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The hair follicle cycle is characterized by a period of growth (anagen), followed by a period of regression and remodeling (catagen), and a period of rest (telogen) During pregnancy, there is an increase in the amount of anagen hairs secondary to the increase in estradiol After giving birth, telogen effluvium is triggered by the rapid drop in estrogen, and is further suppressed in women who breastfeed because of the inhibitory effects of prolactin, a peptide hormone associated with lactation, on estrogen production Postmenopausal women often experience a similar decrease in hair density owing to the decline in estradiol and the subsequent unmasking of androgen effects
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For many decades androgens have dominated hair growth research A commonly prescribed drug for hair loss, finasteride (Propecia ), blocks the conversion of testosterone to DHT by inhibiting the enzyme 5- -reductase type II Regarding treatment of hair loss, finasteride is a pregnancy category X, thus contraindicated for women in their childbearing years who intend to have children It is indicated for men with male pattern hair loss, and may be effective for the treatment of androgenetic alopecia, or male pattern hair loss, in postmenopausal women16 As both androgen and estrogen receptors are found in the hair follicles, theoretically either of them can be targeted for the treatment of patterned hair loss Furthermore, as the aromatase enzyme is located in the hair follicle and the sebaceous gland, these tissues can be both target and source for estrogen or testosterone While ER- is found in the bulge region, ER- and androgen receptors are found in the dermal papilla The hair cycle is self-renewing because of the presence of stem cells in the bulge It is thought that cells in the dermal papilla send a signal to the stem cells in the bulge to differentiate and ultimately restart the anagen phase While it is known that the dermal papillae regulate hair growth and have receptors for androgens and ER- , the sequence of signals that regulate hair growth has not been elucidated What is clear is that estrogens and androgens are intimately involved in this process Gender differences in hair exist as evidenced in the commonality of androgenetic alopecia, which occurs but is much less common in women This gender difference may be attributable more to the inherent enzyme content within hair follicles than to serum hormone levels For instance, Sawaya and Price17 examined the levels of 5- -reductase types I and II, aromatase, and androgen receptors in hair follicles of women and men with androgenetic alopecia and found that the women had a six-fold greater aromatase level in frontal hair follicles than the men, giving them the ability to convert weaker sex hormone precursors into stronger ones These authors also determined that the women had threeand three-and-a-half-fold less 5- -reductase types I and II, respectively, in their hair follicles than the men did in their frontal hair follicles, thus reducing the women s ability to synthesize the more potent form of male hormone, DHT, which is responsible for hair miniaturization and eventual loss17 Sawaya and
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Price17 concluded that these differences in androgen receptor and steroid-converting enzymes may account for the different clinical presentations of androgenetic alopecia in women and men A similar study examining androgen receptor and steroid-converting enzymes should be undertaken in women and men with normal hair growth as well as those with other hair growth disorders
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While skin quality deteriorates because of the synergistic effects of chronologic time, photoaging, and environmental factors such as smoking and poor nutrition, the results of hormonal decline with age on the quality of skin are also significant and worthy of examination Young skin is often associated with acne, oiliness, and thick scar or keloid formation, while the clinically apparent changes associated with aging skin include skin thinning (notably, not in all layers) and atrophy, loss of elasticity, dryness, increased wrinkling, and poor wound healing but cosmetically better surgical scars While androgen and estrogen receptors are found in the epidermis, sebaceous glands, and hair follicles, it is primarily ER- that is localized in the fibroblasts of the dermis, and it is the fibroblasts that synthesize collagen, hyaluronic acid, elastin, and other components of the extracellular matrix10,11 Therefore, of the sex hormones, it is mainly estrogen that controls the fibroblast Collagen is responsible for imparting strength and structure to the skin; elastin confers its elasticity; and hyaluronic acid content directly leads to an increase in waterholding capacity Together, these constituents provide the resilience and fullness to the skin that is associated with youth, while the lack of these constituents leads to wrinkles, the feature most emblematic of aged skin In the fourth and fifth decades of life, many women begin to notice changes in their skin that are associated with changes seen in menopause Most postmenopausal women complain of skin thinning and dryness, an increase in wrinkles, and decreased elasticity of the skin In fact, studies have shown that as much as 30% of skin collagen (both type I, which confers strength to the skin, and type III, which contributes to the elasticity of skin) is lost in the first 5 years after menopause,18 and total
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collagen levels are estimated to decline on an average of 2% per postmenopausal year over a period of 15 years19 In a study by Affinito et al that evaluated the effects of aging and postmenopausal hypoestrogenism on type I and type III collagen content in the skin of premenopausal and postmenopausal women, a decrease in skin collagen was more closely related to years of postmenopause than to chronologic age18 While collagen content seems to quickly diminish with increased postmenopausal years, several studies demonstrate that postmenopausal women who start receiving hormone replacement therapy (HRT) with estrogen have an increase in skin collagen content,19 22 with as much as a 65% increase in skin collagen content after 6 months of estrogen replacement21 In a study by Brincat et al examining different regimens of estrogen replacement therapy in postmenopausal women, the authors found that all regimens of estrogen therapy under consideration increased skin collagen content and that estrogen replacement therapy is prophylactic in women who have higher skin collagen levels and both prophylactic and therapeutic in women with lower skin collagen levels19 Similarly, a study by Castelo-Branco et al examining skin collagen changes and HRT in postmenopausal women at 0 and 12 months of treatment showed that various forms of HRT with estrogeninduced increases in skin collagen content in postmenopausal women, whereas the postmenopausal control
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group had significant decreases when assessed at the same time points22 (Box 5-1) In another study by Brincat et al23 examining skin collagen changes in postmenopausal women receiving topical estradiol applied to the abdomen and thigh, the authors noted a strong correlation between the change in skin collagen content and the original skin collagen content, indicating that the change in response to estrogen therapy is dependent on the original collagen level, and that there is no further increase in collagen production once an optimum skin collagen level is reached This study is particularly noteworthy insofar as it suggests that there is a therapeutic window in which estrogen exerts its maximal effect in stimulating collagen production Estrogen can also combat skin dryness by decreasing transepidermal water loss In a study by Pi rard-Franchimont et al that examined transepidermal water loss in menopausal women, the authors found that women receiving transdermal hormone replacement with estrogen exhibited a significantly increased water-holding capacity of the stratum corneum as compared with menopausal women not receiving hormone replacement24 In addition, in a study examining changes in transepidermal water loss and cutaneous blood flow during the menstrual cycle, Harvell et al found that transepidermal water loss was higher on the day of minimal estrogen/progesterone secretion as compared with the day of maximal estrogen secretion on both back (p 0037) and forearm (p 0021) skin in normal
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