It has been hypothesized that vitamin D and testosterone levels are associated, but the evidence remains unclear. We aimed to investigate the association between hypogonadism and vitamin D deficiency.

A retrospective analysis was performed on 471 men who visited for the first time with lower urinary tract symptoms (LUTS) (mean age 60.56 ± 10.79 years) at two medical centers between 2014 and 2018. Serum 25-hydroxyvitamin D [25(OH)D] and testosterone levels in morning samples were measured. 25(OH)D was classified as sufficiency (>30 ng/mL), insufficiency (30-20 ng/mL), and deficiency (<20 ng/mL). Testosterone was classified as hypogonadism (<300 ng/dL) and non-hypogonadism (≥300 ng/dL). The association between 25(OH)D and total testosterone (T), free testosterone (FT), bioavailable testosterone (BT), prostate volume(PV), uroflowmetry parameters (Maximum flow rate/voided volume/postvoid residual volume), the International Prostate Symptom Score (IPSS), the Overactive Bladder Symptom Score (OABSS), and the International Index of Erectile Function (IIEF)-5 was analyzed using t-tests, partial correlation analysis, and propensity score matching (1:2). The seasonal variation of 25(OH)D and testosterone was analyzed using one-way ANOVA.

The mean testosterone level and age of the hypogonadism group (n=88) were 2.3 ± 0.6 ng/dL and 60.0 ± 10.8 years, respectively. In the non-hypogonadism group (n=383), the mean values were 5.3 ± 1.8 ng/dL and 63.0 ± 10.3 years. The mean value of 25(OH)D was 20.6 ± 11.4 ng/mL in the hypogonadism group compared to 20.1 ± 8.5 ng/mL in the non-hypogonadism group (p=0.649). The distribution of 25(OH)D classifications also did not differ significantly between groups (hypogonadism: sufficiency=13 [14.8%], insufficiency=24 [27.3%], deficiency=51 [58.0%]; non-hypogonadism: sufficiency=52 [13.6%], insufficiency=124 [32.4%], deficiency=207 [54.3%], p=0.648). There was no significant difference in 25(OH)D levels even after propensity matching for age, BMI, diabetes, coronary heart disease, and cerebrovascular disease (p=0.811). 25(OH)D showed no association with T, FT, BT, PV, uroflowmetry parameters, IPSS, OABSS, or IIEF-5 total scores, even after adjusting for age in partial correlation analysis (p>0.05). In one-way ANOVA, 25(OH)D was significantly higher in summer than in winter (26.8 ± 12.5 ng/mL vs. 19.0 ± 8.6 ng/mL, p=0.02), whereas testosterone showed no seasonal variation.

We could not find a significant association between vitamin D deficiency and hypogonadism in older adult LUTS patients, even after adjusting for age, BMI, diabetes, coronary heart disease, and cerebrovascular disease. The relationship between vitamin D levels and sexual function, as well as the seasonal variation of testosterone, remains unclear. Further large and well-designed studies are needed to determine the association between vitamin D and testosterone levels in healthy individuals.