Acne Causes: Beyond Hygiene—Hormones, Genetics, and Inflammation
Acne vulgaris is a multifactorial disease of the pilosebaceous unit. Poor hygiene is not a primary cause. Over-cleansing can worsen it by disrupting the skin barrier.
Core Pathogenic Factors
- Androgen-driven sebum overproduction: Testosterone/DHT stimulate sebaceous glands. Peaks in puberty; persists in adult female acne (PCOS, hormonal fluctuation).
- Follicular hyperkeratinization: Abnormal desquamation of keratinocytes forms a microcomedone (plug).
- Cutibacterium acnes proliferation: Anaerobe thrives in lipid-rich, hypoxic plugged follicle. Biofilms enhance virulence.
- Inflammation: C. acnes activates TLR2 → IL-1, TNF-α, IL-17 → neutrophilic infiltrate → papules, pustules, nodules.
Contributing Factors
- Genetics: Heritability ~80%. Influences sebum composition, follicular keratinization, immune response.
- Diet: High glycemic load, dairy (especially skim milk) associated with severity in some studies.
- Stress: ↑ cortisol/adrenal androgens → sebum; neuropeptides (substance P) → inflammation.
- Medications: Corticosteroids, lithium, anticonvulsants, EGFR inhibitors, anabolic steroids.
- Cosmetics: Comedogenic products (occlusive oils, certain silicones).
- Mechanical: Friction (helmets, masks), picking (acne excoriée).
Effective Management
- Gentle cleanser + non-comedogenic moisturizer.
- Topical retinoids (adapalene, tretinoin) – normalize keratinization (first-line).
- Benzoyl peroxide – bactericidal, anti-inflammatory.
- Topical/oral antibiotics (with BP to prevent resistance).
- Hormonal therapy (COCs, spironolactone) for adult females.
- Isotretinoin for severe, scarring, refractory cases.
See a dermatologist for personalized regimen. Consistency > intensity.
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