INTRODUCTION
Acne vulgaris (AV) is the number one skincare concern of women ages 18-50 years and is in the top 3 complaints dermatologists see in their office, with the prevalence increasing across the globe.1,2 As patients and providers search for effective treatments for such a large portion of the population, the market for treatments is also growing and is expected to increase by 5% compounded annual growth rate by 2030.1
In the pursuit of finding effective therapeutics for AV, conventional medicine has characterized the correlation of pathophysiology of the pilosebaceous unit (PSU) and AV lesion formation with 4 mechanisms: excess sebum production, follicular keratinization causing an obstructed follicular orifice, and the over-proliferation of Cutibacterium acnes, triggering an immune response. With this understanding, options for the management of AV targeting the pathophysiology at the PSU have been developed, from prescription and over-the-counter (OTC) medications to at-home devices.3,4 Current treatment regimens often include azelaic acid, benzoyl peroxide, or retinoids, which all target follicular keratinization, C. acnes proliferation, and inflammation. Oral antibiotics, isotretinoin, hormone therapy, or a combination target all 4 of the underlying mechanisms occurring at the AV lesion site.5
A growing trend in acne management is for a more integrative, systemic approach, driven by both patients and providers. In addition to the local inflammation at the PSU, there is now a growing body of evidence that suggests that AV may be driven by underlying systemic, immune-inflammatory pathways. Some purported mechanisms include: psycho-emotional stress leads to a neuroendocrine response and the release of inflammatory cytokines in the skin; diet and metabolism, such as high glycemic diets, insulin, and aberrant vitamin levels are associated with inflammatory pathways in the skin; dysbiosis of the gut and skin microbiome can lead to the overgrowth of pathogenic microbes, triggering an immune response; excess androgens and hormonal fluctuations may stimulate sebocytes and PSU inflammation; oxidative stress triggered by
In the pursuit of finding effective therapeutics for AV, conventional medicine has characterized the correlation of pathophysiology of the pilosebaceous unit (PSU) and AV lesion formation with 4 mechanisms: excess sebum production, follicular keratinization causing an obstructed follicular orifice, and the over-proliferation of Cutibacterium acnes, triggering an immune response. With this understanding, options for the management of AV targeting the pathophysiology at the PSU have been developed, from prescription and over-the-counter (OTC) medications to at-home devices.3,4 Current treatment regimens often include azelaic acid, benzoyl peroxide, or retinoids, which all target follicular keratinization, C. acnes proliferation, and inflammation. Oral antibiotics, isotretinoin, hormone therapy, or a combination target all 4 of the underlying mechanisms occurring at the AV lesion site.5
While benzoyl peroxide, retinoids, and antibiotics are known to be effective in treating AV, some of these therapeutics are limited in their use as more attention is being paid to the secondary effects associated with their use. For example, dermatologists prescribe antibiotics almost twice as much as providers of other specialties, with strong implications for the rise of antibiotic resistance.6 Additionally, approximately 37% of acne patients discontinue using acne products because of the side effects.2
A growing trend in acne management is for a more integrative, systemic approach, driven by both patients and providers. In addition to the local inflammation at the PSU, there is now a growing body of evidence that suggests that AV may be driven by underlying systemic, immune-inflammatory pathways. Some purported mechanisms include: psycho-emotional stress leads to a neuroendocrine response and the release of inflammatory cytokines in the skin; diet and metabolism, such as high glycemic diets, insulin, and aberrant vitamin levels are associated with inflammatory pathways in the skin; dysbiosis of the gut and skin microbiome can lead to the overgrowth of pathogenic microbes, triggering an immune response; excess androgens and hormonal fluctuations may stimulate sebocytes and PSU inflammation; oxidative stress triggered by
