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Menopause HRT basics

The median age for onset of menopausal symptoms is 45-52 years.[1, 2] Symptoms of menopause are a significant problem, affecting nearly 80% of women in the United States between 40 and 65 years of age. [3] HRT (hormone replacement therapy) with estrogen and progesterone is often prescribed to treat symptoms associated with menopause, including hot flushes, night sweats and sleep disturbances.[4] As outlined below, adding testosterone to HRT confers additional benefits.
 

Quick facts about menopausal HRT (Hormone Replacement Therapy) preparations

 
* Transdermal administration of hormones, especially estrogen, provides a more beneficial effect on cardiovascular risk factors [5] and less risk of blood clots and thromboembolic complications [6] compared to oral estrogen. In addition, transdermal estrogen doesn’t stimulate SHBG (sex hormone binding globulin) production as much as oral estrogen [7], and thus causes less reduction in blood levels of free “active” testosterone. Therefore, women with low testosterone or those experiencing sexual dysfunction and/or depression, may benefit even more from transdermal estrogen than oral estrogen.[8-10]
 
* The HRT window of opportunity suggests that younger symptomatic women (below 60 years of age) who start HRT around the onset of menopause or within 10 years after the last period, get the greatest overall health benefits, whereas older women treated with HRT for the first time get no overall benefit and may experience more harm.[11-13]
 
* Bioidentical hormone preparations often come from compounding pharmacies. The benefit of compounded hormone preparations is that they allow for customization of both hormone dosages and hormone mixes (estrogen, progesterone, testosterone and DHEA).[14]
 
* Progestogen is a term encompassing both bioidentical and non-bioidentical progesterone:
 
- Progesterone is bioidentical.
 
- Progestin is non-bioidentical (some examples are norethindrone and MPA [medroxy-progesterone acetate] brand name Provera®).
 
* The most common non-bioidentical HRT are:
 
- Premarin® (horse urine-derived estrogens, also called conjugated equine estrogen [CEE])
 
- Prempro® (a combination of CEE + and a synthetic progestin called medroxy-progesterone acetate [MPA]).
 
* For women with contraindications for estrogen HRT, supplementation with DHEA and/or testosterone is a viable alternative.
 

The three types of estrogens - estradiol, estrone and estriol

 
In daily parlance, estrogen is used as a synonym for estradiol. However, there are three biologically active forms of estrogens: estrone, estradiol and estriol.[15, 16] 
 
Among women at reproductive age, the main estrogen with the highest biological activity is estradiol. Estrone is about 5–10 times less active than estradiol, and only a small amount is produced in the ovaries. It mainly arises from the peripheral conversion of androstenedione. The least active estrogen is estriol. Most estriol is produced by metabolism of estradiol and estrone in the liver, but small amounts may also be produced by the ovaries.[15]
 
Conventional menopause HRT contains only estradiol (either non-bioidentical or bioidentical). Estriol is recommended by some doctors and may be included in compounded bioidentical HRT preparations. However, it is it controversial among practitioners, even among those who advocate bioidentical HRT.[16-19]
 

Do menopausal symptoms reflect a woman’s health status?

 
Vasomotor symptoms (hot flashes and night sweats) are among the most notable and bothersome menopausal symptoms, along with mood and sleep disturbances.[20, 21] Vasomotor symptoms may significantly impair quality of life and are also considered risk markers of chronic illnesses such as osteoporosis [22] and cardiovascular disease.[23] 
 
Specifically, hot flashes may mark adverse underlying vascular changes among midlife women.[23] It has been shown that women with hot flashes have impaired blood vessel function (aka endothelial dysfunction) and a greater degree of calcification of the main artery in the body (aorta) [23], which predicts an increased incidence of cardiovascular events.[24] Other data also indicated that hot flashes seem to be a marker for physiological alterations that could be associated with cardiovascular disease.[25]
 

Do menopausal symptoms subside over time?

 
A recent meta-analysis found that 2 years before menopause, vasomotor symptoms are present in 14% of premenopausal women (which may come as surprise to many), peaking 1 year (56%) after menopause onset, and then decreasing over the following 5 years (28.9%).[26] In most women vasomotor symptoms has subsided 8 years after final menstrual, but 10% of women reported symptoms up to 12 years after final menstrual period.[26]  A more recent study also shows that the prevalence of bothersome vasomotor symptoms decreases from 51% at 1 year after menopause to 23% at 4 years after menopause.[27]
 
However, one also need to consider menopause risk factors that aren’t visible, including but not limited to, osteoporosis and cardiovascular risk factors. Even though a correlation has been found between menopausal symptoms (hot flashes) and osteoporosis and cardiovascular risk factors, it is important that these invisible risk factors are being monitored also in menopausal women who do not suffer from vasomotor symptoms. Postmenopausal women who have low levels testosterone (due to low DHEA levels and/or surgical removal of the ovaries) are more likely to develop osteoporotic fractures, depression and deterioration in wellbeing (see below).
 

Can menopausal symptoms be affected by lifestyle habits?

 
Another factor contributing to inter-individual variability in menopause symptoms is lifestyle. Obesity, lack of exercise and smoking are related to more severe symptoms.[28] Weight loss induced by a healthy dietary modification may help eliminate vasomotor symptoms among postmenopausal women not taking HRT.[29] Exercise is another greatly influential lifestyle factor affecting the duration of hot flushes seems; more regular exercise I associated with shorter symptom duration.[30]
 

Why do some women suffer more than others from menopausal symptoms? 

 
Menopausal symptoms, especially hot flashes, shown a great deal of variability in frequency and severity between women.[27, 28, 31] Aside lifestyle factors, one major contribution to this inter-individual variability is the wide distribution of DHEA levels.[32, 33] DHEA (dehydroepiandrosterone) is a natural pro-hormone which the body gets converted to both estrogen and testosterone. In women DHEA is secreted by the adrenal gland and the ovaries, even after menopause.[33, 34]
 
A notable study investigated the inter-individual variability of DHEA blood levels and the contribution of the ovary to sex hormone (estrogen and testosterone) metabolism in postmenopausal women.[33] DHEA blood levels and its metabolites, estrogen and testosterone, were measured in postmenopausal women aged 42 to 74 years. It was found that the lowest and highest recorded levels of DHEA varied 8-fold between women.[33] The inter-individual variability in testosterone and estrogen levels was even greater, 10-fold for testosterone and 12-fold estrogen.[33] These results explain the lack of menopausal symptoms in some women, and also provide an indication for DHEA supplementation in women with menopausal symptoms. In accordance with this, a study that compared traditional estrogen therapy (CEE) with DHEA found that DHEA was as effective as CEE in alleviating menopausal symptoms, without causing side effects seen with CEE (headache and nausea).[35] 

 

It is not just about estrogen – DHEA, testosterone and cortisol also impact women’s health

 
The almost exclusive focus on the role of ovarian estrogens for women’s health and menopause issues has overshadowed the dramatic 60-70% fall in blood levels of DHEA, which already occurs between the ages of 20-30 and 40 -50 years.[36-38] Because DHEA is transformed to both androgens and estrogens in tissues, such a fall in blood levels of DHEA(S) explains why women at menopause are not only lacking estrogens but are also likely to have been deprived of testosterone for several years.[37] 
 
Testosterone levels in women decrease progressively from the age of 30 years in parallel with the decrease in DHEA(S) levels.[37, 39] Consequently, it appears logical to use both testosterone and estrogen replacement therapy at peri- and post-menopause in order to maintain a physiological balance between these two classes of sex hormones. This can be accomplished by DHEA supplementation, or by adding testosterone to estrogen replacement therapy (see below).
 
Another menopause related hormonal change is an elevation of cortisol levels.[40, 41] Studies of women experiencing hot flashes in laboratory situations indicate that a cortisol spike follows hot flashes.[42] In line with this, it has been shown that climacteric symptoms are associated with increased 24-hour urinary cortisol level and risk factors for cardiovascular disease, such as insulin resistance and decreased HDL-cholesterol level.[43] As cortisol promotes development and progression of atherosclerosis [43-45], the elevated cardiovascular risk in post-menopausal women may be due not only to withdrawal from estrogen, but also due to elevation of cortisol. In the same way, menopausal elevation of cortisol may contribute to the increased accumulation of abdominal body fat that comply occurs in women after menopause.[46-50]
 

Why is Progesterone added to Estrogen in HRT?

 
Progesterone is the "other" female hormone (the main one is estrogen) naturally produced by the ovaries in women. Progesterone balances out the effects of estrogen in certain tissues, such as the endometrium (i.e. the mucous membrane lining the walls of the uterus).
 
Progestogens (either progesterone or progestin, see explanation of terminology below) are added to estrogen in HRT in order to counteract the development of endometrial cancer, which is an important risk with estrogen therapy alone (known as unopposed estrogen therapy).[51, 52] However, the addition of non-bioidential progesterone (i.e. progestin) to estrogen HRT markedly increases the risk of breast cancer relative to estrogen use alone.[53-55]
 
However, bioidential progesterone does not have this detrimental impact on breast cancer risk; it may even reduce breast cancer risk.[56] Bioidential progesterone also has neuro-protective effects.[57] The benefits of bioidential progesterone will be covered in an upcoming article.
 
Another reason to add progesterone to menopausal HRT is that hormone replacement with estrogen alone may cause and/or exacerbate migraine.[58-60] Higher levels of estradiol and an elevated estradiol:progesterone ratio are directly correlated to worsening of migraine attacks [61] and progesterone deficiency has been linked to migraine.[62] Therefore, adding progesterone to estrogen in HRT can help alleviate menstrual migraine [63] and tailored hormonal replacement therapy that minimizes estrogen/progesterone imbalance are recommended.[64]
 
Summary of progesterone
 
Progestagens (either progesterone or progestin) are added to estrogen in HRT in order to counteract the development of endometrial cancer, which is a risk with estrogen therapy. While non-bioidential progesterone increases breast cancer risk, bioidential progesterone may reduce breast cancer risk. In addition bioidential progesterone has neuro-protective effects and helps alleviate menstrual migraine.
 

Should testosterone be added to estrogen HRT?

 
The prevalence of sexual dysfunction among all women is estimated to be between 25% and 63%; in postmenopausal women the prevalence is even higher, with rates between 68% and 86.5%.[65] Menopausal HRT effectively relieves menopausal symptoms, and for women suffering from painful intercourse (dyspareunia) due to vaginal dryness, estrogen therapy enhances sexual pleasure and desire.[66] However, progestins can oppose these changes and lead to a recurrence of vaginal dryness and pain.[66] 
 
For some women, sexual difficulties respond initially to estrogen therapy but subsequently revert to their initial problems, especially when the problem has been loss of libido.[66] Another group of women have sexual difficulties that remain unresponsive to estrogen therapy.[66, 67] For these women, the addition of testosterone to HRT increases libido and well-being.[68, 69]
 
One reason for the lack of, or negative, effect on sexual function in many women taking HRT is that estrogen and progesterone treatment reduces testosterone “the libido hormone” levels [70-72], and women with lower testosterone levels often report low libido.[73] However, it should be noted that some women may be more sensitive to changes in testosterone levels than others.[74]
 
For example, one study gave naturally menopausal women 2 mg/day of oral micronized estradiol for 12 weeks.[72] It was found that this reduced testosterone levels by 42% and DHEA(S) levels by 23%, while elevating the level of sex hormone binding globulin (SHBG) by 160%. Because SHBG binds to and “inactivates” testosterone, this large elevation in SHBG likely reduced bioavailable testosterone (the active testosterone fraction) even more profoundly.[72] Progestins (levonorgestrel and norethindrone acetate) also lower testosterone levels.[70, 71]
 
Many studies show that the addition of testosterone to estrogen treatment improves sexual function more than treatment with estrogen alone in postmenopausal women.[8, 75, 76] Consequently, even though there is no universal threshold for testosterone below which sexual dysfunction appears, testosterone deficiency is considered among the underlying causes of hypoactive sexual desire disorder (HSDD).[77]
 
Another reason to add testosterone to estrogen/progesterone therapy is that testosterone prevents development and progression of breast cancer.[78-87] We will cover this in more depth in an upcoming article.
 
Summary of combined HRT + testosterone
 
Menopausal estrogen therapy may induce testosterone deficiency, and combined estrogen + testosterone treatment shows additional benefits on sexual function and wellbeing over estrogen treatment alone. Testosterone also confers protection against breast cancer. This provides a strong argument for concurrent estrogen and testosterone replacement therapy.
 

Are there any contraindications for estrogen therapy?

 
Clinical guidelines consider the following clinical situations to be contraindications for traditional HRT treatment (i.e. reasons to withhold treatment): [88, 89]
 
A family history of breast cancer
 
A family history of endometrial cancer 
 
Hypertriglyceridemia (elevated triglycerides, aka blood fats)
 
Thromboembolic disorders (eg. venous thrombosis and pulmonary embolism)
 
Undiagnosed vaginal bleeding (eg. dysfunctional uterine bleeding)
 
Endometriosis (a disorder in which tissue that normally lines the inside of the uterus (aka endometrium) grows outside the uterus)
 
Fibroids (noncancerous (benign) tumors that develop in the womb (uterus)
 
Severe liver disease
 

Menopause hormone therapy with only testosterone?

 
For women who have contraindications for estrogen therapy, or who refuse estrogen therapy, there are effective alternatives. Clinical studies show that both DHEA supplementation and testosterone therapy effectively alleviate menopausal symptoms, and also confer significant health benefits.
 
In an upcoming article we will cover the importance of DHEA supplementation for women’s health, and its use to alleviate menopausal symptoms.
 
For more info on use of testosterone therapy as a possible alternative to traditional HRT, see our previous articles:
 
 
 
 
(this article refutes the old myth that testosterone is supposedly un-physiological for women)


 

References:

1.            Morris, E.P. and N. Burbos, Menopausal symptoms. Clin Evid (Online), 2010. 2010.

2.            Palacios, S., et al., Age of menopause and impact of climacteric symptoms by geographical region. Climacteric, 2010. 13(5): p. 419-28.

3.            Williams, R.E., et al., Frequency and severity of vasomotor symptoms among peri- and postmenopausal women in the United States. Climacteric, 2008. 11(1): p. 32-43.

4.            Jokinen, K., et al., Experience of climacteric symptoms among 42-46 and 52-56-year-old women. Maturitas, 2003. 46(3): p. 199-205.

5.            Kopper, N.W., J. Gudeman, and D.J. Thompson, Transdermal hormone therapy in postmenopausal women: a review of metabolic effects and drug delivery technologies. Drug Des Devel Ther, 2009. 2: p. 193-202.

6.            Canonico, M., et al., Hormone therapy and venous thromboembolism among postmenopausal women: impact of the route of estrogen administration and progestogens: the ESTHER study. Circulation, 2007. 115(7): p. 840-5.

7.            Campagnoli, C., et al., Differential effects of oral conjugated estrogens and transdermal estradiol on insulin-like growth factor 1, growth hormone and sex hormone binding globulin serum levels. Gynecol Endocrinol, 1993. 7(4): p. 251-8.

8.            Somboonporn, W., et al., Testosterone for peri- and postmenopausal women. Cochrane Database Syst Rev, 2005(4): p. CD004509.

9.            Rohr, U.D., The impact of testosterone imbalance on depression and women's health. Maturitas, 2002. 41 Suppl 1: p. S25-46.

10.          Nappi, R.E., et al., Menopause and sexual desire: the role of testosterone. Menopause Int, 2010. 16(4): p. 162-8.

11.          Rossouw, J.E., et al., Lessons learned from the Women's Health Initiative trials of menopausal hormone therapy. Obstet Gynecol, 2013. 121(1): p. 172-6.

12.          Lobo, R.A., Where are we 10 years after the Women's Health Initiative? J Clin Endocrinol Metab, 2013. 98(5): p. 1771-80.

13.          Wharton, W., et al., Rationale and design of the Kronos Early Estrogen Prevention Study (KEEPS) and the KEEPS Cognitive and Affective sub study (KEEPS Cog). Brain Res, 2013. 1514: p. 12-7.

14.          McBane, S.E., et al., Use of compounded bioidentical hormone therapy in menopausal women: an opinion statement of the Women's Health Practice and Research Network of the American College of Clinical Pharmacy. Pharmacotherapy, 2014. 34(4): p. 410-23.

15.          Krolik, M. and H. Milnerowicz, The effect of using estrogens in the light of scientific research. Adv Clin Exp Med, 2012. 21(4): p. 535-43.

16.          Taylor, M., Unconventional estrogens: estriol, biest, and triest. Clinical Obstetrics and Gynecology, 2001. 44(4): p. 864-79.

17.          Head, K.A., Estriol: safety and efficacy. Alternative Medicine Review, 1998. 3(2): p. 101-13.

18.          Esposito, G., Estriol: a weak estrogen or a different hormone? Gynecological Endocrinology, 1991. 5(2): p. 131-53.

19.          Heimer, G.M., Estriol in the postmenopause. Acta Obstetricia et Gynecologica Scandinavica. Supplement, 1987. 139: p. 1-23.

20.          Rapkin, A.J., Vasomotor symptoms in menopause: physiologic condition and central nervous system approaches to treatment. Am J Obstet Gynecol, 2007. 196(2): p. 97-106.

21.          Pinkerton, J.V. and A.S. Zion, Vasomotor symptoms in menopause: where we've been and where we're going. J Womens Health (Larchmt), 2006. 15(2): p. 135-45.

22.          Crandall, C.J., et al., Presence of vasomotor symptoms is associated with lower bone mineral density: a longitudinal analysis. Menopause, 2009. 16(2): p. 239-46.

23.          Thurston, R.C., et al., Hot flashes and subclinical cardiovascular disease: findings from the Study of Women's Health Across the Nation Heart Study. Circulation, 2008. 118(12): p. 1234-40.

24.          Jayalath, R.W., S.H. Mangan, and J. Golledge, Aortic calcification. Eur J Vasc Endovasc Surg, 2005. 30(5): p. 476-88.

25.          Pines, A., Vasomotor symptoms and cardiovascular disease risk. Climacteric, 2011. 14(5): p. 535-6.

26.          Politi, M.C., M.D. Schleinitz, and N.F. Col, Revisiting the duration of vasomotor symptoms of menopause: a meta-analysis. J Gen Intern Med, 2008. 23(9): p. 1507-13.

27.          Hemminki, E., et al., Variability of bothersome menopausal symptoms over time--a longitudinal analysis using the Estonian postmenopausal hormone therapy trial (EPHT). BMC Womens Health, 2012. 12: p. 44.

28.          Gold, E.B., et al., Relation of demographic and lifestyle factors to symptoms in a multi-racial/ethnic population of women 40-55 years of age. Am J Epidemiol, 2000. 152(5): p. 463-73.

29.          Kroenke, C.H., et al., Effects of a dietary intervention and weight change on vasomotor symptoms in the Women's Health Initiative. Menopause, 2012. 19(9): p. 980-8.

30.          Col, N.F., et al., Duration of vasomotor symptoms in middle-aged women: a longitudinal study. Menopause, 2009. 16(3): p. 453-7.

31.          Utian, W.H., Psychosocial and socioeconomic burden of vasomotor symptoms in menopause: a comprehensive review. Health Qual Life Outcomes, 2005. 3: p. 47.

32.          Labrie, F., Impact of circulating dehydroepiandrosterone on androgen formation in women. Menopause, 2011. 18(5): p. 471-3.

33.          Labrie, F., C. Martel, and J. Balser, Wide distribution of the serum dehydroepiandrosterone and sex steroid levels in postmenopausal women: role of the ovary? Menopause, 2011. 18(1): p. 30-43.

34.          Labrie, F., DHEA, important source of sex steroids in men and even more in women. Prog Brain Res, 2010. 182: p. 97-148.

35.          Gupta, B., et al., A Comparative Study of CEE, Tibolone, and DHEA as Hormone Replacement Therapy for Surgical Menopause. J Obstet Gynaecol India, 2013. 63(3): p. 194-8.

36.          Orentreich, N., et al., Age changes and sex differences in serum dehydroepiandrosterone sulfate concentrations throughout adulthood. J Clin Endocrinol Metab, 1984. 59(3): p. 551-5.

37.          Labrie, F., et al., Marked decline in serum concentrations of adrenal C19 sex steroid precursors and conjugated androgen metabolites during aging. J Clin Endocrinol Metab, 1997. 82(8): p. 2396-402.

38.          Migeon, C.J., et al., Dehydroepiandrosterone and androsterone levels in human plasma: effect of age and sex; day-to-day and diurnal variations. J Clin Endocrinol Metab, 1957. 17(9): p. 1051-62.

39.          Davison, S.L., et al., Androgen levels in adult females: changes with age, menopause, and oophorectomy. J Clin Endocrinol Metab, 2005. 90(7): p. 3847-53.

40.          Woods, N.F., et al., Increased urinary cortisol levels during the menopausal transition. Menopause, 2006. 13(2): p. 212-21.

41.          Woods, N.F., E.S. Mitchell, and K. Smith-Dijulio, Cortisol levels during the menopausal transition and early postmenopause: observations from the Seattle Midlife Women's Health Study. Menopause, 2009. 16(4): p. 708-18.

42.          Meldrum, D.R., et al., Pituitary hormones during the menopausal hot flash. Obstet Gynecol, 1984. 64(6): p. 752-6.

43.          Cagnacci, A., et al., Increased cortisol level: a possible link between climacteric symptoms and cardiovascular risk factors. Menopause, 2011. 18(3): p. 273-8.

44.          Hadoke, P.W., J. Iqbal, and B.R. Walker, Therapeutic manipulation of glucocorticoid metabolism in cardiovascular disease. Br J Pharmacol, 2009. 156(5): p. 689-712.

45.          Whitworth, J.A., et al., Cardiovascular consequences of cortisol excess. Vasc Health Risk Manag, 2005. 1(4): p. 291-9.

46.          Duclos, M., et al., Increased cortisol bioavailability, abdominal obesity, and the metabolic syndrome in obese women. Obes Res, 2005. 13(7): p. 1157-66.

47.          Wallerius, S., et al., Rise in morning saliva cortisol is associated with abdominal obesity in men: a preliminary report. J Endocrinol Invest, 2003. 26(7): p. 616-9.

48.          Poehlman, E.T., Menopause, energy expenditure, and body composition. Acta Obstet Gynecol Scand, 2002. 81(7): p. 603-11.

49.          Toth, M.J., et al., Menopause-related changes in body fat distribution. Ann N Y Acad Sci, 2000. 904: p. 502-6.

50.          Shi, H. and D.J. Clegg, Sex differences in the regulation of body weight. Physiol Behav, 2009. 97(2): p. 199-204.

51.          Archer, D.F., The effect of the duration of progestin use on the occurrence of endometrial cancer in postmenopausal women. Menopause, 2001. 8(4): p. 245-51.

52.          Lacey, J.V., Jr., et al., Endometrial carcinoma risks among menopausal estrogen plus progestin and unopposed estrogen users in a cohort of postmenopausal women. Cancer Epidemiology, Biomarkers and Prevention, 2005. 14(7): p. 1724-31.

53.          Ross, R.K., et al., Effect of hormone replacement therapy on breast cancer risk: estrogen versus estrogen plus progestin. Journal of the National Cancer Institute, 2000. 92(4): p. 328-32.

54.          Anderson, G.L., et al., Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women's Health Initiative randomized controlled trial. JAMA, 2004. 291(14): p. 1701-12.

55.          Rossouw, J.E., et al., Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial. JAMA, 2002. 288(3): p. 321-33.

56.          Formby, B. and T.S. Wiley, Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53. Annals of Clinical Laboratory Science, 1998. 28(6): p. 360-9.

57.          Stein, D.G., The case for progesterone. Annals of the New York Academy of Sciences, 2005. 1052: p. 152-69.

58.          Silberstein, S.D. and G.R. Merriam, Sex hormones and headache. Journal of Pain and Symptom Management, 1993. 8(2): p. 98-114.

59.          Silberstein, S.D., The role of sex hormones in headache. Neurology, 1992. 42(3 Suppl 2): p. 37-42.

60.          Silberstein, S.D., Sex hormones and headache. Revue Neurologique, 2000. 156 Suppl 4: p. 4S30-41.

61.          Beckham, J.C., et al., The relationship of ovarian steroids, headache activity and menstrual distress: a pilot study with female migraineurs. Headache, 1992. 32(6): p. 292-7.

62.          Colson, N.J., et al., Investigation of hormone receptor genes in migraine. Neurogenetics, 2005. 6(1): p. 17-23.

63.          Somerville, B.W., The role of progesterone in menstrual migraine. Neurology, 1971. 21(8): p. 853-9.

64.          Nappi, R.E., et al., Hormonal management of migraine at menopause. Menopause Int, 2009. 15(2): p. 82-6.

65.          Ambler, D.R., E.J. Bieber, and M.P. Diamond, Sexual function in elderly women: a review of current literature. Rev Obstet Gynecol, 2012. 5(1): p. 16-27.

66.          Sarrel, P.M., Effects of hormone replacement therapy on sexual psychophysiology and behavior in postmenopause. J Womens Health Gend Based Med, 2000. 9 Suppl 1: p. S25-32.

67.          Sarrel, P.M., Androgen deficiency: menopause and estrogen-related factors. Fertil Steril, 2002. 77 Suppl 4: p. S63-7.

68.          DeCherney, A.H., Hormone receptors and sexuality in the human female. J Womens Health Gend Based Med, 2000. 9 Suppl 1: p. S9-13.

69.          Maia, H., Jr., J. Casoy, and J. Valente, Testosterone replacement therapy in the climacteric: benefits beyond sexuality. Gynecol Endocrinol, 2009. 25(1): p. 12-20.

70.          Thorneycroft, I.H., et al., Effect of low-dose oral contraceptives on androgenic markers and acne. Contraception, 1999. 60(5): p. 255-62.

71.          Strufaldi, R., et al., Effects of two combined hormonal contraceptives with the same composition and different doses on female sexual function and plasma androgen levels. Contraception, 2010. 82(2): p. 147-54.

72.          Casson, P.R., et al., Effect of postmenopausal estrogen replacement on circulating androgens. Obstet Gynecol, 1997. 90(6): p. 995-8.

73.          Turna, B., et al., Women with low libido: correlation of decreased androgen levels with female sexual function index. Int J Impot Res, 2005. 17(2): p. 148-53.

74.          Graham, C.A., et al., Does oral contraceptive-induced reduction in free testosterone adversely affect the sexuality or mood of women? Psychoneuroendocrinology, 2007. 32(3): p. 246-55.

75.          Floter, A., et al., Addition of testosterone to estrogen replacement therapy in oophorectomized women: effects on sexuality and well-being. Climacteric, 2002. 5(4): p. 357-65.

76.          Simon, J., et al., Testosterone patch increases sexual activity and desire in surgically menopausal women with hypoactive sexual desire disorder. J Clin Endocrinol Metab, 2005. 90(9): p. 5226-33.

77.          Kingsberg, S.A., J.A. Simon, and I. Goldstein, The current outlook for testosterone in the management of hypoactive sexual desire disorder in postmenopausal women. J Sex Med, 2008. 5 Suppl 4: p. 182-93; quiz 193.

78.          Dimitrakakis, C. and C. Bondy, Androgens and the breast. Breast Cancer Res, 2009. 11(5): p. 212.

79.          Dimitrakakis, C., et al., A physiologic role for testosterone in limiting estrogenic stimulation of the breast. Menopause, 2003. 10(4): p. 292-8.

80.          Hofling, M., et al., Testosterone inhibits estrogen/progestogen-induced breast cell proliferation in postmenopausal women. Menopause, 2007. 14(2): p. 183-90.

81.          Zhou, J., et al., Testosterone inhibits estrogen-induced mammary epithelial proliferation and suppresses estrogen receptor expression. FASEB J, 2000. 14(12): p. 1725-30.

82.          Glaser, R.L. and C. Dimitrakakis, Reduced breast cancer incidence in women treated with subcutaneous testosterone, or testosterone with anastrozole: a prospective, observational study. Maturitas, 2013. 76(4): p. 342-9.

83.          Davis, S.R., et al., The effect of transdermal testosterone on mammographic density in postmenopausal women not receiving systemic estrogen therapy. J Clin Endocrinol Metab, 2009. 94(12): p. 4907-13.

84.          Davis, S.R., et al., The incidence of invasive breast cancer among women prescribed testosterone for low libido. J Sex Med, 2009. 6(7): p. 1850-6.

85.          Schwartz, A.G., Inhibition of spontaneous breast cancer formation in female C3H(Avy/a) mice by long-term treatment with dehydroepiandrosterone. Cancer Res, 1979. 39(3): p. 1129-32.

86.          Labrie, F., et al., Endocrine and intracrine sources of androgens in women: inhibition of breast cancer and other roles of androgens and their precursor dehydroepiandrosterone. Endocr Rev, 2003. 24(2): p. 152-82.

87.          Glaser, R.L. and C. Dimitrakakis, Rapid response of breast cancer to neoadjuvant intramammary testosterone-anastrozole therapy: neoadjuvant hormone therapy in breast cancer. Menopause, 2014. 21(6): p. 673-8.

88.          de Villiers, T.J., et al., Updated 2013 International Menopause Society recommendations on menopausal hormone therapy and preventive strategies for midlife health. Climacteric, 2013. 16(3): p. 316-37.

89.          Santen, R.J., et al., Postmenopausal hormone therapy: an Endocrine Society scientific statement. J Clin Endocrinol Metab, 2010. 95(7 Suppl 1): p. s1-s66.

 
 

Tags: Hormone Replacement Therapy (HRT) bioidentical hormones menopause estrogen progesterone testosterone therapy women

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This module can not work without the AcyMailing Component