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Misc Tolerance to most drugs can easily be prevented

I assumed it all was due to DXM's depressant effects adding on to the alprazolam's effects, I never even considered the increase in glutamate and then the reduction of its transmission from DXM's NDMA antagonism to have played a role but that makes a lot of sense. This is why I joined here, and I'm sure as I get farther along in my major I'm gonna be accessing the wealth of knowledge you guys have a lot more :)

While I don't doubt DXM can boost the analgesic effect of morphine, increased analgesia doesn't correspond to increased euphoria IMO, maybe that's why I didn't notice much. I am a chronic pain patient and I can attest DXM definitely does modulate pain signals in some way, with it alone I notice the nerve pain from my herniated disc is taken down a small but noticeable amount. Combined with morphine/H there was plenty of times it felt like I was never injured, but there was no increase in euphoria that (maybe I'm mistaken in thinking) would signal a lower tolerance with equal doses. Maybe if I had stuck with it longer it could have prevented my tolerance from growing down the line but during those 2-3 weeks my dose crept up pretty much the same as it normally would with daily use.

I'm currently on about 2mg of Suboxone daily, what effects did you notice while taking them together? Is there a noticeable boost in mu opioid effect that you would say is more than what could be considered placebo? If Suboxone + DXM can dull my pain enough that I can get even a 2 point drop on the 1-10 pain scale that would be a godsend.
 
DXM itself is actually a very weak NMDA antagonist, its metabolite DXO is responsible for most of the NMDA blockade. DXM's major effect at low doses is more like that of a SNRI plus sigma agonist.
 
sekio said:
DXM itself is actually a very weak NMDA antagonist, its metabolite DXO is responsible for most of the NMDA blockade. DXM's major effect at low doses is more like that of a SNRI plus sigma agonist.
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Keep goingg..... i actually trust your information somewhat...
 
Posted in another thread:
It should also be noted that methadone is itself an NMDA antagonist.

NMDA antagonists work wonders for tolerance and dependence, and as was said earlier in the thread, seem to completely cancel out acute opioid withdrawal. Whilst I still require continual pain medication for my knee/hip problems, after a while taking diphenidine, at up to 1-1.5g/day whilst subject to an opioid tolerance sufficient to make required several shots of at least 120mg morphine sulfate (IV) per day, with between 20-30 and 70mg or so of oxy added to said shots, between 3-4xdaily, I was able to quite literally jump straight off the opioids, to 0mg daily, taking just the diphenidine and continue this for a week or so, and then find myself totally free of opioid withdrawal.

Most impressed. Now, my opiate tolerance has crashed through the floor, the doses of morphine/oxy I was formerly taking, if I take the same amount now, its enough with the reduced tolerance courtesy of the NMDA antagonist diphenidine to hit me like a runaway freight train and have me nodding harder than ever. If I combine the two, opiates AND diphenidine, then I actually feel I need to be somewhat careful in my dosing, so as to stay safe.

I'd rate it a life-changing wonder drug in fact, and not feel like that description was approaching being hyperbole, or overselling it in any way.
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sekio said:
DXM itself is actually a very weak NMDA antagonist, its metabolite DXO is responsible for most of the NMDA blockade. DXM's major effect at low doses is more like that of a SNRI plus sigma agonist.
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In the other thread most ppl took memantine, that may explain the difference in succes rates.
 
DXM only works for this purpose if it is dextromethorphan polistirex. The regular HBr metabolism is not appropriate for tolerance reduction as the DXO gets rapidly chewed up.

Memantine works very well and has far fewer side effects than DXM does.

I'm considering adding memantine to my taper because I'm completely stuck at 10mg of diazepam right now and I used it in the past to drop from 60mg to 20mg in the course of a month.

DXM + memantine together are a knockout combo. Memantine shows much more limited success in reducing tolerance and withdrawal if you are still using the drug while DXM will drop tolerance either way but combining them seems to work the best.
 
ThePredecessor said:
What about gabapentin ? Does dxm reverse the tolerance? That would be great becUse tolerance is rapid.
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PCP does so I think DXM would too.

Actually I seem to have created some kind of loop by using too much PCP while on gabapentin and I've felt dissociated for over half a year even though I haven't done any drugs besides my meds and some smoking. I'd be wary of doing this combo too much, it seems to interfere with the bodys ability to reboot the NMDA receptors. The gabapentin triggers dissociation again every time I take them now it's like doing a small dose of PCP too and this is affecting my day to day life pretty severely at this point and unfortunately I can not quit the meds because of horrific withdrawals and neuropathic pain.
 
DXM and GBP potentiate each other greatly... Be really careful with it. I was fucked up for like 18 hours after taking 600mg of GBP after being on 60mg of Delsym twice a day for three weeks. Really messed me up to the point everyone was thinking I was tripping on acid and not in the good way.
 
MagickalKat777 said:
DXM and GBP potentiate each other greatly... Be really careful with it. I was fucked up for like 18 hours after taking 600mg of GBP after being on 60mg of Delsym twice a day for three weeks. Really messed me up to the point everyone was thinking I was tripping on acid and not in the good way.
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Can you give me a simple (if that's possible) rundown of how NMDA antagonism correlates with mu-receptor upregulation? and also any more info on why polistrex is better than instant release DXM?
All of this thread is somewhat questionable in validity to me but i still seem to have success with taking DXM for tolerance reduction so i guess i really don't require any explanation if the shit works ahahahaha but then again i am very curious
 
I have heard quite a bit of success stories with maintaining Adderall tolerance with DXM, magnesium citrate, etc.

Yet, after repeated tries over a good period of time, I myself have had zero success. Perhaps I'm the exception? Sigh
 
OlahAcaciah said:
I have heard quite a bit of success stories with maintaining Adderall tolerance with DXM, magnesium citrate, etc.

Yet, after repeated tries over a good period of time, I myself have had zero success. Perhaps I'm the exception? Sigh
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What doses did you use? I suggest that you try memantine 40mg a day.
 
MeDieVil what you think about reverse tolerance to NDRI by NDRA and vice versa?
Competent person wrote me this:

„The subject is very simple: taking NDRI for years creates a tolerance not only in dopaminergic and noradrenergic receptors (their sensitivity or even quantities), but also in protein reuptake. NDRI no longer work as you need to. Taking DXM, etc. little bit helps, but not enough.
Of course break from NDRI helps, but turns tolerance very slowly.


I think a little about that and below I wrote what I suspect (not necessarily have to be truthful, I did not find adequate research on this topic):
Tolerance to NDRI formed on the specific substances and also includes a tolerance reuptake transporters (DAT, NET and sometimes SERT for SNDRI). For example, a dextromethylphenidate (d-MPH) have Ki value for DAT = 161, for NET = 206. In my opinion, the tolerance undermines this factor and so, for example, after a while the occurrence of tolerance, Ki DAT may be, for example 300-400, and add higher doses refutes for example to 250. In turn tolerance to NET can grow slowly and, for example at the normal dose will DAT Ki = 400, the NET = 206. Therefore, taking the higher dose did not give full effect, and only a partial improvement, but the deterioration of other effects (which is also certainly additional substrate [de]sensitization of receptors). I noticed that at methylphenidate and ethylphenidate there is cross-tolerance, due to the similarity of molecules.


I noticed that at metylofenidacie and metylofenidacie there is cross-tolerance, due to the similarity of molecules.
However, when given another NDRI this tolerance has not occurred (!!!). I tested this with a variety of other NDRI and NRI, including bupropion, reboxetine, 2-DPMP, even low doses of cocaine.
I conclude that tolerance to transporters (I note that this is still only my theory) is selective for certain substances, or one substance can no longer give full effect, but the second one did. That means that it is possible to administering of other NDRI also reverses tolerance to the NDRI which we taken for a long time, but are not just as strong as amphetamines (as describe below).


But this is not the end, another suspect is the acceleration transport reuptake (RE). I suspect that when administered to specified NDRI for a long time reuptake works faster and faster pulls back monoamine from synapses. It is known that type substances NDRI not block 100% monoamine transporter proteins, so some of them still active despite the action of the substance, and I suspect that this part increases the rate of uptake for reduce the effect of transporters blocked.






Here it comes the magical effect of amphetamines, or reversing the direction reuptake. For example, the PEA running on the DAT and the NET in such a way that the uptake is not blocked, but its direction is reversed. So DAT protein, and the NET "take" monoamines with bubbles nerve endings and "throw" them to synapses. PEA is therefore an indirect releaser (through reuptake transporters) and "blocker" (in quotes because uptake is not blocked, but it does not work in the usual way - throw monoamines to the synapse rather than take them into bubbles for future use).


Thus, DAT and NET if they are not blocked by the administration of amphetamine probably slow down the release of monoamines was not so strong. After a long time formed a kind of tolerance on the action of amphetamines on the uptake, but this tolerance is reverse tolerance to NDRI. Not enough, that tolerance to specific substance falls (eg on methylphenidate), it is still probable tolerance "speed" reuptake also falling. As a result, when will occur tolerance for amphetamine, repeated administration of NDRI should have a very strong effect.


I tested this process several times taking in cycles NDRI and PEA + sele. Every time I cycled the PEA when I back to NDRI everything work as it should. So far in my experience, it is the most effective way to reverse tolerance, no other has given me such spectacular results.


If anyone has other suspicions or any other explanation for this effect, let him write go ahead. For me the most important thing is that it works


I think that after such a cycle PEA few months could additionally increase the sensitivity of DA receptors by the administration of light neuroleptics / dopamine receptor antagonists. Currently, I am during administering tests PEA together with such antagonists. The effects of PEA are weaker (eg no euphoria), but still noticeable. For some time I'll report how this process will be effective (I plan to shorten the time needed to reverse tolerance to NDRI from a few months to eg. 2-weeks - months). I am happy to hear your views on this topic, because maybe something I missed and it should be taken into consideration.


Action PEA reversal of tolerance NDRI may also have a relationship with agonism TAAR1.


It is worth to look at the mechanism of action NET frontal lobe. While in other areas of the brain DAT rules the roost as the reuptake of dopamine, but in prefrontal cortex dopamine majority is captured by NET. And this part of the brain is responsible for, among others, planning, logical thinking, problem solving, etc., and is the most stimulating this part we feel eg. the after taken NDRI.”
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What are you think?
 
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