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Social Determinants of Health as a Predictor of Psoriasis Risk: Preliminary Findings from a National Survey

Authors Lin X, Li C, Wang J

Received 5 October 2025

Accepted for publication 2 January 2026

Published 23 January 2026 Volume 2026:19 572283

DOI https://doi.org/10.2147/CCID.S572283

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Jeffrey Weinberg



Xiaoqiong Lin, Changchang Li, Jinhui Wang

Department of Dermatology, Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine, Wenzhou, Zhejiang Province, People’s Republic of China

Correspondence: Xiaoqiong Lin, Department of Dermatology, Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine, No. 75, Jinxiu Road, Wenzhou, Zhejiang Province, 325000, People’s Republic of China, Email [email protected]

Background: Social determinants of health (SDOH) profoundly influence disease risk, but their specific relationship with psoriasis remains unclear. This study aimed to examine the association between SDOH with psoriasis risk, as well as the mediating role of metabolic syndrome.
Methods: We analyzed data of 16,083 adults participating in the 2003– 2006 and 2009– 2014 National Health and Nutrition Examination Survey. A composite SDOH score (range 0– 8) was constructed from eight subcomponents across five domains: economic stability, neighborhood and built environment, education, social context, and healthcare access. The association between the SDOH score and psoriasis was assessed using multivariable logistic regression, and a mediation analysis was conducted to quantify the contribution of metabolic syndrome.
Results: The overall prevalence of psoriasis was 2.46%. Restricted cubic spline curves indicated a non-linear relationship between SDOH and psoriasis. Piece-wise regression analysis indicated that the odds ratios (95% confidence intervals) for SDOH of 0– 2, 3– 5 and 6– 8 were 0.57 (0.35– 0.94), 1.13 (0.93– 1.36), and 0.48 (0.36– 0.63), respectively. The protective effect of a higher SDOH for psoriasis risk was stronger in participants taking statins (P for interaction = 0.03). Mediation analysis indicated that metabolic syndrome explained a modest yet significant 5.92% (95% CI 1.43– 20.63%) of the association.
Conclusion: The SDOH score exhibits a non-linear association with psoriasis risk in US adults, which is partially mediated by metabolic syndrome. These findings underscore the complex role of socioeconomic and environmental factors in psoriasis etiology. Future prospective studies are needed to establish temporality and assess whether SDOH-targeted interventions can mitigate psoriasis risk.

Keywords: mediation, metabolic syndrome, NHANES, psoriasis, social determinants of health

Introduction

Psoriasis is a chronic, immune-mediated inflammatory dermatopathy that affects approximately 2–4% of the global population.1 Beyond its physical manifestations, psoriasis imposes a substantial socioeconomic and psychological burden on both patients and their caregivers, impacting healthcare costs, work productivity, and overall quality of life. Furthermore, psoriasis patients exhibit a significantly higher prevalence of metabolic syndrome, a comorbidity that substantially increases their risk of cardiovascular mortality.2 Current understanding suggests psoriasis is a multifactorial disorder arising from the complex interplay between genetic predisposition and environmental triggers.3

Emerging evidence suggests that socioeconomic status may influence both the development and management of psoriasis. For instance, a large-scale population-based study demonstrated that a higher socioeconomic status was associated with an increased risk of psoriasis.4 Moreover, a case-control study reported that patients with higher socioeconomic status had greater adherence to biological treatment, while those with a lower socioeconomic status experienced significantly higher rates of treatment failure and were less likely to receive systemic treatments.5 These findings underscore the critical role of socioeconomic status in psoriasis development and therapeutic outcomes. In this context, the social determinants of health (SDOH) provides a more comprehensive framework for understanding the environmental and social factors that shape health. SDOH encompass the broad conditions in which people are born, live, work, and age, making it a more robust tool for assessing the full spectrum of environmental exposures relevant to psoriasis.6

We are aware that the majority of previous studies have focused on the relationship between individual SDOH factor and psoriasis, while their synergistic effects on psoriasis remain understudied. To address this knowledge gap, we conducted a large population-based, cross-sectional study to investigate the association between SDOH and psoriasis prevalence. Given the well-established bidirectional relationship between psoriasis and metabolic syndrome,7 we further assessed whether metabolic syndrome mediates the link between SDOH and psoriasis risk.

Methods

Data Source and Participant Selection

This cross-sectional analysis included a nationally representative sample of non-institutionalized US population from the US National Health and Nutrition Examination Survey spanning from 2003–2006 and 2009–2014 cycles, as these were the only cycles containing psoriasis assessment data. Ethical oversight for this study included approval of the NHANES protocols by the National Center for Health Statistics Research Ethics Review Board. As our analysis used de-identified, publicly available data, it was exempt from further institutional review board approval per Items 1 and 2, Article 32 of China’s Measures for Ethical Review of Life Science and Medical Research Involving Human Subjects (February 18, 2023). All participants in the original survey provided informed consent.

The inclusion criteria were adult participants (aged ≥ 20 years). Participants were excluded for pregnancy, history of cancer, missing data of SDOH, missing data of psoriasis, missing data of metabolic syndrome, and missing covariates. The participant selection and exclusion process was presented in Figure 1, and a total of 16,083 participants were finally included for analysis.

Figure 1 Flowchart of participant selection.

Abbreviations: NHANES, National Health and Nutrition Examination Survey; SDOH, social determinants of health.

Assessment of SDOH

Following established methodology in NHANES population,8,9 we operationalized eight SDOH sub-items across five domains as defined by the Healthy People 2030 framework: 1) economic stability (including employment status, food security status, and family poverty-income ratio), 2) neighborhood and built environment (ie, home ownership), 3) education access and quality (ie, education level), 4) social and community context (ie, marital status), and 5) healthcare access and quality (health insurance coverage and type of health insurance). Each sub-item was dichotomized to represent favorable (scored as 1) or unfavorable (scored as 0) status. The cumulative SDOH score (range: 0–8) was calculated by summing all sub-item scores, with higher scores indicating more favorable overall SDOH status. Detailed method for calculating SDOH was provided in Supplementary Table 1.

Determination of Psoriasis Status

Participants were considered to have psoriasis if responded positively to the question “Have you ever been told by a doctor or other health care professional that you had psoriasis (sore-eye-asis)?”.2 Those who declined to answer this question or unsure were excluded.

Covariate Measurements

We selected the following covariates based on their established pathophysiological relevance to psoriasis or SDOH, as well as their use in previous similar studies: age (continuous), sex (men/women), race/ethnicity (Mexican American/non-Hispanic White/non-Hispanic Black/Other Hispanics/Other, including multiracial), smoking (never/former/current), drinking (never/former/mild/moderate/severe), physical activity (no/moderate/vigorous), statin use (yes/no), and history of cardiovascular disease (yes/no).10–12 Smoking and drinking was categorized based on previous criteria in the NHANES population.13 Moderate and vigorous physical activity was defined as self-reported activities that require moderate and vigorous physical effort (≥ 10 consecutive minutes) and cause a small and large increase in breathing or heart rate, respectively, either at work or during leisure time, in a typical week.14 History of cardiovascular disease was self-reported and included stroke, coronary heart disease, congestive heart failure, heart attack, and angina pectoris.

Diagnosis of Metabolic Syndrome

Metabolic syndrome was defined according to the National Cholesterol Education Program Adult Treatment Panel III criteria,15 requiring at least three of the five following components: 1) hypertension, with systolic blood pressure  ≥ 130 mmHg or diastolic blood pressure ≥ 85 mmHg or current use of antihypertensive medications; 2) central obesity, with waist circumference  ≥ 102 cm for men or ≥ 88 cm for women; 3) hypertriglyceridemia, with blood triglycerides ≥ 150 mg/dL or current use of medications to treat hypertriglyceridemia; 4) hyperglycemia, defined as fasting blood glucose ≥ 110 mg/dL or current use of anti-diabetic medications; 5) reduced high-density lipoprotein cholesterol levels < 40 mg/dl for men or < 50 mg/dl for women.

Statistical Analysis

Participants were categorized into four groups based on their SDOH score (0–2, 3–4, 5–6, and 7–8). Baseline characteristics were compared using one-way analysis of variance or chi-squared test, as appropriate. Multivariate logistic regression analysis was conducted to calculate the odds ratios (OR) and corresponding 95% confidence intervals (CI) for the association between SDOH score and psoriasis prevalence. We constructed three models in total, in which the crude model was unadjusted. Model 1 was adjusted for participants’ age, sex, and race/ethnicity, and the final model 2 was further adjusted for variables of smoking, drinking, physical activity, statin use, and history of cardiovascular disease. Restricted cubic spline curves were generated to evaluate the dose-response relationship between SDOH score and psoriasis prevalence. Stratified analyses were also conducted to examine the relationship between SDOH score and psoriasis prevalence in subgroups stratified by age (< 60 vs ≥ 60 years), sex (men vs women), race (White vs Black vs Mexican Americans vs Other Hispanics vs Other), smoking (never vs former vs current), drinking (never vs former vs mild vs moderate vs heavy), physical activity (no vs moderate vs vigorous), statin use (yes vs no), and cardiovascular disease status (yes vs no). Finally, a mediation analysis was performed to explore whether metabolic syndrome mediated the association between SDOH score and psoriasis prevalence by adjusting for covariates listed in Model 2. Appropriate sampling weights were applied in all analyses. Statistical significance was set at P < 0.05.

Results

Comparison of Baseline Characteristics

The final analytic sample comprised 16,083 participants (mean age 43.86 years, 50.67% men), including 405 cases of psoriasis, leading to an overall prevalence of 2.46%. As summarized in Table 1, compared with participants with a SDOH score of 7–8, those with lower SDOH scores were significantly younger, less likely to be non-Hispanic white, more likely to be current smokers and heavy drinkers, and associated with higher prevalence of cardiovascular disease.

Table 1 Comparison of Baseline Characteristics Among US Adults Stratified by the Social Determinants of Health Score

Associations Between SDOH Score and Psoriasis Risk

Table 2 presents the associations between SDOH score and psoriasis risk. In brief, each one-score increase in SDOH score was associated with 9% reduction in psoriasis risk. When SDOH was analyzed as a categorical variable, compared to those with a SDOH of 7–8, those with a SDOH score of 5–6 had the highest risk, followed by SDOH of 0–2 and 3–4. Similar trends were observed in the fully adjusted model 2.

Table 2 Associations Between Social Determinants of Health Score and Prevalence of Psoriasis in US Adults from the 2003–2006 and 2009–2014 National Health and Nutrition Examination Survey

The dose-response relationship between SDOH and psoriasis prevalence was presented in Figure 2, which showed a non-linear relationship. Piece-wise regression analysis indicated that the ORs (95% CIs) for SDOH of 0–2, 3–5 and 6–8 were 0.57 (0.35–0.94), 1.13 (0.93–1.36), and 0.48 (0.36–0.63), respectively.

Figure 2 Restricted cubic spline curves showing the dose-response relationship between social determinants of health and psoriasis risk. The solid red line depicts the smooth curve fit between the variables, and the shadow represents the corresponding 95% confidence intervals.

Abbreviation: CI, confidence interval.

Subsequent logistic regression for the association between individual SDOH component and psoriasis prevalence (Table 3) showed that poverty-income ratio ≥ 3 (OR=1.41, 95% CI 1.02–1.95) and no routine place to go for healthcare (OR=1.45, 95% CI 1.07–1.97) were independently associated with an increased prevalence of psoriasis.

Table 3 Associations Between Individual Component of Social Determinants of Health and Prevalence of Psoriasis in US Adults

Subgroup Analysis

Stratified analysis (Figure 3) indicated that participants’ age, sex, race/ethnicity, smoking, drinking, physical activity, and cardiovascular status did not significantly modify the association between SDOH score and psoriasis prevalence. The protective effect of a higher SDOH for psoriasis risk was stronger in participants taking statins than those who did not (P for interaction = 0.03).

Figure 3 Forest plots depicting the odds ratio (OR) and 95% confidence intervals (CI) for psoriasis in each subgroup.

Mediation Analysis

The mediation analysis (Figure 4) showed that metabolic syndrome accounted for 5.92% (95% CI 1.43–20.63%) of the association between SDOH score and psoriasis risk.

Figure 4 Decomposition of the total association between social determinants of health (SDOH) and psoriasis prevalence into total, direct, and indirect associations mediated by the metabolic syndrome.

Abbreviations: CI, confidence interval; DE, direct effect; IE, indirect effect; PM, proportion mediated; TE, total effect.

Discussion

The findings of the current cross-sectional, nationwide survey demonstrated that the SDOH score is non-linearly associated with psoriasis prevalence in US adults. Notably, psoriasis risk exhibited a triphasic relationship: initially decreasing with SDOH scores of 0–2, then increasing through scores of 3–6, before declining again at scores > 6. Subsequent analysis of individual SDOH component revealed that both poverty-income ratio ≥ 3 and lack of routine healthcare access independently predicted elevated psoriasis risk. Stratified analysis indicated that the protective effect of a higher SDOH for psoriasis risk was more pronounced in participants taking statins than those who did not. Mediation analysis further demonstrated that metabolic syndrome explained 5.92% of the observed association between SDOH and psoriasis. Collectively, these findings highlight the clinical relevance of SDOH screening for psoriasis risk assessment, while underscoring income disparities and healthcare accessibility as potentially modifiable risk factors.

The overall prevalence of psoriasis in this nationwide survey is 2.46%, which is largely compatible with rates reported in Western populations.16 Furthermore, our study revealed a significant nonlinear association between composite SDOH scores and psoriasis prevalence, extending beyond previous studies that primarily examined individual SDOH components. For instance, Dagan et al demonstrated that medium and high socioeconomic status groups had a 1.2- and 1.43-fold higher psoriasis risk, respectively, compared to the lowest socioeconomic status group, a finding that parallels our observation of a 41% increased risk among participants with poverty-income ratio ≥ 3 versus those with lower ratios.17 Bardazzi and colleagues further reinforced these socioeconomic links by reporting that lower educational attainment and income were associated with more severe psoriasis phenotypes.18 Notably, a Mendelian randomization study provided evidence for a causal relationship between lower educational attainment and psoriasis risk, while another NHANES analysis identified food insecurity - a marker of financial hardship - as an independent risk factor.19,20 Our analysis only observed higher poverty-income ratio and healthcare inaccessibility to be significantly associated with psoriasis risk, raising the possibility that underdiagnosis and subsequently lower reporting rates may potentially partially explain this association. Alternatively, it is also possible that other factors associated with a higher economic status, such as smaller families and urban communities, may also contribute to increased psoriasis risk.21 Collectively, these studies substantiate our finding that structural socioeconomic determinants significantly influence psoriasis risk, though our composite SDOH approach reveals a more complex, nonlinear risk relationship that may reflect threshold effects and synergistic interactions between multiple disadvantage domains.

Although biologically plausible explanations for the association between SDOH and psoriasis risk are scarce, previous preliminary studies have explored potential links between individual factors and psoriasis risk. For instance, cross-sectional analysis has established associations between food insecurity, support isolation and psoriasis prevalence.20,22 In our study, there was a trend toward increased psoriasis prevalence among individuals experiencing food insecurity and those not living with a partner. It is reasonable to speculate that both pathophysiological and psychological pathways have been implicated in the association between SDOH and psoriasis risk. First, those with a lower SDOH may have poorer diet quality, including higher consumption of ultra-processed foods, which has been linked to an increased psoriasis risk.23 Second, low socioeconomic status communities are often exposed to higher concentrations of air pollutants, a known trigger for psoriasis development.24,25 Third, prior research supports a plausible temporal association between psychological stress and the onset, recurrence, and severity of psoriasis.26 Mounting evidence has consistently established a robust association between adverse SDOH and elevated psychological stress, mediated through interconnected pathways of chronic financial strain, environmental adversity, and constrained access to psychosocial resources.27,28

Stratified analysis revealed that the protective association between higher SDOH and reduced psoriasis risk was significantly more pronounced among statin users. This finding aligns with existing evidence demonstrating statins’ beneficial effects on psoriasis severity and patient-reported outcomes.29 Congruently, a large epidemiological study of 36,702 incident psoriasis cases and matched controls reported reduced psoriasis risk among statin users, potentially mediated through statins’ anti-inflammatory properties - particularly via inhibition of T-cell activation and cutaneous migration, key pathogenic mechanisms in psoriasis.30,31 These findings collectively suggest that patients with dyslipidemia receiving statin therapy may represent a target population for SDOH-targeted interventions, where combined pharmacological and socioeconomic approaches could yield synergistic benefits.

Mediation analysis suggested metabolic syndrome may partially mediate the association between adverse SDOH and increased psoriasis risk. This finding aligns with population-based evidence demonstrating that unfavorable social risk profiles correlate with both prevalence and severity of cardiovascular-kidney-metabolic syndrome.32 Longitudinal data further support this relationship, with Kim et al reporting a dose-dependent association between metabolic syndrome components and psoriasis incidence over 8 years of follow-up.33 The potential mechanisms underlying this mediation may include: 1) chronic low-grade inflammation characterized by elevated interleukin-6 and tumor necrosis factor α; 2) insulin resistance and hyperinsulinemia; 3) dysregulated adipokine secretion, particularly increased leptin and decreased adiponectin, and 4) shared genetic susceptibility loci identified in recent genome-wide association studies.34,35

This study has several implications for public health policy and clinical patient management. Policymakers should recognize SDOH as a modifiable risk factor for psoriasis development and prioritize interventions targeting key socioeconomic disparities, particularly in communities with dual burdens of high SDOH disadvantage and elevated psoriasis prevalence. For clinical practice, healthcare providers should integrate SDOH screening into standard dermatological care and facilitate referrals to appropriate social services.

Notable strengths of this study include use of a nationwide survey that ensures national representativeness and broader generalizability. Meanwhile, it also suffers from several limitations that should be acknowledged. First, the cross-sectional design precludes establishing causal relationships between social determinants of health and psoriasis risk. Although we adjusted for multiple covariates, residual confounding by unmeasured factors may persist. For instance, we did not account for genetic susceptibility, which has been linked to variants in the interleukin-19 subfamily, the ATG16L1 gene, and loci encoding key therapeutic targets such as interleukin-17 receptor A and the aryl hydrocarbon receptor.36–38 Similarly, seasonal variation, which influences disease through sunlight exposure and mood, was not considered.39 Investigating these biological and environmental interplays represents an important direction for future research. Second, the reliance on self-reported data for both SDOH measures and psoriasis diagnosis introduces potential recall bias and outcome misclassification, though previous validation studies have demonstrated reasonable agreement between self-reported psoriasis and physician diagnosis.40 Third, whether these findings extend to other populations with different characteristics or genetic backgrounds is yet to be determined. Finally, our analysis was limited to individual-level SDOH factors and did not incorporate important neighborhood-level determinants such as air quality, social vulnerability indices, or built environment characteristics, which have been implicated in psoriasis pathogenesis.41 These limitations highlight the need for future longitudinal studies incorporating both individual and community-level SDOH measures, along with objective clinical confirmation of psoriasis diagnosis.

Conclusions

In conclusion, this nationally representative analysis revealed a non-linear association between SDOH and psoriasis prevalence in US adults, which is partially mediated by metabolic syndrome. Poverty-income ratio ≥ 3 and no routine place to go for healthcare were SDOH components independently associated with a higher risk of psoriasis. Prospective studies that incorporate critical unmeasured factors, such as genetic susceptibility and seasonal variation, are needed to elucidate the temporal relationship between SDOH and psoriasis risk and to assess the efficacy of SDOH-targeted interventions.

Data Sharing Statement

Data used for the analysis of this study are publicly available from the CDC’s website at https://wwwn.cdc.gov/nchs/nhanes/Default.aspx.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare no competing interests in this work.

References

1. Parisi R, Iskandar IYK, Kontopantelis E, et al. National, regional, and worldwide epidemiology of psoriasis: systematic analysis and modelling study. BMJ. 2020;369:m1590. doi:10.1136/bmj.m1590

2. Kong X, Wang W. Synergistic effect of psoriasis and metabolic syndrome on risk of all-cause and cardiovascular mortality in US adults: a nationwide cohort study. Clin Exp Dermatol. 2024;50(1):113–12. doi:10.1093/ced/llae340

3. Roszkiewicz M, Dopytalska K, Szymańska E, Jakimiuk A, Walecka I. Environmental risk factors and epigenetic alternations in psoriasis. Ann Agric Environ Med. 2020;27(3):335–342. doi:10.26444/aaem/112107

4. Heikkilä A, Sliz E, Huilaja L, et al. Genetic study of psoriasis highlights its close link with socioeconomic status and affective symptoms. J Invest Dermatol. 2024;144(12):2719–2729. doi:10.1016/j.jid.2024.03.043

5. Norlin JM, Löfvendahl S, Schmitt-Egenolf M. The influence of socioeconomic factors on access to biologics in psoriasis. J Clin Med. 2023;12(23):7234. doi:10.3390/jcm12237234

6. Lau DT, Ahluwalia N, Fryar CD, Kaufman M, Arispe IE, Paulose-Ram R. Data related to social determinants of health captured in the national health and nutrition examination survey. Am J Public Health. 2023;113(12):1290–1295. doi:10.2105/AJPH.2023.307490

7. Liu L, Wang W, Si Y, Li X. Genetic insights into the risk of metabolic syndrome and its components on psoriasis: a bidirectional Mendelian randomization. J Dermatol. 2023;50(11):1392–1400. doi:10.1111/1346-8138.16910

8. Yang ZG, Sun X, Han X, Wang X, Wang L. Relationship between social determinants of health and cognitive performance in an older American population: a cross-sectional NHANES study. BMC Geriatr. 2025;25(1):25. doi:10.1186/s12877-024-05672-0

9. Liang L, Chen CY, Aris IM. Association of the life’s essential 8 cardiovascular health score with periodontitis among US adults. J Clin Periodontol. 2024;51(11):1502–1510. doi:10.1111/jcpe.14042

10. Li M, Gan Y, Cheng H, Wang Z. Correlation between cardiometabolic index and psoriasis: a cross-sectional analysis using NHANES data. Front Physiol. 2025;16:1552269. doi:10.3389/fphys.2025.1552269

11. Lin Z, Wang HF, Yu LY, et al. The relationship between biological aging and psoriasis: evidence from three observational studies. Immun Ageing. 2025;22(1):6. doi:10.1186/s12979-025-00500-4

12. Zhenfu S, Wenting S, Xi W, Shiyu T, Zhenlin C. Metabolic syndrome and the risk of psoriasis: a population-based cross-sectional study and Mendelian randomization analysis. Eur J Dermatol. 2024;34(6):632–639. doi:10.1684/ejd.2024.4800

13. Kong X, Wang W. Estimated glucose disposal rate and risk of cardiovascular disease and mortality in U.S. adults with prediabetes: a nationwide cross-sectional and prospective cohort study. Acta Diabetol. 2024;61(11):1413–1421. doi:10.1007/s00592-024-02305-1

14. Liu W, Liu Z, Ding C, Li J, Jiang H. Associations of the gap between 2-hour post-load plasma glucose and fasting blood glucose with all-cause or cardiovascular mortality in US normoglycemic adults. Biol Res Nurs. 2025;27(3):391–399. doi:10.1177/10998004251316688

15. Lipsy RJ. The national cholesterol education program adult treatment panel III guidelines. J Manag Care Pharm. 2003;9(1 Suppl):2–5. doi:10.18553/jmcp.2003.9.s1.2

16. Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis prevalence among adults in the United States. J Am Acad Dermatol. 2014;70(3):512–516. doi:10.1016/j.jaad.2013.11.013

17. Dagan O, Schonmann Y, Shavit E, Cohen AD, Valdman-Grinshpoun Y, Czarnowicki T. High socioeconomic status is significantly associated with psoriasis: results from a cross-sectional, population-based study of 129 855 patients. Clin Exp Dermatol. 2025;50(6):1138–1145. doi:10.1093/ced/llae286

18. Bardazzi F, Tengattini V, Rucci P, et al. Socio-economic status and severity of plaque psoriasis: a cross-sectional study in the metropolitan city of Bologna. Eur J Dermatol. 2019;29(2):197–202. doi:10.1684/ejd.2019.3524

19. Dai Q, Zhang Y, Liu Q, Zhang C. Causal effect of educational attainment on psoriasis risk mediated by obesity-related traits: Mendelian randomization study. Arch Dermatol Res. 2023;316(1):29. doi:10.1007/s00403-023-02780-6

20. Shin L, Laborada J, Lee C, Egeberg A, Wu JJ. Association between psoriasis and food insecurity among United States adults. J Clin Aesthet Dermatol. 2022;15(12):47–48.

21. Chen L, Chen H, Mo L, et al. Spatial distribution of residential environment, genetic susceptibility, and psoriasis: a prospective cohort study. J Glob Health. 2024;14:04139. doi:10.7189/jogh.14.04139

22. Picardi A, Mazzotti E, Gaetano P, et al. Stress, social support, emotional regulation, and exacerbation of diffuse plaque psoriasis. Psychosomatics. 2005;46(6):556–564. doi:10.1176/appi.psy.46.6.556

23. Penso L, Touvier M, Srour B, Ezzedine K, Sbidian E. Ultraprocessed food intake and psoriasis. JAMA Dermatol. 2025;161(1):105–108. doi:10.1001/jamadermatol.2024.4832

24. Hajat A, Hsia C, O’Neill MS. Socioeconomic disparities and air pollution exposure: a global review. Curr Environ Health Rep. 2015;2(4):440–450. doi:10.1007/s40572-015-0069-5

25. Bellinato F, Adami G, Vaienti S, et al. Association between short-term exposure to environmental air pollution and psoriasis flare. JAMA Dermatol. 2022;158(4):375–381. doi:10.1001/jamadermatol.2021.6019

26. Stewart TJ, Tong W, Whitfeld MJ. The associations between psychological stress and psoriasis: a systematic review. Int J Dermatol. 2018;57(11):1275–1282. doi:10.1111/ijd.13956

27. Tanarsuwongkul S, Liu J, Spaulding M, Perea-Schmittle K, Lohman M, Wang Q. Associations between social determinants of health and mental health disorders among U.S. population: a cross-sectional study. Epidemiol Psychiatr Sci. 2025;34:e4. doi:10.1017/S2045796024000866

28. Mayorga NA, Smit T, Salwa A, et al. Examining financial strain and subjective social status in terms of behavioral health among latinx adults in a federally qualified health center. J Racial Ethn Health Disparities. 2025;12(5):3429–3441. doi:10.1007/s40615-024-02146-2

29. Aleid AM, Almutairi G, Alrizqi R, et al. The impact of statins on disease severity and quality of life in patients with psoriasis: a systematic review and meta-analysis. Healthcare. 2024;12(15):1526. doi:10.3390/healthcare12151526

30. Brauchli YB, Jick SS, Meier CR. Statin use and risk of first-time psoriasis diagnosis. J Am Acad Dermatol. 2011;65(1):77–83. doi:10.1016/j.jaad.2010.05.039

31. Weitz-Schmidt G, Welzenbach K, Brinkmann V, et al. Statins selectively inhibit leukocyte function antigen-1 by binding to a novel regulatory integrin site. Nat Med. 2001;7(6):687–692. doi:10.1038/89058

32. Zhu R, Wang R, He J, et al. Prevalence of cardiovascular-kidney-metabolic syndrome stages by social determinants of health. JAMA Netw Open. 2024;7(11):e2445309. doi:10.1001/jamanetworkopen.2024.45309

33. Kim HN, Han K, Park YG, Lee JH. Metabolic syndrome is associated with an increased risk of psoriasis: a nationwide population-based study. Metabolism. 2019;99:19–24. doi:10.1016/j.metabol.2019.07.001

34. Hao Y, Zhu YJ, Zou S, et al. Metabolic syndrome and psoriasis: mechanisms and future directions. Front Immunol. 2021;12:711060. doi:10.3389/fimmu.2021.711060

35. Oh SM, Kim SK, Ahn HJ, Jeong KH. A pilot genome-wide association study identifies novel markers of metabolic syndrome in patients with psoriasis. Ann Dermatol. 2023;35(4):285–292. doi:10.5021/ad.22.196

36. Kingo K, Mössner R, Kõks S, et al. Association analysis of IL19, IL20 and IL24 genes in palmoplantar pustulosis. Br J Dermatol. 2007;156(4):646–652. doi:10.1111/j.1365-2133.2006.07731.x

37. Dand N, Stuart PE, Bowes J, et al. GWAS meta-analysis of psoriasis identifies new susceptibility alleles impacting disease mechanisms and therapeutic targets. Nat Commun. 2025;16(1):2051. doi:10.1038/s41467-025-56719-8

38. Douroudis K, Kingo K, Traks T, et al. Polymorphisms in the ATG16L1 gene are associated with psoriasis vulgaris. Acta Derm Venereol. 2012;92(1):85–87. doi:10.2340/00015555-1183

39. Zheng X, Wang Q, Luo Y, et al. Seasonal variation of psoriasis and its impact in the therapeutic management: a retrospective study on chinese patients. Clin Cosmet Investig Dermatol. 2021;14:459–465. doi:10.2147/CCID.S312556

40. Modalsli EH, Snekvik I, Åsvold BO, Romundstad PR, Naldi L, Saunes M. Validity of self-reported psoriasis in a general population: the hunt study, Norway. J Invest Dermatol. 2016;136(1):323–325. doi:10.1038/JID.2015.386

41. Muntyanu A, Milan R, Kaouache M, et al. Tree-based machine learning to identify predictors of psoriasis incidence at the neighborhood level: a populational study from Quebec, Canada. Am J Clin Dermatol. 2024;25(3):497–508. doi:10.1007/s40257-024-00854-3

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