Psoriasis Diet & Natural Treatment: Evidence Guide

A Mediterranean diet can clear psoriasis lesions by 75% or more in nearly half of patients, according to the MEDIPSO trial published in JAMA Dermatology in 2025. Mindfulness meditation accelerates phototherapy clearance by a factor of four (Kabat-Zinn, 1998). These are not fringe findings. They represent the strongest evidence for dietary and lifestyle interventions in psoriasis to date. Every recommendation below carries an evidence grade (A, B, or C) so you can prioritize what the clinical data actually supports. All dosage recommendations should be discussed with your doctor before starting.

Can Diet Really Improve Psoriasis?

The skepticism is understandable. Psoriasis is a chronic, genetically mediated inflammatory disease driven by the IL-23/IL-17 immune axis. How could food choices alter a pathway targeted by biologic drugs costing $50,000 per year?

The MEDIPSO trial (2025, JAMA Dermatology) answered that question with the first rigorous randomized controlled trial of dietary intervention in psoriasis. Researchers randomized patients with moderate-to-severe plaque psoriasis to either a Mediterranean diet intervention or standard dietary counseling. At 16 weeks, 47.4% of the Mediterranean diet group achieved PASI 75 (a 75% reduction in psoriasis severity). Zero percent of the control group reached that threshold.

The finding that stunned dermatologists: the improvement was independent of weight loss. Both groups lost similar amounts of weight. The skin cleared because of what patients ate, not because they weighed less. This overturns a decade of assumptions that dietary benefits in psoriasis operate solely through obesity reduction.

PASI 75 is the same clinical benchmark used to evaluate biologic drugs. When adalimumab (Humira) won FDA approval for psoriasis, it achieved PASI 75 in roughly 70% of patients. A dietary intervention reaching nearly half that response rate, with zero drug side effects, zero cost beyond groceries, and no immunosuppression risk, reframes the treatment conversation. Diet is no longer a "maybe it helps" footnote. The MEDIPSO data places it in the evidence-based treatment toolkit.

Earlier observational data had pointed in the same direction. Barrea et al. (2015, Journal of Translational Medicine) demonstrated that lower Mediterranean diet adherence scores correlated directly with higher psoriasis severity and elevated inflammatory markers. Afifi et al. (2017, Dermatology and Therapy) surveyed 1,206 psoriasis patients through the National Psoriasis Foundation and found that 86% had tried dietary modifications. Among those who did, specific patterns emerged: 53.8% improved after reducing alcohol, 53.4% improved after eliminating gluten, and 52.1% improved after removing nightshade vegetables.

Survey data carries significant limitations (recall bias, placebo effect, no controls). The MEDIPSO trial's randomized design moves the conversation from anecdote to evidence.

The Gut-Skin Axis: Why Diet Affects Your Skin

The connection between gut health and psoriasis is not metaphorical. Psoriasis patients harbor a measurably different intestinal microbiome compared to healthy controls.

Studies published in Frontiers in Microbiology (2025) and Biomedicines (2022) have documented reduced populations of Faecalibacterium prausnitzii, a keystone anti-inflammatory bacterium that produces butyrate, in psoriasis patients. Simultaneously, potentially inflammatory species like Prevotella copri are overrepresented. This dysbiosis pattern mirrors what researchers observe in inflammatory bowel disease, which shares the IL-23/IL-17 pathway with psoriasis and co-occurs in 7-11% of psoriasis patients.

The mechanism connecting gut bacteria to skin involves intestinal permeability. When the gut barrier weakens (a process mediated by zonulin, as described by Fasano et al.), bacterial components like lipopolysaccharide (LPS) enter systemic circulation. LPS activates dendritic cells, which migrate to skin and produce IL-23. IL-23 drives the differentiation of Th17 cells, which release IL-17, the cytokine directly responsible for keratinocyte hyperproliferation and plaque formation.

This is the same pathway that biologic drugs like secukinumab (IL-17 inhibitor) and guselkumab (IL-23 inhibitor) target at a cost of tens of thousands of dollars annually. Dietary interventions work upstream, reducing the inflammatory input rather than blocking the output.

The clinical overlap between psoriasis and inflammatory bowel disease makes this axis hard to dismiss. Patients with psoriasis develop IBD at two to three times the rate of the general population. Psoriatic arthritis patients face even higher IBD risk. Both conditions respond to the same biologic drugs because both run on the IL-23/IL-17 circuit. When a patient with psoriasis develops gut symptoms, the gut-skin axis has become bidirectional: gut inflammation worsens skin, and systemic inflammation from skin worsens gut. Addressing the gut microbiome breaks this cycle from the inside out. If you experience gastrointestinal symptoms alongside psoriasis (bloating, irregular bowel habits, food intolerances), investigating your gut health becomes especially relevant. See our overview of autoimmune disease symptoms for more on overlapping conditions.

For a deeper understanding of gut barrier repair strategies, including the 4R protocol and compounds like zinc carnosine, see our BPC-157 and gut healing guide.

The Anti-Psoriasis Diet: What to Eat

Mediterranean Framework (Grade A)

The MEDIPSO trial's intervention centered on a traditional Mediterranean pattern: abundant extra-virgin olive oil, fatty fish at least three times per week, five or more daily servings of colorful vegetables and fruits, legumes, nuts, and whole grains. Red meat was minimized. Processed foods were eliminated.

A practical daily framework looks like this: breakfast built around fruit, nuts, and plain yogurt or oats. Lunch and dinner centered on vegetables, legumes, or fish with olive oil as the primary fat. Snacks of raw nuts, olives, or fresh fruit. Cooking methods favor roasting, grilling, and sauteing in olive oil over deep frying.

Olive oil deserves specific attention. It contains oleocanthal, a compound that inhibits both COX-1 and COX-2 enzymes through the same mechanism as ibuprofen. Four tablespoons of extra-virgin olive oil delivers roughly 10% of the ibuprofen dose, sustained daily over months and years rather than as an acute intervention. The polyphenol content of high-quality olive oil also suppresses NF-kB activation. Choose extra-virgin varieties in dark glass bottles. Refined olive oil lacks most of the polyphenol content that provides the anti-inflammatory benefit.

Omega-3 Rich Foods (Grade A)

EPA (eicosapentaenoic acid) competes directly with arachidonic acid for the COX and LOX enzyme systems. Arachidonic acid, concentrated in red meat and dairy, generates pro-inflammatory prostaglandins (PGE2) and leukotrienes (LTB4) that amplify psoriatic inflammation. EPA generates anti-inflammatory resolvins and protectins instead. Shifting this balance requires consistent intake.

Wild-caught salmon, sardines, mackerel, and anchovies provide the highest EPA/DHA concentrations per serving. Two to three servings per week from food, supplemented to reach 3-4 g/day total EPA+DHA, represents the evidence-based target. For cross-condition supplement guidance, see our best supplements for autoimmune disease guide.

Polyphenol-Rich Plant Foods

Berries (particularly blueberries and blackberries), dark leafy greens, cruciferous vegetables, and green tea contain polyphenols that modulate NF-kB signaling and reduce oxidative stress. These compounds also serve as prebiotics, feeding beneficial gut bacteria like F. prausnitzii and promoting butyrate production.

Fermented foods (sauerkraut, kimchi, kefir, plain yogurt) directly introduce beneficial bacterial strains. A Stanford study demonstrated that a high-fermented-food diet increased microbial diversity and reduced 19 inflammatory markers over 10 weeks. Microbial diversity is precisely what psoriasis patients lack.

Fiber and Resistant Starch

Dietary fiber feeds beneficial gut bacteria and promotes short-chain fatty acid production, particularly butyrate. Butyrate strengthens intestinal tight junctions (reducing the permeability that feeds the gut-skin axis), suppresses NF-kB in colonocytes, and promotes regulatory T cell expansion. Psoriasis patients produce less butyrate than healthy controls.

Sources with the highest prebiotic impact: cooked and cooled potatoes (resistant starch, though note the nightshade consideration below), oats, lentils, chickpeas, garlic, onions, leeks, and asparagus. If nightshades are not a personal trigger, cooked and cooled potatoes provide one of the richest sources of resistant starch available. Aim for 25-35 grams of total dietary fiber per day, increasing gradually to minimize GI discomfort.

Foods That Worsen Psoriasis

Red and Processed Meat (Grade B)

A 2025 King's College London study found that plant-rich dietary patterns were associated with lower psoriasis severity, while diets high in red and processed meat correlated with worse outcomes. The mechanism is straightforward: red meat is the primary dietary source of arachidonic acid, the precursor to pro-inflammatory eicosanoids that drive psoriatic plaque formation.

Processed meats add a second insult. Nitrates, advanced glycation end products (AGEs), and saturated fat independently activate NF-kB and toll-like receptors on innate immune cells. The combination of arachidonic acid plus NF-kB activation creates a compounding inflammatory effect.

Alcohol (Grade B)

The dose-response relationship between alcohol and psoriasis is well quantified. A 2024 meta-analysis calculated a 4% increase in psoriasis odds per gram of alcohol consumed daily. One standard drink contains approximately 14 grams of alcohol. Three drinks per day increases risk by roughly 56%.

Alcohol worsens psoriasis through multiple simultaneous mechanisms. It increases intestinal permeability (the gut-skin axis described above), impairs liver detoxification of inflammatory mediators, depletes folate and zinc (both relevant to skin cell turnover), and directly stimulates keratinocyte proliferation. The Afifi survey found that 53.8% of patients who reduced alcohol intake reported improvement, making it the single dietary change with the highest self-reported success rate.

Complete elimination produces the clearest results. Even moderate drinking maintains the gut permeability disruption.

For patients with psoriatic arthritis (which affects up to 30% of psoriasis patients), the case for alcohol elimination is even stronger. Alcohol's pro-inflammatory effects compound the joint inflammation already driven by the IL-17 pathway. The combination of impaired gut barrier, systemic inflammation, and joint destruction creates a cycle that moderate drinking perpetuates.

Refined Sugar and Ultra-Processed Foods (Grade C)

High-glycemic diets increase insulin and IGF-1, both of which stimulate keratinocyte proliferation and inflammatory cytokine production. No psoriasis-specific RCT has isolated refined sugar as a variable, which keeps the grade at C. The mechanistic evidence is strong enough to warrant elimination as part of a Mediterranean transition.

Nightshade Vegetables (Grade C)

Tomatoes, peppers, potatoes, and eggplant contain glycoalkaloids, compounds that may increase intestinal permeability in susceptible individuals. The Afifi survey reported that 52.1% of patients who eliminated nightshades noticed improvement. The absence of controlled trials prevents a higher grade.

A practical approach: run an 8-week elimination trial. Remove all nightshades completely. Reintroduce each one individually over three-day windows. Track PASI changes, joint symptoms, and subjective skin assessment. If no improvement occurs after 8 weeks, nightshades are unlikely to be a personal trigger.

Gluten (Grade C)

The 53.4% improvement rate from the Afifi survey is notable but uncontrolled. Stronger evidence exists for the subset of psoriasis patients with elevated anti-gliadin antibodies (present in approximately 14% of psoriasis patients). In this subgroup, gluten elimination has shown clearer benefit.

Request anti-gliadin and anti-tissue transglutaminase (anti-tTG) antibody testing before committing to long-term gluten elimination. If positive, a strict 3-month trial is warranted. For patients without these markers, the evidence does not justify the significant dietary restriction. For more on elimination diet protocols in autoimmunity, see our AIP diet guide.

Stress and Psoriasis: The Psychoneuroimmunology

Sixty-nine percent of psoriasis patients identify psychological stress as their primary flare trigger. The connection is biological, not psychological.

The HPA (hypothalamic-pituitary-adrenal) axis in psoriasis patients behaves paradoxically. Under acute stress, healthy individuals mount a cortisol response that restrains inflammation. Psoriasis patients show a blunted cortisol response: the stress occurs, but the normal anti-inflammatory brake fails to engage. Researchers have identified a "stress responder" phenotype within the psoriasis population. These patients experience measurably worse flares following stressful events compared to psoriasis patients with normal HPA function.

The brain-skin connection extends beyond cortisol. Keratinocytes (the skin cells that proliferate excessively in psoriasis) express receptors for neuropeptides including substance P, calcitonin gene-related peptide (CGRP), and nerve growth factor (NGF). During psychological stress, sensory nerve endings in the skin release these neuropeptides, directly stimulating keratinocyte proliferation and immune cell recruitment. The skin is, in a measurable sense, a neuroimmune organ.

This makes stress management a biological intervention for psoriasis, not a lifestyle suggestion.

The practical consequence: telling a psoriasis patient to "reduce stress" without providing a specific, evidence-tested technique is as unhelpful as telling them to "eat better" without specifying what to eat. The next section covers the one stress intervention with RCT-level evidence in psoriasis.

Meditation for Psoriasis: The Kabat-Zinn Study and Beyond

Jon Kabat-Zinn's 1998 study, published in Psychosomatic Medicine, remains one of the most striking findings in psoriasis research. Thirty-seven patients undergoing ultraviolet phototherapy (UVB) or photochemotherapy (PUVA) were randomized to either standard treatment or standard treatment plus a mindfulness meditation audio intervention played during light sessions. The meditation group reached skin clearing at four times the rate of the control group (p = .013 for UVB, p = .033 for PUVA).

Four times faster. From a meditation tape.

A 2022 systematic review of mindfulness-based interventions in psoriasis confirmed the direction of Kabat-Zinn's finding across multiple study designs. Consistent psychological benefit (reduced stress, anxiety, and depression) was accompanied by measurable skin improvement in the majority of studies reviewed.

The mechanism aligns with the psychoneuroimmunology described above. Mindfulness-Based Stress Reduction (MBSR) normalizes HPA axis function, reduces circulating cortisol variability, and decreases neuropeptide release from cutaneous nerve endings. By restoring the cortisol response to stress, MBSR re-engages the anti-inflammatory brake that psoriasis patients have lost.

A Practical MBSR Protocol

The clinical trials used structured 8-week MBSR programs. A simplified daily practice captures most of the benefit:

Weeks 1-2: 10 minutes daily. Sit comfortably. Focus attention on the breath at the nostrils. When the mind wanders (it will, repeatedly), return attention to the breath without judgment. This is the practice, not a failure of the practice.

Weeks 3-4: Extend to 15 minutes. Add a body scan: systematically move attention from feet to head, noticing sensation in each region without attempting to change it. Psoriatic plaques will draw attention. Observe them as sensation rather than problem.

Week 5 onward: 15-20 minutes daily. Alternate between breath awareness and body scan sessions. Consistency matters more than duration. Ten minutes every day outperforms 45 minutes twice a week.

Apps like Insight Timer or the UCLA Mindful app provide free guided sessions calibrated to these timeframes.

The Kabat-Zinn protocol specifically paired meditation with phototherapy sessions. If you undergo UVB or PUVA treatment, practicing mindfulness during the light session replicates the study conditions most closely. The original study used audio-guided meditation tapes played during treatment. Ask your dermatologist about using headphones during phototherapy sessions. Even without phototherapy, daily meditation practice addresses the HPA axis dysregulation and neuropeptide release that drive flares independently.

Supplements for Psoriasis (Evidence-Graded)

Omega-3 EPA + DHA (Grade A)

The omega-3 evidence for psoriasis rests on the arachidonic acid competition described above. Supplementation at 3-4 g/day of combined EPA + DHA shifts the eicosanoid balance from pro-inflammatory (PGE2, LTB4) toward anti-inflammatory (PGE3, LTB5) and pro-resolving (resolvins, protectins) mediators.

Multiple RCTs have demonstrated PASI score improvements with high-dose fish oil. The effect size is modest compared to biologics but meaningful as an adjunct, particularly when combined with dietary omega-3 from fatty fish. The supplemental dose adds to what food provides, compounding the shift in eicosanoid balance over weeks and months.

Triglyceride-form fish oil has better bioavailability than ethyl ester forms. Check the supplement label: if it lists "fish oil concentrate" without specifying form, it is likely ethyl ester. Algal omega-3 is an option for vegetarian patients, though most clinical trials used fish-derived EPA+DHA. Doses above 3 g/day have mild anticoagulant properties. Discuss with your doctor if you take blood thinners or methotrexate.

Dosing: 3-4 g combined EPA + DHA per day, split across meals. Take with food containing fat for absorption. Choose products tested for heavy metals (look for IFOS or NSF certification). Expect 8-12 weeks before measurable PASI changes.

Curcumin (Grade B)

Curcumin inhibits NF-kB, the master inflammatory transcription factor activated in psoriatic plaques. An RCT demonstrated a 33% PASI reduction with curcumin supplementation. The compound also suppresses TNF-alpha, IL-17, and IL-23, the specific cytokines driving psoriasis pathology. The NF-kB pathway is the same target as many biologic psoriasis drugs, though curcumin acts as a broad modulator rather than a precision-targeted monoclonal antibody.

Beyond systemic anti-inflammatory effects, curcumin has demonstrated direct anti-proliferative activity on keratinocytes in vitro. It downregulates cyclin D1 and CDK4, proteins that drive the accelerated cell division defining psoriatic plaques. Whether oral curcumin achieves sufficient skin concentrations to replicate this effect in vivo remains unclear. The PASI improvements documented in trials suggest some degree of systemic-to-local translation.

Standard turmeric powder delivers only 3% curcumin by weight, with poor absorption. The liver rapidly metabolizes unformulated curcumin through glucuronidation, clearing it from the bloodstream before it reaches therapeutic concentrations. Clinical trials used bioavailability-enhanced formulations: curcumin with piperine (black pepper extract, which inhibits hepatic glucuronidation and increases absorption by approximately 2,000%), phytosomal forms (Meriva), or liposomal delivery systems. Cooking with turmeric provides trace amounts but does not approach therapeutic dosing.

Dosing: 500-1,000 mg/day of bioavailable curcumin with meals. Curcumin has mild anticoagulant properties. Do not combine high-dose curcumin with high-dose omega-3 (above 3 g/day) without discussing both with your doctor. Patients on methotrexate should discuss curcumin with their rheumatologist or dermatologist before starting.

Zinc (Grade B)

Zinc deficiency is prevalent among psoriasis patients. Zinc regulates keratinocyte proliferation, T cell differentiation, and wound healing. Correcting deficiency may help normalize the accelerated skin cell turnover (28 days in healthy skin, 3-4 days in psoriatic plaques) that defines the disease.

Psoriasis lesions themselves lose zinc at an accelerated rate through increased skin cell shedding, creating a localized depletion that systemic testing may underestimate. Serum zinc levels reflect circulating zinc but not tissue stores. RBC zinc testing provides a better picture of intracellular status.

Dosing: 15-30 mg/day as zinc picolinate or bisglycinate, taken with food to minimize nausea. Long-term zinc supplementation above 30 mg/day can deplete copper. Add 1-2 mg copper if using zinc for more than 3 months. Test serum zinc and RBC zinc before starting. Discuss with your doctor, particularly if you take immunosuppressants.

Vitamin D: An Honest Assessment (Grade C for Oral Supplementation)

This finding surprises many patients: four randomized controlled trials have tested oral vitamin D supplementation for psoriasis. None showed significant improvement in PASI scores.

Topical vitamin D analogues (calcipotriol, calcitriol) are effective, well-established psoriasis treatments. They work through direct contact with keratinocytes, inhibiting proliferation and promoting differentiation. Oral supplementation does not achieve the same local concentrations in skin.

Correct vitamin D deficiency for general autoimmune health (the VITAL trial showed a 22% reduction in autoimmune disease incidence with supplementation). Do not expect oral vitamin D to clear psoriatic plaques. The distinction between topical pharmaceutical analogues and oral supplements is critical and rarely explained clearly.

Dosing: 2,000-4,000 IU/day if deficient. Target serum 25(OH)D of 40-60 ng/mL. Test every 3 months until stable. Discuss with your doctor.

Action Plan: Putting It Together

The interventions above span diet, supplementation, stress management, and elimination testing. Implementing everything simultaneously is overwhelming and makes it impossible to identify which changes produce benefit. A staged approach solves both problems.

Weeks 1-2: Foundation

Transition to a Mediterranean dietary pattern. Replace cooking oils with extra-virgin olive oil. Add fatty fish three times per week. Increase vegetable intake to five or more servings daily. Eliminate alcohol completely. Remove processed foods and refined sugar.

Begin a 10-minute daily meditation practice using the breath awareness technique described above. Photograph your plaques on day 1 under consistent lighting to establish a visual baseline.

Weeks 3-4: Supplementation

Add omega-3 supplementation (3 g/day EPA + DHA) and curcumin (500 mg/day bioavailable form). If zinc testing reveals deficiency, begin 15-30 mg/day zinc picolinate.

Continue daily meditation. Extend to 15 minutes if comfortable.

Weeks 4-8: Elimination Trial

Begin nightshade elimination if you suspect they contribute to flares. Remove tomatoes, peppers, potatoes, and eggplant completely for 8 weeks. Track symptoms weekly.

If anti-gliadin antibodies are positive, begin a concurrent gluten elimination trial. Three months of strict avoidance is the minimum to evaluate response.

Ongoing Monitoring

Photograph plaques weekly under consistent lighting. Use the same camera distance and angle. Visual documentation reveals gradual changes that daily observation misses. A simple smartphone camera works. Place a ruler or coin in the frame for scale consistency.

Track PASI changes at 4-week intervals if your dermatologist performs scoring, or use the self-assessment SAPASI tool. Expect dietary interventions to require 8-16 weeks before measurable skin changes appear. The MEDIPSO trial measured outcomes at 16 weeks. If you see zero improvement at 16 weeks despite full adherence, the dietary component may not be a significant driver for your particular psoriasis.

Maintain daily meditation indefinitely. The Kabat-Zinn data shows benefit during active treatment. Ongoing stress management prevents flares between treatments.

Keep a brief daily log noting diet adherence (0-10 scale), meditation completion (yes/no), alcohol intake, and subjective skin assessment. Patterns emerge over weeks that are invisible day to day. Many patients discover specific triggers (a stressful week, a weekend of dietary deviation) that correlate with flares on a 5-14 day delay.

For a personalized protocol that accounts for your specific psoriasis severity, current medications, gut health status, and stress patterns, take our free quiz. The protocol engine builds condition-specific recommendations graded by evidence quality.

FAQ

Does the Mediterranean diet work for psoriasis even without weight loss?

Yes. The MEDIPSO trial (2025) specifically demonstrated this. Both the intervention and control groups lost similar amounts of weight. The Mediterranean diet group achieved PASI 75 in 47.4% of patients versus 0% in controls. The benefit came from the anti-inflammatory composition of the diet (omega-3 fatty acids, polyphenols, fiber for microbiome support), not from caloric restriction or weight reduction.

How long does it take for dietary changes to improve psoriasis?

Most patients need 8-16 weeks of consistent dietary change before seeing measurable skin improvement. The MEDIPSO trial measured outcomes at 16 weeks. Keratinocyte turnover in psoriatic plaques runs on a 3-4 day cycle, but altering the systemic inflammatory environment that drives that turnover takes longer. Alcohol elimination and stress reduction tend to show earlier effects (4-6 weeks) because they remove active triggers rather than building anti-inflammatory reserves.

Should psoriasis patients take vitamin D supplements?

Correct deficiency, but do not expect oral vitamin D to clear plaques. Four RCTs have tested oral vitamin D for psoriasis with no significant PASI improvement. Topical vitamin D analogues (calcipotriol) are effective prescription treatments that work by direct contact with skin cells. Oral supplementation supports general autoimmune health (the VITAL trial demonstrated a 22% reduction in autoimmune disease incidence) but does not replicate the topical effect.

Can meditation really help psoriasis?

Kabat-Zinn's 1998 RCT demonstrated that patients who meditated during phototherapy cleared skin lesions at four times the rate of patients receiving phototherapy alone. A 2022 systematic review confirmed consistent benefits across study designs. The mechanism involves normalizing the blunted cortisol stress response and reducing neuropeptide release from cutaneous nerves, both documented biological pathways in psoriasis.

What foods should I eliminate first for psoriasis?

Alcohol produces the highest self-reported improvement rate (53.8% in the Afifi survey of 1,206 patients) and has strong mechanistic support including a dose-response meta-analysis. Eliminate alcohol first. Processed and red meat rank second based on the King's College London 2025 data linking arachidonic acid intake to psoriasis severity. Nightshade and gluten elimination require longer trials (8-12 weeks) and benefit a subset of patients rather than the majority.

Take the Next Step

Diet, supplements, and stress management form one layer of an evidence-based psoriasis protocol. For deeper coverage, see our psoriasis diet guide and psoriasis supplement protocol. Condition-specific interventions like low dose naltrexone, gut barrier repair, and advanced protocols can complement these foundational changes. Our free quiz builds a personalized, evidence-graded protocol based on your psoriasis severity, current medications, and health profile.

This article is for educational purposes only. It does not constitute medical advice and should not replace consultation with your physician. Always discuss dietary changes and supplement use with your healthcare provider, particularly if you take prescription medications for psoriasis or other conditions.