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.
Some anti-aging physicians also use sublingual ( taken under the tongue) forms of non-bioidentical testosterone like oxandrolone. I took oxandrolone with a physician’s guidance for about two weeks, and I got pimples and hair loss. I quit and was bummed that it didn’t generate enough impact to write a blog post about it. I have continued to recommend bioidentical testosterone since.
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. 

I’m telling you all of this because no matter who you are, keeping your testosterone levels balanced is more important now than ever before. Modern living has not been kind to our hormones. In American men, serum testosterone levels have declined by about 1% each year for the past 30 years [5], and you can make a few educated guesses about why. Hormone-disrupting chemicals are more prevalent than ever before, physical activity is less and less common, veganism is popular (I was a raw vegan for a while), and many doctors insist on pushing a low-fat, low-cholesterol diet for health (by the way, the concept of a low-fat diet began in the mid-70s, shortly before the nationwide testosterone decline. It could be a coincidence, but I doubt it).
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.
Look, ED can have many causes. Most of the time, it’s physiological. But there are also lots of psychological reasons why someone may experience ED. Treating ED isn’t all about medication. Dealing with some of these psychological issues can help you battle ED, too. I’m talking about depression, anxiety, loss of desire, sense of inadequacy, guilt, fatigue, anger, relationship dysfunction. Working through these types of psychological challenges can help you achieve the happy, healthy manhood you deserve.
"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.
"A lot of the symptoms are mirrored by other medical problems," Hedges says. "And for a long time, we were not attributing them to low testosterone, but to diabetes, depression, high blood pressure, and coronary artery disease. But awareness and appreciation of low testosterone has risen. We recognize now that low testosterone may be at the root of problems."
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).
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.
Unfortunately, some patients may have an overly simplified understanding of the role of PDE5 inhibitors in ED management. Such patients may not expect or be willing to undergo a long evaluation and testing process to obtain a better understanding of their sexual problem, and they may be less likely to involve their partner in discussing their sexual relationship with the physician. They may expect to obtain medications through a phone call to their doctor or even over the Internet, with minimal or no physician contact at all.
This is similar to magnetic resonance imaging. Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. Doctors may inject a "contrast agent" into the person's bloodstream that causes vascular tissues to stand out against other tissues. The contrast agent provides for enhanced information regarding blood supply and vascular anomalies.
Alcohol is a depressant, not an aphrodisiac or a libido enhancer. Excessive consumption can interfere with the ability to achieve an erection at any age, and even occasional drinking can make erectile dysfunction worse in older men. Feloney advises using alcohol in moderation: "In small amounts, alcohol can relieve anxiety and may help with erectile dysfunction, but if you drink too much, it can cause erectile dysfunction or make the problem worse."
Unlike women, who experience a rapid drop in hormone levels at menopause, men experience a more gradual decrease of testosterone levels over time. The older the man, the more likely he is to experience below-normal testosterone levels. Men with testosterone levels below 300 ng/dL may experience some degree of low T symptoms. Your doctor can conduct a blood test and recommend treatment if needed. They can discuss the potential benefits and risks of testosterone medication, as well.
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. 

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.
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." 

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.
^ Jump up to: a b Lazaridis I, Charalampopoulos I, Alexaki VI, Avlonitis N, Pediaditakis I, Efstathopoulos P, Calogeropoulou T, Castanas E, Gravanis A (2011). "Neurosteroid dehydroepiandrosterone interacts with nerve growth factor (NGF) receptors, preventing neuronal apoptosis". PLoS Biol. 9 (4): e1001051. doi:10.1371/journal.pbio.1001051. PMC 3082517. PMID 21541365.

A vacuum erection device is a plastic tube that slips over the penis, making a seal with the skin of the body. A pump at the other end of the tube makes a low-pressure vacuum around the erectile tissue, which results in an erection. An elastic ring is then slipped onto the base of the penis. This holds the blood in the penis (and keeps it hard) for up to 30 minutes. With proper training, 75 out of 100 men can get a working erection using a vacuum erection device.
But if a man with sleep apnea is diagnosed with low testosterone alone, taking the supplemental hormone can worsen sleep apnea. That's why it's crucial for men with low testosterone to get a thorough workup by an endocrinologist so underlying conditions that can cause low testosterone, such as sleep apnea or pituitary-gland tumors, don't go undiagnosed, Dr. Goodman says. 

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.
Erections occur in response to tactile, olfactory, and visual stimuli. The ability to achieve and maintain a full erection depends not only on the penile portion of the process but also on the status of the peripheral nerves, the integrity of the vascular supply, and biochemical events within the corpora. The autonomic nervous system is involved in erection, orgasm, and tumescence. The parasympathetic nervous system is primarily involved in sustaining and maintaining an erection, which is derived from S2-S4 nerve roots.
This penile tumescence monitor is placed at the base and near the corona of the penis. It is connected to a monitor that records a continuous graph depicting the force and duration of erections that occur during sleep. The monitor is strapped to the leg. The nocturnal penile tumescence test is conducted on several nights to obtain an accurate indication of erections that normally occur during the alpha phase of sleep.
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.

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.
Knowing about your history of ED will help your health provider learn if your problems are because of your desire for sex, erection function, ejaculation, or orgasm (climax). Some of these questions may seem private or even embarrassing. However, be assured that your doctor is a professional and your honest answers will help find the cause and best treatment for you.
Testosterone does a lot more than you’d think, whether we’re talking about male or female biology. It’s the hormone that helps you burn fat, build muscle [1], and increase your sex drive [2], and its power doesn’t stop there. Keeping your testosterone levels in a normal range can make you happier, too [3], and testosterone can even improve your cardiovascular health and decrease your risk of mortality (from all causes!), according to a study of 83,000 older men who underwent testosterone replacement therapy [4].
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.

"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.


In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats.[40] This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.
Medications for erectile dysfunction don't work for everyone and may cause side effects that make a particular drug hard to take. "Work with your doctor to find the right treatment. There are still options for people who fail at medical treatment," advises Feloney. Alternatives to erectile dysfunction drugs include vacuum pump devices, medications injected into the penis, testosterone replacement if needed, and a surgical penile implant.
Alprostadil is injected into the side of penis with a very fine needle. It's of great value to have the first shot in the doctor's office before doing this on your own. Self-injection lessons should be given in your doctor's office by an experienced professional. The success rate for getting an erection firm enough to have sex is as high as 85% with this treatment. Many men who do not respond to oral PDE5 inhibitors can be ‘rescued' with ICI.
This post can absolutely change your life, and probably help you avoid some pitfalls. Like shrunken balls. (I am not an expert in the synthetic anabolic testosterone drugs used by bodybuilders — they carry lots of risks but pack a big punch if you want to get swole. Bulletproof is all about having massive clean energy, looking good, and living a very long time…so anabolic steroids aren’t on my roadmap.)
Sleep apnea is another frequently listed contraindication to testosterone treatment. There have been a few reports of the development, or worsening, of sleep apnea during testosterone therapy (Matsumoto et al 1985) but sleep apnea is actually associated with lower serum testosterone levels (Luboshitzky et al 2002). The reduction in fat mass during treatment with testosterone could potentially be beneficial for sleep apnea, so many specialists will still consider patients for treatment with appropriate monitoring. It is wise to take a clinical history for sleep apnea during testosterone treatment in all men and perform sleep studies in those who develop symptoms.
In males, testosterone is synthesized primarily in Leydig cells. The number of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In addition, the amount of testosterone produced by existing Leydig cells is under the control of LH, which regulates the expression of 17β-hydroxysteroid dehydrogenase.[124]
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).
Studies also show a consistent negative correlation of testosterone with blood pressure (Barrett-Connor and Khaw 1988; Khaw and Barrett-Connor 1988; Svartberg, von Muhlen, Schirmer et al 2004). Data specific to the ageing male population suggests that this relationship is particularly powerful for systolic hypertension (Fogari et al 2005). Interventional trials have not found a significant effect of testosterone replacement on blood pressure (Kapoor et al 2006).
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).
This evidence, together with the beneficial effects of testosterone replacement on central obesity and diabetes, raises the question whether testosterone treatment could be beneficial in preventing or treating atherosclerosis. No trial of sufficient size or duration has investigated the effect of testosterone replacement in primary or secondary prevention cardiovascular disease. The absence of such data leads us to examine the relationship of testosterone to other cardiovascular risk factors, such as adverse lipid parameters, blood pressure, endothelial dysfunction, coagulation factors, inflammatory markers and cytokines. This analysis can supply evidence of the likely effects of testosterone on overall cardiovascular risk. This has limitations, however, including the potential for diverging effects of testosterone on the various factors involved and the resultant impossibility of accurately predicting the relative impact of such changes.
Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen positions respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites.[5] It exerts its action through binding to and activation of the androgen receptor.[5] In humans and most other vertebrates, testosterone is secreted primarily by the testicles of males and, to a lesser extent, the ovaries of females. On average, in adult males, levels of testosterone are about 7 to 8 times as great as in adult females.[6] As the metabolism of testosterone in males is greater, the daily production is about 20 times greater in men.[7][8] Females are also more sensitive to the hormone.[9]
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.
Following a detailed discussion about the history of erectile dysfunction and its risk factors, your doctor will examine the testicles and penis to help determine the cause of erectile dysfunction. Your doctor will check reflexes and pulses in the area to see if problems with blood vessels or nerves are contributing to the erectile dysfunction. If necessary, your doctor will order tests to help diagnose erectile dysfunction.
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).

Alprostadil (also known as prostaglandin E1 [PGE1]) is the prominent known smooth-muscle dilator of the corpus cavernosum. Its mechanism of action is believed to be the promotion of intracellular accumulation of cyclic adenosine monophosphate, thereby causing decreased intracellular accumulation of calcium and resulting smooth muscle relaxation. Alprostadil can be delivered to the erectile tissue either via an intraurethral suppository that is massaged and then absorbed across the corpus spongiosum of the urethra to the corpora cavernosa, or directly injected into the corpora cavernosa. When administered urethrally, doses are substantially higher than when directly injected (typical dosing is 500 mcg to 1 mg intraurethral compared with 2.5 mcg to 20 mcg intracavernosal).
Hormone deficiency or hypogonadism, whether primary or secondary, has been thought to impact erectile function. Approximately a third of men in the European Male Aging Study demonstrated low testosterone, suggesting that hypogonadism is overrepresented among men with ED.11 Hormone deficiency, however, is less frequently the cause of ED than diabetes or vascular disease. Many entities with a strong relationship to ED also diminish bioavailable testosterone, including obesity, diabetes, and opioid use. Other hormones involved in testosterone metabolism or availability, like thyroid stimulating hormone and gonadotropins, also may impact erectile quality, presumably through regulating bioavailable testosterone. Understanding the relationship between testosterone and ED has been impaired by a lack of standardized measurement of this hormone and the cyclic nature of its release and consumption.

Oral/buccal (by mouth). The buccal dose comes in a patch that you place above your incisor (canine or "eyetooth"). The medication looks like a tablet but you should not chew or swallow it. The drug is released over 12 hours. This method has fewer harmful side effects on the liver than if the drug is swallowed, but it may cause headaches or cause irritation where you place it.

Commercials do mention other potential side-effects for the male user, calling them "rare," including swollen and painful breasts, blood clots in the legs, increased risk for prostate cancer, problems breathing during sleep (sleep apnea), change in the size and shape of the testicles, and a low sperm count. But you're not supposed to focus on the details. Instead, just think of the energy you'll have. The great sex you'll have. And the muscles. It will be a veritable second adolescence as your aging body bursts into new bloom.


It is essential to discuss erectile dysfunction with your doctor, so any serious underlying causes can be excluded and treatment options can be discussed. Many men are embarrassed discussing this issue with their doctor, or even their partner. Open communication with your doctor, and in your relationship, is important for effectively managing this common problem.
An analysis of 14 studies involving more than 90,000 patients with ED confirmed the relation between ED and an increased risk of cardiovascular events and mortality. [56] Compared with patients without ED, those with ED had a 44% increased risk of cardiovascular events, a 25% increased risk of all-cause mortality, a 62% increased risk of MI, and a 39% increased risk of cerebrovascular events. Treatment of ED, either through lifestyle interventions or by pharmacologic means, may improve prognosis and reduce risk.
“Although having sex at 70 is not the same as having sex at 20, erectile dysfunction is not a normal part of aging,” according to Michael Feloney, MD, urologic surgeon and expert on sexual dysfunction issues at the Nebraska Medical Center in Omaha. “You should still be able to have a satisfying sex life as you age." If you are experiencing erectile dysfunction, these 10 dos and don'ts may help.
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.
Performance anxiety can be another cause of impotence. If a person wasn’t able to achieve an erection in the past, he may fear he won’t be able to achieve an erection in the future. A person may also find he can’t achieve an erection with a certain partner. Someone with ED related to performance anxiety may be able to have full erections when masturbating or when sleeping, yet he isn’t able to maintain an erection during intercourse.
Erectile dysfunction - (ED) or impotence is sexual dysfunction characterized by the inability to develop or maintain an erection of the penis during sexual activity. A penile erection is the hydraulic effect of blood entering and being retained in sponge-like bodies within the penis. The process is most often initiated as a result of sexual arousal, when signals are transmitted from the brain to nerves in the penis.
According to a review of all randomized controlled trials evaluating sildenafil by the American Urological Association (AUA) Consensus Panel on Erectile Dysfunction, 36% to 76% of patients receiving the drug were "able to achieve intercourse" during treatment. For tadalafil, four randomized controlled trials revealed that 11% to 47% of patients were "able to achieve intercourse." Similar efficacy has been observed with vardenafil, although studies are fewer.19 A meta-analysis published in 2013 clearly demonstrated increased efficacy over placebo for all PDE5 inhibitors.24 Head-to-head comparison suggested that tadalafil outperforms sildenafil on validated measures of erectile dysfunction, including the international index of erectile function and sexual encounter profile-2 and -3.
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]
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.
Oral/buccal (by mouth). The buccal dose comes in a patch that you place above your incisor (canine or "eyetooth"). The medication looks like a tablet but you should not chew or swallow it. The drug is released over 12 hours. This method has fewer harmful side effects on the liver than if the drug is swallowed, but it may cause headaches or cause irritation where you place it.
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