Seriously, the authors really, honestly do recommend against consuming tudei. They and the South Pacific governments also support differentiating between tudei and noble. Consumers agree and choose kavas determined to be 100% noble.
What is your point, honestly? Is it to say that a session with traditional kava is probably not lethal, but might still be very unpleasant? Fine. So what, Garry has never argued that "tudei kills people". If this is what you think you are fighting again then you've built yourself a nice straw man. The idea behind True Kava has always been that people should have the right to demand 100% pure, noble kava, which is something that hardly any vendor sold before Garry's testing. Many vendors called their kava noble, but it contained tudei, tudei peelings etc. Regardless of how dangerous or safe tudei is long-term, many people find it to be extremely undesirable and they have welcome the ability to avoid it. Are you upset that some people who mix tudei and noble have lost customers? C'est la vie. Surely it would be either stupid or evil (or both) to demand that the whole world stops pushing for quality so that some businesses can continue to sell crap.
In any case I actually do not believe you represent any vendors. No vendor voices support for your position (and no, your assertions that they do, but in complete secrecy) is not credible, no scientist backs your position.
Other quotes from the article you quote:
"Among these, pure flavokavin B [37] and further flavokavins [51] were found to be potentially liver toxic in mice, whereas dihydrome- thysticin was shown to be nontoxic. Toxicity seems to be triggered only at relatively high concentrations, too high to be of relevance with the use of noble kava or its corresponding extract preparations [42].
Based on the analyses of this still ongoing project, flavokavin B could be used as a marker for the determination of kava quality. From a practical point of view, a limitation of flavokavin B con- tent to 2 mg/g of dried material would be sufficient to assure the use of noble kava and thus the possibility to lean on traditional safety experience.
Results from a currently ongoing research program in the South Pacific so far confirm these findings. Roots and peeled stumps of noble kava varieties usually contain less than 1 mg/g of flavokavin B in the dry matter, whereas the bark (“peelings”) frequently contains higher quantities than 2 mg/g in noble varieties, mostly exceeding 5 mg/g in non-noble varieties, especially in plant parts exposed to sunlight (unpublished data). These findings corroborrate the traditional use of roots and peeled rhizome stumps only and the avoidance of non-peeled materials and sun-exposed plant parts.
Such unsuitable plant parts, especially peelings of two-day kava, are unfortunately still sold by certain traders in Vanuatu and Fiji (in the latter case, with re-exported material from Vanuatu). Vanuatu has officially banned exports of two-day kava through the Vanuatu kava act, but does not have the means to control the qual- ity of the exports. Furthermore, this law unfortunately makes an exception from this prohibition of exporting two-day kava plant materials when the client specifically demands such a quality – a loophole in the legislation extensively used by some traders.
The other kava-producing South Pacific nations, i.e., Fiji, Samoa, and Tonga, do not have two-day varieties.
(..)
The current state of ethnopharmacological and phytochemical research still does not confirm a causal relationship between the consumption of kava preparations and the occurrence of adverse liver reactions. With the assumption of the (albeit very rare) ex- istence of such a type of reaction, manufacturers should seek guidance for the quality of plant material known to be safe through centuries of traditional experience. The problem of possible hepatotoxicity of kava preparations was potentially caused by ill-defined herbal drug identity, a lack of appropriate quality control, and misguided regulatory politics.
Thus, in order to re-establish “noble” kava to its rightful place as an essential anxiolytic drug in the European market, its botanical and phytochemical differentiation from the “non-noble” kava varieties has to be established by pharmacopoeial regulations. This should be a minor problem, as there are already several plant drugs where the pharmacopoeia does already differentiate be- tween closely related and easily misidentified species (e.g., Illic- ium verum vs. Illicium anisatum). With the circumstantial evidence supporting a raw drug identity/quality issue at the base of the problem of hepatotoxicity, the definition of appropriate quality standards should, in any case, be helpful.
There is, however, not much time to act on the problem of drug identity of pharmaceutically suitable kava varieties. In the past 10 years, kava exports from the South Pacific islands have again multiplied, reaching the same level as at the time before the kava ban in 2001. The United States have especially evolved as a kava market, with currently more than 90 kava bars serving kava of frequently highly doubtful quality. Similarly, the market of New Caledonia has shifted to the import of large quantities of two- day kava roots and (mainly) peelings from Vanuatu, with the ar- gument that the higher kavalactone concentrations and, at the same time, relatively low costs allow for the production of more kava drinks at lesser expenses. If the flavokavins or other as yet non-identified constituents of non-noble kava are truly responsi- ble for liver toxicity, this could be playing with fire. There are al- ready isolated reports of liver toxicity related to kava use from New Caledonia – cases that are now discussed in the context of potential mould-related toxicity [54], but even this aspect would have to be part of quality specifications."
, I got a better idea. 
