Plant-Based Foods for Chronic Skin Diseases: A Focus on the Mediterranean Diet

Abstract

Purpose of Review

In this narrative review, we provide an overview of how adherence to a Mediterranean dietary pattern can complement traditional treatment strategies for psoriasis, acne, and hidradenitis suppurativa. We emphasize the importance of an integrated approach, with dietary interventions as a key component of holistic patient care.

Recent Findings

Psoriasis, acne, and hidradenitis suppurativa are immune-mediated chronic diseases marked by systemic inflammation, with genetic and environmental factors influencing their onset. The Mediterranean diet, rich in plant-based foods with antioxidant and anti-inflammatory properties—such as whole-grain cereals, extra-virgin olive oil, vegetables, legumes, fruits, and nuts—has been shown to reduce the clinical severity of these conditions. It also supports weight control and positively impacts metabolic and cardiovascular risk factors, which are closely linked to these diseases.

Summary

Dietary education, particularly about the Mediterranean diet, plays a crucial role in the management of these skin diseases and serves as an important non-pharmacological treatment option that can influence patient prognosis. This review offers specific nutrition recommendations for prescribing the Mediterranean diet to patients with chronic inflammatory skin diseases.

Introduction

Chronic inflammatory skin disorders such as psoriasis, acne, and hidradenitis suppurativa (HS) significantly impact both physical and mental well-being [1–3].

Psoriasis and HS share several underlying features, including impaired skin barrier function, disrupted skin homeostasis, neutrophil-rich inflammation, and activation of the Th17 immune pathway [4, 5]. However, HS is distinct in that it leads to hypertrophic scarring and the formation of dermal tunnels, highlighting a unique role for fibroblasts in its pathology [6]. In contrast, acne is driven by factors such as excessive sebum production, hyperkeratinization (thickening of the skin around hair follicles), increased growth of the bacteria Propionibacterium acnes (P. acnes), and inflammation [7]. All three conditions are characterized by elevated levels of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)−1, and IL-17, which contribute to increased inflammation and severity of symptoms [6, 8–10].

Because these skin disorders are chronic, they typically necessitate ongoing management rather than a complete cure. Treatment options often lead to significant side effects, which can limit their long-term use. Additionally, individual responses to therapy can vary, often necessitating multiple approaches that extend the management process. Effective treatment generally involves a comprehensive strategy that combines medications with non-drug interventions, especially dietary changes, to improve symptoms and promote skin health [11–13].

The Mediterranean diet (MD), known for its distinctive nutritional characteristics, is widely recognised as one of the most studied dietary patterns for its health-promoting properties. In fact, it was awarded the title of Intangible Heritage of Humanity by UNESCO in 2010 [14]. The benefits of MD are well-documented, largely to its food composition and the frequency of consumption, as outlined in the traditional Mediterranean food pyramid [14]. Examining this pyramid reveals specific foods that are not always present in other dietary patterns, giving the MD added value through its richness in bioactive compounds. These foods provide significant nutraceutical potential. The concept of MD's nutraceutical potential is not new; as early as 2016, it was noted that many of MD’s key benefits, such as antioxidant and anti-inflammatory effects, are mediated by the bioactive compounds found in typical Mediterranean foods [15].

Thus, the added value of MD, reflected in its intrinsic nutraceutical potential, is highlighted. The MD is based on the regular consumption of vegetables, fruits, legumes, cereals (preferably wholegrain), nuts, fish, and extra virgin olive oil (EVOO) as the primary fat for seasoning, with a low-to-moderate consumption of meat, eggs and dairy products. Red wine may be consumed in moderation, in line with social habits. Adherence to MD's nutritional guidelines ensures the regular intake of specific bioactives, particularly monounsaturated fatty acids (MUFAs) (abundant in EVOO), polyunsaturated fatty acids (PUFAs) (especially the omega-3 fatty acids found in fish and certain nuts), and polyphenols (abundant in fruit, vegetables, EVOO, nuts, wine, spices and herbal teas) [14, 16]. The main beneficial effects of these bioactive compounds are their antioxidant and anti-inflammatory actions, which occur through various mechanisms, such as the inhibition of IκB/NFκB and MAPK signalling pathways by polyphenols [17] and the stimulation of eicosanoid synthesis with anti-inflammatory effect by omega-3 PUFAs [18].

MD is thus a predominantly antioxidant and anti-inflammatory dietary pattern, with mechanisms that also include modulation of the gut microbiota and immune system [19, 20]. This makes it a valid medical nutrition therapy (MNT) in managing inflammatory dermatological diseases and their associated complications. High adherence to MD has been shown to have beneficial effects on obesity [21], metabolic syndrome [22], systemic inflammation [23] and cardiovascular health [24]. Additionally, high adherence to MD in pregnancy has been linked to a reduced risk of atopy in unborn child [25], further emphasizing its broad health benefits.

In this narrative article, we provide an overview of the current understanding of the MD and its impact on reducing flare-ups and disease severity in chronic inflammatory skin disorders. We present evidence supporting the importance of a holistic approach in managing these conditions.

Psoriasis

Psoriasis is an immune-mediated skin disease characterized by a chronic relapsing–remitting course, affecting approximately 2–3% of the global population [26]. It can onset at any age but is most observed between the ages of 20–40, and 50–70 [27].

Both genetic and environmental factors are thought to contribute to psoriasis onset [28]. The HLA-Cw6 allele is genetically associated with the highest risk of developing the disease [29]. A study involving 112 randomly selected patients found that the HLA-Cw6 marker was present in 85.3% of those with early onset, compared to only 14.7% of patients with late onset [30].

Environmental factors, such as physical trauma and bacterial or viral infections, may trigger innate immune responses, activating the release of nucleic acid/autoantigen complexes from damaged skin cells. For instance, complexes formed by cathelicidin LL37 and self-DNA/RNA fragments activate plasmacytoid dendritic cells (pDCs), which release high levels of interferon (IFN)-α and TNF-α [31]. This local production of IFN-α and other type I IFNs triggers keratinocyte immune activation and myeloid DC (mDC) maturation, initiating the adaptive immune response. Consequently, an inflammatory environment rich in IL-23/IL-17 cytokines is established in psoriatic skin, with IL-23 promoting type 17 helper (Th17) and cytotoxic (Tc17) effector responses [32, 33]. The subsequent expansion of effector T cells and increased production of IL-17 and IL-22 in psoriatic skin leads to epidermal hyperplasia and abnormal cornification processes [34]. IL-17 also activates keratinocytes to produce chemokines (CXCL1/CXCL2/CXCL8 and CCL20) and antimicrobial peptides (S100 family members), which recruit neutrophils, T cells, and contribute to the immune response [35, 36]. IL-17 thus plays a key role in linking T cells and keratinocytes in psoriasis. Despite this, analyses of transcriptional profiles in psoriatic lesions show that the IFN-γ signature predominates, even though IL-17 and TNF-α induce a wide array of genes [35, 36]. Additionally, IL-22 is crucial in psoriasis pathogenesis, activating STAT3-dependent genes involved in differentiation and proliferation. However, IL-22 induces fewer genes than IL-17 in psoriatic lesions [37]. Among the genes activated by IL-22 are CXCL8, CCL20 and antimicrobial peptides (HBD-2, HBD-3, and S100).

The clinical diagnosis of psoriasis generally involves identifying characteristic skin lesions, with plaque psoriasis being the most common type, affecting 80–90% of patients [38]. Psoriasis plaques are typically well-defined, symmetrical, erythematous, and covered with silvery scales, often found on the scalp, trunk, buttocks, and limbs, although they may appear anywhere on the body. Active lesions can be itchy or painful [38, 39]. Disease severity and eligibility for systemic treatment are often assessed using the Psoriasis Area and Severity Index (PASI), with a cut-off score of 10 being commonly used in several European countries [40]. However, it is unclear whether this cut-off accurately reflects systemic inflammation or the risk of comorbidity.

Psoriasis is not only a skin condition but also a systemic disease that can impact the cardiovascular system [41]. Individuals with psoriasis have a higher prevalence of cardiovascular diseases (CV), especially with severe disease, which increases the risk of heart attacks and strokes [42]. A 2006 population-based study in the U.K. showed that psoriasis is associated with an increased risk of myocardial infarction, independent of traditional risk factors such as body mass index (BMI), smoking, hypertension, type 2 diabetes, and dyslipidemia [43]. Later, Flammer and Ruschitzka [44] proposed the theory of “two plaques for one syndrome”, noting similarities in the molecular mechanisms and pro-inflammatory cytokine profiles between psoriatic lesions and atherosclerosis, including a similar inflammatory infiltrate of T cells, macrophages, and monocytes. Elevated levels of TNF-α and soluble TNF receptors have been detected in psoriatic lesions and serum of patients with severe psoriasis, resembling those found in congestive heart failure patients [42, 45]. Research has also shown increased pro-atherogenic markers, such as C-reactive protein (CRP) and soluble intercellular adhesion molecule-1 (ICAM-1), in psoriasis patients without traditional CV risk factors [46].

Up to 40% of psoriasis patients may develop psoriatic arthritis (PsA), an inflammatory arthritis that often accompanies the skin manifestations of psoriasis [47, 48]. Studies have found that certain psoriasis body sites localizations, such as scalp lesions, nail dystrophy, and intergluteal/perianal involvement, are associated with a higher risk of developing PsA [49, 50]. Specific mediators from psoriatic skin, such as IL-33, OPN, IL-17, and TNF-α, contribute to bone damage by releasing pro-osteoclastogenic factors that promote osteoclast formation and recruitment, initiating bone damage [51].

Obesity is a significant risk factor for psoriasis, and vice versa, as both conditions share a chronic inflammatory state [28]. A meta-analysis has shown that psoriasis patients have a more than 50% increased risk of obesity compared to the general population [52]. Elevated leptin levels and M1-polarized macrophages in visceral adipose tissue are implicated in this relationship [28, 53]. Moreover, psoriasis patients may experience low physical activity due to reluctance to expose their skin, which can contribute to obesity [54, 55]. Obesity can also negatively affect the efficacy of both conventional and biological treatments, especially those with fixed dosages due to altered pharmacokinetics [56].

Traditional systemic therapies for psoriasis include methotrexate, acitretin, cyclosporine, and phototherapy [57, 58]. However, patients, particularly those with obesity, may be at increased risk for liver steatosis and toxicity. For instance, methotrexate can be harmful to the liver, and acitretin should be used cautiously in obese patients due to increased risk of hypertriglyceridemia and hypercholesterolemia, especially in those with diabetes or alcohol abuse. Cyclosporine, dosed according to body weight, carries a nephrotoxicity risk in obese patients, older patients, and those with hypertension. Photochemotherapy with psoralen plus UVA is unaffected by body weight, though patients with abdominal obesity may be more susceptible to skin reactions and burns due to their proximity to the bulbs [28]. Systemic therapy is frequently used when PsA is present, with methotrexate being a common choice; however, its long-term use can cause serious side effects, including teratogenicity and bone marrow toxicity [59].

Biologic therapies, which target specific cytokines or immune pathways, are the first-line treatment for moderate-to-severe psoriasis, aiming to reduce systemic inflammation and prevent future complications [58, 60]. Approved biologics include TNF-α inhibitors (e.g., infliximab, etanercept, certolizumab, and adalimumab), IL-12/23 inhibitors (ustekinumab), IL-17 inhibitors (e.g., bimekizumab, ixekizumab, secukinumab, brodalumab); and IL-23 inhibitors (e.g., guselkumab, tildrakizumab, risankizumab) [28]. Notably, certolizumab is the only biologic approved for moderate-to-severe psoriasis treatment in women of childbearing potential [61]. However, biologic treatments do not provide a permanent solution, and many patients may lose their response over time, necessitating a switch to a different biologic medication [62].

Recent network meta-analysis that anti-IL-17 therapies are among the most effective for achieving PASI 90 (90% reduction in PASI score), compared to other biological agents except for anti-IL23 therapies [63]. Biologics targeting IL17, IL23, and TNF-α all demonstrated higher PASI 90 rates compared to non-biological agents [63, 64]. However, individual responses may vary, and biologics come with potential side effects and costs that must be considered. Biologics such as TNF-α inhibitors can reactivate latent tuberculosis, while IL-17 inhibition can lead to mucocutaneous candidiasis [64].

Treatment strategies for psoriasis must balance the benefits for skin manifestations and comorbidities like obesity, which can impair the efficacy of biological therapies. Research on how these therapies affect weight and metabolic health is ongoing, and dietary modifications alongside biologics may improve disease management and overall outcomes [28, 65].

Being a complex disease from an etiopathogenic point of view, it is clear that diet plays a central role in the management of psoriasis and its associated comorbidities [66], primarily by counteracting oxidative stress, which is reflected in improvements in severity indices such as the PASI score [55]. One of the first studies conducted on this topic demonstrated how the MD is associated with psoriasis severity [12]. In this study, 62 patients with mild-to-severe psoriasis were compared with an equal number of healthy subjects matched for age, sex and BMI. Adherence to MD was assessed using the 14-item PREvención con DIeta MEDiterránea (PREDIMED) questionnaire. The results showed that a lower PREDIMED score (indicating lower adherence to the MD) was found in a higher percentage of patients with psoriasis compared to controls. Interestingly, the PREDIMED score was negatively correlated with the PASI score and was the strongest predictor of psoriasis severity. Furthermore, analysing the PREDIMED questionnaire revelead that the consumption of EVOO (a source of MUFAs) and fish (a source of omega-3 s) were independent predictors of PASI score and CRP levels [12], suggesting the anti-inflammatory and protective role of the MD as a whole, as well as the individual components of its characteristic foods. Similarly, other observational studies confirmed both (i) a lower adherence to the MD in patients with psoriasis compared to controls and (ii) its negative association with disease severity [67–69], allowing this diet to be considered a MNT in the management of psoriasis, given its strong antioxidant and anti-inflammatory actions. The beneficial effects of diet on the clinical outcomes of psoriasis are mainly attribuited to the bioactive components of specific foods, such as minerals and vitamins, which possess anti-inflammatory and antioxidant properties. Among the vitamins, vitamin D plays a key role, influencing the proliferation and maturation of keratinocytes [55, 70]. Among macronutrients, MUFAs (particularly those abundant in EVOO) exert important protective effects, primarily by protecting biological membranes from oxidative damage, resulting in improvements in the PASI score in patients with psoriasis [55].

Table 1 reports the main studies that have investigated the role of the MD on psoriasis.

Table 1.

Observation studies investigating the role of Mediterranean diet on skin diseases

Skin disease	Number of patients	Adherence to MD	Main results	Reference
Psoriasis	62 vs 62 controls	PREDIMED	- Low PREDIMED score in a higher percentage of patients than control - PREDIMED score negatively correlated with psoriasis severity - PREDIMED was the stronger predictor of psoriasis severity - Consumption of EVOO and omega-3 were independent predictors of psoriasis severity and CRP levels	[12]
Psoriasis	3557	MEDI-LITE	- A higher percentage of patients with severe psoriasis were in the lower tertile of adherence to the MD	[67]
Psoriasis	89	PREDIMED	- A high adherence to MD were found in patients with a low degree of psoriasis severity and CRP levels	[68]
Psoriasis	69 vs 69 controls	MedDietScore	- Psoriasis severity was negatively associated with adherence to the MD and consumption of legumes, fish, and EVOO	[69]
Acne	51 vs 51 controls	PREDIMED	- PREDIMED scores were lower in patients than controls, and negatively correlated with the degree of acne severity - PREDIMED score was a major determinant of acne severity - A PREDIMED score of ≤ 9 predicted the higher degree of acne severity	[130]
Acne	121 vs 121 controls	MEDAS	- The largest percentage of subjects had low adherence to the MD in both patients and controls - No significant association was found between adherence to the MD and diagnosis or severity of disease	[131]
Acne	40 vs 40 controls	PREDIMED	- PREDIMED score was negatively correlated with acne severity	[132]
Acne	35	PREDIMED	- Lower levels of IGF-1 were found in patients with higher adherence to the MD	[129]
HS	41 vs 41 controls	PREDIMED	- Adherence to the MD was lower in patients than in controls - The degree of HS severity was negatively correlated with PREDIMED - A PREDIMED score of ≤ 5 predicted a higher degree of HS severity - HS had a lower complex carbohydrate, MUFAs, omega-3 and higher of saturated fatty acids and omega-6	[171]
HS	35 vs 35 controls	MedDietScore	- HS patients had a lower adherence to the MD than controls	[172]
HS	221	PREDIMED	- The HS severity was negatively correlated to PREDIMED score - Use of EVOO and preference of poultry over red meat were the major influencers of this correlation	[173]

Abbreviations: PREvención con DIeta MEDiterránea, PREDIMED; extravirgin olive oil, EVOO; C-reactive protein, CRP; Mediterranean diet, MD; 14-Item Mediterranean Diet Adherence Screener, MEDAS; monounsaturated fatty acids, MUFAs; Hidradenitis suppurativa, HS

Acne

Acne is a very common skin condition characterized by the presence of comedones, papules, pustules and/or nodules, primarily affecting the face and trunk [71, 72]. Its high prevalence and localization in body areas of cosmetic concern contribute to its significant social burden. Approximately 70–80% of adolescents are affected [73], with 64% and 43% of individuals experiencing persistence into their twenties and thirties, respectively [74]. Acne is more prevalent in males during adolescence due to higher androgen levels, which stimulate sebaceous gland activity. In contrast, adult acne, particularly in women, is often linked to hormonal fluctuations and/or metabolic disturbances [75]. Although acne affects individuals across all ethnic groups, studies suggest that presentation and scarring tendencies may differ based on skin type and genetic factors [76]. Variations in age of onset and ethnic distribution may also be influenced by lifestyle factors [77].

Acne is a chronic inflammatory disorder that affects the pilosebaceous unit [78]. Its pathogenesis is multifactorial and involves several factors, including genetics, excessive sebum production, hyperkeratinization of the sebaceous duct, colonization by Cutibacterium Acnes (formerly called Propionibacterium acnes), and perifollicular inflammation [7]. Various immunological and inflammatory mediators, such as cytokines, defensins, and neuropeptides, play a significant role in its development [79]. Increased levels of prostaglandin E2 and Peroxisome proliferator-activated receptors (PPAR)-γ can trigger sebaceous gland hyperplasia, sebum overproduction, and subsequent inflammation, contributing to the characteristic acne lesions [80, 81]. Additionally, C. acnes triggers the release of pro-inflammatory cytokines [82].

The follicular occlusion process in acne is a central pathogenic event that initiates comedone formation and sets the stage for further inflammation and lesion development [83]. Hyperkeratinization within the pilosebaceous unit is thought to result from both increased keratinocyte proliferation and reduced shedding, leading to the accumulation of keratinocytes and sebum, which forms a microcomedo [84]. The follicular occlusion creates an anaerobic environment that favors the growth of C. acnes, a commensal bacterium that becomes pathogenic under these conditions [85]. The proliferation of C. acnes triggers the release of pro-inflammatory mediators, further disrupting the follicular wall and leading to the development of papules, pustules and/or nodules [86]. Recent studies have shown that acne severity is associated with a reduction in the diversity of C. acnes strains compared to healthy individuals [87–89]. However, no significant differences in the distribution of C. acnes strains were found between patients with mild (n = 29) and severe acne (n = 34) [90].

The clinical manifestation of acne can vary depending on the severity, type, and number of predominant lesions, greatly affecting quality of life [2]. Patients typically exhibit pleomorphism in their lesions, which can be classified as inflammatory or non-inflammatory [7]. Treatment is tailored to the severity of the condition, ranging from mild comedonal acne to severe inflammatory forms.

The diagnosis of acne is mostly clinical, relying on the recognition of the typical skin lesions, whether inflammatory or not. Accurate assessment scales are crucial for effective treatment and management. Several grading systems for assessing acne severity have been developed, including the Pillsbury scale, Leeds acne grading system, Cook’s acne grading scale, Global Acne Grading System, and the investigator’s global assessment, among others [91]. Emerging technologies, such as artificial intelligence, hold promise for enhancing acne assessment and developing advanced grading systems [92].

Comedonal lesions are a hallmark of acne, with both open and closed comedones generally accompanied by minimal or no inflammation in mild forms. Treatment focuses on preventing pore blockage and addressing these early-stage lesions. Topical retinoids, such as adapalene or tretinoin, regulate keratinization and are effective in reducing comedone formation [93, 94]. Inflammatory lesions, including papules, pustules, and nodules, are tipically associated with more severe forms of acne. In the milder cases, topical treatments like benzoyl peroxide and topical antibiotics (e.g., clindamycin) are used to reduce inflammation and bacterial colonization by C. acnes, often combined with topical retinoids to address comedonal components [93, 95]. If topical therapies are insufficient, oral antibiotics like doxycycline, lymecycline, or minocycline may be added for systemic anti-inflammatory and antibacterial effects [96]. Oral isotretinoin is considered the gold standard for severe acne, addressing excessive sebum production, inflammation, and keratinization abnormalities [93, 97]. Oral antibiotics may be used for patients who cannot tolerate isotretinoin. Hormonal treatments, such as combined oral contraceptives and anti-androgens like spironolactone, can be effective in lowering androgen-driven sebum production [98]. In case of scarring or resistant acne, procedural interventions like chemical peels, laser treatments, or cyst drainage may complement pharmacologic therapies [99–101].

Acne is a multifactorial condition influenced by genetic, hormonal, lifestyle, and environmental factors. Genetics play a significant role, with individuals who have a family history of acne being more likely to experience it themselves, often with earlier onset and greater severity [102, 103]. Acne is also linked to rare genetically determined syndromes, such as PAPA (Pyogenic Arthritis, Pyoderma gangrenosum, Acnes) and other autoinflammatory disorders [103–105]. Hormonal influences and nutritional factors also contribute to acne development and exacerbation [13, 106]. Hormonal fluctuations, especially during puberty, stimulate sebaceous glands to produce excess sebum, leading to clogged pores and bacterial overgrowth [107]. Women may also experience hormonal acne during menstrual cycles, pregnancy, or due to conditions like polycystic ovary syndrome (PCOS). Lifestyle factors further modulate acne risk [108]. Like other inflammatory skin diseases, metabolic factors play a role in acne pathogenesis, with conditions like diabetes, metabolic syndrome and obesity often being comorbidities [109]. Stress can exacerbate acne by influencing hormones and inflammation, while improper skincare, such as using comedogenic products, may worsen skin congestion [110, 111]. Environmental factors like humidity, pollution, and exposure to oils or chemicals can also trigger or worsen acne [112]. Recognizing these risk factors is essential for understanding the acne’s complexity and tailoring prevention and treatment strategies.

As of now, approximately 900 studies are ongoing in the field of acne treatment (https://clinicaltrials.gov) with several specifically focusing on dietary interventions.

The understanding of acne as a food-related disease has evolved significantly. In the 19th and early twentieth centuries, acne was often attributed to poor dietary choices, with foods like chocolate, fried items, and sweets commonly blamed for breakouts. This view was largely anecdotal, rooted in broader ideas about diet and health. By the mid-twentieth century, studies like those conducted by Fulton and colleagues dismissed the role of diet, asserting that acne was primarily driven by hormonal and genetic factors [113, 114]. As a result, patients were frequently told that diet had no impact on their skin. However, by the late 1990s and early 2000s, new research revisited the diet-acne connection,identifying potential links between high-glycemic diets, dairy consumption, and acne severity [115, 116]. High-glycemic foods were found to exacerbate acne by increasing insulin levels and triggering hormonal changes, while dairy products were implicated due to hormones and bioactive molecules that may influence oil production and inflammation [117, 118]. Today, diet is recognized as one of many factors influencing acne, though the exact relationship remains complex and is not universally agreed upon [119, 120]. Modern perspectives emphasize the need for personalized approaches and caution against overstating the dietary impacts, despite growing public interest in "skin-friendly" diets fueled by social media and wellness trends, which sometimes lead to misinformation or restrictive eating habits [121, 122].

The importance of diet in acne is supported by the role of obesity in its development and exacerbation [123]. One key link between obesity and acne is the effect of excess body fat on hormonal activity. Obesity is associated with increased levels of androgens and insulin-like growth factor 1 (IGF-1), both of which stimulate sebaceous gland activity and promote the production of sebum, a key factor in acne development [109, 124]. Elevated IGF-1 levels, often seen in individuals with obesity, also influence keratinocyte proliferation, increasing the likelihood of follicular occlusion and comedo formation [102, 125]. Obesity is also associated with a pro-inflammatory state due to the chronic release of inflammatory cytokines such as IL-1, IL-6 and TNF-α from adipose tissue [126, 127]. Cytokines have also been implicated in acne pathogenesis [128]. The connection between obesity and dietary habits, such as the consumption of high-glycemic foods and dairy, may further exacerbate acne by causing hormonal fluctuations and increasing inflammation. Obesity may also influence acne indirectly through psychological and lifestyle factors. Thus, obesity contributes to acne through hormonal dysregulation, chronic inflammation, and lifestyle factors, underscoring the importance of addressing diet and weight management as part of a comprehensive acne treatment plan.

It is now well established that, in addition to genetic and hormonal factors, nutrition plays a central role in the onset and exacerbation of acne [66, 119]. Scientific evidence has clarified the bidirectional role of nutrition, showing that high-glycaemic index foods, fats, dairy products, and chocolate negatively affect acne, while fruit, vegetables, and PUFAs offer protective benefits [119]. The negative effects of certain foods are primarily associated with hyperinsulinaemia and increased IGF-1 levels, which stimulate androgen production and, in turn, sebum production. Diets rich in these foods appear to promote inflammation and comedogenesis through activation of mTORC1 and suppression of FOXO1. Similarly, hyperinsulinaemia leads to a reduction in IGFBF-3, stimulating cell proliferation and worsening clinical acne outcomes [119]. Lower IGF-1 levels have been observed in patients with acne who have high adherence to the MD compared to those with low adherence [129]. In contrast, diets rich in low-glycaemic foods and antioxidant, such as the MD have been shown to protect against acne. In a case–control study, the role of MD, evaluated using PREDIMED score, was investigated in 51 patients matched with 51 controls [130]. The authors first observed that the PREDIMED score was significantly lower in patients with acne than in controls. Patients generally followed a less healthy diet, characterised by lower consumption of fruit and vegetables, pulses, fish and nuts. Adherence to MD, therefore, was the major determinant of disease severity, as assessed using the global acne grading system (GAGS) score. This observation was corroborated by an inverse correlation between PREDIMED score and GAGS. Regarding individual PREDIMED items, low GAGS score values were significantly associated with higher odds ratios for the consumption of fruit, EVOO and fish. Finally, using receiver operating characteristic analysis, the authors identified a PREDIMED score value of ≤ 9 as a cut-off for the identifying patients with higher GAGS scores [130]. Further studies in this area show conflicting results. On one hand, a study of 121 university students with acne, compared with 121 healthy controls, showed that although low MD adherence (assessed with the 14-Item Mediterranean Diet Adherence Screener, MEDAS) was found in the highest percentage of both cases and controls, there was no significant association between MEDAS and acne diagnosis or severity [131]. On the other hand, in line with Barrea's observations, a study of 40 French women with acne reported a significant negative correlation between PREDIMED and Global Evaluation Acne Severity score [132].

Table 1 reports the main studies that have investigated the role of the Mediterranean diet on acne.

Hidradenitis Suppurativa

HS, or acne inversa, is a chronic inflammatory skin condition that affects around 1% of the global population [3]. It typically affects areas of the body rich in apocrine glands, such as the armpits, breasts, groin, genitals, and anal regions [4]. Clinically, HS is characterized by painful subcutaneous nodules, abscesses, and scarring, often emerging after puberty [133, 134]. Due to its chronic and painful nature, HS significantly impacts the quality of life for those affected [135, 136].

Diagnosis of HS primarily relies on observations of lesion, and a total body skin examination is required to assess the severity and extent of the disease. The Hurley score, introduced in 1989, is the first severity scoring system and is widely used in clinical practice [137]. It allows for quick classification based on clinical findings: Stage I, which involves single or multiple abscesses without scars or sinus tracts; Stage II, with recurrent abscesses and sinus tracts/scarring; and Stage III, with diffuse lesions interconnected by sinus tracts throughout the affected area. While easy to use, the Hurley score is static and not ideal for assessing disease progression or treatment response. For these purposes, the Sartorius score system is more suitable [138], although it is not commonly used in clinical practice. More recent scoring systems have emerged, such as the Physician Global Assessment (PGA) for HS [139], which evaluates lesions on a scale from clear to very severe (depending on visible abscesses, tunnels, drainage and inflammatory nodules), and the International Hidradenitis Suppurativa Severity Score System (IHS4), which counts the number of inflammatory nodules, tunnels, and abscesses [140]. Additional scoring systems are also used in clinical trials [141]. Other tools assess tools the impact on quality of life, among other factors. Despite the availability of new tools, there remains insufficient precision in HS assessment, making it difficult to track treatment progress and compare study outcomes. For instance, current scoring systems fail to account for non-visible or deeper inflammatory activity. Therefore, identifying relevant blood biomarkers is essential for more accurate severity assessment, treatment selection, and follow-up.

The pathophysiology of HS involves follicular occlusion, inflammation, immune system dysregulation, bacterial infection and colonization, abnormal secretion from apocrine glands, and alterations in antimicrobial peptide expression [4]. Chronic inflammation is a key feature, often exacerbated by concurrent endocrine and metabolic disturbances such as obesity [142, 143]. HS has an autoinflammatory nature, linked to a deficiency in the Notch signaling pathway, which leads to the conversion of hair follicles into keratin-rich epidermal cysts and stimulates innate immunity through Toll-like receptor (TLR) pathways, thereby sustaining chronic inflammation [144–146].

Skin lesions in HS show increased levels of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-17, which are primarily produced by macrophages and dendritic cells and promote Th17 cell polarization [4, 5]. TNF-α plays a central role in HS, and its expression levels correlate with disease severity [147, 148].

HS is also closely associated with various endocrine disorders, such as obesity, PCOS, and thyroid dysfunction [149]. In HS patients, particularly those with obesity, there is an imbalance in adipokine expression, resulting in elevated levels of pro-inflammatory adipokines like resistin and leptin, and reduced levels of anti-inflammatory adiponectin, further exacerbating inflammation [150, 151]. The dysregulation of adipokines, such as leptin and resistin (associated with obesity), combined with reduced adiponectin levels (linked to insulin resistance), highlights the endocrine and metabolic disturbances in HS [152, 153]. Additionally, obesity contributes to vitamin D deficiency, which is crucial for immune modulation and skin homeostasis, influencing epidermal differentiation, proliferation, and immune response regulation [154]. Patients with HS often have lower vitamin D levels, which are associated with increased disease severity and inflammation [155]. Vitamin D deficiency may also link HS to other conditions, such as PCOS, as it is frequently observed in patients with both conditions [155].

The relationship between vitamin D and the development and outcomes of HS has been extensively studied [156, 157]. Research suggests that vitamin D supplementation can improve clinical outcomes in HS [156, 157]. For example, Guillet et al. [158] reported therapeutic success in 11 (79%) out of 14 supplemented patients, with a reduction in the number of inflammatory nodules. Similarly, Fabbrocini et al. [159] observed a significant reduction in symptoms in 27 (75%) of 36 supplemented patients, indicating decreased disease severity. In another study, Lim et al. [160] conducted a randomized controlled trial in which patients with HS received vitamin D supplementation for two months, resulting in a 34.6% decrease in the number of inflammatory lesions compared to the placebo group (p < 0.05). Vitamin D appears to influence immune regulation by promoting the production of antimicrobial peptides in sebocytes, exerting anti-inflammatory effects in skin conditions [161]. These findings suggest that vitamin D may play a vital role in treating HS and other inflammatory skin diseases by reducing inflammation. However, further research is needed to determine optimal dosing and assess the protective effects of vitamin D supplementation in managing HS.

Treatment options for HS are limited, mostly off-label, and often require surgical interventions to achieve remission [4]. Currently, adalimumab is approved for HS, with its efficacy and safety supported by several clinical trials and real-world data [162–164]. Secukinumab has also shown promising results in both clinical trials and real-world studies [165, 166]. Recently, the European Commission approved secukinumab for adults with active moderate-to-severe HS who have not responded adequately to conventional systemic therapies [165]. However, these treatments do not provide a definitive solution for resolving the disease. Therefore, identifying new therapeutic targets is essential, who may need adjusted medication doses, similar to those with psoriasis. Frew and colleagues [167] studied data from 578 participants with HS in the PIONEER Phase 3 trial and found that those who were overweight or obese had significantly lower chances (58% and 67%, respectively) of achieving a clinically meaningful response compared to those with a BMI under 25. These results indicate that BMI plays a crucial role in treatment outcomes and underscore the variability in disease severity and response to adalimumab.

Hormonal factors are thought to play a role in the pathogenesis of HS, although the relationship remains complex. From an immunological perspective, sex hormones such as estrogens and androgens can influence skin immune responses, including the activation of the inflammasome and the enhancement of Th1/Th17 responses [149]. However, the exact mechanisms underlying this connection are not yet fully understood.

Thyroid dysfunction is commonly observed in patients with HS and may impact disease severity and management [168, 169]. A meta-analysis of case–control studies, including 36,103 individuals with HS and 170,517 control subjects, found a significant association between HS and thyroid disease, with an odds ratio of 1.36 (95% CI: 1.13–1.64, I² = 78%, p = 0.001). In a case–control study by Rached et al. [169], which involved 160 participants (108 HS patients and 52 age- and sex-matched controls), no significant link was found between HS severity and thyroid hormone levels or antibodies (p > 0.05). However, regardless of hypothyroidism, HS patients exhibited lower FT4 levels and reduced thyroid secretory capacity (SPINA-GT). Smoking HS patients had significantly higher levels of TSH receptor autoantibodies (TRAb) compared to non-smokers (median: 1.18 vs. 1.08; p = 0.042). Additionally, the prevalence of subclinical hypothyroidism was notably higher in the HS group. These findings suggest that HS should be considered in a dermato-endocrinological context to guide more effective therapeutic strategies.

As with other dermato-endocrine disorders, diet plays a crucial role in the management of HS, exerting bidirectional effects [66, 170]. The inflammatory processes underlying the pathogenesis of HS appear to be exacerbated by the consumption of foods rich in simple carbohydrates (e.g. fructose), cholesterol, saturated fatty acids, and trans-fatty acids, while they are counteracted by the regular intake of foods rich in MUFAs, PUFAs and polyphenols [66, 170]. It seems clear that a Mediterranean-style nutritional approach significantly contributes to the improvement of clinical outcomes in HS, as demonstrated by observational studies that have reported a negative relationship between adherence to the MD and disease severity [171–173].

Among the first studies to investigate the role of the MD in this clinical context, Barrea et al. (2019) [171] conducted a cross-sectional study involving 41 treatment-naive patients with HS and an equal number of controls. This study revealed two important observations: (i) patients with HS had lower adherence to the MD (assessed by the PREDIMED score) than controls, and (ii) adherence to the MD was negatively correlated with disease severity (assessed by the Sartorius score). The PREDIMED score had the greatest influence of the Sartorius score, suggesting the central role of diet in disease progression. Based on this, the authors proposed that a PREDIMED score ≤ 5 might predictive a higher Sartorius score. To further understand the relationship between diet and disease severity, the nutritional characteristics of the participants' habitual diets were analysed. It was found that patients with HS, compared to controls, followed a dietary pattern characterized by lower intake of complex carbohydrates, MUFAs and omega-3 fatty acids, and higher consumption of saturated fatty acids and omega-6 fatty acids, despite consuming the same total calories [171]. These findings were later confirmed by other studies. Specifically, a case–control study demonstrated that adherence to the MD (assessed by Med Diet Score) was lower in 35 patients with HS compared to healthy controls [172]. Similarly, a larger cross-sectional study confirmed the inverse association between the PREDIMED score and disease severity (assessed by International Hidradenitis Suppurativa Severity Score System), and when analysing the 14 items of the MD adherence questionnaire, it was found that the use of EVOO and a preference for poultry over red meat were the key factors influencing this correlation [173].

Taken together, these studies suggest that the MD significantly influences the severity of HS, primarly through its anti-inflammatory and antioxidant effects, which are exerted both via modulation of the intestinal microbiota [174, 175] and at the systemic level due to its intrinsic nutritional components. Specifically, the regular consumption of complex carbohydrates and reduced intake of simple carbohydrates modulate pathways involving IGF-1, FOXO1, and mTORC1 [174, 176, 177], while the direct effects of MUFAs, omega-3 fatty acids, and polyphenols help counteract inflammation and oxidative stress [173], and contribute to immunomodulation [178].

Table 1 summarizes the main studies that have investigated the role of the MD in HS.

Prescription of the Mediterranean diet in Dermatological Clinical Practice

Although the MD is well-established and widely practiced in most countries around the Mediterranean basin, its adoption in clinical practice can be challenging if not tailored to the individual's daily life [21]. Therefore, it is essential for physicians and nutritionists to prescribe a Mediterranean-type MNT that incorporates the patient's dietary habits and preferences to improve adherence. This approach avoids simply providing patients with lists of foods to include or eliminate, which can be difficult to follow. Instead, the focus should be on educating the patient about the basic principles of the MD and offering a nutritional plan that aligns with these principles. The role of the physician and nutritionist is, therefore, to create personalised Mediterranean-type plans. The following suggestions can help guide this process:

• Develop diet plans based on the individual’s nutritional and metabolic needs: In cases of co-existing obesity and/or endocrine-metabolic disorders, a calorie deficit of 500–750 kcal/day is recommended to promote weight loss, in line with official guidelines [179, 180].

• Ensure an optimal macronutrient distribution: According to the MD, daily calorie intake should consist of approximately 30% fat (with no more than 9% saturated fatty acids), ~ 15–16% protein (preferably from lean animal sources and plant-based proteins), and the remaining percentage carbohydrates (preferably complex, whole-grain carbs) [16].

• Promote proper fiber intake: Given their role in maintaining a low glycemic index for meals and the overall daily diet, fiber intake should be between 25 and 30 g per day.

• Modulate the intake of Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols (FODMAPs): Recent studies have shown that certain dermato-endocrine disorders, such as HS, share pathological features with intestinal conditions like irritable bowel syndrome and inflammatory bowel disease, where leaky gut may trigger both systemic and local symptoms. For this reason, a Mediterranean-style low-FODMAP diet has been suggested as an effective MNT for managing these disorders [181].

• Ensure adequate intake of specific nutrients for skin health: Focus on foods that provide essential nutrients such as MUFAs, PUFAs (especially omega-3), vitamin D, A, B12, zinc, and selenium. Recommended foods include EVOO, cold-water fish, flaxseed, chia seeds, evening primrose oil, pumpkin seeds, brewer's yeast, legumes, whole grains, fruits, and vegetables. If needed, supplementation should be considered [181, 182].

• Divide the daily diet into multiple meals: A diet plan that includes breakfast, a mid-morning snack, lunch, a mid-afternoon snack, dinner, and possibly a portion-controlled, balanced post-dinner snack is recommended [183]. This strategy helps control emotional eating episodes and reduces the glycaemic load (and consequently the glycemic index) of the individual meals. Additionally, a multi-meal approach allows for better protein distribution throught the day, aiding in its absorption [184].

• Educate on the avoidance of specific foods: Without being overly restrictive, it’s important to educate the patient on avoiding regular or large portion consumption of foods that may negatively impact skin health. This includes foods high in saturated fatty acids (e.g., dairy products and red meat), irritants (e.g., spicy foods), nerve stimulants (e.g., tea, coffee, chocolate), and alcohol [181, 182].

Conclusion

In conclusion, the Mediterranean diet is a promising complementary strategy for managing chronic inflammatory skin disorders, contributing to both clinical improvement and overall metabolic and cardiovascular health. Incorporating dietary education and tailored nutrition recommendations into patient care can enhance treatment outcomes and support long-term disease management, making it an essential aspect of a holistic approach to these conditions.

Author Contribution

E. S. and L. B. drafted and revised the manuscript. G. A. and L. V. wrote the main manuscript text and prepared the Table 1. The literature review and manuscript writing involved also A.Z., G.M., C.A., and A.P. All authors have read and approved the final version.

Funding

This study was funded by the Italian Ministry of Health, Current Research Program RC 2025.

Data Availability

No datasets were generated or analysed during the current study.

Declarations

Conflicts of Interest

The authors declare no competing interests.

Human and Animal Rights and Informed Consent

This article does not not contain any studies with human or animal subjects performed by any of the authors.