Lara Pizzorno, MDiv, MA, LMT
Integr Med (Encinitas). 2015 Aug; 14(4): 35–48.
The trace mineral boron is a micronutrient with diverse and vitally important roles in metabolism that render it necessary for plant, animal, and human health, and as recent research suggests, possibly for the evolution of life on Earth. As the current article shows, boron has been proven to be an important trace mineral because it (1) is essential for the growth and maintenance of bone; (2) greatly improves wound healing; (3) beneficially impacts the body’s use of estrogen, testosterone, and vitamin D; (4) boosts magnesium absorption; (5) reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor a (TNF-a); (6) raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase; (7) protects against pesticide-induced oxidative stress and heavy-metal toxicity; (8) improves the brains electrical activity, cognitive performance, and short-term memory for elders; (9) influences the formation and activity of key biomolecules, such as S-adenosyl methionine (SAM-e) and nicotinamide adenine dinucleotide (NAD+); (10) has demonstrated preventive and therapeutic effects in a number of cancers, such as prostate, cervical, and lung cancers, and multiple and non-Hodgkin’s lymphoma; and (11) may help ameliorate the adverse effects of traditional chemotherapeutic agents. In none of the numerous studies conducted to date, however, do boron’s beneficial effects appear at intakes > 3 mg/d. No estimated average requirements (EARs) or dietary reference intakes (DRIs) have been set for boron—only an upper intake level (UL) of 20 mg/d for individuals aged = 18 y. The absence of studies showing harm in conjunction with the substantial number of articles showing benefits support the consideration of boron supplementation of 3 mg/d for any individual who is consuming a diet lacking in fruits and vegetables or who is at risk for or has osteopenia; osteoporosis; osteoarthritis (OA); or breast, prostate, or lung cancer.
The article highlights:
Bone Growth and Maintenance
Scientists have known for many years that boron is essential for healthy bones. In 1985, the US Department of Agriculture (USDA) conducted an experiment in which postmenopausal women (n = 12) who had been put on a low-boron diet (0.25 mg/d for 119 d) were supplemented with 3 mg/d of boron during two 28-day trials. In one trial, magnesium intake was low; in the other, magnesium intake was adequate. With boron supplementation, the women’s daily urinary excretion of calcium was reduced by 44%. The reduction in calcium loss resulting from boron supplementation was 52 mg/d when the women were low in magnesium and 22 mg/d when magnesium levels were adequate.1
Boron plays an important role in osteogenesis, and its deficiency has been shown to adversely impact bone development and regeneration.2 Boron influences the production and activity of steroid hormones, actions via which this trace mineral is involved in the prevention of calcium loss and bone demineralization. Boron supplementation has repeatedly been shown to markedly reduce urinary excretion of both calcium and magnesium and to increase serum levels of estradiol and calcium absorption in peri- and postmenopausal women.1,3 Boron also beneficially impacts vitamin-D utilization. Supplementation with boron stimulates bone growth in vitamin-D deficient animals and alleviates dysfunctions in mineral metabolism characteristic of vitamin-D deficiency.4
Animal studies published in 20085 and 20096 found that healing of the alveolar bone—a ridge of compact bone that contains the tooth sockets on the maxillae and mandible (ie, the bones that hold teeth)—was inhibited in boron-deficient rats. Compared with boron-adequate rats (3 mg/kg/d of boron in the diet) when evaluated at 7 and 14 days, boron-deficient animals (0.07 mg/kg/d boron in the diet) had significant reductions in osteoblast surface (57% and 87% at 7 d and 14 d, respectively) concomitant with increases in quiescent surface (120% and 126% at 7 d and 14 d, respectively), indicating that boron deficiency can result in impaired bone healing due to a marked reduction in osteogenesis.
In 2010, Hakki et al7 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 (17ß-estradiol [E2], 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.
Anti-inflammatory Effects in Osteoarthritis
Epidemiological evidence, case reports, and controlled animal and human studies have provided evidence for the use of boron as a safe and effective treatment for osteoarthritis (OA).52–54 Examining the relationship between boron administration and OA prevalence around the world, researchers discovered that in areas where boron intake is greater than or equal to 1 mg/d, the estimated incidence of arthritis ranges from 20% to 70%. In contrast, in areas where boron intake is usually 3 to 10 mg/d, estimated incidence of arthritis ranges from 0% to 10%.55 The boron concentration has been found to be lower in the femur heads, bones, and synovial fluid of OA patients compared with individuals without OA.56
Analysis of animal studies, in which rats with induced arthritis benefited from orally or intraperitoneally administered boron, revealed that boron downregulates production and activity of serine protease enzymes involved in the inflammatory response.57 Human studies of boron deprivation and repletion have shown that boron significantly increases erythrocyte superoxide dismutase (SOD) activity. In a study in which 63 days of boron depletion were followed by 49 days of boron supplementation 3 mg/d, SOD rose from 3091 U/g Hb to 3231 U/g Hb in men older than 45 years, from 2666 U/g Hb to 3169 U/g Hb in postmenopausal women, and from 2520 U/g Hb to 3327 U/g Hb in postmenopausal women on estrogen therapy.58
Human clinical evidence for boron’s use in the treatment of OA patients was first provided by a doubleblind, placebo-controlled supplementation trial conducted in Australia, in which a significantly favorable response to a supplement of 6 mg of boron per day (sodium tetraborate decahydrate) was seen in 20 subjects with OA; 50% of subjects receiving supplemental boron improved compared with only 10% of those receiving the placebo.61
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