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Constantin, C.; Surcel, M.; Munteanu, A.; Neagu, M. Psoriatic Patients and Obesity. Encyclopedia. Available online: https://encyclopedia.pub/entry/48038 (accessed on 07 August 2024).
Constantin C, Surcel M, Munteanu A, Neagu M. Psoriatic Patients and Obesity. Encyclopedia. Available at: https://encyclopedia.pub/entry/48038. Accessed August 07, 2024.
Constantin, Carolina, Mihaela Surcel, Adriana Munteanu, Monica Neagu. "Psoriatic Patients and Obesity" Encyclopedia, https://encyclopedia.pub/entry/48038 (accessed August 07, 2024).
Constantin, C., Surcel, M., Munteanu, A., & Neagu, M. (2023, August 14). Psoriatic Patients and Obesity. In Encyclopedia. https://encyclopedia.pub/entry/48038
Constantin, Carolina, et al. "Psoriatic Patients and Obesity." Encyclopedia. Web. 14 August, 2023.
Psoriatic Patients and Obesity
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This entry is adapted from the peer-reviewed paper 10.3390/nu15163528

Psoriasis, an autoimmune chronic inflammatory skin condition, has a high incidence in the general population, reaching 2–4%. Its pathogenesis involves an interplay of genetic factors, immune disturbances, and environmental factors. Within the environmental factors that aid the appearance of this autoimmune skin disease, the Western lifestyle and overall diet play important roles in the steady growth in psoriasis prevalence. Furthermore, psoriasis is associated with comorbidities such as psoriatic arthritis, cardiovascular disease, metabolic syndrome, and obesity. Accumulating evidence suggests that obesity is an important risk factor for psoriasis. 

psoriasis obesity nutrition diet microbiome

1. Introduction

The multifactorial nature of Ps pathogenesis includes metabolic process disruption, among which obesity has been recognized as a novel risk factor with rising importance in Ps onset and severity. Both obesity and Ps are associated with a chronic pro-inflammatory status in which microbiome deregulation has been identified to play a leading role [1].

2. Obesity in Psoriasis Onset

Obesity is defined as a body mass index (BMI) of ≥30 kg/m2, and this metabolic status poses both a significant global health concern and an economic burden [2]. In recent years, accumulating data has connected Ps incidence to excess body weight, as people suffering from Ps are usually overweight in comparison to the rest of the population. Interestingly, in May 2022, the WHO released a complex report that emphasized that obesity prevalence has almost tripled since 1975, and furthermore, over 60% of European citizens are overweight or even obese. The report highlights the cumulative inferences of the COVID-19 pandemic in respect of obesity, with all the repercussions that have resulted in terms of morbidity and mortality [3]. Obesity has thus acquired the roles of both a trigger and a contributor in the development of various diseases in which metabolic deregulation plays an important role, and Ps is one of these diseases. Moreover, a large meta-analysis of observational studies has suggested that obese people suffering from Ps have a higher risk of psoriatic arthritis, with a 6% surge in complications for every 1 kg/m2 increase in BMI [4].
Various studies have underlined novel insights regarding the severity of Ps lesions and the risk of obesity. Armstrong et al. explored the link between these two parameters in a meta-analysis that included over 2 million participants, of whom over 200,000 were patients with Ps. The authors showed that in Ps patients, the risk of obesity is over 50% compared to healthy subjects. Going further into the analysis, patients with more serious forms of Ps present a higher risk of obesity compared to patients diagnosed with the mild form. In addition, patients with Ps and normal body weight are prone to becoming obese in the future [5]. Along with more severe psoriatic lesions, psoriatic obese patients can also encounter several metabolic comorbidities (e.g., fatty liver, hyperlipidemia, etc.) that worsen their clinical disease profile. Additionally, an elevated BMI is a significant risk factor for many other disorders with a chronic autoimmune background, such as psoriatic arthritis (PsA) [2]. Moreover, patients with PsA experience serious metabolic- and inflammatory-driven comorbidities such as obesity, hypertension, or diabetes, as well as cardiovascular disease, in comparison with the general healthy population. The inflammatory milieu in PsA is attributed to adipose tissue, whose dysregulation maintains chronic low-grade systemic inflammation [6]. Therefore, in order to reduce the risk of developing metabolic complications, it is mandatory for Ps and PsA patients to control their BMI primarily through losing weight [7]. The most accessible strategy for lowering BMI and reducing adipose tissue in Ps patients is a low-calorie diet. Recently, diet as a potential therapeutic support method in Ps management has been exploited through the on-going Diet and Psoriasis Project, which aims to assess whether dietary factors are related to Ps severity (e.g., time-restricted eating vs. Mediterranean diet) [8].
According to various studies, body composition and body fat distribution are parameters that are more reliable than BMI, reflecting more accurately the patient’s nutritional status, and thus allowing observation of the in-depth correlation between weight and lesion severity, and monitoring the disease course. By using various refined methods that assess the nutritional status of psoriatic patients (e.g., bioimpedance analysis), the analysis of body composition has revealed that Ps is associated with elevated levels of body fat, visceral fat, and a diminished muscle mass [9], and thus bioimpedance analysis is endorsed as having a much better diagnostic power compared to BMI assessment alone [10].
Thus, the obesity–psoriasis–nutrition axis could be explored to decrease inflammation at the gut and skin levels. The result of such a strategy in terms of the disease course could be evaluated by measuring specific markers, such as decreases in C-reactive protein, TNF-α, and IL-6 levels; these parameters have been linked to a diet rich in soluble fibers [11].

3. Adipose Tissue Dysregulation in Psoriatic Patients

There are two forms of adipose tissue in humans: white tissue, which is the most abundant form and stores energy, and brown tissue, which is found especially in human newborns and plays an important role in regulating body temperature. Adipocytes are the most abundant cell type in white adipose tissue, along with pre-adipocytes (adipocytes that are unloaded yet contain lipids), endothelial cells, fibroblasts, leukocytes, and macrophages. Moreover, the number of macrophages in white adipose tissue has been found to be directly correlated with the degree of obesity [12].
Obesity can also be defined as an overbalance in the ratio between energy intake and energy consumption. As obesity evolves, body fat will excessively accumulate, giving rise to unhealthy white adipose tissue that becomes inflamed [13]. This adipose-related inflammation correlates further with chronic low-grade systemic inflammation. The specific low-inflammatory status is now a well-recognized mechanism for an increased risk of many serious pathologies (e.g., cardiovascular diseases), including those related to skin manifestation as Ps is [14][15].
In obesity, the alteration of adipogenesis is the leading step to the hypertrophy of adipocytes and further inflammation [16]. In this context, the modified adipose tissue will start to release a specific category of bioactive factor known as adipokines, whose types and levels depend on various factors such as the types of activated adipocytes (white or brown cells), number of cells, site, and interaction with other immune and non-immune cells. Moreover, in light of recent studies, adipose tissue should be considered not only a simple energy storage deposit but also a dynamic endocrine organ that actively intercedes in the regulation of inflammation, metabolism, and immunity, as well as in other physiological processes [17].
Studies in the last decade focusing on obesity onset have identified the entire flow of cellular processes involved in normal to hypertrophic adipose tissue transition, resulting in increased systemic inflammation and inhibition of adipogenesis. Excessive, unbalanced nutrition associated with other factors such as stress and/or a lack of physical exercise can lead to hypertrophy of adipocytes and eventually to obesity. Subsequently, mature adipocytes start to secrete free fatty acids and express an important array of pro-inflammatory adipokines (e.g., leptin, resistin, visfatin, chemerin, etc.) [18]. In addition, the expression of anti-inflammatory adiponectin is inhibited, which causes local inflammation and the recruitment of immune cells. There are increased numbers of locally infiltrating macrophages in obese adipose tissue, a process associated with fibrosis that also alters hormonal equilibrium [19]. Moreover, adipocytes and pre-adipocytes secrete a panel of pro-inflammatory cytokines and chemokines, including IL-6, CCL2, IL-1β, and TNF-α, which fuel low-grade systemic inflammation in obese individuals and induce metabolic syndrome [20].
In Ps patients with a severe course of the disease, increased blood levels of pro-inflammatory adipokines have been observed, and during lesion remission, these levels were found to be decreased. Additionally, serum levels of the anti-inflammatory adipokines omentin and adiponectin are significantly lower in patients with severe disease compared to patients with mild forms of Ps [20].
Considering the role of obesity in Ps development, some adipokines have been thoroughly studied in relation to the inflammatory milieu and severity of lesions. Studies from the last decade have claimed a role for adiponectin in the pathogenesis of Ps [21].
Adiponectin levels control a series of cytokines and the immune cellular balance of certain T lymphocyte subsets. Thus, in keratinocytes from Ps lesions, adiponectin inhibits pro-inflammatory cytokine synthesis and increases the release of anti-inflammatory cytokines [22][23]. At a cellular level, this would be translated as a restoration of the Th1-Th17/Th2 lymphocyte ratio, hindering IL-17A synthesis as a key part of adiponectin’s anti-inflammatory effects [24].
Adiponectin plasma levels correlate with a Ps patient’s weight and clinical outcomes. In the plasma of Ps patients, there are lower levels of adiponectin, resulting in an increased pro-inflammatory cytokine pattern and a decreased anti-inflammatory cytokine milieu [25], which may aggravate the severity of skin lesions [4]. Alternatively, with weight loss, the concentration of circulating adiponectin increases, concomitant with psoriatic lesion improvement [26].
Another adipokine, leptin, is involved in regulating the body’s energy balance and weight [27] by raising lipolysis and lowering hepatic lipogenesis [28]. In patients with obesity and psoriatic patients, leptin levels were found to be significantly increased, with a high level of leptin being directly correlated with BMI and with the PASI score [29]. Like adiponectin, leptin is responsible for increasing the pro-inflammatory cytokine pattern, which causes and favors keratinocyte proliferation. In addition, at the cellular level, leptin can impact T helper and dendritic cell functions, thus affecting the immunity processes in Ps [30].
Resistin is another adipokine currently regarded as a potential biomarker in Ps pathogenesis, as it induces a series of molecular and cellular events in psoriatic skin. Resistin is synthesized in adipose tissue mostly by macrophages and monocytes under pro-inflammatory conditions [31]. Further, resistin can induce keratinocyte proliferation via pro-inflammatory factors secreted by B lymphocytes [24]. Impacting the cellular immune network at the skin level, resistin plays an important role in Ps, as resistin can affect both the number and proliferation capacity of Foxp3+ regulatory T (Treg) cells. These deficiencies in Treg cell functionality reinforce the immune-related deregulation in Ps [32]. Prior studies have indicated a direct correlation between Ps severity and plasma resistin levels [33], while elevated plasma resistin levels in patients with Ps were strongly correlated with the DLQ index [24].
Chemerin is an adipokine produced mainly in white fat adipocytes, but is also produced by hepatocytes, and plays a role in the pathophysiology of Ps [34][35]. Although the precise function and mechanism of Ps pathogenesis are still in debate, positive correlations between systemic chemerin and obesity-related phenotypes (insulin resistance, BMI, serum triglycerides, etc.) have been registered, suggesting an important function of chemerin in metabolic diseases [36]. Another positive correlation between chemerin levels, inflammatory cytokines, and C-reactive protein was reported in Ps [37][38]. Chemerin acts as a chemotactic factor for human blood plasmacytoid dendritic cells (pDCs), promoting their migration and recruitment in psoriatic skin [39]. Skin exhibiting early and active lesions shows high expression of chemerin in the dermis, while skin exhibiting chronic lesions has low chemerin expression, associated with few pDCs in the dermis. Chemerin expression has been found to be upregulated mainly in fibroblasts linked with higher levels of chemerin mRNA than fibroblasts from healthy or unaffected psoriatic skin. Therefore, chemerin expression specifically labels the early phases of evolving skin psoriatic lesions [40]. The upregulation of chemerin in Ps was assessed in a recent study involving an imiquimod-induced mouse model of Ps. It was observed that intraperitoneal inoculation of an anti-chemerin antibody reduced epidermal proliferation and inflammation in the experimental mice, indicating that chemerin promotes keratinocyte proliferation and enhances the production of inflammatory cytokines, thereby aggravating the Ps. That study proposes chemerin as a forthcoming target for Ps treatment [41].
Other important adipokines, including retinol-binding protein-4, fetuin-A, and lipocalin-2, are being studied as potential mediators in obesity and Ps, although further studies are needed to support this hypothesis [26]. Nevertheless, apart from the cellular and molecular events that cause prolonged inflammation fueled by an array of pro-inflammatory markers, there is another component that impacts the behavior and lifestyle of obese psoriatic patients. Hence, the comorbidity picture of these individuals is completed by depression as a psychological stressor that contributes to the development of anxiety disorders [42][43]. Therefore, understanding the molecular mechanisms of the alterations suffered by adipose tissue in obesity is important because, through the metabolic and functional disorders suffered during the onset of obesity and through maintaining an inflammatory environment, adipose tissue could be analyzed as a potential multifaceted target in the management of obesity in Ps [19].

4. Microbiota in Obese Psoriatic Patients

Contributing to the multifactorial etiology of Ps, an altered microbiota can be an important trigger in obesity development, as a strong relationship has been documented between the microorganisms that inhabit internal and external body surfaces and are present in autoimmune diseases [44]. Firmicutes, Bacteroides, Proteobacteria, and Actinobacteria represent >98% of the gut microbiota. In respect of Ps, several studies have demonstrated that the relative abundances of Proteobacteria and Bacteroides decrease while the relative abundances of Actinobacteria and Firmicutes increase [45][46]. Like in Ps, in obese subjects, changes in the gut microbiota composition have been registered and significant alterations have been observed in the Firmicutes and Bacteroidota (F/R) ratio compared to normal-weight subjects. The F/B ratio is now broadly recognized as a critical marker in controlling normal gut homeostasis and is an important indicator of the gut microbiota’s status [45]. Variations in F/B lead to dysbiosis, and this ratio was found to be increased in obesity and decreased in some inflammatory conditions, such as Ps [47] and inflammatory bowel disease [48][49]. Some microbiota disturbances at the level of Clostridium innocuum, Eubacterium dolichum, Catenibacterium mitsuokai, Lactobacillus reuteri, Lactobacillus sakei, and Actinobacteria have also been described in obesity, reinforcing gut microbiota dysbiosis as one of the crucial characteristics of this condition [50]. Moreover, in obese psoriatic patients, a state of chronic inflammation is fueled by pro-inflammatory cytokines and adipokines generated by white fat adipocytes and characterized by high levels of IL-17, IL-23, TNFα, and IFNγ, supporting the relation between the microbiome and obesity in psoriatic individuals [51][52][53]. The volume of research in the field that is focused on the comorbidities of Ps is increasing, and recent studies have proved that the intestinal microbiota in patients with obesity suffering from Ps undergoes changes in terms of composition and abundance [54].

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Subjects: Dermatology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Carolina Constantin
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Mihaela Surcel
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Adriana Munteanu
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Monica Neagu
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Update Date: 15 Aug 2023
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