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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 cyano[57Co]cobalamin. 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-[14C]histidine. 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.