Androgens &
Androgen Deficiency
The Hormones of Sexual Desire
Illustration by Patsy
Website FromLifeDrawings.com
Androgens &
Androgen Deficiency
The Hormones of Sexual Desire
Illustration by Patsy
Website FromLifeDrawings.com
The sex hormones are divided into two major groups, androgens and estrogens (oestrogens). Traditionally, androgens where considered the "male" sex hormones and estrogens the "female" sex hormones, but both play an active and vital role in the normal function of men and women. There are three types of estrogen that have a role in over 400 bodily functions. The three types of estrogen are estrone (E1), estradiol (E2), and estriol (E3). There are five types of androgens that influence a woman’s sexual desire, mood, and energy, and are necessary for healthy bones and muscles. The five types of androgens are dihydrotestosterone (DHT), testosterone, dehydroepiandrosterone (DHEA), dehydroepiandrosterone-sulfate (DHEA-S), and androstenedione. The total amount of androgens in women is estimated to be about 71% of that of men, which is a level much greater than previously believed.
Androgen levels in girls first start to increase between the ages of six and ten, but do not reach their maximum levels until between the ages of 20 and 30. The onset of increased androgen production is referred to as adrenarche. The first visible indication of this event is the development of pubic hair, which is referred to as pubarche. The increasing level of these hormones at this young age is a possible reason why 47% of women report they experienced sexual desire prior to their first menstrual period, menarche. Menarche is unrelated to andrenarche, and a woman can experience the onset of menstruation without ever developing pubic hair. The fact that androgen levels do not peak until a woman is in her twenties may explain why 68% of women report their level of sexual desire is greater in their twenties than their teens, and why some do not experience the onset of intense sexual desire until they are in their late teens or early twenties. When a woman's level of androgen decrease to 10-20% of their peak level it is referred to as adrenopause, which is independent of menopause.
Medical Quote:
"All agree that dehydroepiandrosterone sulfate (DHEA-S) production from the adrenal gland begins during the preteen years, peaks in the mid 20s, then declines progressively over time. In contrast, ovarian androgen (i.e., testosterone) secretion commences at puberty, is sustained during a woman's peak reproductive years and declines as a woman ages, with a more rapid and steep decrease after surgical menopause. However, there are ample data to suggest that adrenal androgens play a role in the development of axillary and pubic hair, and that testosterone is critical for women's libido and sexual function."
"Interestingly, Davis et al. were unable to demonstrate a correlation between total testosterone plasma [blood] levels and symptoms of sexual function. However, good correlations were found between various parameters of sexual function and the adrenal androgen DHEA-S." [9]
Androgens are initially produced by the ovaries and adrenal glands. After which they enter the blood stream and circulate throughout the body to the tissues and organs that are sensitive to and controlled by them. The amount of estrogens and androgens in the blood, for the most part, indicate the amount of these hormones being produced by the ovaries and adrenals, but these levels do not accurately indicate the amount of these hormones within the actual tissues of the body. The amount of androgens in the blood indicate the general health, menstrual state, and functional age of the ovaries and adrenals.
Schematic representation of the role of ovarian and adrenal
sources of sex steroids in premenopausal women. [8]Relatively recently it was discovered that the conversion of hormones into other types of hormones takes place within the individual cells that use them. As an example, the hormone DHEA is converted into testosterone during a chain of events inside some cells within the tissues of the breast, and other organs. It is now believed that the majority of the testosterone produced and consumed within the female body is done in this manner. These newly converted hormones are consumed by the cell and only the bi-products of that process enter the blood stream.
Only a small fraction of the hormones produced within the cells of the different organs enter into the blood stream where they can be measured by standard blood tests. The amount of androgen in the tissues is measured indirectly through the amount of bi-product within the blood. To determine the total amount of androgens in the body the amount of androsterone glucuronide (ADT-G), androstenediol glucuronide (3α-diol-G), and androsterone-3β (3β-diol-G) in the blood must be measured. The most reliable test methods employ radioimmunoassays; some luminometric assays are reported to be "problematic."
Androgen Levels Decrease
Throughout AdulthoodAs indicated by the following graphs and tables, the amount of androgens in the blood stream decrease throughout adulthood, and have decreased significantly by the completion of menopause. While the androgen output of the ovaries may have decreased during menopause, they do not decrease to zero. This is demonstrated by the fact that postmenopausal women who have had their ovaries surgically removed have significantly lower levels of androgens than women who did not.
Total Testosterone
nmol/liter* After surgical removal of ovaries
Free Testosterone
pmol/liter* After surgical removal of ovaries
DHEAS
μmol/liter* After surgical removal of ovaries
Androstenedione
nmol/liter* After surgical removal of ovaries
The data presented in the above graphs and tables came from the article Androgen Levels in Adult Females: Changes with Age, Menopause, and Oophorectomy The Journal of Clinical Endocrinology & Metabolism 90(7):384-3853 April 12, 2005
Androgens Across a Woman's Lifetime Source
Original Source of Data [7]
Androgen Production & Circulation
The following illustrations reveal how much the ovaries contribute to the amount of androstenedione and testosterone in the blood prior to and after menopause. They also show how some of the DHEA that is converted into androstenedione and testosterone, within the cells of the body, contribute to the amount of these hormones in the blood. [8]
Prior to menopause the ovaries contribute 50% of the androstenedione present in the blood. Women who have had their ovaries removed prior to menopause may experience a 50% decrease in the amount of androstenedione in their blood, but this may not cause a significant change in the overall amount of androstenedione in their body.
After menopause the ovaries contribute 20% of the androstenedione present in the blood. Women who have had their ovaries removed after menopause may experience a 20% decrease in the amount of androstenedione in their blood, but this may not cause a significant change in the overall amount of androstenedione in their body.
The ovaries contribute about half of the amount of testosterone in the blood throughout a woman's lifetime. Surgical removal of the ovaries may result in a 50% decrease in the amount of testosterone present in the blood, but this may not cause a significant change in the overall amount of testosterone in the body. The amount of testosterone in the blood decreases by about 50% between the ages of 21 and 40. This is thought to be the result of the declining quantity of DHEA produced by the adrenals.
The following illustration demonstrates how only 10% of the testosterone present in the tissues of the body originates in the blood stream. The remaining 90% is the result of the conversion of DHEA to testosterone within the tissues of the body. DHEA must be converted into other hormones prior to its conversion into testosterone. When testosterone is converted into DHT, it is most effective.
The information contained in the four illustrations shown above came from the article Endocrine and Intracrine Sources of Androgens in Women: Inhibition of Breast Cancer and Other Roles of Androgens and Their Precursors. Endocrine Reviews 24(2): 152-182 Copyright 2003
Androgen Deficiency
There is no agreement amongst the medical community concerning what constitutes androgen deficiency in women and its roll in sexual dissatisfaction.
The Princeton consensus in 2002 defined it as when a woman meets all three of the following conditions:
1. She believes she is experiencing impaired well-being or libido
2. She has adequate estrogen levels, meaning her ovaries are producing sufficient estrogen or she is on estrogen replacement therapy (ERT)
3. She has blood levels of androgens that are less than or equal to 25% of the normal or average amount. If the average amount is 100, then measured values of 0-25 meet this condition.The Sexual Function Health Council of the American Foundation for Urologic Disease (AFUD) defined Hyposexual Desire Disorder (HSDD) as when the following two conditions exist at the same time:
1. Continuous or recurrent experiences of decreased frequency of or absent sexual fantasies, thoughts and/or desire for or willingness to engage in sexual activity. Basically, little or no sexual feelings or motivations.
2. The existence of the first condition leads to person distress. Meaning you are very unhappy because you are not experiencing sexual feelings or desires as often as you would like or believe you should.Some find fault with the use of any diagnosis that cannot be verified in a medical lab with proven tests, and verifiable results, which is any diagnosis a women determines for herself. Since medical science has not found a clear link between the majority of self reported cases of low sexual desire and measurable androgen deficiencies, this is to be expected. Though women are understandably frustrated by the medical community's apparent lack of action when it comes to resolving their lack of sexual desire, and decreased quality of life.
One study found that having low DHEAS levels did not automatically lead to women reporting lower sexual satisfaction, but women who reported having impaired sexual function were more likely to have a low DHEAS level. The question becomes, do some women experience decreased sexual desire without knowing, or are low DHEAS levels unrelated to sexual desire? Keep in mind that in the past, and to varying degrees today, society said women don't experience innate sexual desire, that they engage in sex for purely non-sexual motives; maternal instinct, love, partner's needs, intimacy, etc. This means women may not be concerned with an absence of purely sexual motives, especially older generations.
Women may also expect their desire for sex to decrease with age, meaning their decreased desire is to be expected, and is normal, and therefore not a reason for concern; it just is. If sexual desire leads to sex, pregnancy, and more children, you may be happy to no longer experience it. If sexual desire leads to sexual frustration, you may be more than happy to do without. A woman may not believe she is experiencing decreased sexual desire until outside forces, partner's sexual demands and the mass media, lead her to believe otherwise. These factors may explain why women and their doctors do not agree when it comes to explaining and treating sexual dissatisfaction, and specifically low sexual desire.
Why then do women routinely experience increased sexual desire when they are prescribed androgens, specifically testosterone? One possible answer is the fact that the prescribed dosages often raised a woman's level of testosterone to above average levels; lower dosages do not appear to have the same affect. It seems possible that you can raise a woman's level of sexual desire to a point that it overcomes other factors that are the true cause for the low desire, specifically environmental factors. If you ring a woman's sexual bell loud enough she cannot help but hear it. This scenario becomes a real possibility when one considers the fact that women frequently do not perceive their true level of physical sexual arousal when they are exposed to sexual stimulus. The problem with too much testosterone is that it has undesired side affects.
The following is a list of conditions and causes that may lead to some degree of androgen deficiency.
Low androgen levels may be indicated by:
- Diminished feelings of well-being
- Lethargy (exhaustion, low energy)
- Loss of sex drive and interest
- Unexplained fatigue
- Reduced motivation, pubic hair, and bone and muscle mass
- Poor quality of life
- Problems with blood vessel constriction and dilation
- Insomnia
- Depression
- HeadachesLow androgen levels may be caused by:
- Increasing age2
- Low ovarian output caused by medical factors or surgical removal of the ovaries
- Low adrenal gland output
- Hypopituitarism2
- Glucocorticoid therapy2 (Used to treat asthma and rheumatic diseases.)
- Use of oral contraceptives and oral estrogens2
- Addison's disease4
- Corticosteroid therapy4
- Chronic illness4
- Chronic stress6
- Estrogen replacement (leads to elevated SHBG and, therefore, low free testosterone)4
- Premenopausal ovarian failure4
- Oophorectomy4 (Removal of the ovaries)
- Progestin; cyproterone or drospirenone used in oral contraceptives6Low androgen levels may be associated with3:
- Osteoporosis
- Obesity
- Type 2 diabetes
- Sexual dysfunction
- Loss of muscular strength
- Turner's syndrome6
Treatment of Androgen Deficiency
Note: A summary of the current state of Testosterone Replacement Therapy in Naturally and Surgically Menopausal Women, as of January 2009, is available online from the Journal of Sexual Medicine. Medical terminology is used in the article so you may have to discuss what is stated with your doctor, to gain a full understanding. Online medical dictionaries are also available if you want to read the article for yourself.
It is now believed that decreasing DHEA levels may account for some of the symptoms associated with androgen deficiency, rather than the measurable decrease in the other four types of androgens found in the blood. This is because the amount of androgens in the blood does not accurately reflect the total amount of androgens in the tissues of the body. This may explain why current research has not found a clear correlation between the amount of androgens in the blood and female sexual dissatisfaction. I am not aware of research that has looked for or found a specific correlation between DHEA and sexual dissatisfaction, as of November 2006.
Studies have found that when women experiencing adrenal insufficiency took 50mg of DHEA daily, it brought their levels of androgens and estrogens up to normal premenopausal levels, "without significant side affects." DHEA can also be administered in the form of a topical cream. DHEA is available without a prescription, but such products are not under Food and Drug Administration (FDA) control. A study conducted in 1998 found that over the counter products that were said to contain 25mg of DHEA actually had anywhere between 0 and 140 mg; partial testing results from 2006 can be seen by clicking here.
If a woman chooses to take DHEA, it is highly advisable for her to consult her doctor so they can monitor her hormone levels to ensure they increase to the desired levels without becoming too high. The use of DHEA is believed to avoid some of the adverse side affects associated with Estrogen Replacement Therapy (ERT) and Hormone Replacement Therapy (HRT), because the resulting increased hormone levels in the tissues are not circulating throughout the body in the blood stream, where they can affect tissues and organs in undesired ways. I would caution women against taking DHEA unless laboratory testing has indicated their androgen levels are significantly lower than they should be.
You can learn more about DHEA, as a medical treatment, at the following web sites:
http://www.mayoclinic.com/health/dhea/NS_patient-dhea
http://www.nlm.nih.gov/medlineplus/druginfo/natural/patient-dhea.html
My layman's interpretation of the current body of knowledge, as of June 2009, concerning androgen replacement therapy is that it is beneficial, as long as the resulting level of androgens do not exceed those considered normal for women of reproductive age. This is my personal opinion and should not be construed as medical advice.
There are risks associated with androgen replacement therapy, but based on my interpretation of the medical information presented below, those risks are lesser if the resulting androgens levels do not exceed what is considered normal or typical for women of reproductive age. This means a woman's androgens levels should be accurately determined and monitored throughout the period of treatment, and the lowest dosage necessary to achieve the desired result utilized, without exceeding normal levels. Androgen replacement therapy is not a guaranteed solution for sexual dissatisfaction and decreased quality of life.
Something to consider, postmenopausal women naturally have decreased androgen levels, and what is quote unquote normal for them isn't necessarily the same as it is for women of reproductive age. At this time, I don't believe we know the minimum androgen levels required for postmenopausal women to experience sexual satisfaction, and a satisfactory quality of life. The recommended dosages appear to conform to the expectation that one size fits all, regardless of age, which sends up a red flag for me; they are likely the only dosage readily available for prescription, and possibly based on recommended dosages for men. This is why it is important to monitor the resulting androgen levels in the body.
Elevated estrogen and androgen levels, even those occurring naturally within the body, are linked to an increased risk for cancer (see reference). That risk is likely greater for those who are already at an increased risk for developing cancer. You and your doctor should consider all risk factors prior to initiating androgen replacement therapy.
The following medical abstracts presents some of the current and somewhat conflicting body of knowledge available. I have not included information on why androgens may increase the risk for cancer, as that information is of an even greater technical nature. This is not a complete body of knowledge, if you are wanting to know more, or up to date information, you can access that information at PubMed.gov. Perform keyword searches using words like "androgens breast cancer", "androgens hsdd", and "androgens female desire"
Medical Abstract:
Originally Published: July 2009
Approved Hormonal Treatments for HSDD: An Unmet Medical Need
Introduction. Despite a high prevalence of hypoactive sexual desire disorder (HSDD), no medical treatment is available in the United States for this condition.
Aim. To identify the current prescribing pattern of off-label testosterone use in treating HSDD.
Main Outcome Measures. Quantitation of Intercontinental Marketing Services (IMS) prescription data to identify testosterone prescriptions written for women and a summary of response to queries to opinion leaders and practicing physicians.
Methods. Interviews and an opinion poll of gynecologists and family medicine physicians on current medical treatment of HSDD.
Results. The IMS prescription review showed that: two million testosterone prescriptions were written for women in 2006 and 2007—many physicians have prescribed compounded testosterone. Based on a summary of the physicians' survey: on average, patients of all ages, but particularly menopausal women, have at least moderate awareness of HSDD. More than 80% of physicians believe there is a need or great need for a Food and Drug Administration- (FDA) approved HSDD treatment. Ninety percent of physicians surveyed would prescribe an approved HSDD product over currently prescribed therapy.
Conclusions. In the context of increased regulatory scrutiny, increasing off-label use of testosterone, formulation and dosing issues, increased patient awareness of FSD and HSDD, and overall favorable physician sentiment, the completion of the LibiGel® clinical development program and an FDA approval will meet the demand for the first safe and effective FDA-approved treatment of HSDD in postmenopausal women. [20]Medical Abstract:
Originally Published: June 20, 2009
Role of testosterone in the treatment of hypoactive sexual desire disorder.
Hypoactive sexual desire disorder (HSDD) is a common clinical problem that may have a very negative impact on a woman's quality of life. Diagnosis and treatment is challenging, as one must keep in mind the complex web of factors influencing sexual functioning alone or in concert. Data suggest that androgens are significant independent factors affecting sexual desire, sexual activity and satisfaction, as well as other components of women's health such as mood and energy. For decades, physicians used various androgen preparations to improve sexual function in women, based on the results of smaller clinical trials and personal clinical observations when taking care of patients. Today, there is substantial body of evidence from randomized placebo-controlled trials that low-dose testosterone treatment is efficacious in women with HSDD who have an established cause of androgen deficiency such as surgical menopause. Recent data support the hypotheses that androgens may also be beneficial in naturally menopausal women or in premenopausal women with low circulating testosterone levels and a decrease in satisfying sexual activity. No single testosterone level has been found to be predictive for low female sexual function, even though women suffering from HSDD commonly have low testosterone levels. The most frequently reported side effects of testosterone treatment are mild hirsutism or acne. Long-term safety is not yet established. Several clinical trials are in progress to further investigate potential benefits and risks of androgen treatment in women with sexual dysfunction. [13]
Originally Published: May 30, 2009
The role of testosterone in the management of hypoactive sexual desire disorder in postmenopausal women.
At least 16 million women over the age of 50 currently experience low sexual desire, with approximately 4 million women exhibiting hypoactive sexual desire disorder (HSDD). Although early research established that testosterone therapy improves sexual desire in postmenopausal women, safer and more efficacious administration routes were explored. Large randomized, double-blinded placebo-controlled studies demonstrate that transdermal testosterone improves sexual function and activity in postmenopausal women with HSDD. Large multi-center Phase III trials further confirm the positive effects of the testosterone patch in the treatment of HSDD. More recent studies are exploring the utility of testosterone gels. Based upon data from two recent clinical relevance studies, physicians can be reassured that postmenopausal women with HSDD report a meaningful benefit with testosterone therapy, and further, women will only continue therapy if they experience a meaningful benefit. Although most trials combined testosterone with estrogen/progesterone therapy, the recent APHRODITE trial examined testosterone alone, showing increased sexual desire with mild adverse events. Concerns regarding the long-term safety profile of transdermal testosterone must be addressed before the FDA will approve a testosterone product for women. Although some fear an increased risk of breast cancer with exogenous [applied to skin] testosterone administration, recent studies support the idea that androgens can play a role in suppressing the proliferative effects of estrogen and progesterone. Long-term safety data is now being collected and analyzed and Phase III trials focusing on long-term risks are underway. In the meantime, transdermal testosterone appears to be a safe and effective therapy for postmenopausal women with HSDD. [14]
Originally Published: May 20, 2009
Safety of testosterone use in women.
Female sexual desire appears to be in part androgen dependent, which has lead to the use of testosterone in women for low libido. Despite this benefit, the long-term safety of testosterone as a hormone replacement or therapy has not been well established. Side effects of testosterone therapy include mild and reversible acne and hirsuitism, as well as changes to the lipid profile with oral, but not transdermal testosterone. Short-term studies, up to 2 years, have shown that for serum plasma [blood] testosterone levels at the upper portion or slightly above the reference range for reproductive-aged women, testosterone does not increase the risk of hepatotoxicity, endometrial hyperplasia, or behavioral hostility. No adverse cardiovascular effects including changes in blood pressure, blood viscosity, arterial vascular reactivity, hypercoagulable states, and polycythemia have been shown. Data is mixed with outcomes of breast cancer risk, with some experimental studies suggesting a decrease in estrogen-induced breast epithelial proliferation with low dose testosterone. Additionally, models of superphysiologic [elevated] testosterone levels, such as polycystic ovarian disease, have not shown an increased risk of breast cancer. As with all hormone therapy in postmenopausal women, testosterone therapy should be individualized and requires that each woman weigh the risk and benefits. Nevertheless, only long-term safety studies will provide conclusive evidence as to testosterone safety in women. [15]
Medical Abstract:
Originally Published: April 30, 2009
The safety of 52 weeks [1 year] of oral DHEA therapy for postmenopausal women.
OBJECTIVE: The aim of this study was to evaluate the safety of 52 weeks of DHEA 50mg daily oral dose given to postmenopausal women with low libido to improve sexual function.
METHOD: 93 postmenopausal women were enrolled in a 52-week randomised, double-blind, placebo-controlled trial and received either DHEA 50mg or placebo (PL) daily. The effects of DHEA versus placebo on lipid profile, insulin-glucose homeostasis and the endomentrium were assessed over 52 weeks.
RESULTS: Oral DHEA, 50mg/day, was not associated with any effects on blood lipids or insulin resistance. The pattern of breakthrough bleeding did not substantially differ between the DHEA and PL groups and no significant adverse endometrial effects were apparent.
CONCLUSIONS: The use of 50mg oral DHEA did not significantly alter lipid profile, insulin sensitivity or adversely affect the endometrium in postmenopausal women. [10]
Originally Published: April 24, 2009
The Incidence of Invasive Breast Cancer Among Women Prescribed Testosterone for Low Libido.
Introduction. Although the efficacy of testosterone for the treatment of hypoactive sexual desire disorder is well established, the effect of testosterone therapy on breast cancer risk remains uncertain.
Aim. The incidence of invasive breast cancer among past and current testosterone users. Methods. Retrospective cohort study of 631 women ever treated with testosterone between January 1989 and December 2007 in a clinical endocrinology practice.
Main Outcome Measure. The incidence of invasive breast cancer since first exposure, and the standardized incidence rate ratio (IRR) calculated using Australian age-specific incidence rates for 2005. Results. The mean age of the women at first exposure to testosterone therapy was 49.1 +/- 8.2 years, median treatment duration, 1.3 years, and mean follow-up of 6.7 +/- 4.6 years, providing 4,015 woman-years of follow-up. Twelve cases of invasive breast cancer occurred among 599 women breast cancer-free before treatment, giving an age adjusted IRR of 1.35 (95% confidence interval 0.76-2.38). There was no evidence of an independent effect of duration of exposure on breast cancer risk.
Conclusion. In this study, testosterone use was not associated with a significant increase in breast cancer risk. [16]
Originally Published: April 15, 2009
Does the increase of endogenous steroid hormone levels also affect breast cancer risk in Chinese women?
Accumulating epidemiological evidence suggests that sex steroid hormones are positively associated with the development of breast cancer. However, most of these studies were conducted among Caucasian women and few have been carried out in China. To determine whether the associations of sex steroid hormone levels with breast cancer risk observed by and large in Caucasian populations are also evident in Chinese women, we conducted a case-control study in Chongqing, China. The study included 367 incident breast cancer patients and 367 healthy controls matched on menstrual status, age and periods of blood collection in the menstrual cycle. Plasma concentrations of estradiol, progesterone, testosterone, dehydroepiandrosterone sulfate (DHEAS) and sex hormone binding globulin (SHBG) were determined by electrochemiluminescene immunoassay (ECLIA). Conditional logistic regression analysis was performed to examine their associations with breast cancer risk. From comparisons of upper and lower tertiles, we observed statistically significant positive associations with breast cancer risk for plasma estradiol levels in follicular phase (adjusted odds ratio [OR] = 5.48, 95% confidence interval [CI] = 1.58-18.97), luteal phase (OR = 4.23, CI = 1.65-10.87) and postmenopausal (OR = 2.67, CI = 1.20-5.93); for progesterone levels in luteal phase (OR = 3.11, CI = 1.28-7.56), and for testosterone levels in postmenopausal (OR = 2.83, CI = 1.26-6.35). No significant association was found with DHEAS or SHBG.
Our study suggests that high circulating levels of estradiol and testosterone are positively associated with increased breast cancer risk in Chinese women, which are generally consistent with the observations in Caucasian populations. [18]
Originally Published: January 20, 2009
Study of adverse outcomes in women using testosterone therapy.
OBJECTIVES: There are concerns that exogenous [applied to skin] testosterone therapy may be associated with adverse cardiovascular effects, increases in risk of breast or uterus cancer and alterations in insulin sensitivity. Objective of this study was to explore the safety of testosterone therapy in actual clinical practice.
METHODS: Data from the General Practice Research Database and the Health Improvement Network was used, including computerised medical records of UK general practitioners. The study population included women aged 18+ years prescribed testosterone, administered through implants (72.2%), tablets (18.4%) or injections (7.9%). Each testosterone user was matched by age and practice to three control patients. Cox proportional hazards models were used to compare the rates of several outcomes.
RESULTS: The study population included 8412 women, 2103 testosterone users and 6309 controls. There were no statistically significant differences between the cohorts in the rates of cerebrovascular disease, ischemic heart disease, breast cancer, deep venous thrombosis/pulmonary embolism, diabetes mellitus or acute hepatitis. The rate of breast cancer was comparable between testosterone users and control patients. The rate of androgenic events was increased in the testosterone cohort (relative rate of 1.55 [95% CI 1.21-1.97]). Differences in outcomes between the cohorts were generally comparable across subgroups based on age and use of hormone therapy.
CONCLUSIONS: This study found no major increase in the risk of cardiovascular diseases or breast cancer in women using testosterone (implants, tablets, or injections), while the risk of androgenic events was increased. It would be useful to conduct similar studies at lower doses with transdermal testosterone. [17]
Originally Published: January 12, 2009
Influence of estrogen plus testosterone supplementation on breast cancer.
BACKGROUND: Concern that the use of exogenous testosterone may increase breast cancer risk coexists with rising use of this medication in the United States. We sought to examine the relationship between the use of estrogen plus testosterone (E + T) therapy (esterified estradiol plus methyltestosterone) and the occurrence of breast cancer.
METHODS: A total of 31,842 postmenopausal participants in the Women's Health Initiative Observational Study were followed for a mean of 4.6 years. At the 3-year visit, E + T users were compared with non-hormone therapy users for time to incident invasive breast cancer. Cox proportional hazards estimates were adjusted for known predictors of breast cancer including prior hormone use and screening mammography.
RESULTS: Thirty five women using E + T at visit 3 developed invasive breast cancer. Use of E + T had a nonsignificant impact on invasive breast cancer risk (adjusted hazard ratio, 1.42; 95% confidence interval, 0.95-2.11). The most commonly used E + T preparation, Estratest, was associated with a significant elevation in invasive breast cancer (adjusted hazard ratio, 1.78; 95% confidence interval, 1.05-3.01). However, rates of breast cancer were lower in longer-term E + T users than in shorter-term E + T users.
CONCLUSION: Although our results have less strength than an initial report linking E + T [estrogen plus testosterone] to breast cancer, we found a modest, albeit nonsignificant, elevation in breast cancer risk associated with E + T use. [19]
Medical Abstract:
Originally Published: November 6, 2008
Testosterone for low libido in postmenopausal women not taking estrogen.
BACKGROUND: The efficacy and safety of testosterone treatment for hypoactive sexual desire disorder in postmenopausal women not receiving estrogen therapy are unknown.
METHODS: We conducted a double-blind, placebo-controlled, 52-week trial in which 814 women with hypoactive sexual desire disorder were randomly assigned to receive a patch delivering 150 or 300 microg of testosterone per day or placebo. Efficacy was measured to week 24; safety was evaluated over a period of 52 weeks, with a subgroup of participants followed for an additional year. The primary end point was the change from baseline to week 24 in the 4-week frequency of satisfying sexual episodes.
RESULTS: At 24 weeks, the increase in the 4-week frequency of satisfying sexual episodes was significantly greater in the group receiving 300 microg of testosterone per day than in the placebo group (an increase of 2.1 episodes vs. 0.7, P<0.001) but not in the group receiving 150 microg per day (1.2 episodes, P=0.11). As compared with placebo, both doses of testosterone were associated with significant increases in desire (300 microg per day, P<0.001; 150 microg per day, P=0.04) and decreases in distress (300 microg per day, P<0.001; 150 microg per day, P=0.04). The rate of androgenic adverse events - primarily unwanted hair growth - was higher in the group receiving 300 microg of testosterone per day than in the placebo group (30.0% vs. 23.1%). Breast cancer was diagnosed in four women who received testosterone (as compared with none who received placebo); one of the four received the diagnosis in the first 4 months of the study period, and one, in retrospect, had symptoms before undergoing randomization. [See Abstract 1, Abstract 2, Abstract 3, Abstract 4, Abstract 5, Abstract 6, and Abstract 7]
CONCLUSIONS: In postmenopausal women not receiving estrogen therapy, treatment with a patch delivering 300 microg of testosterone per day resulted in a modest but meaningful improvement in sexual function. The long-term effects of testosterone, including effects on the breast, remain uncertain. [11]
Medical Abstract:
Originally Published: September-October 2008
Testosterone enhances estradiol's effects on postmenopausal bone density and sexuality.
To investigate the role of androgens in increasing bone density and improving low libido in postmenopausal women, we have studied the long-term effects of estradiol and testosterone implants on bone mineral density and sexuality in a prospective, 2 year, single-blind randomised trial.
Thirty-four postmenopausal volunteers were randomised to treatment with either estradiol implants 50 mg alone (E) or estradiol 50 mg plus testosterone 50 mg (E&T), administered 3-monthly for 2 years. Cyclical oral progestins were taken by those women with an intact uterus. Thirty-two women completed the study.
BMD (DEXA) of total body, lumbar vertebrae (L1-L4) and hip area increased significantly in both treatment groups. BMD increased more rapidly in the testosterone treated group at all sites. A substantially greater increase in BMD occurred in the E&T group for total body (P < 0.008), vertebral L1-L4 (P < 0.001) and trochanteric (P < 0.005) measurements. All sexual parameters (Sabbatsberg sexual self-rating scale) improved significantly in both groups. Addition of testosterone resulted in a significantly greater improvement compared to E for sexual activity (P < 0.03), satisfaction (P < 0.03), pleasure (P < 0.01), orgasm (P < 0.035) and relevancy (P < 0.05). Total cholesterol and LDL-cholesterol fell in both groups as did total body fat. Total body fat-free mass (DEXA, anthropometry, impedance) increased in the E&T group only.
We concluded that in postmenopausal women, treatment with combined estradiol and testosterone implants was more effective in increasing bone mineral density in the hip and lumbar spine than estradiol implants alone. Significantly greater improvement in sexuality was observed with combined therapy, verifying the therapeutic value of testosterone implants for diminished libido in postmenopausal women. The favourable estrogenic effects on lipids were preserved in women treated with T, in association with beneficial changes in body composition. [12]
Originally Published: August 22, 2007
"In a recent editorial by Burger entitled "Should testosterone be added to estrogen ad progesterone therapy for breast protection" the author discussed the potential protective effect of testosterone in women with regard to breast cancer. Considerable evidence is emerging suggesting that testosterone counteracts the proliferative effects of estrogen and progestins in the mammary gland. Several studies [4 studies cited] have suggested that there is no evidence that testosterone is implicated in breast cancer and provide a protective effect, contrary to fear implied in the [Endocrine] Society Guidelines." [9]
References:
1 Assessment and Management of Women's Sexual Dysfunctions: Problematic Desire and Arousal. The Journal of Sexual Medicine Volume 2 Number 3 2005
2 A clinical update on female androgen insufficiency-testosterone testing and treatment in women presenting with low sexual desire. Sex Health. 2006 May;3(2):73-8.
3 Androgen glucuronides, instead of testosterone, as the new markers of androgenic activity in women. The Journal of Steroid Biochemistry and Molecular Biology. 2006 Jun;99(4-5):182-8.
4 Androgen production in women. Fertility and Sterility 2002 Apr; 77 Supplement 4:S3-5
5 Menstrual cycle irregularities are associated with testosterone levels in healthy premenopausal women. Am J Hum Biol. 2006 Nov-Dec;18(6):841-4
6 Androgen Therapy in Women European Journal of Endocrinology 2006 154 1-11 See Text File or PDF File
7 Androgen Levels in Adult Females: Changes with Age, Menopause, and Oophorectomy The Journal of Clinical Endocrinology & Metabolism 90(7):384-3853 April 12, 2005.
8 Endocrine and Intracrine Sources of Androgens in Women: Inhibition of Breast Cancer and Other Roles of Androgens and Their Precursors. Endocrine Reviews 24(2): 152-182 Copyright 2003. See Text File or PDF File
9 Are the Endocrine Society's Clinical Practice Guidelines on Androgen Therapy in Women Misguided? A Commentary, Journal of Sexual Medicine Volume 4 Issue 5, Pages 1223 - 1235
10 The safety of 52 weeks of oral DHEA therapy for postmenopausal women. Maturitas. 2009 Apr 30
11 Testosterone for low libido in postmenopausal women not taking estrogen. N Engl J Med. 2008 Nov 6;359(19):2005-17.
12 Testosterone enhances estradiol's effects on postmenopausal bone density and sexuality. Maturitas. 2008 Sep-Oct;61(1-2):17-26.
13 Role of testosterone in the treatment of hypoactive sexual desire disorder. Maturitas. 2009 Jun 20;63(2):152-9.
14 The role of testosterone in the management of hypoactive sexual desire disorder in postmenopausal women. Maturitas. 2009 May 30.
15 Safety of testosterone use in women. Maturitas. 2009 May 20;63(1):63-6.
16 The Incidence of Invasive Breast Cancer Among Women Prescribed Testosterone for Low Libido. J Sex Med. 2009 Apr 24.
17 Study of adverse outcomes in women using testosterone therapy. Maturitas. 2009 Jan 20;62(1):76-80.
18 Does the increase of endogenous steroid hormone levels also affect breast cancer risk in Chinese women? Int J Cancer. 2009 Apr 15;124(8):1892-9.
19 Influence of estrogen plus testosterone supplementation on breast cancer. Arch Intern Med. 2009 Jan 12;169(1):41-6.
20 Approved Hormonal Treatments for HSDD: An Unmet Medical Need. Journal of Sexual Medicine Volume 6 Issue 7, Pages 1846 - 1849
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