R SKIN CARE 97


H O


WAX ESTER 26%-30%


CHOLESTEROL 1-3%


TRIGLYCERIDE 30-55%


HO O Figure 4: The main lipid components of normal human sebum


acnes. These recent results suggest a pathway whereby oxidation of squalene by follicular epithelium may trigger a series of cellular events that lead to both a chronic inflammatory response and overgrowth of C. acnes, the hallmarks of acne. Clinical studies have supported the


experimental evidence for a key role of squalene peroxides. Tochio et al found that the contents of lipid peroxides and the inflammatory cytokine IL-1α were raised in comedones relative to the adjacent stratum corneum of the same subjects.39 Capitanio et al reported that squalene


peroxides in comedones and IL-1α in sebum were raised in mildly affected sufferers,40 and that application of a vitamin E-retinoid combination reduced both, accompanied by clinical improvement, despite no change in sebum or squalene secretion. Plasma levels of malondialdehyde, an advanced lipid peroxidation product, are raised on average by almost five-fold in acne sufferers.41 Furthermore, in the only randomised


controlled trial of its type to date, significant reductions in acne severity were observed


during treatment with oral or topical simvastatin, an inhibitor of squalene (and cholesterol) synthesis by reducing HMG CoA reductase activity.42 If oxidised squalene is the true initiator of the chain of cellular, biochemical, and immune events that leads to acne, one would expect molecules that neutralise their effects would reduce the lesions. Preliminary evidence that this may be the case has been obtained in a pilot study of palmitoyl tetrapeptide-114, a small peptide that binds lipid peroxides.44 Commencing two weeks after stopping all


other treatment, 24 acne sufferers applied a cosmetic serum containing the peptide twice daily to one side of the face. The numbers of comedones were quantified objectively by digitization of images generated by a Bio3D structured-light scanner (Bionos Biotech SL, Valencia). The results showed that after 28 days the number of lesions on the treated side was reduced by 15% relative to the untreated side (P<0.01).


Conclusion Discussion of the relative roles of sebum and


C. acnes infection in the aetiology of acne has a long history. The presence of the organism in inflamed pilosebaceous units was first described by Gilchrist in 1900,45


but it was not


until 1986 that Saint-Leger et al detected the presence of oxidised squalene.46 After finding that the lesions with the


highest concentrations also contained the greatest numbers of C. acnes (and the lowest concentrations of squalene), they proposed that oxidation of squalene in some way creates the conditions for overgrowth of the bacterium. In the absence of sufficient evidence for or against the hypothesis, the debate has continued on and off ever since. Although the body of evidence is still not


enough to unequivocally convict squalene peroxidation as the villain, Saint-Leger‘s original idea has never been stronger. Hopefully, further basic and clinical research in the near future will resolve the issue.


References References for this article can be found online at https://personalcaremagazine.com/story/46741/ do-squalene-peroxides-cause-acne-references


SQUALENE 12-20%


O


FATTY ACIDS 15-30%


C=O H O O H O O O


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PC


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