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Acne during perimenopause develops from the same core mechanisms seen in other life stages, including excess sebum production, abnormal follicular keratinization, clogged pores, and inflammation. However, hormonal fluctuations characteristic of perimenopause can alter sebaceous gland activity in ways that make breakouts more unpredictable. As estrogen levels gradually decline and fluctuate, the relative influence of androgens may become more pronounced. Because androgens stimulate sebaceous glands, this hormonal shift can increase oil production, particularly along the jawline, chin, and lower face.
Perimenopause is marked by irregular hormonal patterns rather than a steady decline. Estrogen levels may vary significantly from month to month, while progesterone and androgen activity can shift in response. Even if total androgen levels are not elevated, increased sensitivity of sebaceous glands to these hormones may contribute to oily skin and clogged pores. In some individuals, skin that was previously balanced may begin to experience blackheads, whiteheads, or deeper inflammatory lesions. At the same time, collagen production declines with age, and the skin barrier may become more fragile, increasing susceptibility to irritation.
Environmental and lifestyle factors can compound these changes. Chronic stress, which is common during midlife transitions, may elevate cortisol levels and indirectly influence oil production and inflammatory signaling. Sleep disruption can further affect hormonal balance. Additionally, skincare routines designed for younger, oilier skin may become too harsh as barrier resilience declines. Overuse of exfoliating acids or aggressive cleansing may disrupt barrier integrity, leading to irritation that worsens inflammation and delays healing.
Management strategies during perimenopause often require balancing acne control with barrier support. Topical retinoids are commonly recommended because they normalize follicular keratinization, reduce clogged pores, and may also support collagen production. However, gradual introduction is important to minimize dryness and sensitivity. Salicylic acid can penetrate oil-rich follicles and assist in dissolving debris, making it useful for comedonal acne. Benzoyl peroxide may help reduce inflammatory lesions linked to bacterial overgrowth, though lower concentrations may be better tolerated. Niacinamide is frequently included in routines because it may help regulate sebum production while reinforcing the skin barrier and reducing visible redness.
For persistent or hormonally driven acne, professional evaluation may be appropriate. Dermatologists may consider prescription-strength retinoids, short-term oral antibiotics for inflammatory control, or hormonal therapies when clinically indicated. Treatment decisions should be individualized, particularly as perimenopausal skin may be more reactive and prone to dryness than adolescent skin.
Realistic expectations are essential. Hormonal fluctuations during perimenopause can make breakouts cyclical and unpredictable. Improvement often requires consistent, gentle care rather than aggressive oil stripping. With a balanced approach that addresses excess sebum, clogged pores, and barrier health, many individuals can achieve meaningful control of acne during this transitional stage. Persistent, painful, or scarring lesions should be evaluated by a qualified dermatology professional to ensure appropriate long-term management
