Men with medical conditions that may cause a sustained erection, such as sickle cell anemia, leukemia, or multiple myeloma, or a man who has an abnormally-shaped penis, may not benefit from these medications. Also, men with liver diseases or a disease of the retina, such as macular degeneration or retinitis pigmentosa, may not be able to take these medications, or may need to take the lowest dosage.
In men with hypogonadism, a low level of testosterone is produced due to a problem in the testicles or the pituitary gland. According to Harvard Medical School, determining exactly what constitutes a low testosterone level is a controversial matter. Levels of this hormone fluctuate wildly and even vary according to the time of day. However, generally physicians only decide to treat a patient for hypogonadism if the blood testosterone level is below 300 ng/dL and the following symptoms outlined by The National Institutes of Health are present.    
Erectile dysfunction (ED) affects 50% of men older than 40 years, [4] exerting substantial effects on quality of life. [5] This common problem is complex and involves multiple pathways. Penile erections are produced by an integration of physiologic processes involving the central nervous, peripheral nervous, hormonal, and vascular systems. Any abnormality in these systems, whether from medication or disease, has a significant impact on the ability to develop and sustain an erection, ejaculate, and experience orgasm.
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.

The nerves and endothelium of sinusoids and vessels in the penis produce and release transmitters and modulators that control the contractile state of corporal smooth muscles. Although the membrane receptors play an important role, downstream signaling pathways are also important. The RhoA–Rho kinase pathway is involved in the regulation of cavernosal smooth muscle contraction. [12]

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.


Hypogonadism (as well as age-related low testosterone) is diagnosed with blood tests that measure the level of testosterone in the body. The Endocrine Society recommends testing for suspected low T with a total testosterone test. It may be performed in the morning when testosterone levels tend to be highest in young men, although this isn't necessarily the case in older men. The test may be repeated on another day if the results show a low T level. (5)

In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][147] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][147] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][147] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[149][150] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[148]
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.

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.
The first period occurs between 4 and 6 weeks of the gestation. Examples include genital virilisation such as midline fusion, phallic urethra, scrotal thinning and rugation, and phallic enlargement; although the role of testosterone is far smaller than that of dihydrotestosterone. There is also development of the prostate gland and seminal vesicles.
Impotence, also known as erectile dysfunction or ED, is a very common problem, affecting up to half of 40-70 year old men in Australia.Treatment techniques for impotence have varied through the years, from external steel mechanical attachments, to static electricity attached to the penis and testicles, to simple aphrodisiacs such as oysters. Until as recently as 1970, erectile failure was almost always seen as being due to psychological causes and was usually treated with psychotherapy.Since then, the medical causes contributing to impotence have been recognised and the treatment of impotence has been revolutionised, providing a range of options which are far more acceptable and very much more successful.Treatment options for impotenceTreatment choices for erectile dysfunction include:medicines;self-injection therapy;devices such as vacuum pumps;penile implant surgery;hormone therapy; andcounselling.If you have erectile dysfunction, the treatment your doctor recommends will depend on the severity of symptoms and the underlying cause of your impotence.Your doctor will want to check that any conditions that could be contributing to or causing erectile dysfunction are being treated.Your doctor may also suggest that you make some lifestyle adjustments, such as:increasing the amount of physical activity you get;losing weight if you are overweight;reducing the amount of alcohol you drink;quitting smoking; andnot taking illicit drugs.These lifestyle recommendations can help improve impotence related to several causes and improve your health in general.Medicines for erectile dysfunctionThe first tablet available for erectile dysfunction, sildenafil (brand name Viagra), has been largely responsible for helping to bring the topic of erectile dysfunction out into the open. Similar medications — tadalafil (Cialis) and vardenafil ( Levitra) — are also available. These medicines all work in a similar way, although there is some difference in how long their effect lasts. Sildenafil, tadalafil and vardenafil belong to a group of medicines called phosphodiesterase type 5 (PDE5) inhibitors because they block the PDE5 enzyme.How do oral medicines help treat erectile dysfunction?PDE5 inhibitors help in the process of getting and keeping an erection by working on chemicals in the body that are involved in erections. These medicines work by stopping PDE5 from breaking down an erection-producing chemical called cyclic guanosine monophosphate (cGMP). cGMP helps to relax the smooth muscle cells in the penis's erectile tissue, allowing more blood to flow into the penis to cause an erection. When PDE5 is temporarily blocked by these medicines, it can’t break down the erection producing cGMP, so an erection can be achieved and maintained. PDE5 inhibitors can be used in the treatment of erectile dysfunction that is due to physical or psychological causes.Medications such as Viagra, Cialis and Levitra will work only if you are sexually stimulated. They are not aphrodisiacs and won’t increase your sex drive.Side effects of PDE5 inhibitorsSide effects of these medicines can include headaches, flushes, blocked nose, indigestion and dizziness.In rare situations, sildenafil and vardenafil can cause a distortion of vision or change in colour vision.Tadalafil has been associated with back pain.Who can take medicines for impotence?PDE5 inhibitors cannot be taken by all men, so your doctor will need to evaluate your suitability before prescribing either of these medications.Men taking nitrates (often used to treat angina) should never take phosphodiesterase type 5 (PDE5) inhibitors. PDE5 inhibitors should also not be taken with some medicines used to treat high blood pressure.PDE5 inhibitors may also not be suitable for men with certain heart conditions or low blood pressure. Check with your doctor to find out if this type of medication may be suitable for you.Self-injection therapySelf-injection therapy delivers a medicine called alprostadil (brand name Caverject), also known as prostaglandin E-1, to the erectile tissue of the penis. Prostaglandin E-1 occurs naturally in the body and helps increase the blood flow to the penis to cause an erection. Unlike the PDE5 inhibitors, alprostadil will cause an erection whether the penis is stimulated or not.Self-injection therapy is usually recommended if PDE5 inhibitor medicines are not suitable or have not been effective in the treatment of erectile dysfunction.How to use self-injection therapyAlprostadil is injected into either of the 2 cigar-shaped chambers of the penis known as the corpora cavernosa, which run along the length of the penis, one on either side. Your doctor or urologist (specialist in problems with male reproductive organs and the urinary tract) will give you instructions on how to do this.Alprostadil should produce an erection in 5 to 20 minutes and, generally, the erection will last for 30 to 60 minutes.You should not use alprostadil more than once in a 24-hour period, and you should use it no more than 3 times a week.Don’t try to use more than the recommended dose of alprostadil, as your erection may last longer than is medically safe.Who can use self-injection therapy?You should ask your doctor if alprostadil is suitable for you. Your doctor will also be able to tell you how much alprostadil to use, depending on your condition and whether or not you are taking any other medications, and also how to use alprostadil properly.People with certain illnesses, such as leukaemia and sickle cell anaemia, or who have a penile implant or Peyronie’s disease, where the penis may be scarred and produces erections that are not straight, should not use alprostadil.Men for whom sexual activity is not advised should not use alprostadil.Side effects of injection therapyThe most common side effects of alprostadil include pain in the penis or bruising in the penis at the site of injection. Fibrosis (the development of fibrous tissue) can also develop following injections into the penis.The most serious side effect is priapism (a persistent erection), which is a medical emergency. Your doctor will inform you of what to do if you have an erection that persists for 2 hours or more. It is very important that you follow your doctor’s instructions and inform them that you have experienced this side effect.Vacuum erection devicesVacuum erection devices work by creating a vacuum, which increases blood flow to the penis, producing an erection.The penis is lubricated and placed inside a hollow plastic chamber. Air is pumped out of the chamber, either manually or by a battery powered pump. This creates a vacuum which pulls blood into the penis to cause an erection. This takes about 5 minutes.Once the penis is erect, the man fits a rubber ring around the base of his penis to keep the blood trapped inside the penis when the cylinder is removed. After intercourse, the ring can be removed to return the penis to a limp state.Vacuum erection devices avoid surgery and can be used as often as required. However, they may be difficult to use, and many men and their partners feel they take much of the pleasure and spontaneity away from sexual activities. Vacuum pumps are not suitable for men who have problems with blood clotting, or blood disorders such as leukaemia.Penile implant surgery for impotencePenile implant surgery is not a common procedure but in some cases it may be the most appropriate treatment for erectile dysfunction.The procedure involves placing an implant inside the penis, along its length, so that it can become erect. The implant may be a pair of semi-rigid rods or a pair of inflatable cylinders.The inflatable implants allow the penis to look and feel limp (flaccid) or erect, depending on how much the cylinders are inflated. The cylinders in an inflatable implant are hollow, and the man gets an erection by squeezing a pump located in his scrotum to fill the cylinders with salt water (saline) stored in a reservoir implanted in his lower abdomen. A release valve drains the saline out of the cylinders and back into the reservoir.With the semi-rigid, malleable rod type of implant, the rods run along the length of the penis and can be bent upwards to produce an erect penis, or downwards when an erect penis is not required.Like all surgery, there are some risks, such as infection or bleeding. If you have had surgery and have severe pain, fever, swelling or excessive bleeding, you should contact your doctor as soon as possible.Vascular surgery for erectile dysfunctionIn cases where a man’s anatomy prevents blood flow into or out of the penis, vascular surgery may be an option. This treatment option is rarely recommended, and is usually only successful in younger men.If there is a blockage that prevents blood from flowing into the penis, a doctor may recommend an operation that bypasses the blocked blood vessels, using a length of vein or manufactured tubing, to allow more blood to flow into the penis and help produce an erection.If the problem is that blood leaks back out of the penis, this can be corrected by tying off the major veins that drain the penis, a procedure known as venous ligation.Hormone treatments for impotenceIn a small number of men, blood tests may show abnormally low levels of testosterone, the male sex hormone. In such cases your doctor might prescribe a course of testosterone injections or a testosterone implant. The supplements can help boost sex drive as well as increasing the ability to have erections. Testosterone gel or patches, applied daily to the skin, are another option.Complementary medicines for erectile dysfunctionThere is a lack of scientific evidence supporting the effectiveness of complementary therapies for the treatment of impotence.Always check with your doctor before taking any herbal medicines or supplements for impotence. These formulations may contain ingredients that can interact with other medicines or cause dangerous side effects.Counselling for men with impotenceErectile dysfunction often has physical causes, but sometimes there is a psychological basis for erection problems. Often this is a form of performance anxiety. A man may have had an episode of erectile dysfunction due to some passing cause like fatigue, stress, relationship difficulty or intoxication. This may have led to embarrassment or a feeling of failure. Even if the physical cause does not remain, future attempts to have sex may trigger memories of this embarrassment and acute anxiety that it will happen again. This anxiety itself is capable of causing erectile dysfunction, and so a man may get trapped in a self-reinforcing cycle of anxiety and erectile dysfunction. In these instances, seeing a GP, counsellor or psychologist can be very helpful.Stress, anxiety, depression and low self-esteem, in fact, almost all significant emotional problems, can have a major effect on sexuality. So do many chronic physical illnesses, even if they don't directly affect genital function. Counsellors and psychologists can assist with these and a wide range of other sexual and relationship problems and can also help female partners suffering from sexual problems. They are particularly skilled in helping patients to overcome guilt or anxiety relating to sexual abuse, and in helping couples to sort out relationship difficulties. Simple problems can be dealt with in a few visits, but more complex problems may require several months or even years of therapy.Your doctor may be able to recommend a psychologist or counsellor who specialises in sexual and relationship problems. Last Reviewed: 12 December 2016
Sharma, R., Oni, O. A., Gupta, K., Chen, G., Sharma, M., Dawn, B., … & Barua, R. S. (2015, August 6). Normalization of testosterone level is associated with reduced incidence of myocardial infarction. European Heart Journal, 36(40), 2706-2715. Retrieved from https://academic.oup.com/eurheartj/article/36/40/2706/2293361/Normalization-of-testosterone-level-is-associated
You may find this hard to believe, but some common breakfast foods like Kellogg’s corn flakes and Graham crackers were invented 100 years ago to lower male libido. Kellogg and Graham believed that male sexual desire was the root of society’s problems, so they set out to make bland foods that would take away libido (this is absolutely true; look it up). That low fat, grain-based thing absolutely works wonders for lowering testosterone.
In addition to its role as a natural hormone, testosterone is used as a medication, for instance in the treatment of low testosterone levels in men and breast cancer in women.[10] Since testosterone levels decrease as men age, testosterone is sometimes used in older men to counteract this deficiency. It is also used illicitly to enhance physique and performance, for instance in athletes.
ED can also occur among younger men. A 2013 study found that one in four men seeking their first treatment for ED were under the age of 40. The researchers found a stronger correlation between smoking and illicit drug use and ED in men under 40 than among older men. That suggests that lifestyle choices may be a main contributing factor for ED in younger men.
ED usually has something physical behind it, particularly in older men. But psychological factors can be a factor in many cases of ED. Experts say stress, depression, poor self-esteem, and performance anxiety can short-circuit the process that leads to an erection. These factors can also make the problem worse in men whose ED stems from something physical.
Dr. Wyne told me that although she has seen an increase in male patients asking about low testosterone, she hasn't seen an actual increase in the condition itself. "I do see an increase in guys who are fatter," she said. "The question is whether, if you lose 15 or 20 pounds, your testosterone would revert [to normal]. We know that even 15 pounds makes a huge difference to their level. Most of these guys actually have 50 pounds to lose."
A number of research groups have tried to further define the relationship of testosterone and body composition by artificial alteration of testosterone levels in eugonadal populations. Induction of a hypogonadal state in healthy men (Mauras et al 1998) or men with prostate cancer (Smith et al 2001) using a gonadotrophin-releasing-hormone (GnRH) analogue was shown to produce increases in fat mass and decreased fat free mass. Another experimental approach in healthy men featured suppression of endogenous testosterone production with a GnRH analogue, followed by treatment with different doses of weekly intramuscular testosterone esters for 20 weeks. Initially the experiments involved men aged 18–35 years (Bhasin et al 2001) but subsequently the study was repeated with a similar protocol in men aged 60–75 years (Bhasin et al 2005). The different doses given were shown to produce a range of serum concentrations from subphysiological to supraphysiological (Bhasin et al 2001). A given testosterone dose produced higher serum concentrations of testosterone in the older age group (Bhasin et al 2005). Subphysiological dosing of testosterone produced a gain in fat mass and loss of fat free mass during the study. There were sequential decreases in fat mass and increases in fat free mass with each increase of testosterone dose. These changes in body composition were seen in physiological and supraphysiological treatment doses. The trend was similar in younger versus older men but the gain of fat mass at the lowest testosterone dose was less prominent in older patients (Bhasin et al 2001; Bhasin et al 2005). With regard to muscle function, the investigators showed dose dependent increases in leg strength and power with testosterone treatment in young and older men but there was no improvement in fatigability (Storer et al 2003; Bhasin et al 2005).
There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).

Psychological factors — Psychological issues such as depression, anxiety, guilt or fear can sometimes cause sexual problems. At one time, these factors were thought to be the major cause of impotence. Doctors now know that physical factors cause impotence in most men with the problem. However, embarrassment or "performance anxiety" can make a physical problem worse.
^ Southren AL, Gordon GG, Tochimoto S, Pinzon G, Lane DR, Stypulkowski W (May 1967). "Mean plasma concentration, metabolic clearance and basal plasma production rates of testosterone in normal young men and women using a constant infusion procedure: effect of time of day and plasma concentration on the metabolic clearance rate of testosterone". The Journal of Clinical Endocrinology and Metabolism. 27 (5): 686–94. doi:10.1210/jcem-27-5-686. PMID 6025472.
Intramuscular testosterone injections were first used around fifty years ago. Commercially available preparations contain testosterone esters in an oily vehicle. Esterification is designed to retard the release of testosterone from the depot site into the blood because the half life of unmodified testosterone would be very short. For many years intramuscular preparations were the most commonly used testosterone therapy and this is still the case in some centers. Pain can occur at injection sites, but the injections are generally well tolerated and free of major side effects. Until recently, the available intramuscular injections were designed for use at a frequency of between weekly and once every four weeks. These preparations are the cheapest mode of testosterone treatment available, but often cause supraphysiological testosterone levels in the days immediately following injection and/or low trough levels prior to the next injection during which time the symptoms of hypogonadism may return (Nieschlag et al 1976). More recently, a commercial preparation of testosterone undecanoate for intramuscular injection has become available. This has a much longer half life and produces testosterone levels in the physiological range throughout each treatment cycle (Schubert et al 2004). The usual dose frequency is once every three months. This is much more convenient for patients but does not allow prompt cessation of treatment if a contraindication to testosterone develops. The most common example of this would be prostate cancer and it has therefore been suggested that shorter acting testosterone preparations should preferably used for treating older patients (Nieschlag et al 2005). Similar considerations apply to the use of subcutaneous implants which take the form of cylindrical pellets injected under the skin of the abdominal wall and steadily release testosterone to provide physiological testosterone levels for up to six months. Problems also include pellet extrusion and infection (Handelsman et al 1997).
Growth of spermatogenic tissue in testicles, male fertility, penis or clitoris enlargement, increased libido and frequency of erection or clitoral engorgement. Growth of jaw, brow, chin, nose, and remodeling of facial bone contours, in conjunction with human growth hormone.[21] Completion of bone maturation and termination of growth. This occurs indirectly via estradiol metabolites and hence more gradually in men than women. Increased muscle strength and mass, shoulders become broader and rib cage expands, deepening of voice, growth of the Adam's apple. Enlargement of sebaceous glands. This might cause acne, subcutaneous fat in face decreases. Pubic hair extends to thighs and up toward umbilicus, development of facial hair (sideburns, beard, moustache), loss of scalp hair (androgenetic alopecia), increase in chest hair, periareolar hair, perianal hair, leg hair, armpit hair.
Both testosterone and 5α-DHT are metabolized mainly in the liver.[1][147] Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively.[1] An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order.[1][147][148] Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone.[1][147] The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile.[1][147][148] Only a small fraction (2%) of testosterone is excreted unchanged in the urine.[147]

A related issue is the potential use of testosterone as a coronary vasodilator and anti-anginal agent. Testosterone has been shown to act as a vasodilator of coronary arteries at physiological concentrations during angiography (Webb, McNeill et al 1999). Furthermore men given a testosterone injection prior to exercise testing showed improved performance, as assessed by ST changes compared to placebo (Rosano et al 1999; Webb, Adamson et al 1999). Administration of one to three months of testosterone treatment has also been shown to improve symptoms of angina and exercise test performance (Wu and Weng 1993; English et al 2000; Malkin, Pugh, Morris et al 2004). Longer term studies are underway. It is thought that testosterone improves angina due its vasodilatory action, which occurs independently of the androgen receptor, via blockade of L-type calcium channels at the cell membrane of the vascular smooth muscle in an action similar to the dihydropyridine calcium-channel blockers such as nifedipine (Hall et al 2006).
×