| 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 manifests additional integrative
effects on bone metabolism in its actions relating to vitamin D (cholecalciferol).
Vitamin D affects absorption and utilization of calcium and also has
major anti-cancer effects relating to slowing tumor cell proliferation.13 Vitamin D enhances calcium absorption through the stomach and small
intestine. The effect of boron on raising plasma calcium levels may,
in part, be due to its enhancing effect on vitamin D.14 Again, boron
is acting as a helper, backup agent, and/or facilitator to maintain
bone integrity in its actions on vitamin D and calcium.
BORON’S EFFECT ON ARTHRITIS
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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
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Boron is a trace mineral that is found in non-citrus fruits such as plums,
red grapes, apples, pears, and avocados, as well as in legumes and
nuts. It is also present in significant amounts in coffee and red
wine. Dried fruits contain a much higher amount of boron than fresh
fruit. For example, fresh plums contain 0.45 mg of boron per 100
grams (g), but the same weight of dried prunes (about 12 prunes)
contains 2.15 mg of boron.1 Although boron currently is not considered
an essential element in the diet of humans, many scientists believe
it merits the status as an essential “ultratrace” element.35
The usual dietary boron consumption in humans is 1-2 mg/day for adults.
But boron requirements may be as high as 9-12 mg per day.
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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
|
Manual dexterity
Eye-hand coordination
Attention
Perception
Encoding and short-term memory
Long-term memory |
Decreased |
Normal |
<0.5 |
Electroencephalogram (EEG)
spectral analysis
|
|
|
|
Low-frequency activity |
Higher |
Lower |
<0.5 |
High-frequency activity
|
Lower |
Higher |
TABLE 2: Effects of
Boron Deprivation on Cognitive Performance and Brain Activity. In multiple studies, older men and
women showed statistically significant impairment in cognitive function
on a low-boron diet in comparison to a diet ample in boron. EEG
activity was also abnormal in patients on the low-boron diet.26 |
BORON TOXICITY 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.
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