Psoriasis
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Psoriasis
Psoriasis is a chronic autoimmune skin disease characterized by rapid keratinocyte hyperproliferation, resulting in thick, silvery-scaled plaques on the skin. It stems from dysregulated Th17 cell activity, with IL-17 and IL-23 driving excessive inflammation and abnormal skin cell turnover. This condition affects approximately 2-3% of the global population and can significantly impact quality of life, with up to 30% of patients developing psoriatic arthritis.
Recognizing Psoriasis
Common symptoms and warning signs to look for
Red, raised plaques with silvery-white scales - typically on elbows, knees, and scalp
Thickened, pitted, or detached nails (nail psoriasis)
Scaly patches on the scalp with flaking resembling dandruff
Joint pain, stiffness, and swelling (psoriatic arthritis)
Cracked, bleeding skin that may be painful or itchy
Koebner phenomenon - new lesions appearing at sites of skin trauma
What a Healthy System Looks Like
In a healthy individual, keratinocytes undergo a carefully regulated lifecycle: basal keratinocytes in the stratum basale divide and migrate upward through the stratum spinosum and granulosum over approximately 28 days, ultimately forming the stratum corneum where they flatten, lose their nuclei, and desquamate. This balanced turnover maintains epidermal homeostasis at approximately 3.5 billion cells daily. The normal epidermis maintains tight regulation through cytokines, growth factors, and cell cycle controls, with keratinocyte proliferation rate matching desquamation rate. Resident immune cells (Langerhans cells, dermal dendrocytes, T lymphocytes) maintain surveillance without triggering inflammatory cascades. The dermal-epidermal junction remains intact, and blood vessels in the papillary dermis supply adequate nutrients without dilation or tortuosity.
How the Condition Develops
Understanding the biological mechanisms
Psoriasis involves a self-sustaining inflammatory loop: (1) Th17 cell activation - Unknown triggers (stress, infection, trauma) activate dendritic cells to produce IL-23, which stimulates and expands Th17 cells; (2) IL-17/IL-22 release - Th17 cells secrete IL-17A, IL-17F, and IL-22, which stimulate keratinocyte hyperproliferation and pro-inflammatory mediator production; (3) Keratinocyte hyperproliferation - Abnormal keratinocyte proliferation reduces turnover time from 28 days to 3-4 days, causing acanthosis (epidermal thickening) and parakeratosis (retained nuclei in stratum corneum); (4) Scale formation - Excess keratinocyte production combined with failed desquamation creates characteristic silvery scales; (5) Angiogenesis - VEGF and other growth factors promote new blood vessel formation in dermal papillae, causing plaque redness and warmth; (6) Neutrophil infiltration - Munro microabscesses form as neutrophils migrate into the stratum corneum; (7) Systemic inflammation - Elevated TNF-alpha, IL-17, and IL-23 circulate systemically, explaining extra-cutaneous manifestations; (8) Koebner phenomenon - Isomorphic response triggers lesions at sites of physical trauma due to increased growth factor expression.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| TNF-Alpha | <8 pg/mL | <4 pg/mL | Key inflammatory cytokine elevated in psoriasis; correlates with disease severity; target of infliximab, adalimumab, etanercept |
| IL-17 (Interleukin-17) | <5 pg/mL | <2 pg/mL | Primary driver of keratinocyte proliferation; target of secukinumab, ixekizumab, brodalumab; levels correlate with PASI score |
| IL-23 (Interleukin-23) | <10 pg/mL | <5 pg/mL | Th17 cell survival and expansion cytokine; target of guselkumab, tildrakizumab, risankizumab; elevated in active disease |
| IL-6 (Interleukin-6) | <5 pg/mL | <2 pg/mL | Pro-inflammatory cytokine elevated in psoriasis; correlates with cardiovascular comorbidity risk; acute phase reactant |
| CRP (C-Reactive Protein) | <3 mg/L | <1 mg/L | Non-specific inflammation marker; elevated in moderate-severe psoriasis; cardiovascular risk predictor |
| Uric Acid | 3.5-7.2 mg/dL | 4.0-6.0 mg/dL | Elevated in psoriasis due to increased nucleic acid turnover; may contribute to gout comorbidity |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Genetic Predisposition","contribution":"40-60% heritability - HLA-C*06:02 allele strongly associated; PSORS1-9 susceptibility loci identified; family history increases risk 3-4x; first-degree relatives have 10% lifetime risk","assessment":"Family history assessment; HLA-C*06:02 testing (research); clinical examination of relatives"}
{"cause":"Th17/IL-23 Pathway Dysregulation","contribution":"Core mechanism - IL-23 drives Th17 expansion; IL-17A/F stimulates keratinocyte proliferation; IL-22 promotes epidermal hyperplasia; creates self-sustaining inflammatory loop","assessment":"Serum cytokine panels (IL-17, IL-23, IL-22); clinical disease severity (PASI); response to biologics confirms pathway involvement"}
{"cause":"Environmental Triggers","contribution":"30-50% of flare triggers - Stress (psychological, physical), infections (streptococcal pharyngitis triggers guttate), trauma (Koebner), medications (beta-blockers, lithium, antimalarials), smoking, alcohol","assessment":"Detailed trigger history; symptom diary; infection workup for acute flares"}
{"cause":"Immune System Dysfunction","contribution":"Core mechanism - Dendritic cell activation, Th1/Th17 polarization, neutrophil infiltration, mast cell activation; impaired regulatory T-cell function","assessment":"Immunologic panel; T-cell subset analysis; clinical assessment of infection history"}
{"cause":"Metabolic Factors","contribution":"Obesity - Adipose tissue secretes pro-inflammatory adipokines; insulin resistance increases inflammation; mechanical stress on skin folds triggers lesions","assessment":"BMI, waist circumference; fasting glucose, HbA1c; lipid panel"}
{"cause":"Environmental Exposures","contribution":"Smoking - Direct trigger; 3x increased risk in smokers; dose-dependent; alcohol - worsens disease severity, impairs treatment response","assessment":"Smoking history (pack-years); alcohol use assessment; occupation exposures"}
{"cause":"Nutritional Deficiencies","contribution":"Vitamin D deficiency - Immuno-modulatory role; associated with disease severity; omega-3 deficiency - reduced anti-inflammatory mediators; zinc deficiency - impaired wound healing","assessment":"Serum 25-OH vitamin D; omega-3 index; zinc levels; dietary assessment"}
Risks of Inaction
What happens if left untreated
{"complication":"Psoriatic Arthritis","timeline":"Within 5-10 years in 30% of patients","impact":"Progressive joint damage, erosions, deformities, disability; early treatment critical as damage often irreversible; functional impairment affects work and daily activities"}
{"complication":"Cardiovascular Disease","timeline":"Lifetime elevated risk","impact":"2-3x increased risk of myocardial infarction, stroke, peripheral vascular disease; accelerated atherosclerosis from chronic inflammation; increased cardiovascular mortality"}
{"complication":"Metabolic Syndrome","timeline":"Progressive with disease duration","impact":"Type 2 diabetes, hypertension, dyslipidemia, obesity cluster; creates vicious cycle with psoriasis inflammation; increases cardiovascular risk exponentially"}
{"complication":"Psychological Morbidity","timeline":"Chronic, progressive","impact":"Depression (2x increased risk), anxiety, social isolation, reduced quality of life; unemployment rates 3x higher; relationship strain and social withdrawal"}
{"complication":"Ocular Complications","timeline":"Variable, often concurrent with flares","impact":"Uveitis (acute anterior), conjunctivitis, blepharitis, keratitis; can lead to vision loss if untreated; requires ophthalmologic monitoring"}
{"complication":"Reduced Life Expectancy","timeline":"Lifetime cumulative effect","impact":"3-4 year reduced life expectancy from cardiovascular disease, metabolic syndrome, and psychological comorbidities; quality-adjusted life years significantly impacted"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"PASI Score Assessment","purpose":"Standardize disease severity measurement","whatItShows":"Psoriasis Area and Severity Index measures erythema, induration, scaling, and body surface area; PASI 75/90/98 response defines treatment success; guides treatment escalation"}
{"test":"Cytokine Panel (IL-17, IL-23, TNF-alpha)","purpose":"Assess inflammatory burden and guide biologic selection","whatItShows":"Elevated Th17-axis cytokines confirm disease activity; helps predict response to specific biologic classes; serial measurements track treatment response"}
{"test":"Cardiovascular Risk Assessment","purpose":"Screen for comorbidity burden","whatItShows":"Lipid panel, fasting glucose, HbA1c, blood pressure, BMI; identifies metabolic syndrome; informs holistic treatment planning"}
{"test":"Nutritional Panel","purpose":"Identify modifiable nutritional contributors","whatItShows":"Vitamin D, omega-3 index, zinc, selenium; deficiencies impair immune regulation and barrier function; guides supplementation"}
{"test":"Psoriatic Arthritis Screening","purpose":"Early detection of joint involvement","whatItShows":"Physical exam for enthesitis, dactylitis; rheumatologic referral if symptoms; early imaging (X-ray, ultrasound, MRI) for subclinical disease"}
{"test":"Inflammatory Markers","purpose":"Objective measure of systemic inflammation","whatItShows":"CRP, ESR, IL-6; correlates with disease severity; cardiovascular risk stratification"}
Our Treatment Approach
How we help you overcome Psoriasis
Healers Psoriasis Immune Reset Protocol
Healers Psoriasis Immune Reset Protocol
Diet & Lifestyle
Recommendations for optimal recovery
Recovery Timeline
What to expect on your healing journey
{"initialImprovement":"2-4 weeks - Reduced scaling and plaque thickness, decreased redness, improved pruritus, early PASI score reduction","significantChanges":"3-6 months - Marked plaque clearance (PASI 75-90), normalized nail changes, reduced systemic inflammation markers, improved quality of life scores, decreased cardiovascular risk markers","maintenancePhase":"6-12 months - Sustained remission with clear or nearly clear skin, stable PASI scores, reduced treatment requirements, managed comorbidities, improved overall health metrics"}
How We Measure Success
Outcomes that matter
PASI 75 response (75% improvement in PASI score)
PASI 90 response (90% improvement, near clearance)
Body surface area affected reduced to <3%
Nail psoriasis improvement (reduced pitting, onycholysis)
Pruritus severity reduced by >50%
Quality of life improvement (Dermatology Life Quality Index)
Reduced systemic inflammation (CRP, IL-6 normalization)
Comorbidity risk reduction (metabolic markers improvement)
Maintenance of remission with minimal treatment
Patient-reported satisfaction and well-being
Frequently Asked Questions
Common questions from patients
What is the most effective treatment for psoriasis?
The most effective psoriasis treatment depends on disease severity and patient factors. For mild disease, topical corticosteroids and vitamin D analogs work well. For moderate-severe disease, biologic therapies targeting specific cytokines (IL-17 inhibitors like secukinumab, IL-23 inhibitors like guselkumab, or TNF-alpha inhibitors like adalimumab) offer the highest efficacy, with PASI 90 responses in 50-80% of patients. At Healers Clinic, we use advanced cytokine testing to select the most appropriate biologic for your specific inflammatory profile, combined with lifestyle interventions to optimize outcomes.
Can psoriasis be cured completely?
While there is no definitive cure for psoriasis, it can be effectively controlled to the point of achieving clear or nearly clear skin. Modern biologic therapies have revolutionized treatment, with many patients experiencing 90-100% clearance. Some patients achieve long-term remission after years of treatment and can eventually discontinue therapy. The goal shifts from 'cure' to 'sustained remission with minimal treatment burden.' Early aggressive treatment may alter the natural disease course and improve long-term outcomes.
Does psoriasis affect internal organs?
Psoriasis is a systemic inflammatory disease, not just a skin condition. It affects multiple organ systems: joints (psoriatic arthritis in 30% of patients), cardiovascular system (2-3x increased heart attack and stroke risk), metabolism (increased diabetes, obesity, metabolic syndrome), eyes (uveitis, conjunctivitis), and potentially the liver and kidneys in severe disease. This is why comprehensive care at Healers Clinic includes cardiovascular screening, metabolic monitoring, and rheumatologic assessment.
Is psoriasis hereditary?
Yes, genetics play a significant role in psoriasis. Having a parent with psoriasis increases your risk 3-fold, while having both parents affected increases risk 10-fold. The HLA-C*06:02 gene is strongly associated. However, genetics alone don't determine fate - environmental triggers (stress, infections, medications, smoking) often precipitate disease in genetically susceptible individuals. Understanding your family history helps with early detection and proactive management.
What foods should I avoid with psoriasis?
While triggers vary individually, foods to limit or avoid include: red and processed meats, high-fat dairy, refined carbohydrates and sugars, fried foods, excessive omega-6 vegetable oils, and alcohol. These foods can increase systemic inflammation. Many patients also report improvement on anti-inflammatory diets like Mediterranean diet. Nightshades (tomatoes, peppers) trigger some patients but not others. At Healers Clinic, we offer food sensitivity testing and personalized nutritional guidance.
How long does it take for psoriasis treatment to work?
Treatment response timelines vary by therapy: topical treatments show improvement in 2-4 weeks; phototherapy in 4-8 weeks; oral systemics in 4-12 weeks; biologics often show significant improvement within 4-12 weeks, with maximum effect at 16-24 weeks. It's important to give each treatment adequate time before evaluating efficacy. At Healers Clinic, we establish clear expectations and monitor progress regularly to optimize your treatment protocol.
Medical References
- 1.Greb JE, Goldminz AM, Elder JT, et al. Psoriasis. Nat Rev Dis Primers. 2016;2:16082. doi:10.1038/nrdp.2016.82
- 2.Griffiths CEM, Armstrong AW, Gudjonsson JE, Barker J. Psoriasis. Lancet. 2021;397(10273):1301-1315. doi:10.1016/S0140-6736(20)32549-6
- 3.Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361(5):496-509. doi:10.1056/NEJMra0804595
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