Psoriasis

Condition: Psoriasis  |  Category: Autoimmune and Inflammatory Health  |  Reviewed by: Brian Lamkin, DO

What Is Psoriasis?

Psoriasis is a chronic autoimmune inflammatory disease in which Th17-mediated immune activation drives keratinocyte hyperproliferation, producing the characteristic raised, scaly, erythematous plaques on the skin. Normal skin cell turnover occurs over 28 to 30 days. In psoriatic skin, this cycle accelerates to 3 to 4 days, producing the thickened, silvery-white scale over inflamed, reddened skin. Psoriasis affects approximately 8 million Americans and presents most commonly as plaque psoriasis (80 to 90 percent of cases), with guttate, inverse, pustular, and erythrodermic variants comprising the remainder.

The conventional narrative treats psoriasis as a dermatologic condition requiring topical or systemic immune suppression. This framing is incomplete. The Th17-driven inflammation producing the skin plaques is the same inflammation that accelerates atherosclerosis (psoriasis patients have 2 to 3 times higher cardiovascular event risk), drives metabolic syndrome (psoriasis patients have significantly higher rates of insulin resistance, obesity, and dyslipidemia), and produces psoriatic arthritis in 30 percent of cases. Treating only the skin ignores the systemic inflammatory disease that is simultaneously producing cardiovascular, metabolic, and joint damage.

Why Psoriasis Matters

Common Symptoms

Root Causes: A Functional Medicine Perspective

Psoriasis is a genetically predisposed autoimmune condition that requires environmental activation. The environmental triggers are modifiable.

Gut Permeability and the Gut-Skin Axis

The gut-skin axis is well-documented in psoriasis. Intestinal permeability allows microbial and food antigens to enter the bloodstream, activating dendritic cells that drive Th17 differentiation and IL-17/IL-23 production. Psoriasis patients have documented higher rates of gut permeability, microbiome disruption (reduced Faecalibacterium prausnitzii and Akkermansia, increased Firmicutes/Bacteroidetes ratio), and increased rates of SIBO compared to healthy controls. Gut restoration reduces the antigenic load driving the Th17 activation.

Vitamin D Deficiency

Vitamin D regulates keratinocyte differentiation (slowing the hyperproliferative cycle), supports regulatory T cell function, and directly suppresses IL-17 production. Psoriasis patients are frequently deficient. Topical vitamin D analogs (calcipotriene) are a first-line psoriasis treatment, confirming the mechanistic role. Systemic vitamin D optimization to 60 to 80 ng/mL provides the immune regulatory and keratinocyte-normalizing benefit that topical application alone cannot achieve.

Chronic Stress and Cortisol

Psychological stress is one of the most commonly reported psoriasis flare triggers, with 40 to 80 percent of patients identifying stress as a precipitant. Cortisol produces a paradoxical effect in psoriasis: acute cortisol elevation is anti-inflammatory and can suppress flares (hence why corticosteroids work), but chronic cortisol dysregulation impairs immune regulation and promotes the Th17 shift that drives psoriasis progression.

Food Sensitivities and Dietary Triggers

Gluten is the most studied dietary trigger in psoriasis. Anti-gliadin antibodies are present in a significantly higher proportion of psoriasis patients compared to controls, and gluten elimination produces measurable PASI improvement in this subset. Alcohol worsens psoriasis through multiple mechanisms: increased gut permeability, liver-mediated inflammatory cytokine production, and direct keratinocyte proliferation effects. Individual food sensitivities identified through elimination or IgG testing can significantly reduce flare frequency.

Conventional vs Functional Medicine Approach

Key Labs to Evaluate

How to Interpret These Labs Together

Common Patterns Seen in Patients

• The patient on biologics with persistent metabolic syndrome: IL-17 inhibitor producing good skin clearance (PASI 90 response). But fasting insulin 18, triglycerides elevated, BMI 31, hs-CRP 3.8. The biologic is controlling the skin disease but the systemic metabolic inflammation is untreated. Insulin sensitization, dietary modification, and cardiovascular risk management alongside the biologic addresses the metabolic disease that the dermatologic treatment cannot.
• The patient whose psoriasis flares with every stressful period: stress is identified by 40 to 80 percent of psoriasis patients as a flare trigger. Cortisol dysregulation confirmed on 4-point salivary cortisol. HPA axis support, stress management techniques, and magnesium glycinate for cortisol and GABA support reduced stress-triggered flare frequency from every 4 to 6 weeks to every 4 to 5 months.
• The patient who cleared on a Mediterranean diet vacation and relapsed at home: two weeks in Greece: psoriasis improved by 60 percent. Home: full relapse within 3 weeks. The Mediterranean dietary pattern (high omega-3, polyphenols, fiber; low processed food, alcohol, sugar) reduced the inflammatory trigger burden. Systematic adoption of anti-inflammatory dietary principles at home with food sensitivity identification produced sustained improvement that vacation alone could not maintain.

Treatment and Optimization Strategy

Trigger Reduction Alongside Conventional Treatment

What Most Doctors Miss

• Psoriasis is a systemic inflammatory disease, not a skin disease: the same Th17 inflammation producing the plaques accelerates atherosclerosis, drives metabolic syndrome, and produces psoriatic arthritis. Treating only the skin ignores the systemic disease.
• Gut health directly modulates psoriasis severity: intestinal permeability and dysbiosis are documented in psoriasis and drive the Th17 activation producing the disease. Gut restoration is not standard care but has direct disease-modifying potential.
• Vitamin D systemic optimization exceeds topical benefit: topical vitamin D analogs are first-line treatment, confirming the mechanism. But systemic optimization to 60 to 80 ng/mL provides immune regulatory benefit throughout the body that topical application to individual plaques cannot achieve.
• Cardiovascular risk assessment should be standard: psoriasis is an independent cardiovascular risk factor with event rates comparable to diabetes in severe disease. Proactive cardiovascular evaluation should accompany every psoriasis treatment plan.

When to Seek Medical Care

If you have psoriasis that is not adequately controlled, experience joint symptoms (potential psoriatic arthritis), have metabolic syndrome components alongside your psoriasis, or want to identify and reduce the environmental triggers driving your flares, a comprehensive functional medicine evaluation alongside your dermatologic care is warranted.

Recommended Testing

Frequently Asked Questions

How The Lamkin Clinic Approaches Psoriasis

At The Lamkin Clinic, psoriasis evaluation includes comprehensive inflammatory markers (hs-CRP), vitamin D with a target of 60 to 80 ng/mL, gut microbiome and permeability assessment, food sensitivity evaluation (including anti-gliadin antibodies), metabolic assessment (fasting insulin, HbA1c), and cardiovascular risk evaluation. Treatment combines vitamin D optimization, omega-3 supplementation, gut restoration, dietary modification, and stress management alongside appropriate conventional dermatologic treatment to reduce the environmental trigger burden and improve outcomes beyond what immune suppression alone achieves.

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