Recent studies have uncovered that unseen (but measurable) inflammatory events precede even the clogging of pores and proliferation of P. acnes that then causes noticeable inflammation. Although it is not completely understood, decades of research and new findings support the theory that the degradation of cell lipids by free radicals may trigger some of the inflammatory reactions of acne. Measurements of lipid peroxidation in comedones show free radical damage is present even at the earliest stages of pimple development and continues to rise dramatically with inflammation as the condition progresses.¹

In fact, controlled studies measuring blood levels of antioxidants show that acne patients have much lower levels of antioxidants and significantly higher levels of free radicals than people without acne—both of which correlate to severity of the condition. Studies have shown that not only do acne patients produce about 59% more sebum than healthy controls, but the sebum from those with acne contain significantly greater amounts of the lipid squalene. Squalene peroxide free radicals were shown to promote certain inflammatory processes that are linked to acne inflammation, even without P. acnes.¹

All of these findings may explain the results of clinical studies that demonstrate the effectiveness of retinoids (e.g., isotretinoin) and antioxidants like green tea catechins against acne. Retinoids strongly inhibit the production of these lipid free radicals, and catechin antioxidants help prevent the decrease in blood antioxidant enzymes by scavenging for these free radicals.¹

Inflammation in acne has also recently been implicated in scarring from acne. Studies show that patients prone to scars from acne exhibit a delayed immune response and a chronic sensitivity reaction. This causes different types of inflammatory responses than those in patients not prone to scars.²