Talk:Acorus calamus/Archives/2020/March

Safety and toxicity

The reversion here was done because it over-interpreted the rat data and made assumptions about metabolism and toxicity that remain unproven, as stated in the EC document. This is WP:OR and is discouraged. The detail of the edit is unencyclopedic per WP:NOTJOURNAL, #6-8, i.e., although this discussion might be appropriate for a thesis or journal article, it is not established as fact, and is therefore unencyclopedic for such detail. The EC conclusion - the most authoritative source used - was that a safe level could not be established. The previous paragraph, including an FDA source, already discusses that succinctly. Reverted again per WP:BRD for review by other editors and consensus, WP:CON. --Zefr (talk) 15:37, 4 August 2019 (UTC)

I fail to understand how data can over-interpret itself, since data is what was posted. But thank you for taking the time to edit this article. It would be interesting to discuss with you further about this subject.

In my humble opinion, the deleted information was important, therefore I would like to give readers an opportunity to decide for themselves if it is relevant. The removed section is conveniently posted below for those who may wish to review the information:

"The original FDA ban was the result of lab studies that involved supplementing the diets of lab animals over a prolonged period of time with massive doses of isolated chemicals (β-asarone) from the Indian Jammu strain of calamus. The animals developed tumors, and the plant was labeled procarcinogenic.[1] Wichtl says "It is not clear whether the observed carcinogenic effects in rats are relevant to the human organism."[2] However, most sources advise caution in ingesting strains other than the diploid strain. Again, limits on consumption of any type of calamus in food or alcoholic beverages (115 micrograms per day) were recommended in a 2001 ruling by the European Commission, without defining degrees of safe exposure.[3]

The diploid strains of A. calamus in parts of Mongolia, in parts of the western Himalayas and C Siberia, and the Acorus americanus does not contain the procarcinogenic β-asarone.[4][5][6]

In reality β-asarone is neither hepatotoxic nor directly hepatocarcinogenic. It must first undergo metabolic l'-hydroxylation in the liver before achieving toxicity. Cytochrome P450 in the hepatocytes is responsible for secreting the hydrolyzing enzymes that convert β-asarone into genotoxic epoxide structure.[7] Even with the activation of these metabolites, the carcinogenic potency is very low because of the rapid breakdown of epoxide residues with hydrolase which leaves these compounds inert.[8] Additionally, the major metabolite of β-asarone is 2,4,5-trimethoxycinnamic acid, a derivative which is not a carcinogen.[9]

References

1. Natural carcinogenic products, EK Weisburger – Environmental Science & Technology, 1979 – ACS Publications

2. Wichtl, Max (2004). Herbal drugs and phytopharmaceuticals: a handbook.

3. Opinion of the Scientific Committee on Food on the presence of beta-asarone in flavourings and other food ingredients with flavouring properties" (PDF). European Commission, Scientific Committee on Food. 12 December 2001. Retrieved 28 January 2019.

4. Chemical composition of the essential oil and supercritical CO2 extract of Commiphora myrrha (Nees) Engl. and of Acorus calamus L.B Marongiu, A Piras, S Porcedda… - J. Agric., 2005 - ACS Publications

5. (Rost and Bos, 1979)

6. Antimicrobial activities of the crude methanol extract of Acorus calamus Linn., S Phongpaichit, N Pujenjob, J. Songklanakarin

7. McGuffin, Michael, ed. (1997). American Herbal Products Association's Botanical Safety Handbook. Boca Raton, Florida: CRC Press. p. 135. ISBN 978-0- 8493-1675-3.

8. Luo, G. A. N. G., MAZEN K. Qato, and THOMAS M. Guenthner. "Hydrolysis of the 2', 3'-allylic epoxides of allylbenzene, estragole, eugenol, and safrole by both microsomal and cytosolic epoxide hydrolases." Drug Metabolism and Disposition 20.3 (1992): 440-445.

9. Hasheminejad, G., and J. Caldwell. "Genotoxicity of the alkenylbenzenes α− and β-asarone, myristicin and elemicin as determined by the UDS assay in cultured rat hepatocytes." Food and chemical toxicology 32.3 (1994): 223-231."

CWatchman (talk) 16:47, 4 August 2019 (UTC)

I don't think any of this should be added except the sentence referenced by reference 3. That's a good source and clear enough. The rest is problematic because it's trying to lead readers into a potentially dangerous conclusion. The sentence referenced by 4, 5 & 6 is simply untrue (it's more complicated that that, some genotypes from this region are in fact more toxic, see ref. 1 for example). 7, 8 & 9 is nonsensical (it's a precursor to a genotoxin and will harm your liver when you ingest it, the point is people ingest it -fossil fuel doesn't cause global warming no matter how much you extract by the same argument) and not about the subject matter (the plant Acorus). Ref 2 is nonsense. Sentences referenced by 1 are not neutral, stretching material beyond citation and uninformed. Science behind toxicity of asarone (it occurs in a number of other unsafe traditional herbal medicines) is pretty solid, and not only based on that one study. The same bad argument could be made about why rhino horn is frowned upon in western medicine despite centuries of anecdotal efficiency: I could pick one study and say it's a bad study -the criticism doesn't mean rhino horn is any better at giving people a bigger penis or whatnot. 2 cents, Leo Breman (talk) 23:01, 12 March 2020 (UTC)