What causes oily skin?
Excess sebum production—commonly referred to as oily skin—is primarily driven by the activity of the sebaceous glands, which are microscopic oil-producing structures located in the dermis and connected to hair follicles. These glands secrete sebum, a complex mixture of triglycerides, wax esters, squalene, and cholesterol esters that helps maintain skin barrier integrity and hydration. Several interrelated factors influence sebum output:
Hormonal influences play the most significant role. Androgens—including testosterone, dihydrotestosterone (DHT), and dehydroepiandrosterone sulfate (DHEA-S)—stimulate sebaceous gland proliferation and lipid synthesis via androgen receptors expressed on sebocytes. This explains why oily skin often intensifies during puberty, pregnancy, or in conditions such as polycystic ovary syndrome (PCOS) or congenital adrenal hyperplasia.
Genetic predisposition strongly contributes: individuals with a family history of acne or seborrhea frequently exhibit higher baseline sebum excretion rates due to inherited variations in sebaceous gland density, size, and hormonal sensitivity.
Environmental and behavioral factors also modulate sebum secretion. High ambient humidity and temperature can increase surface oiliness—not by boosting sebum synthesis, but by reducing evaporation and enhancing sebum spread across the epidermis. Conversely, over-cleansing or using harsh, stripping agents may trigger compensatory sebum overproduction through feedback mechanisms involving peroxisome proliferator-activated receptors (PPARs) and endocannabinoid signaling.
Other contributors include certain medications (e.g., corticosteroids, lithium, or androgenic progestins), dietary patterns high in refined carbohydrates and dairy (which may elevate insulin-like growth factor 1 [IGF-1] and promote androgen bioavailability), and chronic stress—via cortisol-induced upregulation of sebocyte activity. Importantly, oily skin itself is not pathological; however, when combined with follicular hyperkeratinization and Propionibacterium acnes (now Cutibacterium acnes) colonization, it creates the pathophysiological triad underlying acne vulgaris.