Kava Research Opportunities and Challenges of Kava in Lung Cancer Prevention

[The Kap'n]

New Review on Kava's effect on Lung Cancer​

Opportunities and Challenges of Kava in Lung Cancer Prevention Lung cancer is the leading cause of cancer-related deaths due to its high incidence, late diagnosis, and limited success in clinical treatment. Prevention therefore is critical to help improve lung cancer management. Although tobacco control and tobacco cessation are effective strategies for... www.mdpi.com Freeman, Breanne, Jessica Mamallapalli, Tengfei Bian, Kayleigh Ballas, Allison Lynch, Alexander Scala, Zhiguang Huo, et al. 2023. “Opportunities and Challenges of Kava in Lung Cancer Prevention.” International Journal of Molecular Sciences, May. https://doi.org/10.3390/ijms24119539. ​

This is an excellent review of the supporting evidence of kava's possible anticarcinogenic properties.

I only had issues with one section, and that was section 4.4 (predictably).

This section is titled "Potential Risks Associated with Kava Use, Particularly in the Chronic Use".

I'm going to go through them sentence by sentence.

Sentence #1 also cited as 148:

Besides these potential benefits, kava has been associated with hepatotoxic potential even though the risk was rated extremely rare and idiosyncratic with a wide range of mechanisms and responsible ingredients proposed, including chalcone-based flavokavains and various kavalactones [148].

This source literally speaks about the Pacific kava paradox being rejected. 180° from what the author is attempting to use it for.

"At present, little evidence exists that the primary psychoactive constituents (kavalactones) or other constituents (pipermethystine and flavokavain B) of the kava plants are the toxicological culprits for kava hepatotoxicity"

Sentence #2 cited as 149:

Specifically, chalcone-based flavokavains A and B have been demonstrated to induce hepatotoxicity in animal models or potentiate acetaminophen (APAP)-induced hepatotoxicity, potentially via the depletion or reduction in endogenous glutathione level [149].

This part is actually from two totally different sources than 149.

They are: Narayanapillai, Sreekanth C., Pablo Leitzman, M. Gerard O’Sullivan, and Chengguo Xing. 2014. “Flavokawains a and B in Kava, Not Dihydromethysticin, Potentiate Acetaminophen-Induced Hepatotoxicity in C57BL/6 Mice.” Chemical Research in Toxicology 27 (10): 1871–76. https://doi.org/10.1021/tx5003194.

Yang, Xi, and William F. Salminen. 2011. “Kava Extract, an Herbal Alternative for Anxiety Relief, Potentiates Acetaminophen-Induced Cytotoxicity in Rat Hepatic Cells.” Phytomedicine: International Journal of Phytotherapy and Phytopharmacology 18 (7): 592–600. https://doi.org/10.1016/j.phymed.2011.02.006.

The first source uses levels of FKB 100 to 1,000 fold higher than what could be seen drinking an entire kilo of noble kava powder.

The second source uses APAP at a human equivalence of 16,000mg. Neither of these two studies can be said to replicate what is happening in-vivo.

Sentence #3 is correct:

The content of flavokavains A and B indeed were found to be higher in kava plants not recommended for human use in comparison to those popular for traditional consumption.

Sentence #4 cited as 150 & 151:

Kavalactones have also been suspected to contribute to kava’s hepatotoxic risk, potentially through drug herb interactions since various kavalactones have been reported to modulate several CYP enzymes [150,151]

Source 150: Uses Almeida's trash document to suggest pharmacodynamic interactions with benzodiazepine and kava. Also uses 100µM directly applied to cells, a concentration level we would never see in the human body.

Results of 150&151 are not reproducible in-vivo.

Sentence #5 cited as 87:

The concentrations or doses of kavalactones evaluated in the biochemical or cell-based models may have limited human physiological relevance based on our recent pharmacokinetic studies of kava [87]

The authors here go back and attempt to explain that these cell-based models may not coincide with what actually happens in the human body. No issues here.

Sentence #6:

Nonetheless, the safety of kava needs to be closely monitored in future human translation, particularly for its potential chronic use in lung cancer risk reduction.

Kava's safety has been monitored quite closely for the last 25 years. Considering we've had no credible instances of adverse events involving the liver in the last 20 years (Per the FDA adverse events database), I would say the "safety" of kava has been proven quite continuously over the last two decades.

Other than this one section, this is an excellent review. Highly suggest giving it a read over.

 

[Alia]

New Review on Kava's effect on Lung Cancer​

Opportunities and Challenges of Kava in Lung Cancer Prevention Lung cancer is the leading cause of cancer-related deaths due to its high incidence, late diagnosis, and limited success in clinical treatment. Prevention therefore is critical to help improve lung cancer management. Although tobacco control and tobacco cessation are effective strategies for... www.mdpi.com Freeman, Breanne, Jessica Mamallapalli, Tengfei Bian, Kayleigh Ballas, Allison Lynch, Alexander Scala, Zhiguang Huo, et al. 2023. “Opportunities and Challenges of Kava in Lung Cancer Prevention.” International Journal of Molecular Sciences, May. https://doi.org/10.3390/ijms24119539.​

This is an excellent review of the supporting evidence of kava's possible anticarcinogenic properties.

I only had issues with one section, and that was section 4.4 (predictably).

This section is titled "Potential Risks Associated with Kava Use, Particularly in the Chronic Use".

I'm going to go through them sentence by sentence.

Sentence #1 also cited as 148:


This source literally speaks about the Pacific kava paradox being rejected. 180° from what the author is attempting to use it for.

"At present, little evidence exists that the primary psychoactive constituents (kavalactones) or other constituents (pipermethystine and flavokavain B) of the kava plants are the toxicological culprits for kava hepatotoxicity"

Sentence #2 cited as 149:


This part is actually from two totally different sources than 149.

They are: Narayanapillai, Sreekanth C., Pablo Leitzman, M. Gerard O’Sullivan, and Chengguo Xing. 2014. “Flavokawains a and B in Kava, Not Dihydromethysticin, Potentiate Acetaminophen-Induced Hepatotoxicity in C57BL/6 Mice.” Chemical Research in Toxicology 27 (10): 1871–76. https://doi.org/10.1021/tx5003194.

Yang, Xi, and William F. Salminen. 2011. “Kava Extract, an Herbal Alternative for Anxiety Relief, Potentiates Acetaminophen-Induced Cytotoxicity in Rat Hepatic Cells.” Phytomedicine: International Journal of Phytotherapy and Phytopharmacology 18 (7): 592–600. https://doi.org/10.1016/j.phymed.2011.02.006.

The first source uses levels of FKB 100 to 1,000 fold higher than what could be seen drinking an entire kilo of noble kava powder.

The second source uses APAP at a human equivalence of 16,000mg. Neither of these two studies can be said to replicate what is happening in-vivo.

Sentence #3 is correct:


Sentence #4 cited as 150 & 151:


Source 150: Uses Almeida's trash document to suggest pharmacodynamic interactions with benzodiazepine and kava. Also uses 100µM directly applied to cells, a concentration level we would never see in the human body.

Results of 150&151 are not reproducible in-vivo.

Sentence #5 cited as 87:


The authors here go back and attempt to explain that these cell-based models may not coincide with what actually happens in the human body. No issues here.

Sentence #6:


Kava's safety has been monitored quite closely for the last 25 years. Considering we've had no credible instances of adverse events involving the liver in the last 20 years (Per the FDA adverse events database), I would say the "safety" of kava has been proven quite continuously over the last two decades.

Other than this one section, this is an excellent review. Highly suggest giving it a read over.

You have written a great review and I hope others read it as well as the new paper.
The evolution of the "kava as cancer prevention" is remarkable. It goes from the
keen statistical (Dr. Steiner) to what I now estimate to be more scientific research that
kava can stop the formation of many forms of cancer than there is research of kava as
" anxiolytic " (a medication or other intervention that reduces anxiety). Correct me
if I'm wrong. This evolution has gone from attempts to create the "perfect" cancer
prevention kava-extract- capsule, tinctures. Attempt to patent, get FDA approval,
unsuccessful I believe. NOW in this latest paper it seems the BEST is traditional kava
beverage!

 

[JohnMichael]

New Review on Kava's effect on Lung Cancer​

Opportunities and Challenges of Kava in Lung Cancer Prevention Lung cancer is the leading cause of cancer-related deaths due to its high incidence, late diagnosis, and limited success in clinical treatment. Prevention therefore is critical to help improve lung cancer management. Although tobacco control and tobacco cessation are effective strategies for... www.mdpi.com Freeman, Breanne, Jessica Mamallapalli, Tengfei Bian, Kayleigh Ballas, Allison Lynch, Alexander Scala, Zhiguang Huo, et al. 2023. “Opportunities and Challenges of Kava in Lung Cancer Prevention.” International Journal of Molecular Sciences, May. https://doi.org/10.3390/ijms24119539.​

This is an excellent review of the supporting evidence of kava's possible anticarcinogenic properties.

I only had issues with one section, and that was section 4.4 (predictably).

This section is titled "Potential Risks Associated with Kava Use, Particularly in the Chronic Use".

I'm going to go through them sentence by sentence.

Sentence #1 also cited as 148:


This source literally speaks about the Pacific kava paradox being rejected. 180° from what the author is attempting to use it for.

"At present, little evidence exists that the primary psychoactive constituents (kavalactones) or other constituents (pipermethystine and flavokavain B) of the kava plants are the toxicological culprits for kava hepatotoxicity"

Sentence #2 cited as 149:


This part is actually from two totally different sources than 149.

They are: Narayanapillai, Sreekanth C., Pablo Leitzman, M. Gerard O’Sullivan, and Chengguo Xing. 2014. “Flavokawains a and B in Kava, Not Dihydromethysticin, Potentiate Acetaminophen-Induced Hepatotoxicity in C57BL/6 Mice.” Chemical Research in Toxicology 27 (10): 1871–76. https://doi.org/10.1021/tx5003194.

Yang, Xi, and William F. Salminen. 2011. “Kava Extract, an Herbal Alternative for Anxiety Relief, Potentiates Acetaminophen-Induced Cytotoxicity in Rat Hepatic Cells.” Phytomedicine: International Journal of Phytotherapy and Phytopharmacology 18 (7): 592–600. https://doi.org/10.1016/j.phymed.2011.02.006.

The first source uses levels of FKB 100 to 1,000 fold higher than what could be seen drinking an entire kilo of noble kava powder.

The second source uses APAP at a human equivalence of 16,000mg. Neither of these two studies can be said to replicate what is happening in-vivo.

Sentence #3 is correct:


Sentence #4 cited as 150 & 151:


Source 150: Uses Almeida's trash document to suggest pharmacodynamic interactions with benzodiazepine and kava. Also uses 100µM directly applied to cells, a concentration level we would never see in the human body.

Results of 150&151 are not reproducible in-vivo.

Sentence #5 cited as 87:


The authors here go back and attempt to explain that these cell-based models may not coincide with what actually happens in the human body. No issues here.

Sentence #6:


Kava's safety has been monitored quite closely for the last 25 years. Considering we've had no credible instances of adverse events involving the liver in the last 20 years (Per the FDA adverse events database), I would say the "safety" of kava has been proven quite continuously over the last two decades.

Other than this one section, this is an excellent review. Highly suggest giving it a read over.

One of the most significant sentences in this review was: "It should be noted that the dose range of kava and natural dihydromethysticin, with effective lung cancer prevention in these animal studies, was comparable to the levels of traditional kava consumption in humans." This statement is very significant since so many studies employ extravagant amounts of whatever they're investigating. In this case, the "effective lung cancer prevention" amount was basically the same as "traditional kava consumption in humans." That's really meaningful.

 

[KavaTasteGood]

Thanks for pointing that out, John! What I also see is that it's not just lung cancer, but other types of cancer too. Interestingly, the highest consumption group in Table 1 is at 6.7 kg/year/person. I do double since I started haha. So much benefits to this root! The IMAO-B effect should also decrease neurodegenerative pathologies in my understanding. This is cool!