Swimmingdancer
Bluelight Crew
I know there is a kava thread but I don't think many people would see this there and it's a more specific topic, however if the OD mods would rather this not have it's own thread please feel free to move it there.
So I've been doing some reading about how in animal tests kava has been found to cause upregulation of GABA receptors. What exactly that means for humans is still far from conclusive, but I think this possibility has some very interesting potential applications for withdrawal from GABAergic pharmaceuticals, which generally cause receptor downregulation, which is a big contributor to tolerance and withdrawal.
I have heard anecdotal evidence of and have seen in myself a sensitization to kava over time, as opposed to a tolerance, which seems to support the idea that kava could cause receptor upregulation.
Anyone have any relevant personal experience? For example using kava for benzo withdrawal/PAWS?
These animal studies report that kava causes upregulation of GABA receptors:
So I've been doing some reading about how in animal tests kava has been found to cause upregulation of GABA receptors. What exactly that means for humans is still far from conclusive, but I think this possibility has some very interesting potential applications for withdrawal from GABAergic pharmaceuticals, which generally cause receptor downregulation, which is a big contributor to tolerance and withdrawal.
I have heard anecdotal evidence of and have seen in myself a sensitization to kava over time, as opposed to a tolerance, which seems to support the idea that kava could cause receptor upregulation.
Anyone have any relevant personal experience? For example using kava for benzo withdrawal/PAWS?
These animal studies report that kava causes upregulation of GABA receptors:
Kavapyrone enriched extract from Piper methysticum as modulator of the GABA
binding site in different regions of rat brain.
Scatchard analysis revealed that the observed effects of kavapyrones were due to an increase in the number of binding sites (Bmax), rather than to a change in affinity. [Source: Kavapyrone enriched extract from Piper methysticum as modulator of the GABA binding site in different regions of rat brain.]
Kavalactones increase GABA receptor density in specific areas of rodent brain (especially hippocampus and amygdala) suggesting GABA-a receptor mediation of the sedative effects of kava, although earlier studies did not find GABA or benzodiazepine receptor binding. German EEG studies have confirmed the limbic structures, especially the amygdylar complex, mediate the sedative effects of kava [Source: The action profile of D,L-kavain. Cerebral sites and sleep-wakefulness-rhythm in
animals. *only the abstract is shown in this link]