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'.
"I am very cautious about committing someone for life to medication," said Dr. Kathleen L. Wyne, who directs research on diabetes and metabolism at Houston's Methodist Hospital Research Institute and serves on the Sex Hormone and Reproductive Endocrinology Scientific Committee for the American Association of Clinical Endocrinologists. "That does frustrate patients because they have heard about [Low T] from TV and friends."
The device consists of an acrylic cylinder placed over the penis that uses a lubricant to achieve a good seal between the penile body and cylinder. An erection is then achieved by creating a vacuum inside the cylinder with a pump connected to the cylinder. Once an erection is achieved, a constriction band is applied to the base of the penis to maintain the erection. The cylinder can then be removed and the patient can engage in intercourse with the constriction band at the base of the penis maintaining the erection. The band can remain on for approximately 30 minutes and then must be removed. The erection produced by the device differs from a normal erection likely because of venous occlusion from the constriction band resulting in generalized swelling of the entire penis, with probable preservation of arterial inflow.
Low testosterone levels may contribute to decreased sex drive, erectile dysfunction, fragile bones, and other health issues. Having low testosterone levels may also indicate an underlying medical condition. See your doctor if you suspect you have low testosterone. A simple blood test is all it takes to check if your testosterone falls within the normal range.
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.
Your doctor will ask you questions about your symptoms and health history. They may do tests to determine if your symptoms are caused by an underlying condition. You should expect a physical exam where your doctor will listen to your heart and lungs, check your blood pressure, and examine your testicles and penis. They may also recommend a rectal exam to check your prostate. Additionally, you may need blood or urine tests to rule out other conditions.
When stimulated by the nerves, the spongy tissue arranges itself in such a way that more blood can be stored in the penis. The veins running through the outer sheath of the penis then compress which stops the blood from leaving the penis. As the blood is stopped from flowing out, the penis fills with blood and stretches within the outer casing, giving an erection.
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.
The most common treatment for erectile dysfunction is drugs known as phosphodiesterase-5 (PDE-5) inhibitors. These include tadalafil (Cialis), vardenafil (Levitra), and sildenafil citrate (Viagra). These are effective for about 75% of men with erectile dysfunction. They are tablets that are taken around an hour before sex, and last between 4 and 36 hours. Sexual stimulation is required before an erection will occur. The PDE-5 inhibitors cause dilation of blood vessels in the penis to allow erection to occur, and help it to stay rigid. Men using nitrate medication (e.g. GTN spray or sublingual tablets for angina) should not use PDE-5 inhibitors.
ED usually has a multifactorial etiology. Organic, physiologic, endocrine, and psychogenic factors are involved in the ability to obtain and maintain erections. In general, ED is divided into 2 broad categories, organic and psychogenic. Although most ED was once attributed to psychological factors, pure psychogenic ED is in fact uncommon; however, many men with organic etiologies may also have an associated psychogenic component.
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.
Clinical studies have suggested that these devices are effective and acceptable to a large number of patients with ED of varying causes, including psychogenic erectile failure. These devices are safe and can restore a man’s ability to achieve penetrative intercourse, with one study suggesting nearly 95% success with adequate instruction and support.30 However, satisfaction with this treatment modality typically wanes with time, as patients report dissatisfaction with how cumbersome or unnatural the devices are to use, hinging or buckling of the erection with thrusting, and dissatisfaction with the fact that the erection is ischemic and therefore cold, which can be off-putting to the partner.
The main surgical treatment of ED involves insertion of a penile implant (also called penile prostheses). Because penile vascular surgery is not recommended for aging males who have failed oral PDE5 inhibitors, ICI or IU therapies, implants are the next step for these patients. Although placement of a penile implant is a surgery which carries risks, they have the highest rates of success and satisfaction among ED treatment options.
Recently, a panel with cooperation from international andrology and urology societies, published specific recommendations with regard to the diagnosis of Late-onset Hypogonadism (Nieschlag et al 2005). These are summarized in the following text. It is advised that at least two serum testosterone measurements, taken before 11 am on different mornings, are necessary to confirm the diagnosis. The second sample should also include measurement of gonadotrophin and prolactin levels, which may indicate the need for further investigations for pituitary disease. Patients with serum total testosterone consistently below 8 nmol/l invariably demonstrate the clinical syndrome of hypogonadism and are likely to benefit from treatment. Patients with serum total testosterone in the range 8–12 nmol/l often have symptoms attributable to hypogonadism and it may be decided to offer either a clinical trial of testosterone treatment or to make further efforts to define serum bioavailable or free testosterone and then reconsider treatment. Patients with serum total testosterone persistently above 12 nmol/l do not have hypogonadism and symptoms are likely to be due to other disease states or ageing per se so testosterone treatment is not indicated.
A physical cause can be identified in about 80% of cases. These include cardiovascular disease, diabetes mellitus, neurological problems such as following prostatectomy, hypogonadism, and drug side effects. Psychological impotence is where erection or penetration fails due to thoughts or feelings; this is somewhat less frequent, in the order of about 10% of cases. In psychological impotence, there is a strong response to placebo treatment.
Many experts believe that atrophy, a partial or complete wasting away of tissue, and fibrosis, the growth of excess tissue, of the smooth muscle tissue in the body of the penis (cavernous smooth muscle) triggers problems with being able to maintain a firm erection. Poor ability to maintain an erection is often an early symptom of erectile dysfunction. Although the condition is called venous leak, the real problem is not with the veins but malfunction of the smooth muscle that surrounds the veins. The end result is difficulty with maintain a firm erection (losing an erection too quickly) that is now believe to be an early manifestation of atherosclerosis and vascular disease.
Recognized risk factors for ED include cardiovascular disease (CVD) (hypertension, atherosclerosis, and hyperlipidemia), diabetes, depression, alcohol use, smoking, pelvic/perineal surgery or trauma, neurologic disease, obesity, pelvic radiation, and Peyronie’s disease. One study suggested that the relationship between arterial disease and ED is very strong, with 49% (147 of 300) of patients with coronary artery disease noted on cardiac catheterization reporting significant erectile dysfunction.6 Endothelial dysfunction has been indicated as the pathophysiologic mechanism responsible for both CVD and ED.7 The Boston Area Community Health survey demonstrated a dose-response between smoking and incidence of erectile dysfunction.8 Animal studies have demonstrated both smooth-muscle disruption and decreased production of neural nitric oxide synthase in cigarette-exposed animals.9
There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).
Replacement therapy may produce desired results, such as greater muscle mass and a stronger sex drive. However, the treatment does carry some side effects. Oily skin and fluid retention are common. The testicles may also shrink, and sperm production could decrease significantly. Some studies have found no greater risk of prostate cancer with testosterone replacement therapy, but it continues to be a topic of ongoing research.
Instead of the hesitation with which he had accosted the cardinal a quarter of an hour before, there might be read in the eyes of the young king that will against which a struggle might be maintained, and which might be crushed by its own impotence, but which, at least, would preserve, like a wound in the depth of the heart, the remembrance of its defeat.
Epidemiological data has associated low testosterone levels with atherogenic lipid parameters, including lower HDL cholesterol (Lichtenstein et al 1987; Haffner et al 1993; Van Pottelbergh et al 2003) and higher total cholesterol (Haffner et al 1993; Van Pottelbergh et al 2003), LDL cholesterol (Haffner et al 1993) and triglyceride levels (Lichtenstein et al 1987; Haffner et al 1993). Furthermore, these relationships are independent of other factors such as age, obesity and glucose levels (Haffner et al 1993; Van Pottelbergh et al 2003). Interventional trails of testosterone replacement have shown that treatment causes a decrease in total cholesterol. A recent meta-analysis of 17 randomized controlled trials confirmed this and found that the magnitude of changes was larger in trials of patients with lower baseline testosterone levels (Isidori et al 2005). The same meta-analysis found no significant overall change in LDL or HDL cholesterol levels but in trials with baseline testosterone levels greater than 10 nmol/l, there was a small reduction in HDL cholesterol with testosterone treatment.
The PDE5 inhibitors sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis) are prescription drugs which are taken orally.:20–21 Additionally, a cream combining alprostadil with the permeation enhancer DDAIP has been approved in Canada as a first line treatment for erectile dysfunction. Penile injections, on the other hand, can involve one of the following medications: papaverine, phentolamine, and prostaglandin E1.:25
If you have unstable heart disease of any kind, heart failure or unstable, what we call angina, contraindication to using the medications. All right? So if you’re in an unstable medical state, these medications are not a good idea. Now, there are relative issues. If you may be taking a blood pressure medicine or a medicine for your prostate which dilates your blood vessel a little bit– you know, the typical ones are what we call the alpha blockers– you may have an additive effect from the medication. But for the most part, the medicines are incredibly safe.
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Patients at high cardiovascular risk should not be treated for ED until their cardiac condition is stabilize. These conditions include unstable or refractory angina, myocardial infarction or cerebrovascular accident within the past 2 weeks, uncontrolled hypertension, New York Heart Association (NYHA) Functional Classification III-IV congestive heart failure, high-risk arrhythmias, hypertrophic obstructive cardiomyopathies, and moderate-to-severe valvular disease.25 This class of drugs is also contraindicated in patients who use nitroglycerin or nitrate-containing compounds.26, 27
Psychosocial problems are important and may cause erectile dysfunction by themselves or together with other causes of erectile dysfunction, such as diabetes and heart disease. Relationships are complicated and many factors cause tensions, which can affect sexual relations. For some men, these problems can become ongoing and it can help to talk through the issue with a skilled counsellor. It is important to know that the longer erectile dysfunction is left untreated, the greater the effect on relationships. This is another reason why early treatment of erectile dysfunction is important.
Several studies accessed the prevalence of ED. The Massachusetts Male Aging Study reported a prevalence of 52%.2 The study demonstrated that ED is increasingly prevalent with age: approximately 40% of men are affected at age 40 and nearly 70% of men are affected at age 70. The prevalence of complete ED increased from 5% at age 40 to 15% at age 70.2 Age was the variable most strongly associated with ED.
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.)
Although not proven, it is likely that erectile dysfunction can be prevented by good general health, paying particular attention to body weight, exercise, and cigarette smoking. For example, heart disease and diabetes are problems that can cause erectile dysfunction, and both are preventable through lifestyle changes such as sensible eating and regular exercise. Furthermore, early diagnosis and treatment of associated conditions like diabetes, hypertension and high cholesterol may prevent or delay erectile dysfunction, or stop the erectile dysfunction from getting more serious.
"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.
Surgical intervention for a number of conditions may remove anatomical structures necessary to erection, damage nerves, or impair blood supply. Erectile dysfunction is a common complication of treatments for prostate cancer, including prostatectomy and destruction of the prostate by external beam radiation, although the prostate gland itself is not necessary to achieve an erection. As far as inguinal hernia surgery is concerned, in most cases, and in the absence of postoperative complications, the operative repair can lead to a recovery of the sexual life of people with preoperative sexual dysfunction, while, in most cases, it does not affect people with a preoperative normal sexual life.
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.
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.  A limitation of existing studies are their heterogeneous nature and methodological drawbacks.
The hypogonadal-obesity-adipocytokine cycle hypothesis. Adipose tissue contains the enzyme aromatase which metabolises testosterone to oestrogen. This results in reduced testosterone levels, which increase the action of lipoprotein lipase and increase fat mass, thus increasing aromatisation of testosterone and completing the cycle. Visceral fat also promotes lower testosterone levels by reducing pituitary LH pulse amplitude via leptin and/or other factors. In vitro studies have shown that leptin also inhibits testosterone production directly at the testes. Visceral adiposity could also provide the link between testosterone and insulin resistance (Jones 2007).
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.
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).