This section explains what testosterone is, in which forms it is present in the human body, the roles of testosterone throughout our life-stages, how testosterone affects erectile functioning as well as how a lack of it can lead to erectile dysfunction and a reduced libido.
Testosterone is what is called a steroid hormone and which belongs to the androgen group. Androgens stimulate and control the development and maintenance of male characteristics and sexual development. A small percentage of testosterone is made in the adrenal glands on top of our kidneys, however about 95% of it is made in the testicles. Levels of testosterone are about 7–8 times greater in adult males than in adult females, but, as the consumption of testosterone in males is greater, the daily production is about 20 times greater in men. On average, a man’s body produces about 7 mg of testosterone a day, but not all of that testosterone can be immediately used by the body because it is bound to proteins and therefore made inactive. Testosterone is present in the body in the following three forms:
- Free Testosterone: This is testosterone in its optimal and purest form. The reason it’s called ‘free’ is because there aren’t any proteins attached to it. Unbound to other molecules, free testosterone can go about carrying out its functions freely by entering cells and activating receptors. Free testosterone normally makes up only 1-3% of a man’s total testosterone levels.
- SHBG-bound Testosterone: About 40-50% of a man’s total testosterone is bound to a protein called sex hormone-binding-globulin (SHBG). SHBG is produced mostly in our livers and plays an important role in regulating the amount of free testosterone in our bodies. SHBG binds to testosterone in order to transport it to somewhere else in the body where it can be used, or simply for storage for later use. While testosterone is bound to SHBG it is biologically inert.
- Albumin-bound Testosterone: The remainder of our testosterone is bound to a protein called albumin. It is bound to albumin for the same reasons: transport and storage. Albumin is a protein also produced in the liver, and its job is to regulate blood pressure by binding to water, fatty acids, hormones and a number of other compounds. Like SHBG-bound testosterone, albumin-bound testosterone is biologically inactive. However, unlike SHBG-bound testosterone, the bond between albumin and testosterone is weak and can be easily broken in order to create free testosterone when needed.
The testosterone production process starts in the brain. When our hypothalamus detects that our body needs more testosterone to fulfill some task, it secretes a hormone called gonadotropin-releasing hormone. This hormone makes its way over to the pituitary gland in the back of the brain. When the pituitary gland detects the gonadotropin-releasing hormone, it starts producing a hormone called luteinizing hormone. This hormone is then transported through the bloodstream to the testicles. In the testicles, it stimulates the leydig cells to convert cholesterol to testosterone. Once testosterone is produced, it is released into our bloodstream. Most of it immediately gets bound to SHBG and albumin and become biologically inert.
The small percentage of testosterone that remains free and unbound (1-3%) circulates around the blood vessels and carries out the normal functions of testosterone. When the brain detects that there is enough testosterone in the blood, it signals the pituitary gland to stop secreting luteinizing hormone so that the testicles can slow down or stop testosterone production.
Testosterone production takes place primarily at night when the body is sleeping. This manufacturing of testosterone normally peaks about three hours into the sleep, and also normally continues for as long as a person is sleeping. Therefore, testosterone levels are typically highest in the morning right after a person wakes up, and are also normally lowest in the evening before bedtime.
Testosterone and cholesterol are both called steroids because they share a similar chemical structure, and both are also important for many bodily functions. Cholesterol is part of every cell‘s outer membrane, responsible for its fluid nature and helping determine which molecules can enter the cells. The body can obtain cholesterol from animal-based foods, but it’s also made as needed by the liver and other organs. Cholesterol has a bad reputation primarily for causing cardiovascular disease, however it is an absolutely essential molecule for healthy bodily functions.
Whereas testosterone is transported through the blood bound to SHGB and albumin, cholesterol is combined with proteins called lipoproteins, which transport cholesterol through the blood vessels to reach cells and tissues. Low-density lipoproteins and high-density lipoproteins both transport cholesterol in the blood, but they deliver cholesterol to different parts of the body.
Low-density lipoproteins, the primary carriers of cholesterol and also called ‘bad’ cholesterol, bring cholesterol to cells throughout the body as all cells need cholesterol to function optimally. It is called ‘bad’ because it may cause cholesterol to build up in the arteries if there is more supply of cholesterol than there is demand for it from the body. High-density lipoproteins, called ‘good’ cholesterol, carry cholesterol away from the heart and other organs and deliver it back to the liver, where it is broken down and removed from the bloodstream.
The body needs a healthy balance of cholesterol and testosterone to function optimally, and too much of one normally means too little of the other. For instance, an important role of testosterone is to enable and support high-density lipoproteins in the removal of excess cholesterol from the arteries and transport it to the liver for destruction. Inadequate testosterone may therefore cause a build-up of excess cholesterol. In addition, obesity, which will normally be accompanied by excess cholesterol, will often lead to decreased testosterone levels.
The Roles of Testosterone
As early as during prenatal development, testosterone takes part in human formation by playing a key role in determining the gender of the embryo. After birth, the presence of testosterone stimulates the development of the male sex organs and the prostate gland.
In very young boys, testosterone impacts brain development leading to development of characteristics such as high levels of activity, increased risk taking, exploration, need for dominance, etc.
In late childhood, testosterone contributes to the growth of pubic hair, axillary hair, facial hair, increased oiliness of skin and hair and acne formation. Boys will often also witness a sudden growth and lengthening of arms and legs due to bone maturation just before reaching adolescence.
During adolescence, testosterone makes boys acquire a deeper voice, makes facial features take on a more defined contour, increases muscle mass, makes shoulders broader, makes hair growth increase overall, and makes the Adam’s apple appear. During adolescence, testosterone will also cause young men to experience an increase in sexual desire.
During adulthood, one of testosterone‘s key functions is to regulate sperm production. Testosterone is also a requirement for protein synthesis and production of growth hormone, both of which are needed for maintaining muscle mass, tissue growth, hair growth and bone formation.
Testosterone also assists with oxygen uptake throughout the body, helps control blood sugar, regulates cholesterol, and maintains the immune system. In addition, the body requires testosterone to maintain efficient bloodflow from the heart (cardiac output) and for the bone marrow to manufacture red blood cells. Testosterone also plays an important role in regulating glucose and fat metabolism.
Testosterone also plays a role in development of certain behaviors, including aggression, dominance, tolerance for risk-taking and the desire for power. It also helps to spark competitiveness, increase self-esteem and contribute to higher levels of energy.
Testosterone levels peak in the late teens and then gradually decline over time, typically by about 1% a year after age 30. By age 60 to 65, though usually earlier, most men notice that their sexual inclinations and sexual abilities have changed; it takes longer for the penis to become erect and erections may not be as firm as before. It may also take longer to achieve orgasm and to ejaculate. Erectile dysfunction also becomes more common. This decline in testosterone plays an important role in a series of signs and symptoms that accompany the ageing process, such as a decline in virility, libido, sexual activity, muscle mass, strength and bone mass (osteoporosis) as well as an increase in abdominal fat.
Many people are probably aware that testosterone is somehow a key ingredient needed for a man to function sexually. But how exactly does testosterone support erections, libido and how does it impact erectile dysfunction?
When the penis is in a flaccid state, the smooth muscles in the penis are in a state of contraction and therefore clench around the blood vessels. When this happens, blood is squeezed out of the penis and the only blood that is allowed to enter is for maintenance purposes. In order for a penis to become erect, blood needs to flow into the penis to fill it to its capacity. For this to happen, help is needed from a molecule called nitric oxide. Nitric oxide, when diffused into the smooth muscles of the penis, makes these smooth muscles start to relax and therefore give up the tight grip around the blood vessels. When this happens, blood is allowed to flow into the penis and an erection can be built. This nitric oxide is created by an enzyme called nitric oxide synthase. To learn more about nitric oxide on Truelibido, please go here.
Nitric oxide synthase is highly dependent on testosterone to function properly, and low levels of testosterone will normally cause these enzymes to produce low levels of nitric oxide. The reason is that low levels of testosterone will normally lead to a decrease in the number of active nitric oxide synthase neurons in the brain. In other words, these neurons that communicate with nitric oxide need testosterone to operate. Studies on animals and humans have shown that castrated individuals (castration will normally lead to a significant reduction in testosterone production) tend to lose a significant amount of nitric oxide synthase activity compared to uncastrated individuals. Additionally, castrated subjects that have later undergone testosterone replacement therapy, have seen their nitric oxide synthase activity increase substantially.
Not only is nitric oxide synthase dependent on testosterone to carry out its tasks and function properly, but so is the messenger molecule dopamine. In order for adequate levels of dopamine to be produced, testosterone is needed. An environment with adequate levels of testosterone provides the basis for dopamine synthesis. Dopamine is a key element in libido and is also paramount for a penile erection to take place. It provides the basis for libido and is one of the first chemicals to act in the erection process by setting off a cascade of events among chemicals such as nitric oxide, serotonin, testosterone and others. In addition, these three molecules – testosterone, dopamine and nitric oxide – are interconnected and impact each other further as increased nitric oxide production in turn causes further dopamine release, which again further support both libido and erectile functioning. To learn more about dopamine on Truelibido, please go here.
Research has also found that testosterone has a profound effect on the functional and structural integrity of the corpus cavernosum, nerves and connective tissues in the penis, and particularly on the regulation of smooth muscle relaxation and contraction that allows for appropriate bloodflow in and out of the penis. In other words, if there is a lack of testosterone over a significant period of time, a person may experience a decay of integral features of the penis – the penis may stop working properly – and erectile dysfunction may kick in as a result. To learn more about erectile dysfunction on Truelibido, please go here.
Anderson RA, Bancroft J, Wu FC. The effects of exogenous testosterone on sexuality and mood of normal men. J Clin Endocrinol Metab. 1992;75:1503–1507.
Aversa A, Isidori AM, De Martino MU et al. Androgens and penile erection: evidence for a direct relationship between free testosterone and cavernous vasodilation in men with erectile dysfunction. Clin Endocrinol (Oxf) 2000; 53: 517-22.
Azadzoi KM, Kim N, Brown ML, Goldstein I, Cohen RA, Saenz de Tejada I. Endothelium-derived nitric oxide and cyclooxygenase products modulate corpus cavernosum smooth muscle tone. J Urol 1992; 147: 220-5.
Baba K, Yajima M, Carrier S, Morgan DM, Nunes L, Lue TF, Iwamoto T. Delayed testosterone replacement restores nitric oxide synthase-containing nerve fibres and the erectile response in rat penis. BJU Int. 2000 May; 85(7):953-8.
Bagatelle C, Heiman JR, Rivier RE, Bremmer WJ. Effects of endogenous testosterone and estradiol on sexual behavior in normal young men. J Clin Endocrinol Metab. 1994; 78:711–716.
Benkert O, Witt W, Adam W, Leitz A. Effects of testosterone undecanoate on sexual potency and the hypothalamic-pituitary-gonadal axis of impotent males. Arch Sex Behav. 1979; 8:471–480.
Blute M, Hakimian P, Kashanian J, Shteynshluyger A, Lee M, Shabsigh R. Erectile dysfunction and testosterone deficiency. Front Horm Res. 2009; 37:108-22. DOI: 10.1159/000176048.
Boloña ER, Uraga MV, Haddad RM, Tracz MJ, Sideras K, Kennedy CC, Caples SM, Erwin PJ, Montori VM. Testosterone Use in Men With Sexual Dysfunction: A Systematic Review and Meta-analysis of Randomized Placebo-Controlled Trials. Mayo Clinic Proceedings, Jan 2007,82(1):20-28.
Buena F, Swerdloff R, Steiner BS, et al. Sexual function does not change when serum testosterone levels are pharmacologically varied within the normal male range. Fertil Steril. 1993; 59:1118–1123.
Burnett AL. Novel nitric oxide signaling mechanisms regulate the erectile response. Int J Impot Res 2004; 16 (Suppl. 1): S15-9.
Buvat J, Lemaire A, Buvat-Herbaut M. Human chorionic gonadotropin treatment of nonorganic erectile failure and lack of sexual desire: a double-blind study. Urology. 1987; 30:216–219.
Chamness SL, Ricker DD, Crone JK, Dembeck CL, Maguire MP, Burnett AL, Chang TS. The effect of androgen on nitric oxide synthase in the male reproductive tract of the rat. Fertil Steril, 1995 May, 63(5):1101-7.
Davidson JM, Camargo CA, Smith ER. Effects of androgen on sexual behavior in hypogonadal men. J Clin Endocrinol Metab. 1979; 48:935–941.
Du J, Hull EM. Effects of testosterone on neuronal nitric oxide synthase and tyrosine hydroxylase. Brain Res. 1999 Jul 31; 836(1-2):90-8.
Foresta C, Caretta N, Rossato M, Garolla A, Ferlin A. Role of androgens in erectile function. J Urol 2004; 171: 2358-62.
Goh VH, Tong TY. Sleep, sex steroid hormones, sexual activities, and aging in Asian men. J Androl. 2010 Mar-Apr; 31(2):131-7. DOI: 10.2164/jandrol.109.007856.
Granata AR, Rochira V, Lerchl A, Marrama P, Carani C. Relationship between sleep-related erections and testosterone levels in men. Journal of Andrology, 18(5):522-527.
Gray PB, Singh AB, Woodhouse LJ, Storer TW, Casaburi R, Dzekov J, Dzekov C, Sinha-Hikim I, Bhasin S. Dose-Dependent Effects of Testosterone on Sexual Function, Mood, and Visuospatial Cognition in Older Men. J Clin Endocrinol Metab. 2005 Jul; 90(7):3838-46.
Handelsman DJ, Zajac JD. Androgen deficiency and replacement therapy in men. Med J Aust 2004; 180: 529-35.
Isidori AM, Giannetta E, Gianfrilli D et al. Effects of testosterone on sexual function in men: results of a meta-analysis. Clin Endocrinol (Oxf) 2005; 63: 381-94.
Jannini EA, Screponi E, Carosa E et al. Lack of sexual activity from erectile dysfunction is associated with a reversible reduction in serum testosterone. Int J Androl 1999; 22: 385-92.
Morales A, Johnston B, Heaton JP, Lundie M. Testosterone supplementation for hypogonadal impotence: assessment of biochemical measures and therapeutic outcomes. J Urol. 1997; 157:849–854.
Morelli A, Filippi S, Mancina R et al. Androgens regulate phosphodiesterase type 5 expression and functional activity in corpora cavernosa. Endocrinology 2004; 145: 2253-63.
Morley JE, Kaiser FE, Perry HM, et al. Longitudinal changes in testosterone, luteinizing hormone and follicle stimulating hormone in healthy old men. Metabolism. 1997; 46:410–413.
Mulhall JP, Valenzuela R, Aviv N, Parker M. Effect of testosterone supplementation on sexual function in hypogonadal men with erectile dysfunction. Urology 2004; 63: 348-52.
O’Carroll R, Bancroft J. Testosterone therapy for low sexual interest and erectile dysfunction in men: a controlled study. Br J Psychiatry. 1984; 145:146–151.
Park KH, Kim SW, Kim KD, Paick JS. Effects of androgens on the expression of nitric oxide synthase mRNAs in rat corpus cavernosum. BJU Int 1999; 83: 327-33.
Penev PD. Association between sleep and morning testosterone levels in older men. Sleep. 2007 Apr; 30(4):427-32.
Pirke KM, Kockott G, Aldenhoff J, et al. Pituitary gonadal system function in patients with erectile impotence and premature ejaculation. Arch Sex Behav. 1979; 8:41–48.
Rajfer J. Relationship Between Testosterone and Erectile Dysfunction. Rev Urol. 2000 Spring; 2(2): 122–128.
Salminies S, Kockott G, Pirke KM, et al. Effects of testosterone replacement on sexual behavior in hypogonadal men. Arch Sex Behav. 1982; 11:345–353.
Schiavi RC, White D, Mandeli J, Levine AC. Effect of testosterone administration on sexual behavior and mood in men with erectile dysfunction. Arch Sex Behav 1997; 26: 231-41.
Shabsigh R. The effects of testosterone on the cavernous tissue and erectile function. World Journal of Urology, 15(1):21-26.
Shabsigh R. The role of testosterone in the cavernous tissue and its neural supply. World J Urol 1997; 15: 21-6.
Sternbach H. Age-Associated Testosterone Decline in Men: Clinical Issues for Psychiatry. Am J Psychiatry. 1998 Oct; 155(10):1310-8.
Tenover JL. Testosterone and the aging male. J Androl. 1997; 18:103–106.
Travison TG, Morley JE, Araujo AB, O’Donnell AB, McKinlay JB. The Relationship between Libido and Testosterone Levels in Aging Men. J Clin Endocrinol Metab. 2006 Jul; 91(7):2509-13.
Wheeler MJ. The determination of bio-available testosterone. Ann Clin Biochem. 1995; 32:345–357.
Yassin AA, Saad F. Improvement of Sexual Function in Men with Late-Onset Hypogonadism Treated with Testosterone Only. The Journal of Sexual Medicine, Mar 2007, 4(2):497-501.
Zhang XH, Morelli A, Luconi M, Vignozzi L, Filippi S, Marini M, Vannelli GB, Mancina R, Forti G, Maggi M. Testosterone regulates PDE5 expression and in vivo responsiveness to tadalafil in rat corpus cavernosum. Eur Urol 2005; 47: 409-16.
Zvara P, Sioufi R, Schipper HM, Begin LR, Brock GB. Nitric oxide mediated erectile activity is a testosterone dependent event: a rat erection model. Int J Impot Res. 1995 Dec; 7(4):209-19.