• Log in with Facebook Log in with Twitter Log In with Google      Sign In    
  • Create Account
  LongeCity
              Advocacy & Research for Unlimited Lifespans

Photo
- - - - -

Which to choose


  • Please log in to reply
6 replies to this topic

#1 darksanity

  • Guest
  • 47 posts
  • 3
  • Location:Vancouver, BC

Posted 16 July 2006 - 04:26 PM


I have thought of some nootropics supplements I could start taking to repair & protect my brain from drug induced brain damage and something that would snyergize with my ADD medication (Adderall XR, Time-Released Amphetamine salts). The problem I don't want to spend a huge amount of money since it's my first experimentation with nootropics. So I need help to choose from this list :

Piracetam 800mg
Idebenone 90mg
Inositol 500mg
Vinpocetine 10mg
Standardized Mucuna Pruriens Extract (100mg 99% L-dopa and 150mg of 20% L-dopa giving 130mg pure L-dopa)
Centrophenoxine 500mg
Pyritinol 400mg
Alpha GPC 300mg

I would like to keep like 4-5 of the above products. I also need help with dosage, I weight 140lbs and workout 4 days per week. I have some ginkgo, ginseng, full vitamins and minerals and omega 3-6-9 already. Oh and I have just read that L-dopa mixed with Vitamin B6 is not recommended... I was wondering if l-tyrosine was still a good dopamine precursor and if it's true it's not recommended to mix B6 with L-dopa.

Thank you

Edited by zoolander, 18 July 2006 - 01:50 AM.


#2 darksanity

  • Topic Starter
  • Guest
  • 47 posts
  • 3
  • Location:Vancouver, BC

Posted 17 July 2006 - 11:34 AM

Actually I would like to know wich to choose as a ACh precursor... Centrophenoxine or Alpha GPC??? Should I stay with the Mucuna Pruriens L-dopa Extract or get L-Tyrosine?? ... Please someone answer! =(

Thank you

sponsored ad

  • Advert
Click HERE to rent this advertising spot for BRAIN HEALTH to support LongeCity (this will replace the google ad above).

#3 doug123

  • Guest
  • 2,424 posts
  • -1
  • Location:Nowhere

Posted 17 July 2006 - 08:48 PM

If you are already taking Adderall, you might consider a tyrosine supplement (2 or 3 grams a day): amphetamine tends to deplete tyrosine from the dopamine system; and high tyrosine blood levels have been correlated with high dopamine levels. And, as you will see below; high prolactin levels, too (in males). :o

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]


However, WARNING! High dose tyrosine blood levels have also been correlated with higher prolactin levels. So if you are male, you might want to not engage in high dose tryosine... :) This trials' results contradict the results from above; and both of these trials were randomized (and included many of the same researchers); so it makes you wonder if tyrosine really works as a stimulant by itself....


Nutr Neurosci. 2003 Aug;6(4):221-35. 

A comparison of tyrosine against placebo, phentermine, caffeine, and D-amphetamine during sleep deprivation.


Waters WF, Magill RA, Bray GA, Volaufova J, Smith SR, Lieberman HR, Rood J, Hurry M, Anderson T, Ryan DH.

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

Sleep deprivation can impair alertness and cognitive and motor performance. We hypothesized that the amino acid tyrosine might reduce deleterious effects of sleep deprivation. Seventy-six healthy males, age 18-35 years, participated in a four-day protocol that included a habituation night, a baseline night, a 40.5 h period without sleep, and a recovery night. Tyrosine 150 mg/kg, caffeine 300 mg/70 kg, phentermine 37.5 mg, D-amphetamine 20 mg and placebo were administered in a double-blind, randomized fashion to compare their effects on the time it took to fall asleep, on endocrine responses during sleep deprivation, and on sleep quantity, quality and architecture as measured by polysomnography during recovery sleep. When given after 36 h without sleep, tyrosine had no significant effect on any parameter of sleep. D-amphetamine produced marked decrease in sleep drive but caused deleterious effects on many aspects of recovery sleep. Still, D-amphetamine was associated with increased alertness on the first recovery day. Phentermine and caffeine both decreased sleep drive during sleep deprivation, but phentermine impaired rapid-eye-movement (REM) recovery sleep. Tyrosine (when compared to placebo) had no effect on any sleep related measure, but it did stimulate prolactin release.

Publication Types:

* Clinical Trial
* Randomized Controlled Trial


PMID: 12887139 [PubMed - indexed for MEDLINE]


let's keep looking....

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]


I might suggest 2 or 3 grams tyrosine a day; on an empty stomach (maybe right after you awaken).

#4 darksanity

  • Topic Starter
  • Guest
  • 47 posts
  • 3
  • Location:Vancouver, BC

Posted 18 July 2006 - 01:27 AM

ok, and what about Centrophenoxine or Alpha GPC for ACh precurosr??? I know Alpha GPC is a better ACh precursor but would Centrophenoxine be enough since it seems to have more other fonctions and seems better overall but I want to be sure. I also would like to know wich to choose between Piracetam, Oxiracetam and Aniracetam?? I never took any 'racetams and want to choose a single one...
Thank you

Edited by darksanity, 18 July 2006 - 11:50 AM.


#5 senseix

  • Guest
  • 250 posts
  • 1

Posted 23 July 2006 - 11:55 PM

ok, and what about Centrophenoxine or Alpha GPC for ACh precurosr??? I know Alpha GPC is a better ACh precursor but would Centrophenoxine be enough since it seems to have more other fonctions and seems better overall but I want to be sure. I also would like to know wich to choose between Piracetam, Oxiracetam and Aniracetam?? I never took any 'racetams and want to choose a single one...
Thank you


Being pretty new to the scene, I wouldn't mind an answer to his question:) specifically what i'd like to know is:

1. Is Centrophenoxine enough of a precursor when using Piracetam or should you use CDP-choline too?
2. I've read that Aniracetam is stronger and lasts longer than Piracetam due to it being fat soluble, so lets say one was to switch from Piracetam to Aniracetam, would you be ok with Using Centrophenoxine 500mg as a Precursor or should you use CDP-choline too?

Any clear input on this would be greatly appreciated.

#6 Ghostrider

  • Guest
  • 1,996 posts
  • 56
  • Location:USA

Posted 24 July 2006 - 01:57 AM

Have you spoken with your doctor about a possible substitute for Adderall XR? There might be something less neurotoxic such as Modafinil.

sponsored ad

  • Advert
Click HERE to rent this advertising spot for BRAIN HEALTH to support LongeCity (this will replace the google ad above).

#7 doug123

  • Guest
  • 2,424 posts
  • -1
  • Location:Nowhere

Posted 24 July 2006 - 07:22 AM

Have you spoken with your doctor about a possible substitute for Adderall XR?  There might be something less neurotoxic such as Modafinil.


A healthy person should never take amphetmine without a doctor's care. However, for many people with serious ADD/ADHD, nothing works quite the same. I think it's always best to start with non stimulants like Wellbutrin, strattera, modafinil, etc. before trying amphetmaine. Have you tried strattera, Ghostrider?

The amphetamine compounds can be dangerous, and in particular patients, they can be deadly...however, ampetamines have been used since the early 1900s safely in far too many patients to be considered "unsafe"..and D-amphetamine seems to be as effective than Adderall..it's, however, Adderall was easy way to make money, mixing up four isomers of amphetmine and patenting it...D-amp is available in generic and on the cheap.

Deadly side-effects earn ADHD drugs warning
http://www.canada.co...953c8cb&k=97407

I also think it's safer to say: "amphetamines may be neurotoxic" rather than they "are." More research needs to be conducted to say anything definitive it seems.

J Pharmacol Exp Ther. 2005 Oct;315(1):91-8. Epub 2005 Jul 13.

Amphetamine treatment similar to that used in the treatment of adult attention-deficit/hyperactivity disorder damages dopaminergic nerve endings in the striatum of adult nonhuman primates.

Ricaurte GA, Mechan AO, Yuan J, Hatzidimitriou G, Xie T, Mayne AH, McCann UD.

Department of Neurology, Johns Hopkins Medical Institutions, 5501 Hopkins Bayview Circle, Rm. 5B.71E, Baltimore, MD 21224, USA. ricaurte@jhmi.edu

Pharmacotherapy with amphetamine is effective in the management of attention-deficit/hyperactivity disorder (ADHD), now recognized in adults as well as in children and adolescents. 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. Furthermore, plasma concentrations of amphetamine associated with dopaminergic neurotoxicity in nonhuman primates are on the order of those reported in young patients receiving amphetamine for the management of ADHD. These findings may have implications for the pathophysiology and treatment of ADHD. Further preclinical and clinical studies are needed to evaluate the dopaminergic neurotoxic potential of therapeutic doses of amphetamine in children as well as adults.

PMID: 16014752 [PubMed - in process]


When I take a full load of classes at UC, to compete at the top of my class I need to take Atomoxetine HCL (strattera) AND modafinil (under doctor's care, of course). It helps me focus with only the tax of a negative sexual side effect...things happen...uh, too early. When not in school, I stop taking it altogether.

Ann Pharmacother. 2006 Jun;40(6):1134-42. Epub 2006 May 30
Atomoxetine versus stimulants for treatment of attention deficit/hyperactivity disorder.

        * Gibson AP,
        * Bettinger TL,
        * Patel NC,
        * Crismon ML.

College of Pharmacy, The University of Texas at Austin, 78712, USA.

OBJECTIVE: To identify, review, and analyze studies comparing atomoxetine with psychostimulants with the intent of determining the role of atomoxetine in the pharmacologic management of attention deficit/hyperactivity disorder (ADHD). DATA SOURCES: Primary, review, and meta-analysis articles were identified by a MEDLINE search (1966-December 2005). MeSH headings used in the search include: attention deficit/hyperactivity disorder, ADHD, atomoxetine, stimulants, psychostimulants, methylphenidate, and amphetamine salts. Relevant data presented at professional meetings that we attended were also identified. STUDY SELECTION AND EXTRACTION: All clinical studies comparing atomoxetine with psychostimulants, regardless of study design, were evaluated. Relevant efficacy and safety data from these studies were included in the discussion. DATA SYNTHESIS: At time of writing, 5 head-to-head trials had compared psychostimulants and atomoxetine in the treatment of ADHD. No significant difference between atomoxetine and methylphenidate immediate-release were found on the ADHD Rating Scale total score. Osmotic oral release system (OROS) methylphenidate showed significantly greater improvement at weeks 1 and 2, and significantly more patients treated with OROS methylphenidate were classified as responders. Patients on both atomoxetine and mixed amphetamine salts extended-release (MAS XR) showed significant improvements at endpoint over baseline; however, Swanson, Kotkin, Agler, M-Flynn, and Pelham (SKAMP) scores were significantly better with MAS XR. Tolerability was similar between atomoxetine and stimulant medications. CONCLUSIONS: Based on available evidence, psychostimulants are regarded as first-line pharmacologic treatment for children and adolescents with ADHD, as the efficacy and safety of these agents have been well established based on clinical trials and extensive naturalistic use. Adverse effects in some patients and abuse potential have led to the search for new treatments. Atomoxetine represents an alternative treatment for ADHD and is unlikely to be associated with abuse; however, long-term safety data are needed to further establish its place in therapy.
PMID: 16735655 [PubMed - in process]






1 user(s) are reading this topic

0 members, 1 guests, 0 anonymous users