Homestead mailing list

[Juliana Dutra <kila01 AT yahoo.com>]

Bill watch out for Comfrey as livestock feed. It has
been considered carcinogenic and toxic even for
humans:

Comfrey (Symphytum officinale or Symphytum x
uplandicum), has a long history of medicinal use. Yet
Comfrey is a herb surrounded by controversy. To some
it is virtually a panacea, to others it is a dangerous
and poisonous weed. .. in the scientific literature
are studies which claim to demonstrate harmful effects
and this has led to the use of Comfrey being
restricted by its classification as a poison.
Australia was the first country to do this but others
have followed. The reason is that Comfrey contains
pyrrolizidine alkaloids — these are toxic substances.

The pyrrxolizidine alkaloids (PA’s) found in Comfrey
are not responsible for its therapeutic effects.
Alkaloids are plant substances which contain nitrogen,
and can have high phamacological activities —
morphine, quinine and nicotine are examples. Comfrey
leaves contain about 0.06% alkaloids, and roots about
0.2 to 0.4%. Pyrrolizidine alkaloids ..form a highly
diverse group of chemicals and are widespread in the
plant kingdom. Some, but not all, are quite toxic,
particularly to the liver. There are many
well-documented cases of livestock poisonings. Human
poisoning occurs largely in the third world from
contaminated food or herbal teas and a liver disorder
known as veno-occlusive disease often follows.

http://forums2.gardenweb.com/forums/load/herbal/msg080635098259.html

TOXIC PLANTS II

PYRROLIZIDINE ALKALOIDS

The pyrrolizidine alkaloids (PA's) are a group of
naturally occurring chemicals synthesized by many
plant species. The ingestion of PA's in plant material
has produced widespread toxicity problems in both
humans and food producing animals. The PA's occur in
plants that are eaten by livestock and occasionally
used by humans as herbal remedies. Pyrrolizidine
alkaloids usually produce a chronic delayed toxicity,
thus the signs and symptoms of PA toxicity are not
seen until a long time after ingestion has occurred.
Because of this long delay between ingestion and the
appearance of toxic symptoms, in many instances it is
very difficult to diagnose PA intoxication. Currently
there is no known remedy to counteract the toxic
effects of the PA, thus preventing intoxication is the
best method to control the problem.

Pyrrolizidine alkaloid poisoning has been reported in
all parts of the world. Poisoning of livestock was
first reported in South Africa in the early 1900's. In
California, PA poisoning of livestock may be the most
important plant related veterinary problem at this
time. Pyrrolizidine alkaloid poisoning is not limited
to veterinary species however. Recent outbreaks in
1976 of human poisoning in Afghanistan and in India
serve as dramatic examples. In both instances food
grain had become contaminated with weed seeds that
contained PA's. In India 67 cases were reported with a
mortality rate of 42%. In Afghanistan more than 1600
cases were reported.

In California the most prominent plants involved are
fiddleneck, tansy ragwort and common groundsel.
Pyrrolizidine alkaloid content of these plants ranges
from less than 0.5% up to 1.2% dry weight. Comfrey,
which is used as an animal feed and human herbal
remedy, also contains small quantities of PA's. Plant
parts ranked in decreasing concentration of PA's are:
flowers and seeds > leaves > stems > roots. The plants
contain PA's at all stages of growth. The PA's are
resistant to heat, and also maintain their toxicity in
dried plant material and hay.

The PA's toxic action is principally exerted on the
liver, and depending on the animal species, the kidney
and lungs may also be affected but to a lesser extent
than the liver. Pyrrolizidine alkaloids are activated
by liver metabolism to toxic pyrrole metabolites which
have been shown to be carcinogenic, mutagenic, and
embryotoxic. Most of the toxic effects of the PA's can
be traced to their destructive effect on liver cells,
and thus the clinical signs and symptoms of PA
intoxication are those of progressive liver failure. 

http://extoxnet.orst.edu/newsletters/n14_81.htm