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Re: on the contrary » linkadge

Posted by chemist on June 22, 2004, at 15:37:24

In reply to on the contrary, posted by linkadge on June 22, 2004, at 13:06:57

hello the, chemist here...my comments/questions delineated by ***

> I would definately say that cocaine is a much more potent stimulant than tobacco is. I do not suppose that ginkgo could even come close to reducing the cocaine craving in the heavy users.

*** if you look at the LD_{50} for cocaine hydrochloride and nicotine, you will find that on a mg/kg basis (i.v.), cocaine is about 50 times less likely to cause death than nicotine ***
>
> Kava is an anxiolitic but also a potent MAO-B inhibitor. From what I hear more potent than Ginkgo and SJW - similar to smoking. It does have nootropic properties. Let us remember that GABA potentiation has nootropic properties.

*** the component(s) you are referring to as potent MAO-B inhibitors isolated from kava kava were from one study that was done in vitro. the K_{i}s of the strongest 2 component was in the sub-micromolar to micromolar range. a potent inhibitor binds in (at least) the nanomolar to sub-nanomolar range. how is taking kava kava ``similar to smoking?'' any references would be appreciated. also, which component of kava kava are you referring to when you implicate the GABAnergic potentiation? any references are appreciated, because i am unaware of direct GABA modulation by binding to the BZ site (although there is weak affinity for GABA_{A}), rather, there are ways to do so by interaction of nootropics with AMPA. i assume you are talking about the aspartate/glutamate pathway, but please clarify. the nootropic properties of kava kava are from methysticin, but unfortunately, this component exhibits the greatest hepatic cyctotoxicity of the P450 class of isoenzymes. ***
>
> Ginkgo has been shown to be of some use to smoking ceasation, because it does have a mild dopimanergic action.

*** can you provide any references that implicate binding of nicotine to neuronal nicotine receptors (alpha_{7} or alpha_{4}beta_{2} substypes) followed by dopanergic agonism/antagonism? many thanks! *****
>
> The reason I suggest Kava is because MAO-B action would mimic cigarettes and GABA action would mimic alchohol.

*** again, how does MAO-B action ``mimic cigarettes?'' could you please clarify? i am unaware of any monoamineoxidase inhibition - reversible or not - by nicotine. thanks! ****
>
>
> I know a friend that quit both smoking and drinking with Kava. It may not be a long term solution however, since it may casue hepatotoxicity, (the jury is still out on that one)
>
>
**** the jury is in: kava extracts were banned in the EU and Canada in january, 2003 thanks to 11 cases of hepatic failure (4 deaths resultant) and, according to ``Kava kava: examining new reports of toxicity,'' Toxicology Letters 150:85-96 (2004), there are a ``a total of 78 cases of hepatotoxicity reputedly linked to kava ingestion,'' also for reasons i cannot understand, the author concludes that the risk-to-benefit ratio remains good compared to other anxiolytics. in an abstract from Integ. Cancer Ther 3:128-148 (2004), the phrase ``Studies of better-known herbal sedatives, notably valarien and kava, showed moderate evidence for both safety and efficacy for valerian while revealing disturbing toxicity concerns for kava.'' there is evidence (in vitro) to support moderate to little toxicity (Planta Med. 70:289-292, 2004); that pipermethystine ``is capable of causing cell death, probably in part by disrupting mitochondrial function'' (Toxicol. Sci. 79:106-111, 2004); and there is evidence that hepatotoxicity is reversible. still, i'm not taking my chances.....all the best, chemist ****

*** and please do forward references in re: the connection with nicotine and MAO inhibition? many thanks, chemist *******
> Linkadge
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