Statins improve ED

madman

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Erectile dysfunction and statins: The assorted view of preponderance
Hayder M. Al-Kuraishy, Ali I. Al-Gareeb, Thabat J. Al-Maiahy




ABSTRACT

Objective
: To explore the association between statin therapy and the risk of erectile dysfunction by literature review.

Methods: We conducted diversities of search strategies including electronic database searches of MEDLINE, Scopus, Pubmed, and Web of Science using MeSH terms, keywords, and title words during the search. Reference lists of identified and public articles were reviewed. In addition, only English articles were considered and case reports were not concerned in the review. The key features of recognized applicable search studies were considered and the conclusions were summarized in a narrative review.

Results: Different studies gave a consensus that erectile dysfunction was regarded as an early sign of silent cardiovascular disorder and hidden atherosclerosis. Different studies reported that statins might induce erectile dysfunction through induction of peripheral neuropathy, cognitive deficits, and reduction of circulating testosterone. However, most recent studies illustrated that statins led to a significant improvement in erectile function and sexual health in men age over forty years. Atorvastatin advanced endothelial nitric oxide concentrations through activation and upregulation of endothelial nitric oxide synthase and rescued phosphodiesterase-5 inhibitors non-responders since nitric oxide and cyclic guanosine monophosphate increased penile blood flow and improved erectile function.

Conclusions: According to the assorted view of preponderance, statins improved erectile dysfunction is more dominant than statins induced erectile dysfunction. Therefore, statins regardless of their property improve erectile dysfunction through amelioration of penile endothelial dysfunction, and penile neuronal reflexes that are inter-related during sexual excitation and penile erection.




1. Introduction

Erectile dysfunction is defined as a failure or inability to maintain a penile erection for suitable pleasure during sexual intercourse[1]. It affects more than 150 million worldwide, which may be doubled by 2025. Erectile dysfunction is often linked with different cardiometabolic disorders such as type 2 diabetes mellitus (T2DM), hypertension, ischemic heart disease, and hypogonadism. It has been reported that erectile dysfunction is associated with ischemic heart disease since erectile dysfunction proceeds and heralds the onset of ischemic heart disease[2].

The prevalence of erectile dysfunction is surprisingly high, affecting 40% of the population. This prevalence is affected by population characteristics and methods used for the assessment of erectile dysfunction. Since single question may be used for assessment of erectile function while other trials used more sophisticated and validated questionnaires[3]. Although erectile dysfunction affects sexual and mental health, the rates of consultation for erectile dysfunction remain low and not all patients respond to the phosphodiesterase inhibitors[4].

Vasculogenic erectile dysfunction is related to different risk factors including T2DM, hypertension, smoking, and dyslipidemia. Moreover, the presence of erectile dysfunction indicates the underlying cardiovascular disorders and complications; thus, assessment of erectile function should be part of the evaluation of hypertensive patients mainly those over 50 years[5]. Medical literature and different epidemiological trials illustrated that age is strongly linked to erectile dysfunction. Also, modifiable risk factors such as smoking, sedentary life, and dyslipidemia are regarded as second main causes of erectile dysfunction which could be reversed[6]

Dyslipidemia is strongly associated with erectile dysfunction since every mmol/L increase in serum cholesterol is associated with a 32% increase in erectile dysfunction. Therefore, hyperlipidemia is correlated with erectile dysfunction due to the development of endothelial dysfunction through the impairment of nitric oxide (NO) synthesis and release[7].

Statins that are 3-hydroxy-3-methylglutaryl-coenzyme A (HMGCoA) reductase inhibitors are the first-line in the treatment of hyperlipidemia and major cardiac events regardless of lipid profile due to pleiotropic properties. Statins improve endothelial function prior to the improvement of total cholesterol[8,9]. However, there are conflicting reports regarding the impact of statins on sexual function. The negative effects of many drugs on male sexual function are well-known. However, the relationship between statins and male sexual function is not clear. A number of studies have hypothesized that statins were associated with erectile dysfunction; whereas, some others advocated that statins improve erectile dysfunction[10]. Therefore, the objective of the present study was to elucidate the potential effect of statins therapy on erectile dysfunction regarding the assorted view of preponderance.





3. Statins induced-erectile dysfunction
3.1. Statins induced-hormonal changes
3.2. Statins induced-neuropathy
3.3. Statins induced-cognitive impairment


4. Statins improved-erectile dysfunction




5. Conclusion

In this review, there are conflicting findings regarding the potential effect of statins therapy on erectile dysfunction.
Some studies implicate statins as a causative cause of erectile dysfunction, while most of the studies report the beneficial effect of statins in the prevention of erectile dysfunction. Therefore, this study concludes that statins, regardless of their property, improve erectile dysfunction through amelioration of penile endothelial dysfunction, penile neuronal reflexes, and antidepressant effects which are interrelated during sexual excitation and penile erection. For these reasons, the assorted view of preponderance confirms that statins improve erectile dysfunction mainly through the enhancement of erectile endothelial functions.
 

madman

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In reality, testosterone plays an essential role in the regulation of endothelial and vascular functions. Testosterone prevents vascular remodeling through inhibition of vascular inflammation and oxidative stress. Physiological testosterone leads to vasodilatation through activation of NO production and by increasing endothelial nitric oxide synthase (eNOS) expression, these effects are partly mediated by the endothelial androgen receptors[23]. Therefore, low testosterone due to different reasons leads to endothelial dysfunction and induction of oxidative stress. So, testosterone replacement therapy inhibits oxidative stress, vascular inflammations, and intima-media thickness in men patients with ischemic heart disease[24]. Therefore, testosterone is very important for erectile function since it increases neuronal activations toward the penis stimulates the releases of oxytocin and dopamine from the brain's medial pre-optic area (which are involved in the sexual arousal), and preservation of penile blood flow through activation of NO synthase[25]. Therefore, theoretically, a reduction of testosterone levels by statin therapy leads to penile endothelial dysfunction and decreases the responsiveness during sexual excitation which eventually causes erectile dysfunction. Although it was statistically non-significant, hypoandrogenemia may be a reasonable cause. Rearrangement of the two different types of fibers in the penis may be associated with a decrease in the intracavernosal pressure. However, further comprehensive experimental studies investigating the effect of cavernosal collagen and elastic fibers on erection with longer follow-up periods are needed to judge this hypothesis[26]
 

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