SYSTEMIC ASPECTS OF PSORIASIS:
AN INTEGRATIVE MODEL BASED ON INTESTINAL ETIOLOGY
David L. McMillin, MA, Douglas G. Richards, PhD,
Eric A. Mein, MD, Carl D. Nelson, DC
Meridian Institute
Virginia Beach, VA 23454
[NOTE: This article was published in Integrative Medicine; Vol.
2, No. 2/3, 1999; see
below for continuing
education credit for this article.]
ABSTRACT
Psoriasis can best be understood from a multifactorial
approach that recognizes the systemic aspects of the disorder. Among
the various factors thought to be involved in the etiology and pathogenesis
of psoriasis, bowel pathology has assumed a noteworthy position in the
literature. This article reviews the psoriasis/bowel connection with
regard to abnormal bowel structure and physiology in psoriasis patients.
Clinical implications of bowel involvement in psoriasis are discussed within
the framework of an integrative medicine model that emphasizes natural
therapeutics for addressing the systemic aspects of the illness.
Psoriasis is a chronic cutaneous disease of unknown
causation [1]. Although there is no generally recognized cure for
psoriasis, a variety of treatments are commonly used to reduce the severity
of symptoms and lessen their impact on the patient's quality of life.
Topical therapy may be helpful for symptomatic relief, especially for mild
psoriasis. For moderate to severe psoriasis, phototherapy and systemic
therapies are the standard medical therapies. However, these treatments
are all associated with significant adverse effects. Phototherapy
may produce erythema, pruritus, wrinkling, solar elastosis, and an increased
risk of skin cancer. Systemic therapies such as acitretin, methotrexate,
cyclosporine, hydroxyurea, and thioguanine are all associated with significant
systemic toxicity and must be closely monitored [2].
The cost of standard medical treatment for psoriasis
is substantial, currently estimated at approximately $1.6 billion to $3.2
billion per year in the United States [3]. There continues to be
a need for effective, affordable therapies with fewer side-effects.
Understanding the etiology and pathogenesis of psoriasis may lead to economical
therapies which address the underlying causes of the disease while decreasing
adverse effects.
Considered to be an autoimmune disorder with systemic
features, psoriasis is known to be associated with joint and bowel disease.
This article explores the concept of intestinal pathology as a significant
etiological factor in psoriasis. The conceptual basis of the integrative
approach advocated in this article is derived from the systems approach
of Edgar Cayce as described by Landsford, Mein, and Pagano [4-6].
In essence, the model focuses on intestinal permeability as a primary factor
in the pathogenesis of psoriasis. The Cayce hypothesis is that various
factors produce a "thinning of the walls of the small intestine - specifically,
the jejunum and the lower duodenum . This thinning allows toxic products
to leak from the intestinal tract into the circulation; these eventually
find their way into the superficial circulation and lymphatics and are
eliminated through the skin, producing the plaques of psoriasis" [5, p.
176]. Therapeutically, a variety of natural remedies (such as diet,
herbal teas, hydrotherapies, and topical applications) are utilized to
heal the gut, decrease systemic toxicity, and provide symptomatic relief.
The literature on bowel structure and function suggests
that systemic autointoxication is a plausible pathophysiological pattern
in psoriasis. A literature review is provided on the systemic aspects
of psoriasis with special emphasis on comorbidity with other systemic disorders.
Consideration of the systemic patterns associated with psoriasis may contribute
to an understanding of the various pathophysiological processes producing
this illness. With this broader perspective in mind, the review will
consider the abundant body of information on bowel pathology in psoriasis.
For completeness, this review draws on sources with differing levels of
quality and strength of evidence: experimental reports, clinical studies,
and case studies. Most are in peer reviewed journals; a few are not.
It is particularly important to include this diversity of sources in an
area where some practitioners may not conduct controlled studies or may
be outside mainstream medicine, yet have contributed valuable clinical
insights.
A discussion then follows which outlines an intestinal
model of psoriasis causation and suggests an integrative medicine approach
to psoriasis. Integrative medicine emphasizes cooperation between
health care professionals of conventional and alternative therapies.
From an integrative medicine approach, natural therapeutics directed to
internal cleansing and intestinal healing hold promise in the treatment
of psoriasis, in addition to standard medical therapies for this condition.
COMORBIDITY OF PSORIASIS WITH OTHER SYSTEMIC DISORDERS
The term "comorbidity" has been used to describe
the overlap of illnesses which tend to occur together. In reviewing
the possible sources of comorbidity, Weissman et al. [7] have concluded:
"In comorbidity there is an underlying assumption that separate
diagnoses may co-occur for several reasons: one disorder increases vulnerability
to the other; one disorder is a different expression of the other; both
disorders are due to some third underlying cause, or by chance alone ..."
[7, p. 433].
Henseler and Christophers [8] have documented a significant
comorbidity of psoriasis with several other conditions including obesity,
diabetes and heart disease. They hypothesized that the concomitance
of these systemic disorders may be related to dietary habits, nutritional
status or common genetic factors. Numerous case reports suggest
a comorbidity of psoriasis and kidney disease [9-11]. The conceptual
significance of this association with regard to autointoxication will be
discussed in a later section.
The comorbidity of skin disease with bowel pathology
is particular noteworthy. Person and Bernhard [12] observed that
the pustular dermatitis associated with small bowel bypass surgery and
the cutaneous manifestations of inflammatory bowel disease are well known.
These manifestations of skin disease are generally assumed to be due to
the absorption of microbial antigens from the bowel. Thus, autointoxication
is described as a primary pathophysiological process in the cormorbidity
of bowel and skin disease.
Other clinicians have described the association of
digestive system surgery with skin disease. D'Amico et al. [13] reported
an association of primary biliary cirrhosis and psoriasis. Following
implantation of a porto-caval anatomosis, the patient experienced remission
of psoriasis and psoriatic arthritis. The physicians hypothesized
that the blood flow redistribution reduced bowel congestion and decreased
the involvement of pathological intestinal flora, particularly with regard
to hepatic functioning. Porres [14] noted that jejuno-ilio
bypass surgery resulted in improvement of psoriasis symptoms in a 44-year-old
woman. The woman was able to discontinue her psoriasis medication.
Yates et al. [15] also emphasized the comorbidity
of psoriasis and bowel disease. To test the hypothesis that these
disorders are related, they studied 204 patients with inflammatory bowel
disease (116 with Crohn's disease and 88 with ulcerative colitis) and 204
age- and sex-matched controls. They concluded: "The prevalance of
psoriasis in Crohn's disease (11.2%) and in ulcerative colitis (5.7%) was
significantly greater than in the control group (1.5%). The prevalence
of psoriasis in first-degree relatives of patients with inflammatory bowel
disease was also increased. It is suggested that there is a relationship
between psoriasis, ankylosing spondylitis, sacroiliitis, peripheral arthropathy
and inflammatory bowel disease ." [p. 323].
Menzel and Holzmann [16] analyzed stool samples
of patients suffering from seborrheic eczema of the scalp, psoriasis capitis,
or seborrhiasis. The researchers measured pathological flora of the
bowel to a high degree in all patients. The flora were predominantly
pathogenic yeasts. With regard to treatment, they observed that therapy
for the intestine is helpful for the skin disease as well. Numerous
studies have emphasized the significance of pathological intestinal microorganisms
in the etiology of psoriasis [17-20].
The comorbidity of psoriasis and joint disease is
also well known. Approximately 5 - 7% of psoriasis patients
suffer from a specific form of arthritis linked to psoriasis [21].
Although the relationship between these diverse manifestations is unknown,
the bowel has been implicated as a possible link between skin and joint
disease. Most notably, inflammatory bowel disease has been shown
to be comorbid with psoriatic arthritis and other illnesses classified
as spondyloarthropathies. The concept of spondyloarthropathy links
diseases with common clinical, radiological, and genetic features.
In addition to psoriatic arthritis, other diseases in this category include
ankylosing spondylitis, reactive arthritis caused by urogenital or enterogenic
infection, inflammatory bowel disease [ulcerative colitis and Crohn's disease],
some forms of juvenile chronic arthritis, and acute anterior uveitis [22].
Furthermore, gut inflammation has been specifically cited as a likely causative
factor in certain forms of psoriatic arthritis based on ileocolonoscopic
studies of patients with psoriatic arthritis [23].
Fry [24] theorized that the association of small
intestine and skin disease may be considered under the following subgroups.
1. A non-specific relationship in which a primary disease
of the small intestine causes non-specific changes in the skin [e.g., acquired
ichthyosis] or, a primary disease of the skin produces non-specific changes
in the small intestine [e.g. dermatogenic enteropathy].
2. A specific relationship in which a particular disease-entity
of the skin is associated with a particular disorder of the small intestine
[e.g. dermatitis herpetiformis].
3. A generalized disease process which affects both the skin and
the gut but which is not necessarily confined to these two organs [e.g.
systemic sclerosis or polyarteritis nodosa].
Depending upon the orientation of the investigator,
psoriasis has been placed within each of these subgroups. Pagano
[6] regards psoriasis as a nonspecific manifestation of bowel pathology
[intestinal permeability] in which toxins leak out of the gut and are eventually
relayed to the skin for elimination from the body. Marks and Shuster
[25] have emphasized a nonspecific process in which psoriasis is the primary
disease producing secondary pathology in the small bowel. De Vos
et al. [26] have noted that psoriasis may be associated with a particular
disorder of the small intestine (coeliac disease). The growing literature
on the spondyloarthropathies [22] reflects an interest in the systemic
manifestations of auto-immune diseases including psoriatic arthritis.
ABNORMALITIES OF INTESTINAL MUCOSAL STRUCTURE IN PSORIASIS
Pursuing the pathophysiology of bowel and skin
disease comorbidity, researchers have investigated intestinal permeability
as a possible etiological factor. Hamilton et al. [27] explored passive
small intestinal permeability in 29 patients with psoriasis using the cellobiose/mannitol
differential sugar absorption test which measures urinary recovery ratio
of cellobiose and mannitol. The recovery ratio was abnormal
in seven patients. However the researchers concluded that these rates
were similar to values in a control population, and were not affected by
the extent or activity of the skin disease.
Using a different assessment technique, Humbert,
et al. [28] studied the intestines of 15 psoriatic patients and 15 healthy
subjects. Intestinal permeability was evaluated using the 51Cr-labeled
EDTA absorption test. The psoriasis group was found to exhibit significantly
increased bowel permeability compared to the controls. The researchers
concluded: "The difference in intestinal permeability between psoriatic
patients and controls could be due to alterations in the small intestinal
epithelium of psoriatics" [p. 324].
In seeking to reconcile these inconsistent findings
with regard to intestinal permeability in psoriasis, a possible explanation
is that absorption of antigens through the bowel wall is primarily through
the lymphatic system. The 51Cr-labelled EDTA absorption test is sensitive
to lymph movement [29, 30]. Thus, the apparent contradiction may
provide a valuable clue to the pathophysiology of psoriasis. Absorption
of antigens via the intestinal lymphatics may be a significant source of
systemic autointoxication. Because the intestinal lymphatic
absorption vessels (lacteals) drain fats and proteins from the bowel, increased
permeability through the lacteals should lead to increased serum levels
for fats and proteins. Hyperlipoproteinaemia has been documented
in psoriasis [31] and is thought to be a primary factor in the comorbidity
of psoriasis and heart disease [32]. The role of the lymphatic/immune
system in psoriasis will be reviewed in a later section.
In addition to bowel permeability, the intestinal
mucosal structure of psoriatic patients has also been investigated.
Using microscopic analysis of the gut, Shuster and Marks [33] initially
reported structural abnormalities of the jejunal mucosa in psoriasis, but
later withdrew the claim citing faulty analysis technique and small sample
size [25]. Barry et al. [34,35] created a more precise grading
system for measuring bowel mucosal architecture pathology which demonstrated
differences in jejunal mucosa in psoriatic patients as compared to normal
controls. The researchers focused on severe psoriasis (greater than
50% surface area involved). "Both the structural and functional intestinal
changes described suggest that there is a decrease in the small bowel surface
area in patients with severe psoriasis" [35, p. 877]. Thus, smoothing
of the intestinal wall in the jejunal area of the bowel is regarded as
a feature of severe psoriasis. In addition to the normal controls,
an additional comparison group included sick and wasting individuals.
The results indicated that pathological changes in the small bowel mucosal
architecture are not specific to psoriasis, but may also be found in patients
who are sick and losing weight from other causes. The nonspecific
aspect of intestinal permeability is consistent with the Pagano hypothesis
cited above [6]. More recently, Hendel et al. [36] reported that
6 of 15 patients had abnormal jejunal histology, with short villi.
Michaelsson et al. [37] found that 37 psoriasis patients
had highly increased numbers of tryptase-positive mast cells in the duodenal
stroma. The authors hypothesized "that there are at least two types
of abnormalities in the duodenal mucosa in psoriasis, one type that is
present in most psoriasis patients and characterized by an increase in
mast cells and eosinophils, and another that is present in a subgroup of
patients with antibodies to gliadin and an increased number of duodenal
intraepithelial lymphocytes" [p. 866]. Michaelsson et al. had previously
noted physiological abnormalities in the duodenal mucosa of psoriasis patients
involving increased lymphocyte infiltration and IgA antibodies to gliadin
[38], and elevated serum eosinophil cationic protein with increased numbers
of EG2 positive eosinophils in the duodenal mucosa of psoriasis patients
[39].
AUTOINTOXICATION IN PSORIASIS
Autointoxication is an ancient theory based on the
belief that intestinal toxins can enter the circulation and poison the
body. The concept probably originated in Egypt or Greece. The
Greek version recognized a broad range of pathological agents including
residues of food, bile and phelgm as portrayed in the humoral theory of
disease [40]. Until the early 20th century, autointoxication was
widely accepted and various therapies (such as colonic irrigation) were
commonly used for a variety of systemic disorders [41]. Unsupported
by scientific evidence, the autointoxication concept fell out of favor
several decades ago. However, the growing body of information linking
intestinal disease, excessive intestinal permeability, and systemic illness
has revived the theory [12, 42]. Similar concepts such as multiple
chemical sensitivities [43] and endotoxins [40] are also now gaining in
favor.
The concept of autointoxication in psoriasis gained
support from numerous case reports suggesting that dialysis is efficacious
in the treatment of psoriasis. As early as 1965, dialysis was used
by Russian clinicians for the treatment of psoriasis [11]. In 1976
McEvoy and Kelly reported that a uremic patient with psoriasis experienced
clearing of skin lesions while being treated with hemodialysis [44].
Numerous subsequent reports documented the efficacy of dialysis in decreasing
psoriatic lesions [45-50]. However, a controlled trial with 7 patients
by Nissenson et al. [51] failed to confirm the efficacy of dialysis for
psoriasis. Halevy et al. [52] pointed out methodological flaws in
the Nissenson et al. study, especially a predominance of patients with
psoriatic erythroderma, a form regarded as particularly unresponsive to
dialysis. A notable double-blind crossover study of 5 patients [53]
resulted in two patients with complete clearing, two patients had greater
than 75% clearing, and one patient had no substantial response. None
of the five patients responded to the sham dialysis procedure.
A study by Sobh et al. [54] compared hemodialysis,
peritoneal dialysis, and Goeckerman treatment (coal tar dressings and ultraviolet
light). Forty patients with severe psoriasis (greater than 50% body
surface area affected) were randomly assigned to treatment groups.
Statistical analysis of the data obtained following ten dialysis sessions
showed better response in peritoneal than hemodialysis, and both were better
than Goeckerman treatment. The researchers concluded that dialysis
treatment is a good therapeutic modality, especially for those with severe
lesions in whom mortality and morbidity are high, especially if other potent
therapeutic modalities are contraindicated.
Practically speaking, dialysis has not assumed a
prominent position among the various therapeutic options available to clinicians.
In reviewing the literature, Halevy et al. concluded that "dialysis does
have an effect on psoriasis and that this effect is more prominent after
peritoneal dialysis than after hemodialysis. The clinical response
is not always complete, however, and in most cases short lasting.
For these reasons, and because such therapy is not a simple procedure,
dialysis is not a practical mode of treatment for psoriasis" [10,
p. 72].
From a conceptual standpoint, the apparent therapeutic
efficacy of dialysis is supportive of an autointoxication model of psoriasis.
"The mechanism by which dialysis affects psoriasis is unknown. Removal
of some substances from the bloodstream is the most likely explanation.
These substances could be carried free in plasma or on white blood cells
and removed in the peritoneal dialysate during treatment" [55, p.
1179]. The reported increased efficacy of peritoneal dialysis
over hemodialysis may be linked to the fact that peritoneal dialysis can
remove solutes of higher molecular weight in larger quantities than hemodialysis
[56]. Although the psoriasis/dialysis literature is complex
and at times conflicting, the overall thrust of this body of data supports
the plausibility of an intestinal etiology in psoriasis which involves
autointoxication via the absorption and circulation of toxins from the
digestive tract. One possible explanation is that, for psoriasis
patients whose kidneys are weak or overtaxed, the overload of toxins may
enter the superficial circulation and eventually provoke an immune response
in the skin.
LYMPHATIC AND IMMUNE SYSTEM INVOLVEMENT IN PSORIASIS
Recently, psoriasis has been grouped with numerous
other systemic disorders which are related to immune system dysfunction.
One of the seminal events in drawing attention to the autoimmune aspects
of psoriasis was the chance clinical observation that psoriasis improved
in patients treated with cyclosporine, a drug used to prevent rejection
of transplanted organs. Immunotherapeutic drugs have since been used
extensively to suppress immune reactions in psoriasis.
Autoimmune diseases are caused by over stimulation
of the body's own immune defenses, in which the immune cells attack healthy
cells. In psoriasis, immune system T cells become activated and stay
turned on causing the skin to constantly regenerate itself. The specific
trigger for T cell activation is unknown, but may be an antigen, a bacterial
or viral infection, or an environmental factor. Even bacterial DNA,
previously considered immunologically inert, has been recently shown to
trigger immune responses [57].
Although there is no animal model imitating psoriasis
completely, some aspects of psorasis (particularly arthritis) may be mirrored
in HLA-B27 transgenic animals [58]. Similar to human disease, experimental
animals with HLA-B27 transgene also develop spontaneous inflammatory disease.
In addition to HLA-B27, the role of environmental antigens has been implicated
in the animal models. Many B27-linked diseases begin after an infection
with an enterobacteria, suggesting a role for environmental antigens in
addition to an HLA-B27 molecule, but how bacteria interact with HLA-B27
is not yet clearly understood [59].
The human body is in continuous relationship with
the outer environment. Various allergens are known to trigger autoimmune
responses. Furthermore, autoimmune disorders have inner, self-perpetuating
causes, such as medicines and food materials. It is important
to keep in mind that food is a primary source of the external environment
that interacts with the immune system within the body. In addition
to inherently toxic substances that may be ingested, intact peptides and
proteins are absorbed into the circulation [60]. Thus, diet may play
a significant role in autoimmune diseases.
The bowel has protection from harmful materials which
are ingested. The process of absorption takes place via the microvilli
of the intestinal walls. Normal bowel permeability permits assimilation
of nutrients while providing protection against pathogens being absorbed
into the systemic circulation.
Food-enriched blood from the bowel is processed in
the liver where most immune-complexes are removed. The other pathway
of intestinal absorption is through lymphatic circulation. The abdominal
lymph vessels are channeled into the thoracic duct, which drains the lymph
into the subclavian vein. In both circulatory patterns (blood and
lymph), antigens are eventually directed to the liver where they may be
removed from the circulation or made harmless to the body's tissues.
If the antigens are passed beyond the liver, they will circulate through
the lungs, heart, kidneys, and then to the rest of the body where they
may disrupt the functioning of various systems. In a healthy body,
appropriate bowel permeability and adequate liver and kidney functioning
are able to maintain a level of minimal systemic toxicity which can be
easily managed by the immune system.
Intestinal permeability can become excessive (so-called
"leaky gut syndrome") due to a wide variety of factors including alcohol
consumption, bacterial or viral infection, reduced blood flow (resulting
from injury, surgery or atherosclerosis), certain drugs (NSAIDS), etc.
If the amount of circulating toxins becomes excessive, and if the liver
and kidneys are unable to keep up, autointoxication can result. The
immune system reacts to antigens producing the characteristic inflammation
associated with autoimmune diseases. Psoriatic skin lesions and arthritis
are two possible outcomes from this process.
The immune and lymphatic systems are key factors
in this process. In addition to the lymphatic vessels in the intestinal
microvilli, the intestinal tract is a mucosal immune system lined with
lymph nodes (Peyer's patches) and solitary lymphoid nodules [61].
Thus, the mucosal epithelial surfaces of the intestine are important mediators
in the interaction between external and internal milieus.
Beyond the intestinal tract, lymphatic circulation
has been implicated in the pathophysiology of skin disease with regard
to lymphoctye migration into the skin. Jalkanen et al. [62] studied
lymphatic circulation patterns in celiac disease (CD) and dermatitis herpetiformis
(DH). They observed that "the staining results of inflamed duodenum
in DH and CD were identical with those obtained from inflamed skin.
Because more specific markers are not presently available in the human
system, we cannot exclude the possibility that there is a common lymphocyte-endothelial
cell-interaction system for differing sites of inflammation" [p.
791]. Lymphatic/immune system involvement in psoriasis is well established,
although the precise homing mechanism by which lymphocytes migrate to the
skin remains unknown [63-65].
The concept of autoimmune inflammatory response produced
by leaky gut and the ensuing autointoxication is not limited to psoriasis
and other inflammatory skin diseases, but may also apply to various systemic
conditions. For example, Swank and Deitch [42] described the relationship
between intestinal permeability, autoimmune inflammatory reactions, systemic
disease, and comorbidity in multiple organ failure as a complex process
of bacterial translocation.
"It is clear that increased gut permeability and bacterial
translocation play a role in multiple organ failure (MOF). Failure
of the gut barrier remains central to the hypothesis that toxins escaping
from the gut lumen contribute to activation of the host's immune inflammatory
defense mechanisms, subsequently leading to the autointoxication and tissue
destruction seen in the septic response characteristic of MOF. However,
the role of the gut is more than that of a sieve, which simply allows passage
of bacteria and endotoxin from the gut lumen to the portal or systemic
circulation. It appears, in addition, that the translocation of bacteria
and endotoxin may lead to local activation of the immune inflammatory system
and the local production of cytokines and other immune inflammatory mediators
." [42, p. 411].
Thus, in viewing psoriasis as a systemic disorder
involving increased autoimmune reactivity in the skin (and to the joints
in psoriatic arthritis), the intestinal tract and lymphatic system take
on important roles with regard to etiology and pathophysiology of the disorder.
Naturally, diet and nutrition also become important in the cause
and treatment of psoriasis.
DIET AND PSORIASIS
Based on the substantial literature linking bowel
pathology to skin disease, it is not surprising that dietary factors are
well represented in the psoriasis literature. There have been numerous
dietary approaches for psoriasis dating back many years. Although
the literature does support the idea that diet can have significant positive
effects on psoriatic symptoms, the evidence is complex and open to various
interpretations.
For example, Schamberg [66] reported remarkable
treatment efficacy using a low-protein diet. The typical diet contained
about 30 gm of protein. Typically, patients were hospitalized
for three to four weeks. Lerner and Lerner [67] reported a 69-year-old
man whose psoriasis improved on a low-protein diet and exacerbated on a
high-protein steak diet. Roe [68,69] reported good results with a
low-taurine diet in psoriasis. Because the principal source of taurine
is animal protein, a low-taurine diet is necessarily a low-protein diet.
However, reports from some observers do not support
the efficacy of a low-protein diet for psoriais. Zackheim and Farber
[70] failed to see significant improvement in 13 psoriatic patients who
were hospitalized for periods of 4 to 17 weeks. Kwitten and Kantor
[71] reported on a 37-year-old man whose psoriasis failed to improve on
a starvation diet consisting of one head of lettuce, two medium-sized tomatoes,
one cucumber, tea, and 12 ounces of soda daily for six days a week.
The estimated protein consumption was 4.7 gm per day. Interestingly,
Pagano [6] believes that certain foods (including carbonated beverages
and tomatoes) contribute significantly to psoriasis. Simplistic models
of dietary effects in psoriasis invariably fall short of validation.
Food deprivation has been associated with improvement
in psoriatic symptoms. Simons [72] reported that 8 of 13 Dutch prisoners
with psoriasis improved in Japanese concentration camps in Java in World
War II, while on a near starvation diet. Some observers feel
that psoriasis is exacerbated with weight gain [73, 74]. Others have
reported remissions with weight loss under conditions of prolonged food
deprivation [72]. Although some physicians feel that psoriasis diminishes
during periods of food deprivation or poor nutrition, there is no consensus
on this point [70].
Spiera and Lefkovits [75] reported dramatic improvement
in four psoriatic patients who were placed on a diet believed to be low
in tryptophan. The patients substituted turkey meat for regular sources
of meat. Symptoms decreased while on the turkey diet and increased
when the previous diet was resumed. Later measurements of the tryptophan
levels of turkey meat indicated an error in the original calculations -
turkey meat is not devoid of tryptophan. Although tryptophan level
was probably not a factor in the clinical improvement, perhaps the change
in protein sources was influential.
Dietary supplementation with fatty acids (fish oil)
has been credited for the improvement of psoriatic patients. Kromann
and Green [76] observed a decreased incidence of psoriasis in fish-eating
Greenland Eskimos. This finding, combined with evidence for epidermally
derived eicosanoids in the pathogenesis of psoriasis [77], led Ziboh et
al. [78] to investigate the effect of fish oil dietary supplementation
on psoriatic symptoms. Global evaluation showed that 8 of 13 patients
demonstrated mild to moderate improvement of their psoriatic lesions.
Further studies [79-82] supported the claim for modest improvement in psoriasis
for patients consuming daily dosages of fish oil. As with much
of the psoriasis literature, the effects of fish oil supplementation are
variable. Fish oil has been found to be no better than corn oil [83]
or olive oil [84] in reducing psoriasis symptoms. Kettler et al.
[85] noted that although 25 patients with plaque-type psoriasis vulgaris
showed no significant clinical improvement while taking fish oil supplement,
one patient with generalized pustular psoriasis show marked improvement.
It may be that fish oil is most helpful for certain individuals or specific
forms of psoriasis.
Pagano [6] reports significant improvement of psoriasis
in patients using a restrictive diet (discussed below) and dietary supplementation
with herbal teas (most often yellow saffron and slippery elm) and olive
oil. Yellow saffron (Carthamus tinctorius) has been shown to possess
anti-inflammatory [86, 87] and immunosuppressive properties [88].
Slippery elm (Ulmus fulva) is an herb used traditionally for digestive
difficulties, stomach and intestinal ulcers, and colitis. Slippery elm
is a demulcent, high in mucilage, noted for its ability to soothe or protect
irritated mucous membranes [89-91]. Although herbal therapy has been
used effectively for atopic dermatitis [92-95], Pagano appears to be the
primary advocate of herbal therapy for psoriasis.
In an epidemiological study of the association between
diet and psoriasis, Naldi et al. [96] noted that dietary factors may influence
psoriasis and modulate its clinical expression in an Italian population.
Notably, increased intake of fresh vegetables and fruit was linked to a
decreased prevalence of psoriasis. This study is in agreement with
a similar prevalence survey in a Norwegian population [97].
In summary, diet does seem to play a role in the
etiology and treatment of psoriasis. In general, a diet of fresh
fruits and vegetables and low protein seems helpful. On the other
hand, diet is a highly individual matter. Food allergies and sensitivities
(e.g. coeliac disease) may play a role for certain individuals while others
may be relatively unaffected by the same foods. The degree of gut
permeability and the system's ability to handle autointoxication are important
factors in this regard. The use of dietary supplements (e.g., fish
oil) may be helpful for specific individuals. Research has tended
to look for "the" dietary factor (whether protein, taurine, fatty oils)
which is problematic for psoriatics. A multifactorial model which
recognizes human diversity and systemic interactions will probably be most
useful in clinical practice. Assessment of individual dietary patterns
and reactions could be of use in understanding the process, in both research
and clinical settings.
DISCUSSION
Psoriasis is a complex disorder involving a variety
of factors. Therefore a multifactorial approach is needed to integrate
the various aspects of psoriasis into a plausible model which addresses
both the theoretical and clinical dimensions of the illness. The
sources cited above point to the bowel as one possible integrative factor
in the etiology, pathogenesis and treatment of psoriasis. The section
which follows is speculative, and focuses on the central themes of an intestinal
model. These include:
-
Bowel Pathology: Due to injury, illness and/or poor dietary habits, a variety
of abnormalities in the upper small bowel (duodenum and/or jejunum) compromise
the integrity of the intestinal tract. Various microorganisms may
be involved in bowel pathology in psoriasis. From a clinical standpoint,
screening for microorganisms is an appropriate early step in the assessment
process [20, 98].
-
Intestinal permeability and autointoxication: Deterioration of the intestinal
wall results in a smoothing effect to intestinal villi and a thinning of
the intestinal wall, particularly in the upper portion of the small bowel.
Microorganisms and/or other toxins that would normally be eliminated or
restricted to the bowel are absorbed into the circulation (autointoxication).
Additional bowel permeability studies using the 51Cr-labeled EDTA absorption
test as per Humbert et al. [28] are needed to determine the prevalence
of intestinal permeability in psoriasis.
-
Lymphatic/Immune System Involvement: The lymphatic/immune system is a likely
channel by which the pathogens enter the systemic circulation. An
immune response to the misplaced pathogens produces the various forms of
psoriatic lesion, depending upon the type of pathogen and the unique response
of the individual system.
-
Comorbidity: Because the systemic toxicity associated with intestinal permeability
provides access to various organs in the body, toxicity can manifest in
a variety of conditions in addition to psoriasis, most notably joint disease.
There is a need for further research to clarify the extent of comorbidity
and the specific causal relationships between psoriasis and other systemic
illnesses.
-
Natural Therapeutics: "Cure by removal of cause" via natural healing
modalities such as diet and nutritional supplementation can assist with
internal cleansing and healing the gut. The sources cited in the
preceding section support the notion that a diet consisting primarily of
fresh fruits and vegetables and low in protein can be helpful for some
individuals suffering from psoriasis. In addition to a cleansing
diet, the work of Pagano [6] suggests that herbal teas may be helpful in
healing the intestine. Specifically, yellow saffron tea and slippery
elm are mainstays of Pagano's approach. Avoidance of foods which
contribute to systemic toxicity may require careful monitoring of the effects
of specific foods or food groups. For example, Pagano observed that
the nightshade group (tomatoes, eggplant, peppers, etc.) tends to exacerbate
psoriasis.
Psoriasis has a genetic aspect which can best be regarded
as a predisposition or vulnerability. The diathesis/stress concept
in which a genetic vulnerability is triggered into action via environmental
or endogenous stressor is an excellent model of this view of hereditary
factors in psoriasis. In addition to a predisposition for skin disease,
an individual may also possess hereditary predispositions for other conditions
which are known to be comorbid with psoriasis. In other words, the
autointoxication manifests most obviously in weak systems of the body.
The genetic diathesis may involve a predisposition for increased bowel
permeability or a tendency to for the immune system to react to certain
toxins. Stressors may be physical, social or psychological.
Although not directly related to intestinal etiology
in psoriasis, treatment compliance is a practical concern for anyone attempting
significant lifestyle changes (such as diet). Psychosocial support
should be considered as an adjunct to clinical interventions for any condition
requiring substantial lifestyle changes. For example, Ornish et al.
[99] convincingly demonstrated the role of group support with regard to
intensive lifestyle changes for reversing coronary heart disease.
Abel et al., [100] recognized the beneficial effects of psychosocial support
for stress reduction, improvement of coping skills, and health education
in psoriasis patients. Because stress has been linked to increased
psoriatic symptoms [101-103], psychosocial support and stress reduction
training are reasonable adjuncts to any psoriasis treatment program.
Thus, the therapeutic model advocated in this article
is holistic and integrative. The diet is intended to avoid foods
that irritate the gut or increase autointoxication. Although each
individual is unique, in general the diet is intended to improve assimilation
of nutrients and elimination of toxins. Essentially, the diet consists
mainly of fruits and vegetables while avoiding fried foods and refined
carbohydrates ("junk food"). The nightshade vegetables (such as tomatoes
and peppers) are avoided [6]. For some individuals, colonic irrigation
may be helpful for cleansing the lower bowel and decreasing autointoxication
[4,5].
Evidence of the efficacy of this intestinal model
rests largely on the numerous case reports documented by Pagano [6].
Pagano has conducted over 15 years of clinical studies resulting in impressive
before-and-after photography of the total clearing of severe psoriatic
lesions in numerous individuals. Longitudinal case reports of these
patients strongly support the contention that the model is effective in
healing psoriasis.
Our own clinical observations in cases of psoriasis
treated according to Pagano's protocol lend some support to his approach.
Seven of the nine patients in one group exhibited decreased psoriasis symptoms;
three had essentially complete clearing of skin lesions. In a later group
of five patients, all five showed improvement when treated according to
the Pagano protocol. More case studies from other investigators and controlled
clinical studies will be necessary to confirm these observations.
CONCLUSION
The etiology of psoriasis involves varied factors,
both specific and nonspecific. Based on the literature, the bowel
pathology model described in this article provides a conceptual framework
for understanding certain systemic features of psoriasis. Clearly,
intestinal etiology in psoriasis does not account for all the varied manifestations
of the illness. Yet it does provide a plausible approach for integration
of some of the diverse research and clinical information in the literature.
An integrative medicine model, in which standard
medical treatments (which can often provide temporary symptomatic relief)
are integrated with natural therapeutics (intended to address more fundamental
causes), is proposed as a plausible next step in the treatment of psoriasis.
Additional research is needed to further document the clinical effectiveness
of this model, to evaluate the role of bowel permeability in psoriasis,
and to determine which elements of the treatment protocol contribute to
the improvement in symptoms.
REFERENCES
1. Espinoza LR, van Solingen R, Cuellar ML, Angulo J. Insights into
the pathogenesis of psoriasis and psoriatic arthritis. Am J Med Sci 1998;316:271-6.
2. Tristani-Firouzi P, Krueger GG. Efficacy and safety of treatment
modalities for psoriasis. Cutis 1998;61(2 Suppl):11-21.
3. Sander HM, Morris LF, Phillips CM, Harrison PE, Menter A. The annual
cost of psoriasis. J Am Acad Dermatol 1993;28:422-5.
4. Landsford, FD. Psoriasis. In: McGarey W, editor. Physicians
reference notebook. Virginia Beach, VA: A.R.E. Press, 1983. p. 303-11.
5. Mein E. Keys to health. New York: Harper & Row,
1989.
6. Pagano J. Healing psoriasis: the natural alternative. Englewood
Cliffs, NJ: The Pagano Organization, Inc., 1991.
7. Weissman MM, Merikangas KR, Wickramaratne P, Kidd KK, Prusoff BA,
Leckman JF, Pauls DL. Understanding the clinical heterogeniety of major
depression using family data. Arch Gen Psychiatry 1986;43:430-4.
8. Henseler T, Christophers E. Disease concomitance in psoriasis. J
Am Acad Dermatol 1995; 32:982-6.
9. Anderson PC. Dialysis treatment of psoriasis. Arch Dermatol 1981;117:67-8
10. Halevy S, Halevy J, Boner G, Rosenfeld JB, Feuerman EJ. Dialysis
therapy for psoriasis. Report of three cases and review of the literature.
Arch Dermatol 1981;117:69-72.
11. Kramer P, Brunner FP, Brynger H, Chantler C, Donckerwolcke RA,
Jacobs C, Selwood NH, Wing AJ. Dialysis treatment and psoriasis in Europe.
Clin Nephrol 1982;18:62-8.
12. Person JR, Bernhard JD. Autointoxication revisited. J Am Acad Dermatol
1986;15:559-63.
13. D'Amico E, Palazzi C, Capani F. Remission of psoriatic arthritis
after porto-caval anastomosis in a patient with primary biliary cirrhosis.
J Rheumatol 1999;26:236.
14. Porres JM. Jejunoileal bypass and psoriasis. Arch Dermatol
1977;113:983.
15. Yates VM, Watkinson G, Kelman A. Further evidence for an association
between psoriasis, Crohn's disease and ulcerative colitis. Br J Dermatol
1982;106:323-30.
16. Menzel I, Holzmann H. Uberlegungen zum seborrhoischen Kopfekzem
und der Psoriasis capillitii im Zusammenhang mit intestinalen Mykosen.
Z Hautkr 1986;61:451-4.
17. Yaffee HS. Relationships of microorganisms to psoriasis - toxic
or allergic? Arch Dermatol 1971;104:560-1.
18. Buslau M, Menzel I, Holzmann H. Fungal flora of human faeces in
psoriais and atopic dermatitis. Mycoses 1990;33:90-4.
19. Senff H, Bothe C, Busacker J, Reinel D. Studies on the yeast flora
in patients suffering from psoriasis capillitii or seborrhoic dermatitis
of the scalp. Mycoses 1990;33:29-32.
20. Rosenberg EW, Noah PW, Skinner RB. Microorganisms and psoriasis.
J Natl Med Assoc 1994;86:305-10.
21. Espinoza LR. Psoriatic arthritis. Further epidemiological
and genetic considerations. In: Gerber LH, Espinoza LR, editors.
Psoriatic Arthritis, New York: Grune & Stratton, 1985.
22. Mielants H, Veys EM, Cuvelier C, De Vos M, Goemaere S, De Clercq
L, Schatteman L, Gyselbrecht L, Elewaut D J. The evolution of spondyloarthropathies
in relation to gut histology. III. Relation between gut and joint. Rheumatol
1995;22:2279-84.
23. Schatteman L, Mielants H, Veys EM, Cuvelier C, de Vos M, Gyselbrecht
L, Elewaut D, Goemaere S. Gut inflammation in psoriatic arthritis: a prospective
ileocolonoscopic study. J Rheumatol 1995;22:680-83.
24. Fry L. The gut and the skin. Postgrad Med J 1970;46(541):664-70.
25. Marks J, Shuster S. Small-intestinal mucosal abnormalities in various
skin diseases - fact or fancy? Gut 1970;11:281-91.
26. De Vos R J, De Boer, WA, Haas FD. Is there a relationship
between psoriasis and coeliac disease? J Intern Med 1995;237:118.
27. Hamilton I, Fairris GM, Rothwell J, Cunliffe WJ, Dixon MF, Axon
AT. Small intestinal permeability in dermatological disease. Q J Med 1985;56(221):559-67.
28. Humbert P, Bidet A, Treffel P, Drobacheff C, Agache P. Intestinal
permeability in patients with psoriasis. J Dermatol Sci 1991;2:324-6.
29. MacDonald HR. Early detection of potentially lethal events in T
cell-mediated cytolysis. Eur J Immunol 1975;5:251-4.
30. Freitas AA, de Sousa M. Control mechanism of lymphocyte traffic.
Altered migration of 51Cr- labeled mouse lymph node cells pretreated in
vitro with phospholipases. Eur J Immunol 1976;6:703-11.
31. Brustein DM, Scher RK, Auerbach R. Hyperlipoproteinaemia and psoriasis.
Lancet 1976;1(7951):154.
32. Seishima M, Seishima M, Mori S, Noma, A. Serum lipid and apolipoprotein
levels in patients with psoriasis. Br J Dermatol 1994;130:738-42.
33. Shuster S, Marks J. Psoriatic enteropathy, a new cause of steatorrhoea.
Lancet 1965;1:1367-8.
34. Barry RE, Salmon PR, Read AE, Warin RP. Mucosal architecture of
the small bowel in cases of psoriasis. Gut 1971;12:873-7.
35. Barry RM, Salmon PR, Read, AE. Small bowel mucosal changes
in psoriasis. Gut 1971;12:495.
36. Hendel L, Hendel J, Johnsen A, Gudmand-Hoyer E. Intestinal function
and methotrexate absorption in psoriatic patients. Clin Exp Dermatol 1982;7:491-8.
37. Michaelsson G, Kraaz W, Hagforsen E, Pihl-Lundin I, Loof L.
Psoriasis patients have highly increased numbers of tryptase-positive mast
cells in the duodenal stroma. Br J Dermatol 1997;136:866-70.
38. Michaelsson G, Kraaz W, Gerden B, Hagforsen E, Hjelmqvist G, Loof
L, Sjoberg O, Scheynius A. Increased lymphocyte infiltration in duodenal
mucosa from patients with psoriasis and serum IgA antibodies to gliadin.
Br J Dermatol 1995;133:896-904.
39. Michaelsson G, Kraaz W, Gerden B, Hagforsen E, Lundin IP, Loof
L, Sjoberg O, Scheynius A. Patients with psoriasis have elevated levels
of serum eosinophil cationic protein and increased numbers of EG2 positive
eosinophils in the duodenal stroma. Br J Dermatol 1996;135:371-8.
40. Chen TS, Chen PS. Intestinal autointoxication: a medical leitmotif.
J Clin Gastroenterol 1989;11:434-41.
41. Ernst EJ. Colonic irrigation and the theory of autointoxication:
a triumph of ignorance over science. J Clin Gastroenterol 1997;24:196-8.
42. Swank GM, Deitch EA. Role of the gut in multiple organ failure:
bacterial translocation and permeability changes. World J Surg 1996;20:411-7.
43. Gots RE. Medical hypothesis and medical practice: autointoxication
and multiple chemical sensitivities. Regul Toxicol Pharmacol 1993;18:2-12.
44. McEvoy J, Kelly AMT. Psoriatic clearance during hemodialisis. Ulster
Med J 1976;45:76-8.
45. Twardowski ZJ. Abatement of psoriasis and repeated dialysis. Ann
Intern Med 1977;86:509-10.
46. Twardowski ZJ, Nolph KD, Rubin J, Anderson PC. Peritoneal dialysis
for psoriasis. An uncontrolled study. Ann Intern Med 1978;88:349-51.
47. Buselmeier TJ, Kjellstrand CM, Dahl MV, Cantieri JS, Nelson RS,
Burgdorf WC, Bentley CR, Najarian JS, Goltz RW. Treatment of psoriasis
with dialysis. Proc Eur Dial Transplant Assoc 1978;15:171-7.
48. Chen WT, Hu CH, Schiltz JR, Nakamoto S. In search of "psoriasis
factor(s)": a new approach by extracorporeal treatment. Artif Organs 1978;2:203-5.
49. Muston HL, Conceico S. Remission of psoriasis during haemodialysis.
Br Med J 1978;1(6111):480-1.
50. Glinski W, Jablonska S, Imiela J, Nosarzewski J, Jarzabek-Chorzelska
M, Haftek M, Obalek S. Continuous peritoneal dialysis for treatment of
psoriasis. I. Depletion of PMNL as a possible factor for clearing of psoriatic
lesions. Arch Dermatol Res 1979;265:337-41.
51. Nissenson AR, Rapaport M, Gordon A, Narins RG. Hemodialysis in
the treatment of psoriasis. A controlled trial. Ann Intern Med 1979;91:218-20.
52. Halevy S, Halevy J, Rosenfeld JB, Feuerman E. Dialysis for psoriasis.
Ann Intern Med 1980;92:263.
53. Whittier FC, Evans DH, Anderson PC, Nolph KD. Peritoneal dialysis
for psoriasis: a controlled study. Ann Intern Med 1983;99:165-8.
54. Sobh MA, Abdel Rasik MM, Moustafa FE, el-Sharabasy MM, Rezk RA,
el-Shamy SI. Dialysis therapy of severe psoriasis: a random study
of forty cases. Nephrol Dial Transplant 1987;2:351-8.
55. Twardowski ZJ, Lempert KD, Lankhorst BJ, Welton WA, Whittier FC,
Anderson PC, Nolph KD, Khanna R, Prowant BF, Schmidt LM. Continuous ambulatory
peritoneal dialysis for psoriasis. A report of four cases. Arch Intern
Med 1986;146:1177-9.
56. Steck WD, Nakamoto S, Bailin PL, Paganini E, Chang K, Becker JM,
Matkaluk RM, Vidt DG. Hemofiltration treatment of psoriasis. J Am Acad
Dermatol 1982;6:346-9.
57. Pisetsky DS. DNA and the immune system. Ann Intern Med 1997;126:169-71
58. Taurog JD. Arthritis in HLA-B27 transgenic animals. Am J Med Sci
1998;316:250-6.
59. Khare SD, Luthra HS, David CS. Unraveling the mystery of HLA-B27
association with human spondyloarthropathies using transgenic and knock
out mice. Semin Immunol 1998;10:15-23.
60. Gardner ML. Gastrointestinal absorption of intact proteins. Ann
Rev Nutr 1988; 8:329-50.
61. Bienenstock J, Ernst PB, Underdown, BJ. The gastrointestinal tract
as an immunologic organ - state of the art. Ann Allergy 1987;59:17-20.
62. Jalkanen S, Saari S, Kalimo H, Lammintausta K, Vainio E, Leino
R, Duijvestijn AM, Kalimo K. Lymphocyte migration into the skin: the role
of lymphocyte homing receptor (CD44) and endothelial cell antigen (HECA-452).
J Invest Dermatol 1990;94:786-92.
63. Chin YH, Falanga V, Streilin JW, Sackstein R. Lymphocyte recognition
of psoriatic endothelium: evidence for a tissue-specific receptor/ligand
interaction. J Invest Dermatol 1989;93 supplement:82S-87S.
64. Bacon KB, Camp RDR. Lipid lymphocyte chemoattractants in psoriasis.
Prostaglandins 1990;40:603-14.
65. Arvilommi A, Salmi M, Kalimo K, Jalkanen S. Lymphocyte binding
to vascular endothelium in inflamed skin revisited: a central role for
vascular adhesion protein-1(VAP-1). Eur J Immunol 1996;26:825-33.
66. Schamberg JF. Dietary treatment of psoriasis. JAMA 1932;98:1633.
67. Lerner MR, Lerner AB. Psoriasis and protein intake. Arch Dermat
1964;90: 217.
68. Roe DA. Nutrient requirements in psoriasis. New York J Med 1965;65:1319-26.
69. Roe DA. Current concepts of the low taurine diet in psoriasis.
Cutis 1966;2:1013-20.
70. Zackheim HS, Farber EM. Low-protein diet and psoriasis. A hospital
study. Arch Dermatol 1969;99:580-6.
71. Kwitten J, Kantor I. Psoriasis and diet. N Y State J Med
1967;67:587-8.
72. Simons RD. Additional studies on psoriasis in the tropics and in
starvation camps. J Invest Dermat 1949;12:285.
73. Baden HP. The treatment of psoriasis. N Eng J Med. 1963;269: 907.
74. Farber EM, Roth RJ. Current concepts in the diagnosis and treatment
of psoriasis, GP 1964;29:94-9.
75. Spiera H, Lefkovitz AM. Remission of psoriasis with low dietary
tryptophan. Lancet 1967; 2(7507):137-9.
76. Kromann N, Green A. Epidemiological studies in the Upemavik District,
Greenland. Acta Med Scand 1980;200:401-6.
77. Voorhees JJ. Leukotrienes and other lipoxygenase products in the
pathogenesis and therapy of psoriasis and other dermatoses. Arch Dermatol
1983;119:541-7.
78. Ziboh VA, Cohen KA, Ellis CN, et al. Effects of dietary supplementation
of fish oil on neutrophil and epidermal fatty acids. Arch Dermatol 1986;122:1277-82.
79. Maurice PDL, Allen BR, Barkley ASJ, et al. The effects of dietary
supplementation with fish oil in patients with psoriasis. Br J Dermatol
1987;117:599-606.
80. Bittiner SB, Tucker WFG, Cartwright L, Bleehen S. A double-blind,
randomized, placebo-controlled study of fish oil in psoriasis. Lancet 1988;1(8582):378-80.
81. Kragballe K, Fogh K. A low-fat diet supplemented with dietary fish
oil (Max-EPA) results in improvement of psoriasis and in formation of leukotriene
B5. Acta Derm Venereol 1989;69:23-8.
82. Collier PM, Payne CR. The dietary effect of oil fish consumption
on psoriasis. Br J Dermatol 1996;135:858.
83. Soyland E, Funk J, Rajka G, Sandberg M, Thune P, Rustad L, Helland
S, Middelfart K, Odu S, Falk ES, Solvoll K, Bjorneboe GE, Drevon CA. Dietary
supplementation with very long-chain n-3 fatty acids in patients with atopic
dermatitis. A double-blind multicentre study. Br J Dermatol 1994;130:757-64.
84. Bjorneboe A, Smith AK, Bjorneboe GA, Thune PO, Drevon CA. Effect
of dietary supplementation with n-3 fatty acids on clinical manifestations
of psoriasis. Br J Dermatol 1988; 188:77-83.
85. Kettler AH, Baughn RE, Orengo IF, Black H, Wolf, JE. The effect
of dietary fish oil supplementation on psoriasis. J Am Acad Dermatol 1988;8:1267-73.
86. Xu SX. Anti-inflammatory active constituents of Carthamus
tinctorius. Chung Yao Tung Pao 1986;11:42-4.
87. Akihisa T, Yasukawa K, Oinuma H, Kasahara Y, Yamanouchi S, Takido
M, Kumaki K,
Tamura T. Triterpene alcohols from the flowers of compositae and their
anti-inflammatory effects. Phytochemistry 1996;43:1255-60.
88. Lu ZW, Liu F, Hu J, Bian D, Li FG. Suppressive effects of safflower
yellow on immune functions. Chung Kuo Yao Li Hsueh Pao 1991;12:537-42.
89. Duke JA. The green pharmacy. Emmaus, PA: Rodale Press, 1997.
90. Golan R. Optimal wellness. New York: Ballantine Books, 1995.
91. Tierra L. The herbs of life. Crossing, CA: The Freedom Press, 1992.
92. Atherton DJ, Sheehan MP, Rustin MHA, et al. Chinese herbs for eczema.
Lancet 1990;336:1254.
93. Sheehan MP, Atherton DJ. A controlled trial of traditional Chinese
medicinal plants in widespread non-exudative atopic eczema. Br J Dermatol
1992;126:179-84.
94. Sheehan MP, Rustin MHA, Atherton DJ, et al. Efficacy of traditional
Chinese herbal therapy in adult atopic dermatitis. Lancet 1992;340:13-7.
95. Atherton DJ, Sheehan MP, Rustin MHA, et al. Treatment of atopic
eczema with traditional Chinese medicinal plants. Pediatr Dermatol 1992;9:373-5.
96. Naldi L, Parazzini F, Peli L, Chatenoud L, Cainelli T. Dietary
factors and the risk of psoriasis. Results of an Italian case-control study.
Br J Dermatol 1996;134:101-6.
97. Kavli G, Forde OH, Arnesen E et al. Psoriasis: familial predisposition
and environmental factors. Br Med J 1985;291:999-1000.
98. Skinner RB Jr, Rosenberg EW, Noah PW. Antimicrobial treatment
of psoriasis. Dermatol Clin 1995;13:909-13.
99. Ornish D, Scherwitz LW, Billings JH, Gould KL, Merritt TA, Sparler
S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ. Intensive
lifestyle changes for reversal of coronary heart disease. JAMA 1998;280:2001-7.
100. Abel EA, Moore US, Glathe JP. Psoriasis patient support group
and self-care efficacy as an adjunct to day care center treatment. Int
J Dermatol 1990;29:640-3.
101. Winchell SA, Watts RA. Relaxation therapies in the treatment of
psoriasis and possible pathophysiologic mechanisms. J Am Acad Dermatol
1988;18:101-104.
102. Kantor SD. Stress and psoriasis. Cutis 1990;46:321-2.
103. Zachariae R, Oster H, Bjerring P, Kragballe K. Effects of psychologic
interventions on psoriasis: A preliminary report. J Am Acad Dermatol 1996;34:1008-15.
CONTINUING
EDUCATION CREDITS ASSOCIATED WITH THIS MATERIAL
As a service to health professionals
who are required to obtain continuing education, an exam is provided to
test your understanding of some of the key concepts discussed above.
These CEUs are designed to qualify as "Type 2" as required by the Virginia
Board of Medicine for MDs, DOs, and DCs. If you don't practice in
Virginia, check with your state medical board or professional organization
for applicable requirements for continuing education. It is your
responsibility to determine the applicability of this CEU material to your
situation.
-
For more information on the Meridian Institute
Continuing Education Program, click here.
-
To take the EXAM
for this material, click here.
|
|