What Triggers Psoriatic Disease? Dietary, Infectious, Allergenic, Physical, and Environmental Exposures in Psoriasis and Psoriatic Arthritis: A Narrative Review

Ori Scott, M.Sc., Registered Dietitian (Israel)Independent Researcher, New York, NY, USA

Abstract

Background and Objectives

Patients with psoriasis and psoriatic arthritis (PsA) frequently attribute disease onset or worsening to foods, infections, allergens, weather, pollution, household exposures, or physical trauma. However, the term trigger is often applied to relationships supported by fundamentally different types of evidence. An exposure associated with disease development is not necessarily an acute flare trigger, and a factor associated with chronic disease severity or progression from psoriasis to PsA should not automatically be interpreted as a trigger of established disease. This narrative review evaluates dietary, infectious, allergenic, physical, seasonal, household, and environmental exposures proposed to influence psoriatic disease while distinguishing psoriasis development, acute exacerbation, chronic disease modification, PsA activity, and transition from psoriasis to PsA.

Methods

A structured narrative literature search was undertaken primarily using PubMed/MEDLINE and supplemented by reference tracing from relevant systematic reviews and verification against PubMed and publisher records. Searches were conducted by exposure domain and updated through September 2026. Systematic reviews and meta-analyses were used primarily to map the literature, while primary human studies were prioritized for specific quantitative findings. Evidence was interpreted according to study design and the clinical outcome measured and was considered direct/established, indirect/supportive, emerging/hypothesis-generating, or insufficient. These categories are descriptive and do not constitute formal certainty grading. This was a narrative review; protocol registration, duplicate independent screening, formal risk-of-bias assessment, certainty grading, and meta-analysis were not performed.

Results

Streptococcal infection in relevant psoriasis phenotypes and cutaneous trauma through the Koebner phenomenon have comparatively direct clinical support as triggers. Weight reduction in people with overweight or obesity and Mediterranean dietary intervention may improve psoriasis outcomes, but these findings support disease modification rather than establishing individual foods as acute flare triggers. Gluten restriction is best supported in selected patients with celiac disease or relevant positive serology rather than universally. Smoking and alcohol have epidemiologic associations with psoriasis, while emerging observational evidence links particulate air pollution and selected environmental contaminants with psoriasis incidence, prevalence, severity, or exacerbation. Microbiome alterations are repeatedly reported, but their causal significance remains uncertain. Current evidence is insufficient to classify nuts or peanuts, eggs, seafood or shellfish, dairy products, honey or bee products, pollen, household pets, animal dander, indoor mold, or nonspecific contaminated household water as general psoriasis or PsA flare triggers. Evidence concerning external triggers of established PsA is particularly limited, and flare definitions remain heterogeneous.

Conclusions

The evidence does not support a universal list of psoriasis or PsA triggers. Proposed exposures should be distinguished according to whether the evidence concerns acute triggering, disease risk, chronic disease modification, disease progression, or biological plausibility. Greater precision in these distinctions may reduce unsupported avoidance behaviors, improve clinical counseling, and provide a clearer framework for future prospective research.

Keywords: psoriasis; psoriatic arthritis; flare; diet; infection; Koebner phenomenon; environmental exposure; air pollution; food allergy; microbiome

1. Introduction

Psoriasis is a chronic immune-mediated inflammatory disease resulting from interactions among genetic susceptibility, immune dysregulation, and environmental influences. Psoriatic arthritis (PsA) is a heterogeneous inflammatory musculoskeletal disease occurring in a subset of people with psoriasis. Because both conditions can fluctuate over time, patients frequently seek potentially modifiable explanations for disease onset or worsening.

Diet is particularly prominent in patient perceptions. Surveys show that people with psoriasis commonly experiment with dietary modification and report perceived benefit after eliminating particular foods or changing overall dietary patterns [11]. Such observations are clinically relevant but do not by themselves establish causality because they are susceptible to recall bias, self-selection, concurrent lifestyle changes, and placebo or expectation effects.

Similar uncertainty surrounds infection, physical trauma, pollen, season, pets, indoor exposures, air pollution, and environmental contaminants. A fundamental problem is that the word trigger is frequently used for biologically and epidemiologically different relationships. An exposure associated with incident psoriasis is not necessarily an acute flare trigger. A factor associated with higher chronic disease severity may be a disease modifier rather than a trigger, and a predictor of progression from psoriasis to PsA should not automatically be interpreted as a trigger of established PsA.

The objective of this narrative review is therefore to evaluate commonly suspected dietary, infectious, allergenic, physical, household, and environmental exposures in psoriatic disease while explicitly distinguishing evidence for psoriasis development, psoriasis exacerbation, chronic severity, PsA activity, and psoriasis-to-PsA transition.

2. Methods

2.1. Review Design and Information Sources

This work was conducted as a narrative review.

A structured literature search was undertaken primarily using PubMed/MEDLINE, supplemented by reference tracing from relevant systematic reviews and verification against PubMed and publisher records. Searches were conducted by exposure domain rather than as a single combined search and were updated through September 2026.

Search concepts combined psoriasis or psoriatic arthritis with terms relating to diet, obesity, weight loss, Mediterranean diet, ultra-processed foods, gluten, celiac disease, food allergy, nuts, eggs, seafood, shellfish, dairy products, honey, alcohol, smoking, microbiome, streptococcal infection, trauma, Koebner phenomenon, mechanical stress, seasonality, ultraviolet exposure, temperature, humidity, pollen, aeroallergens, pets, animal dander, mold, air pollution, particulate matter, per- and polyfluoroalkyl substances (PFAS), metals, environmental contaminants, and water exposure.

Systematic reviews and meta-analyses were used primarily to map the literature, while primary human studies were prioritized for specific quantitative statements. Older studies were retained when they provided direct or historically important evidence. Evidence was interpreted according to study design and the outcome actually measured.

2.2. Evidence Interpretation

For synthesis, evidence was considered direct/established when it directly addressed the exposure–outcome relationship; indirect/supportive when it informed but did not establish triggering; emerging/hypothesis-generating when preliminary, mechanistic, or exploratory; and insufficient when direct clinical evidence was inadequate.

These categories are descriptive and do not constitute formal certainty grading.

Because this is a narrative rather than systematic review, protocol registration, duplicate independent screening, formal study-level risk-of-bias assessment, certainty grading, and meta-analysis were not performed. The search should therefore not be interpreted as an exhaustive systematic evidence synthesis.

3. What Constitutes a Trigger?

A clinically meaningful trigger is most reasonably defined as an exposure temporally related to disease expression or exacerbation. This differs from a risk factor, which predicts disease development; a disease modifier, which influences chronic activity or treatment response; and a mechanistically plausible exposure, for which biological evidence exists without demonstrated clinical triggering.

This distinction substantially changes interpretation of the literature. Cross-sectional associations cannot establish temporal direction and are particularly vulnerable to confounding. Diet, adiposity, smoking, alcohol use, physical activity, socioeconomic factors, and environmental exposures frequently cluster.

Strong evidence for triggering therefore benefits from temporal proximity, reproducibility, objective disease assessment, and an appropriate comparator. Where clinically and ethically feasible, elimination followed by rechallenge can strengthen causal inference.

4. Diet, Obesity, and Dietary Patterns

The strongest nutritional evidence in psoriasis concerns weight management and overall dietary patterns rather than avoidance of individual foods. Evidence syntheses and intervention studies have examined weight reduction, dietary patterns, supplements, and other nutritional interventions [1–9,40–48].

The National Psoriasis Foundation systematic review identified 55 studies representing 77,557 unique participants, including 4,534 with psoriasis. It strongly recommended hypocaloric dietary weight reduction for patients with psoriasis who have overweight or obesity and weakly recommended gluten-free diets only in patients with positive serologic markers of gluten sensitivity [1].

Randomized intervention studies also support weight reduction as an adjunctive strategy [2–4], with longer-term follow-up suggesting that sustained weight reduction may remain relevant to psoriasis severity [5]. Systematic reviews of lifestyle and weight-loss interventions provide additional contextual support while also reflecting heterogeneity among interventions and populations [40,42].

In the randomized trial by Jensen and colleagues, adults with psoriasis and excess body weight assigned to a low-energy diet achieved substantially greater weight loss than controls. At 16 weeks, the between-group difference in weight loss was 15.4 kg. The between-group PASI difference was −2.0 points but did not reach conventional statistical significance (P=0.06), whereas Dermatology Life Quality Index improvement was statistically significant [2]. This distinction is important: the study supports potential clinical benefit of weight reduction but should not be represented as unequivocal proof of a statistically significant PASI effect.

Dietary-pattern evidence has also developed. Observational studies have examined adherence to Mediterranean dietary patterns in relation to psoriasis severity [7,8]. More recently, the MEDIPSO randomized clinical trial evaluated a dietitian-guided Mediterranean dietary intervention [6]. In that trial, 38 adults with mild-to-moderate psoriasis receiving stable topical therapy were randomized to a 16-week Mediterranean dietary intervention or standard low-fat dietary advice; 37 completed the study. The between-group estimated marginal mean difference in PASI change was −3.4 points (95% CI −4.8 to −2.0), and 9 of 19 intervention participants achieved PASI75 compared with none in the control group [6].

These findings support Mediterranean dietary intervention as a potentially useful adjunct. They do not establish that individual foods excluded or consumed less frequently within the dietary pattern were responsible for disease activity.

Prospective observational evidence has also associated higher consumption of ultra-processed foods with psoriasis risk [9]. Such findings should presently be classified as risk associations rather than evidence that an individual ultra-processed meal precipitates a flare.

Taken together, the nutritional literature supports a role for weight management and potentially overall dietary pattern in disease modification. It does not support reducing psoriasis to a simple list of foods that universally trigger acute disease activity.

5. Gluten, Food Allergy, and Individual Foods

Gluten represents an important subgroup-specific issue.

Clinical evidence has reported improvement during a gluten-free diet among some patients with psoriasis and antigliadin antibodies [10]. Reviews of psoriasis and celiac disease have likewise considered the relevance of gluten-related disorders [43], and the National Psoriasis Foundation synthesis weakly supported gluten-free diets specifically in patients with positive serologic markers of gluten sensitivity [1].

This evidence does not justify characterizing gluten as a universal psoriasis trigger or recommending gluten avoidance to all people with psoriasis.

Evidence is substantially weaker for nuts or peanuts, eggs, seafood or shellfish, dairy products, and honey or bee products. Patient reports and isolated observations can generate hypotheses, but they cannot demonstrate population-level psoriasis triggering. Broader reviews addressing nutritional factors, food allergy, supplements, and diet in psoriasis illustrate both continuing interest and the limitations of this evidence base [44–48,53,54].

Similarly, IgE-mediated food allergy in an individual patient should be diagnosed and managed on its own clinical merits. The existence of food allergy does not establish the allergen as a psoriasis-specific trigger.

Broad elimination diets therefore should not be inferred from current psoriasis evidence. Where an individual reports a reproducible food relationship, alternative explanations—including allergy, intolerance, changes in total energy intake, body weight, alcohol intake, and other simultaneous dietary or behavioral changes—should be considered.

Fish oil illustrates another important distinction. Nutritional supplementation has been investigated in randomized trials and meta-analysis [41,44], but evidence concerning a supplement's therapeutic effect addresses a different question from whether the corresponding food is an acute disease trigger.

The appropriate conclusion is therefore not that individual food-related experiences are impossible. Rather, current evidence does not justify generalizing the commonly suspected foods considered here as established psoriasis or PsA triggers.

6. Alcohol and Smoking

Smoking has repeatedly been associated with psoriasis in observational literature and meta-analysis [14]. These data are most appropriately interpreted as evidence concerning psoriasis risk and potentially disease severity rather than proof that an individual smoking exposure triggers an immediate flare.

Alcohol also shows an epidemiologic association. Earlier systematic review evidence documented the complexity and limitations of the relationship [13]. A 2024 systematic review and dose-response meta-analysis subsequently included 48 studies involving 1,702,847 individuals from 24 countries and reported a positive overall association between alcohol consumption and psoriasis [12]. Important heterogeneity and limitations inherent to observational exposure assessment remain.

Smoking and alcohol are therefore clinically relevant behavioral exposures, but epidemiologic association should not be converted into an unsupported claim that every exposure produces an acute flare.

7. Gut and Skin Microbiome

Differences in gut and skin microbial composition have repeatedly been reported between people with psoriasis and controls [15–17]. Proposed pathways include intestinal-barrier alterations, microbial metabolites, and effects on immune signaling, including Th17-related pathways.

However, microbiome studies are heterogeneous in population, sampling, analytical methodology, medication exposure, geography, and reported microbial signatures. Recent systematic reviews continue to document this heterogeneity [16,17]. Treatment itself may also modify microbial composition, making temporal and causal interpretation difficult.

Dysbiosis could consequently represent a cause, consequence, correlate, or treatment-responsive feature of disease. Current evidence supports biological plausibility and continued investigation but does not establish a particular microbial signature—or a particular food presumed to alter that signature—as a clinical psoriasis trigger.

This distinction is important because mechanistic plausibility should not be treated as evidence of clinical effectiveness or clinical triggering.

8. Infectious Triggers

Infection provides some of the strongest evidence for genuine triggering in selected psoriasis phenotypes.

Streptococcal infection has a long-recognized relationship with guttate psoriasis. Telfer and colleagues documented recent streptococcal infection among patients presenting with acute guttate psoriasis [18]. Prospective evidence has also associated streptococcal throat infection with exacerbation of chronic plaque psoriasis in susceptible individuals [19].

This temporal relationship is qualitatively stronger than the evidence supporting most proposed individual food triggers.

However, evidence that an infection can precipitate psoriasis should not be confused with evidence that antimicrobial treatment reliably improves established psoriasis. A Cochrane review of antistreptococcal interventions [20] and a later systematic review of antistreptococcal treatment [21] illustrate the heterogeneity and uncertainty of the treatment literature.

Accordingly, the evidence supports streptococcal infection as a relevant trigger in particular clinical contexts, but it does not follow that antibiotics or other antistreptococcal interventions are universally effective psoriasis treatments.

9. Physical Trauma and Mechanical Stress

The Koebner phenomenon—the development of psoriatic lesions at sites of cutaneous injury—is one of the clearest examples of a physical trigger in psoriasis [22].

This distinction helps interpret household exposures. A scratch from a cat or dog, for example, could potentially precipitate a lesion through trauma in a Koebner-responsive patient. Such an event would support trauma as the mechanism; it would not establish the animal, its fur, or its dander as a psoriasis trigger.

Mechanical and traumatic exposures have also been investigated in relation to progression from psoriasis to PsA [23–26].

A systematic review and meta-analysis of 16 observational studies involving 322,967 people with psoriasis found associations between subsequent PsA and obesity (OR 1.75, 95% CI 1.42–2.16), overweight (OR 1.50, 95% CI 1.08–2.09), physical trauma (OR 1.33, 95% CI 1.16–1.54), and fracture (OR 1.46, 95% CI 1.22–1.74). Each 1-kg/m² increase in body mass index was associated with an approximately 6% increase in the odds of PsA [26].

These findings concern development of PsA among people with psoriasis. They do not establish that trauma produces an acute flare in a person with established PsA.

10. Season, Climate, and Pollen

Seasonal variation in psoriasis occurs, but the pattern is heterogeneous [27,28].

A systematic review of 13 studies from Northern and Central Europe reported that approximately 50% of patients experienced no important seasonal difference, about 30% improved during summer, and approximately 20% did better during winter [27].

Season is not a single exposure. It incorporates changes in ultraviolet radiation, temperature, humidity, infection patterns, behavior, and potentially psychological and other environmental factors. Seasonal worsening therefore cannot establish pollen causality.

Despite the common perception that pollen or aeroallergens may trigger inflammatory skin disease, direct psoriasis-specific evidence demonstrating pollen-induced psoriasis flares remains insufficient based on the literature evaluated for this review.

Pollen should therefore remain a research question rather than being presented as an established psoriasis trigger.

11. Household Pets and Indoor Exposures

Evidence that cat or dog ownership, animal dander, or routine household pet exposure precipitates psoriasis or PsA flares is insufficient.

This should not be confused with evidence connecting animal allergens with classical allergic disorders. Nor should it obscure plausible indirect mechanisms. Animal scratches can produce cutaneous trauma and potentially provoke a Koebner response. Animal exposure can occasionally be associated with infection, and pets can modify indoor microbial and allergen environments.

None of these mechanisms demonstrates that pet ownership itself causes psoriatic disease activity.

Evidence for indoor mold as a psoriasis-specific trigger is similarly inadequate based on the literature evaluated for this review.

The evidence therefore does not support routine avoidance of household pets or indoor allergens specifically for psoriasis or PsA in the absence of another established clinical indication.

12. Air Pollution and Environmental Contaminants

Air pollution represents an increasingly important research domain. Observational studies have examined particulate matter and gaseous pollutants in relation to psoriasis incidence, prevalence, severity, and exacerbation [29,30].

Recent large-scale research has strengthened the temporal literature concerning particulate exposure. A 2026 nationwide cohort study examined long-term particulate-matter exposure in relation to psoriasis incidence and short-term exposure in relation to exacerbation [30].

These findings increase interest in air pollution as a potentially relevant environmental exposure, but the evidence remains observational. Residual confounding, exposure misclassification, and correlations among individual pollutants complicate causal interpretation.

Environmental chemical research has also examined PFAS and mixtures of environmental contaminants in relation to psoriasis [31,32]. Additional studies have examined cadmium and other metals [33,34]. These findings support continued investigation but require careful interpretation according to design.

Cross-sectional biomonitoring studies can identify exposure–disease associations but generally cannot determine whether exposure preceded disease or precipitated an individual flare.

The frequently used phrase polluted water is therefore scientifically imprecise. Drinking and household water can contain diverse microbial, chemical, and mineral exposures with different biological properties. Evidence concerning a defined contaminant cannot automatically be generalized to all forms of water contamination.

Current evidence does not establish nonspecific contaminated household water as a general psoriasis or PsA flare trigger. Research should instead evaluate defined contaminants, exposure routes, doses, timing, and clinically specified outcomes.

13. Psoriatic Arthritis and the Psoriasis-to-PsA Transition

Evidence concerning external triggers of established PsA is much less developed than the corresponding psoriasis literature.

A 2025 systematic review included 54 studies addressing PsA flare. Forty-four studies provided a definition of flare, but definitions varied considerably. In higher-quality studies, current patient-reported flare prevalence was approximately 10%, physician-reported prevalence approximately 7%, and annual flare incidence approximately 22–23%. The review concluded that risk-factor evidence was limited or unclear and that no consensus flare definition existed [35].

This uncertainty makes claims about specific dietary or environmental PsA flare triggers particularly vulnerable to overinterpretation.

Dietary intervention and weight loss have also been examined in PsA [36,37], while broader reviews have considered nutritional approaches in inflammatory arthritides [49]. These studies address potential disease modification and should not automatically be interpreted as evidence for specific acute food triggers.

By contrast, several studies and evidence syntheses have evaluated predictors of the development of PsA among people with psoriasis [23–26,38,39]. Obesity, overweight, and previous physical trauma have been associated with PsA onset, but these relationships concern disease transition rather than acute fluctuation of established PsA.

PsA onset, chronic PsA activity, and an acute PsA flare are therefore separate outcomes and should remain analytically distinct.

14. Clinical Interpretation

The available evidence supports a hierarchy rather than a universal list of psoriasis and PsA triggers.

Comparatively direct evidence exists for streptococcal infection in relevant psoriasis phenotypes and for cutaneous trauma through the Koebner phenomenon [18,19,22].

Disease-modifying evidence supports consideration of weight reduction in people with overweight or obesity and suggests potential benefit from Mediterranean dietary intervention [1–8,40,42,48]. These findings should not be converted into claims that individual foods are acute triggers.

Subgroup-specific evidence supports consideration of gluten restriction primarily in patients with celiac disease or relevant positive serology rather than universally [1,10,43].

Epidemiologic associations exist for smoking and alcohol [12–14], while obesity and trauma have been associated with transition from psoriasis to PsA [23–26,38].

Emerging environmental evidence concerns air pollution, PFAS, metals, and other environmental contaminants [29–34]. These studies frequently address incidence, prevalence, or chronic disease relationships rather than experimentally demonstrated acute triggering.

Mechanistic or hypothesis-generating evidence concerns the microbiome [15–17]. Repeated observation of dysbiosis does not yet establish causality.

In contrast, current evidence is insufficient to classify nuts or peanuts, eggs, seafood or shellfish, dairy products, honey or bee products, pollen, pets, animal dander, indoor mold, or nonspecific household water contamination as general psoriasis or PsA flare triggers.

Importantly, insufficient population-level evidence does not prove that an individual patient's observation is false. It means that reproducibility, timing, allergy, infection, trauma, treatment changes, weight changes, and alternative explanations should be considered before an individual experience is generalized into a clinical recommendation.

The appropriate response to an individual suspected trigger is therefore neither automatic dismissal nor automatic acceptance. It is careful evaluation of temporal relationships, reproducibility, competing explanations, and the strength and applicability of the relevant clinical evidence.

15. Research Gaps and Future Directions

Future trigger studies require prospective exposure measurement before disease worsening and standardized definitions of flare.

Dietary research should distinguish food allergy, celiac disease, intolerance, dietary pattern, energy balance, body-weight change, and individual foods. When safe and ethically appropriate, controlled elimination–rechallenge designs could provide stronger evidence than retrospective surveys.

Pollen research should simultaneously measure aeroallergen concentrations, sensitization, ultraviolet exposure, temperature, and humidity. Without such measurements, apparent seasonal relationships may be incorrectly attributed to pollen.

Pet studies should distinguish ownership from direct allergen exposure, allergic sensitization, trauma, infection, and changes in the indoor microbiome.

Air-pollution research would benefit from more precise personal exposure measurements and repeated objective disease assessments. Studies of water and environmental contaminants should identify specific agents rather than treating pollution or contaminated water as homogeneous exposures.

For PsA, consensus flare definitions and prospective cohorts following people with psoriasis through transition to PsA are particularly important. Studies of established PsA flare and studies of psoriasis-to-PsA transition should be treated as separate clinical questions.

16. Strengths and Limitations

A principal strength of this narrative review is its explicit separation of acute triggering from disease incidence, chronic severity, disease modification, and psoriasis-to-PsA transition. This addresses an important source of overinterpretation in discussions of psoriasis triggers.

The review also deliberately considers commonly suspected exposures for which evidence may be weak or absent rather than restricting discussion to exposures already supported by positive studies.

The review has important limitations. It is a narrative rather than systematic review. Although the literature search was structured, it was not designed to guarantee exhaustive retrieval. Formal duplicate screening, study-level risk-of-bias assessment, prospective protocol registration, certainty grading, and meta-analysis were not performed.

The underlying literature is heterogeneous. Several exposure domains rely heavily on observational or cross-sectional studies. Exposure definitions, psoriasis outcomes, populations, treatment status, and adjustment for confounding vary substantially among studies.

Evidence concerning PsA triggers is particularly limited, in part because definitions of PsA flare remain inconsistent.

Finally, absence of convincing published evidence should not be interpreted as evidence that an exposure can never affect an individual patient. It indicates that the exposure has not been established as a general clinical trigger at the population level based on the evidence evaluated.

17. Conclusions

The term trigger is used too broadly in psoriatic disease.

Streptococcal infection in relevant psoriasis phenotypes and cutaneous trauma through the Koebner phenomenon have comparatively direct clinical support. Weight reduction and Mediterranean dietary intervention may modify psoriasis severity in selected populations, while gluten restriction is best targeted to patients with celiac disease or evidence of gluten sensitivity.

Smoking, alcohol, obesity, air pollution, environmental contaminants, and mechanical exposures have varying associations with psoriasis or PsA, but much of this evidence concerns disease risk, chronic severity, or disease development rather than acute flares.

Direct evidence remains insufficient to classify nuts or peanuts, eggs, seafood or shellfish, dairy products, honey or bee products, pollen, household pets, animal dander, indoor mold, or nonspecific contaminated water as general psoriasis or PsA flare triggers.

Microbiome alterations provide biologically interesting hypotheses but do not currently establish a particular microbial profile or microbiome-modifying food as a clinical trigger.

For PsA, additional caution is required because evidence concerning external triggers of established disease is limited and flare definitions remain heterogeneous.

Greater precision in distinguishing acute triggers, disease risk factors, chronic disease modifiers, progression factors, and mechanistically plausible exposures may improve clinical counseling, reduce unsupported avoidance behaviors, and provide a clearer framework for future research.

References

1. Ford AR, Siegel M, Bagel J, et al. Dietary recommendations for adults with psoriasis or psoriatic arthritis from the Medical Board of the National Psoriasis Foundation: a systematic review. JAMA Dermatol. 2018;154:934–950. doi:10.1001/jamadermatol.2018.1412.

2. Jensen P, Zachariae C, Christensen R, et al. Effect of weight loss on the severity of psoriasis: a randomized clinical study. JAMA Dermatol. 2013;149:795–801. PMID:23752669. [Erratum published in JAMA Dermatol. 2013;149:997.]

3. Gisondi P, Del Giglio M, Di Francesco V, et al. Weight loss improves the response of obese patients with moderate-to-severe chronic plaque psoriasis to low-dose cyclosporine therapy: a randomized, controlled, investigator-blinded clinical trial. Am J Clin Nutr. 2008. PMID:18996858. doi:10.3945/ajcn.2008.26427.

4. Naldi L, Conti A, Cazzaniga S, et al. Diet and physical exercise in psoriasis: a randomized controlled trial. Br J Dermatol. 2014. PMID:24641585.

5. Jensen P, et al. Long-term effects of weight reduction on the severity of psoriasis in a cohort derived from a randomized trial. Am J Clin Nutr. 2016. PMID:27334236.

6. Perez-Bootello J, Berna-Rico E, Abbad-Jaime de Aragon C, et al. Mediterranean diet and patients with psoriasis: the MEDIPSO randomized clinical trial. JAMA Dermatol. 2025;161:1215–1223. PMID:40991259.

7. Barrea L, et al. Nutrition and psoriasis: is there any association between the severity of the disease and adherence to the Mediterranean diet? J Transl Med. 2015.

8. Phan C, et al. Association between Mediterranean anti-inflammatory dietary profile and severity of psoriasis: results from the NutriNet-Santé cohort. JAMA Dermatol. 2018.

9. Peng X, Li X, He J, et al. Ultra-processed food consumption and the risk of psoriasis: a large prospective cohort study. Nutrients. 2025;17:1473. PMID:40362782. doi:10.3390/nu17091473.

10. Michaëlsson 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. PMID:10651693. doi:10.1046/j.1365-2133.2000.03240.x.

11. Afifi L, Danesh MJ, Lee KM, et al. Dietary behaviors in psoriasis: patient-reported outcomes from a US national survey. Dermatol Ther (Heidelb). 2017. PMID:28526915.

12. Choi J, Han I, Min J, et al. Dose-response analysis between alcohol consumption and psoriasis: a systematic review and meta-analysis. J Dtsch Dermatol Ges. 2024;22:641–652. PMID:38679782. doi:10.1111/ddg.15380.

13. Brenaut E, Horreau C, Pouplard C, et al. Alcohol consumption and psoriasis: a systematic literature review. J Eur Acad Dermatol Venereol. 2013. PMID:23845150. doi:10.1111/jdv.12164.

14. Armstrong AW, Harskamp CT, Dhillon JS, Armstrong EJ. Psoriasis and smoking: a systematic review and meta-analysis. Br J Dermatol. 2014;170:304–314. PMID:24117435.

15. Benhadou F, Mintoff D, Schnebert B, Thio HB. Psoriasis and microbiota: a systematic review. Diseases. 2018;6:47.

16. Gao Y, Lou Y, Hui Y, et al. Characterization of the gut microbiota in patients with psoriasis: a systematic review. Pathogens. 2025;14:358. PMID:40333159. doi:10.3390/pathogens14040358.

17. Xue M, Deng Q, Deng L, et al. Alterations of gut microbiota for the onset and treatment of psoriasis: a systematic review. Eur J Pharmacol. 2025;998:177521. PMID:40107339.

18. Telfer NR, Chalmers RJ, Whale K, Colman G. The role of streptococcal infection in the initiation of guttate psoriasis. Arch Dermatol. 1992;128:39–42. PMID:1739285.

19. Gudjonsson JE, Thorarinsson AM, Sigurgeirsson B, Kristinsson KG, Valdimarsson H. Streptococcal throat infections and exacerbation of chronic plaque psoriasis: a prospective study. Br J Dermatol. 2003;149:530–534. PMID:14510985. doi:10.1046/j.1365-2133.2003.05552.x.

20. Antistreptococcal interventions for guttate and chronic plaque psoriasis. Cochrane Database Syst Rev. 2019. PMID:30835819.

21. Antistreptococcal treatment of psoriasis: a systematic review. Arch Dermatol Res. 2024. PMID:38850287. doi:10.1007/s00403-024-03051-8.

22. Weiss G, Shemer A, Trau H. The Koebner phenomenon: review of the literature. J Eur Acad Dermatol Venereol. 2002;16:241–248. PMID:12195563. doi:10.1046/j.1473-2165.2002.00406.x.

23. Pattison E, Harrison BJ, Griffiths CEM, et al. Environmental risk factors for the development of psoriatic arthritis: results from a case-control study. Ann Rheum Dis. 2008. PMID:17823200. doi:10.1136/ard.2007.073932.

24. Physical trauma recorded in primary care is associated with the onset of psoriatic arthritis among patients with psoriasis. Ann Rheum Dis. PMID:27457510. doi:10.1136/annrheumdis-2016-209334.

25. Eder L, et al. Environmental risk factors for psoriatic arthritis among patients with psoriasis. Arthritis Care Res. 2011. PMID:21560259. doi:10.1002/acr.20496.

26. Xie W, Huang H, Deng X, Gao D, Zhang Z. Modifiable lifestyle and environmental factors associated with onset of psoriatic arthritis in patients with psoriasis: a systematic review and meta-analysis of observational studies. J Am Acad Dermatol. 2021;84:701–711. PMID:32827608. doi:10.1016/j.jaad.2020.08.060.

27. Jensen KK, Serup J, Alsing KK. Psoriasis and seasonal variation: a systematic review on reports from Northern and Central Europe—little overall variation but distinctive subsets with improvement in summer or wintertime. Skin Res Technol. 2022;28:180–186. PMID:34758175. doi:10.1111/srt.13102.

28. The impacts of seasonal factors on psoriasis. 2025. PMID:40103264.

29. Environmental and neighborhood determinants of psoriasis: a systematic review of pollution, built environment, and socioeconomic vulnerability. Dermatol Ther (Heidelb). 2026. PMID:41922878. doi:10.1007/s13555-026-01725-x.

30. Long-term particulate matter exposure and risk of psoriasis incidence, and short-term exposure and risk of exacerbation: a nationwide cohort study. J Dermatol. 2026. PMID:42050799. doi:10.1111/1346-8138.70283.

31. Zhang Q, Zhang M, Zhao C. Exposure to per- and polyfluoroalkyl substances and risk of psoriasis: a population-based study. Toxics. 2024. PMID:39591006.

32. Association between United States environmental contaminants and the prevalence of psoriasis derived from the National Health and Nutrition Examination Survey. Toxics. 2024. PMID:39058174.

33. Liaw FY, et al. Exploring the link between cadmium and psoriasis in a nationally representative sample. Sci Rep. 2017. PMID:28496169. doi:10.1038/s41598-017-01827-9.

34. Wacewicz-Muczyńska M, et al. Cadmium, lead and mercury in the blood of psoriatic and non-psoriatic patients. Sci Total Environ. 2021. PMID:33302005. doi:10.1016/j.scitotenv.2020.143967.

35. Hojeij B, Koc GH, Luime JJ, et al. Psoriatic arthritis flare incidence, definition and risk factors: a systematic review. Rheumatology (Oxford). 2025;64:4886–4901. PMID:40392198. doi:10.1093/rheumatology/keaf247.

36. Leite BF, et al. Dietetic intervention in psoriatic arthritis: the DIETA trial. Adv Rheumatol. 2022;62:12.

37. Effect of weight loss on activity in psoriatic arthritis: a systematic review. 2017. PMID:28262478.

38. Predictors, risk factors, and incidence rates of psoriatic arthritis development in psoriasis patients: a systematic literature review and meta-analysis. 2021. PMID:34596875. doi:10.1007/s40744-021-00378-w.

39. Predicting and preventing clinical psoriatic arthritis. 2026. PMID:41862404.

40. Ko SH, Chi CC, Yeh ML, et al. Lifestyle changes for treating psoriasis. Cochrane Database Syst Rev. 2019;7.

41. Yang SJ, Chi CC. Effects of fish oil supplement on psoriasis: a meta-analysis of randomized controlled trials. BMC Complement Altern Med. 2019;19:354.

42. Upala S, Sanguankeo A. Effect of lifestyle weight loss intervention on disease severity in patients with psoriasis: a systematic review and meta-analysis. Int J Obes (Lond). 2015;39:1197–1202.

43. Diet and psoriasis, part II: celiac disease and role of a gluten-free diet. 2014. PMID:24780176.

44. Diet and psoriasis, part III: role of nutritional supplements. 2014. PMID:24780177.

45. The role of nutritional factors and food allergy in the development of psoriasis. 2020. PMID:32083821.

46. The role of lifestyle and nutrition in psoriasis: current status of knowledge and interventions. 2022. PMID:35790061.

47. The role of diet in the management of psoriasis: a scoping review. 2023. PMID:37726103.

48. Evidence-based dietary recommendations for patients with psoriasis: a systematic review. Clin Nutr. 2025. PMID:39987781. doi:10.1016/j.clnu.2025.02.005.

49. Nutrition and diet in rheumatoid arthritis, axial spondyloarthritis, and psoriatic arthritis: a systematic review. Front Med (Lausanne). 2025.