Hypogonadism is a disease in which the body is unable to produce normal amounts of testosterone due to a problem with the testicles or with the pituitary gland that controls the testicles. Testosterone replacement therapy can improve the signs and symptoms of low testosterone in these men. Doctors may prescribe testosterone as injections, pellets, patches or gels.
Instead of the hesitation with which he had accosted the cardinal a quarter of an hour before, there might be read in the eyes of the young king that will against which a struggle might be maintained, and which might be crushed by its own impotence, but which, at least, would preserve, like a wound in the depth of the heart, the remembrance of its defeat.
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Common side effects from testosterone medication include acne, swelling, and breast enlargement in males.[10] Serious side effects may include liver toxicity, heart disease, and behavioral changes.[10] Women and children who are exposed may develop virilization.[10] It is recommended that individuals with prostate cancer not use the medication.[10] It can cause harm if used during pregnancy or breastfeeding.[10]

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What you need to know about STDs Sexually transmitted diseases (STDs) are infections that are passed on from one person to another through sexual contact. There are many STDs, including chlamydia, genital warts, syphilis, and trich. This article looks at some of the most common STDs, the symptoms, and how to avoid getting or passing an STD one on. Read now
Now, there are lots of ways that you can reduce stress and anxiety in your life. One of those things you can do is exercising daily. Now, it doesn’t mean getting into a gym all the time, but it can just be doing sit-ups at home, long walks at the grocery store, bicycling, and if you can afford the gym, getting there maybe two to three days a week. But don’t forget, a healthy body equals a healthy mind. Meditation, yoga, breathing exercises– now, here’s where you can take a few moments to be centered and communicate with your inner self, peace. Healthy eating– now, taking control of the intake of what goes into your body makes you to start feeling better and looking better. That wellness is the opposite of anxiety. And treating issues and tackling things that are weighing you down, taking that very first step is liberating.

Common side effects from testosterone medication include acne, swelling, and breast enlargement in males.[10] Serious side effects may include liver toxicity, heart disease, and behavioral changes.[10] Women and children who are exposed may develop virilization.[10] It is recommended that individuals with prostate cancer not use the medication.[10] It can cause harm if used during pregnancy or breastfeeding.[10]


Other factors leading to erectile dysfunction are diabetes mellitus, which is a well-known cause of neuropathy).[1] ED is also related to generally poor physical health, poor dietary habits, obesity, and most specifically cardiovascular disease, such as coronary artery disease and peripheral vascular disease.[1] Screening for cardiovascular risk factors, such as smoking, dyslipidemia, hypertension, and alcoholism is helpful.[1]
Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and others not yet identified. Factors that mediate relaxation include acetylcholine, nitric oxide (NO), vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.

Additionally, the physiologic processes involving erections begin at the genetic level. Certain genes become activated at critical times to produce proteins vital to sustaining this pathway. Some researchers have focused on identifying particular genes that place men at risk for ED. At present, these studies are limited to animal models, and little success has been reported to date. [4] Nevertheless, this research has given rise to many new treatment targets and a better understanding of the entire process.


The mechanism of age related decreases in serum testosterone levels has also been the subject of investigation. Metabolic clearance declines with age but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels. Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced (Mulligan et al 1999, 2001). This implies that the reduced production may be caused by primary testicular failure but in fact these changes are not adequate to fully explain the fall in testosterone levels. There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved (Mulligan et al 1999). It therefore seems likely that there are changes in endogenous production of GnRH which underlie the changes in LH secretion and have a role in the age related decline in testosterone. Thus the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis. With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH (Ono et al 1988; Gallon et al 1989).


There is a negative correlation of testosterone levels with plasminogen activator inhibitor-1 (PAI-1) (Glueck et al 1993; Phillips 1993), which is a major prothrombotic factor and known to be associated with progression of atherosclerosis, as well as other prothrombotic factors fibrinogen, α2-antiplasmin and factor VII (Bonithon-Kopp et al 1988; Glueck et al 1993; Phillips 1993; De Pergola et al 1997). There is a positive correlation with tissue plasminogen activator (tPA) which is one of the major fibrinolytic agents (Glueck et al 1993). Interventional trials have shown a neutral effect of physiological testosterone replacement on the major clotting factors (Smith et al 2005) but supraphysiological androgen administration can produce a temporary mild pro-coagulant effect (Anderson et al 1995).
However, in contrast, a recent systematic review of published studies, the authors concluded that overall, the addition of testosterone to PDE-5 inhibitors might benefit patients with ED associated with testosterone levels of less than 300 ng/dL (10.4 nmol/L) who failed monotherapy. [20] A limitation of existing studies are their heterogeneous nature and methodological drawbacks.

The mechanism of age related decreases in serum testosterone levels has also been the subject of investigation. Metabolic clearance declines with age but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels. Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced (Mulligan et al 1999, 2001). This implies that the reduced production may be caused by primary testicular failure but in fact these changes are not adequate to fully explain the fall in testosterone levels. There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved (Mulligan et al 1999). It therefore seems likely that there are changes in endogenous production of GnRH which underlie the changes in LH secretion and have a role in the age related decline in testosterone. Thus the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis. With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH (Ono et al 1988; Gallon et al 1989).
The effects of testosterone in humans and other vertebrates occur by way of multiple mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.[105][106] Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors.[107][108][109]
At the present time, it is suggested that androgen replacement should take the form of natural testosterone. Some of the effects of testosterone are mediated after conversion to estrogen or dihydrotestosterone by the enzymes aromatase and 5a-reductase enzymes respectively. Other effects occur independently of the traditional action of testosterone via the classical androgen receptor- for example, its action as a vasodilator via a cell membrane action as described previously. It is therefore important that the androgen used to treat hypogonadism is amenable to the action of these metabolizing enzymes and can also mediate the non-androgen receptor actions of testosterone. Use of natural testosterone ensures this and reduces the chance of non-testosterone mediated adverse effects. There are now a number of testosterone preparations which can meet these recommendations and the main factor in deciding between them is patient choice.

Important future developments will include selective androgen receptor modulators (SARMs). These drugs will be able to produce isolated effects of testosterone at androgen receptors. They are likely to become useful clinical drugs, but their initial worth may lie in facilitating research into the relative importance of testosterone’s action at the androgen receptor compared to at other sites or after conversion to other hormones. Testosterone will remain the treatment of choice for late onset hypogonadism for some time to come.
Erections are more complicated than you think. Your brain, nerves, heart, blood vessels, and a whole lot of hormones have to work together perfectly or nothing happens. It’s a lot to ask, and sometimes things break down. And while ED happens to most guys at some point in their lives, erectile dysfunction isn’t something you can just ignore and hope it goes away.
Testosterone belongs to a class of male hormones called androgens, which are sometimes called steroids or anabolic steroids. In men, testosterone is produced mainly in the testes, with a small amount made in the adrenal glands. The brain's hypothalamus and pituitary gland control testosterone production. The hypothalamus instructs the pituitary gland on how much testosterone to produce, and the pituitary gland passes the message on to the testes. These communications happen through chemicals and hormones in the bloodstream.
However, testosterone is only one of many factors that aid in adequate erections. Research is inconclusive regarding the role of testosterone replacement in the treatment of erectile dysfunction. In a review of studies that looked at the benefit of testosterone in men with erection difficulties, nearly half showed no improvement with testosterone treatment. Many times, other health problems play a role in erectile difficulties. These can include:
Fatherhood decreases testosterone levels in men, suggesting that the emotions and behavior tied to decreased testosterone promote paternal care. In humans and other species that utilize allomaternal care, paternal investment in offspring is beneficial to said offspring's survival because it allows the parental dyad to raise multiple children simultaneously. This increases the reproductive fitness of the parents, because their offspring are more likely to survive and reproduce. Paternal care increases offspring survival due to increased access to higher quality food and reduced physical and immunological threats.[60] This is particularly beneficial for humans since offspring are dependent on parents for extended periods of time and mothers have relatively short inter-birth intervals,[61] While extent of paternal care varies between cultures, higher investment in direct child care has been seen to be correlated with lower average testosterone levels[62] as well as temporary fluctuations. For instance, fluctuation in testosterone levels when a child is in distress has been found to be indicative of fathering styles. If a father's testosterone levels decrease in response to hearing their baby cry, it is an indication of empathizing with the baby. This is associated with increased nurturing behavior and better outcomes for the infant[63].
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Conflicting results have been obtained concerning the importance of testosterone in maintaining cardiovascular health.[29][30] Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters that are thought to reduce cardiovascular disease risk, such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control.[31]
More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.
Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels.[138] Behavior: Dominance challenges can, in some cases, stimulate increased testosterone release in men.[139] Drugs: Natural or man-made antiandrogens including spearmint tea reduce testosterone levels.[140][141][142] Licorice can decrease the production of testosterone and this effect is greater in females.[143]

Testosterone belongs to a class of male hormones called androgens, which are sometimes called steroids or anabolic steroids. In men, testosterone is produced mainly in the testes, with a small amount made in the adrenal glands. The brain's hypothalamus and pituitary gland control testosterone production. The hypothalamus instructs the pituitary gland on how much testosterone to produce, and the pituitary gland passes the message on to the testes. These communications happen through chemicals and hormones in the bloodstream.
The doctor regularly measured my levels to be sure they were within the normal range for a male my age. In other words, I wasn’t taking ‘roids to get big; I was getting control of hormones that were not functioning well. This is how you should look at testosterone therapy – it is a gentle nudge to help you be in normal ranges, not a big push to get you huuu-yge. If you’re like me, you want “normal ranges” of a 27-year-old, not of a 60-year-old. It’s my plan to keep my testosterone where it is now (around 700) no matter what it takes. Right now, the Bulletproof Diet and the other biohacks I’ve written about do that! I’m 43.

A testicular action was linked to circulating blood fractions – now understood to be a family of androgenic hormones – in the early work on castration and testicular transplantation in fowl by Arnold Adolph Berthold (1803–1861).[174] Research on the action of testosterone received a brief boost in 1889, when the Harvard professor Charles-Édouard Brown-Séquard (1817–1894), then in Paris, self-injected subcutaneously a "rejuvenating elixir" consisting of an extract of dog and guinea pig testicle. He reported in The Lancet that his vigor and feeling of well-being were markedly restored but the effects were transient,[175] and Brown-Séquard's hopes for the compound were dashed. Suffering the ridicule of his colleagues, he abandoned his work on the mechanisms and effects of androgens in human beings.
Transdermal preparations of testosterone utilize the fact that the skin readily absorbs steroid hormones. Initial transdermal preparations took the form of scrotal patches with testosterone loaded on to a membranous patch. Absorption from the scrotal skin was particularly good and physiological levels of testosterone with diurnal variation were reliably attained. The scrotal patches are now rarely used because they require regular shaving or clipping of scrotal hair and because they produce rather high levels of dihydrotestosterone compared to testosterone (Behre et al 1999). Subsequently, non-scrotal patches were developed but the absorptive capacity of non-scrotal skin is much lower, so these patches contain additional chemicals which enhance absorption. The non-scrotal skin patches produce physiological testosterone levels without supraphysiological dihydrotestosterone levels. Unfortunately, the patches produce a high rate of local skin reactions often leading to discontinuation (Parker and Armitage 1999). In the last few years, transdermal testosterone gel preparations have become available. These require daily application by patients and produce steady state physiological testosterone levels within a few days in most patients (Swerdloff et al 2000; Steidle et al 2003). The advantages compared with testosterone patches include invisibility, reduced skin irritation and the ability to adjust dosage, but concerns about transfer to women and children on close skin contact necessitate showering after application or coverage with clothes.
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