• BASIC DRUG
    DISCUSSION
    Welcome to Bluelight!
    Posting Rules Bluelight Rules
    Benzo Chart Opioids Chart
    Drug Terms Need Help??
    Drugs 101 Brain & Addiction
    Tired of your habit? Struggling to cope?
    Want to regain control or get sober?
    Visit our Recovery Support Forums
  • BDD Moderators: Keif’ Richards | negrogesic

Can't get high..?

btrswiet7u4ia

Bluelighter
Joined
Jun 6, 2008
Messages
411
Location
Here and there
Since my addiction to stimulants (that's as detailed as I feel comfortable with) I can't seem to get any kind of rush at all. I get high per say, but there's no notable euphoric rush.. Is that normal?
This is with my usual ROA - snorting. If I were to smoke it it may be different...
When I was on it (before I quit and went back) it was like every time I used I got this energy rush crazy.. awesome feeling. But now it's just like hardly there.

Has anyone else experienced this? To go back to your drug and have one good go with it and then not feel any rush?



BTW, potency not a factor with me- not street drugs
 
It sort of happened with me and opiates. The feeling was there but not the fast pickup. Change your method of administration and that will change. That of course has its own set of complications.
 
Yeah..
I'm scared to smoke because I did that for a couple weeks and I was just... deteriorating. I don't want to get back to how I was, yet, I want that feeling. Typical of addiction I suppose. Things are going so good for me too.
 
Are you sure that the quality and dosage is on par with what you "should" be doing? You might be underestimating your dose.
 
Are u sober at the time of using, or under the influence of any other Drug? Tolerance might be coming into play if u were indeed sober at the times of using but if u were high, the other drugs might be counter-acting against what ur using...Don't know =/ Just figured id throw that out there =/
 
Last edited:
I know exactly what you mean, and if your avatar says anything about your DOC, then I'm right there with you. I can't do coke anymore because that overwhelming euphoric onset that was once present is now gone :( (and I too will not resort to smoking or shooting it in order to regain that high). I think it's for the best
 
Are you sure that the quality and dosage is on par with what you "should" be doing? You might be underestimating your dose.

Quality's good, but I may not be getting 'enough'
But then again, I don't want to do so much that I just skip the whole pleasant part of it and have seizures instead (it's happened)
Are u sober at the time of using, or under the influence of any other Drug? Tolerance might be coming into play if u were indeed sober at the times of using but if u were high, the other drugs might be counter-acting against what ur using...Don't know =/ Just figured id throw that out there =/
Totally sober. Is there a possibility that coffee, tea, mtn. dew etc can create a cross tolerance to stimulants in general? I know that when I was drinking like a pot of coffee a day it took more amp to get me goin'...

I know exactly what you mean, and if your avatar says anything about your DOC, then I'm right there with you. I can't do coke anymore because that overwhelming euphoric onset that was once present is now gone :( (and I too will not resort to smoking or shooting it in order to regain that high). I think it's for the best
Not coke, but close enough. All stimulants have a very similar abuse pattern. I've noticed this in my 'friends', birds of a feather flock together.

sounds to me like a tolerance issue.. all you got to do is take a long(ish) breack from the stims to get those rushes you got before, maybe 1 or 2 months
8 months is a long break :(
 
Is there a possibility that coffee, tea, mtn. dew etc can create a cross tolerance to stimulants in general?

No. Caffeine has a completely distinct mechanism of action.
 
Caffeine is a stimulant.. so it's got to have some similarities. I don't think it would cause a cross tolerance like D-amphetamine vs. meth would, but there's got to be something
 
That's like saying that alcohol and heroin cause a cross-tolerance because both are depressants.

That's simply not how it works.

Caffeine is a CNS adenosine antagonist. It might prolong other drugs because of secondary mechanisms but it does not cause a cross tolerance with amphetamines.
 
That's like saying that alcohol and heroin cause a cross-tolerance because both are depressants.

That's simply not how it works.

Caffeine is a CNS adenosine antagonist. It might prolong other drugs because of secondary mechanisms but it does not cause a cross tolerance with amphetamines.

:Face palm: There is some cross tolerance between alcohol and heroin. Alcohol doesn't act directly upon mu-opioid receptors, but there's such a thing as downstream modulation. By some mechanism or another which I do not entirely understand, alcohol's antagonistic activity at voltage-gated sodium channels as well as at NMDA receptors results in an increase in opioidergic neurotransmission.

A similar thing happens with caffeine. Yes, it is an antagonist at adenosine receptors, but to look no further than that and conclude that there can't be cross tolerance between caffeine and amphetaminergics is simplistic and naive. Adenosine receptors are inhibitory, meaning that when activated then diminish the rate of release of certain neurotransmitters from storage vesicles, dopamine, epinephrine, norepinephrine, and others. An antagonist then would promote the release of these neurotransmitters.
 
Oh, I can't get high either, by the way. It's extremely frustrating. My situation is even more grim in that when I first started abusing drugs, my ability to experience pleasure was already greatly impaired on account of a long-standing depression.

My life consists now in sitting around wondering how long it will take for these FUCKING receptors to upregulate and whether or not I will be able to wait that long. In the mean time, I guess it's total boredom and anhedonia for me. Fun.
 
:Face palm: There is some cross tolerance between alcohol and heroin. Alcohol doesn't act directly upon mu-opioid receptors, but there's such a thing as downstream modulation. By some mechanism or another which I do not entirely understand, alcohol's antagonistic activity at voltage-gated sodium channels as well as at NMDA receptors results in an increase in opioidergic neurotransmission.

A similar thing happens with caffeine. Yes, it is an antagonist at adenosine receptors, but to look no further than that and conclude that there can't be cross tolerance between caffeine and amphetaminergics is simplistic and naive. Adenosine receptors are inhibitory, meaning that when activated then diminish the rate of release of certain neurotransmitters from storage vesicles, dopamine, epinephrine, norepinephrine, and others. An antagonist then would promote the release of these neurotransmitters.

It's true that indirect mechanisms of action exist with these drugs but their impact is so negligible that in terms of tolerance they are almost completely irrelevant.

With the example that you cite with alcohol, NMDA receptors are not activated by alcohol except in very high doses, and even then alcohol is still an extremely weak ligand. Anyone will argue that because of its clearly negligible effects on this receptor, its corresponding endogenous opioidergic effects are equally negligible.

The same rings true in the case of adenosine antagonism in the case of caffeine. The release of these neurotransmitters is a weak secondary effect. To argue that even heavy caffeine use would cause enough of a cross-tolerance with a potent drug acting on the DAT and SERT like methamphetamine to be noticeable would be foolish.
 
With the example that you cite with alcohol, NMDA receptors are not activated by alcohol except in very high doses, and even then alcohol is still an extremely weak ligand. Anyone will argue that because of its clearly negligible effects on this receptor, its corresponding endogenous opioidergic effects are equally negligible.

One of the principal pharmacological treatments for alcohol dependence is naltrexone. And opioid addicts typically express a total disinterest in alcohol on account the fact that a vast majority of the pleasure of alcohol intoxication is mediated by mu-opioid receptors but alcohol only produces mild downstream activation of those receptors. So... cross tolerance.

To argue that even heavy caffeine use would cause enough of a cross-tolerance with a potent drug acting on the DAT and SERT like methamphetamine to be noticeable would be foolish.

I never said that the cross-tolerance would be noticeable, but it probably does occur. How would one even measure this cross tolerance, by the way? If your first use of some amphetamine-like substance follows years of caffeine use, how can you say whether the experience would have been more stimulating or euphoric than if you hadn't used the caffeine? And if your first use of caffeine follows the use of some amphetamine, and then after having used caffeine for some time you once again betake yourself to the use of that amphetamine and you find it not to be as euphoric as the first time, how could you be certain whether it was the caffeine use or your first use of amphetamine that resulted in the downregulation necessary for a diminution of the hedonic effect or, indeed, whether or not it was some other factor entirely?

What I am saying is that you can't be certain of the veracity of your claims.

For what it's worth, I have experienced rather considerable euphoria and mania-like reactions as a result of caffeine use. I have experienced far more euphoria with caffeine than I ever did with dextroamphetamine. In fact, dextroamphetamine, which I used for the first time only after many years of very heavy caffeine use, didn't produce in me even a whit of pleasure or euphoria - not at 10mg nor even at 60mg. I got NOTHING out of it. I realize that that's anecdote and not proof, but it's better than nothing.
 
The mechanism through which naltrexone helps manage alcohol dependence is not known. Also, the second claim that you make in that paragraph is completely based on anecdotal evidence.

In response to your second paragraph, you are clearly splitting hairs at this point. The poster asked if caffeine tolerance would cause a corresponding tolerance to methamphetamine. The clear answer here is simply no. And I see that you are once again citing purely anecdotal evidence.
 
Top