We found a trend towards increased risk of hypogonadism in men within the lowest 25(OH)D quintile (≤43.9 nmol/L). In conclusion, our data suggest that men with very high 25(OH)D levels (>102 nmol/L) might be at an increased risk of hypogonadism. Furthermore, we observed a trend towards increased risk of hypogonadism in men with very low vitamin D levels indicating a U-shaped association of vitamin D levels and hypogonadism. With respect to risk of male hypogonadism, our results suggest optimal serum 25(OH)D concentrations of 82-102 nmol/L.
This, in my opinion my explain why some guys do well on vitamin D, but when they overdo it they may in up in a crash. Me myself I felt some overall improvements, but I also had terribly low vitamin D although I try to get as much sun as possible.
" Thus, it can be concluded that vitamin D3 delays testicular senescence by regulating proliferation and apoptosis."
https://www.nature.com/articles/s41598-019-50679-y
“The testes of vit. D-deficient rats showed incomplete spermatogenesis and degenerative changes. Although interpretation is complicated by the intricate communication among testis cell types, these data suggest that the Sertoli cell is a primary site of action of 1,25(OH)2D in the testis. Moreover, these data indicate that 1,25(OH)2D receptor function in the testis relates to germ cell division/maturation, although this may be an indirect effect via the Sertoli cells.”
https://www.sciencedirect.com/science/article/abs/pii/0022473189901052
“Vitamin D may have a stimulatory role on androgen production in men”
https://www.sciencedirect.com/science/article/abs/pii/S0960076019305680
" Epidemiological data have shown that vitamin-D deficiency is also associated with erectile dysfunction. In this review, our aim is to interpret the mechanisms by which vitamin-D might regulate anatomy and physiology of penis. Evidence showed that vitamin-D is needed for an adequate erectile function"
- Vitamin-D and androgen receptors
An extra mechanism of VD on erectile function seems to function via binding to T receptors. Computer ( in silico ) modeling shows that besides activating the VDR, 1,25-D displays high affinity for some of the body’s other nuclear receptors. This suggests that when 1,25-D increases above its normal range, it binds the α/β thyroid, the glucocorticoid, and the T receptors, displacing their native ligands [53]. Marshall [54] showed the symmetry with which endogenous ligands exhibited very similar affinities across some members of the type 1 nuclear receptor family [54]. For example, 1,25-D docked into the VDR with a (nanomolar) Kd of 8.48, but also exhibited a Kd of 8.05 into the T receptor.
VD is positively associated with T, exhibits a concordant seasonal changeability [47], elevates when T was supplemented in hypogonadism [48]. Surprisingly, the reverse situation is also true, suggesting that VD supplementation might increase T levels [49]. In a clinical randomized controlled trial, which is the first on this topic in literature, Pilz et al [49] investigated the effect of VD supplementation on androgens in men. The results were significant and the researchers observed that overweight men with VDD had a clinically meaningful increase in serum T levels after VD supplementation for 1 year [49]. Recently, it was also demonstrated that VD supplementation improves T levels, metabolic syndrome and erectile function in middle-aged VD deficient men [8]. Canguven