Comfrey - The Facts
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. The world of herbalism abounds with anecdotal accounts of its virtues, but there have been few serious studies of ts medicinal use. What has instead appeared in the scientific literature are studies which claim to emonstrate 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 (PAÂs) found in Comfrey are not responsible for its therapeutic effects. Alkaloids are plant substances which contain nitrogen, and can have high phamacological activities Â morphine, quinine and nicotine are examples. Comfrey leaves contain about 0.06% alkaloids, and roots about 0.2 to 0.4%. Pyrrolizidine alkaloids contain two fused five-membered rings with a nitrogen atom common to both rings. They 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.
A number of important issues are embodied in the Comfrey dilemma, issues which have much broader implications for herbal medicine. Should a medicinal plant which has a long history of safe use be regarded as dangerous because it contains low levels of toxic chemicals? Should a medicinal plant be regarded as carcinogenic because it produces a few malignant tumours in inbred, susceptible laboratory animals when fed to them at unrealistically high levels over a whole lifetime? To address these issues requires rationality and good science, but above all common sense. So far these have been lacking from the Comfrey debate. It has been a debate argued from extremes.
On the one hand a group of well-meaning scientists actively lobbied the Australian government to have Comfrey restricted. The basis for their concern was just two toxicological studies, both of which have doubtful relevance to normal human use. The arguments generally used were related to pyrrolizidine alkaloids, not Comfrey itself, and their theme was that pyrrolizidine alkaloids should be entirely eliminated from human diet and human medicine.
Their zeal saw Comfrey in some states of Australia receive a higher poisons classification than arsenic, hemlock,belladonna and strychnine. In Victoria Comfrey
was restricted from external use when there is no evidence
that this is harmful. The hysteria generated by their crusade saw a coroner file a report in Australia attributing a human death to just a few meals containing
On the other hand the defence for Comfrey has been at times emotional and irrational. It is not enough for herbalists and naturopaths to say, "I have used it and
never seen any harm," or for a consumer to say, ÂIÂve taken
50g every day for 10 years and IÂm normal."Valid as these
observations may be, similar arguments have been used
to defend, for example, cigarette smoking. It does not
impress the scientific community to argue emotionally
or from personal experience.What does impress are new,
objective facts, or a critical interpretation of the existing facts.
So what are the facts? The relevant issues can be embodied in the form of six questions. By dealing with these questions, the facts can emerge. How do the toxicological studies on Comfrey compare with those for commonly used plant substances?
The first study by Culvenor and associates was concerned
with the acute and sub-acute toxicity of the PAÂs
extracted from Russian Comfrey (Symphytum x uplandicum) leaves.4 These PAÂ s were administered by injection, so it is difficult to relate this to the oral use of the Comfrey leaf, but ignoring this we can still arrive at some pertinent facts.
We can convert the injected dose of alkaloids in rats
to the equivalent oral human dose of leaves based on the
fact that a leaf consistently contains 0.33mg of alkaloids
whether it is old (large) or young (small).5 These projections are given in Table 1. Clearly from this information, normal human consumption of a few leaves per day does not pose an immediate threat to health, a fact acknowledged by Culvenor.
The dose needed for death is impossibly high. How could anyone possibly consume 66,300 Comfrey leaves at one sitting Â more than the personÂs body weight in Comfrey? How could one even consume this amount over 10 days? Yet a coroner has reported, on the basis of medical opinion, that someone died of acute Comfrey poisoning.6 This is a travesty of common sense. Clearly it is impossible to die from acute Comfrey toxicity. Other factors must have been at play.7
Even to show some mild impairment of liver function one would need to consume 4.5kg of leaves per day for 3 weeks (assuming 5g per leaf). Yet there are 2 medical papers associating, by hearsay only, acute PA toxicity in the form of veno-occlusive disease with Comfrey medications.8,9 In neither case was it verified scientifically that herbal preparations used by the subjects contained Comfrey. Also it was not ascertained
that this was their only source of PA intake. This is a
travesty of scientific method and a poor reflection on the
journals which accepted these articles for publication.
Doubly so, because once something is in print in a journal it is often quoted in a superficial way as fact, with no analysis of the validity of the original information (as is the case in some internet forums).
Is Comfrey carcinogenic?
Here we refer to the second toxicological study on Comfrey by Japanese workers entitled, "Carcinogenic Activity of Symphytum officinale".10 A foregone conclusion, isnÂt it? The title says it all. But is it a fact? Although this is a relatively recent study, it does not satisfy many of How carcinogenic are pyrrolizidine alkaloids? The question of the carcinogenicity of PAÂs is a controversial area. In laboratory animals only a handful of the large number of PAÂs have been studied and while malignant tumours have been induced in many organs, usually it has only been in a small percentage of the test population. Most studies have reported the induction of liver tumours, but there is controversy as to whether these are malignant. Chronic PA poisoning gives rise to liver nodules, and the tumours found in these are probably benign not malignant.1 One scientist in the field concluded, "As far as pyrrolizidine alkaloid carcinogenesis is concerned then, an important part of the argument rests on the disputed identity of the lesions reported as hepatoma".1 The study of PA toxicity is not a crowded field, so there has not been exhaustive examination of carcinogenicity Â often preliminary studies are not followed up. This can result in things being taken for proven facts which are far from properly studied. No-one, for example, has repeated the original arcinogenicity study on Comfrey, despite all the controversy. Given the controversy over the carcinogenicity of PAÂs as observed in the laboratory, it is noteworthy that there has never been a link with PA intake and cancer in human or in veterinary studies, despite the many recorded cases of livestock poisoning.1 PA poisoning (venoocclusive disease), is high in JamaicaÂdue to indigenous herbal teas Â yet the incidence of primary liver cancer is lower than in western countries. Also primary liver cancer is not more common in people with livers damaged by PAÂs than in people with cirrhotic livers due to alcoholism.2
Is it valid to generalise about PAÂs in terms of
their toxicity and carcinogenicity?
In one study rats were fed green leaves of Senecio jacobea
(Oxford Ragwort) and Comfrey in their diet.3 At 5% Comfrey leaves there was no sign of toxicity, but at 1% Ragwort leaves in the diet there were many signs of toxicity, including changes in liver enzyme activity.3 Even 20% Comfrey leaf in the diet did not cause the liver enzyme changes from 1% Ragwort.3 Comfrey PAÂs are therefore much less toxic to the liver than those of Ragwort. This would explain why Ragwort causes livestock poisoning whereas Comfrey is used as a livestock feed, with excellent results. In fact there are no recorded cases of livestock poisoning due to Comfrey.
What do the toxicological studies on Comfrey
Despite all the rhetoric there are in fact only two full-scale toxicological studies on Comfrey. To quote other publications which merely interpret the findings of these two studies does not constitute additional evidence. 2 Professional Review
Alkaloid Dose Effect Equivalent Human
for Rat Dose of Leaves
284mg/kg Deaths 66,300 Jeaves
71 mg/kg No effect 16,600 leaves
8.9mg/kg Reduced liver 890 leaves/day
(9 doses over 3 weeks) function
Toxicity Studies of Symphytum x uplandicum Leaf alkaloids.4 the criteria demanded for a rigorous assessment of carcinogenicity. Rats were fed Comfrey leaf from 8 to 33% of their diet, thus all test levels exceeded the 5% maximum recommended by the EC. Test levels for the
root were 0.5 to 4%. Liver tumours were observed in all
test groups, but the vast majority were probably benign tumours (hepatomas), indicating hepatotoxicity at the
levels tested. For the rats fed 8% Comfrey leaf only one
benign tumour occurred late in the study, indicating low
toxicity and absence of carcinogenicity. Only 3 definite
liver cancers (haemangioendothelial sarcomas) occurred
randomly throughout the 7 test groups, a level which has
neither statistical nor biological significance.
In order to prove biological significance for a carcinogen
the following criteria must be demonstrated:11
A dose-response relationship
A decreased latency period for the tumours
A more anaplastic tumour type than controls
Early or pre-neoplastic lesions
Capability to produce a reliable and consistent
increase in tumour incidence
None of these criteria was satisfied for the liver
sarcomas. The fact that rats could be fed 33% Comfrey
leaves in their diet and still survive to old age is testimony to its relatively low toxicity.How many drugs could survive such scrutiny?
Let us take everyday tea as an example. Tea is the dried fermented leaves of Thea sinensis, a herb indigenous to the Indian sub-continent. Tea contains caffeine and tannins, including tannic acid, as its main constituents.(12) A superficial examination of the literature reveals the following: Caffeine is a known teratogen,(13) a suspected carcinogen,(14) and in animal feeding studies causes severe weight loss and thymic and testicular atrophy.15 Tannins have demonstrated carcinogenic effects, they inhibit digestive enzymes, inhibit mineral absorption and are highly toxic to the liver and kidneys.16 Human deaths have resulted
from the administration of tannic acid.17 The carcinogenic
activity18 and toxicity19 of the tannins from tea have
been demonstrated in animal experiments. In human
studies tea can cause thiamine deficiency,20 constipation21
and epidemiological studies have linked black tea with
rectal22 and oesophageal cancers.18 Of course, common
sense tells us normal use of tea is safe, but the scientific information taken out of context is quite damning, in fact more alarming than that for Comfrey.
It is worthwhile to examine why this considerable
scientific evidence for the toxic nature of tea has not made headlines and has not resulted in tea being restricted or entirely banned in the public interest. Just as a series of promising pharmacological studies does not imply the birth of a new wonder drug, the findings of toxicological studies can be of only minor relevance to the common experience. Differences such as species studied, dose, form a dose, interaction with nutrients, and duration of dose all combine to explain why the results for tea and its components should have little bearing on the moderate consumption of the beverage. Qualified herbalists can therefore be forgiven for taking a similar stance about Comfrey. The main difference is that toxicologists and legislators are familiar with tea, but to them Comfrey is alien and unnecessary so they are prepared to believe the worst.
Assuming Comfrey was a proven carcinogen,
what is the relative risk of drinking Comfrey tea?
Life is carcinogenic Â so it has been said. Here we are
undertaking an assessment of relative risk. Dr Bruce
Ames, a respected scientist in the fields of carcinogenicity and mutagenicity has published an article in the journal Science entitled "Ranking Possible Carcinogenic Hazards".23 The review discusses reasons why animal cancer tests cannot be conclusively used to predict human risks but such tests may be used to indicate that some chemicals might be of greater concern than others. An
index was developed called HERP Â Human exposure dose/Rodent potency dose. In this study it was found that inhaling air in the home absopbs 598mcg of Formaldahyde, and that cooking bacon causes the inhalation of .4 mcgs of nitrosamines which puts the 750mcgs of PA's you'd ingest from a cup of comfrey tea in perspective.
So now we have the facts:
1. There is some doubt that pyrrolizidine alkaloids
cause cancer outside of laboratory experiments.
2. The pyrrolizidine alkaloids in Comfrey are qualitatively
and quantitatively less toxic than pyrrolizidine
alkaloids found in known poisonous plants, e.g.
3. Atoxicological study has shown that normal human
use of Comfrey cannot cause death or toxicity.
4. The incidence of malignant tumours induced by
long-term experimental feeding of high levels ofComfrey to rats is neither statistically nor biologically
5. Toxicological studies of tea are far more extensive
and alarming than those on Comfrey, yet tea is widely
used without apparent harm or restriction to its use.
6. Even assuming that Comfrey was carcinogenic, the
relative risk from its normal use is insignificant when
compared to normal exposure to other carcinogens.
A recent study of long-term Comfrey users tends to
confirm the premise that normal use of Comfrey is not
hepatotoxic.24 Biochemical tests revealed no evidence of
liver damage in 29 users, even for those who had been
regularly taking up to 25g/day for more than 20 years.24
Comfrey was never regarded as a poisonous plant.
Despite the findings of two laboratory studies, it should
maintain this status. However, in the interests of the public and the herbal profession, a rigorous study of its longterm toxicity should be undertaken. Otherwise the
Comfrey issue will continue to damage the credibility of
herbal medicine in many countries.
1. McLean, E.A: Pharmacol Rev 22, 429 (1970); 2. Bras, G. et al: J Patho Bacteriol
82, 503 (1961); 3. Garrett, B.J. et al: Toxicol Lett 10, 183 (1982); 4. Culvenor, C. C.
J et al: Experientia 36, 377 (1980); 5. Mattocks, A.R: Lancet 2, 1136 (1980); 6. NZ
Dept of Justice, CoronerÂs report on the death of Paul Edward Neutz, March 12,
1986; 7. Beckham, N: Wellbeing, April (1988); 8. Weston, C.F.M. et al: BMJ 295,
183; 9. Ridker, P.M. et al: Gastroenterology 88, 1050 (1985); 10. Hirono, I. et al:
JNCI 61, 865 (1978) 11. Borzelleca, J.F. et al: Fd Chem Toxic 23, 551 (1985); 12,
Trease, G.E. and Evans,W.C: Pharmacognosy, 12th ed., Balliere Tindall, London, P
622 (1983); 13. Collins, T.F.X. et al: Fd Chem Toxic 25, 647 (1987); 14. Rozenkranz,
H.S. and Ennerver, F.K: ibid 25, 247 (1987); 15. Gans, J.H: ibid 22, 365 (1984); 16.
Deshpande, S.S. et al: Adv in Exptal Med and Biol 177, 457 (1984); 17. Kreanoski,
J.Z: Radiology 87, 655 (1966); 18. Morton, J.F: Science 204, 909 (1979); 19. Panda,
N.C. et al: Ind J Nutr and Diet, p97 (1981 ); 20. Ruenwongsa, P. and Patannavibag,
S: Experientia 38, 787 (1982); 21. Hojyaard, L. et al: BMJ 282, 864 (1981); 22.
Heilbrun, L. K. et al: Br J Cancer 54, 677 (1986); 23. Ames, B.N. et al: Science 236,
271 (1987); 24. Anderson, P.C. and McLean, A.E.M.: Human Toxicology 8 (1)
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