Does abuse of amphetamines cause long-term anxiety? And if so, through what action?

[New]

I'm just wondering because I have massive anxiety and a history of massive amphetamine abuse. It would be nice to know if there is at least a correlation.

 

[lenses]

For some people long term heavy AMP use can cause dopamine receptor downregulation . Probally has something to do with my love affair with opiates after my two year AMP binge. I think I have some sort of long term anxiety issues from it , and the opiates helped . Doing better now though. I will comment more when i'm not posting from my phone.

-lenses

 

[negrogesic]

Possibly, but maybe not...

My past ultra high dose benzo abuse resulted in an increased level of anxiety, of which i still can feel. GABAergic damage, possibly?

 

[seep]

I wish someone would come through with some kind of explanation as to what permanent changes are brought about by chronic amp abuse. I'm very curiois about this too, but all there seems to be as far as research is amp used as a control for chronic murine mdma administration. And these don't even elaborate on what systems/regions the drug actually destroys.

I don't know that a permanent shift in DA receptor density is significant after chronic amp abuse. If so, how/why/where does this happen and why is it permanent? We can answer these questions for Parkinson's, Alzheimer's and even tardive dyskinesia, so if amp abuse did bring about permanent neurophysiological changes, we should be able to have some sort of info on pathophysiology.

Also remember that anxiety is an epiphenomenon and part of an out-of-control stress response, which itself is a blanket term for a suite of physiological processes that prepare an animal for self-defense. Anxiety is to a large part mediated by conscious activity. Answering this thread's question might be as hard as answering "What is consciousness?"

 

[kaskelot]

I wish someone would come through with some kind of explanation as to what permanent changes are brought about by chronic amp abuse. I'm very curiois about this too, but all there seems to be as far as research is amp used as a control for chronic murine mdma administration. And these don't even elaborate on what systems/regions the drug actually destroys.

I don't know that a permanent shift in DA receptor density is significant after chronic amp abuse. If so, how/why/where does this happen and why is it permanent? We can answer these questions for Parkinson's, Alzheimer's and even tardive dyskinesia, so if amp abuse did bring about permanent neurophysiological changes, we should be able to have some sort of info on pathophysiology.

Also remember that anxiety is an epiphenomenon and part of an out-of-control stress response, which itself is a blanket term for a suite of physiological processes that prepare an animal for self-defense. Anxiety is to a large part mediated by conscious activity. Answering this thread's question might be as hard as answering "What is consciousness?"

This is a good point, I feel.

 

[Lupus]

Its totally subjective.

If you're heavily using methamp than the residual effects will be far more pronounced than if you were just using straight oral dexedrine. Longevity of "runs" and if you eat and drink (water) during the period of said runs plays a large part also. Psychosis is the real enemy and all the strains and things it does to your brain.

 

[PsychedelicPeptide]

Also remember that anxiety is an epiphenomenon and part of an out-of-control stress response, which itself is a blanket term for a suite of physiological processes that prepare an animal for self-defense. Anxiety is to a large part mediated by conscious activity.

I'd have to look towards the stimulatory effect of amphetamine as an instigator of anxiety-type behavior over the long-term. Think about what amphetamine does: it speeds up your behavior & thinking, it is a stimulant.

Now ask yourself what anxiety is like. Anxiety is a sped-up behavior where you worry excessively about one thing or another. Kind of like you are on speed in terms of how your brain is thinking about the issue at hand, but there is no euphoria and if we are talking events that "induce anxiety" we are probably talking stressful or unpleasant ones.

So lets come back to amphetamine, what if you keep taking and taking amphetamine so that you're sped up all the time. Well eventually your brain is going to become accustomed to that behavior. With enough abuse you may become prone to displaying the phenotype of being high on amphetamine, ie being stimulated or sped up, even without taking the drug. Think about how stoners sometimes "act high" even when they have not smoked pot that day. They display residual effects of the drug even after it is gone from their system. But now in sobriety, without the drug in your system, you have no pleasure, no high, or any other effect. However your abuse has induced changes in your brain and it either needs the drug for you to "feel normal" or it will display residual effects and possibly result in you mimicking the lack of amphetamine, since you are now not using.

But what can you do that allows you to recreate the amphetamine high in your brain without actually having the drug? Well you can speed up your thinking for one, but how many of us really speed up our thinking past what we do when we are sober without the assistance of drugs? None of us pretty much right? UNLESS ... we are full of anxiety! Hence "amp withdrawal" = increased susceptibility to anxiety because your brain just wants to be high and sped up again. And unfortunately it just can't do it like that little amphetamine molecule can.

And there you have it a reasonable explanation to link the two. Of course I've never abused amphetamines nor have I seen anyone with these specific symptoms so I may or may not be even close to what kind of explanation you all are looking for. I have however used amps and have gone through many of my own anxiety bouts over the years so it's not like I haven't had a little taste of what is being discussed. I can relate with the stoner thing a lot though where you "feel burnt" or "slightly still high but not just slow" when sober.

So what do you all think about that explanation? Satisfactory? Or were you looking for more of a specific biochemical reason? I don't think much of anything could be said in that respect because the issue is much more grandly complex and we would probably have a hard time trying to say "Well it is the dopamine receptors in brain area XX specifically" because if what we are talking about is an actual change in behavioral phenotype then we are probably talking changes throughout the entire brain and consciousness machinery (ie, rewired brain circuits or loss of existing ones) as well as changes in protein expression and regulation beyond just the dopamine receptor itself.

 

[pofacedhoe]

from what i can tell with my own abuse and that of others damage to dopamine receptors occurs in the higher thinking areas-prefrontal cortex

http://content.karger.com/ProdukteD...t&ArtikelNr=193395&Ausgabe=0&ProduktNr=224107

the thing about doing speed is that after abuse it really messes up your ability to think clearly, organise things, remember stuff, control yourself and delay gratification

 

[Sturnam]

Anxiety is to a large part mediated by conscious activity.

Normally I would totally agree, but I think that amphetamine abuse might cause physiological changes that would greatly enhance anxiety. Somewhat relatedly, I recently read a review of PTSD and the related pathophysiology. Sufferers of PTSD have enlarged amygdalas and a smaller prefront cortex. This means that the PFC is less able to regulate the amygdala and the amygdala is much more active than in healthy controls. Thus, the amygdala is activated by much more subtle cues, that the person is unaware of consciously. This can lead to anxiety/panic attacks where conscious activity has nothing to do with it.

Now, AFAIK, there is nothing showing this same type of thing in chronic amphetamine abusers. However, I'd be really surprised if there wasn't some type of physiological change that had this effect. It's well proven that addiction can have permanent changes to several different areas of the brain, so I'm sure one of them would have this type of effect upon ceasing use of the drug.

 

[PARooolller]

Its totally subjective.

If you're heavily using methamp than the residual effects will be far more pronounced than if you were just using straight oral dexedrine. Longevity of "runs" and if you eat and drink (water) during the period of said runs plays a large part also. Psychosis is the real enemy and all the strains and things it does to your brain.

Agree...The exacerbated symptoms of anxiety from heavy abuse of dextroamp (doses over 300 mgs in 24 hours) seemed to only last about 4 months...

 

[seep]

I don't think much of anything could be said in that respect because the issue is much more grandly complex and we would probably have a hard time trying to say "Well it is the dopamine receptors in brain area XX specifically" because if what we are talking about is an actual change in behavioral phenotype then we are probably talking changes throughout the entire brain and consciousness machinery (ie, rewired brain circuits or loss of existing ones) as well as changes in protein expression and regulation beyond just the dopamine receptor itself.

This last paragraph is begging for some discussion of chronic amp's effect on neurotrophic factors. The rest is just Pavlovian conitioning (which isn't without merit: I still get the shits every time I decide to go out and cop some heroin [bell=salivating dog]).

 

[seep]

Sufferers of PTSD have enlarged amygdalas and a smaller prefront cortex. This means that the PFC is less able to regulate the amygdala and the amygdala is much more active than in healthy controls. Thus, the amygdala is activated by much more subtle cues, that the person is unaware of consciously. This can lead to anxiety/panic attacks where conscious activity has nothing to do with it.

Hey, this sounds really familiar. Didn't this series of symptoms lead to the development of some drug?

 

[Sturnam]

Hey, this sounds really familiar. Didn't this series of symptoms lead to the development of some drug?

I'm not sure if it did. It seems like all the studies dealing with this issue in humans are from 2005 on, so if they did develop some drug, then it would have to be really new and experimental.

 

[seep]

I'm not sure if it did. It seems like all the studies dealing with this issue in humans are from 2005 on, so if they did develop some drug, then it would have to be really new and experimental.

Oh it came to me. It's THC, which temporarily shrinks the amygdala. I can't remember if there's actual research going into this or if its just a drummed-up rumor. In the US, dronabinol can be prescribed for any number of reasons with varying amounts of regulatory scrutiny, so it wouldn't be surprising if this is already being used on patients (not saying its effective, just saying).