A hormonally sensitive skin losing its capacity to sustain regular skin water loss is the fundamental cause of acne. The obstruction of the hair follicle duct is caused by the skin's reaction to excessive trans epidermal water loss, which also causes bacterial colonising, breeding, and feeding under the plug, which results in inflammation and the spot.
Dihydrotestosterone (DHT), a hormone continuously generated as part of the natural breakdown of testosterone throughout the body, is made more sensitive to the skin by underlying physiological changes.
At certain life stages, the skin becomes aware of and sensitised to DHT hormone and this causes a depletion of skin fatty acids; linoleic acid in particular. Sensitivity appears to occur with normal hormonal balance. In 100% of men and 75% of women, there is no change to hormonal levels before, during, or after the acne phase. Apart from women with polycystic ovary syndrome.
This depletion can cause up to a 10 fold reduction in linoleic acid content in the skin and sebum which compromises barrier function increasing trans epidermal water loss (skin loses water faster).
The skin responds to this increase in trans epidermal water loss:
The sebaceous gland in hair follicle increases sebum production to compensate (hyper- seborrhea) - Slows water loss
Increased keratin deposition in skin, thickens and makes skin more impermeable - Slows water loss
Skin cell production and also cell turnover accelerates to thicken the stratum corneum (SC) but as epidermal also line the hair follicle duct (pilo-sebaceous opening) then this causes a narrowing of the duct - Slows water loss.
So in summary, faster skin cell turnover results in more dead skin on the surface. These are mixing with increased oil production trying to get out of a narrowing duct. The dead skin merge with oil, this leads to plugs forming in the hair follicle duct opening – causing acne breakouts.