https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712861/
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Boron has been shown to increase serum levels of 25-hydroxyvitamin D3 (25[OH]D3) in animal studies and of vitamin D–deficient individuals in human studies. In a clinical trial in which middle-aged men and women (n = 15) were placed on a low-boron diet, which was also marginal in magnesium and copper status, for 63 days (0.23 mg B/2000 kcal), 25(OH)D3 rose significantly after boron supplementation (3 mg/d as sodium borate) for an additional 49 days. Levels of 25(OH)D3 rose from an average of 44.9 nM after the 63 days of boron deprivation to 62.4 nM after the 49 days of boron repletion, a 39% increase.
Similar results were seen in an open pilot study of middle-aged individuals (n = 13) predetermined to be vitamin D deficient (serum 25[OH]D3 < 12 ng/mL). Levels of 25(OH)D3 were studied during boron supplementation of 6 mg/d for 60 days using calcium fructoborate, Ca([C6H10O6]2B)2·4H2O, a boron-containing complex that occurs naturally in fruit. The study took place in Serbia with supplementation beginning in October and concluding by January; in other words, the study occurred during the fall transition to winter, a time when vitamin-D status would be expected to worsen. Yet, with boron supplementation, 25(OH)D3 levels rose significantly, with an average rise of 20%.
How does boron exert its hormonal effects? In sum, boron increases the biological half-life and bioavailability of E2 and vitamin D.
Boron Increases Half-life and Bioavailability of Sex Hormones and Vitamin D
Boron’s beneficial effects on bone metabolism are due in part to the roles it plays in both producing E2 and in increasing its biological half-life and that of vitamin D. Regarding 17β-estradiol, the simplest and preferred pathway for its production is reduction of the keto group of estrone by a tetrahydroborate salt, potassium borohydride.
Regarding vitamin D, Miljkovic et al proposed in an excellent paper in Medical Hypotheses that boron suppresses the activity of 24-hydroxylase, the microsomal enzyme primarily responsible for catabolism of 25(OH)D3. A number of recent papers, which are discussed in the following text, have provided evidence to support this hypothesis.
The hypothesis by Milijkovic et al also accounts for boron’s well-recognized upregulation of 17β-estradiol levels in women, including postmenopausal women receiving hormone replacement therapy, because catabolism of 17β-estradiol is also achieved by microsomal enzymes catalyzing vicinal hydroxylations (eg, 24-hydroxylase). This suggests a more general hypothesis: Nutritional boron can inhibit a range of microsomal enzymes that insert hydroxyl groups vicinal to existing hydroxyls in steroids, which include enzymes that catabolize 17β-estradiol, 25(OH)D3, and 1α,25-dihydroxyvitamin D3 (1α,25[OH]2D3). As noted by Miljkovic et al:
Boron readily forms covalent complexes with cis-vicinal dihydroxy compounds. Thus, it is conceivable that it can form such a complex with 24,25-dihydroxyvitamin D, the end product of the reaction of 25(OH)D3 with 24-hydroxylase. This postulated complex might either act as a competitive inhibitor of the 24-hydroxylase reaction, or alternatively, perhaps could act to down-regulate expression of the enzyme. Another possibility is that boron is a direct inhibitor of the enzyme at very modest concentrations; indeed, boron can inhibit numerous enzymes …
Therefore, boron’s beneficial hormonal effects are likely to be a result of its general impact on vicinal hydroxylations of steroids.
