lymeHerx001
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posted
Ok, so if I look up B12 the list of things it does in the body is staggering. I cant follow it.
I feel slightlly better on it and I read that taking it with folic acid is necesarry especailly for detox.
Whats the deal? Is it really that good as a long term solution?
What about the mercury issue.
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lymeHerx001
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This is taken from wikipedia ***************
Vitamin B12 is normally involved in the metabolism of every cell of the body, especially affecting the DNA synthesis and regulation but also fatty acid synthesis and energy production. However, many (though not all) of the effects of functions of B12 can be replaced by sufficient quantities of folic acid (another B vitamin), since B12 is used to regenerate folate in the body. Most "B12 deficient symptoms" are actually folate deficient symptoms, since they include all the effects of pernicious anemia and megaloblastosis, which are due to poor synthesis of DNA when the body does not have a proper supply of folic acid for the production of thymine. When sufficient folic acid is available, all known B12 related deficiency syndromes normalize, save those narrowly connected with the B12 dependent enzymes Methylmalonyl Coenzyme A mutase (MUT), and 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR), also known as methionine synthase; and the buildup of their respective substrates (methylmalonic acid, MMA) and homocysteine.
Coenzyme B12's reactive C-Co bond participates in two types of enzyme-catalyzed reactions.[10]
Rearrangements in which a hydrogen atom is directly transferred between two adjacent atoms with concomitant exchange of the second substituent, X, which may be a carbon atom with substituents, an oxygen atom of an alcohol, or an amine. Methyl (-CH3) group transfers between two molecules. In humans, only two corresponding coenzyme B12-dependent enzymes are known:
Methylmalonyl Coenzyme A mutase (MUT) which uses the AdoB12 form and reaction type 1 to catalyze a carbon skeleton rearrangement (the X group is -COSCoA). MUT's reaction converts MMl-CoA to Su-CoA, an important step in the extraction of energy from proteins and fats (for more see MUT's reaction mechanism). This functionality is lost in vitamin B12 deficiency, and can be measured clinically as an increased methylmalonic acid (MMA) level. Unfortunately, an elevated MMA, though sensitive to B12 deficiency, is probably overly sensitive, and not all who have it actually have B12 deficiency. For example, MMA is elevated in 90-98% of patients with B12 deficiency; however 25-20% of patients over the age of 70 have elevated levels of MMA, yet 25-33% of them do not have B12 deficiency. For this reason, assessment of MMA levels is not routinely recommended in the elderly.[11] The "gold standard" test for B12 deficiency continues to be low blood levels of the vitamin. The MUT function cannot be affected by folate supplementation, which is necessary for myelin synthesis (see mechanism below) and certain other functions of the central nervous system. Other functions of B12 related to DNA synthesis related to MTR dysfunction (see below) can often be corrected with supplementation with the vitamin folic acid, but not the elevated levels of homocysteine, which is normally converted to methionine by MTR. 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR), also known as methionine synthase. This is a methyl transfer enzyme, which uses the MeB12 and reaction type 2 to catalyze the conversion of the amino acid Hcy back into Met (for more see MTR's reaction mechanism).[12] This functionality is lost in vitamin B12 deficiency, and can be measured clinically as an increased homocysteine level in vitro. Increased homocysteine can also be caused by a folic acid deficiency, since B12 helps to regenerate the tetrahydrofolate (THF) active form of folic acid. Without B12, folate is trapped as 5-methyl-folate, from which THF cannot be recovered unless a MTR process reacts the 5-methyl-folate with homocysteine to produce methionine and THF, thus decreasing the need for fresh sources of THF from the diet. THF may be produced in the conversion of homocysteine to methionine, or may be obtained in the diet. It is converted by a non-B12-dependent process to 5,10-methylene-THF, which is involved in the synthesis of thymine. Reduced availability of 5,10-methylene-THF results in problems with DNA synthesis, and ultimately in ineffective production cells with rapid turnover, in particular blood cells, and also intestinal wall cells which are responsible for absorption. The failure of blood cell production results in the once-dreaded and fatal disease, pernicious anemia. All of the DNA synthetic effects, including the megaloblastic anemia of pernicious anemia, resolve if sufficient folate is present (since levels of 5,10-methylene-THF still remain adequate with enough dietary folate). Thus the best known function of B12 (that which is indirectly involved with DNA synthesis and restoration of cell-division and anemia) is actually a facultative function which is mediated by B12 conservation of active folate which can be used for DNA production.[13] If folate is present in quantity, then of the two absolutely B12 dependent reactions, the MUT reaction shows the most direct and characteristic secondary effects, focusing on the nervous system. Since the late 1990s folic acid has begun to be added to fortify flour in many countries, so that folate deficiency is now more rare. At the same time, since DNA synthetic-sensitive tests for anemia and erythrocyte size are routinely done in even simple medical test clinics (so that these folate mediated-biochemical effects are more often directly detected), the MTR dependent effects of B12 deficiency are becoming apparent not as anemia (as they were classically), but now mainly as an elevation of homocysteine in the blood and urine (homocysteinuria). This condition may result in long term damage to arteries and in clotting (stroke and heart attack), but is difficult to separate from other processes associated with atherosclerosis and aging.
The B12 dependent MTR reactions may have neurological effects through an indirect mechanism. Adequate methionine (which must otherwise be obtained in the diet) is needed to make S-adenosyl-methionine, which is in turn necessary for methylation of myelin sheath phospholipids. In addition, SAMe is involved in the manufacture of certain neurotransmitters, catecholamines and in brain metabolism. These neurotransmitters are important for maintaining mood, possibly explaining why depression is associated with B12 deficiency. Methylation of the myelin sheath phospholipids may also depend on adequate folate, which in turn is dependent on MTR recycling, unless ingested in relatively high amounts.
The specific myelin damage resulting from B12 deficiency has also been connected to B12 reactions related to MUT, which is needed to convert methylmalonyl coenzyme A into succinyl coenzyme A. Failure of this second reaction to occur results in elevated levels of methylmalonic acid (MMA), a myelin destabilizer. Excessive MMA will prevent normal fatty acid synthesis, or it will be incorporated into fatty acid itself rather than normal malonic acid. If this abnormal fatty acid subsequently is incorporated into myelin, the resulting myelin will be too fragile, and demyelination will occur. Although the precise mechanism(s) are not known with certainty, the result is subacute combined degeneration of central nervous system and spinal cord.[14] Whatever the cause, it is known that B12 deficiency causes neuropathies, even if folic acid is present in good supply, and therefore anemia is not present.
[edit] Human absorption and distribution The human physiology of vitamin B12 is complex, and therefore is prone to mishaps leading to vitamin B12 deficiency. The vitamin as it occurs in foods enters the digestive tract bound to proteins, known as salivary R-binders. Stomach proteolysis of these proteins requires an acid pH, and also requires proper parietal cell release of proteolytic enzymes referred to as pepsin. (Even small amounts of B12 taken in supplements bypasses these steps and thus any need for gastric acid, which may be blocked by antacid drugs).
The free B12 then attaches to gastric intrinsic factor, which is generated by the gastric parietal cells in response to histamine, gastrin and pentagastrin, as well as the presence of food. The generation of this intrinsic factor-B12 complex will allow absorption of the vitamin as well as protect the vitamin from catabolism by intestinal bacteria. If this step fails due to gastric parietal cell atrophy (the problem in pernicious anemia), sufficient B12 is not absorbed later on, unless administered orally in relatively massive doses (500 to 1000 mcg/day). Due to the complexity of B12 absorption, geriatric patients, many of whom are hypoacidic due to reduced parietal cell function, have an increased risk of B12 deficiency.[15]
The conjugated vitamin B12-intrinsic factor complex (IF/B12) is then normally absorbed by the terminal ileum of the small bowel. Absorption of food vitamin B12 therefore requires an intact and functioning stomach, exocrine pancreas, intrinsic factor, and small bowel. Problems with any one of these organs makes a vitamin B12 deficiency possible.
Once the IF/B12 complex is recognized by specialized ileal receptors, it is transported into the portal circulation. The vitamin is then transferred to transcobalamin II (TC-II/B12), which serves as the plasma transporter of the vitamin. Genetic deficiencies of this protein are known, also leading to functional B12 deficiency.
For the vitamin to serve inside cells, the TC-II/B12 complex must bind to a cell receptor, and be endocytosed. The transcobalamin-II is degraded within a lysozyme, and free B12 is finally released into the cytoplasm, where it may be transformed into the proper coenzyme, by certain cellular enzymes (see above).
Hereditary defects in production of the transcobalamins and their receptors may produce functional deficiencies in B12 and infantile megaloblastic anemia, and abnormal B12 related biochemistry, even in some cases with normal blood B12 levels.[16]
Individuals who lack intrinsic factor have a decreased ability to absorb B12. This results in 80-100% excretion of oral doses in the feces versus 30-60% excretion in feces as seen in individuals with adequate intrinsic factor.[15]
The total amount of vitamin B12 stored in body is about 2,000-5,000 mcg in adults. Around 80% of this is stored in the liver[17]. Approximately 0.1% of this is lost per day by secretions into the gut as not all these secretions are reabsorbed. How fast B12 levels change depends on the balance between how much B12 is obtained from the diet, how much is secreted and how much is absorbed. B12 deficiency may arise in a year if initial stores are low and genetic factors unfavourable or may not appear for decades. In infants, B12 deficiency can appear much more quickly[18].
[edit] History of B12 as a treatment for pernicious anemia B12 deficiency is the cause of pernicious anemia, a usually-fatal disease of unknown etiology when it was first described in medicine. The cure was discovered by accident. George Whipple had been inducing anemia in dogs by bleeding them, and then conducting experiments in which he fed them various foods to observe which diets allowed them fastest recovery from the anemia produced. In the process, he discovered that ingesting large amounts of liver seemed to most-rapidly cure the anemia of blood loss, and hypothesized that therefore liver ingestion be tried for pernicious anemia, an anemic disease of the time with no known cause or cure. He tried this and reported some signs of success in 1920. After a series of careful clinical studies George Minot and William Murphy set out to partly isolate the substance in liver which cured anemia in dogs, and found that it was iron. They found further that the partly isolated water-soluble liver-substance which cured pernicious anemia in humans was something else entirely different--and which had no effect at all on canines under the conditions used. The specific factor treatment for pernicious anemia, found in liver juice, had been found by this coincidence. These experiments were reported by Minot and Murphy in 1926, marking the date of the first real progress with this disease, though for several years, patients were still required to eat large amounts of raw liver or to drink considerable amounts of liver juice.
In 1928, the chemist Edwin Cohn prepared a liver extract that was 50 to 100 times more potent than the natural liver products. The extract was the first workable treatment for the disease. For their initial work in pointing the way to a working treatment, Whipple, Minot, and Murphy shared the 1934 Nobel Prize in Physiology or Medicine.
The active ingredient in liver was not isolated until 1948 by the chemists Karl A. Folkers of the United States and Alexander R. Todd of Great Britain. The substance was a cobalamin called vitamin B12. It could also be injected directly into muscle, making it possible to treat pernicious anemia more easily.[19]
The chemical structure of the molecule was determined by Dorothy Crowfoot Hodgkin and her team in 1956, based on crystallographic data. Eventually, methods of producing the vitamin in large quantities from bacteria cultures were developed in the 1950s, and these led to the modern form of treatment for the disease.
[edit] Symptoms and damage from deficiency
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map1131
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I have two good brands of B12 and both contain folic acid listed on the ingredients. Are you doing a sublingual?
I can't answer you question on metals??? I know it makes a difference for me. I take it in large doses also.
Pam
-------------------- "Never, never, never, never, never give up" Winston Churchill Posts: 6478 | From Louisville, Ky | Registered: Jan 2002
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lymeHerx001
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Yes taking subligual.
Any other people have any info?
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disturbedme
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I don't know much about it... but I do know that having a B12 deficiency can give a person a lot of lyme-like symptoms... So it's good to have your B12 levels checked... I also think everyone would benefit (maybe not noticeably though) from taking at least sublingual B12 and folic acid daily.
When I first went downhill I thought maybe I had B12 deficiency because I am vegan... my levels were normal though. But I take sublingual B12 and folic acid before bed every day.
The symptoms of B12 deficiency:
Numbness or tingling in the hands or feet Insomnia Loss of memory Loss of appetite Dizziness Lack of balance Depression Digestive problems Diarrhea Dizziness Liver enlargement Eye problems Fatigue Headaches Hallucinations Inflamed tongue Breathing difficulties Shortness of breath Paleness Palpitations Neurological damage Tinitus or ringing in the ears etc.
-------------------- One can never consent to creep when one feels an impulse to soar. ~ Helen Keller
My Lyme Story Posts: 2965 | From Land of Confusion (bitten in KS, moved to PA, now living in MD) | Registered: Jun 2007
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lymeHerx001
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Thanks
From what I understand b12 helps our cells use iron. Iron is needed to use oxygen.
Too much oxygen is not good because it oxydizes our cells, (rust). But no oxygen is also not good because then we die.
Posts: 2905 | From New England | Registered: Sep 2004
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lymeHerx001
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^
Posts: 2905 | From New England | Registered: Sep 2004
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lymeHerx001
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More info on B12
Protection via Methylcobalamin
Protective effects of a vitamin B12 analogue, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons Akaike A Tamura Y Sato Y Yokota T, Eur J Pharmacol 1993 Sep 7) 2411-6
The effects of methylcobalamin, a vitamin B12 analogue, on glutamate-induced neurotoxicity were examined using cultured rat cortical neurons. Cell viability was markedly reduced by a brief exposure to glutamate followed by incubation with glutamate-free medium for 1 h. Glutamate cytotoxicity was prevented when the cultures were maintained in methylcobalamin-containing medium. Glutamate cytotoxicity was also prevented by chronic exposure to S-adenosylmethionine, which is formed in the metabolic pathway of methylcobalamin. Chronic exposure to methylcobalamin and S- adenosylmethionine also inhibited the cytotoxicity induced by methyl-D-aspartate or sodium nitroprusside that releases nitric oxide. In cultures maintained in a standard medium, glutamate cytotoxicity was not affected by adding methylcobalamin to the glutamate-containing medium. In contrast, acute exposure to MK-801, a NMDA receptor antagonist, prevented glutamate cytotoxicity. These results indicate that chronic exposure to methylcobalamin protects cortical neurons against NMDA receptor-mediated glutamate cytotoxicity.
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lymeHerx001
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Protection via Methylcobalamin
Methylcobalamin and Diabetic Neuropathy
Clinical usefulness of intrathecal injection of methylcobalamin in patients with diabetic neuropathy Ide H Fujiya S Asanuma Y Tsuji M Sakai H Agishi Y, Clin Ther (1987) 9(2):183-92
Seven men and four women with symptomatic diabetic neuropathy were treated with methylcobalamin (2,500 micrograms in 10 ml of saline) injected intrathecally. Treatment was begun when patients had good metabolic control, as determined by measurements of plasma glucose and hemoglobin, and was repeated several times with a one-month interval between injections. Three patients were re-treated one year after the last intrathecal injection. Symptoms in the legs, such as paresthesia, burning pains, and heaviness, dramatically improved. The effect appeared within a few hours to one week and lasted from several months to four years. The mean peroneal motor-nerve conduction velocity did not change significantly. The mean (+/- SD) concentration of methylcobalamin in spinal fluid was 114 +/- 32 pg/ml before intrathecal injection (n = 5) and 4,752 +/- 2,504 pg/ml one month after intrathecal methylcobalamin treatment (n = 11). Methylcobalamin caused no side effects with respect to subjective symptoms or characteristics of spinal fluid. These findings suggest that a high concentration of methylcobalamin in spinal fluid is highly effective and safe for treating the symptoms of diabetic neuropathy.
-------------------------------------------------------------------------------- Nerve Regeneration with Methylcobalamin
Ultra-high dose methylcobalamin promotes nerve regeneration in experimental acrylamide neuropathy. Watanabe T Kaji R Oka N Bara W Kimura J, J Neurol Sci (1994 Apr) 122(2):140-3
Despite intensive searches for therapeutic agents, few substances have been convincingly shown to enhance nerve regeneration in patients with peripheral neuropathies. Recent biochemical evidence suggests that an ultra-high dose of methylcobalamin (methyl-B12) may up-regulate gene transcription and thereby protein synthesis. We examined the effects of ultra-high dose of methyl-B12 on the rate of nerve regeneration in rats with acrylamide neuropathy, using the amplitudes of compound muscle action potentials (CMAPs) after tibial nerve stimulation as an index of the number of regenerating motor fibers. After intoxication with acrylamide, all the rats showed equally decreased CMAP amplitudes. The animals were then divided into 3 groups; rats treated with ultra-high (500 micrograms/kg body weight, intraperitoneally) and low (50 micrograms/kg) doses of methyl- B12, and saline-treated control rats. Those treated with ultra-high dose showed significantly faster CMAP recovery than saline-treated control rats, whereas the low-dose group showed no difference from the control. Morphometric analysis revealed a similar difference in fiber density between these groups. Ultra-high doses of methyl-B12 may be of clinical use for patients with peripheral neuropathies.
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map1131
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I have to do higher doses than recommended for "normal healthy folks". I do 3000mcg methyl b-12 a day.
Pam
-------------------- "Never, never, never, never, never give up" Winston Churchill Posts: 6478 | From Louisville, Ky | Registered: Jan 2002
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lymeHerx001
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I have the tabs that are 1000mcg. I can take 10 or more a day!
Apparently they are water soluble so there is no upper dosage limit.
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lymeHerx001
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^
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treepatrol
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quote:Originally posted by disturbedme: I don't know much about it... but I do know that having a B12 deficiency can give a person a lot of lyme-like symptoms... So it's good to have your B12 levels checked... I also think everyone would benefit (maybe not noticeably though) from taking at least sublingual B12 and folic acid daily.
When I first went downhill I thought maybe I had B12 deficiency because I am vegan... my levels were normal though. But I take sublingual B12 and folic acid before bed every day.
The symptoms of B12 deficiency:
Numbness or tingling in the hands or feet Insomnia Loss of memory Loss of appetite Dizziness Lack of balance Depression Digestive problems Diarrhea Dizziness Liver enlargement Eye problems Fatigue Headaches Hallucinations Inflamed tongue Breathing difficulties Shortness of breath Paleness Palpitations Neurological damage Tinitus or ringing in the ears etc.
Add in
Achey all over low level acheyness for lymies at least this one. Also bones get brittle I broke a molar believe it or not chewing a apple and there was no filling in it.
I suspect also eye problems.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
posted
Methyl-B12 is important for myelin formation. Myelin is the insulation around your nerves and in your brain. I'm pretty sure that lyme interferes with myelin formation.
Jennifer
Posts: 236 | From Illinois | Registered: Feb 2009
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-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
posted
I believe I am anemic from Babesia due to having elevated MCV on my labs each month. I have never had my B-12 checked but I recently started taking B complex Plus. I am hoping it helps my heart issues.
-------------------- Lyme, Babesia Microti, possible Bart. Posts: 173 | From A little south of sanity - PA | Registered: Jan 2009
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