Acne is an inflammatory skin condition with lesions commonly blamed on increased sebum production, hyperkeratinisation, and colonization of Cutibacterium acnes (formerly called Propionibacterium acnes).
Acne lesions range from noninflammatory open or closed comedones (blackheads and whiteheads) to inflammatory papules, pustules, or nodules. Lesions typically occur on the face, neck, chest, and back, where there is a higher concentration of sebaceous glands. Contributing to acne for adolescents is change in androgenic hormones that stimulates sebum over-production. Sebum can then block hair follicles and result in a lesion. Common treatments for acne include topical and oral antibiotics, in some cases. The risk of antimicrobial resistance is a noted concern.
New acne research, however, has focused on the “gut-brain-skin axis” exploring the intersection of dysbiosis, stress and skin microbiota:
…the cutaneous microbiota in acne patients and acne-free individuals differ at the virulent-specific lineage level. Acne also has close connections with the gastrointestinal tract, and many argue that the gut microbiota could be involved in the pathogenic process of acne.
Emotions play a significant role in the immunobiology of acne:
The emotions of stress (e.g., depression and anxiety), for instance, have been hypothesized to aggravate acne by altering the gut microbiota and increasing intestinal permeability, potentially contributing to skin inflammation.
Research suggests that stress and nervous system deregulation can also promote changes in gut physiology, leading to problems like dysbiosis, intestinal inflammation and permeability, small intestinal bacterial overgrowth (SIBO) and other functional bowel disorders through “…the reduction of gastric acid production, impairment of GI motility and gut mucosal immunity, enhanced bacterial growth and virulence, and the formation of biofilm.”
LWP Bacteria 2
Exocrine System / Body Fluids