Psoriasis is a common, chronic skin condition occurring worldwide, presenting at any age, and leading to a substantial burden for individuals and society. It is associated with several important medical conditions, including depression, psoriatic arthritis, and cardiometabolic syndrome, impacting millions of people around the world.
Understanding this skin condition is essential for its effective management.
Psoriasis has a complex origin that can be attributed to both genetic and non-genetic factors. While genetics play a significant role in predisposing individuals to psoriasis, it’s only one piece of the puzzle. Environmental triggers and lifestyle choices also contribute to the development and progression of this condition.
Understanding both genetic and environmental factors contributing to psoriasis is vital for a better grasp of the condition and for improving support and treatment options for those affected.
Researchers have found specific gene variations related to our immune system and the skin’s protective barrier that can make the skin more sensitive and vulnerable to triggers.
In a family, if one parent has psoriasis, there’s a 20% chance their child will develop it, and this risk increases to 65% if both parents are affected.
Studies involving twins have shown that if one identical twin has psoriasis, there’s a 70% chance that the other twin will also develop the condition. In non-identical twins, this likelihood is lower, at 20%.
These findings highlight the relevance of hereditary factors in psoriasis.
The PSORS1 locus, located on chromosome 6, is one of the key genetic areas linked to psoriasis. Recent genetic studies have highlighted the significance of HLA-C, specifically the variant HLA-Cw6 (rs1131118), in psoriasis development, but the precise role is still under study. Additionally, SNP rs10484554 in the HLA-C region has been associated with a higher risk of psoriasis in some studies. It’s worth noting that psoriasis shares genetic overlaps with other conditions, such as type 2 diabetes, indicating complex genetic interactions. The specific mechanisms through which SNP rs10484554 influences psoriasis development are an active area of research, contributing to our understanding of the genetic complexities underlying this condition.
While many genes may contribute to psoriasis risk, specific gene mutations like those in IL36RN and CARD14 have been found to independently trigger psoriasis. These mutations affect both the skin and the immune system. Also, polymorphisms (SNPs) in the IL36RN gene on chromosome 2 can lead to variations in the IL-36Ra protein, which plays a role in regulating inflammation. IL36RN mutations and polymorphisms are particularly associated with pustular psoriasis.
On chromosome 17, the PSORS2 region has also been associated with psoriasis. Recent research has identified rare mutations in the CARD14 gene, contributing to overactive immune responses in familial psoriasis cases.
A comprehensive genetic study of psoriasis and psoriatic arthritis uncovered 10 regions significantly associated with psoriatic arthritis (PsA) and 11 with cutaneous-only psoriasis (PsC), further pinpointing the genetic distinctions between these conditions. Additionally, the study identified the previously unreported genome-wide significant association of TRAF3IP2 with PsC, adding new insights into the genetic underpinnings of these related conditions.
In a broader genetic analysis of psoriasis, a meta-analysis encompassing multiple genome-wide association studies revealed 15 novel susceptibility loci, expanding the total number of psoriasis-associated loci in European populations to 36. Moreover, this study unveiled candidate genes involved in immune regulation and innate host defense, contributing to our understanding of the genetic factors influencing immune-mediated inflammatory conditions, and emphasizing the skin’s significance in host defense mechanisms.
These findings underscore the consistent role of the TRAF3IP2 gene in psoriasis and its subtypes. This genetic factor has emerged as a critical component in understanding the genetic architecture of psoriasis.
In addition to nucleotide variation in specific genes, scientists have studied SNPs in non-coding regions of the genome. These SNPs are genetic markers that may indicate potential gene regulatory regions related to psoriasis, many of which involve the immune system’s role in the condition.
LifeDNA’s Skincare Report can provide valuable insights to help you determine if you have a genetic predisposition (potential) for developing psoriasis and offer suggestions on managing this skin condition.
Several non-genetic elements have been associated with a predisposition to the development and exacerbation of this skin condition.
In an intriguing historical discovery, Heinrich Koebner observed that physical trauma, like cuts, burns, insect bites, and even tattoos, could trigger and worsen psoriasis. This response, known as the Koebner response, often results in new psoriatic lesions that closely mirror the type of injury sustained.
The prevalence of this response in psoriasis patients ranges from 24% to 51%. The development of psoriasis following an injury can take anywhere from 3 days to 2 years and may depend on factors like the season and the severity of the skin condition.
Some medications have been linked to the onset and worsening of psoriasis. Common causes include drugs such as lithium, beta-blockers, antimalarials, tetracyclines, and non-steroidal anti-inflammatory medications.
More recently, medications that include TNFα blockers, IL-6R blockers, and certain interferons, along with the TLR7 agonist imiquimod, have also been reported to induce or exacerbate psoriasis. Other medications such as ACE inhibitors, calcium channel blockers, and IL-2 in the form of cancer immunotherapy have also been associated with psoriasis worsening.
Infections, especially in children, have been identified as significant triggers for psoriasis. Guttate psoriasis, characterized by small, drop-like lesions, has been linked to Streptococcus pyogenes infections through both the throat and skin routes. Additionally, infections like Staphylococcus aureus, Malassezia, and Candida albicans in the gut or on the skin have been associated with psoriasis worsening. In some cases, Helicobacter pylori infection has been observed to correlate with psoriasis severity.
Researchers suspect that toxins from these microorganisms and bacterial components could activate T cells and lead to abnormal immune responses, thus contributing to psoriasis development.
Psychological stress is known to exacerbate psoriasis by affecting the immune system. Stress hormone levels can increase due to the activation of the hypothalamus–pituitary–adrenal axis, potentially leading to psoriasis worsening.
In particular, cutaneous CRH and CRH-receptor 1 have been shown to regulate local homeostasis in the skin, and in psoriasis, expression of CRH is significantly increased. The pro-inflammatory effects of CRH on the skin are still being studied, but it may stimulate the production of key cytokines, further exacerbating psoriasis.
The relationship between alcohol and psoriasis is multifaceted and debated. Studies suggest that alcohol abuse is associated with a higher prevalence of psoriasis. Furthermore, moderate to severe psoriasis patients are at an increased risk of alcohol-related conditions and mortality.
While the exact mechanisms remain unclear, laboratory studies have shown that ethanol can stimulate T cells and induce keratinocyte hyperproliferation. Smoking is another risk factor for psoriasis, with a stronger correlation among women and former or current smokers. Recent research indicates that genetic susceptibility to psoriasis, combined with smoking and alcohol use, can significantly increase the risk.
Obesity has been identified as a risk factor for psoriasis, and studies have also suggested a connection between obesity and psoriasis severity. The mechanism behind this link is not fully understood, but it may involve adipokines such as leptin and resistin, which are often found in higher concentrations in psoriasis patients and obese individuals.
These adipokines can stimulate the production of proinflammatory cytokines, leading to skin inflammation. However, the relationship between obesity, weight loss, and psoriasis is complex, and more research is needed to understand their interactions fully.
Curious about your genetic predisposition to psoriasis and seeking personalized skincare advice to proactively address and manage this skin condition? Unlock LifeDNA’s DNA skincare report today.
Psoriasis is not contagious; it doesn’t spread through air or touch. It’s rooted in immune system dysfunction, where skin cells grow at an accelerated rate, leading to the formation of dry, scaly patches. This rapid cell turnover contributes to the hallmark plaques of psoriasis.
Regrettably, psoriasis has no permanent cure. It falls under the category of chronic conditions. While symptoms can be managed, they typically persist over the long term. New treatment approaches, like biologics targeting immune responses, have revolutionized psoriasis management, enhancing patients’ quality of life.
Psoriasis is indeed an immune-mediated genetic skin condition. The interplay of the innate and adaptive immune systems, orchestrated by various cells such as T cells, dendritic cells, macrophages, and keratinocytes, play a central role. Recent years have seen the development of biologics, which are drugs created from living organisms and are designed to focus on specific molecules or pathways in the body.
These target various cytokines, such as tumor necrosis factor-α, interleukin-23, and interleukin-17, drastically altering psoriasis treatment. While genetics are involved, various environmental factors also influence psoriasis onset and exacerbation. Furthermore, psoriasis has been associated with systemic inflammation, cardiovascular comorbidities, and other autoimmune and auto-inflammatory conditions.
Psoriasis has a history of several treatment options that have proven effective in managing this condition. These include:
Advanced psoriasis treatments, including biologic therapies such as infliximab, ustekinumab, adalimumab, and etanercept, have transformed psoriasis management. These highly effective treatments target specific proteins or pathways in the body, providing personalized and safe care. These therapies represent promising advancements in the field of psoriasis treatment.
*Understanding your genetics can offer valuable insights into your well-being, but it is not deterministic. Your traits can be influenced by the complex interplay involving nature, lifestyle, family history, and others.
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