Existing evidence suggests that its pathogenesis may be associated with dysregulation of the neuro-hormone-immune network within the skin-gut-brain axis framework. In erythematotelangiectatic rosacea, glucocorticoid resistance within keratinocytes may induce CCL20-driven Th17 inflammation, while catecholamines released by sympathetic nerves are associated with neurovascular flushing. Ocular rosacea is associated with gut-derived low-grade systemic inflammation and neurogenic inflammation.
Relevant if you experience acne and rosacea.
If you're targeting acne, this research adds to the evidence base, look at the key findings for the mechanism the study describes.
Translated from this study's findings, not a personal prescription. Pair with your existing protocol and your practitioner's guidance.
1. Drug Des Devel Ther. 2026 Jun 16;20:608151. doi: 10.2147/DDDT.S608151. eCollection 2026. Neurohormonal-Immune Dysregulation in Rosacea: Emerging Perspectives from the Skin-Gut-Brain Axis. Shi L(1), Li S(1), Yao X(1), Zhang Z(2), Dong Q(2), Zhang H(1), Wang X(1), Bai J(1), Han H(1), Fu X(2), Zheng K(1), Liang L(1)(2).
1. Drug Des Devel Ther. 2026 Jun 16;20:608151. doi: 10.2147/DDDT.S608151. eCollection 2026. Neurohormonal-Immune Dysregulation in Rosacea: Emerging Perspectives from the Skin-Gut-Brain Axis. Shi L(1), Li S(1), Yao X(1), Zhang Z(2), Dong Q(2), Zhang H(1), Wang X(1), Bai J(1), Han H(1), Fu X(2), Zheng K(1), Liang L(1)(2). Author information: (1)The Cosmetic and Plastic Surgery, Department of Shanxi Provincial People' s Hospital, Shanxi Medical University, Taiyuan, 030012, People's Republic of China. (2)The Third Clinical College, Shanxi University of Chinese Medicine, Taiyuan, People's Republic of China. Rosacea is a chronic inflammatory skin disease with a global prevalence of approximately 5.1%. Existing evidence suggests that its pathogenesis may be associated with dysregulation of the neuro-hormone-immune network within the skin-gut-brain axis framework. This review summarizes the potential roles of stress hormones, sex hormones, and insulin-like growth factor-1 in the four major subtypes. In erythematotelangiectatic rosacea, glucocorticoid resistance within keratinocytes may induce CCL20-driven Th17 inflammation, while catecholamines released by sympathetic nerves are associated with neurovascular flushing. In papulopustular rosacea, androgen excess, relative estrogen deficiency, LL-37-mediated innate immune activation, and gut microbiota dysbiosis may collectively contribute to the formation of inflammatory skin lesions.In the phymatous type, insulin-like growth factor-1 and androgens may interact through the PI3K/Akt/mTOR and FoxO1 pathways, promoting sebaceous gland hyperplasia and fibrosis. Ocular rosacea is associated with gut-derived low-grade systemic inflammation and neurogenic inflammation. For treatment, β-receptor blockers such as carvedilol and selective serotonin reuptake inhibitors such as paroxetine can be used for erythematotelangiectatic rosacea; anti-androgen drugs like spironolactone and metformin may be explored for papulopustular rosacea; metformin for the phymatous type; and for ocular rosacea, topical corticosteroids can be used cautiously for a short term under ophthalmological supervision. Adjunctive interventions such as eradication of small intestinal bacterial overgrowth, a low glycemic index diet, and mindfulness-based stress reduction therapy also demonstrate potential.Taken together, existing evidence supports viewing rosacea as a systemic disease potentially mediated by the skin-gut-brain axis and characterized by dysregulation of the neuro-hormone-immune network. However, more high-quality randomized controlled trials and stratified studies guided by hormone-related biomarkers are currently needed to further validate its mechanisms and advance precision treatment. © 2026 Shi et al. DOI: 10.2147/DDDT.S608151 PMCID: PMC13282955 PMID: 42325915 [Indexed for MEDLINE] Conflict of interest statement: The authors report no conflicts of interest in this work.
Original source →Recent preclinical studies have shown that nicotinamide adenine dinucleotide (NAD+) plays a critical role in molecular mechanisms of axon degeneration, and reductions in NAD+ levels are associated with axonal degeneration. Nicotinamide riboside (NR) is a safe and widely available pyridine-nucleoside form of vitamin B3 and is an NAD+ precursor. To investigate if oral supplementation of synthetic NR can act as a therapeutic agent to prevent degeneration of small somatic sensory axons innervating the skin or promote regeneration of these same fibers in humans, we utilized a validated experimental model of cutaneous nerve degeneration and regeneration and conducted a placebo-controlled, double-blinded Phase 2 study.
Nicotinamide (NAM) and Polypodium leucotomos extract (PL) have demonstrated photoprotective effects, but their role in preventing UVA-induced DNA damage in humans remains unclear. To evaluate the effects of oral NAM and PL on UVA-induced erythema and thymidine dimer (TT-dimer) formation. In this intraindividual trial, 50 healthy volunteers (phototypes I-III) were randomized (1:1) to receive either NAM (2000 mg daily) or PL (Heliocare Advanced: 480 mg daily) for 30 days.
Friedreich's ataxia is a rare, chronic, progressive, neurodegenerative condition affecting multiple organ systems, including neurological, musculoskeletal, cardiac, and endocrine systems, and is marked by low cardiopulmonary fitness. We tested the effect of exercise and NAD+ precursor supplementation with nicotinamide riboside, which have each shown benefits in animal and early clinical studies, on cardiopulmonary fitness in individuals with Friedreich's ataxia. This 12-week, outpatient, phase 2, single-site (Children's Hospital of Philadelphia, Philadelphia, PA, USA), randomised, 2 × 2 factorial clinical trial recruited individuals aged 10-40 years with an ejection fraction of 45% or greater who were able to exercise.
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