Hormonal imbalance can cause oil glands to overproduce, leading to acne breakouts. Furthermore, hormones can alter skin cells near hair follicles which clog up pores and result in breakouts.
Stress affects acne through multiple mechanisms, including hormonal fluctuations, inflammation, impaired skin barrier function, immune modulation, oxidative stress, insulin resistance, altered skin pH levels and lifestyle changes. Understanding these influences is key in creating more effective acne management strategies.
Androgens
Androgens such as testosterone and dihydrotestosterone modulate sebocyte proliferation, lipid synthesis and sebum secretion via their interactions with androgen receptor (AR), with insulin-like growth factor 1 ligands such as IGF-1 or the PI3 K/Akt/FoxO1/mTOR pathway augmenting these effects further. Acne is further complicated by overactive enzymes type II 17b-hydroxysteroid dehydrogenase/5a-reductase 5a-reductase which convert testosterone to its more tissue active tissue-active form dihydrotestosterone. This increase in androgens is central to its inflammation process.
Acne is often caused by locally produced androgens, with higher incidence during puberty as hormonal changes take effect. Current treatments for acne include medications to decrease production by the adrenal gland or ovary by inhibiting gonadotropin secretion, or by blocking their action at targeted sites in skin (SG). Furthermore, these therapies suppress androgen activity at cellular level either directly via nuclear blockade or increasing levels of SHBG which reduces AR binding.
Insulin
Insulin resistance is an established risk factor for multiple metabolic conditions and forms part of the metabolic syndrome. According to one recent study, an association was observed between insulin resistance biomarkers and acne severity, specifically showing significant correlations between C-peptide and TyG index levels and acne severity.
Insulin regulates sebaceous gland activity by stimulating ovarian and adrenal glands to produce androgens, lowering serum sex hormone-binding globulin levels, stimulating androgen metabolite production and stimulating keratinocyte proliferation and apoptosis and decreasing elastin production.
Although progesterone’s exact role in acne remains controversial, it can certainly be considered preventive as it reduces sebaceous gland activity by inhibiting 5 alpha reductase. Furthermore, progesterone boosts keratinocytes’ production of ceramides while simultaneously decreasing C. acnes-induced TLR2 activation.
Cortisol
Cortisol, the stress hormone, regulates numerous activities within the body. It has an approximately 24-hour rhythm with its highest levels occurring first thing in the morning and gradually decreasing throughout the day to reach their lowest point by evening time. A range of factors, including food intake, alcohol consumption, glucose levels in blood oxygenated tissues such as muscles or organs such as skin or muscle exercise as well as anxiety can impact cortisol secretion; its receptors being most prominently expressed on basal epidermal keratinocytes basal epidermal keratinocytes as well as dermal fibroblasts cells.
Normal stress reactions involve cortisol and adrenaline being released as part of a fight-or-flight response that eventually self-limits when the threat has passed. This system delays nonessential or potentially harmful functions like inflammation responses as well as digestive, reproductive and growth processes that might otherwise otherwise accelerate during times of extreme tension.
Over-active endocrine systems can lead to hyperandrogenism (acne, excess hair growth and hirsutism). Common causes for hyperandrogenism include polycystic ovary syndrome, Cushing’s disease and adrenal androgen secreting tumors.
Estrogen
Estrogen, often referred to as the “sex hormone” among both women and men who menstruate, plays an essential role in sebaceous gland activity. Studies indicate that dysregulation of nuclear androgen receptor (AR) occurs among those suffering from severe acne [6, 11]. Corticotrophin-releasing hormone and cortisol are stress hormones which increase sebaceous gland activity by increasing expression levels for 5a-DHT and transforming growth factor beta (TGFb).
Exposure to multiple EDCs has been found to decrease several enzymes necessary for estradiol biosynthesis, possibly altering its ratio and increasing sebaceous gland activity. Genistein has been shown to restore skin cells’ ability to express TGFb and reduce sebaceous gland activity [78].
Hyperandrogenism plays an integral part in the cause of hormonal acne, often manifesting itself through cysts and nodules. Treatment options for hormonal acne may include androgen receptor blockers such as spironolactone, flutamide, cyproterone acetate or oral contraceptives and anti-androgens such as clascoterone; alternatively limiting dairy consumption while increasing intake of low glycemic plants may help ease symptoms of acne.