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What Is the Endocrine System? Hormones, Glands, and How They Affect Your Skin

Written by: Lindsey Walsh

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Time to read 16 min

Your skin does not operate in isolation. It is in constant communication with your body's hormonal system — receiving signals that regulate how much oil it produces, how quickly it renews itself, how firmly it holds collagen, and how it responds to stress, aging, and environmental challenge. The endocrine system is the body's chemical messaging network, and the skin is one of its most hormone-responsive organs.


Understanding the endocrine system — how it works, which hormones matter for skin, and what happens when it is disrupted — is foundational to understanding why skin changes at puberty, pregnancy, menopause, during illness, under stress, and in response to the endocrine-disrupting chemicals that are increasingly present in the modern environment. It is also foundational to understanding the skin consequences of cancer treatments that deliberately alter hormone levels.

What the Endocrine System Is

The endocrine system is a network of glands and organs that produce, store, and secrete hormones — chemical messengers that travel through the bloodstream to target cells throughout the body, regulating a vast range of physiological processes.


Unlike the nervous system, which communicates through electrical signals at speeds of milliseconds, the endocrine system communicates through chemical signals that may take minutes to hours to produce their effects — but those effects can last for days, months, or years. Hormones regulate growth and development, metabolism, reproduction, sleep, mood, immune function, and the behavior of every organ system in the body — including the skin.


The skin is not a passive recipient of hormonal signals. It expresses receptors for numerous hormones — estrogen, testosterone, cortisol, thyroid hormones, insulin, and others — and it can also produce and metabolize hormones locally. The skin is, in this sense, both a target organ and an endocrine organ. [1]

The Major Glands and What They Produce

The endocrine system is distributed throughout the body. Its primary glands and their skin-relevant hormones:


The Hypothalamus and Pituitary Gland — The Master Regulators

The hypothalamus, located in the brain, and the pituitary gland, just below it, form the control center of the endocrine system. The hypothalamus produces releasing hormones that signal the pituitary to produce its own hormones, which in turn signal peripheral glands throughout the body.


The pituitary produces:

  • Growth hormone (GH) — stimulates cell growth and proliferation throughout the body, including keratinocytes and fibroblasts. Growth hormone-driven collagen synthesis is highest during sleep, making sleep quality directly relevant to skin structural maintenance.
  • Melanocyte-stimulating hormone (MSH) — directly regulates melanocyte activity and pigmentation.
  • Thyroid-stimulating hormone (TSH) — signals the thyroid to produce thyroid hormones.
  • Adrenocorticotropic hormone (ACTH) — signals the adrenal glands to produce cortisol.
  • Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) — regulate sex hormone production in the ovaries and testes. [1]

The Thyroid Gland

Located in the neck, the thyroid produces thyroxine (T4) and triiodothyronine (T3) — the metabolic hormones that regulate the rate of cellular activity throughout the body. The skin is highly sensitive to thyroid hormone levels — both excess (hyperthyroidism) and deficiency (hypothyroidism) produce characteristic and often dramatic skin, hair, and nail changes.


The Adrenal Glands

The adrenal glands, sitting atop each kidney, produce:

  • Cortisol — the primary stress hormone, with profound effects on skin barrier function, collagen, inflammation, and immune response
  • DHEA (dehydroepiandrosterone) — a precursor to both estrogen and testosterone, with its own skin effects
  • Aldosterone — regulates fluid balance, relevant to skin hydration
  • Adrenaline (epinephrine) — triggers the acute stress response, including the vascular changes that produce stress-related skin flushing and pallor [2]

The Ovaries and Testes

The gonads produce the sex hormones:

  • Estrogens (primarily estradiol in premenopausal women) — the most important hormones for skin health in female-assigned individuals
  • Progesterone — has its own skin effects, particularly relevant to cyclical skin changes
  • Testosterone and other androgens — produced by both ovaries and testes (and adrenal glands), with significant effects on sebum production and hair follicle behavior

The Pancreas

The pancreatic islets of Langerhans produce:

  • Insulin — regulates blood glucose; has significant indirect effects on skin through glycation and inflammation mechanisms
  • Glucagon — regulates blood glucose in the opposite direction to insulin [1]

The Skin Itself

The skin is increasingly recognized as an endocrine organ in its own right. It produces:

  • Vitamin D3 (from UV-driven synthesis) — technically a hormone, not a vitamin
  • Local estrogens — peripheral conversion of androgens to estrogens by aromatase in skin cells
  • Cortisol — the skin can produce cortisol locally in response to stress
  • Neuropeptides — including substance P and CGRP, produced by skin nerve endings in response to stimuli [2]
  • Oxytocin — the "love hormone" is also produced locally by epidermal keratinocytes, where it modulates inflammation, oxidative stress, and skin aging. Higher oxytocin levels have been correlated with more youthful-appearing skin in clinical studies. [10, 11, 12]

How Hormones Work — Receptors, Signaling, and Feedback

A hormone exerts its effects only on cells that express the appropriate receptor for it. Hormones circulate throughout the bloodstream — but only cells with the matching receptor respond. This receptor-ligand specificity is why estrogen affects skin collagen but does not affect all cells equally, and why androgens affect sebaceous glands more than other skin structures.


Two primary receptor mechanisms:

  • Nuclear receptors — used by steroid hormones (estrogen, testosterone, cortisol, thyroid hormones). These hormones are lipid-soluble and can pass through cell membranes to bind receptors inside the nucleus, directly regulating gene expression. This mechanism produces effects that are slower to develop but longer-lasting — hours to days.
  • Cell surface receptors — used by peptide hormones (insulin, growth hormone, MSH). These hormones cannot cross cell membranes and bind to receptors on the cell surface, triggering intracellular signaling cascades. Effects develop faster but are shorter-lived.

Feedback loops:

Hormone production is regulated by feedback loops — mechanisms that maintain hormonal balance by adjusting production in response to circulating levels. The hypothalamic-pituitary-adrenal (HPA) axis is the classic example: the hypothalamus produces CRH, which signals the pituitary to produce ACTH, which signals the adrenal glands to produce cortisol. Rising cortisol levels signal back to the hypothalamus and pituitary to reduce CRH and ACTH production — preventing cortisol from rising indefinitely.


Endocrine disruption occurs when this feedback system is interfered with — by exogenous chemicals that mimic or block hormone signals, by disease affecting glandular function, or by medical treatments that deliberately alter hormone levels. [3]

Estrogen and Skin

Estrogen is the most important hormone for skin health in female-assigned individuals — and its effects are so significant that the dramatic skin changes of menopause, when estrogen levels fall, are among the most visible manifestations of any hormonal transition.


The skin expresses estrogen receptors throughout — in keratinocytes, fibroblasts, melanocytes, sebaceous glands, and hair follicles. Estrogen's effects on skin are comprehensive:

  • Collagen synthesis — estrogen directly stimulates fibroblast collagen production and inhibits the matrix metalloproteinases (MMPs) that degrade it. The 30% collagen loss women experience in the first five years after menopause is directly attributable to the loss of this estrogenic support. Estrogen replacement therapy has been shown to significantly reduce this post-menopausal collagen loss. [4]
  • Skin thickness — estrogen supports dermal thickness by stimulating fibroblast activity and hyaluronic acid production. Post-menopausal skin is measurably thinner than pre-menopausal skin, with the difference attributable primarily to estrogen loss.
  • Barrier function — estrogen supports ceramide synthesis and barrier lipid production. The impaired barrier function that many women experience at menopause reflects the loss of estrogen's support for these processes.
  • Sebaceous activity — estrogen has an anti-androgenic effect on sebaceous glands, moderating sebum production. Its loss at menopause can paradoxically produce both increased dryness (from barrier impairment) and, in some women, increased oiliness or adult-onset acne (from the relative shift toward androgenic dominance).
  • Pigmentation — estrogen stimulates melanocyte activity and regulates melanin distribution. Estrogen-driven pigmentation changes include the melasma of pregnancy and hormonal contraceptive use, and the post-menopausal shift in skin tone. [2]
  • Wound healing — estrogen accelerates wound healing through effects on keratinocyte proliferation, inflammatory regulation, and angiogenesis. Post-menopausal women heal more slowly than pre-menopausal women, with estrogen replacement restoring healing rates.

Testosterone and Androgens — Sebum, Acne, and Hair

Androgens — testosterone and its more potent derivative DHT — have their most visible skin effects through sebaceous glands and hair follicles.

  • Sebum production — sebaceous glands are exquisitely sensitive to androgenic stimulation. The surge in androgen production at puberty is the primary driver of increased sebum production and the acne that follows. Sebaceous glands express 5-alpha reductase — the enzyme that converts testosterone to DHT — locally, making them responsive to both circulating and locally produced androgens. [3]
  • Androgenetic alopecia — DHT binding to androgen receptors in hair follicle dermal papilla cells triggers the follicle miniaturization process that produces pattern hair loss. This is covered in depth in the Hair Growth Serum ingredient posts — particularly the posts on saw palmetto, soybean germ, and scutellaria baicalensis.
  • Acne — the relationship between androgens and acne involves both sebum overproduction and the downstream changes in follicular environment that favor Cutibacterium acnes overgrowth and inflammatory responses. Anti-androgenic approaches — including 5-alpha reductase inhibitors and androgen receptor blockers — are foundational to both pharmaceutical and botanical acne treatments.
  • In Women — androgens are produced in smaller amounts by the ovaries and adrenal glands, but even these lower levels are sufficient to drive sebaceous activity. Conditions of androgen excess — PCOS, congenital adrenal hyperplasia — produce acne, hirsutism, and androgenetic hair loss in women through the same mechanisms. [2]

Cortisol — The Stress Hormone and Skin

Cortisol is the body's primary stress hormone — produced by the adrenal cortex in response to ACTH signaling, with production increasing dramatically during physical or psychological stress. Its effects on skin are significant and multiple:

  • Barrier function — cortisol reduces ceramide synthesis and impairs barrier enzyme function, increasing transepidermal water loss and reducing barrier resilience. This explains the well-documented observation that stress worsens skin barrier function and exacerbates conditions like eczema and rosacea.
  • Collagen degradation — cortisol suppresses fibroblast collagen synthesis and upregulates MMP expression, accelerating collagen loss under chronic stress conditions.
  • Immune modulation — cortisol has complex, dose-dependent immune effects. Acutely, it is anti-inflammatory. Chronically elevated, it impairs the skin's immune defenses and alters the inflammatory response in ways that worsen chronic inflammatory skin conditions.
  • Wound healing — chronic cortisol elevation impairs wound healing through multiple mechanisms — reduced immune function, impaired keratinocyte proliferation, and reduced growth factor expression.
  • Microbiome — as discussed in the microbiome post, cortisol alters sebum composition and skin surface chemistry in ways that shift the microbiome toward pathogenic compositions. [1]

The skin's own capacity to produce cortisol locally — independent of the adrenal glands — means that skin stress responses can occur without systemic stress, adding a local dimension to the stress-skin relationship.

Thyroid Hormones and Skin

Thyroid hormones (T3 and T4) regulate metabolic rate in virtually every cell — and the skin is no exception. Both excess and deficiency of thyroid hormones produce characteristic skin changes:


Hypothyroidism (too little thyroid hormone):

  • Dry, rough, cool skin from reduced sweating and sebaceous activity
  • Coarse, brittle hair and diffuse hair loss
  • Puffy face from glycosaminoglycan accumulation in the dermis
  • Slow wound healing
  • Pale or yellowish skin tone from carotenoid accumulation and reduced melanin synthesis

Hyperthyroidism (too much thyroid hormone):

  • Warm, moist, flushed skin from increased metabolic activity and vasodilation
  • Fine, silky hair that may fall out (diffuse alopecia)
  • Increased sweating
  • Pretibial myxedema in Graves' disease — a specific skin thickening on the lower legs [4]

Subclinical thyroid dysfunction — levels outside the ideal range but not classified as clinical disease — is common and can produce subtler versions of these skin changes that are often attributed to other causes.




Insulin, Blood Sugar, and Skin

Insulin's skin effects operate primarily through two mechanisms:

  • Glycation — as covered in the collagen and elastin post, excess blood glucose reacts with collagen and elastin through non-enzymatic glycation, producing advanced glycation end-products (AGEs) that cross-link proteins in a disordered way, making them rigid, brittle, and dysfunctional. Chronically elevated blood sugar — from insulin resistance or diabetes — significantly accelerates this process.
  • IGF-1 signaling — insulin and IGF-1 (insulin-like growth factor 1) share signaling pathways. High insulin levels, associated with high-glycemic diets and insulin resistance, upregulate IGF-1 signaling in skin cells — stimulating sebaceous gland activity, keratinocyte proliferation, and androgen production. This IGF-1 pathway is one of the mechanisms connecting high-glycemic diets to acne. [3]
  • Acanthosis nigricans — a characteristic skin darkening and thickening in body folds (neck, armpits, groin) associated with insulin resistance — is one of the most visible skin manifestations of metabolic hormonal dysregulation.

Is the Endocrine System Different for Different People?

Yes — individual hormonal profiles vary significantly based on genetics, sex, age, body composition, and health status, producing meaningful differences in skin behavior across individuals.

  • Biological sex and hormonal profileThe most significant source of hormonal variation for skin is the difference between estrogen-dominant and androgen-dominant hormonal profiles. Femen generally have more estrogen-responsive skin — thicker dermis at reproductive ages, more collagen relative to androgens, more dramatic skin changes at hormonal transitions. Men have androgen-dominant profiles that produce higher sebum production, thicker skin overall, and different patterns of aging.
  • Genetic variation in hormone receptorsIndividuals vary in the sensitivity of their hormone receptors — the same circulating estrogen level may produce stronger or weaker effects depending on receptor expression and sensitivity. This receptor-level variation contributes to the wide range of skin responses to hormonal events like puberty, pregnancy, and menopause.
  • Body compositionAdipose (fat) tissue is a site of peripheral estrogen production — aromatase in fat cells converts androgens to estrogens. Individuals with higher body fat percentages produce more peripheral estrogen, which can moderately influence skin behavior, particularly post-menopause.
  • Hormonal conditionsPCOS, thyroid disorders, adrenal conditions, and other endocrine diseases produce distinct and often dramatic skin presentations that reflect their specific hormonal signatures. [2]

How the Endocrine System Changes With Age

Hormonal changes with age are among the most significant drivers of skin aging — often more impactful than chronological time alone.

  • Puberty — the surge in sex hormone production produces the characteristic skin changes of adolescence: increased sebum, acne, body hair development, and the beginning of the hormonal skin cycle.
  • Reproductive years — cyclical hormonal fluctuations produce predictable monthly skin changes in many women — increased sebum and acne in the luteal phase (premenstrual), improved skin clarity in the follicular phase.
  • Pregnancy — dramatic hormonal shifts produce diverse skin changes: melasma (estrogen-driven pigmentation), the "pregnancy glow" (increased blood volume and skin circulation), linea nigra, and sometimes improved or worsened acne depending on the individual hormonal response.
  • Perimenopause and menopause — the most significant hormonal transition for skin in women. Estrogen levels fall dramatically over 2-10 years, producing accelerated collagen loss, barrier impairment, increased dryness, altered microbiome, and changes in pigmentation and sebum production.
  • Andropause (Men) — the more gradual decline in testosterone in men produces slower skin changes: reduced sebum production, some reduction in skin thickness, and gradual changes in hair follicle behavior.
  • Late aging — growth hormone, DHEA, and other hormones continue to decline with age, contributing to the progressive skin thinning, reduced renewal, and impaired repair capacity of very old skin. [4]

What Disrupts the Endocrine System

Endocrine-Disrupting Chemicals (EDCs)

EDCs are exogenous chemicals that interfere with hormone signaling — by mimicking hormones, blocking hormone receptors, altering hormone synthesis or metabolism, or disrupting transport proteins. They are found in plastics, pesticides, industrial chemicals, and — critically for Juventude's audience — some personal care product ingredients.


Read the Deep Dive On This Topic: Endocrine Disrupting Chemicals in Skincare: What T hey Are, Where They Hide, and How to Actually Avoid Them


EDCs relevant to personal care products include certain parabens, phthalates, benzophenones (oxybenzone), and other synthetic chemicals that have demonstrated endocrine-disrupting activity in laboratory and epidemiological studies. The avoidance of these compounds is a central pillar of Juventude's formulation philosophy. EDCs and their skin-relevant mechanisms are covered in depth in a dedicated post in this series.



Chronic Stress

Chronic psychological stress maintains elevated cortisol through sustained HPA axis activation — with the skin consequences detailed above. The stress-hormone-skin connection is one of the most clinically significant and least-addressed aspects of skin health.


Sleep Disruption

Sleep is the primary window for growth hormone release and cortisol reduction. Chronic sleep disruption elevates average cortisol levels, reduces growth hormone pulses, and impairs the hormonal repair signaling that maintains skin structure overnight.


Diet

High-glycemic diets elevate insulin and IGF-1, influencing sebum production and acne. Nutrient deficiencies affect hormone synthesis — iodine for thyroid hormones, zinc for testosterone metabolism, essential fatty acids for steroid hormone production. Extreme caloric restriction reduces sex hormone production.


Environmental and Chemical Exposures

Beyond personal care products, EDC exposure from food packaging, drinking water, agricultural chemicals, and industrial pollution represents a significant source of endocrine disruption in the modern environment. [3]



Cancer Treatment and the Endocrine System

For people undergoing or recovering from cancer treatment, the endocrine system faces specific and significant challenges:

  • Hormone therapy for breast cancer — aromatase inhibitors (anastrozole, letrozole, exemestane) block peripheral estrogen synthesis through inhibition of the aromatase enzyme, reducing circulating estrogen by up to 97-99% in postmenopausal women. Tamoxifen and other selective estrogen receptor modulators (SERMs) competitively block estrogen receptor activity in breast tissue while having variable estrogenic effects in other tissues. Both approaches produce skin changes that closely mirror accelerated menopause: rapid collagen loss, barrier impairment, increased dryness, altered pigmentation, and hair thinning. Clinical studies document skin collagen loss of up to 1.7% per month in women on aromatase inhibitors — significantly faster than the age-related rate. [5]
  • Hormone therapy for prostate cancer — androgen deprivation therapy (ADT) reduces testosterone to castrate levels through either surgical orchiectomy or pharmacological suppression using GnRH agonists or antagonists. The resulting androgen deficiency produces skin thinning, dramatically reduced sebum production, changes in body hair distribution, and loss of the skin-supporting properties of testosterone. Studies document significant reductions in skin thickness and sebaceous gland activity within 3-6 months of ADT initiation. [6]
  • Chemotherapy-induced ovarian failure — alkylating agents (cyclophosphamide, melphalan) and certain platinum-based agents are particularly gonadotoxic, causing premature ovarian failure in premenopausal women. Unlike natural menopause, which unfolds over years, chemotherapy-induced ovarian failure can occur abruptly — producing the full constellation of estrogen-withdrawal skin changes within weeks. The younger the patient, the more dramatic the relative hormonal shift. Studies report rates of chemotherapy-induced premature menopause of 40-68% depending on regimen and patient age. [7]
  • Corticosteroid medications — dexamethasone and prednisone are routinely used in cancer treatment protocols as antiemetics, anti-inflammatories, and components of some chemotherapy regimens. Systemic corticosteroids at therapeutic doses produce the cutaneous effects of hypercortisolism: barrier impairment through reduced ceramide synthesis, collagen loss through fibroblast suppression and MMP upregulation, skin atrophy and thinning, impaired wound healing, striae formation, and altered immune surveillance. These effects are dose- and duration-dependent. [5]
  • Thyroid effects of cancer treatment — thyroid dysfunction is a documented side effect of multiple cancer treatment modalities. Checkpoint inhibitor immunotherapy (anti-PD1, anti-CTLA4) causes immune-related thyroiditis in 5-10% of patients. Tyrosine kinase inhibitors (sorafenib, sunitinib) are associated with hypothyroidism in up to 53% of patients with prolonged use. Head and neck radiation fields frequently include the thyroid gland, with radiation-induced hypothyroidism occurring in 20-30% of patients within 5 years. Each of these mechanisms produces the characteristic cutaneous features of thyroid dysfunction — dryness, coarseness, altered hair quality, and impaired skin renewal. [8]
  • Stress and HPA axis dysregulation — cancer diagnosis and treatment represent one of the most significant sources of chronic psychological stress encountered in clinical practice. Sustained HPA axis activation maintains chronically elevated cortisol, producing the barrier, collagen, immune, and microbiome consequences detailed throughout this series. Studies measuring cortisol patterns in cancer patients document flattened diurnal rhythms and elevated baseline levels that persist for months to years after treatment completion. [9]
  • Insulin resistance and metabolic effects — several chemotherapy regimens, corticosteroid use, and treatment-related weight changes can induce or worsen insulin resistance, increasing circulating insulin and IGF-1 levels with the downstream effects on skin inflammation, sebaceous activity, and glycation described above. [6]

The skin changes experienced during and after cancer treatment are not arbitrary or unrelated — they follow directly from the specific hormonal disruptions each treatment produces. Understanding the endocrine mechanisms behind them is the foundation for understanding both why they occur and how to address them through targeted skincare strategies.



The Bottom Line

The endocrine system is the body's chemical messaging network — and the skin is one of its most hormone-responsive target organs. Estrogen drives collagen synthesis, barrier function, and skin thickness; androgens regulate sebum and hair follicle behavior; cortisol impairs barrier and collagen under stress; thyroid hormones regulate skin metabolic rate; insulin connects blood sugar to glycation and sebaceous activity. These hormonal influences vary by individual, change throughout life, and are disrupted by EDCs, stress, sleep deprivation, diet, and cancer treatment. Understanding the endocrine system is not peripheral to understanding skin health — it is central to it, and it provides the biological context that makes sense of skin changes that might otherwise seem random or unrelated.



Array of antioxidant-rich plants for skincare products

This article is for educational purposes only and does not constitute medical advice. Consult with healthcare professionals before starting any new skincare regimen, especially if you have existing skin conditions or are undergoing medical treatment.

Image of Lindsey Walsh, Founder of Juventude

The Author: Lindsey Walsh

Lindsey is founder and CEO of Juventude. A breast cancer survivor and cancer advocate. Lindsey built Juventude to provide effective skin care based on antioxidant-rich plants and without endocrine disrupting toxins. 

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References

  1. Zouboulis CC. "The skin as an endocrine organ." Dermato-Endocrinology, 2009; 1(5):250-252. https://doi.org/10.4161/derm.1.5.9499
  2. Thornton MJ. "Oestrogens and ageing skin." Dermato-Endocrinology, 2013; 5(2):264-270. https://doi.org/10.4161/derm.23872
  3. Katta R, Desai SP. "Diet and dermatology: The role of dietary intervention in skin disease." Journal of Clinical and Aesthetic Dermatology, 2014; 7(7):46-51.
  4. Verdier-Sevrain S. "Effect of estrogens on skin aging and the potential role of selective estrogen receptor modulators." Climacteric, 2007; 10(4):289-297. https://doi.org/10.1080/13697130701467157
  5. Bines J, Oleske DM, Cobleigh MA. "Ovarian function in premenopausal women treated with adjuvant chemotherapy for breast cancer." Journal of Clinical Oncology, 1996; 14(5):1718-1729. https://doi.org/10.1200/JCO.1996.14.5.1718
  6. Higano CS. "Side effects of androgen deprivation therapy: Monitoring and minimizing toxicity." Urology, 2003; 61(1 Suppl 1):32-38. https://doi.org/10.1016/S0090-4295(02)02397-X
  7. Petrek JA, et al. "Incidence, time course, and determinants of menstrual bleeding after breast cancer treatment." Journal of Clinical Oncology, 2006; 24(7):1045-1051. https://doi.org/10.1200/JCO.2005.03.3969
  8. Delivanis DA, et al. "Thyroid dysfunction in the context of immune checkpoint inhibitor treatment." Journal of Clinical Endocrinology and Metabolism, 2017; 102(7):2777-2782. https://doi.org/10.1210/jc.2017-00258
  9. Bower JE, et al. "Fatigue and proinflammatory cytokine activity in breast cancer survivors." Psychosomatic Medicine, 2002; 64(4):604-611. https://doi.org/10.1097/00006842-200207000-00010
  10. Denda S, et al. "Oxytocin is expressed in epidermal keratinocytes and released upon stimulation with adenosine 5'-(γ-thio)triphosphate in vitro." Experimental Dermatology, 2012; 21(7):535-537. https://doi.org/10.1111/j.1600-0625.2012.01507.x
  11. Deing V, et al. "Oxytocin modulates proliferation and stress responses of human skin cells: Implications for atopic dermatitis." Experimental Dermatology, 2013; 22(6):399-405. https://doi.org/10.1111/exd.12155
  12. Hayre N. "Oxytocin levels inversely correlate with skin age score and solar damage." Journal of Drugs in Dermatology, 2020; 19(12):1146-1148. https://doi.org/10.36849/JDD.2020.5063
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