Phytother Res. 2013 Mar;27(3):472-4. doi: 10.1002/ptr.4729. Epub 2012 May 14.
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.
如果由于某些个体在使用卡瓦后的代谢异常，导致其潜在的不良反应具有独特性、不可预测性和剂量独立性，那么卡瓦肝毒性的罪魁祸首在人类中仍将是一个谜。此外，目前在临床前模型中无法重现卡瓦肝毒性的实验性研究，这表明研究表明全卡瓦提取物没有肝毒性。这使我们提出了我们的“工作假设”，即包括霉菌在内的污染物肝毒素可能导致了人类罕见的卡瓦肝毒性。现在需要进一步的研究来证明或反驳我们的工作假设，因为基于污染物肝毒素的卡瓦肝毒性可能是一种可预防的疾病。然而，与此同时，为了最大限度地降低卡瓦使用者的毒性风险，一种务实的方法应该侧重于使用一种源自去皮根茎和无霉菌优质卡瓦品种的根部的水提物，每日最大剂量为 250 毫克卡瓦内酯，用于急性或间歇性使用。
