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Health Protocols

Erectile Dysfunction

Causes Of Erectile Dysfunction


Achieving an erection requires coordination between many body systems, so there are several ways the process can go wrong (Ritchie 2011). The cause of erectile dysfunction can be biological, psychological, or both (Heidelbaugh 2010).
Biological causes of erectile dysfunction include hormonal, vascular, and neurologic disorders (McVary 2007).

  • Cardiovascular disease accounts for up to 80% of erectile dysfunction cases (Paroni 2012). Atherosclerosis, the most common vascular disease, impedes blood flow to the penis (Ginsberg 2010). Cardiovascular disease and high blood pressure contribute to endothelial dysfunction, which is the most common contributing mechanism to erectile dysfunction overall (Kolodny 2011; Sadeghi-Nejad 2007).
  • Age-related decline in hormone levels (eg, testosterone and dehydroepiandrosterone [DHEA]) is associated with erectile dysfunction (Morales 2011; Kolodny 2011; Mackay 2004). (See “Erectile Dysfunction and Hormones”, below.)
  • Diabetes can interfere with penile blood flow and damage nerves in the penis, leading to erectile dysfunction (Ginsberg 2010).
  • Age-related decline in penile elastic fibers also contributes to erectile dysfunction (Sadeghi-Nejad 2007).
  • Medication-induced erectile dysfunction can occur from several drugs including antihistamines, benzodiazepines, tricyclic antidepressants, and others (Heidelbaugh 2010; Fortney 2012).

Psychological causes such as depression, anxiety, stress, low self-esteem, and various other conditions can contribute to erectile dysfunction as well (Ginsberg 2010; NIH 1992). Psychological problems are often to blame for intermittent erectile dysfunction among young men, while older men with erectile dysfunction frequently have a mixture of both psychological and biological causes (Sadeghi-Nejad 2007).

The Link Between Erectile Dysfunction and Cardiovascular Disease

It is important for men suffering from erectile dysfunction to discuss their symptoms with their physician (Hackett 2009). In addition to recommending an effective treatment for the primary complaint of erectile dysfunction, physicians should also screen for cardiovascular disease (CVD) (Nehra 2012; Sadeghi-Nejad 2007; NIH 1992). This is because erectile dysfunction and CVD share similar risk factors, including aging, hypertension, obesity, and a sedentary lifestyle (Hannan 2009; Ewane 2012; Nunes 2012). Furthermore, erectile dysfunction itself has been shown to independently increase the risk of CVD, stroke, and all-cause death (Kolodny 2011; Heidelbaugh 2010).
Since erectile dysfunction often precedes some cardiovascular events by 2-5 years (Nehra 2012), erectile dysfunction is viewed as a potential early warning sign for CVD (Meldrum 2011). Early detection is critical since CVD is a major cause of disability and death (Ewane 2012).
The abbreviation “ED” can help make this issue easy to understand and remember. For instance, “ED” stands not only for “Erectile Dysfunction”, but also “Endothelial Dysfunction”, “Exercise & Diet” (for prevention), and “Early Detection” of risk factors, which can help avoid “Early Death” due to CVD(Jackson 2006). 

Erectile Dysfunction and Hormones


Many facets of male sexual function depend upon male hormones (androgens) such as testosterone (Morales 2011). Testosterone helps support the production of nitric oxide (Kolodny 2011), but also helps maintain libido (Morales 2011). As men age their androgen levels decline. Low androgen levels are observed in as many as one-third of men with erectile dysfunction (Burnett 2011).

Androgen deficiency can directly contribute to erectile dysfunction by negatively impacting penile blood flow and increasing breakdown of cGMP (Martin 2012; Heidelbaugh 2010). Low testosterone is the most common reason for failure to respond to Phosphodiesterase-5 (PDE5) inhibitors (eg, Viagra® and Cialis®), which are drugs that slow the breakdown of cGMP (Hackett 2012).

Clinical guidelines recommend hormone level testing for aging men who suffer from sexual dysfunction. Maintaining optimal testosterone levels is not only important for sexual function, but also for cardiovascular health (Cattabiani 2012). Moreover, low androgen levels are associated with depression, osteoporosis, insulin resistance, increased fat mass, decreased lean body mass, and cognitive dysfunction (Morales 2011; Kolodny 2011). Life Extension recommends that ageing men target optimal free testosterone blood levels of 20 – 25 pg/mL and total testosterone levels of 700 – 900 ng/dL.

Testosterone restoration can lead to improved erectile function and libido in men with low androgen levels (Heidelbaugh 2010). In fact, when PDE5 inhibitors fail, the addition of testosterone therapy is associated with substantial improvement in erectile function among men with low testosterone and may eliminate the need for PDE5 inhibitors altogether (Heidelbaugh 2010; Kolodny 2011; Morales 2011; Hackett 2012). Refer to Life Extension’s Male Hormone Restoration protocol for more information. 


Dehydroepiandrosterone (DHEA) is a precursor to testosterone (Oloyo 2011; Maggi 2012). As with testosterone, aging is associated with decreased levels of DHEA. Circulating levels of DHEA can decline by up to 80% from age 25 to 80 (Maggi 2012). Low DHEA levels have been linked to erectile dysfunction (Mackay 2004; Feldman 1994). Studies have shown that oral DHEA supplementation may improve sexual performance, as measured by erectile function, orgasmic function, sexual desire, intercourse satisfaction, and overall satisfaction in some men (Reiter 1999; Reiter 2001). Life Extension recommends an optimal target blood level for DHEA-sulfate of 350 – 490 µg/dL.

Aromatase Inhibitors, Testosterone Restoration, and Testosterone/ Estrogen Balance

Physicians versed in male hormone restoration know that exogenous administration of testosterone may increase estrogen (estradiol) levels in aging men, in particular aging men with significant amounts of visceral fat. The conversion of testosterone into estrogen is called aromatization and is mediated by an enzyme called aromatase (Traish 2007). Aromatase inhibitors (eg, anastrozole [Arimidex®]) are drugs that inhibit the activity of the aromatase enzyme, thereby reducing the amount of testosterone converted into estradiol.

When used concurrently with testosterone supplementation, aromatase inhibitors allow testosterone levels to rise without being converted into excess estrogen. Reports suggest that aromatase inhibitor therapy can improve sexual function in men (Traish 2007).

Maintaining healthy testosterone/estrogen balance has other important implications for aging males. For example, in a study among men with heart failure, both low and high estradiol levels were associated with significantly increased chances of death compared to “balanced” levels (Jankowska 2009). More about estrogen/testosterone balance in men is available in the Life Extension Magazine article entitled “Why Estrogen Balance is Critical to Aging Men”.
Life Extension suggests an optimal estrogen level (measured as estradiol) of 20 – 30 pg/mL for men.