Psoriasis is a widespread and complex disorder that results from an interplay between multiple genetic and environmental factors (Parisi et al., 2013; Griffiths & Barker, 2007).

Psoriasis has a wide range of clinical manifestations and although worldwide incidence and prevalence is poorly understood, psoriasis is estimated to affect around 2–4% of the population in Western countries (Parisi et al., 2013).

Like many chronic inflammatory disorders, genetics plays a key role in psoriasis development (Parisi et al., 2013). In addition, the manifestation of psoriasis may also be dependent environmental factors (Griffiths & Barker, 2007). Monozygotic twins demonstrate a concordance rate of 65–72% for psoriasis, supporting this hypothesis (Boehncke & Schön, 2015; Chandra et al., 2015).

Suggested environmental triggers responsible for the pathogenesis or intensification of psoriasis (Boehncke & Schön, 2015; Chandra et al., 2015):

  • Infections
  • Psychological stress 
  • Cigarette smoking 
  • Alcohol consumption 
  • Obesity
  • Exposure to some pharmacologic agents

Learn more about some of the important factors in the variation of psoriasis incidence and prevalence rates: (Parisi et al., 2013)

Factors in the variation of psoriasis incidence and prevalence rates


Globally, psoriasis prevalence increases with age. Studies from the United Kingdom, Germany, Russia, and United States found an increasing trend with age until around 60 years, after which the prevalence reduced (Parisi et al., 2013).

In a recent Mediterranean regional study, a corrected database analysis that included 6,868 patients with a psoriasis diagnosis, the highest prevalence of psoriasis was found in the 61–70 year old group (2.90%). Psoriasis prevalence was just 0.30% among those under 18 years of age (Fernández-Armenteros et al., 2019). However, further studies need to determine the relationship between patients age and psoriasis prevalence after accounting for confounders.

Find out how age influences treatment selection from Professor Andrew Blauvelt.

Geographical location and ethnicity

Higher prevalence rates have been reported at higher latitudes and in Caucasians compared with other ethnic groups. This is likely due to a combination of genetic and environmental factors (Parisi et al., 2013). In addition, prevalence estimates may depend on the sampling method (eg medical databases or patient questionnaires).

Prevalence of psoriasis by location

Figure 1. Prevalence of psoriasis by location (Lee et al., 2017; Richard et al., 2018; Valent et al., 2018).

Understanding country-specific prevalence and incidence of psoriasis provides useful insights and may allow future resources to be allocated appropriately and adequately (Parisi et al., 2013). 


Areas of chromosomes thought to harbour psoriasis genes are named psoriasis-susceptibility (PSORS) loci. Understanding the genetic variations in psoriasis and how these may influence the immunological disease-causing pathways may help in the development of novel and targeted personalised psoriasis therapies (Gunter et al., 2019).

Find out more about targeted and personalised therapies from Professor Andrew Blauvelt. He describes targeting therapy as a challenge, and stresses the importance of onset of action.

The HLA-C gene

There are at least 15 different PSORS loci responsible for susceptibility of psoriasis and the HLA-C gene has been consistently indicated as the most likely ‘psoriasis-susceptibility region 1’ (PSORS1) gene associated with psoriasis. HLA-C is a class I major histocompatibility complex (MHC) molecule and the locus at 6p21 within the MHC region has been shown to exhibit the strongest association with psoriasis development; abnormalities in this locus account for 35–50% of psoriasis susceptibility (Lowes et al., 2014; Singh et al., 2019).

Genome-wide association study findings 

Genome-wide association studies (GWAS) have identified psoriasis-associated genes; a recent review of genomic databases found 424 genes to have single nucleotide polymorphisms (SNPs) associated with psoriasis (Singh et al., 2019). Many of these genes are involved in skin barrier defence and the induction of innate or adaptive immunity. This has allowed GWAS to provide insights into the biological mechanisms associated with psoriasis susceptibility (Capon et al., 2012; Boehncke & Schön, 2015; Chandra et al., 2015; Aterido et al., 2016). 

GWAS have also discovered psoriasis-linked genes outside of the PSORS segments. Epigenetic changes have also been associated with the development of psoriasis (Singh et al., 2019).


Despite its decline since the 1960s, smoking remains a common part of westernised culture and is increasing in developing countries. A 2018 review paper by Pezzolo & Naldi reported smoking to be a risk factor for the development of psoriasis and a possible reduction to treatment adherence (Pezzolo & Naldi, 2019). One study included in the review – a pooled analysis of three studies (the Nurses’ Health Study [NHS], the Nurses’ Health Study II [NHS II], and the Health Professionals’ Follow-Up Study [HPFS]) – found that current smokers were twice as likely to develop psoriasis than non-smokers (adjusted OR 1.94, 95% CI 1.64–2.28). The likelihood of developing psoriasis was also seen to increase with an increase in the number of daily cigarettes (Armstrong et al., 2014).


Obesity has also been associated with the risk of developing psoriasis. A recent systematic review confirmed that different adiposity measures such as BMI, waist circumference, waist-to-hip ratio, and weight gain positively correlated with increased risk of psoriasis (Aune et al., 2018).

A retrospective study of medical records between 1970–2014 found children diagnosed with psoriasis were more likely to be obese at the time of diagnosis than a control group without psoriasis (OR = 2.58, 95% Cl 1.48–4.52) (Hunjan et.al., 2018).

A previous study found obesity preceded psoriasis in 93% of paediatric patients with psoriasis who were either overweight or obese (Becker et.al., 2014)

Cross-talk between adipocytes and the immune system via various mediators such as adipokines have been proposed as a pathological explanation for the association between obesity and psoriasis (Wong et al., 2019).

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