Boron is obtained by eating a diet rich in fruits, vegetables, nuts and legumes. The daily intake has been estimated between 0.5 and 40 mg per day. Large amounts of boron are well tolerated, while consistent signs of deficiency include depressed growth and reductions in some blood parameters, especially steroid hormone concentrations. Through its effect on steroid hormones and interaction with mineral metabolism, boron may be involved in a number of clinical conditions, such as arthritis or osteoporosis. Numerous studies suggest that boron interacts with other nutrients and plays a regulatory role in mineral metabolism, and subsequently bone metabolism. Although the mechanism of action has not been defined, it can be mediated by increasing the concentration of steroid hormones such as testosterone and beta-estradiol.
In animals, the need for boron was improved when responding to nutritional stress that adversely affected calcium metabolism, including magnesium deficiency. A combined deficiency of boron and magnesium causes changes in the animals’ bones. In two human studies, boron deprivation caused changes in variables associated with calcium metabolism in a way that could be interpreted as detrimental to bone formation and maintenance; these changes were apparently enhanced by low dietary magnesium. Alterations caused by boron deprivation included depressed plasma calcium and calcitonin, as well as increased urinary calcium excretion. Because boron and/or magnesium deprivation cause changes similar to those seen in osteoporosis and postmenopausal women, these elements are apparently required to optimize calcium metabolism. They are therefore needed to prevent the excessive bone loss that often occurs in postmenopausal women and older men.
Increasing dietary boron intake from 0.25 to 3.25 mg/day has been reported to increase plasma estradiol and testosterone and decrease urinary calcium excretion in postmenopausal women. Consequently, it is thought that the higher level of boron intake could reduce bone loss associated with menopause and loss of ovarian function. Additionally, women on a low-boron diet appeared to experience hyper-absorption of calcium. Nutritional intakes of boron have been shown to reduce the negative consequences of vitamin D deficiency in rodents. Pilot clinical studies suggest that this effect could be partially mediated by an increase in serum vitamin D. An impact of boron on vitamin D is potentially beneficial in light of the fact that many individuals’ vitamin D is in short supply during the winter; and traditional supplemental doses of this vitamin are often too low to correct this problem.
There is clinical evidence, very small per recruited cohort, that proves dietary supplementation improves estrogen and vitamin D levels in postmenopausal women. It seems that boron, among the mechanisms connected to vitamin D, can prevent its enzymatic degradation but how this happens is still unknown. In addition to estrogens, a direct effect of borate ions on bone cells cannot be excluded. Boron regulates the production of RUNX2, a protein essential for osteoblastic differentiation, bone formation and its maintenance. It is a transcription factor that works cooperatively with BMPs to stimulate osteoblast gene expression, remaining active in mature osteoblasts. BMPs are embryonic proteins that shape bones (Bone Morphogenetic Proteins) and belong to the family of transforming growth factor (TGF-beta), the same one that builds scars.
Treatment with boric acid affected the metabolism of cultured human dermal fibroblasts, reducing the synthesis of extracellular matrix macromolecules such as proteoglycans, collagen and total proteins. The effects of boric acid on cartilage cells or fibroblasts were proven at least twenty years ago and more recently confirmed. Boron decreased the activity of elastase and alkaline phosphatase, but had no effect on trypsin and collagenase activities. The effect of boron on enzymatic activity was also tested in fibroblasts considered as an in vivo test. In contrast to the results obtained in vitro, boron enhanced the activities of collagenase and cathepsin D; it also stimulates the synthesis of TNF-alpha, a cytokine which, apart from its inflammatory action, is also involved in wound healing.
In 2010, Hakki et al. published research investigating the mechanisms underlying boron’s effects on osteogenesis. Boron was determined to induce mineralization of osteoblasts by regulating the expression of genes related to tissue mineralization and the actions of key hormones (17β-estradiol, testosterone, and vitamin D) involved in bone growth and turnover. Boron’s induction of tissue mineralization also underlies boron’s beneficial effects on wound healing. Boron supplementation has repeatedly been shown to markedly increase serum levels of estradiol and calcium absorption in peri- and postmenopausal women. Boron also beneficially impacts vitamin-D utilization. Supplementation with boron stimulates bone growth in vitamin-D deficient animals and alleviates the consequent dysfunctions in mineral metabolism.
Finally, it seems that organic boron can exert anti-inflammatory effects by acting directly on white blood cells. Human leukocytes exposed in vitro to organoborates (calcium fructoborate, which occurs naturally in fruit) elevate their antioxidant enzymes (catalase, SOD1, G6PDH, GST, etc.) and do not fully meet the triggered “oxidative burst” usually from bacteria. Perhaps because boron somehow controls the synthesis of enzymatic cofactors of intermediate metabolism: in fact, it influences the formation and activity of biomolecules such as SAM and NAD+. The latter is all the rage as a supplement even among health enthusiasts and sportsmen, because it is recognized to have an anti-aging action. Quite recently, finally, boron has been proven its immune-directed effects to be (at least) partially mediated by GPR30 protein, a cell surface receptor able to bind female estrogens.
The effects were seen at low levels, very similar to those obtained by a diet well-balanced in boron content. This may enhance the original hypothesis that the “feminine side” shown by this element could be actually tue.
- edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.
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