I copyd this from bluelight, its very interesting;


"Amphetamine tolerance is caused by an excess Ca++ influx through the NDMA receptor gated calcium channels. Too much Ca++ entering these channels is what causes your amphetamine tolerance to build.

Taking a NDMA partial antagonist has been shown to inhibit Ca++ flow into the NDMA receptor thus lowering amphetamine tolerance. Taking NDMA antagonists can also prevent future brain damage from too much amphetamines.

DXM, PCP, Ketamine and Magnesium are the most well-known NDMA antagonists and I would recommend only using the last one to treat amphetamine tolerance. Magnesium is responsible for maintaining stress levels . During periods of stress your body's magnesium levels are below normal and this in turn affects your mood as well. Research has shown that children with aphetamine-type medication have lower levels of magnesium in their body.

Magnesium is naturally found in banannas and peanuts. In order to lower amphetamine tolerance 500mg of magnesium a day should be taken.

I don't mean to self-promote but I did a bit of research on this subject when I was writing my FAQ I made a couple of years ago. There is more information on that FAQ if your interested."

Methylphenidate isn't an amphetamine.

1: J Biomed Sci. 2006 Sep;13(5):695-702. Epub 2006 Jul 23.
Links
Co-administration of dextromethorphan with methamphetamine attenuates methamphetamine-induced rewarding and behavioral sensitization.
Yang PP, Huang EY, Yeh GC, Tao PL.

Department of Pharmacology, National Defense Medical Center, P.O. Box 90048-504, Nei-Hu 114, Taipei, Taiwan, R.O.C.

Methamphetamine (MA) is well known as a potent CNS stimulant, which produces strong rewarding and behavioral sensitization after repeated administration. In the present study, we investigated whether co-administration of (DM) with MA could suppress these effects induced by acute and chronic MA treatment. The conditioned place preference (CPP) test was used to examine the rewarding/drug seeking effects and locomotor and stereotypic activities were measured to investigate behavioral sensitization induced by chronic MA. Our results revealed that co-administration of DM (20 mg/kg, ip) with MA (2 mg/kg, ip) almost completely abolished the MA-induced CPP and behavioral sensitization. Furthermore, both of the acute and chronic MA could result in an increase of dopamine (DA) turnover rate in the NAc and mPFC. The acute effects of MA on DA turnover rate could be attenuated by the co-administration of DM in both regions. The chronic effect of MA on DA turnover rate in the mPFC was also attenuated by the co-administration of DM. These results suggest that the effect of DM on blocking MA-induced rewarding and behavioral sensitization may be related to its effect on inhibiting the activity of DA neurons projected to mPFC and/or NAc.

PMID: 16865411 [PubMed - indexed for MEDLINE]

My layman interpretation of that is DXM might reduce a person developing tolerance to amphetamines by reducing their effectiveness. Which would be
pointless.

My layman interpretation of that is DXM might reduce a person developing tolerance to amphetamines by reducing their effectiveness. Which would be
pointless.

20mg/kg is a VERRY high dose. That would be well above the gram range for the avarage person. Im talking about low dose nmda antogonists supplementation. You can use magnesium instead wich is quite safe. Stimulants also deplete magnesium.

I posted some links to more about this but they have been removed.

Methylphenidate isn't an amphetamine.

I know , I didnt say it is

Alternate take one for a period of time and switch

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.

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.

This is could be verry good news people, why doesnt it excite anyone

I posted some links to more about this but they have been removed.

Yeah I wish I had seen them. Been searching online for a basis for the hypothesis.

1: Pharmacol Biochem Behav. 1990 Jul;36(3):531-8.
Links
Postconditioning effects of magnesium on cocaine conditioned place preference in mice.
Lawley SI, Kantak KM.

Department of Psychology, Boston University, MA 02215.

Magnesium chloride (MgCl2) has recently been shown to have stimulant-like properties. Because stimulants are known to induce conditioned place preference (CPP), the CPP procedure was used to test the hypothesis that cocaine and MgCl2 share similar stimulus properties. This would be shown if cocaine-induced CPP could be enhanced in a postconditioning preference test by MgCl2 and other stimulants. Mice were conditioned with 5.0 mg/kg cocaine to the nonpreferred end of a three-compartment straight shuttle box. All groups showed significant shifts in preference from the preconditioning test to the postconditioning test. There were no changes in place preference over test days in mice that were injected only with saline and therefore not conditioned. When animals were given acute injections of either saline, 5.0 mg/kg cocaine, 1.0 mg/kg amphetamine, 30 mg/kg MgCl2, 10 mg/kg pentobarbital, or 0.25 mg/kg haloperidol following conditioning with cocaine, amphetamine and MgCl2 elevated the conditioned cocaine effect, and pentobarbital and haloperidol decreased the conditioned cocaine effect compared to saline. In addition, there was a dose-dependent influence of MgCl2, with 30 mg/kg producing the maximum effect on the conditioned cocaine effect.

PMID: 2377655 [PubMed - indexed for MEDLINE]

1: Pharmacol Biochem Behav. 1990 Jul;36(3):539-45.
Links
Magnesium-induced conditioned place preference in mice.
Lawley SI, Kantak KM.

Department of Psychology, Boston University, MA 02115.

A conditioned place preference procedure was used in mice to test the hypothesis that magnesium possesses reinforcing properties. Mice were conditioned to the nonpreferred end of a three-compartment straight shuttle box with MgCl2 injections alternating with saline injections on the preferred end. Dose of MgCl2 was varied (0, 15, 30, 125 mg/kg) as well as number of conditioning trials (8 or 16). On the day after the first postconditioning test, animals were given acute injections of 5 mg/kg cocaine, or other test drug, to determine if the conditioned effect on behavior would be potentiated, maintained or blocked by these test drugs. Results demonstrated that 15 mg/kg MgCl2 induced the greatest amount of conditioning and that increasing the number of MgCl2/place pairings did not enhance the amount of conditioning, but rather, it decreased it. Amphetamine potentiated MgCl2-induced place preference; cocaine and pentobarbital maintained it; and haloperidol blocked it. These data indicate that MgCl2 has some primary reinforcing properties in mice and that MgCl2 shares stimulus properties with other stimulants and reinforcing substances.

PMID: 2377656 [PubMed - indexed for MEDLINE]

15-30 mg MgCl2 per kg works out to 3.8-7.7 mg Mg per Kg. A supplement that was 80% bioavialable from oral intake would put the dose at 4.8-9.5 mg of Mg from magnesium glycinate per kg. In my case at 73 kg that would be 350-700 mg of magnesium a day.

mohawk, i'm excited

has anyone actually tried this?

So if I understand correctly, most side effects should go away if you combine Ritalin with Magnesium? If so I'll try it out and let you guys know.

Methylphenidate isn't an amphetamine.

Actually, I read somewhere that "Methylphenidate" does come under the "Amphetamine" family.

Methylphenidate has it's own family now, it is referred to as a methylphenidate, ther are two methylphenidate class medications which is probably why they were branched into their own group.

Ritalin and Focalin are part of that group. Focalin is Dexmethylphenidate.

Actually, I read somewhere that "Methylphenidate" does come under the "Amphetamine" family.

Its mostly pointless semantics there is no official nomenclature. But my layman's answer is methylphenidate is in the amphetamine family. For two reason one Methylphenidate is a strong CNS stimulant and second it's structure is related to amphetamine and methamphetamine.

http://img175.imageshack.us/img175/153/92070414yi6.png

Mohawk 1984, I'm very excited about this. I'll try it out and let you know how it works out. Thanks!!!

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.

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.

This is could be verry good news people, why doesnt it excite anyone


This study has been cited before in these fora. It's old news. Moreover, its authors are mistaken regarding the causes of tolerance.

and why is that?

Drinking a teaspoon of baking soda, or taking a tums will reduce tolerance as well.

Drinking a teaspoon of baking soda, or taking a tums will reduce tolerance as well.

This will not reduce tolerance. However, what it will do is potentiate the medication and potentially cause someone to experience a much longer effect from their medication, in fact it's impossible for a person to know exactly how long the effect will last. This can be a bad thing, and a potentially unhealthy thing for someone who was anticipating their medication to where off by a certain time. This will not cause an increase in potency, and it is ill advised for anyone to try this without talking to their Dr about it first.

Tolerance to a medication is only reduced by the absence of the medication which caused the tolerance to develop.

People who abuse these medications do not take drug holidays to reduce tolerance. They periodically increase their dosage until they overcome their tolerance. That's not to say that everyone who increases their dosage is abusing these medications.

When I first started taking medication, I was quite content at a 5mg dose for quite some time. However, my Dr and I both decided that it would be wise to try a larger dose. Turns out we were right. This process went on for quite some time, but eventually I reached a point where I achieved a dose that was ideal for me and did not (or has not) caused me to need anymore dose adjustments.

It's best to discuss any issues concerning tolerance with your Dr to see if maybe you might be in need of a dosage adjustment, or perhaps a drug holiday, or perhaps a different drug all together.

PCP? Really?

Anyways, thank you. I asked recently on the adderall board and people reccomended magnesium so I'm on 500 mg/day. I don't get the calcium thing though. If we have too much calcium in our blood, will it cause tollerance?

PCP? Really?

Anyways, thank you. I asked recently on the adderall board and people recommended magnesium so I'm on 500 mg/day. I don't get the calcium thing though. If we have too much calcium in our blood, will it cause tolerance?
Nobody has mentioned PCP here. Perhaps you are confusing what was mentioned in the first page of this thread when someone talked about "CPP" or "conditioned place preference."

Calcium is not the catalyst here. The bicarbonate is the catalyst here, and I am fearing that this thread is starting to flow in a direction that would violate the rules of the medications forum. In this forum we only discuss prescribed therapeutic uses of these medications, and potentiating these drugs is not something that lowers tolerance, nor is it something that falls under the defiition of prescribed use, unless under a Dr's orders.

Potentiating these drugs with other things is something that is discussed in the addictions/substance abuse forum. Please feel free to start a thread discussing these things in that forum. For now, lets just focus on things that will reduce tolerance in this thread. Thanks.

Magnesium supplementation (not oxide) within a reasonable range is an excellent idea for numerous reasons.

Nobody has mentioned PCP here. Perhaps you are confusing what was mentioned in the first page of this thread when someone talked about "CPP" or "conditioned place preference."

Original post says... DXM, PCP, Ketamine and Magnesium are the most well-known NDMA antagonists and I would recommend only using the last one to treat amphetamine tolerance.

Eh.

Calcium is not the catalyst here. The bicarbonate is the catalyst here, and I am fearing that this thread is starting to flow in a direction that would violate the rules of the medications forum. In this forum we only discuss prescribed therapeutic uses of these medications, and potentiating these drugs is not something that lowers tolerance, nor is it something that falls under the defiition of prescribed use, unless under a Dr's orders.

Potentiating these drugs with other things is something that is discussed in the addictions/substance abuse forum. Please feel free to start a thread discussing these things in that forum. For now, lets just focus on things that will reduce tolerance in this thread. Thanks.
Oh ok. Thanks. I didn't realize it was something bad, just a way to reduce the acid in your stomach so it works properly. People were recommending it on the board below this one at some point.

Original post says... DXM, PCP, Ketamine and Magnesium are the most well-known NDMA antagonists and I would recommend only using the last one to treat amphetamine tolerance. Sorry about that, I didn't notice it when I was skimming back through the thread. :o





Oh ok. Thanks. I didn't realize it was something bad
Please don't assume that I think it's bad. I am not saying that it's a bad thing. I was just trying to point out that it's usually something that is done by those who abuse drugs like these to increase the duration of these medications.

Unless a persons Dr instructs them to do that, then it is not appropriate for this forum. This forum is for the discussion of prescribed treatments.

Even if this was being discussed in the addictions forum I would not necessarily see it as a bad thing. I am not easily offended by addictive behavior, because I recognize it as a medical problem first and foremost. Fortunately there is a forum here at the ADHDF for just about everyone, and I am very grateful for that fact.

Sorry about that, I didn't notice it when I was skimming back through the thread. :o


Please don't assume that I think it's bad. I am not saying that it's a bad thing. I was just trying to point out that it's usually something that is done by those who abuse drugs like these to increase the duration of these medications.

Unless a persons Dr instructs them to do that, then it is not appropriate for this forum. This forum is for the discussion of prescribed treatments.

Even if this was being discussed in the addictions forum I would not necessarily see it as a bad thing. I am not easily offended by addictive behavior, because I recognize it as a medical problem first and foremost. Fortunately there is a forum here at the ADHDF for just about everyone, and I am very grateful for that fact.
Well alright. I thought it just would make it so that you got the dose you were supposed to since it's all that's in the pill.

This will not reduce tolerance. However, what it will do is potentiate the medication and potentially cause someone to experience a much longer effect from their medication, in fact it's impossible for a person to know exactly how long the effect will last.

According to this the difference in half-life for acidic and basic urine for a
basic drug was basic urine gave twice the half-life. The compound in the study
was 2-methoxymethamphetamine.

1: J Pharm Sci. 1987 Jun;76(6):427-32.
Links
Influence of urinary pH on the disposition of methoxyphenamine and three metabolites in humans.
Roy SD, Hawes EM, Midha KK.

The disposition of methoxyphenamine (o-methoxy-N,alpha-dimethylphenethylamine) and three of its metabolites was studied in five healthy volunteers on three occasions, with the urine pH separately under uncontrolled, acidic, and basic conditions. All five volunteers were extensive metabolizers of debrisoquine and methoxyphenamine, the latter with respect to O-demethylation and aromatic 5-hydroxylation. The plasma peak concentration and the area under the curve of methoxyphenamine from 0 to infinity did not differ significantly during the three phases of the study. However, on the average, its renal clearance increased by fivefold and its plasma terminal half-life decreased by twofold in the acidic as compared with the alkaline urine condition. The urinary excretions of methoxyphenamine and its metabolites N-desmethylmethoxyphenamine and O-desmethylmethoxyphenamine were significantly enhanced in the uncontrolled pH and the acidic urine conditions as compared with the alkaline urine condition. By contrast, the urinary excretion of the 5-hydroxymethoxyphenamine metabolite was not significantly affected by urinary pH variations. The mean urinary excretion ratios methoxyphenamine: O-desmethylmethoxyphenamine and N-desmethylmethoxyphenamine: O-desmethylmethoxyphenamine did not differ significantly during the three phases of the study, whereas the methoxyphenamine:5-hydroxymethoxyphenamine and N-desmethylmethoxyphenamine:5-hydroxymethoxyphenamine ratios were significantly altered during the alkaline phase as compared with the other two phases. Therefore, the ratios in terms of O-desmethylmethoxyphenamine are recommended for phenotyping individuals when using methoxyphenamine as a metabolic probe.

PMID: 3625484 [PubMed - indexed for MEDLINE]

According to this the difference in half-life for acidic and basic urine for a
basic drug was basic urine gave twice the half-life. The compound in the study
was 2-methoxymethamphetamine.
Very interesting, however, for starters that is not a drug that is used in the treatment of ADHD.

Secondly, where are the methods for that study indicating just how those subjects received the 2-methoxymethamphetamine?

Instead of spending a lot of time explaining what I want to say here, let me just say that back in the summer/fall of 2006 I got into a similar discussion about urinary pH and how it can or can't extend the half life of Dexedrine. To make a long story short, I ended up emailing one of my best friends who was in his final year of pharmacy school, and I asked him to explain things to me so that I might be able to explain things to the other member here at the forums who had misunderstood the effect of urinary pH on a drug like Dexedrine. Below was his response from the email he sent me:

"the short answer is that absorption of an oral drug takes place in the GI tract through the small intestine. The only way that urine pH would be affected is if some of the free base did not absorb. Thus, dexedrine as a free base would raise the urine pH if it did not absorb. The stomach pH is low, and that converts the amine base dexedrine into a hydrochloric acid salt. Entities passing through the small intestine into the blood are polar, and a salt is the best case scenario of polarity. Lowering the urine pH has no appreciable effect on drug absorption through the GI. If anything, it means that absorption was poor. Dexedrine will already be an HCL, H2SO4, tartrate, or maleate salt in the pill form to aid in shelf life and GI absorption. Kidneys are only for blood filtration of metabolites of a given drug, and in that sense, If dexedrine were in free base form, it would stay away from the kidneys longer since they filter ions. But freebase dexedrine would also have very poor absorption through the GI. So the person at that forum who told you this is absolutely wrong."<!-- / message -->

Very interesting, however, for starters that is not a drug that is used in the treatment of ADHD.

Secondly, where are the methods for that study indicating just how those subjects received the 2-methoxymethamphetamine?

Instead of spending a lot of time explaining what I want to say here, let me just say that back in the summer/fall of 2006 I got into a similar discussion about urinary pH and how it can or can't extend the half life of Dexedrine. To make a long story short, I ended up emailing one of my best friends who was in his final year of pharmacy school, and I asked him to explain things to me so that I might be able to explain things to the other member here at the forums who had misunderstood the effect of urinary pH on a drug like Dexedrine. Below was his response from the email he sent me:

"the short answer is that absorption of an oral drug takes place in the GI tract through the small intestine. The only way that urine pH would be affected is if some of the free base did not absorb. Thus, dexedrine as a free base would raise the urine pH if it did not absorb. The stomach pH is low, and that converts the amine base dexedrine into a hydrochloric acid salt. Entities passing through the small intestine into the blood are polar, and a salt is the best case scenario of polarity. Lowering the urine pH has no appreciable effect on drug absorption through the GI. If anything, it means that absorption was poor. Dexedrine will already be an HCL, H2SO4, tartrate, or maleate salt in the pill form to aid in shelf life and GI absorption. Kidneys are only for blood filtration of metabolites of a given drug, and in that sense, If dexedrine were in free base form, it would stay away from the kidneys longer since they filter ions. But freebase dexedrine would also have very poor absorption through the GI. So the person at that forum who told you this is absolutely wrong."<!-- / message -->

We are talking about two different things though. Your friend is talking about
absorption of dexedrine. Variables in absorption may or may not effect the half-life of the drug in the blood. They certainly could effect initial blood levels.
Ounce in the blood though dexedrine half-life will largely be determine by how
fast the kidneys can remove it or its metabolites. Acidic urine will likely remove dexedrine twice as fast from the blood. Also note from the study that
the 5-hydroxy (a phenol)metabolite was not effected by urine pH as much. That is because phenols are acidic and would have improved excretion in
basic urine in the same way aspirin would and the amino base part of the metabolite would have improved excreation in acidic urine.

The rate the liver can oxidize dexedrine to a weak or inactive metabolite like 4-hydroxylamphetamine that could be excreting efficiently in a wide range of urine pHs would determine the maximum half-life.

You're right, we are talking about two different things. I am talking about drugs (specifically prescription stimulants) that are taken orally, which are then absorbed primarily in the G.I. tract (small intestine primarily).

You are referring to something that dose not indicate how the subjects in that study were dosed with 2-methoxymethamphetamine. Perhaps it could it have been through an IV? Trans dermal patch? Insulfating (this would be the least likely)? etc. Drugs absorbed through the G.I. tract are not significantly impacted by urinary pH.

Can you confirm how the subjects in that study were dosed? If you go back to the study, it will be clearly stated under the methods section.

PS Instead of responding in this thread, I would ask that you either please send me a PM and let me know the method that the 2-methoxymethamphetamine was dosed into those subjects, or just start a new thread in a forum where the discussion of illegal drugs is appropriate. The medications forum is a forum for the discussion of legally available prescription drug therapies used in the treatment of ADHD. This thread has gone off topic enough at this point, and I do not want to see it go any further off topic. This thread is about preventing "amphetamine/methylphenidate tolerance," which means it is a thread about two drugs which are legally prescribed for the treatment of ADHD. In contrast, 2-methoxymethamphetamine is not only a schedule I controlled drug (meaning it's highly illegal with no known therapeutic use), but it has never been approved for the treatment of ADHD.

You're right, we are talking about two different things. I am talking about drugs (specifically prescription stimulants) that are taken orally, which are then absorbed primarily in the G.I. tract (small intestine primarily).

You are referring to something that dose not indicate how the subjects in that study were dosed with 2-methoxymethamphetamine. Perhaps it could it have been through an IV? Trans dermal patch? Insulfating (this would be the least likely)? etc. Drugs absorbed through the G.I. tract are not significantly impacted by urinary pH.

Can you confirm how the subjects in that study were dosed? If you go back to the study, it will be clearly stated under the methods section.

PS Instead of responding in this thread, I would ask that you either please send me a PM and let me know the method that the 2-methoxymethamphetamine was dosed into those subjects, or just start a new thread in a forum where the discussion of illegal drugs is appropriate. The medications forum is a forum for the discussion of legally available prescription drug therapies used in the treatment of ADHD. This thread has gone off topic enough at this point, and I do not want to see it go any further off topic. This thread is about preventing "amphetamine/methylphenidate tolerance," which means it is a thread about two drugs which are legally prescribed for the treatment of ADHD. In contrast, 2-methoxymethamphetamine is not only a schedule I controlled drug (meaning it's highly illegal with no known therapeutic use), but it has never been approved for the treatment of ADHD.

2-methoxymethamphetamine is not a schedule I drug its a prescription
sympathomimetric drug like ephedrine. It has about zero abuse potential.
I assume the study used IV injection. I think your missing the point absorption
and excretion are two different things. Absorption effect how much drug gets to the blood excreting effect how long it stays in the blood.

2-methoxymethamphetamine is not a schedule I drug its a prescription sympathomimetric drug like ephedrine. It has about zero abuse potential. You're right. I apologize, but I mistakenly thought I read "2,5-Dimethoxyamphetamine" which is a schedule I controlled substance. My mistake, it's getting late. :o






I assume the study used IV injection. I think your missing the point absorption and excretion are two different things.You're right, I was missing the point. I was thrown off by an earlier post (by another member concerning how absorption could be altered with bicarbonates). I had not responded to this thread prior to that post, but I honestly should have read the first page of this thread before responding to your post. I'm sorry for not following along with the thread better than I did, and for making the wrong assumption after reading your post.





Absorption effect how much drug gets to the blood excreting effect how long it stays in the blood. Well said. I knew the difference between the two already, I am just not on top of my game tonight. Sorry for the confusion, and thank you for being so patient with me.

It's not you, it's me...:o

, I am just not on top of my game tonight. Sorry for the confusion, and thank you for being so patient with me.



Yeah I can understand when I'm tired or stressed my productivity is limited to laying in a fetal position and shaking. ADD meds are good at getting you through the day but when they wear off its hard. Which may explain alot why
addicts will use them in non-stop binges.

Thanks for understanding Theta, and thanks for posting so many informative post like you do. ;)

15-30 mg MgCl2 per kg works out to 3.8-7.7 mg Mg per Kg. A supplement that was 80% bioavialable from oral intake would put the dose at 4.8-9.5 mg of Mg from magnesium glycinate per kg. In my case at 73 kg that would be 350-700 mg of magnesium a day.
I'm about 100 kg, which meant a 500mg-1g dose. It's 2.5 times of RDA at the higher end-- are you sure it's not a problem?

I'm about 100 kg, which meant a 500mg-1g dose. It's 2.5 times of RDA at the higher end-- are you sure it's not a problem?

Not sure but taking too much magnesium can have a laxative effect. As for as the problems of too much in the blood:

http://dietary-supplements.info.nih.gov/factsheets/magnesium.asp

What is the health risk of too much magnesium?
Dietary magnesium does not pose a health risk, however pharmacologic doses of magnesium in supplements can promote adverse effects such as diarrhea and abdominal cramping. Risk of magnesium toxicity increases with kidney failure, when the kidney loses the ability to remove excess magnesium. Very large doses of magnesium-containing laxatives and antacids also have been associated with magnesium toxicity [25]. For example, a case of hypermagnesemia after unsupervised intake of aluminum magnesia oral suspension occurred after a 16 year old girl decided to take the antacid every two hours rather than four times per day, as prescribed. Three days later, she became unresponsive and demonstrated loss of deep tendon reflex [57]. Doctors were unable to determine her exact magnesium intake, but the young lady presented with blood levels of magnesium five times higher than normal [25]. Therefore, it is important for medical professionals to be aware of the use of any magnesium-containing laxatives or antacids. Signs of excess magnesium can be similar to magnesium deficiency and include changes in mental status, nausea, diarrhea, appetite loss, muscle weakness, difficulty breathing, extremely low blood pressure, and irregular heartbeat [5,57-60].

Clearly if you have kidney problems you should avoid taking too much.

OTOH, I take up to 1600mg (400mg 4x, various forms -- citrate, malate, a little glycinate and orotate when I'm feelin' extra special) daily. It works very well for me. I do not take psychostimulants at this time -- its effects are evinced in a strong resistance to stress, which I have never had, and vastly improved sleep quality. I can ascribe these changes with strong confidence to the magnesium supplementation. I do not typically make these kind of gushing claims for any substance (except lysergic acid diethylamide, whoops) but it has worked well for me. Note that I believe many people would get diarrhea at these doses, and some people also respond with a feeling of tiredness. So it's not good for everyone.

a 500mg-1g dose. It's 2.5 times of RDA at the higher end-- are you sure it's not a problem?

If I recall correctly there has been discussion of raising the RDA to 1000mg, but perhaps considering that so many people are already deficient at the current setting, this seemed excessive.

I don't know anything about how magnesium effects amphetamine tolerance, but I have read studies that state that better that 80% of ADDers are deficient in it, and that by adding it to the diets of children being studied there was an improvement in their symptoms.

to support what Scattered wrote above, taken from: http://www.smart-nutrition.net/JamesSouth-ADHD.htm

Magnesium: Mineral For The Mind<?XML:NAMESPACE PREFIX = O /><O:P></O:P>
Magnesium is the activator mineral for over 300 different enzymes - more than any other mineral. (53) Magnesium serves as the mineral activator for most of the enzymes of the glycolytic and Krebs' cycles. (54) Once ATP is produced, it is normally complexed with magnesium for stable storage. (55) Magnesium activates sodium potassium ATPase, the membrane pump which transfers sodium and potassium across neural membranes to allow repeated bursts of electrical nerve activity (56), and which consumes up to 40% of neural ATP. (10) Magnesium regulates the activity of NMDA glutamate receptors, and thus glutamate nerve activity. (57 (excitotoxins:%20the%20Ultimate%20Brainslayer)) Glutamate nerves are the chief excitatory nerves, and are the primary neurons, along with the GABA nerves, in the brain areas connected with attention: the frontal cortex, hippocampus, striatum, thalamus, hypothalamus, and posterior cortex. (58) <O:P> </O:P>
Given magnesium’s myriad roles in human physiology, it is perhaps not surprising that cellular magnesium deficiency leads to a wide variety of symptoms: anxiety, fear, restlessness, poor attention, confusion, memory loss, mood changes including depression, lack of co-ordination, appetite loss, weakness, insomnia, muscle tremors, disorientation, learning disability, apathy, fatigue, heart disturbances, problems in nerve conduction and muscle contraction, muscle cramps, and predisposition to stress, to name just a few! (59-62) Note that many of these symptoms are common to ADHD.<O:P> </O:P><O:P></O:P>
Is magnesium deficiency common enough to think that it might play a role in difficulties with attention, memory, learning abilities, restlessness, etc.? Actually, most people in the Western world are probably at least marginally magnesium deficient. Dietary surveys show women on typical Western diets to average 175-225mg magnesium /day, men 225-275mg magnesium /day. A typical modern "junk food" diet, consisting primarily of soft drinks, hot dogs, hamburgers, white bread, French fries, cheese, pastries, candy, pizza, snack chips, etc. might fail to provide even 200mg Mg/day. The RDA for magnesium has been set at 300-400mg/day. Yet magnesium "guru" Mildred Seelig, M.D., has done extensive research which indicates that 8mg/kg bodyweight is probably a more optimal intake level. (63) This would be a 560mg/day requirement for a 70kg (154 pound) person.<O:P> </O:P><O:P></O:P>
In addition, there are many factors that impair intestinal absorption of magnesium. High intake of phosphate (common in meat, soft drinks and baked goods) calcium, fat, phytate (found in unleavened bread and wheat bran), lactose (milk sugar), oxalate (found in spinach, rhubarb, chocolate), and alcohol, as well as laxative abuse, all inhibit intestinal magnesium absorption. (53, 59, 60) Healthy kidneys may reabsorb up to 95% of magnesium before it is lost in the urine, yet many factors promote magnesium urinary loss: the stress hormones adrenaline and cortisol, diuretics (including caffeine), some antibiotics, digoxin, alcohol, high sodium/calcium/sugar intake (i.e. the typical western diet) and birth control pills, among others. (53, 59, 64) Thus anyone who lives the typical modern high stress/ high fat and sugar/ high soft drink/ high coffee and alcohol lifestyle may be an appropriate candidate for magnesium supplementation, with increased focus, attention, stress resistance, memory and learning powers as possible benefits. However, magnesium repletion at the cellular level is a slow process, and may take weeks to months to achieve maximum benefit. Most people can safely and beneficially take 100 - 200mg magnesium 2 - 3 times daily (with some at bedtime for insomniacs). If diarrhea develops, reduce dosage and /or frequency. Anyone with serious kidney disease should check with a nutritionally knowledgeable physician before adding magnesium. Best supplement forms are magnesium malate, orotate, succinate, taurinate, glycinate, aspartate, and chloride.<O:P> </O:P>

Sorry to those who are writting chemical novels I am curently un-medicated and lack the attention span to absorb such . . . complex confusion. I am just going to bottom line it here okay.

Drinking a teaspoon of baking soda, or taking a tums will reduce tolerance as well.


Actually they decrease the acid in the stomach which increases absorption effectiveness - however one must also be careful when ingesting things like baking soda - Sodium hydrogen carbonate - is the chemical name for this - sodium is normally in a over abundance in our foods any way I am unsure recommending adding more is such a wonderful idea here.

People which kidney problems may find clearing these chemicals difficult and sodium is one of the four electrolytes - electrolytes effect the induction of electrical impulses - including but not limited to the heart beat.

Females with PMS issue the last thing we need is MORE sodium - swelling from "mother nature" and her progesterone is bad enough -

Increasing the sodium may also decrease other necessary chemicals - potassium comes to mind. Although young healthy people will probably have no problems one must remember not all ADDF members are young / healthy.



Although Tums has calcium - over use could lead to constipation - calcium even in supplements taken in the recommended amounts can cause constipation in some -

Just as use of these acid reducing products can increase the absorption of things like ADD medications antacids can also reduce the absorption of other medications - some people are treating more than just ADD - therefore any more than occasion usage should be discussed with your doctor before hand Any use of anti-acids by those who have other conditions and/or who are on other medications should be discussed with your doctor or pharmacist first.




Not sure but taking too much magnesium can have a laxative effect

MOM - Milk of Magnesia {magnesium}

Mag-citrate - Magnesium and citrate

Both above named over the counter medications are laxatives therefore I am sensing there is a connection between magnesium intake and looser bowel movements.

I am not scientist, doctor or genius I have just :rolleyes: been constipated from too much calcium . .. ..:o


The tolerance issue I believe some may experience this however I believe it to happen less than believed. So many equate the effectiveness of ADD medications with "feelings" they believe if they do not feel the effects then the medication can't possibly be working - Here a bit of news:

Just because you no longer feel the medications does NOT mean they are no longer working. Do not go on feelings go on your ability to function. . . .


If you take any medications long enough you will become used to it I have been on Adderall for over ten years and I no longer "feel" the effects. I haven't in years. . . because I am used to the changes they make in my chemistry. . . .

Analogy

A man who has always kept a bread will notice the change in the feeling of his face when he first begin shaving it . He will notice the feeling in his face because it is different than it was when he had a beard, However if he continues to shave every day he will remain clean shaven. Just because he becomes used to the feeling of being clean shaven doesn't mean his razor has quit working. . . .the same principle applies to ADD medication. . .




Function is the way to go in telling weather or not your medications are working however if one is convinced the medication isn't working because there is no longer a certain feeling or is one preoccupied by the worry of medication tolerance then the lack of focus is due to ones own thoughts not a medication tolerance.

A man who has always kept a beard will notice the change in the feeling of his face when he first begin shaving it . He will notice the feeling in his face because it is different than it was when he had a beard, However if he continues to shave every day he will remain clean shaven. Just because he becomes used to the feeling of being clean shaven doesn't mean his razor has quit working. . . .the same principle applies to ADD medication. . .
When you first realize you need glasses and get that brand-new pair, you notice a remarkable difference in your vision...then you get used to that and it no longer seems remarkable. You do not need another prescription unless your vision actually gets worse.



Just because you no longer feel the medications does NOT mean they are no longer working. Do not go on feelings go on your ability to function. . . .
YATTA!

Here here!

Huzzah!

Hurray!

Etc!

:cool: