Plant PAs Pyrrolizidine alkaloid HoS 301

>>Pyrrolizidine alkaloids (PAs), sometimes referred to as necine bases, are a group of naturally occurring alkaloids based on the structure of pyrrolizidine. Pyrrolizidine alkaloids are produced by plants as a defense mechanism against insect herbivores. More than 660 PAs and PA N-oxides have been identified in over 6,000 plants, and about half of them exhibit hepatotoxicity.^[1] They are found frequently in plants in the Boraginaceae, Asteraceae, Orchidaceaeand Fabaceae families; less frequently in the Convolvulaceae and Poaceae, and in at least one species in the Lamiaceae. It has been estimated that 3% of the world’s flowering plants contain pyrrolizidine alkaloids.^[2] Honey can contain pyrrolizidine alkaloids,^[3][4] as can grains, milk, offal and eggs.^[5] To date (2011), there is no international regulation of PAs in food, unlike those for herbs and medicines.^[6][7]

Unsaturated pyrrolizidine alkaloids are hepatotoxic, that is, damaging to the liver.^[8][9] PAs also cause hepatic veno-occlusive disease and liver cancer.^[10] PAs are tumorigenic.^[11] Disease associated with consumption of PAs is known as pyrrolizidine alkaloidosis.

Of concern is the health risk associated with the use of medicinal herbs that contain PAs, notably borageleaf, comfrey and coltsfoot in the West, and some Chinese medicinal herbs.^[11]

Some ruminant animals, for example cattle, showed no change in liver enzyme activities or any clinical signs of poisoning when fed plants containing pyrrolizidine alkaloids.^[12] Yet Australian studies have demonstrated toxicity^[13] Sheep, goats and cattle are much more resistant and tolerate much higher PA dosages, thought to be due to thorough detoxification via PA-destroying rumen microbes.^[14] Males react more sensitively than females and fetuses and children.^[15]

PA is also used as a defense mechanism for some organisms such as Utetheisa ornatrix. Utetheisa ornatrixcaterpillars obtain these toxins from their food plants and use them as a deterrent for predators. PAs protect them from most of their natural enemies. The toxins stay in these organisms even when they metamorphose into adult moths, continuing to protect them throughout their adult stage.<sup>[16]<<

Ref.</sup> https://en.wikipedia.org/wiki/Pyrrolizidine_alkaloid?fbclid=IwAR3KvC4b33bkkPF0UIA6Xdo7EgpAoOmaAtE_TE_MLiwPtGmsAuHzvUrYIIg

Shawn Power If someone is pregnant or has pre-existing liver damage then maybe PAs would be a concern however I presumed anyone in such a condition would naturally think very carefully about anything that they may ingest and there would be no need for any kind of scare-story disclaimer. 
It seems PA fear is a smear campaign that has been kicking around since the 19th/20th century doctors and chemists chose to use chemical extracts of synthesised versions of active properties in plants rather than the traditional herbal remedies. 

The reputation of Comfrey is one of the worst affected by this fear which is sad because Symphytum officinale is a very effective healer for all kinds of ailments ranging from broken bones to bronchial disorders.

The hepatoxin (liver-damaging) content in Joe Pye (Gravel Root), if any, is minimal which my small pets have proven. From my experience it is also the most effective plant for kidney stones and urinary tract infections. IMO such ailments wouldn't require long term treatment/usage of PA containing herbs. 

In herbal medicine the application of discernment, adequate research and practical experience rather than hearsay are vital tools for making your own medicine.

*I did purposefully add that Yellow Dock ROOT is good to use with this herb as it seems to be the best plant for the liver.*

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Comfrey

Another recent development involves the use of comfrey (Symphytum officinale).  Comfrey has a long track record of safe and effective use as a medicine.  It has also been used safely as food for both humans and animals.  This aside, comfrey has been the subject of recent controversy.  One of the constituents of comfrey is a pyrrolizidine alkaloid that, if taken in large amounts, under certain conditions, may cause liver damage.  This is a very rare occurrence and need not concern the average comfrey user.  People who need to exercise caution with comfrey are those with chronic liver conditions (such as hepatitis, or cirrhosis) and those who are taking liver compromising medications.  Due to new government policy, no herbal product containing comfrey may be sold for internal use.  Because of this, some herbal recipes have been re-formulated to include other healing herbs to replace comfrey (bulk formulas with comfrey are still available for external use).  The author maintains that this wonderful healing herb should be available to all who would like to use it, and looks forward to the day that comfrey will be once again be accessible to everyone.  In this index, the formulas are listed both in their original form (with comfrey) and with the recent changes.

http://online.snh.cc/files/2100/HTML/hlc_appendix.htm?fbclid=IwAR32DhJvvIImsqA4e7U2UI6JXCeI-SARza6L32FLXDcCQOuAwitiSwRfCf8

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Pyrrolizidine Alkaloids
This page is an adaption of the U S FDA Bad Bug Book, permission given by the author Mark
Walderhaug, PhD.
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1. Name of Toxin: Pyrrolizidine Alkaloids

2. Name of Acute Disease: Pyrrolizidine Alkaloids Poisoning
Pyrrolizidine alkaloid intoxication is caused by consumption of plant
material containing these alkaloids. The plants may be consumed as
food, for medicinal purposes, or as contaminants of other agricultural
crops. Cereal crops and forage crops are sometimes contaminated with
pyrrolizidine-producing weeds, and the alkaloids find their way into
flour and other foods, including milk from cows feeding on these
plants. Many plants from the Boraginaceae, Compositae, and Leguminosae
families are contain well over 100 hepatotoxic pyrrolizidine alkaloids.

3. Normal Course of Disease
Most cases of pyrrolizidine alkaloid toxicity result in moderate to
severe liver damage. Gastrointestinal symptoms are usually the first
sign of intoxication, and consist predominantly of abdominal pain with
vomiting and the development of ascites. Death may ensue from 2 weeks
to more than 2 years after poisoning, but patients may recover almost
completely if the alkaloid intake is discontinued and the liver damage
has not been too severe.

4. Diagnosis of Human Illness:
Evidence of toxicity may not become apparent until sometime after the
alkaloid is ingested. The acute illness has been compared to the
Budd-Chiari syndrome (thrombosis of hepatic veins, leading to liver
enlargement, portal hypertension, and ascites). Early clinical signs
include nausea and acute upper gastric pain, acute abdominal distension
with prominent dilated veins on the abdominal wall, fever, and
biochemical evidence of liver disfunction. Fever and jaundice may be
present. In some cases the lungs are affected; pulmonary edema and
pleural effusions have been observed. Lung damage may be prominent and
has been fatal. Chronic illness from ingestion of small amounts of the
alkaloids over a long period proceeds through fibrosis of the liver to
cirrhosis, which is indistinguishable from cirrhosis of other etiology.

5. Associated Foods:
The plants most frequently implicated in pyrrolizidine poisoning are
members of the Boraginacea, Asteraceae/Compositae, and
Fabaceae/Leguminosae families. Consumption of the alkaloid-containing
plants as food, contaminants of food, or as medicinals has occurred.

6. Relative Frequency of Disease:
Reports of acute poisoning in the United States among humans are
relatively rare. Most result from the use of medicinal preparations as
home remedies. However, intoxications of range animals sometimes occur
in areas under drought stress, where plants containing alkaloids are
common. Milk from dairy animals can become contaminated with the
alkaloids, and alkaloids have been found in the honey collected by bees
foraging on toxic plants. Mass human poisonings have occurred in other
countries when cereal crops used to prepare food were contaminated with
seeds containing pyrrolizidine alkaloid.

7. Target Population:
All humans are believed to be susceptible to the hepatotoxic
pyrrolizidine alkaloids. Home remedies and consumption of herbal teas
in large quantities can be a risk factor and are the most likely causes
of alkaloid poisonings in the United States.

8. Analysis in Foods:
The pyrrolizidine alkaloids can be isolated from the suspect commodity
by any of several standard alkaloid extraction procedures. The toxins
are identified by thin layer chromatography. The pyrrolizidine ring is
first oxidized to a pyrrole followed by spraying with Ehrlich reagent,
which gives a characteristic purple spot. Gas chromatography and mass
spectral methods also are available for identifying the alkaloids.

9. History of Recent Outbreaks:
There have been relatively few reports of human poisonings in the
United States. Worldwide, however, a number of cases have been
documented. Most of the intoxications in the USA involved the
consumption of herbal preparations either as a tea or as a medicine.
The first patient diagnosed in the USA was a female who had used a
medicinal tea for 6 months while in Ecuador. She developed typical
hepatic veno-occlusive disease, with voluminous ascites, centrilobular
congestion of the liver, and increased portal vein pressure.
Interestingly, the patient completely recovered within one year after
ceasing to consume the tea. Another herbal tea poisoning occurred when
Senecio longilobus was mistaken for a harmless plant (called "gordolobo
yerba" by Mexican Americans) and used to make herbal cough medicine.
Two infants were given this medication for several days. The
2-month-old boy was ill for 2 weeks before being admitted to the
hospital and died 6 days later. His condition was first diagnosed as
Reye's syndrome, but was changed when jaundice, ascites, and liver
necrosis were observed. The second child, a 6-month-old female, had
acute hepatocellular disease, ascites, portal hypertension, and a right
pleural effusion. The patient improved with treatment; however, after 6
months, a liver biopsy revealed extensive hepatic fibrosis, progressing
to cirrhosis over 6 months. Another case of hepatic veno-occlusive
disease was recently described in a 47-year-old nonalcoholic woman who
had consumed large quantities of comfrey (Symphytum species) tea and
pills for more than one year. Liver damage was still present 20 months
after the comfrey consumption ceased

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