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An Introduction To Cobalamin Metabolism-

I am not a health and nutrition expert, nor am I an expert at

biochemistry. But to the best of my knowledge the information here is

correct, being derived from well informed sources, but given some of

my own interpretations and deductions. Some information is based on

reading and knowledge gained from sources not mentioned in the

references, such as the well known food chain effect in concentrating

toxins up the food chain.

Introduction

Most vegans, sooner or later, will discover the Vitamin B12

(cobalamin) requirement stories that circulate and often form the

basis for demonstrating the alleged dangers of veganism. This text

aims to demonstrate that it is not so much a lack of B12 that causes

ill health, but that rather it is the modern western lifestyle that

may generate excess requirements of this micronutrient. In particular

this text will look at the little known issue of mercury, and how it

interferes with normal cobalamin metabolism.

I hope to encourage people to read about, examine and challenge

popular nutritional and health issues, because my experience has

tought me that only learning the issues for yourself frees one from

the many misleading schools of thought that surround dietary

practices. Perhaps most people will be satisfied just to know that

they get enough B12, but this text is for those who want to

understand what the real health issues are.

I suggest that rather than focusing always on B12 intake, a far more

health giving practice is to ensure that the B12 in your body is used

effectively. The human body can only absorb about 8 µg of B12 from

any one oral dose. If one lives a conventional " toxic " lifestyle it

would seem sensible to take a modest B12 supplement if you are a

vegan. I have yet to see any strong evidence that this is necessary

or what levels of intake may be required depending on lifestyle

factors.

Lifestyle risks other than your heavy metal load

· meat or other animal products and refined carbohydrates

(sugars) when used generously may more than double B12 needs

· persons who use drugs (eg Losec), chemicals, or beverages

which destroy or remove B12 (e.g., tobacco*, alcohol, caffeine,

laxatives, etc.)

· egg albumin and egg yolk decrease B12 absorption

· heavy metals present in food decrease dietary uptake

· a lack of calcium in food may decrease dietary uptake

· intestinal disorders or surgery affecting the intestines

· washing, cooking and light exposure of food containing B12

[adapted from; Thrash & Thrash, " NUTRITION FOR VEGETARIANS " ,

1982, " Heavy Metal Bulletin " Vol 2, Iss 3, Dec 1995 and

Thorsons " Complete Guide To Vitamins and Minerals " ]

*B12 detoxifies cyanide in food and also tobacco smoke

The primary loss of B12 in the human body seems to be through bile

excretion, which is a greater factor amongst meat eaters. Also

failure of intrinsic factor or poor production of stomach acid

(usually due to aging) can contribute to B12 deficiency.

B12 is a vitamin required for blood formation and rapidly growing

tissues. Methylcobalamin production requires cobalamin and is the

cobalamin found in the central nervous system (CNS) and brain where

it transports methyl groups (-CH3) to proteins in the myelin. It is

for these reasons that B12 deficiency leads to anaemia (blood

disorders include macrocytos and pernicious anaemia) and neurological

disorders (Alzheimer's disease and suspected amalgam related

disorders). There are, as with many diseases, usually more than one

factor which may be involved with causation. Given that the former

disorders are rare, even in vegans who have low B12 intakes, what I

am more concerned about is the potential for neurological disorders

that may be subclinical. This occurs because it is possible to have a

deficiency of B12 in the CNS even when blood levels of B12

are " normal " , or what is called non-anaemic deficiencies. These occur

for meat eaters with huge B12 intakes as well as for vegans. So

laying the blame for neurological problems on veganism or indeed any

alleged B12 intake deficiency is not always accurate, since increased

B12 dietary intake will evidently, not always work. In these serious

cases B12 is usually injected since dietary availability of B12 can

be as low as 1% of the total ingested for mega B12 doses, and some

patients do not convert dietary B12 to the methylcobalamin required

for normal neurological activity so well.

Myelin is the insulating layer which, along with fatty acids*,

surrounds nerve fibres. This protects nerves just like the insulation

arround electrical cables. In B12 deficiency, toxic 15-17 coal atom

fatty acids have a demyelinating effect on nerves, and electrical

impulse transmission is disturbed. Large doses of B12 supplements may

help to repair damage to the myelin given time, but once a nerve cell

is destroyed it will not " grow back " . Essential fatty acids and

antioxidants will also assist with protection and regeneration of

myelin.

*Myelin is made up of; cholesterol, polyunsaturated fats (PUFA), and

phosphatidyl choline complex with lipid call sphingosine. (L. Mervyn)

What Is Cobalamin and What Does It Do?

Cobalamin (vitamin B12) is the largest B vitamin and was the last one

to be isolated in 1948 by Dr E. Lester in the UK from liver. It

is a red crystalline substance. It had been known as early as 1926,

that something in raw liver was a treatment for anaemia. There are

various forms of the cobalamin (so called due to the presence of

cobalt) molecule, some of these are; methyl-, cyano, adnosyl- and

hydroxocobalamin (B12b). There are also nitrit (B12c), sulphito and

aquacobalamins. The human body can normally convert from one to the

other. The human body typically contains 5000-10000 µg of B12

distributed about equally between the liver, kidneys and nervous

system. Indeed the liver can store enough B12 for many years of

supply, so that daily ingestion of B12 is not required. Most of the

B12 present in animal tissues is in one of the two coenzyme forms,

adnosylcobalamin or methylcobalamin, and not actual vitamin B12

(cobalamin), which may be present due to diffusion from gut bacteria

or active transport using intrinsic factor. Vitamin B12 is also water

soluble and therefore easily lost, whereas cobalamin coenzymes will

remain in the liver and nerve cells, and can be effectively recycled.

B12 is now obtained by deep fermentation. According to Leonard

Mervyn, B.Sc., PH.D., C.Chem F.R.S.C, in Thorsons Complete Guide to

Vitamins & Minerals, pp42, 8 µg of B12 can be absorbed at any one

time by the intrinsic factor and calcium mechanism, only 1% being

absorbed by simple diffusion following oral dose. According to

Mervyn, pig's liver contains 25.0µg/100g of B12, therefore 100g of

pigs liver will result in 8.017µg of B12 absorbed, assuming digestion

is healthy.

Vitamin B12 is produced exclusively by microorganisms, but is also

found in animal flesh due to ingestion, or presence of the micro

organisms in the gut. However, since grazing " meat animals " tend to

accumulate heavy metals from the environment, it might be suggested

that animal sources of B12 are not as " good " a source as might be

supposed. Poultry, especially chickens, are routinely fed fishmeal,

which may contain significant amounts of mercury and other heavy

metals. Bottom feeding rather than deep sea fish contain the most

mercury. Vegans, by avoiding eating higher on the food chain, will

therefore accumulate less heavy metals (via diet) and may require far

less B12 as a result of that risk factor. We may therefore expect to

find a lower incidence of dementia, caused by heavy metal

intoxication, amongst amalgam free vegans.

Detailed structure of cobalamin showing the corrin ring (in black),

cobalt (in red) and 5,6-di-methylbenzimidazole ribonucleotide (in

blue). The corrin ring coordinates the metal cobalt and the

benzimidazole ribonucleotide is coordinated with the cobalt of the

corrin ring and also via the phosphoester linkage to a side chain of

the corrin ring system

Vitamin B12 is converted to 2 coenzyme forms of cobalamin (methyl and

adenosyl) by enzyme catalysis to catalyse reactions in the human

body. The vitamin is therefore a precursor, and not the active

substance. Cobalamin coenzymes are part of the prosthetic group, that

is the tightly bound group of coenzymes. This refelects the strength

of interactions with their apoenzymes (proteins), which are inactive

without the cobalamin cofactors, but convert to active holoenzymes

when bound (The coenzymes bind to help form the active sites of their

apoenzymes thus making an active enzyme). So, if methylcobalamin is

inhibited, then the building and repair of nervous tissues is

inhibited due to enzyme inactivity. Read literally, we get a " nervous

breakdown " !

Methylcobalamin participates in the transfer of methyl groups as in

the regeneration of methionine from homocysteine in mammals, as shown

here. The methyl group of 5-methyltetrahydrofolate is passed to a

reactive reduced form of cobalamin to form methylcobalamin, which

transfers the methyl group to the thiol side chain of homocystein

Symptoms would include: disturbed sense of co-ordination,

paraesthesiae, loss of memory, abnormal reflexes, weakness, loss of

muscle strength, exhaustion, confusion, low self-confidence,

spacticity, incontinence, impaired vision, abnormal gait, frequent

need to pass water and psychological deviances. Non-anaemic

deficiencies play a role in diseases such as Multiple Sclerosis,

Fibromyalgia, Diabetes and Chronic Fatigue Syndrome. Schizophrenia

has also been successfully treated with B12 plus other supplements,

and cardiovascular disease is linked to B12 deficiency while herpes

zoster used to be treated with B12 injections back in the 1950s.

What May Cause Non-Anaemic Deficiency?

The transport of vitamin B12 into the brain can be disturbed or

prevented by heavy metals such as inorganic mercury or lead. These

affect the blood-brain barrier by causing leakage and restricting the

active transport of nutrients. Also exposure to nitrous oxide (N2O),

often called laughing gas, can cause cobalamin deficiencies in the

brain. This may occur to women given the gas in labour or otherwise

during use of this anaesthetic, and may result in permanant brain

damage to someone with B12 deficiency. It is also worth bearing in

mind that since metals can cause deficiency, then anyone exposed to

sufficient quantity of metals may suffer permanent brain damage, even

when ingesting RDA levels of the vitamin.

Heavy metals such as mercury, lead and cadmium can be detoxified by

high doses of vitamin C (3000mg/day) plus supplementary essential

minerals. (L. Mervyn)

The stock method of measuring vitamin B12 levels is not going to

reveal deficiencies of the coenzymes required for healthy

neurological functioning since it measures blood levels of vitamin

B12 and not the CNS levels. These are not necessarily related to

blood levels of B12. Deficiencies in the brain and CNS can be

measured by checking " increased homocystein in LIQUOR " , (liquor

cerebrospinalis). However it would be expected that lower B12 levels

in serum would indicate lower levels in the CNS.

The precise mechanism of brain B12 deficiency causation is theorised

to be the oxidation of cobalt from CO2+ to CO3+ due to heavy metal

action. The denatured and thus enlarged cobalt molecule will

therefore not pass through the blood-brain barrier, the molecules

size being already large. Meanwhile the heavy metal molecule will

have been reduced. The result is a biologically inactive B12, and a

modified heavy metal.

Dr. Britt Ahlrot-Westerlund from Stockholm is an advocate of this

hypothesis. She recommends high doses of B12 for those suffering from

heavy metal exposure, such as from dental amalgam, since in the

presence of metals in the blood-brain barrier (plexus chorioideus),

most of the vitamin B12 is consumed depending on the level of metal,

such that regular B12 intake will not be sufficient.

Mercury (Hg) seems to change valency and binding site in the body,

and therefore causes increased formation of free radicals. Maybe Hg

valency change in pro-oxidative direction oxidizes cobalt atoms. To

confirm this theory, electron spin resonance investigation was

planned at Stockholm University's Department of Biophysics.

With dental amalgam now banned in Sweden and Germany, we can only

wonder at the fate of populations who are continually exposed to this

major mercury source in other nations. It would be sensible for

people with amalgam fillings to have them replaced by a non-metal

material. Vegans should also be careful to avoid alocohol, refined

sugar, smoking and the other risk factors listed above. It would also

be advisable to filter tap water. Dietary fibre helps to remove heavy

metals from the body as does sweating. Unfortunately the half life of

Hg in the brain/CNS is 25 years, thus steady accumulation, leading to

neurological disorders is virtually guaranteed.

Alcohol May Cause Tissue Cobalamin Deficiency

Just as mercury may cause cobalamin deficiency in the nervous system,

so alcohol can cause deficiency in tissues. Even worse, alcohol seems

to raise serum levels of vitamin B12, so that the deficiency is

masked and the subject may look like they have higher than normal B12

levels! Whether these effects correlate to alcohol intake, or are

only found in " alcoholics " is not clear.

Serum, erythrocyte, and liver levels of total corrinoids, cobalamin

(vitamin B12), and cobalamin analogues were determined by

differential radioassay in 27 patients with alcoholism. Compared with

normal subjects, liver content of total corrinoids and cobalamin in

alcoholics was low. Conversely, serum total corrinoids and cobalamin

were high. Compared with normal, levels of erythrocyte cobalamin

analogue in alcoholics were elevated, but levels of cobalamin were

not. Analogues in liver represented a similar percentage of total

corrinoids in alcoholics as in normals. The data confirm prior work

suggesting that, in alcoholism and in liver disease, cobalamin

depletion in tissues may be masked by normal to high serum cobalamin

and analogue levels. The failure of damaged liver to take up from the

serum cobalamin and analogues, compounded by release of these

compounds and their binders from damaged liver into the serum, can

account for these findings.

Kanazawa S; Herbert V,Total corrinoid, cobalamin (vitamin B12), and

cobalamin analogue levels may be normal in serum despite cobalamin in

liver depletion in patients with alcoholism, Lab Invest, 53:1, 1985

Jul, 108-10

Upon investigating Victor Herberts research I found useful background

information at the Journal of Optimum Nutrition (JON) web site. Also

the book Dirty Medicine by J contains some critique of

Herberts research methods and his political actions against the

alternative health movement. Elaborating upon the quality of his

studies is beyond the scope of this article and is covered by the

JON.

Mercury Sources

Table 2 on page 36 of the WHO Health Criteria 118 has the following

table:

Estimated average daily intake and retention (ug/day) of total

mercury and mercury compounds in the general population exposed to

mercury

Exposure Elemental mercury vapour Inorganic Mercury

vapour Methylmercury

Air 0.030(0.024) 0.002(0.001) 0.008(0.0064)

Diet/Fish 0 0.600(0.042) 2.4(2.3)

Diet/Non-Fish 0 3.6(0.25) 0

Drinking Water 0 0.050(0.0035) 0

Dental Amalgam 3.8-21(3-17) 0 0

TOTAL 3.9-21(3.1-17) 4.3(0.3) 2.41(2.31)

From: Environmental Health Criteria 101: Methylmercury (WHO 1990)

Values given are the estimated average daily intake; the figures in

parentheses

represent the estimated amount retained in the body of an adult.

Values are quoted to 2 s.fs.

More alarming than these WHO figures is the conclusion of Prof.

Aposhian and his colleagues at the University of Arizona who

demonstrated that two-thirds of the body load of mercury with those

with dental amalgam, comes from mercury vapour released from the

amalgam.

[Aposhian HV; Bruce DC; Alter W; Dart RC; Hurlbut KM; and Aposhian MM.

Urinary mercury after administration of 2,3-dimercaptopropane-1-

sulfonic acid:

correlation with dental amalgam score. FASEB J. 6:2472-2476,1 1992]

A similar study in Germany by Zander et al, provides data to show

that release of mercury from amalgam fillings represents the main

source of mercury exposure in subjects with amalgam fillings.

[Zander D; Ewers U; Freier I; Brockhaus. Studies on human exposure to

mercury. 3.

DMPS induced mobilization of mercuy in subjects with and without

amalgam fillings.

Zentralblatt fur Hygiene und Umwelmedizin 192(5):447-454, Feb 1992.]

Most of the scientific evidence used by the pro-amalgam " experts " to

justify the continued use of amalgam represent gross underestimates

of mercury exposure because they only measure exposure during dental

visits, and do not include the exposure due to vapour found

otherwise!

Psychological and Neurological symptoms Related To Amalgam

Psychological Neurological/Neuromuscular

Irritability Numbness

Nervousness Sensitivity to EMF

Sleeping Difficulties Tingling Sensation

Anxiety Headaches

Sudden Anger Dizziness

Rapid mood swings Chronic fatigue

Forgetfulness Tremor

Impaired shortterm memory Speech problems

Suicidal tendancies Restless legs

Concentraion difficulties Cramps

Hallucinations Stiffness

Lack of self-control Feeling of pressure in the body

Depression Fainting

Conclusion

Talking about B12 deficiencies is a reversal of the scientific facts.

The real dangers are due to exposure to toxins in industrialised

populations. Taking vitamin B12 will not protect you from heavy

metals, but it will help in the short terms. However a high intake of

vitamin C and essential minerals along with dietary fibre will assist

with reducing your heavy metal load, and therefore improving

methylcobalamin status in the brain.

Meat, fish and dairy products may be " good " sources of vitamin B12,

but expect them to also be good sources of heavy metals that will

accumulate in tissues over time. Winding up in a hospital dribbling

and with dimentia is perhaps the worst way to go out. Going vegan is

a good way to significantly reduce your heavy metal intake.

High dietary intakes of vitamin B12 do not always guarantee safety

from neurological disorders, as metal patients with " normal " B12

serum levels exist. In contrast, vegans with " low " serum levels of

B12 do not always display medical problems associated with B12

deficiency.

Many factors inhibit cobalamin bioavailability and function. These

have been highlighted and should be eliminated or heavily restricted

for a healthy mind and body. How much B12 we each need will vary

widely depending on your lifestyle. We can only absorb small

quantities of B12 via digestion, so it is safest to reduce the B12

expendature. Consider the risk factors indicated, and if you fit any

of the groups, then supplementation may be required. If you have

mercury " amalgam " fillings your B12 requirements may be drastically

increased to the point that only injected B12 will help you. Some

nutritional supplement providers suggest that hydroxocobalamin rather

than cyanocobalamin is preferable.

Since the various state, medical and nutritional bodies are evidently

aware of the problems, but do not inform the public of the dangers,

one can only conclude that there is a conspiracy of silence to

protect economic interests and credability to the public. This comes

at the expense to the publics health and wealth, and the future

viability of the affected populations.

Links

The links below will fill you in on many other environmental hazards,

and what you can do to help yourself avoid them.

· Aluminum: Human Neurophysiology, Behavior, Alzheimers

· Chemical Control of the Human Population

· Leading Edge Research Group: Biological Effect of Mercury

Amalgam

· http://www.algonet.se/~leif/AmFAQigr.html (A good FAQ on the

subject)

· http://emporium.turnpike.net/P/PDHA/health.htm ( IAOMT's web

page)

· http://home.sol.no/reiersol/amalgam.htm (Recent amalgam

research)

· http://vest.gu.se/~bosse/MercuryPage.html (Mercury page)

· http://203.23.131.20/wholmed/lphs18.htm (Amalgam in your

teeth)

· http://netvoyage.net/~daveq/amalgam.htm (Amalgam and MS?)

Bibliography

Much of this text was adapted from an article Vitamin B12- metals

disturb transport by Kauppi, assisted by Dr. Ahlrot-

Westerlund, which appeared in " Heavy Metal Bulletin " dec 1995 vol 2,

3:8-10.

HMB is available from Lilla Aspuddsv. 10, S-12649 STOCKHOLM, SWEDEN,

tel/fax: +46 8 184086.

· Dr. Ahlrot-Westerlund was the first physician in Sweden to

identify the need for Selenium supplementation due to very low soil

levels in Sweden. In the 70's she suspected that there might be a

connection with heavy metals and Multiple Sclerosis. In 1978 she was

invited by the Norwegian Scientific Acadamy to speak about selenium

and vitamin E deficiency, as she had found that these were involved

in the lipid peroxidation of cells in MS patients. Free radicals and

dental amalgam are, according to her, an important part in explaining

the MS syndrome. From 1980 she worked at the Institute for

Neurochemistry and Neurotoxicology. She has been studying the effects

of B12 mainly in heavy metal patients since 1987. In 1990 she was

associated to the Karolinska Institutes Department of Applied

Biochemistry.

The original references for this article are:

· Cees J.H./van Tiggelen. Alzheimers Disease/Alcohol Dementia:

Association with Zinc Deficiency and Cerebral vitamin B12 Deficiency.

J. of Orthomolecular Psychiatry, 1983, vol 12, No. 2, 97-104.

· sson S/Svensson.A, Catalytic effects by thiotransferase

on the transfer of methylmercury and p-mercury-benzoate from

macromolecules to low molecule weight thiol compounds. Toxicology 10,

1978, 115-122.

· Gran B. B12 i hög dos vid neuropsykiatriska symtom hos

misstäktamalgamsjuka patienter. Swedish Medical Journal, 1994

· Hanson M. Vitamin B12, TF-bladet, 4, 1992

· Ideda T. et al. Vitamin B12 levels in serum and cerebrospinal

fluid of people with Alzheimer's disease. Acta-Psychatr. Scand 1990,

82:337-329

· Lind/Friberg/Nylander. Demethylation of mercury in brain,

National Institute of Environmental Medicine and Dept. of

Environmental Hygiene, Presented at the First Meeting of the

International Society for Trace Element Research in humans, Palm

Springs, Dec.8-12., 1986.

· Lindenbaum J. et al. Neuropsychiatric disorders caused by

cobalamin deficiency in the absence of anaemia of macrocytos. The new

England Journal of Medicine, June 30, 1988.

· Metz J. Cobalamin Defciciency and the pathogensis of Nervous

System Disease. Ann Ren Nub., 1992, 12:59-79.

· Mottet K. et al. Effects of Methylmercury Exposure in

Primates, Presented at the First Meeting of the International Meeting

of the International Society for Trace Element Research in humans,

Palm Springs, Dec. 8-12, 1986.

· Mörnstad H/Norberg B. Paradigmskifte för bedömning och

behandling av vitamin B12-brist, Swedish Dental Journal, nr 1 1994.

· Patridge W. Inorganic mercury; selective effects on blood-

brain barrier transport systems. J. of Neurochemistry, 1976, No.

27:333-335.

· Reynalds E.H. Multiple Sclerosis and vitamin B12 metabolism.

J, of Neuroimmunol. 40 (1992):225-230.

· Rochelle et al. Interactions between Hydroxocobalamin and

Nitric Oxide (NO): Evidence of Redox Reaction between NO and Reduced

Cobalamin and Reversible NO Binding to Oxidized Cobalamin, 1995,

Journal of Pharm. and Exp. Terapheutics, vol 275, 1995, No. 1:48-52.

The article also goes in to some detail on explaining how B12 levels

are assessed and the use of methylcobalamin to treat metal patients,

and the problems associated with non methylcobalamin treatment.

Details on B12 testing and supply of methylcobalamin were also given.

Multiple deficiencies/excesses can also obscure diagnosis of B12

deficiency, ie. folic acid and B1 and other B vitamins.

Dr. Ahlrot-Westerlund also presents some case studies of successful

methylcobalamin treatments.

The following publications were also used:

· Sam Ziff, F. Ziff, DDS Dentistry Without Mercury, Bio-

Probe, Inc. Available from Bio-Probe web site.

· Horton/Moran/Ochs/Rawn/Scrimgeour Principles of Biochemistry

2nd Ed., Prentice-Hall International, Inc. Available from Prentice-

Halls web site.

· Leonard Mervyn, B.Sc., PH.D., C.Chem F.R.S.CThorsons Complete

Guide to Vitamins & Minerals, Published by Thorsons available via

Harper web site.

· Leibovitz, Ph.D. Journal of Optimal Nutrition

Editorials, Journal of Optimal Nutrition (contains useful critique of

Victor Herbert)