Phytother Res. 2013 Mar;27(3):472-4. doi: 10.1002/ptr.4729. Epub 2012 May 14.
Abstract
The
culprit of kava hepatotoxicity will continue to remain a mystery in
humans, if the underlying reaction is of idiosyncratic, unpredictable,
and dose-independent nature due potentially to some metabolic aberration
in a few individuals emerging from kava use. In addition, kava
hepatotoxicity is presently not reproducible experimentally in
preclinical models, as demonstrated by studies showing whole kava
extracts are not hepatotoxic. This led us to propose our 'working
hypothesis' that contaminant hepatotoxins including moulds might have
caused rare kava hepatotoxicity in humans. Further studies are now
warranted to proof or disproof our working hypothesis, because kava
hepatotoxicity possibly based on contaminant hepatotoxins could be a
preventable disease. In the meantime, however, for minimizing toxicity
risk in kava users, a pragmatic approach should focus on the medicinal
use of an aqueous extract derived from peeled rhizomes and roots of a
non-mouldy noble kava cultivar, limited to maximum 250-mg kavalactones
daily for acute or intermittent use.
Copyright © 2012 John Wiley & Sons, Ltd.
Copyright © 2012 John Wiley & Sons, Ltd.
