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.
An international consensus document was recently published and provides guidance on the diagnosis, treatment and monitoring of late-onset hypogonadism (LOH) in men. The diagnosis of LOH requires biochemical and clinical components. Controversy in defining the clinical syndrome continues due to the high prevalence of hypogonadal symptoms in the aging male population and the non-specific nature of these symptoms. Further controversy surrounds setting a lower limit of normal testosterone, the limitations of the commonly available total testosterone result in assessing some patients and the unavailability of reliable measures of bioavailable or free testosterone for general clinical use. As with any clinical intervention testosterone treatment should be judged on a balance of risk versus benefit. The traditional benefits of testosterone on sexual function, mood, strength and quality of life remain the primary goals of treatment but possible beneficial effects on other parameters such as bone density, obesity, insulin resistance and angina are emerging and will be reviewed. Potential concerns regarding the effects of testosterone on prostate disease, aggression and polycythaemia will also be addressed. The options available for treatment have increased in recent years with the availability of a number of testosterone preparations which can reliably produce physiological serum concentrations.
One study examined the role of testosterone supplementation in hypogonadal men with ED. These men were considered nonresponders to sildenafil, and their erections were monitored by assessing nocturnal penile tumescence (NPT). After these men were given testosterone transdermally for 6 months, the number of NPTs increased, as did the maximum rigidity with sildenafil. [18] This study suggests that a certain level of testosterone may be necessary for PDE5 inhibitors to function properly.
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Erectile dysfunction, also known as ED or impotence, is the inability to attain or maintain an erection of the penis adequate for the sexual satisfaction of both partners. It can be devastating to the self-esteem of a man and of his partner. As many as 30 million American men are afflicted on a continuing basis, and transient episodes affect nearly all adult males. But nearly all men who seek treatment find some measure of relief.


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.

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]
Effective treatment for erectile dysfunction is available, and for most men will allow the return to a fulfilling sex life. The side effects of the treatment for erectile dysfunction vary depending on the treatment that is used. Some may interrupt the spontaneity of sexual activity. For example, PDE-5 inhibitors typically need to be taken one hour before sex. Side effects may include headaches, indigestion, vasodilation, diarrhoea and blue tinge to vision. Other treatments such as penile injections may cause pain at the injection site, or an erection that will not go down. Treatment options need to be carefully discussed with your doctor to determine which one is best suited to you.
"Stress and anxiety can adversely affect sexual performance and are common causes of erectile dysfunction,” warns Feloney. “Feelings of stress and anxiety can also lead to depression and a loss of interest in sex." It's important to get these feelings out in the open where you can deal with them. Issues that can lead to erectile dysfunction include fear from previous bad experiences with sex, family or work related stress, poor communication with your partner, and unrealistic goals and expectations.
However, in contrast, a recent systematic review of published studies, the authors concluded that overall, the addition of testosterone to PDE-5 inhibitors might benefit patients with ED associated with testosterone levels of less than 300 ng/dL (10.4 nmol/L) who failed monotherapy. [20] A limitation of existing studies are their heterogeneous nature and methodological drawbacks.
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Interestingly, the Belgian company Solvay, acquired for €4.5 billion in 2010 by American pharmaceutical giant Abbott, didn't put its own or its product's name on the website. As AdWeek pointed out when the campaign launched, "One of the advantages of taking the unbranded route for Androgel is that the company does not have to warn consumers quite so prominently about Androgel's side effects."

If you have low testosterone, your functional medicine or anti-aging physician will help you diagnose it. There are several different hormones your physician should measure, but the most important two are your free testosterone and estrogen levels, because converting too much testosterone to estrogen is a problem that’s different from not making enough testosterone in the first place. In my case, I wasn’t making very much testosterone, and what I was making my body converted to estrogen way too effectively.


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]
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.
Overall, few patients have a compelling contraindication to testosterone treatment. The majority of men with late onset hypogonadism can be safely treated with testosterone but all will require monitoring of prostate parameters HDL cholesterol, hematocrit and psychological state. It is also wise to monitor symptoms of sleep apnea. Other specific concerns may be raised by the mode of delivery such as local side effects from transdermal testosterone.
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.)
The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.
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.

But when a premenopausal woman’s testosterone levels are too high, it can lead to polycystic ovary syndrome (PCOS), a condition that increases the risk of irregular or absent menstrual cycles, infertility, excess hair growth, skin problems, and miscarriage. High levels of testosterone in women, whether caused by PCOS or by another condition, can cause serious health conditions such as insulin resistance, diabetes, high cholesterol, high blood pressure, and heart disease. (12)
Testosterone is most commonly associated with sex drive in men. It also affects mental health, bone and muscle mass, fat storage, and red blood cell production. Abnormally low or high levels can affect a man’s mental and physical health. Your doctor can check your testosterone levels with a simple blood test. Testosterone therapy is available to treat men with low levels of testosterone. If you have low T, ask your doctor if this type of therapy might benefit you.
Relationship problems often complicate erectile dysfunction. Improving your relationship may be part of the solution. It may be a good idea to get counseling together from a sex therapist, marriage counselor, or a medical specialist. "I almost always see couples together to discuss erectile dysfunction. It often turns out that both partners have issues regarding the sexual relationship and once they are out in the open, couples can work together on a more satisfying sexual experience," says Feloney.

Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).

The sexual hormone can encourage fair behavior. For the study, subjects took part in a behavioral experiment where the distribution of a real amount of money was decided. The rules allowed both fair and unfair offers. The negotiating partner could subsequently accept or decline the offer. The fairer the offer, the less probable a refusal by the negotiating partner. If no agreement was reached, neither party earned anything. Test subjects with an artificially enhanced testosterone level generally made better, fairer offers than those who received placebos, thus reducing the risk of a rejection of their offer to a minimum. Two later studies have empirically confirmed these results.[71][72][73] However men with high testosterone were significantly 27% less generous in an ultimatum game.[74] The Annual NY Academy of Sciences has also found anabolic steroid use which increase testosterone to be higher in teenagers, and this was associated with increased violence.[75] Studies have also found administered testosterone to increase verbal aggression and anger in some participants.[76]
The effects of testosterone in humans and other vertebrates occur by way of multiple mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.[105][106] Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors.[107][108][109]
Lifestyle choices that impair blood circulation can contribute to ED. Smoking, excessive drinking, and drug abuse may damage the blood vessels and reduce blood flow to the penis. Smoking makes men with atherosclerosis particularly vulnerable to ED. Being overweight and getting too little exercise also contribute to ED.  Studies indicate that men who exercise regularly have a lower risk of ED.
Sexual stimulation causes the release of neurotransmitters from cavernosal nerve endings and relaxation factors from endothelial cells lining the sinusoids. NOS produces NO from L-arginine, and this, in turn, produces other muscle-relaxing chemicals, such as cGMP and cyclic adenosine monophosphate (cAMP), which work via calcium channel and protein kinase mechanisms (see the image below). This results in the relaxation of smooth muscle in the arteries and arterioles that supply the erectile tissue, producing a dramatic increase in penile blood flow.
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.
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
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.

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Studies of the effects on cognition of testosterone treatment in non-cognitively impaired eugonadal and hypogonadal ageing males have shown varying results, with some showing beneficial effects on spatial cognition (Janowsky et al 1994; Cherrier et al 2001), verbal memory (Cherrier et al 2001) and working memory (Janowsky et al 2000), and others showing no effects (Sih et al 1997; Kenny et al 2002). Other trials have examined the effects of testosterone treatment in older men with Alzheimer’s disease or cognitive decline. Results have been promising, with two studies showing beneficial effects of testosterone treatment on spatial and verbal memory (Cherrier et al 2005b) and cognitive assessments including visual-spatial memory (Tan and Pu 2003), and a recent randomized controlled trial comparing placebo versus testosterone versus testosterone and an aromatase inhibitor suggesting that testosterone treatment improves spatial memory directly and verbal memory after conversion to estrogen (Cherrier et al 2005a). Not all studies have shown positive results (Kenny et al 2004; Lu et al 2005), and variations could be due to the different measures of cognitive abilities that were used and the cognitive state of men at baseline. The data from clinical trials offers evidence that testosterone may be beneficial for certain elements of cognitive function in the aging male with or without cognitive decline. Larger studies are needed to confirm and clarify these effects.

Diabetes is an example of an endocrine disease that can cause a person to experience impotence. Diabetes affects the body’s ability to utilize the hormone insulin. One of the side effects associated with chronic diabetes is nerve damage. This affects penis sensations. Other complications associated with diabetes are impaired blood flow and hormone levels. Both of these factors can contribute to impotence.
Erectile dysfunction or ED (It used to be called impotence) is the inability to achieve or sustain an erection suitable for sexual intercourse. Problems with erections may stem from medications, chronic illnesses, poor blood flow to the penis, drinking too much alcohol, or being too tired. Erectile dysfunction can occur at any age, but it is more common in men older than 75.
Autopsy studies have found histological prostate cancer to be very common, with one series showing a prevalence of greater than fifty percent in men over age sixty (Holund 1980). The majority of histological cancers go undetected so that the clinical incidence of the disease is much lower, but it is still the most prevalent non-skin cancer in men (Jemal et al 2003). Prostate cancer is also unusual in comparison to other adult cancers in that the majority of those with the disease will die of other causes. Treatment of prostate cancer with androgen deprivation is known to be successful and is widely practiced, indicating an important role for testosterone in modifying the behavior of prostate cancer. In view of this, testosterone treatment is absolutely contraindicated in any case of known or suspected prostate cancer. The question of whether testosterone treatment could cause new cases of prostate cancer, or more likely cause progression of undiagnosed histological prostate cancer that would otherwise have remained occult, is an important consideration when treating ageing males with testosterone.
Studies of the effects on cognition of testosterone treatment in non-cognitively impaired eugonadal and hypogonadal ageing males have shown varying results, with some showing beneficial effects on spatial cognition (Janowsky et al 1994; Cherrier et al 2001), verbal memory (Cherrier et al 2001) and working memory (Janowsky et al 2000), and others showing no effects (Sih et al 1997; Kenny et al 2002). Other trials have examined the effects of testosterone treatment in older men with Alzheimer’s disease or cognitive decline. Results have been promising, with two studies showing beneficial effects of testosterone treatment on spatial and verbal memory (Cherrier et al 2005b) and cognitive assessments including visual-spatial memory (Tan and Pu 2003), and a recent randomized controlled trial comparing placebo versus testosterone versus testosterone and an aromatase inhibitor suggesting that testosterone treatment improves spatial memory directly and verbal memory after conversion to estrogen (Cherrier et al 2005a). Not all studies have shown positive results (Kenny et al 2004; Lu et al 2005), and variations could be due to the different measures of cognitive abilities that were used and the cognitive state of men at baseline. The data from clinical trials offers evidence that testosterone may be beneficial for certain elements of cognitive function in the aging male with or without cognitive decline. Larger studies are needed to confirm and clarify these effects.
In one study, 9.6% reported ‘occasional’ erectile dysfunction, 8.9% reported erectile dysfunction occurring ‘often’, and 18.6% reported erectile dysfunction occurring ‘all the time’. Of these, only 11.6% had received treatment.In another study, only 14.1% of men reported that they had received treatment, despite experiencing erectile dysfunction for longer than 12 months.
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.
In non-human primates, it may be that testosterone in puberty stimulates sexual arousal, which allows the primate to increasingly seek out sexual experiences with females and thus creates a sexual preference for females.[39] Some research has also indicated that if testosterone is eliminated in an adult male human or other adult male primate's system, its sexual motivation decreases, but there is no corresponding decrease in ability to engage in sexual activity (mounting, ejaculating, etc.).[39]

The aim of treatment for hypogonadism is to normalize serum testosterone levels and abolish symptoms or pathological states that are due to low testosterone levels. The exact target testosterone level is a matter of debate, but current recommendations advocate levels in the mid-lower normal adult range (Nieschlag et al 2005). Truly physiological testosterone replacement would require replication of the diurnal rhythm of serum testosterone levels, but there is no current evidence that this is beneficial (Nieschlag et al 2005).

Richard J. Wassersug, PhD, an adjunct professor of urology at the University of British Columbia, described his personal experience with androgen deprivation therapy (ADT). "If you are on ADT," he said, "and you see those Low T ads, what are you supposed to make of it? This produces a cognitive dissonance." He called the ads "hurtful" for suggesting that low testosterone makes a man less of a man.
Erectile dysfunction can be embarrassing and difficult to talk about for some men. Many men may feel like they need to hide their diagnosis from their partner. "Failure to communicate openly about erectile dysfunction can result in both partners drawing away from the relationship," warns Feloney. Remember that your partner is also affected by your problem; being open and honest is the best way to decrease fear and anxiety. Discuss options for achieving sexual satisfaction together, and be positive — most erectile dysfunction problems can be treated.

However, testosterone is only one of many factors that aid in adequate erections. Research is inconclusive regarding the role of testosterone replacement in the treatment of erectile dysfunction. In a review of studies that looked at the benefit of testosterone in men with erection difficulties, nearly half showed no improvement with testosterone treatment. Many times, other health problems play a role in erectile difficulties. These can include: 

It doesn’t get more natural than getting a good night’s sleep. Research published in the Journal of the American Medical Association showed that lack of sleep can greatly reduce a healthy young man’s testosterone levels. That effect is clear after only one week of reduced sleep. Testosterone levels were particularly low between 2 and 10 p.m. on sleep-restricted days. Study participants also reported a decreased sense of wellbeing as their blood testosterone levels dropped.
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.
Some of the effects of testosterone treatment are well recognised and it seems clear that testosterone treatment for aging hypogonadal men can be expected to increase lean body mass, decrease visceral fat mass, increase bone mineral density and decrease total cholesterol. Beneficial effects have been seen in many trials on other parameters such as glycemic control in diabetes, erectile dysfunction, cardiovascular risk factors, angina, mood and cognition. These potentially important effects require confirmation in larger clinical trials. Indeed, it is apparent that longer duration randomized controlled trials of testosterone treatment in large numbers of men are needed to confirm the effects of testosterone on many aspects of aging male health including cardiovascular health, psychiatric health, prostate cancer and functional capacity. In the absence of such studies, it is necessary to balance risk and benefit on the best available data. At the present time the data supports the treatment of hypogonadal men with testosterone to normalize testosterone levels and improve symptoms. Most men with hypogonadism do not have a contraindication to treatment, but it is important to monitor for adverse consequences including prostate complications and polycythemia.

^ 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.
Testosterone replacement therapy may improve energy, mood, and bone density, increase muscle mass and weight, and heighten sexual interest in older men who may have deficient levels of testosterone. Testosterone supplementation is not recommended for men who have normal testosterone levels for their age group due to the risk of prostate enlargement and other side effects. Testosterone replacement therapy is available as a cream or gel, topical solution, skin patch, injectable form and pellet form placed under the skin.
Testosterone is included in the World Health Organization's list of essential medicines, which are the most important medications needed in a basic health system.[172] It is available as a generic medication.[10] The price depends on the form of testosterone used.[173] It can be administered as a cream or transdermal patch that is applied to the skin, by injection into a muscle, as a tablet that is placed in the cheek, or by ingestion.[10] 

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]
The FDA recommends that men follow general precautions before taking a medication for ED. Men who are taking medications that contain nitrates, such as nitroglycerin, should NOT use these medications. Taking nitrates with one of these medications can lower blood pressure too much. In addition, men who take tadalafil or vardenfil should use alpha blockers with care and only as instructed by their physician, as they could result in hypotension (abnormally low blood pressure). Experts recommend that men have a complete medical history and physical examination to determine the cause of ED. Men should tell their doctor about all the medications they are taking, including over-the-counter medications.
Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels.[138] Behavior: Dominance challenges can, in some cases, stimulate increased testosterone release in men.[139] Drugs: Natural or man-made antiandrogens including spearmint tea reduce testosterone levels.[140][141][142] Licorice can decrease the production of testosterone and this effect is greater in females.[143]
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.
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Organic ED involves abnormalities the penile arteries, veins, or both and is the most common cause of ED, especially in older men. When the problem is arterial, it is usually caused by arteriosclerosis, or hardening of the arteries, although trauma to the arteries may be the cause. The controllable risk factors for arteriosclerosis--being overweight, lack of exercise, high cholesterol, high blood pressure, and cigarette smoking--can cause erectile failure often before progressing to affect the heart. 
The views expressed in this article intend to highlight alternative studies and induce conversation. They are the views of the author and do not necessarily represent the views of hims, and are for informational purposes only, even if and to the extent that this article features the advice of physicians and medical practitioners. This article is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment, and should never be relied upon for specific medical advice.

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.


Treatment involves addressing the underlying causes, lifestyle modifications, and addressing psychosocial issues.[1] In many cases, a trial of pharmacological therapy with a PDE5 inhibitor, such as sildenafil, can be attempted. In some cases, treatment can involve inserting prostaglandin pellets into the urethra, injecting smooth muscle relaxants and vasodilators into the penis, a penile prosthesis, a penis pump, or vascular reconstructive surgery.[1][2] It is the most common sexual problem in men.[3]
CONDITIONS OF USE: The information in this database is intended to supplement, not substitute for, the expertise and judgment of healthcare professionals. The information is not intended to cover all possible uses, directions, precautions, drug interactions or adverse effects, nor should it be construed to indicate that use of a particular drug is sage, appropriate or effective for you or anyone else. A healthcare professional should be consulted before taking any drug, changing any diet or commencing or discontinuing any course of treatment.
4. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Erectile dysfunction (updated Nov 2015). https://www.niddk.nih.gov/health-information/health-topics/urologic-disease/erectile-dysfunction/Pages/facts.aspx (accessed Nov 2016). myDr myDr provides comprehensive Australian health and medical information, images and tools covering symptoms, diseases, tests, medicines and treatments, and nutrition and fitness.Related ArticlesImpotence causesFind out the physical and psychological causes of impotence, also called erectile dysfunction or ED.Erectile dysfunction: visiting your doctorFind out what questions a doctor may ask when discussing erectile dysfunction (ED, or impotence8 Surprising causes of erectile dysfunctionOccasional erectile dysfunction is not uncommon, but if it's persistent, erectile dysfunction caAdvertisement

Now, there are lots of ways that you can reduce stress and anxiety in your life. One of those things you can do is exercising daily. Now, it doesn’t mean getting into a gym all the time, but it can just be doing sit-ups at home, long walks at the grocery store, bicycling, and if you can afford the gym, getting there maybe two to three days a week. But don’t forget, a healthy body equals a healthy mind. Meditation, yoga, breathing exercises– now, here’s where you can take a few moments to be centered and communicate with your inner self, peace. Healthy eating– now, taking control of the intake of what goes into your body makes you to start feeling better and looking better. That wellness is the opposite of anxiety. And treating issues and tackling things that are weighing you down, taking that very first step is liberating.
Testosterone is also important for maintaining bone strength and lean muscle mass in women, as well as contributing to overall well-being and energy levels. This hormone plays a key role in a woman’s sex drive and is responsible for enhancing sexual pleasure during intercourse. However, the levels of testosterone produced by females is still between ten and times less than the amount produced by men.
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.
With sex therapy, your counselor looks at the sexual problems you and your partner are having. Sex therapy works with problems such as performance anxiety, which means that you worry so much about whether you will be able to have sex that you are not able to. It also helps when you have erection problems that are not due to physical or drug problems, or premature ejaculation (you come too quickly). It may help you to reach orgasm or to learn to relax enough to avoid pain during sex. Counseling can help you to adjust to the treatment you and your doctor choose.
Professional-athlete-turned-biohacker Maximilian Gotzler gave a speech about boosting testosterone at the 2015 Bulletproof Conference. He started by leading the room through the Haka, a Maori war dance that New Zealand’s pro rugby team has made popular. The Pasadena Conference Center trembled as over 100 people shouted and stomped in unison. It was awesome.

In 1927, the University of Chicago's Professor of Physiologic Chemistry, Fred C. Koch, established easy access to a large source of bovine testicles — the Chicago stockyards — and recruited students willing to endure the tedious work of extracting their isolates. In that year, Koch and his student, Lemuel McGee, derived 20 mg of a substance from a supply of 40 pounds of bovine testicles that, when administered to castrated roosters, pigs and rats, remasculinized them.[176] The group of Ernst Laqueur at the University of Amsterdam purified testosterone from bovine testicles in a similar manner in 1934, but isolation of the hormone from animal tissues in amounts permitting serious study in humans was not feasible until three European pharmaceutical giants—Schering (Berlin, Germany), Organon (Oss, Netherlands) and Ciba (Basel, Switzerland)—began full-scale steroid research and development programs in the 1930s.
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).
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.
Overall, it seems that both estrogen and testosterone are important for normal bone growth and maintenance. Deficiency or failure of action of the sex hormones is associated with osteoporosis and minimal trauma fractures. Estrogen in males is produced via metabolism of testosterone by aromatase and it is therefore important that androgens used for the treatment of hypogonadism be amenable to the action of aromatase to yield maximal positive effects on bone. There is data showing that testosterone treatment increases bone mineral density in aging males but that these benefits are confined to hypogonadal men. The magnitude of this improvement is greater in the spine than in the hip and further studies are warranted to confirm or refute any differential effects of testosterone at these important sites. Improvements seen in randomized controlled trials to date may underestimate true positive effects due to relatively short duration and/or baseline characteristics of the patients involved. There is no data as yet to confirm that the improvement in bone density with testosterone treatment reduces fractures in men and this is an important area for future study.
Stanley A Brosman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Association for the Advancement of Science, American Association for Cancer Research, American College of Surgeons, American Medical Association, American Urological Association, Society for Basic Urologic Research, Society of Surgical Oncology, Society of Urologic Oncology, Western Section of the American Urological Association, Association of Clinical Research Professionals, American Society of Clinical Oncology, International Society of Urology, International Society of Urological Pathology
ICI therapy often produces a reliable erection, which comes down after 20-30 minutes or with climax. Since the ICI erection is not regulated by your penile nerves, you should not be surprised if the erection lasts after orgasm. The most common side effect of ICI therapy is a prolonged erection. Prolonged erections (>1 hour) can be reversed by a second injection (antidote) in the office.

However, in contrast, a recent systematic review of published studies, the authors concluded that overall, the addition of testosterone to PDE-5 inhibitors might benefit patients with ED associated with testosterone levels of less than 300 ng/dL (10.4 nmol/L) who failed monotherapy. [20] A limitation of existing studies are their heterogeneous nature and methodological drawbacks.

Surgery: If neither drugs nor the vacuum pump works, your doctor may suggest surgery. With surgery, the doctor can place a device in your penis that will cause enough hardness for intercourse. In a few cases, infections may develop after the operation, and the doctor may have to remove the device. Another operation that may help you is rebuilding the blood vessels in the penis to increase blood flow into the penis or decrease blood flow out of the penis. These procedures can help you to get and maintain an erection.
In males, the majority of testosterone is secreted from the testes, hence the term “testosterone”. The hormone is also produced in small amounts by the adrenal gland. The production of this hormone is controlled by the hypothalamus and pituitary gland in the brain. The pituitary gland receives instructions from the hypothalamus on how much testosterone needs producing and passes this information onto the testicles via chemicals and hormones circulating in the bloodstream.

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.
A recent study compared total and bioavailable testosterone levels with inflammatory cytokines in men aged 65 and over. There was an inverse correlation with the pro-inflammatory soluble interleukin-6 receptor, but no association with interleukin-6 (IL-6), highly sensitive CRP (hsCRP), tumor necrosis factor-α (TNF-α) or interleukin-1β (IL-1β (Maggio et al 2006). Another trial found that young men with idiopathic hypogonadotrophic hypogonadism had higher levels of proinflammatory factors interleukin-2 (IL-2), interleukin-4 (IL-4), complement C3c and total immunoglobulin in comparison to controls (Yesilova et al 2000). Testosterone treatment in a group of hypogonadal men, mostly with known coronary artery disease, induced anti-inflammatory changes in the cytokine profile of reduced IL-1β and TNF-α and increased IL-10 (Malkin, Pugh, Jones et al 2004).
For best results, men with ED take these pills about an hour or two before having sex. The drugs require normal nerve function to the penis. PDE5 inhibitors improve on normal erectile responses helping blood flow into the penis. Use these drugs as directed. About 7 out of 10 men do well and have better erections. Response rates are lower for Diabetics and cancer patients.
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