Cui Bono ?
The Comfrey Scandal
By Ivor Hughes

Cui Bono? The Comfrey Scandal

The Emperors New Set of Clothes, by Hans Christian Anderson is a charming European folk tale for children. It is a story about cupidity and stupidity

I have just written a new one; It is called  'Comfrey and Humphrey'.  Humphrey is the high ranking minister from the  British televison farce 'Yes Minister' whilst Comfrey is the pharmaceutically abused 'Symphytum officinale', who after thousands of years of service to mankind  was framed by the authorities on a trumped up charge, of  'Assault on the Liver'. 

The jury comprised of 12 Ph D,s appointed by Carnage, Killem and Slaughter International, (The worlds leading supplier of 'Ethicals') had gathered at the Atheaneum Club to be addressed by the Trial Judge Lord R.U.A. Bad Egg, KC VD and Scar (known affectionately by his friends as 'Roger the Dodger')

"Harrumph !" Bad Egg cleared his throat and  commenced, "Never in the field of human conflict" here he paused, realising that  he was playing the wrong tape. He began again, "Ok you herd of porkers, lift  your snouts from the trough ! I trust you have all received your thirty pieces  of silver" ? On assent, Bad Egg continued, "Tomorrow we will strike a telling  blow for Scientific, Academic and Corporate freedom, The First Armoured  Battalion 'The Royal Establishment' have surrounded the Old Bailey with a  bristling ring of steel, their orders are, to shoot to kill dissenters,  furthermore, England expects that every man will do his duty"

Bad Egg continued,  "I understand that the evidence is shonky, not that I can understand a word that you bunch of blithering idiots say, so I cannot say whether it is shonky or not. However we have all been well paid to ensure justice is done. The only acceptable verdict for the 1st Armoured  Battalion The Royal Establishment, is 'Guilty' Do you understand ?" As a man the  jury stood, and raising their arms in the Facist salute broke into a rousing  rendition of 'Red Star uber alles' swiftly followed by the 'Rockafella Rothschild Polka', and human decency danced in its grave. Bad Egg popped another antacid laxative combo and rinsed it down with a snifter of brandy, and muttered  "Blithering idiots".

As Comfrey was led away to the dungeons beneath the  Old Bailey he cried out "CUI BONO?" but it was drowned out in the hysterical applause from all the little Cui Bono,s who packed the well of the court  room.

The Scientific case against Comfrey appears to be based upon some very cleverly massaged quantative analysis. This original  hatchet job was quickly, and unquestioned, taken up by the establishment who unleashed a blizzard of similar studies that went around and round in circles,  each new study cited the one before it. This occurred because the pharmaceutical companies fed green backs to the pigeons. When looking at the available evidence we must understand that there are some very serious conflicts of interest at  work. There is an old saying "A man is known by the company he keeps". in other words guilty by association ! In the not to distant future this unholy alliance of the Pharmaceutical, Medical Establishment will be called to task. Thus all of  those men and women of integrity, scientists and doctors who have been ruined  and imprisoned because they dared to dissent will be vindicated. Then the honour of Science and Medicine will be restored.

The following is a montage of material taken from  the WHO site and other scientific sites on the Internet. I will not bore you  with the usual blah blah citations. I am sure you are all capable of doing your  own research in an honest manner

Comfrey is a member of the plant family  Boraginaceae. The major constituent of the comfrey plant is mucilage; other  constituents include allantoin, polyphenols, amino acids, phytosterols,  triterpenoids, saccharides, and pyrrolizidine alkaloids. The major unsaturated  pyrrolizidine alkaloids in comfrey are lycopsamine, intermedine,  7-acetyllycopsamine, 7-acetylintermedine, and symphytine. One kilogram of  comfrey contains 1.7-2.5 grams of symphytine.

9.0 TOXICOLOGICAL DATA
Summary: Although, there  was no evidence of liver damage in a group of people who had regularly consumed  comfrey, there are a number of case reports that implicate consumption of  comfrey in the development of liver toxicity, predominantly hepatic  veno-occlusive disease.

Unsaturated pyrrolizidine alkaloids are  metabolically activated to toxic compounds in the liver. In experimental animal  studies, pyrrolizidine alkaloids are almost completely excreted within 24 hours  following a single acute exposure. Sprague-Dawley rats treated orally by gavage  or dermally with reduced crude comfrey alkaloids or unreduced crude alkaloid  N-oxides of comfrey extract excreted a number of pyrrolizidine alkaloids in  urine collected over the first 24 hours; the urine of rats treated dermally with  the reduced alkaloid extract contained about 20 times less total alkaloids than  did urine from rats dosed by gavage.

No acute exposure data on comfrey were located. In mice, the intraperitoneal (i.p.) LD50 dose for symphytine is 300 mg/kg (0.786  mmol/kg); in rats the i.p. LD50 is 130 mg/kg (0.341 mmol/kg). Rats fed a 30%  comfrey diet for 21 days exhibited a decrease in body weight gain and an  increase in hepatic aminopyrine N-demethylase activity, but had no change in  hepatic glutathione S-transferase or epoxide hydrolase activities.

The incidence of hepatocellular adenoma was  increased in rats fed comfrey leaves in the diet daily for 480-600 days or  comfrey roots in the diet daily for 245 or 280 days, or until death. The  incidence of liver tumors were also increased, but not significantly, in rats  injected i.p. with symphytine once or twice per week for 56 weeks.

Comfrey did not induce X-linked recessive lethal  mutations in Drosophila melanogaster, and an acetone extract of comfrey was not  mutagenic in Salmonella typhimurium strains TA98 and TA100 with or without  metabolic activation. However, incubation of human lymphocytes with an extract  of comfrey induced an increase in sister chromatid exchanges in both the absence  and presence of metabolic activation. Symphytine induced gene mutations in S.  typhimurium strain TA100 with metabolic activation and in V79 Chinese hamster  cells (metabolic activation conditions not provided) and was positive for the  induction of wing spot mutations in D. melanogaster. Symphytine did not induce  morphological transformation in Syrian hamster embryo cells. Extracts of comfrey  suppressed the mutagenic activity of benzo[a]pyrene and heated extracts  suppressed the mutagenic activity of 3-amino-1,4-dimethyl-5H-pyrido [4,3-�] indole  in S. typhimurium (metabolic activation condition not provided), while a crude  comfrey extract suppressed the genotoxic activity of  N-methyl-N-nitro-N-nitrosoguanidine in Bacillus subtilis.

An ethanol extract of comfrey roots inhibited both  the classical and alternative pathways of complement in vitro. In another study,  a crude aqueous extract of comfrey root and 2 of its fractions inhibited the in  vitro proliferation of human peripheral blood lymphocytes stimulated with  phytohemagglutinin. The same crude aqueous comfrey extract and one of its  fractions enhanced the generation and release of O2- by unstimulated and  stimulated granulocytes and increased the total respiratory burst of the  unstimulated granulocytes, but had an inhibitory effect on the respiratory burst  of the stimulated granulocytes.

A crude aqueous extract of comfrey and 2 of its  fractions had no effect on the in vitro proliferation of Ehrlich tumor cells.  However, symphytine exhibited cytotoxic activity towards Ehrlich ascites  carcinoma cells in vitro. In mice inoculated i.p. with EL-4 or Ehrlich ascites  cells, proliferation of the tumor cells was stimulated by a crude aqueous  extract of comfrey and by one of its fractions, but was inhibited by another  fraction.

9.1 General Toxicology

9.1.1 Human Data

9.1.1.1 Clinical Studies    
There was no evidence  of liver damage in a group of 29 people who had regularly consumed comfrey  (Anderson and McLean, 1989, abstr.). 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). 

9.1.1.2 Case Reports
A number of case reports  implicate consumption of comfrey in the development of liver toxicity,  predominantly hepatic veno-occlusive disease.

Veno-occlusive disease was reported in a woman who  took 2 comfrey-pepsin tablets per meal for 2 months (Ridker et al., 1985; cited  by Huxtable et al., 1986), in a woman who took 6 comfrey-pepsin tablets containing 280 mg/kg total pyrrolizidine alkaloids for 6 months, and in a woman  who took 6 comfrey-pepsin tablets containing 988 mg/kg total pyrrolizidine  alkaloids for 6 months (Huxtable, 1987 abstr.). No other details were given. 

In New Zealand, a newspaper article described the  death of a young man from liver collapse following regular consumption of comfrey leaves (The Press, 1986; cited by Vollmer et al., 1987).

A 13-year-old boy previously diagnosed with Crohn's disease and treated first with prednisolone and sulphasalazine, and then with  comfrey tea and acupuncture, presented with hepatomegaly and ascites (Weston et  al., 1987). A liver biopsy revealed hepatic veno-occlusive disease. The  duration, quantity, and frequency of comfrey use were not reported. 

A 47-year-old woman with no history of blood  transfusion or alcohol use also developed hepatic veno-occlusive disease after a  number of years of comfrey consumption (Bach et al., 1989). The patient had  previously complained of vague abdominal pain, fatigue, and allergies to a  homeopathic doctor who recommended comfrey. The patient then began consuming as  many as 10 cups of comfrey tea per day and also took comfrey pills "by the  handful" for more than a year. Four years later, she had abnormally high  aminotransferase levels; 8 years later she had developed ascites. Liver biopsies  performed 9 and 10 years after the start of comfrey use revealed fibrosis and  proliferation of bile ductules.

A liver biopsy of a 49-year-old woman who had  consumed a "large amount" of comfrey tea (amount and duration not specified) was  consistent with hepatic veno-occlusive disease (McDermott and Ridker, 1990). A  follow-up 7 years later revealed that her symptoms had improved after  discontinuing the use of comfrey tea.

Serious liver and pulmonary disease was observed in  a 77-year-old woman who took herbal remedies containing comfrey and skullcap  (Scutelleria galericulata) for 6 months (Miskelly and Goodyear, 1992). The  patient's conditions returned to normal 4 months after use of the remedies were  discontinued.

A 30-year-old man experienced light-headedness,  agitation, confusion, difficulty in urinating, dry mouth, rapid heart beat, and  dilated pupils immediately after consuming several cups of comfrey tea (28 g in  boiling water) (Routledge and Spriggs, 1989). Twenty-four hours later his  symptoms had subsided. Based on previous analyses of other batches of comfrey,  the authors noted that the comfrey was possibly contaminated with  atropine.

9.1.2 Chemical Disposition, Metabolism, and  Toxicokinetics
Unsaturated pyrrolizidine alkaloids are metabolically  activated to toxic compounds in the liver by mixed function oxidases (Vollmer et  al., 1987). This process involves dehydrogenation of the pyrrolizidine to form  the corresponding pyrrole, a potent alkylating agent (Vollmer et al., 1987; WHO,  1988; McDermott and Ridker, 1990). In experimental animals, pyrrolizidine  alkaloids are almost completely excreted within 24 hours (method of  administration not provided) (WHO, 1988).

In a study conducted by Brauchli et al. (1982),  Sprague-Dawley rats were treated orally by gavage (single dose) or dermally  (44-hour contact time) with reduced crude comfrey alkaloids or unreduced crude  alkaloid N-oxides of comfrey. Rats treated orally or dermally with the reduced  alkaloid extract excreted 7-acetyllycopsamine, 7-acetylintermedine, lycopsamine,  intermedine, and retronecine in urine collected over the first 24 hours. The  urine of rats treated dermally with the reduced alkaloid extract contained about  20 times less total alkaloids than did urine from rats dosed by gavage. 

In the urine of rats treated with the alkaloid  N-oxide extract and collected over the second 24-hours, 7-acetylintermedine,  7-acetyllycopsamine, intermedine, lycopsamine, and the N-oxides intermedine and  lycopsamine were detected following oral but not dermal exposure. However, the  N-oxides of 7-acetylintermedine and 7-acetyllycopsamine were detected following  either oral or dermal treatment. In a chemical analysis of the comfrey used in  this study, 7-acetyllycopsamine, 7-acetylintermedine, lycopsamine, and  intermedine were detected. Only trace amounts of symphytine were  present.

9.1.3 Acute Exposure
Acute toxicity values for  comfrey were not available; acute toxicity values for symphytine are presented  in Table 1.

Table 1. Acute Toxicity Values for Symphytine

Route Species (sex and strain) LD50  Reference
i.p. mouse (sex and strain not provided) 300 mg/kg
(0.786  mmol/kg)
Culvenor et al. (1980)
- rat (male inbred ACI)  130 mg/kg
(0.341 mmol/kg)
Hirono et al. (1979a)

9.1.4 Short-Term and Subchronic Exposure
The short-term exposure  study described in this section is presented in Table 2; no information on  subchronic exposure was located.

Table 2. Short-Term Toxicity of Comfrey
Species Strain, Age  Number of Animals Chemical Form Dose&; Exposure/ Observation  Period Results/Comments Reference
rat (Long-Evans; age  n.p.) exposed: 6 M
controls: 6 M (basal diet); 6 M (basal diet with  30% alfalfa)
comfrey, harvested in prebloom vegetative state and  finely ground 5, 10, or 30% in diet 21 days; rats were killed at end  of treatment period. There was a significant decrease in weight gain in  rats fed 30% comfrey diet. Rats fed 10 or 30% comfrey or 30% alfalfa diet  exhibited an increase in hepatic aminopyrine N-demethylase activity, but had no  change in hepatic glutathione S-transferase or epoxide hydrolase activities, as  compared to rats fed a basal diet alone. (Garrett et al. 1982)

Abbreviations: M = males; n.p. = not provided

Male Long-Evans rats fed a 10 or 30% comfrey diet or a 30% alfalfa diet for  21 days exhibited an increase in hepatic aminopyrine N-demethylase activity, but  had no change in hepatic glutathione S-transferase or epoxide hydrolase  activities, as compared to rats fed the basal diet (Garrett
et al., 1982). Rats  fed a 30% comfrey diet exhibited a significant decrease in body weight gain, but  a 5 or 10% comfrey diet or a 30% alfalfa diet did not affect body weight gains.  There was no change in enzyme activities in
rats fed a 5% comfrey diet. The  comfrey used in this study was harvested in the prebloom vegetative state.

9.1.5 Chronic Exposure
Other than carcinogenicity studies (see Section  9.3), no chronic exposure studies on comfrey and symphytine were located.

9.2 Teratogenicity and Embryotoxicity
No data was found.

9.3 Carcinogenicity
The studies described in this section are presented  in Table 3.

9.3.1 Oral Administration
Inbred male and female ACI rats were fed comfrey leaves in the diet for 480-600 days or comfrey roots in the diet for 245  or 280 days, or until death (Hirono et al., 1978). Comfrey leaves were administered as 8, 16, or 33% of the diet. Comfrey roots were administered according to one of the following 5 schedules: 8% diet; 4% diet (185 days), 2%  diet (30 days), then 1% diet; 4% diet (180 days), 0.5% (65 days), then basal diet; 2% (190 days), 0.5% (90 days), then basal diet; or 1% diet (275 days),  then alternating 0.5% diet and basal diet at 3-wk intervals. A control group was  fed the basal diet alone. There was a dose-response increase in the incidence of  liver tumors among rats fed comfrey leaves for 600 days; this relationship was only suggestive in rats fed comfrey roots. The investigators noted that the incidence of urinary bladder tumors in rats fed comfrey leaves was too small to draw any conclusion, while the incidence in rats fed comfrey roots was not  significant. A very small number of tumors were detected in other organs, but  these were concluded to be spontaneously occurring.                       

9.3.2 Intraperitoneal Injection
Liver tumors were detected in 4/20  male inbred ACI rats injected i.p. with symphytine (13 mg/kg [0.034 mmol/kg])  twice per week for 4 weeks and then once per week for 52 weeks while no liver  tumors were detected in a control group of 20 rats similarly administered 0.9%  sodium chloride solution (Hirono et al., 1979a). The rats were observed for up  to 650 days after the first injection. While suggestive, the increase in liver tumors was not statistically significant. Rats treated with symphytine also had  megalocytosis and proliferation of oval cells and endothelium of the sinusoids  (incidences not given). It was not specified whether other organs were  examined.

9.4 Genotoxicity
The studies described in this section are presented in  Table 4.

9.4.1 Prokaryotic Systems
An acetone extract of comfrey (0.1 mL extract  per 0.1 mL culture; extract not characterized) did not induce his gene mutations  in S. typhimurium strain TA98 or TA100 with or without S9 metabolic activation  (White et al., 1983).  Symphytine (doses not given) induced his gene mutations in S. typhimurium  strain TA100 in the presence but not the absence of S9, and was negative in  strain TA98 with or without S9 (Hirono et al., 1979b).

9.4.2 Lower Eukaryotic Systems
Comfrey did not induce X-linked recessive  lethal mutations in D. melanogaster (Canton-S wild type, Basc stock) (Clark,  1982). Dried chopped comfrey leaves were administered by cooking them in the  food medium on which larvae were reared or by allowing adult males to feed on  Kleenex tissue soaked in 10% aqueous sucrose solution containing comfrey (doses  not provided).

Symphytine induced a significant increase in wing spots, indicative of  somatic mutations or recombination, in D. melanogaster (cell marker heterozygous  mwh flr+/mhw+ flr ) when administered to larva in food at a dose of 0.1 or 0.25  mM, but not at 0.05 mM (Frei et al., 1992).

9.4.3In Vitro Mammalian Systems
Incubation of human lymphocytes with  1.4, 14, 140, or 1400 g/mL of a crude extract of comfrey increased the frequency  of sister chromatid exchanges (SCE) at the two highest doses in the absence and  presence of S9 (Behninger et al., 1989). The extract contained 19% lycopsamine,  13% intermedine, 19% acetyllycopsamine, 20% acetylintermedine, and 4%  symphytine; the remainder was comprised of unidentified alkaloids.

Symphytine (doses not given) induced mutations at the hypoxanthine  phosphoribosyl transferase (HPRT) locus in V79 Chinese hamster cells, but did  not induce morphological transformation in Syrian hamster embryo cells (Hirono  et al., 1979b).

9.5 Antimutagenicity
The studies described in this section are  presented in Table 5.

Crude comfrey extract (nature of extract not specified) suppressed  approximately 43% and 52% of benzo[a]pyrene-induced his gene mutations in S.  typhimurium strains TA98 and TA100, respectively (Ham et al., 1992, abstr.).  When heated, the comfrey extract suppressed approximately 75% and 76% of 3-amino-1,4-dimethyl-5H-pyrido[4,3-�]indole-induced mutations in strains TA98  and TA100, respectively (Ham et al., 1992, abstr.). No other experimental  details were given.

In B. subtilis H17 (rec+) and M45 (rec-), it was reported that a crude comfrey extract (40 L/disc) "showed strong antimutagenic effects" against  N-methyl-N'-nitro-N-nitrosoguanidine-induced genotoxicity (Ham et al., 1992, abstr.). The spore rec-assay was used [this assay measures differential killing  as a result of DNA repair or damage and is not a measure of mutagenicity]. No  other experimental details were given.

9.6 Immunotoxicity
The studies described in this section are presented  in Table 6.

In a study conducted by van den Dungen et al. (1991), an ethanol extract of  comfrey roots strongly inhibited both the classical and alternative pathways of  complement in vitro. The extract was shown to contain amino acids and sugars,  but was not further characterized.

Olinescu et al. (1993) concluded that a crude aqueous extract of comfrey  root and 2 of its fractions extracted with (NH4)2SO4 strongly inhibited the in  vitro proliferation of human peripheral blood lymphocytes stimulated with  phytohemagglutinin (PHA). One of the comfrey fractions (fraction V) was rich in  carbohydrates and contained no detectable proteins, whereas the other fraction  (fraction VI) contained mucus, carbohydrates, and proteins. The crude extract  was not characterized. Doses were as follows: 1 mg/mL (extract); 100 L (fraction  V); 1 mg/mL (fraction VI). The blood lymphocytes in this first experiment were  obtained from healthy human volunteers. In another experiment, when the blood  lymphocytes were obtained from volunteers with chronic staphylococcal infections  or rheumatoid polyarthritis, or with solid tumors, the inhibition of  proliferation was more moderate (staphylococcal infections or rheumatoid  polyarthritis) or did not occur at all (solid tumors).

Olinescu et al. (1993) also evaluated the effect of the comfrey extract and  fractions described above on the respiratory burst of human granulocytes. The  granulocytes were either unstimulated or stimulated with opsonized-zymosan  particles via Fc receptors. The crude comfrey extract (100 g) and fraction VI  (100 g) enhanced the generation and release of O2- by the unstimulated and  stimulated granulocytes, whereas fraction V (100 L) had virtually no effect. The  crude extract and fraction VI also increased the total respiratory burst of the  unstimulated granulocytes, but had an inhibitory effect on the respiratory burst  of the stimulated granulocytes. Fraction V inhibited the total respiratory burst  of both unstimulated and stimulated granulocytes.

Radu et al. (1994) reported that a 5% solution of an aqueous extract of  comfrey root (chemical composition not provided) enhanced the generation and  release of oxygen free radicals by unstimulated granulocytes isolated from the  heparinized venous blood of healthy volunteers. When the granulocytes were stimulated either with opsonized-zymosan or Concanavalin A, however, the comfrey extract inhibited oxygen free radical production. It was noted that neither the stimulatory nor inhibitory effect of the extract on oxygen free radical  production was due to the presence of enzymes such as superoxide dismutase,  catalase, or xantinoxidase, because the effects were present even after heating  of the reaction mixture.

9.7 Other Data
A crude aqueous extract of comfrey and 2 fractions  extracted with (NH4)2SO4 had no effect on the proliferation of Ehrlich tumor  cells in vitro when treated for 24, 48, or 72 hours (Olinescu et al., 1993). One  of the fractions was rich in carbohydrates and contained no detectable proteins,  whereas the other fraction contained mucus, carbohydrates, and proteins. The  crude extract was not characterized.

Wassel et al. (1987) reported that symphytine was cytotoxic to Ehrlich  ascites carcinoma cells in vitro. No other experimental details were given. 

In female A2G mice inoculated i.p. with EL-4 or Ehrlich ascites cells,  proliferation of the tumor cells was stimulated by a crude aqueous extract of  comfrey and by one of its fractions (fraction VI) extracted with (NH4)2SO4, but  was inhibited by another (NH4)2SO4-extracted fraction (fraction V) (Olinescu et  al., 1993). Fraction V was rich in carbohydrates and contained no detectable  proteins, whereas fraction VI contained mucus, carbohydrates, and proteins. The  crude extract was not characterized. The comfrey extract and fractions were  administered i.p. concurrently with the tumor cells. The mice were killed 7 or  10 days after inoculation. Ascites fluid and cells from the peritoneal cavity  were removed and the volume of tumor cells was determined.

Exposure to comfrey occurs orally, via ingestion of teas or capsules, or  dermally via the application of comfrey-containing poultices or cosmetics. The  concern over the health effects of comfrey is based on the presence of toxic  pyrrolizidine alkaloids as constituents (D'Arcy, 1991). Oral exposure to comfrey  has been associated with toxic effects in the liver, while dermal exposure is  believed to pose little or no hepatotoxicity because of limited absorption  (Awang, 1987) (see Section 9.1.2).

Huxtable et al. (1986) estimated that a person who consumes two comfrey-pepsin capsules per meal for 6 months would ingest a total of 162 mg  pyrrolizidine alkaloids from a preparation made from comfrey leaves and 1740 mg  alkaloids from a preparation made from comfrey roots. Bach et al. (1989)  reported that comfrey-pepsin capsules may contain as much as 2.9 mg total  pyrrolizidines per gram.

Roitman (1981) detected 8.5 mg total pyrrolizidine alkaloids in one cup of  comfrey root tea with the gelatinous residue removed. Inclusion of the residue  resulted in a total pyrrolizidine alkaloid content of 26 mg/cup. Bach et al.  (1989) reported that comfrey root tea contains as much as 26 mg total  pyrrolizidine alkaloids per cup. Corrigan (1987), however, reported that some  commercial comfrey products (not specified) contained no detectable pyrrolzidine  alkaloids.

There are no reports of intentional consumption of symphytine, but the  compound is a component of a number of herbs. Ames et al. (1988) estimated that a person who consumes 1 cup of comfrey herb tea is exposed to 38 g  symphytine.

Now anyone who cares to root around in that heap will find there are some serious anomalies. However it was all received with breathless reverence as  though it came down from the mount engraved on tablets of stone.

I will give you a clue .... 1Kg of dried Comfrey root approximates 3 Kg of  fresh. 1 Kg of Comfrey leaves approximates 4 Kg of fresh. One cup of Comfrey herb tea approximates (Dry leaf 1.5 g) of Symphytine, 38 �g..

In addition these Scientists had been using the isolated alkaloids freed  from the parent material, this is dishonest. It is dishonest, because the  isolated alkaloids behave in a very different fashion to the same alkaloids  within its parent body. I refer of course to the synergistic effect.

Now given the shonky science that has surrounded the 'Comfrey Scandal' the  very first question that should be asked is 'Cui Bono'? (Who profits)  Forget  about all of the tiresome bleatings, about the safety and efficacy of crude  herbal drugs, because that is not what it is all about.

What it is all about, is who controls the market. ? Cui Bono, who profits ?  Well one thing is for sure, if the WHO is successful it will not be the indigenous peoples. Once again they will have been robbed and the last resort of health care taken from them. They cannot afford the pharmaceutical companies offerings. Neither will they be able to afford the herbs which was once their  heritage. 

To sin by silence, when they should protest makes cowards out of  men.
Abraham Lincoln

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