Subject: Re: comfrey

From: [email-masked] (Camilla Cracchiolo)
Date: 23 Dec 1994 09:56:17 GMT

Hilda Marshall ([email-masked]) wrote:

: Well, comfrey HAS been linked to liver damage in rats - in continuous,
: force-fed, lab-rat doses.

Comfrey has been linked to rather more than just liver damage in rats.  
There are a number of deaths from severe liver damage in humans as well.
Attached is a factsheet on comfrey and other liver toxic herbs.

: The fact that somebody even bothered to DO a study on a folk medicine
: like comfrey, and the dire reports of its fairly predictable results,
: strike me as evidence that this particular folk medicne might
: constitute a threat to medbiz profits if people weren't frightened of
: it.  But then I'm a very opinionated person.  ;-)

Ah yes, when you don't know the facts, blame the vast MD conspiracy.  Any 
adverse effects of herbs just have to be lies.  Right.  The studies were 
done because of the reports of toxicity in humans, not the other way around.

                        HOW MUCH COMFREY IS SAFE?
 
                   Copyright 1994 by Jay D Mann
             Feel free to quote this but with acknowledgment

          There has been much discussion on this newsgroup about whether
          comfrey and related plants are or are not safe. At the risk of
          committing a breach of good net manners, I'm going to
          introduce some numerical data into the discussion. Apologies
          for the length.  Please try to read this if you plan on using
          or recommending comfrey, coltsfoot, or gordolobo; it might
          save a life.
 
          My figures are all presented in metrics, as gm, kg, etc.
          Apologies if you prefer ounces and pounds; they're too
          complicated for me.  For a quick seat-of-the-pants estimate,
          an adult man weighs  70-80 kg.  One kg is about two pounds;
          one pound is about half a kilogram. One teaspoon of water
          weighs about 5  gm.  One milligram (mg) is one-thousandth of a
          gram.  One microgram (ug) is one-thousandth of a milligram, or
          one-millionth of a gram.  1% is 1 part in a hundred, or 10 mg
          in a gram.  0.1% = 1 mg per gram, and 0.01% = 0.1 mg per gram
          which is also 100 ug per gram.
 
          The abbreviation PA is used to significy pyrrolizidine
          alkaloids.   The overall structure of these is:
                R1
                O  R2     where R1 and R2 are all kinds of chains
               /\ /\\
              /  |  \\
              \  N  /
               \/ \/

          There are three main questions
          A) How much alkaloid is present in different plants?
          B) What is this "VOD" liver disease?
          C) How much alkaloid can people tolerate before developing
          VOD?

 A. THE CONTENT OF PYRROLIZIDINE ALKALOIDS
 =========================================
 
 1. COLTSFOOT (Tussilago farafara) contains  0.015% senkirkine
 (a PA) in flowers (Tyler 1993 pg 96).  The same alkaloid is
 also present in leaves, but I don't have quantitative data.
 
 A herbal tea purchased from a Swiss pharmacy, sold as an
 expectorant, contained 0.6 mg senecionine (PA) per kg dry wt,
 that is, 0.6 ug per gm in a mix that was 9% coltsfoot by
 weight. (Roulet et al 1988).  Coltsfoot was the source of PA
 in the tea blend. Thus the coltsfoot leaves would have had
 only 100/9 * 0.6 =~ 7 ug per gr.  (This was enough to kill the
 infant with daily usage by the mother.)
 
 2. COMFREY (Symphytum sp)
    Three different plants are marketed as "comfrey".
    Symphytum officinale, is smooth comfrey.
    S. asperum is prickly comfrey.
    S. x uplandicum (a hybrid) is Russian comfrey.
 
 Smooth comfrey has PA's called 7-acetylintermedine and
 7-acetyllycopsamine, which may be slightly less toxic.
 Russian and prickly comfrey have echimidine, which is quite
 dangerous, as well as symphytine and 6 other alkaloids (Tyler
 1993). There could be some doubt as to the relative toxicities
 because they were probably obtained with rat or mouse tests.
 All PA's should be regarded as liver-damaging in humans.
 
 Just because a product is marketed as "comfrey" or even as
 "Symphytum officinalis" doesn't mean that it is genuine smooth
 comfrey.  A study in Canada showed that 6 out of 13 commercial
 "comfreys" contained prickly or Russian comfrey (Tyler, pg
 96).  (In case you feel that you'd rather collect your own
 comfrey, note that there have been several deaths from people
 who mistook foxglove (Digitalis) or Aconitum for comfrey.  How
 good is your botany?)
 
 Comfrey leaves have from 0.003% to 0.115% alkaloids; the roots
 0.14% to 0.4% alkaloids.  There are about 7 times more
 N-oxides than free alkaloids, and the N-oxides are nearly as
 toxic as the free bases (Ridker et al 1984).  Young leaves of
 Russian comfrey had 0.15% PA's (dry wt) compared to 0.01% in
 mature leaves, and 0.05% in a bulk collection of
 intermediate-sized leaves (Culvenor et al, 1980).  Earlier
 reports showed a range of 0.013% to 0.053% PA in dried mature
 leaves, and 0.9% in unspecified leaves. Culvenor et al did not
 measure the N-oxides which could well have been 5 to 7-times
 higher than the free alkaloids.
 
 For the sake of ballpark calculations, assume 0.1% alkaloid
 and 0.5% N-oxide.  One gram of dried comfrey leaves would then
 contain 0.6% total PA, or 6 mg of liver toxins.
 
 More details are given below on what amounts would be damaging
 to humans.
 
 3. SENECIO (ragwort, groundsel) is well-known as a dangerous
 plant for grazing animals in Australia and some parts of the
 Southern USA.  In areas with many other plants, grazing
 animals avoid senecio, but hungry animals will eat it. Horses,
 cattle and sheep are susceptible.  Senecio causes cirrhosis of
 the liver and hepatitis in South American and U S horses
 (Kraybill 1974). "Senecio disease" in humans was described as
 long ago as 1920, in South Africa (Bach et al 1989).  A toxic
 gorodolobo yerba tea in Arizona, is sometimes made from
 Senecio longilobus that contained 3 mg PA and 10 mg of equally
 toxic N-oxide derivatives per g dry wt.  The final tea, as
 prepared, contained from 70 to 147 mg total toxins per dose
 (Stillman et al 1977).
 
 4. HELIOTROPIUM contains two PA's called heliotrine  and
 monocrotaline, although Culvenor says they are not much more
 toxic than other PA's. Heliotropium lasiocarpum, which killed
 one young chinese woman in Hong Kong and damaged three others,
 contained 1.6% PA, that is, 16 mg per gm dry wt (Culvenor et
 al 1986). This particular species had caused an epidemic of
 liver disease in Uzbekistan when grain had been contaminated
 with Heliotrope seed.
 
 5. CROTOLORIA and other plants.  I don't have detailed
 information; hopefully no one would think of using any of
 these as herbal medication.  In Jamaica the young victims of a
 crotolaria "bush-tea" are said to have "swell belly". In South
 Africa, the victims of Crotolaria fulva die of "white back".
 Children and infants are almost invariably the main victims of
 Jamaican bush teas made from Crotolaria fulva (McLean, 1974).

 B. What is VOD (Veno-occlusive disease)?
 ========================================
 
 VOD is characterised by a blockage of the smallest passages
 (venules) in the liver. Cirrhosis is a general term "applied
 to diffuse liver damage of multiple aetiology" (causation).
 VOD is, thus, a form of cirrhosis but has a unique set of
 diagnostic attributes. The most common cause of VOD is
 poisoning from PA's. In addition, cancer chemotherapy and
 radiation therapy can cause VOD.  An exceedingly uncommon
 cause is use of oral contraceptives.  In non-cancer patients,
 a diagnosis of VOD automatically leads to a search for dietary
 factors.
 
 The symptoms of VOD are a greatly swollen belly (ascites)
 caused by accumulation of ascitic fluid.  In one case, a
 49-year-old woman lost 16 lb when the fluid was drained by an
 operation (Ridker et al 1984).  A Chinese womea  in Hong Kongwho
 died from PA had 3 liters of ascitic fluid at autopsy (Kumana
 et al 1985). A 38-day-old infant had 500 ml of yellow ascitic
 fluid in his abdomen (Roulet et al 1988).
 
 Typical medical findings (McLean 1974) are of a child with
 abdominal pain, or discomfort and distension, large hard liver
 and a large spleen, severe ascites (liquid in the belly).
 Examination of the liver in VOD shows that small vessels have
 been blocked by growth of fibrous tissue, that is, something
 like scar tissue. The distribution of this blockage is
 characteristic of VOD compared to other liver diseases. There
 can be portal hypertension (high blood pressure in the blood
 vessels feeding the liver) because flow of blood through the
 liver has been blocked.

 C. How much PA does it take to make a human being sick?
 =======================================================
 
 First off, we have to say that most of the laboratory studies
 on PA's are worthless because they used rats or mice.  PA's do
 not cause VOD in rodents at the same low concentrations in
 which they affect humans and cattle (Cornelius and Himes,
 1974). Rodents can get cancer or pre-cancerous conditions from
 PA's but no case of human cancer from PA has been shown. There
 has already been a lot of discussion of the fallacy of using
 high-dose tests on rodents for estimating human cancer risks,
 and I won't add to it.  Suffice it to say that the reasons for
 worrying about PA's have nothing to do with cancer. The
 article by Cornelius and Himes was buried in an obscure
 symposium volume, and I've never seen it cited elsewhere.
 (Remember, you read about it here first.)
 
 Cows, man, and macaca monkeys can get VOD from PA's.  The
 symptoms in cattle and sheep are different from humans,
 because the grazing animals show liver cell enlargement
 (megalocytosis) in additon to VOD (McLean 1974). There is a
 suggestion that male animals might more susceptible than
 females (Huxtable 1990) but those studies involve rats, which
 as said earlier are not the correct animal models.
 
 PA's are relatively harmless to animal tissue, until an effort
 is made to inactivate them by microsomal oxidases. Because
 these enzymes are in the liver, the main organ that removes
 dietary toxins, damage is greatest in the liver.  The
 attempted detoxification results in formation of highly
 reactive molecules that bind to the liver cells, causing their
 death and also damage to liver tubules downstream (McLean
 1974). This seems to be contradictory to the oft-stated theory
 that our bodies are expert in detoxifying natural compounds;
 the PA's have been around for a long while in all parts of the
 world, yet our bodies handle them inappropriately.

 D. Examination of individual PA-containing plants
 =================================================
 It seems generally accepted that children and infants are more
 likely to be victims of PA than adults.  Their livers are more
 susceptible to damage.
 
 1. COLTSFOOT:
 The only known death from coltsfoot occurred in a newborn
 Swiss infant (Roulet et al 1988).  The mother had bought a
 herbal expectorant from a local pharmacy, and had used it
 throughout her pregnancy.  This tea had 9% coltsfoot leaves in
 it, with a concentration of only 0.6 ug PA(senecionine) per gm
 dry wt. She apparently drank one cup of this tea every day.
 The infant was born with liver damage and died at 38 days.
 There was apparently one other case of VOD reported "after
 consuming herbal teas containing traces of PA for 2 years"
 (McGee et al, 1976, J Clin Pathol 29: 788-94, not seen by me).
 The mother's liver was entirely normal; it was the foetal
 liver that was damaged.

 2. COMFREY:
 There have been several recorded illnesses or deaths from
 comfrey. The amounts of PA's involved were summarised by
 Culvenor (1992) as follows:
 
 USA, 49 yr old woman, 14 ug/kg/day => 85 mg total.  VOD only
 NZ, 23 yr old man,   750 ug/kg/day => 200-1000 mg.  Death
 USA, 50 yr woman,     70 ug/kg/day => 360 mg        Edema,kidney disease
 
 The first case cited was a 49-year-old woman who had been
 taking 1 quart a day of "MU-16 herbal beverage with ginseng"
 for six months (Ridker et al 1984). Analysis showed that the
 tea contained 24-80 nmole of the pyrrolizidine alkaloids per
 gram dry weight.  Over six months, she consumed 480 gram of
 dried tea, equal to 0.5 to 1.5 ug/kg/day.  If her body weight
 was  50 kg, six months at this rate calculates. out as 0.5 to
 1.5 mg PA).
 
 This same woman had also taken two capsules of comfrey-pepsin
 with each meal in the last four months.  These pills had
 provided 85 mg of PA total, at a rate of 14 ug/kg/day. Note
 that the pills, perhaps made with comfrey root rather than
 leaves, provided most of the PA.  Her symptoms were
 progressive swelling of abdomen and extremities over the
 previous four months.  The ascites liquid in her abdomen
 weighed about 15 lb.
 
 Another woman, this time a 47-year-old social worker,
 illustrates how long a delay can elapse between taking a
 PA-containing plant and the onset of VOD (Bach et al 1989).
 The woman had been recommended comfrey tea by a homeopathic
 doctor. In 1978, "she began consuming as many as 10 cups of
 tea per day in addition to taking comfrey pills by the
 handful, which continued for more than one year."  Four years
 later, in 1982, a medical exam disclosed abnormal blood enzyme
 levels indicative of liver disorder. Still later, in December
 1986, she was hospitalised for massive ascites, hyponatremia
 (drop in blood sodium levels) and confusion.  An operation to
 drain the liquid was successful.  The total amount of PA's
 consumed was not known.
 
 This case supports the statement of Croom (1983) that:
 "Although folk practitioners and their patients recognize
 acute signs of poisoning, it is improbable that they can
 detect toxicity due to long term or chronic exposure to drug
 plants.  Without the diagnostic tools and techniques of
 Western medicine . . ., the practitioner is in a poor position
 to find untoward effects such as suppression of the immune
 system, the induction or stimulation of cancer, and damage to
 internal organs such as the liver and kidneys."  [The full
 article shows that Croom is an enthusiast for further but
 better documented studies of herbal remedies.]
 
 An elderly woman, hospitalised with VOD, had been taking 6
 comfrey-pepsin pills a day.  The total amount of PA consumed
 was unknown, but the latest batch of pills contained 988 mg
 PA/kg, that is, about 0.1% PA (Huxtable 1990).

 3. SENECIO:
 
 "Senecio disease" was first described in South Africa in 1920.
 Senecio (Ragwort) is a hazard to grazing animals on the range.
 In the U.S., the main risk to people comes from gordolobo
 yerba tea, commonly used by Mexican-Americans.  This tea may
 be made either from harmless Gnaphalium macounii, or the
 dangerous Senecio longilobus (Huxtable 1990).  In one case, a
 six-month-old baby girl had been given gordolobo yerba tea.
 The plant used for the tea contained 3 mg of PA and 10.5 mg of
 equally toxic N-oxide derivatives per gram.  As prepared by
 the girl's mother, the tea contained from 70 to 147 mg of
 combined alkaloid + N-oxide.  This little girl survived
 (Stillman et al 1977).  A second apparently independent case,
 of a two-month-old boy, proved fatal after six days in
 hospital.  The little boy had been given Senecio longilobus
 (gordolobo yerba) tea as a cough medicine for only 5 days.
 The authors suggested that PA poisoning may be an "iceberg
 disease" in the US, often being misdiagnosed as "atypical
 hepatitis".

 4. HELIOTROPIUM:
 This is a highly dangerous plant, which of course has never
 stopped some people from including it in herbal remedies.
 
 Culvenor (1992) says "Heliotrine and monocrotaline are of
 higher acute toxicity than comfrey alkaloid but not greatly
 so.  The data support the conclusion that intakes above 0.5
 mg/kg/day [500 ug/kg/day] induce serious, possibly fatal,
 effects if sustained for 2-7 weeks; intakes below 100
 ug/kg/day may still induce liver damage over a period of
 months.  The lowest figure, 14 ug/kg/day, is an intake which
 might lead to disease in some people."
 
 There were four young Chinese women who took an Indian tea as
 a purported psoriasis remedy (Kumana et al, 1985).  This
 episode has some of the best quantitative data in the field,
 although the story is a bit complicated. I'll use the authors'
 original numbering system.  Patient 3 took the mixture for
 only 21 days, because she developed a skin rash.  Later, lab
 tests showed that she had suffered some liver damage but with
 no obvious symptoms. (She still might show a delayed illness
 years from now.)  She consumed 630 mg of PA (base plus
 N-oxide) over 21 days.
 
 Patient 1 took the tea for 45 days; patient 3 for 19 days.
 Both stopped when disturbing side-effects occurred.  Although
 they were no longer using the tea, patient 1 had to be
 admitted to hospital 16 days later, patient 3 after 49 days.
 In other words, 45+16=61 days, and 19+49=68 days from first
 day of taking the tea until the victims were hospitalised.
 Both of these women survived.  Patient 1 had consumed 1350 mg
 PA over 45 days; patient 3 had taken 570 mg over 19 days.
 Clearly there are individual differences in susceptibility.
 
 Patient 2 developed symptoms 30 days after starting the tea,
 but she kept on using the herbal tea for a further 16 days (46
 days total), against medical advice.   She did not go to
 hospital until day 66, and she eventually died.  Necropsy
 (autopsy) showed liver cell atrophy and necrosis (death),
 three liters of ascites fluid, a single oozing oesophageal
 varix (enlarged and tortuous vein), and bloody mucus in the
 stomach.  This victim had consumed 900 mg PA over 30 days,
 less than that taken by Patient 1, who had survived.
 
 At the time of the original publication, the plant responsible
 was not known. Then Culvenor et al (1986) manually separated
 bits of leaves and seeds from the mixture. The mixed leaves
 contained 0.47% PA, all from Heliotropium lasiocarpum Fisch
 and Mey (sorry, that's the botanical identification).  They
 raised plants from the heliotrope seeds in the mixture, and
 found that the leaves contained 1.6% PA (dry wt).  This
 particular species was known to have caused an epidemic of
 liver disease in Uzbekistan when grain was contaminated by
 heliotrope seed.

 5. CROTOLARIA and OTHERS:
 There are reports of "numerous" children being killed by
 Jamaican bush teas.  McLean (1974) writes of West Indian
 children with VOD as though it is a common finding, but gives
 no indication of how many.  She says that such children have
 usually "been treated at home for some childhood ailment with
 'bush tea', and if you ask his parents to bring you samples of
 the plants from which his tea was made, you can often find
 Crotolaria fulva among them."  This suggests that a single
 course of "treatment" is enough to trigger liver damage in the
 children.

 6. MISLABELLING:
 It's all very well being careful about the ingredients of any
 medicine that you consume, but what if the labels are false?
 I've already mentioned that about half the so-called "comfrey"
 samples in Canada were Russian or prickly comfrey rather than
 smooth comfrey.  In England, what was supposed to be mate' tea
 (Ilex paraguaensis) killed someone with VOD.  The particular
 PA-containing plant that had been substituted was not
 identified (Huxtable 1990).  There are other instances of
 mislabelling in the herbal area, but they don't involve PA's,
 to the best of my recollection.

 D. CONCLUSIONS:
 ===============
 
 Coltsfoot seems to be relatively safe.  The one confirmed
 death was from exposure of a foetus during the whole of
 pregnancy, although the amount seems to have been only from
 one cup a day.
 
 Comfrey has caused VOD with as little as 85 mg of accumulated
 PA dose.   There seems no documented case of infant mortality,
 which is not the same as saying there has been no such case.
 Onset of VOD could be years after the comfrey is consumed.
 Comfrey-pepsin pills and capsules have, quite appropriately,
 been taken off the market; they were the biggest source of
 PA's from comfrey.  Comfrey root is nearly ten times more
 risky than the leaves.  Old leaves are probably safer than
 young ones.
 
 Senecio (ragwort) caused death of a young child with perhaps
 as little as 70 mg total alkaloid. Most deaths of children
 from Senecio occur in the Third World, and don't get
 documented in formal medical journals.  The same applies to
 Crotolaria.
 
 Heiotropium caused VOD with total intakes in the range of
 630-1350 mg total alkaloids including N-Oxides). Although the
 heliotropium alkaloids are supposed to be more toxic than PA's
 from other plants, these results suggest that larger
 quantities are needed, although perhaps liver damage was
 faster. Almost certainly the comparative toxicity tests were
 run with rats or mice, which are inappropriate.    Perhaps the
 simple reason why heliotropium leaves and seeds are so
 dangerous is that they contain such high concentrations of
 alkaloids, over 1%.
 
 All PA plants: The N-oxides should be included in the total
 PA's as far as hazard is concerned. This means that analyses
 reported only in terms of pure PA free base should be
 multiplied by at least 5 to estimate human risk.
 
 I don't want to make medical recommendations, but clearly any
 use of PA-containing herbal medicines by pregnant women is
 out.  (Pregnant women probably should not take any drugs at
 all, and that includes both nicotine and alcohol.) Children,
 especially young ones, should not be given PA-containing
 medicines. Whether adults want to use coltsfoot and comfrey
 occasionally for specific short-term problems, is up to them.
 Personally I use a coltsfoot tea for coughs.  Note that the
 German health authorities allow sale of low-PA comfrey, so
 long as it is not used for more than six weeks per year
 (Tyler, pg 96). Also note that in Germany the PA content has
 to be analysed before material can be sold; U.S. and N.Z.
 consumers don't have that protection.

 E. REFERENCES
 =============
 
 Bach, N, S Nz Thung, and F Schaffner. 1989.  Comfrey herb
 tea-induced hepatic veno-occlusive disease.  The Amer J
 Medicine 87:97-99.
 
 Cornelius, C E and J A Himes. 1974. Species differences in
 hepatotoxicity. Intl Symposium on Hepatotoxicity (Ed: M
 Eliakim, J Eshchar, and H J Zimmerman). Academic Press (NY).
 pp 132-137.
 
 Croom, E M.  1983. Documenting and evaluating herbal remedies.
 Economic Botany 37: 13-27.
 
 Culvenor, C C J, J A Edgar, L W Smith, C R Kumana and J H Lin.
 1986. Heliotropium lasiocarpum fisch and Mey identified as
 cause of veno-occlusive disease due to a herbal tea.  Lancet
 April 26, 1986, pg 978 only.
 
 Culvenor, C C J. 1992.  Toxic plant consituents in foods.
 Food Australia 44(2): 73-75.
 
 Culvenor, C C J, J A Edgar, J L Frahn, and L W Smith. 1980.
 The alkaloids of Symphytum x uplandium (Russian comfrey).
 Aust J Chem 33: 1105-1113.
 
 Huxtable, R J.  1990.  The harmful potential of herbal and
 other plant products.  Drug Safety 5 (suppl 1):126-136.
 
 Kraybill, H F. 1974. The toxicology and epidemiology of
 natural hepatotoxin exposure.  Intl Symp on Hepatotoxicity. pp
 122-230.
 
 Kumana, C R, M Ng, H Ju Lin, W Ko, Pui-Chee Wo, and D Todd.
 1985. Herbal tea induced hepatic veno-occlusive disease:
 quantification of toxic alkaloid exposure in adults.  Gut 26:
 101-104.
 
 McLean, E K. 1974.  Senecio and other plants as liver poisons.
 Intl Symp on Hepatotoxicity, pg 142-146.
 
 Ridker, P M, S Ohkuma, W V McDermott,s C Trey, and R J
 Huxtable.  1984. Hepatic venocclusive disease associated with
 the consumption of pyrrolizidine-containing dietary
 supplements.  Gastroenterology 1985:88:1050-4.
 
 Roulet, M, L Ricardo, L Rivier, and A Calame. 1988.  Hepatic
 veno-occlusive disease in newborn infant of a woman drinking
 herbal tea. Journal of Pediatrics 112(3): 433-436.
 
 Stillman, A E, R Huxtable, P Consroe, P Kohnen and S Smith.
 1977. Veno-occlusive disease due to pyrrolizidine poisoning in
 Arizona. Gastroenterology 73:349-352.
 
 Tyler, V E. "The Honest Herbal:  A Sensible Guide to the Use
 of Herbs and Related Remedies"  (Hawthorn Press, 1993).  Page
 citations refer to the 3rd edition.
 
 ==========================================
 
 Jay D Mann
 Christchurch, New Zealand
 [email-masked]

--

-----------------------------------------------------------------------
           Camilla Cracchiolo, RN   [email-masked]

        Shrine of the Cybernetic Madonna BBS  213-766-1356
        "The Board that Hates Rush Limbaugh With A Passion"
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---

From: [email-masked]
Date: Wed, 21 Dec 1994 22:33:30 GMT

Comfrey -- particularly the root -- contains pyrolizidine alkaloids, which
are poisonous for the liver. Drinking comfrey tea for a while, in moderation,
is probably okay -- unless your liver is already weak or damaged. But I
wouldn't drink more than 3 cups a day for a month or so.

A safe alternative is to make a comfrey poultice, or use comfrey tincture
externally, or to make comfrey oil and rub thãt into the wounded area (but
probably not into deep open wounds, because of the pyrolizidine problem).

Rick
In article <[email-masked]>, [email-masked] (Hilda Marshall) writes:
>> Hilda Marshall <[email-masked]> writes:
>>
>>>Diane - Drink comfrey tea after your surgery to speed your healing
>>>time.  And feel better soon!  Love, Hilda
>>
>>Hi, Hilda.
>>
>>I've read in several books that comfrey has been pulled off the
>>market as being dangerously toxic. Yes? No?
>>
>>Tom
>
>Well, comfrey HAS been linked to liver damage in rats - in continuous,
>force-fed, lab-rat doses.
>
>The fact that somebody even bothered to DO a study on a folk medicine
>like comfrey, and the dire reports of its fairly predictable results,
>strike me as evidence that this particular folk medicne might
>constitute a threat to medbiz profits if people weren't frightened of
>it.  But then I'm a very opinionated person.  ;-)
>
>Love, Hilda
>
>
>

---

From: [email-masked] (Hilda Marshall)
Date: 23 Dec 1994 15:27:04 GMT

Interesting article!  Three questions:

Coltsfoot is often SMOKED - would this make similar levels of PA's
enter the body, and/or a similar risk for VOD?

Are PA's accumulated in the body over time?  Are they ever
eliminated?

Is VOD reversible?  (i.e. if a patient stops ingesting PA's does
it clear up?)

Love, Hilda

---

From: [email-masked] (Jay Mann)
Date: 23 Dec 1994 19:46:51 GMT

Hilda Marshall ([email-masked]) wrote:
: > Hilda Marshall <[email-masked]> writes:
[snip]
: >I've read in several books that comfrey has been pulled off the
: >market as being dangerously toxic. Yes? No?

Opinionated but not informed.  Comfrey has been shown to cause serious and
sometimes fatal liver disease, not cancer.  Technically known as VOD,
veno-occlusive disease.  Yes, it takes a lot of hard, dedicated work for a
human to consume enough comfrey alkaloids to kill himself or herself.  It's
easier to poison a child.

In Germany, where herbal medicines are widely available and used, with a
pretty good background of popular knowledge, the demand for comfrey
("Beinwurz") is just about nil.  

Jay D Mann  <[email-masked]>
Christchurch, New Zealand

---

From: [email-masked] (Hilda Marshall)
Date: 21 Dec 1994 14:25:53 GMT

Love, Hilda

---

From: [email-masked] (PlantMed)
Date: 23 Dec 1994 17:13:38 -0500

Comfrey is available without the P.A.'s (toxic alkaloids) from Herb Pharm.