Prostate Restored
Prostate Restored
Photo: Hatice Noğman
Jorde et al. showed that supplementation with even high-dose vitamin D (20,000–40,000 IU/week for 6–12 months) does not lead to an increase in serum testosterone levels in healthy men.
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Read More »Vitamin D deficiency is becoming a public health problem in all age groups in developing and developed countries1. From an evolutionary point of view, vitamin D is one of the oldest biologically active compounds. It has had various metabolic functions throughout the history of the species’ development, in different cells. This is echoed by the presence of its receptors in many tissues, organs, and systems, such as the skeletal muscles2, the thyroid gland3, the cardiovascular system4, the immune system5, and the reproductive system6. Vitamin D is not actually an amine (as the name might imply), and its molecule is cyclopentanoperhydrophenanthrene, with a broken B ring. The biological action of vitamin D takes place in cells via specific receptors and genomic and extragenic mechanisms7. Vitamin D is assumed to affect the function of approximately 3% of the human genome by modulating tissue metabolism8. Vitamin D has been suggested to play a role in sex steroid production, based on the evidence of the expression of vitamin D receptors (VDR) and vitamin D metabolizing enzymes, which are simultaneously expressed in Leydig cells and also in Sertoli cells, germ cells, spermatozoa and in the epithelial cells lining the male reproductive tract6,9. Testosterone production, by the Leydig cells that reside in the interstitial compartment, is under strict control of LH, which induces steroidogenesis by increasing cyclic AMP production and the intracellular concentration of calcium ions (Ca2+) in Leydig cells and 1α,25-dihydroxyvitamin D might exert an influence by modulating this calcium-dependent LH response10. A possible mechanism for the effect of vitamin D on testosterone production might be indirectly hypothesized from the results of an in vivo study in vitamin D-depleted and vitamin D-repleted chickens, investigating on the testis expression of calbindin-D28K, a cytosolic calcium-binding protein involved in the regulation of intracellular calcium homeostasis, and proposed to be involved in testis hormone production in rats6. The active biological form of vitamin D (known as calcitriol) is synthesized starting in the skin, with the initial synthesis of pre-vitamin D 3 through a nonenzymatic reaction initialized by UV light, using 7-dehydrocholesterol7. As a part of vitamin D synthesis, human skin also expresses genes which encode enzymes participating in sequential cholesterol metabolism leading to pregnenolone and to corticosteroids. Androgen production, activation and metabolism also occurs in the skin, acting as an important site for the entire process. These molecules are involved in intra-, auto- or paracrine fashion to adjust local homeostasis. The skin can produce signals to induce rapid (neural) or slow (humoral or immune) effects at the local and systemic levels. These local and systemic responses are coordinated as mediated by the skin neuroendocrine system, employing local equivalents of the hypothalamo-pituitary-adrenal axis (HPA)11,12. It has been proved that, in response to a variety of stressors, skin can produce numerous hormonal elements which are expressed in systemic responses to stressors in the environment. Furthermore, it has been shown that the key corticosteroid synthesis enzymes resulting in dermal corticosterone and cortisol production are expressed in the skin13. Human exposure to sunlight led to increased vitamin D serum levels, UVR-mediated central HPA axis activation may be used as a rational basis for phototherapy in systemic autoimmune disorders, as well as different pathologies12,13,14. Vitamin D exhibits features of endocrine action in the regulation of phosphate and calcium and parathormone metabolism, whereas it shows signs of an auto-, para- or juxtacrine signalling molecule in the remainder of its biological effects. With these mechanisms, it can affect the function of many cells, tissues, and systems, including Leydig cells15, which are the main source of testosterone in the male body.
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Learn More »It should be emphasised that the influence of vitamin D (mainly auto- and paracrine) is usually local and that studying them requires tissue analysis. The local effects of this type are generally not discernible at the blood serum level (they are not endocrine in the classic sense, and therefore do not affect the entire organism). Exceptions may include situations where there is a high level in a specific substrate or a specific tissue, such as adipose tissue. Testosterone is the primary androgenic–anabolic hormone in the male body, the role of which is well known and unquestioned. Vitamin D, on the other hand, is receiving increased interest and is the subject of numerous studies with inconclusive results. This raises the question of whether vitamin D levels can modulate testosterone levels in men, and thus the functioning of the hypothalamic–pituitary–gonadal axis (HPA). The answer is currently unknown. The aim of our study was to evaluate the effects of different 25(OH)D levels (deficient and insufficient) on the functioning of the HPA, i.e. on the levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), total testosterone (TT), free testosterone (FT), bioavailable testosterone (BT), and sex hormone binding globulin (SHBG) levels in young, healthy men.
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