by Paul Bergner
Medical Herbalism 03-31-97 9(1): 1, 11-14
The Eclectic physicians used echinacea clinically for about fifty years, and today we still possess an extensive record of their observations in their medical literature. In that literature, they make no mention of contraindications for its use. However, a German regulatory commission has recently suggested several contraindications, including “progressive systemic diseases like tuberculosis, leukosis, collagen disorders, or multiple sclerosis.” This class of diseases would include autoimmune conditions such as systemic lupus or rheumatoid arthritis. Rumors also abound in North American herbal circles that echinacea is contraindicated in AIDS. The commission also suggest limiting echinacea administration to no longer than eight weeks. These contraindications do not appear to be based on clinical facts.
Multiple sclerosis is suspected to have an autoimmune component in which the immune system attacks the sheath that encases the nerves. Leukosis is abnormal proliferation of the white blood cells or the tissues that produce them, and includes diseases like leukemia. The reasoning here is that if the disease is due to over activity or imbalance of the immune or collagen-making systems, then it does not make sense to stimulate them. The commission also lists contraindications for injectable forms of echinacea in diabetes or pregnancy. In this article, I’ll discuss the commission’s contraindications for tuberculosis, leukemia, AIDS, and is restriction on long term use. In the next issue of Medical Herbalism, I’ll discuss Echinacea and autoimmune diseases in detail.
Tuberculosis is not a simple infection. In complicated cases the patient’s own immune system destroys lung tissue in a process similar to autoimmunity, perhaps explaining the caution of the German commission. Tuberculosis is usually passed through coughing. Bits of bacteria, suspended in droplets of mucous, linger in the air, especially in crowded living conditions. When they are taken into the lung they are treated like any other invader — the macrophages in the lung engulf them. In some instances, tuberculosis may be stronger than the macrophages, and actually take up residence inside a macrophage, reproducing inside it, and turning it into a tuberculosis breeding factory. The macrophage bursts after a while, releasing newly born tuberculosis germs into the lung. More macrophages are attracted to the site to engulf these additional bacteria. The disease can stabilize at this point, with the macrophages winning the battle.
If the macrophages have attracted the
attention of a wandering T-cell from of the blood stream, however,
another course of action ensues. The T-cell finds the remains of
macrophage-eaten tuberculosis germs and secretes chemicals that attract
more macrophages to the site and stimulate the local macrophages to a
feeding frenzy. These activated macrophages cause scar tissue to form
around the area, walling it off from the rest of the body. They also
send fever-inducing chemical messages to the brain. At this point,
again, the immune system may win the battle and defeat the invading
If not, however, progressed tuberculosis become a nightmare. The T-cells eventually recognize that tuberculosis germs are “hiding out” inside the macrophages, and begin killing off the infected macrophages. This releases even more germs into the surrounding tissues where they now take up residence in the cells of the lung. The T-cells then begin destroying the infected lung tissue. This stage of the disease is called “liquefaction and cavitation” — portions of the lung are literally liquefied by the immune response to the infection, similar to the reaction that causes the body to reject organ transplants. At this point, most of the destruction is coming from the immune system rather than the tuberculosis infection, and it is a valid question whether to stimulate immunity or not.
However, clinical reports do not show a worsening of tuberculosis at any stage with echinacea treatment. If fact, echinacea seems to be an effective therapy, either along or as an adjunct to conventional treatments. Among the first published echinacea research was that of Dr. Victor Von Unruh of New York, who used echinacea to treat tuberculosis patients. He reported normalization of the body temperature, increase in phagocytosis, destruction of the tuberculosis germs, and shorter duration or else stabilization of the disease (Von Unruh 1915). German clinicians Heesen and Schroeder have also used echinacea as adjunct therapy in tuberculosis (Heesen and Schroeder 1960; Heesen 1964), and report that overall health and X-ray findings improved in a group of several hundred tuberculosis patients receiving echinacea, and especially among those with therapy-resistant progressive tuberculosis. The German commission’s decision to list a contraindication for echinacea in tuberculosis seems to overlook these clinical reports. They may have felt that the clinical reports did not carry the weight of well-designed clinical trial, or the decision may have been intended to protect the public from self-medication without proper supervision.
The German Commission’s
contraindication in leukemia and related diseases is likely based on
the ability of echinacea to cause a proliferation of the white blood
cells. Since these diseases are characterized by elevated white blood
cells, it seems prudent not to stimulate their growth. The immune
system is quite complex, however, with its own internal balancing
mechanisms. Echinacea acts on many areas of the system, not just on
white blood cells, and it only elevates white blood cell count for a
few days. David McLeod, naturopathic doctor, herbalist, and President
of the National Herbalist Association of Australia has reported a case
study of long term echinacea use in a patient with leukemia (McLeod
1996a). Leukemia is a cancer of the bone marrow. The majority of
patients who die do so from infections because of their weakened immune
system. McLeod treated a sixty-eight year-old leukemia patient for
eighteen months, using mainly herbal treatments. The patient took half
an ounce a day of each of two remedies, one a combination of
immunomodulating herbs, which was adjusted from time to time during the
course of treatment, and the other a strong tincture of Echinacea
angustifolia. An M.D. hematologist monitored blood status every three
months. At the beginning of treatment, with white blood cell count was
11.8, with the normal range being between 4.0 and 10.5. After six
months, the count was 13.2. By eighteen months, however, the white
blood cell count had fallen into the normal range, and has remained
there ever since (McLeod 1996b). The patient’s platelet count, another
measure of the progression of leukemia, also returned to the normal
range. I don’t suggest that echinacea “cured” the leukemia, because
many herbs were administered in the other formulas. But this patient
took about a half ounce of a strong echinacea preparation for more than
a year and a half, and it certainly had no adverse effect on his
A debate has gone back and forth in herbal circles for at least the last ten years in the U.S. about whether echinacea is contraindicated in HIV infection or AIDS. I’ve been unable to locate any published case reports where echinacea worsened the symptoms of AIDS, even though AIDS patients commonly take echinacea (Kassler et al 1991; Gowan et al 1993). Objections to the use of echinacea in AIDS have been theoretical, not based on empirical evidence.
T-4 cell levels
I was partly responsible for spreading the rumor that echinacea can lower T-4 cell counts, when I stated such a contraindication in an article in East-West magazine in August 1986. My reasoning was based on a just-published article showing that echinacea administration could lower T-4 cell counts, with T-8 cells remaining stable (Gaisbauer and Zimmerman, 1986). Since AIDS is characterized by a decline in T-4:T-8 cell ratios, it seemed reasonable to avoid echinacea. Further examination, however, shows that this trial was done with daily injections for seven days, rather than oral use. It’s is now well-known that frequently-repeated injections have this effect, although it has not been noted with oral use. In fact, one clinical trial showed a steady improvement in cell-mediated immunity over a period of ten weeks with oral echinacea administration (Coeugniet and Künast 1986). Another trial showed that oral echinacea was most effective at preventing infections in those with low T-4:T-8 ratios (Schöneberger 1992). There is no evidence of any need to avoid the oral use of echinacea to maintain T-4 cell levels.
Autoimmunity and AIDS
The second theoretical objection to
using echinacea in AIDS comes from the theory that AIDS has an
autoimmune component. In the 1990s the theory emerged among leading
AIDS researchers that the HIV virus initiated a series of events that
left parts of the immune system attacking itself. So the objection is
that immune stimulation by echinacea could hasten this autoimmune
attack. This autoimmune component of AIDS no longer plays a prominent
role in the theory of the dynamics of the disease. Current opinion is
that vital replication in massive amounts is countered by likewise
large formation of T-cells, until gradually, usually over years, the
virus wins the battle (Wei 1995). The declining number of T-cells
leaves the immune system fatally weakened. This theory is supported by
newer drug therapies which have led in the last two years to a decline
m AIDS deaths in the U.S. and France, and, if this theory is correct,
there is no theoretical reason to avoid echinacea on the basis of fears
of stimulating autoimmunity. It may remain prudent to monitor the
status of AIDS patients taking echinacea
The final objection is quite convoluted, but has become widespread in herbal circles in the U.S. in the last few years. It is based on research showing that echinacea polysaccharides increased the secretion of a substance called tumor-necrosis-factor-alpha in animals (Roesler et al 1991a,b). A rise in TNF-alpha has been associated with increased replication of HIV as well as wasting syndrome in the later stages of AIDS. The weakness of this argument lies in the form of “echinacea” that was used in the trial. It was not “echinacea” at all, but rather purified polysaccharides derived from Echinacea purpurea cells cultured in the laboratory. These were injected into mice. These polysaccharides, being insoluble in alcohol, are not present in most commercial products. If this trial says anything, it is that you should use caution before injecting concentrated echinacea polysaccharides if you have AIDS. Subsequent research has demonstrated that echinacea tincture, taken orally for four weeks, had no effect on tumor-necrosis-factor in humans (Elsasser-Beile et al 1996).
Finally, the clinical trial by Schöneberger I discussed in Chapter Six showed that echinacea, taken orally, benefited patients with lowered T4/T8 cell ratios — the same profile as the AIDS patient — the most. Of course this does not prove anything about contraindication, but it hints that, in the absence of any evidence for contraindication, echinacea might in fact be helpful for transient opportunistic infections in AIDS.
Is echinacea immunosuppressive over time?
Another controversy among North American herbalists is whether echinacea loses it potency after several weeks, or in fact becomes immunosuppressive if taken for too long, and is contraindicated for long term use. The official German regulatory commission for herbal medicines says that echinacea should not be taken for longer than eight weeks. As with the above contraindications, there seems to be no clinical evidence that oral doses of echinacea lose their ability to stimulate the immune system, or become immunosuppressive over time. in fact, clinical data shows the opposite. Separate clinical trials by Coeugniet and Schöneberger lasted ten and eight weeks, respectively. Each measured the immune parameters of the participants. The Coeugniet trial showed steadily increasing immunity between weeks two and ten. Schöneberger did not report on immunity, but measured it at the eight-week endpoint of the trial, and presumably would have noted any decline.
No evidence of immunosuppression has ever been found for oral doses of echinacea, but both Coeugniet and Jurcic found suggestions that echinacea injections, if repeated too frequently, may cause an initial depression of immune response. Coeugniet and Elek found, however, that even this depression was followed by a rise above the initial levels on discontinuation of the injections.
Herbal traditions and modern case
studies also contradict the idea that echinacea becomes
immunosuppressive over time. The Eclectics report using it daily for as
long as nine months with no ill effects (Ellingwood). In the leukemia
case by McLeod cited above. Half-ounce doses of echinacea for eighteen
months showed no ill effects. A German medical text by R.F. Weiss,
M.D., known as the “grandfather of phytotherapy” in Germany, who
probably used echinacea clinically for more than fifty years, says that
oral doses of echinacea: “should be continued for many weeks and even
months, if necessary, even for years. This is inevitable with many
chronic conditions where physical resistance has been reduced.” (Weiss
1988) Weiss also states that, even though the exact chemistry of its
action is not known, echinacea can be taken anyway because it
“certainly can do no harm.”
Bauer, R and Wagner, H. Echinacea: Handbuch für Ärzie, Apotheker, und andere Naturwissenschaftler. 1990. Stuttgart: Wissenschaftliche Verlagsgessellschaft, mbH.
Bergner P. Contraindications for echiancea? Medical Herbalism 1990;2(3):6
Couegniet E.G. and Kühnast. Therapiewoche 1986;36(33):3352-3358
Coeugniet E.G. and Elek E. “Immunomodulation with Viscum album and Echiancea purpurea extracts. Onkologie 1987;10(3):27-33
Elsasser-Beile, U., Willenbacher, W., Bartsch, H.H, Gallati, H., et al. Cytokine production in leukocyte cultures during therapy with Echinacea extract. J Clin Lab Anal 1996;10(6):441-5
Felter, H.W. The Eclectic Materia Medica, Phrmacology, and Therapeutics. Cincinnati, Ohio, 1922. Reprinted 1985. Portland, Oregon: Eclectic Medical Publications
Gaisbauer M. and Zimmerman W. Natura Med 1986;1:6-10
Gowen S.L., Erskine D., McAskill R., Hawkins D. An assessment of the usage of non-prescribed medication by HIV Int Conf AIDS. 1993 Jun 6-11;9(1):497 (abstract no. PO-B29-2174).
Heesen W. und Schroeder C. Die Bedeutung des Echiancin in der Tuberculöse-Therapie. Med Monatsschr 1960;14:251256
Heesen W. Unspecifische Behandlungsmöglichkeiten bei tuberkulöse Erkrankungen. Erfahrungsheilkunde 1964;13(5):209-217 [cited in Bauer and Wagner 1990]
Heesen W. und Schroeder C. Die Bedeutung des Echiancin in der Tuberculöse-Therapie. Med Monatsschr 1960;14:251256
Kassler W.J., Blanc P., Greenblatt R., The use of medicinal herbs by human immunodeficiency virus-infected patients. Arch Intern Med. 1991 Nov;151(11):2281-8.
McLeod, D. Case History of Chronic Lymphocytic Leukaemia, The Modern Phytotherapist 1996a;2(3):10
McLeod, D. Personal communication. December 1996b
Roesler J., Steinmuller C., Kiderlen A., Emmendorffer A., Wagner H., Lohmann-Matthes M.L. Application of purified polysaccharides from cell cultures of the plant Echinacea purpurea to mice mediates protection against systemic infections with Listeria monocytogenes and Candida albicans. Int J Immunopharmacol 1991 (a); 13(1):27-37
Roesler J., Emmendorffer A.,
Steinmuller C., Luettig B., Wagner H., Lohmann-Matthes M.L. Application
of purified polysaccharides from cell cultures of the plant Echinacea
purpurea to test subjects mediates activation of the phagocyte system.
Int J Immunopharmacol 1991 (b);13(7):931-41
Schöneberger D. The influence of immune-stimulating effects of pressed juice from Echinacea purpurea on the course and severity of colds. Results of a double-blind study. Forum Immunologie 1992;8:2-12 [German Language]
Von Unruh, V. Echiancea angustifolia and Inula helenium in the treatment of tuberculosis. Nat Eclect Med Assoc Quart. 1915;7:63
Wei X., Ghosh S.K., Taylor M.E., Johnson V.A., et al. Viral dynamics in human immunodeficiency virus type 1 infection Nature 1995 Jan 12;373(6510):117-22.