An occasional problem achieving an erection is nothing to worry about. But failure to do so more than 50% of the time at any age may indicate a condition that needs treatment. About 40% of men in their 40s report at least occasional problems getting and maintaining erections. So do more than half (52%) of men aged 40 to 70, and about 70% of men in their 70s.
Before assessing the evidence of testosterone’s action in the aging male it is important to note certain methodological considerations which are common to the interpretation of any clinical trial of testosterone replacement. Many interventional trials of the effects of testosterone on human health and disease have been conducted. There is considerable heterogenicity in terms of study design and these differences have a potential to significantly affect the results seen in various studies. Gonadal status at baseline and the testosterone level produced by testosterone treatment in the study are of particular importance because the effects of altering testosterone from subphysiological to physiological levels may be different from those of altering physiological levels to supraphysiological. Another important factor is the length of treatment. Randomised controlled trials of testosterone have ranged from one to thirty-six months in duration (Isidori et al 2005) although some uncontrolled studies have lasted up to 42 months. Many effects of testosterone are thought to fully develop in the first few months of treatment but effects on bone, for example, have been shown to continue over two years or more (Snyder et al 2000; Wang, Cunningham et al 2004).
Erectile dysfunction - (ED) or impotence is sexual dysfunction characterized by the inability to develop or maintain an erection of the penis during sexual activity. A penile erection is the hydraulic effect of blood entering and being retained in sponge-like bodies within the penis. The process is most often initiated as a result of sexual arousal, when signals are transmitted from the brain to nerves in the penis.
It appears that testosterone has NOS-independent pathways as well. In one study, castrated rats were implanted with testosterone pellets and then divided into a group that received an NOS inhibitor (L-nitro-L-arginine methyl ester [L-NAME]) and a control group that received no enzyme. [24] The castrated rats that were given testosterone pellets and L-NAME still had partial erections, a result suggesting the presence of a pathway independent of NOS activity.
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 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.
^ 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.
It may also become a treatment for anemia, bone density and strength problems. In a 2017 study published in the journal of the American Medical Association (JAMA), testosterone treatments corrected anemia in older men with low testosterone levels better than a placebo. Another 2017 study published in JAMA found that older men with low testosterone had increased bone strength and density after treatment when compared with a placebo. 
All devices that are currently approved by the FDA are considered safe for use in magnetic resonance imaging environments. However, 2 previously approved devices–the OmniPhase and the DuraPhase penile prostheses–are not considered safe in this environment. Other surgical procedures–including venous ligation to limit penile venous outflow and penile revascularization procedures–are rarely successful and are not recommended.19 These surgeries are only indicated when a patient demonstrates recent-onset ED and an occlusive lesion seen on angiogram or magnetic resonance angiography and should be performed only in centers of excellence for ED.
The primary nerve fibers to the penis are from the dorsal nerve of the penis, a branch of the pudendal nerve. The cavernosal nerves are a part of the autonomic nervous system and incorporate both sympathetic and parasympathetic fibers. They travel posterolaterally along the prostate and enter the corpora cavernosa and corpus spongiosum to regulate blood flow during erection and detumescence. The dorsal somatic nerves are also branches of the pudendal nerves. They are primarily responsible for penile sensation. [10]
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).
"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."
Vascular damage may result from radiation therapy to the pelvis and prostate in the treatment of prostate cancer. [36] Both the blood vessels and the nerves to the penis may be affected. Radiation damage to the crura of the penis, which are highly susceptible to radiation damage, can induce ED. Data indicate that 50% of men undergoing radiation therapy lose erectile function within 5 years after completing therapy; fortunately, some respond to one of the PDE5 inhibitors.
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).
"The hope," explained Dr. Swerdloff in a telephone interview, "is this will provide some clarity as to whether testosterone replacement therapy will benefit men in this older age group who clearly have abnormal testosterone and have some symptoms." He added, "We don't know whether it will be beneficial at all the endpoints we are studying, or be beneficial to some and not others. We don't know if the benefits occur at different blood levels that are attained in the individuals."
Rest and recovery is just as important as exercise, if not more so. Every time you do an intense workout, give yourself a minimum of 2 days to recuperate afterward, if not more. And don’t mix exercise with sleep hacking. If you’re exercising, get at least 8 hours of sleep every night. Your body uses it to rebuild, and you can throw your hormones out of whack if you don’t rest up properly. Here’s a more in-depth guide to Bulletproof weight training, complete with sample workouts.
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).
Testosterone is necessary for normal sperm development. It activates genes in Sertoli cells, which promote differentiation of spermatogonia. It regulates acute HPA (hypothalamic–pituitary–adrenal axis) response under dominance challenge.[22] Androgen including testosterone enhances muscle growth. Testosterone also regulates the population of thromboxane A2 receptors on megakaryocytes and platelets and hence platelet aggregation in humans.[23][24]
Usually there will not be a specific treatment that will lead to the improvement of erectile dysfunction. However, there are treatments that will allow erections to happen and can be used to allow sexual activity to take place. There are three main types of treatments: non-invasive treatments such as tablet medicines and external devices (e.g. vacuum device); penile injections; or for men who have not had success with other treatments, surgery may be an option.
If a trial of oral therapy and withdrawal of offending medications do not restore erectile function or if a patient has medical or financial contraindications to pharmacologic therapy, most primary care practitioners should consider referring the patient to a specialist for additional evaluation and discussion of alternative treatment options. However, some primary care practitioners may recommend vacuum constriction devices.
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.
There is a dirty little secret about testosterone cream that almost no one knows, and I’m going to share it here. Please don’t abuse it. If you take a vanishingly small dose of testosterone cream and apply it to your labia and the vulva (or your partner’s), you will witness a form of vasodilation rarely seen no matter how good you are in bed. It has a profound local effect and will produce a night you won’t forget for years.
The mechanism of age related decreases in serum testosterone levels has also been the subject of investigation. Metabolic clearance declines with age but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels. Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced (Mulligan et al 1999, 2001). This implies that the reduced production may be caused by primary testicular failure but in fact these changes are not adequate to fully explain the fall in testosterone levels. There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved (Mulligan et al 1999). It therefore seems likely that there are changes in endogenous production of GnRH which underlie the changes in LH secretion and have a role in the age related decline in testosterone. Thus the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis. With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH (Ono et al 1988; Gallon et al 1989).
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In a prospective study from the Prostate Cancer Prevention Trial database, Thompson et al reported that men presenting with ED had a significantly higher chance of developing a cardiovascular event over a 7-year follow-up period. [55] The hazard ratio was 1.45, which is in the range of risk associated with current smoking or a family history of MI.
In a recent study of male workers, men with low testosterone levels had an increased chance of severe erectile dysfunction (Kratzik et al 2005), although such a link had not been found previously (Rhoden et al 2002). Certainly erectile dysfunction is considered part of the clinical syndrome of hypogonadism, and questions regarding erectile dysfunction form part of the clinical assessment of patients with hypogonadism (Morley et al 2000; Moore et al 2004).
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