Boron (B) - General Discussion
Boron (B) References|
B - Boron is found in igneous rocks shale 100 ppm; sandstones at 35 PPM; limestone at 20 ppm; fresh water at 0.0 13 ppm; sea water at 4.0 to 6.0 ppm; soil 2.0 to 100 ppm (highest in saline and alkaline soils); in California certain deserts have toxic levels; marine plants 120 ppm (highest in brown algae); land plants a at 5 0 ppm; Chenopodiaceae and Plumboginaceae are indicator plant families; marine animals at 20 to 50 ppm; land animals 0.5 ppm; boron is essential for bone metabolism including efficient use of calcium and magnesium and proper function of endocrine glands (i.e. ovaries, testes and adrenals).
Pure boron is hard and gray and melts at over 4,000 degrees F. Boron, a non-metallic mineral, occurs as a combination in nature, i.e. borax, boric acid (sassolite), ulexite, colemanite, boracite and tourmaline.
Large deposits of borax or "diamond boron" were discovered in Death Valley in 1881. The Death Valley deposits were made famous by the 20-mule team wagons that hauled out the mined borax. The rear wheels were 7 foot high, each wagon bed was 16 foot long and could carry 24,000 pounds (12 tons) of borax. Each 20 mule team pulled two wagons plus a 1,200 gallon water wagon (36.5 tons in each load! 1), the total length of the team and equipment was 120 foot long. The railhead in Mojave was 165 miles from the Death Valley mine site.
Prior to 1981, boron was not considered an essential nutrient; boron was first shown to be an essential mineral for growing chicks. It was not until 1990 that boron was accepted as an essential nutrient for humans.
Boron is required for the maintenance of bone and normal blood levels of estrogen and testosterone; within eight days of supplementing boron women lost 40 percent less calcium, 33 percent less magnesium and less phosphorus through their urine.
Women getting boron supplementation had blood levels of estradiol 17B doubled to 1evels found in women on estrogen replacement therapy," the at 10 ppm; levels of testosterone almost doubles.
More is becoming known of the biochemical function of boron in human and animal tissues. Because boron affects steroid hormone metabolism in humans and animals, and because the response of experimental animals to boron deficiency seems to be enhanced by nutritional stressors that induce secondary hyperparathyroidism (i.e. magnesium deficiency and aluminum toxicity, it would not be surprising to find that boron affects major mineral metabolism via a regulatory role involving a hormone.
The signs of boron deficiency in animals vary in nature and severity as the dietary content of aluminum, calcium, cholecalciferol, magnesium, methionine and potassium is varied. Variables affected by dietary boron include plasma and organ calcium and magnesium concentrations, plasma alkaline phosphatase, and bone calcification. Two studies showing a response to boron deprivation in humans have been reported. The first, on postmenopausal women housed in a metabolic unit, indicated that a low boron diet (0.25 mg/2000 kcal) elevated urinary excretion of calcium and magnesium, and depressed serum concentrations of 17fl-estradiol and ionized calcium. The second, in which five men, nine postmenopausal women (five on estrogen therapy) and one premenopausal woman were fed a low-magnesium, marginal copper diet, showed that plasma ionized calcium and serum 25-hydroxycholecalciferol were lower and serum calcitonin and osteocalcin were higher during boron depletion (0.23 mg/2000 kcal) than during boron repletion. Brain function was affected in these 15 adults; electroencephalograms indicated that they were less mentally alert during boron depletion than during boron repletion. In these experiments the first 21 days of depletion were not included in the statistical analyses because there were no apparent changes in variables of interest. Peace et al. also failed to find any significant effects in postmenopausal women fed a low-boron diet (0.33 mg/day) for 21 days.
Boron is an essential mineral nutrient found in trace amounts in most tissues. Although its precise role is unclear, boron may function in bone formation in both women and men and may also help prevent CALCIUM and MAGNESIUM losses in postmenopausal women. Boron seems to aid in the formation of steroid hormones (estrogen) and vitamin D and estrogen, and it improves COPPER metabolism. A magnesium deficiency accentuates the effects of boron. As yet there is no Recommended Dietary Allowance (RDA) for boron because a requirement has not yet been quantified. An estimated safe and adequate daily intake is I to 3 mg for adults. Sources of boron include legumes, leafy vegetables and fruit; APPLES, GRAPES and PEARS are good sources. A varied diet would be expected to supply adequate amounts of this mineral. Excessive use of boron supplements can cause a dangerous overdose of boron.
Newnham, R.E., "'Essentiality of Boron for Healthy Bones and joints,"' Environmental Health Perspectives, 102:supplement (November 1994), pp. 83-85.
The Clinical Effects of Boron (B)
by E. Blaurock-Busch, PhD
Boric acid was mentioned by the famous Arab researcher Geber who died in 776 AD. Latin scriptures and translations dating from the early Middle Ages referred to it as "Borach," "Baurauch," or "Bauracon," a precious commodity that was imported from Tibet under the name of Tinkal or Tinkar. Elemental boron wasn't discovered until 1810 by Davy, and was finally produced in pure form by Moissan at the end of the 19th century.
Boron is considered a catalytic trace element in humans and animals. The works of Albrecht and others have shown that boron has considerable involvement in glycogen synthesis in the liver. Bersin demonstrated that boron deficiency in humans with a tendency to skin allergies can trigger eczema, acne, and enteritis. Russian researchers emphasized the relationship of boron to adrenaline, carbohydrate and lipid metabolism. More recently, it has been recognized that this trace element plays a role in the prevention and treatment of osteoporosis and it has been suggested that it be involved in the formation of specific steroid hormones. There is some evidence that osteoporotic women who take boron supplements increase their serum hormone levels.
Plenty of data supports the hypothesis that boron is an essential element and that it is involved in regulating parathormone action. Therefore, it is likely that boron influences the metabolism of calcium, phosphorus, magnesium and cholecalciferol. Animal studies have indicated that cholecalciferol deficiency enhances the need for boron, and that boron might interact in some manner other than through an effect on cholecalciferol metabolism. The relationship seemed strongest between boron and magnesium, because boron supplementation alleviated magnesium deficiency signs in chicks. Boron does not seem to consistently alleviate signs of calcium and phosphorus deficiency. Elsair and co-workers found that a high dietary boron intake partially alleviated fluoride induced secondary hyperparathyroidism signs of hypercalcemia, hypophosphatemia, and depressed renal absorption of phosphorus in rabbits.
Boron and boron compounds can influence calcium metabolism, and tissue boron level changes in animals with abnormal calcium metabolism. In humans, a low caries incidence has been associated with adequate boron levels; however other studies indicated that high levels of orally administered boron increased dental caries. Boron has been shown to affect the activity of numerous enzymes in both plants and animals. Lewin and Chen stated that boron might have a role as a cofactor for some enzymatic reactions and also inhibits some enzymes, namely the pyridine or flavin I nucleotide-requiring oxidoreductases, cytochrome b5 reductase, and chymotrypsin.
Boron is rapidly absorbed, and excreted mainly in urine. Urinary recoveries depend on the dietary intake and may range from 30-90%. Kidney problems reduce excretion, causing potential boron accumulation in the heart, lungs, kidneys, brain, reproductive glands and adipose tissues. Years ago, boric acid was administered at 0.5 g/day to achieve weight loss. This dosage caused boric acid diarrhea, in addition to considerable deterioration of nutrient absorption.
Selected reported deficiency signs of Boron
Decreased calcium content and force required to break vertebrae of calcium-deficient rats; more severe signs of rickets in cholecalciferol (Vit. D)-deficient chicks; decreased apparent absorption and balance of calcium, magnesium and phosphorus; increased calcium concentration in brain cortex and increased phosphorus concentration in cerebellum of Vitamin D - deprived rats; decreased Red Blood Cell superoxide dismutase levels; increased plasma calcium, serum creatinine, and blood urea nitrogen (BUN); impaired performance in computer tasks and electroencephalograms indicating depressed mental alertness in postmenopausal women and men over the age of 45.
Possible functions of Boron
Through reactions with certain biosubstances to maintain proper cell membrane function or stability and influences hormone reception and transmembrane signaling.
Dietary need and sources
Human requirement of Boron most likely between 0.5 and 1.0 mg/day; rich food sources include noncitrus fruits, leafy vegetables, nuts, pulses and legumes.
Toxic effects appear at intakes of about 100 mg. The World Health Organization has banned boron (in the form of boric acid) as a food additive and preservative. Toxic effects include a red rash with weeping skin, vomiting, diarrhea characterized by a blue green color, depressed blood circulation, coma and convulsions. A fatal dose in adults is 15 to 20 g and in children 3 to 6 g. Repeated intakes of small amounts can cause accumulative toxicity. Signs of toxicity include nausea, vomiting, diarrhea, dermatitis, and lethargy. In addition, excess boron intake induces riboflavinuria. Landauer found that boron-induced teratogenic problems include skeletal abnormalities and were reduced with riboflavin therapy.
Oral administration of boron has low toxicity. A maximum tolerable level of 150 ug boron (as borax) per gram of dry diet has been suggested for cattle. Continuous feeding tests with rats have shown that boron levels in food of 73 ppm cause growth problems. When food contained 385 ppm boron, which corresponds to an uptake of 60.7 mg/kg, histological organ changes were observed, especially testicular atrophy. Cows consuming 150-300 mg/L of boron exhibited inflammation and edema in the legs and around the dewclaws. Furthermore, reduced feed intake, growth, hematocrit, hemoglobin, and plasma phosphorus was observed. Green et al. found that when boron levels of drinking water exceed 150 mg/L, rats exhibit depressed growth, continued prepubescent fur, aspermia, and impaired ovarian development. When drinking' water levels exceeded 300 mg/L, rats exhibit depressed plasma triglycerides, protein and alkaline phosphates, and depressed bone calcium.
Therapeutic considerations: check calcium, magnesium, phosphorus and riboflavin levels. Vitamin B6 reduces or abolishes the teratogenic effects of boric acid.
Distribution and Laboratory Analysis
Although boron is distributed throughout the tissues and organs of animals and humans, boron is mainly stored in bones. The ashes of human bones yield between 16 and 138 ppm of boron. Dental enamel varies widely in boron content and the concentration found in hair is similar to that of soft tissue. Plasma boron levels are apparently relatively high at birth, and decrease by about 50% within five days. Human milk contains boron at about one tenth the levels found in blood. Water containing 150-300 mg/L seems to cause inflammation and edema in the legs and other health problems.
A study was conducted to examine the effects of aluminum, magnesium, and boron on major mineral metabolism in postmenopausal women. This communication describes some of the effects of dietary boron on 12 women between the ages of 48 and 82. A boron supplement of three mg/day markedly affected several indices of mineral metabolism in seven women consuming a low-magnesium diet and five women consuming a diet adequate in magnesium. An adequate-magnesium diet was considered to be about 0.25 mg boron/day for 119 days. Boron supplementation markedly reduced the urinary excretion of calcium and magnesium. The reduction in calcium and magnesium excretion was greater when dietary magnesium was low. Boron supplementation depressed the urinary excretion of phosphorus only in women with low-magnesium diets. Boron supplementation markedly elevated the serum concentrations of 170-estradiol and testosterone. The elevation was more dramatic when dietary magnesium was low. Neither high dietary aluminum (1,000 mg/day) nor an interaction between boron and aluminum affected the variables presented. The findings suggest that supplementation of low-boron diets with a typical amount of boron induces changes in postmenopausal women, consistent with the prevention of calcium loss and bone demineralization.