61.Testosterone Sex & Society

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61.Testosterone Sex & Society




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Testosterone Sex & Society

What is testosterone?
Testosterone is produced by the gonads (by the Leydig cells in testes in men and by the ovaries in women), although small quantities are also produced by the adrenal glands in both sexes. It is an androgen, meaning that it stimulates the development of male characteristics.

Present in much greater levels in men than women, testosterone initiates the development of the male internal and external reproductive organs during foetal development and is essential for the production of sperm in adult life. This hormone also signals the body to make new blood cells, ensures that muscles and bones stay strong during and after puberty and enhances libido both in men and women. Testosterone is linked to many of the changes seen in boys during puberty (including an increase in height, body and pubic hair growth, enlargement of the penis, testes and prostate gland, and changes in sexual and aggressive behaviour). It also regulates the secretion of luteinising hormone and follicle stimulating hormone. To effect these changes, testosterone is often converted into another androgen called dihydrotestosterone.
In women, testosterone is produced by the ovaries and adrenal glands. The majority of testosterone produced in the ovary is converted to the principle female sex hormone, oestradiol.

How is testosterone controlled?
The regulation of testosterone production is tightly controlled to maintain normal levels in blood, although levels are usually highest in the morning and fall after that. The hypothalamus and the pituitary gland are important in controlling the amount of testosterone produced by the testes. In response to gonadotrophin-releasing hormone from the hypothalamus, the pituitary gland produces luteinising hormone which travels in the bloodstream to the gonads and stimulates the production and release of testosterone.

As blood levels of testosterone increase, this feeds back to suppress the production of gonadotrophin-releasing hormone from the hypothalamus which, in turn, suppresses production of luteinising hormone by the pituitary gland. Levels of testosterone begin to fall as a result, so negative feedback decreases and the hypothalamus resumes secretion of gonadotrophin-releasing hormone.

What happens if I have too much testosterone?
The effect excess testosterone has on the body depends on both age and sex. It is unlikely that adult men will develop a disorder in which they produce too much testosterone and it is often difficult to spot that an adult male has too much testosterone. More obviously, young children with too much testosterone may enter a false growth spurt and show signs of early puberty and young girls may experience abnormal changes to their genitalia. In both males and females, too much testosterone can lead to precocious puberty and result in infertility.

In women, high blood levels of testosterone may also be an indicator of polycystic ovary syndrome. Women with this condition may notice increased acne, body and facial hair (called hirsutism), balding at the front of the hairline, increased muscle bulk and a deepening voice.

There are also several conditions that cause the body to produce too much testosterone. These include androgen resistance, congenital adrenal hyperplasia and ovarian cancer.

The use of anabolic steroids (manufactured androgenic hormones) shuts down the release of luteinising hormone and follicle stimulating hormone secretion from the pituitary gland, which in turn decreases the amount of testosterone and sperm produced within the testes. In men, prolonged exposure to anabolic steroids results in infertility, a decreased sex drive, shrinking of the testes and breast development. Liver damage may result from its prolonged attempts to detoxify the anabolic steroids. Behavioural changes (such as increased irritability) may also be observed. Undesirable reactions also occur in women who take anabolic steroids regularly, as a high concentration of testosterone, either natural or manufactured, can cause masculinisation (virilisation) of women.

What happens if I have too little testosterone?
If testosterone deficiency occurs during fetal development, then male characteristics may not completely develop. If testosterone deficiency occurs during puberty, a boy’s growth may slow and no growth spurt will be seen. The child may have reduced development of pubic hair, growth of the penis and testes, and deepening of the voice. Around the time of puberty, boys with too little testosterone may also have less than normal strength and endurance, and their arms and legs may continue to grow out of proportion with the rest of their body.

In adult men, low testosterone may lead to a reduction in muscle bulk, loss of body hair and a wrinkled ‘parchment-like’ appearance of the skin. Testosterone levels in men decline naturally as they age. In the media, this is sometimes referred to as the male menopause (andropause).

Low testosterone levels can cause mood disturbances, increased body fat, loss of muscle tone, inadequate erections and poor sexual performance, osteoporosis, difficulty with concentration, memory loss and sleep difficulties. Current research suggests that this effect occurs in only a minority (about 2%) of ageing men. However, there is a lot of research currently in progress to find out more about the effects of testosterone in older men and also whether the use of testosterone replacement therapy would have any benefits.
Sexual function in women is a complex issue, impacted upon by several factors. Female testosterone levels decrease slightly during the reproductive years, but do not change substantially after menopause, because the ovaries continue to produce androgens after depletion of follicular capital (1,2). Reduced androgen levels have been frequently associated with reduced libido in women, mainly in the peri- and postmenopausal periods (1-4). While testosterone has been frequently prescribed to women with low sexual desire, there is no evidence of a consistent association between low testosterone levels and low libido, nor of consistent improvement in sexual problems when testosterone therapy is administered. Therefore, testosterone therapy is not routinely recommended for women with low androgen levels caused by adrenal insufficiency, hypopituitarism, or surgical menopause, nor to enhance cardio-metabolic parameters, cognitive health, or general well-being in healthy women. In fact, the use of androgens in postmenopausal women remains controversial, with strong positions being taken by a variety of sexual medicine experts and professional societies (5-9).

In 1997 and 1998, two meetings were held in Cape Cod, Massachusetts, to discuss the clinical detection and management of female sexual dysfunction. These two meetings, and their subsequent iterations, would lead to the formation of the International Society for the Study of Women’s Sexual Health (ISSWSH) in 2001 (10). Later in 2002, the Princeton Consensus proposed the existence of a female androgen insufficiency syndrome, defined as a pattern of clinical symptoms in the presence of decreased bioavailable testosterone and normal estrogen status (11). The diagnostic criteria were criticized because the syndrome definition implied that sexual dysfunction, the predominant clinical finding, was a consequence of androgen insufficiency (12). In 2005, a study revealed that, while serum androgen levels decline steeply in the early reproductive years, they do not vary as a direct consequence of natural menopause. The investigators pointed out that the significant age-related variations in androgens must be taken into account when normal ranges are reported and in studies on the role of androgens in women (1).

Recently, a systematic review assessed the available evidence regarding the evaluation of serum testosterone levels and testosterone treatment for premenopausal women with low libido from 1995 to 2015. Nine out of ten studies failed to find a correlation between total testosterone levels and sexual desire, and four small studies showed little, if any, improvement in libido when compared to placebo (13). Therefore, the present position statement was developed to review the existing literature on the off-label use of testosterone to treat low sexual desire in women.

Nine members of the Female Endocrinology and Andrology Department of the Brazilian Society of Endocrinology and Metabolism, experts in clinical practice, clinical research and/or translational research in the field, were asked to critically review the topic of testosterone use and develop a position statement on testosterone therapy for women with low sexual desire. MEDLINE and SciELO/LILACS databases were searched for relevant studies and clinical practice guidelines regarding testosterone therapy in women. The level of evidence of each publication was graded using the Oxford Centre for Evidence-Based Medicine recommendations (14). In the present position statement, these levels of evidence are reported as: A: experimental or observational studies with consistent results; B: experimental or observational studies with less consistent results; C: case reports (uncontrolled studies); D: opinion lacking critical evaluation or based on guidelines, physiological studies, or animal models (15).

Testosterone levels in women across the lifespan
During childhood, testosterone levels are very low. At puberty, kisspeptin triggers pulsatile gonadotropin releasing hormone (GnRH) secretion in the medial basal hypothalamus and preoptic area (16), enhancing luteinizing hormone (LH) secretion and consequently stimulating estradiol and testosterone secretion. Upon puberty and during the reproductive years, mainly in young adult women, testosterone is produced equally by the ovarian theca cells and the adrenal cortex, accounting for approximately 300 mcg daily (17,18).
Only one-third of circulating testosterone results from direct ovarian and adrenal secretion; the remaining two-thirds arise from peripheral conversion of precursors, including delta 4-androstenedione (A4) and DHEA, in non-steroid-producing tissues. Testosterone is converted to estradiol by aromatase and to dihydrotestosterone (DHT) by 5-alpha reductase, in target tissues as well as in the periphery (mainly in adipose tissue) (19).

As in men, testosterone production in women follows a circadian rhythm, with higher levels in the morning and a nadir around midnight (20). Moreover, a modest mid-cycle testosterone peak, coincident with the LH surge in ovulatory cycles, has been confirmed by recent high-sensitivity assays (21). Apart from this mid-cycle peak, testosterone levels in the follicular and luteal phases seem to be stable (1,21,22). During the late reproductive years, the increment of anovulatory cycles leads to a failure of this mid-cycle rise, despite preservation of baseline physiological ovarian testosterone secretion at other phases of the cycle (3). Aging promotes a progressive reduction in testosterone production by the ovaries and adrenal glands (Table 1). At that stage, the peripheral conversion of A4 and DHEA into testosterone becomes more important (23-25). DHEA serves as an intermediate steroid within the testosterone and estradiol biosynthetic pathways. Peripheral tissues involved with DHEA/DHEA-S uptake from the circulation typically generate more potent androgens and estrogens that act locally (26,27).

Hormones can matter a lot when explaining sexual diversity in humans. However, just because hormones might be linked to some feature of sexuality doesn’t mean the hormones caused it. In many cases, hormones change as a result of sexual behaviors, rather than sexual behaviors being the consequence of hormone variations (Goldey & van Anders, 2014; Muller et al., 2009).

Some sexual diversity scholars have suggested many of the hormonal differences between men and women (and most of the psychological sex differences that seem connected to hormonal differences) largely result from men and women undergoing differential socialization experiences and inhabiting different social roles (e.g., Wood & Eagly, 2012). If men and women were raised exactly the same, and held identical positions and roles across society, for instance, it is expected there would be little to no sex differences in hormones such as testosterone (Butler, 2002).

In a recent paper, van Anders and her colleagues (2015) tried to experimentally test certain facets of this view. They measured testosterone levels in 26 men and 15 women who were trained actors. They asked the actors to portray a “boss” in different workplace scenes on different days. Participants were asked either to play a boss who fires someone in a “stereotypically masculine way” such as taking up space, using dominance posturing, and displaying infrequent smiles or in a “stereotypically feminine way” such as upending sentences, hesitating, and displaying infrequent eye contact. All participants also were asked to engage in a presumably hormone-neutral control activity (i.e., watching a travel documentary).

What happened to their hormone levels on these different days? For the men, not a lot. Relative to the hormone-neutral control condition, playing a role in which they were a boss firing people raised men’s testosterone about 3% or so, and it didn’t matter whether they did so in a masculine or feminine way. The average 29 year old man (the average participant age) has a total testosterone level of about 600ng/dL (nanograms per deciliter), so this would represent a jump to about 618ng/dl (this is just an estimation, actual jumps in mean testosterone levels were unreported in the paper). The testosterone jumps in men due to acting like a boss were statistically insignificant, though, and very small in terms of effect size. Not a whole lot there.

For women, it was a different story. Relative to the hormone-neutral control condition, playing a role in which they were a boss firing people raised women’s testosterone about 13% or so, and again it didn’t matter whether they did so in a masculine or feminine way. The average 29 year old woman (the average participant age) has a total testosterone level of about 60ng/dL, so this is a jump to about 68ng/dl. These effects were statistically significant, and had (d) effect sizes in the .50 to .70 range—rather impressive effect sizes.



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