Skip to content
Psoriasis: The Missing Manual

Environmental Triggers

Psoriasis develops when environmental factors interact with genetic susceptibility to kick off (or ramp up) the immune cascade described above. The following triggers are well-characterised in the literature.

8.1 Infections

Streptococcal infection (particularly pharyngitis/strep throat) is the best-established infectious trigger for psoriasis and is especially linked to the onset of guttate psoriasis. Streptococcal M protein shares structural similarity with keratin in human skin, potentially leading to cross-reactive T cell activation, a form of molecular mimicry where the immune system confuses a bacterial protein with a similar-looking human protein and attacks both (Griffiths et al., 2021). Other infections, including HIV, may also trigger or exacerbate psoriasis.

8.2 Obesity

Obesity is both a risk factor for developing psoriasis and a factor that worsens existing disease. Adipose tissue (body fat) is metabolically active and produces pro-inflammatory cytokines called adipokines, including TNF-a and IL-6, which contribute to systemic inflammation. Obesity also reduces the efficacy of many psoriasis treatments, and weight loss improves disease severity and treatment response (Zhu et al., 2024; Al-Kufi et al., 2025).

8.3 Psychological Stress

Stress is one of the most commonly cited triggers for psoriasis flares, reported by a significant proportion of patients. The mechanism may involve promotion of neurogenic inflammation (inflammation triggered by the nervous system), changes in the neuroendocrine system, particularly the hypothalamic-pituitary-adrenal (HPA) axis (the body’s central stress-response system connecting the brain to the adrenal glands), and redistribution of immune cells to the skin (Ko et al., 2019).

8.4 Smoking

Smoking is an independent risk factor for psoriasis onset and severity. Tobacco smoke causes oxidative stress and free radical production, interfering with signalling pathways relevant to psoriasis including NF-kB, MAPK, and JAK-STAT (Naldi, 2016). Smokers with psoriasis also show reduced treatment response. One study found that patients with longer smoking duration and higher smoking intensity had significantly lower rates of achieving PASI 75 after eight weeks of treatment (Zhou et al., 2024). Smoking also alters the gut microbiota in ways that may promote psoriatic inflammation (Luca et al., 2024).

8.5 Alcohol

Excessive alcohol consumption increases the expression of TNF-a-converting enzyme (TACE) and plasma levels of TNF-a receptor, upregulates genes promoting lymphocyte and keratinocyte proliferation, and may facilitate skin infections that act as psoriasis triggers. Alcohol misuse affects approximately one-third of people with psoriasis and worsens therapeutic compliance (Brenaut et al., 2022; cited in Caso et al., 2022).

8.6 Medications

Several classes of medications can trigger or exacerbate psoriasis, including beta-blockers, lithium, antimalarials (chloroquine, hydroxychloroquine), interferon-alpha, ACE inhibitors, and rapid withdrawal of systemic corticosteroids (Griffiths et al., 2021).

8.7 COVID-19 Infection

SARS-CoV-2 infection has been documented as both a trigger for new-onset psoriasis and a cause of severe flares in existing disease. A systematic review identified cases of de novo guttate, plaque, and pustular psoriasis following COVID-19 infection, with onset typically 2-8 weeks after acute illness (Gananandan et al., 2022). The mechanisms likely involve the intense cytokine release during COVID-19 (particularly IL-6, TNF-α, and IFN-γ) priming the same inflammatory pathways that drive psoriasis. COVID-19 vaccination has also been associated with psoriasis flares in case reports, most commonly after mRNA vaccines, though the absolute risk is very low and the benefits of vaccination far outweigh this risk (Section 30). Interestingly, some patients on biologic therapy reported improvement in their COVID-19 course, possibly because IL-17 and IL-23 inhibitors dampen the excessive inflammatory response.

8.8 Hormonal Changes

Hormonal transitions can trigger or modify psoriasis activity. The most documented is pregnancy (covered in detail in Section 21.1), where 40-60% of women improve due to the Th2 shift that protects the foetus, while 10-20% worsen and postpartum flares are common. But other hormonal transitions also matter:

  • Puberty: Psoriasis onset peaks during adolescence, coinciding with the surge in sex hormones. Androgens may promote keratinocyte proliferation and inflammatory cytokine production, potentially explaining the adolescent onset peak (Ceovic et al., 2013).
  • Menopause: Some women report new-onset or worsening psoriasis around menopause. The decline in oestrogen, which has anti-inflammatory and immunomodulatory properties, may remove a protective brake on Th17-mediated inflammation. Hormone replacement therapy has shown mixed results in case reports.
  • Menstrual cycle: Premenstrual flares are reported by some women with psoriasis, likely reflecting the drop in oestrogen and progesterone in the late luteal phase.

The interplay between sex hormones and psoriasis is understudied relative to its clinical impact. Most psoriasis clinical trials don’t stratify results by hormonal status, and specific hormonal interventions haven’t been tested in rigorous trials.

8.9 Physical Trauma (Koebner Phenomenon)

Skin injury (cuts, burns, tattoos, surgical wounds, or even friction) can trigger psoriatic lesions at the site of trauma. This is the Koebner phenomenon or isomorphic response, and it occurs in approximately 25-30% of psoriasis patients (Boyd & Neldner, 1990).

8.10 Climate and UV Exposure

Cold, dry climates tend to worsen psoriasis, while moderate sunlight exposure (particularly UV-B radiation) can improve symptoms, forming the basis for phototherapy treatments. Sunburn, on the other hand, can trigger flares. The geographic gradient of psoriasis prevalence (higher at higher latitudes) may partly reflect reduced UV exposure and lower vitamin D levels (Dairov et al., 2024).

8.11 Air Pollution

Ambient air pollution is an increasingly recognised environmental trigger for psoriasis. A 2024 meta-analysis found significant associations between particulate matter and nitrogen dioxide exposure and psoriasis prevalence and flares: an excess risk of 3.0% per 10 ug/m3 increase in NO2, 1.2% for PM10, and 0.2% for PM2.5 (Chen et al., 2024). Effects were more pronounced in cold seasons and in females.

How does air pollution actually get from your lungs (or skin) to your immune system? Several pathways:

  • AhR activation: Polycyclic aromatic hydrocarbons and dioxins in particulate matter activate the aryl hydrocarbon receptor (AhR) on keratinocytes and immune cells, driving Th17 polarisation and IL-22 production.
  • Skin barrier impairment: Fine particulate matter deposits on the skin surface, disrupting the lipid barrier and increasing transepidermal water loss.
  • Oxidative stress: PM2.5 generates reactive oxygen species that amplify NF-kB signalling (Section 6.5) and lipid peroxidation (Section 7.6).
  • Microbiome disruption: Air pollutants alter the skin microbiome composition, potentially promoting pathogenic colonisation.
  • Epigenetic modification: A study using UK Biobank data found that PM2.5-related DNA methylation changes at the ZMIZ1 locus, a known psoriasis susceptibility gene (Section 5), correlate with increased psoriasis risk (Huang et al., 2024).

Research stage: Emerging. Evidence strength: Moderate. Meta-analyses and longitudinal studies with plausible biological mechanisms; specific pollutant-pathway links being characterised.

8.12 Climate Change

Climate change is anticipated to affect psoriasis through several interconnected mechanisms (Frontiers in Immunology, 2025):

  • Heat stress: Rising temperatures trigger psoriasis flares through vasodilation, increased sweating (which can irritate intertriginous psoriasis), and upregulation of heat shock proteins that activate innate immune pathways.
  • Humidity changes: Low humidity worsens skin barrier dysfunction and promotes scale formation; conversely, high humidity in tropical zones may foster microbial growth (particularly Malassezia, Section 6.6) and maceration in skin folds.
  • UV radiation changes: Ozone depletion increases UV exposure, which in moderate doses improves psoriasis but in excessive doses causes sunburn and Koebner phenomenon (Section 8.7).
  • Seasonal variation in treatment outcomes: A 2025 multicentre longitudinal study is examining how temperature-trend-defined seasonality affects biologic treatment outcomes across European centres (PMC, 2025).

The net effect of climate change on psoriasis is likely to be regionally variable, with worsening in areas experiencing extreme heat and low humidity, and potentially modest improvement in currently cold, dark climates that see increased UV exposure.

Research stage: Emerging. Evidence strength: Low-Moderate. Primarily epidemiological and mechanistic reasoning; prospective climate-psoriasis studies are underway but not yet completed.