Introduction
Psoriasis is a chronic autoimmune disease that affects 1–3% of the population, predominantly Caucasians between 20 and 30 years of age, and between 50 and 60 years [1, 2]. The pathomechanism underlying the development of psoriasis is complex, but genetic factors play a key role [3]. Nine different regions of genes implicated in the development of psoriasis (PSORS 1–9) have been located, the most important of which is PSORS 1, located on chromosome 6p21, where the major histocompatibility genes are also present [4].
Activation of interleukin-12/Th1/interferon g (INF-g) (IL-12/Th1/IFN-g) and Th17/interleukin-23 (IL-23) axes is observed, in which IL-12 induces the formation of Th1 lymphocyte subpopulations and IL-23 stimulates the activity of Th17 lymphocyte subpopulations. Moreover, Th17 lymphocyte differentiation induces transforming growth factor b (TGF-b) in the presence of IL-6, while Th17 lymphocytes affect the secretion of interleukin-17 (IL-17) and interleukin-22 (IL-22), which are keratinocyte proliferation simulators [5, 6]. A characteristic feature is the phenomenon of parakeratosis, or accelerated and incomplete keratinization, which is associated with an 8-fold shortening of the cell cycle [7].
The most common clinical form is psoriasis vulgaris, accounting for 90% of cases [8]. It is characterized by the presence of papular lesions on an erythematous base covered with silvery-white scales and located on the scalp (most common), symmetrically on the upright parts of the upper and lower extremities, as well as in the lumbosacral region. The diagnosis of psoriasis is typically made based on the clinical picture [9]. When the diagnosis cannot be made based on the clinical picture and dermoscopy, a skin biopsy from the lesion and histopathological confirmation are indicated [10–12].
The objective of this narrative review was to analyse the influence of dietary habits, alcohol consumption, and smoking on the clinical course of psoriasis.
The importance of environmental factors in the course of psoriasis
Environmental factors can influence both the onset and course of psoriasis and can have a decisive impact on the risk of exacerbations [13, 14]. Patients with psoriasis often have a strong sense of the cosmetic defect and social stigma due to their skin lesions, which significantly affects their quality of life and increases their risk of exacerbations [10, 15].
Effects of diet on the clinical course of psoriasis
Although the importance of diet in the clinical course of psoriasis has been evaluated since the 1950s, no clear dietary recommendations have been developed to date [16–18].
The rationale for a reduced-calorie diet in patients with psoriasis is that obesity is a risk factor for the disease [12]. In addition, the concomitant presence of obesity and HLA-Cw*06 increases the risk of psoriasis 35-fold compared to individuals with normal body weight [11, 19]. Studies conducted to date indicate that a body mass index (BMI) of 26–29 kg/m2 slightly increases the risk of psoriasis, while a body mass index (BMI) > 29 kg/m2 significantly increases the risk of the disease. At the same time, a reduction in body weight results in an alleviation of symptoms [20, 21]. Hsieh et al. showed that reducing caloric intake from food by one third for 4 weeks resulted in a reduction in excessive epidermal proliferation by 45% in a mouse model [22]. The link between weight reduction and relieving the clinical symptoms of psoriasis is most likely due to a reduction in the volume of visceral fat, which consists not only of adipocytes but also a large number of macrophages [23, 24]. Studies indicate that patients with psoriasis have decreased concentrations of adipokines with protective effects, which include adiponectin and omentin, and increased concentrations of leptin, chemerin, visfatin, and resistin [23–28].
Further, macrophages are a source of a number of pro-inflammatory cytokines, which are responsible for the onset of psoriasis, , as well as other adipokines, such as resistin, visfatin, and retinol-4-binding protein [29, 30]. An increase in the concentration and secretion of TNF-a from visceral adipose tissue is responsible for free fatty acids (FFAs), which, by exerting an activating effect on the Janus kinase pathway and stimulation of Toll-like receptors (TLR-4), contribute to the further development of inflammation and the “vicious circle” mechanism of inflammation [31–33]. FFAs may also exacerbate oxidative stress. An important action of TNF-a is to exert a suppressive effect on the expression of genes encoding enzymes in adipocytes, such as acetyl-CoA carboxylase, lipoprotein lipase, and glycerol phosphate dehydrogenase, which are responsible for the uptake of fatty acids from the blood, resulting in an increase in the concentration of FFAs and triglycerides in the blood [34, 35]. This concept explains the phenomenon of “psoriasis march” and the frequent coexistence of psoriasis with obesity [36].
Low-calorie diet
Serum levels of pro-inflammatory cytokines have been shown to decrease in patients who have experienced weight loss [37]. Patients with psoriasis should consume a diet rich in omega-3 fatty acids that are not synthesized by humans and must be obtained from food. The main representatives of omega-3 acids are eicosapentaenoic acid and docosahexaenoic acid [38]. Omega-3 fatty acids reduce the inflammatory process by affecting the expression of genes that encode proteins crucial to the etiopathogenesis of psoriasis [39]. Inuit people are much less likely to develop psoriasis due to their traditional diet of marine fish, which is an excellent source of eicosapentaenoic acid and docosahexaenoic acid. Similarly, fewer cases of psoriasis have been reported in West Africans, whose diet is also rich in omega-3 fatty acids [32]. Significant improvements in the skin condition and a reduction in lesion severity have been observed in patients with psoriasis who consume omega-3 fatty acids [40]. Gisondi et al. showed that weight reduction among obese patients with psoriasis resulting from a low-calorie diet can be a valuable adjunct to traditional pharmacotherapy [41]. Pona et al. and Wu et al. showed that a low-calorie diet combined with topical or general treatment significantly reduced psoriasis activity and severity index (PASI) and dermatology life quality index values [18, 42]. Al-Mutairi et al., who conducted a randomized prospective study in a group of 262 patients with psoriasis receiving biologic therapy, reported significant reductions in body weight and PASI and Body Surface Area (BSA) values after 24 weeks of follow-up in patients on a low-calorie diet (< 1000 kcal; n = 131) compared to a group of patients whose dietary habits were not changed (control; n = 131) [43]. This finding provides further evidence of the synergistic effect of pharmacotherapy and a reduction diet in patients with psoriasis [43].
The improvement in clinical indicators of psoriasis progression in patients on a low-calorie diet may also be due to a reduced dietary supply of pro-inflammatory arachidonic acid, which, in turn, translates into lower levels of arachidonic acid metabolites, such as leukotriene B4 and prostaglandin 2, and lower CD4+ lymphocyte activity [44].
Gluten-free diet
The National Psoriasis Foundation’s 2018 Medical Council indicated that it “weakly recommend[s] a gluten-free diet (GFD) only in patients who test positive for serologic markers of gluten sensitivity” [45]. The first reports of a link between enteropathy, malabsorption syndrome, and psoriasis were published in the 1980s [46]. The common denominator of the three diseases appears to be an increased permeability of the intestinal mucosa in individuals with celiac disease, which affects the increased migration of bacteria acting as superantigens, causing the onset or exacerbation of psoriatic lesions [47]. Acharya et al. conducted a systematic review and meta-analysis of 18 articles that examined the association between celiac disease, GFD, and psoriasis [48]. Only one of the two studies on the prevalence of celiac disease in patients with psoriasis showed a significantly higher prevalence of this dermatosis in patients with gluten intolerance (odds ratio, OR = 1.9, 95% CI = 1.6–2.2 and OR = 1.20, 95% CI = 0.91–1.59 [49]). Two studies also confirmed a significantly higher risk of psoriasis in patients with celiac disease (OR = 1.72, 95% CI = 1.54–1.92 [45] and OR = 1.9, 95% CI = 1.5–2.3 [46]). By contrast, the risk of celiac disease in patients with psoriasis vulgaris or psoriatic arthritis was reported in five [45, 47–50] out of nine [51–54] studies (meta-analysis: OR = 2.16, 95% CI = 1.74–2.69 [48]).
Similarly, the incidence of psoriasis among patients with celiac disease appeared to increase according to four [50–53] out of eight [54–57] studies (meta-analysis: odds ratio = 1.8; 95% CI = 1.36–2.38 [48]). In a questionnaire study, Affifi et al. showed that 38% of surveyed (n = 1206) patients with psoriasis declared the use of GFD, and another 53.4% (n = 247) indicated an improvement in their clinical condition after eliminating gluten from their diet. In the vast majority of cases, celiac disease occurs in people with other autoimmune diseases. Among patients with psoriasis, a subpopulation with coexisting visceral disease has been observed [15]. A study by Michaëlsson et al. showed that in psoriasis patients with serum antigliadin antibodies (AGA), the use of a gluten-free diet improves their clinical status [58].
In a screening study by Michaelsson et al., 16% of 302 patients with psoriasis had elevated titres of IgA-class AGA antibodies [59]. However, other researchers found no statistically significant differences in AGA antibody titres in IgA and IgG classes in patients with psoriasis compared to healthy controls [60]. Moreover, in a study by Zamani et al., only 3 of 328 patients with psoriasis had elevated transglutaminase antibodies and anti-endomysial antibodies, which are specific for celiac disease [61].
Further, Kolchak et al. showed a significant reduction in PASI values in 56% and 36% of patients with psoriasis who had very high (> 30 U/ml, n = 5) or high (11.5–30.0 U/ml, n = 8) IgA AGA, respectively. Nevertheless, it was not indicated whether these patients suffered from gluten intolerance [62]. De Bastiani et al. confirmed the effectiveness of GFD use in patients with psoriasis and coexisting celiac disease, noting during a 3-month follow-up, a reduction in PASI values in 9 patients (n = 2, a reduction in PASI two of at least 50%; n = 5 of at least 75%; n = 1, complete resolution of lesions) [63]. Qiu et al. showed that out of 75 antigens in the serum of patients with psoriasis, significantly higher concentrations were recorded only for IgG4 against antigliadin. The concentration of these antibodies positively correlated with the PASI score (r = 0.65, p < 0.001), suggesting that the determination of their levels may be a valuable diagnostic biomarker of psoriasis [64]. Nevertheless, a relatively large number of case-control studies do not indicate an association between GFD and psoriasis severity. Nevertheless, the studies presented have low power (global seroprevalence of celiac disease at 1.4%) [65].
Vegetarian diet
By contrast, the premise of a vegetarian diet is to eschew meat and meat products in favour of large amounts of groats, cereals, legumes, vegetables, fruits, nuts, and mushrooms, reduces the supply of arachidonic acid and its derivatives, prostaglandins and leukotriene B4, which have pro-inflammatory effects [66]. A vegetarian diet benefits weight maintenance, as it results in a lower intake of saturated fatty acids and cholesterol, which is important for patients with psoriasis. It contributes to regulating uric acid, C-reactive protein, and triacylglycerols [67]. People who give up eating meat should introduce a substitute in the form of fish, which supplements omega-3 fatty acids [18]. Elevated markers of lipid peroxidation and oxidized low-density lipoprotein are found in patients with psoriasis, indicating an overproduction of oxygen free radicals in this condition [68]. Thus, people with psoriasis who consume a diet rich in fruits and vegetables, a source of antioxidants, may have less severe psoriatic lesions [69].
Mediterranean diet
The Mediterranean diet, considered a healthy diet, can be a valuable adjunct to the treatment of chronic inflammatory diseases because it is low in saturated fatty acids and trans-fatty acids, and rich in polyunsaturated fatty acids of the omega-3 family, antioxidants and flavonoids [70].
There are many variants of the Mediterranean diet, varying in the quality and quantity of total fat consumed, the type of meat, milk, cheese, fruits and vegetables, and wine [70]. The traditional Mediterranean diet is characterized by a high proportion of olive oil and products of plant origin, such as cereals, fruits, vegetables, legumes, potatoes, nuts and seeds [71]. Fish and poultry are consumed in moderation, and red meat is eaten only a few times a month. Dairy products are mainly consumed in the form of yogurt and cheese [71, 72].
The study evaluated the convergence of the dietary habits of 62 patients with psoriasis with the Mediterranean diet, based on the score obtained from the questionnaire used in the Prevention with Mediterranean Diet study (PREDIMED) [73]. It was assessed that people with psoriasis followed diets significantly less similar to the Mediterranean diet (lower point scores) compared to healthy subjects [73]. In addition, lower levels of similarity to the Mediterranean diet were associated with higher PASI scores and CRP levels [73]. Consumption of olive oil, fruits, vegetables, legumes, fish and nuts negatively correlated with PASI score [73].
Alcohol consumption, addiction, and association with psoriasis
According to available statistics, more than 10% of the adult population in Poland has consumed alcohol in a harmful way at some point in their lives [74]. The main reasons for not attempting or discontinuing alcohol treatment are psychological barriers in addicts, who are ashamed of their disease, fear being associated with a facility, and may face social ostracism [75]. It should be emphasized that alcohol consumption, especially in a risky manner, significantly restricts possible therapeutic options for psoriasis [8, 76]. For example, aztrethin and methotrexate may also have hepatotoxic effects, limiting their usefulness in the treatment of psoriasis in patients with chronic alcohol abuse [77]. The exacerbation of psoriasis in alcoholics appears to be associated with more frequent mechanical trauma, a greater susceptibility to infections, and the exertion of adverse changes in the differentiation of specific T-lymphocyte subpopulations that disrupt the immune response [78]. Alcohol can both initiate and exacerbate inflammation by stimulating lymphocyte proliferation and the production of pro-inflammatory cytokines [79]. A study by Gerdes et al. of 1203 patients hospitalized for psoriasis found an association between the severity of psoriatic lesions expressed on the PASI scale and alcohol consumption [80].
Brenaut et al. reported that patients with psoriasis consumed alcohol more frequently and in greater amounts compared to those without dermatosis [81]. Poikolainen et al. reported that men with psoriasis consumed an average of 42.9 g of alcohol per day, whereas healthy volunteers drank an average of 21 g of alcohol per day. By contrast, the average annual frequency of alcoholic beverage consumption was 61.6 g in the psoriasis group and 42.6 g in the control group [82]. In subsequent observations, Poikolainen et al. observed that in women, the incidence of psoriasis was significantly associated with alcohol consumption, smoking, and the occurrence of negative life events, but the degree of skin surface involvement was only significantly associated with alcohol consumption [83].
Wolk et al. also observed a statistically significant association between alcohol intake and the onset of psoriasis in men but not in women. In men, the odds ratio was 3.4 for 5–19 drinks per month and 3.1 for more than 20 drinks per month [84]. Svanström et al. also observed that alcohol consumption among patients with psoriasis was significantly above average and concluded that alcohol consumption is associated with a more severe and frequent incidence of psoriasis. They also emphasized that in patients with psoriasis who abuse alcohol, skin lesions are located primarily on the face, groin, knee, and elbow flexures, and acral localization [85, 86].
Smoking and psoriasis
Nicotine is absorbed both through the alveoli in the lungs and through the skin and intestinal mucosa. Nicotine receptors, through which nicotinism effects on the human body are exerted, are located in the central nervous system, as well as in the adrenal medulla, keratinocytes, and cells of the immune system [87]. Patients with psoriasis often declare current or previous nicotine addictions. Smoking may not only worsen the course of already existing psoriasis but also increase the risk of disease [88]. Fortes et al. showed that patients who smoked more than 20 cigarettes per day had twice the risk of developing severe psoriasis and a reduced likelihood of periods of remission compared to those who smoked less than 10 cigarettes per day [88]. By contrast, in a retrospective study of patients with psoriasis vulgaris and psoriatic arthritis, Kinahan et al. observed no effect of cigarette smoking on clinical responses to general treatment [89]. Nevertheless, it is important to remember that smoking is a risk factor for the development of psoriasis; it is positively associated with the disease at the population level but negatively associated with patients with psoriasis, a phenomenon referred to as the “smoking paradox” in psoriasis [87, 89].
It is important to note that many studies have not confirmed a worse clinical response to biological treatment in patients with psoriasis who smoked cigarettes compared to those who were not smokers [88–94]. Zhou et al. pointed out that the inconclusive association between smoking and psoriasis progression and response to treatment is due to the relatively small number of studies on the relationship between psoriasis and cigarette smoking [94].
Conclusions
Psoriasis is a dermatosis that affects 1–3% of the adult population. It has a complex etiopathogenesis that is becoming increasingly well understood. The risk of onset and clinical course of psoriasis is influenced by factors beyond our control (genetic factors) and can be modified to reduce the risk of the disease and possible exacerbations. Therefore, in addition to the correct selection of therapy, it is extremely important to educate patients about the impact of alcohol consumption, smoking, stress, physical activity, and a well-balanced diet on the onset and progression of psoriasis. This literature review confirms that a holistic and multidisciplinary approach is required when treating patients with psoriasis. It seems that the best complement to pharmacotherapy is a well-balanced diet, attention to a healthy lifestyle, and avoidance of common stimulants.
Of course, this review of the literature does not fully address the topic, but it does highlight the validity of Hippocrates’ thesis, “Let food be thy medicine, and medicine be thy food” [95].
