Skin care professionals that are committed to caring for mature skin are undoubtedly challenged by unexpected skin problems such as acne, pigmentation, sensitivities, hair growth, wrinkles, and more. Unfortunately, many of these challenges often fail to respond to conventional product formulations and professional aesthetic remedies.
A complicated immune organ, our skin is exposed to extrinsic and intrinsic assaults that lead to an imbalance of its intelligent ecosystem, resulting in varying cosmetic injuries benchmarked by pigmentation, acnelesions, dryness and wrinkles. It also has the ability to communicate its physiological requirements such as temperature control, water balance, excretory activity, sensory output, physical defense, immunological protection and central hormone activation, triggering various skin reactions.
Our skin is regarded as the target for several hormones whose effects have long been recognized. For example, hair follicles and sebaceous glands are the targets for androgen steroids secreted by the gonads and the adrenal cortex with the melanocytes (central pigmentation cell) directly influenced by polypeptidehormones of the pituitary. Hormones are involved in intrinsic aging accompanied by the reduced secretion of the pituitary and adrenal glands and the gonads. As the skin begins to experience hormonal withdrawal, consequences arise including, but not limited to, a decrease in intellectual activity, lean body mass, bone mineral density, increases in fatigue, depression and alterations in skin.
Multicellular organisms depend on communication among cells for regulation of metabolic processes, control of cell growth, differentiation and integration of physiological function. Cell-to-cell communication is mediated by the action of molecules in the endocrine, paracrine, autocrine and neurotransmitter systems. The primary signals of cellular communication are hormones. Therefore, in the pursuit of ongoing personal and professional growth, aestheticians benefit by learning to understand the language of hormones and their direct impact on skin.
Facts about Menopause
Hormonal consequences due to a lack of estrogen affect over 50 million women currently experiencing menopause. Systemic alterations cumulatively impact and compound complexities of the aging process. When trauma to the skin occurs, it initiates cell movement, cell death, and the formation of intercellular substances. For optimal skin health, proper aesthetic practices are required to cleanse, treat, balance and protect the systematic skin care routine. Menopause is not affected by race, use of oral contraception, number of pregnancies, or age. Furthermore, climacteric skin becomes proactive during the three phases of menopause: perimenopause, menopause and postmenopause.
The Language of Hormones
Hormones are the chemical messengers that give specific instructions to cells. They perform an important role in the development and physiological function of human skin and aestheticians clinically treat and subsequently recommend continuance of a particular home care regimen based on a thorough examination, making sure to record the findings on the client's intake form.
From the archives of modern dermato-endocrinological studies, the skin is not only the recipient of signals from distant transmitters but it is also an organized community where cells and organelles emit, receive and coordinate molecular signals. In the widest sense, the human skin and its cells are the targets, as well as the producers, of hormones.
Hormones take on many forms; some are chains of amino acids (peptides) while others are simple or slightly modified single amines (monoamines) or diamines (two amines). Nonetheless, many hormones often belong to different chemical classes altogether.
Steroid hormones are produced in the ovaries, testes, adrenal cortex and the fetal-placental unit. They are produced from cholesterol, readily synthesized by the body. Peptide hormones are created by the hypothalamus, anterior pituitary gland, parathyroid gland, pancreas, kidney and gastrointestinal tract. Although glands are often thought of as the synthesizers of their respective hormones, this is not the case with most peptide hormones. Current research has revealed a system whereby large polypeptide prohormones consisting of many amino acid sequences are synthesized initially.
Specific skin language biomarkers for estrogen show an increase of the mitotic rate in the epidermis, a reduction in size and activity of the sebaceous glands, a slower rate of hair growth, stimulated synthesis, a turnover of collagen, and an increase in the production of hyaluronic acid. Skin cells express estrogen receptors, making them directly susceptible to estrogens, but a cross-communication between estrogen and insulin-like growth factor (IGF-1) signaling pathways. IGF-1 plays a major role in regulating lipid synthesis in sebocytes, proliferation in fibroblasts, and modulating the estrogen activity on normal and aged skin cells.
Estrogen earned its name because it plays an important role in the estrous cycle. The term is from the Latin word(s) estrus/oistros which means a period of fertility for female mammals, plus the Latin word(s) gen/gonos meaning to generate. Estrogens are steroid compounds that diffuse across the cell membrane. Once inside, they bind to the estrogen receptors present in the nucleus of the cells where DNA resides. They also act by activating G protein-coupled receptor (GPR30). Their main action is to regulate the expression of certain genes that maintain fertility and assist in the development of the female reproductive system.
The primary molecule that begins the synthesis of estrogen is cholesterol. It forms a substance of moderate an-drogenic activity known as androstenedione. This compound crosses the basal membrane into the surrounding granulosa cells where it is converted to estrone or estradiol either immediately or through testosterone. This conversion of testosterone to estradiol, and androstenedione to estrone, is catalyzed by the enzyme aromatase. Estradiol levels vary through the menstrual cycle, with levels at their highest just before ovulation.
Some of the estrogens are also produced in smaller amounts by other tissues such as the liver, adrenal glands and the breasts. These secondary sources are important in women who have already been through menopause. Fat cells are also sources of estrogen. This is the reason why underweight or overweight women are at risk of infertility; a delicate balance of estrogen is important for fertility. Excess or deficiency of this hormone may adversely affect fertility.
Estrogens stimulate fat deposits in the female body mass and as this estrogen drops, fat deposits relocate and fat is lost on the face, neck, hands and arms. Aestheticians should observe the loss of fat in these specific areas when assessing clients and note any changes on their client intake form. The loss of fat can provide significant insight to the aging of the skin, directly affecting your decision for the proper clinical treatment option(s) and the continuance of a daily at-home care regimen.
WHAT IS Dermato-Endocrinology?
“From its dawn probably in 1855 as Thomas Addison described skin pigmentation in patients with adrenal insufficiency followed by identification of the melanotropic effect of a melanocyte-stimulating hormone, until our current ever-changing concept on how hormones affect cutaneous cells, the skin has been defined as a target for hormones. Through the definition of novel biological activities of hormones and their diversity on different skin cell types, it has become apparent that the skin itself possesses the capacity to generate several hormones and substances with hormone-like activity. These substances appear to act through paracrine, autocrine, intracrine and endocrine mechanisms to fulfill their pleiotropic effects. Also new is the knowledge that the skin can metabolize hormones and produce derivatives with potentially systemic activity. These findings point towards novel concepts in our understanding of the skin role and of its hormones as important players in homeostasis and disorders of the entire human organism. Finally, the scientists active in the field of Dermato-Endocrinology expect that their activities will exploit the pharmacological and therapeutic function of hormone mediators, their receptors and antagonists.”
Blackwell Munksgaard; Experimental Dermatology; 2004: 13 (Suppl. 4): 3–4.
Side effects of estrogen withdrawal include a decrease in dermalglycosaminoglycans (GAGS). GAGS are hydrophilic molecules that draw moisture into the dermis. Decreased dermal GAGS are associated with aging and are believed to contribute to dry skin, wrinkling and atrophy. Thickness and suppleness of skin may also occur, creating an imbalance of androgen that causes acne flare-ups, terminal facial hairs, enlarged sebaceous glands, increased pore size, and additional sebum production.
Changes in the lipid layer of the epidermis are frequently associated with aging and may affect the water holding capacity of the skin. Significant variations in the stratumcorneum sphingolipids have been noted among women of varying ages leading to a possible hormonal influence. Laxity and wrinkling are cutaneous signs of aging related to the loss of skin elasticity. Aging is an inevitable process and affects all organ systems, including skin. A decrease of estrogen accompanies aging and contributes to age-related skin changes.
Scientific studies regarding menopause indicate skin sensitivity increases in the years of the onset of menopause. This increase in sensitivity is not attributed to stratumcorneum (SC) thickness or barring corneocyte buildup, which is known to stay the same once a woman turns 18. It was also indicated that no SC thickness alterations occurred in perimenopausal (Climacteric I), menopause (Climacteric II) or early postmenopausal (Climacteric III) women.
Although SC thickness for the most part remains intact, there is a link between skin moisturization and skin sensitivity. This important fact requires aestheticians to use skin care formulations for menopausal skin rich in human identical ceramides (50 percent of SC lipids), amino acids, and other indigenous stratumcorneumlipids such as cholesterol and free fatty acids. Ceramides are sphingolipids consisting of a long chain amino alcohol to which a long chain fatty acid is linked via an amide bond.
The biochemical nature of difference between sensitive and non-sensitive skin is not yet completely understood, however, it has been established that the relative amount of lipid molecules in the SC barrier is the significant distinction. Skin sensitivity is associated with an impaired barrier function and this correlation is true for mature women, especially those affected by menopause.
Testosterone is a steroid hormone from the androgen group and is found in mammals, reptiles, birds, and other vertebrates. In mammals, testosterone is primarily secreted in the testicles of males and the ovaries of females, although small amounts are also secreted by the adrenal glands. It is the principal male sex hormone and an anabolic steroid. In men, testosterone plays a key role in the development of male reproductive tissues such as the testes and prostate, as well as promoting secondary sexual characteristics such as increased muscle, bone mass, and the growth of body hair. In addition, testosterone is essential for health and well-being, as well as the prevention of osteoporosis.
The skin is a major site of androgen metabolism and a primary object for the effects of androgens. Under the influence of androgens, mitotic activity, intracellular lipid synthesis, and the thickness of the epidermis increases. In addition, hair growth and pigmentation are influenced. Sebaceous glands are stimulated by both systemic and topical application of androgens and sebum production is a sensitive indicator of androgenic activity. Androgenreceptor levels are similar in men and women with acne, as well as in acnelesions and lesion-free skin. Neither in acne nor in unconventional hirsutism conditions does a correlation exist between androgenreceptors and androgen serum levels.
"Endocrine factors play an important role in the control of the secretory activity of sebaceous glands, as well as proliferation and lipogenic activity of sebocytes influenced"
Climacteric Skin Phases
Estrogens are produced primarily by the ovaries. They are released by the follicles on the ovaries and secreted by the corpus luteum after the egg has been released from the follicle and the placenta. The stimulation for secretion of estrogen comes from the luteinizing hormone (LH) from the anterior pituitary gland.
Skin becomes proactive during three phases of menopause as histologic and clinical changes begin to occur. Reduced blood supply to the stratum germinativum leads to impaired capillaries. Estrogens partially influence growth and maintenance of capillaries and blood flow is reduced during menopause. Nutrients are compromised and oxygen is less available to the stratum germinativum. Dry skin transpires and becomes problematic as alterations in elasticity and suppleness are compromised. A thinning epidermis is a consequence of a slower cell turnover, a reduction of the barrier repair function (BRF), leading to transepidermal water loss (TEWL).
Menopausal skin exposed to ultraviolet radiation (UVR) starts melanin synthesis and age spots increase on face, hands, neck, arms and chest. Lipid peroxidation caused by free radical injury from UVR could be responsible for the pigment lipofuscin accumulation that produces age spots. UVR sensitivities increase and melanocytes are under the control of estrogens. As menopause progresses, melanocyte volume decreases and leads to climacteric melanocyte degeneration (CMD), a marbled hyperpigmentation condition tempered by estrogens. In global skin Types I and II, loss of melanocyte protection can become serious, leading to further UVR damage and increased photoaging. A good recommendation for aestheticians would be to incorporate a minimum of SPF 30 and a healthy skin makeup protection for daily UVR protection.
Phase I of the menopausal period is a pre-menopause transition from years of fertility to the end of a woman's menstrual cycle; this phase is classified as Climacteric 1 Skin. During this transition, the skin has a decrease in sweat and sebaceous gland activity. An itching or crawling feeling may be a side effect during this transitional stage related to the vasomotor system. Phase II is a menopause completion of 12 months after the end of the menstrual cycle and classified as Climacteric 2 Skin. Phase III is postmenopause and the years following 12 months are classified as Climacteric 3 Skin. At this juncture, the skin becomes drier and thinner, leading to more wrinkles which cause the skin to look older than its chronological age. Postmenopausal clients may require more ceramide and hylauronic acid as part of their clinical treatment and home care. It becomes evident that the skin is easily compressed and loses its mobility. The breasts also begin to lose turgor, resulting in a saggy, flat appearance. An efficacious firming body cream can be recommended to help reduce the effects of the loss of turgor brought on by menopause.
"Estrogens in females decrease rapidly after menopause and up to the 60th year of their life, and then show a low level"
There is also an increase in Hirsutism and women with high levels of androgens will exhibit more hair during menopause as estrogen decreases. This condition is excessive hair growth in androgen-dependent hair patterns on the face, chest, lower back, buttocks, inner thighs, et cetera. The epidemiology in this situation is familial, ethnic and has racial influence. There seems to be an association with postmenopausal (Climacteric 3) hirsutism of the chin and upper lip. The vellus hairs of the beard and cheek area tend to be long, creating unwanted facial hair. Aesthetic remedies to treat this condition can range from waxing, tweezing or laser hair removal.
In addition, Climacteric 3 skin exhibits skin atrophy due to the loss of estrogen impacting collagen. Moreover, skin collagen increases with estrogen and Type I is 60 to 80 percent of the dermis extracellular matrix (ECM). Age related atrophy of the skin has been correlated with decreases in dermalcollagen which occurs at a rate of one to two percent per year after menopause. There is a reduction of skin thickness and symptoms could indicate osteoporosis. Specific aesthetic peel treatments and dermasound applications help to increase dermalcollagen and rebalance skin via homeostasis.
During the transitions of Climacteric 1, 2 and 3, an active oil phase manifests within the sebaceous environment triggering a phenomenon that ultimately contributes to menopausal acne in adult women. Climacteric skin is influenced by decreased estrogen
levels and affects testosterone, an action influenced by the adrenal glands. Then, the sebaceous glands are stimulated by testosterone which triggers thicker sebum production. Additionally, skin appendages are targets for androgens and have an active role in the production of these hormones which result from pre-hormones and are considered the cause of menopausal acne (also known as postmenopausal acne).
Menopausal acne affects women currently experiencing menopause, mostly within the first two years of ovarian failure. In fact, it may precede the last menstruation, often in association with other menopausal symptoms like hot flashes. During female clients' initial consulation, it is important to note any acnelesions, hot flashes, et cetera.
One explanation of menopausal acne is that the ovaries are no longer producing estrogen, but they continue to synthesize androgens along with the adrenals causing a state of unopposed hyperandrogenism to develop. However, keep in mind that hormonal imbalance may also incite menopausal acne.
Generally characterized as low-grade acne, menopausal acne has small, closed comedones that become more visible as the skin is stretched. When examining skin for menopausal acne, the aesthetician should stretch the skin and record any lesion information on an accompanying facial map. Open comedones appear to not be as prevalent in menopausal acne but they do exist. These lesions can be extremely resistive and may require a more aggressive means of extraction and treatment. Most of these women do not exhibit scarring from adolescent acne but have large facial pores, especially around the nose and malar areas. Excessive oiliness juxtaposed with dry skin is also a common complaint, leaving the aesthetician to treat both conditions at the same time.
Menopausal acne appears to be most common in Mediterranean women with thick, darker, oilier skin and is rarely encountered with skin phototype (SPT) I. However, your intake form should include a thorough background check on your client's ethnic heritage, since skin color should never be the determining factor for any skin condition.
Acne treatments for menopausal acne may vary. Aesthetic acne treatments are a challenge and must be administered with skill and a complete understanding of menopause and its affects and consequences on the skin. Additionally, medical physicians use estrogens as a part of oral contraceptive, hormone replacement therapy, and other treatment disorders on the endocrine system. Therefore, it is important to document when a client has been prescribed estrogens by their physician in the form of a female hormone dominate oral contraceptive to treat acne. Estrogens do not significantly affect the proliferation of the sebaceous glands. However, they may act by suppressing the secretion of pituitary gonadotropins thereby affecting the production of androgens. Significant differences exist with regard to the number of estrogen receptors between normal and acne-bearing skin. When administered systemically, estrogens bring about a reduction in the size and secretion of the sebaceous glands, yet it is unlikely that estrogens play a physiological role in the regulation of sebaceous gland activity.
"In the pursuit of ongoing personal and professional growth, aestheticians benefit by learning to understand the language of hormones and their direct impact"
Skin pigmentation is stimulated by menopausal hyperpigmentation and it has also been associated with female hormones, especially estrogens. Progesterone also affects skin pigmentation and the effects of testosterone have also been widely studied. However, despite the common and misunderstood data linking estrogen preparations to postmenopausal women, studies indicate that this hormone is not the cause of melasma despite sun exposure. Melasma is mainly attributed to pregnancy and combinations of estrogen and progestational agents used for contraception.
Millions of women enter menopause every day. Even so, there are only a few educational courses available for aestheticians to learn about menopausal climacteric skin. Due to the nature of this subject, it is impossible to assimilate all there is to know from reading one article. Therefore, it is imperative that aestheticians who are passionate in pursuing excellence in the aesthetics field seek out credible and established training courses taught by experienced and knowledgeable educators. Remember that skill and knowledge go hand in hand, so invest in yourself! Take advanced courses to press forward your proficiency and do not settle for product hype as a means of your schooling. Education is not a destination; it is a continued journey!
As a licensed mater aesthetician who has procaticed skin care for over 25 years, Christine Heathman C.M.E., L.M.T. is an aesthetic pioneer and nominated legend in American aesthetics. She is a powerful speaker, world-wide lecturer, educator, author of several skin manuals, has written hundreds of skin science editorials, selected to the editorial board of a leading skin journal and is an innovator in the research and development of unconventional and progressive skin care and protocols used in the most prestigious skin care and medical clinics all over the world. As the owner and CEO of GlyMed Plus, she has appeared several times on the popular health care program, The Doctors.