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  • BDD Moderators: Keif’ Richards

Amphetamine harm reduction

The mechanics and "proof" behind the neurotoxicity of oral amphetamine is vague at best. The lack of sleeping and eating is probably the true culprit in the whole affair. As it is with amphetamine psychosis.

I've been taking oral dexedrine (the dextro isomer) for years and the most important advice is "less is more". Amphetamine is not about chasing the euphoria and it will forcefully make you understand that, with very real psychological consequences if you push it. Treat it like a tool and respect it, you'll find it to be one of the most helpful substances when it comes to intensely intellectual jobs or activities.
 
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I really wanna try shooting amphetamine-laced water up my rectum... lol... Im actually serious, How do you go about this? I tried to plug E once, and the pill just fell out 8 hours later and some kid was willing to eat it lol
 
I havent read anything but the OP.

But by amphetamine do you mean actual speed (literal amphetamine?), keep in mind most "speed" these days is actually methamphetamine (from testing me and friends have done, the amount of actual amphetamine has all but dwindled to a rarity in the past 5 years)

Now, if you mean amphetamine as a catch all for mdma, mda, meth, speed etc etc then what are you specifically wanting to do, as realistically there are different methods for protecting yourself on each, and rightfully so.

Why couldnt I have just stuck to chemicals *sigh*, then I wouldnt be on methadone now :(
 
motiv311 said:
I really wanna try shooting amphetamine-laced water up my rectum... lol... Im actually serious, How do you go about this? I tried to plug E once, and the pill just fell out 8 hours later and some kid was willing to eat it lol
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It's incredibly easy.. crush substance and dissolve into some water. Draw the water into a needleless syringe and squirt it up into your bowels.

The quick onset, rush, long duration and high are easily better then oral/snorting. Less side effects too, feels alot smoother and cleaner.
 
Lupus said:
The mechanics and "proof" behind the neurotoxicity of oral amphetamine is vague at best. The lack of sleeping and eating is probably the true culprit in the whole affair. As it is with amphetamine psychosis.
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I'm sorry, but this is far from true. Neurotoxicity caused by amphetamines is a side-effect of the overproduction of dopamine that they cause. The neurons become stressed as the metabolic processes inside them that produce dopamine are ramped up significantly, and they are also harmed by several of dopamines toxic metabolites that form because dopamine is being released in quantities beyond what the cells can re-uptake or destroy via enzymes.

An earlier poster asked about "how much" of an amphetamine drug has to be taken before neurotoxicity kicks in. This would be a recreational amount of the drug, because this causes the excess flood of dopamine. So, virtually every time an amphetamine is used recreationally, dopaminergic neurons die.

This is a problem for people, because long-term use kills of these dopaminergic neurons throughout the body, including those in the subtantia nigra which are necessary for motor function and movement. Individuals with parkinsons disease have experienced accelerated death of these neurons, which causes their symptoms. An individual needs to lose around 70-80% of these cells in the substantia nigra to start exhibiting Parkinsonian symptoms. We lose these cells at a rate of 0.5%-1% a year as a normal process of aging, but using amphetamines speeds this process up by killing off these neurons more quickly. These neurons do not re-grow or recover.

The substantia nigra is just one area of the body where dopaminergic neurons are found, and there are many more. I just wanted to bring this up, because people seem to think that what doesnt kill them didn't do any harm, and in this case it can do alot of harm.

Here is a PET scan showing the extent of damage that use can cause. Note that when these scans were taken, the methamphetamine user had been completely off of the drug for 3 years, as was the methcathinone user. To the far right is an individual newly diagnosed with parkinsons disease.

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^thats a meth abuser. . . What about normal adderall usage? Plus if you take proper supplements. Neurotransmitter supports *5htp tyrosine sam-e , b12, etc. with the proper hydration and REM sleep, I would say your brain would grow.
 
motiv311 said:
^thats a meth abuser. . . What about normal adderall usage? Plus if you take proper supplements. Neurotransmitter supports *5htp tyrosine sam-e , b12, etc. with the proper hydration and REM sleep, I would say your brain would grow.
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It's a fundamental fact of neurophysiology that neurons do not regrow. No matter how many supplements they take, a quadriplegic will always be quadriplegic.

And as I said in my post, unless a recreational dosage is taken where there will be an overabundance of dopamine produced, normal therapeutic dosage probably will not cause neurotoxicity.
 
good post dokomo. that helped me a lot.

so basically everytime we get high off of amphetamines we increase our chances of getting parkinson's at a later stage in life?

And is there anyway to lower the .5%- 1% of neurons that we lose each year?

and this applies to coke, adderall, ritalin, and benzedrex as well?
 
dokomo said:
I'm sorry, but this is far from true. Neurotoxicity caused by amphetamines is a side-effect of the overproduction of dopamine that they cause. The neurons become stressed as the metabolic processes inside them that produce dopamine are ramped up significantly, and they are also harmed by several of dopamines toxic metabolites that form because dopamine is being released in quantities beyond what the cells can re-uptake or destroy via enzymes.
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You should note that i said oral amphetamine, route of administration is the determining factor. The faster blood/serum levels the quicker the cascade of dopamine being released from DAT cells and damaging receptor sites.

Dont bother trying to quote one of ricaurte's studies on the subject.

The level of 5-HT release is what causes such a drastic difference in damage done to amphetamine vs methamphetamine users.

You were clearly confused about the content of my post and while your post was informative it was misleading.
 
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Lupus said:
You should note that i said oral amphetamine, route of administration is the determining factor. The faster blood/serum levels the quicker the cascade of dopamine being released from DAT cells and damaging receptor sites.

Dont bother trying to quote one of ricaurte's studies on the subject.

The level of 5-HT release is what causes such a drastic difference in damage done to amphetamine vs methamphetamine users.

You were clearly confused about the content of my post and while your post was informative it was misleading.
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ROA is A determining factor, certainly not THE determining factor. Oral amphetamine can still cause neurotoxicity. Amphetamine has excellent oral bioavailability.

What is your problem with Ricaurte? Its a bit foolish to tell me not to mention him when he's one of the leading researchers in specifically what we're talking about. If you're referring to the MDMA study, the problems there are still under investigation and are just as likely attributable to the experimental supplier as anything else.

I was not confused with the content of your post, I simply disagree with it based on my understanding of the mechanisms involved. Methamphetamine is certainly more readily toxic to dopaminergic neurons than amphetamine, but amphetamine is still neurotoxic.
 
Korn3x said:
good post dokomo. that helped me a lot.

so basically everytime we get high off of amphetamines we increase our chances of getting parkinson's at a later stage in life?

And is there anyway to lower the .5%- 1% of neurons that we lose each year?

and this applies to coke, adderall, ritalin, and benzedrex as well?
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Well technically not Parkinson's, just Parkinsonian symptoms. Parkinson's disease itself is a bit more of a mystery as we don't fully understand what mechanism causes the neurons to die in individuals with this disease.

As far as I know there isn't any way to lower that decline. Certainly preventing exposures to known neurotoxins such as herbicides and pesticides would help, but there will always be some amount lost as we age. With few exceptions, we're born with all of the neurons we will ever have so its important to protect what we've got.

It applies to adderall and ritalin at least, cocaine does act on dopamine, but moreso on 5-HT or serotonin receptors. I believe the active ingredient in Benzedrex is adrenergic so it would act on ephinephrine or norepinephrine, I can't remember which off the top of my head. Its important to note that some amphetamines are more neurotoxic than others, but they all can cause neurotoxicity at recreational doses.
 
motiv311 said:
Are you sure about this? ^^ Any scientific support for that ?
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Positive. I'll try to look it up in my old textbooks. There are only two exceptions, one is a specialized type of neuron in the olfactory cortex and I can't remember what the other one was.
 
my shrink says thats not really true. . and that no one has proven neurons are not regenerated
 
motiv311 said:
my shrink says thats not really true. . and that no one has proven neurons are not regenerated
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Havent had time to scan the old textbooks yet, but how long ago did your shrink go to medical school? The advances of the last 10 years or so have been pretty incredible as far as our ability to see into the brain and look at some of the minute details and function.

The information that I've given here regarding neurons regrowing comes from a neuroscience course I took three semesters ago.
 
ya ^ but is it not expected of any decent doctor to keep himself updated and constantly reeducated. however possible?
 
the brain is plastic and new connections can be formed

BDNF acts on certain neurons of the central nervous system and the peripheral nervous system, helping to support the survival of existing neurons, and encourage the growth and differentiation of new neurons and synapses.[4][5] In the brain, it is active in the hippocampus, cortex, and basal forebrain—areas vital to learning, memory, and higher thinking.[6] BDNF itself is important for long-term memory.[7] BDNF was the second neurotrophic factor to be characterized after nerve growth factor (NGF).

they wont grow like a babys brain but new growth does occur and even if new neurons dont replace the old ones, new connections will somewhat encourage recovery


# ^ Acheson A, Conover JC, Fandl JP, DeChiara TM, Russell M, Thadani A, Squinto SP, Yancopoulos GD, Lindsay RM (March 1995). "A BDNF autocrine loop in adult sensory neurons prevents cell death". Nature 374 (6521): 450–3. doi:10.1038/374450a0. PMID 7700353.
# ^ Huang EJ, Reichardt LF (2001). "Neurotrophins: roles in neuronal development and function". Annu. Rev. Neurosci. 24: 677–736. doi:10.1146/annurev.neuro.24.1.677. PMID 11520916.
 
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