- Gabapentin :-
- It is used to treat painful nerve diseases.
- It may be given to you for other reasons. Talk with the doctor.
Gabapentin is used with other medications to prevent and control seizures. It is also used to relieve nerve pain following shingles (a painful rash due to herpes zoster infection) in adults. Gabapentin is known as an anticonvulsant or antiepileptic drug.
Is Gabapentin a good painkiller?
How is this medication given for pain when its a drug for fits? I have femoral nerve palsy in my left leg and bad pain in both my arms,and my lower back, i am undergoing tests but no results yet. I am on 1800mgs per day of Gabapentin and 30mg of Amitriptyline (which is a drug for depression) i am very confused and still in alot of pain, in fact these pills arnt making any difference, should i stop taking them?
Gabapentin is a neurological drug, so it helps with nerve pain. Don’t stop taking meds right away. Nerve pain is hard to get rid of and it may take a dose change eventually. Anti depressents are used to treat pain, however cymbalta is the usual one that is used.
Methylcobalamin is equivalent physiologically to vitamin B12, and can be used to prevent or treat pathology arising from a lack of vitamin B12 (vitamin B12 deficiency), such as pernicious anemia.
Methylcobalamin B12 supplement benefit and side effects, proper dosage, 5mg pills – Cobalamin information
September 22 2016 by Ray Sahelian, M.D.
Methylcobalamin is one of the two coenzyme forms of vitamin B12 (cobalamin). Vitamin B12 plays an important role in red blood cells, prevention and treatment of anemia, methylation reactions, and immune system regulation. Evidence indicates it has some metabolic and therapeutic applications not shared by the other forms of vitamin B12.
Rev Prat. Oct 2013. Vitamin B12 cobalamin. The term “vitamin B12” refers to four cobalamins (Cbl), including methyl-Cbl and adenosyl-Cbl, the two enzyme co-factors of methionine synthase and methylmalonyl-CoA mutase, respectively. Vitamin B12 deficiency produces clinical disorders that include mainly megaloblastic anaemia, peripheral and central neurological manifestations. The clinical significance of low blood B12 concentrations in the absence of manifestations of deficiency is a matter of debate. The biochemical diagnosis of the subclinical and clinical deficiency of vitamin B12 has been enriched by several parameters, including serum methylmalonic acid, homocysteine, and holo-transcobalamine, which have been evaluated over the past two decades.
Methylcobalamin is the active form of vitamin B12 that acts as a cofactor for methionine synthase in the conversion of homocysteine to methionine, thus lowering blood levels of homocysteine. It acts as a methyl donor and participates in the synthesis of SAM-e (S-adenosylmethionine), a nutrient that has powerful mood elevating properties. Vitamin B12 can be absorbed sublingually, orally, and in a doctor’s office it can be given by injection.
Clinical Uses and benefits
Methylcobalamin supplements increase alertness and body temperature.
May slightly help those with diabetic neuropathy. A better nutrient for this condition is lipoic acid.
It has been found to be helpful in Bell’s palsy. However, I don’t have personal experience to determine whether when given in a doctor’s office to actual patients with Bell’s palsy it really helps or not.
Methylcobalamin taken orally is effective in the treatment of pernicious anemia, says a Japanese study.
Methylcobalamin may inhibit the ototoxic (hearing damage) side effects of the antibiotic gentamicin.
Vitamin B-12 is essential for brain development, neural myelination, and cognitive function. Inadequate vitamin B-12 status during pregnancy and early childhood has been associated with adverse child health outcomes, including impaired cognitive development.
Neural Plast. 2013. Methylcobalamin: A Potential Vitamin of Pain Killer. Methylcobalamin (MeCbl), the activated form of vitamin B12, has been used to treat some nutritional diseases and other diseases in clinic, such as Alzheimer’s disease and rheumatoid arthritis. As an auxiliary agent, it exerts neuronal protection by promoting regeneration of injured nerves and antagonizing glutamate-induced neurotoxicity. Recently several lines of evidence demonstrated that MeCbl may have potential analgesic effects in experimental and clinical studies. For example, MeCbl alleviated pain behaviors in diabetic neuropathy, low back pain and neuralgia. MeCbl improved nerve conduction, promoted the regeneration of injured nerves, and inhibited ectopic spontaneous discharges of injured primary sensory neurons. This review aims to summarize the analgesic effect and mechanisms of MeCbl at the present.
Curr Med Res Opin. 2015 . Nutritional management of patients with diabetic peripheral neuropathy with L-methylfolate-methylcobalamin-pyridoxal-5-phosphate: results of a real-world patient experience trial.
Cobalamin and methylcobalamin biochemistry
The B12 or cobalamin coenzymes are complex macrocycles whose reactivity is associated with a unique cobalt-carbon bond. The two biologically active forms are methylcobalamin and AdoCbl and their closely related cobamide forms. Methylcobalamin participates as the intermediate carrier of activated methyl groups. During the catalytic cycle the coenzyme shuttles between methylcobalamin and the highly nucleophilic cob(I)alamin form. Examples of methylcobalamin -dependent enzymes include methionine synthase and Me-H4-MPT: coenzyme M methyl transferase. AdoCbl functions as a source of carbon-based free radicals that are unmasked by homolysis of the coenzyme’s cobalt-carbon bond. The free radicals are subsequently used to remove non-acid hydrogen atoms from substrates to facilitate a variety of reactions involving cleavage of carbon-carbon, carbon-oxygen and carbon-nitrogen bonds.
Coenzyme B12 (cobalamin)-dependent enzymes.
Essays Biochem. 1999.
The B12 or cobalamin coenzymes are complex macrocycles whose reactivity is associated with a unique cobalt-carbon bond. The two biologically active forms are methylcobalamin and AdoCbl and their closely related cobamide forms. Methylcobalamin participates as the intermediate carrier of activated methyl groups. During the catalytic cycle the coenzyme shuttles between methylcobalamin and the highly nucleophilic cob(I)alamin form. Examples of methylcobalamin -dependent enzymes include methionine synthase and Me-H4-MPT: coenzyme M methyl transferase.
Dibencozide is an active coenzyme form of vitamin B-12. It is required for processing branched chain amino acids through the Krebs cycle.
Vitamin B12, or cobalamin, is one of the most structurally complex small molecules made in Nature. Adenosyltransferase converts cobalamin to coenzyme B(12).
Four cobalamines (methyl-, hydroxy-, adenosyl- and cyancobalamines) are considered as natural forms of vitamin B12 in human and animal tissues. Methyl- and adenosylcobalamines are the coenzymes of more than 10 enzymes, catalyzing important reactions of lipid, carbohydrate and protein metabolism. The four natural forms of vitamin B12 are interconverted in presence of corresponding enzymatic systems. Content of individual forms of cobalamines and of corresponding coenzymes depends on the function of enzymatic systems involved in their synthesis as well as on the enzymes, which use these derivatives as coenzymes. Spectra of cobalamines in human and animal bodies are dynamic systems, distinctly and specifically responding to various effects.
The biosynthetic route to adenosylcobalamin from its five-carbon precursor, 5-aminolaevulinic acid, can be divided into three sections: (1) the biosynthesis of uroporphyrinogen III from 5-aminolaevulinic acid, which is common to both pathways; (2) the conversion of uroporphyrinogen III into the ring-contracted, deacylated intermediate precorrin 6 or cobalt-precorrin 6, which includes the primary differences between the two pathways; and (3) the transformation of this intermediate to form adenosylcobalamin.
Deficiency due to medication use
Proton pump inhibitors also reduce the absorption of vitamin B12 probably by inhibiting intragastric proteolysis and, thus, its release from food required prior to binding to R-proteins and gastric intrinsic factor.
Metformin, a drug used for diabetes management, could cause deficiency.
Oral supplements of vitamin B12 appear to correct vitamin B12 deficiencies as well as B12 injections. However, in order to correct a deficiency, oral doses need to contain more than 200 times the recommended daily allowance (RDA) of vitamin B12. Study author Dr. Lisette C. P. G. M. de Groot of Wageningen University in the Netherlands explained that most people develop vitamin B12 deficiencies as a result of “malabsorption,” in which their bodies become unable to extract vitamin B12 from food. The deficiency typically strikes older people, she added, and takes years to develop. In some instances, people who avoid animal products — such as vegans and followers of a macrobiotic diet — can also develop a deficiency in vitamin B12 as a result of not eating enough B12-rich foods. A vitamin B12 deficiency is typically treated by monthly, often painful, shots. To investigate whether an oral dose of vitamin B12 works, as well, they tested various daily doses of oral vitamin B12 supplements in 120 people aged 70 and older. They found that daily oral doses of 647 to 1032 micrograms of vitamin B12 appeared to correct the deficiency. The current RDA for vitamin B12 is 3 micrograms per day. Archives of Internal Medicine, May 23, 2005.
Mothers with low levels of vitamin B12 in their blood are at increased risk of having an infant with spina bifida — a birth defect in which the spinal cord fails to form properly. Based on previous research, pregnancy guidelines recommend that women consume enough folic acid to reduce the risk of spina bifida and related problems. The new findings suggest that these guidelines should also include recommendations about vitamin B12.
The many faces of vitamin B12: catalysis by cobalamin-dependent enzymes.
Annu Rev Biochem. 2003.
Vitamin B12 is a complex organometallic cofactor associated with three subfamilies of enzymes: the adenosylcobalamin-dependent isomerases, the methylcobalamin -dependent methyltransferases, and the dehalogenases. Different chemical aspects of the cofactor are exploited during catalysis by the isomerases and the methyltransferases. Thus, the cobalt-carbon bond ruptures homolytically in the isomerases, whereas it is cleaved heterolytically in the methyltransferases. The reaction mechanism of the dehalogenases, the most recently discovered class of B12 enzymes, is poorly understood. Over the past decade our understanding of the reaction mechanisms of B12 enzymes has been greatly enhanced by the availability of large amounts of enzyme that have afforded detailed structure-function studies, and these recent advances are the subject of this review.
Acc Chem Res. 2001.
Cobalamin cofactors play critical roles in radical-catalyzed rearrangements and in methyl transfers. This Account focuses on the role of methylcobalamin and its structural homologues, the methylcorrinoids, as intermediaries in methyl transfer reactions, and particularly on the reaction catalyzed by cobalamin-dependent methionine synthase. In these methyl transfer reactions, the cobalt(I) form of the cofactor serves as the methyl acceptor. Biological methyl donors to cobalamin include N5-methyltetrahydrofolate, other methylamines, methanol, aromatic methyl ethers, acetate, and dimethyl sulfide. The challenge for chemists is to determine the enzymatic mechanisms for activation of these unreactive methyl donors and to mimic these amazing biological reactions.
Effects of vitamin B12 on performance and circadian rhythm in normal subjects.
This preliminary study investigates effects of methyl- and cyanocobalamin on circadian rhythms, well-being, alertness, and concentration in healthy subjects. Six women (mean age 35 years) and 14 men (mean age 37 years) were randomly assigned to treatment for 14 days with 3 mg cyano-(CB12) or methylcobalamin (MB12) after 9 days of pre-treatment observation. Levels in the CB12 group increased rapidly in the first, then slowly in the second treatment week, whereas increase in the MB12 group was linear. Urinary aMT6s excretion was reduced by both forms of vitamin B12 over 24 hours with a significant decrease between 0700-1100 hours, whereas urinary excretion of potassium was significantly increased between 0700-1100 hours. Activity from 2300-0700 hours increased significantly under both forms of vitamin B12. Sleep time was significantly reduced under MB12 intake. In this group the change in the visual analogue scales items “sleep quality,” “concentration,” and “feeling refreshed” between pretreatment and the first week of treatment showed significant correlations with vitamin B12 plasma levels. Cortisol excretion and temperature were not affected by either medication. We conclude that vitamin B12 exerts a direct influence on melatonin. Only MB12 has a positive psychotropic alerting effect with a distribution of the sleep-wake cycle toward sleep reduction.