Maintains Bones, Joints, Neurons and May Reduce Prostate Cancer Risk
by Stephen B. Strum, M.D., FACP
Medical Oncologist Specializing in Prostate Cancer
The effect of boron intake was analyzed in a human study involving 12 post-menopausal women not on estrogen replacement therapy. Patients were first given a boron-deficient diet consisting of 0.25 mg of boron daily for 119 days. This was followed by a 48-day period in which the same patients received boron supplementation at a dose of 3 mg per day. Patients were also studied during periods of adequate magnesium intake versus magnesium deficiency. Deprivation of boron and/or magnesium caused changes that are similar to those seen in women with post-menopausal osteoporosis, including increased loss of urinary calcium. However, in women receiving 3 mg of boron per day, urinary losses of both calcium and magnesium were significantly diminished, especially if dietary magnesium was low. Also noted were increased levels of plasma ionized calcium, beta estradiol, and testosterone.12
Vitamin D <=> Boron Interactions
BORON’S EFFECT ON ARTHRITIS
The inhibition of enzymes such as serine proteases (e.g., PSA) was mentioned in relation to the anti-cancer effects of boron. In a review of the literature on boron’s metabolic activities, Hunt et al also emphasized the down-regulation of other enzyme activities by boron.15 For example, boron has been shown to inhibit cyclooxygenase (COX) and lipoxygenase (LOX). These two enzymes mediate the inflammatory cascade and are pertinent to therapies directed against inflammatory conditions. Such anti-inflammatory capabilities of boron are clearly pertinent to its anti-cancer effect, because the reduction of COX II and LOX enzymes leads to a decrease in prostaglandin E2 (PGE2) and other unfavorable eicosanoids such as leukotrienes. These hormonal breakdown products of arachidonic acid were discussed and illustrated in an article on prostate cancer in the June 2003 Life Extension magazine. We now know that omega-6 fatty acid metabolism that is allowed to continue down this pathway represents a vital stimulus for angiogenesis and cancer growth.
The very same prostaglandins and leukotrienes are mediators of inflammatory conditions such as degenerative joint disease and osteoarthritis. PGE2 and leukotrienes have been implicated in causing problems with joint swelling, restricted joint motion, and other arthritic complaints. Anti-arthritic agents like glucosamine sulfate work through inhibition of COX II and PGE2 by suppressing nuclear factor kappa beta (NfkappaB)—a proinflammatory cytokine.18,19 There is also evidence that boron has similar modes of action in reducing arthritic conditions.20-22 These findings are clinically supported by evidence showing that areas of the world with low levels of boron in the soil have a higher percentage of people suffering from arthritis in comparison to regions with higher soil levels of boron. There is also epidemiologic evidence that in areas of the world where boron intake is 1 mg or less per day, the estimated incidence of arthritis ranges from 20% to 70%, whereas in areas of the world where boron intake is usually 3-10 mg, the estimated incidence of arthritis ranges from 0 to 10%.23 In a study of 20 patients with osteoarthritis, the 50% who received a daily supplement of 6 mg of boron noted subjective improvement (less pain on movement), while only 10% of those who had received placebo improved over the same time interval.24
In another study, bone adjacent to joints with osteoarthritis tends to be less mineralized than control bone and bone from fracture patients. Interestingly, bone samples in such instances have significantly lower concentrations of boron.25
Lastly, there have been studies that show the anti-arthritic effects of S-adenosylmethionine (SAMe) are equivalent to those seen with non-steroidal anti-inflammatory agents (NSAIDs) but without the toxicity seen with NSAIDs.27-29 Also interesting is a report indicating a very high affinity of SAMe for boron.30 An interesting consideration would be to evaluate the efficacy of SAMe in reducing arthritic symptoms in relationship to boron consumption and boron blood levels.
BORON’S EFFECT ON BRAIN FUNCTION
There are many parallels between the medical applications of NSAIDs and the biological properties of boron. These shared benefits may be due to the common mechanisms involved in the down-regulation of pro-inflammatory cytokines and the subsequent reduction in COX II and LOX enzymes. These mechanisms provide some explanation for the positive clinical benefits of boron such as those seen in patients with arthritis and boron’s relation to the reduction in the incidence of prostate cancer, and hopefully in the use of boron in prostate cancer treatment. Since it is now commonly accepted that the routine use of NSAIDs significantly reduces the incidence of Alzheimer’s disease,31,32 it is not surprising that papers have been published on boron’s positive effect on cognitive function.33
Penland et al conducted experiments in men and women to investigate the functional role of boron in relation to brain electrophysiology and cognitive performance (see Table 2). Findings were compared in healthy older men and women while on a diet deprived of boron versus a diet with ample boron (approximately 0.25 mg boron/2000 kcal/day versus approximately 3.25 mg boron/2000 kcal/day). The ability of patients to perform skills involving cognition and psychomotor tasks were assessed and showed significant impairment during the boron-deprived diet. Brain-wave patterns were evaluated using an electroencephalogram (EEG) and showed an increased proportion of low-frequency activity in patients on the boron-deprived diet. Similar findings are often observed in response to general malnutrition and heavy metal toxicity. The authors concluded from such data that boron appears to play a significant role in human brain function and cognitive performance, and that boron is an essential nutrient for humans.26
BORON: OTHER FUNCTIONS
Boric acid solution (3%) dramatically improves wound healing through action on the extracellular matrix, a finding that has been obtained in vitro.34
In the 1870s, it was determined that sodium borate (borax, a form of boron) had the ability to preserve foods. Over the next 50 years, borates were valued as preservatives and used to extend the palatability of fish, meat, cream, and butter.35 The first evidence of the potential for toxicity associated with borate consumption occurred in 1904. Human volunteers, consuming over 500 mg per day of boric acid, had symptoms of decreased appetite, nausea, abdominal discomfort, and diarrhea. After this was reported, the use of boron as a food preservative and taste enhancer greatly declined, and by the mid-1950s boron was essentially banned worldwide in the food industry. Ironically, boron has been replaced with monosodium glutamate that has been shown to be neurotoxic36 yet remain in widespread use.
Boron compounds are toxic to all species tested at high doses, but they are not carcinogenic or mutagenic.37 A rat developmental toxicity study of boron determined a “no observed adverse effect level (NOAEL) of 9.6 mg of boron per kg per day. Toxicology studies of boron in humans have shown safety up to a maximal daily intake of 0.3 mg/kg of boron, which equates with a daily intake of 18 mg of boron for a 60-kg (132-pound)individual.38
Four patients with elevated serum boric acid levels after single, acute ingestions of 10-297 grams were reported to the Rocky Mountain Poison and Drug Center (RMPDC) between January 1983 and August 1985. In these cases, systemic effects were absent. In 1983-4, 364 cases of boric acid exposure were reported to the RMPDC, with only one fatality from a probable chronic ingestion. In this case, vomiting, nausea, diarrhea, and abdominal cramps were present. These observations suggest that significant poisoning is unlikely to result from a single, acute ingestion of boric acid.39
A report by Pinto et al showed that boric acid ingestion can induce urinary losses of vitamin B2 (riboflavin).40 Patients taking boron supplements may wish to also consider B vitamin supplementation. Gordon et al reported a case of two infants using pacifiers dipped in a honey-borax solution over a period of several weeks in 1973. These infants had findings of hair loss, anemia, and seizures. All signs and symptoms disappeared after discontinuation of the borax and honey preparation.41
The critical effects of boron in several species involve male reproductive toxicity and developmental toxicity. Testicular effects occurred at approximately 26 milligrams of boron equivalents per kilogram of body weight per day. Data on endocrine toxicity include altered follicle stimulating hormone and testosterone levels within 14 days of treatment.37 It is important to emphasize that the doses that cause these effects are far higher than the levels to which the human population could be exposed. Humans would need to consume daily approximately 3.3 grams of boric acid (or 5.0 grams of borax) to ingest the same dose level as the lowest animal NOAEL. No effects on fertility were seen in a population of workers exposed to borates or to a population exposed to high environmental borate levels.42 Therefore, the likelihood of boron toxicity caused by boric acid and inorganic borates is remote.