17 replies to this topic

[jdog]

Gunna get this in quick before I miss the bus for class.

Is it posssible to reset/restore the dopamine and other receptors which become inhibited as a result of taking adderall? Its effects tend to wear off after a short while, requiring an increase in dosage. Any suggestions? Oh, and I'm thinking along the lines other than just taking a 2 week break to restore natural function.

[doug123]

I might suggest taking an L-tyrosine supplement (at least 2 grams a day, on an empty stomach):

Amphetamine tends to deplete tyrosine from the dopamine system; and some evidence suggests high tyrosine blood levels seem to have been correlated with high dopamine levels.

Nutr Neurosci. 2003 Aug;6(4):237-46. 

Effects of tyrosine, phentermine, caffeine D-amphetamine, and placebo on cognitive and motor performance deficits during sleep deprivation.

Magill RA, Waters WF, Bray GA, Volaufova J, Smith SR, Lieberman HR, McNevin N, Ryan DH.

Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808, USA.

Cognitive and motor performance are critical in many circumstances and are impaired by sleep deprivation. We administered placebo, tyrosine 150 mg/kg, caffeine 300 mg/70 kg, phentermine 37.5 mg and D-amphetamine 20 mg at 15.30 h following overnight sleep deprivation and compare their effects on cognitive and motor performance in healthy young men. Tests of visual scanning, running memory, logical reasoning, mathematical processing, the Stroop task, four-choice serial reaction time, time wall take, pursuit tracking, visual vigilance, Trails (B) task and long-term memory were evaluated at standardized intervals before, during and after sleep deprivation and drugs. Performance decrements with sleep deprivation occurred in visual scanning, running memory, logical reasoning, mathematical processing, the Stroop test, the time wall test, tracking and visual vigilance. Interestingly, with sleep deprivation some tests improved and others did not deteriorate. Improvements with medication following sleep deprivation were seen in running memory, logical reasoning, mathematical processing, tracking and visual vigilance. Although less effective than D-amphetamine, tyrosine improved performance on several tests. We conclude that all drugs tested improved at least some aspects of cognitive and motor performance after sleep deprivation. As a naturally occurring amino acid, and thus amenable to nutritional strategies, tyrosine may deserve further testing.
Publication Types:

* Clinical Trial
* Randomized Controlled Trial


PMID: 12887140 [PubMed - indexed for MEDLINE]

Neuropsychopharmacology. 2004 Feb;29(2):427-32. 
 
Decreasing amphetamine-induced dopamine release by acute phenylalanine/tyrosine depletion: A PET/[11C]raclopride study in healthy men.

Leyton M, Dagher A, Boileau I, Casey K, Baker GB, Diksic M, Gunn R, Young SN, Benkelfat C.

Department of Psychiatry, McGill University, Montreal, Quebec, Canada. marco.leyton@mcgill.ca

Acute phenylalanine/tyrosine depletion (APTD) has been proposed as a new method to decrease catecholamine neurotransmission safely, rapidly, and transiently. Validation studies in animals are encouraging, but direct evidence in human brain is lacking. In the present study, we tested the hypothesis that APTD would reduce stimulated dopamine (DA) release, as assessed by positron emission tomography (PET) and changes in [(11)C]raclopride binding potential (BP), a measure of DA D2/D3 receptor availability. Eight healthy men received two PET scans, both following d-amphetamine, 0.3 mg/kg, p.o., an oral dose known to decrease [(11)C]raclopride BP in ventral striatum. On the morning before each scan, subjects ingested, in counter-balanced order, an amino-acid mixture deficient in the catecholamine precursors, phenylalanine, and tyrosine, or a nutritionally balanced mixture. Brain parametric images were generated by calculating [(11)C]raclopride BP at each voxel. BP values were extracted from the t-map (threshold: t=4.2, equivalent to p<0.05, Bonferroni corrected) and a priori identified regions of interest from each individual's coregistered magnetic resonance images. Both receptor parametric mapping and region of interest analyses indicated that [(11)C]raclopride binding was significantly different on the two test days in the ventral striatum (peak t=6.31; x=-25, y=-8, and z=0.1). In the t-map defined cluster, [(11)C]raclopride BP values were 11.8+/-11.9% higher during the APTD session (p<0.05). The reduction in d-amphetamine-induced DA release exhibited a linear association with the reduction in plasma tyrosine levels (r=-0.82, p<0.05). Together, the results provide the first direct evidence that APTD decreases stimulated DA release in human brain. APTD may be a suitable new tool for human neuropsychopharmacology research.
    PMID: 14583741 [PubMed - indexed for MEDLINE]

J Psychopharmacol. 1999;13(2):144-7. 
   
Attenuation of some subjective effects of amphetamine following tyrosine depletion.

McTavish SF, McPherson MH, Sharp T, Cowen PJ.

University Department of Psychiatry, Warneford Hospital, Oxford, UK. sarah.mctavish@psyc.ox.ac.uk

Fifteen healthy volunteers received d-amphetamine (20 mg orally) 2 h after ingesting either a nutritionally balanced amino acid mixture or one lacking the catecholamine precursors, tyrosine and phenylalanine (TYR-free). Plasma tyrosine levels were significantly lowered in subjects who received the TYR-free mixture but mean plasma amphetamine levels were higher. Despite this, the TYR-free mixture appeared to decrease the subjective psychostimulant effects of amphetamine, as determined by visual analogue scales. In contrast, the TYR-free mixture failed to lower the subjective anorectic effect of amphetamine. These findings are consistent with animal experimental studies indicating that tyrosine depletion attenuates the release of dopamine produced by amphetamine but not the release of noradrenaline.
Publication Types:

* Clinical Trial
* Randomized Controlled Trial

PMID: 10475719 [PubMed - indexed for MEDLINE]

However, one study suggests that amphetamine like compounds used to treat ADD/ADHD may be neurotoxic:

So you might want to add r-alpha-lipoic acid and alcar as a possible strategy for neuroprotection.

[purerealm]

i want to know as well, i dont know anything about resetting, but i know that you can minimize tolerance by taking a specific other claass of drug

[fast turtle]

http://www.bluelight...&threadid=97021

[purerealm]

godsend

[xanadu]

I hate it when someone posts a huge link or something and the whole thread is stretched out sideways. Then I have to scroll side to side to read it or use tiny text that is hard to read.

[ajnast4r]

I hate it when someone posts a huge link or something and the whole thread is stretched out sideways. Then I have to scroll side to side to read it or use tiny text that is hard to read.

increase your screen resolution

[jdog]

Thanks a lot for the info Adam. I'm thinking about dropping adderall in favor of a different medication that is less neurotoxic. Any suggestions other than the typical noots?

[doug123]

Thanks a lot for the info Adam. I'm thinking about dropping adderall in favor of a different medication that is less neurotoxic. Any suggestions other than the typical noots?

jdog, do I perhaps know you from another forum?

Onto your question...

The study I pasted above that suggests that amphetamine medications used to treat ADD/ADHD are neurotoxic was in adult non human primates.

Again:

You might try asking your doctor to try Provigil (modafinil), Strattera, Wellbutrin, or perhaps a combination of these. Maybe print out this page on Strattera and bring it into your next visit. Strattera seems to work on NE meanwhile the amphetamines work mostly on DA.

I know a lot of people who have been taking amphetamines for many years and can't function in society without them. However, for some people (like me) they are just bad news. Provigil (modafinil) is, in my opinion, one of the best drugs available for attention...and it's the most well documented "smart drug." See this topic to understand why.

[doug123]

Jeez, I hate these editing bugs! I meant "I know a lot of people who have been taking amphetamines for many years and claim they can't function in society without them."

It is still up in the air whether or not amphetamine treatments are neurotoxic in humans or not...note:

Further preclinical and clinical studies are needed to evaluate the dopaminergic neurotoxic potential of therapeutic doses of amphetamine in children as well as adults.

[salesman]

I would agree with that statement about not being able to function without amphetamines but i havent tried provigil yet so we will see.

[ikaros]

It is still up in the air whether or not amphetamine treatments are neurotoxic in humans or not...note:

QUOTE 

Further preclinical and clinical studies are needed to evaluate the dopaminergic neurotoxic potential of therapeutic doses of amphetamine in children as well as adults.

If it damages the nerve endings of primates, then with 90% likelihood it does the same in humans. As much as I've understood the mainstream medical oppinion is that low-dose amphetamine treatment for ADHD does not result in long-term damage or at least it does not really ever surface to the level of functioning or consciousness of those individuals. The damage depends probably on how much activity is produced at a time. If you take for example methylphenidate and methamphetamine, then the latter does obvious damage and the former doesn't, even though they are basically identically acting drugs. Anyway for example 10 mg of methylphenidate (Ritalin) might not be neurotoxic for ADHDers (whose DA system is somewhat very low), but may be for normal individuals (whose DA system is working optimally).

[ikaros]

http://www.bnl.gov/b...nlpr092998.html

An article which discusses the safety of reasonable Ritalin consumption.

[xanadu]

Ajnast wrote:

"increase your screen resolution"

All that does is make the text smaller. I can do that directly but tiny text is hard on the eyes. There are coding fixes that will make long URL's fit within a normal page. But, they can't even fix the quote bug so no way will they do something like that. No one else is annoyed by having to scroll left and right?

As for the topic at hand, as usual the stimulant users jump in to say it's safe and the dangers are downplayed. Stimulants are addictive and I believe they are not good in the long term.

[Shepard]

No one else is annoyed by having to scroll left and right?

Doesn't happen with me. I do have a widescreen, but it wasn't an issue when I had my CRT.

[purerealm]

firefox

[fast turtle]

As far as non-neurotoxic replacements for AMP (amphetamine) I'd recommend a dopamine reuptake inhibitor (DARI) like buproprion, methylphenidate, pyrovalerone, 2-(1-pyrrolidinyl)valerophenone, or 3,4'-methylenedioxy-2-(1-pyrrolidinyl)valerophenone. The former two are available easily from a doctor if you have ADHD, and the latter three are more experimental highly selective DARIs. If that doesn't work well try adding an SSRI like sertraline or atomoxetine to the mix.

I wouldn't worry all too much about the neurotoxicity induced by amphetamines though, it's all probably easily preventable by adding strong antioxidants like cocoa powder, r-ALA, or idebenone to your diet.

If you take for example methylphenidate and methamphetamine, then the latter does obvious damage and the former doesn't, even though they are basically identically acting drugs.

Methylphenidate and methamphetamine are very differently acting drugs; the former is a DARI and the latter reverses transport of SER and DA, effectively freeing both from their cytoplasmic stores. AMP works similar to methamphetamine but mostly only at DA receptors. Subjectively I would say all three feel fairly different, though I would characterize all these as stimulants.

[power.bulls.x]

i am thinking of glutamate blocker like aka the news alzimer class of drug memantine i think. not sure