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Phytotherapy for Ankylosing Spondylitis and Inflammatory
Bowel Disease
In previous editions of the Townsend
Letter, I proposed an approach
to the phytotherapy of autoimmune disease in general1 and
elaborated on this approach for multiple sclerosis.2 In
this article the further application of this treatment model to
the herbal therapy for ankylosing
spondylitis, Crohn's disease and ulcerative colitis are described.
Ankylosing Spondylitis — Good
Evidence to Implicate Molecular Mimicry
There is good evidence to implicate molecular mimicry in the cause of ankylosing
spondylitis (AS). This has direct implications for its treatment.
Ankylosing spondylitis is often grouped with reactive arthritis. Both diseases
occur predominantly in individuals who are positive for the HLA-B27 tissue
marker. For cases of reactive arthritis and Reiter's syndrome, a clear
association with an infecting organism such as Salmonella, Shigella, Chlamydia,
Yersinia or Campylobacter is observed. Reactive arthritis can follow urogenital
or intestinal infection with these bacteria.
In the case of AS there is no clear proof of infection, and considerable controversy
still surrounds the concept of an infectious etiology. AS almost always follows
a chronic course, whereas only 10% of patients with reactive arthritis have
evidence of active disease 20 years after the onset. However, evidence is growing
that AS is triggered by the asymptomatic presence of pathogenic bacteria, particularly
in the intestine. The bacteria may not occur in sufficient numbers to cause
a frank infection, but this fact may also help to sustain their persistence
in the body, a persistence which can lead to a chronic course of disease.
The following evidence exists for a bacterial trigger for AS:
-
Considerable evidence exists that bacteria such as Klebsiella, Enterobacter,
Salmonella, Shigella and Yersinia immunologically cross-react with HLA-B27.3
(It is doubtful whether severe disease occurs in the small number of AS
patients who are HLA-B27 negative.)3
- More than 50% of AS patients
with peripheral arthritis have inflammatory gut lesions.4 The
degree of gastrointestinal inflammation was significantly correlated
with the degree of joint inflammation in 45 patients
with AS.5 The chronic
gut lesions resemble inflammatory bowel disease.4 It was demonstrated
that the intestinal secretory immune system was significantly overstimulated
in
active AS, and this was reflected by raised serum levels of IgA.6 When
the gastrointestinal anti-inflammatory drug sulfasalazine was given,
there was
normalization of immune activity in those patients who responded clinically.
Another study found that chronic lesions of the gut were frequently found
in patients with AS.7
- Of the above micro-organisms, Dr Alan
Ebringer found that only Klebsiella could be consistently isolated
from fecal cultures obtained from British patients
with AS.3 In a study of 63 AS patients by Ebringer's group,
an increased recovery of Klebsiella could be obtained during the clinically
active phases
of the disease.8 A second study showed that a positive culture
of Klebsiella in patients with inactive disease was subsequently followed
by a relapse.9
The same research team found that the presence of Klebsiella was strongly
associated with episodes of anterior uveitis in AS patients.10 Some
scientists in other countries have confirmed this association with
Klebsiella, but several other
research groups have not. It is possible that other organisms might
be associated with AS in other countries (see below).
- Another group
of scientists found that a substantial portion of patients
with AS have antibodies which react to both HLA-B27 and Klebsiella pneumoniae
nitrogenase.11 Amino acid sequence similarities (ie molecular
mimicry) had previously been demonstrated between the Klebsiella nitrogenase
and HLA-B27. However
molecular
mimicry between the two proteins was not confirmed by a research team
from Finland.12
- Since 1980, the British group led by Ebringer
has concentrated on finding antibodies to Klebsiella in the bloodstream
of patients with active AS.
This association
has been confirmed in several controlled studies using several different
techniques to measure anti-Klebsiella antibodies.3 However, in
a New Zealand study, antibodies to Yersinia were also associated with AS
in 4 out of 15 cases.13 Twenty-nine
control subjects had no serum antibodies to Yersinia.
- In what has been
described as "the missing link" in the cause
of the HLA-B27-associated arthropathies, B27-restricted CD8+ cells,
which showed specificity for both autoantigens and arthritogenic
bacteria such
as Yersinia,
have been isolated from the synovial fluids of patients with reactive
arthritis and AS.14
- Nonsecretors of ABO blood group antigens are more
susceptible to infection. The fact that nonsecretors of ABO are 2.6 times
more likely to have
AS supports an infectious etiology for AS.15
- The site of the bacterial trigger
for AS is not necessarily always the bowel. An association between
AS and chronic bacterial prostatitis
has long been observed.
The incidence of chronic prostatitis in male AS patients was 83%,
compared to 33% in patients with rheumatoid arthritis.16 This association was
confirmed in a later study.17 The fact that the prostate may harbor a bacteria
which
contributes to AS could explain the higher incidence of this disorder
in males.
Consideration of the above and other similar
findings led Dr. John Vaughan to conclude in a recent review: "The
probability that AS is due to a peculiar immunologic relationship between
the patient and his enteric organisms,
and that this is determined by his HLA-B27 molecules, seems great."18
The information on possible sources of immune dysregulation in
AS is less clear. However, enhanced gastrointestinal permeability,
the
so-called
leaky gut, could
be such a source. Normally, small amounts of lipopolysaccharides
(endotoxin) enter portal venous blood and are eliminated by phagocytic
cells in
the liver.19 Increased mucosal permeability may result in the increased
exposure of the
body to such pro-inflammatory bacterial fragments.
Studies have demonstrated an increased intestinal permeability
in AS.20-22 These findings also support the notion that asymptomatic
gut inflammation,
possibly due to pathogenic bacteria, is a factor in the pathogenesis
of AS.
Other factors which have been associated with AS and may reflect
on immune dysregulation include trauma23 and delayed hypersensitivity.24
Reactive arthritis
and Reiter's syndrome have been reported after hepatitis B vaccination25,26
and this could also be a factor in some cases of AS. Eliminating
cow's
milk products from the diet caused symptomatic improvement in AS
in one study.27
Treatment Approach
From the above, a key part of the treatment approach to AS is to reduce the
presence of Klebsiella or other potentially pathogenic organisms. This will
not only reduce the stimulus for immune cross-reactivity, but will also decrease
gastrointestinal inflammation and the resultant increased permeability.
Klebsiella in the bowel uses resistant starch processed to oligosaccharides
by friendly bacteria as a major source of nutrition. So a low starch diet should
decrease its numbers. Ebringer recommends that patients with AS should avoid
bread, pasta, cereals of all sorts, rice, potatoes and sugary foods. They can
eat unrestricted amounts of vegetables (excluding starchy root vegetables such
as potatoes and yams), fruit, eggs, cheese, fish and meat.28 Legumes such as
soy beans and uncooked bananas contain a significant proportion of indigestible
starch which may act as a food source for Klebsiella. They should also be avoided.
Ebringer claims that the majority of 200 patients on this diet had their disease
process halted. However a significant result may take 6 months or more.28
Herbal treatment for AS should be selected from the following:
- Immune-enhancing
herbs such as Echinacea, Andrographis and Astragalus to
eliminate pathogenic organisms.
- Gastrointestinal antiseptics such as Berberis
(barberry), Hydrastis (golden seal), Allium sativum (garlic) and
propolis to eliminate pathogenic organisms
from the bowel.
- Gastrointestinal healing and anti-inflammatory agents
such as Calendula, Filipendula (meadowsweet), Matricaria (chamomile)
and propolis to reduce
inflammation and
heal the gut wall.
- Echinacea and Silybum (milk thistle) to reduce the
systemic impact of a leaky gut wall by improving hepatic phagocytosis
(Kupffer cells).
- Suitable treatment for the prostate if chronic prostatitis
is present, using herbs such as saw palmetto.
- Anti-inflammatory herbs
such as Salix (willow bark), Glycyrrhiza (licorice) and Bupleurum
to help control symptoms and break the vicious cycle sustaining
the tissue destruction. A key anti-inflammatory herb is Boswellia,
which can help to alleviate both the gut (see later) and the joint
inflammation.
Crohn's Disease
Evidence exists to support the hypothesis of a microbial trigger for Crohn's
disease (CD). Although the association of bacteria, viruses and bowel flora
with CD may confound a clear infectious cause, such a multiplicity of factors
is consistent with the proposed model for the development of autoimmune disease.
In the case of CD, a virus could provide the primary lesion but bacteria are
more likely to be involved. A combination of effects from bacteria, imbalanced
bowel flora, diet and stress trigger a state of immune dysregulation which
results in active disease. A similar theory for the cause of CD has been proposed
by French scientists.29 Viruses
A group led by Dr Andrew Wakefield at the Royal Free Hospital in London completed
a study of CD tissue specimens. Based on this study they proposed that the
primary lesion in CD was a vasculitis caused by multifocal intestinal infarction.30
They further proposed that this injury was consistent with a cell-mediated
response to a persistent viral infection of mesenteric microvascular endothelium.
Of the viruses known to infect vascular endothelium, the measles virus was
of particular interest for two reasons: it localizes to the intestine and
it can persist for many years. They began to search for the measles virus.
Intestinal tissue from 10 patients with CD were all found to contain measles
virus RNA.31 Moreover, measles virus RNA was found within vascular endothelial
cells associated with inflammatory foci in 9 out of the 10 CD patients. Other
tests also supported the presence of measles virus.31
A Swedish epidemiological study subsequently found that children born during
the three-month period following a measles epidemic were significantly more
likely to develop CD in later life.32 However no association with measles was
observed for UC.32
Wakefield is of the opinion that measles vaccination may be responsible for
the rise of CD cases in children. This rise is seven-fold in Scotland over
the last 20 years, whereas cases of measles infections there have dropped dramatically.
However, vaccination may not be the only explanation for this rise. Moreover,
fewer cases of measles infection might not necessarily reflect that general
exposure to the virus is less. Generally there is controversy over the association
of CD with measles vaccination and several studies which could not find any
association have been subsequently published.
Mycobacteria
Research attention has been given to the possible association of mycobacteria
with CD. The original account by Crohn described a disease that closely resembled
intestinal tuberculosis. Johne's disease, which occurs in cattle and
other ruminants, is very similar to Crohn's disease and is caused
by Mycobacterium paratuberculosis. In 1984 Chiodini and co-workers reported
the isolation of a strain resembling M. paratuberculosis from the intestinal
tissue of three patients with CD.33 This report initiated both interest and
controversy about a mycobacterial etiology for CD. One problem is that, on
culture, mycobacteria isolated from CD tissue initially appear as cell wall-deficient
forms that are difficult to identify by conventional techniques.34 With the
development of the enzyme PCR (polymerase chain reaction), which replicates
DNA, DNA from M. paratuberculosis has been detected in cultures from CD patients.34
M. avium has also been identified in the intestinal tissue of patients with
CD.35
Many other groups of investigators have isolated mycobacteria from CD patients,36,37
although not all patients and not all studies have yielded positive results.35-39
In a study reported by Sanderson and co-workers, M. paratuberculosis DNA was
identified in gut wall tissues from 65% of CD patients, 4.3% of patients with
UC and 12.5% of control patients.40 Other researchers found raised antibodies
specific to M. paratuberculosis in 84% of patients with CD.41 Such findings
led a scientist working in the field to conclude that the evidence for a mycobacterial
association with CD is "stronger now than it has been before."37
One problem which has led to skepticism about the above statement is that there
is inconclusive evidence that CD results from an actual mycobacterial infection.
Only the presence of mycobacteria has been proven. PCR technology can detect
very small amounts of bacterial DNA, as low as several hundred bacteria per
g of tissue. From an immunological point of view, it is difficult to see how
so few organisms alone could elicit such a strong inflammatory response, especially
since the form of M. paratuberculosis implicated in CD may lack a cell wall.42
However, in accordance with the proposed model, mycobacteria are possibly acting
as a source of immune cross-reactivity or immune dysregulation, and the main
inflammatory stimulus is elsewhere. Therefore the presence of mycobacteria
is still a significant finding, despite their low numbers.
Other Bacteria
Other bacteria have been implicated in CD, but results are often conflicting.
For example, one study found that 93% of patients with CD had antibodies
against Chlamydia, compared to 26% in the control group.43 However, another
study failed to find evidence of Chlamydia infection in CD patients.44 This
discrepancy could be due to the testing of different patient populations.
That is, depending on environmental circumstances, Chlamydia may act as a
pathogenic factor in CD. Antibodies to Klebsiella were also higher in a population
of CD patients.45
Mollicute-like organisms (MLO) are cell wall-deficient intracellular bacterial
pathogens. They cannot be cultured by microbiological techniques and can only
be detected in cells with an electron microscope. MLO were found in the white
blood cells of patients with CD.46
Bowel Flora
There is little doubt that the fecal stream plays an important part in the
progression of CD.47-49 Bowel flora are likely to be a strong source of immune
dysregulation in CD. Monocytes from CD patients showed enhanced stimulation
by bacterial cell wall products such as lipopolysaccharide.50 Bacterial wall
fragments in the bowel wall of CD patients caused enhanced immune responsiveness
of monocytes.51 When 36 tissues from 16 patients with CD were examined, no
evidence of the presence of many pathogenic bacteria and viruses were found.52
However, E. coli and streptococcal antigens were found in 69% and 63% of
the 16 cases studied, respectively. Both E. coli and streptococci are normal
inhabitants of bowel flora. The above results suggest that some of the granulomas
in CD may result from the immunological processing of bowel flora antigens
following their penetration through a compromised mucosa.52 Serum antibodies
to bowel flora bacteria are increased in CD patients.53
Pathogenic forms of E. coli adhere to the gut mucosa. E. coli isolated from
patients with UC and CD showed a significantly greater index of adhesion when
compared to normal controls.54
Bowel Permeability
A leaky gut would enable enteric antigens to penetrate the mucosa to an increased
extent, and the capacity for removal or degradation of this antigenic load
could then be exceeded. This would create a state of immune dysregulation.
Several studies indicate permeability abnormalities for both the small and
large intestine in CD.55In fact, so characteristic is this enhanced permeability
that it is considered a good marker of active inflammation occurring in CD
patients in remission.56 Circulating levels of lipopolysaccharide are increased
in patients with active CD.57 There is a general leakiness of the intestinal
mucosa in CD which is not dependent on the presence of inflammatory lesions.55
It has been postulated that increased permeability may be a primary expression
of CD and an important pathological factor.55
In support of the concept that increased permeability is a pathogenic factor,
CD has been associated with the use of nonsteroidal anti-inflammatory drugs
(NSAIDs). These drugs are responsible for increased gut permeability and small
intestinal inflammation.58,59 A group of researchers from Jersey reported that
of 60 new cases of colitis, 23 had developed while the patient was taking NSAIDs.60
None of these 23 patients had a known pre-existing IBD. Diclofenac (Voltaren)
and mefenamic acid (Ponstan) were the most frequently observed associations.
On endoscopic examination, some cases were indistinguishable from UC.
Diet
Food is a potential source of many immune-provoking antigens, and food is probably
therefore a potent source of immune dysregulation in CD. It is a well-accepted
observation that many patients with CD improve substantially when they are
placed on an elemental diet, that is, a predigested liquid diet free of antigenic
challenge consisting of amino acids, dextrin, vitamins, vegetable oil, minerals
and so on.61 An elemental diet also decreases small intestinal permeability
in CD.62
The concept of using an exclusion diet to treat CD was first proposed by a
group at Cambridge,63 and subsequent publications have originated from England.
The Cambridge group found that during a controlled trial of 20 patients with
CD, 7 of 10 patients on an exclusion diet remained in remission for 6 months,
compared to none of the 10 on a normal fiber-rich diet.63 In an uncontrolled
study, an exclusion diet allowed 51 of 77 patients to remain well on diet alone
for periods up to 51 months, with an average annual relapse rate of less than
10%.63
These results were confirmed in a controlled trial on 78 patients.64 Corticosteroid
therapy was compared to an exclusion diet. Patients on the exclusion diet also
received placebo. Results for diet treatment were favorable, median remission
periods were 3.8 months in the corticosteroid group and 7.5 months in the group
treated by diet. Intolerances discovered were predominantly to cereals, dairy
products and yeast. The authors concluded that diet provides a further therapeutic
strategy in active CD.64
Patients with CD but not UC were found to have significantly high levels of
antibodies to baker's yeast in blood samples. These results were confirmed
in a later study which also found that raised antibodies to yeast occurred
in CD patients regardless of whether they were yeast intolerant or not.65 The
pathogenic importance of these findings has not been established.
Phytotherapy for Crohn's Disease
Diet
An individually determined exclusion diet, as outlined above, is an important
part of therapy. However, if this is not practical, the case history may
provide clues to food sensitivities. In particular, dairy or wheat avoidance
should be considered. Supplementation with fish oil can be beneficial in
CD.66-68
Bowel Flora Regime
A correction of bowel flora in CD may reduce the dysregulation caused by an
abnormal flora, and could also create an unfavorable environment for intracellular
pathogens such as mycobacteria and viruses. Phytotherapist Hein Zeylstra
has developed a successful treatment regime for IBD. The regime is outlined
in Table 1. This approach originated from the naturopathic approach to Johne's
disease in cows described by Roger Newman-Turner, Sr. Although Hein Zeylstra
provides no explanation as to why this approach may work, it is my interpretation
that the regime has a favorable influence on bowel flora.
Basically, the routine is to periodically fast, taking fresh garlic (Allium
sativum) and slippery elm (Ulmus rubra). Pathogenic bacteria in the bowel
lumen would be weakened by fasting, since they rely on a ready source of
nutrients.
The garlic then reduces the population of all bacteria in the bowel lumen,
and the slippery elm encourages only the growth of favorable bacteria. This
last aspect of the therapy takes advantage of the ability of favorable organisms,
such as bifidobacteria, to utilize the mucilage in the slippery elm as a
food source, whereas pathogenic bacteria cannot. Thus there is an increase
in favorable
bacteria. If the routine is repeated several times over a few months, a "normalization" of
bowel flora will result. According to Zeylstra the regime works faster in
CD than UC, possibly because of the favorable effect of fasting on CD.
The Bowel Flora Regime as
developed by phytotherapist Hein Zeylstra. This may need to be followed
for several months.
Day 1: Fast — no food, but water
and medicines are allowed.
Day 2 and 3: Continue as for Day 1. Twice during the day take one to
two cloves of crushed fresh garlic with a copious quantity of water.
This has the effect of flushing the fresh garlic quickly into the
small intestine. At different times take one to two teaspoons of
slippery elm powder with copious water.
Day 4: Gradually introduce allowed foods and continue with medicines
and slippery elm.
Day 5 to 14: Follow exclusion diet and take medicines and slippery
elm.
Day 15: Begin again as for Day 1, etc.
Herbs for CD
Immune enhancement with herbs such as Echinacea, Andrographis and Astragalus
will help resolve the presence of any virus, mycobacteria and abnormal bowel
flora. If any virus involved is enveloped, hypericin found in Hypericum would
be active against the virus. Hypericum has also been shown to be active against
mycobacteria in vitro.69 Other herbs with such in vitro activity against
mycobacteria include Allium sativum and Cinnamomum zeylanicum.69 Berberine-containing
herbs such as Berberis species and Hydrastis have a good broad-spectrum antimicrobial
activity and are useful to help correct bowel flora. Matricaria is useful
for the symptoms of spasm and together with Calendula will help to repair
a leaky gut. Because of the leaky gut, phagocytic screening by the liver
should be increased using Echinacea and Silybum. Anti-inflammatory herbs
which inhibit leukotriene production such as Boswellia are also strongly
indicated. Cell-mediated immunity is a factor in the pathogenesis of CD,
so selective use of Tylophora 1:5 (for 10 days of each month) may be useful
in the early stages of treatment. As with all autoimmune diseases, best results
come with long-term treatment.
Ulcerative Colitis
In contrast to Crohn's disease, studies have consistently associated
ulcerative colitis (UC) with cytomegalovirus (CMV).70 A clear association between
onset of UC and primary CMV infection was confirmed by virus studies in two
patients.71,72 Higher frequency and amount of antibodies to CMV was found in
patients with UC.70 The simultaneous presence of DNA from several herpes viruses,
including CMV, was much greater in UC patients compared to those with CD or
normal controls.73
E. coli with specific surface hairs or pili that promote adhesion are found
in significant amounts in patients with UC compared to controls.54 (This phenomenon
was also observed for CD but was less marked.) Pathogenic E. coli show mucosal
adhesion, and this is a necessary condition for their pathogenicity. Several
workers have shown that isolates of E. coli obtained from patients with UC
can degrade mucins and produce toxins.
Serological tests of patients with IBD found a connection between antibodies
against Chlamydia (93% for CD and 45% for UC) compared to controls (26%).74
A patient with AIDS developed UC after an episode of amebic dysentery.75
UC patients receiving probiotic therapy with a live nonpathogenic strain of
E. coli (enteric coated capsules), following a one-week course of an antibiotic,
experienced a similar benefit to therapy with mesalazine in maintaining remission.76
The authors suggested that this finding confirms a link between UC and bowel
flora. Implantation of normal colonic flora from a donor following reduction
of endogenous bowel flora led to a favorable outcome in one patient with UC.77
Hypothesis
Cytomegalovirus (an enveloped virus) or similar viruses provide the source
of the primary antigen in UC, possibly by molecular mimicry. Adhesive E.
coli and other bacterial factors in bowel flora and elsewhere promote immune
dysregulation.
Diet and UC
Studies have shown that elimination diets can help reduce symptoms of UC78
and clinical trials of fish oil supplementation have shown positive results.79
The association between a low-sulfur diet and a clinical benefit in UC has
already been described. One study found that the metabolic effects of sodium
hydrogen sulfide on butyrate oxidation along the length of the colon closely
mirror metabolic abnormalities observed in active UC.80 The authors suggested
that increased production of sulfide in UC suggests that the action of mercaptides
(sulfur compounds) may be involved in the genesis of UC.
Herbal Therapy
The suggested herbal therapeutic approach for UC is similar to that for CD,
although there should be a greater emphasis on antiviral treatments, especially
St John's wort. Bowel flora modification by whatever means (for example
by the regime described in Table 1 although the sulfur in garlic could be
detrimental) is an essential part of the treatment. Boswellia is an important
anti-inflammatory herb for both CD and UC as outlined below.
A Key Role for Boswellia in Inflammatory Bowel Disease
Pharmacological studies have found that extracts from the gum resin of Boswellia
serrata (Indian olibanum, a relative of frankincense) possess anti-inflammatory
properties. In particular, the boswellic acids inhibit the enzyme 5-lipoxygenase
which is responsible for the production of leukotrienes. Since the inflammatory
process in inflammatory bowel disease (IBD) is associated with increased
function of leukotrienes, the benefits of Boswellia in the treatment of both
chronic colitis (ulcerative colitis) and Crohn's disease have been
recently investigated.
Twenty patients with chronic colitis received Boswellia gum resin (900 mg per
day for 6 weeks) and another 10 patients were given sulfasalazine (3 g per
day for 6 weeks).1 Out of 20 patients treated with Boswellia, 14 went into
remission (70% compared to 40% for sulfasalazine).
The safety and efficacy of a Boswellia extract was compared against mesalazine
for the treatment of 102 patients with active Crohn's disease in an
eight-week randomized, double-blind study.2 The primary clinical outcome measured
was the change in Crohn's Disease Activity Index (CDAI). After therapy
with Boswellia extract (3.6 g per day) the average CDAI was reduced by 90,
compared to a reduction of 53 for the mesalazine group (4.5 g per day). The
authors concluded that the Boswellia extract was as effective as mesalazine,
which is the state-of-the-art treatment for this disorder. Considering the
observed fewer side effects and better safety profile of Boswellia, they suggested
that this novel herbal treatment appears to be superior to mesalazine in terms
of a risk-benefit evaluation.
The chronic colitis study described above follows from a similar, earlier study
of the efficacy of Boswellia for this disorder. Unfortunately, the design flaws
in the earlier study (fewer patients in the control treatment group, study
was open) are reflected in the current trial. In contrast, the study on Crohn's
disease was well designed and conducted in Europe. It adds serious weight to
the suggestion that Boswellia is a useful anti-inflammatory agent for IBD.
Ulcerative Colitis: A Brief Case History
A female patient aged 55 presented with ulcerative colitis (12 years of history).
Her drug treatment was 6 tablets per day of Salazopyrin (sulfasalazine).
She was also on prednisone due to an episode of severe bleeding (but was
tapering off). Over the past 15 months her condition had become much worse.
Based on recent research she was placed on a low sulfur diet (no dairy, no
cabbage family, no eggs, no onions or garlic, reduced red meat, no sulfur-based
additives).
The following herbs were prescribed (tablets were used because alcohol made
her bowel worse):
-
St John's wort: 3 tablets per day, each tablet containing Hypericum
perforatum (St John's wort) extract standardized to contain hypericin
990 mcg and hyperforin 9 mg, equivalent to 1.8 g of herb flowering top.
- Boswellia:
3 tablets per day, each tablet containing: Boswellia serrata extract
standardized to contain boswellic acids 180 mg, equivalent to 1.2
g of Boswellia
gum resin; Apium graveolens (celery) extract equivalent to 1 g of fruit;
Zingiber officinale (ginger) extract equivalent to 300 mg of rhizome; and Curcuma
longa
(turmeric) extract standardized to contain curcuminoids 70.4 mg, equivalent
to 2 g of rhizome.
- Echinacea: 2 tablets per day, each tablet containing:
Echinacea angustifolia extract standardized to contain 2.0 mg of
alkylamides, equivalent to
600 mg of root; Echinacea purpurea extract standardized to 2.1 mg of alkylamides,
equivalent to 675 mg of root.
- Slippery elm powder: 2 teaspoons per day.
The rationale for the treatment:
-
St John's wort: antiviral, nervine tonic
- Slippery elm: demulcent and improves
bowel flora
- Echinacea: balance immunity
- Boswellia, ginger, celery and turmeric:
anti-inflammatory
Her progress was as follows:
- After 2 months — stopped
prednisone and no blood, drug down to 4 per day
- Two months later — bowel
a lot better, fewer motions, biopsy normal, drug down to 2 per
day
- Two months later — bowel
action up (but no blood or cramping), drug back to 3 per day
- Two months
later — everything OK, drug down to 2 per day
- Six months later
there were no symptoms and biopsy showed no sign of ulcerative colitis,
drug at 2 per day
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