- Email: [email protected]
Integrative dermatology for psoriasis: facts and controversies
Clinics in Dermatology (2010) 28, 93–99
Integrative dermatology for psoriasis: facts and controversies Valori Treloar, MD, CNS Integrative Dermatology, 1172 Beacon St, Ste 402, Newton, MA 02461
Abstract Recommendations for changes in diet and lifestyle are not meant to supplant conventional therapy but to integrate with it and, hopefully, improve response to treatment. At the same time, integrative approaches permit the patient to depend less on more expensive and potentially harmful pharmaceutical and medical approaches. Manipulation of diet and lifestyle may actually diminish the effect of underlying predisposing or etiologic factors and simultaneously treat serious comorbidities. Topics include alcohol, smoking, body composition, sleep and stress, diet and nutrients, and exercise. © 2010 Published by Elsevier Inc.
Psoriasis is a destination that our patients reach by taking different paths. In some, guttate psoriasis develops in childhood a week or so after streptococcal pharyngitis. Others find silvery plaques evolving on their elbows and knees only after they reach their fifth or sixth decade of life. Some unfortunate folks experience erythroderma suddenly one day and are plagued with severe psoriasis thereafter. And so on. Our patients’ responses to our treatments show comparable variability. Many do very well for years using topical steroid creams or phototherapy intermittently. Others require rotations of corticosteroids and topical analogs of vitamin D and vitamin A. The more unfortunate need aggressive therapy with additional immunosuppressive drugs that must also be rotated or combined. The wide range of clinical presentations combined with the striking variability in response to treatments vividly demonstrates the concept of biochemical individuality. Now that the human genome has been deciphered, we are beginning to appreciate the extent of variability attributed to single nucleotide polymorphisms (SNPs). These small
E-mail address: [email protected]. 0738-081X/$ – see front matter © 2010 Published by Elsevier Inc. doi:10.1016/j.clindermatol.2009.03.016
genetic mistakes translate into proteins with slightly altered structure or enzymes that have higher or lower levels of activity. Some abnormal enzymes or proteins can be normalized by increasing their cofactors, such as vitamins or minerals. The new field of epigenetics helps elucidate the influence of the environment on genetic expression. Environmental effects derive not only from air and water pollution but also from the cellular environment created by our diets and lifestyle choices. This contribution explores the evidence that lifestyle and diet can influence psoriasis. Recommendations for changes in diet and lifestyle are not meant to supplant conventional therapy but to integrate with it and, hopefully, improve response to treatment while allowing our patients to depend less on pharmaceutical solutions. Topics include alcohol, smoking, body composition, sleep and stress, diet and nutrients, and exercise.
Alcohol Patients with active psoriasis have elevated levels of a serum receptor for tumor necrosis factor-α (TNF-α). This
94 receptor (sTNF-α-R1) up-regulates in response to the TNFα–converting enzyme (TACE) from peripheral blood monocytes. TACE can serve as a sensitive marker of the disease severity.1 Alcohol abuse may contribute to the increase of TACE expression and also to the elevated plasma sTNF-R1 concentration in psoriasis patients.2 This mechanism may help explain the epidemiologic association seen in a number of studies. One demonstrated a modest but significant association between physical severity of psoriasis and weekly alcohol consumption.3 A Finnish study showed that young men with psoriasis drank twice as much alcohol as controls in the year preceding the onset of psoriasis, suggesting that alcohol may have a causative role.4 Another review showed relative risk factors up to 8.01 in men.5 To the best of my knowledge, a study assessing the effect of abstinence from alcohol on psoriasis has not been published.
Smoking Alcohol-controlled studies suggest that women who are smokers have an up to 3.3-fold increased risk of developing plaque-type psoriasis. Smoking among both men and women who are psoriasis patients has been shown to reduce improvement rates.6 For current smokers compared with never smokers, the odds ratio for psoriasis was 1.49 for men and 1.48 for women.7 Smoking more than 20 cigarettes daily compared with 10 or fewer cigarettes was associated with a more than twofold increased risk of clinically more severe psoriasis.8 The Nurses’ Health Study data shows that the relative risk of psoriasis increases as the number of pack-years of smoking rises. On an optimistic note, the authors state, “The risk of incident psoriasis among former smokers decreases nearly to that of never smokers 20 years after cessation.”9 The only prospective trial of smoking cessation in psoriasis, performed in a group of patients with palmoplantar pustulosis, showed significant improvement in those who quit smoking, whereas those who did not quit had no improvement.10 Smoking does not have the same effect on all patients. The hepatic P450 enzyme CYP1A1 metabolizes nicotine as well as many xenobiotic molecules. The wild-type genotype codes for lower activity of the enzyme than the variant genotypes. The lower activity correlates with psoriasis in smokers, but not in nonsmokers. This genetic susceptibility indirectly points to nonmetabolized xenobiotics, and perhaps nicotine, as etiologic agents in psoriasis.11 Smoking and alcohol both have a more profound effect on men who carry the HLA-DQA1*0201 gene variant.12
Body composition The large prospective Nurses’ Health Study provided data to show that weight gain after the age of 18, higher waist
V. Treloar circumference, hip circumference, and waist-hip ratio were all associated with a higher risk of incident psoriasis.13 A review in the British Journal of Dermatology concluded “More severely affected patients with psoriasis are much more likely to be obese.”14 Serum resistin levels, elevated with increased adiposity correlate with psoriasis severity. Resistin induces in vitro production of TNF-α by peripheral blood monocytes as well as elevations of other inflammatory and angiogenic cytokines.15 Circulating levels of TNF-α, soluble TNF-α receptors, and in vitro TNF-α production are all significantly increased in obese compared with nonobese individuals.16 The T-cell responses and previously reduced T-cell subsets increase significantly after weight reduction.16 When population-attributable risk was assigned to several variables, an elevated body mass index accounted for 16% of psoriasis.17 The only study to assess the effect of weight loss on psoriasis did so indirectly. The study combined a substandard dose of cyclosporine with a supervised weight loss diet in obese patients with severe chronic plaque psoriasis. The control group received the same low dose of cyclosporine and met with a physician instead of receiving dietary counseling. Dr Paolo Gisondi reported his unpublished findings at the annual meeting of the European Society for Dermatological Research in 2008. In the weight loss group, 67% achieved a Psoriasis Area and Severity Index (PASI) reduction of 75% compared with 21% of controls.18 Dr Gisondi concluded, “A global approach to obese patients with severe psoriasis should include body weight reduction.”
Sleep and stress Numerous studies have correlated stress and psoriasis. A positive correlation was documented between the severity of psoriasis symptoms and psychologic distress prospectively during a 20-week period.19 An Italian version of the Holmes and Rahe Social Readjustment Rating Scale was used to assess stressful life events during the year before diagnosis, and the highest quartile compared with the lowest had an odds ratio of 2.2 for the risk of developing psoriasis.17 Compared with patients with other skin diseases, those with psoriasis reported that the experience of stress predated the onset and exacerbations of their condition, and chronic difficulties were also more common.20 In another study, patients with psoriasis had lower perceived social support.21 “Actively spreading psoriasis was significantly associated with stressful life events for men but not for women. Compared to the low-stress group, the patients in the highstress group had more severe skin and joint symptoms and a higher score” (Psoriasis Area and Severity Index, activity of psoriasis, and the presence of joint symptoms).22 The rate of skin clearing in patients with moderate to severe psoriasis accelerated when they “engaged in an
Integrative dermatology for psoriasis audiotape-guided, meditative stress reduction exercise during their UVB [ultraviolet B] or PUVA [psoralen + ultraviolet A] treatment sessions.”23 Studies in mice suggest that the risk of squamous cell carcinoma may be greater in patients whose ultraviolet (UV) exposure is combined with emotional or physiologic stress.24 Phototherapy may carry greater skin cancer risk in patients whose stress levels are higher. Adding stress reduction training to phototherapy may improve not only therapeutic response to treatment but also decrease the skin cancer risk associated with UV exposure. Although they have not been studied specifically, other activities that similarly evoke the relaxation response may benefit our psoriasis patients. They may choose among a variety of options, including yoga, tai chi, meditation, biofeedback, self-hypnosis, and prayer. Regardless of the clinical outcome, the benefit far outweighs the risk of this therapy. Sleep and stress interweave tightly. Sleep deprivation increases stress hormone production,25 and stress disturbs sleep patterns.26 “Sleep deprivation increases the activity of the autonomic sympatho-adrenal system and the hypothalamic-pituitary-adrenal axis and may gradually change certain brain systems and neuroendocrine systems in a manner that is similar to what is seen in stress-related disorders.” 27 Sleep disturbance decreases skin barrier function recovery and increases plasma TNF-α.28 Good sleep hygiene may improve sleep duration and quality and the guidelines are straightforward (see Addendum 1).29
Diet and nutrition The relative dearth of research in the area of diet and nutrition in psoriasis contributes to the controversy surrounding the subject. Most human studies are epidemiologic, making it difficult to attribute cause and effect to diet. Intervention studies have been performed largely in animals, and extrapolation to humans is questioned. Similar limitations are found in in vitro studies; however, the evidence is slowly building. Diets high in fresh fruits and vegetables are associated with a lower risk of psoriasis.30 Given that increased consumption of fruit and vegetables can increase the plasma antioxidant capacity in humans,31 this corresponds well with the finding of decreased antioxidant capacity and increased oxidative stress in patients with psoriasis.32 There may not be double-blinded, placebo-controlled trials showing that a diet rich in fruits and vegetables improves psoriasis, but the risk of such a diet is minimal. Even if no cutaneous improvement follows, the health of a psoriasis patient is likely to improve with this dietary change. Oily fish and fish oil supplements appear to provide moderate improvement in mild to moderate psoriasis, but the data are contradictory.33 Dietary lipids, incorporated into cell membranes, serve as the precursors for prostaglandins and
95 leukotrienes. The omega-3 fatty acids from fish oil convert into inflammatory mediators in odd-numbered classes (eg, leukotriene B5, prostaglandin E3). The odd-numbered eicosanoids tend to counteract the more inflammatory even-numbered mediators derived from arachidonic acid (eg, leukotriene B4 and prostaglandin E2), with the end result of a less inflammatory milieu.34 Theoretically, this should be therapeutically useful in an inflammatory disease like psoriasis. The lack of conclusive evidence is likely to be due to individual variability and may be explained in part by the following. One of the reported anti-inflammatory actions of fish oil is a reduction in the production of TNF-α peripheral blood mononuclear cells. Data suggest that a person's sensitivity to the suppressive effects of omega-3 fatty acids on TNF-α production is linked to both the inherent level of production of the cytokine and to genetic variation of the lymphotoxin-α+252 SNP. TNF-α production decreased after fish oil supplementation in 22%, 43%, and 86% of the healthy participants in the lowest, middle, and highest inherent TNF-α level tertiles, respectively. The highest incidence of the homozygous variant lymphotoxin-α (B2/B2) occurred in the tertile with the highest inherent TNF-α levels. Fish oil supplementation appears to be most effective in those patients who produce the most TNF-α and the tendency to produce high levels appears to be associated with the lymphotoxin-α B2/B2 SNP.35 Fish oil may be more useful as an adjunct to other therapies. A study of 18 persons with stable plaque psoriasis found that low-dose UVB treatment combined with oral fish oil produced a significantly greater decrease in the total body surface area of psoriasis compared with patients who received UVB and olive oil.36 Supplementation of lowdose etretinate with eicosapentaenoic acid reduced the mean time required for a favorable response and led to significantly more improvement rated as excellent compared with etretinate alone.37 Psoriasis is more common in people who have higher insulin levels/insulin resistance.38 A significant correlation was found between insulin secretion and the PASI score.39 Indirect evidence suggests that diet, by affecting insulin levels, may affect psoriasis. A diet with a high glycemic index contains foods that cause insulin levels to rise high and fast and appears to increase insulin resistance.40 In patients with metabolic syndrome, a rye-pasta diet, characterized by a low postprandial insulin response, down-regulated genetic expression in the subcutaneous tissue. An otherwise identical oat-wheat-potato diet, characterized by a high postprandial insulin response, up-regulated subcutaneous tissue genes related to inflammation, interleukin cytokines, and oxidative stress.41 Theoretically, dietary manipulation to lower insulin levels could improve psoriasis, but no study has assessed this approach. Eating small meals consisting of fiber-rich, whole foods containing few refined carbohydrates every 2 to 3 hours will modulate glucose and insulin levels.
96 Even if it has no salutary effect on psoriasis, it is a healthy way to eat. Positive antigliadin antibodies were found in about one out of seven Swedish psoriasis patients42 compared with an incidence of about one in 120 in the general population. A clinical trial of a 3-month, gluten-free diet in 30 antibodypositive patients, only two of whom had classic microscopic findings of celiac disease, showed clinical improvement in 22. When rechallenged with a normal diet, two flared so dramatically that they had to be returned to the gluten-free diet, and 18 needed to increase their psoriasis medications because of worsening disease. Two patients worsened and opted to return to the diet after the study was completed. Both cleared with no relapse during a 4-year follow-up period.43 The results of that study illustrate the variability among psoriasis patients and their variable responses to treatment, a point further emphasized by a recent study in the United States showing no increased prevalence of antigliadin antibodies in psoriasis patients.44 The psoriasis in a patient who has elevated antigliadin antibodies may improve on a gluten-free diet. About one in seven may have dramatic clearing. As long as patients eat appropriate replacements for gluten-containing foods, they can maintain a healthy diet and bear no risk while exploring this option.
Exercise If exercise were a pill, doctors would prescribe it to everyone. Proper exercise, performed safely, improves mental health and vitality, strength and body composition,45 improves sleep,46 and helps with insulin control.47 It improves at least three or four risk factors for psoriasis. TNF-α was significantly lower in wounds from exercised old mice compared with control mice.48 “The exercise the mice received corresponds with a human taking a brisk walk for 30 minutes a day 5-6 times a week.”49 Heat intolerance may be a problem for people with psoriasis,50 so they must be taught to stay well hydrated and avoid exercising in warm, humid environments. They should keep exertion at a level that does not induce heavy sweating and always check with their primary care physician before embarking on an exercise program. Exercise is a double-edged sword. When practiced strenuously it causes oxidative stress and cell damage. When practiced in moderation, it increases the expression of antioxidant enzymes and thus should be considered an antioxidant.51 If a physician provides a written prescription for exercise in contrast to verbal instruction, the proportion of people performing any activity rises from 51% to 86%.52 A good exercise prescription will include strength training, aerobic exercise, and balance and flexibility training, and will
V. Treloar specify duration, frequency, and intensity. See Addendum 2 for an exercise prescription template.
Comorbidities Comorbid diseases associated with psoriasis include heart disease, diabetes, metabolic syndrome, lipid abnormalities,53 depression,54 alcoholism,3 and gastrointestinal disease. 55 Whether the association is due to shared mechanisms of disease or one disease predisposes to others is not clear, but the severity of the comorbidities is impressive. The lifestyle therapeutic approach discussed in this essay has salutatory effects on the comorbid conditions, as well.
Conclusions The search for “psoriasis genes” implies that the disease is a mark of inherited weakness. It may seem to be rather bad luck, but an evolutionary perspective suggests that our psoriasis patients come from biologic warrior stock.56 Gene variants that occur with high frequency may have been selected because they confer protection against environmental hazards. Sickle cell anemia protection against malaria is the classic example. The incidence of psoriasis, at 1:100 in northern latitudes, meets the criteria for a common gene variant occurring with high frequency. What protection might it confer? Those with psoriasis have a reduction in erythema and induration in response to streptococcal antigen dermal injection skin testing; their immune systems amplify the delayed-type hypersensitivity reaction far less dramatically. The potentially lethal shock that follows scarlet fever, until recently associated with high childhood mortality, is partly due to the delayed-type hypersensitivity reaction to the streptococcal antigen. Those with psoriasis are less likely to produce the snowballing immunologic cascade that characterizes shock and devastates the young body. Psoriasis may confer protection against death in scarlet fever. Our psoriasis patients, rather than being victims of an unlucky genetic draw, may be descended from survivors whose genes brought them down a path of protection and miraculously kept them alive. Psoriasis was the price extracted for survival. Giving a patient the evolutionary perspective of their disease may help them feel less victimized and confer a sense of worth rather than shame. As descendants of victorious warriors in the battle against a lethal disease, they may be more willing to choose healthier care for the inner warrior and exercise regularly, eat wisely, nurture their faithful bodies with sound sleep, and seek centered calm through peaceful relaxation.
Integrative dermatology for psoriasis
Integrative dermatology for psoriasis 1. 2. 3. 4.
Quit smoking. Limit alcohol intake. Improve body composition. Sleep 8 uninterrupted hours nightly (see sleep hygiene information, Addendum 1). 5. Learn and practice daily an activity that elicits the relaxation response. 6. Exercise five to seven times weekly at a moderate level for 20 minutes (see exercise prescription, Addendum 2). 7. Eat a nutrient-dense diet at the three main meals, and two to three small-meal snacks daily. a. Five or more servings of vegetables daily b. Two servings of fruit daily c. 8 to 12 ounces of protein-rich food daily (fish, chicken, turkey, lean meat, eggs) d. Whole grains, squash, sweet potatoes, beans; minimal refined carbohydrates e. Olive oil, coconut oil for cooking f. Small amounts of butter, cheese, and other dairy products g. Nuts and seeds if allergy is not an issue h. Consider a 3-month trial of a gluten-free diet i. Consider working with a nutritionist
References 1. Serwin AB, Sokolowska M, Chodynicka B. Tumour necrosis factor alpha (TNF-alpha)-converting enzyme (TACE) and soluble TNFalpha receptor type 1 in psoriasis patients treated with narrowband ultraviolet B. Photodermatol Photoimmunol Photomed 2007;23: 130-4. 2. Serwin AB, Sokolowska M, Dylejko E, Chodynicka B. Tumour necrosis factor (TNF-alpha) alpha converting enzyme and soluble TNF-alpha receptor type 1 in psoriasis patients in relation to the chronic alcohol consumption. J Eur Acad Dermatol Venereol 2008;22: 712-7. 3. Kirby B, Richards HL, Mason DL, Fortune DG, Main CJ, Griffiths CE. Alcohol consumption and psychological distress in patients with psoriasis. Br J Dermatol 2008;158:138-40. 4. Poikolainen K, Reunala T, Karvonen J, Lauharanta J, Kärkkäinen P. Alcohol intake: a risk factor for psoriasis in young and middle aged men? BMJ 1990;300:780-3. 5. Behnam SM, Behnam SE, Koo JY. Alcohol as a risk factor for plaquetype psoriasis. Cutis 2005;76:181-5. 6. Behnam SM, Behnam SE, Koo JY. Smoking and psoriasis. Skinmed 2005;4:174-6. 7. Bø K, Thoresen M, Dalgard F. Smokers report more psoriasis, but not atopic dermatitis or hand eczema: results from a Norwegian population survey among adults. Dermatology 2008;216:40-5. 8. Fortes C, Mastroeni S, Leffondré K, et al. Relationship between smoking and the clinical severity of psoriasis. Arch Dermatol 2005;141: 1580-4. 9. Setty AR, Curhan G, Choi HK. Smoking and the risk of psoriasis in women: Nurses’ Health Study II. Am J Med 2007;120:953-9. 10. Michaëlsson G, Gustafsson K, Hagforsen E. The psoriasis variant palmoplantar pustulosis can be improved after cessation of smoking. J Am Acad Dermatol 2006;54:737-8.
97 11. Kramer U, Esser C. Cigarette smoking, metabolic gene polymorphism, and psoriasis. J Invest Dermatol 2006;126:693-4 author reply 695. 12. Zheng GY, Wei SC, Shi TL, Li YX. Association between alcohol, smoking and HLA-DQA1*0201 genotype in psoriasis. Acta Biochim Biophys Sin (Shanghai) 2004;36:597-602. 13. Setty AR, Curhan G, Choi HK. Obesity, waist circumference, weight change, and the risk of psoriasis in women. Nurses’ Health Study II Arch Intern Med 2007;167:1670-5. 14. Sterry W, Strober BE, Menter A. Obesity in psoriasis: the metabolic, clinical and therapeutic implications. Report of an interdisciplinary conference and review. Br J Dermatol 2007;157:649-55. 15. Johnston A, Arnadottir S, Gudjonsson JE, et al. Obesity in psoriasis: leptin and resistin as mediators of cutaneous inflammation. Br J Dermatol 2008;159:342-50. 16. Tanaka S, Isoda F, Ishihara Y, Kimura M, Yamakawa T. T lymphopaenia in relation to body mass index and TNF-alpha in human obesity: adequate weight reduction can be corrective. Clin Endocrinol (Oxf) 2001;54:347-54. 17. Naldi L, Chatenoud L, Linder D, et al. Cigarette smoking, body mass index, and stressful life events as risk factors for psoriasis: results from an Italian case-control study. J Invest Dermatol 2005; 125:61-7. 18. Jancin B. Diet increases effect of low-dose cyclosporine in psoriasis patients. Skin Allergy News 2007:9. 19. Gaston L, Lassonde M, Bernier-Buzzanga J, Hodgins S, Crombez JC. Psoriasis and stress: a prospective study. J Am Acad Dermatol 1987;17: 82-6. 20. Al'Abadie MS, Keng GG, Gawkrodger DJ. The relationship between stress and the onset and exacerbation of psoriasis and other skin conditions. Br J Dermatol 1994;130:199-203. 21. Picardi A, Mazzotti E, Gaetano P, et al. Stress, social support, emotional regulation, and exacerbation of diffuse plaque psoriasis. Psychosomatics 2005;46:556-64. 22. Harvima RJ, Viinamäki H, Harvima IT, et al. Association of psychic stress with clinical severity and symptoms of psoriatic patients. Acta Derm Venereol 1996;76:467-71. 23. Kabat-Zinn J, Wheeler E, Light T, et al. Influence of a mindfulness meditation-based stress reduction intervention on rates of skin clearing in patients with moderate to severe psoriasis undergoing phototherapy (UVB) and photochemotherapy (PUVA). Psychosom Med 1998;60: 625-32. 24. Parker J, Klein SL, McClintock MK, et al. Chronic stress accelerates ultraviolet-induced cutaneous carcinogenesis. J Am Acad Dermatol 2004;51:919-22. 25. Adam K, Tomeny M, Oswald I. Physiological and psychological differences between good and poor sleepers. J Psychiatr Res 1986;20: 301-16. 26. Healey ES, Kales A, Monroe LJ, Bixler EO, Chamberlin K, Soldatos CR. Onset of insomnia: role of life-stress events. Psychosom Med 1981; 43:439-51. 27. Meerlo P, Sgoifo A, Suchecki D. Restricted and disrupted sleep: effects on autonomic function, neuroendocrine stress systems and stress responsivity. Sleep Med Rev 2008;12:197-210. 28. Altemus M, Rao B, Dhabhar FS, Ding W, Granstein RD. Stress-induced changes in skin barrier function in healthy women. J Invest Dermatol 2001;117:309-17. 29. Lam JC, Mason TB. Treatment of sleep disorders in children. Curr Treat Options Neurol 2007;9:404-13. 30. 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. 31. Cao G, Booth SL, Sadowski JA, Prior RL. Increases in human plasma antioxidant capacity after consumption of controlled diets high in fruit and vegetables. Am J Clin Nutr 1998;68:1081-7. 32. Vanizor Kural B, Orem A, Cimşit G, Yandi YE, Calapoglu M. Evaluation of the atherogenic tendency of lipids and lipoprotein content
98
33. 34. 35.
36.
37.
38.
39.
40.
41.
42.
43.
V. Treloar and their relationships with oxidant-antioxidant system in patients with psoriasis. Clin Chim Acta 2003;328:71-82. Mayser P, Grimm H, Grimminger F. n-3 fatty acids in psoriasis. Br J Nutr 2002;87(suppl 1):S77-82. Lands WE. Biochemistry and physiology of n-3 fatty acids. FASEB J 1992;6:2530-6. Grimble RF, Howell WM, O'Reilly G, et al. The ability of fish oil to suppress tumor necrosis factor alpha production by peripheral blood mononuclear cells in healthy men is associated with polymorphisms in genes that influence tumor necrosis factor alpha production. Am J Clin Nutr 2002;76:454-9. Gupta AK, Ellis CN, Tellner DC, Anderson TF, Voorhees JJ. Doubleblind, placebo-controlled study to evaluate the efficacy of fish oil and low-dose UVB in the treatment of psoriasis. Br J Dermatol 1989;120: 801-7. Danno K, Sugie N. Combination therapy with low-dose etretinate and eicosapentaenoic acid for psoriasis vulgaris. J Dermatol 1998;25: 703-5. Reynoso-von Drateln C, Martínez-Abundis E, Balcázar-Muñoz BR, Bustos-Saldaña R, González-Ortiz M. Lipid profile, insulin secretion, and insulin sensitivity in psoriasis. J Am Acad Dermatol 2003;48: 882-5. Boehncke S, Thaci D, Beschmann H, et al. Psoriasis patients show signs of insulin resistance. Br J Dermatol 2007;157: 1249-51. McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PW, Jacques PF. Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort. Diabetes Care 2004;27:538-46. Kallio P, Kolehmainen M, Laaksonen DE, et al. Dietary carbohydrate modification induces alterations in gene expression in abdominal subcutaneous adipose tissue in persons with the metabolic syndrome: the FUNGENUT Study. Am J Clin Nutr 2007;85: 1417-27. Michaelsson G, Gerdén B, Ottosson M, et al. Patients with psoriasis often have increased serum levels of IgA antibodies to gliadin. Br J Dermatol 1993;129:667-73. Michaelsson G, Gerdén B, Hagforsen E, et al. Psoriasis patients with antibodies to gliadin can be improved by a gluten-free diet. Br J Dermatol 2000;142:44-51.
44. Kia KF, Nair RP, Ike RW, Hiremagalore R, Elder JT, Ellis CN. Prevalence of antigliadin antibodies in patients with psoriasis is not elevated compared with controls. Am J Clin Dermatol 2007;8: 301-5. 45. Smith TP, Kennedy SL, Smith M, Orent S, Fleshner M. Physiological improvements and health benefits during an exercise-based comprehensive rehabilitation program in medically complex patients. Exerc Immunol Rev 2006;12:86-96. 46. Santana MG, Poyares D, Tufik S, Mello MT. Physical exercise can improve sleep quality of insomniac patients. Abstract 737. Presented at: Associated Professional Sleep Societies Meeting 2008; 2008 [Baltimore (MD)]. 47. Hawley JA, Lessard SJ. Exercise training-induced improvements in insulin action. Acta Physiol (Oxf) 2008;192:127-35. 48. Keylock KT, DiPietro LA, Schrementi M, Woods JA. Exercise accelerates cutaneous wound healing and decreases wound inflammation in aged mice. Am J Physiol Regul Integr Comp Physiol 2008;294: R179-84. 49. Roehr B. Get moving! Exercise decreases inflammation, facilitates wound healing. Dermatol Times 2008:41. 50. Leibowitz E, Seidman DS, Laor A, Shapiro Y, Epstein Y. Are psoriatic patients at risk of heat intolerance? Br J Dermatol 1991;124: 439-42. 51. Gomez-Cabrera MC, Domenech E, Viña J. Moderate exercise is an antioxidant: upregulation of antioxidant genes by training. Free Radic Biol Med 2008;44:126-31. 52. Swinburn BA, Walter LG, Arroll B, Tilyard MW, Russell DG. The green prescription study: a randomized controlled trial of written exercise advice provided by general practitioners. Am J Public Health 1998;88:288-91. 53. Kourosh AS, Miner A, Menter A. Psoriasis as the marker of underlying systemic disease. Skin Therapy Lett 2008;13:1-5. 54. Nasreen S, Ahmed I, Effendi S. Frequency and magnitude of anxiety and depression in patients with psoriasis vulgaris. J Coll Physicians Surg Pak 2008;18:397-400. 55. Bernstein CN, Wajda A, Blanchard JF. The clustering of other chronic inflammatory diseases in inflammatory bowel disease: a populationbased study. Gastroenterology 2005;129:827-36. 56. McFadden J. Hypothesis - the natural selection of psoriasis. Clin Exp Dermatol 1990;15:39-43.
Addendum 1. Good sleep hygiene 1. Devote the time to sleep. Arrange consistent bedtimes and waking times to allow 7 to 8 hours of uninterrupted sleep. 2. Begin unwinding 30 to 45 minutes before sleep should begin. Do not use this time to finish tasks, tidy up the house, or make to do lists. 3. If you have worries, write them down and leave them for tomorrow. 4. Try relaxation techniques as your prepare for bed. 5. Do not eat 1 to 2 hours before bed. Do not drink a lot of fluids. 6. Avoid caffeine (coffee, tea, chocolate) after 4 PM. 7. Avoid alcohol 4 to 6 hours before bedtime. 8. Avoid daytime naps. 9. Exercise regularly and moderately. Do not engage in vigorous exercise after 6 PM. 10. Do not keep the television in your bedroom. 11. Use the bedroom only for sleep (and sex). 12. Keep the bedroom quiet. 13. Pull the shades so the room is dark. Light disturbs melatonin release. 14. Ensure that the temperature of the bedroom is optimal for you. 15. Consider putting a few drops of a high-quality lavender essential oil on a handkerchief under your pillow. 16. Consider a bedtime ritual, such as a warm bath or a few pages of reading.
Integrative dermatology for psoriasis
99
Addendum 2. Exercise prescription Name________________________________ Date___________________ Cautions: Diabetic retinopathy or neuropathy–avoid vigorous exercise Diabetic patients must monitor blood sugar before and after exercise. Delayed hypoglycemia can occur up to 6 to 15 hours after exercise. Framingham Cardiac Risk Score N 10% may require a graded exercise electrocardiogram before beginning an exercise program. Risk calculator at: http://www.mdcalc.com/cardiacrisk If you have the conditions listed above or have any concerns or questions, be sure to consult your physician before embarking on an exercise program. Consider working with a trainer. 30 minutes of moderate* activity 5 times weekly; or 20 minutes of vigorous** activity 3 times weekly Exertion scale Exertion of sitting = 1. . . . .2. . . . .3. . . . .4 . . . . . 5. . . . .6. . . . .7. . . . .8. . . . .9. . . . .10 = Maximal exertion *Moderate = 5 to 6 = noticeable increase in heart rate. **Vigorous = 7 to 8 = rapid breathing and greater increase in heart rate. 1. Walking / Jogging / Running / Swimming / Dancing / Yard work / Biking / Exercise class _____________________ ________________________________________________________ 2. Strength training / Muscle building / Resistance training / Weight lifting / Body weight training ________________ _____________________________________________________ 2-3 sets of 8-12 repetitions, with the last rep being extremely difficult. Work upper body, lower body, core; both front body and back body. [Consider facial muscle resistance exercise, too] 3. Flexibility / Stretching / Yoga / Tai chi / Pilates / ______________________________ Work through the full range of motion for all joints. 4. Balance training / Tai chi / Yoga / Dance / ____________________________________
Integrative dermatology for psoriasis: facts and controversies Valori Treloar, MD, CNS Integrative Dermatology, 1172 Beacon St, Ste 402, Newton, MA 02461
Abstract Recommendations for changes in diet and lifestyle are not meant to supplant conventional therapy but to integrate with it and, hopefully, improve response to treatment. At the same time, integrative approaches permit the patient to depend less on more expensive and potentially harmful pharmaceutical and medical approaches. Manipulation of diet and lifestyle may actually diminish the effect of underlying predisposing or etiologic factors and simultaneously treat serious comorbidities. Topics include alcohol, smoking, body composition, sleep and stress, diet and nutrients, and exercise. © 2010 Published by Elsevier Inc.
Psoriasis is a destination that our patients reach by taking different paths. In some, guttate psoriasis develops in childhood a week or so after streptococcal pharyngitis. Others find silvery plaques evolving on their elbows and knees only after they reach their fifth or sixth decade of life. Some unfortunate folks experience erythroderma suddenly one day and are plagued with severe psoriasis thereafter. And so on. Our patients’ responses to our treatments show comparable variability. Many do very well for years using topical steroid creams or phototherapy intermittently. Others require rotations of corticosteroids and topical analogs of vitamin D and vitamin A. The more unfortunate need aggressive therapy with additional immunosuppressive drugs that must also be rotated or combined. The wide range of clinical presentations combined with the striking variability in response to treatments vividly demonstrates the concept of biochemical individuality. Now that the human genome has been deciphered, we are beginning to appreciate the extent of variability attributed to single nucleotide polymorphisms (SNPs). These small
E-mail address: [email protected]. 0738-081X/$ – see front matter © 2010 Published by Elsevier Inc. doi:10.1016/j.clindermatol.2009.03.016
genetic mistakes translate into proteins with slightly altered structure or enzymes that have higher or lower levels of activity. Some abnormal enzymes or proteins can be normalized by increasing their cofactors, such as vitamins or minerals. The new field of epigenetics helps elucidate the influence of the environment on genetic expression. Environmental effects derive not only from air and water pollution but also from the cellular environment created by our diets and lifestyle choices. This contribution explores the evidence that lifestyle and diet can influence psoriasis. Recommendations for changes in diet and lifestyle are not meant to supplant conventional therapy but to integrate with it and, hopefully, improve response to treatment while allowing our patients to depend less on pharmaceutical solutions. Topics include alcohol, smoking, body composition, sleep and stress, diet and nutrients, and exercise.
Alcohol Patients with active psoriasis have elevated levels of a serum receptor for tumor necrosis factor-α (TNF-α). This
94 receptor (sTNF-α-R1) up-regulates in response to the TNFα–converting enzyme (TACE) from peripheral blood monocytes. TACE can serve as a sensitive marker of the disease severity.1 Alcohol abuse may contribute to the increase of TACE expression and also to the elevated plasma sTNF-R1 concentration in psoriasis patients.2 This mechanism may help explain the epidemiologic association seen in a number of studies. One demonstrated a modest but significant association between physical severity of psoriasis and weekly alcohol consumption.3 A Finnish study showed that young men with psoriasis drank twice as much alcohol as controls in the year preceding the onset of psoriasis, suggesting that alcohol may have a causative role.4 Another review showed relative risk factors up to 8.01 in men.5 To the best of my knowledge, a study assessing the effect of abstinence from alcohol on psoriasis has not been published.
Smoking Alcohol-controlled studies suggest that women who are smokers have an up to 3.3-fold increased risk of developing plaque-type psoriasis. Smoking among both men and women who are psoriasis patients has been shown to reduce improvement rates.6 For current smokers compared with never smokers, the odds ratio for psoriasis was 1.49 for men and 1.48 for women.7 Smoking more than 20 cigarettes daily compared with 10 or fewer cigarettes was associated with a more than twofold increased risk of clinically more severe psoriasis.8 The Nurses’ Health Study data shows that the relative risk of psoriasis increases as the number of pack-years of smoking rises. On an optimistic note, the authors state, “The risk of incident psoriasis among former smokers decreases nearly to that of never smokers 20 years after cessation.”9 The only prospective trial of smoking cessation in psoriasis, performed in a group of patients with palmoplantar pustulosis, showed significant improvement in those who quit smoking, whereas those who did not quit had no improvement.10 Smoking does not have the same effect on all patients. The hepatic P450 enzyme CYP1A1 metabolizes nicotine as well as many xenobiotic molecules. The wild-type genotype codes for lower activity of the enzyme than the variant genotypes. The lower activity correlates with psoriasis in smokers, but not in nonsmokers. This genetic susceptibility indirectly points to nonmetabolized xenobiotics, and perhaps nicotine, as etiologic agents in psoriasis.11 Smoking and alcohol both have a more profound effect on men who carry the HLA-DQA1*0201 gene variant.12
Body composition The large prospective Nurses’ Health Study provided data to show that weight gain after the age of 18, higher waist
V. Treloar circumference, hip circumference, and waist-hip ratio were all associated with a higher risk of incident psoriasis.13 A review in the British Journal of Dermatology concluded “More severely affected patients with psoriasis are much more likely to be obese.”14 Serum resistin levels, elevated with increased adiposity correlate with psoriasis severity. Resistin induces in vitro production of TNF-α by peripheral blood monocytes as well as elevations of other inflammatory and angiogenic cytokines.15 Circulating levels of TNF-α, soluble TNF-α receptors, and in vitro TNF-α production are all significantly increased in obese compared with nonobese individuals.16 The T-cell responses and previously reduced T-cell subsets increase significantly after weight reduction.16 When population-attributable risk was assigned to several variables, an elevated body mass index accounted for 16% of psoriasis.17 The only study to assess the effect of weight loss on psoriasis did so indirectly. The study combined a substandard dose of cyclosporine with a supervised weight loss diet in obese patients with severe chronic plaque psoriasis. The control group received the same low dose of cyclosporine and met with a physician instead of receiving dietary counseling. Dr Paolo Gisondi reported his unpublished findings at the annual meeting of the European Society for Dermatological Research in 2008. In the weight loss group, 67% achieved a Psoriasis Area and Severity Index (PASI) reduction of 75% compared with 21% of controls.18 Dr Gisondi concluded, “A global approach to obese patients with severe psoriasis should include body weight reduction.”
Sleep and stress Numerous studies have correlated stress and psoriasis. A positive correlation was documented between the severity of psoriasis symptoms and psychologic distress prospectively during a 20-week period.19 An Italian version of the Holmes and Rahe Social Readjustment Rating Scale was used to assess stressful life events during the year before diagnosis, and the highest quartile compared with the lowest had an odds ratio of 2.2 for the risk of developing psoriasis.17 Compared with patients with other skin diseases, those with psoriasis reported that the experience of stress predated the onset and exacerbations of their condition, and chronic difficulties were also more common.20 In another study, patients with psoriasis had lower perceived social support.21 “Actively spreading psoriasis was significantly associated with stressful life events for men but not for women. Compared to the low-stress group, the patients in the highstress group had more severe skin and joint symptoms and a higher score” (Psoriasis Area and Severity Index, activity of psoriasis, and the presence of joint symptoms).22 The rate of skin clearing in patients with moderate to severe psoriasis accelerated when they “engaged in an
Integrative dermatology for psoriasis audiotape-guided, meditative stress reduction exercise during their UVB [ultraviolet B] or PUVA [psoralen + ultraviolet A] treatment sessions.”23 Studies in mice suggest that the risk of squamous cell carcinoma may be greater in patients whose ultraviolet (UV) exposure is combined with emotional or physiologic stress.24 Phototherapy may carry greater skin cancer risk in patients whose stress levels are higher. Adding stress reduction training to phototherapy may improve not only therapeutic response to treatment but also decrease the skin cancer risk associated with UV exposure. Although they have not been studied specifically, other activities that similarly evoke the relaxation response may benefit our psoriasis patients. They may choose among a variety of options, including yoga, tai chi, meditation, biofeedback, self-hypnosis, and prayer. Regardless of the clinical outcome, the benefit far outweighs the risk of this therapy. Sleep and stress interweave tightly. Sleep deprivation increases stress hormone production,25 and stress disturbs sleep patterns.26 “Sleep deprivation increases the activity of the autonomic sympatho-adrenal system and the hypothalamic-pituitary-adrenal axis and may gradually change certain brain systems and neuroendocrine systems in a manner that is similar to what is seen in stress-related disorders.” 27 Sleep disturbance decreases skin barrier function recovery and increases plasma TNF-α.28 Good sleep hygiene may improve sleep duration and quality and the guidelines are straightforward (see Addendum 1).29
Diet and nutrition The relative dearth of research in the area of diet and nutrition in psoriasis contributes to the controversy surrounding the subject. Most human studies are epidemiologic, making it difficult to attribute cause and effect to diet. Intervention studies have been performed largely in animals, and extrapolation to humans is questioned. Similar limitations are found in in vitro studies; however, the evidence is slowly building. Diets high in fresh fruits and vegetables are associated with a lower risk of psoriasis.30 Given that increased consumption of fruit and vegetables can increase the plasma antioxidant capacity in humans,31 this corresponds well with the finding of decreased antioxidant capacity and increased oxidative stress in patients with psoriasis.32 There may not be double-blinded, placebo-controlled trials showing that a diet rich in fruits and vegetables improves psoriasis, but the risk of such a diet is minimal. Even if no cutaneous improvement follows, the health of a psoriasis patient is likely to improve with this dietary change. Oily fish and fish oil supplements appear to provide moderate improvement in mild to moderate psoriasis, but the data are contradictory.33 Dietary lipids, incorporated into cell membranes, serve as the precursors for prostaglandins and
95 leukotrienes. The omega-3 fatty acids from fish oil convert into inflammatory mediators in odd-numbered classes (eg, leukotriene B5, prostaglandin E3). The odd-numbered eicosanoids tend to counteract the more inflammatory even-numbered mediators derived from arachidonic acid (eg, leukotriene B4 and prostaglandin E2), with the end result of a less inflammatory milieu.34 Theoretically, this should be therapeutically useful in an inflammatory disease like psoriasis. The lack of conclusive evidence is likely to be due to individual variability and may be explained in part by the following. One of the reported anti-inflammatory actions of fish oil is a reduction in the production of TNF-α peripheral blood mononuclear cells. Data suggest that a person's sensitivity to the suppressive effects of omega-3 fatty acids on TNF-α production is linked to both the inherent level of production of the cytokine and to genetic variation of the lymphotoxin-α+252 SNP. TNF-α production decreased after fish oil supplementation in 22%, 43%, and 86% of the healthy participants in the lowest, middle, and highest inherent TNF-α level tertiles, respectively. The highest incidence of the homozygous variant lymphotoxin-α (B2/B2) occurred in the tertile with the highest inherent TNF-α levels. Fish oil supplementation appears to be most effective in those patients who produce the most TNF-α and the tendency to produce high levels appears to be associated with the lymphotoxin-α B2/B2 SNP.35 Fish oil may be more useful as an adjunct to other therapies. A study of 18 persons with stable plaque psoriasis found that low-dose UVB treatment combined with oral fish oil produced a significantly greater decrease in the total body surface area of psoriasis compared with patients who received UVB and olive oil.36 Supplementation of lowdose etretinate with eicosapentaenoic acid reduced the mean time required for a favorable response and led to significantly more improvement rated as excellent compared with etretinate alone.37 Psoriasis is more common in people who have higher insulin levels/insulin resistance.38 A significant correlation was found between insulin secretion and the PASI score.39 Indirect evidence suggests that diet, by affecting insulin levels, may affect psoriasis. A diet with a high glycemic index contains foods that cause insulin levels to rise high and fast and appears to increase insulin resistance.40 In patients with metabolic syndrome, a rye-pasta diet, characterized by a low postprandial insulin response, down-regulated genetic expression in the subcutaneous tissue. An otherwise identical oat-wheat-potato diet, characterized by a high postprandial insulin response, up-regulated subcutaneous tissue genes related to inflammation, interleukin cytokines, and oxidative stress.41 Theoretically, dietary manipulation to lower insulin levels could improve psoriasis, but no study has assessed this approach. Eating small meals consisting of fiber-rich, whole foods containing few refined carbohydrates every 2 to 3 hours will modulate glucose and insulin levels.
96 Even if it has no salutary effect on psoriasis, it is a healthy way to eat. Positive antigliadin antibodies were found in about one out of seven Swedish psoriasis patients42 compared with an incidence of about one in 120 in the general population. A clinical trial of a 3-month, gluten-free diet in 30 antibodypositive patients, only two of whom had classic microscopic findings of celiac disease, showed clinical improvement in 22. When rechallenged with a normal diet, two flared so dramatically that they had to be returned to the gluten-free diet, and 18 needed to increase their psoriasis medications because of worsening disease. Two patients worsened and opted to return to the diet after the study was completed. Both cleared with no relapse during a 4-year follow-up period.43 The results of that study illustrate the variability among psoriasis patients and their variable responses to treatment, a point further emphasized by a recent study in the United States showing no increased prevalence of antigliadin antibodies in psoriasis patients.44 The psoriasis in a patient who has elevated antigliadin antibodies may improve on a gluten-free diet. About one in seven may have dramatic clearing. As long as patients eat appropriate replacements for gluten-containing foods, they can maintain a healthy diet and bear no risk while exploring this option.
Exercise If exercise were a pill, doctors would prescribe it to everyone. Proper exercise, performed safely, improves mental health and vitality, strength and body composition,45 improves sleep,46 and helps with insulin control.47 It improves at least three or four risk factors for psoriasis. TNF-α was significantly lower in wounds from exercised old mice compared with control mice.48 “The exercise the mice received corresponds with a human taking a brisk walk for 30 minutes a day 5-6 times a week.”49 Heat intolerance may be a problem for people with psoriasis,50 so they must be taught to stay well hydrated and avoid exercising in warm, humid environments. They should keep exertion at a level that does not induce heavy sweating and always check with their primary care physician before embarking on an exercise program. Exercise is a double-edged sword. When practiced strenuously it causes oxidative stress and cell damage. When practiced in moderation, it increases the expression of antioxidant enzymes and thus should be considered an antioxidant.51 If a physician provides a written prescription for exercise in contrast to verbal instruction, the proportion of people performing any activity rises from 51% to 86%.52 A good exercise prescription will include strength training, aerobic exercise, and balance and flexibility training, and will
V. Treloar specify duration, frequency, and intensity. See Addendum 2 for an exercise prescription template.
Comorbidities Comorbid diseases associated with psoriasis include heart disease, diabetes, metabolic syndrome, lipid abnormalities,53 depression,54 alcoholism,3 and gastrointestinal disease. 55 Whether the association is due to shared mechanisms of disease or one disease predisposes to others is not clear, but the severity of the comorbidities is impressive. The lifestyle therapeutic approach discussed in this essay has salutatory effects on the comorbid conditions, as well.
Conclusions The search for “psoriasis genes” implies that the disease is a mark of inherited weakness. It may seem to be rather bad luck, but an evolutionary perspective suggests that our psoriasis patients come from biologic warrior stock.56 Gene variants that occur with high frequency may have been selected because they confer protection against environmental hazards. Sickle cell anemia protection against malaria is the classic example. The incidence of psoriasis, at 1:100 in northern latitudes, meets the criteria for a common gene variant occurring with high frequency. What protection might it confer? Those with psoriasis have a reduction in erythema and induration in response to streptococcal antigen dermal injection skin testing; their immune systems amplify the delayed-type hypersensitivity reaction far less dramatically. The potentially lethal shock that follows scarlet fever, until recently associated with high childhood mortality, is partly due to the delayed-type hypersensitivity reaction to the streptococcal antigen. Those with psoriasis are less likely to produce the snowballing immunologic cascade that characterizes shock and devastates the young body. Psoriasis may confer protection against death in scarlet fever. Our psoriasis patients, rather than being victims of an unlucky genetic draw, may be descended from survivors whose genes brought them down a path of protection and miraculously kept them alive. Psoriasis was the price extracted for survival. Giving a patient the evolutionary perspective of their disease may help them feel less victimized and confer a sense of worth rather than shame. As descendants of victorious warriors in the battle against a lethal disease, they may be more willing to choose healthier care for the inner warrior and exercise regularly, eat wisely, nurture their faithful bodies with sound sleep, and seek centered calm through peaceful relaxation.
Integrative dermatology for psoriasis
Integrative dermatology for psoriasis 1. 2. 3. 4.
Quit smoking. Limit alcohol intake. Improve body composition. Sleep 8 uninterrupted hours nightly (see sleep hygiene information, Addendum 1). 5. Learn and practice daily an activity that elicits the relaxation response. 6. Exercise five to seven times weekly at a moderate level for 20 minutes (see exercise prescription, Addendum 2). 7. Eat a nutrient-dense diet at the three main meals, and two to three small-meal snacks daily. a. Five or more servings of vegetables daily b. Two servings of fruit daily c. 8 to 12 ounces of protein-rich food daily (fish, chicken, turkey, lean meat, eggs) d. Whole grains, squash, sweet potatoes, beans; minimal refined carbohydrates e. Olive oil, coconut oil for cooking f. Small amounts of butter, cheese, and other dairy products g. Nuts and seeds if allergy is not an issue h. Consider a 3-month trial of a gluten-free diet i. Consider working with a nutritionist
References 1. Serwin AB, Sokolowska M, Chodynicka B. Tumour necrosis factor alpha (TNF-alpha)-converting enzyme (TACE) and soluble TNFalpha receptor type 1 in psoriasis patients treated with narrowband ultraviolet B. Photodermatol Photoimmunol Photomed 2007;23: 130-4. 2. Serwin AB, Sokolowska M, Dylejko E, Chodynicka B. Tumour necrosis factor (TNF-alpha) alpha converting enzyme and soluble TNF-alpha receptor type 1 in psoriasis patients in relation to the chronic alcohol consumption. J Eur Acad Dermatol Venereol 2008;22: 712-7. 3. Kirby B, Richards HL, Mason DL, Fortune DG, Main CJ, Griffiths CE. Alcohol consumption and psychological distress in patients with psoriasis. Br J Dermatol 2008;158:138-40. 4. Poikolainen K, Reunala T, Karvonen J, Lauharanta J, Kärkkäinen P. Alcohol intake: a risk factor for psoriasis in young and middle aged men? BMJ 1990;300:780-3. 5. Behnam SM, Behnam SE, Koo JY. Alcohol as a risk factor for plaquetype psoriasis. Cutis 2005;76:181-5. 6. Behnam SM, Behnam SE, Koo JY. Smoking and psoriasis. Skinmed 2005;4:174-6. 7. Bø K, Thoresen M, Dalgard F. Smokers report more psoriasis, but not atopic dermatitis or hand eczema: results from a Norwegian population survey among adults. Dermatology 2008;216:40-5. 8. Fortes C, Mastroeni S, Leffondré K, et al. Relationship between smoking and the clinical severity of psoriasis. Arch Dermatol 2005;141: 1580-4. 9. Setty AR, Curhan G, Choi HK. Smoking and the risk of psoriasis in women: Nurses’ Health Study II. Am J Med 2007;120:953-9. 10. Michaëlsson G, Gustafsson K, Hagforsen E. The psoriasis variant palmoplantar pustulosis can be improved after cessation of smoking. J Am Acad Dermatol 2006;54:737-8.
97 11. Kramer U, Esser C. Cigarette smoking, metabolic gene polymorphism, and psoriasis. J Invest Dermatol 2006;126:693-4 author reply 695. 12. Zheng GY, Wei SC, Shi TL, Li YX. Association between alcohol, smoking and HLA-DQA1*0201 genotype in psoriasis. Acta Biochim Biophys Sin (Shanghai) 2004;36:597-602. 13. Setty AR, Curhan G, Choi HK. Obesity, waist circumference, weight change, and the risk of psoriasis in women. Nurses’ Health Study II Arch Intern Med 2007;167:1670-5. 14. Sterry W, Strober BE, Menter A. Obesity in psoriasis: the metabolic, clinical and therapeutic implications. Report of an interdisciplinary conference and review. Br J Dermatol 2007;157:649-55. 15. Johnston A, Arnadottir S, Gudjonsson JE, et al. Obesity in psoriasis: leptin and resistin as mediators of cutaneous inflammation. Br J Dermatol 2008;159:342-50. 16. Tanaka S, Isoda F, Ishihara Y, Kimura M, Yamakawa T. T lymphopaenia in relation to body mass index and TNF-alpha in human obesity: adequate weight reduction can be corrective. Clin Endocrinol (Oxf) 2001;54:347-54. 17. Naldi L, Chatenoud L, Linder D, et al. Cigarette smoking, body mass index, and stressful life events as risk factors for psoriasis: results from an Italian case-control study. J Invest Dermatol 2005; 125:61-7. 18. Jancin B. Diet increases effect of low-dose cyclosporine in psoriasis patients. Skin Allergy News 2007:9. 19. Gaston L, Lassonde M, Bernier-Buzzanga J, Hodgins S, Crombez JC. Psoriasis and stress: a prospective study. J Am Acad Dermatol 1987;17: 82-6. 20. Al'Abadie MS, Keng GG, Gawkrodger DJ. The relationship between stress and the onset and exacerbation of psoriasis and other skin conditions. Br J Dermatol 1994;130:199-203. 21. Picardi A, Mazzotti E, Gaetano P, et al. Stress, social support, emotional regulation, and exacerbation of diffuse plaque psoriasis. Psychosomatics 2005;46:556-64. 22. Harvima RJ, Viinamäki H, Harvima IT, et al. Association of psychic stress with clinical severity and symptoms of psoriatic patients. Acta Derm Venereol 1996;76:467-71. 23. Kabat-Zinn J, Wheeler E, Light T, et al. Influence of a mindfulness meditation-based stress reduction intervention on rates of skin clearing in patients with moderate to severe psoriasis undergoing phototherapy (UVB) and photochemotherapy (PUVA). Psychosom Med 1998;60: 625-32. 24. Parker J, Klein SL, McClintock MK, et al. Chronic stress accelerates ultraviolet-induced cutaneous carcinogenesis. J Am Acad Dermatol 2004;51:919-22. 25. Adam K, Tomeny M, Oswald I. Physiological and psychological differences between good and poor sleepers. J Psychiatr Res 1986;20: 301-16. 26. Healey ES, Kales A, Monroe LJ, Bixler EO, Chamberlin K, Soldatos CR. Onset of insomnia: role of life-stress events. Psychosom Med 1981; 43:439-51. 27. Meerlo P, Sgoifo A, Suchecki D. Restricted and disrupted sleep: effects on autonomic function, neuroendocrine stress systems and stress responsivity. Sleep Med Rev 2008;12:197-210. 28. Altemus M, Rao B, Dhabhar FS, Ding W, Granstein RD. Stress-induced changes in skin barrier function in healthy women. J Invest Dermatol 2001;117:309-17. 29. Lam JC, Mason TB. Treatment of sleep disorders in children. Curr Treat Options Neurol 2007;9:404-13. 30. 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. 31. Cao G, Booth SL, Sadowski JA, Prior RL. Increases in human plasma antioxidant capacity after consumption of controlled diets high in fruit and vegetables. Am J Clin Nutr 1998;68:1081-7. 32. Vanizor Kural B, Orem A, Cimşit G, Yandi YE, Calapoglu M. Evaluation of the atherogenic tendency of lipids and lipoprotein content
98
33. 34. 35.
36.
37.
38.
39.
40.
41.
42.
43.
V. Treloar and their relationships with oxidant-antioxidant system in patients with psoriasis. Clin Chim Acta 2003;328:71-82. Mayser P, Grimm H, Grimminger F. n-3 fatty acids in psoriasis. Br J Nutr 2002;87(suppl 1):S77-82. Lands WE. Biochemistry and physiology of n-3 fatty acids. FASEB J 1992;6:2530-6. Grimble RF, Howell WM, O'Reilly G, et al. The ability of fish oil to suppress tumor necrosis factor alpha production by peripheral blood mononuclear cells in healthy men is associated with polymorphisms in genes that influence tumor necrosis factor alpha production. Am J Clin Nutr 2002;76:454-9. Gupta AK, Ellis CN, Tellner DC, Anderson TF, Voorhees JJ. Doubleblind, placebo-controlled study to evaluate the efficacy of fish oil and low-dose UVB in the treatment of psoriasis. Br J Dermatol 1989;120: 801-7. Danno K, Sugie N. Combination therapy with low-dose etretinate and eicosapentaenoic acid for psoriasis vulgaris. J Dermatol 1998;25: 703-5. Reynoso-von Drateln C, Martínez-Abundis E, Balcázar-Muñoz BR, Bustos-Saldaña R, González-Ortiz M. Lipid profile, insulin secretion, and insulin sensitivity in psoriasis. J Am Acad Dermatol 2003;48: 882-5. Boehncke S, Thaci D, Beschmann H, et al. Psoriasis patients show signs of insulin resistance. Br J Dermatol 2007;157: 1249-51. McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PW, Jacques PF. Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort. Diabetes Care 2004;27:538-46. Kallio P, Kolehmainen M, Laaksonen DE, et al. Dietary carbohydrate modification induces alterations in gene expression in abdominal subcutaneous adipose tissue in persons with the metabolic syndrome: the FUNGENUT Study. Am J Clin Nutr 2007;85: 1417-27. Michaelsson G, Gerdén B, Ottosson M, et al. Patients with psoriasis often have increased serum levels of IgA antibodies to gliadin. Br J Dermatol 1993;129:667-73. Michaelsson G, Gerdén B, Hagforsen E, et al. Psoriasis patients with antibodies to gliadin can be improved by a gluten-free diet. Br J Dermatol 2000;142:44-51.
44. Kia KF, Nair RP, Ike RW, Hiremagalore R, Elder JT, Ellis CN. Prevalence of antigliadin antibodies in patients with psoriasis is not elevated compared with controls. Am J Clin Dermatol 2007;8: 301-5. 45. Smith TP, Kennedy SL, Smith M, Orent S, Fleshner M. Physiological improvements and health benefits during an exercise-based comprehensive rehabilitation program in medically complex patients. Exerc Immunol Rev 2006;12:86-96. 46. Santana MG, Poyares D, Tufik S, Mello MT. Physical exercise can improve sleep quality of insomniac patients. Abstract 737. Presented at: Associated Professional Sleep Societies Meeting 2008; 2008 [Baltimore (MD)]. 47. Hawley JA, Lessard SJ. Exercise training-induced improvements in insulin action. Acta Physiol (Oxf) 2008;192:127-35. 48. Keylock KT, DiPietro LA, Schrementi M, Woods JA. Exercise accelerates cutaneous wound healing and decreases wound inflammation in aged mice. Am J Physiol Regul Integr Comp Physiol 2008;294: R179-84. 49. Roehr B. Get moving! Exercise decreases inflammation, facilitates wound healing. Dermatol Times 2008:41. 50. Leibowitz E, Seidman DS, Laor A, Shapiro Y, Epstein Y. Are psoriatic patients at risk of heat intolerance? Br J Dermatol 1991;124: 439-42. 51. Gomez-Cabrera MC, Domenech E, Viña J. Moderate exercise is an antioxidant: upregulation of antioxidant genes by training. Free Radic Biol Med 2008;44:126-31. 52. Swinburn BA, Walter LG, Arroll B, Tilyard MW, Russell DG. The green prescription study: a randomized controlled trial of written exercise advice provided by general practitioners. Am J Public Health 1998;88:288-91. 53. Kourosh AS, Miner A, Menter A. Psoriasis as the marker of underlying systemic disease. Skin Therapy Lett 2008;13:1-5. 54. Nasreen S, Ahmed I, Effendi S. Frequency and magnitude of anxiety and depression in patients with psoriasis vulgaris. J Coll Physicians Surg Pak 2008;18:397-400. 55. Bernstein CN, Wajda A, Blanchard JF. The clustering of other chronic inflammatory diseases in inflammatory bowel disease: a populationbased study. Gastroenterology 2005;129:827-36. 56. McFadden J. Hypothesis - the natural selection of psoriasis. Clin Exp Dermatol 1990;15:39-43.
Addendum 1. Good sleep hygiene 1. Devote the time to sleep. Arrange consistent bedtimes and waking times to allow 7 to 8 hours of uninterrupted sleep. 2. Begin unwinding 30 to 45 minutes before sleep should begin. Do not use this time to finish tasks, tidy up the house, or make to do lists. 3. If you have worries, write them down and leave them for tomorrow. 4. Try relaxation techniques as your prepare for bed. 5. Do not eat 1 to 2 hours before bed. Do not drink a lot of fluids. 6. Avoid caffeine (coffee, tea, chocolate) after 4 PM. 7. Avoid alcohol 4 to 6 hours before bedtime. 8. Avoid daytime naps. 9. Exercise regularly and moderately. Do not engage in vigorous exercise after 6 PM. 10. Do not keep the television in your bedroom. 11. Use the bedroom only for sleep (and sex). 12. Keep the bedroom quiet. 13. Pull the shades so the room is dark. Light disturbs melatonin release. 14. Ensure that the temperature of the bedroom is optimal for you. 15. Consider putting a few drops of a high-quality lavender essential oil on a handkerchief under your pillow. 16. Consider a bedtime ritual, such as a warm bath or a few pages of reading.
Integrative dermatology for psoriasis
99
Addendum 2. Exercise prescription Name________________________________ Date___________________ Cautions: Diabetic retinopathy or neuropathy–avoid vigorous exercise Diabetic patients must monitor blood sugar before and after exercise. Delayed hypoglycemia can occur up to 6 to 15 hours after exercise. Framingham Cardiac Risk Score N 10% may require a graded exercise electrocardiogram before beginning an exercise program. Risk calculator at: http://www.mdcalc.com/cardiacrisk If you have the conditions listed above or have any concerns or questions, be sure to consult your physician before embarking on an exercise program. Consider working with a trainer. 30 minutes of moderate* activity 5 times weekly; or 20 minutes of vigorous** activity 3 times weekly Exertion scale Exertion of sitting = 1. . . . .2. . . . .3. . . . .4 . . . . . 5. . . . .6. . . . .7. . . . .8. . . . .9. . . . .10 = Maximal exertion *Moderate = 5 to 6 = noticeable increase in heart rate. **Vigorous = 7 to 8 = rapid breathing and greater increase in heart rate. 1. Walking / Jogging / Running / Swimming / Dancing / Yard work / Biking / Exercise class _____________________ ________________________________________________________ 2. Strength training / Muscle building / Resistance training / Weight lifting / Body weight training ________________ _____________________________________________________ 2-3 sets of 8-12 repetitions, with the last rep being extremely difficult. Work upper body, lower body, core; both front body and back body. [Consider facial muscle resistance exercise, too] 3. Flexibility / Stretching / Yoga / Tai chi / Pilates / ______________________________ Work through the full range of motion for all joints. 4. Balance training / Tai chi / Yoga / Dance / ____________________________________