Shown: posts 21 to 45 of 45. Go back in thread:
Posted by dbc on August 10, 2008, at 11:53:00
In reply to Re: So concluding......, posted by SLS on August 10, 2008, at 11:28:09
> The UK has a real problem with the abuse of amphetamine provided by illicit sources. It seems far worse there than in the USA. Perhaps this motivates the search for neurotoxicity. I would just like to see more evidence and more discussion before scaring the hell out of people.
>From first hand accounts of users in the UK the amphetamine is very subpar and meth is pretty much non-existant as is any substantial quanity of dexedrine. Neurotoxic effects of the amphetamine available may be the result of impurities created during production.
I've heard recently though that research chemicals such as MDPV (Methylenedioxypyrovalerone) and Methylone (2-methylamino-1-(3,4-methylenedioxyphenyl)propan-1-one)
have gained popularity as grey market stimulants and they may result in damage being attributed to amphetamine as absolutely nothing is known about they substances beyond initial research.The UK also always has a plentiful supply of cheap and pure MDMA given its proximity to holland.
Posted by Deputy Dinah on August 10, 2008, at 12:06:25
In reply to Re: Freud, Cocaine, and Adderall, posted by West on August 10, 2008, at 9:15:49
> Do you realise how crazy you all sound?
Please don't post anything that could lead others to feel accused or put down.
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Posted by Deputy Dinah on August 10, 2008, at 12:12:03
In reply to Re: Freud, Cocaine, and Adderall, posted by dbc on August 10, 2008, at 11:10:46
> I wonder why a refined and intellectual dr like Mrs. Ashton allows your people to use her name for this agenda of misinformation and cherry picked studies. Do you ever wonder what sort of damage you do to ill people looking for help?
Please respect the views of others even if you think they're wrong. Please don't post anything that could lead others to feel accused or put down.
If you or others have questions about this or about posting policies in general, or are interested in alternative ways of expressing yourself, please see the FAQ:
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Follow-ups regarding these issues should be redirected to Psycho-Babble Administration. They, as well as replies to the above posts, should of course themselves be civil.
Dr. Bob is always free to override deputy decisions. His email is on the bottom of each page. Please feel free to email him if you believe this decision was made in error.
Dinah, acting as deputy to Dr. Bob
Posted by Deputy Dinah on August 10, 2008, at 12:18:23
In reply to Please be civil » dbc, posted by Deputy Dinah on August 10, 2008, at 12:12:03
Thanks for responding in a civil manner.
Dr. Bob really appreciates it when posters present a balancing point of view in a civil and respectful manner. Thanks, Nadezda and Scott for the following:
Well, I'm sure it is not just you alone.
It never seemed bizarre to me. I think one must be careful to not generalize to the majority what one as an individual experiences with treatment. It is possible to be angry at a drug for mistreating you, thus your wanting to take it away from people who need it.
Taking Adderall is a necessity for people for whom it works to improve their condition, whether it be ADD/ADHD or depression. Some people respond well to Adderall whom failed to respond to Dexedrine or Ritalin. Clinically, Adderall is useful and not nearly as addicting as cocaine.- Scott
You need to distinguish between medications that didn't help one or some people and medications that don't help anyone-- or, alternatively, medications that you had problems with and medications that everyone has problems with.
I wouldn't make a useful med unavailable to everyone because some people have problems with it.
I've used adderall for several years and it's been of great help to me. I'm sure, from reading this board, that I"m not the only person who has.Nadezda
Dinah, acting as deputy to Dr. Bob
Posted by West on August 10, 2008, at 16:22:05
In reply to Re: Freud, Cocaine, and Adderall, posted by West on August 10, 2008, at 9:15:49
Scott you rightly say the onus is on me to prove it. I am under the impression, as might have become clear, that the deleterious effects are common scientific knowledge, in the same way one would no longer dispute global climate change. Clearly this is not the case.
West
http://www.ncbi.nlm.nih.gov/pubmed/16014752?dopt=AbstractPlushttp://jpet.aspetjournals.org/cgi/reprint/jpet.105.087916v1.pdf
Also amphetamine neurotoxicity is not a peculiarly Britain concept relegated to an underclass of so called street-drug users. Speculating that impurities or the addition of other much rarer stimulants like 4-mar seem rather baseless when the primary constituents found in sold speed int his country are glucose and caffeine. I may be wring but what sense would there be in cutting a low cost £5-10 a gramme drug with hard to manufacture and rarer, more expensive, chemicals?
Posted by West on August 10, 2008, at 16:32:40
In reply to Amphetamine neurotoxicity in therapeutic doses, posted by West on August 10, 2008, at 16:22:05
My crap english is i hope uncharacteristic, i have heavy hands today. apologies (read 'British' instead of 'Britain')
Posted by SLS on August 10, 2008, at 16:37:19
In reply to Amphetamine neurotoxicity in therapeutic doses, posted by West on August 10, 2008, at 16:22:05
Thanks for the citations. I wish you had not been able to come up with any.
:-(
I'll have to give this a lot more thought.
- Scott
Posted by West on August 10, 2008, at 16:40:32
In reply to Amphetamine neurotoxicity in therapeutic doses, posted by West on August 10, 2008, at 16:22:05
The second link, yes, is a study in adult non-human primates. To be honest i didn't even read it, you'll find it on the second page of google.
I don't think i am fear mongering but providing information where it may be of some help, however marginal.
Posted by dbc on August 10, 2008, at 16:46:38
In reply to Re: Amphetamine neurotoxicity in therapeutic doses, posted by West on August 10, 2008, at 16:40:32
But what is the point? I wonder what Anon would think of benzo.org, im sure they'd be interested in the forum.
Posted by desolationrower on August 10, 2008, at 16:50:58
In reply to Re: Amphetamine neurotoxicity in therapeutic doses, posted by West on August 10, 2008, at 16:40:32
There is evidence of change in dopamine neurones after use of amphetamines, little of it is clearly applicable to human and therapeutic doses. Calling this 'neurotoxic' is not warranted from the evidence currently availible though. For instance, DATs are overexpressed for people with ADHD and reducing there number would be a benefit from chronic treatment. This would be consistent with the therapeutic benefit often extending past the time one takes the drug.
Posted by West on August 10, 2008, at 17:08:38
In reply to Re: Amphetamine neurotoxicity in therapeutic doses, posted by desolationrower on August 10, 2008, at 16:50:58
Potentially yes, and the theory is a neat one. Since I do not have ADD I cannot comment on how effective something like adderall is in treating that condition. I can say i still think that from a safety perspective, all other existing agents should be tried before taking it.
Posted by cumulative on August 10, 2008, at 23:58:27
In reply to Amphetamine neurotoxicity in therapeutic doses, posted by West on August 10, 2008, at 16:22:05
It is my opinion that the changes in dopamine transporters in that study reflect plastic changes, not neurotoxicity. Homeostatic changes in the dopamine transporter (and many other systems -- some of which seem to sensitize) are well-known to occur with dopaminergic psychostimulants, and that study does not show anything different. Also, ever since his hysterical MDMA mess-ups (where it was later found that they accidently used methamphetamine instead of MDMA, later being long after MDMA's neurotoxicity was trumpeted all over the news media) I don't really trust anything coming out of Ricaurte's lab. Other than that study, neurotoxicity from dextroamphetamine (unlike dextromethamphetamine, which has an additional mechanism of neurotoxicity that has a good chance of being active at therapeutic dosing, due to its serotonergic affinity) neurotoxicity is not known to occur at anything near human therapeutic doses of amphetamine.
Posted by West on August 11, 2008, at 16:00:05
In reply to Re: Amphetamine neurotoxicity in therapeutic doses, posted by dbc on August 10, 2008, at 16:46:38
>>But what is the point? I wonder what Anon would think of benzo.org, im sure they'd be interested in the forum.
I originally decided to ignore this post since the one you posted prior to it seemed rather confused and off-topic, i thought you'd lost your way a bit since we were discussing amphetamines not benzos. If you're trying to portray me as some kind of extremist out to chastise unwell people then i can promise you that i am not that person having suffered depression and anxiety for 6 years myself.
My concern is that tons of americans and their children are taking this drug in good faith without knowing about its neuropharmacology and i'm sure that, if they knew more about its action, they would open themselves up to making more educated decisions when it comes to treating their ADD/ADHD. The layman for instance might, when asked which treatment he preferred, settle on adderall, perhaps saying 'it was the only one that worked' for him when plausibly he might just have preferred the feeling it engendered in him, unaware of amphetamine's euphoric effects. Who wouldn't prefer a drug which directly arouses feelings of interest and pleasure- it's a neurochemical non sequitur.
So a second issue exists with their safety which is marginalised by the drug's strong reinforcing effects, to me nothing spells trouble like a potent releaser of monoamines. MDMA + MDA are both examples of phenylethlamines known to induce the redistribution and release of chemicals in the brain; both are well documented neurotoxins.
I just read a study which i will look for again which attributed d-amphetamine's primary neurotoxic effects at room temperature to hypothermia, similar effects were seen with ephedrine I believe.
Posted by linkadge on August 12, 2008, at 15:56:22
In reply to Re: Amphetamine neurotoxicity in therapeutic doses, posted by desolationrower on August 10, 2008, at 16:50:58
I don't think this study should be shrugged off. I think this study is applicable to human usage, and I would personally be very concerned about the potential for theraputic use of amphetamines and other related compounds to cause neurotoxicity.
You can bet though that its not Shire that is going to be rushing out any time soon to fund follow up studies.
Also, DAT transporters are *not* upregulated in ADHD. This is a stupid hypothesis (which is not supported by the majority of studies) based on the mechanism of action of the stimulants. Its just about as believable as the notion that serotonin transporters are elevated in depression.
Linkadge
Posted by linkadge on August 12, 2008, at 16:01:25
In reply to Re: Amphetamine neurotoxicity in therapeutic doses, posted by linkadge on August 12, 2008, at 15:56:22
In defense though, I do not believe that euphoria is the mechanism of action of the amphetamines in ADHD. There are plenty of euphoriants which do not improve ADHD symptoms.
A fixed dose of amphetamine will only provide mood improvement for a short length of time (days or weeks at best), but they can be effective in ADHD for years.
I am still concerned though about the potential for neurotoxicity. There are other issues too which concern me, namely the long term cardiac side effects of stimulants and atomoxetine. Also a metabolite of methylphenidate has strong binding to 5-ht2b receptors and could pose risk to cardiac valves in a similar manner to the withdrawn dopamine agonists permax and cabergoline.
Linakdge
Posted by Dade on August 13, 2008, at 18:48:20
In reply to Re: Amphetamine neurotoxicity in therapeutic doses, posted by linkadge on August 12, 2008, at 15:56:22
"Also, DAT transporters are *not* upregulated in ADHD".Perhaps not *all* ADHD patients but *some*?
"This is a stupid hypothesis (which is not supported by the majority of studies) based on the mechanism of action of the stimulants. Its just about as believable as the notion that serotonin transporters are elevated in depression."
LinkadgeAgreed, similar to the theory that Schizophrenia is caused by overactive dopamine systems.
Thou studies have often shown high doses of amphetamines cause notorious shaking and loss of balance, low doses (10-15mgs) D-amp improve steadiness and balance, alertness, attention, hand eye coordination, especially in fatigued persons. long distance truckers call amphetamines "co-pilots".
Posted by Dade on August 13, 2008, at 18:56:29
In reply to re: Ricaurte therapeutic dose study., posted by cumulative on August 10, 2008, at 23:58:27
> It is my opinion that the changes in dopamine transporters in that study reflect plastic changes, not neurotoxicity. Homeostatic changes in the dopamine transporter (and many other systems -- some of which seem to sensitize) are well-known to occur with dopaminergic psychostimulants, and that study does not show anything different. Also, ever since his hysterical MDMA mess-ups (where it was later found that they accidently used methamphetamine instead of MDMA, later being long after MDMA's neurotoxicity was trumpeted all over the news media) I don't really trust anything coming out of Ricaurte's lab. Other than that study, neurotoxicity from dextroamphetamine (unlike dextromethamphetamine, which has an additional mechanism of neurotoxicity that has a good chance of being active at therapeutic dosing, due to its serotonergic affinity) neurotoxicity is not known to occur at anything near human therapeutic doses of amphetamine.
hi there....desoxyn = (S)-methamphetamine, and dexedrine = d-amphetamine. There is a body of literature that reports that methamphetamine is about twice as potent as d-amphetamine. potency is derived from dose/response evaluations of subjects, and i can point you to several citations that conclude that (S)-methamphetamine and d-amphetamine are actually equipotent. HOWEVER, it turns out that (in at least 1 study examining a D_{1} antagonist) the mechanisms of neurotoxicity at high doses of desoxyn and dexedrine are different, as the antagonist protected against death from dexedrine in a dose-dependent fashion but not for desoxyn. (Derlet et al., Life Sci. 47:821-827 (2000)). but, the equipotency has been established, too. [e.g., Woolverton et al., Pharmacol. Biochem. Behav. 13:869-876 (1980)]. but then, see Peachey et al., Psychopharmacology 51:137-140 (1977) for evidence of greater stimulation (not potency) of desoxyn than dexedrine. more recently, Melega et al. JPET 274:90-96 (1995) concluded that low doses of either drug exhibited similar pharmacokinetics and dopamine response, although this is not a measure of potency nor were the doses extreme. from an abstract by Ellison and Switzer in Neuroreport. 25:17-20 (1993), they report (i quote) ``Both [dexedrine] and [cocaine] induced pronounced degeneeration in fasciculus retroflexus, but only [dexedrine] further induced substantial degeneration in striatum...[Desoxyn] administered in the very high dose but less prolonged drug regimen often employed in studies of dopamine toxicity induce pronounced degeneration in striatum, but widespread degeneration in many other regions as well.'' and then there is one paper by the man who instigated the FDA to make MDMA illegal: Ricaurte et al., Neuropharmacology 22:1165-1169 (1983), in which ``Repeated administration of large doses of [desoxyn] produce long-lasting depletion of brain dopamine and serotonin, as well as persistent decreases in the activity of their respective biosynthetic enzymes...'' interestingly, dexedrine - in ``a comparable regimen'' to the desoxyn dosing - ``did not did not produce long-lasting depletion of 5-HT in either the neostriatum or hippocampus.'' but, it turns out (and not just in this ref) that pretreatment with fluoxetine likely inhibits metabolism of amphetamines in general. so, in summary: potency is derived from dose/response curves, and in low doses, it appears as if desoxyn and dexedrine exhibit similar pharmacokinetics and are somewhat equipotent. however, at high doses of both drugs, the potency of desoxyn is greater and the toxicity is, as well, due to the larger amount of the brain affected in re: dopamine and 5-HT response. most drugs exhibit linear pharacokinetics/dynamics in the recommended dose ranges. the LD_{50} for desoxyn and dexedrine are almost identical, but at higher doses, desoxyn is more lethal. finally, as i posted some time ago, the study by (again) Ricaurte et al. in Science 297:2260-2263 (2003) entitled ``Severe dopaminergic neurotoxicity in primates after a common recreational dose regimen of MDMA (``ecstact'')'' - which was later retracted because the drugs given to the 5 monkeys tunred out to be methamphetamine and not MDMA - is actually testament to the neurotoxicity to methamphetamine (desoxyn). the dose was 6 mg/kg over 6 hours. recalling that this was pure methamphetamine, this means that your 100 mg desoxyn would correspond to your weight at about 16 kg, or about 35 lbs. 1 monkey died, 1 was unable to continue after the second dose (dosing was 2 mg/kg tid), and the 3 surviving monkeys were examined over several weeks after the acute dosing (there's more, and i can send you the PDF of the article if you desire, or anyone else). conclusions: severe dopaminergic injury and serotonergic neuortoxicity (for subjects using methamphetamine in repeated doses over several hours). the implication is that using desoxyn for a prolonged period - which is essentially what this last study showed - is bad news compared to dexedrine. hope this helps, and all the best,
Posted by linkadge on August 13, 2008, at 19:16:27
In reply to Re: Amphetamine neurotoxicity in therapeutic doses » linkadge, posted by Dade on August 13, 2008, at 18:48:20
Oh, I suppose dopamine transporters could be elevated in some patients with ADHD, but far fewer than I think would indicate that this is really the etiology of the disorder.
Some studies show decreased DAT transporters in ADHD, and mice with a genetic loss of DAT function display symptoms of hyperactivity.
Linkadge
Posted by dcruik518 on August 14, 2008, at 15:17:51
In reply to Re: Amphetamine neurotoxicity in therapeutic doses » Dade, posted by linkadge on August 13, 2008, at 19:16:27
Can NAC prevent or even reverse any of this neurotoxicity you all are talking about? I saw some posts about that earlier. I've been on fairly high dose adderall for about eight years now and am a little disturbed by these studies. DRC
Posted by West on August 15, 2008, at 12:35:29
In reply to D-amp M-amp MDMA toxicity » cumulative, posted by Dade on August 13, 2008, at 18:56:29
>>Thou studies have often shown high doses of amphetamines cause notorious shaking and loss of balance, low doses (10-15mgs) D-amp improve steadiness and balance, alertness, attention, hand eye coordination, especially in fatigued persons. long distance truckers call amphetamines "co-pilots".
Which studies? How is that relevant?
> > It is my opinion that the changes in dopamine transporters in that study reflect plastic changes, not neurotoxicity.
Your opinion appears to contradict current clinical evidence.
>>Homeostatic changes in the dopamine transporter (and many other systems -- some of which seem to sensitize) are well-known to occur with dopaminergic psychostimulants, and that study does not show anything different.
Which dopaminergic psychostimulants other than the amphetamines show these homeostatic changes? Please provide some examples. The second (non Ricaurte) study seemed quite clear:
'Here we demonstrate that amphetamine treatment, similar to that used clinically for adult ADHD, damages dopaminergic nerve endings in the striatum of adult nonhuman primates.'
How does that show evidence of merely 'plastic changes'?
>>Also, ever since his hysterical MDMA mess-ups (where it was later found that they accidently used methamphetamine instead of MDMA, later being long after MDMA's neurotoxicity was trumpeted all over the news media) I don't really trust anything coming out of Ricaurte's lab.>>Other than that study, neurotoxicity from dextroamphetamine (unlike dextromethamphetamine, which has an additional mechanism of neurotoxicity that has a good chance of being active at therapeutic dosing, due to its serotonergic affinity) neurotoxicity is not known to occur at anything near human therapeutic doses of amphetamine.
Please cite evidence. From 'Update on amphetamine neurotoxicity and its relevance to the treatment of ADHD.':
'In early studies, high doses of amphetamine, comparable to amounts used by addicts, were shown to damage dopaminergic pathways. More recent studies, using therapeutic regimens, appear contradictory. One paradigm shows significant decreases in striatal dopamine and transporter density after oral administration of "therapeutic" doses in primates. Another shows morphological evidence of "trophic" dendritic growth in the brains of adult and juvenile rats given systemic injections mimicking "therapeutic" treatment. Imaging studies of ADHD-diagnosed individuals show an increase in striatal dopamine transporter availability that may be reduced by methylphenidate treatment.'
Finally in respect to the previous post about hyperthermia being a contributing factor in d-amphetamine and l-ephedrine induced neurotoxicity - From 'An Evalutaion of l-Ephedrine Neurotoxicity with respect to Hyperthermia and Caudate/Putamen Microdialysate Levels of Ephedrine, Dopamine, Serotonin, and Glutamate':
Although the 3 x 40 mg/kg dose of l-ephedrine should produce CPu extracellular dopamine levels more comparable to the 4 x 5 mg/kg d-amphetamine dose, the excessive cooling necessary to prevent lethality would obtund dopamine and 5-HT levels. The reduction in dopamine and 5-HT levels is not the only mechanism by which cooling would reduce long-term dopamine depletions. We have previously observed that animals dosed with 4 x 10 mg/kg d-amphetamine in a cold environment have higher CPu microdialysate dopamine levels than animals dosed with 4 x 5 mg/kg d-amphetamine at 23°C temperature but no significant long-term dopamine depletions (Bowyer et al., 1993Go). The cooling should also reduce oxidative stress, since indices of oxidative stress produced by quinones of dopamine are decreased when hyperthermia does not occur during methamphetamine exposure (LaVoie and Hastings, 1999Go). Increased oxidative stress and reactive oxidative species of dopamine, such as 6-hydroxy-dopamine and quinones of dopamine, have been postulated to be mediators of dopamine neurotoxicity in the CPu (Graham, 1978Go; O'Dell et al., 1991Go; Seiden and Sabol, 1995Go; Stokes et al., 1999Go; Yamamoto and Zhu, 1998Go). Thus, from these previous studies, it seems likely that the greater the dopamine release and hyperthermia the greater the generation of reactive dopamine-like species. However, it is possible that the increase of dopamine within the dopaminergic terminals of the CPu is primarily mediating long-term neurotoxicity (LaVoie and Hastings, 1999Go).
http://toxsci.oxfordjournals.org/cgi/content/full/55/1/133
In regards to preventing brain damage (besides the use of memantine) here is one study I found using neuroprotective agents to prevent monoamine depletion after methamphetamine:
Striatal dopamine release in vivo following neurotoxic doses of methamphetamine and effect of the neuroprotective drugs, chlormethiazole and dizocilpine.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1908047>
>
Posted by Dade on August 15, 2008, at 17:49:54
In reply to Re: D-amp M-amp MDMA toxicity, posted by West on August 15, 2008, at 12:35:29
> >>Thou studies have often shown high doses of amphetamines cause notorious shaking and loss of balance, low doses (10-15mgs) D-amp improve steadiness and balance, alertness, attention, hand eye coordination, especially in fatigued persons. long distance truckers call amphetamines "co-pilots".
>
> Which studies? How is that relevant?I suspect you have had unfavourable experience with amps mdma?
Sure most psych drugs cause changes in neurotransmitter function, benzos, ssris- but the desired effect is to help.
Use of ams for medically indicated reasons has beeen use for decades, USE NOT ABUSE.
Posted by West on August 16, 2008, at 12:17:15
In reply to Re: D-amp M-amp MDMA toxicity, posted by Dade on August 15, 2008, at 17:49:54
> > >>Thou studies have often shown high doses of amphetamines cause notorious shaking and loss of balance, low doses (10-15mgs) D-amp improve steadiness and balance, alertness, attention, hand eye coordination, especially in fatigued persons. long distance truckers call amphetamines "co-pilots".
> >
> > Which studies? How is that relevant?
>
> I suspect you have had unfavourable experience with amps mdma?You seem to be missing the point, and the few experiences i have had with the substituted amphetamines have been great, thanks. My input throughout the thread has tried to show that people taking amphetamines at theraputic doses on a daily basis might be giving themselves brain damage. I suppose there would be little benefit in stopping for those who have been doing this for the past twenty years. However for somebody about to take adderall, the evidence provides some orientation on the subject, and helps to raise awareness where no dispute seems to exist in the public consciousness as to their safety.
> Sure most psych drugs cause changes in neurotransmitter function, benzos, ssris- but the desired effect is to help.
The drugs you mention have totally different mechanisms of action and are therefore completely unsuitable for comparison. Please do not continue to make erroneous statements which might mislead others. Any safety issues that exist with SSRIs are marginal in comparison, some issues have been raised with the benzos.
>
> Use of ams for medically indicated reasons has beeen use for decades, USE NOT ABUSE.It is exactly their 'use' which poses a danger since at prescribed doses evidence exists for their causing brain damage, sometimes termed 'neurotoxicity'.
In addition, although continuing to use amphetamine daily in doses prescribed is achievable, increased use or what you call 'abuse' ('misuse' might be a more suitable word for use in wide circulation) is common. Why?
Although an individual's personality will have some bearing over whether or not dose-escalation occurs, drug craving as a result of it's reinforcing effect is great, brutal even: once the brain has been directly aroused it will continue to fixate on those feelings of pleasure, often down regulating the frequency of cue-prompted tonic firing of dopamine neurons, (naturally occurring in daily life) which, if you follow, there will be less of originally because of their prior vesicular release. This combination might make the user feel more tired or 'run down' or on the other hand and at the other end of the scale worsen existing depression and exacerbate mental illness.
Posted by West on November 6, 2015, at 14:20:23
In reply to Re: Freud, Cocaine, and Adderall » West, posted by SLS on August 10, 2008, at 9:34:52
Hi
This was a while ago, I'm very ashamed to be reading it now. Unexcusably rude and scaremongery. I was on my high horse refusing to back down. Worst part of all is I went on to take Vyvanse for about 3 years! I no longer take it because it made me worse later in the day. But I completely see it helps lots of people live their lives. Very wrong of me to try and scare people away. If it helps, it helps. Sorry everyone.
Posted by mocharain on November 16, 2015, at 12:10:13
In reply to Re: Freud, Cocaine, and Adderall, posted by West on November 6, 2015, at 14:20:23
Adderall neurotoxicity is definitely controversial. You might find this comprehensive review on the subject helpful: http://www.brainprotips.com/article/adderall-neurotoxicity/
It is possible for high-dose Adderall to both be neurotoxic but also beneficial to the brain's of people with ADHD. For example, patients with ADHD treated with psychostimulants during development have normalized brain volumes compared to controls (patients with untreated ADHD).
Posted by West on November 21, 2015, at 3:50:40
In reply to Re: Freud, Cocaine, and Adderall, posted by mocharain on November 16, 2015, at 12:10:13
Very interesting article, thanks.
It would be good to see more studies of stimulant use with memantine and other NMDA antagonists.
One idea - what if tolerance (to stimulants) is a form of neuroprotection, which if reversed could expose the brain to sudden 'insult' (injury) on resuming an amphetamine dose?
This is the end of the thread.
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