Interest in testosterone began when farmers of old first noticed that castrated animals were more docile than their intact peers. Ditto for castrated humans. For human males with intact gonads, testosterone increases during puberty. It deepens the voice, increases muscle growth, promotes facial and body hair, and spurs the sex drive. Testosterone also is associated with personality traits related to power and dominance.

Interest in testosterone began when farmers of old first noticed that castrated animals were more docile than their intact peers. Ditto for castrated humans. For human males with intact gonads, testosterone increases during puberty. It deepens the voice, increases muscle growth, promotes facial and body hair, and spurs the sex drive. Testosterone also is associated with personality traits related to power and dominance.

The neurovascular events that ultimately occur result in the inhibition of adrenergic tone and the release of the nonadrenergic, noncholinergic neurotransmitter, nitric oxide. Nitric oxide is believed to be released from nonadrenergic, noncholinergic nerves and endothelial cells. It subsequently stimulates the guanylate cyclase enzyme system in penile smooth muscle. This results in increased levels of cyclic guanosine monophosphate (cGMP) and ultimately in smooth muscle relaxation, enhancement of arterial inflow, and veno-occlusion, producing adequate firmness for sexual activity.


Longitudinal studies in male aging studies have shown that serum testosterone levels decline with age (Harman et al 2001; Feldman et al 2002). Total testosterone levels fall at an average of 1.6% per year whilst free and bioavailable levels fall by 2%–3% per year. The reduction in free and bioavailable testosterone levels is larger because aging is also associated with increases in SHBG levels (Feldman et al 2002). Cross-sectional data supports these trends but has usually shown smaller reductions in testosterone levels with aging (Feldman et al 2002). This is likely to reflect strict entry criteria to cross-sectional studies so that young healthy men are compared to older healthy men. During the course of longitudinal studies some men may develop pathologies which accentuate decreases in testosterone levels.


When a man becomes sexually excited, muscles in their penis relax. This relaxation allows for increased blood flow through the penile arteries. This blood fills two chambers inside the penis called the corpora cavernosa. As the chambers fill with blood, the penis grows rigid. Erection ends when the muscles contract and the accumulated blood can flow out through the penile veins.
Once a complete sexual and medical history has been completed, appropriate laboratory studies should be conducted. In the initial evaluation of ED, sophisticated laboratory testing is rarely necessary. For example, serum testosterone (and sometimes prolactin) is typically only useful when the patient demonstrates hypogonadal features or testicular atrophy, or when clinical history is suggestive. Additional hormonal evaluation may include thyroid stimulating hormone in those with a clinical suspicion of hypothyroidism or appropriate diabetes screening in those presenting with a concern for impaired glucose metabolism. If the patient has not been evaluated with a lipid panel and hyperlipidemia is suspected, measurement and appropriate referral to internal medicine or cardiology is recommended. In most cases, a tentative diagnosis can be established with a complete sexual and medical history, physical examination, and limited or no laboratory testing.
Some men report being helped by an oral medication called yohimbine, which comes from the bark of a tree that grows in India and Africa. This drug, which needs to be taken every day, has been reported to help about 20 to 25 percent of the men taking it. A relatively new but widely used oral medication called Viagra requires a careful medical evaluation by your doctor.
Patients at high cardiovascular risk should not be treated for ED until their cardiac condition is stabilize. These conditions include unstable or refractory angina, myocardial infarction or cerebrovascular accident within the past 2 weeks, uncontrolled hypertension, New York Heart Association (NYHA) Functional Classification III-IV congestive heart failure, high-risk arrhythmias, hypertrophic obstructive cardiomyopathies, and moderate-to-severe valvular disease.25 This class of drugs is also contraindicated in patients who use nitroglycerin or nitrate-containing compounds.26, 27
In a randomized double-blind, parallel, placebo-controlled trial, sildenafil plus testosterone was not superior to sildenafil plus placebo in improving erectile function in men with ED and low testosterone levels. [19] The objective of the study was to determine whether the addition of testosterone to sildenafil therapy improves erectile response in men with ED and low testosterone levels.
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
THIS TOOL DOES NOT PROVIDE MEDICAL ADVICE. It is intended for general informational purposes only and does not address individual circumstances. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. Never ignore professional medical advice in seeking treatment because of something you have read on the WebMD Site. If you think you may have a medical emergency, immediately call your doctor or dial 911.
A physical exam checks your total health. Examination focusing on your genitals (penis and testicles) is often done to check for ED. Based on your age and risk factors, the exam may also focus on your heart and blood system: heart, peripheral pulses and blood pressure. Based on your age and family history your doctor may do a rectal exam to check the prostate. These tests are not painful. Most patients do not need a lot of testing before starting treatment.
After bombarding consumers with advertising, and massaging physicians with free meals and medical "information," the stage is set to seal the deal. "The fat guy has been seeing the ads on TV," said Fugh-Berman. "The doc has just come from a medical meeting where they were talking about how using testosterone can fight depression, etc., and they are being primed in a different way."
The hypogonadal-obesity-adipocytokine cycle hypothesis. Adipose tissue contains the enzyme aromatase which metabolises testosterone to oestrogen. This results in reduced testosterone levels, which increase the action of lipoprotein lipase and increase fat mass, thus increasing aromatisation of testosterone and completing the cycle. Visceral fat also promotes lower testosterone levels by reducing pituitary LH pulse amplitude via leptin and/or other factors. In vitro studies have shown that leptin also inhibits testosterone production directly at the testes. Visceral adiposity could also provide the link between testosterone and insulin resistance (Jones 2007).

The changes in average serum testosterone levels with aging mean that the proportion of men fulfilling a biochemically defined diagnosis of hypogonadism increases with aging. Twenty percent of men aged over 60 have total testosterone levels below the normal range and the figure rises to 50% in those aged over 80. The figures concerning free testosterone are even higher as would be expected in view of the concurrent decrease in SHBG levels (Harman et al 2001).


The partial synthesis in the 1930s of abundant, potent testosterone esters permitted the characterization of the hormone's effects, so that Kochakian and Murlin (1936) were able to show that testosterone raised nitrogen retention (a mechanism central to anabolism) in the dog, after which Allan Kenyon's group[183] was able to demonstrate both anabolic and androgenic effects of testosterone propionate in eunuchoidal men, boys, and women. The period of the early 1930s to the 1950s has been called "The Golden Age of Steroid Chemistry",[184] and work during this period progressed quickly. Research in this golden age proved that this newly synthesized compound—testosterone—or rather family of compounds (for many derivatives were developed from 1940 to 1960), was a potent multiplier of muscle, strength, and well-being.[185]


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.
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.
Qaseem, A., Snow, V., Denberg, T. D., Casey, D. E., Forciea, M. A., Owens, D. K., & Shekelle, P. (2009). Hormonal testing and pharmacologic treatment of erectile dysfunction: A clinical practice guideline from the American College of Physicians. Annals of internal medicine, 151(9), 639-649. Retrieved from http://annals.org/aim/article/745155/hormonal-testing-pharmacologic-treatment-erectile-dysfunction-clinical-practice-guideline-from
Cavernosography measurement of the vascular pressure in the corpus cavernosum. Saline is infused under pressure into the corpus cavernosum with a butterfly needle, and the flow rate needed to maintain an erection indicates the degree of venous leakage. The leaking veins responsible may be visualized by infusing a mixture of saline and x-ray contrast medium and performing a cavernosogram.[21] In Digital Subtraction Angiography (DSA), the images are acquired digitally.
ICI Alprostadil may be used as a mixture with two other drugs to treat ED. This combination therapy called "bimix or trimix" is stronger than alprostadil alone and has become standard treatment for ED. Only the Alprostadil ingredient is FDA approved for ED. The amount of each drug used can be changed based on the severity of your ED, by an experienced health professional. You will be trained by your health professional on how to inject, how much to inject and how to safely raise the drug's dosage if necessary.
Impotence, also known as erectile dysfunction or ED, is a condition in which a man is unable to get or hold an erection long enough to have a satisfactory sex life. Impotence is a common problem, affecting up to half of Australian men between the ages of 40 and 70 years. The risk of developing erectile dysfunction increases as you get older.In the past, doctors considered impotence to be a mainly psychological problem, caused by performance anxiety or stress. Now, doctors know that many cases of impotence have a physical cause, which usually can be treated. Often, a combination of physical and psychological factors contributes to erectile dysfunction.Physical causes of impotencePhysical causes of impotence can include:problems with blood to flow into and out of the penis;damage to the nerves that send signals from the body’s central nervous system to the penis; and, more rarely,a deficiency in testosterone or other hormones.Some medicines can contribute to impotence, as can some types of surgery and radiotherapy treatments.Blocked blood vessels to the penisA very common cause of impotence is when blood flow into the penis is reduced. This can be due to atherosclerosis, also known as hardening of the arteries. In atherosclerosis, the arteries are clogged and narrowed, resulting in reduced blood flow.Risk factors for atherosclerosis include:high cholesterol;high blood pressure;obesity;sleep apnoea;diabetes; andsmoking.If your erection problems are caused by atherosclerosis, there is a chance that the arteries in other parts of your body (e.g. the coronary arteries that supply your heart) are also affected by atherosclerosis. In fact, erection problems may be the first sign that you are at risk of coronary heart disease.Because the arteries to the penis are narrower than those to the heart, you may develop symptoms of erectile dysfunction before you experience any symptoms of heart disease, such as angina. So seeing your doctor about erection problems may be important for your overall physical health.Impotence can also be caused by a blood clot that prevents enough blood from flowing into the penis to cause an erection.Venous leakageIn some men, blood can flow in to the penis easily, but the problem is that it leaks out again, so an erection cannot be sustained. This is called venous leakage. Doctors aren’t certain of the cause of venous leakage, but they can perform surgery to help repair it.Medicines that can cause impotenceMany medicines can cause erection problems as a side effect, including:diuretics (sometimes known as ‘water tablets’ - often used for high blood pressure);high blood pressure medications;cholesterol-lowering medicines (including statins);some types of antipsychotics;antidepressants;cancer treatments;some medicines used to treat heartburn and stomach ulcers;antihistamines;some pain medicines; andcertain epilepsy medications.If you experience impotence after starting a new medication, tell your doctor, who may be able to prescribe a different medicine for you. Don’t stop taking a medicine without first consulting your doctor. You should also tell your doctor about any over-the-counter medicines or complementary remedies you may be taking.The following table contains a list of specific medicines that may cause or contribute to erectile dysfunction. This list may not cover all types of medicines that can cause erectile dysfunction, so always ask your doctor if you are in doubt. Also, for some of these medicines ED is a very rare side effect. Most men taking these medicines do not experience erectile dysfunction.Medicines that may cause erectile dysfunctionType of medicineExamplesACE inhibitorscaptopril (Capoten), enalapril (Renitec), perindopril (Perindo), ramipril (Tritace), and othersAntidepressantsamitriptyline (Endep), clomipramine (Anafranil), desvenlafaxine (Pristiq), fluoxetine (Prozac), paroxetine (Aropax), sertraline (Zoloft), venlafaxine (Altven, Efexor), and othersAnti-epilepticsclonazepam (Rivotril), pregabalin (Lyrica)Antifungalsitraconazole (Sporanox)Anti-ulcer drugscimetidine (Magicul), nizatidine (Tazac), ranitidine (Zantac), and othersBeta-blockerspropranolol (Inderal), metoprolol (Betaloc, Lopresor), and othersOther blood pressure-lowering medicinesclonidine (Catapres), lercanidipine/enalapril (Zan-Extra), losartan (Cozaar), perindopril/amlodipine (Coveram), olmesartan/amlodipine (Sevikar), telmisartan/amlodipine (Twynsta), valsartan/hydrochlorothiazide (Co-Diovan)Calcium-channel blockersdiltiazem (Cardizem), felodipine (Plendil), nifedipine (Adalat)Cholesterol-lowering drugsatorvastatin (Lipitor), ezetimibe/simvastatin (Vytorin), fluvastatin (Lescol, Vastin), gemfibrozil (Ausgem), pravastatin (Pravachol), simvastatin (APO-simvastatin, Lipex, Zocor), and othersDiuretics ('water tablets')bumetanide (Burinex), chlorthalidone (Hygroton), spironolactone (Aldactone), and othersSchizophrenia drugsamisulpride (Solian, Sulprix), haloperidol (Haldol, Serenace), olanzapine (Lanzek, Ozin, Zypine, Zyprexa), paliperidone (Invega), risperidone (Rispa, Risperdal), ziprasidone (Zeldox)Combination cholesterol-lowering and anti-hypertensiveamlodipine/atorvastatin (Caduet, Cadatin)Pain medicinesfentanyl (Denpax, Durogesic), hydromorphone (Jurnista), morphine (Momex SR, MS Contin), oxycodone (OxyContin, OxyNorm, Targin), tramadolMiscellaneousoestrogens, antiandrogens, anticancer drugs and some chemotherapy treatments, baclofen (Clofen, Lioresal); cyproterone (Androcur, Cyprohexal, Cyprostat), degarelix (Firmagon), etoricoxib (Arcoxia), finasteride (Proscar and Propecia), flutamide (Flutamin), rotigotine (Neupro), triptorelin (Diphereline)*The names in brackets are just some examples of the trade names each specific medicine is marketed under in Australia. The medicine may also be known by other trade names.Diabetes and erectile dysfunctionMen who have diabetes have a higher risk of developing impotence than other men. Diabetes contributes to impotence because it can damage blood vessels and cause a type of nerve damage known as peripheral neuropathy.Hormones and impotenceLow levels of the male hormone, testosterone, are more commonly linked to a lowered sex drive, rather than impotence itself. Only a small percentage of cases of impotence are caused by hormone deficiency.Low testosterone levels may be the result of a condition called hypogonadism, in which the testicles don’t produce enough testosterone. More rarely, low testosterone can be caused by the pituitary (a small gland at the base of the brain) not secreting sufficient hormones to stimulate the testes to produce testosterone. The pituitary is also sometimes affected by small benign (non-cancerous) tumours that secrete prolactin, another hormone that can cause impotence.Mildly decreased levels of testosterone are often not due to specific testicular or pituitary problems, but rather stress or depression. In this situation, testosterone replacement is rarely of any benefit.Other hormone problems, including thyroid disease, can also cause impotence.Prostate cancer and erectile dysfunctionThe advanced stages of prostate cancer can affect the nerves and arteries that are vital for an erection.Radiation treatment for prostate cancer can harm the erectile tissues of the penis, and prostate cancer surgery can cause nerve or artery damage to the penis.Treatment for advanced prostate cancer often includes medicines that counteract testosterone, and commonly cause erectile dysfunction as well as loss of sexual interest.Peyronie’s diseasePeyronie’s disease is an uncommon condition that affects a man’s sex life because his penis curves abnormally and causes pain when he has an erection. He might also be unable to have a hard erection. The curvature of the penis is caused by a scar, called a plaque, that forms in the penis.Other physical causes of impotenceSeveral other factors and conditions can contribute to erectile dysfunction, including the following.Depression. Many men find that when they’re suffering from depression, they lose interest in sex and can’t get or keep an erection. Asking your doctor for treatments for depression may help alleviate your erection problems as well.Smoking contributes to vascular disease (disease of the blood vessels), so it can contribute to erectile dysfunction by affecting blood flow to the penis. Giving up smoking often has a beneficial effect on erectile function.Excessive alcohol use. Alcoholism can cause permanent nerve damage, resulting in impotence. This nerve damage is called peripheral neuropathy. Long-term alcohol use can impair the liver’s ability to function, resulting in a hormone imbalance in which a man has too much of the female sex hormone, oestrogen. On a day-to-day level, alcohol dulls the central nervous system, adversely affecting sexual response.Illicit drug use. Illicit drugs such as marijuana, cocaine, heroin, barbiturates, and amphetamines act on the central nervous system, impairing the body’s ability to respond sexually.Certain exercises. Nerve and artery damage can be caused by prolonged cycling, rodeo riding, or use of a rowing machine, resulting in the inability to get an erection. Often, minimising the use of hard bicycle seats and exercise machine seats, as well as correct positioning of the seat, will help restore sexual function.Surgery to organs near the nerve pathways of the penis, such as the bladder, rectum and prostate, can cause nerve or artery damage to the penis, resulting in the inability to have an erection.Injuries. Impotence can be caused by spinal cord injury; injury to your sex organs; or a pelvic fracture, which can cause damage to the nerves of the penis, or damage the blood vessels, resulting in reduced blood flow to the penis.Conditions affecting the nervous system. Multiple sclerosis (MS) and other degenerative diseases of the nervous system, such as Parkinson’s disease, can damage the nerves involved in erections.Psychological causes of impotenceMost cases of impotence have physical causes, but, in some men, psychological factors are the main contributors to impotence.Impotence that’s triggered by psychological factors is more common in men who are sexually inexperienced. Psychological erectile dysfunction may only occur when you’re with just one particular person. You’re also more likely to have morning erections, and be able to have an erection when you masturbate, than men whose impotence has a physical cause.Here are some psychological factors that can have an impact on your erections.Stress and anxietyWhen you’re stressed and focusing on other issues apart from sex, you might find that you don’t want to have sex as often and there might be a drop in your ability to perform when you do try. You might find that tackling the source of your stress can have benefits in the bedroom as well.Fear of failureAnxiety about your sexual prowess (commonly called performance anxiety) can, in itself, contribute to failure. By putting pressure on yourself, you become too anxious to get an adequate erection.Most men experience isolated episodes of erectile failure. Even when the transient physical cause has passed, anxiety that it may recur is sufficient to prevent erection. Anxiety, whether about something specifically sexual or part of a wider anxiety syndrome, is never helpful to good sexual function.Problems with your relationship and impotenceImpotence may be a manifestation of a poor relationship, or a problematic time in a relationship. Sexual boredom, tension or anger among partners, and lack of intimacy and communication are all possible triggers of erectile dysfunction. In these cases, seeing a counsellor may help.It’s worth remembering that impotence is a complex medical condition, which may have more than one cause. For example, if impotence is the result of a side effect of medicine or an underlying disease, the anxiety caused by lack of performance may perpetuate the erectile dysfunction even after the physical cause has been dealt with.Almost any chronic (ongoing) physical or mental health disorder, including those with no direct effect on penile nerves or blood supply, can have a powerful effect on sexuality, sexual self-image and erectile function.If you’re worried about your sexual response or the quality of your erections, don’t be afraid to talk to your doctor, who has access to treatments that can help. Last Reviewed: 16 December 2016
The reliable measurement of serum free testosterone requires equilibrium dialysis. This is not appropriate for clinical use as it is very time consuming and therefore expensive. The amount of bioavailable testosterone can be measured as a percentage of the total testosterone after precipitation of the SHBG bound fraction using ammonium sulphate. The bioavailable testosterone is then calculated from the total testosterone level. This method has an excellent correlation with free testosterone (Tremblay and Dube 1974) but is not widely available for clinical use. In most clinical situations the available tests are total testosterone and SHBG which are both easily and reliably measured. Total testosterone is appropriate for the diagnosis of overt male hypogonadism where testosterone levels are very low and also in excluding hypogonadism in patients with normal/high-normal testosterone levels. With increasing age, a greater number of men have total testosterone levels just below the normal range or in the low-normal range. In these patients total testosterone can be an unreliable indicator of hypogonadal status. There are a number of formulae that calculate an estimated bioavailable or free testosterone level using the SHBG and total testosterone levels. Some of these have been shown to correlate well with laboratory measures and there is evidence that they more reliably indicate hypogonadism than total testosterone in cases of borderline biochemical hypogonadism (Vermeulen et al 1971; Morris et al 2004). It is important that such tests are validated for use in patient populations relevant to the patient under consideration.

The participants were seen every 4 weeks. Blood was taken to measure hormone levels, and questionnaires were given to assess physical function, health status, vitality, and sexual function. Body fat and muscle measurements were also taken at the beginning and end of the 16 weeks. The study was funded in part by NIH’s National Institute on Aging (NIA) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results appeared in the September 12, 2013, issue of the New England Journal of Medicine.
Having learned a great deal more about erectile dysfunction including its risk factors and causes, you should be equipped to assess your own erectile function. If you have experienced erectile issues or you have some of the risk factors mentioned above, it may be worth making a trip to your doctor’s office. If you choose to seek help, give your doctor as much information as you can about your symptoms including their frequency and severity as well as the onset. With your doctor’s help, you can determine the best course of treatment to restore sexual function.
Dr. Ronald Swerdloff, chief of the endocrinology division at the Harbor-UCLA Medical Center and a professor of medicine at UCLA's David Geffen School of Medicine, served on the panel of experts who developed the Endocrine Society's guidelines. He is also the principal investigator for one of the 12 sites of The Testosterone Trial in Older Men, a nationwide study funded mainly by the National Institute on Aging. The study of 800 men over age 65 with low testosterone is looking at whether men using AndroGel for one year, compared to placebo, will show improvements in walking speed, sexual activity, vitality, memory, and anemia. The study will be completed in June 2015.
Sugar is to testosterone what kryptonite is to Superman. Eliminating sugar is probably the single most powerful way to increase your performance, in part because sugar absolutely devastates your testosterone levels (but all carbs do not, especially under heavy training.) In one study of 74 men, a 75g dose of sugar – about the equivalent of a bottle of soda – decreased serum testosterone by 25% in under an hour, and levels stayed low for at least 2 hours [7]. On top of that, 15% of the men who started with normal testosterone dipped into the hypogonadal range after they ate sugar – that’s the range in which doctors diagnose men’s testes and women’s ovaries as failing. When you do eat carbs, stick to Bulletproof ones like sweet potatoes and squash. My recommendations for types of carbs and how often to eat them are here. 

Mood disturbance and dysthymia are part of the clinical syndrome of hypogonadism. Epidemiological studies have found a positive association between testosterone levels and mood, and depressed aging males have lower testosterone levels than controls (Barrett-Connor, Von Muhlen et al 1999). Furthermore, induction of a hypogonadal state during treatment of men for prostate cancer leads to an increase in depression scores (Almeida et al 2004). Trials of testosterone treatment effects on mood have varied in outcome. Data on the effects on men with depression are conflicting (Seidman et al 2001; Pope et al 2003) but there is evidence that testosterone treatment of older hypogonadal men does result in improvements in mood (Wang et al 1996) and that this may occur through changes in regional brain perfusion (Azad et al 2003).
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.
A vacuum erection device helps draw blood into the penis by applying negative pressure. This type of device is sometimes referred to as penis pump and may be used just prior to sexual intercourse. Several types of FDA approved vacuum therapy devices are available under prescription. When pharmacological methods fail, a purpose-designed external vacuum pump can be used to attain erection, with a separate compression ring fitted to the base of the penis to maintain it. These pumps should be distinguished from other penis pumps (supplied without compression rings) which, rather than being used for temporary treatment of impotence, are claimed to increase penis length if used frequently, or vibrate as an aid to masturbation. More drastically, inflatable or rigid penile implants may be fitted surgically.
Causes of impotence are many and include heart disease, high cholesterol, high blood pressure, obesity, metabolic syndrome, Parkinson's disease, Peyronie's disease, substance abuse, sleep disorders, BPH treatments, relationship problems, blood vessel diseases (such as peripheral vascular disease and others), systemic disease, hormonal imbalance, and medications (such as blood pressure and heart medications).
show that total testosterone levels increase after exercising, especially after resistance training. Low testosterone levels can affect your sex drive and your mood. The good news is that exercise improves mood and stimulates brain chemicals to help you feel happier and more confident. Exercise also boosts energy and endurance, and helps you to sleep better. Fitness experts recommend 30 minutes of exercise every day.
There are relatively few contraindications to the use of vacuum devices. Some conditions can predispose to priapism or perhaps bleeding with constriction, such as sickle cell disease, polycythemia, and other blood dyscrasias. Patients taking anticoagulants can safely use vacuum constriction devices but need to accept a higher risk of bleeding (ecchymosis). Good manual dexterity is also needed to use the device; if manual dexterity is impaired, a willing sexual partner can learn to apply the device.
The normal development of the prostate gland is dependent on the action of testosterone via the androgen receptor, and abnormal biosynthesis of the hormone or inactivating mutations of the androgen receptor are associated with a rudimentary prostate gland. Testosterone also requires conversion to dihydrotestosterone in the prostate gland for full activity. In view of this link between testosterone and prostate development, it is important to consider the impact that testosterone replacement may have on the prevalence and morbidity associated with benign prostatic hypertrophy (BPH) and prostate cancer, which are the common conditions related to pathological growth of the prostate gland.
^ David KG, Dingemanse E, Freud JL (May 1935). "Über krystallinisches mannliches Hormon aus Hoden (Testosteron) wirksamer als aus harn oder aus Cholesterin bereitetes Androsteron" [On crystalline male hormone from testicles (testosterone) effective as from urine or from cholesterol]. Hoppe-Seyler's Z Physiol Chem (in German). 233 (5–6): 281–83. doi:10.1515/bchm2.1935.233.5-6.281.
Testosterone was first used as a clinical drug as early as 1937, but with little understanding of its mechanisms. The hormone is now widely prescribed to men whose bodies naturally produce low levels. But the levels at which testosterone deficiency become medically relevant still aren’t well understood. Normal testosterone production varies widely in men, so it’s difficult to know what levels have medical significance. The hormone’s mechanisms of action are also unclear.
Clinical trials of the effect of testosterone on glucose metabolism in men have occurred in diabetic and non-diabetic populations. Data specific to aging males is not available. A series of studies investigated the effects of testosterone or dihydrotestosterone given for 6 weeks or 3 months to middle aged, non-diabetic obese men (Marin, Holmang et al 1992; Marin, Krotkiewski et al 1992; Marin et al 1993). It was found that physiological treatment doses led to improved insulin resistance, as measured by the gold standard technique using a euglycemic clamp and/or serum glucose and insulin responses during glucose tolerance test. These improvements were associated with decreased central obesity, measured by computered tomography (CT) or waist-hip ratio, without reduced total fat mass. Insulin resistance improved more with testosterone than dihydrotestosterone treatment and beneficial effects were greater in men with lower baseline testosterone levels. Increasing testosterone levels into the supraphysiological range lead to decreased glucose tolerance.
Findings that improvements in serum glucose, serum insulin, insulin resistance or glycemic control, in men treated with testosterone are accompanied by reduced measures of central obesity, are in line with other studies showing a specific effect of testosterone in reducing central or visceral obesity (Rebuffe-Scrive et al 1991; Marin, Holmang et al 1992). Furthermore, studies that have shown neutral effects of testosterone on glucose metabolism have not measured (Corrales et al 2004), or shown neutral effects (Lee et al 2005) (Tripathy et al 1998; Bhasin et al 2005) on central obesity. Given the known association of visceral obesity with insulin resistance, it is possible that testosterone treatment of hypogonadal men acts to improve insulin resistance and diabetes through an effect in reducing central obesity. This effect can be explained by the action of testosterone in inhibiting lipoprotein lipase and thereby reducing triglyceride uptake into adipocytes (Sorva et al 1988), an action which seems to occur preferentially in visceral fat (Marin et al 1995; Marin et al 1996). Visceral fat is thought to be more responsive to hormonal changes due to a greater concentration of androgen receptors and increased vascularity compared with subcutaneous fat (Bjorntorp 1996). Further explanation of the links between hypogonadism and obesity is offered by the hypogonadal-obesity-adipocytokine cycle hypothesis (see Figure 1). In this model, increases in body fat lead to increases in aromatase levels, in addition to insulin resistance, adverse lipid profiles and increased leptin levels. Increased action of aromatase in metabolizing testosterone to estrogen, reduces testosterone levels which induces further accumulation of visceral fat. Higher leptin levels and possibly other factors, act at the pituitary to suppress gonadotrophin release and exacerbate hypogonadism (Cohen 1999; Kapoor et al 2005). Leptin has also been shown to reduce testosterone secretion from rodent testes in vitro (Tena-Sempere et al 1999). A full review of the relationship between testosterone, insulin resistance and diabetes can be found elsewhere (Kapoor et al 2005; Jones 2007).
In the last few years, a lot of men and women have switched over to a pellet that goes under your skin. This is probably the best way to take testosterone now. The pellet is life-changing for both men and women (the dose for women is much lower than it is for men). Women, you won’t get bulky and grow a beard when you take testosterone to achieve normal levels, but you will probably lean out a little without losing your curves, and your energy and sex drive will be amazing. Female bodybuilders who experience weird scary side effects are taking anabolic steroids.
"One of the reasons erectile dysfunction increases with age is that the diseases that lead to it also increase with age," notes Dr. Feloney. Evaluating the causes of erectile dysfunction starts with your doctor taking a good health history and giving you a physical exam. Common medical issues that can lead to erectile dysfunction include diabetes, high blood pressure, hardening of the arteries, low testosterone, and neurological disease. Talk to your doctor about better managing these health conditions.
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