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6 are known, what percentages are in kava. What are their names, what do the molecules look like? The article doesn't say... heres 3 of the kavalactones. Needs expansion. --x1987x(talk) 04:40, 16 January 2007 (UTC)

Probably "(+)-methysticin, (+)-dihydromethysticin, (+)-kavain, (+)-dihydrokavain, yangonin, and desmethoxyyangonin" ( It'd be nice if someone knew what they did. On the main page desmethoxyyangonin is identified as a reversible mao-b inhibitor. I'd like to know what the other 5 do. —Preceding unsigned comment added by (talk) 08:01, 10 February 2008 (UTC)

Last three chemical structures[edit]

Looking at the last 3 structures of kavalactones, by their substitution there seems to be no difference between them...could there be a mistake here, or is there some sort of sterics thing I'm missing here? 17:14, 15 August 2007 (UTC)

Double bonds (in the rings) are in different places --x1987x(talk) 01:42, 27 October 2008 (UTC)

Removed content[edit]

Removed content

Kavalactones are the active ingredient in the tranquilizing beverage Kava. They are the main psychoactive components of the roots of Piper methysticum (kava), a shrub common on some Pacific Ocean islands. Another class of compounds found in P. methysticum are the Flavokavains, which are substituted chalcones in nature and not lactones, and thus they are not kavalactones.

The rhizome and roots of the shrub are ground, grated and steeped in water to produce a non-alcoholic drink which is said to promote sociability, mental clarity, and reduction of anxiety (see main kava entry). The quantity and ratio of kavalactones present vary dramatically and are highest when roots are extracted with solvents rather than by conventional tea preparation (but note safety issues; see kava).[1]

Some use lipids to aid in kavalactone extraction. (ie; whole milk, oils, etc.)

Effects of kavalactones include mild sedation, a slight numbing of the gums and mouth, and vivid dreams.[citation needed] Kava has been reported to improve cognitive performance and promote a cheerful mood. [2] Muscle relaxant, anaesthetic, anticonvulsive and anxiolytic effects are thought to result from direct interactions of kavalactones with voltage-gated ion channels. [3] Research currently suggests that kavalactones potentiate GABAA activity but do not alter levels of dopamine and serotonin in the CNS. [4] Heavy, long-term kava use does not cause any reduction of ability in saccade and cognitive tests but is associated with elevated liver enzymes. [5]

Desmethoxyyangonin, one of the six major kavalactones, is a reversible MAO-B inhibitor (Ki 280 nM)[6] and is able to increase dopamine levels in the nucleus accumbens. This finding might correspond to the slightly euphoric action of kava.[7]

Kavain in both enantiomeric forms inhibit the reuptake of noradrenalin at the transporter (NAT), but not of serotonin (SERT).[8] An elevated extracellular NA level in the brain may account for the reported enhancement of attention and focus with kava.

The United States Food and Drug Administration (FDA) has warned that very rare cases of liver damage or fulminant liver failure may be caused by kava-containing supplements. However, these injuries might result from pipermethystine[9], an alkaloid present in portions of the plant used industrially but normally discarded in traditional preparations (see kava).

Some researchers have theorized that that there may be differences in hepatoxicity based on whether aqueous extraction or ethanolic extraction is used.[who?] In a study conducted by South Dakota State University, researchers found that aqueous kava extracts did not affect liver function tests in rats.[10] Another study conducted by MediHerb Research Laboratories found that extraction method influenced the total (but not relative) concentration of kavalactones, but concluded that it did not markedly affect bioavailability, and that "any differences between an ethanolic or an aqueous extract in terms of the propensity of kava to cause liver damage is not because of differing kavalactone bioavailabilities."[11]

Much of the content [that was] in this article needs to be reincorporated into the articles about the specific kavalactones referenced.   — C M B J   03:03, 5 September 2009 (UTC)

  1. ^ Hu, A; et al. (2005). "Determination of six kavalactones in dietary supplements and selected functional foods containing Piper methysticum by isocratic liquid chromatography with internal standard". J AOAC Int. 88 (1): 16–25. PMID 15759721. 
  2. ^ Thompson, R; et al. (2004). "Enhanced cognitive performance and cheerful mood by standardized extracts of Piper methysticum (Kava-kava)". Hum Psychopharmacol. 19 (4): 243–250. doi:10.1002/hup.581. PMID 15181652. 
  3. ^ Cairney, S; et al. (2002). "The neurobehavioural effects of kava". Aust N Z J Psychiatry. 36 (5): 657–652. doi:10.1046/j.1440-1614.2002.01027.x. PMID 12225450. 
  4. ^ Hunter, A (2006). "Kava (Piper methysticum) back in circulation". Australian Centre for Complementary Medicine. 25 (7): 529. 
  5. ^ Cairney, S; et al. (2003). "Saccade and cognitive function in chronic kava users". Neuropsychopharmacology. 28 (2): 389–396. doi:10.1038/sj.npp.1300052. PMID 12589393. 
  6. ^ Uebelhack R, Franke L, Schewe HJ (1998): “Inhibition of platelet MAO-B by kava pyrone-enriched extract from kava-kava.” Pharmacopsychiatry 31(5):187-92. PMID 9832350
  7. ^ Baum SS, Hill R, Rommelspacher H (1998): “Effect of kava extract and individual kavapyrones on neurotransmitter levels in the nucleus accumbens of rats.” Prog Neuropsychopharmacol Biol Psychiatry 22(7):1105-20. PMID 9829291
  8. ^ Seitz U, Schule A, Gleitz J (1997): "[3H]-monoamine uptake inhibition properties of kava pyrones." Planta Med. 63(6):548-9. PMID 9434608
  9. ^ Nerurkar, PV; et al. (2004). "In vitro toxicity of kava alkaloid, pipermethystine, in HepG2 cells compared to kavalactones". Toxicological Sciences. 79 (1): 106–111. doi:10.1093/toxsci/kfh067. PMID 14737001. 
  10. ^ Singh, Yadhu (2003 June). "Aqueous kava extracts do not affect liver function tests in rats." (PDF). Planta Medica. 69 (6): 496–499. PMID 12865965. Retrieved 2009-09-04.  Unknown parameter |coauthors= ignored (|author= suggested) (help); Check date values in: |date= (help)
  11. ^ Matthias, A. (2007 June). "Permeability studies of Kavalactones using a Caco-2 cell monolayer model". Journal of Clinical Pharmacy and Therapeutics. 32 (3): 233–239. PMID 17489874 doi:10.1111/j.1365-2710.2007.00810.x.  Unknown parameter |coauthors= ignored (|author= suggested) (help); Check date values in: |date= (help);