9 replies to this topic

[ajnast4r]

i have a friend who has pretty nasty food & airborn allergies, one of the supps im gonna put her on is quercetin... im just not sure what form.

i know perque and thorne use quercetin dihydrate which i believe is a water solubule form? every other company ive seen lists simply "quercetin"...

can anyone give me the run-down on this stuff?

[scottl]

It is poorly absorbed and I'm sure you know to use bromelain with it if not (thorne or...no idea who perque is).

[DukeNukem]

Here's the one I have been using:
http://www.pslchiro.....asp?name=SB332

[ajnast4r]

scott; no i didnt know about the bromeline, thanks. do you use it?

duke; ive heard great stuff about the thorne product... what exactly do you use it for, and is it working well for u?

what exactly is "chalcone"

[DukeNukem]

I can't remember which book I read about Thorne's version, but apparently it's a version of quercetin that doesn't have carcinogenic side effects. I read about this a year or two ago, and I do not remember the details.

I do not take it everyday -- maybe one pill every three days or so, and more often as a spot antihistamine, if needed.

[scottl]

I don't use it, but the one Duke uses is a good one, and I like Thorne.

[pycnogenol]

I've been using Source Naturals Activated Quercetin containing bromelain,
vitamin C, magnesium.

[syr_]

I enquired AOR about their Quercetin product and the different forms available.
Below is posted their answer.

BTW, who can point me to the possible carcinogenic effect of Quercetin? That interest me much more then absorbtion.

(headers removed for privacy)

> All forms of quercetin are poorly absorbed including dihydrate and
> chalcone. There is no clinical evidence that chalcone version are any
> superior over dihydrate. This apparent willingness of Nutraceutical
> companies ( which is no better than drug companies) to mislead people
> with word-game is one of many examples to sell their products
> any-way-you-can mentality.
>
> AOR is looking into improving the bioavailabilities of poorly absorbable
> nutraceuticals like quercetin, resveratrol and curcumin in the near
> future. But this wil mean more than includinh bromelain ( as an enzyme)
> to increase bioavailability.

[trh001]

Int J Mol Med. 2005 Aug;16(2):275-8. Related Articles, Links


Safety of quercetin for clinical application (Review).

Okamoto T.

Research Laboratories, Nippon Chemiphar Co., Ltd., 1-22 Hikokawato, Misato, Saitama 341-0005, Japan. t-okamoto@chemiphar.co.jp

Quercetin is the major flavonoid involved in vegetables and fruits. Quercetin is ingested from the daily diet, but in 1970s it was reported as mutagenic. Quercetin possesses a variety of pharmacological activities, and in order for further clinical application, it is important to evaluate its safety. In Ames test, quercetin is regarded as mutagenic. However, recent in vitro studies indicate that quercetin is protective against genotoxicants, and regarded as antimutagenic. Some in vivo studies including National Toxicology Program reported carcinogenic effect of quercetin in F344 rats. However, the method used in the study was unusual and the result was not reproduced. Most of the results of in vivo studies indicate that quercetin is not carcinogenic. Since 1969, the International Agency for Research on Cancer (IARC) has undertaken a program to evaluate the carcinogenic risk of chemicals. In 1999, IARC concluded that quercetin is not classified carcinogenic to humans. In the U.S. and Europe, supplements of quercetin is commercially available, and beneficial effects of quercetin supplements were reported in clinical trials. Overall, quercetin is genotoxic to salmonella, but its safety upon human application is approved.

Publication Types:
Review

PMID: 16012761 [PubMed - indexed for MEDLINE]

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Mutat Res. 2005 Jul 1;574(1-2):124-38. Epub 2005 Mar 31. Related Articles, Links


Flavonoids and alkenylbenzenes: mechanisms of mutagenic action and carcinogenic risk.

Rietjens IM, Boersma MG, van der Woude H, Jeurissen SM, Schutte ME, Alink GM.

Division of Toxicology, Wageningen University, Tuinlaan 5, 6703 HE, Wageningen, The Netherlands. ivonne.rietjens@wur.nl

The present review focuses on the mechanisms of mutagenic action and the carcinogenic risk of two categories of botanical ingredients, namely the flavonoids with quercetin as an important bioactive representative, and the alkenylbenzenes, namely safrole, methyleugenol and estragole. For quercetin a metabolic pathway for activation to DNA-reactive species may include enzymatic and/or chemical oxidation of quercetin to quercetin ortho-quinone, followed by isomerisation of the ortho-quinone to quinone methides. These quinone methides are suggested to be the active alkylating DNA-reactive intermediates. Recent results have demonstrated the formation of quercetin DNA adducts in exposed cells in vitro. The question that remains to be answered is why these genotoxic characteristics of quercetin are not reflected by carcinogenicity. This might in part be related to the transient nature of quercetin quinone methide adducts, and suggests that stability and/or repair of DNA adducts may need increased attention in in vitro genotoxicity studies. Thus, in vitro mutagenicity studies should put more emphasis on the transient nature of the DNA adducts responsible for the mutagenicity in vitro, since this transient nature of the formed DNA adducts may play an essential role in whether the genotoxicity observed in vitro will have any impact in vivo. For alkenylbenzenes the ultimate electrophilic and carcinogenic metabolites are the carbocations formed upon degradation of their 1'-sulfooxy derivatives, so bioactivation of the alkenylbenzenes to their ultimate carcinogens requires the involvement of cytochromes P450 and sulfotransferases. Identification of the cytochrome P450 isoenzymes involved in bioactivation of the alkenylbenzenes identifies the groups within the population possibly at increased risk, due to life style factors or genetic polymorphisms leading to rapid metaboliser phenotypes. Furthermore, toxicokinetics for conversion of the alkenylbenzenes to their carcinogenic metabolites and kinetics for repair of the DNA adducts formed provide other important aspects that have to be taken into account in the high to low dose risk extrapolation in the risk assessment on alkenylbenzenes. Altogether the present review stresses that species differences and mechanistic data have to be taken into account and that new mechanism- and toxicokinetic-based methods and models are required for cancer risk extrapolation from high dose experimental animal data to low dose carcinogenic risks for man.

Publication Types:
Review

PMID: 15914212 [PubMed - indexed for MEDLINE]

[syr_]

Thank you.