Acne: Causes

Pathogenesis (development of disease)

Acne vulgaris is a chronic inflammatory disease of the sebaceous glands. Acne is caused by changes in the skin due to hormonal influences such as those that occur during puberty (androgen production ↑). IGF-1 (insulin-like growth factor 1) seems to be important for the stimulation of androgen signaling. IGF-1 increases the amount of androgens (male hormones) formed and the conversion (transformation) of medium-potent (testosterone) to high-potent androgens (dihydrotestosterone, DHT). Furthermore, IGF-1 activates the food and IGF-1 sensitive kinase mTORC1 (mechanistic target of rapamycin complex 1). mTORC1 is considered the cell’s “master regulator” of growth and proliferation. Hyperseborrhea (increased sebum release) and obstruction of the follicular orifices by the increased sebum (follicular hyperkeratosis) occur. This results in comedones (blackheads), which can become inflamed by bacterial colonization with Propionibacterium acnes and thus lead to pustules (pustular vesicles) and other efflorescences (pathological skin changes). The following factors occur in acne:

  • Development of an inflammatory reaction by various factors, especially Propionibacterium acnes → Development of pustules, papules and other secondary efflorescences.
  • Hyperkeratosis of the follicular epithelium (follicular hyperkeratosis) → formation of microcomedones.
  • Seborrhea → formation of comedones (blackheads).

Pathogen-induced acne

Malassezia furfur induced seborrheic eczema ( oily scaly inflammation of the skin) and rosacea (chronic inflammatory skin disease manifesting on the face) due to overgrowth of Demodex mites can mimic an acneiform lesion (acne-like skin change). Lead efflorescences (pathological skin changes that indicate this) here are erythematous papules (circumscribed skin elevation < 1.0 cm in diameter associated with skin redness) with eczema that is more or less severe. Comedones (whitish small skin entities) are absent in both disorders. Hormone-related acne

It is known that elevated serum androgen levels correlate with increased acne incidence (frequency of new acne cases). Syndromal conditions in which determination of serum androgen concentrations is useful include hirsutism (increased terminal hair (long hair) in women, according to the male distribution pattern), androgenetic alopecia (male-type alopecia/hair loss), or menstrual irregularities (see Laboratory Diagnostics for details).Medications associated with elevated serum androgen concentrations see Medications/Hormones below.

Etiology (causes)

Biographic causes

  • Genetic burden – inheritance of skin factors that promote acne, such as seborrhea (oily skin) or the nature of the sebaceous glandsA multivariate analysis shows the likelihood of developing acne:
    • 2.7-fold increased risk if father had acne (OR: 2.70)
    • 3-fold increased risk if mother had acne (odds ratio [OR]: 3.077).
    • 8-fold increased risk if both parents had acne (OR: 7.887).
  • Gender – boys are slightly more likely to be affected than girls.
  • Hormonal factors – especially testosterone serum levels.
    • Puberty

Behavioral causes

  • Nutrition
    • High intake of mono- and disaccharides (monosaccharides and disaccharides), e.g., white flour products, high-sugar beverages; milk and dairy products; saturated fatty acids (contained in animal products); trans fatty acids (e.g., in fast food products, baked goods, chips, snacks, cookies, fried foods)
    • Consumption of a lot of chocolate (OR: 1.276) compared with the lowest quartile of chocolate consumption
    • Milk consumption
      • High milk consumption; skim milk promotes acne more than whole milk
      • Skim milk consumption (milk with 1% and 0% fat content)/teens.
    • Too little fish consumption (omega-3 fatty acids).
    • Low vegetable consumption (phytochemicals, especially polyphenols, which inhibit mTORC1 (see above)).
  • Drug use
    • Methylenedioxyamphetamine (ecstasy)
  • Incorrect skin care
  • Manipulation of papules, pustules
  • Wearing headbands or chin straps

Medication

  • Antibiotics
    • Aminoglycosides (streptomycin)
    • Tetracycline
  • Antiepileptic drugs (quinine, quinidine, phenobarbital, phenytoin).
  • Antipsychotics (neuroleptics).
    • Conventional (Classical) antipsychotics (neuroleptics) – Phenothiazines.
    • Lithium, hydantoin, trimethadone, amineptines.
  • Beta-blockers (propranolol).
  • Bromide
  • DHEA [for women: only in case of overdose!]
  • Disulfiram
  • D-Penicillamine
  • EGF receptor antagonists.
  • Hormones
    • Anabolic steroids (testosterone ester, metandienone, methandrostenolone, metenolone acetate, mesterolone, stanozolol).
    • Androgens
    • ACTH
    • Glucocorticoids (cortisone, hydrocortisone) [steroid acne].
    • Oral contraceptives (depending on the progestin content: higher risk with norethisterone, dydrogesterone, less with desogestrel or levonorgestrel; also more common with contraceptives with low estrogen content) [no acne risk with chlormadinone acetate and cyproterone acetate]
    • Testosterone
    • Testosterone derivatives (danazol)
    • Thyroxine
  • Immunosuppressants (azathioprine, ciclosporin (cyclosporin A))
  • Iodide
  • Leprosy drug (clofazimine)
  • Lithium
  • 8-methoxypsoralen+ UVA
  • Muscle relaxants (dantrolene)
  • Anesthetics (halothane)
  • Retinoids (acitretin, etretinate, isotretinoin).
  • Sedatives (chloral hydrate, diazepam).
  • Thiourea
  • Tuberculostatics (isoniazid, ethambutol, ethionamide, protionamide, rifampicin).
  • Thyrostatic drugs (thiouracil)
  • Cytostatic drugs (actinomycin-D)

Environmental pollution – intoxications (poisonings).

  • Quinine – an alkaloid extracted from cinchona bark.
  • Halogens – these are fluorine, chlorine, bromine and iodine, as well as the element astatine, which is extremely rare and largely unexplored due to its radioactivity.
  • Contact with substances such as oil, pitch or dioxinNote: Dioxin belongs to the endocrine disruptors (synonym: xenohormones), which even in smallest quantities can damage health by altering the hormonal system.