Posted by vanvog on April 24, 2013, at 21:31:20
In reply to MAOI + Ginkgo Biloba, posted by Tyrannosaur on April 24, 2013, at 3:51:49
You have probably seen this:
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Evidence that gingko biloba extract does not inhibit MAO A and B in living human brain.Abstract
Extracts of Ginkgo biloba have been reported to reversibly inhibit both monoamine oxidase (MAO) A and B in rat brain in vitro leading to speculation that MAO inhibition may contribute to some of its central nervous system effects. Here we have used positron emission tomography (PET) to measure the effects of Ginkgo biloba on human brain MAO A and B in 10 subjects treated for 1 month with 120 mg/day of the Ginkgo biloba extract EGb 761, using [11C]clorgyline and [11C]L-deprenyl-D2 to measure MAO A and B respectively. A three-compartment model was used to calculate the plasma to brain transfer constant K1 which is related to blood flow, and lambdak3, a model term which is a function of the concentration of catalytically active MAO molecules. Ginkgo biloba administration did not produce significant changes in brain MAO A or MAO B suggesting that mechanisms other than MAO inhibition need to be considered as mediating some of its CNS effects.http://www.ncbi.nlm.nih.gov/pubmed/10698362
-------------------I am curious as to where you found this information because I checked on the web and if you read the info from shops selling some kind of Ginkgo Biloba products it's "DO NOT TAKE WITH .... OR MAOI", "Avoid Ginkgo if you are taking MAOI for depression" etc.
**************************************************There might be some truth to it though:
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Effects of herbal components on cDNA-expressed cytochrome P450 enzyme catalytic activity.Abstract
We evaluated the effects of 25 purified components of commonly used herbal products on the catalytic activity of cDNA-expressed cytochrome P450 isoforms in in vitro experiments. Increasing concentrations of the compounds were incubated with a panel of recombinant human CYP isoforms (CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) and their effects on the conversion of specific surrogate substrates measured fluorometrically in a 96-well plate format. For each test substance, the IC50 (the concentration required to inhibit metabolism of surrogate substrates by 50%) was estimated and compared with IC50's for the positive control inhibitory drugs furafylline, sulfaphenazole, tranylcypromine, quinidine, and ketoconazole. Constituents of Ginkgo biloba (ginkgolic acids I and II), kava (desmethoxyyangonin, dihydromethysticin, and methysticin), garlic (allicin), evening primrose oil (cis-linoleic acid), and St. John's wort (hyperforin and quercetin) significantly inhibited one or more of the cDNA human P450 isoforms at concentrations of less than 10 uM. Some of the test compounds (components of Ginkgo biloba, kava, and St. John's wort) were more potent inhibitors of the isoforms 1A2, 2C19, and 2C19 than the positive controls used in each assay (furafylline, sulfaphenazole, and tranylcypromine, respectively), which are known to produce clinically significant drug interactions. The enzyme most sensitive to the inhibitory of effects of these compounds was CYP2C19, while the isoform least effected was CYP2D6. These data suggest that herbal products containing evening primrose oil, Ginkgo biloba, kava, and St. John's Wort could potentially inhibit the metabolism of co-administered medications whose primary route of elimination is via cytochrome P450.http://www.ncbi.nlm.nih.gov/pubmed/12127912
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Let's say metabolism inhibition of the MAOI you take is a good thing, how much Ginkgo do you have to take exactly to have a significant positive effect yet avoid nasty interactions and Ginkgo side effects?
I would still stay away from herbs and Ginkgo in particular but again it's just my opinion and I'm NOT the smartest guy I know.
poster:vanvog
thread:1042572
URL: http://www.dr-bob.org/babble/20130408/msgs/1042619.html