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Dermatology and Skin Diseases · Journal article
Journal of Cutaneous Medicine and Surgery · August 13, 2026
Raises a question worth testing. It does not answer one.
This narrative review integrates mechanistic pathways and correlational observations linking obesity, insulin resistance, and ultra-processed diets to inflammatory skin diseases via adipokine signalling, altered microbiota, and metabolic endotoxemia. The evidence presented is descriptive and hypothesis-generating rather than confirmatory; it proposes a framework for understanding skin inflammation as a manifestation of systemic metabolic dysfunction but does not present definitive clinical trial data or causal proof.
Journal article. Patients with inflammatory dermatoses (hidradenitis suppurativa, acne, psoriasis, atopic dermatitis, acanthosis nigricans, hirsutism, scarring alopecias, intertrigo, chronic idiopathic urticaria); children with atopic dermatitis in the correlational example..
Adipose tissue secretes adipokines and cytokines driving Th1/Th17-skewed chronic inflammation affecting skin Hyperinsulinemia and elevated IGF-1 promote keratinocyte proliferation and sebum production in multiple dermatoses including hidradenitis suppurativa, acne, psoriasis, and atopic dermatitis Fast-food intake ≥3× weekly is associated with increased risk of severe atopic dermatitis in children
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
Dermatologists should consider screening for cutaneous signs of insulin resistance (acanthosis nigricans, acrochordons) and assess lifestyle factors including diet and metabolic status as part of routine care. However, no specific therapeutic recommendations are supported by the evidence presented; GLP-1 agonists are described as emerging and adjunctive only.
A mechanistic review proposing pathways linking metabolic dysfunction to skin inflammation, supported by correlational evidence and emerging data, but lacking primary clinical trial evidence or definitive causal proof.
Quoted from the source exactly as published.
Dermatologists should consider screening for cutaneous signs of insulin resistance (acanthosis nigricans, acrochordons) and assess lifestyle factors including diet and metabolic status as part of routine care. However, no specific therapeutic recommendations are supported by the evidence presented; GLP-1 agonists are described as emerging and adjunctive only.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Inflammatory dermatoses are increasingly linked to systemic metabolic factors. Obesity and insulin resistance create a pro-inflammatory milieu that affects the skin. Adipose tissue functions as an endocrine organ secreting adipokines and cytokines that drive chronic inflammation with notable skewing toward T-helper 1 (Th1)/Th17 signaling. Hyperinsulinemia, elevated insulin-like growth factor-1 promote keratinocyte proliferation, sebum production, and autoinflammation, contributing to a multitude of skin diseases including hidradenitis suppurativa, acne, psoriasis, atopic dermatitis (AD), acanthosis nigricans, hirsutism, scarring alopecias, intertrigo, and chronic idiopathic urticaria. Concomitantly, ultra-processed diets low in fiber and high in additives detrimentally affect the gut-skin axis. Diets rich in emulsifiers, sugars, and fructose alter the gut microbiome and increase intestinal permeability, leading to metabolic endotoxemia and increased systemic inflammation. High-fructose corn syrup in sweetened beverages is metabolized via hepatic fructokinase, promoting de novo lipogenesis and excess uric acid, a cascade implicated in metabolic fatty liver disease and heightened inflammation. These dietary factors have been correlated with aggravated skin diseases, where fast-food intake (≥3× weekly) is associated with increased risk of severe AD in children. Emerging evidence suggests that dietary modifications may help mitigate skin inflammation in select patients. At the same time, the advent of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 receptor agonists may improve metabolic parameters and could represent promising adjunctive therapies in select inflammatory dermatoses. Dermatologists can serve as sentinels, identifying cutaneous signs of insulin resistance (eg, acanthosis nigricans, acrochordons, and other skin diseases driven by insulin resistance) and addressing lifestyle factors as part of routine care.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.