I run a Kava company. Would you consider Kava a Nootropic?

Wait, where do you see it has been officially debunked? I am not seeing any evidence that the possible hepatotoxicity has been proven wrong. In fact, I am seeing much evidence from recent studies not only proving it to be a risk, but the compounds and mechanisms responsible. The one meta analysis rejecting the so called kava paradox is blaming mold hepatotoxins for the damage, due to improper storage or production methods. Even if that is the only case, you would need to be testing for these contaminants before selling to customers. Based on your lack of answer to Shrillthrill above, I would venture to guess you are not testing for these possible contaminants. Am I correct in that assumption?

Here is that meta analysis: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3269575/

However, there have been specific studies into the components of kava root that might be damaging to the liver:

Kavalactones Yangonin and Methysticin Induce Apoptosis in Human Hepatocytes (HepG2) In Vitro

Our data demonstrated increasing kavalactone hepatotoxicity from kavain to methysticin to yangonin. This differs from another study which found yangonin was the least toxic of three purified kavalactones tested on cultured hepatocytes (Zou et al., 2004). The most toxic was methysticin, followed by desmethoxyyangonin.

Studies in HepG2 cells revealed that kavain, methysticin and yangonin have an increasing order of hepatotoxicity. Dual staining with acridine orange/ethidium bromide showed apoptosis was induced by methysticin and yangonin. Apoptosis predominated over necrosis as the mechanism of cell death.

So you have evidence there that multiple compounds in kava are hepatotoxic. Then some people claim those compounds are only found in the leaves, not the root. However, other studies have proven that incorrect.

Comparison of subcritical water and organic solvents for extracting kava lactones from kava root

Here is the graph showing how water temperature has a big effect on the specific kavalactones extracted.

You can see both Yangonin and Dihydromethysticin are present in water extracts of kava root. So it does not take leaf matter or special solvent extraction to pull out these hepatotoxic compounds. It just takes water and heat. The saving grace for the Yangonin is that it takes over boiling temps to pull the compounds out. So most preparations will not have to deal with that. However, the Dihydromethysticin starts to be an issue at only 115*F. These were 10 minute extraction times. So perhaps longer extractions at lower temps could lead to issues as well. It's certainly a possibility.

The big kicker with this study are the following statements:

40 min of subcritical water extraction were sufficient to yield recoveries similar to those obtained with 18 h of sonication with acetone, CH Cl , or methanol for all lactones (Table 3). None of the organic solvents showed significantly higher recoveries than water, or other organic solvents. Table 3 also demonstrates that the addition of CH Cl after the extraction cell has no effect on the extraction efficiencies. No statistically significant change in extraction efficiencies occurs with or without CH Cl , demonstrating that only pure water is needed for quantitative recovery of kava lactones.

So the use of different solvent extraction methods did not lead to appreciable differences in the efficiencies or compounds extracted, compared to water. This means that the argument that only certain solvent extraction methods lead to the toxic compounds is not correct. A purely water-based extraction method is more than enough to pull out the compounds that have been proven to be toxic to human liver cells.

Then you have this study from 2014: Flavokawains A and B in Kava, Not Dihydromethysticin, Potentiate Acetaminophen-Induced Hepatotoxicity in C57BL/6 Mice

The results from this study demonstrated that kava when administered alone via gavage in C57BL/6 mice induced no adverse effect even at a fairly high dose (500 mg/kg bodyweight daily) in a chronic manner, as reflected in mouse growth and serum levels of ALT and AST (Figure 1). These results are consistent with the results from many early studies.(26-29) On the other hand, kava significantly potentiated the hepatotoxicity of APAP in C57BL/6 mice, as indicated by the increase in serum ALT and AST, and the increased severity of liver lesions (Figure 2). The treatment regimen was designed to mimic potential circumstances among human kava users that kava would be consumed on a daily basis while other medications, APAP in this case, were used occasionally when needed. Since the majority of kava-associated hepatotoxic cases consumed other medications or dietary supplements concomitantly, the results from this study may have direct indication to the observed hepatotoxicity among kava users. It remains to be determined whether kava usage can potentiate the hepatotoxic risk of other medications or hepatotoxins, such as alcohol consumption. It also remains to be determined whether other kava treatment regimens, such as prolonged kava usage or in a fasted stage (recommended for traditional kava usage), may potentiate its hepatotoxic risk even at lower kava dosages.

So they are seeing that Flavokawains A and B actually potentiate the liver damage from other compounds, but do not cause it on their own. So this is what could be causing all the reported liver issues around the world. If someone consumes kava, then takes a Tylenol or drinks a beer, then damage to the liver occurs. One could look at this study and claim that it shows kava is not directly causing liver damage. However, the interactions with other compounds are the real risk in that case. This is why the risks need to be stated, and people need to be informed.

So please please please, stop making statements like "All hepatoxin claims have finally been officially debunked," as they are simply not true. Kava root does have a risk of hepatotoxicitiy, whether that be from a direct apoptosis mechanism seen in human liver studies, or from a potentiation of other liver-taxing compounds like Acetominophen. The risk of mold hepatotoxins from improper production and storage of kava has also been brought up. So it is prudent for vendors of kava to be testing for these compounds, to ensure that at least that risk is not something their customers have to worry about.