the case for concerta

[LucidityBane]

Hello all,

I have been seeing so many negative accounts of Concerta that I felt the need to de-lurk and present a counter-argument.
I mean, really,
I am waiting for the next thread titled 'I took Concerta and my arm fell off'.
I am starting to suspect Scientologist infiltration in the BB.



I just do not beleive those who say, 'I took 36 mg of Concerta and nothing happened'.
B.S.
maybe it did not work as well as you wanted,
but it did increase the level of usable Dopamine in your brain, just like most other stimulant ADHD drugs.

If you have a bad attitude about it from the beginning well, then, you are not exactly unbiased.


anyway, let me bring some science in to the mix:

let's start with this;



Deficits in brain's reward system observed in ADHD patients
Low levels of dopamine markers may underlie symptoms; implications for treatment

UPTON, NY — A brain-imaging study conducted at the U.S. Department of Energy's (DOE) Brookhaven National Laboratory provides the first definitive evidence that patients suffering from attention deficit hyperactivity disorder (ADHD) have lower-than-normal levels of certain proteins essential for experiencing reward and motivation.

"These deficits in the brain's reward system may help explain clinical symptoms of ADHD, including inattention and reduced motivation, as well as the propensity for complications such as drug abuse and obesity among ADHD patients," said lead author Nora Volkow, Director of the National Institute on Drug Abuse and a long-time collaborator on neuroimaging research at Brookhaven Lab.

The study, published in the September 9, 2009, issue of the Journal of the American Medical Association, also has important implications for treatment. "Finding ways to address the underlying reward-system deficit could improve the direct clinical outcome of ADHD, and potentially reduce the likelihood of other negative consequences of this condition," said study co-author Gene-Jack Wang, chair of Brookhaven's medical department.

Prior to this study, it was not clear whether people with ADHD had abnormalities in the brain's dopamine-mediated motivation/reward system. Previous studies were relatively small and may have been complicated by the fact that some ADHD patients had undergone treatments, or had a history of drug abuse or other conditions that can affect the dopamine system.

To strengthen the statistics and control for these factors, the current study looked at 53 adult ADHD patients who had never received treatment and 44 healthy control subjects — all of whom had been carefully screened to eliminate potentially confounding variables.

The scientists used positron emission tomography (PET) to measure two markers of the dopamine system — dopamine receptors, to which the chemical messenger binds to propagate the "reward" signal, and dopamine transporters, which take up and recycle excess dopamine after the signal is sent.

Lying in a PET scanner, each patient was injected with a minute amount of a "radiotracer" compound — a chemical labeled with a radioactive form of carbon and designed to bind specifically to one of the targets. Different tracers were used for each target, and patients were scanned for each at separate times. By detecting the signal from the radiotracers, the PET machine can measure the receptor and transporter locations and concentrations in various parts of the brain.

The results clearly showed that, relative to the healthy control subjects, the ADHD patients had lower levels of dopamine receptors and transporters in the accumbens and midbrain — two key regions of the brain directly involved in processing motivation and reward. In addition, the measurements of dopamine markers correlated with measures of behavior and clinical observations of ADHD symptoms, such as reduced levels of attention as measured by standard psychological tests.

"Our findings imply that these deficits in the dopamine reward pathway play a role in the symptoms of inattention in ADHD and could underlie these patients' abnormal responses to reward," Volkow said.

"This pathway plays a key role in reinforcement, motivation, and in learning how to associate various stimuli with rewards," she continued. "Its involvement in ADHD supports the use of interventions to enhance the appeal and relevance of school and work tasks to improve performance.

"Our results also support the continued use of stimulant medications — the most common pharmacological treatment for ADHD — which have been shown to increase attention to cognitive tasks by elevating brain dopamine," she said.

The findings may also help explain why ADHD patients are more likely than control subjects to develop drug-abuse disorders and conditions such as obesity.

Said Wang: "Other studies from our group suggest that patients who abuse drugs or overeat may be unconsciously attempting to compensate for a deficient reward system by boosting their dopamine levels. Understanding how deficits in the dopamine system contribute to ADHD and finding ways to improve the functioning of the reward system could help mitigate these troubling consequences in the ADHD patient population."




ok, so this finding supports the use of 'stimulants' but what about methylphenidate (and it's derivatives) vs. amphetamines;


Brain Res. 1997 Aug 29;767(1):172-5.Click here to read Links
Methylphenidate and brain dopamine neurotoxicity.
Yuan J, McCann U, Ricaurte G.

Department of Neurology, Johns Hopkins Medical Institutions, Baltimore, MD 21224, USA.

To further evaluate the dopamine (DA) neurotoxic potential of the widely prescribed psychostimulant, methylphenidate, mice were treated with various doses (range: 10-120 mg/kg) and treatment schedules of methylphenidate (every 2 h x 4 or twice daily x 4). Higher doses of methylphenidate produced intense stereotypy, as well as short- (5-day), but not long- (2-week), term depletions of striatal DA axonal markers. By contrast, amphetamine caused not only intense stereotypy, but also profound, long-lasting, dose-related DA deficits. These findings indicate that results of studies of amphetamine neurotoxicity using short (5-day) post-drug survival periods are potentially misleading. Further, the present findings confirm and extend previous results indicating that methylphenidate, unlike amphetamine, lacks DA neurotoxic potential, and strongly suggest that DA efflux, although perhaps necessary, is not sufficient for the expression of amphetamine-induced DA neurotoxicity.



Annnd again;

1: J Neural Transm. 2006 Dec;113(12):1927-34. Epub 2006 Jun 1.Click here to read Links

Methylphenidate exerts no neurotoxic, but neuroprotective effects in vitro.
Ludolph AG, Schaz U, Storch A, Liebau S, Fegert JM, Boeckers TM.

Department of Child and Adolescent Psychiatry, University of Ulm, Ulm, Germany. andrea.ludolph@uni-ulm.de

Methylphenidate (MPH) is the most common used drug in child and adolescent psychiatry. Despite of this fact, however, little is known about its exact pharmacological mechanisms.Here we investigated the toxic effects of MPH in vitro in human embryonic kidney (HEK-293) cells stably expressing the human dopamine transporter (HEK-hDAT cells) and in cultured rat embryonic (E14.5) mesencephalic cultures. MPH alone (up to 1 mM) affected neither the growth of HEK-hDAT cells nor the survival of dopaminergic (DA) neurons in primary cultures after treatment up to 72 h. No differences in neuronal arborisation or in the density of synapses were detected. 1-methyl-4-phenylpyridinium (MPP(+)) showed no toxic effect in HEK-293 cells, but had significant toxic effects in HEK-hDAT cells and DA neurons. MPH (1 microM - 1 mM) dose-dependently reduced this cytotoxicity in HEK-hDAT cells and primary mesencephalic DA neurons.The presented results show that application of MPH alone does not have any toxic effect on DA cells in vitro. The neurotoxic effects of MPP(+) could be significantly reduced by co-application of MPH, an effect that is most likely explained by MPH blocking the DAT.




sooo, I know that ADDerall, etc an be more effective in some individuals, but if they are equally effective in an individual I would think MPH is the better choice.



Comments?


/!uciditY

[Krys]

Originally Posted by LucidityBane

Hello all,

I have been seeing so many negative accounts of Concerta that I felt the need to de-lurk and present a counter-argument.
I mean, really,
I am waiting for the next thread titled 'I took Concerta and my arm fell off'.
I am starting to suspect Scientologist infiltration in the BB.

Oh god, this made me spit out my water! Haha.

Originally Posted by LucidityBane

just do not beleive those who say, 'I took 36 mg of Concerta and nothing happened'.
B.S.
maybe it did not work as well as you wanted,
but it did increase the level of usable Dopamine in your brain, just like most other stimulant ADHD drugs.

I've just started on 27 mg and don't really notice much, so I don't know. Logically I understand what you're saying though.

And thank you for posting the article.

[LucidityBane]

Glad I was good for a laugh, but seriously some people on here are attributing all kinds of side-effects to Concerta that just do no seem likely.

Since Concerta is usually the first ADHD drug that is prescribed, I think some individuals rebel against the whole idea of medication.

Also I think some want Adderall and complain about Concerta in order to get that other med.

The medication is not meant to get one 'high' it is supposed to increase your ability to stay on task and concentrate. Concerta has a slow onset and a slow release so there is less of a 'rebound' than that of other drugs.

I do not experience side effects other than an occasional mild headache, and that may result from combining caffeine with the med.

Also, Focalin XR is a more refined version of methylphenidate that may have less side-effects. I have tried it but feel that I get more done with Concerta, but it is similar.

Actually Focalin seems a bit more 'psychoactive' than Concerta, not sure why.

Anyway I also take 27 mg 4 days a week.. hope it works for you, but if not try Focalin XR before the amphetamine salts.

/!uciditY

[Peterr]

I am still finding out what works best for me. I've done MPH (Concerta and generic mph) and AMP (dex in my case). I can definately feel that they are in the same class of drugs.

MPH works by blocking the reuptake of dopamine, AMP works by releasing more dopamine into the brain. Net effect in both cases: more dopamine.

MPH to me feels stronger. More effective but more side effects. AMP is smoother and works longer (not as long as concerta though), has less side effects (in ME) but it seems that I must take much more of it to get the desired effect.

Neither give me a 'high'.

[daydreamer84]

My arm did fall off but only for the first week or so. This side effect will go away after a while. Life's great, I now have more arms than I did before!