82 replies to this topic

[bgwithadd]

DOesn't theanine have the same mechanism as memantine? Since I can't get any memantine easily it would be nice to find a substitute.

[Jacovis]

Nicotinamide/NAD may be useful for D-amphetamine (AMPH)-induced dopamine (DA) depletion and energy metabolism change at least according to this study focusing on the rat striatum...

1: Brain Res Bull. 1999 Oct;50(3):167-71.
D-amphetamine-induced depletion of energy and dopamine in the rat striatum is attenuated by nicotinamide pretreatment.

Wan FJ, Lin HC, Kang BH, Tseng CJ, Tung CS.
Institute of Undersea and Hyperbaric Medicine, Taipei, Taiwan, Republic of China.
The present study examined the effects of nicotinamide on the D-amphetamine (AMPH)-induced dopamine (DA) depletion and energy metabolism change in the rat striatum. In chronic studies, co-administration of AMPH with desipramine, a drug that retards the metabolism of AMPH, (10 mg/kg, intraperitoneal [i.p.], respectively) caused a significant decrease of striatal DA content measured 7 days later. Pretreatment with nicotinamide (500 mg/kg, i.p.), the precursor molecule for the electron carrier molecule nicotinamide adenine dinucleotide (NAD), attenuated this effect of AMPH, whereas itself exerted no long-term effect on striatal DA content. In acute studies, a decrease in striatal adenosine triphospate/adenosine diphosphate (ATP/ADP) ratio was found 3 h after co-injection of AMPH and desipramine. However, nicotinamide pretreatment blocked the reduced striatal ATP/ADP ratio and resulted in a striking increase in striatal NAD content in AMPH-treated rats. Furthermore, nicotinamide was noted to increase striatal ATP/ADP ratio and NAD content in saline-treated rats. These findings suggest that nicotinamide protects against AMPH-induced DAergic neurotoxicity in the striatum of rats via energy supplement.
PMID: 10566977 [PubMed - indexed for MEDLINE]


NOW has an interesting NAD lozenge/sublingual product (see below). Some people have seen decent results with it. Tryptophan (Trp), nicotinic acid (Na), nicotinamide (Nam), nicotinamide riboside (NR), and possibly nicotinic acid riboside (NaR) are the only known metabolic pathways to form NAD+ in the cell. Other interesting 'related' substances are 'No Flush Niacin' (Inositol Hexanicotinate), Trigonelline (N-methylnicotinate), Xanthinol Nicotinate, and ENADA NADH. In addition, Benagene (3-carboxy-3-oxopropanoic acid) is said to increase the amount of NAD+ available as well. Interventions known to produce a favourable NAD+/NADH ratio include R(+)- lipoic acid, carnosine, 3-carboxy-3-oxopropanoic acid, and Calorie Restriction (CR). Resveratrol should be helpful in this area as well...


http://www.nowfoods....lly/M011571.htm
NAD 25 mg - 60 Lozenges

Serving Size: 1 Lozenge
Servings Per Container: 60

Amount Per Serving % Daily Value
Niacin (as Nictinamide) 4 mg 20%
NAD (ß Nicotinamide Adenine Dinucleotide) 25 mg †
Stevia rebaudiana Extract (min. 90% total Steviosides) (leaf) 2.5 mg †
* Percent Daily Values are based on 2,000 calorie diet.
† Daily Value not established.

http://www.imminst.o...howtopic=26043
Lufega (December 4, 2008):
"...NAD by NOW also gives me an unexpected focus and concentration..."

neogenic (December 5, 2008):
"...I get that from NAD+ from NOW as well. I got bashed in a thread about niacinamide/nicotinamide in the supplements section, for suggesting it. A poster stated it just gets broken down in to niacin and made it seem like it'd have no unique action unto itself. I don't get this from niacin or niacinamide. I do like xanthinol nicotinate. I take 2 NAD+ sublinguals and 2 Brain B-12 (5000mcg methylcobalamin) sublinguals by NOW and I feel great. Any thoughts?"

Lufega (December 9, 2008):
"...I also use the NAD with methyl B-12 and feel good. I think in the niacinamide thread, they are looking at niacin/NAD from a life -extension point of view. We don't seem to know what happens to NAD when it gets into the blood and whether it gets converted to NADH, decreasing the NAD/NADH ratio. That aside, it makes me feel awsome. I also feel like all my muscles have morel tone. I'm curious to try sublingual NADH to see if I get the same effect as NAD. Maybe that'll be a subjective way to say that NAD DOES get converted to NADH. Anyways, I have no idea beyond this. There's very little info about this supplement and the interest in it died with the gap in knowledge. I'll keep using it in the meanwhile.

Heck, my brother is into theather. I gave him two NAD before an audition, he said it was the best he'd ever had. That's one amazing little pill I tell ya. I also wrote a thread wonder if NAD can be used in place of niacin to increase stomach acid but no one seems to know....yet."

http://www.imminst.o...o...25586&st=30
100YearsToGo (November 24, 2008):
"All plant, animal, and fungal inputs in our diet contain cellular NAD+ and NAD+ metabolites, foods provide NAD+, NADH, NADP, and NADPH, which are considered nutritional "niacin equivalents. NOW's NAD is more of the same.

It is broken down to niacin equivalents before entering the (intra) cellular process. You can not import NAD+ into a cell. It has to be "made" through the known pathways. Researchers such as Brenner would not be wasting their time if there was a short cut. As to xanthinol nocotinate please explain why do you think it would work to increase NAD and activate sirtuins. I asks this because as far as I know, Tryptophan (Trp), nicotinic acid (Na), nicotinamide (Nam), nicotinamide riboside (NR), and possibly nicotinic acid riboside (NaR) are the only known metabolic pathways to form NAD+ in the cell.

Regards,
100YTG"

http://www.imminst.o...o...25586&st=60
FunkOdyssey (February 10, 2009):
"...But -- what if NAD is absorbed sublingually? The Now NAD product is a lozenge that you can dissolve under your tongue. If you absorb the NAD directly through the lining of the mouth, wouldn't this change the picture?

[url="http://www.iherb.com/ProductDetails.aspx?c=1&pid=711&at=0""]http://www.iherb.com/ProductDetails.aspx?c...&at=0"[/url]

neogenic (February 10, 2009):
"...I asked that very question a few months ago. I love that NOW product and it blows away NADH for me. I take 2 sublinguals of NAD+ and 2 5mg methylcobalamin sublinguals (and I've dosed the two separately and love them both) together and it is awesome for a natural energy lift. Very noticeable. I quite enjoy that "stack"."

100YearsToGo (February 10, 2009):
"It's nice to see navigators revive threads. Good job.

The cell membrane can take up extracellular NAD. So sublingually you probably have a good chance untill the liver breaks it up.

http://www.jbc.org/c...act/283/10/6367

Once in the cell it could be used by cell organelles. Mainly the mitochondria does not produce NAD and NAD must be transported into it. So the boost of energy feeling could be explained that way."

geddarkstorm (February 11, 2009):
"...Hm, yes, using a lozenge greatly increases the chance of taking in actual NAD without it being stripped down to niacinamide first, it seems. Great catch, FunkOdyssey. Makes this product and system actually sound interesting and useful, and not a gimmick. Hopefully NAD taken into the system this way will be able to disseminate throughout the body before breakdown. If so, then we would expect it to effectively stimulate Sirt1 activity - as long as the NAD dose from the lozenge was high enough to push the NAD/niacinamide ratio over the tipping point. You wouldn't want to take this at the same time as a niacinamide containing pill."

100YearsToGo (February 22, 2009):
"Be carefull. Extracellular NAD+ seems to affect the immune response. Cells seems to transport NAD outside the cell when under stress to enlist the immune system. I'm not sure yet if the immune system response to extracellular NAD is beneficial. It could be pro inflamation among others. Take a look at these two:

http://www.biochemj....849/3820849.pdf

and

[url="http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2096762""]http://www.pubmedcentral.nih.gov/articlere...d=2096762"[/url]

FunkOdyssey (February 22, 2009):
"Interesting, nice find. I could not discern any subjective benefit of the NAD lozenges, even while taking them 4x daily. This may be related to the fact that I already supplement with 100mg nicotinic acid 4x daily, I'm not sure. I am no longer using the lozenges."

Edited by Visionary7903, 09 May 2009 - 06:26 AM.

[Jacovis]

Interesting study mentioned below on rats: "Calcitriol protects against the dopamine and serotonin-depleting effects of neurotoxic doses of methamphetamine."
So Vitamin D3 may be another useful supplement to guard against Amphetamine toxicity (along with sublingual NAD or NAD precursors like Niacin and Memantine among others)...

http://www.michaelmo...ineToxicity.htm
Michael Mooney's Note:

Like the study that showed less anxiety for drug addicts when given high doses of omega-3 (fish oil) fats, this study indicated that optimal-dose vitamin D3 supplementation might reduce decreases in dopamine and serotonin when methamphetamine is used and thus, potentially reduce craving for the drug.

Vitamin D's active metabolite has potent effects in upregulating dopamine and serotonin and protecting against damage to neurons (nerve cells). Rats were given 16 times the dose of methamphetamine (speed) that human substance abusers typically use, which amounts to about 400 mg four times a day. While a radical increase in body temperature that occurs with methamphetamine use that might cause damage to neurons still happened, the neurotoxic damage to the dopamamine and serotonin cells in the brain was reduced significantly.

Caveat: This is a study that was conducted using rats, not humans, so one of my medical doctor friends criticized me for promoting the idea it might work in humans before it is proven. To him and others with that perspective I say: In its optimal dosage range, Vitamin D is not toxic like prescription drugs or some over-the-counter drugs can be. Medical doctors are taught to make decisions with prudence guiding them and they are dealing with more critical situations, drugs, procedures and the like. In this case, the benefit-to-risk potential greatly favors my going out on a limb with this hypothesis. As has occurred in the past, I'd wager that if someone does a study based on my hypothesis, my position will be validated. This happened when I published a hypothesis that ketoconazole shampoo might reduce hair loss and allow a bit of hair re-growth in my column in Muscle Media magazine in 1995. A few years later, two published studies supported my hypothesis. (1,2)

If people who suffer have to wait for a more specific study to prove this hypothesis, many, many people will continue to suffer. Why wait for a study to prove something like this if the information might help even one person have more quality of life without toxicity or deleterious effects?

The question is what dose might help? The No Observed Adverse Effect Level for Vitamin D is 2400 IU per day. So this is safe. I take 7,500 IU per day to prevent cancers based on blood tests showing that the vitamin D blood test called OH-vitamin D does not rise to the most ideal "anti-cancer" range between 50 and 60 ng/mL unless I take this dosage. Since the Lowest Observed Adverse Effect Level for Vitamin D for long-term use is 3800 IU I would not recommend taking doses at or as high as 3800 IU without your doctor's approval and monitoring. I do suggest that people ask their doctor for a "25-OH vitamin D" blood test and work with their doctor to find a best dose for them. Everyone is different, so it is best to get a blood test and work with a qualified medical doctor. Ask your doctor to work with you to find an optimal dose that works for you.

One question this study did not answer, that seems logical to me, is since vitamin D reduces the decrease in brain dopamine and serotonin caused by methamphetamine administration, does vitamin D administration also reduce the rise in dopamine and serotonin that methamphetamine produces. This would cause less of a "high" for the drug abuser, which might make the drug experience less attractive.
-----------------------------------------------------------------------
Cass, WA, et al. Calcitriol protects against the dopamine and serotonin-depleting effects of neurotoxic doses of methamphetamine. Ann N Y Acad Sci. 2006 Aug;1074:261-71.

Abstract:
Repeated methamphetamine (METH) administration to animals can result in long-lasting decreases in brain dopamine (DA) and serotonin (5-HT) content. Calcitriol, the active metabolite of vitamin D, has potent effects on brain cells, both in vitro and in vivo, including the ability to upregulate trophic factors and protect against various lesions. The present experiments were designed to examine the ability of calcitriol to protect against METH-induced reductions in striatal and nucleus accumbens levels of DA [dopamine]and 5-HT [serotonin]. Male Fischer-344 rats were administered vehicle or calcitriol (1 microg/kg, s.c.) once a day for eight consecutive days. After the seventh day of treatment the animals were given METH (5 mg/kg, s.c.) or saline four times in 1 day at 2-h intervals. Seven days later the striata and accumbens were harvested from the animals for high-performance liquid chromatography (HPLC) analysis of monoamines and metabolites. In animals treated with vehicle and METH, there were significant reductions in DA, 5-HT, and their metabolites in both the striatum and accumbens. In animals treated with calcitriol and METH, the magnitude of the METH-induced reductions in DA, 5-HT, and metabolites was substantially and significantly attenuated. The calcitriol treatments did not reduce the hyperthermia associated with multiple injections of METH, indicating that the neuroprotective effects of calcitriol are not due to the prevention of increases in body temperature. These results suggest that calcitriol can provide significant protection against the DA- and 5-HT-depleting effects of neurotoxic doses of METH.

References:
1. Piérard-Franchimont C, etal. Ketoconazole Shampoo: Effect of Long-Term Use in Androgenic Alopecia. Dermatology 1998;196:474.
2. Ju Jiang, et al. Topical Application of Ketoconazole Stimulates Hair Growth in C3H/HeN Mice. J Dermatol 32 (4): 243-247, 2005.

Be well,
Michael Mooney
www.michaelmooney.net

[ricardodias]

Hi,

i'm a portuguese journalist from Sábado newsmagazine, and i'm working on using estimulants to study like Adderall and Ritalin. You're one of the few cases that it seems to have taken but do regrett that. I would like to know more about you, if you're interested (how did you started, what do you study, how do you get the drugues, does your friends take it to, and so on...). In Portugal the fenomena is starting now and i think it's important to wright about it. I would be very please if you could answer to my email ricardofelner@gmail.com. Best regards, Ricardo Dias Felner

i'm not saying that it happens to everybody but the state-dependent learning is common to a certain degree with every drug, and for me it is especially poignant with stimulants. It is common sense. If you are using stimulants to help w/ memory and concentration, it is only logical that when you are not on it, your memory and concentration are going to be even worse than before. The thing with the adderall is that it stopped losing its effectiveness after about 30 mg. After the 30 mg, I had to take 50 mg.
After that, I decided to wait a week to see if my tolerance would die down, it didn't.
I waited 4 more days but I had finals to study for so instead I opted to up the dosage, half-knowing that the dose would be unsustainable to carry me through all of my finals.

Before that my dosage was at around 20 mg, I waited the entire summer (2.5 months) and coming back my tolerance was a little better but nowhere near as good as before.

So to reiterate, the number of doses it took me to get from ~30 to ~200 mg was something like 4 doses. 4 DOSES.

Sure the stimulants might do you good, but why risk your mind and body? Wouldn't it be better to err in favor of your health? For some reason some of the members of this life-extension related forum don't seem to be concerned about harm reduction. But before you go decide to go the stimulant route go visit some ADD forums, there are many people out there who do not take adderall anymore, because they cannot take it anymore.

[bgwithadd]

i'm not saying that it happens to everybody but the state-dependent learning is common to a certain degree with every drug, and for me it is especially poignant with stimulants. It is common sense. If you are using stimulants to help w/ memory and concentration, it is only logical that when you are not on it, your memory and concentration are going to be even worse than before. The thing with the adderall is that it stopped losing its effectiveness after about 30 mg. After the 30 mg, I had to take 50 mg.
After that, I decided to wait a week to see if my tolerance would die down, it didn't.
I waited 4 more days but I had finals to study for so instead I opted to up the dosage, half-knowing that the dose would be unsustainable to carry me through all of my finals.

Before that my dosage was at around 20 mg, I waited the entire summer (2.5 months) and coming back my tolerance was a little better but nowhere near as good as before.

So to reiterate, the number of doses it took me to get from ~30 to ~200 mg was something like 4 doses. 4 DOSES.

Sure the stimulants might do you good, but why risk your mind and body? Wouldn't it be better to err in favor of your health? For some reason some of the members of this life-extension related forum don't seem to be concerned about harm reduction. But before you go decide to go the stimulant route go visit some ADD forums, there are many people out there who do not take adderall anymore, because they cannot take it anymore.

You are expecting to be superman, and that's the problem. You don't take adderall for better general memory, but attention. Stims don't work for everyone, and it's probably not what you need. Most people, though, don't then take 200mg. Sorry, but I hear all the scare stories but when you come down and look at it people who have problems are almost always people who misue it. Did you get prescribed 200mg? I highly doubt that...so you are basically using it to get a high or expecting a complete miracle cure and of course you were disappointed.

[VoidPointer]

Guest_Isochroma_*

needs to get his/her facts straight & give up Scientology;

http://www.imminst.o...ate-t40206.html


Included are the largest non-drug co studies done on MPH.

[Rage]

I have been taking Modafinil (Modalert) from Sun pharma for around 8 months now. I take 100 mg once or twice a week depending on the how tired and sleepy I am feeling, or when I feel that coffee cant simply cut it, or if my schedule is really loaded.

The effects remain almost the same, I know I may increase tolerance to it if I abuse it. Because it is a little bit less effective than it used to be. I used to take 100mg and was awake as a light bulb for around 14 hrs straight. Now it doesn't give the kick it used to but it can still do its stuff for some 6-8hrs or so.

I do feel really tired after that so I plan things around it..

[kikai93]

Guest_Isochroma_*

needs to get his/her facts straight & give up Scientology;

http://www.imminst.o...ate-t40206.html


Included are the largest non-drug co studies done on MPH.

Dead link?

[kikai93]

what does that even mean, that drugs are not proven to be toxic? you'd have to be missing a few chromosomes to seroiusly believe that amphetamines are non-toxic. in fact, they are very toxic, they permanent deplete dopamine in rhesus monkeys

on bbc there was just an article reporting on how adhd drugs are more often than not NOT effective in the long run.

LOL, none of these drugs are proven toxic, not provezn to be non toxic too but i dont beleive they are

@purerealm
look into DXM
however it prevents a tolerance,i dont know how you can reverse one

None of these drugs? lol Here's the potential toxic effects of amphetamines (including Dextroamphetamine and Methamphetamine):

Amphetamine compounds cause a general efflux of biogenic amines from neuronal synaptic terminals (indirect sympathomimetics). They inhibit specific transporters responsible for reuptake of biogenic amines from the synaptic nerve ending and presynaptic vesicles. Amphetamines also inhibit monoamine oxidase, which degrades biogenic amine neurotransmitters intracellularly. The net effect is an increase of neurotransmitter release into the synapse. Physiological adaptation occurs through receptor or coupling down-regulation; this tolerance and an accompanying psychological tolerance can lead to escalating use of the drug and increased toxicity. Chronic use can lead to a depletion of biogenic amine stores and a paradoxical reverse effect of the drug—a wash out.

Elevated catecholamine levels usually lead to a state of increased arousal and decreased fatigue. Increased dopamine levels at synapses in the CNS may be responsible for movement disorders, schizophrenia, and euphoria. Serotonergic signals may play a role in the hallucinogenic and anorexic aspects of these drugs.

Other serotonergic and dopaminergic effects may include resetting the thermal regulatory circuits upward in the hypothalamus and causing hyperthermia. The hyperthermia produced by amphetamines is similar to that of the serotonin syndrome.

Laboratory studies reveal that amphetamines interfere with the normal control of the neurohumoral (hypothalamopituitary) axis, affecting secretion of such factors as adrenocorticotropic hormone (ACTH). Amphetamines may alter other neural functions such as complex behavioral and learning patternings; this may be important for understanding effects of amphetamine use during pregnancy.

Animal studies indicate that amphetamines interact with N -methyl-D-aspartate (NMDA) receptors on serotonergic neurons, leading to neuronal destruction. This interaction may contribute to seizure activity.

In vitro, amphetamines have been found to stimulate regulatory molecules, such as the oncogenes c-fos and rasand cyclic adenosine monophosphate (cAMP) response element binding (CREB) protein. These proteins are responsible for signaling long-term changes at the transcriptional level.

Catecholaminergic (sympathomimetic) effects of amphetamines include inotropic and chronotropic effects on the heart, which can lead to tachycardia and other dysrhythmias. The vasoconstrictive properties of the drugs can lead to hypertension and/or coronary vasospasm.

Serotonergic action of amphetamines on peripheral vasculature can lead to vasoconstriction, which is especially problematic in placental vessels. Animal studies have shown that serotonergic actions of amphetamines effect changes in plasma levels of oxytocin, somatostatin, gastrin, and cholecystokinin.

Long-term use of the drugs can lead to myonecrosis and dilated cardiomyopathy. Amphetamine use is also associated with increased risk of pulmonary hypertension.




The package inserts talk about the need for blood monitoring, increased risk of stroke and cardiac events, etc FFS.

[VoidPointer]

what does that even mean, that drugs are not proven to be toxic? you'd have to be missing a few chromosomes to seroiusly believe that amphetamines are non-toxic. in fact, they are very toxic, they permanent deplete dopamine in rhesus monkeys

on bbc there was just an article reporting on how adhd drugs are more often than not NOT effective in the long run.

LOL, none of these drugs are proven toxic, not provezn to be non toxic too but i dont beleive they are

@purerealm
look into DXM
however it prevents a tolerance,i dont know how you can reverse one

None of these drugs? lol Here's the potential toxic effects of amphetamines (including Dextroamphetamine and Methamphetamine):

Amphetamine compounds cause a general efflux of biogenic amines from neuronal synaptic terminals (indirect sympathomimetics). They inhibit specific transporters responsible for reuptake of biogenic amines from the synaptic nerve ending and presynaptic vesicles. Amphetamines also inhibit monoamine oxidase, which degrades biogenic amine neurotransmitters intracellularly. The net effect is an increase of neurotransmitter release into the synapse. Physiological adaptation occurs through receptor or coupling down-regulation; this tolerance and an accompanying psychological tolerance can lead to escalating use of the drug and increased toxicity. Chronic use can lead to a depletion of biogenic amine stores and a paradoxical reverse effect of the drug—a wash out.

Elevated catecholamine levels usually lead to a state of increased arousal and decreased fatigue. Increased dopamine levels at synapses in the CNS may be responsible for movement disorders, schizophrenia, and euphoria. Serotonergic signals may play a role in the hallucinogenic and anorexic aspects of these drugs.

Other serotonergic and dopaminergic effects may include resetting the thermal regulatory circuits upward in the hypothalamus and causing hyperthermia. The hyperthermia produced by amphetamines is similar to that of the serotonin syndrome.

Laboratory studies reveal that amphetamines interfere with the normal control of the neurohumoral (hypothalamopituitary) axis, affecting secretion of such factors as adrenocorticotropic hormone (ACTH). Amphetamines may alter other neural functions such as complex behavioral and learning patternings; this may be important for understanding effects of amphetamine use during pregnancy.

Animal studies indicate that amphetamines interact with N -methyl-D-aspartate (NMDA) receptors on serotonergic neurons, leading to neuronal destruction. This interaction may contribute to seizure activity.

In vitro, amphetamines have been found to stimulate regulatory molecules, such as the oncogenes c-fos and rasand cyclic adenosine monophosphate (cAMP) response element binding (CREB) protein. These proteins are responsible for signaling long-term changes at the transcriptional level.

Catecholaminergic (sympathomimetic) effects of amphetamines include inotropic and chronotropic effects on the heart, which can lead to tachycardia and other dysrhythmias. The vasoconstrictive properties of the drugs can lead to hypertension and/or coronary vasospasm.

Serotonergic action of amphetamines on peripheral vasculature can lead to vasoconstriction, which is especially problematic in placental vessels. Animal studies have shown that serotonergic actions of amphetamines effect changes in plasma levels of oxytocin, somatostatin, gastrin, and cholecystokinin.

Long-term use of the drugs can lead to myonecrosis and dilated cardiomyopathy. Amphetamine use is also associated with increased risk of pulmonary hypertension.




The package inserts talk about the need for blood monitoring, increased risk of stroke and cardiac events, etc FFS.

http://www.imminst.o...__1#entry397890

thanks for the notice about the dead link..

[kikai93]

http://www.imminst.o...__1#entry397890

thanks for the notice about the dead link..

Thanks! I read the studies you have linked in that thread that I have not linked previously. I admit I have less reservations concerning MPH (particularly the dextro/focalin version) than concerning Amphetamines (which I was discussing above).
However, a quick search of Methylphenidate/Death, Methylphenidate/Side Effects, Methylphenidate/Cardiomyopathy, or similar search terms should yield the reasons why I'm not a fan of the MPH either. And I'm not a Scientologist. :P
My own experience with psychostimulants supports the commentary of TophetLOL on the thread you've linked, so I'll repeat the relevant comments I support, here.

1) Often the improvements noticed in medium-term (5 year) studies are not statistically significant. (.29? Really?)
2) From my own experience with the gamut of psychostimulants I would agree that lower-order functioning is improved.
BUT
Higher order functions are not improved, and in fact some higher order functions suffer. (The infamous loss of creativity, repetitious rhetoric, et al.)
3) There are significant risks and side effects with any psychostimulant, even dexmethylphenidate. Even methylhexamine (a relatively innocuous psychostimulant with a safety profile near that of caffeine).
4) Psychostimulants may be beneficial for some cases, but they aren't necessary.
5) Psychostimulants address symptoms, not causes. This is true of most, but certainly not all, modern pharmaceutical treatment options.

My position is that psychostimulants, like anti-depressants, should be used as a band-aid to allow the treatment of the underlying causes of the symptoms. This means short term treatment. I also think that monitoring is necessary, per the recommendations of both the manufacturers and the medical research community. Particularly cardiac function and liver function. Of course in a perfect world, everyone could have regular monitoring of all their major vital signs and systems. After the failure of traditional therapies, I successfully treated my own ADD symptoms. I realized that for many ADD is a conditioned behavior, and that it can be addressed without drugs, or with drugs as a temporary adjunct. Our brains can be retrained with sufficient will to do so. Meditation, physical exercise, and focus-building exercise did more for me than any psychostimulant ever did. I do not believe that any extant psychostimulant will be efficacious at a consistent dosage over the long term. Thus, I do not believe that any extant psychostimulant is a long term solution.

[VoidPointer]

http://www.imminst.o...__1#entry397890

thanks for the notice about the dead link..

Thanks! I read the studies you have linked in that thread that I have not linked previously. I admit I have less reservations concerning MPH (particularly the dextro/focalin version) than concerning Amphetamines (which I was discussing above).
However, a quick search of Methylphenidate/Death, Methylphenidate/Side Effects, Methylphenidate/Cardiomyopathy, or similar search terms should yield the reasons why I'm not a fan of the MPH either. And I'm not a Scientologist. :P
My own experience with psychostimulants supports the commentary of TophetLOL on the thread you've linked, so I'll repeat the relevant comments I support, here.

1) Often the improvements noticed in medium-term (5 year) studies are not statistically significant. (.29? Really?)
2) From my own experience with the gamut of psychostimulants I would agree that lower-order functioning is improved.
BUT
Higher order functions are not improved, and in fact some higher order functions suffer. (The infamous loss of creativity, repetitious rhetoric, et al.)
3) There are significant risks and side effects with any psychostimulant, even dexmethylphenidate. Even methylhexamine (a relatively innocuous psychostimulant with a safety profile near that of caffeine).
4) Psychostimulants may be beneficial for some cases, but they aren't necessary.
5) Psychostimulants address symptoms, not causes. This is true of most, but certainly not all, modern pharmaceutical treatment options.

My position is that psychostimulants, like anti-depressants, should be used as a band-aid to allow the treatment of the underlying causes of the symptoms. This means short term treatment. I also think that monitoring is necessary, per the recommendations of both the manufacturers and the medical research community. Particularly cardiac function and liver function. Of course in a perfect world, everyone could have regular monitoring of all their major vital signs and systems. After the failure of traditional therapies, I successfully treated my own ADD symptoms. I realized that for many ADD is a conditioned behavior, and that it can be addressed without drugs, or with drugs as a temporary adjunct. Our brains can be retrained with sufficient will to do so. Meditation, physical exercise, and focus-building exercise did more for me than any psychostimulant ever did. I do not believe that any extant psychostimulant will be efficacious at a consistent dosage over the long term. Thus, I do not believe that any extant psychostimulant is a long term solution.

I understand your position, but my position is that you are vastly overstating the risk of MPH. The few deaths from stimulant medications that have occurred were almost exclusively in patients who already had pre-existing heart conditions.

More people have been killed from alcohol, tylenol, after-school sports, driving in cars, alligators etc than from stimulant medications.

ADD has genetic links, and to suggest that meditation will cure this condition is a stretch;

http://www.highlight...dhd-identified/


As a child my mother (who was much a hippy-yoga-hollistic type) ignored the advice of my doctors and did not put me on Ritalin when I was in school. As a result I did poorly in all classes other than math, and got into a bunch of trouble.

Now I lead a healthy lifestyle with exercise 4 times a week, and a very good diet. But that alone is no where near enough to improve my ADD symptoms.

I do agree that in the very long run stimulants lose efficacy and do not cure the problem, but life is short and if one can get a few years of diminished symptoms that may be worth the small risk associated with such meds. Believe me there are many kids out there who are much better off on meds, than without. It can make the critical difference between a student flunking out of school or moving on to college. Also the fact that students who stay on their ADD meds are less likely to get into car accidents, and are less likely to abuse alcohol or other drugs does mean something.


Also please show me literature to support your assertion of liver problems associated with MPH. I have never heard that before, and was told by my doc that MPH was not toxic to the liver

Few drugs have been subject to more critical examination that methylphenidate, and the vast majority of all research in different countries has shown MPH to be effective in most patients.

In a perfect world no person would need any meds, but this is not a perfect world and risks must be taken. Good for you that you are able to control your ADD symptoms with natural means. But one size does not fit all.

[kikai93]

ADD has genetic links, and to suggest that meditation will cure this condition is a stretch;

http://www.highlight...dhd-identified/

Correlation does not equal causation, identical CNV's were not observed in all of the subjects, and CNV's have been correlated to a number of disorders. Also, the findings of the study have yet to be duplicated. If CNV's are actually a cause, we need therapies that will directly address that cause.

As a child my mother (who was much a hippy-yoga-hollistic type) ignored the advice of my doctors and did not put me on Ritalin when I was in school. As a result I did poorly in all classes other than math, and got into a bunch of trouble.

That sucks. Were you in therapy at all? I would be surprised if behavioral therapy had no positive effect. I had a somewhat opposite experience. My mother thought drugs were all that were necessary so I was prescribed ritalin, then dexedrine, then adderall, and so on through the gamut of ADD drugs. They weren't effective.

Now I lead a healthy lifestyle with exercise 4 times a week, and a very good diet. But that alone is no where near enough to improve my ADD symptoms.

Again, I'd be surprised if that didn't improve your ADD symptoms at all. I understand this to mean these changes alone didn't improve your symptoms enough, but if I misunderstand please clarify.

I do agree that in the very long run stimulants lose efficacy and do not cure the problem, but life is short and if one can get a few years of diminished symptoms that may be worth the small risk associated with such meds.

If one could use the time bought by medication to institute behavioral and cognitive changes that would further ameliorate the condition to the point that it is no longer a nuisance, wouldn't that be better? It's possible. That's why multi-modal therapy is the way to go. As I was just saying to kassem23, with whom I am having a similar discussion:

I am of the mind of the many clinicians who prescribe this course:
1) Try behavioral therapy. Often this works, all by itself. For child patients, Parenting Skills Education is also helpful, as well as special modifications in the school environment.
2) If behavioral therapy alone isn't working, try behavioral therapy with medication. You will be informed of all potential risks and side effects of the proposed medication.
3) Any potential adjunct you want to try that won't negatively impact your well-being or prescribed therapy is ok.
4) If you are on medication, we will do more than a cursory follow up with you to ensure you are getting the desired results and that your health is not being negatively impacted.


I base this on a thorough review of the literature, the written and verbal opinions of a number of physicians in the field, anecdotal reports including my own, the findings of the NIMH Multimodal Treatment of Attention Deficit Hyperactivity Disorder (MTA) Study and its 3 and 8 year followups. (read it if you haven't, best study to date).

Believe me there are many kids out there who are much better off on meds, than without. It can make the critical difference between a student flunking out of school or moving on to college. Also the fact that students who stay on their ADD meds are less likely to get into car accidents, and are less likely to abuse alcohol or other drugs does mean something.

I believe you, and even agree with you to a point. I just don't believe that medication alone is a solution, or always required to treat ADD.

Also please show me literature to support your assertion of liver problems associated with MPH. I have never heard that before, and was told by my doc that MPH was not toxic to the liver

Rarely, some patients have shown elevated enzymes. It's pemoline that can be hepatotoxic. Search "ritalin liver damage" on pubmed.

Few drugs have been subject to more critical examination that methylphenidate, and the vast majority of all research in different countries has shown MPH to be effective in most patients.

That's actually not true. A tentative majority of research points to methylphenidate's effectiveness (about 75%) in treating symptoms of ADD for about a year. After that, research points to diminishing effectiveness until, at about the three year mark it's difficult to see any lasting positive benefits. Seriously, read the NIMH MTA and its followups, and the corroborating research (yes, the results have been corroborated). It's not that I hate the methylphenidate or other psychostimulants, but rather that I don't see them as first-line treatments. I'm sure they can be useful adjuncts in many cases.

In a perfect world no person would need any meds, but this is not a perfect world and risks must be taken. Good for you that you are able to control your ADD symptoms with natural means. But one size does not fit all.

I agree. Meds were counterproductive for me. They are apparently working for you. I would advise seeing a behavioral therapist to make the most of it. Also, it can't hurt to take up meditation and focus visualization, force yourself to read books without skimming, etc.

Edited by kikai93, 09 January 2011 - 10:42 PM.

[VoidPointer]

Reading in particular has always been difficult, not sure how to address that problem. I took the LSAT many years ago and got 65% wrong on the reading comprehension section, but also got an almost perfect score on the logical reasoning section.

Exercise does help a bit, as does green tea. Would be willing to try meditation if you can direct me towards a link.

[kikai93]

Reading in particular has always been difficult, not sure how to address that problem. I took the LSAT many years ago and got 65% wrong on the reading comprehension section, but also got an almost perfect score on the logical reasoning section.

Exercise does help a bit, as does green tea. Would be willing to try meditation if you can direct me towards a link.

Sure. There are a few different "sorts" of meditation. Here are the ones I find useful:
Zen: http://www.mro.org/z.../meditation.php http://www.beyondzen...tate-on-a-koan/
Mindfulness: http://stress.about....a/exercises.htmhttp://www.upmc.com/...meditation.aspx
Raja Yoga: http://hermetic.com/...ook-4/aba1.html (Try to ignore the mystical mumbo jumbo and focus on his excellent summary of technique)

[Tukotih Doji]

Guest_Isochroma_*

needs to get his/her facts straight & give up Scientology;

http://www.imminst.o...ate-t40206.html


Included are the largest non-drug co studies done on MPH.

Dead link?

http://www.longecity.org/forum/topic/40206-why-so-much-methylphenidate-hate/

Does anyone think MDPV, which has the same mechanism, could be far more dangerous?
It works good for my ADD since it also has an active metabolite which makes me only need one morning dose and then I'll be fine for 6h+.

But I'm not sure for how long I will continue the use since there may be unwanted side-effects from long term use. Like neurotoxicity.
I've read somewhere that amphetamine (Adderal) expresses neurotoxicity since it works as an releasing agent. Although, new potential mechanisms of action may exist. I've read about it somewhere but can't remember the exact context of the statement...

[medievil]

MDPV is not neurotoxic, and has very low toxiticy, it should be safe to use (other then possible unknown complications from it being a research chemical).

[Construct]

MDPV is not neurotoxic, and has very low toxiticy, it should be safe to use (other then possible unknown complications from it being a research chemical).

MPDV is a research chemical. You can't claim it has no neurotoxic side effects and point out that it is a research chemical with unknown complications in the same sentence.

If safety and long-term well-being are your goals, stay far, far away from research chemicals.

[medievil]

MDPV is not neurotoxic, and has very low toxiticy, it should be safe to use (other then possible unknown complications from it being a research chemical).

MPDV is a research chemical. You can't claim it has no neurotoxic side effects and point out that it is a research chemical with unknown complications in the same sentence.

If safety and long-term well-being are your goals, stay far, far away from research chemicals.

It has been tested for toxiticy in rodents, so i dont see why i wont be able to claim that, i also pointed out its a rc and can have unknown complications, i stand by my point.

[longevitynow]

Long-term effects of Ritalin, Adderall, Modafanil: Adrenal fatigue, Adrenal exhaustion, fried HPA axis.

Occasional use might not be so depleting, but regular use is very heavy on the adrenals and HPA axis. Daily use by children/teenagers=brain and body burn-out later. Actually, college age 17-22 years is probably the time when the body is most resilient to the negative effects, but the daily use part is IMO what make them such a bad idea.

[VoidPointer]

Long-term effects of Ritalin, Adderall, Modafanil: Adrenal fatigue, Adrenal exhaustion, fried HPA axis.

Occasional use might not be so depleting, but regular use is very heavy on the adrenals and HPA axis. Daily use by children/teenagers=brain and body burn-out later. Actually, college age 17-22 years is probably the time when the body is most resilient to the negative effects, but the daily use part is IMO what make them such a bad idea.

I agree that everyday use should be avoided, but those three drugs are not the same.. Also what you describe as the long-term effects can be measured by scientific studies, and I have not seen an abundance of evidence that supports this claim.

[medievil]

Daily use by children/teenagers=brain and body burn-out later.

You have references for those claims i assume?

[medievil]

MDPV is not neurotoxic, and has very low toxiticy, it should be safe to use (other then possible unknown complications from it being a research chemical).

MPDV is a research chemical. You can't claim it has no neurotoxic side effects and point out that it is a research chemical with unknown complications in the same sentence.

If safety and long-term well-being are your goals, stay far, far away from research chemicals.

Your concerns are legit, but lets not forget that many compounds being discussed here have no safety data on humans at all, even tough it makes the rats live a long and happy life! There seem to be a bias here for compounds that shows health benefits in rodents, however they can just like any other chemical, have adverse effects in humans.