11 replies to this topic

[Phreak]

Is there any benefit of adding L-DOPA to a standard -racetam stack?
I've looked into it a bit but haven't found much info on it being a Nootropic of any sort. I was thinking along the lines that, if it help increase dopamine levels in the brain, it might synergise with some of the other drugs, making them last longer or potentiating them...

Anyone had any experience with this stuff, either alone or in combination??

[abelard lindsay]

Is there any benefit of adding L-DOPA to a standard -racetam stack?
I've looked into it a bit but haven't found much info on it being a Nootropic of any sort. I was thinking along the lines that, if it help increase dopamine levels in the brain, it might synergise with some of the other drugs, making them last longer or potentiating them...

Anyone had any experience with this stuff, either alone or in combination??

L-Dopa is not something you should take unless you have Parkinsons. Even if you do, you stand a high risk of getting tardive dyskinesia. If you want to stimulate dopamine I'd go for so L-Phenylalanine or L-Tyrosine as needed.

http://en.wikipedia.org/wiki/L-Dopa
http://www.ncbi.nlm....Pubmed_RVDocSum

Dyskinesia: L-dopa-induced and tardive dyskinesia.
Rascol O, Fabre N.

Department of Clinical Pharmacology, Clinical Investigation Center, INSERM U 455, Toulouse University-Hospital, 37 allees J. Guesde, 31073 Toulouse Cedex, France.

Neuroleptic induced tardive dyskinesia and L-dopa-induced dyskinesia are the two most common types of drug-induced abnormal involuntary movements. These two drug-induced dyskinesias are clearly different with respect to the offending drugs and the underlying disease, but they both share a number of intriguing similarities in terms of clinical phenomenology, epidemiology, risk factors, pathophysiological mechanisms and therapeutic responses. In both instances, it is believed that some dysregulation occurring at the level of the striatal dopaminergic receptors, and related non-dopaminergic neurotransmitters systems are playing a crucial role in the development and persistence of the mechanisms causing dyskinesia. These long-lasting functional changes, known as the "priming" phenomenon, are responsible for an impaired balance within the relays of the cortico-subcortical motor loops that release an inadequate output from the basal ganglia leading to an abnormal motor behavior. From a therapeutic perspective, there are also many similarities in the strategies proposed to manage these two dyskinesias. In both cases, unprimed patients not previously exposed to the offending drugs, are offered alternative medications to reduce, at least partly, the risk of occurrence of future dyskinesia: "atypical" neuroleptics in the place of "typical" neuroleptics, and dopamine agonists in the place of L-dopa. In both cases, once dyskinesias are present, in already "primed" patients, both types of dyskinesia appear to be poorly and only partly reversible. Based on limited clinical evidence, it is a common proposal to switch the dyskinetic subject from "typical" to "atypical" neuroleptics for tardive dyskinesia, or to switch from (or more pragmatically to substitute as much as possible) L-dopa to a dopamine agonist for L-dopa-induced dyskinesia. In both cases, efficacious symptomatic antidyskinetic interventions, to reduce the severity of a ready present dyskinesia, are rare. There are some uncontrolled data suggesting that dopamine depleting agents, like tetrabenazine, are possibly useful for tardive dyskinesia; however, there is more clinical evidence to support the efficacy of amantadine and functional surgery in parkinsonian patients with L-dopa-induced dyskinesia.

[Ghostrider]

Is there any benefit of adding L-DOPA to a standard -racetam stack?
I've looked into it a bit but haven't found much info on it being a Nootropic of any sort. I was thinking along the lines that, if it help increase dopamine levels in the brain, it might synergise with some of the other drugs, making them last longer or potentiating them...

Anyone had any experience with this stuff, either alone or in combination??

L-Dopa is not something you should take unless you have Parkinsons. Even if you do, you stand a high risk of getting tardive dyskinesia. If you want to stimulate dopamine I'd go for so L-Phenylalanine or L-Tyrosine as needed.

http://en.wikipedia.org/wiki/L-Dopa
http://www.ncbi.nlm....Pubmed_RVDocSum

Dyskinesia: L-dopa-induced and tardive dyskinesia.
Rascol O, Fabre N.

Department of Clinical Pharmacology, Clinical Investigation Center, INSERM U 455, Toulouse University-Hospital, 37 allees J. Guesde, 31073 Toulouse Cedex, France.

Neuroleptic induced tardive dyskinesia and L-dopa-induced dyskinesia are the two most common types of drug-induced abnormal involuntary movements. These two drug-induced dyskinesias are clearly different with respect to the offending drugs and the underlying disease, but they both share a number of intriguing similarities in terms of clinical phenomenology, epidemiology, risk factors, pathophysiological mechanisms and therapeutic responses. In both instances, it is believed that some dysregulation occurring at the level of the striatal dopaminergic receptors, and related non-dopaminergic neurotransmitters systems are playing a crucial role in the development and persistence of the mechanisms causing dyskinesia. These long-lasting functional changes, known as the "priming" phenomenon, are responsible for an impaired balance within the relays of the cortico-subcortical motor loops that release an inadequate output from the basal ganglia leading to an abnormal motor behavior. From a therapeutic perspective, there are also many similarities in the strategies proposed to manage these two dyskinesias. In both cases, unprimed patients not previously exposed to the offending drugs, are offered alternative medications to reduce, at least partly, the risk of occurrence of future dyskinesia: "atypical" neuroleptics in the place of "typical" neuroleptics, and dopamine agonists in the place of L-dopa. In both cases, once dyskinesias are present, in already "primed" patients, both types of dyskinesia appear to be poorly and only partly reversible. Based on limited clinical evidence, it is a common proposal to switch the dyskinetic subject from "typical" to "atypical" neuroleptics for tardive dyskinesia, or to switch from (or more pragmatically to substitute as much as possible) L-dopa to a dopamine agonist for L-dopa-induced dyskinesia. In both cases, efficacious symptomatic antidyskinetic interventions, to reduce the severity of a ready present dyskinesia, are rare. There are some uncontrolled data suggesting that dopamine depleting agents, like tetrabenazine, are possibly useful for tardive dyskinesia; however, there is more clinical evidence to support the efficacy of amantadine and functional surgery in parkinsonian patients with L-dopa-induced dyskinesia.

Kind of off the topic, but how does deprenyl relate to Phenylalanine or Tyrosine? All stimulate dopamine.

[Phreak]

Oops, well I ordered a whole load of it :S

I've seen reports of people who take it daily as a sort of 5-HTP substitute (even though it works on a different neurotransmitter), so surely it must be okay?
I was just thinking of adding a small amount to a -racetam stack to boost endurance of focus...

[abelard lindsay]

Oops, well I ordered a whole load of it :S

I've seen reports of people who take it daily as a sort of 5-HTP substitute (even though it works on a different neurotransmitter), so surely it must be okay?
I was just thinking of adding a small amount to a -racetam stack to boost endurance of focus...

Tryptophan =~ L-Phenylalanine
5-HTP =~ L-Tyrosine

Tyrosine is just one metabolic step after Phenylalanine on the way to what your brain ultimately turns into dopamine. This is similar to how 5-HTP is one more metabolic step after Tryptophan on the way to what your brain ultimately turns into serotonin. BTW, I've thrown out supplements I ordered without ever taking them because I did more research while they shipped and decided they weren't something I wanted to take.

Edited by abelard lindsay, 08 April 2008 - 04:52 PM.

[FunkOdyssey]

Dopamine metabolism is a cause of oxidative stress in the brain, so to the extent that l-dopa supplementation results in increased dopamine metabolism, it could be considered pro-aging. I think this is the primary argument against its use by healthy individuals.

[Phreak]

Hmmm, I've been doing some more research and, yes, there are risks, but I have read some really good anecdotal reports of using L-DOPA as a gentle mood booster or to enhance other Nootropics. If it is a precursor just like 5-HTP I don't see how it can se so bad. I'm particularly interested in it's ability to increase hGH(RH) - Human Growth Hormone Release Hormones....

Surely it can't be all negative stuff surrounding l-DOPA...?

EDIT - Also, what is 'oxidative stress', FunkOdyssey?

Edited by phreak, 08 April 2008 - 09:08 PM.

[FunkOdyssey]

EDIT - Also, what is 'oxidative stress', FunkOdyssey?

http://parkinsons.bs...view/Causes.htm

Pathogenesis of Parkinson's disease ( the process by which dopaminergic cells degenerate)

...<clipped>...

* Oxidative stress - This is an attractive theory that is gaining increasing acceptance as a major contributor in the causation of Parkinson’s disease. When molecules contain unpaired electrons they are called free radicals. Oxidative stress occurs when the formation of free radicals is increased. Free radicals can kill the surrounding brain cells contributing to progression of the disease. Free radicals of relevance in Parkinson’s disease include superoxide, peroxide, nitric oxide and hydroxyl species. Iron may play a role in oxidative stress. Perhaps of most importance, metabolism of dopamine can contribute to free radical formation. An understanding of this concept is altering our treatment strategies in Parkinson’s disease.

When they say the understanding of this concept is altering treatment strategies, they are referring to the recent realization that loading up the patient's brain with large amounts of dopamine using l-dopa is accelerating the disease process via increased dopamine metabolism and the oxidative stress that follows.

Edited by FunkOdyssey, 08 April 2008 - 09:25 PM.

[dopamine]

L-Dopa is definitely not a good idea for otherwise healthy individuals, and will probably not even increase brain dopamine levels to a significant degree without a decarboxylase inhibitor. See this thread I created at M&M on the topic. A snippet -

From a very different perspective, Khan, et al (2005) demonstrated an inhibition of rat brain mitochondrial activity in electron transport chain complexes I and IV, and indicates the involvement of DA-specific quinoproteins, rather than that of reactive oxygen species (ROS) in the neurotoxic effects of L-Dopa, as reported recently by Chen L, et al (2008) and earlier by Lai CT, et al (1997) (despite the partially protective effect of glutathione, an oxygen singlet free-radical scavenger). The interesting effect noted toward the end of the abstract is the ameliorating effect of the MAO-A inhibitor clorgyline on DA-induced generation of neuronal quinones, consistent with the hypothesis that prevention of de-amination may afford some neuroprotective effects against the metabolic byproducts of certain neurotransmitters (a concept reviewed most recently by Baker G, et al (2007).

[FunkOdyssey]

L-Dopa is definitely not a good idea for otherwise healthy individuals, and will probably not even increase brain dopamine levels to a significant degree without a decarboxylase inhibitor. See this thread I created at M&M on the topic.

Wow! Forget my little blurb from the University of Chicago, dopamine's thread on M&M is the new authority on L-Dopa toxicity. I doubt anyone who reads through that information will willingly ingest it again.

[Phreak]

I may be being dense, and admittedly I haven't read dopamine's link yet (I've bookmarked it for tomorrow morning), but if excessive free radical production is the problem (I don't really know what free radicals are but I will Wiki them, again, tomorrow morning), then surely some sort of of anti-oxidant co-administered with L-DOPA would reduce adverse effects...? Loads of Vitamin E, C and B etc...

Like I said, I'm very ignorant to all this and it's my own fault - I will do my homework on the subject tomorrow - but I know that free radical damage can be prevented with several herbs/vitamins/supplements, so surely this would at least reduce risks associated with ingesting L-DOPA...no...? :S

[Lurker]

http://www.scienceda...70427072318.htm

Interesting article about l-dopa.

The negatives seem pretty scary though.