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    Meth/speed and Opiates Tolerance Prevention/Reduction 
    #1
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    Almost everyone's opinion on using speed/amphetamine/meth is that the best highs were the first two (or three). That is also the case with me.
    When I first tried speed I've used very small amount (I'd say it was around 50 mg) of rather pure amphetamine and damn, it was the best day of my life :] I remember that I was euphoric for around 12 hours, I couldn't stop talking, the music sounded extremely well, I was full of motivation and never felt better in my whole life. Afterwards I had no comedown.
    My second attempt wasn't as fantastic, but also wonderful. Since then I've never achieved that extremely euphoric sensation with my head tingling from pleasure and my insides screaming "DAMN I FEEL FUCKING AWESOME!!!". After a year of my speed usage and trying doses even four times as high as the 1st amount I tried - I never came close to that feeling. Sure, I can be motivated, energetic, have a great time during the tweak, be very sociable, but it is still not like during the first two times. I'm aware that amphetamine tolerance develops very quickly and stays at that level for a long period of time (even when taking breaks), so lately I've been doing some online reading on that subject.

    Amphetamine tolerance is caused by excess Ca++ influx through the NMDA receptor gated calcium channels on the outer membranes of the dopamine cells bodies in the ventral tegental area, one of two areas in the brain with concentrations of dopamine producing neurons.
    As alluded to above, taking an appropriate NMDA (partial) antagonist will prevent the development of a tolerance for the effects of an amphetamine or amphetamine-like stimulant. Also, by preventing excess Ca++ influx into the neuron, an NMDA antagonist will prevent associated brain alterations and damage (excitotoxicity).

    Studies have indicated that amphetamine tolerance is prevented by exogenous or endogenous agents that are able to inhibit excess Ca++ influx into the neuron through the gated calcium channels on the neuronal membrane that have NMDA subtype glutamate receptors.Glutamate , the body’s major excitatory neurotransmitter, opens the gated calcium ion channels upon attaching to the NMDA receptor. A number of other receptors are also expressed on these calcium channels, which, when stimulated, either facilitate or inhibit glutamate’s action.

    It is also important that agents that inhibit calcium channel activity not also cause deficient Ca++ influx. For example, ketamine is a full NMDA receptor antagonist, that prevents excess Ca++ influx and amphetamine tolerance. But being a full NMDA antagonist, ketamine in excessive doses results in deficient Ca++ influx. This could be one of the reasons it leaves K-user in a state of disassociation.

    So basically we have following NDMA antagonists:
    1. Memantine (Akatinol/Axura)
    2. Acamprosate (Campral)
    3. Amantadine (Symmetrel/Amantix)
    4. Magnesium (supplement)
    5. Dextrometorphan/DXM
    6. Ketamine
    7. PCP
    (funny that 5,6,7 are recreational drugs)

    Two of them have minimal (or none) side effects and have been identified (and verified by one anecdotal person, which has been taking amphetamine-type stimulants and NDMA antagonist with same beneficial effects for a period of 2 years) as preventing amphetamine tolerance: 1) Memantine and 2) Acamprosate.

    1) Memantine is a partial NMDA antagonist that effectively puts an upper limit on Ca++ influx without compromising healthy levels of Ca++ influx. Memantine is not available in the US at this time. It is in stage 3 trials for Alzheimer’s disease. US approval may come within the next 2 years. Memantine is now approved in the European Union for the treatment of Alzheimer’s. It has been marketed in Germany since 1978 for the treatment of dementia and other cognitive disorders. It comes in 10mg tablets. One or two tablets/day are sufficient to prevent amphetamine tolerance, overactivity of the NMDA receptor and consequent free radical stress inside the neuron. The most expensive option though.

    2) Acamprosate (n-acetyl-homo-taurine) analogue of the amino acid taurine. Alternatively, it may be termed as a carrier molecule for taurine, that allows taurine to readily cross the blood brain barrier, unlike taurine itself. Taurine is a NMDA receptor antagonist. Acamprosate is an investigational drug in the US, undergoing stage 2 (?) trials for the treatment of alcoholics. It is available in most European countries as a treatment for alcoholism, with great efficiacy. Cheaper than memantine, however efficiacy should be the same.

    3) Amantadine, originally used in the treatment and prophylaxis of influenza infection and drug-induced Parkinsonism, also blocks NMDA receptors. Besides it is beneficial in traumatic head injury, dementia, multiple sclerosis,cocaine withdrawal and depression. Amantadine appears to act through several pharmacological mechanisms, none of which have been identified as the one chief mode of action. It is a dopaminergic, noradrenergic and serotonergic substance, blocks monoaminoxidase A and NMDA receptors, and seems to raise beta-endorphin/beta-lipotropin levels. I couldn't find what amount of the drug should be used to block NDMA. Cheaper than Acamprosate. No one has tested it yet, but I think it would be a good choice.

    4) Magnesium is also an NMDA antagonist. Most people are deficient in magnesium, and stress reduces magnesium levels. Whether or not one takes amphetamines, magnesium supplementation is very important for mood, general well-being and keeping stress levels under control. It is also important to take magnesium in efficient form, with adequate bioavailability. The best type is magnesium glycinate (chelated) with bioavailability at around 80%. Second best is magnesium carbonate with (I don't remember exactly) bioavailability at little above 30%. Supplemented magnesium should be at 500 mg/day level. Also there is a study which shows that children who use amphetamine-type stimulants have bad magnesium/calcium balance. Calcium levels stay the same with amphetamine usage, but magnesium levels drop.

    5) DXM - definitely the cheapest option of all NDMA antagonists, but I'd rather use Memantine or Acamprosate. Although, I've heard anecdotes that doses as low as 70 mg/day are enough to block NDMA - I couldn't find those amounts in abstracts/studies.

    6) and 7) I wouldn't use as an amphetamine tolerance prevention. Ketamine for its known effects (you wouldn't want to be in a K-hole during the tweak just for the sake of prevention tolerance)
    PCP - this one doesn't need explanation. It has nasty side-effects and I've mentioned it just because it is a NDMA antagonist. I wouldn't touch it even if it was dirt cheap.


    So basically combination of partial NDMA antagonist and amphetamines should prevent tolerance. But I'm curious whether NDMA antagonists are able to *reduce* amphetamine tolerance. If yes then my goal would be to reduce it as far as to the point of first speed experience :] Right now, I have high amphetamine tolerance (too much tweaking during short time in the summer) so I will be using Acamprosate to try and reduce my tolerance. I'll post my results here.
    And sorry for the length of the post - but I just wanted to write down everything I researched during last few days (I skipped PubMed abstracts).
    Take care.
    Last edited by MattPD; 21-06-2004 at 22:29.
     

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    #2
    dag, I appreciate youor entry so much. my only question to u is, do u have to take this with the dose of the amphetamine or can u take it apart from it, and what doses of magnesium exactly?
    this always begs to question whether or not jaw clenching (subtly known to be less intense while taking magnesium) is due to the influx of calcium. damn, and thanks again.
     

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    #3
    Thumbs up
    Excellent post Dag !! Thanks for sharing your research !!
    during your research did you come across any other negative effects other than tolerance from the excess Ca++ influx!!
    B interested in what results you get from Acamprosate ! any reverse in tolerance and/or negatives sounds like something I'd lik too know about. LoL
    which magnesium supplement r u using ? magnesium glycinate ?
    Keep us posted

     

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    #4
    Here's good post from another board (www.dr-bob.org) :


    > I'm not concerned with development of tolerance as I've been able to maintain a constant effect from amphetamines for months now without raising dose. In all fairness, I do take 60mg Delsym (dextromethorphan polystirex) twice daily, which is quite likely preventing tolerance. My pdoc endorses the use of DXM to all his stimulant-treated patients now, ever since I brought it to his attention months ago. He's seeing many patients finally stabilized on doses of amphetamines whereas they used to escalate monthly or even weekly. It doesn't seem to be working as well for his patients taking methylphenidate.
     

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    #5
    ^^You are lucky my friend, I told my pdoc about it and basically just shrugged it off and told me to just stick to my adderall.
     

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    #6
    Actually I (DaG was my old nick) have been using three things to keep my amphetamine tolerance.
    3 NDMA antagonists: DXM (60mg/day), Magnesium Glycinate (300-500mg/day), L-Theanine (100mg/day).

    The last NDMA antagonist hasn't been mentioned in the above post, because I didn't know about it at that time. Here's some info:

    1)
    Inhibition by theanine of binding of [3H]AMPA, [3H]kainate, and [3H]MDL 105,519 to glutamate receptors.

    http://www.ncbi.nlm.nih.gov:80/entre...&dopt=Abstract

    2)
    Inhibition of glutamate transporter by theanine enhances the therapeutic efficacy of doxorubicin.

    http://www.ncbi.nlm.nih.gov:80/entre...&dopt=Abstract

    3)
    Theanine as a glutamate antagonist at a crayfish neuromuscular junction.

    http://www.ncbi.nlm.nih.gov:80/entre...&dopt=Abstract


    There are also studies showing that L-Theanine increases dopamine (and to a lesser degree 5HT) , especially in striatum, hypothalamus and hippocampus. (DA is depleted after amphetamine stops working - so this combination could be of significance as far as "comedown")
    In addition, L-Theanine shows neuro-protective activity, see study below.

    1)
    Effect of theanine, r-glutamylethylamide, on brain monoamines and striatal dopamine release in conscious rats.

    http://www.ncbi.nlm.nih.gov:80/entre...&dopt=Abstract

    2)
    Neuroprotective effects of the green tea components theanine and catechins.

    http://www.ncbi.nlm.nih.gov:80/entre...&dopt=Abstract


    Many net resources also mention that L-Theanine increases GABA levels (just like benzodiazepines). I couldn't find any abstracts/studies about it though.
    All in all - it is a great supplement, costs not so much at BAC in powdered form.


    Well, as far as my results with my regime my Adderall usage has been steady at 40mg/day (most of the time, not always - I like to use more than what is needed for my ADD, for rec purposes of course ;-)

    I also know 2 guys who have used NDMA antagonists successfully for keeping the amphetamine tolerance at steady level.
    Ok just my 2 cents.
     

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    #7
    Here is some *great* update on the usage of DXM for amphetamine tolerance. Seems like the cheapest NDMA antagonist might be enough for the blockade of tolerance.

    Check this out (the first part was written by the poster from another board):



    I've been using Delsym (dextromethorphan polistirex, DXM, a sustained-release preparation of DXM) to prevent amphetamine-tolerance as long as I've been taking them. So that would be about 8-9 months of use without breaks, and the proof is in the pudding. :-)

    I haven't developed any tolerance whatsoever to any of the drug's effects. The dose started at 30mg/day (of the XR formulation), but an extra 30mg capsule later in the day was added onto that after a few weeks because they seemed to wear off too quickly for me. I stayed on that until a couple months ago when I switched to the immediate-release formulation, which I find lasts about eight hours per dose (quite surprisingly!), with a come-up beginning at approximately T+0:15 hours post-dose, a pronounced effect at T+1:00 pursuant, the peak at T+2:00 through T+7:00, followed by a gentle comedown which ends about T+9:00. The only difference I find between the IR and XR formulations of the drug is actually that the IR form lacks the mid-dose sluggishness and consequent "second-wind". So one dose at 6AM *really* kicks in at 8AM, beginning to wear off at 1PM; taking the second dose at noon times everything just perfectly. If I'm planning on making rounds of the bars with friends at night or practicing/playing a gig with my band, I just pop an extra 30mg in the early evening as needed.

    But back to the Delsym -- I used to take a full teaspoon of the 12-hour suspension twice daily (that's equivalent to 15mg Robitussin Maximum Strength Cough every six hours). This dose completely prevented any development of tolerance and *may* have even allayed some of the nastier stim side effects by antagonizing some excitatory neurotransmission via glutamate et al. For six weeks now though I've been taking Prozac at 40mg daily, which (along with its ultra-long-half-life metabolite, norfluoxetine) is among the most potent inhibitors of cytochrome P450 IID6 (aka debrisoquine 4-hydroxylase), along with quinidine and paroxetine. CYPIID6 is responsible for the metabolism via O-demethylation (removal of the methyl group at the sixth position in the structure) of dextromethorphan, which primarily acts upon PCP2 and sigma receptors, to the potent NMDA antagonist dextrorphan (DXO; the dextroratory form of the opioid levorphan, which is about equipotent to morphine). Thus I now take twice as much Delsym to ensure a more normal ratio of DXM to DXO in the blood. My doctor and all reseach I've done has assured me that this is perfectly safe (i.e. not nearly a dose sufficient to cause Olney's lesions, etc.). I would use another NMDA antagonist like Emenda (memantine HCl) if it were available to me, even if simply to avoid the simple carbohydrates in the syrup, but Medicaid will only cover three prescriptions monthly now that I've turned 21. I may, on the other hand, finally put my lab scale to good use and order pure dextrorphan tartrate from Sigma-Aldrich (0.5 grams = $63.30) so as to avoid the unnecessary PCP2/sigma activation associated with DXM. Another chemical I'm interested in is Merck, Sharpe and Dome Inc.'s (+)-MK-801 hydrogen maleate (dizocilpine hydrogen maleate), for which the Sigma-Aldrich "Cell Signalling and Neuroscience" catalog provides the following synopsis: "Highly potent and selective non-competitive NMDA receptor antagonist that acts at the NMDA receptor-operated ion channel as an open channel blocker. Inhibits behavioral sensitization to psychostimulants and ethanol." The cost is prohibitive, though -- $43.10/5mg. A more plausible idea may be any one of the following:

    Ifenprodil tartrate salt (alpha-(4-Hydroxyphenyl)beta-methyl-4-benzyl-1-piperidineethanol tartrate salt) -- "NMDA antagonist acting at the polyamine site; neuroprotective agent; alpha-adrenergic central and peripheral vasodilator; alpha-2-adrenergic receptor ligand."

    Arcaine sulfate salt (1,4-Diguanidinobutane sulfate salt) -- "Potent antagonist at the polyamine site of the NMDA receptor."

    7-Chlorokynurenic acid (7-Chloro-4-hydroxyquinoline-2-carboxylic acid; 7-Cl-KYNA) -- "Potent NMDA receptor antagonist; antagonizes the strychnine-insensitive glycine site of the NMDA receptor; prevents neurodegeneration produced by quinolinic acid."

    5,7-Dichlorokynurenic acid (5,7-Dichloro-4-hydroxyquinoline-2-carboxylic acid) -- "Potent excitatory amino acid receptor antagonist; active at the strychnine-insensitive glycine binding site of the NMDA receptor."

    d-3-Methoxy-N-methylmorphinanhydrobromide -- "Allosteric antagonist at NMDA-controlled ion channels; antagonist at voltage-dependent channels."

    Pentamidine isethionate salt (1,5-Bis(p-amidinophenoxy)pentane bis(2-hydroxyethanesulfonate salt)) -- "Neuroprotective; inhibits constitutive nitric acid synthase in the brain; NMDA glutamate receptor antagonist. Antimicrobial against 'Pneumocystis carinii'."

    Also important, I feel, is protection from neurotoxic levels of homocysteine -- I take quite a few vitamin/mineral/amino acid/herbal supplements, but B-12 and its cofactors are undoubtedly most important for this (not to mention avoidance of neurotoxic excitatory substances such as monosodium glutamate and aspartame).
     

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    #8
    And here's some scientific info on NDMA, DXM, Morphine & whole process of tolerance development etc. ( not only NDMA antagonists block amphetamine tolerance, but in theory they could also block opiate tolerance).



    ~Dextromethorphan Potentiates the Antinociceptive Effects of Morphine and the delta-Opioid Agonist SNC80 in Squirrel Monkeys

    http://jpet.aspetjournals.org/cgi/co...full/300/2/435

    ~Clinically Available NMDA Receptor Antagonists Memantine and Dextromethorphan Reverse Existing Tolerance to the Antinociceptive Effects of Morphine in Mice

    http://opioids.com/nmda/memantine.html

    ~The Uses and Psychoactive Properties of Dextromethorphan

    http://sulcus.berkeley.edu/mcb/165_0...ripts/_67.html

    ~MorphiDex (MSM) Double-Blind, Multiple-Dose Studies in Chronic Pain Patients

    http://opioids.com/morphidex/
     

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    Magnesium Taurate 
    #9
    Bluelighter
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    The best and only stop on the internet for any information you will ever need on magnesium is : http://www.coldcure.com/html/dep.html#kefir

    The best form of magnesium if Magnesium Taurate, it is SO important to supplement with Mag Taurate whether or not you use amphetamines. BUT - if you are a tweaker, the supplementation of Magnesium Taurate is *tremendously* beneficial: Here is some info from that site:

    "When I purchased my first bottle of magnesium glycinate, it was not from intelligence that I chose that particular compound of magnesium. It was just what was available on the shelf at the store I visited. After considerable research, I found that the store provided the second best form of magnesium that I could have chosen to treat depression. Only magnesium taurate (a form of magnesium that decreases chances of diarrhea) is superior to all other forms of magnesium. Both glycine and taurine have been used to effectively treat depression. Also taurine (the ligand in magnesium taurate) has been shown to be low or absent in 100 percent of people with depression and chronic pain according to Shealy.

    I quit taking and quit recommending magnesium glycinate because glycine, in the doses taken and while taken for a protracted period of time, will damage its delicate balance with another amino acid, taurine. Taurine is vital to mental and cardiac health and must not be disturbed, while glycine is ubiquitous and appears highly unlikely to be bothered by too much taurine. For example, diets with up to 1% as taurine had no adverse effect on test animals. Long term high doses of glycinate will eventually cause ever worsening cardiac arrhythmias and will never allow total recovery from depression or other mood disorders, although most people will find that it works miracles for them in the short-term. Also, both magnesium and taurine have been proven to be low in depression in about 80% and 100% of cases respectively. Read Shealy's article starting here. See sentence immediately before the Discussion section. This does not mean magnesium glycinate is harmful in the short- or near-term, it just means one shouldn't use it year in and year out, and it must be IMMEDIATELY stopped if side effects, particularly cardiac arrhythmias (PVCs and/or PACs) occur.

    Glycine (the second component of magnesium glycinate) chelates (removes) mercury from the body, and may be superior to even magnesium taurate for people with heavy metal poisoning in the short- or near-term. Citric acid and cysteine also remove mercury and appear safer for long term use than glycine. The first stability constants for glycine, cysteine and citric acid are in the log 10 to log 14 range, which are vastly stronger bindings than can be broken by any natural biology or chemistry event occurring in the body. Glycine is a non-essential amino acid, but for people with mercury poisoning, it, cysteine and citric acid may be highly important. Because of these amazing chelating, sequestering or binding powers, if they reacted with mercury in any form in the body, they should be able to bind them much more tightly, making mercury biologically unavailable in the body. Perhaps, consumption of large amounts of these amino acids from high quality protein sources, and consumption of citrus help protect from the toxic effects of mercury. Mercury is extremely toxic and can cause depression and many symptoms associated with depression. These symptoms include, insomnia, nervousness, memory loss, dizziness, anxiety, loss of self-confidence, irritability, drowsiness, weight loss, tremors, paraesthesia (numbness and tingling), hallucinations, headaches, fatigue, muscle weakness, hearing difficulties, emotional instability, skin inflammation, incoordination and kidney damage. The common areas where mercury is found are: auto exhaust emissions, used motor oils, pesticides, fertilizers, dental amalgams (silver fillings), drinking water (tap and well), leather tanning chemicals, felt, bleached flour, processed foods, fabric softeners, fish (tuna, swordfish, shark, king mackerel and tile fish), calomel (mercury chloride contaminant in talc, body powder), paint pigments and solvents, cinnabar (mercury sulfide - used in red jewelry items), inorganic mercury laxatives, mercurochrome/methiolate anti-infectives, cosmetics (mascara), floor waxes and polishes, wood preservatives, water plumbing & piping, adhesives, batteries, used air conditioner filters (better here than in the air), broken thermometers, and some electronic equipment. Consequently, supplementing several grams of these chelating agents daily is a good idea regardless of current mental health."

    Basically, the amount of magnesium that we ingest is not as important as the amount we absorb. Most absorbable: Taurate.

    I am using about 1000mg / day of Magnesium Taurate. Magnesium with B-6 is also recommended because it raises serotonin levels. The benefits it has had for me are:

    Muscles no longer hurt
    Happier
    Amphetamine tolerance way up

    this also might be due to the other supplements I am taking, which are many, but Mag Taurate is by far the best as far as amphetamine tolerance goes (for me).

    I am really really interested in this L-theanine. I will be buying it and supplementing it in the morning, will post results soon.
    Attached Images Attached Images
     

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    #10
    this is too much for me to work through. could someone dumb it down for me?
     

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    #11
    Wow. Well i have a bunch of amantadine around maybe i'll give that a try. I''d love to find a way to stop amph. tolerance or even reduce it. I'll be getting some dxm powder soon, which well it was cheap, not that i like to trip off it, got it cause it was cheap. I could make up capsules of doses of it, starting low maybe just so any effects i'd notice would go away, and try taking it every day and use dexedrine as i usually do and see if i notice a difference after a while.

    If that doesn't work good i'll give the amantadine a shot since i have a shitload laying around, i think they are 100mg each.

    Amphetamine tolerance sucks..
     

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    #12
    This thread = gold.
     

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    #13
    Psychopharmacology (Berl). 2002 Dec;164(4):376-84. Epub 2002 Oct 05. Related Articles, Links


    Effects of the NMDA antagonist memantine on human methamphetamine discrimination.


    Hart CL, Haney M, Foltin RW, Fischman MW.

    New York State Psychiatric Institute, Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA. clh42@columbia.edu


    RATIONALE: The discriminative stimulus effects of N-methyl- D-aspartate (NMDA) antagonists have been assessed in laboratory animals. To date, no published study has assessed their ability to alter methamphetamine-related discriminative stimulus effects in humans. OBJECTIVE: This study investigated the discriminative stimulus, subjective (e.g. "Good Drug Effect"), psychomotor performance, and cardiovascular effects (e.g. blood pressure) of oral methamphetamine following acute oral memantine (a non-competitive NMDA antagonist) in humans.

    METHODS: Initially, participants were trained to discriminate 10 mg methamphetamine from placebo using a standard two-response procedure (drug versus placebo). Then, the effects of memantine (0, 40 mg) on methamphetamine discrimination were examined across several methamphetamine doses (0, 5, 10, 20 mg) using a novel-response procedure (drug versus placebo versus novel).

    RESULTS: Following placebo pretreatment, 10 mg methamphetamine produced 99% methamphetamine-appropriate responding and placebo produced 75% placebo-appropriate responding. Following memantine pretreatment, participants responded as if they had been given a novel compound, although memantine did not significantly alter most subjective-effects ratings following methamphetamine. Memantine alone produced "positive" subjective effects and novel drug-appropriate responding.

    CONCLUSION: These data indicate that the memantine-methamphetamine combination produced novel discriminative stimulus effects and that memantine produced some stimulant-like subjective effects.
     

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    Re: Magnesium Taurate 
    #14
    Originally posted by DoctorDoctor
    The best and only stop on the internet for any information you will ever need on magnesium is : http://www.coldcure.com/html/dep.html#kefir

    The best form of magnesium if Magnesium Taurate, it is SO important to supplement with Mag Taurate whether or not you use amphetamines.

    I don't know about all that.
    Taurate doesn't really seem like something everyone should be needing to take in any doses.

    Generally calcium/magnesium are bound together, becaues 50% of magnesium or so that you absorb, is absorbed with calcium.




    From research, and my experience trying the supplements.

    Magnesium/calcium Citrate "Capsules" 125MG mag in them. Will absorb about the same amount amount in to your body, as most of those "500mg" "1000mg" magnesium supplement gimmicks.


    But most important seems to be the fact its a capsule, and a citrate combined with calcium supposingly. I never took the combo with calcium until recently.
    But before that, it was simply Magnesium Citrate Capsules - Which i still prefer as #1 choice, being only one element i'm taking at a time.


    Easy to find at any store, Absorbs well. no side effects, stoped many side effects of tweaking... to a nice balance.. and without any marketing ploys in it...over exaggerating on some additive they discovered worked well heh.



    -That is an extrememly good source, or at least intresting to read by the way doctordoctor. Thanks.


    It words alot of different facts, differntly to better understand for most.
    "one such drug is the amphetamine dextroamphetamine which has the unique property of elevating magnesium in serum and significantly reducing the calcium to magnesium ratio"


    Basically, this is reason i had started on the cal/mag combo already. I take large amounts of dextroamphetamine daily.


    Last edited by Synapse999; 16-06-2004 at 17:12.
     

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    #15
    Bluelight Crew snolly's Avatar
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    Thanks, that's been pretty useful. My tolerance to speed's been building up for awhile, though mainly my fault due to the parties I've been to.
    It would be very interesting to find out if tolerance could be reduced, rather than just prevented, cos I've been wanting to feel a repeat of my first few experiences with 'phet, as they were brilliant.
    I wouldn't say I've got a high tolerance to the stuff, but whereas it only used to take me a very small line to be absolutely buzzing, now it'll take quite a few.
    Quite annoying and bloody expensive too, so yeah...
     

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    #16
    Originally posted by bouncer

    ~Dextromethorphan Potentiates the Antinociceptive Effects of Morphine and the delta-Opioid Agonist SNC80 in Squirrel Monkeys

    http://jpet.aspetjournals.org/cgi/co...full/300/2/435

    ~MorphiDex (MS : DM) Double-Blind, Multiple-Dose Studies in Chronic Pain Patients

    http://opioids.com/morphidex/

    ---> ...but in theory they could also block opiate tolerance


    I don't know if anyone noticed but NDMA antagonists (at least DXM from the info above) can also "fool around" with opiate tolerance. Meaning reduce it or prevent. I wish someone being into opiates, would give a shot at 60mg DXM + his/her opiate/opioid of choice (Vicodin/Oxy/H/...) and see what kind of results would get. It would be *VERY* interesting..
     

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    #17
    More about Magnesium (from another forum)

    Magnesium
    --------------

    Dextroamphetamine can increase blood levels of magnesium, which causes significant lowering of the calcium to magnesium ratio in the blood. The change in this ratio may in part explain the effectiveness of stimulants like dextroamphetamine in hyperactive boys.

    1 Another magnesium-amphetamine interaction involves supplements of magnesium hydroxide, which are known to cause retention of amphetamines in the body.

    2 This could theoretically result in increased blood levels of these drugs. Finally, animal studies have suggested that magnesium supplements can increase learning and enhance the behavioral response to stimulants.

    3 For these reasons, the use of magnesium along with amphetamines may enhance the effectiveness of these drugs in the treatment of ADD, but controlled studies of this possibility are needed.

    References:

    1. Schmidt ME, Kruesi MJ, Elia J, et al. Effect of dextroamphetamine and methylphenidate on calcium and magnesium concentration in hyperactive boys. Psychiatry Res 1994;54:199–210.

    2. Hurwitz A. Antacid therapy and drug kinetics. Clin Pharmacokinet 1977;2:269–80.

    3. Reviewed in Schmidt ME, Kruesi MJ, Elia J, et al. Effect of dextroamphetamine and methylphenidate on calcium and magnesium concentration in hyperactive boys. Psychiatry Res 1994;54:199–210.
     

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    #18
    Bluelighter
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    when should these supplements be taken? ie if someone speeded just every once in awhile, should they use DXM/Magnesium...
    every day?
    for a few days before/after they take *amphetamine?
    at the same time they take *amphetamine ?
     

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    #19
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    I'd say no more than every day..though I dunno how good it is to multidose on mineral supplements a few times a day.
     

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    #20
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    oh my god....i need speed to be up to read this! guys...y do i feel like i won't be able to quit spped cold turkey? And most definatly my tolerance has increased.. help!! what do i do????
    ...start by reading all that info. can't understand all terminology...but....ive benn a speed user for almost a year. coke addict for almost 10yrs. smoker for too long. im doomed ah? (can u tell im canadian? ah?) **beautifly was here **
     

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    #21
    *BUMP*!

    This is a good thread..

    I'm wondering how some of you have been doing with this.

    I take dexedrine daily (almost daily), and although the tolerance is NOTHING near as bad as Adderall was, it still sucks.

    I was trying the dextromethorphan thing, like 30mg twice a day, then i guess i got sick of putting the stuff in capsules/measuring and stopped.

    But I just lately got a 'bulk' thing of l-theanine, and have been taking that at least once if not 2-3 times a day or whenever i take dex. Also almost daily but not quite, a big magnesium/calcium pill.

    Also while I was going to order l-theanine online anyway, I wanted to get some Aniracetam powder, because I do like the effect piracetam is doing (seems to potentiate amphetamines, aniracetam too). Also while "there" i grabbed some l-carnitine which i've been taking "just for the fuck of it, its good for me so why not" along with sometimes if i feel like capping up a capsule of Alpha Lipoic Acid.

    Now, I am not sure if its the combination of things lately, but.. anyway, I started taking amisulpride (about 50mg/day) a couple weeks or so ago, and just the last few days been taking the mao-a inhibitor moclobemide (actually was used to potentiate a mushroom trip, and experiment with other tryptamines, but just ended up taking 150mg or so a day, maybe sometimes 2 tabs/300mg). I've noticed my sleep has improved, usually its real hard for me to fall asleep, and then, real hard to wake up (dex!). Lately I haven't needed much dexedrine compared to before, if any really "needed" at all, but i'll just go on but notice i'll get tired at better times, and easily dose off. Usually after just a few hours of sleep, or 6-7hrs, i'm good, and I wake right up without the need to pop a dex. Usually, once i do fall asleep, i can sleep for SO long, and its hard to wake up.. not lately.

    Also I wanted to know if there is a certain amount of l-theanine that is "good" for this? If it helps prevent tolerance, after you take some how long does this effect last? I've just been putting a sorta random amount in a capsule, anywhere from 100-300mg when i take it, less if i take it more than once a day (less meaning around 100mg), usually a bit while before i take any dexedrine (if any at all, i just take it anyway).

    I know the amisulpride is probably giving me some 'energy' and motivation, and that may be the main reason, might be finally really 'kicking in' who knows. Also I do know that after taking piracetam for a while (I already had an old big bulk amount of that, which i thought was useless until i kept taking it daily) i've noticed what thats doing up there in the ol' head, and I like aniracetam too, and know that probably has something to do with the extra energy. I notice the dexedrine lasts longer and dont really notice it 'come down' suddenly like before, just kinda slowly lingers/wears off i guess.

    Anyway I highly recommend the 'racetams! I thought they were useless til lately. Even such things as, my eyes focusing on an object from near to far is like twice as fast. My memory and coming up with what to say, its like snap, faster than I can get it out. My internal mental image/"movie" of a memory is nice and vivid and clear, all senses vision/hearing/the wind blowing/how i felt is all nice and clear. Without dexedrine I have much better focus than normal, "faster mind" and "easier access" to ..more areas of the brain. Easier "access" to the right side where i can bring out more creativity when needed. Wierd shit, i like it hehe.

    Anyway this is a good thread, noticed nothing has been posted in it in a while, and its probably just floating along down not being seen anymore..
     

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    #22
    for us recreational speed users, would I want to just take some DXM or such medicines just before any uses, or is it something that I would have to maintain constantly?
     

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    #23
    Originally posted by toolazy2think
    for us recreational speed users, would I want to just take some DXM or such medicines just before any uses, or is it something that I would have to maintain constantly?

    You don't want to take any DXM with speed.

    Only thing worth considering to take with speed is maybe magnesium citrate/capsules.
    to reduce some of the neurotoxic effects, slow tolerance kinda.


    Other then that.....some people are just mixing way to many medications lately at once. They can/do conflict with eachother regardless of what there labeled "purpose" is.
     

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    #24
    Bluelighter Riemann Zeta's Avatar
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    I also enjoy amphetamines, but worry about neurotoxicity. Hence, I take methylphenidate for ADD, instead of Adderall. I have read about (from many of the articles cited in this thread) the tolerance-preventing effects of NMDA receptor antagonists. The issue of NMDA receptor antagonism preventing amphetamine-mediated dopaminergic neurotoxicity, however, has not really been addressed. Since the putative pathway for DA neurotoxicity is increased intracellular oxidation of DA to quinone species (which might interfere with the cellular cytochrome c oxidative phosphorylation chain), I don't seem how an NMDA receptor antagonist would help in this situation. That is, if the cellular damage is not Ca++ dependent and is ameliorated by DA reuptake transporter blockers.

    However, if I could have my cake and eat it too: take (d)-amphetamine and prevent neurotoxicity, I would be very happy. (D)-amphetamine lasts much longer than methylphenidate for ADD. I already have to take 3 of the bloody little Ritalin pills per day. (D)-amphetamine is also more fun recreationally.

    PS: What is the PCP2 receptor? I have heard this mentioned in papers and always thought that it was bullshit. PCP has significant affinity for the NMDA pore (the PCP1 receptor of old) and the dopamine reuptake transporter (the PCP2 receptor?), which dextromethorphan (but not dextrorphan) also binds to at high enough concentrations.
     

  25. Collapse Details
     
    #25
    Originally posted by Riemann Zeta
    I also enjoy amphetamines, but worry about neurotoxicity. Hence, I take methylphenidate for ADD, instead of Adderall. I have read about (from many of the articles cited in this thread) the tolerance-preventing effects of NMDA receptor antagonists. The issue of NMDA receptor antagonism preventing amphetamine-mediated dopaminergic neurotoxicity, however, has not really been addressed. Since the putative pathway for DA neurotoxicity is increased intracellular oxidation of DA to quinone species (which might interfere with the cellular cytochrome c oxidative phosphorylation chain), I don't seem how an NMDA receptor antagonist would help in this situation. That is, if the cellular damage is not Ca++ dependent and is ameliorated by DA reuptake transporter blockers.

    However, if I could have my cake and eat it too: take (d)-amphetamine and prevent neurotoxicity, I would be very happy. (D)-amphetamine lasts much longer than methylphenidate for ADD. I already have to take 3 of the bloody little Ritalin pills per day. (D)-amphetamine is also more fun recreationally.

    PS: What is the PCP2 receptor? I have heard this mentioned in papers and always thought that it was bullshit. PCP has significant affinity for the NMDA pore (the PCP1 receptor of old) and the dopamine reuptake transporter (the PCP2 receptor?), which dextromethorphan (but not dextrorphan) also binds to at high enough concentrations.

    isnt the entire structure, and how it works different with ritalin - compared to the amphetamines.
    and also, in the same effect is potentialy more toxic? (or am i getting confused due to the fact there is a billion anti-ritalin sites, and really none for d-amphetamine heh-
     

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