Chronic Fatigue Syndrome Support Group
Chronic Fatigue Syndrome (ME/CFS) describes a sense of exhaustion and post-exertion malaise, even when you have gotten enough rest and sleep. The disease is characterized by six months of incapacitating fatigue experienced as profound exhaustion and extremely poor stamina, and problems with concentration and short-term memory. The cause is unknown, but it is a...
Ali5tair
I've known for 3 years that B12 shots help me. Recently I found that I am Mercury Poisened with 94 parts per million so I went looking on the web for the relationship between Heavy metals and B12.
Heres a beaut article.
Al
Vitamin B12
- metals disturb transport!
The administration of relatively high doses of vitamin B12, in the form of methylcobalamin, in the treatment of fibromyalgia, diabetics, Multiple Sclerosis and amalgam-related disorders has been gradually increasing in Sweden since the end of the 80's. The results are remarkable...
Essential for blood formation and rapidly growing tissues, vitamin B12 is mainly present in animal food. A healthy person requires approximately 3-5 ug of vitamin B12 per day, the amount usually available in a normal diet. For strict vegetarians, however, blue-green algae and bean sprouts are suitable sources.
The human body normally contains approx. 5000-10000 ug of vitamin B12, equally distributed in the liver and the nervous system. Due to the presence of the cobalt atom (trace element), vitamin B12 is also called cobalamin.
Anaemia
Vitamin B12 deficiencies have been mainly related to blood deficiency diseases, such as macrocytos and pernicious aneamia. First described in 1855, the latter was usually lethal. The connection with cobalamin was not established until after vitamin B12 was first isolated in 1948. (As early as 1926, however, it was found that raw liver, which later proved to be rich in vitamin B12, could effectively cure anaemia).
Causes and Symptoms
Deficiencies can be caused by low intestinal B12 uptake (intestinal disorders), low intrinsic factor (a substance essential for its transport to the blood) in the stomach, deficiency of hydrochloric acid in the gastric juices (increasing with old age), regular use of laxatives or medicines like Losec (for treatment of peptic ulcer), low uptake in the central nervous system (CNS) or excessive B12 degradation. Lack of calcium in the food can also reduce the uptake and so can heavy metals.
Vitamin B12 deficiencies are followed by neurological and psychological disorders, such as 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, psychological deviances.
Non-anaemic deficiencies
Lately it has been discovered that anaemia is not always present in neurogical and psychological disturbances associated with B12 deficiencies. In diseases such as Alzheimer's and suspected amalgam-related disorders, hidden B12 deficiencies in the CNS (without low blood values) have been found.
The transport of vitamin B12 to the brain can be disturbed or interrupted by heavy metals such as inorganic mercury, which affects the blood-brain barrier by causing leakage and hampering the active transport of nutrients. Exposure to laughing gas (N2O), commonly given to women in labour, causes similar B12 deficiencies in the brain of the infant, and sometimes in mothers with low B12 levels (and the anaesthetist). When used as a sedative in connection with an operation, the gas can cause irreparable damage in an individual with B12 deficiency.
Non-anaemic vitamin B12 deficiencies also play a role in diseases like Multiple Sclerosis, Fibromyalgia, Diabetes and Chronic Fatigue Syndrome. Schizophrenia, a psychotic condition, has been successfully treated with B12 injections in combination with other supplements. There also seems to be a connection between B12 deficiencies and cardiovascular diseases
In the 1950's, it was common practice to treat a patient with the first signs of herpes zoster with a vitamin B12 injection which effectively reversed the symptoms. This knowledge has fallen into oblivion. Ongoing research will most probably further increase the area of use of vitamin B12.
Test methods
Rarely detectable through normal testing procedures, such as blood serum or methyl malonic acid, B12 deficiencies in the brain and CNS can be determined by checking "increased homocystein in LIQUOR", (liquor cerebrospinalis)*, the most appropriate test method.
*) In rare cases, mainly very young patients, side-effects such as headaches may occur. It is therefore recommended to drink water and rest immediately after the spinal test.
If the blood serum B12 value is low, it can be expected that the B12 in the CNS is even lower. If B12 in methyl malonic acid is elevated while the serum value is normal, there are probably B12 deficiencies at a cellular level.
The LIQUOR-test method is rather complicated. Ordinary equipment can be used, but at the Uddevalla Hospital in Sweden, the method of analysis has been especially designed for the purpose. According to Dr. Bo Nilsson, Chief Physician, it is important to measure with an exactness of 1 pmol/L**. The secret is to extract the minute quantity of B12 available without changing the molecule.
**) One thousand of a millionth of a millionth mol per litre, which makes one millionth of a millionth of a gram/litre.
However, many amalgam patients use the trial-and-error method, and initiate the treatment without previous testing.
High doses
It has been suggested that in the presence of heavy metals the cobalt atom is oxidized from CO2+ to CO3+ (denaturation) at the same time as the heavy metal is reduced. The properties of the cobalamin are hypothetically changed and B12 has lost its biological properties. Due to its molecular size, B12 normally has difficulties in crossing the blood-brain barrier and it is possible that denaturation make this even more difficult. This process is analogous to the behaviour of laughing gas.
One of the advocates of this hypothesis is Dr. Britt Ahlrot-Westerlund in Stockholm. The reason why high doses are recommended is that, in the presence of heavy metals in the blood-brain-barrier (more specifically in the plexus chorioideus), most of the vitamin B12 seems to be consumed (for reasons we don't know) and, depending on the level of heavy metal exposure, part of the supplemented B12 will most probably also be consumed in this way until the surplus can be used in the brain where it is needed.
Hg seems to change valency and binding site in the body, and this causes increased free radical formation. It is possible that the Hg change in valency in prooxidative direction oxidizes the cobalt atom. There is, according to Dr. Westerlund, reason to believe that the process of Hg oxidation of the cobalt atom is analogous to the way in which Fe2+ in haemoglobulin is oxidized to Fe3+ in methaemoglobulin (incapable of releasing oxygen) by exogene toxic substances.
To confirm this, an in vitro investigation using electron spin resonance is planned at Stockholm University, Department of Biophysics.
Many different forms
The active vitamin comes in many different forms, i.e. methyl-, cyano-, adnosyl- and hydroxocobalamin, freely transformed into each other in the body. However, vitamin B12 in the brain and CNS is only present as methylcobalamin, which effectively transports methyl groups (-CH3) to proteins in the myelin, the insulating layer which together with fatty acids surrounds the nerve fibers, protecting them just like insulation on electric cables.
In cases of B12 deficiency, toxic fatty acids with 15-17 carbon atoms with a demyelinating effect on the myelin are formed, and the transmission of electrical impulses is disturbed. If enough B12 is supplied, the myelin might be repaired in the course of time.
Methylcobalamin
The uptake from oral B12 supplementation is usually very low, approx. 1 %. Vitamin B12 is therefore often given intramuscularly.
Although vitamin B12 can be supplemented in any of its forms, it is given as hydroxo- or sometimes as cyanocobalamin in many countries. In the south of Europe, however, methylcobalamin is generally used to treat disorders such as neuritis and polyneuropathia. Highly recommended by the Swedish Association of Dental Mercury Patients, it is usually the drug of choice for the treatment of patients with amalgam-induced disorders.
In the experience of Dr. Ahlrot-Westerlund among others, B12 in its active form, methylcobalamin, gives a much better result than other forms which have to be transformed into methylcobalamin. It is possible that the process of transformation itself is inefficient in many patients.
It has been suspected that the supplementation of methylcobalamin in the presence of mercury could lead to the formation of methyl mercury. Inorganic mercury steals methyl groups from methylcobalamin, and methyl mercury is formed. However, methyl mercury is not more toxic than inorganic in mercury and the positive effects of B12 supplementation in this form seem to outweigh the possible disadvantages.
Preservatives
Methylcobalamin should be obtained with dry substance and liquid packed separately to increase the shelf life. The preparation should be kept in the dark stored at a temperature below 25 degees C and used within a year. (Premixed preparations, on the other hand, should be kept in a refrigerator).
Many of the vitamin B12 preparations on the market contain preservatives which can cause problems in sensitive patients. However, the methylcobalamin available under the product names "Algobaz" from Portugal or "Cobamet" produced by a French company (Roussel) also in Portugal do not.
The corresponding Japanese preparation, Esai's Mecobal, contains only 0.5 mg B12. According to Dr. Bo Nilsson, it is probable that, given daily, the transport between the blood-brain barrier is saturated even by such a small dose. In Dr. Ahlrot-Westerlund's opinion, however, methylcobalamin for patients with metal-induced disorders should be given daily intramuscularly* in doses of 10 mg with 8 x 5 mg oral folic acid and 300 mg vitamin B6 for 6 days a week until a positive effect is achieved and then continued until no further peak is achieved. This can take as long as 1/2-1 year or perhaps even longer. The dose should then be gradually diminished (given every other day for example).
*) given subcutaneously, the B12 treatment is, according to Dr. Westerlund, not as effective.
Multiple deficiencies
In many cases it can be assumed that multiple deficiencies, not always easily separable, are present. For example, lack of folic acid can also cause anaemia and its supplementation can mask a B12 deficiency. Therefore it is important that both vitamins are supplied, and to some extent also the other vitamins in the B-complex. Some of the symptoms of B12 deficiency are also present in B1 deficiency** and both deficiencies can be present at the same time.
**) diagnosed by testing thiamin pyrimydine phosphate in serum (expensive)
For a successful recovery from amalgam-poisoning among other disorders, the importance of additional supplementation of essential fatty acids (fish oil etc.) and anti-oxidants should be emphasized.
Some addresses and prices: Methylcobalamin: The two recommended preparations are of equal quality. Both can be ordered from a pharmacy in Lisbon, phone number: +351 1 342 3821. Ask for the head pharmacist, Maria Augusta. Since the preparation is prescription free, it can also easily be obtained during a trip to Portugal. However it should be ordered at least one week ahead.
B12 testing: Uddevalla Hospital in Sweden fax No: +46 522 93101
Test facilities available at the cost of SEK 130:- for B12, 200:- for homocystein and 200:- for methylmalonic acid (MMA). 1 USD is approx. 7 SEK.
According to the Charing Cross & Westminster Medical School, B12 Unit, Dr. Bhatt, there are "a handful" of laboratories worldwide, specialized in vitamin B12 testing. For further information: Tel: +44 (0)181 746 8625, Fax No.:+44 (0)181 746 8860
Monica Kauppi (with thanks to Dr. Westerlund for her kind assistance)
References:
Cees J.H./van Tiggelen. Alzheimers Disease/Alcohol Dementia: Association with Zinc Deficiency and Cerebral vitamin B12 Deficiency. J. of Orthomolecular Psychiatry, 1983, vol 13, No. 2, 97-104.
Eriksson S/Svensson.A, Catalytic effects by thioltransferase on the transfer of methylmercury and p-mercurybenzoate from macromolecules to low molecule weigth thiol compounds. Toxicology 10, 1978, 115-122.
Gran B. B12 i hg dos vid neuropsykiatriska symtom hos misstnkt amalgamsjuka patienter. Swedish Medical Journal, 1994.
Hanson M. Vitamin B12, TF-bladet, 4-1992.
Ideda T. et al. Vitamin B12 levels in serum and cerbrospinal 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 anemia or macrocytos. The new England Journal of Medicine, June 30, 1988
Metz J. Cobalamin Deficiency 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 Society for Trace Element Research in humans, Palm Springs, Dec. 8-12, 1986.
Mrnstad H/Norberg B. Paradigmskifte fr bedmning 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 for 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
Heres a beaut article.
Al
Vitamin B12
- metals disturb transport!
The administration of relatively high doses of vitamin B12, in the form of methylcobalamin, in the treatment of fibromyalgia, diabetics, Multiple Sclerosis and amalgam-related disorders has been gradually increasing in Sweden since the end of the 80's. The results are remarkable...
Essential for blood formation and rapidly growing tissues, vitamin B12 is mainly present in animal food. A healthy person requires approximately 3-5 ug of vitamin B12 per day, the amount usually available in a normal diet. For strict vegetarians, however, blue-green algae and bean sprouts are suitable sources.
The human body normally contains approx. 5000-10000 ug of vitamin B12, equally distributed in the liver and the nervous system. Due to the presence of the cobalt atom (trace element), vitamin B12 is also called cobalamin.
Anaemia
Vitamin B12 deficiencies have been mainly related to blood deficiency diseases, such as macrocytos and pernicious aneamia. First described in 1855, the latter was usually lethal. The connection with cobalamin was not established until after vitamin B12 was first isolated in 1948. (As early as 1926, however, it was found that raw liver, which later proved to be rich in vitamin B12, could effectively cure anaemia).
Causes and Symptoms
Deficiencies can be caused by low intestinal B12 uptake (intestinal disorders), low intrinsic factor (a substance essential for its transport to the blood) in the stomach, deficiency of hydrochloric acid in the gastric juices (increasing with old age), regular use of laxatives or medicines like Losec (for treatment of peptic ulcer), low uptake in the central nervous system (CNS) or excessive B12 degradation. Lack of calcium in the food can also reduce the uptake and so can heavy metals.
Vitamin B12 deficiencies are followed by neurological and psychological disorders, such as 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, psychological deviances.
Non-anaemic deficiencies
Lately it has been discovered that anaemia is not always present in neurogical and psychological disturbances associated with B12 deficiencies. In diseases such as Alzheimer's and suspected amalgam-related disorders, hidden B12 deficiencies in the CNS (without low blood values) have been found.
The transport of vitamin B12 to the brain can be disturbed or interrupted by heavy metals such as inorganic mercury, which affects the blood-brain barrier by causing leakage and hampering the active transport of nutrients. Exposure to laughing gas (N2O), commonly given to women in labour, causes similar B12 deficiencies in the brain of the infant, and sometimes in mothers with low B12 levels (and the anaesthetist). When used as a sedative in connection with an operation, the gas can cause irreparable damage in an individual with B12 deficiency.
Non-anaemic vitamin B12 deficiencies also play a role in diseases like Multiple Sclerosis, Fibromyalgia, Diabetes and Chronic Fatigue Syndrome. Schizophrenia, a psychotic condition, has been successfully treated with B12 injections in combination with other supplements. There also seems to be a connection between B12 deficiencies and cardiovascular diseases
In the 1950's, it was common practice to treat a patient with the first signs of herpes zoster with a vitamin B12 injection which effectively reversed the symptoms. This knowledge has fallen into oblivion. Ongoing research will most probably further increase the area of use of vitamin B12.
Test methods
Rarely detectable through normal testing procedures, such as blood serum or methyl malonic acid, B12 deficiencies in the brain and CNS can be determined by checking "increased homocystein in LIQUOR", (liquor cerebrospinalis)*, the most appropriate test method.
*) In rare cases, mainly very young patients, side-effects such as headaches may occur. It is therefore recommended to drink water and rest immediately after the spinal test.
If the blood serum B12 value is low, it can be expected that the B12 in the CNS is even lower. If B12 in methyl malonic acid is elevated while the serum value is normal, there are probably B12 deficiencies at a cellular level.
The LIQUOR-test method is rather complicated. Ordinary equipment can be used, but at the Uddevalla Hospital in Sweden, the method of analysis has been especially designed for the purpose. According to Dr. Bo Nilsson, Chief Physician, it is important to measure with an exactness of 1 pmol/L**. The secret is to extract the minute quantity of B12 available without changing the molecule.
**) One thousand of a millionth of a millionth mol per litre, which makes one millionth of a millionth of a gram/litre.
However, many amalgam patients use the trial-and-error method, and initiate the treatment without previous testing.
High doses
It has been suggested that in the presence of heavy metals the cobalt atom is oxidized from CO2+ to CO3+ (denaturation) at the same time as the heavy metal is reduced. The properties of the cobalamin are hypothetically changed and B12 has lost its biological properties. Due to its molecular size, B12 normally has difficulties in crossing the blood-brain barrier and it is possible that denaturation make this even more difficult. This process is analogous to the behaviour of laughing gas.
One of the advocates of this hypothesis is Dr. Britt Ahlrot-Westerlund in Stockholm. The reason why high doses are recommended is that, in the presence of heavy metals in the blood-brain-barrier (more specifically in the plexus chorioideus), most of the vitamin B12 seems to be consumed (for reasons we don't know) and, depending on the level of heavy metal exposure, part of the supplemented B12 will most probably also be consumed in this way until the surplus can be used in the brain where it is needed.
Hg seems to change valency and binding site in the body, and this causes increased free radical formation. It is possible that the Hg change in valency in prooxidative direction oxidizes the cobalt atom. There is, according to Dr. Westerlund, reason to believe that the process of Hg oxidation of the cobalt atom is analogous to the way in which Fe2+ in haemoglobulin is oxidized to Fe3+ in methaemoglobulin (incapable of releasing oxygen) by exogene toxic substances.
To confirm this, an in vitro investigation using electron spin resonance is planned at Stockholm University, Department of Biophysics.
Many different forms
The active vitamin comes in many different forms, i.e. methyl-, cyano-, adnosyl- and hydroxocobalamin, freely transformed into each other in the body. However, vitamin B12 in the brain and CNS is only present as methylcobalamin, which effectively transports methyl groups (-CH3) to proteins in the myelin, the insulating layer which together with fatty acids surrounds the nerve fibers, protecting them just like insulation on electric cables.
In cases of B12 deficiency, toxic fatty acids with 15-17 carbon atoms with a demyelinating effect on the myelin are formed, and the transmission of electrical impulses is disturbed. If enough B12 is supplied, the myelin might be repaired in the course of time.
Methylcobalamin
The uptake from oral B12 supplementation is usually very low, approx. 1 %. Vitamin B12 is therefore often given intramuscularly.
Although vitamin B12 can be supplemented in any of its forms, it is given as hydroxo- or sometimes as cyanocobalamin in many countries. In the south of Europe, however, methylcobalamin is generally used to treat disorders such as neuritis and polyneuropathia. Highly recommended by the Swedish Association of Dental Mercury Patients, it is usually the drug of choice for the treatment of patients with amalgam-induced disorders.
In the experience of Dr. Ahlrot-Westerlund among others, B12 in its active form, methylcobalamin, gives a much better result than other forms which have to be transformed into methylcobalamin. It is possible that the process of transformation itself is inefficient in many patients.
It has been suspected that the supplementation of methylcobalamin in the presence of mercury could lead to the formation of methyl mercury. Inorganic mercury steals methyl groups from methylcobalamin, and methyl mercury is formed. However, methyl mercury is not more toxic than inorganic in mercury and the positive effects of B12 supplementation in this form seem to outweigh the possible disadvantages.
Preservatives
Methylcobalamin should be obtained with dry substance and liquid packed separately to increase the shelf life. The preparation should be kept in the dark stored at a temperature below 25 degees C and used within a year. (Premixed preparations, on the other hand, should be kept in a refrigerator).
Many of the vitamin B12 preparations on the market contain preservatives which can cause problems in sensitive patients. However, the methylcobalamin available under the product names "Algobaz" from Portugal or "Cobamet" produced by a French company (Roussel) also in Portugal do not.
The corresponding Japanese preparation, Esai's Mecobal, contains only 0.5 mg B12. According to Dr. Bo Nilsson, it is probable that, given daily, the transport between the blood-brain barrier is saturated even by such a small dose. In Dr. Ahlrot-Westerlund's opinion, however, methylcobalamin for patients with metal-induced disorders should be given daily intramuscularly* in doses of 10 mg with 8 x 5 mg oral folic acid and 300 mg vitamin B6 for 6 days a week until a positive effect is achieved and then continued until no further peak is achieved. This can take as long as 1/2-1 year or perhaps even longer. The dose should then be gradually diminished (given every other day for example).
*) given subcutaneously, the B12 treatment is, according to Dr. Westerlund, not as effective.
Multiple deficiencies
In many cases it can be assumed that multiple deficiencies, not always easily separable, are present. For example, lack of folic acid can also cause anaemia and its supplementation can mask a B12 deficiency. Therefore it is important that both vitamins are supplied, and to some extent also the other vitamins in the B-complex. Some of the symptoms of B12 deficiency are also present in B1 deficiency** and both deficiencies can be present at the same time.
**) diagnosed by testing thiamin pyrimydine phosphate in serum (expensive)
For a successful recovery from amalgam-poisoning among other disorders, the importance of additional supplementation of essential fatty acids (fish oil etc.) and anti-oxidants should be emphasized.
Some addresses and prices: Methylcobalamin: The two recommended preparations are of equal quality. Both can be ordered from a pharmacy in Lisbon, phone number: +351 1 342 3821. Ask for the head pharmacist, Maria Augusta. Since the preparation is prescription free, it can also easily be obtained during a trip to Portugal. However it should be ordered at least one week ahead.
B12 testing: Uddevalla Hospital in Sweden fax No: +46 522 93101
Test facilities available at the cost of SEK 130:- for B12, 200:- for homocystein and 200:- for methylmalonic acid (MMA). 1 USD is approx. 7 SEK.
According to the Charing Cross & Westminster Medical School, B12 Unit, Dr. Bhatt, there are "a handful" of laboratories worldwide, specialized in vitamin B12 testing. For further information: Tel: +44 (0)181 746 8625, Fax No.:+44 (0)181 746 8860
Monica Kauppi (with thanks to Dr. Westerlund for her kind assistance)
References:
Cees J.H./van Tiggelen. Alzheimers Disease/Alcohol Dementia: Association with Zinc Deficiency and Cerebral vitamin B12 Deficiency. J. of Orthomolecular Psychiatry, 1983, vol 13, No. 2, 97-104.
Eriksson S/Svensson.A, Catalytic effects by thioltransferase on the transfer of methylmercury and p-mercurybenzoate from macromolecules to low molecule weigth thiol compounds. Toxicology 10, 1978, 115-122.
Gran B. B12 i hg dos vid neuropsykiatriska symtom hos misstnkt amalgamsjuka patienter. Swedish Medical Journal, 1994.
Hanson M. Vitamin B12, TF-bladet, 4-1992.
Ideda T. et al. Vitamin B12 levels in serum and cerbrospinal 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 anemia or macrocytos. The new England Journal of Medicine, June 30, 1988
Metz J. Cobalamin Deficiency 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 Society for Trace Element Research in humans, Palm Springs, Dec. 8-12, 1986.
Mrnstad H/Norberg B. Paradigmskifte fr bedmning 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 for 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
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My 6mo twin DD's are EBF and just started rice cereal on the first. Everything has been going fine except this morning one of them had a diaper rash (lots of redness around her anus). I read this as one of the signs of an allergy. BUT I did just buy a different brand diaper yesterday (which they have used randomly before w/no issues). Do you think its the cereal or the diaper? Im ready to start...
Recently an article I read somewhere here suggested that B12 shots could lead to methyl mercury being formed when mercury was present and I was a little worried about this.
This article clears that problem, and I thank you for finding it and posting it.
jazzy
I have good levels of B12 anyway, so not sure they'd help.
I have been close to amemic all my life. I used to give blood 20 years ago and my hemaglobin level was always an issue. I just put it down to the heap of sport I used to play but it was probably something else.
I have had an extream fatty liver for about 7 years now, coincidently this occured soon after I was DX with depression in 2001. I only becameaware of it two weeks ago but both liver damage (Fatty liver) and depression are side affects of mercury poisening. I'm only speculating but I have stomach ulscers and this may have something to do with my bodys lowability to manufacture B12. So far as diet is concerned I'm married to a Neutritionalist. We eat low fat red meat 3or 4 times per week, I cant drink milk but I do eat eggs about once per week aswell as a decent amount of fresh fruit and veg so I am satisfied that its not a dietry cause. The following is taken from WIkipedia and it describes all the most likley causes of Vitamin B12 Deficiency;
[edit] Causes
Inadequate dietary intake of vitamin B12. As the vitamin B12 occurs naturally only in animal products (eggs, meat, milk), and a particular strain of nutritional yeast; a vegan diet can produce a deficiency unless one uses supplements or eats enriched food.[9][10]
Selective impaired absorption of vitamin B12 due to intrinsic factor deficiency. This may depend on loss of gastric parietal cells in chronic atrophic gastritis (in which case, the resulting megaloblastic anaemia takes the name of "pernicious anaemia"), or on wide surgical resection of stomach (such as in bariatric surgery), or on rare hereditary causes of impaired synthesis of intrinsic factor.
Impaired absorption of vitamin B12 in the setting of a more generalised malabsorption or maldigestion syndrome. This includes any form of structural damage or wide surgical resection of the terminal ileum (the principal site of vitamin B12 absorption), forms of achlorhydria (including that artificially induced by drugs such as proton pump inhibitors), as well as bacterial overgrowth (such as in blind loop syndrome).
Chronic intestinal infestation by the fish tapeworm Diphyllobothrium, that competes for vitamin B12, seizing it for its own use and therefore leaving insufficient amount for the host organism. This is mostly confined to Scandinavia and parts of Eastern Europe (for example, in preparers of gefilte fish, who would acquire the tapeworm by sneaking bits of fish before it was cooked while making the Eastern European delicacy).
The diabetes medication, metformin may interfere with B12 dietary absorption.[11]
Hereditary causes such as severe MTHFR deficiency, homocystinuria, and transcobalamin deficiency.
Some studies have shown that giardiasis, or similar parasite should be considered as a cause of Vitamin B12 deficiency, this a result of the problems caused within the intestinal absorption system. [12]
End quote
Lastly there was some one in my fathers family tree who died of Pernicious Anemia in the 1850's so there is a remote possibilit that its a DNA issue. I though think its got more to do with the ulscers in my digestive system ans something to do with the terminal ileum. I would'nt be supprised if mercury rich saliva has damaged signifigant parts of my gut over the years. IBS-D is also a main symptom of mercury poisening. All these thaughts are onlymy speculation though.
Cheers
Al
I think they can hurt if you take too much at once, however. I think it's better to take smaller shots more often than large shots over a monthly or bi-monthly period.
I can only tolerate 1 cc at one time. Otherwise, my blood level of B12 is too high, and I throw up after the shot . . . . But 1 cc once/month does help energy level FOR ME.
None of us are same. We all have in common a constellation of symptoms and immune system dysfunction . . . .
That's why I laugh when I see daily postings asking "have you ever had [a specific symptom]"?
We have all had hundreds of weird symptoms, if we haven't, then we don't have CFIDS.
And it comes down to what YOU have, not what other people have . . . . .
But thanks for your post about a general aid, vitamin B12. It probably would do some good for all of us . . . . . .
Emma, some of us do not absorb things as well as we should. Of those of us who are middle aged we may remember getting shots of penicillin as youngsters when OTHER times we just got that liquid. The shots got into our systems faster ...
Al
I inject 1cc B12 and 1cc of Glutithyione, once a week for 5 weeks, every six months. it helps a lot, clearer thinking, a lot of energy. It is a lot of fun self injecting this stuff, burns... I have been a vegetarian for over 30 years, so I guess that might have something to do with my need for B12.
Be well!
Jon
You need to be aware of the fact that all artificial forms of vitamin B-12 (cyanocobalamin, methylcobalamin and hydroxo cobalamin) methylate mercury. Methylated ionic mercury is probably the most neurotoxic substance there is. The article is correct in noting that methyl mercury is no more toxic than inorganic mercury; however when ionic mercury is methylated it will convert back to ionic once it it transported to the cell. Ionic mercury is cytotoxic, and one atom of it can kill a cell. The danger of methyl mercury is that it crosses all barriers and then converts to its non-methyl form. In other words, methy mercury just allows the mercury to travel anywhere in the body. The ionic (organic mercury as a result of combining with a carbon) can enter the cell or cell membrane, and if it combines with a protein it will form a hapten which can attach to the cell membrane and re-identify the cell marking it for an autoimmune attack.
More current research has been conducted by the Univ. of Kentucky under the chair of Dr. Boyd Haley 1999-2001 in conjuction with the masters work and thesis of Dr. Hal Huggins ("Monographs of Mercury" 1987). Dr. Huggins has treated almost 4,000 cases of mercury toxic diseases (over 1,500 MS with over an 80% success rate), and has evaluated over 35,000 body chemistries of mercury toxic cases. He has written numerous times in many of his published books and works about the clinical evaluations of patients that received B-12 IVs, shots and orally (including sublingual)whose symptoms recured. Not all mercury toxic people will methylate the ionic mercury in their systems from taking B-12 in excess of 25mcg because ionic mercury is very difficult to remove from deep tissue. The ones at risk are the ones who have considerable amounts of ionic mercury in their subcutaneous layers.
Although I was mercury toxic for over twenty years and used B-12 intravenously, I don't recall having any serious long term negative effects. According to Dr. Huggins, the world's leading authority on mercury toxicity, The risk to an individual can not be predetermined. The amount of or frequency is indeterminant. Unfortunately, they will suffer the consequences as a result.
I am not trying to be an alarmist. Just as 95% to 97% of people that have amalgams seem to be in good health, that 3% to %5 who contract serious disorders and diseases from it were also unable to predetermine their fate. There is a thousand times more credible support of how mercury from amalgams cannot cause harm than the support of B-12 from the article that you cited.
I wish you the best, and hope that you do not suffer any serious problems as a result.
wellatlast
Al
I have had consistently low RBC (Red Blood Cell Count) and high MCV (Mean corpuscular volume) for at least last 10 years (other blood tests are mostly fine except thyroid antibodies which have been high for at least last 10 years also) . I have had bouts of low energy and foggy brain since about 14. Life really went down the hill since last spring. Extreme brain fog, heavy head, really slow, balance problems, sometimes numbness in various parts of my head. Bouts of extreme irritability and impatience.
My doctor prescribed B12 injections every other week, because my B12 was rather low, although it did not seem to be out of range (361 pg/mL, when normal is considered 211-911). Nonetheless B12 helps enormously, just not long enough. My brain would clear up, my sense of balance and energy level would get better, my irritability would go away after every injection, but after about 5 to 7 days I would start sliding back to my old sickly state. And since my last blood test showed high B12 (around 800), my doctor told me to cut back the B12 injections to once a month.
While looking for answers on the web I found the same Swedish research data (Dr. Britt Ahlrot-Westerlund) http://www.whale.to/w/b12.html
that links low B12 in the brain to mercury poisoning.
What is really interesting about it they say that a person might have perfectly fine B12 level in his blood, but low B12 in the brain, and high doses of B12 will reach the brain if given at least every few days.
Of course then there is danger of all the methylated mercury that gets created when B12 and mercury react. But the Swedish researchers seem to show that the toxic effect of mercury to humans is mostly due to causing B12 deficiency in the brain, so I guess if you just keep bombarding brain with B12 you are fine. But you cant stop, otherwise all the methylated mercury will quickly starve the brain.
I have quite a few amalgam fillings, and about a year and a half ago I had quite a few of them drilled out and replaced with no precautions taken whatsoever. I suspect that I might have quite a load of mercury stashed in various parts of my body, but I am not sure how to test for that, since blood or urine tests will only show an acute poisoning. Anyway, I am planning to do these tests as well as a hair test. And even if the tests dont show much, Ill try high doses of B12 every few days for a few months, because the way I feel when I am not on B12 seems to show that I will end up in a wheelchair pretty soon if I dont act. I will also try to see if there are any laboratories in the US, that test for B12 deficiency in liquor cerebrospinalis.
This, for him did not do as much for him. I must say he does NOT have any brain fog. I think if you have brain fog or muscle issues then it is much more likely B's will help.
He has D deficiency even after taking 1400IU D2 so we put him on 2400 D3 day and 4 months later he is 10 points higher, not at mid normal but getting there.
I do think though that there are subclasses of these diseases: MS, RA, CFS, Fibro. Different deficiencies that lead to tissue degrade.
I agree with much of what Alistar has said. If you want you can look at my website
http://www.ramswebsite.net/Flowcharts.html then double click the B12 & D, flowcharts to get a visual of how these vitamins are processed.
I bring up D because these TWO vitamins are very key to MANY functions in the body. Both should be checked. Realize you can get a B panel of the BLOOD done but this does NOT tell you what is getting to the cell. A methyl malic acid and homcysteine test tells you in general what B is in the cell. The problem with this test is that there are about 17 B vitamins and it just gives you an overview of all B so if you are taking too much of a few B vitamins ie folic acid(b9) Then it can mask a B12 or other B deficiency.
Also if you take B vitamins orally less than 5% is used by the body because it is such a fragile vitamin the enzymes and acids break it down before it can be used. So you either have to tkae higher oral doses, OR use subligual spray in the mouth that goes directly to the bloodstream OR injectins from a doc. The interesting part is that certain gut bacteria can MAKE B vitamins. I am still researching to find which ones do this. If I can then I'll just have my hubby use this probacteria strain.
FYI Choline (good for nerves and MUSCLE function) is also a Methyl compound but in few vitamins. Many B vitamins work best when taken with other B vitamins. So just taking B12 is NOT neraly as good as taking many different B's together
Best wishes to all
EP