Boron is an ultratrace element that is present in the human body at concentrations of approximately 0.5mg/kg (with a total body boron content of approximately 3-4mg), and it is found primarily in the bone, the teeth, and the nails, where it is incorporated into the hydroxyapatite crystal lattice in place of the carbonate or the phosphate groups. The biological functions of boron are less well characterised than those of the other trace elements, but the evidence from animal studies and from human clinical trials suggests that boron is a critical regulator of the vitamin D metabolism, of the bone cell function, and of the inflammatory response — and that its deficiency produces the bone loss, the osteoporosis, and the increased fracture risk that are the hallmark of the boron deficiency, particularly in postmenopausal women who are already at increased risk of osteoporosis because of the oestrogen deficiency that follows the menopause. The primary dietary sources of boron are the fruits (particularly the avocado, the banana, the raisins, and the grapes), the vegetables (particularly the leafy green vegetables, the legumes, and the root vegetables), the nuts (particularly the almonds and the peanuts), and the whole grains — and the dietary boron intake in the typical Western diet is approximately 1-3mg daily, which is generally adequate for the prevention of the boron deficiency symptoms.
Boron and the Vitamin D Metabolism
The most important biological function of boron is its role as a regulator of the vitamin D metabolism — specifically, boron is required for the conversion of the vitamin D3 (cholecalciferol) to the 25-hydroxyvitamin D3 (calcidiol) in the liver and for the subsequent conversion of the calcidiol to the 1,25-dihydroxyvitamin D3 (calcitriol, the hormonally active form) in the kidney. The enzymes that catalyse these conversions — the vitamin D-25-hydroxylase and the 1-alpha-hydroxylase — are both cytochrome P450 enzymes that require the P450 enzyme system for their activity, and boron has been shown to stimulate the activity of these enzymes and to increase the production of the calcitriol in the kidney cells. When boron is deficient, the conversion of the vitamin D3 to the calcitriol is impaired, the calcitriol levels fall, and the calcium absorption from the gut is reduced — leading to the bone loss, the hypocalcaemia, and the secondary hyperparathyroidism that are the clinical manifestations of the boron deficiency. This boron-vitamin D interaction is one of the most important and least appreciated aspects of the bone health nutrition, and it explains why boron supplementation has been shown to improve the bone density in postmenopausal women who are vitamin D deficient.
The clinical importance of the boron-vitamin D interaction for the bone health is underscored by the observation that boron supplementation reduces the urinary calcium excretion and increases the serum calcitriol levels in postmenopausal women — indicating that boron reduces the bone resorption by improving the calcium economy through the stimulation of the vitamin D metabolism. A study in 12 postmenopausal women found that boron supplementation at 3mg daily for 8 weeks reduced the urinary calcium excretion by 25% and increased the serum calcitriol levels by 50%, without any change in the serum calcium or parathyroid hormone levels — suggesting that boron improves the calcium economy through a vitamin D-dependent mechanism that does not involve the parathyroid hormone. These findings are consistent with the hypothesis that boron is an essential cofactor for the vitamin D metabolism, and that boron deficiency contributes to the osteoporosis of the postmenopausal women who are already at increased risk because of the oestrogen deficiency.
Boron and the Bone Cell Function
Beyond its effects on the vitamin D metabolism, boron also has direct effects on the bone cells — it has been shown to stimulate the proliferation and the differentiation of the osteoblasts (the bone-forming cells) and to inhibit the formation and the activity of the osteoclasts (the bone-resorbing cells). The mechanism of these effects involves the boron-dependent modulation of the NF-kappaB signalling pathway — boron inhibits the activation of the NF-kappaB transcription factor, which is the primary regulator of the osteoclast differentiation and of the osteoclast-mediated bone resorption. When NF-kappaB is inhibited by boron, the osteoclast differentiation is reduced, the bone resorption is suppressed, and the bone mass is maintained — this is the primary mechanism of the boron-induced suppression of the bone resorption and of the boron-induced improvement in the bone density in postmenopausal women with osteoporosis.
Practical Application
For general boron supplementation, the evidence-based approach is to supplement with 3-9mg of boron daily (as the boric acid or as the sodium borate form), which is the dose range that has been used in the majority of the clinical trials of boron supplementation for the bone health. The safe upper intake level for boron is 20mg daily for adults (above which the boron can produce the gastrointestinal symptoms, the skin eruptions, and the renal dysfunction). The boron is particularly effective for the postmenopausal women who are vitamin D deficient and who have the osteoporosis that is associated with the oestrogen deficiency — in these women, the boron supplementation at 3-6mg daily improves the vitamin D metabolism, reduces the bone resorption, and increases the bone density. For comprehensive bone health support, boron pairs well with vitamin D3 (which is required for the calcium absorption and for the bone mineralisation), with vitamin K2 (which directs the calcium to the bone and away from the soft tissues by activating the osteocalcin and the matrix Gla protein), with the calcium (which is the primary mineral component of the bone), and with the strontium (which is a bone-seeking element that has been shown to reduce the fracture risk in postmenopausal women with osteoporosis).
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