Acne and its causes

Acne develops as a result of blockages in follicles. Hyperkeratinization and formation of a plug of keratin and sebum is the earliest change. Enlargement of sebaceous glands and an increase in sebum production occur with increased androgen (DHEA-S) production at adrenarche. The micro comedo may enlarge to form an open comedo (blackhead) or closed comedo (whitehead). In these conditions the naturally occurring largely commensurable bacteria Propioni bacterium acnes can cause inflammation, leading to inflammatory lesions (papules, infected pustules, or nodules) in the dermis around the microcomedo or comedo, which results in redness and may result in scarring or hyper pigmentation. Exactly why some people get acne and some do not, is not fully known. It is known to be partly hereditary. Several factors that are linked to acne are:

Family/Genetic history:
The tendency to develop acne runs in families. For example, school-age boys with acne have other members of their family with acne. A family history of acne is associated with an earlier occurrence of acne and an increased number of retention acne lesions.

Hormonal activity:

  • Stress through increased output of hormones from the adrenal (stress) glands.
  • Hyperactive sebaceous glands, secondary to the three hormone sources above.
  • Accumulation of dead skin cells.
  • Bacteria in the pores, Propionibacterium acnes is the anaerobic bacterium that causes acne. In-vitro resistance of P. acnes to commonly used antibiotics has been increasing.
  • Skin irritation or scratching of any sort will activate inflammation.
  • Use of anabolic steroids.
  • Any medication containing halogens (iodides, chlorides, bromides), lithium, barbiturates, or androgens.
  • Exposure to certain chemical compounds. Chloracne is particularly linked to toxic exposure to dioxins, namely Chlorinated dioxins.

Several hormones have been linked to acne such as the androgens testosterone, di-hydro-testosterone (DHT) and de-hydro-epi-andro-sterone sulfate (DHEAS), as well as insulin-like growth factor 1 (IGF-I). In addition, acne-prone skin has been shown to be insulin resistant.

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