Vitamin D deficiency is independently associated with greater prevalence of erectile dysfunction: The National Health and Nutrition Examination Survey (NHANES) 2001–2004

Abstract

Background and Aims Erectile dysfunction (ED) and atherosclerotic cardiovascular disease (ASCVD) share many common risk factors, and vascular ED is a marker for increased ASCVD risk. Low 25-hydroxyvitamin D [25(OH)D] concentrations have been associated with increased ASCVD risk, but less is known regarding the relationship of low 25(OH)D with ED. We determined whether 25(OH)D deficiency is associated with ED independent of ASCVD risk factors. Methods We performed cross-sectional analyses of 3,390 men aged ≥20 years free of ASCVD who participated in NHANES 2001-2004. Serum 25(OH)D was measured by the DiaSorin radioimmunoassay; deficiency was defined as levels <20 ng/mL (<50 nmol/L). Self-reported ED, assessed by a single validated question, was defined as men who reported being “never” or “sometimes able” to maintain an erection. We assessed the relationship between 25(OH)D deficiency and ED prevalence using adjusted Poisson regression methods. Results After accounting for NHANES sampling, the weighted prevalence of 25(OH)D deficiency and of ED were 30% and 15.2%, respectively. 25(OH)D levels were lower in men with vs. those without ED (mean 22.8 vs 24.3 ng/mL, respectively; p=0.0005). After adjusting for lifestyle variables, comorbidities, and medication use, men with 25(OH)D deficiency had a higher prevalence of ED compared to those with levels ≥30 ng/ml (Prevalence Ratio 1.30, 95% CI 1.08-1.57). Conclusion In this cross-sectional analysis of a representative sample of U.S. men, vitamin D deficiency was associated with an increased prevalence of ED independent of ASCVD risk factors. Additional research is needed to evaluate whether treating vitamin D deficiency improves erectile function.

The role of vitamin D supplementation on erectile function

“…[31] An increased risk for prevalent ED was seen for deficient levels of 25(OH)D below 20 ng/mL, while prevalence of ED decreases when VD levels are over 35 ng/mL. [9] The researchers of the latter study restricted their analysis to the 562 men (among 3,390 men) and found even stronger association between VD status and ED. [9] Unfortunately, the available literature evaluating VD supplementation and its relationship to cardiovascular health are limited in number.…”

“…[13] Vitamin D deficiency is one of several conditions that is associated with increased CV disease. [9,14] Research in The United States has shown that low serum VD levels are associated with a higher prevalence of peripheral arterial disease in the general population. [30] Database information of more than 7,000 VD deficient patients showed an association between VDD, many CV disease states, including hypertension, coronary artery disease, and ASCV risk factors, such as hypertension, diabetes mellitus (DM), and hyperlipidemia.…”

“…According to a cross-sectional analysis of 3,390 men aged >20 years, free of ASCV disease, VDD was associated with an increased prevalence of ED. [9] Normal levels of VD [25(OH)D] range between 30-80 ng/mL; and mild to moderate, and severe deficiencies are typically observed when VD levels drop to21 to 29 ng/mL, and <20 ng/mL, respectively. [31] An increased risk for prevalent ED was seen for deficient levels of 25(OH)D below 20 ng/mL, while prevalence of ED decreases when VD levels are over 35 ng/mL.…”

“…Strikingly, over 3,000 genes are responsive to VD [7] and its biological effects are mediated through binding to the VD receptor and inducing either genomic or non-genomic downstream effects (Figure 1). [4,5,[8][9][10] Once bound with VD, the VD-receptor moiety translocates from the plasma membrane to the nucleus where it transcriptionally activates genes via the VD response element, thereby affecting transcription of other genes. [8] When a man is sexually stimulated, neuronal nitric oxide (NO) synthase is triggered, inducing a smooth muscle dilatory effect of NO, which is then, amplified by the release of endothelial NO synthase (eNOS) and endothelial stimulated release of additional NO.…”

“…[14] Although there are many links between ED, ASCV disease and VD, to date, there are no prospective studies evaluating VD supplementation in patients with ED. [9] The questions might be asked "What is the connection between "VD and ED?" and "Could VD supplementation offer further advantage in ED treatment?…”