Testosterone in the Treatment of Women with Low Sex Drive

Written by BIH of Decatur on . Posted in Women

Transdermal Testosterone

Transdermal testosterone has been evaluated over the last decade for treatment of sexual dysfunction in women. A randomized, double-blind, placebo-controlled, crossover trial evaluated the use of transdermal testosterone for surgically induced postmenopausal women with low testosterone levels and decreased sexual desire. Seventy-five women with surgically induced menopause were randomly assigned to placebo, testosterone 150 μg/day patch applied twice/week and testosterone 300 μg/day patch applied twice/week for 12 weeks in addition to oral estrogen. The placebo group was noted to have an increase in the overall BISF-W score from 52 ± 27% of normal to 72 ± 38% over 12 weeks. The investigators determined that the transdermal testosterone 300-μg/day group had significantly improved frequency of sexual activity and orgasm (p=0.03) on the BISF-W, but the 150-μg/day group did not differ significantly from the placebo group. This study indicates women with low testosterone levels have a positive physical sexual response to exogenous testosterone.

The testosterone patch was further evaluated in 447 surgically induced postmenopausal women with HSDD who were taking estrogen. HSDD was assessed using questions that compared sexual desire before and after menopause and an interest in increasing sexual activity…….. At a dose of 300 μg/day over a period of 6 months, transdermal testosterone increased the frequency by 0.58 satisfying sexual episodes/week………. The number of sexual events and orgasms on the PFSF were also increased along with desire and arousal. The sexual desire score increased 67% from baseline in the 300-μg/day group compared with 48% in the placebo group. The other active groups did not demonstrate a significant change compared with placebo. These results demonstrate a positive effect on both the psychologic and physical aspects of sex with 300 μg/day of transdermal testosterone.

Further studies of the 300-μg/day testosterone patch in surgically induced postmenopausal women with HSDD demonstrated a benefit for testosterone on increasing total satisfying sexual activity by 1.5 (p=0.001) to 2 (p=0.0003) events over 4 weeks compared with placebo, although one study did not demonstrate an increase. Significant benefit was also demonstrated for other aspects of HSDD, including improved self-image, decreased personal distress, decreased concerns, and increased responsiveness. The studies also confirmed previous significant results indicating an increase of arousal, pleasure, desire, sexual activity, and orgasm.

A phase III trial of the 300-μg/day testosterone patch was conducted in surgically induced postmenopausal women with HSDD. When asked if they found a “meaningful benefit” from the testosterone patch, 33 (52%) of 64 women who received the active patch reported “yes” compared with 21 (31%) of 68 women receiving placebo (p=0.025). The women also reported increased desire (p=0.041) and activity (p=0.011) and decreased personal distress (p<0.001 ).
A significant increase in total satisfying sexual activity at 24 weeks was seen in both trials, with INITIMATE SM 1 showing a mean increase of 2.10 sexually satisfying event episodes/4 weeks with testosterone versus 0.98 events/4 weeks with placebo (p=0.0003), whereas INTIMATE SM 2 reported 1.56 and 0.73 episodes/4 weeks in the testosterone and placebo groups, respectively (p=0.001). Skin site reactions were the most commonly reported adverse effects.

The A Study in Women with Low Sexual Desire to Evaluate the Efficacy and Safety of Oral Transdermal Testosterone Therapy in Naturally Menopausal Women Receiving Transdermal Estrogen Therapy (ADORE) study was a double-blind, parallel-group study investigating the use of a transdermal testosterone patch………….. Women assigned to testosterone patch 300 μg/day experienced a mean increase of 1.69 total sexually satisfying episodes/4-week period versus an increase of 0.53 episodes/4-week period in women who received placebo (p=0.0089). Overall, more adverse events were reported by women in the placebo group versus those in the testosterone patch 300-μg/day group. However, there were greater occurrences of both acne (4.6% vs 1.4%) and hair growth (18.5% vs 12%) in the testosterone patch 300-μg/day group versus the placebo group.

Efficacy in Premenopausal Women
Although most studies investigated the use of testosterone in postmenopausal women, questions remain about the efficacy of testosterone in premenopausal women with decreased sexual desire. A small, randomized, double-blind, placebo-controlled crossover study of topical testosterone cream was evaluated in premenopausal women with low libido. Thirty-four women were given either testosterone 1% cream 10 mg/day or a placebo to apply daily. Testosterone cream demonstrated a significant effect versus placebo on the SRS score on sexual interest, satisfaction, pleasure, fantasy, activity, and orgasm. Although this study involved a small number of participants, these results suggest that women with low sexual desire may benefit from testosterone whether before or after menopause. Additional large, randomized, controlled trials are needed to assess benefit in premenopausal women.

Testosterone Supplementation for Hypoactive Sexual Desire Disorder in Women

Written by BIH of Decatur on . Posted in Women


Injectable Testosterone

In 1984, an implant of estradiol 40 mg and testosterone 100 mg was used in a small pilot study for 6 months in 17 postmenopausal women with decreased libido while taking oral estrogen. The testosterone implant demonstrated an improvement from baseline on self-reported libido and enjoyment of sex. At baseline, 94% of women reported absent or reduced libido compared with 43% of women 3 months after testosterone implantation (p<0.01). All women reported absent or reduced enjoyment of sex at baseline compared with 29% of women after 3 months (p<0.01). The effects returned to baseline levels 4 months after implantation. A placebo effect could not be ruled out due to the lack of a control group, but a follow-up study was published in 1987. This small 6-month study of 20 postmenopausal women with decreased libido while taking estrogen evaluated the effect of an estradiol 40 mg–testosterone 50-mg implant compared with estrogen alone and repeated the results of the pilot study with a significant effect of testosterone on self-reported libido and enjoyment of sex. Sexual symptoms were rated by using a visual analog scale from 0–100. Across both trials, one woman reported hirsutism and weight gain, but no other significant adverse events were reported.

A follow-up study published in 1987 evaluated the impact of an estrogen 8.5 mg–testosterone 150 mg combination (22 women) versus estrogen 10 mg (11) and placebo (11) in women who had been receiving hormones once/month since their hysterectomy and oophorectomy 4 years earlier. Women who received the combination with testosterone reported significantly more sexual desire, arousal, fantasies, and coitus and orgasm on the DMRS than women who received estrogen alone or placebo. The largest increase in coitus and orgasm was reported within the first 2 weeks of the estrogen-testosterone injection and decreased the following 2 weeks before the next injection. This suggests that the physical acts of sex may correlate with testosterone levels.

In 1995, an evaluation of a testosterone 50 mg– estradiol 50 mg implant (17 women) versus an estradiol 50 mg implant alone (16 women) every 3 months for 2 years in postmenopausal women was reported. Women who received the combination treatment with testosterone reported increased orgasm (p<0.035), sexual satisfaction (p<0.03), and sexual activity on the SRS compared with women who received estrogen alone, demonstrating long-term effects for testosterone on sexual desire and function.

Hormones and Risk of Breast Cancer

Written by BIH of Decatur on . Posted in Women

Attached is an article that is very detailed explaining the risk of breast cancer depending on the type of hormone replacement therapy used.  In a quick summary, in this study when estrogen is used alone the risk of breast cancer increases to 1.3 with normal being 1.00.  This differs from the Women’s Health Initiative Study in which conjugated estrogen alone showed no increased risk and actually slightly lower risk of breast cancer.  However, usually when estrogen is given a type of progestagen is given along with the estrogen especially in women who still have a uterus.  And this is the key:  Which type of progestagen is used with estrogen.

When estrogen is used with a synthetic progestagen (the most commonly used in the USA is Provera or medroxyprogesterone) the incidence of breast cancer rises dramatically.  The risk rises to 1.69 with 1.00 being normal.  If estrogen iHGH-Testosterone-Hormone-Replacement-Therapys used with the natural progestagen (progesterone as seen in the normally functioning female during menstruating years) the risk is 1.00, equal to non-uses of HRT.

At our clinic, natural estradiol and natural progesterone are used, never the synthetic.

The article is very long.  There are large portions that are deleted as they are technical and may not add to what can be gained by reading all the details.  However, the article in its entirety can be found on the internet.

Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study
Agnès Fournier, Franco Berrino, and Françoise Clavel-Chapelon, E3N, Nutrition, hormones et cancer: épidémiologie et prévention, Université Paris Sud – Paris XI, EA4045, Institut Gustave-Roussy, Department of Preventive and Predictive Medicine Istituto Nazionale Tumori, Milan,IT

Large numbers of hormone replacement therapies (HRTs) are available for the treatment of menopausal symptoms. It is still unclear whether some are more deleterious than others regarding breast cancer risk. The goal of this study was to assess and compare the association between different HRTs and breast cancer risk, using data from the French E3N cohort study. Invasive breast cancer cases were identified through biennial self-administered questionnaires completed from 1990 to 2002. During follow-up (mean duration 8.1 postmenopausal years), 2,354 cases of invasive breast cancer occurred among 80,377 postmenopausal women. Compared with HRT never-use, use of estrogen alone was associated with a significant 1.29-fold increased risk (95% confidence interval 1.02–1.65). The association of estrogen-progestagen combinations with breast cancer risk varied significantly according to the type of progestagen: the relative risk was 1.00 (0.83–1.22) for estrogen–progesterone, 1.16 (0.94–1.43) for estrogen–dydrogesterone, and 1.69 (1.50–1.91) for estrogen combined with other progestagens. This latter category involves progestins with different physiologic activities (androgenic, nonandrogenic, antiandrogenic), but their associations with breast cancer risk did not differ significantly from one another. This study found no evidence of an association with risk according to the route of estrogen administration (oral or transdermal/percutaneous). These findings suggest that the choice of the progestagen component in combined HRT is of importance regarding breast cancer risk; it could be preferable to use progesterone or dydrogesterone.

Estrogen–progestagen postmenopausal hormone replacement therapy (HRT) has been classified as carcinogenic to humans with respect to breast cancer, on the basis of both observational studies and randomized controlled trials [1]. However, small structural changes in progestagens may considerably alter their effects [2, 3]. The relationship between estrogen-only therapy and breast cancer risk is also the subject of intense debate: unopposed estrogen use was associated with a decreased risk of breast cancer in the Women’s Health Initiative (WHI) trial [6], but not in some observational studies [7–14].

Millions of women are still using HRTs, as estrogen remains the most effective treatment to alleviate menopausal symptoms [15]. It is therefore crucial to evaluate the effect of different HRTs on breast cancer risk and identify the safest preparations. images

In France, estrogen, mostly estradiol administered through the skin, is used alone or combined with a variety of progestagens. Further to our earlier report (2005), in which we discussed the breast cancer risk associated with three broad categories of HRTs (estrogens alone, combined with progesterone, or with synthetic progestins) [16], we now report on the association between various other HRTs and breast cancer risk in 80,377 postmenopausal women after up to 12 years of follow-up. In what follows, “other progestagens” should be understood to mean “progestagens other than progesterone and dydrogesterone”.

Compared with women who had never used HRT, women in the estrogen alone and estrogen–other progestagens groups had a significantly increased breast cancer risk (relative risks 1.29 (95% confidence interval 1.02–1.65), and 1.69 (1.50–1.91), respectively). Estrogen-progesterone was associated with a relative risk of 1.00 (0.83–1.22), and estrogen–dydrogesterone with a relative risk of 1.16 (0.94–1.43). Estrogen alone, estrogen–progesterone and estrogen–dydrogesterone were associated with breast cancer risks that did not differ significantly from one another, but that were all significantly lower than that of estrogen–other progestagens (P for homogeneity 0.03, <0.001, and <0.001, respectively). There were significant trends of increased risk with increased duration of use of estrogen–progesterone and estrogen–other progestagens. However, even short spells of estrogen–other progestagens use (<2 years) were associated with a significant 1.36-fold increase in breast cancer risk.

When analyses were restricted to women with the most accurate age at menopause (i.e., derived from information on age at last menstrual period—unless due to hysterectomy, and/or self-reported age at menopause), our main conclusions remained unchanged. This sensitivity analysis  yielded relative risks of 1.2, 1.0, 1.2, and 1.6 for estrogen alone, estrogen–progesterone, estrogen–dydrogesterone, and estrogen–other progestagens, respectively, compared with HRT never-use.

We found that the risk of invasive breast cancer was significantly lower with estrogen–progestagen HRTs containing progesterone or dydrogesterone than with HRTs containing other progestagens. The latter group involved a variety of progestins whose associations with breast cancer risk did not differ significantly from one another. We also observed a significantly increased risk of breast cancer with the use of estrogen alone.

The effect of progestagens on breast tissue is complex and not completely understood. The mechanisms by which they act on cell proliferation include interaction with steroid receptors, growth factors and oncogenes, and with the cell-cycle and estrogen metabolizing enzymes [3]. Because progestagens differ widely in their chemical structure, metabolism, pharmacokinetics and potency, it is reasonable to expect them to induce different responses in the breast [2].

Recently, Wood et al. [22] compared the effects of estradiol given with either medroxyprogesterone acetate or micronized progesterone on risk biomarkers for breast cancer in a postmenopausal primate model. In this randomized crossover trial, they found that, compared to placebo, estradiol + medroxyprogesterone acetate resulted in significantly greater proliferation (as measured by Ki67 expression) in lobular and ductal breast epithelium, while estradiol + micronized progesterone did not. This result supports our findings suggesting that, when combined with an estrogen, progesterone may have a safer risk profile in the breast compared with some other progestagens.

The high degree of androgenicity of progestins used in certain HRTs has been hypothesized to play a role in the increased risk of breast cancer [5]. Our results do not support this hypothesis, as, when combined with an estrogen, neither promegestone, nomegestrol acetate, chlormadinone acetate or medrogestone (all nonandrogenic progestagens) nor cyproterone acetate (an antiandrogenic progestagen) had effects that differed significantly from tarticle-1334609-0C1DFD35000005DC-942_468x313hat of norethisterone acetate (the most androgenic progestagen cited). These results are in line with those of two other European studies [10, 11], which found no difference between the effect of 19-nortestosterone derivatives and medroxyprogesterone acetate (a 17-hydroxyprogesterone derivative with lower androgenic potential than 19-nortestosterone derivatives), implying that other parameters must be involved. However, possible preferential prescribing of the nonandrogenic or antiandrogenic HRTs to women with signs of insulin resistance or hyperandrogenism, who are at higher risk of breast cancer [23], could partly explain our findings.

In our study, estrogen alone was associated with a significantly lower increase in breast cancer risk than estrogen opposed with a progestagen (with the exception of progesterone or dydrogesterone), in line with the growing evidence that adding certain progestins to estrogen has an adverse impact on breast cancer risk [24]. However, our finding of a 1.3-fold increased breast cancer risk associated with the use of estrogen alone (almost exclusively estradiol compounds, and mostly administered through the skin) differs with that of the WHI estrogen-alone trial which found a decreased risk when oral conjugated equine estrogens were used in a population of older and often overweight women [6].

E3N is the first epidemiological study that we know of to be providing results indicating that estrogen–progesterone and estrogen–dydrogesterone combinations may be the least harmful estrogen–progestagen HRTs regarding breast cancer risk. However, more evidence is required before these results can be translated into firm clinical recommendations for the management of menopausal symptoms. In addition, the effect of these combinations in other diseases (e.g., coronary heart disease, venous thromboembolism and colorectal cancer) has also to be evaluated.



1. Cogliano V, Grosse Y, Baan R, Straif K, Secretan B, El Ghissassi F. Carcinogenicity of combined oestrogenprogestagen contraceptives and menopausal treatment. Lancet Oncol. 2005;6:552–553. [PubMed]

2. Stanczyk FZ. All progestins are not created equal. Steroids. 2003;68:879–890. [PubMed]

3. Pasqualini JR, Paris J, Sitruk-Ware R, Chetrite G, Botella J. Progestins and breast cancer. J Steroid Biochem Mol Biol. 1998;65:225–235. [PubMed]

4. Lee SA, Ross RK, Pike MC. An overview of menopausal oestrogen-progestin hormone therapy and breast cancer risk. Br J Cancer. 2005;92:2049–2058. [PMC free article] [PubMed]

5. Campagnoli C, Abba C, Ambroggio S, Peris C. Pregnancy, progesterone and progestins in relation to breast cancer risk. J Steroid Biochem Mol Biol. 2005;97:441–450. [PubMed]

6. Stefanick ML, Anderson GL, Margolis KL, et al. Effects of conjugated equine estrogens on breast cancer and mammography screening in postmenopausal women with hysterectomy. JAMA. 2006;295:1647–1657. [PubMed]

7. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormone replacement therapy: collaborative reanalysis of data from 51 epidemic logical studies of 52,705 women with breast cancer and 108,411 women without breast cancer. Lancet. 1997;350:1047–1059. [PubMed]

8. Magnusson C, Baron JA, Correia N, Bergstrom R, Adami HO, Persson I. Breast-cancer risk following long-term oestrogen- and oestrogen-progestin-replacement therapy. Int J Cancer. 1999;81:339–344. [PubMed]

9. Newcomb PA, Titus-Ernstoff L, Egan KM, et al. Postmenopausal estrogen and progestin use in relation to breast cancer risk. Cancer Epidemiol Biomarkers Prev. 2002;11:593–600.

10. Beral V. Breast cancer and hormone-replacement therapy in the Million Women Study. Lancet. 2003;362:419–427. [PubMed]

11. Stahlberg C, Pedersen AT, Lynge E, et al. Increased risk of breast cancer following different regimens of hormone replacement therapy frequently used in Europe. Int J Cancer. 2004;109:721–727. [PubMed]

12. Bakken K, Alsaker E, Eggen AE, Lund E. Hormone replacement therapy and incidence of hormone-dependent cancers in the Norwegian Women and Cancer study. Int J Cancer. 2004;112:130–134. [PubMed]

13. Ewertz M, Mellemkjaer L, Poulsen AH, et al. Hormone use for menopausal symptoms and risk of breast cancer. A Danish cohort study. Br J Cancer. 2005;92:1293–1297.

14. Lee S, Kolonel L, Wilkens L, Wan P, Henderson B, Pike M. Postmenopausal hormone therapy and breast cancer risk: the multiethnic cohort. Int J Cancer. 2006;118:1285–1291.

15. Hickey M, Davis SR, Sturdee DW. Treatment of menopausal symptoms: what shall we do now? Lancet. 2005;366:409–421. [PubMed]

16. Fournier A, Berrino F, Riboli E, Avenel V, Clavel-Chapelon F. Breast cancer risk in relation to different types of hormone replacement therapy in the E3N-EPIC cohort. Int J Cancer. 2005;114:448–454. [PubMed]

17. Riboli E, Hunt KJ, Slimani N, et al. European Prospective Investigation into Cancer and Nutrition (EPIC): study populations and data collection. Public Health Nutr. 2002;5:1113–1124.

18. Weiss NS, Rossing MA. Healthy screenee bias in epidemiologic studies of cancer incidence. Epidemiology. 1996;7:319–322. [PubMed]

19. Santen RJ. Risk of breast cancer with progestins: critical assessment of current data. Steroids. 2003;68:953–964. [PubMed]

20. de Lignieres B. Effects of progestogens on the postmenopausal breast. Climacteric. 2002;5:229–235. [PubMed]

21. Graham JD, Clarke CL. Physiological action of progesterone in target tissues. Endocr Rev. 1997;18:502–519. [PubMed]

22. Wood CE, Register TC, Lees CJ, Chen H, Kimrey S, Mark CJ. Effects of estradiol with micronized progesterone or medroxyprogesterone acetate on risk markers for breast cancer in postmenopausal monkeys. Breast Cancer Res Treat. 2007;101:125–134. [PubMed]

23. Muti P, Stanulla M, Micheli A, et al. Markers of insulin resistance and sex steroid hormone activity in relation to breast cancer risk: a prospective analysis of abdominal adiposity, sebum production, and hirsutism (Italy) Cancer Causes Control. 2000;11:721–730. [PubMed]

24. Li CI. Postmenopausal hormone therapy and the risk of breast cancer: the view of an epidemiologist. Maturitas. 2004;49:44–50. [PubMed]

25. Ray WA. Evaluating medication effects outside of clinical trials: new-user designs. Am J Epidemiol. 2003;158:915–920. [PubMed]

26. Greendale GA, Reboussin BA, Slone S, Wasilauskas C, Pike MC, Ursin G. Postmenopausal hormone therapy and change in mammographic density. J Natl Cancer Inst. 2003;95:30–37.

Testosterone And Sexual Function In Women

Written by BIH of Decatur on . Posted in Menopausal Research, Women

The impact of testosterone treatment on sexual dysfunction was first described in the 1950s in studies of postmenopausal women who received testosterone in combination with estrogen. Although sexual function was not a primary outcome of these trials, improved libido was self-reported by 23–42% of the subjects. Studies performed in the 1980s and 1990s further elucidated the role of testosterone therapy in female sexual behavior. Screen-shot-2013-06-17-at-7.42.34-PM-380x247

Another trial compared oral estrogens alone with the combination of estrogen and testosterone (esterified estrogens 1.25 mg and methyltestosterone 2.5 mg once/day) in 20 postmenopausal women taking estrogen at baseline. Objective sexual arousal was measured by using vaginal blood flow velocity and fingertip blood flow. This study did not find a significant impact of testosterone on either vaginal or fingertip blood flow velocity. However, a study of eight premenopausal women receiving a single dose of sublingual testosterone undeconate 0.5 mg in a double-blind, randomized, placebo-controlled, crossover design demonstrated increased vaginal blood flow, self-reported sensations  and sexual lust on a visual analog scale within 5 hours of the testosterone dose. A small crossover trial in 10 postmenopausal women without sexual dysfunction demonstrated a benefit for methyltestosterone 5 mg on genital sexual response with increased vaginal blood flow 4.5 hours after the dose.  However, the women did not report a subjective increase in sexual response with testosterone.

Testosterone has rarely been evaluated alone in postmenopausal women but has been investigated in several studies as an addition to estrogen therapy. Twenty postmenopausal women with menopausal or sexual symptoms unrelieved by estrogen were enrolled in a small, randomized, double-blind, parallel-group study to evaluate the effects of testosterone in addition to estrogen therapy. Participants were randomly assigned to either esterified estrogens 1.25 mg/day or estrogen plus methyltestosterone 2.5 mg/day for 8 weeks. The Sexual Activity and Libido Scale (11 questions) was completed weekly by each subject. This scale evaluates vaginal dryness, sexual desire, pain with intercourse, clitoral sensation, and sensitivity on a scale from 0–4; vaginal moisture, orgasm, sexual fantasy, sexual response in the last 24 hours as yes or no; and sexual intercourse as none, once, twice, 3 times, or 4 or more times/week. Sexual desire and clitoral sensation were significantly increased from baseline at 8 weeks in the testosterone group. The frequency of sexual activity was significantly increased at week 4; however, this increase was no longer observed at 8 weeks.
A longer (16-wk), double-blind, randomized, parallel-group study comparing esterified estrogens 1.25 mg/day (19 women) with estrogen plus methyltestosterone 2.5 mg/day (18 women) was conducted to determine effects on fat and muscle mass and muscle strength. Sexual function was evaluated as a secondary objective by using three self-report questionnaires. A significant change from baseline was noted on each scale in the estrogen-testosterone group. A significant increase for pleasure/orgasm was noted on the BISF-W and for interest in sex on the SIQ scale in the estrogen-testosterone group.shutterstock-couple

Sexual function was the primary outcome in one crossover study involving 50 women with surgically induced menopause who were randomly assigned to estradiol 2 mg/day or estradiol and testosterone undecanoate 40 mg/day. McCoy’s sex scale questionnaire, a 14-item scale evaluating the previous 30 days, was used to compare sexual function at baseline and after 6 months of treatment. No significant difference was found between treatment groups for lubrication, pain with intercourse, interest in sex, or sexual thoughts and fantasies.

Although significant improvement from baseline was noted in the testosterone group on: enjoyment, satisfaction with frequency of sexual activity, arousal, frequency  and satisfaction of orgasm, and feeling of attractiveness to partner), only the domains of enjoyment, satisfaction with frequency, and interest in sex were significantly improved in the testosterone group compared with the other groups.

Women receiving the formulation with testosterone reported a significant increase in responsiveness, which was more than twice that of women taking estrogen alone. Sexual interest or desire and frequency of desire were also greater in the testosterone combination group, with an increase noted at 4 weeks of therapy and maintained throughout 16 weeks. This study further solidified the role of testosterone in increasing sexual motivation in women with lack of sexual interest or desire.

Testosterone Supplementation for Hypoactive Sexual Desire Disorder in Women
C. Brock Woodis, Pharm.D, Amber N. McLendon, Pharm.D., Andrew J. Muzyk, Pharm.D.
Pharmacotherapy. 2012;32(1):38-53

Menopause and What to Do About It

Written by BIH of Decatur on . Posted in Menopausal Research, Women

Most women do not like the effects of menopause.  That is not news.  Who would want to have hot flashes, vaginal dryness, and depression?  The really sad thing is that so very many women now are on medications for depression, anxiety and sleep in an effort to counter the horrible consequences of loss of hormones.  This does not have to happen.  Your declining hormones can be replaced easily without the documented side effects of synthetic non-natural hormones.

Menopause is a condition in women resulting in loss of sex hormones.  Testosterone begins to drop off in most women by age 30.  Progesterone declines at age 35.  And finally estradiol declines by age 40 in most women.  Eight percent of women will go through menopause before age 40.
Menopause is defined as not having a period for 6 to 12 months.  Another indication is when follicular stimulating hormone (FSH), a pituitary hormone, goes up to 23 whether she is menstruation or not.   Women may have significant hot flashes and increased sexual dysfunction, as well as depressive symptoms which can cause psychosocial impairment.  Portrait of mature woman sitting in countryside

The commonly used synthetic conjugated estrogen for menopausal symptoms has inherent problems, namely an increased incidence of breast and cervical cancer, blood clots and heart disease as noted by the Women’s Health Initiative.  The erroneous assumptions of this study implied that ALL estrogens given with progestin or progesterone produce an increase in breast cancer.  Oral hormone replacement therapy cannot produce normal, steady physiologic levels of estrogen and maintain the physiologic ratio of estradiol to estrone 2:1.(1)

Bio-identical hormone replacement is safer than synthetic artificial hormones.  There have never been noted the health risks as with the use of synthetic estrogens especially when used with synthetic progestin.  Replacing the natural hormones we once had when we were 20 can be protective.  Dr. Gino Tutera performed a study of 976 women over a period of 10 years (1992 through 2002) who all had the bio-equivalent pellet hormone insertions of estradiol and/or testosterone.  After 10 years there was only 1 lady who had breast cancer.  The patient with breast cancer was discovered less than 1 year after the insertion.  Most likely she already she had a microscopic cancer before the implants.  There were no cases of ovarian cancer, and only one case of endometrial cancer.  The endometrial cancer was found after the patient’s first six months in therapy.  The patient had Stage 3 Grade 1, well differentiated tumor who has remained disease free three years after therapy.(2)

These were patients in the years of a woman’s life where she would most likely find breast cancer.  With the law of averages one would expect to find 60 or 70 women from a study group like this to develop breast cancer over a 10 year period.
Subcutaneous bio-identical hormone replacement therapy with estradiol and testosterone with oral progesterone, imparts a protective physiologic environment that can reduce the risks of breast, endometrial and ovarian cancer.  We know that breast cancer is extremely rare in an 18-year-old.  An 18-year-old has normal levels of sex hormones to protect her.  Subcutaneous pellet therapy causes the release of minute amounts of estradiol steadily over a 24-hour period for up to 4 to 6 months giving a protective physiologic ratio of estradiol to estrone at 2:1.
Equally, ovarian cancer shows marked reduction in those on oral contraceptive therapy as noted in the National Nurses Study.  OC therapy produces suppression of serum FSH thereby halting follicular development.  This produces a dormant state in the ovaries therefore a lower risk of ovarian cancer.

Natural Pellet Bio-Identical Hormone Replacement Therapy more closely simulates the sought-after healthy state found in young men and women.


1. Thom, M.H.; Studd, J.W.W., Estrogen and Testosterone Implant Therapy.  Whitehead, M., Campbell , Estrogen and the Menopause. Queensboorough, Kent;  Abbott Laboratories, Ltd., 1978: 85-88.

2. Tutera, G. Subcutaneous hormone therapy reduces breast cancer incidence. Rediscover You. Scottsdale, AZ.

Get Directions