism).

Search BL for more info on NMDA antagonists being used to "lower" tolerance (again, what that really means is keeping tolerance from forming), especially: NMDA Antagonists for Tolerance, A Collection of the Evidence and Anecdotal