too much vitamin b12

Vitamin B-12
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VITAMIN B-12

Vitamin B-12 is the cobalt-containing vitamin and levels can be judged
by cobalt levels in the hair analysis. B-12 is critical for iron
metabolism and a deficiency of B-12 will lead to anemia and probable
hypothyroidism.

If you are hypo and supplementation with iron causes a problem, then
suspect either a B-12 deficiency or a copper deficiency. If you are
hyper and B-12 causes an increase in hyper symptoms, then suspect a
copper deficiency (because B-12 will push iron metabolism and thereby
suppress copper).

B-12 deficiency is very likely in persons with hypothyroidism and
persons who have been taking copper and iron to recover from
hyperthyroidism. Supplementation with high amounts of the other B
vitamins, iron, and possibly manganese may use up B-12 creating a
deficiency. This may be detected by experiencing adverse reactions to
copper, iron, manganese, B vitamins, and many foods.

It is easy to determine a B-12 deficiency by taking a large dose (5000
mcg) since B-12 will have noticeable effects within several hours in a
person who is deficient. If you are hypo, feel tingling in the hands,
feet, or face, have a low pulse rate, feel your heart beating hard but
not excessively rapid at night, or have adverse effects to iron,
copper, or zinc, then try some B-12. If you are hyper and just
commencing supplementation of copper and other supplements, do not
take B-12. You may need to take some later as your hyper symptoms
subside and you begin iron supplementation, but avoid it at the
beginning.

Find an enteric coated 5000 mcg B-12 tablet. B-12 is destroyed by
stomach acid so the enteric coating preserves it until it reaches the
intestines where is can be absorbed. The sublingual types of B-12
apparently do not contribute a significant amount of B-12 to the body,
but will provide a small but quicker energy boost.

Studies:

This powerful vitamin is essential for those who are strict
vegetarians or those with nervous complaints. It is a great energiser
of the nervous system and can reduce depression and fatigue. It is
required for phase one detoxification of chemicals in the liver, and
can help people who are allergic to sulphites, which are common food
and wine additives. A study showed that vitamin B12 can effectively
block most of the adverse reactions to sulphites such as hay fever,
sinus, headache and bronchial spasms. B12 is required in increased
amounts by those who use alcohol excessively or in liver disease.

Metal-free, zinc, copper, and rhodium analogues of vitamin B12 were
synthesized to further characterize structural requirements for the
binding to human intrinsic factor, transcobalamin I, and
transcobalamin II. Binding affinities of the various analogues were
studied by competition against cyano57Cocobalamin. When
albumin-coated charcoal was used for the separation of free and bound
corrinoids, the relative 50% inhibition indexes were determined. The
influence of metal substitution was similar among the three binding
proteins. For analogues with a strong coordinative linkage between the
heterocyclic base and the central metal ion, similar to that with
cobalt (e.g., zincobalamin and cyanorhodibalamin), the indexes range
from 0.65 to 2.35 for all three binding proteins. Analogues in which
coordination is impossible (hydrogenobalamin and dicyanorhodibalamin)
exhibit markedly reduced binding with indexes between 10 and 160.
Cupribalamin shows 50% inhibition indexes ranging from 2.3 to 5.0,
thus suggesting a weak coordinative bond between the copper ion and
the 5,6-dimethylbenzimidazole moiety. These results emphasize the
importance of the coordinative linkage between the central metal ion
and the nucleotide moiety for optimal recognition by vitamin B12
binding proteins.

vitamin B12 analogues of cu, zn, rh.doc

The following study shows that pectin can rapidly decrease body levels
of B-12. Pectin is found in fruit.

J Nutr 1988 Dec;118(12):1495-501

Effect of hypothyroidism on methylmalonate excretion and hepatic
vitamin B-12 levels in rats.

Stokstad EL, Nair CP

Department of Nutritional Sciences, University of California,
Berkeley 94720.

The effect of hypo- and hyperthyroidism on vitamin B-12
metabolism in the rat was studied by measuring methylmalonic
acid excretion, B-12 content of liver and oxidation of
2-14Chistidine. Ten percent pectin was added to increase
severity of B-12 deficiency. The addition of thiouracil to a
diet containing 10% pectin decreased the excretion of
methylmalonic acid suggesting an amelioration of the B-12
deficiency. It was found that part of this decreased
methylmalonic acid excretion was due to a decreased food
consumption with a correspondingly decreased intake of
branched-chain amino acids which are precursors of methylmalonic
acid. When attempts were made to increase the protein intake of
animals receiving thiouracil so their amino acid intake was
equal to that of the control animals, methylmalonic acid
excretion was still lower than that of the controls. It was also
found that the vitamin B-12 content of the liver was higher in
the animals receiving thiouracil than in the controls.
Thyroidectomy had the same effect as feeding thiouracil. Liver
B-12 levels are rapidly depleted on a B-12 deficient diet
containing 10% pectin. It appears that hypothyroidism, induced
either by thyroidectomy or by feeding thiouracil, slows the rate
of depletion of hepatic B-12 which in turn facilitates the
metabolism of methylmalonic acid and decreases its excretion in
the urine.

Annu Rev Nutr 1985;5:115-41

Vitamin B12-folate interrelationships.

Shane B, Stokstad EL

The studies discussed in this review support the view that
biochemical and clinical symptoms common to both folate and
vitamin B12 deficiency are due to the induction of a functional
folate deficiency, which in turn is induced by cobalamin
deprivation. The interrelationship between these two vitamins is
best explained by the methyl trap hypothesis stating that
vitamin B12 deficiency can lead to lowered levels of methionine
synthetase, which results in a functional folate deficiency by
trapping an increased proportion of folate as the 5-methyl
derivative. In addition, as 5-methyl-H4PteGlu is a poor
substrate for folylpolyglutamate synthetase, there is a
decreased synthesis of folylpolyglutamates and consequently a
decreased retention of folates by tissues. The real folate
deficiency that ensues because of decreased tissue folate levels
is probably as important physiologically as the functional
deficiency caused by the methyl trap. The sparing effect of
methionine can be explained by adenosylmethionine inhibition of
methylenetetrahydrofolate reductase, which would prevent the
buildup of 5-methyl-H4PteGlun. A deficiency in vitamin B12 would
not, in itself, be sufficient to cause a disturbance in folate
metabolism. The deficiency would have to result in lowered
methyltransferase levels before any such disturbance would be
manifest.

Nuklearmedizin 1979;18(6):278-82

Serum vitamin B12 and folic acid levels in hyperthyroidism.

Gyftaki H, Kesse-Elias M, Koutras D, Pandos P, Papazoglou S,
Moulopoulos S

Serum vitamin B12 and folic acid levels were measured in 48
hyperthyroid patients and in a group of euthyroid controls. The
levels of vitamin B12 ranged from 120-900 pg/ml with a mean of
429.3 +/- 30.9 pg/ml (SE). The mean serum vitamin B12 level was
lower in hyperthyroid patients than in normal controls, the
difference being statistically significant (t = 2.584, p less
than 0.025). Serum vitamin B12 levels showed a statistically
significant negative correlation with the clinical index of
Grooks et al. (r = 0.344, p less than 0.05). The findings,
although not excluding the involvement of auto-immune gastritis
in patients with low serum vitamin B12 levels, suggest a direct
action of increased thyroid hormone concentrations. Serum folic
acid levels ranged from 0.5-13.8 ng/ml with a mean of 6.8 +/-
0.46 ng/ml (SE). The mean serum folic acid levels were higher in
the hyperthyroid patients than in normal controls but the
difference was not statistically significant (t = 1.2, p greater
than 0.2). The serum folic acid levels did not show any
statistically significant correlation with the clinical index of
Grooks et al. The fact that no statistically significant
difference was found between the mean value in hyperthyroid
patients and the mean value in normal controls is probably due
to the high folic acid intake in Greece.

Brain Res 1996 Jul 15;727(1-2):31-9

Vitamin B12 affects non-photic entrainment of circadian
locomotor activity rhythms in mice.

Ebihara S, Mano N, Kurono N, Komuro G, Yoshimura T

Department of Animal Physiology, School of Agricultural
Sciences, Nagoya University, Japan.

Administration of vitamin B12 (VB12) has been reported to
normalize human sleep-wake rhythm disorders such as non-24-h
sleep-wake syndrome (HNS), delayed sleep phase syndrome (DSPS)
or insomnia. However, the mechanisms of the action of VB12 on
the rhythm disorders are unknown. In the present study,
therefore, effects of VB12 on circadian rhythms of locomotor
activity were examined in mice. In the first experiment, CBA/J
mice were maintained under continuous light condition (LL) or
blinded, and after free-running rhythms became stable, the mice
were intraperitoneally injected with either VB12 or saline at a
fixed time every day. In all the mice with tau > 24 h, saline
injections resulted in entrainment of circadian rhythms, whereas
not all the mice with tau < 24 h entrained to the injection. In
contrast to saline injections, VB12 injections did not always
induce entrainment and about half of the mice with tau > 24 h
free-ran during the injection. In the second experiment, the
amount of phase advances of circadian rhythms induced by a
single injection of saline at circadian time (CT) 11 under LL
was compared between the mice with and without VB12 silastic
tubes. The results showed that the amplitude of phase advances
was smaller in the mice with VB12 than those without VB12. In
the third experiment, daily injections of saline were given to
the mice with VB12 silastic tubes maintained under LL. In this
chronic treatment of VB12 as well, attenuating effects of VB12
on saline-induced entrainment were observed. These results
suggest that VB12 affects the mechanisms implicated in
non-photic entrainment of circadian rhythms in mice.

Physiol Behav 1995 Jun;57(6):1019-24

Effects of intravenously administered vitamin B12 on sleep in
the rat.

Chang HY, Sei H, Morita Y

Department of Physiology, School of Medicine, University of
Tokushima, Japan.

Vitamin B12 (VB12) has been reported to normalize the
entrainment of circadian rhythms in the non-24-h sleep wake
cycle and delayed sleep phase insomnia in humans. The purpose of
this work was to clarify whether the peripheral administration
of VB12 has any sleep-promoting effect on the sleep-wake rhythm
in freely moving rats. After a baseline day of saline infusion.
VB12 (500 micrograms/kg/day) was administered continuously for 4
days via the jugular vein. Polysomnographic recordings were
carried out concurrently. In both the light and the 24-h
periods, the amount of non-rapid eye movement (NREM) sleep
increased significantly on VB12-days 2 and 3, while the amount
of REM sleep increased significantly on VB12-day 2. In the light
period, the increase in NREM sleep was due to increased duration
of the episode, while the tendency to an increase in REM sleep
was due to an increased number of episodes. Changes in the
diurnal sleep-wake rhythm tended to appear in the earlier light
period. The serum VB12 concentrations in the VB12 group were 40
times higher than in controls. These findings suggest that
peripherally infused VB12 has promoting effects on the rat's
sleep, especially in the light period.

The following is novel and interesting. I would advise against
supplementing with too much B12 because there is the possibility that
too much B12 could deplete iron if iron is not concurrently
supplemented.

DMSO and Vitamin B12

by Dr. David Gregg

There have been a number of publications reporting studies showing
that breathing nitrous oxide may destroy a person's vitamin B12. This
has been reported not only in journal articles, but has finally been
incorporated in the latest books on nutritional supplements as well as
books on biochemistry.

What first came to my mind was the use of this gas by dentists.
Nitrous oxide, often called "laughing gas," is commonly used by
dentists to help mitigate pain. This could present a risk to patients,
but probably more often it presents a risk to people working in the
office who would be exposed every day.

However, a far greater potential concern came to mind when I recently
read a news article that stated that the catalytic converters in
automobiles are creating enough nitrous oxide emissions to contribute
significantly to the greenhouse effect. It is also known to be a very
stable molecule that has a lifetime in the atmosphere of approximately
150 years.

With cars continuing to produce it, one would expect the concentration
in the atmosphere, world wide, to be increasing every year, and it
appears to be doing so. Is this already producing B12 deficiencies
world wide, which will increase with time? This would not be
surprising because we require (and absorb) only a few micrograms of
vitamin B12 per day and our livers store only a few micrograms in
reserve. It would take only a very low concentration of nitrous oxide
in the atmosphere to destroy this if the destruction process is
efficient, and the individual's dietary absorption process is
inefficient. What are the potential health consequences and what can
we as individuals do to protect against this potential problem? I have
had some personal experience, which I will discuss below that makes me
believe I have discovered a significant fraction of the population is
B12 deficient. It is a far greater fraction that I would have
expected, since it even exists in young people who should have healthy
B12 absorption systems. Is this the effect of the atmospheric nitrous
oxide emissions already showing up? I believe it is a definite
possibility which deserves some serious attention.

Health Consequences of a Vitamin B12 Deficiency

It is widely recognized that vitamin B12 in combination with folic
acid is essential for your body to synthesize hemoglobin. A deficiency
can result in a particular form of anemia called pernicious anemia.
However, as we continually expand our knowledge of biochemistry, it is
being recognized that these vitamins fill far more broad ranging
requirements. It is doubtful that all their functions been identified,
but it is reasonable to conclude that a deficiency could result in or
contribute to a broad range of degenerative processes.

The absorption of vitamin B12 requires a highly specialized process,
which tends to become less effective with age. For this reason it is
common for doctors to give elderly people B12 shots which result in
them feeling much better and more energetic. It is also common for the
elderly to develop numerous degenerative diseases. (They don't all get
shots.) Does a B12 (and folic acid) deficiency contribute to the
development of many degenerative diseases that we commonly associate
with aging? It would not surprise me at all if it does. It doesn't
appear to be so common to give vitamin B12 shots to young people, so
we may have not discovered a deficiency that may exist. Is there a
similar deficiency in younger people resulting in a different set of
medical problems? I have reason to believe there might be, and my only
explanation for such a surprising and unnatural development is the
growing nitrous oxide concentration in the atmosphere.

The individual solutions and my evidence that the problem might be
broad ranging over all age groups.

If a serious vitamin B12 deficiency is being caused by automobile
emissions, we certainly want to change that process. However, this
will require changes in cars that are beyond our individual control.
So, what can we do individually?

I am a strong believer in oral dietary supplements. It is the best
start. You can get B12 and folic acid supplements at any health food
store and follow the directions on the label. Since vitamin B12
requires a special absorption system that may not be healthy in a
particular individual, some people may not benefit from oral
supplements. For such people, one form of B12 is available, called
sublingual tablets, which are designed to be held under the tongue
while the B12 is absorbed through the skin. Many may find this
approach to be advantageous. Available by prescription are B12 shots,
which may have to be administered by a doctor.

I discovered another approach which I experimented with personally and
which eventually led me to discover what I interpreted to be a very
common Vitamin B12 deficiency, independent of the age group. This
surprised and puzzled me very much.

Back in 1994 when I was focusing on learning as much as I could about
vitamin B12, an experiment came to mind, which I decided to try on
myself. I saw a bottle of DMSO (dimethylsulfoxide) on the shelf of my
health food store and remembered that DMSO is not only absorbed
directly through the skin, but it also would carry with it any
impurities dissolved in it. This can be a serious problem if the
impurities are toxic. However, I also realized that if I dissolved
vitamin B12 in it, it might carry it directly to my blood stream
through my skin. I tried it and the results were dramatic for me, far
greater than any impact I had ever felt from oral or sublingual
tablets. I put some of my vitamin B12 tablets obtained at a health
food store into a two liquid ounce bottle with an eyedropper and
filled it with DMSO. It took a couple of days for the tablets to fall
apart. Once they did, I put an eyedropper load on one arm and rubbed
it in. In approximately one hour I started to feel very good, which
was a sense of general strength and well being. This lasted all day.
When I tried it again the next day, I got no such feeling. I also
didn't experience any bad effects either. Since I knew that
approximately one month's requirement of B12 is stored in the liver, I
reasoned that my system was simply fully supplied with Vitamin B12 and
that I wouldn't need to use it again for a month or so. When I tried
it again a month or so later, I got a significant boost from it again.
Since then I have continued to use it on a once every month or so
basis.

With time I decided to also add folic acid and a
multiviamin-multimineral tablet to give the solution a broader base of
nutritional support. I use a two ounce bottle with an eyedropper, add
10mg of vitamin B12 (ten 1000 mcg tablets), 9.6 mg of folic acid
(twelve 800 mcg tablets) and a single multivitamin-multimineral tablet
and fill it with 99.9% DMSO (leaving a bubble at the top so it can be
mixed when shaken). All ingredients were obtained from my local health
food store. The tablets are mostly binder and take a few days to fall
apart. They don't fully dissolve, but that doesn't seem to matter in
terms of potency.

I now use this regularly on approximately a once every month or two
basis. It serves as a reasonable mood elevator for me, and I believe
it contributes significantly to my general health. My interpretation
is I seem to become deficient in vitamin B12 even though I take oral
supplements regularly.

Over time I have told a number of other people about this home method
and many have chosen to try it. (I strongly recommended that they
consult their physician first.) Of those who have chosen to make up
solutions and try it, approximately 50% have told me that they noticed
a very significant energy boost, and this was not limited to elderly
people. It seemed to be independent of age, from age 25 and up.

Some also found a benefit if they used it as frequently as once every
two weeks and others were like me, finding the best time span between
use to be in the once-a-month or so range. If I interpret this to
indicate B12 deficiencies, the 50% number is much higher than I would
have expected, and the impact on young people was particularly
unexpected. Is this an indication that there is something happening in
our environment that is causing a broad base of Vitamin B12
deficiencies? When I read the news article about automobile exhaust
and the production of enough nitrous oxide to affect the greenhouse
effect, a light turned on. This may the cause. If so, it is a very
important issue.

It is my hope that this article will stimulate a thorough
investigation into this issue to systematically evaluate if it is
true, and result in an organized effort towards a solution.

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