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These patients experienced shorter menstrual cycles post-treatment without adverse reactions, offering a new therapeutic option for those unsuitable for hormone therapy [188]

Here's how the cascade typically unfolds: Genetic Predisposition Sets the Stage: You inherit genes that make your skin barrier less effective or your immune system more reactive [4] Hormones Create the Environment: Androgens stimulate sebaceous glands, producing the oily environment Malassezia loves [1] Malassezia Thrives: In this oil-rich environment, Malassezia populations grow and produce irritating byproducts [5] Barrier Breakdown Begins: Fatty acids from Malassezia metabolism start damaging your skin barrier Immune System Activates: Dendritic cells detect the threat and trigger inflammation [6] Inflammation Damages Further: The inflammatory response itself damages surrounding skin cells Barrier Function Worsens: Damaged skin can't protect itself, allowing more irritants to penetrate Cycle Continues: Poor barrier function leads to more Malassezia penetration, more inflammation, more damage

On the other hand, the levels of the C-C motif chemokine ligand 2 (CCL2) were downregulated following sertraline and irradiation treatment ( p = 0.0279)

a 55% increase compared to the prior year

mBio 12:e02401-20