Is Comfrey Safe to Eat?
Common comfrey is a wild-growing herb that has a long tradition as both an edible and a medicinal species. It is a nutritious plant, being very high in Vitamin A, riboflavin, potassium, manganese and dietary fibre, and also a source of other vitamins and minerals such as magnesium and selenium needed by our bodies. It isn’t eaten a lot, as it has a slightly hairy, rough texture as the leaves age, but the young leaves and buds are very tender and delicious in recipes such as Comfrey Leaf Lemonade Fritters. The leaves are used a lot as a herbal tea. In other countries it has been grown as a vegetable and prepared as a ratatouille – and very tasty it is too!
In herbal medicine, comfrey is traditionally used to repair damaged joints, broken bones and torn tendons. This is because comfrey is very high in both vitamin K and vitamin K2 which promote fracture healing (Hodges, 1995). Incidentally, comfrey is one of the few plants that takes up vitamin B12 from the soil, the vitamin that vegans need to supplement with to avoid pernicious anaemia. The name comfrey comes from the Latin ‘confera’ which means to knit together, hence the old country name for comfrey of Knitbone. (It’s botanical name comes from the Greek word symphyo meaning to unite.) Comfrey root ointment is used to treat painful osteoarthritis of the knee. A clinical trial showed that the ointment works significantly better than a placebo ointment, with five times the effect in pain reduction and four times improvement in quality of life (Grube, Grünwald, Krug & Staiger, 2007).
It is also used in cosmetics because comfrey contains substances that help skin regrow, including allantoin, rosmarinic acid and tannins.
Although herbal medicines are widely considered by the scientific community to be of lower risk than synthetic drugs, they can still sometimes cause toxicity or side effects (De Smet, 2004).
What are pyrrolizidine alkaloids (PAs)?
You may have found warnings or restrictions on the internal use of comfrey on the internet. This is because comfrey contains pyrrolizidine alkaloids (PAs). Pyrrolizidine alkaloids are a group of 660 phytochemicals found in over 6,000 plants. PAs can also found in honey, grains, milk, offal and eggs. In the case of some species of comfrey, a particular PA called echimidine has caused special concern as it is toxic to the liver in animals. Due to this, medicinal or food products for internal use containing comfrey root, are restricted in many countries, with a few also restricting comfrey leaf, although it contains far fewer alkaloids.
The species really matters!
There are several species of comfrey plant. I only eat common comfrey, Symphytum officinale (leaf not root) which rarely contains echimidine and tuberous comfrey (Symphytum tuberosum) which has less than 0.02% PAs. The difficulty nowadays is that common comfrey hybridises to Russian comfrey and some modern analysis shows echimidine appearing in common comfrey too.
Up until now (2018), Common comfrey leaf Symphytum officinale has been allowed in over-the-counter preparations in the USA, UK, Canada, Germany. Canada’s Food and Drug Regulations prohibits the sale, for medicinal purposes, of any products containing echimidine (Canada Gazette, 30 March 1988). Canada’s Cosmetic Regulations ban Symphytum species EXCEPT for Symphytum officinale which is allowed. Echimidine, considered to be the most toxic of the PAs found in comfrey (Brauchli-Theotokis 1987), is rarely found in most samples of common comfrey (Symphytum officinale L.) (Couet et al. 1996; Roitman 1981) but seems to appear more often in later studies. This may be due to the ability of common comfrey to hybridise with prickly comfrey creating a hybrid called Russian comfrey (Symphytum x uplandicum).
Look at the photo at the top of this post – it shows the difference between tuberous comfrey and Russian comfrey. Here in Scotland, tuberous comfrey always has cream flowers.
Common comfrey has flowers that range from white to purple. This make identification a little more difficult. Common comfrey in England mainly has strong coloured pink-purple flowers and lance shaped leaves, while Russian comfrey, which tends to be a bigger plant with broader pointed leaves, has paler violet or blue-purple flowers. Russian comfrey is widely sold to gardeners as the Bocking 14 hybrid for fertiliser. Due to the concerns about PAs, it is important to be able to identify the different comfrey species and it is not easy to tell them apart – except for the tuberous comfrey.
British herbalists use, common comfrey Symphytum officinale. Please see the following excerpt from American Botanical Council research in 1994 when the first concerns were raised.
“The first Canadian action was taken in 1982, when the Health Protection Branch of Health and Welfare Canada introduced an amendment to Canada’s Food and Drug Regulations which prohibits the sale, for medicinal purposes, of any products containing echimidine (Canada Gazette, 30 March 1988).
Echimidine, considered to be the most toxic of comfrey PAs (Brauchli-Theotokis 1987), is not found in common comfrey (Symphytum officinale L.). However, it is present in prickly comfrey (S. asperum Lepechin) and its hybrids with S. officinale (Huizing, Gadella, and Kliphuis 1982), including Russian comfrey (S. x uplandicum Nyman), which is the most commonly encountered commercial comfrey in Britain (Clapham, Tutin and Warburg 1962) due to its popularity as a garden fertiliser especially the strain called Bocking.
The intent of the Canadian legislation is to have more careful attention paid to identification of botanical species by the herbal industry, and to alert the Canadian public to the potential danger of PA consumption. There was no intent to underestimate the relative potential danger of echimidine-free S. officinale. Both root and leaf of Symphytum officinale have been shown to be carcinogenic in rats (Hirono et al. 1978), though again in this paper there is species confusion because the authors equate common comfrey and Russian comfrey!”
Animal testing – is it like for like?
Apart from the species mix up, these theoretical dangers quoted above in Hirono et al. 1978 are not without controversy. Dangerous actions are sometimes attributed to herbs because of in vitro or animal studies. And yet many papers that demonstrate actions in vitro or in animals cannot always be replicated in vivo – i.e. in humans. Animals and humans are not the same. In the Hirono study, the researchers found that forcing rats to eat huge quantities of ground comfrey leaves and roots did them no good at all – especially the 2 week old baby rats. Of note, out of 28 rats fed 8% of diet as dry weight comfrey, one showed a liver tumour at 600 days (a long life for a rat!). The average adult human would probably need to ingest 20,000 comfrey leaves to produce a comparative dose. Assuming 3 dried leaves of comfrey per cup of leaf tea, this equates to drinking 6,666 cups of tea. If you drank a cup of comfrey leaf tea every single day, it would take you over 18 years to reach this level of consumption!
A respected research herbalist, Margaret Whitelegg MNIMH wrote a paper in January 1993 called “In Defence of Comfrey” that was submitted to the Department of Health and Ministry of Agriculture, Fisheries and Food by the National Institute of Medical Herbalists – when these issues first surfaced. If you use her reference below of 5,607 leaves in a man-sized rat being equivalent to the injections of isolated PAs in another animal study, you’d need 1,867 cups of tea, so 5 years if drunk at a cup a day to match the study dose.
There are actually very few cases of comfrey toxicity in humans and they are all more complex than occasional consumption of comfrey as a vegetable. One of the 4 actual human cases known at the time, was a woman who took comfrey in excess – a.k.a. overdosing. She was a forty-seven year old non-alcoholic woman who began to feel unwell in 1978 with vague abdominal pain, fatigue and allergies (Bach, Swan et al (37)). She drank as many as ten cups of comfrey tea per day in addition to taking handfuls of comfrey pills, for over a year. Four years later, her serum aminotransferase levels were twice normal range. Eight years later she had further signs of liver disease. Despite the obvious abuse of comfrey and its use in a very unusual way, nevertheless this case is used to condemn the plant when taken in normal, moderate doses. I wonder what the effects of 10 cans of Red Bull or Coke drunk every day for four years would be on your liver? However, that doesn’t result in a ban of soft drinks.
In her paper, Margaret Whitelegg made the following points that I find significant:
“While evidence on pyrrolizidine alkaloid (PA) toxicity is mounting and the case against any PA-containing plant appears increasingly clear, the controversy over comfrey deserves closer inspection. It appears to be damned by its association with the effects of other PA containing plants, by the effects of its alkaloids on laboratory animals and by certain cases of hepatotoxicity through ingestion of the plant by humans. Yet I would argue that the case against comfrey is by no means proven in the scientific literature.”
She goes on to say:
“Effects on Animals.
Papers on the harmful effects of PAs on laboratory animals are legion, both those in other plant species (1-7) and in comfrey itself (8-11). One of the most often cited papers to this effect is that of Culvenor et al, “The structure and toxicity of the alkaloids of Russian Comfrey, a medicinal herb and item of human diet (12)”. He reported on an experiment in which alkaloids of comfrey were administered intraperitoneally to two-week old rats, either as a single dose or as multiple doses beginning at two weeks old over intervals of nine weeks. Evidence of hepatotoxicity was found. Bone (13) and Pembery (14) criticise this paper. Their criticisms reflect certain problems that occur repeatedly throughout the literature, whether proposing hepatotoxic, genotoxic or carcinogenic effects. Both authors suggest that two-week old rats are more vulnerable to the effects of PAs and, according to Jago, (15) are particularly susceptible to the induction of megalocytosis. Pembery, for the Doubleday Institute, looks more closely at the numerical data and extrapolates equivalent quantities of PAs for humans, suggesting that exposure in humans at such levels is unlikely : “…it can be seen that the dose required to produce the least effect in the rats, reduced liver function, detectable by a change in the proportion of the plasma proteins, is equivalent to the alkaloid from 5,607 leaves if administered to a “man-sized rat” That is, if we assume that the effect of the alkaloid in man (sic) is going to be the same as in a young rat, apparently the most susceptible of any so far tested. If an average comfrey leaf is taken as 100g (and older leaves are much more than this), this dose level represents about eight times the body weight of the man-sized rat. Deaths occurred at levels equivalent to the alkaloid from 19,880 leaves or equivalent to 28 times the bodyweight of the man-sized rat.” [My bold emphasis.]
“More importantly, however – and this applies to all experiments with isolated alkaloids – both authors argue that to give alkaloids in isolation and injected intraperitoneally into animals, cannot reflect the effects in humans of the entire plant taken orally. This reflects one of the central tenets of herbal medicine, that an isolated chemical of a plant, while useful for certain indications, cannot define the action of the whole herb, where the herb is more than the sum of the individual parts, its constituents working synergistically to create its healing effects. A press release by the National Institute of Medical Herbalists (16), written by F. Fletcher Hyde, FNIMH, speaks of “…two insupportable assumptions. First, that the naturally occurring complex in the plant … can be regarded as a mere physical dilution of alkaloids that the human metabolism is identical with that of the rat which is susceptible to these alkaloids, and not with the sheep which is resistant to them.”
“…Tea, almonds, apples, pears, mustard, radishes and hops, to list only a few items, all contain substances which, if extracted, can be shown to be poisonous when tested under conditions similar to those used in the comfrey experiments. Must we then ignore our experience of the usefulness and wholesomeness of these foods because controlled trials and scientific evidence have not been published to establish their safety?”
Personally, I would have also added honey to that list as it often contains the highest levels of PAs in your local supermarket. I also think that there is an extremely valid point to be made that extrapolating results to determine the safety of humans eating comfrey, from results of animals being injected with high concentrations of the alkaloids extracted from comfrey, is not sound.
The plant part matters: leaf not root
“Health and Welfare Canada has for many years refused to register comfrey root products for any medicinal application, in recognition of the much greater risk presented by root material as compared to leaf. Comfrey root has been consistently observed to contain roughly ten times the concentration of PA found in leaves (Mattocks 1986, Roitman 1981). Manufacturers have been advised that the inclusion of comfrey root in herbal preparations is no longer acceptable.” Again, this refers to the root not the leaf.
Research can be contradictory
Comfrey was banned in Australia because of a paper called, The structure and toxicity of the alkaloids of Russian comfrey (S. x uplandicum) a medicinal herb and item of human diet by Dr. C. Culvenor, et al, Australia, 1980. Although Culvenor and his associates identified eight alkaloids in comfrey, four being new to science; there does seem to be inaccuracy, when he quoted the results of Pederson (1975 ). Quotes indicated that he found a 9% concentration of alkaloids in leaves, when Pederson’s actual figures were 0.9 parts per thousand when estimated by titration, and 1.9 parts per thousand when estimated gravimetrically.
Theoretical dangers are often attributed to herbs because of the singular action of one constituent, although herbs are a complex blend of hundreds of phytochemicals whose combined beneficial and protective action often negate the harmful action of one compund. For example, meadowsweet contains salicylic acid (naturally) which is what aspirin is made of (chemically). Aspirin can upset stomachs yet meadowsweet is used by medical herbalists to treat stomach ulcers. Meadowsweet, unlike aspirin, contains many other phytochemicals which have a soothing effect. Read more here about the use of comfrey in creams and ointments.
Reported side effects
There have been some side effects reported from:
• taking comfrey medication (species not recorded) – a woman (1985) taking two comfrey medicines, one for four months and one for six months, and 2 women (1987) who took comfrey-pepsin tablets for 6 months.
• drinking comfrey tea (species not recorded) – a boy with Crohn’s disease (1987) who regularly drank comfrey tea and a woman (1989) who drank 10 cups of comfrey tea daily for 4 years
• eating comfrey (species not recorded) – one single case of a man (1990) who ate 4-5 cooked comfrey leaves a day for 2 weeks where comfrey may have contributed to his death by liver failure (he also had some other very bizarre dietary habits).
These few case studies do support that underlying illness, poor nutrition and the concurrent use of hepatotoxic drugs, increase the likelihood that veno-occlusive (liver) disease may develop when using PA-containing drugs or eating PA-containing plants (Rode, 2002). In particular, they point out that you should avoid taking comfrey in excess – the feature that unites this handful of reports.
To put this in perspective, according to the Office for National Statistics, between 1993 and 2011 around 23,630 people have died in the UK from drug-related poisoning not including drug misuse! (The total deaths if you include drug misuse being 52,732.) Where the cause of death is mentioned on the death certificate, this includes:
• 8606 deaths due to paracetamol poisoning
• 8324 deaths due to antidepressants
• 4611 deaths due to benzodiazepines (Diazepam (Valium), Temazepam and Nitrazepam
• 3079 deaths due to Tramadol
• 872 deaths due to aspirin
• 0 deaths due to comfrey
Note for people taking medication
An obvious recommendation with comfrey is not to eat or drink it excessively. I would add that you should definitely not eat it if you already take a drug that is known to harm the liver. This includes: acetaminophen (Tylenol and others), amiodarone (Cordarone), carbamazepine (Tegretol), isoniazid (INH), methotrexate (Rheumatrex), methyldopa (Aldomet), fluconazole (Diflucan), itraconazole (Sporanox), erythromycin (Erythrocin, Ilosone, others), phenytoin (Dilantin), lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), and many others. If you are on other medication, especially carbamazepine (Tegretol), phenobarbital, phenytoin (Dilantin), rifampin, or rifabutin (Mycobutin), speak to your doctor or medical herbalist before using comfrey, as like other herbs, it may compete with the drug in your liver, the combination of which can cause side-effects.
Using comfrey in pregnancy
Warnings about use in pregnancy, breast-feeding and children found on medicinal/drug advice websites will always caution against use in these conditions without the advice of a doctor unless specific clinical trials have been done on children or pregnant women – which they rarely are! So this is a default warning. To be quite honest very few doctors would even know the answer as without specific genotox/clinical trials this information does not exist. To be on the safe side, pregnant or breastfeeding women should not eat or drink comfrey. Externally, the tiny amount used in a cosmetic cream would be negligible. If you are pregnant or planning to conceive, and wish to use herbal medicines, please err on the side of caution and seek the advice of a qualified medical herbalist.
Why I eat comfrey
There are many issues with the way that research is reported on the internet and many people scare themselves by reading badly referenced and poorly interpreted reports. I eat comfrey personally because I cannot find a single published case history of a healthy human actually experiencing (as opposed to theoretically being at risk from) liver damage from eating identified common comfrey. Nor do I intend to ever consume 20,000 leaves nor drink a cup a day for 18 years.
I also have a huge amount of cream-flowered tuberous comfrey growing here in Scotland (less than 0.02% PAs). So this is mainly the species I eat, in season.
I’m not saying that comfrey is totally safe or denying the presence of PAs. That would be to discredit science and just be ignorant! However, it is all a question of perspective. I believe that I will be doing less harm to my body by occasionally eating or using comfrey than I would from, for example, drinking caffeinated drinks daily, eating processed foods full of chemicals, eating non-organic food sprayed with pesticides, breathing in fragrance chemicals from electric “air fresheners”, traffic fumes, pharmaceutical drug side-effects… the list goes on.
One point that I also find particularly relevant is that not only does the comfrey species matter but the animal species that are studied matters too. Rats are not like humans. Especially 2 week old baby rats. Rode, 2002 points out that as not all animals are susceptible to PA toxicity, comparing humans to rats is not comparing like for like. Using ragwort (Senecio) as an example, as it contains high levels of PAs, she says “The response of different animal species to PAs varies tremendously. Pigs, chickens and rats are highly sensitive to poisoning by Senecio, whereas mice and sheep are resistant. Moreover, the response of a species to Senecio might not reflect its susceptibility to other PAs. For example, guinea-pigs are susceptible to Senecio, but resistant to monocrotaline. Additionally, 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. Despite their sensitivity to PAs, pigs readily accept comfrey and show no adverse effects, even when comfrey represents 40% of their diet. Chickens, another sensitive species, also show no ill effects when fed comfrey. By contrast, rats appear to be sensitive to the PAs in comfrey. Indeed, when rats consume high levels of comfrey or are injected with purified comfrey PAs, they develop liver tumours and hepatic lesions indicative of PA poisoning. However, rats might not be an appropriate human model because their hepatic response to PAs seems to differ from the human response.”
Significantly, a trial by Dr. Clare Anderson, from the Laboratory of Pharmakinetics and Toxicology, School of Medicine, University College, London, tested forty long-term comfrey consumers, who then submitted for liver function tests (Anderson, 1981). This was a small group for a clinical trial but with prolonged consumption of comfrey leaf (0.5–25 g day for 1–30 years).
This is the only study that I can find that has actually tested humans! The abstract from the subsequent paper (Anderson & McLean, 1989) states that: There was no evidence of liver damage in a group of 29 people who had regularly consumed comfrey. Twenty-nine volunteers responded to mailed questionnaires regarding duration, amount, and form of comfrey used. At the same time, liver function tests (bilirubin, transaminase, and GGT) were performed on the volunteers. Most volunteers (21/29) had used comfrey for 1-10 years (mean intake 3.0 g dry leaf/day); 5/29 used it for 11-20 years (mean intake 2.6 g dry leaf/day); and 3/29 used it for 21-30 years (mean intake 11 g dry leaf/day).
All were found to have perfectly fit livers!
Update: Later in 2019 there is a NIMH seminar on comfrey with an update on modern evidence. So we shall see what new thinking comes to light on the question “is comfrey toxic?”.
Monica Wilde works at Napiers the Herbalists. She is a Research Herbalist with a Masters Degree from UCLAN and an advocate for quality, safety and research in herbal medicine. Her special interest is researching drug-herb interactions. At weekends, Monica runs foraging courses and events specialising in wild food and wild medicine.
Anderson, C. (1981) Comfrey in Perspective. The Lancet, 1(8235): 1424
Anderson, P.C. & McLean, A.E.M. (1989). Comfrey and liver damage. Hum Toxicol
Couet, C., Crews, C. & Hanley, A. (1996) Analysis, separation, and bioassay of pyrrolizidine alkaloids from comfrey (Symphytum officinale). Nat Toxins. 4(4):163-7. PubMed PMID: 8887946.
De Smet, P. (2004) Health risks of herbal remedies: an update. Clin. Pharmacol. Ther., 76: 1–17
Grube, J., Grünwald, L., Krug, C. & Staiger. (2007) Efﬁcacy of a comfrey root (Symphyti ofﬁc. radix) extract ointment in the treatment of patients with painful osteoarthritis of the knee: Results of a double-blind, randomised, bicenter, placebo-controlled trial. Phytomedicine, 14: 2-10
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