SYSTEMIC ASPECTS OF PSORIASIS:
AN INTEGRATIVE MODEL BASED ON
David L. McMillin, M.A., Douglas G. Richards,
Eric A. Mein, M.D., Carl D. Nelson, D.C.
Virginia Beach, VA 23454
Copyright 1999, Meridian Institute
All Rights Reserved.
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.
Key Words: psoriasis, intestinal permeability,
Psoriasis is a chronic cutaneous
disease of unknown causation . 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 .
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 . 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
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. According to this
theory, 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.
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 a 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.  have
"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 
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 
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.  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  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.  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  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 .
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 . 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 .
Fry  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 nonspecific 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  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 
have emphasized a nonspecific process in which psoriasis is the primary
disease producing secondary pathology in the small bowel. De Vos et al.
 have noted that psoriasis may be associated with a particular disorder
of the small intestine (coeliac disease). The growing literature on the
spondyloarthropathies  reflects an interest in the systemic manifestations
of auto-immune diseases including psoriatic arthritis.
ABNORMALITIES OF INTESTINAL MUCOSAL STRUCTURE
Pursuing the pathophysiology
of bowel and skin disease comorbidity, researchers have investigated intestinal
permeability as a possible etiological factor. Hamilton et al.  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.  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  and
is thought to be a primary factor in the comorbidity of psoriasis and heart
disease . 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  initially
reported structural abnormalities of the jejunal mucosa in psoriasis, but
later withdrew the claim citing faulty analysis technique and small sample
size . 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 . More recently,
Hendel et al.  reported that 6 of 15 patients had abnormal jejunal
histology, with short villi.
Michaelsson et al.  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
psoriais patients involving increased lymphocyte infiltration and IgA antibodies
to gliadin , and elevated serum eosinophil cationic protein with increased
numbers of EG2 positive eosinophils in the duodenal mucosa of psoriasis
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 . 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 . 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
 and endotoxins  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
. In 1976 McEvoy and Kelly reported that a uremic patient with psoriasis
experienced clearing of skin lesions while being treated with hemodialysis
. 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.  failed to confirm the efficacy of dialysis
for psoriasis. Halevy et al.  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  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. 
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
. 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.
For psoriasis patients whose kidneys are weak or overtaxed, the overload
of toxins may be allowed to 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.
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 . 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
. 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.  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 [60-62].
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 
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
For example, Schamberg 
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  reported a 69-year-old
man whose psoriasis improved on a low-protein diet and exacerbated on a
high-protein steak diet. Roe [65,66] 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  failed to see significant improvement in 13 psoriatic
patients who were hospitalized for periods of 4 to 17 weeks. Kwitten and
Kantor  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  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  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 [70, 71]. Others have
reported remissions with weight loss under conditions of prolonged food
deprivation . Although some physicians feel that psoriasis diminishes
during periods of food deprivation or poor nutrition, there is no consensus
on this point .
Spiera and Lefkovits  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. Kroman and Green  observed a decreased incidence of psoriasis
in fish-eating Greenland Eskimos. This finding, combined with evidence
for a epidermally derived eicosanoids in the pathogenesis of psoriasis
, led Ziboh et al.  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 [76-79] 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 
or olive oil  in reducing psoriasis symptoms. Kettler et al.  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  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 [83, 84] and immunosuppressive
properties . 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 [86-88]. Although herbal therapy
has been used effectively for atopic dermatitis [89-92], Pagano's work
appears to be the primary documentation of herbal therapy for psoriasis.
In an epidemiological study
of the association between diet and psoriasis, Naldi et al.  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
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) play a role for certain individuals
while other 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
is essential, in both research or clinical settings.
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 central
themes of an intestinal model of psoriasis are:
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, 95].
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.  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 are absorbed and transported
for elimination through the skin. 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.
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 tendency
to eliminate circulating toxins through the skin. Stressors may be physical,
social or psychological.
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  documents the efficacy of herbal teas to assist
with 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.
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.  convincingly demonstrated the role of group support
with regard to intensive lifestyle changes for reversing coronary heart
disease. Abel et al.,  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 [98-100], 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 which 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 . For some individuals, colonic irrigation
is helpful for cleansing the lower bowel and decreasing autointoxication
The efficacy of this intestinal
model rests largely on the numerous case reports documented by Pagano .
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
A small pilot study by Meridian
Institute  also investigated the efficacy of the intestinal model.
The study included nine participants with psoriasis (1 man, 8 women, mean
age 50.4 years, age range 12-75 years). They were given the lactulose/mannitol
test for bowel permeability, and the Psoriasis Area and Severity Index
(PASI) examination for psoriatic symptoms. Five of the nine subjects had
abnormal intestinal permeability according to the norms provided by the
Great Smokies Laboratory (63 Zillicoa Street, Asheville, NC 28801-1074).
The subjects were educated and trained in the use of the therapies. They
returned home and applied the protocol on a daily basis, keeping daily
log sheets. Upon return six months later, the assessments were repeated.
Seven of the nine subjects exhibited decreased psoriatic symptoms; three
had essentially complete clearing of the skin lesions. The mean PASI score
decreased from 10.1 to 6.4. There were alterations in bowel permeability
as well, but eight of the nine subjects had permeability outside the normal
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.
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.
5. Mein E. Keys to health. New York: Harper &
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
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
24. Fry L. The gut and the skin. Postgrad Med
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
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
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
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
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
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
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. Gardner ML. Gastrointestinal absorption of
intact proteins. Ann Rev Nutr 1988; 8:329-50.
58. Bienenstock J, Ernst PB, Underdown, BJ. The
gastrointestinal tract as an immunologic organ - state of the art. Ann
59. 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.
60. 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.
61. Bacon KB, Camp RDR. Lipid lymphocyte chemoattractants
in psoriasis. Prostaglandins 1990;40:603-14.
62. 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.
63. Schamberg JF. Dietary treatment of psoriasis.
64. Lerner MR, Lerner AB. Psoriasis and protein
intake. Arch Dermat 1964;90: 217.
65. Roe DA. Nutrient requirements in psoriasis.
New York J Med 1965;65:1319-26.
66. Roe DA. Current concepts of the low taurine
diet in psoriasis. Cutis 1966;2:1013-20.
67. Zackheim HS, Farber EM. Low-protein diet
and psoriasis. A hospital study. Arch Dermatol 1969;99:580-6.
68. Kwitten J, Kantor I. Psoriasis and diet.
N Y State J Med 1967;67:587-8.
69. Simons RD. Additional studies on psoriasis
in the tropics and in starvation camps. J Invest Dermat 1949;12:285.
70. Baden HP. The treatment of psoriasis. N Eng
J Med. 1963;269: 907.
71. Farber EM, Roth RJ. Current concepts in the
diagnosis and treatment of psoriasis, GP 1964;29:94-9.
72. Spiera H, Lefkovitz AM. Remission of psoriasis
with low dietary tryptophan. Lancet 1967; 2(7507):137-9.
73. Kromann N, Green A. Epidemiological studies
in the Upemavik District, Greenland. Acta Med Scand 1980;200:401-6.
74. Voorhees JJ. Leukotrienes and other lipoxygenase
products in the pathogenesis and therapy of psoriasis and other dermatoses.
Arch Dermatol 1983;119:541-7.
75. 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.
76. 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.
77. 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.
78. 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.
79. Collier PM, Payne CR. The dietary effect
of oil fish consumption on psoriasis. Br J Dermatol 1996;135:858.
80. 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.
81. 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.
82. 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.
83. Xu SX. Anti-inflammatory active constituents
of Carthamus tinctorius. Chung Yao Tung Pao 1986;11:42-4.
84. 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
85. Lu ZW, Liu F, Hu J, Bian D, Li FG. Suppressive
effects of safflower yellow on immune functions. Chung Kuo Yao Li Hsueh
86. Duke JA. The green pharmacy. Emmaus, PA:
Rodale Press; 1997.
87. Golan R. Optimal wellness. New York: Ballantine
88. Tierra L. The herbs of life. Crossing, CA:
The Freedom Press; 1992.
89. Atherton DJ, Sheehan MP, Rustin MHA, et al.
Chinese herbs for eczema. Lancet 1990;336:1254.
90. 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.
91. Sheehan MP, Rustin MHA, Atherton DJ, et al.
Efficacy of traditional Chinese herbal therapy in adult atopic dermatitis.
92. Atherton DJ, Sheehan MP, Rustin MHA, et al.
Treatment of atopic eczema with traditional Chinese medicinal plants. Pediatr
93. 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.
94. Kavli G, Forde OH, Arnesen E et al. Psoriasis:
familial predisposition and environmental factors. Br Med J 1985;291:999-1000.
95. Skinner RB Jr, Rosenberg EW, Noah PW. Antimicrobial
treatment of psoriasis. Dermatol Clin 1995;13:909-13.
96. 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.
97. 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.
98. Winchell SA, Watts RA. Relaxation therapies
in the treatment of psoriasis and possible pathophysiologic mechanisms.
J Am Acad Dermatol 1988;18:101-104.
99. Kantor SD. Stress and psoriasis. Cutis 1990;46:321-2.
100. 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.
101. Taylor DS. Psoriasis program is a success.
Venture Inward 1996;12(2):14.