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The kava kava scare Another false herbal scare arose over kava kava, the South Pacific Island herb that helps to overcome mild cases of depression. Pharmaceutical companies in Europe were selling kava kava and reported, without adequate substantiation, that there were reports of liver toxicity in less than 100 people and withdrew the herb (a drug in Europe) from distribution in 2002. US sales of kava kava were then about $34 million a year. The American Herbal Products Association was put on the defensive to prove a long-used herbal extract was safe when there were only specious reports of liver toxicity from Europe. Then the US Food & Drug Administration destroyed US sales of kava kava by issuing a warning of a ‘potential’ hazard and asked health professionals to report any cases of liver toxicity associated with this herb.
(For comparison, the US Poison Control Centers report that acetaminophen (Tylenol) causes 70,000 reported cases of liver toxicity annually which results in 70-100 deaths per year.) Only a handful of adverse reports were submitted to the FDA by US physicians. None panned out to be of concern. But consumers taking kava kava for anxiety and depression were getting more anxious and depressed every time they heard another negative news reports about kava. Dr. Donald Waller, a toxicologist and professor at the University of Illinois, reviewed the reported cases of liver toxicity associated with the use of kava kava and concluded “there was no clear evidence that the liver damage reported in the US and Europe was caused by the consumption of kava.” Other researchers also could not find a link between kava and the reported cases of liver toxicity. [Planta Med. 2004 Mar; 70: 193-6] In many of these cases the kava patients were also taking prescription drugs that are known to be toxic to the liver. But the May 2004 issue of Consumer Reports still listed kava among its list of “Dangerous Supplements Still at Large. Dr. Marvin Lipman, Consumer Reports’ chief medical advisor said: “Given the weight of the evidence against Kava, we would urge everyone to avoid its use.” In March of 2004 Canadian researchers were horrified that health food stores were still recommending kava kava to their customers. [J Gen Intern Med. 2004 Mar; 19: 269-72] “There was no clear evidence that the liver damage reported in the US and Europe was caused by the consumption of kava.” –Dr. Donald Waller, toxicologist Among Hawaiian farmers, sales of kava kava raw material dropped by 87% in just one year. [Hawaii Dept. of Agriculture] Thousands of jobs were wiped out. An efficacious anti-anxiety herb was cast into question, and most consumers didn’t suspect that there were competing commercial interests behind this whole fiasco. 7/04 Integr Med Res. 2019 Jun;8(2):123-128. doi: 10.1016/j.imr.2019.04.007. Epub 2019 Apr 20. A Naturalistic Study of Herbal Medicine for Self-Reported Depression and/or Anxiety a Protocol David Casteleijn 1, Amie Steel 1, Diana Bowman 1, Romy Lauche 2, Jon Wardle 1 PMID: 31193603 PMCID: PMC6536771 Abstract Background: Mental health conditions including anxiety and depression account for around 8% of the global disease burden. Anxiety and depression often coexist and impose a high individual and social burden. Patients with mental and behavioral conditions may be at increased risk of co-morbidities and are often high health-care utilizers. Herbal medicine is estimated to be used by up to 80% of the worlds population, and by 22% of Australian women seeking care for depression. The holistic and tailored treatment approach offered by practitioners of herbal medicine is difficult to capture in randomized controlled trials and as such there is a paucity of research demonstrating the outcomes of real-life practice. This project aims to address this gap with a whole practice, observational model. Methods/design: The study will employ a naturalistic observational design. Two-hundred patient participants will be recruited to be treated by 15 clinician participants from different naturopathic clinics. The observed changes in anxiety and depression symptoms of patients will be documented across three consultations using validated patient-reported outcome measures (SF-36, DASS-21, GHQ-28 and POMS-2). Conclusion: Clinical studies investigating the efficacy of individualized herbal medicine treatment as prescribed by a naturopath are rare. Our study attempts to fill this gap with a longitudinal observation of individualized care as practiced by naturopaths in Australia; to offer valuable insights into the effectiveness of individualized herbal medicine practice and provide contextualization of data currently focused on individual herbal medicines in specific conditions. Trial Registration: Australian and New Zealand Clinical Trials Registry: ACTRN12616000010493. Kava feeding in rats does not cause liver injury nor enhance galactosamine-induced hepatitis Robert A. DiSilvestro, a, Wenyi Zhanga and David J. DiSilvestroa aHuman Nutrition, The Ohio State University, 345 Campbell Hall, 1787 Neil Avenue, Columbus, OH 43210-1295, United States Abstract Kava, like a number of herbals, has been associated with causing liver damage based on limited evidence. In contrast, the present study found that in rats, 3 mo feedings of two types of kava extracts (an acetone extract and an ethanol extract of the Samoan kava cultivar Ava Laau) at three different doses (31.25, 62.5 and 133 mg/kg diet) produced no liver injury based on serum markers of liver damage (sorbitol dehydrogenase activities, bile acid concentrations, and â-glucuronidase activities) and serum lipid peroxide readings. In fact, for some measurements and some kava doses, the injury marker readings were below control values. Moreover, for these same parameters, kava feeding did not enhance the effects of the hepatotoxin galacatosamine (500 mg/kg ip); some kava doses even showed modest protection against liver injury. Liver histology analysis showed no signs of kava causing or enhancing liver injury. Thus, this study does not support the concept that kava produces or aggravates liver injury. Food and Chemical Toxicology Volume 45, Issue 7, July 2007, Pages 1293-1300 doi:10.1016/j.fct.2007.01.015 Author Ann FonfaCategorie
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