Ever since undergoing my training as
a medical herbalist, I have maintained a particular interest in
the cause and treatment of autoimmune disease. The term "autoimmune"
is applied to a very wide spectrum of human disease, sometimes tentatively.
However, many of these diseases do tend to share common factors
in their pathophysiology. But we can confidently state that autoimmune
disease does not arise from a single cause. In fact, it is quite
possible that the same autoimmune disease will have different causes
from person to person. The current approach in medical science is
not very comfortable with such an idea. However traditionally based
systems of medicine such as phytotherapy place great emphasis on
the treatment of the individual.
In order to better treat autoimmune disease, it is necessary to
have an understanding of its causes. This in turn would lead to
a systematic approach to defining the key causative and sustaining
factors operating in each case. For each individual, it is likely
that the autoimmune process has been precipitated by a unique and
complex interaction of causative events. What we therefore need
is a multi-factorial model that allows us to individualize treatments,
yet at the same time takes into account the most likely factors
operating in each particular disease. This requires a blend of traditional
understanding with the latest research findings. Such a synthesis
is the goal of the modern phytotherapist.
– Is it Looking In The Wrong Direction?
Much of the current research into autoimmune disease is centered
on two main areas:
a) the development of immune tolerance
b) the search for a pre-established defect in either immune cells
or immune function that gives rise to autoimmunity.
Particularly with regard to the first
area of research, I wonder if the wrong question is being asked.
Rather than looking at how self-tolerance develops in a human being,
perhaps the question should be, "How does loss of immune tolerance
to self arise?" Scientists are very interested to learn how
the embryo acquires self tolerance. But how relevant is this to
a previously well 50-year-old who suddenly develops an autoimmune
disease? In fact, self recognition by the immune system is part
of its normal function. It is not appropriate to go into detail
here but phenomena such as clonal anergy, idiotypic networks, and
MHC antigens are all examples of the immune system recognizing self
tissue. But it does this in a regulated non-destructive way. We
need to understand the circumstances that cause the capacity for
self recognition to become destructive.
Is there a pre-established defect in the immune system that causes
autoimmune disease? Do some people have a biological time bomb pre-programmed
to explode into tissue destruction at some point in their lives?
We do not know for certain, but other scenarios are also possible.
Consider the immune system as a computer. It has input and output.
The former is antigenic material, and the latter is the immune response.
It has hardware in the form of the white blood cells, and the software
is the way these cells interact. The bias of current scientific
investigations into autoimmunity is that there is some defect in
the hardware or software that is awaiting discovery. But anyone
who has worked with computers knows the old saying – garbage
in equals garbage out. Using this analogy, we can see that it is
possible that the inappropriate response of the immune system, which
is autoimmunity, may be due to aberrant input.
A New Theory of
In 1986, two American scientists, Fred Westall and Robert Root-Bernstein
published a paper in the Lancet
entitled "Cause and Prevention of Postinfectious and Postvaccinal
Neuropathies in Light of a New Theory of Autoimmunity."1
The authors were most interested in the incidence of postinfectious
neuropathies, such as Guillain-Barré syndrome, and postvaccinal
neuropathies, such as the potential reaction to measles vaccination.
But they also linked this interest to a new theory about the development
of autoimmunity in general. As far as I know, this paper did not
cause much lasting interest in scientific circles, but their theory
provides the basis for a practical multifactorial model for the
treatment of autoimmune disease.
The basic rationale for their theory comes from experimental animal
models of autoimmunity. Take, for example, experimental allergic
encephalomyelitis (EAE), an autoimmune disease of the brain. If
myelin basic protein (a brain protein) is injected into an animal,
it does not cause EAE, no matter how often it is injected. The development
of EAE only occurs when the myelin basic protein is injected together
with Freund's complete adjuvant. Freund's complete adjuvant is a
water in oil emulsion containing antigen in the aqueous phase, in
this case myelin basic protein, and dead tuberculosis bacteria in
the oil phase.
Extending this model to humans, the basic hypothesis is that three
requirements must be met to induce autoimmune disease:
1) There must be an antigen present
which is the same as or similar to some fragment of self tissue.
We can call this the primary lesion.
2) There must be a second antigen which is chemically complementary
to the first antigen (for EAE, this is the tuberculosis bacteria).
3) Both antigens must be present and immunologically active in
the host at the same time.
I would like to extend this theory by
examining the role of the second complementary antigen. The presence
of this antigen probably confuses the immune system and causes an
inappropriate response to the first antigen. Once this process is
triggered, it becomes self-sustaining due to the inflammation and
tissue damage that occurs. (This aspect is known as the "Hit
and Run Hypothesis" of autoimmunity.) This tendency for the
immune system to respond inappropriately can be called a state of
immune dysregulation. The immune system is confused, but this need
not always be due to a complementary antigen. It is possible that
other inputs can cause a state of immune confusion.
The obvious implication of the above model is that we need to find
and eradicate the causes of the primary lesion and the immune dysregulation.
What may not be as obvious is that the autoimmune disease may still
continue for a considerable time after these causes have been treated,
since to some extent, the process can become self-sustaining. Therefore
control of sustaining causes should also be sought, and this may
involve symptomatic treatment and even the judicious use of natural
agents that depress immunity.
The Primary Lesion
The primary lesion might often be created by the presence of a micro-organism
(Table 1).2 This need not necessarily be a clinical infection, but
for the sake of brevity I will use this term. How can an infection
create the primary lesion? Micro-organisms contain or produce proteins,
which are antigenic; that is, the immune system is capable of recognizing
parts of these proteins as foreign and mounting a reaction against
them. One protein might provide many antigenic regions known as
epitopes, and each micro-organism might have many antigenic proteins.
It is now known that some of these foreign epitopes exactly resemble
human epitopes. This phenomenon has been described as "molecular
mimicry."2 Originally, the term molecular mimicry was coined
to describe the way that a micro-organism might escape detection
from the immune system. It was felt that proteins from micro-organisms
evolved to be antigenically similar to their hosts in order to escape
immune detection and thereby enhance survival. Molecular mimicry
certainly occurs more often than could be attributed to chance.
(The probability that a random six amino acid sequence will be identical
in two proteins is one in 20 million.)
Table 1: Factors
That May Provide The Primary Lesion
Chronic Tissue Destruction
It is now recognized that molecular
mimicry may be an important factor in the etiology of autoimmune
disease.2 An immune reaction directed against the micro-organism
cross-reacts with a similar self antigen. The evidence for molecular
mimicry is summarized in Table 2. Many examples of the points listed
in the table are documented in the literature.2
Table 2: Evidence
For Molecular Mimicry
Amino acid sequence similarities between
microbial and human proteins
Antibodies to viruses cross-react with uninfected host cells
Animal models of autoimmunity often involve viral infection
Post-infectious auto-antibody production is a common phenomenon
Some examples of the amino acid sequence
similarities between microbial and human proteins are provided in
Table 3.3 The similarity between a Klebsiella protein and HLA B27,
and its implications for autoimmune disease, are supported by other
research. The incidence of ankylosing spondylitis (AS) shows a high
correlation with HLA B27. More than 90% of patients with AS are
HLA B27-positive. Research has demonstrated that a substantial proportion
of patients with AS have antibodies in their blood that react to
the epitope shared by HLA B27 and Klebsiella pneumoniae nitrogenase.4
There was no reaction from antibodies in control subjects. Moreover
antibodies to Klebsiella, but not to other bacteria, have been shown
to be present in patients with active AS by seven different techniques.5
In this context, HLA B27 may be the self antigen that is the site
of the cross-reactivity. The particular sites of inflammation in
AS are also the tissues, which can express a relatively higher concentration
of HLA B27 as a surface antigen.
Table 3: Sequence
Similarities between Microbial Proteins and Human Host Proteins.3
Immunological cross-reactivity between
the indicated pairs of proteins has been demonstrated in all but
the last two cases.
Papilloma virus E2
Rabies virus glycoprotein
Klebsiella pneumoniae nitrogenase
Measles virus P3
Measles virus P3
|Human Host Protein
Human IgG constant region
Myelin basic protein
Dr. Alan Ebringer of King's College Hospital,
London, decided to test this association clinically. Patients with
AS were placed on a low starch and sugar diet, because it was postulated
that this would reduce the number of Klebsiella in the gut.6 Most
patients on this program had their disease process halted, but the
diet must be adhered to for at least six months.
Micro-organisms might provide the primary lesion in other ways.
For example, haptenization may occur, where a fragment from the
infecting agent may bind to a larger endogenous protein. This protein-hapten
complex becomes antigenic, and an immune reaction may be directed
against part of the protein and hence is a reaction to self.2 Drugs
can also produce autoimmune reactions in this way.
"Altered self" is another theory of autoimmunity involving
micro-organisms.2 An infecting agent, particularly a virus, may
cause self tissue to change. The virus harnesses the host cell to
make self-like proteins that are sufficiently close to self to create
cross-reactivities, but different enough to enable strong immune
recognition and attack.
Organisms that can provide the primary lesion include bacteria,
viruses, protozoa, or fungi. The bacteria can be endogenous, that
is they may be present in the gut flora or on the skin or mucous
membranes. Although they may be endogenous, their presence could
still be abnormal. Infestation could also provide the primary lesion.
When I was studying in England, I met a herbalist who claimed good
results in the treatment of juvenile arthritis, an autoimmune disease.
His approach was to treat the child for worms. That was his particular
insight into the problem, which is consistent with the proposed
Why is there not clear evidence for the role of micro-organisms
in most autoimmune diseases? There are many aspects to this problem.
Perhaps the best answer is that micro-organisms have been implicated
in many autoimmune diseases, but the results have not been consistent.
However, this meshes well with the multifactorial model. Autoimmune
disease is not an infection per se, but it may be a response to
an infection under particular circumstances. As such, it would be
unreasonable to expect a single infectious agent to be implicated
in any given autoimmune disease. Furthermore, if the micro-organisms
involved are present at low levels or exist in unusual forms such
as cell wall-deficient variants, they may be very difficult to detect.
Some endogenous microflora that might be involved in autoimmune
disease could also present in healthy subjects. Consequently, it
would be difficult to define their significance in someone who was
Some additional examples of the association of infection with the
autoimmune destruction of tissue are described below. This is not
a comprehensive review of this topic. Guillain-Barré syndrome
is viewed as a reactive, self-limited, autoimmune disease triggered
by a preceding bacterial or viral infection. Campylobacter jejuni,
a major cause of bacterial gastroenteritis, is the most frequent
antecedent pathogen.7 The syndrome has also been linked to influenza
vaccination in isolated instances.8
Patients with rheumatoid arthritis placed on a vegetarian diet for
one year had a significant reduction in anti-Proteus mirabilis antibody
levels, which was correlated with decreased disease activity.9 Patients
with autoimmune thrombocytopenia (low platelet count) who also were
positive for Helicobacter pylori experienced a significant increase
in platelet count when the bacterium was eradicated from their stomachs.10
Eighty-nine percent of patients with untreated celiac disease were
positive for the presence of human adenovirus serotype12, an adenovirus
isolated from the human intestinal tract, whereas the incidence
in controls was 0 to 12.8%.11 Amino acid sequence homology (and
potential for molecular mimicry) was noted between a protein in
gluten and this virus. Infection with Coxsackie B viruses has been
linked to the development of insulin-dependent diabetes mellitus
in children.12 Other viruses have been linked to this disorder.12
A case was reported of a woman who developed ulcerative colitis
during primary cytomegalovirus infection. She subsequently developed
chronic recurrent disease.13 Retroviruses have been implicated in
the development of various autoimmune diseases. For example, retroviral
antibodies were detected in patients with primary biliary cirrhosis
and other biliary disorders of unknown cause.14
Chronic tissue destruction can also potentially provide the primary
lesion. This tissue damage may be due to an infection or may have
other causes such as a tumor or toxins. The destruction creates
facilitatory signals to the immune system. Local macrophages are
induced to attack anything in the region thereby creating a snowball
effect. This is known as the "bystander theory" since
the macrophages are actually bystanders and are not involved in
the initiation process.2
The multiplicity and the diversity of pathogenic auto-antibodies
found in patients with systemic lupus erythematosus (SLE) has fascinated
immunologists for decades. Surface blebs on apoptotic cells (cells
partaking in programmed self destruction) now appear to provide
antigenic material, together with the nuclear material released
from apoptotic cells.15 It has thereby been suggested that the first
event in lupus is an increased tendency towards apoptosis of certain
cell populations, possibly lymphoid cells. What in turn causes this
is an important question, but a high antioxidant status may hinder
this process. Low antioxidant status has certainly been identified
as a risk factor for lupus.16
As well as the primary lesion, the model also requires a state of
immune system dysregulation (Table 4). Concurrent infection may
cause immune dysregulation via several possible pathways. It may
provide a complementary antigen as in animal models of autoimmunity.
A state of endotoxinemia could result from some bacterial infection
or from abnormal bowel flora combined with a leaky gut wall. Endotoxin
is a potent general stimulator of the immune system. Many infecting
agents, particularly viruses, can create a state of generalized
activity of B lymphocytes known as polyclonal activation.2
Table 4: Factors
That May Cause Immune System Dysregulation
Infection or Infestation
Allergy or Chemical Sensitivity
Injury or Foreign Body
Other mechanisms are also possible.
Viral infection may create abnormal expression of immunoregulatory
molecules, such as the MHC antigens, on the surface of somatic cells
(that is, cells that are not part of the immune system). This then
causes these cells to be attacked and destroyed by the immune system
even though they may not actually be infected with the virus.2
Allergy and chemical sensitivity have the potential to cause immune
dysregulation. There is a university in the UK where the medical
treatment of multiple sclerosis includes the removal of amalgam
fillings from patients. Allergy to the mercury in the fillings could
create a state of immune imbalance. A direct toxic effect from the
mercury could also be significant. Hair dyes have been implicated
in autoimmune disease in women, and this could be another example
of chemical sensitivity causing a state of immune dysregulation.
This association has been recently questioned.17
Diet may be a factor. It is often observed that patients with Crohn's
disease respond well to an elemental diet.18 This diet is free of
antigens. Similarly there are anecdotal accounts of amelioration
of multiple sclerosis after following a gluten-free diet. Antigens
in the diet could therefore create a state of immune dysregulation.
Consumption of cow’s milk by infants has been linked to insulin-dependent
diabetes,19 and a dairy-free diet effected a substantial improvement
in more than half of a group of patients with ankylosing spondylitis.20
Injury or foreign bodies may be a factor. Cases of SLE due to breast
implants were documented in the literature. When the implants were
removed (they were not leaking), the SLE was cured. However, this
association has been questioned in recent studies.21 In another
example, a rose thorn was not effectively removed after injury,
and the person developed rheumatoid arthritis.22 Miners with silicosis
also suffer a higher incidence of systemic sclerosis compared to
the general population.
Stress could create immune dysregulation. Many autoimmune diseases
are precipitated during periods of extreme stress.2 The best documented
examples are for insulin-dependent diabetes.
Cancer increases the likelihood of developing autoimmune disease.
It is possible that the mechanisms employed by the tumor to escape
immune detection create a state of immune dysregulation.2
Some additional factors may contribute to the development of autoimmunity
and need to be considered. Although these factors cannot be included
under the above headings, they may facilitate the processes involved
in the proposed model. As such they can be classified as auxiliary
Table 5: Possible
Auxiliary Factors in Autoimmunity
Intestinal Wall Hyperpermeability
Reduced Hepatic Integrity
Reduced Phagocytic Capacity
Reduced Proteolytic Activity
Intestinal wall hyperpermeability, or
a leaky gut, increases the antigen and endotoxin load in the body.
Blood from the digestive tract is screened by the phagocytic Kupffer
cells in the liver. Kupffer cells have the special property of sequestering
engulfed material. That is, they do not readily present such material
to helper T cells in order to enlist an immune reaction. As such,
they have a dampening effect on the reactivity of the immune system.
If phagocytic activity is generally reduced due to poor health,
or the liver is damaged and the activity of the Kupffer cells is
thereby compromised, then the risk for antigen or endotoxin spillover
into the general circulation is substantially increased.
Poor proteolytic capacity may also be an auxiliary factor in the
development of autoimmunity. To understand the significance of this,
we need to consider the theories of Pierre Grabar, who was a respected
immunologist at the famous Pasteur Institute.23 Grabar postulated
that proteolytic enzymes in the body break down immunogenic material
into smaller fragments. He proposed that these smaller fragments
actually induce a state of tolerance in the immune system to their
parent immunogenic proteins. Grabar called these fragments "tolerogens."
He also felt that auto-antibodies were produced when the proteolytic
processing of immunogenic material was overloaded. This in turn
might lead to autoimmune disease in some cases.
Developing a Treatment
from the Model
The proposed model supports many traditional naturopathic concepts
that associate chronic disease with poor immunity, diet, intestinal
dysbiosis, autotoxemia, poor liver function, and chronic infection.
In particular, it stresses the importance of treating chronic disease
by altering bowel flora and improving digestive function and integrity.
This in turn emphasizes the relevance of a wholesome diet.
It is important when approaching autoimmune disease to develop a
detailed case history. Specific causative factors must be identified
for the individual as much as is reasonably possible. Particularly
look for indications of problems in apparently unrelated systems
or organs. Try to identify the process of the primary lesion. Childhood
illnesses, especially serious or atypical ones, are relevant, as
are previous surgery, accidents, or recurrent or chronic illnesses,
especially in the respiratory, urinary, or digestive systems.
Diet is important in the treatment of autoimmune disease for three
main reasons. An inappropriate diet can result in allergies and
intolerances. Imbalanced diets can increase autoimmunity, e.g.,
high-protein or high-fat diets. Finally, diet can contribute to
This association between diet, intestinal dysbiosis, and autoimmune
disease has been highlighted in some recent studies. Excessive bacterial
fermentation of sulfide in the colon could contribute to ulcerative
colitis. In a pilot Australian study, four patients with ulcerative
colitis were placed on a low-sulfur diet that included avoidance
of eggs, dairy, nuts, sulfur-containing food additives, and cruciferous
vegetables. All four patients showed substantial improvement.24
Patients with rheumatoid arthritis assigned to a vegan diet displayed
a significant change in fecal flora, which was correlated with clinical
The cause of any given autoimmune disease will vary from person
to person, so individualization of the case is critical. The primary
lesion and the source or sources of immune dysregulation should
be identified as much as is possible and treated according to the
problems uncovered. However, knowledge of the particular disease
can assist to define these problems. The scientific literature now
contains many publications dealing with the association of various
factors such as micro-organisms, diet, and intestinal dysbiosis
with specific autoimmune diseases.
Autoimmunity – General Strategy
Each heading in this section defines a treatment goal in the phytotherapy
of autoimmune diseases and these treatment goals are based on the
above model. Not all the treatment goals are relevant to every person.
They must be tailored to each individual case at the time of presentation
in the way described above. Moreover, the extensive list of herbs
provided should be regarded as a menu from which items can be selected.
It is not practical or appropriate to attempt to take a large number
of herbs at any one time.
1. Reduce the
Presence of Micro-organisms
Immune-enhancing, antiviral, and antimicrobial herbs are required.
The use of immune-enhancing herbs in autoimmune disease is controversial.
However, the above model clearly justifies their use to resolve
the detrimental influence of micro-organisms. I have never found
immune-enhancing herbs to aggravate an autoimmune disease. Echinacea
root is particularly safe and useful, as it especially works on
the input side of immune activation, mainly phagocytosis. Its influence
will help the body to resolve the presence of micro-organisms that
are having a deleterious influence on health, and yet it will not
stimulate the autoimmune processes. Echinacea will also improve
phagocytic screening of portal blood in the liver. In this case,
it should be combined with Silybum (milk thistle) if there is evidence
of hepatic impairment. Other useful immune-enhancing herbs include
Picrorrhiza, Andrographis, and Astragalus. (Andrographis is contraindicated
Hypericum (St John's wort) and Thuja are two proven antiviral herbs
that have the potential to work systemically (that is they can exert
antiviral activity in the body after oral doses). Hypericum contains
hypericin and pseudohypericin, which are active against enveloped
viruses. Many of the viruses implicated in autoimmune disease have
a viral envelope. To be effective, the daily dose of total hypericins
should be in the range of 2 to 4 mg per day. Therefore, use of a
high hypericin preparation is essential. Thuja is active against
both enveloped and naked viruses.
Some antibacterial herbs are particularly useful against enteric
infections. Herbs to be considered should include Hydrastis (goldenseal)
and other berberine-containing plants, and preparations of Allium
sativum (garlic), which release allicin after ingestion. Propolis,
grapefruit seed extract, and Melaleuca (tea tree) oil may also be
used. Herbs for bacterial contamination of the urinary tract include
Juniperus, Barosma (buchu), and Arctostaphylos uva-ursi (bearberry).
Antiseptics for the respiratory tract include Thymus (thyme) and
Inula (elecampane). Melaleuca oil inhalation may also be useful.
Most of the above antibacterial herbs also have antifungal activity.
Antiprotozoal herbs include Artemisia annua, Euphorbia, and berberine-containing
2. Eliminate Infestation
Infestation may need to be treated. In this case, immune-enhancing
treatment coupled with herbs such as garlic, Tanacetum vulgare (tansy),
and Artemisia absinthium (wormwood) should be applied. Tansy and
wormwood should be taken in controlled doses and for short periods
only. They are contraindicated in pregnancy.
3. Control or
Immune-enhancing herbs again have a role here. A fiber-rich diet
low in refined starch and sugar will encourage healthy bowel flora.
Treat any constipation. Periodic treatment with gastrointestinal
antiseptics (see above) alternating with mucilaginous herbs such
as Ulmus (slippery elm) will also help to normalize gut flora. Chicory
root is a source of inulin that can act as a probiotic.
4. Repair a Leaky
Allergens and alcoholic beverages should be eliminated from the
diet. Demulcent herbs such as Althaea (marshmallow root), anti-inflammatory
herbs such as Matricaria (chamomile), and healing treatments including
propolis and Calendula are indicated. Improving phagocytosis with
Echinacea and hepatic integrity with Silybum will reduce the systemic
impact of a leaky gut wall. Similarly, the normalization of intestinal
dysbiosis will eliminate one of the causes.
5. Reduce the
Impact of Xenobiotic Toxins
Where possible, the source should be removed, e.g., dental amalgam,
hair dyes, insecticide exposure. Otherwise depurative herbs such
as Arctium (burdock) and stimulants of hepatic metabolism such as
Schisandra may reduce the impact of introduced toxins.
6. Support the
If the organs involved in the processes of the primary lesion or
immune dysregulation can be identified, then treatments to improve
their health and function will assist in limiting the overall disease
process. For example, if prostatitis is identified (as can be the
case in ankylosing spondylitis), then treat with saw palmetto as
well as urinary tract antiseptics. If there is a bladder or urethral
"infection," add Glycyrrhiza, Crataeva, and urinary tract
demulcents (e.g., Zea-corn silk) to the normal antiseptic treatment.
Similarly, treat liver damage or "infection" with Silybum
and lung damage or "infection" with anticatarrhal herbs
(e.g., Verbascum – mullein), mucous membrane restoratives
(e.g., Hydrastis) and Equisetum (horsetail) decoction for its silica
7. Improve Proteolytic
According to Grabar, improving the levels of proteolytic enzymes
in the body will help to stabilize the immune system. Enhancing
digestive proteolytic enzymes will decrease the immunogenic nature
of food and possibly increase proteolytic enzymes in tissue fluid.
Digestive stimulant herbs such as bitters and Coleus increase proteolytic
enzyme release from the stomach and pancreas. Melilotus (sweet clover)
contains coumarin, which enhances the breakdown by macrophages of
potentially antigenic protein accumulated in extracellular spaces.
8. Reduce the
The use of anti-inflammatory and immune-depressing herbs is not
just symptom control. Provided the causative factors are also being
treated, judicious use of these herbs will help to break the vicious
cycle sustaining the tissue destruction. Anti-inflammatory herbs
include those containing saponins, which interact with endogenous
corticosteroids. These include Glycyrrhiza (licorice), Bupleurum,
and Aesculus (horsechestnut). Other anti-inflammatory herbs include
Salix (willow bark) and Curcuma (turmeric). Tanacetum parthenium
(feverfew) inhibits inflammatory degranulation of polymorphs. Ginkgo
counters the effects of PAF, and Boswellia, the formation of leukotrienes.
These will help to control inflammation in inflammatory bowel disease.
Picrorrhiza contains apocynin, which is a selective and potent inhibitor
of neutrophil oxidative burst. This selective anti-inflammatory
activity may be important in controlling rheumatoid arthritis. Herbs
with documented immune-depressing activity are Hemidesmus, Tylophora,
and Stephania. Use of Stephania is not recommended due to the high
risk of adulteration with the toxic herb Aristolochia. Neither is
the use of Tripterygium wilfordii (the thunder god vine) due to
the high risk of serious side effects.
Probably the most powerful but safest immune-depressing herb is
Tylophora indica. In excessive (but not high) doses, it will act
as an emetic, and it should not be taken continuously. The best
way to have Tylophora is to take between 20 to 50 drops of a 1:5
tincture (the highest dose in that range which does not cause nausea)
for the first 10 to 14 days of each month.
Desensitization to the original antigen or the cross-reacting antigen
is beyond the scope of phytotherapy. However, it is worth discussing
in the above context since it should also help to break the vicious
cycle of autoimmunity. One way to achieve desensitization is the
gastrointestinal administration of antigen. This technique has been
successfully tested in clinical trials on multiple sclerosis and
rheumatoid arthritis. Breakdown products from bacterial wall fragments
are excreted in the urine, and their oral ingestion may cause desensitization
to their effects. Tolerogens may also be excreted in the urine.
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