Nelson Vergel
Founder, ExcelMale.com
DEHYDROEPIANDROSTERONE AS A TREATMENT FOR ERECTILE DYSFUNCTION
Several studies have reported decreased serum DHEAS levels in patients with ED and denoted that decreased secretions of DHEA and DHEAS are important risk factors for ED in aging men [41]. DHEA levels reach their peak in the third decade of age in men. The serum DHEAS levels were significantly lower in the younger patients with ED compared with non-ED patients. Diminished DHEAS levels, especially in young men with ED, may either be an etiologic factor for ED or a negative consequence of it. However, patients treated with DHEA had a statistically significant increase in all domains of the IIEF in contrast to the placebo group. Interestingly, the serum DHEAS levels increased significantly after sildenafil citrate treatment in the ED group (especially in patients younger than 50 years). Also, patient age was an important factor affecting the sildenafil citrate response [42].
The first clinical effects were reported after 8 weeks of DHEA treatment and a remarkable improvement in maintaining the erection after 16 weeks. Prostate volume, postvoid residual, prolactin and PSA were not significantly changed after DHEA therapy [34]. Despite the evidence that has questioned the validity of improvement in sexual function when treatment relied solely on DHEA administration [43], several previous studies had demonstrated the usefulness of DHEA in treating sexual dysfunction associated with testosterone or DHEA deficiency [34]. A nice explanation of that effect was demonstrated as both testosterone and DHEA are considered central neurosteroids and have been found to modulate endothelial function, which ultimately influence libido and penile erections [44]. Several studies on other organs support the protective role of DHEA and DHEAS i.e., reduction of vascular stenosis in heterotopic heart transplants [45]. Because there is also some experimental evidence for direct effects on the brain, the possibility of a central effect of DHEA might be evident. An interesting mechanism that could better define the role of DHEA in sexual performance is that administration of DHEA results in biosynthesis of active androgens by tissue targets without representation in the peripheral circulation [10].
Although experimental studies had demonstrated that DHEA has direct genomic and nongenomic effects on the vascular endothelium, however its clinical effect as a facilitator of penile erections is not evident [46]. Most of the literature had not confirmed the role of DHEA in the field of sexual medicines [43, 47]. Additionally, other studies questioned the concept of DHEA as a neurosteroid with a central putative effect on libido [48], although this hormone had been found to influence self-esteem and mood in younger individuals [49]. Furthermore, the evidence-based studies supporting an anti-aging, anti-inflammatory, antiatherosclerotic actions, and antidepressant effect of DHEA supplementation are often poor [50, 51] (Table 1).
Source
Several studies have reported decreased serum DHEAS levels in patients with ED and denoted that decreased secretions of DHEA and DHEAS are important risk factors for ED in aging men [41]. DHEA levels reach their peak in the third decade of age in men. The serum DHEAS levels were significantly lower in the younger patients with ED compared with non-ED patients. Diminished DHEAS levels, especially in young men with ED, may either be an etiologic factor for ED or a negative consequence of it. However, patients treated with DHEA had a statistically significant increase in all domains of the IIEF in contrast to the placebo group. Interestingly, the serum DHEAS levels increased significantly after sildenafil citrate treatment in the ED group (especially in patients younger than 50 years). Also, patient age was an important factor affecting the sildenafil citrate response [42].
The first clinical effects were reported after 8 weeks of DHEA treatment and a remarkable improvement in maintaining the erection after 16 weeks. Prostate volume, postvoid residual, prolactin and PSA were not significantly changed after DHEA therapy [34]. Despite the evidence that has questioned the validity of improvement in sexual function when treatment relied solely on DHEA administration [43], several previous studies had demonstrated the usefulness of DHEA in treating sexual dysfunction associated with testosterone or DHEA deficiency [34]. A nice explanation of that effect was demonstrated as both testosterone and DHEA are considered central neurosteroids and have been found to modulate endothelial function, which ultimately influence libido and penile erections [44]. Several studies on other organs support the protective role of DHEA and DHEAS i.e., reduction of vascular stenosis in heterotopic heart transplants [45]. Because there is also some experimental evidence for direct effects on the brain, the possibility of a central effect of DHEA might be evident. An interesting mechanism that could better define the role of DHEA in sexual performance is that administration of DHEA results in biosynthesis of active androgens by tissue targets without representation in the peripheral circulation [10].
Although experimental studies had demonstrated that DHEA has direct genomic and nongenomic effects on the vascular endothelium, however its clinical effect as a facilitator of penile erections is not evident [46]. Most of the literature had not confirmed the role of DHEA in the field of sexual medicines [43, 47]. Additionally, other studies questioned the concept of DHEA as a neurosteroid with a central putative effect on libido [48], although this hormone had been found to influence self-esteem and mood in younger individuals [49]. Furthermore, the evidence-based studies supporting an anti-aging, anti-inflammatory, antiatherosclerotic actions, and antidepressant effect of DHEA supplementation are often poor [50, 51] (Table 1).
Source
