The skin is a powerful organ of communication starting at birth—on the social, psychological, and biologic levels. The skin and its appendages are well innervated with a dense network of afferent sensory nerves and efferent autonomic nerves. The afferent sensory nerves convey sensations of touch, pain, itch, temperature, and other physical stimuli. The efferent autonomic nerves play a role in maintaining cutaneous homeostasis by regulating vasomotor and pilomotor functions and the activity of the apocrine and eccrine sweat glands. The apocrine sweat glands, which produce the protein equivalent of pheromones in humans, become functional at puberty and respond to catecholamines (and not acetylcholine) as do the eccrine sweat glands.
As an organ of communication, the skin plays a vital role in attachment starting in infancy. Freud observed that during early development, the ego is rooted in the body, especially the skin. Bodily sensations and experiences, both internal and from the surface of the body, form the core around which the ego develops. The skin remains a very important organ of communication throughout a person's lifetime. It may react to emotional states such as extreme fear, anxiety and stress, and embarrassment with blanching, increased perspiration, flushing, and blushing reactions.
In addition, the overall appearance of the skin, even when minimally flawed, can have a profound effect on the body image of the person, especially in adolescence, and can result in body image pathology. As an organ of communication, the skin continues to play an important role in later life, when the appearance of the skin projects socially important attributes such as chronologic age and social status. The idea that chronologic age does not necessarily signal the beginning of old age is becoming increasingly widespread, and an attempt to reverse some of the aging-related bodily changes frequently involves medical and surgical procedures on the skin.
Histologically, the skin is composed of 2 main structures—the epidermis and the dermis. The skin and the nervous system share some common embryologic origins. The keratinocytes, hair follicle and sebum-forming sebaceous glands, and apocrine and eccrine sweat glands originate from the embryonic ectoderm. The Merkel cells and melanocytes that migrate to the epidermis from the neural crest are also of ectodermal origin. The dermal components, with the exception of nerves and specialized receptors, are of mesodermal origin.
Cutaneous equivalent of HPA axis
One of the main adaptive responses to systemic stress is mediated by the central hypothalamic-pituitary- adrenal (HPA) axis. Activation of the HPA axis centrally starts with the hypothalamic production of corticotropin-releasing hormone (CRH), which activates the CRH type 1 (CRH-1) receptor in the anterior pituitary and induces the release of proopiomelanocortin (POMC)-derived peptides adrenocorticotropin (ACTH), α-melanocyte stimulating hormone (a-MSH), and ß-endorphin. ACTH stimulates the production and secretion of cortisol in humans by the adrenal cortex.
It has been demonstrated that the skin expresses a neuroendocrine system involving CRH, urocortin (a CRH-like neuropeptide that has been identified in the brain and has a high affinity for the CRH-2 receptor in addition to the CRH-1 receptor), and the POMC-derived peptides ACTH, α-MSH, and ß-endorphin. Skin cells also express functional receptors activated by these neuropeptides.
It has been proposed that the central HPA axis acts as a coordinator of the local cutaneous response to stress, and the local cutaneous effectors of the HPA axis (ie, CRH, urocortin, and the POMC-derived peptides like ACTH and a-MSH) regulate the skin pigmentary, immune, epidermal, adnexal, and dermal systems. In addition, local cholinergic, catecholaminergic, and serotoninergic/ melatoninergic systems and some elements of the pituitary-thyroid axis have been demonstrated in the skin.1,2
Neuroendocrine-immune circuitry and stress-mediated skin disorders
Stress-mediated production of glucocorticoids may induce the suppression of T helper 1 (TH1)-mediated cellular immunity and create a shift towards T helper 2 (TH2)-mediated humoral immunity. Neurohormonal responses to stress also involve the activation of the sympathetic nervous system (SNS) with a subsequent increase of catecholamines. The SNS has been shown to directly participate in cutaneous inflammation. Sympathetic nerve fibers travel with sensory nerves and innervate the dermis and epidermis, where they release norepinephrine.
1. Arck PC, Slominski A, Theoharides TC, et al. Neuroimmunology of stress: skin takes center stage. J Invest Dermatol. 2006;126:1697-1704.
2. Slominski A, Wortsman J. Neuroendocrinology of the skin. Endocr Rev. 2000;21:457-487.
3. Gupta MA, Gupta AK. Psychodermatology: an update. J Am Acad Dermatol. 1996;34:1030-1046.
4. Gupta MA, Gupta AK, Kirkby S, et al. A psychocutaneous profile of psoriasis patients who are stress reactors: a study of 127 patients. Gen Hosp Psychiatry. 1989;11:166-173.
5. Gupta MA, Gupta AK. Depression and suicidal ideation in dermatology patients with acne, alopecia areata, atopic dermatitis and psoriasis. Br J Dermatol. 1998;139:846-850.
6. Hull PR, D'Arcy C. Acne, depression, and suicide. Dermatol Clin. 2005; 23:665-674.
7. Pistiner M, Pitlik S, Rosenfeld J. Psychogenic urticaria. Lancet. 1979;ii:1383.