Abstract
Acne vulgaris is a common skin disease in industrialized countries with Western diet characterized by high glycemic load and milk consumption. Accumulating evidence underlines the role of Western diet as a major cause of enhanced nutrient-mediated mechanistic target of rapamycin complex 1 (mTORC1) signaling that may over-stimulate sebocyte growth and sebaceous lipogenesis resulting in sebaceous gland hyperplasia, hyperseborrhoea, Propionibacterium acnes overgrowth with biofilm formation and inflammatory follicular reactions. Substantial evidence from translational research suggests that all anti-acne agents operate by a common mechanism: the attenuation of exaggerated mTORC1 signal transduction in the pilosebaceous follicle. Future acne therapy should combine dietary and pharmacological interventions attenuating mTORC1 signaling by a paleolithic-type diet supported with natural or synthetic mTOR inhibitors.
Financial & competing interests disclosure
The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Key issues
• Acne is an mTORC1-driven anabolic and inflammatory skin disease.
• High glycemic load and milk/dairy consumption as well as pro-inflammatory signals enhance mTORC1 signaling.
• Anti-acne agents in clinical use operate by indirect or direct mTORC1 inhibition.
• Future anti-acne drugs are either natural or synthetic mTOR-inhibitors.
• Future acne therapy should be a combination of nutrition therapy with a paleolithic-type diet supported by pharmacological attenuation of enhanced mTORC1 signaling.