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.]


    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.


    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.


    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 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.


    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.


    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.


    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.


    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. 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.


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