Skin Care and Treatments of Melbourne Dermatology - Estradiol

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Wednesday, 31 March 2010

Induction of Collagen by Topical Estradiol

Induction of Collagen by Topical Estradiol — Estrogen- and Soy-Containing Skin Care Products.

The basis for systemic and topical estrogen study and use originates in findings that link estrogen depletion and chronologic skin aging.

Decreases in skin thickness following menopause are to be expected without hormone replacement.

Collagen, elastin and dermal hyaluronic acid appear to be highly sensitive to and dependent on hormonal levels — their reduction produces skin dryness, losses in elasticity and volume.

One early study found that within five years of menopause, a large amount (approximately one third) of skin collagen is lost, although other factors — notably free radical damage — are implicated in aging.

Conversely, a controversial trial of a hormone replacement medication ceased in 2002 on grounds it increased the risk of breast cancer, cardiovascular and thromboembolic disease.

Evidence suggests estrogens are stronger antioxidants than Vitamin C and E and that female face and chest skin are especially estrogen-receptive.

Estrogen normally works by signaling genes in cells to be switched on or off, however this recent study has found that sun-damaged skin isn't improved by topical estradiol (Topical 17-beta estradiol in ethanol/propylene glycol (ETOH/PG).

Topical estradiol is included in products such as prescription topical Premarin and OTC Jan Marini Age Intervention (Serum and Cream).

Because photo-aging is superimposed on natural aging in sun-exposed areas of the skin, the results suggest that alterations induced by long-term sun exposure hinder the ability of topical estradiol to stimulate collagen production in aged human skin in vivo.

Comments from Study Co-Author Laure Rittié, PhD

"Frankly, we were very surprised to find that stimulation of collagen production by topical estrogen treatment was restricted to skin not chronically exposed to sunlight. These results suggest that sun exposure alters the ability of skin to respond to topical estrogen, and point out how difficult it is to repair photoaged skin."

An earlier study had found that topical estrogen did repair photodamaged mouse skin.

Estrogens and Phytoestrogens in Skin Care

Topical estrogens (such as estradiol) are more potent than phytoestrogens (found in soy-containing skin care products), however they have a tendency to cause allergies in around a quarter of post-menopausal women.

If you are already taking hormone replacement medication, topical estrogens should not be used without medical attention.

Although they may be purchased through online pharmacies and retailers, neither should topical estrogens be used without medical attention as contraindications exist.

Topically applied soy isoflavones (phytoestrogens) — weaker than estrogens although mimicking their effects — are available in soy-containing foods and many products among which are Skinceuticals Face Cream, Eye Balm, Advanced Body Firming Lotion, Darphin Rose Aromatic Care, Arovita C Cream, Stimulskin Plus Cream, Gernetic Hydra-Men, IS Clinical Youth Complex, Nivea Visage Triple Action Soy, Neutrogena Anti-Aging Hand Cream and J&J's Aveeno Positively Radiant.

Studies in mice suggested systemic and topical soy prevents skin cancer in mice, with the optimal effect reached through a combination of systemic and topical phytoestrogen supplementation, however they are now unlikely to be of any considerable benefit for chronically sun-damaged skin and to be lesser-effective than pure estradiol in any event.

The key components of soy isoflavones are the chemicals genistein and diadzein and are enhanced in the presence of ascorbic acid.

Prescription topical and systemic estrogens, diets and skin care products containing soy may enhance the natural moisturisation, firmness, thickness and antioxidant defenses of post-menopausal female skin in areas of the body which have been consistently photoprotected.

Soy and estradiol-containing skin care formulated to penetrate skin effectively are likely to deliver greater benefit to body skin than facial and hand skin, which more often than not end up chronically photodamaged.

Lifelong photoprotection can enhance skin's positive response to systemic and topical estrogen and soy isoflavones.

Collagen Study Objective

To evaluate the effectiveness of topical estradiol in stimulating collagen I and collagen III production in naturally aged and photoaged human skin of postmenopausal women and age-matched men.

Collagen Study Design

Vehicle-controlled treatment followed by biochemical and immunohistochemical analyses of skin biopsy specimens.

Collagen Study Setting

Academic referral center.

Collagen Study Participants

Seventy healthy volunteers (40 postmenopausal women with a mean age of 75 years, and 30 men with a mean age of 75 years) with photodamaged skin.


Topical application of estradiol, 0.01%, 0.1%, 1%, or 2.5% or vehicle on aged or photoaged skin, with biopsy specimens taken after last treatment.

Main Outcome Measures

De novo synthesis of collagen by quantitative polymerase chain reaction, immunohistochemistry, and enzyme-linked immunosorbent assay.

Collagen Study Results

Topical estradiol increased procollagen I and III messenger RNA and collagen I protein levels in sun-protected aged hip skin in postmenopausal women and, to a lesser extent, in age-matched men.

Surprisingly, no significant changes in production were observed in women or men after 2-week estradiol treatment of photoaged forearm or face skin, despite similar expression of estrogen receptors (ER-, ER-?, and GPR30) in aged and photoaged skin.

Estradiol treatment induced the estrogen-responsive gene GREB1, indicating that penetration of topical estradiol and genomic response to estrogen were similar in the 3 anatomic sites.

Collagen Study Conculsions

Two-week topical estradiol treatment stimulates collagen production in sun-protected hip skin, but not in photoaged forearm or face skin, in postmenopausal women and aged-matched men.

These findings suggest that menopause-associated estrogen decline is involved in reduced collagen production in sun-protected skin.

Interestingly, alterations induced by long-term sun exposure hinder the ability of topical 2-week estradiol to stimulate collagen production in aged skin.

Related Collagen and Estradiol Studies

Skin collagen changes in post-menopausal women receiving oestradiol gel.

Brincat M, Versi E, O'Dowd T, Moniz CF, Magos A, Kabalan S, Studd JW.

Maturitas. 1987; 9:1-5.

Sixteen post-menopausal women who had never previously received any hormonal treatment applied Oestrogel cream 1.5 mg/day percutaneously for 1 yr. Skin biopsies were taken from the abdomen and from the lateral aspect of the thigh at 0, 3, 6 and 12 mth, and the changes in skin collagen content were noted. The abdominal skin collagen content increased significantly (P less than 0.001) over the 1-yr treatment period. The thigh skin collagen content also increased, but did not reach significant levels. There was a strong correlation between the change in skin collagen content (in both the abdomen and the thigh) and the original skin collagen content, indicating that the change in collagen content in response to oestrogen therapy is dependent on the original level. There is no further increase once an 'optimum' skin collagen level has been reached.

The effect of topical oestradiol on skin collagen of postmenopausal women

Eero Varila, Immo Rantala, Aarne Oikarinen, Juha Risteli, Timo Reunala, Hanna Oksanen, Reijo Punnonen.

BJOG: An International Journal of Obstetrics & Gynaecology. 1995; 102(12):985-989

Topical oestradiol treatment increases the amount of skin collagen. The increase in the level of PICP and PIIINP in skin blister fluid indicates that oestradiol treatment stimulates collagen synthesis. Furthermore, our results show that topical ostradiol treatment has a greater influence on the amount than on the quality of skin collagen. On the contrary, in elastic tissue the oestradiol treatment will only result in morphologic improvement.

Estradiol-17beta as an antioxidant: some distinct features when compared with common fat-soluble antioxidants.

Ayres, S : Tang, M : Subbiah, M T

J-Lab-Clin-Med. 1996 Oct; 128(4): 367-75

Estrogens are potent antioxidants both in vitro and in vivo. In this study the antioxidant affect of estradiol-17beta (estradiol) was compared with those of fat-soluble antioxidants (alpha-tocopherol and beta-carotene) in terms of both fatty acid (thiobarbituric acid-reactive substances and diene conjugation) and cholesterol oxidation (oxysterols). The addition of alpha-tocopherol (54 micromol/L) inhibited low-density lipoprotein (LDL) oxidation by 92.6% and high-density lipoprotein (HDL) oxidation by 76.5%. In similar experiments, estradiol (54 micromol/L) inhibited LDL oxidation by 77.5% but inhibited HDL oxidation by only 55.4%. Beta-carotene had no antioxidant effect. Lag times (diene conjugation method) for alpha-tocopherol and beta-carotene increased by 175% and 125%, respectively. Estradiol markedly reduced the maximum formation of diene conjugates as compared with results with alpha-tocopherol and beta-carotene, and it exhibited a linear curve (no change in lag time). In terms of cholesterol oxidation, estradiol was far more effective than alpha-tocopherol or beta-carotene in inhibiting oxysterol formation (microg/ml plasma) (control = 24.56 +/- 2.31, beta-carotene = 20.59 +/- 3.32, alpha-tocopherol = 20.19 +/- 1.58, estradiol = 14.38 +/- 0.70). This study shows that estradiol is as effective an antioxidant as alpha-tocopherol in terms of fatty acid peroxidation but is far more effective than alpha-tocopherol in terms of cholesterol peroxidation.

Estradiol as an antioxidant: incompatible with its physiological concentrations and function.

Santanam N, Shern-Brewer R, McClatchey R, Castellano PZ, Murphy AA, Voelkel S, Parthasarathy S.

Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, GA 30322, USA.

Estradiol has been documented to inhibit the oxidation of low density lipoprotein (LDL). We show that physiological concentrations of estradiol do not inhibit the oxidation of LDL by copper. LDL samples isolated from a) premenopausal and postmenopausal women and from b) women at different time periods during their menstrual cycle, who differ vastly in plasma estradiol levels, were also oxidized at the same rates by copper. In contrast, LDL samples isolated from c) women who were hyperstimulated during in vitro fertilization (IVF), with estradiol concentrations above 2000 pg/ml, were resistant to oxidation by copper. However, these LDL samples were also oxidized at a higher rate by peroxidases. More importantly, subjects with high estradiol levels also showed an increase in myeloperoxidase (MPO) protein in the plasma. Based on these results, we conclude that at physiologic concentrations, it is unlikely that estradiol could act as an antioxidant. In fact, the ability of estradiol to induce MPO and become a prooxidant might instead suggest that MPO-mediated oxidative clearance of LDL from plasma by liver might favorably influence the outcome of atherosclerosis.

Topical estrogens: their effects on connective tissue synthesis in hairless mouse skin

Gerard J. Gendimenico, Vincent J. Mack, Paul A. Siock, James A. Mezick.

Arch Dermatol Res. 2002 Jul;294(5):231-6. 2002 Jun 7.

Skin is an important target organ for estrogens. The major reported effects of estrogens are as regulators of connective tissue molecules, namely collagen and hyaluronic acid. We investigated the regulation of connective tissue synthesis by topical estrogens in a hairless mouse model of photodamaged skin, which has been previously shown to respond to topical retinoids. The naturally occurring estrogen, 17#-estradiol (17#-E) and a close stereoisomer, 17!-estradiol (17!-E), were found to be as effective as all-trans-retinoic acid in stimulating the development of new connective repair zones in photodamaged skin. Furthermore, 17#-E and 17!-E caused a skin thickening response in normal hairless mouse skin after three daily treatments. Skin thickening is due to water accumulation as a result of estrogen-induced hyaluronan synthesis. Our results show that topical estrogens are important regulators of connective tissue synthesis in photodamaged skin as well as normal skin. These findings are consistent with reports from human studies in which estrogen has been found to stimulate collagen production. We also demonstrated that 17!-E, previously thought to be a weak or inactive estrogen, is less potent than 17#-E, but nonetheless topically effective in stimulating connective tissue synthesis.

Induction of Collagen by Estradiol — Authors

Laure Rittié, PhD; Sewon Kang, MD; John J. Voorhees, MD; Gary J. Fisher, PhD

Arch Dermatol. 2008;144(9):1129-1140.

Trial Registration Identifier: NCT00113100

Collagen Study Authors

Laure Rittié, PhD

Laure Rittié is a Research Investigator in the Department of Dermatology Photoaging and Aging Research Program at the University of Michigan in Ann Arbor. Dr. Rittié received her Ph.D. in Biochemistry and Molecular Biology from the Université de Reims Champagne-Ardenne, France in 2001 and her Master of Science in Cell Biology from the Université de Reims Champagne-Ardenne, France in 1996. Dr. Rittié received postdoctoral training at the Université de Reims Champagne, France and at the University of Michigan, Department of Dermatology. She was recruited to join the Dermatology Department faculty in 2006.

Sewon Kang, MD

Clinical Interests: Skin aging, psoriasis, atopic dermatitis, scleroderma, acne and rosacea. Research Interests: Pharmacology of retinoids and immunosuppression. Photomedicine and photoaging.

John J. Voorhees, MD

Dr. Voorhees' research focuses on psoriasis and premature aging of the skin.

Gary J. Fisher, PhD

Dr. Fisher's research studies the molecular mechanisms of sun-induced premature skin aging and the molecular mechanisms of chronological skin aging focusing on four major areas: procollagen biosynthesis, collagen degradation, signal transduction, and inflammation.

Author Affiliations: Department of Dermatology, University of Michigan Medical School, Ann Arbor.

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