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The Massachusetts Male Aging Study (MMAS) documented an inverse correlation between ED risk and high-density lipoprotein (HDL) cholesterol levels but did not identify any effect from elevated total cholesterol levels. [15] Another study involving male subjects aged 45-54 years found a correlation with abnormal HDL cholesterol levels but also found a correlation with elevated total cholesterol levels. The MMAS included a preponderance of older men.
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A number of research groups have tried to further define the relationship of testosterone and body composition by artificial alteration of testosterone levels in eugonadal populations. Induction of a hypogonadal state in healthy men (Mauras et al 1998) or men with prostate cancer (Smith et al 2001) using a gonadotrophin-releasing-hormone (GnRH) analogue was shown to produce increases in fat mass and decreased fat free mass. Another experimental approach in healthy men featured suppression of endogenous testosterone production with a GnRH analogue, followed by treatment with different doses of weekly intramuscular testosterone esters for 20 weeks. Initially the experiments involved men aged 18–35 years (Bhasin et al 2001) but subsequently the study was repeated with a similar protocol in men aged 60–75 years (Bhasin et al 2005). The different doses given were shown to produce a range of serum concentrations from subphysiological to supraphysiological (Bhasin et al 2001). A given testosterone dose produced higher serum concentrations of testosterone in the older age group (Bhasin et al 2005). Subphysiological dosing of testosterone produced a gain in fat mass and loss of fat free mass during the study. There were sequential decreases in fat mass and increases in fat free mass with each increase of testosterone dose. These changes in body composition were seen in physiological and supraphysiological treatment doses. The trend was similar in younger versus older men but the gain of fat mass at the lowest testosterone dose was less prominent in older patients (Bhasin et al 2001; Bhasin et al 2005). With regard to muscle function, the investigators showed dose dependent increases in leg strength and power with testosterone treatment in young and older men but there was no improvement in fatigability (Storer et al 2003; Bhasin et al 2005).
Due to the risk of hypotension, caution should be used in patients using alpha blockers for prostate hyperplasia and patients using other antihypertensive medications and alpha blockers, which should not be co-administered with PDE5 inhibitors. In patients who take 50 mg of sildenafil or more and use alpha blockers, sildenafil dosing should be avoided for at least 4 hours after the dose of the alpha blocker. In patients who take 25 mg of sildenafil, use of any alpha blockers is considered safe.
The medications are extremely effective, which is very good. And the medications are, for the most part, extremely well-tolerated. But there are, like with any medications, a potential downside. The one absolute downside to the use of any of these erection what we call PDE5 medications is if a patient is using a nitroglycerin medication. And nitroglycerins are used for heart disease and for angina, for the most part, although there are some recreational uses of nitrites. And that’s important because your blood vessels will dilate and your blood pressure will drop. And that is an absolute contraindication.
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.

"Low T" is anything but inevitable. BMJ's Drug and Therapeutics Bulletin says that around 80 percent of 60-year-old men, and half of those in their eighties, have testosterone levels within the normal range for younger men. It concluded, "The evidence that an age-related reduction in testosterone levels causes specific symptoms is weak." The Food and Drug Administration (FDA) meanwhile has not approved testosterone use to improve strength, athletic performance, physical appearance, or prevent aging. And a 2004 report from the Institute of Medicine ("Testosterone and Aging: Clinical Research Directions") called TRT for age-related testosterone decline a "scientifically unproven method."


Think of erectile dysfunction as your body’s “check engine light.” The blood vessels in the penis are smaller than other parts of the body, so underlying conditions like blocked arteries, heart disease, or high blood pressure usually show up as ED before something more serious like a heart attack or stroke. ED is your body’s way of saying, “Something is wrong.” And the list of things that cause erectile dysfunction can include:
The development of an erection is a complex event involving integration of psychologic, neurologic, endocrine, vascular, and local anatomic systems. Positron emission tomography scanning studies have suggested that sexual arousal is activated in higher cortical centers that then stimulate the medial preoptic and paraventricular nuclei of the hypothalamus.5 These signals ultimately descend through a complex neural network involving the parasympathetic nervous system and eventually activate parasympathetic nerves in the sacral area (S2 to S4).
The second theory is similar and is known as "evolutionary neuroandrogenic (ENA) theory of male aggression".[78][79] Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate with mates as much as possible.[78] The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb as a fetus. Higher pre-natal testosterone indicated by a low digit ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.[80] Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in males.[81][82][83][84][85]
In rare cases, the drug Viagra ® can cause blue-green shading to vision that lasts for a short time. In rare cases, the drug Cialis® can cause or increase back pain or aching muscles in the back. In most cases, the side effects are linked to PDE5 inhibitor effects on other tissues in the body, meaning they are working to increase blood flow to your penis and at the same time impacting other vascular tissues in your body. These are not ‘allergic reactions'.
Men's levels of testosterone, a hormone known to affect men's mating behaviour, changes depending on whether they are exposed to an ovulating or nonovulating woman's body odour. Men who are exposed to scents of ovulating women maintained a stable testosterone level that was higher than the testosterone level of men exposed to nonovulation cues. Testosterone levels and sexual arousal in men are heavily aware of hormone cycles in females.[46] This may be linked to the ovulatory shift hypothesis,[47] where males are adapted to respond to the ovulation cycles of females by sensing when they are most fertile and whereby females look for preferred male mates when they are the most fertile; both actions may be driven by hormones.
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.
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).
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.
Erections are more complicated than you think. Your brain, nerves, heart, blood vessels, and a whole lot of hormones have to work together perfectly or nothing happens. It’s a lot to ask, and sometimes things break down. And while ED happens to most guys at some point in their lives, erectile dysfunction isn’t something you can just ignore and hope it goes away.

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Male hypogonadism becomes more common with increasing age and is currently an under-treated condition. The diagnosis of hypogonadism in the aging male requires a combination of symptoms and low serum testosterone levels. The currently available testosterone preparations can produce consistent physiological testosterone levels and provide for patient preference.
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).
^ 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.
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.

Testosterone is an androgen hormone produced by the adrenal cortex, the testes (in men), and the ovaries (in women). It is often considered the primary male sex hormone. Testosterone stimulates the development of male secondary sex characteristics (like body hair and muscle growth) and is essential in the production of sperm. In women, testosterone plays a role in egg development and ovulation.
Talk with your doctor before trying supplements for ED. They can contain 10 or more ingredients and may complicate other health conditions. Asian ginseng and ginkgo biloba (seen here) are popular, but there isn't a lot of good research on their effectiveness. Some men find that taking a DHEA supplement improves their ability to have an erection. Unfortunately, the long-term safety of DHEA supplements is unknown. Most doctors do not recommend using it.

Like other steroid hormones, testosterone is derived from cholesterol (see figure).[120] The first step in the biosynthesis involves the oxidative cleavage of the side-chain of cholesterol by cholesterol side-chain cleavage enzyme (P450scc, CYP11A1), a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to give pregnenolone. In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids.[121] In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.

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.

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."
Several pathways have been described to explain how information travels from the hypothalamus to the sacral autonomic centers. One pathway travels from the dorsomedial hypothalamus through the dorsal and central gray matter, descends to the locus ceruleus, and projects ventrally in the mesencephalic reticular formation. Input from the brain is conveyed through the dorsal spinal columns to the thoracolumbar and sacral autonomic nuclei.
The dorsal artery provides for engorgement of the glans during erection, whereas the bulbourethral artery supplies the bulb and the corpus spongiosum. The cavernous artery effects tumescence of the corpus cavernosum and thus is principally responsible for erection. The cavernous artery gives off many helicine arteries, which supply the trabecular erectile tissue and the sinusoids. These helicine arteries are contracted and tortuous in the flaccid state and become dilated and straight during erection. [9]
The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. Copyright 1997-2019, A.D.A.M., Inc. Duplication for commercial use must be authorized in writing by ADAM Health Solutions.
The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch.[180] Only a week later, the Ciba group in Zurich, Leopold Ruzicka (1887–1976) and A. Wettstein, published their synthesis of testosterone.[181] These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry.[179][182] Testosterone was identified as 17β-hydroxyandrost-4-en-3-one (C19H28O2), a solid polycyclic alcohol with a hydroxyl group at the 17th carbon atom. This also made it obvious that additional modifications on the synthesized testosterone could be made, i.e., esterification and alkylation.

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.
Erectile dysfunction is known to be associated with general health status, thus, lifestyle modification improves erectile function and decreases the rate of decline of function with aging. One year after discontinuation of smoking, patients were found to have a 25% improvement in erectile quality.16 In addition, multivariate analysis found obesity is associated with erectile dysfunction with an approximately 50% increase in ED in obese men as compared with normal weight men.17
One of the first steps is to distinguish between physiological and psychological ED. Determining whether involuntary erections are present is important in eliminating the possibility of psychogenic causes for ED.[1] Obtaining full erections occasionally, such as nocturnal penile tumescence when asleep (that is, when the mind and psychological issues, if any, are less present), tends to suggest that the physical structures are functionally working.[19][20] Similarly, performance with manual stimulation, as well as any performance anxiety or acute situational ED, may indicate a psychogenic component to ED.[1]
The brain is also affected by this sexual differentiation;[13] the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.[95]
A larger national study, the National Health and Social Life Survey, looked at sexual function in men and women.4 This study surveyed 1,410 men aged 18 to 59 and also documented an increase in ED with age. Additionally, the study found a decrease in sexual desire with increasing age. Men in the oldest cohort (50 to 59) were more than 3 times as likely to experience erection problems and to report low sexual desire compared with men 18 to 29. Experience of sexual dysfunction was more likely among men in poor physical and emotional health. The study also concluded that sexual dysfunction is an important public health concern and that emotional issues are likely to contribute to the experience sexual dysfunction.
Modern drug therapy for ED made a significant advance in 1983, when British physiologist Giles Brindley dropped his trousers and demonstrated to a shocked Urodynamics Society audience his papaverine-induced erection.[35] The drug Brindley injected into his penis was a non-specific vasodilator, an alpha-blocking agent, and the mechanism of action was clearly corporal smooth muscle relaxation. The effect that Brindley discovered established the fundamentals for the later development of specific, safe, and orally effective drug therapies.[36][better source needed][37][better source needed]

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In my late 20’s, I visited an anti-aging doctor who was one of the pioneers of what we now call functional medicine. I got a full hormone test. Shockingly, my testosterone was lower than my mother’s. No wonder I felt crappy and was overweight. My other sex hormones were out of whack too, especially my estrogen levels. They were high because the little testosterone I did make my body converted into estrogen. I went on a mix of topical replacement testosterone cream, plus small doses of pharmaceuticals like clomid and arimidex in order to keep my other sex hormones functioning properly.
Think of erectile dysfunction as your body’s “check engine light.” The blood vessels in the penis are smaller than other parts of the body, so underlying conditions like blocked arteries, heart disease, or high blood pressure usually show up as ED before something more serious like a heart attack or stroke. ED is your body’s way of saying, “Something is wrong.” And the list of things that cause erectile dysfunction can include:
Men with medical conditions that may cause a sustained erection, such as sickle cell anemia, leukemia, or multiple myeloma, or a man who has an abnormally-shaped penis, may not benefit from these medications. Also, men with liver diseases or a disease of the retina, such as macular degeneration or retinitis pigmentosa, may not be able to take these medications, or may need to take the lowest dosage.
The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.
The hormone also plays a role in sex drive, sperm production, fat distribution, red cell production, and maintenance of muscle strength and mass, according to the Mayo Clinic. For these reasons, testosterone is associated with overall health and well-being in men. One 2008 study published in the journal Frontiers of Hormone Research even linked testosterone to the prevention of osteoporosis in men.
Low-intensity extracorporeal shock wave therapy has been proposed as a new non-invasive treatment for erectile dysfunction caused by problems with blood vessels. Shock wave therapy machines are now available in some medical practices in Australia. Although there is some evidence that it may help a proportion of men with erectile dysfunction, more research is needed before clear recommendations on its use can be made.
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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