Je me sens un peu comme un "climato-sceptique" à te répondre Sebcop, mais je trouve que c'est... Insuffisant pour conclure à la toxicité per se de la consoude. Si tu me trouves biaisé, merci de dire où, parce que je m'en voudrais :x
http://herbcraft.org/hoffmanncomfrey.htmlAlors, je ne sais pas si le mec est fiable mais :
1) Il s'exprime super bien :O
2) Je ne vois pas d'appels au gourou-isme, plus à un réserve scientifique, et il source de nombreux cas & historique.
3) J'ai ses même réserves bien que j'aurais pas eu la capacité de le dire aussi bien.
...Mais même lui voit la consoude sous l'aspect phyto, pas alimentaire, je pense que je peux rayer ça de mes recettes définitivement, par mesure de précaution x)
(voilà un extrait, mais je vous pousse à aller lire le complet sur le site)
The very few specific reports of human toxicity related to comfrey all come from the period between 1980 and 1990, when a number of cases of veno-occiusive disease were reported.[9] There is no question about the diagnoses. However, it is important to note that in these cases, the connection with comfrey was not considered in the context of other contributing factors. For example, concomitant illness, the use of prescription or over- the-counter hepatotoxic drugs (like acetaminophen, for example), and impaired nutritional status clearly increase the likelihood that PA-containing herbs will cause hepatotoxicity.
With minimal epidemiological data, what insights can be garnered from the laboratory research into toxicity? As with many statements about herbal toxicity, the evidence proffered comes primarily from rodent studies that utilized high levels of purified PAs. No systematic toxicity testing or clinical trials of comfrey have been performed. Although PA poisoning in humans does occur, it is most commonly a consequence of consuming plants other than comfrey.[10]
Such reliance on animal experimentation data and toxicity reports about other plants gives us little insight into the risks and therapeutic benefits of the human use of comfrey. Rode enumerates four limitations of the published research.
Not all PAs have similar toxicity. This group of alkaloids do not pose a uniform risk. Based on structure-toxicity studies, it can be concluded that the PAs in comfrey (such as symphytine, a retronecine monoester) are less toxic than those present in the plants Senecio, Crotolaria, and Heliotropium. These have actually caused human toxicity (for example, senecionine, a macrocyclic retronecine diester).[11]
Not all animals are susceptible to PA toxicity. As with most substances, responses to PAs among different animals vary greatly. Pigs, chickens, and rats are highly sensitive to poisoning by Senecio, whereas mice and sheep are resistant. However, and more significant, the response of one species to Senecio might not reflect its susceptibility to other PAs.[12] In addition, the route of administration can dramatically affect the toxic response. For example, rabbits are relatively resistant to chronic feeding of Senecio, but are killed by a single injection of the purified alkaloids.[13] Although theoretically sensitivity to PAs, pigs readily accept comfrey as a food and show no adverse effects, even when comfrey represents 40% of their diet. Rats, however, appear to be very sensitive to the same PAs. When eating large amounts of comfrey or injected with comfrey PAs, rats develop the hepatic lesions indicative of PA poisoning.[14] This calls into question the validity of using rodent animal models as indicators of human response to PAs.
Comfrey species vary in PA content. Between 85% and 97% of the PAs in Symphytum officinale, the corn- frey commonly grown in American gardens, are built around the less toxic retronecine monoester. However, Russian comfrey (Symphytum x uplandicum), contains higher levels of the diester, which, is known to have a greater toxicity.[15] Bearing in mind the differences in toxicity among various PAs, and the variable distribution of PAs in different comfrey species and varieties, we might conclude that extrapolations of research results from one species to another may be unreliable.
Effects of isolated PAs might not be representative of whole plant use. As with many herbs, it is problematic to assume that the pharmacology of a specific constituent can be used to predict the pharmacology of the whole plant. Veterinary studies have shown that the formation of toxic PA metabolites is reduced by concurrent administration of the sulfur-containing amino acid methionine or cysteine.[16] Similarly, protein-deficient dietsenhance the toxicity of PAs.[17] Most toxicity studies used purified PAs, ignoring the potential protective effects of co-occurring nutrients present in the whole plant. This suggests that studies using purified PAs probably overstate the health risks associated with comfrey extracts or the whole plant.
...Il semble que la poule soit pas l'animal le plus compatible avec cet élement toxique qu'est le PA, mais cette substance n'a pas la même qualité selon le type de plante... Pour moi... C'est pas un choix évident.
Je n'aurai aucun mal à donner 10% de consoude dans la diète des poules, mais c'est propre à chacun d'évaluer le bénéfice gain/perte et son esprit critique. Je connais quelques jardiniers qui ajoutent de la consoude aux repas de leurs poules et à l'époque je n'avais jamais rien entendu sur leurs toxicologie, et les poules m'ont toujours semblé littéralement sauter dessus. Mais encore une fois, c'est des arguments faibles, le risque est démontré chez le rat et il y a des composés toxiques qui, purs, sont dangereux chez l'homme si injectés/ingérés, et il y a des cas cliniques autoure de la consommation de la consoude (seulement il y aurait pu avoir d'autres facteur qui n'ont pas été recherchés à l'époque).
Après j'aurais une tolérance 0 sur les enfants avec des doutes gros comme ça, bien entendu x)