Foresta, C., Calogero, A. E., Lombardo, F., Lenzi, A., & Ferlin, A. (2015). Late-onset hypogonadism: beyond testosterone. Asian journal of andrology. https://doi.org/10.4103/1008-682x.135985
Foresta C, Calogero AE, Lombardo F, Lenzi A, Ferlin A. Late-onset hypogonadism: beyond testosterone. Asian journal of andrology. 2015. doi:10.4103/1008-682x.135985
Foresta, Carlo, et al. "Late-onset hypogonadism: beyond testosterone." Asian journal of andrology, 2015.
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Calcidiol raised vitamin D in hypogonadal men, cholecalciferol did not
One form of vitamin D worked. The other did not. A randomized study followed 66 men seen for infertility over three months. Calcidiol raised the men's vitamin D and eased a related hormone, in men with mild low testosterone and in men with marked low testosterone alike. Cholecalciferol, vitamin D's precursor form, made no difference.
Key Findings
The study enrolled 66 men with low 25-hydroxyvitamin D: 26 with classic hypogonadism and 40 with subclinical hypogonadism.
Randomization gave 20 men cholecalciferol and 46 men calcidiol. Researchers checked blood levels after 3 months of therapy.
Calcidiol significantly increased 25-hydroxyvitamin D and significantly decreased parathyroid hormone in both groups of men with hypogonadism (n = 16 and n = 30).
Cholecalciferol did not modify 25-hydroxyvitamin D or parathyroid hormone levels in these men.
Testosterone levels showed no effect after vitamin D supplementation (data not shown).
Interpretation
This randomized study gave men seen for infertility one of two forms of vitamin D. Calcidiol raised the men's vitamin D and eased a second hormone tied to bone health, whether their low testosterone was mild or marked. Cholecalciferol moved neither marker. Testosterone itself stayed steady on both forms. The findings support larger trials of calcidiol as a vitamin D treatment in men seen for fertility care.
RRM Context
Restorative reproductive medicine evaluates both partners together and searches for a cause first. A single testosterone number can miss mild testicular trouble. The authors also check a second hormone and vitamin D status. These men came in through an infertility workup, so their hormones sit inside the couple's shared care from the start.
Our editorial summary of this paper, not the article's abstract.
Abstract
Late-onset hypogonadism is defined as a combination of low testosterone (T) levels and typical symptoms and signs. A major area of uncertainty is whether T concentrations are always really sufficient to fully reflect Leydig cell (dys)function. Mild testicular alteration could be diagnosed only by additional biochemical markers, such as luteinizing hormone (LH) and 25-hydroxyvitamin D levels. These markers help in identifying the so-called "subclinical" hypogonadism (normal T, high LH levels). Patients with hypogonadism have frequently low levels of 25-hydroxyvitamin D due to impairment of the hydroxylating enzyme CYP2R1 in the testis. However, no data have been published dealing with the best treatment option (cholecalciferol - the Vitamin D precursor, or calcidiol - 25-hydroxylated form of Vitamin D) in these patients. We studied 66 patients with classic hypogonadism (total T [TT] <12 nmol l-1 , LH ≥ 8 IU l-1 ) (n = 26) and subclinical hypogonadism (TT ≥ 12 nmol l-1 , LH ≥ 8 IU l-1 ) (n = 40) and low 25-hydroxyvitamin D (<50 nmol l-1 ). Subjects received cholecalciferol (5000 IU per week) (n = 20) or calcidiol (4000 IU per week) (n = 46), and 25-hydroxyvitamin D and parathyroid hormone (PTH) were evaluated after 3 months of therapy. Supplementation with calcidiol significantly increased 25-hydroxyvitamin D and significantly decreased PTH levels in both groups of men with hypogonadism (primary, n = 16 and subclinical, n = 30), whereas supplementation with cholecalciferol did not modify their levels. This study shows for the first time that the administration of the 25-hydroxylated form of Vitamin D (calcidiol), and not the administration of the precursor cholecalciferol, restores 25-hydroxyvitamin D levels in subjects with hypogonadism.
