The link between nutrition and skin health is a focal point of modern clinical practice. Diet influences systemic inflammation, oxidative stress, hormonal balance, sebum composition, and the gut microbiome—all of which communicate with the skin through the complex gut-skin axis [2]. As patients increasingly turn to dietary interventions like the ketogenic diet (KD) to improve their skin, skincare practitioners must be equipped with evidence-based insights. What does science actually tell us about the effect of KD on healthy and diseased skin?

Understanding the ketogenic diet and its popularity

A classic KD is a high-fat (70–80% of total calories), moderate-protein, and very-low-carbohydrate (20–50g per day) regimen. When glucose availability is restricted, the liver synthesizes ketone bodies: beta-hydroxybutyrate (BHB), acetoacetate, and acetone. These serve as alternative energy sources, and the resulting state of nutritional ketosis drives the diet's systemic effects [1].

The diet focuses on plant and animal fats, prioritizing olive, coconut, and avocado oils, alongside medium-chain triglyceride (MCT) oils. Essential fatty acids are sourced from nuts like walnuts, macadamias, and almonds. Proteins are derived from fatty fish (salmon, sardines, mackerel), meats (beef, poultry, pork), and eggs—one of the most recommended KD staples. Dairy intake is limited to full-fat cheeses, heavy cream, butter, and unsweetened Greek yogurt. Carbohydrate sources are primarily leafy greens, cruciferous vegetables, avocados, and low-sugar berries like blueberries or raspberries, while ultra-processed foods are strictly avoided [1].

Initially developed to treat drug-resistant epilepsy, the KD is now widely used for type 2 diabetes, obesity, metabolic syndrome, and neurodegenerative disorders. Its significant impact on weight loss and glycemic control has made it a major topic of discussion within the medical community [1].

The state of dermatological research on KD

Despite its widespread use, the dermatological aspects of KD have long remained under-researched. Most data stem from endocrinology or neurology, with few studies focused specifically on the skin. Existing dermatological research is often fragmented, limited by small sample sizes and short durations. There is a notable lack of large-scale randomized controlled trials (RCTs) with standardized dermatological endpoints [1, 3].

Insights from the 2025 Review

A narrative review published in Frontiers in Nutrition systematically synthesized evidence regarding the KD’s impact on four specific conditions: acne, psoriasis, hidradenitis suppurativa (HS), and cutaneous melanoma [1]. The authors also aimed to map the molecular and cellular mechanisms underlying potential therapeutic outcomes. The work reviewed preclinical data (in vitro and animal models) along with human clinical studies, covering literature published through September 2025.

Acne. KD reduces levels of insulin and insulin-like growth factor-1 (IGF-1). This inhibits the AKT/mTOR signaling pathway—a key intracellular regulator of growth and metabolism. This suppression activates the transcription factor FOXO1 (which inhibits cellular lipid synthesis) and reduces SREBP-1-mediated lipogenesis (a protein controlling fatty acid production, including in sebocytes). The practical outcome is decreased sebum production and a potential reduction in comedones and inflammatory lesions [1].

Psoriasis. Meta-analyses and clinical trials suggest that KD helps reduce body mass index and systemic inflammatory markers like IL-6, IL-17, and IL-23. Some studies recorded improvements in the PASI (Psoriasis Area and Severity Index). These improvements are attributed to the diet’s combined effect on metabolic and inflammatory profiles [1].

Hidradenitis suppurativa (HS). Preliminary data from Very Low-Energy Ketogenic Therapy (VLEKT) show a reduction in inflammatory markers—including trimethylamine-N-oxide (TMAO)—and oxidative stress, alongside weight loss. However, the evidence for HS remains limited [1].

Cutaneous Melanoma. Preclinical models demonstrate that KD may slow tumor growth and decrease metastatic potential. One proposed mechanism involves counteracting the Warburg effect—a characteristic of many cancer cells where they depend on intense glucose fermentation even in the presence of oxygen. Restricting carbohydrates may limit glucose availability for this pathway. The modulation of lipid metabolism, specifically increasing sphingomyelin levels, is also discussed [1]. These findings are currently limited to preclinical work and require human clinical validation.

Molecular and cellular mechanisms

The review highlights three primary biochemical pathways through which the KD may exert its effects [1].

Antioxidant Action. Ketone bodies, particularly BHB, activate the Nrf2-Keap1-ARE signaling pathway. This induces antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and heme oxygenase-1 (HO-1), and improves the NAD+/NADH ratio, thereby mitigating oxidative damage to skin cells.

Anti-inflammatory Action. BHB suppresses the activation of the NLRP3 inflammasome and inhibits the NF-κB transcription factor. This results in decreased production of pro-inflammatory cytokines IL-1β and IL-18—a mechanism fundamental to understanding the KD’s potential role in chronic inflammatory dermatoses.

Gut Microbiome Modulation. KD alters the composition of the intestinal flora, typically increasing the Bacteroidetes-to-Firmicutes ratio and stimulating the production of short-chain fatty acids (SCFAs). These SCFAs strengthen the intestinal barrier and reduce systemic inflammation through the gut-skin axis [1, 5].

Safety and adverse events

The KD is a significant physiological intervention with specific skin-related risks.

Prurigo Pigmentosa (often called "keto rash") is a rare but characteristic dermatological side effect. It presents as itchy, erythematous papules usually localized on the trunk. It typically resolves with dietary modification or tetracycline treatment [1].

Nutrient Deficiencies. Prolonged, unmonitored KD can lead to vitamin C deficiency (leading to scurvy), biotin deficiency (presenting as dermatitis), and zinc deficiency (mimicking acrodermatitis enteropathica). These complications underscore the necessity of laboratory monitoring of nutritional status [1].

Clinical perspectives and practical conclusions

The authors emphasize several methodological limitations: most human studies included fewer than 50 participants, lasted only a few weeks, and lacked standardized KD protocols. Much of the data is still grounded in preclinical models, and high-quality RCTs in dermatology are virtually absent [1, 4].

Nonetheless, the review offers a valuable stance for practitioners. The ketogenic diet has a scientifically sound molecular rationale for use in inflammatory dermatoses, particularly acne and psoriasis. However, it should not be viewed as a standalone dermatological treatment and requires medical supervision. Practitioners should monitor levels of vitamin C, biotin, and zinc [1, 3]. Any new skin eruptions in a patient on KD should be differentially diagnosed with prurigo pigmentosa. Moving forward, large-scale randomized trials with standardized protocols are a high scientific priority in this field.

References

1. Chylińska N., Maciejczyk M. Effects of the ketogenic diet on skin—potential benefits and risks. Front Nutr 2025; 12: 1686056.
2. Agrawal S., Tomecki K.J. Diet and skin: a primer. Cutis 2020; 106(5): 278–9.
3. Fomin D.A., McDaniel B., Crane J. The promising potential role of ketones in inflammatory dermatologic disease: a new frontier in treatment research. J Dermatol Treat 2017; 28(6): 484–7.
4. Mansilla-Polo M., Pisquero-Casals J., Morgado-Carrasco D. Popular diets and skin effects: a narrative review—Actas Dermosifilog 2024; 115(4): T374–86.
5. Gurtler A, Laurenz S. The impact of clinical nutrition on inflammatory skin diseases. J Dtsch Dermatol Ges 2022; 20(2): 185–202.