Super sticky dead skin cells that do not slough off as they should and end up sticking together and clogging sebaceous follicles.
Dead skin cells do not slough off at a normal rate, instead accumulating and clogging pores.
When sebum oxidizes, it turns dark, thick and very comedogenic. Why blackheads are black.
Acneic skin is often deficient in linoleic acid, which changes its composition and makes it stickier and thicker than normal sebum and more prone to clogging pores.
Interleukin-1a has been shown to be present in high concentrations in acneic skin and promotes inflammation as well as encourages hyperkeratinization.
Many ingredients touted to kill acne bacteria (such as tea tree oil) in fact only kill type 1, not type 2. Acne bacteria cause inflammation and damage to the skin.
5a reductase is an enzyme responsible for the conversion of testosterone into DHT – the mega-androgen that is primarily responsible for hormonal acne. Inhibiting 5a Reductase effectively halts the effects of testosterone in the sebaceous follicle.
Collagenases are also known as Matrix Metalloproteinases (MMPs). These are enzymes that destroy collagen and contribute to inflamed, painful acne.
Dehydrated skin is inelastic, which contributes to the formation of microcomedones. An impaired skin barrier allows bacteria in while hydration escapes. It also heals wounds more slowly.
Before a blemish is visible, there are multiple factors that are conspiring to create it, including impactions and micro-comedones in the sebaceous follicles and inflammation and hormonal activity in the skin. Diet can play a large role.
When a blemish surfaces, it is important to reduce as much inflammation as possible and give the skin all the wound healing support it needs. The older a person is and the more compromised their skin health is, the slower the healing process is.
After a blemish stops being inflamed and swollen, it can still leave behind a bump, a scar or hyperpigmentation in the form of red or purple dots. At this stage encouraging cellular renewal and dermal matrix protein regeneration is key.
Even after hyperpigmentation fades (months after the blemish initially surfaced), scarring and collagen damage can remain (even invisibly). To the extent it is possible, supporting the key proteins of the dermal-epidermal junction is most beneficial for the skin at this point.
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