Comfrey: Never Take It Internally

⚠ Do not drink comfrey tea. Do not take comfrey capsules, tinctures, powders, tablets or “green drinks.” Do not eat comfrey leaves as a vegetable or in a soup, however often you have seen it recommended. There is no safe internal dose, no safe preparation method, no safe cultivar, and no amount of drying, boiling or fermenting that removes the danger.

This is not a defensive disclaimer written by lawyers. Comfrey’s pyrrolizidine alkaloids — echimidine, symphytine, lycopsamine, intermedine and their acetylated relatives — are converted by liver enzymes into reactive molecules that destroy the cells lining the smallest veins inside the liver. The resulting condition, hepatic veno-occlusive disease (also called hepatic sinusoidal obstruction syndrome), is often irreversible. It has killed people who took comfrey. One of the published cases was a 23-year-old man. Another involved nothing more exotic than comfrey herb tea.

Oral comfrey products have been removed from the market or restricted in the United States, the United Kingdom, Germany, Canada and Australia. Those regulators did not ban the topical ointment, which is still sold and still studied. They banned the swallowing. That distinction is the whole point.

The rest of this article explains why — the chemistry, the disease, the actual human cases, why herbal tea is a worse route than people assume, and what to do if you have been taking comfrey internally.

Table of Contents

1. What Pyrrolizidine Alkaloids Are
2. How the Liver Turns Them into a Poison
3. Hepatic Veno-Occlusive Disease
4. The Documented Human Cases
5. The Tea Problem
6. Root Versus Leaf, and Which Species
7. DNA Damage and Cancer
8. What Regulators Did, and When
9. The Arguments People Make For Eating It
10. Symptoms, and What to Do
11. Does This Mean Topical Use Is Unsafe?
12. Other Herbs With the Same Problem
13. Key Research Papers
14. Connections

What Pyrrolizidine Alkaloids Are

Pyrrolizidine alkaloids are a family of several hundred plant compounds built on a two-ring “necine” core. Plants make them as a defence against insects and grazing animals, and they occur across the borage family (Boraginaceae, which includes comfrey), the daisy family tribes Senecioneae and Eupatorieae (ragworts, groundsels), and parts of the pea family.

Two structural details determine everything:

• A double bond between positions 1 and 2 of the necine ring. Only the 1,2-unsaturated alkaloids are toxic. Saturated ones are essentially harmless. Comfrey’s are the unsaturated, toxic kind.
• They mostly occur as N-oxides. In the living plant, and in dried herb, much of the alkaloid load exists as an N-oxide — a more water-soluble, less immediately reactive form. This matters twice over: N-oxides are efficiently reduced back to the free alkaloid in the gut, so they are not detoxified, and they are easy to miss in the laboratory unless the analytical method deliberately reduces them first.

Comfrey has been reported to contain as many as fourteen different pyrrolizidine alkaloids, including 7-acetylintermedine, 7-acetyllycopsamine, echimidine, intermedine, lasiocarpine, lycopsamine, myoscorpine, symlandine, symphytine and symviridine. A chemical analysis of one commercial sample of comfrey root found a total alkaloid content of 0.07 % with seven N-oxides present, 7-acetylintermedine and 7-acetyllycopsamine dominating.

There is one more finding worth knowing, because it undercuts a common reassurance. When researchers compared a crude reduced comfrey alkaloid extract against the purified individual alkaloids lycopsamine and intermedine in an animal study, the crude extract was more toxic than either pure compound. The authors concluded that safety recommendations derived from purified compounds may underestimate comfrey’s real toxicity — the mixture behaves worse than its parts. So “my comfrey only contains the milder alkaloids” is not the reassurance it sounds like.

How the Liver Turns Them into a Poison

Pyrrolizidine alkaloids are not particularly dangerous as they arrive. The liver makes them dangerous, which is a bitter irony given that the liver is the organ that suffers.

1. You swallow the alkaloid, or its N-oxide, which gut bacteria and gut-wall enzymes reduce to the free alkaloid.
2. It is absorbed and travels straight to the liver in the portal blood.
3. Liver cytochrome P450 enzymes — principally CYP3A4 — oxidise it. This is the ordinary machinery your liver uses to make foreign molecules easier to excrete. Here it backfires.
4. The product is a highly reactive dehydropyrrolizidine ester (a “pyrrolic” metabolite), which survives long enough to travel a short distance in the bloodstream.
5. That metabolite binds covalently to proteins and to DNA in whatever cell it reaches — and the cells it reaches first, in highest concentration, are the sinusoidal endothelial cells lining the smallest hepatic veins and the hepatocytes around them. The characteristic DNA adducts are derived from 6,7-dihydro-7-hydroxy-1-hydroxymethyl-5H-pyrrolizine, usually abbreviated DHP.

The result is that the venules’ lining cells die and detach. Debris and swollen cells obstruct the vessel, blood cannot leave the liver lobule, pressure backs up, and the tissue downstream congests and dies. This is a dose-cumulative process. There is no threshold below which nothing happens; there is only more or less damage.

Two consequences follow that people routinely get wrong. First, the damage is not an allergy or an idiosyncratic reaction — it is predictable toxicology that will happen to anyone given enough. Second, drying, brewing, boiling and fermenting do not destroy the alkaloids. They are stable, water-soluble compounds. Making tea extracts them into the water rather than removing them.

Hepatic Veno-Occlusive Disease

The clinical picture has a name and a well-described course.

Acute presentation — days to weeks after a substantial exposure: sudden abdominal pain, particularly under the right ribs; nausea and vomiting; rapid weight gain from fluid; a swollen, tender liver; and ascites, fluid accumulating in the abdomen. Liver enzymes and bilirubin rise. In severe cases this progresses to liver failure.

Subacute and chronic presentation — months to years of lower-level intake: a slower slide into portal hypertension, with an enlarging spleen, oesophageal varices that can bleed catastrophically, ascites, and eventually cirrhosis-like scarring. This form is easy to miss, because the early symptoms are vague — tiredness, mild abdominal discomfort, poor appetite — and no one connects them to a daily herbal tea.

What treatment exists. Very little that is specific. Care is supportive: stop the exposure immediately, manage fluid and portal pressure, treat complications. Defibrotide is used for veno-occlusive disease after stem-cell transplantation but is not an established therapy for the plant-alkaloid form. Severe cases have required liver transplantation. Some patients recover if the exposure stops early enough. Others do not: the obliterated venules do not reopen, and the fibrosis is permanent.

This is not a rare disease worldwide. It is only rare where nobody eats these plants. In parts of China, large case series of hepatic sinusoidal obstruction syndrome have been traced to the traditional herb Tusanqi (Gynura species), and outbreaks affecting hundreds or thousands of people have followed contamination of grain with ragwort or heliotrope seed in Afghanistan, India, Ethiopia and Central Asia. The toxicology is the same. Comfrey is simply the version of this problem that appears in Western herb gardens.

The Documented Human Cases

These are published, peer-reviewed reports. They are worth reading as descriptions of real people rather than as citations.

• Gastroenterology, 1985. A 49-year-old woman developed veno-occlusive disease with portal hypertension and obliteration of the smaller hepatic venules; her liver biopsy showed centrilobular necrosis and congestion. Analysis of the food supplements she took regularly found pyrrolizidine alkaloids, and the major source was a powder purporting to contain ground comfrey root. The authors calculated that in the six months before admission she had consumed a minimum of 85 mg of pyrrolizidine alkaloids — about 15 micrograms per kilogram of body weight per day. Their conclusion was explicit: low-level, chronic exposure is sufficient to cause the disease.
• Journal of Gastroenterology and Hepatology, 1990. A 23-year-old man presented with hepatic veno-occlusive disease and severe portal hypertension and subsequently died of liver failure. Microscopy and hepatic angiography showed occlusion of the sublobular veins and small venous radicles with widespread haemorrhagic necrosis of hepatocytes. He had been on a predominantly vegetarian diet and had taken comfrey leaves before his illness. Other causes were excluded.
• American Journal of Medicine, 1989. A case of hepatic veno-occlusive disease attributed to comfrey herb tea — the single most commonly recommended internal preparation.
• British Medical Journal, 1987. Veno-occlusive disease of the liver secondary to ingestion of comfrey, reported from Bristol.
• The Lancet, 1981. An early note on comfrey and liver damage, published while comfrey tea was still being sold freely in health-food shops.
• Perspectives in Biology and Medicine, 1980. A broader account of pyrrolizidine poisoning from herbal teas in the United States, written when the problem was first being recognised.
• Gastroenterology, 1977. An Arizona case of veno-occlusive disease from Senecio tea — a different plant, the identical mechanism, and the report that put pyrrolizidine hepatotoxicity on the map for American clinicians.

You will sometimes see it argued that a handful of case reports is thin evidence. Consider what the alternative would be. Nobody will ever run a randomised trial in which volunteers drink comfrey tea for six months, because no ethics committee would approve it. What exists instead is: a clearly established mechanism, unambiguous animal toxicity and carcinogenicity, a well-characterised human disease with the same histology, case reports where other causes were excluded and the exposure was chemically confirmed, and large-scale human outbreaks from other plants containing the same class of compound. That is a coherent body of evidence, and five national regulators found it sufficient.

The Tea Problem

Tea deserves its own section, because it is the preparation people most often believe is gentle.

A study published in Public Health Nutrition in 2004 bought comfrey leaves from three commercial sources and prepared tea the way a consumer would, then measured the two alkaloids symphytine and echimidine by gas chromatography. Two findings stand out:

1. Alkaloid content varied considerably between vendors. You cannot know what is in a packet of comfrey leaf from the label, the price, or the brand. Growing conditions, plant age, harvest timing and species identity all move the number.
2. Much more symphytine was present than a standard analysis would show. When the researchers included a chemical reduction step to convert N-oxides back to the parent alkaloids, measured symphytine rose substantially. They confirmed that hot water alone does not create the N-oxides, so this was pre-existing alkaloid that ordinary analysis simply does not see.

Their conclusion, stated plainly in the paper, was that consumption of comfrey leaf tea may be ill-advised, and that alkaloid levels in such teas may be substantially underestimated unless N-oxides are accounted for.

The practical implication is important: a product tested by an older or cheaper method and reported as “low in pyrrolizidine alkaloids” may contain several times more than the certificate says. And because the gut converts N-oxides back to free alkaloid, that hidden fraction is fully available to poison you.

Root Versus Leaf, and Which Species

Three practical distinctions, all of which shift risk but none of which makes internal use safe.

• The root contains far more alkaloid than the leaf. This is consistent across analyses and it is why root products — powders, capsules of ground root, root tinctures — are the worst offenders. The fatal-outcome case involving ground comfrey root powder is the illustration.
• Young leaves generally contain more than mature leaves. The tender spring growth that a forager would pick for a “spring tonic” or fry in batter is not the safest part of the plant.
• Species matter. Symphytum officinale (common comfrey) and Symphytum × uplandicum (Russian comfrey, a hybrid of S. officinale and S. asperum) differ in alkaloid profile, and echimidine — among the more toxic members of the group — is characteristic of the Russian hybrid and has also been measured in commercial material sold as common comfrey. Since the two are hard to tell apart in a garden and are freely sold under either name, species identity is not something a consumer can rely on.

One genuine exception exists in the topical world and is worth naming precisely so it is not over-extended. The comfrey herb cream used in several clinical trials is made from a selected cultivar and process specified by its manufacturer as having alkaloid content below the limit of detection. That is a controlled pharmaceutical product with batch testing, sold for external use. It is not a licence to eat comfrey from a garden, and it is not sold for internal use either. Researchers have also explored reducing comfrey’s alkaloid content by silencing the biosynthetic enzyme homospermidine synthase, and by extracting with deep eutectic solvents — both interesting laboratory work, neither of which is in your kitchen.

DNA Damage and Cancer

Beyond the acute liver injury there is a second, slower concern.

The same reactive DHP metabolites that kill endothelial cells also bind DNA and cause mutations. In transgenic rodent studies, comfrey was mutagenic in liver tissue and produced the same profile of DHP-derived DNA adducts as riddelliine, a pyrrolizidine alkaloid that is an established rodent mutagen and carcinogen. Rats fed comfrey developed liver tumours. A 2010 review from the US Food and Drug Administration’s National Center for Toxicological Research concluded that the alkaloids in comfrey appear responsible for both its toxicity and its tumour induction.

Broader analyses of this compound class have raised the possibility that chronic low-level dietary exposure to pyrrolizidine alkaloids — from contaminated honey, herbal teas, grain and salad leaves — contributes to human liver cancer and to some cases of pulmonary hypertension and congenital abnormality. That wider claim is a hypothesis rather than a proven fact, and it is fair to say so. But it is the reason European food-safety bodies have worked to drive background pyrrolizidine exposure in the food supply down, and it makes a decision to add a concentrated dose deliberately look worse rather than better.

What Regulators Did, and When

Note the shape of these decisions. Not one of them banned the ointment. Every one of them targeted swallowing. Regulators are frequently accused of reflexive hostility to herbal medicine; here they did something more discriminating — they left an evidence-supported external use available and closed off the route that kills people.

The Arguments People Make For Eating It

Comfrey has a devoted following in permaculture, foraging and traditional-herbalism circles, and the same handful of arguments recur. They deserve direct answers rather than dismissal.

• “People ate it for two thousand years.” True, and people also drank from lead pipes and dosed themselves with mercury for centuries. Veno-occlusive disease presents as vague fatigue and abdominal swelling, has a long latency, and looks like ordinary liver disease. A traditional society had no way to connect a tea drunk over two years to a swollen abdomen and a death certificate saying “dropsy.” Absence of attribution is not absence of harm.
• “The dose used in the poisoning cases was enormous.” It was not. The best-documented case involved an estimated 15 micrograms per kilogram per day — a supplement dose, taken daily, over six months.
• “My comfrey is the low-alkaloid variety.” Unless you have a certificate of analysis from a laboratory that reduced the N-oxides before measuring, you do not know that. Vendor-to-vendor variation is large and species identification in a garden is unreliable. And the animal comparison of crude extract against purified alkaloids suggests the mixture is worse than its named components.
• “Cooking or fermenting destroys the toxins.” It does not. These are heat-stable, water-soluble compounds. Brewing extracts them.
• “It is fine in small amounts occasionally.” This is the only argument with any force, because risk genuinely is dose-dependent, and a single cup of comfrey tea is very unlikely to harm anyone. But the injury is cumulative and silent, there is no established safe threshold, and people who start with “occasionally” often do not stay there. The plant offers no internal benefit that cannot be obtained elsewhere, so the risk buys nothing.
• “Comfrey heals the gut lining — that is why you take it internally.” There is no human trial of oral comfrey for any gastrointestinal condition. The proposed mechanism is allantoin and mucilage. If you want soothing mucilage for the gut, marshmallow root and slippery elm provide it with no hepatotoxic fraction attached.

One more note for gardeners: comfrey is genuinely excellent as a compost activator, a mulch and a liquid plant feed, and none of that requires eating it. Growing comfrey is fine. Wear gloves when handling large quantities, wash your hands, and keep the leaves away from the kitchen.

Symptoms, and What to Do

If you have been taking comfrey internally — stop today. Not tapering, not finishing the packet. Stop.

Then tell a doctor, and say specifically that you have been taking comfrey and that pyrrolizidine alkaloids cause hepatic veno-occlusive disease. This is not something every clinician sees, and naming it helps. A reasonable initial workup is liver function tests (ALT, AST, ALP, GGT, bilirubin, albumin), a full blood count and platelet count, a coagulation screen, and an abdominal ultrasound with Doppler of the hepatic veins and portal vein.

Seek medical attention promptly if you have any of the following:

• Pain or a dragging ache under the right ribs
• Abdominal swelling, or clothes and belts suddenly feeling tight
• Unexplained weight gain over days to weeks (fluid, not fat)
• Yellowing of the skin or the whites of the eyes
• Dark urine or pale stools
• Persistent nausea, vomiting or loss of appetite
• Unusual fatigue, easy bruising, or bleeding

Go to an emergency department the same day for vomiting blood or passing black tarry stools (possible variceal bleeding), for confusion or drowsiness (possible encephalopathy), or for rapidly worsening jaundice.

Two reassurances that are honestly available. If your exposure was brief — a few cups of tea, once — the probability of harm is very low, and stopping is very likely all that is needed. And some people with early, recognised veno-occlusive disease do recover once the exposure ends. The decisive variable is how quickly the source is removed.

Does This Mean Topical Use Is Unsafe?

No — provided the rules are followed — and it is worth understanding why the same alkaloids are treated so differently by the two routes.

The answer comes from a direct measurement. When a crude alcoholic comfrey extract was applied to the skin of rats at a large dose, urinary excretion of alkaloid N-oxides over two days was 0.1 to 0.4 % of the applied dose. The same material given by mouth produced 20 to 50 times more. Intact skin is a genuinely effective barrier, and the alkaloids that do cross it mostly stay as N-oxides rather than being converted to the free, reactive form. Swallowing bypasses the barrier entirely and delivers the dose straight to the liver.

That is the entire safety case for topical comfrey, and it holds only under conditions:

1. Intact skin only. Broken skin removes the barrier that the whole argument rests on. No cuts, grazes, ulcers, weeping eczema, burns or mucous membranes.
2. Short courses. About 10 days of self-treatment under the European monograph for comfrey root preparations; German rules cap total external use at roughly four to six weeks per year. Absorption is small but it is not zero, and the injury is cumulative.
3. Limited area. Total exposure scales with treated surface. Do not spread it over large parts of the body.
4. No occlusion under a wrap or dressing unless the label directs it — occlusion raises absorption.
5. Never in pregnancy or breastfeeding, and not on children. Alkaloids cross the placenta and enter milk, and the developing liver is the target organ. Children have far more skin per kilogram of body weight, so the same smear is a bigger dose.
6. Not with liver disease or alongside hepatotoxic medication such as methotrexate, azathioprine, isoniazid or high-dose paracetamol.
7. Choose a product that states its alkaloid status — “PA-free,” “below the limit of detection,” or a stated maximum in micrograms.

Used that way, comfrey ointment is a reasonable, evidence-supported choice for a sprain or a sore knee. See Topical Use for Sprains and Bruises and Osteoarthritis and Back Pain.

Other Herbs With the Same Problem

Comfrey is not alone, and if you use herbal products it is worth recognising the family.

• Butterbur (Petasites hybridus) — genuinely useful for migraine prophylaxis, and genuinely alkaloid-bearing. Only PA-free standardized extracts should ever be taken internally, and raw butterbur must not be.
• Coltsfoot (Tussilago farfara) — a traditional cough herb; restricted in several countries for the same reason.
• Borage (Borago officinalis) — the leaf contains alkaloids. Borage seed oil is a different product and is generally certified alkaloid-free; check the label.
• Ragwort and groundsels (Senecio, Jacobaea) — the classic cause of livestock poisoning and of the Arizona human case.
• Tusanqi (Gynura species) — responsible for large numbers of documented hepatic sinusoidal obstruction cases in China.
• Heliotrope (Heliotropium) — implicated in mass poisoning outbreaks through contaminated grain.
• Contaminated products. Honey, herbal teas and even salad leaves can carry background pyrrolizidine alkaloids from weed contamination. This is why European food-safety authorities monitor it, and why deliberately adding a concentrated source is a poor idea.

The general rule: if a herbal product comes from the borage family or the ragwort tribe of the daisy family and is meant to be swallowed, look for an explicit pyrrolizidine-alkaloid-free certification, and do not assume it.

Key Research Papers

Every identifier below was checked live against NCBI E-utilities before it was written — title, first author, journal and year all had to match. Study type is labelled.

Human cases of comfrey and pyrrolizidine liver injury

1. Ridker PM, Ohkuma S, McDermott WV, Trey C, Huxtable RJ. Hepatic venocclusive disease associated with the consumption of pyrrolizidine-containing dietary supplements. Gastroenterology. 1985;88(4):1050–1054. — Human case. 49-year-old woman; minimum 85 mg of alkaloids over 6 months (15 µg/kg/day) from ground comfrey root powder.
2. Yeong ML, Swinburn B, Kennedy M, Nicholson G. Hepatic veno-occlusive disease associated with comfrey ingestion. Journal of Gastroenterology and Hepatology. 1990;5(2):211–214. — Human case, fatal. A 23-year-old man who died of liver failure after taking comfrey leaves.
3. Bach N, Thung SN, Schaffner F. Comfrey herb tea-induced hepatic veno-occlusive disease. American Journal of Medicine. 1989;87(1):97–99. — Human case. Tea alone was sufficient.
4. Weston CF, Cooper BT, Davies JD, Levine DF. Veno-occlusive disease of the liver secondary to ingestion of comfrey. British Medical Journal (Clinical Research Ed.). 1987;295(6591):183. — Human case.
5. Roitman JN. Comfrey and liver damage. The Lancet. 1981;1(8226):944. — Correspondence. An early warning.
6. Stillman AS, Huxtable R, Consroe P, Kohnen P, Smith S. Hepatic veno-occlusive disease due to pyrrolizidine (Senecio) poisoning in Arizona. Gastroenterology. 1977;73(2):349–352. — Human case. A different plant, the same mechanism.
7. Huxtable RJ. Herbal teas and toxins: novel aspects of pyrrolizidine poisoning in the United States. Perspectives in Biology and Medicine. 1980;24(1):1–14.
8. Douros A, Bronder E, Andersohn F, et al. Herb-induced liver injury in the Berlin Case-Control Surveillance Study. International Journal of Molecular Sciences. 2016;17(1):114. — Pharmacovigilance. Herbal liver injury in a systematic surveillance programme.

Mechanism, genotoxicity and carcinogenicity

1. Mei N, Guo L, Fu PP, Fuscoe JC, Luan Y, Chen T. Metabolism, genotoxicity, and carcinogenicity of comfrey. Journal of Toxicology and Environmental Health, Part B. 2010;13(7–8):509–526. — Review, US FDA. Lists the fourteen alkaloids; comfrey is mutagenic in liver and produces the same DHP-derived DNA adducts as the proven carcinogen riddelliine.
2. Fu PP, Xia Q, Lin G, Chou MW. Pyrrolizidine alkaloids — genotoxicity, metabolism enzymes, metabolic activation, and mechanisms. Drug Metabolism Reviews. 2004;36(1):1–55. — Review. The definitive account of the P450 activation step.
3. Mei N, Guo L, Zhang L, et al. Analysis of gene expression changes in relation to toxicity and tumorigenesis in the livers of Big Blue transgenic rats fed comfrey. BMC Bioinformatics. 2006;7(Suppl 2):S16. — Animal study.
4. Yeong ML, Clark SP, Waring JM, Wilson RD, Wakefield SJ. The effects of comfrey derived pyrrolizidine alkaloids on rat liver. Pathology. 1991;23(1):35–38. — Animal study. By the same group that reported the fatal human case.
5. Brown AW, Stegelmeier BL, Colegate SM, et al. The comparative toxicity of a reduced, crude comfrey (Symphytum officinale) alkaloid extract and the pure, comfrey-derived pyrrolizidine alkaloids, lycopsamine and intermedine, in chicks. Journal of Applied Toxicology. 2016;36(5):716–725. — Animal study, USDA. The crude extract was more toxic than the purified alkaloids; safety limits based on pure compounds may underestimate comfrey’s toxicity.
6. Edgar JA, Molyneux RJ, Colegate SM. Pyrrolizidine alkaloids: potential role in the etiology of cancers, pulmonary hypertension, congenital anomalies, and liver disease. Chemical Research in Toxicology. 2015;28(1):4–20. — Review. The broad chronic-exposure hypothesis; read it as hypothesis, not established fact.

Exposure, analysis and risk assessment

1. Oberlies NH, Kim NC, Brine DR, et al. Analysis of herbal teas made from the leaves of comfrey (Symphytum officinale): reduction of N-oxides results in order of magnitude increases in the measurable concentration of pyrrolizidine alkaloids. Public Health Nutrition. 2004;7(7):919–924. — Analytical. The tea study; content varied between vendors and standard analysis underestimates it.
2. Brauchli J, Lüthy J, Zweifel U, Schlatter C. Pyrrolizidine alkaloids from Symphytum officinale L. and their percutaneous absorption in rats. Experientia. 1982;38(9):1085–1087. — Animal study. Dermal dosing gave 0.1–0.4 % urinary excretion; oral dosing gave 20–50 times more. The measurement that justifies topical-only use.
3. Schrenk D, Gao L, Lin G, et al. Pyrrolizidine alkaloids in food and phytomedicine: occurrence, exposure, toxicity, mechanisms, and risk assessment. Food and Chemical Toxicology. 2020;136:111107. — Review. The current European risk-assessment picture.
4. Wiedenfeld H. Plants containing pyrrolizidine alkaloids: toxicity and problems. Food Additives & Contaminants Part A. 2011;28(3):282–292.
5. Edgar JA, Colegate SM, Boppré M, Molyneux RJ. Pyrrolizidine alkaloids in food: a spectrum of potential health consequences. Food Additives & Contaminants Part A. 2011;28(3):308–324.
6. Kim NC, Oberlies NH, Brine DR, et al. Isolation of symlandine from the roots of common comfrey (Symphytum officinale) using countercurrent chromatography. Journal of Natural Products. 2001;64(2):251–253. — Analytical.
7. Rode D. Comfrey toxicity revisited. Trends in Pharmacological Sciences. 2002;23(11):497–499. — Commentary. A useful summary of how the debate settled.
8. Kruse LH, Stegemann T, Jensen-Kroll J, et al. Reduction of pyrrolizidine alkaloid levels in comfrey (Symphytum officinale) hairy roots by RNAi silencing of homospermidine synthase. Planta Medica. 2019;85(14–15):1177–1186. — Laboratory. An attempt to breed the problem out; not a product you can buy.

Live PubMed Searches

1. Comfrey hepatotoxicity
2. Pyrrolizidine alkaloids and veno-occlusive disease
3. Herbal hepatic sinusoidal obstruction syndrome
4. Gynura (Tusanqi) liver injury
5. Alkaloid contamination of honey and herbal tea
6. Butterbur PA-free extracts
7. Herb-induced liver injury
8. Defibrotide for veno-occlusive disease

Connections

• All Herbs
• Comfrey Benefits — hub
• Comfrey — main topic page
• Topical Use for Sprains and Bruises
• Osteoarthritis and Back Pain
• Wound Healing and Allantoin
• Butterbur — the same alkaloids, handled properly
• Marshmallow Root — the safe internal mucilage herb
• Calendula — a topical herb with no hepatotoxic fraction
• Toxins — plant and environmental toxicity

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