The pathogenesis of psoriasis is closely linked to dysregulation of innate and adaptive immune pathways.1 Epigenetic mechanisms may further explain population-level differences in psoriasis prevalence, as environmentally driven changes in gene expression can modulate immune responses without altering genetic background.33–35 One of the most significant genes of interest is the HLA-Cw6 allele, which has a strong association with psoriasis.4,7,9,30–39 HLA-Cw6 is more common in Caucasian patients than in Asian patients, with the presence of HLA-Cw6 conferring a relative risk of 13 for developing psoriasis in the Caucasian population compared to 25 in the Japanese populations.37 Importantly, genetic predisposition appears to be a stronger determinant than geographic location of indigenous groups. Despite their large geographical distance, North American Indians, Aboriginal Australians and the Taiwan Ami people- three indigenous groups that descended from the same ancestor- all have a negligible prevalence compared to non-indigenous populations living in the same areas.3,32

Epigenetics provides a mechanistic link between genetic susceptibility and environmental exposures in psoriasis. Through processes such as DNA methylation, histone modification, and microRNA regulation, external stimuli can induce persistent changes in gene expression that influence key inflammatory pathways, including the IL-23/Th17 axis and keratinocyte proliferation.33,34 Therefore, in genetically predisposed populations, environmental triggers may promote pro-inflammatory modifications that unmask disease expression- conversely, this means in populations without risk alleles, environmental exposures alone may be insufficient to induce the changes required to trigger disease.33–35 This may help explain the persistently low prevalence of psoriasis observed in certain indigenous groups despite increasing exposure to similar environmental risk factors as non-indigenous populations currently.

Studies have demonstrated a positive correlation between psoriasis incidence and heightened innate immune activity, which is hypothesised to have evolved from ancestral exposure to infectious diseases.9,14,32 The majority of indigenous groups with negligible psoriasis prevalence are thought to have experienced delayed exposure to streptococcal and other systemic infections compared to European populations. Evidence suggests that psoriasis was virtually absent in Australia until European settlement in the last 200-years, and similarly in Chile until the Spanish conquests in the 16th and 17th centuries, both of which introduced novel pathogens to these indigenous communities.9,14,32 Similar trends are reported among North American Indians and the Taiwan Ami, whose communities were also impacted by waves of colonisation in the 14th to 16th centuries.3,11

A 1989 study investigating Human Leukocyte Antigen (HLA) and disease associations found that the major histocompatibility complex at HLA-A and HLA-B were nearly identical among indigenous Australians, consistent with an evolutionary history of reduced pathogen exposure and corresponding lower rates of psoriasis.32,36 Such reduced variability likely restricts antigen presentation diversity, influencing how the immune system responds to environmental triggers implicated in psoriasis.32

Exposure to sunlight and UV radiation plays an important part in both disease modulation and therapeutic approaches to psoriasis. A systematic review of 85 papers demonstrated that psoriasis prevalence correlated with increasing distance from the equator, supporting the correlation between UV radiation exposure and clinical improvement.21 This pattern is reflected in our review, where most indigenous communities living closer to the equator, such as the Taiwan Ami, Indigenous Australians, American Samoans, and sub-Saharan African groups, reported no cases of psoriasis.7–9,14,31,32,40 In contrast, Arctic Indigenous populations demonstrated higher prevalence rates, with 5.7% among Inuit people in Greenland and 1.4% among the Sami people in Norway.7,10 Similarly, a study of the rural town of Arctic Kasach’ye demonstrated an outlier prevalence of 11.8%.31

Geographical factors such as altitude, seasonal sunlight availability, and surface reflectivity of snow and water contribute towards shaping the distribution of psoriasis. The widespread and persistent presence of snow cover in circumpolar regions is thought to enhance UV reflectivity and confer a protective effect against psoriasis.31,39 It is also proposed that long-term biological adaptation to the high altitude and extreme cold may contribute to the lack of psoriasis in Peruvian Aboriginals in the Andean Mountains.13 A survey of 555 indigenous people in Brazil, which found no cases of psoriasis, also attributed its findings to the region’s humid and warm climate, high UV exposure, and minimal exposure to external and urban environmental triggers.12

Lifestyle factors such as diet, smoking and alcohol consumption, obesity, physical activity, and stress all play a part in psoriasis by upregulating chronic inflammatory responses.1,29 Indigenous people in the Auaris region of Brazil were reported to have no cases of psoriasis, likely due to abundant natural sunlight exposure and absence of urban lifestyle factors.12 In the Inuit population of Nuuk, patients with psoriasis had higher associations with comorbidities such as metabolic syndrome and cardiovascular diseases.29

Cultural values, traditional therapies, and skin phenotype play an important role in ensuring accurate diagnosis and treatment of psoriasis in Indigenous populations. Women of African ancestry tend to experience more severe forms of scalp psoriasis due to Afro-textured hair, hair care practices (chemical relaxers, braids, weaves), and longer washing intervals, all of which can complicate adherence to topical treatment regimens.38 In Tigray, Ethiopia, a case series reported frequent use of Indigenous therapies, including Hijama (wet cupping) and traditional plants such as Kigelia africana.9 These treatments have inconclusive dermatological outcomes, and in some cases were associated with disease flares or post-inflammatory hyperpigmentation. Access to conventional therapies is limited, with most patients restricted to topical corticosteroids, salicylic acid, or methotrexate.15 Traditional Asian practices such as cupping, coining, moxibustion, and herbal remedies may also exacerbate cutaneous disease activity.38

One of the most important factors that complicates accurate estimation of prevalence is diagnostic accuracy, particularly in skin of colour. In Indigenous populations with darker skin phototypes, psoriasis may present with atypical features, leading to underdiagnosis or misdiagnosis. Erythema in Fitzpatrick type VI skin may appear brown or violaceous, complicating assessment and contributing to underestimation of Psoriasis Area and Severity Index (PASI) scores.32,38 Post-inflammatory hyper- and hypopigmentation are also more prominent in these populations, further complicating clinical evaluation. Among Inuit populations, psoriasis often presents as thin plaques resembling nummular eczema, which may delay diagnosis and result in more advanced disease at presentation.10,15 Delayed recognition not only impacts treatment outcomes but also increases the risk of progression to severe disease, for which systemic therapies may be unavailable or difficult to access in remote communities.

A major limitation of this review is that much of the available data consists of anecdotal descriptions or results from small field studies with limited population numbers. The scarcity of large-scale epidemiological data of indigenous populations is influenced by the underlying issues of reduced access to dermatological services, underrepresentation in clinical trials, and challenges in diagnostic accuracy.

In many low-resource settings, empowering remote and indigenous communities to access mainstream dermatological services can be challenging. In rural regions of Africa, the diagnosis and management of skin conditions, including psoriasis, are often provided by community health workers or non-medical individuals.41 This leads to misdiagnosis of psoriasis (most commonly as tinea corporis) and delays to appropriate treatment, hence resulting in disease progression and greater morbidity.32 Access barriers are also present in high-income nations. In Australia, only 4% of dermatologists are based in rural and remote areas and just 2% in regional areas, despite these areas being home to a large proportion of Indigenous communities.42 Historical and intergenerational trauma further compound these challenges. Among Aboriginal Australians, cultural attitudes toward skin disease, combined with rurality and the enduring legacy of colonisation, have been cited as barriers to engagement with mainstream dermatological services.8

Research gaps also contribute to underrepresentation. Clinical trials and observational studies frequently omit detailed reporting of the racial or ethnic background of participants, limiting the capacity to accurately assess disease burden in indigenous communities.

While biological, environmental, and cultural factors likely contribute to the lower prevalence of psoriasis in Indigenous communities, the lack of standardised, high-quality epidemiological data remains a significant barrier to understanding the true global burden of disease. Improving data collection and reporting practices is, therefore, critical to addressing inequities and informing public health policy.