The Gut-Brain-Skin Axis and Role of Intestinal Dysbiosis in Acne Vulgaris: Therapeutic Effects of Probiotic and Prebiotic Use

    January 2018 in “ Elsevier eBooks ”
    Bryan Tungland
    Studysummary This review discusses the complex mechanisms behind acne vulgaris and suggests that dietary modification, along with pro- and prebiotics, may influence its pathogenesis by addressing stress-induced skin inflammation.
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    Research cited in this study 14

    1. Selected Disorders of Skin Appendages: Acne, Alopecia, Hyperhidrosis Medical Clinics of North America · 2015
    2. Dermatological Manifestations of Stress in Normal and Psychiatric Populations Psychiatric Clinics of North America · 2014
    3. Pathways to Inflammation: Acne Pathophysiology European Journal of Dermatology · 2011
    4. Sebocytes’ Makeup: Novel Mechanisms and Concepts in the Physiology of the Human Sebaceous Glands Pflügers Archiv für die gesamte Physiologie des Menschen und der Tiere/Pflügers Archiv · 2011
    5. Is There a Gut-Brain-Skin Axis? Experimental Dermatology · 2010
    6. The Skin as an Endocrine Organ Dermato-endocrinology · 2009
    7. Role of Insulin, Insulin-Like Growth Factor-1, Hyperglycemic Food, and Milk Consumption in the Pathogenesis of Acne Vulgaris Experimental dermatology · 2009
    8. Influence of Substance P on Cultured Sebocytes Archives of Dermatological Research · 2008
    9. Neuronal Plasticity of the Brain-Skin Connection: Stress-Triggered Up-Regulation of Neuropeptides in Dorsal Root Ganglia and Skin via Nerve Growth Factor-Dependent Pathways Journal of Molecular Medicine · 2007
    10. Neuroimmunology of Stress: Skin Takes Center Stage Journal of Investigative Dermatology · 2006
    11. Acne The New England Journal of Medicine · 2005
    12. Neurogenic Inflammation in Stress-Induced Termination of Murine Hair Growth Is Promoted by Nerve Growth Factor American Journal of Pathology · 2004
    13. The Human Skin as a Hormone Target and an Endocrine Gland Hormones · 2004
    14. Stress Inhibits Hair Growth in Mice by Inducing Premature Catagen Development and Harmful Perifollicular Inflammatory Events via Neuropeptide Substance P-Dependent Pathways American Journal of Pathology · 2003