Discussions By Condition: Medical Stories

Active B12 Basics

Posted In: Medical Stories 51 Replies
  • Posted By: Freddd
  • July 19, 2009
  • 08:01 PM

INTRODUCTION
version 1.0 - 07/19/09


The purpose of this thread is to collect in one place all the basic information somebody new to this idea might need. That way somebody new can be directed to just this one thread to find the basics. Please continue discussing all issues and questions at
http://forums.wrongdiagnosis.com/showthread.php?t=9948&goto=newpost.


The intent is to keep the needed information easy to find and not buried in thousands of posts.

The two active in the human body forms of b12 are methylcobalamin (methylb12, mb12, mecob, mecbl, etc) and adenosylcobalamin (adenosylb12, adb12, adob12, cobalamide, etc). There are many international variations in spelling and the form of the names of these substance. They are tremendously more active and effective than the two more usual forms used in most vitamins and therapies, cyanocobalamin (cyanob12, cb12, cyanideb12, etc) and hydroxycobalamin (hydroxyb12, hb12, hyb12, etc). A third inactive form of b12 is beginning to gain some notariety, glutationylcobalamin (glutathionylb12, gb12, etc). It suffers from the same problems as the other inactive forms of b12. These specific 3 inactive cobalamins can be converted to one or both active forms in very limited quantity by MOST but not all, people.

The other vitamin that we also comes in active and inactive forms is folate. Folic acid is the most common synthetic form of the vitamin. About half the people can't convert it to methylfolate, the active form in the body, in an adequate amount. The other half can barely convert an amount that is considered sufficient. Methylfolate is also known by thew brand name Metafolin. This active form can make a very large difference in effectiveness for many people.

There are a set of relatively subtle deficiency diseases that are common in our society caused by taking the artificial forms of these actiove vitamins. The artificial forms only prevent some problems and symptoms in some people. Because they are thought of as effective, the deficiency diseases that remain are invisible. They can't be seen because of the widespread usage of the synthetic forms obscurring what the lack of the active forms causes because "that problem is already taken care of therefore it must be something else". These many deficiency diseases can exist in persons already taking the synthetic inactive forms of the vitamins. The tests are designed and interpreted with the assumptions of the synthetic versions and do not adequately detect many of the deficiencies. The details of all this will be pointed out in the various specific posts

As the size of each post is limited, there willl be a series of posts covering various aspects of these substances, some very basic, some more advanced. As they will be posted by me and a variety of others as we have the opportunity, they are in no specific order. With a little luck, each post will carry a title, version and date as this page does. Updated versions may supercede earlier versions. For instance I am going to start off with a symptoms list. A month or two from now I may post that list again with just a few minor changes, and so on. So this topic should also be read from the end reading only the most recent version of each posting. I hope this helps. Good luck and good health to everybody.

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  • SYMPTOMS, SIGNS AND CO-CORRELATES OF METHYLB12, ADENOSYLB12, METHYFOLATE AND SELECTED COFACTOR DEFICIENCIESLAST UPDATE - Version 1.0, 07/13/09 mouth sensitive to hot and cold sore burning tonguebeef-red tongue, possibly smoother than normalsore mouth, no infection or apparant reasonteeth sensitive to hot and coldcanker soresburning bladder (no UTI)painful urgency (no UTI)burning urethra (no UTI)burning muscle painaccumulating muscle pains following exertionsore muscleslack of muscle recovery after exerciseexercise does not build muscleextremely sore neck muscles reversing normal curvature of neckexercise deblitates for up to a week, making things much worsepainfully tight muscles, especially legs and/or armsfrequent muscle spasms anywhere in bodymuscle pain especially around attachment points to bonesEighteen severely tender muscle spots of FMSBursitisdyspepsia - sick stomach, nausea, regurgitation, vomiting, bloating, not emptyingflatulencealtered bowel habitsabdominal painloss of appetite for meat, fish, eggs, dairy, the only b12 contining foods, nutrient specific anorexiaintermittent constipationintermittant diarrheairritable bowel syndromeCrohns disease (direction of causality if any not established)Celiac disease (direction of causality if any not established) - gluten sensitivityDairy sensitivitysores, ulcers and lesions along entire GI tract or any partanorexiaBullimiareduced libido - loss of sexual desireloss of orgasmic intensityunsatisfying orgasmsinability to orgasmloss and/or change of genital sensations - "gloved" loss of sensationburning genital skin sensationunable to become arousedreduced testosteroneMENerectile disfunctionlow sperm countpoor sperm motilityPoor sperm qualityZero sperm countWOMENpost partum depressionpost partum psychosisFalse positive pap smears, noncancerous cellular changesmenstrual symptomsFrequent miscarriagechild with neuro tube defectsPMSpalenessrapid heart rateheart arythymiasshortness of breathheart palpitationsweak pulsecongestive heart failurearteriosclerosisWidespread pain throughout bodyHypothyroid (direction of causality if any not established)High homocysteineHigh urinary MMAdizziness - even unable to walkvertigo irritabledepressionSAD - Seasonal Affective Disordermental slowingpersonality changeschronic malaisepoor concentrationmoodinesstirednessmood swingsmemory losslistlessnessimpaired connection to othersmentally fuzzy, foggy, brainfogpsychosis, including many of the most florid psychosis seen in literature, megoblastic madnessAlzheimer'sdeliriumdementiaparanoiadelusionshallucinationsstrange "smells" that are not present like linen being ironed, burnt odors or tidal flats etcstrange "sounds" that are not present, rustlings, mummurings, detonations etcdeja vu experiencesanxiety or tensionnervousnessmaniaimpaired executive functioncognitive impairmentmemory impairmentHypersensitivity to touchHypersensitivity to odorsHypersensitivity to tastesHypersensitivity to clothing textureHypersensitivity to chemicalsHypersensitivity to body malfunctions, symtomsHypersensitivity to sounds and noisesHypersensitivity to light and visual stimuliHypersensitivity to blood sugar changesHypersensitivity to internal metabolic changesHypersensitivity to temperature changesHypersensitivity to foodsmild to extremely severe fatiguecontinuous extremely severe fatigueeasy fatiguabilitysevere abnormal fatigue up to and including apparent paralysis leading to deathspastic paralysisweaknesssleep disordersnon restorative sleeplack of dreamingNight terrorsProlonged hypnogogic state transitioning to sleepSleep paralysisalteration of touch all over body, normal touch can be unpleasant and painfulalterations and loss of tastealterations and loss of smellloss of smell and taste of strawberries specificallyloss or alteration of smell and taste of potato chips specificallyroughening and increased raspiness of voice, mb12 can smooth it outin mid wordblurring of vision - can be sudden onset and sudden returndimmed vision - usually not noticed going into it because change can be very slow or present for lifeVisual impairment can be seen; ophthalmological exam may show bilateral visual lossoptic atrophyoptic neuritisoptic neuropathycentrocecal scotomataintolerance to bright lightdiminished hearing - gradual onset or present for life, sudden return possibleunclear hearing, garbledtinnitus - ringing in earsalways feeling coldintolerance to loud soundsintolerance to multiple soundsinability to pick pick out one voice amongst manyBrainstem or cerebellar signs or even reversible (with mb12) coma may occurneural tube defect not caused by folate deficiency or child with itdemyelinated areas on nervessubacute combined degenerationaxonial degeneration of spinal cordunsteadiness of gaitataxic gait, particularly in darkpositive Rombergpositive Lhermittesneuropathies, many typesprogressive bilateral neuropathiesdemyelination of nerves - white spots on nerves on MRIsloss of detail and sensual aspects of touch all over bodyparesthesias in both feet - burning, tingling,cobwebs, wet, hairs, pain, numbness, etcparesthesias in both legs - burning, tingling, cobwebs, wet, hair, pain, numbness, etcparesthesias in both hands - burning, tingling, cobwebs, wet, hairs, pain, numbness, etcparesthesias in both arms - burning, tingling, cobwebs, wet, hairs, pain, numbness, etcLoss of position sense is the most common abnormality (or vibration sense)Loss of vibration sense is the most common abnormality (or position sense)Loss of sense of joint positionhands feel gloved with loss of sensitivityfeet feel socked by loss of sensitivitytremblingneuropathic bladderunable to release bladder, mild to severeurinary incontenance - occasionally to frequentlyfecal incontinance - occasionally to frequentlysudden electric like shocks/pains shooting down arms, body, legs shooting down from neck movementstanding with eyes closed, a slight nudge or bump causes loss of balancemost patients have signs of both spinal cord and peripheral nerve involvementThe effect on reflexes is quite variableMotor impairment may range from only mild clumsiness to a spastic paraplegiaclumsinessslowed nerve impulsesdecreased reflexesdifficulty swallowingbrisk reflexesdecreased deep tendon reflextoes turn up instead of down in reflex to sole stimulationPositive bilateral Babinski reflexFoot Dropimpaired white blood cell responsepoor resistance to infectionseasy bruisingpronounced anemiamacrocytic anemiamegablastic anemiapernicious anemiadecreased blood clottinglow hematocritMCV > 92-94 first warning, MCV > 97-100 alertelevated MCH (Mean Corpuscular Hemoglobin)elevated LDHbig fat red cells (when said this way usually with happy or healthy modifying it completely misinterpreting results of MCVplatelet dysfunction, low countwhite cell changes, low counthypersegmented neutrophilsmigraine headache cyclesheadachesinflamed epithelial tissues - mucous membranes, skin, GI, vaginal, lungs, bladderinflamed endothelial tissues - lining of veins and arteries, etchigh CRP without infectionmucous becomes thick, jellied and stickydermatitis herpetiformis, chronic intensely burning itching rashfrequent infected folliclesSeborrheic dermatitisdandruffeczemadermatitisskin on face, hands, feet, turns brown or yellow if anemia occurspoor hair conditionthin nailstransverse ridges on nails, can happen as healing startssplits/sores at corners of mouthHyperhidrosis - excessive sweatingBariatric surgeryglutathione, glutathione producing supplements such as NAC/glutamineDilantin, tegretol and some other medicationsRelatives, grandparant, parent, sibling, child, grandchild ever needing b12 shots or supplementcomaseizuresbrain atrophy with ileal tuberculosis preventing b12 absorbtionSTARTING AS INFANT OR CHILDdelayed myelinationfailure to thriveautismdelayed speechdepressionfrequent or continuous toncilitisfrequent strepfrequent pneumoniafrequent longlasting supposed viral illnesses that linger and linger and lingereverything goes to the lungs for extended periodsheadachesgrowing painsskin problemsdandruffallergiesasthmacontinuous swolen glands in necklow grade fever for yearsNight terrorsProlonged hypnogogic state transitioning to sleepSleep paralysisseizurescoma
    Freddd 3,576 Replies Flag this Response
  • REASONS WHY B12 THERAPIES DON'T WORK FOR MANY PEOPLEVersion 1.0 - 07/19/09 1. They take an inactive b12, either cyanob12 or hydroxyb12. The research “validating” their use was primarily for reducing blood cell size in Pernicious Anemia, keeping the serum b12 level over 300pg/ml at the end of the period between injections. They make a statistically significant effect that can be seen in lab tests in a significant percentage of people compared to placebo. They do not heal most damage done by active b12 deficiencies and have little or no effect on the vast majority of symptoms. They may even block active b12 from receptor sites hindering the effects of real b12. They both cause a keyhole effect of having only a very limited amount (estimated at 10mcg/day) that can actually be bound and converted to active forms. They in no way increase the level of unbound active cobalamins which appear required for most healing. They do nothing beneficial in a substantial percentage of people (20-40%) while giving the illusion that the problem is being treated and if it doesn’t work, oh well, that’s the accepted therapy. There is no “dose proportionate” healing with these inactive b12s because it all has to go through this keyhole. Some people are totally incapable of converting these to active forms because they lack the enzyme2. They take active b12 as an oral tablet reducing absorbtion to below 1%. A 1000mcg active b12 oral tablet might bind as much as 10mcg of b12. Again the b12 has to be squeezed through a keyhole that limits the amount and is subject to binding problems in the person whether genetic or acquired.3. They take a sublingual tablet of active b12 and chew it or slurp it down quickly reducing absorbtion back to that same 1% and limited to binding capacity. With sublingual tablets absorbtion is proportionate to time in contact with tissues. I performed a series of absorbtion tests comparing sublingual absorbtion to injection via hypersensitive response and urine colorimetry.4. Of the many brands of sublingual methylb12 only some are very effective. Some are completely ineffective and some have a little effect.5. For injectable methylb12, if it is exposed to too much light (very little light actually is too much) it breaks down. Broken down methylb12 is hydroxyb12. It doesn’t work at healing brain/cord problems of those who have a presumed low CSF cobalamin level. That requires a flood of unbound methylb12 and adenosylb12 (2 separate deficiencies) that can enter by diffusion. Adenosylb12 from sublinguals can ride along with injected methylb12.6. They don’t take BOTH active b12s.7. They don’t take enough active b12s for the purpose.8. Lack of methylfolate9. Lack of other critical cofactors.10. Lack of basic cofactors.
    Freddd 3,576 Replies Flag this Response
  • METHYLB12 STARTUP EFFECTSversion 1.0 - 07/19/09 There are many ideas about what causes the startup effects of methylb12 and some of the other supplements we use in the active b12 protocol. Some may apply specifically to those who have been diagnosed with CFS/FMS or may be more general. As most experimenting with treatments haven't tried a lot of variations there is little mention of how order dependent the startup effects are. Some of the items may appear mutually contradictory. Perhaps there are multiple things going on. Many have offered their ideas about it. I'm trying to summarize here both what I have personally experienced and/or observed and that which others have suggested.Many of these things are order dependent or cofactor dependent. So, methylb12 can cause a significant startup effect of an energetic nature; enough to scare the sox off of some especially when taken as a fearfull thing. So can TMG, methylfolate and SAM-e. In fact, this is order dependent. If one takes hydroxyb12 and/or cyanob12 for a period of time and then starts any of these things the startup effects are amplified. The first of this group of 4 methylators that is started has the biggest startup effect. The fourth one has very little "methylation" startup effect if any. This hypothesis can be deliberately tested and is accidently tested frequently. The roughest startups I have seen are in those on cyanob12 for years switching to methylb12. In that instance you have a very depleted methylation capacity changing to mb12 which increases methylation capacity. So you have at least four kinds of startup effects of starting methylb12. Increase in methylation capacity, large "energized feeling", not due to thyroid.Increased intensity of sensation and symptoms and brightening of the senses as the nervous system starts working better and transmission speed increases; large "energized feeling", not due to thyroid.Mitochondrial startup - In CFS/FMS where abnormal fatigue and/or burning muscle pain exists lactic acid is produced in anorobic metabolism, a sudden increase of 6 times as much energy production occurs as adenosylb12 (converted from mb12) floods back into the mitochondria converting back to oxidation metabolism; large "energized feeling", not due to thyroid.Functional biochemical reactions start suddenly producing suddenly shifting symptoms.When neuropsychiatric healing starts moods and personality can start changing dramatically and suddenly and continue for several months. Functional changes happen immediately, healing takes longer.Hypothetical detox reactionHypothetical bacterial and viral dieoff as immune systyem starts funtioning properly.Hypothetical thyroid reaction often attributed to cause of energetic reactions and changes. As these changes occur faster than T3 and T4 changes occur or can be measured as changing this is questionable. People who try to adjust thyroid hormone doses usually end up making things worse and going back to original dose and being puzzled by the changes not working in expected fashion. When T3 and T4 are measured, usually no significant changes have occurred and maintained.To minimize startup effects, start with adnosylb12. This turns on the mitochondria before the nervous system. There is some nervous system startup due to limited mb12 conversion and due to neuronal mitochondria startup, but only a fraction of what occurs with methylb12. There is no large amount of unbound mb12 which produces large rapid changes. Then add TMG, the gentlest of the methylators. Then add SAM-e, then methylfolate and finally methylb12. By the time the mb12 is added, only those effects due purely to the mb12 itself will occur without the mitochondrial startup and the methylation reaction. After that add the l-carntine to finish the mitochondrial startup. Methylfolate and SAM-e can both give very strong startup reactions if they are the first methylator aboard. L-carnitine can have a strong startup effect if it has been lacking, boosting energy output and endurance.Some people find glutathione or glutathione promoting substances to be benficial. Generally these are people who have been taking it along with hydroxyb12, a non active cobalamin that does not flood the system with unbound active b12s. Those who have been taking active b12s and who have become used to a high level of unbound active b12s find themselves being plunged suddenly back into b12 deficiency states induced by glutathione and glutathione promoting supplements such as NAC/Glutamine but not limited to that specific pair or infused glutathione. This appears hightly dependent upon the actual form of b12s being taken. Those taking glutathione or promotors who change to active b12s don't have a noticable reaction but do not have the anticipated effects of active b12s. The glutathione appears to block the effects of having unbound active coblamins in the system, most specifically methylb12. The effect is only noticable when the effectiveness of methylb12 is suddenly turned off.
    Freddd 3,576 Replies Flag this Response
  • B12 ZONES OF HEALING BY DOSEVersion 1.0 - 07/19/009 Assumptions - Methylcobalamin and adenosylcobalamin are brands tested as 5 star for absorbtion and compared to injection by effect and colorimetry achieving 15% absorbtion or greater in 45 minutes or greater absorbtion in longer times. • ZONE 1 – Cyanob12, oral or injected any size dose, hydroxyb12, oral or injected any size dose, methylb12 oral in doses of 500mcg or less. Limited results largely confined to those changes requiring lab tests to see; reduced hcy, reduced uMMA, sometimes reduced MCV, occasionally mild changes in paresthesias and peripheral neuropathies over time. From literature and experience.• ZONE 2A – methylcobalamin sublingual 1mg to 50mg/day, single sublingual doses to 25mg and IM and SC injections up to 5mg. Dose proportionate healing of widespread symptomology. From literature, tests and experiences. Heals neurology, endothelial tissues, epithelial tissues, energy and mood. Some healing, hematological at least, is dependent upon adequate methylfolate being present. It appears that about 95% of healing takes place in Zone 2A & 2B.• ZONE 2B – adenosylcobalamin sublingual, 3mg to 60mg/day and single doses to 24mg. Less obvious dose proportionate correction and healing of a smaller more specific array of symptoms. Heals muscles, allows them to grow, energy, mood, affects neurology differently from methylb12.• ZONE 3A1 – Methylb12 injection, 7.5mgs SC to 25mgs SC per dose, 1-2 doses per day or 50-60mgs sublingual (Jarrow) saturating oral cavity for 90-120 minutes, 1-2 doses per day. Brain and cord healing, energy and mood, appears dependent upon sufficient methylfolate being present. Neurological deterioration stops, limited amount of healing• ZONE 3A2 – Methylb12 injection, 7.5mgs SC to 25mgs SC per dose, 3-4 doses per day or 50-60mgs sublingual (Jarrow) saturating oral cavity for 90-120 minutes, 3-4 doses per day. Substantial brain and cord healing, energy and mood, appears dependent upon sufficient methylfolate being present.• ZONE 3B1 – Adenosylb12 sublingual (Country Life), 42-60mgs per dose saturating oral cavity for 90-120 minutes, 1 dose per week to 1 dose per month. Brain and cord healing, energy and mood, but different from methylb12 was achieved with adenosylb12• ZONE 3B2 – Adenosylb12 sublingual (Country Life), 15mgs per dose under upper lip for 90-120 minutes, 1 dose per day to 1 dose per week taken in conjunction with 7.5mg mb12 injection, allowing diffusion into CSF with mb12. Brain and cord healing, energy and mood, but different from methylb12 was achieved with adenosylb12• ZONE 4 – Intrathecal injection. Enhanced neurological healing in intentionally damaged rats. From literature. .
    Freddd 3,576 Replies Flag this Response
  • BASIC VITAMINS AND SUPPLEMENTSVersion 1 - 07/23/09 I have divided up the vitamins and supplements in several categories. When brands are mentioned, they are essential as we have performed effectiveness tests and some brands don't work at all, a few work very well and most are mediocre. We are trying to maximize the probability of healing. All needed products are available at www.iherb.com at competitive prices about half of local health food store prices and good service. Using the coupon code RED843 will get a person $5 off their first order. This also gives me a $5 credit I use to supply these vitamins to people unable to afford them. Absolutely critical minimums for basic healing. Jarrow Formulas 5mg Methyl B12, under upper lip or tongue for at least 45 minutes for best effectiveness http://www.iherb.com/Jarrow-Formulas-Methyl-B-12-5000-mcg-60-Lozenges/117?at=0 Country Life Dibencozide (adenosylb12) 3mg under upper lip or tongue for at least 45 minutes for best effectiveness http://www.iherb.com/Country-Life-Active-B-12-Dibencozide-3000-mcg-60-Lozenges/1637?at=0 Solgar Metafolin 800mcg http://www.iherb.com/Solgar-Folate-Metafolin-Folic-Acid-800-mcg-100-Tablets/13961?at=0 Jarrow B-Right b-complex, 1 capsule twice a day http://www.iherb.com/Jarrow-Formulas-B-Right-100-Capsules/110?at=0 Potassium, your choice of brand and form - this is insurance against hypokalemia triggered by sudden healing and potentially fatal - if you have blood tests, potassium is usually checked, midrange, around 4.5 is good. Some people will have problems at bottom of "normal" range, 3.5-4.0. Omega3 fishoils - essential for myelin sheathing for the nerves, many brands will do, 2-6+ capsules per day, I buy it at Costco, house brand. This is available in many supermarkets. Essential, usually needs supplementingZinc - 50 mgCalcium/magnesium supplementD - 3000-5000 IU totalA&D from fish oil, 10,000-(400-800-1000) Vitamin A should be 10,000, D might be any of 3 numbers with additional D to be takenVitamin E, Gamma complex http://www.iherb.com/Now-Foods-Gamma-E-Complex-Advanced-120-Softgels/299?at=0Vitamin C – 4000+mg/day Possibly Critical Cofactors, add after initial stages, any number of these in any combination may be required for maximum effectiveness SAM-e - 200-400mg/day, makes methylb12 more effective, possibly much more effective, increases energy, improves mood TMG - enhances SAM-e, methylb12, l-carnitine L-carnitine fumarate (acetyl might work better for some), works with adenosylb12, lack can completely prevent effectiveness of adenosylb12, increases energy, aerobic endurance, improves mood Alpha Lipoic Acid - enhances l-carnitine and adenosylb12 D-Ribose - enhances adenosylb12, l-carnitine, alpha lipoic acid, improves exercise recovery and energy Additional possibly helpful cofactors SeleniumLecithinChromium GTFmany other supplements THINGS TO AVOID Glutathione and glutathione precursors such as NAC and glutamine, undenatured whey. The glutathione induces immediate active b12 deficiencies, apparently by converting active methylb12 to inactive glutathionylb12 and rapidly excreting it. DEEP NEUROLOGICAL HEALING The most frequent neurological problems are peripheral neuropathies, often in characteristic stocking-glove distribution. Sublingual methylb12 and adenosylb12 appear quite satisfactory in healing these in a sizable percentage of the time. There exists a class of more severe neurological damage. This is sometimes identified as subacute combined degeneration and takes place in the brain and spinal cord. This can occur in people severely deprived of active b12s by diet or lack of absorbtion by other reasons. Another hypothetical cause may occur in people who for unknown reasons have a depressed Cerebral Spinal Fluid cobalamin level compared to their blood serum levels. In addition there may be mood and personality changes, hallucinations, sensory changes, psychosis and an abundance of neuropsychiatric changes. Some of these changes can be corrected with sublingual active b12s but some require much higher levels of active b12s than are usually achieved with sublingual tablets. In these situations usually only injections will help. B12 INJECTIONSThe usual kinds of b12 injections, cyanocobalamin and hydroxycobalamin, are virtually always ineffective on any schedule. The once a month schedule for cyanob12 and the once each three months schedule for hydroxyb12 is useless as well. Daily sublingual active b12s are far superior to these in every way. These occasional injections were developed as a means to prevent people with pernicious anemia from dying. They do not promote neurological healing in any significant way. In order to promote neurological healing methylb12 injections of larger than usual size and greater than usual frequency must be used. My own experience is given below and corresponds with the ZONES defined on another posting. All injections are subcutaneous as that produces a slower diffusion into the blood maintaining a steadier serum peak.1. Single or multiple injections per day to 5mg methylb12, each injection. ZONE 2, fully equivalent to sublingual tablets, did not stop continued neurological deterioration and progressive numbing of feet of 15 years duration.2. Single 7.5mg methylb12 injection per day stopped the progressive numbing of feet of 15 years duration. ZONE 3A13. Two 7.5mg methylb12 injections per day caused some small reversal of numbing of feet and of neuropsychiatric symptoms. ZONE 3A14. Four 7.5mg methylb12 injections per day have caused substantial sustained reversal of numbing in feet and of neuropsychiatric symptoms. ZONE 3A2
    Freddd 3,576 Replies Flag this Response
  • The B12 Issue. Pt1 This is a long posting, divided into three parts (10,000 character limit per posting), because it has to try to encapsulate a wide-ranging subject. A good understanding of what Vitamin B12 Deficiency is, how it harms you, and the major issues surrounding the problem, makes it that much easier to tackle it. There is no "magic wand"; if B12 Deficiency damage is what is wrong, you have to take persistent, logical steps to deal with it; and you have to do so in the understanding that no two of us need precisely the same treatment. The B12 Deficiency thread on WrongDiagnosis works because the people on it are open-minded, critical of the “Because I’m a doctor” brand of authoritative arrogance, inclined towards self-experimentation, willing to share results, and good at doing Net research. We're also pretty good at picking out fraudulent, misleading, and downright dangerous claims. We know that doctors are not infallible, are not omniscient, and don’t necessarily have access to the best forms of treatment; and we also appreciate that most doctors understand those facts too. Once you have read to the end of these three postings, read the thread – from the latest posting backwards - for a good couple of hours, to get an idea of how we work together, what can be achieved, and what needs to be done to achieve it. Starting the thread from the leading edge means that you see the conclusions first, rather than having to wade through the discussions; the arguments – though interesting, reasoned, and relevant at the time - can be a bit tedious when read as history! “Cut to ‘The Chase’” is, therefore, good advice. What the thread does best is to educate people into understanding this thing. Readers suffering serious “brain fog” will find understanding easier with an “unfogged” friend alongside – or, at least, a pencil and paper! “Brain fog” is something every one of us here has been through; we therefore all know what it’s like; however, be assured – it gets better! Almost without exception we are all B12 Deficiency sufferers who - unlike a lot of others out there - are steadily improving. The site started on 17th Feb 2007; by 0600GMT on 28th July 2009, it had received 937,798 visits, and was averaging 1,636 visits/day. B12 Deficiency is a major problem, and the thread helps a very large number of people. There are three tests whose results can point towards (or away from) a diagnosis of B12 Deficiency. They are: a. Serum B12 level. b. Urinary methylmalonic acid level. c. Serum homocysteine level. If you have already been supplementing with forms of Vitamin B12, then the value of doing those tests will have been compromised. Supplementing will make the level of B12 in your blood high, but that does not mean that damage caused by prolonged deficiency will somehow have been instantly rectified. Pulling a knife out doesn’t immediately heal the wound. Serum B12 is merely circulating - it is doing nothing else. It has to make its way from your bloodstream and into your tissues to do its work – and that can take some time. As this process continues, your serum level will steadily fall. Testing serum levels shortly after supplementation is like looking at a river in flood and concluding that it is always that high. In our experience, many doctors do not really understand the extent and variety of damage B12 Deficiency causes; they have difficulty in diagnosing it; and they commonly treat it on the basis of an outmoded protocol which takes no account of current knowledge on the condition. They tend to believe that the condition is uncommon – whereas it is rife; they rely heavily on the Serum B12 Test - without an appreciation of what it actually detects, or of its limitations; and they genuinely believe that a few tiny, infrequent injections will put right the damage done by months, or even years, of deficiency. Doctors will also routinely ignore the evidence of their own eyes and experience, and use the Serum Test to RULE OUT the possibility of B12 Deficiency. The patient’s chances of a correct diagnosis are further hindered by the fact that many countries set “acceptable” B12 levels far too low – typically 200pg/ml. This level is based on the misconception that anaemia is the commonest presenting sign of B12 Deficiency, whereas – in fact – serious neurological signs/symptoms set in at about 550-500. Doctors also tend to believe that there is some kind of “optimum” upper level for Serum B12, and to stop treating it once the patient’s serum level has risen a bit. This notion arises from a fundamental misunderstanding of statistical method. If you define a minimum limit for a quality measured in a population of human beings (serum B12, in this instance) the statistics of nature automatically also throw up a “maximum” which has no relevance. Here’s an easy-to understand analogy. If you recruit men to a drill squad on the basis that “no man is to be less than six feet tall” then – despite the fact that all you have done is to set a minimum height – you still recruit a range of tall men. One of them will be the tallest; he is just thrown up by nature; his stature is not an “upper limit” – it’s simply what happens. Optimum serum B12 level is “as high as possible”. For those of us susceptible to deficiency problems, 1,000pg/ml seems to give a safe leeway. There is no “upper” limit. It is pure nonsense based on misunderstanding. With any other illness, the measure of “cure” would be the extent to which the signs/symptoms retreat. B12 Deficiency problems are no different, and it is difficult to understand the medical profession’s apparent obsession with serum levels. Recovering deficiency sufferers should measure their progress by improvement in health, not by serum level. For reasons not really understood, beginning supplementation often causes neurological symptoms to worsen for a few weeks. The common experience is that the effect soon goes away. One of the advantages of a website such as the thread is that correspondents can obtain support from a community of fellow sufferers. Knowing that you are not alone can be a great help.
    kevinmillhill 1,889 Replies Flag this Response
  • Pt IIThe key to solving this problem lies in understanding it.There is a group of chemical compounds called "cobalamins"; they are structured partially around a single atom of the metal cobalt; and about 38 have been discovered, or manufactured. Almost all of them will give a +ve reading in the simpler B12 Serum Tests. Of these 38, though, only two naturally-occurring ones have immediate mammalian relevance; these are methylcobalamin (m-B12) and adenosylcobalamin (ad-B12). Two other manufactured ones - hydroxocobalamin (h-B12) and cyanocobalamin (c-B12) - can be utilised by mammals, but they first have to be converted to m-B12 or ad-B12 by inefficient metabolic reactions. Both are comparatively ineffective as treatments for B12 Deficiency. Furthermore, cyanocobalamin is known to cause blindness in carriers of a faulty gene leading to a condition called "Leber's Hereditary Retinopathy"; and anecdotal evidence strongly suggests that it also has other low-grade, toxic effects. There have been calls to the World Health Organisation to ban its use. Collectively, these 4 substances get called "Vitamin B12”, or “Cobalamin” and the remainder “B12 Analogues”, or “Cobalamin Analogues”; it can be unhelpful at times.M-B12 and ad-B12 are readily available; we see no good reason to use h-B12 or c-B12 at all, but those are what most doctors will attempt to treat B12 Deficiency with – if they recognize it in the first place. Bear in mind also that one of those two substances is toxic.M-B12 and ad-B12 are present in most cells in tiny quantities. M-B12 is made by bacteria which originate in the soil, and animals can interconvert the two substances. Some animals – particularly ruminants – can harness the bacteria directly, and so obtain B12 internally. Humans, however, can obtain B12 only from animal sources or from supplements. Despite what you may occasionally read, there are NO plant-only sources. M-B12 and ad-B12 are vital to our survival, and are implicated in over 600, widely-differing, metabolic processes; that is why deficiency can lead to so many different, apparently unrelated, signs/symptoms. Above these postings, there is a list of possible signs, symptoms, and predisposing factors related to B12 Deficiency. I realise that it’s breathtaking, but if – by the end of these present postings – you’ve understood what we are driving at – you’ll also understand why there can be so many symptoms. An excellent background to the whole subject is “Could it be B12” by Sally Pacholok and Jeffrey J Stuart. Its availability varies, but you can usually find it on Amazon: http://www.amazon.co.uk/s/ref=nb_ss_b?url=search-alias%3Dstripbooks&field-keywords=Could+it+be+B12%3F&x=15&y=19 (If you do buy this book, bear in mind that it is frozen in time, whereas the thread constantly rolls forward, and is therefore a reflection of the latest research we find on the subject, as well as a showcase for the results of personal experimentation by correspondents.) B12 assimilation is complicated; it is removed from your food and passed on to your metabolism in a series of complex chemical reactions, dependent – in part - on your stomach’s ability to produce hydrochloric acid, but also on its capacity to synthesise a glycoprotein commonly called “Intrinsic Factor”. An inhibited ability to produce this substance tends (for historical reasons now largely irrelevant) to be called “Pernicious Anaemia”. The area of the gut at which B12 passes into the bloodstream is the terminal ileum (Ie the lower end of the small intestine.) Transport from the gut, through the bloodstream, and into the cells depends – to a large degree – on proteins called transcobalamins.Manufactured supplements do not follow this complex assimilation path, but are formulated to achieve direct access to the bloodstream either sublingually, or via injection. Simply eating such supplements causes them to pass through you largely untouched.Ad-B12 (commercially marketed as “dibencozide”) is a lead-player in "Krebs' Cycle" - reactions which maintain energy production in your cells; low ad-B12 leads to chronic fatigue, lassitude, muscle pain, muscle wastage, low exercise tolerance, etc. However, cells need energy, and low intra-cellular "power levels" can affect you in many other ways as well – the speed and efficiency of nerve impulse transmission, for instance.M-B12 is a big-hitter in DNA replication and protein synthesis; low m-B12 means that cells do not repair or replicate efficiently, and/or that they do not produce ligands (things such as hormones, neurotransmitters, enzymes, etc) with the efficiency they should. The myelin of your nervous system becomes patchy, you experience paraesthesias (strange, inappropriate, sensations, and pains), and your co-ordination starts to fail. The cells covering and lining body cavities and organs are not properly replaced (“Beef tongue” tends to be an early sign.) Your immune system cannot churn out white cells quickly enough to cope with infection. Alongside demyelination within the brain, neurotransmitter production slows. These problems cause poor memory, “brain fog”, personality change, paranoia, hallucinations, delusional thinking, etc. B12 Deficiency is – unsurprisingly – frequently misdiagnosed as Alzheimer’s Dementia, Parkinsonism, or Multiple Sclerosis.Vitamin B12 Deficiency can be caused by many different factors; the following list is probably incomplete, since we keep coming across previously unmentioned causes:(a). A diet containing insufficient B12 (Vegetarianism, Veganism).(b). An inadequate supply of Intrinsic Factor due to autoimmune problems, (“Pernicious Anaemia”), or to stomach surgery. (c). An inadequate supply of stomach acid, due either to medical conditions (eg Gastric Atrophy, Hypochloridia), to over-use of Antacids, of H2 Histamine Receptor Antagonists, or of Proton Pump Inhibitors; or to stomach surgery.(d). Coeliac Disease; gastric infection with Helicobacter Pylori. Some forms of intestinal bacterial overgrowth.(e). Genetic Predisposition. (Eg: inadequate synthesis of transcobalamins; inhibited ability to interconvert B12 forms)(f). Some medications (eg Metformin), and many oral contraceptives.(g). Nitrous oxide analgaesia and/or anaesthesia.(h). Pregnancy; breastfeeding.(j). Intestinal parasites – particularly tapeworms.(k). Diets overly-rich in animal products. (l). Gall bladder problemsThose last two demand some explanation: (a). Diets, where meat is the predominating feature - eg those of hunters - have particularly lengthy digestive transit times. This can cause the meat in the gut to putrefy rather than to digest. The bacteria causing this can block the uptake of B12. (b). B12 is difficult to come by, as well as being water soluble. To counter this, animals have evolved a system for scavenging and re-cycling it. The processing is particularly dependent on healthy functioning of the biliary system.
    kevinmillhill 1,889 Replies Flag this Response
  • PtIIIOn the thread, we try to give correspondents the information they need to work in partnership with their doctors; if the doctor either knows the subject, or is receptive, then the partnership will probably flourish, and we see many examples. Unfortunately, there are also altogether too many instances where doctors turn out to be stubbornly unreceptive, or arrogantly opposed, to what the patient has to say. For patients faced with this predicament – and unable to find a more co-operative physician - we can give intelligent advice on dealing with the condition in a more “Do-it-Yourself” manner, based on the experiences, Net research, discussions, and self-experimentation of the people here.There are three fundamental points:(a). What we discuss on the thread is no more than the complex results of a simple nutritional deficiency, which, like any other, you can (if you absolutely have to) treat yourself. Furthermore, the supplements mainly needed – m-B12 and ad-B12 – have no known toxicity, a fact frequently stated in the literature, and borne out by considerable experience on the site.(b). What we discuss and suggest works.(c). The basic substances you need, in order to begin putting matters right, are readily available, throughout most of the world.Most correspondents find using sublingual (let it dissolve under your tongue) methylcobalamin tablets, bought on line from the US, gives a good start on the whole business of rectifying the damaging effects of B12 Deficiency. You have to do a little more besides – but I’ll lay out the basics which most of us have found effective. Many of us (particularly those outside of the US) deal with http://www.iherb.com/ . They're in California, are well-stocked (they have all of the listed items); they're also inexpensive, reliable, and fast. There are sound reasons for the brands mentioned - which we can go into as well, if you want. However, the fact that they work for most people is – in itself – probably good enough.(1) Jarrow Formulas Methyl-B12 5000mcg. http://www.iherb.com/Jarrow-Formulas-Methyl-B-12-5000-mcg-60-Lozenges/117?at=0 (These are sublinguals - most correspondents take 2 - 4 spaced across the day; however, I'd suggest starting on one per day, and gradually working up.) Keep each one dissolving slowly in your mouth for as long as possible. Putting it between your upper lip and upper gum is a good way to do it.(2) Country Life Active B12 Dibencozide 3000mcg. http://www.iherb.com/Country-Life-Active-B-12-Dibencozide-3000-mcg-60-Lozenges/1637?at=0 (Also sublingual.) "Dibencozide" is a commercial name for adenosylcobalamin. One per day seems a good start. Again, make it last.(3) A source of the other B-Vitamins. There are issues with very high doses of Vitamin B6 for some people http://dietarysupplements.info.nih.g.../vitaminb6.asp so we suggest that you read up on the subject. The B-complex form most correspondents use is Jarrow Formulas B-Right. http://www.iherb.com/Jarrow-Formulas-B-Right-100-Capsules/110?at=0 One in the morning, one in the afternoon seems about right.(4) L-methylfolate. Many of us can synthesise this from folic acid, but l-methylfolate itself is actually available on the market, and is a far better idea. Solgar Metafolin 800mcg is adequate – and relatively cheap. http://www.iherb.com/Solgar-Folate-Metafolin-Folic-Acid-800-mcg-100-Tablets/13961?at=0 One per day for a start seems to be enough. (5) At least 500mg of Omega Oils daily. Fish oil capsules will do if you're not a vegetarian. If you are, there’re plenty of veggie alternatives. Omega Oils provoke quite a lot of discussion, and you may have to experiment to find what works best for you. There are other substances as well - you need to find them for yourself on the basis that some things help some people a lot, whilst doing nothing noticeable for others. There is plenty of discussion of them, and Freddd is the expert. A readable book on the subject is “Nutrients for Neuropathy” by John A Senneff. http://www.amazon.co.uk/s/ref=nb_ss_w_h_?url=search-alias%3Dstripbooks&field-keywords=Nutrients+for+Neuropathy&x=16&y=15 Your kidneys perceive "free" B12 as a foreign substance, and will start straining supplementary B12 out of your blood immediately. The transcobalamins have already been mentioned; the task of one of them –TranscobalaminII - is to pick up B12 from the ileum and to move it into the cells of your tissues - in very much the same way that haemoglobin moves oxygen around. B12 bound to transcobalamins is "invisible" to your kidneys. TCII works a sort of shuttle service, picking up B12 from the ileum, moving it into a cell, and then returning – via the circulation – to the ileum to keep on picking up, and dropping off.The binding of B12 to TCII is the nub of a persistent medical argument that there is no point in administering large doses of B12 - because there are only finite numbers of TC molecules. Thus (it is argued) - once all TC molecules are "saturated" - there is no point in adding more B12, because your kidneys will just dump it. The argument makes no sense, because TCII is not actually involved in transporting supplemental B12 within the bloodstream. B12, injected or taken sublingually, creates a concentration gradient between blood and tissues, and therefore simply diffuses into cells through their walls. No biological transportation system is involved. The Laws of Physics are not mocked - although your kidneys will still eventually dump whatever free B12 they can manage to catch.We have learned – from our own experience and from Net research – that increasingly large doses of methylcobalamin, delivered in increasingly aggressive ways – sublingual administration, subcutaneous injection, intravenous infusion - to the target tissues appear to be able to catalyse the reversal of distinctly more “hopeless” and harmful types of deficiency damage. So far as severe, entrenched, unresponsive neurological problems are concerned, intrathecal injection (directly into the CSF within the space surrounding the spinal cord) is probably as far as it is possible to go. However, it is a little bit difficult on a Do-It-Yourself basis!Patients are often told by their doctors that some signs/symptoms are “irreversible” - particularly if left undiagnosed and untreated for a long time. Evidence on the thread, however, is that even the most entrenched of symptoms will retreat if you assault them vigorously enough, and persistently enough. Just what that entails for any given individual tends to be the major subject for discussion.
    kevinmillhill 1,889 Replies Flag this Response
  • Active B12 Titration Methods These methods can be applied to either active b12; adenosylb12 and methylb12. If a person is having a lot of startup reaction to mb12 then I would suggest starting with adb12. Either should be started on a base of the basic vitamins and minerals; A, D, C, E, B-complex that includes P-5-P and pantethine and without Cyanob12 (Jarrow B-Right, twice a day), methylfolate, magnesium, calcium, zinc (50mg) and Omega3 oils. These are so essential that they often go without saying or being taken. They are absolutely essential for healing and tissue formation. There are many other things that may be beneficial and aid healing tremendously and some critical cofactors that are essential but after the active b12s are started as they don’t work as well or at all when the b12 is short. I will use mb12 as an example but this applies in the same way to adb12 (dibencozide). First there are a few general things to consider.Our nervous systems notice differenceUnbound active b12s diffuse into our systemsHigher serum levels of unbound active b12s diffuse “deeper” more quickly making more intense change.Maintained serum levels diffuse “wider” but less intense change.After a period at a given dosage level equilibrium is reached and change is maintained but not increased, healing continues at that level but not more. Healing is dose proportionate but not linearly so.An estimated 250mcg of unbound active b12 accounts for almost all of the perceived intensity until very high levels are reached. That is a 5mg tablet is not particularly perceived as more intense than a 1mg but a 1mg is more intense than ¼ of a 1mg.If a particular level is maintained all day equilibrium is reached more quickly that if that level happens once a day for 1 hour.When equilibrium is reached, perceived intensity diminishes quickly.When a sublingual tablet is removed from the mouth via physical removal or chewing and swallowing the increase in intensity stops within minutes. One can actually hold at a certain level of intensity this way.Approximately 15% is absorbed in the first 45 minutes of tissue contact time, about 1% each 3 minutes. After 45 minutes that drops to about an additional 1% each 5 to 10 minutes until gone. Maximum absorbtion appears to be in the area of 25%. This applies only to the 5 star brands. A fine degree of control can be obtained via a timed method as well as cutting the tablets.Slow titration Start on day 1 with 1 quarter tablet of Enzymatic Therapy 1mg or Jarrow 1mg mb12 or Country Life adb12. This can amount to a 30-60mcg absorbtion, 3x that for the adb12. Much of this will go into the tissues within the actual period of absorbtion. Taking additional quarters can be timed so as not to increase intensity. Taking a half will increase the intensity. If one only takes 1 quarter a day it is unlikely to ever reach equilibrium. I would suggest, that as long as the intensity is tolerable to take at least 8 quarters a day. After a few days, as long as comfort is maintained try ½ tablet. It’s not that there won’t be symptoms shifting and intensification, there will be. We are just trying to keep the intensity under control. Rapid titrationDo as above with ½ or whole tablets. Over the days increase to ¼ of a 5mg, then ½ of a 5 mg tablet and finally to a 5mg tablet. At 5mg tablet 4 times a day most people will reach a stable equilibrium that is at the maximum short of injections or multiple tablets per dose. However, once one reaches this point, 2 x 5mg tablets at a time or 4x5 may be a just barely noticeable difference from 1 tablet, if there is any additional effect at all. At around the point of 50mg in 2-3 hours with multiple tablets at a time a threshold effect may be noticed. This is the point approximately equivalent to a 7.5mg injection, the point at which the Japanese research and my own experience indicates up regulated neurological healing may occur. Above that dose no additional noticeable effect occurs at up to at least 25mg injection. This may only apply to people with CNS/CSF deficiencies. That is unknown at this time. There are current Japanese studies being done with 50mg IV infusions that may define this zone more clearly. This is the area I’ve labeled as ZONE 3 on some other posts which I’ll repost here. A fast high dose repeated for several days will soon loose it’s startup effects and will rapidly diminish that of smaller doses. Approximately 20mg on day one may cause a lack of startup effect on day two for any dose less than approximately 2-5mg.
    Freddd 3,576 Replies Flag this Response
  • Hi I have had an issue with my doctor over not giving me vitamin b12 injections, i had my colon recently removed and im 34. I am now exhausted all the time, get pins and needles in one arm, my memory is awful where as I used to be very sharp, my concentration is weak just to describe a few symptoms. Having the colon removed changes all the make up in the small intestines and body. MY GP point blank refused as my blood test is at 245..still the lower end. In Japan theirs start at 800 as normal ours is 180. I want to be treated symptomatically. The idiot said its all in line with a low mood, im on antidepressants as Ive been severely ill for 4 years after a surgeon did the wrong op on me, 11 ops later and I lose my colon. My doctor is trying to say Im depressed, since my colon came out ive never been so pleased. My moods are stabilised, its just a cop out and boy did I tell him, they see depression and they home in on it..it infuriates me. Its not just slight tiredness its exhaustion, I want to get up and do things but i sleep loads. I know when im depressed & because I asked for a trail course he said as my test was normal he cant do that. My iron was low as lost alot of blood in op but my body just isnt functioning properly, I get my 9 yr old correcting me on what I say as sometimes it comes out wrong. Ive been informed the B12 Tablets cannot be absorbed properly and are a waste of time, hence why I try the patches...help
    crunchiejoe 61 Replies Flag this Response
  • Hi I have had an issue with my doctor over not giving me vitamin b12 injections, i had my colon recently removed and im 34. I am now exhausted all the time, get pins and needles in one arm, my memory is awful where as I used to be very sharp, my concentration is weak just to describe a few symptoms. Having the colon removed changes all the make up in the small intestines and body. MY GP point blank refused as my blood test is at 245..still the lower end. In Japan theirs start at 800 as normal ours is 180. I want to be treated symptomatically. The idiot said its all in line with a low mood, im on antidepressants as Ive been severely ill for 4 years after a surgeon did the wrong op on me, 11 ops later and I lose my colon. My doctor is trying to say Im depressed, since my colon came out ive never been so pleased. My moods are stabilised, its just a cop out and boy did I tell him, they see depression and they home in on it..it infuriates me. Its not just slight tiredness its exhaustion, I want to get up and do things but i sleep loads. I know when im depressed & because I asked for a trail course he said as my test was normal he cant do that. My iron was low as lost alot of blood in op but my body just isnt functioning properly, I get my 9 yr old correcting me on what I say as sometimes it comes out wrong. Ive been informed the B12 Tablets cannot be absorbed properly and are a waste of time, hence why I try the patches...help\ Hi Crunchiejoe, Come on over to http://forums.wrongdiagnosis.com/showthread.php?p=192093&posted=1#post192093 and repost your message. We can help you.
    Freddd 3,576 Replies Flag this Response
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  • Hi Ive read your posts but think il need to read it a few times as alot of medical jargon. I have bought Vitamin b12 patches but they are expensive...not sure ive had much benefit as yet. What would you suggest my first port of call would be? My GP would not give me Vitamin B12 even for a trail as mine was 245, he made out morally he couldnt as I didnt test positive for being 180 or below & because of the side effects. More like the costs in my opinion, I bet they cost alot but my GP is pretty ignorant on this subject, Ive been ill for 4 years because of my condition, I have had 11 ops in 4 years and copious amounts of antibiotics every month, my system is in complete turmoil, esp now my colon is gone, it is so difficult getting it across to my GP the exhaustion it brings & my memory being so foggy. Ive looked on the net before I found this site and seen you can have a test called the schillings test, Ive emailed my doctors secretary & asked him to look into it. I just want to feel normal, I see old ladies marching into town & i envy the energy they have, now that is sad...
    crunchiejoe 61 Replies Flag this Response
  • Hi Ive read your posts but think il need to read it a few times as alot of medical jargon. I have bought Vitamin b12 patches but they are expensive...not sure ive had much benefit as yet. What would you suggest my first port of call would be? My GP would not give me Vitamin B12 even for a trail as mine was 245, he made out morally he couldnt as I didnt test positive for being 180 or below & because of the side effects. More like the costs in my opinion, I bet they cost alot but my GP is pretty ignorant on this subject, Ive been ill for 4 years because of my condition, I have had 11 ops in 4 years and copious amounts of antibiotics every month, my system is in complete turmoil, esp now my colon is gone, it is so difficult getting it across to my GP the exhaustion it brings & my memory being so foggy. Ive looked on the net before I found this site and seen you can have a test called the schillings test, Ive emailed my doctors secretary & asked him to look into it. I just want to feel normal, I see old ladies marching into town & i envy the energy they have, now that is sad... Please repost this for discussion on http://forums.wrongdiagnosis.com/showthread.php?p=192181#post192181 We are trying to maintain this one for easy reading of the basics instead of haing the basics buried in discussion. I'm copying it over there for you and answering.
    Freddd 3,576 Replies Flag this Response
  • Dear crunchiejoe, Please use the main B12 thread for correpondence; if you go to http://forums.wrongdiagnosis.com/showthread.php?p=192209&posted=1#post192209 you'll find comprehensive answers there at 9497 and 9498 from Freddd and myself.
    kevinmillhill 1,889 Replies Flag this Response
  • These are the two specific defects leading to inability to make adenosylcobalamin in the brain. Again, treatment of cbl B is only 40% effective when treated with hydroxyb12. Why don't they use their brain and use adenosylb12 for trewatment instead of hydroxyb12? Carnitine is also suggested for use to aid the functinality. This is beginning to sound like obstinate stupidity on the part of those insisting that the only treatment is hydroxyb12. Cobalamin C disease is concermed with homocysteine (mb12) rather than mma as for these two. Cobalamin D is concerned with a combination of a/b and c so a person has 2 defects affecting inability to synthecize both forms of active b12s. cblA- They have the best prognosis because the biochemical and clinical abnormalities reverse in about 90% of patients when they are provided pharmacological doses of hydroxy-cobalamin (OH-cbl) injections. cblB- Equal fractions of affected patients are alive and well, alive and impaired or deceased. Age of onset of symptoms can help prognosticate, those with later onset tend to have a more benign course. About 40% of these patients will respond with a drop in MMA level when given pharmacological doses of OH-cbl injections. Missing Enzyme & Location:Cobalamin A (cblA) deficiency: defect in the mitochondrial cobalamin reductase. These patients are unable to make adenosylcobalamin. Cobalamin B (cblB) deficiency: defect of mitochondrial cob(I)alamin adenosyltransferase and the patients are unable to make adenosylcobalamin http://66.102.1.104/scholar?hl=en&lr...n+mitochondria Patients with congenital malabsorption develop megaloblastic anemia and failure to thrive in the first years of life and may later develop a myelopathy.2-3 In the first months of life, most patients with TCII deficiency present with severe megaloblastic anemia, failure to thrive, and diarrhea, but neurological involvement is not present at diagnosis.2-3 On the basis of complementation studies performed in cultured skin fibroblasts, failure in the synthesis of cellular AdoCbl and/or MetCbl has been divided into disease groups, Cbl A to Cbl H.1, 4 Isolated increased levels of MMA in the blood and urine characterizes Cbl A, Cbl B, and Cbl H diseases. Most of these patients present in infancy with recurrent episodes of ketoacidosis without megaloblastic anemia. Hyperhomocysteinemia and hypomethioninemia without methylmalonic aciduria characterize Cbl E and Cbl G diseases. Most patients who have these 2 diseases present in the first months of life with megaloblastic anemia, poor feeding, and, if their disease is not promptly diagnosed, with various neurological deficits such as tonus abnormalities or seizures. Cobalamin C, Cbl D, and Cbl F diseases are due to defective synthesis of both MetCbl (resulting in hyperhomocysteinemia and hypomethioninemia) and AdoCbl (resulting in methylmalonic aciduria). Most of these patients present in the neonatal period with feeding difficulties, failure to thrive, neurological deterioration, and megaloblastic anemia. In addition, they may have renal and liver failure, cardiomyopathy, pneumonia, and retinopathy.3, 5 http://archneur.ama-assn.org/cgi/con...ull/60/10/1457 Our patients presented no evidence of having defective vitamin B12 supplies, malabsorption, or transport since they had normal vitamin B12 and TCII levels in their serum. Despite the absence of megaloblastic anemia and the presence of normal vitamin B12 serum levels, they were both clearly affected with a neurological form of vitamin B12 deficiency only diagnosed by the demonstration of homocystinuria and methylmalonic aciduria. Patient 1 exhibited a subacute combined degeneration of the spinal cord, which is highly suggestive of a vitamin B12 deficiency. Nevertheless, the diagnosis of functional vitamin B12 deficiency had been long delayed because of normal serum vitamin B12 levels although a metabolic investigation of the cellular vitamin B12 status had not been performed. The metabolic disorder of these sisters can probably be included in the Cbl C group, although no complementation studies were done with fibroblasts from patients identified with Cbl D or Cbl F. First, Cbl C is the most common of these diseases; to our knowledge, only 2 cases in a sibship have been reported as Cbl D disease and fewer than 10 cases as Cbl F disease.6 Second, in contrast to fibroblasts from patients with Cbl F, which accumulate excess unmetabolized cyanocobalamin, fibroblasts from our patient had a low incorporation of cyanocobalamin (in accordance with our findings in other patients with Cbl C disease) compared with healthy control subjects. Similar therapeutic approaches are proposed for these 3 groups of Cbl disease and aim to normalize all metabolite values including methionine levels Most patients with Cbl C disease respond biochemically and clinically when treated with high-dose systemic hydroxocobalamin.7-11 As with pernicious anemia, myelopathy and peripheral neuropathy improved more slowly and less completely than cortical signs (Table 3). Because this treatable condition can lead to death or irreversible neurological damage, it requires prompt diagnosis and treatment. This article emphasizes the need, at any age, for extensive investigation of the vitamin B12 status in patients with neurological symptoms whose clinical picture is consistent with vitamin B12 deficiency and in whom the serum vitamin B12 level is normal. This article is a must read. It is free.
    Freddd 3,576 Replies
    • August 15, 2009
    • 05:45 PM
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  • And More: Department of Digestive Diseases, VA Medical Center, West Haven, CT 06516, USA.All of vitamin B12 in nature is of microbial origin. Cobalamin, as vitamin B12 should correctly be termed, is a large polar molecule that must be bound to specialized transport proteins to gain entry into cells. Entry from the lumen of the intestine under physiological conditions occurs only in the ileum and only when bound to intrinsic factor. It is transported into all other cells only when bound to another transport protein, transcobalamin II. Congenital absence or defective synthesis of intrinsic factor or transcobalamin II result in megaloblastic anemia. The Immerslund-Graesbeck syndrome, a congenital defect in the transcellular transport of cobalamin through the ileal cell during absorption, also presents with megaloblastic anemia, but with accompanying albuminuria. In most bacteria and in all mammals, cobalamin regulates DNA synthesis indirectly through its effect on a step in folate metabolism, the conversion of N5-methyltetrahydrofolate to tetrahydrofolate, which in turn is linked to the conversion of homocysteine to methionine. This reaction occurs in the cytoplasm, and it is catalyzed by methionine synthase, which requires methyl cobalamin (MeCbl), one of the two coenzyme forms of the vitamin, as a cofactor. Defects in the generation of MeCbl (cobalamin E and G diseases) result in homocystinuria; affected infants present with megaloblastic anemia, retardation, and neurological and ocular defects. 5'-Deoxyadenosyl cobalamin (AdoCbl), the other coenzyme form of cobalamin, is present within mitochondria, and it is an essential cofactor for the enzyme Methylmalonyl-CoA mutase, which converts L-methylmalonyl CoA to succinyl CoA. This reaction is in the pathway for the metabolism of odd chain fatty acids via propionic acid, as well as that of the amino acids isoleucine, methionine, threonine, and valine. Impaired synthesis of AdoCbl (cobalamin A or B disease) results in infants with methylmalonic aciduria who are mentally retarded, hypotonic, and who present with metabolic acidosis, hypoglycemia, ketonemia, hyperglycinemia, and hyperammonemia. Megaloblastic anemia does not develop in these children because adequate amounts of MeCbl are present, but the effect of methylmalonic acid on marrow stem cells may give rise to pancytopenia. Congenital absence of reductases in the cytoplasm, which normally reduce the cobalt atom in cobalamin from its oxidized to its reduced state (cobalamin C and D diseases), results in impaired synthesis of both MeCbl and AdoCbl. Both methylmalonic aciduria and homocystinuria therefore develop in these children, and they present with megaloblastosis, mental retardation, a host of neurological and ocular disorders, and failure to thrive; however, they do not have hyperglycinemia or hyperammonemia. A similar biochemical profile and clinical presentation is also seen in cobalamin F disease, which results from a defect in the release of cobalamin from lysosomes, following receptor-mediated endocytosis of the transcobalamin II-cobalamin complex into cells. It is important to recognize these inborn errors of cobalamin absorption, transport, or function as soon after birth as possible, because most respond (in some patients more fully than others) to parenteral administration of cobalamin. Delays in diagnosis can lead to grave clinical consequences.PMID: 8775094 http://www.ncbi.nlm.nih.gov/pubmed/8...gdbfrom=pubmed This gives a good breakdown of the many variations of the lettered cobalamin diseases. The presumed "late onset" forms are not well defined and are considered rare, or perhaps merely rarely recognized.
    Freddd 3,576 Replies
    • August 15, 2009
    • 05:48 PM
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  • And Folate - Cobalamin deficiency in the newborn usually results from cobalamin deficiency in the mother. Megaloblastic anaemia, pancytopenia and failure to thrive can be present, accompanied by neurological deficits if the diagnosis is delayed. Most cases of spina bifida and other neural tube defects result from maternal folate and/or cobalamin insufficiency in the periconceptual period. Polymorphisms in a number of genes involved in folate and cobalamin metabolism exacerbate the risk. Inborn errors of cobalamin metabolism affect its absorption, (intrinsic factor deficiency, Imerslund-Gräsbeck syndrome) and transport (transcobalamin deficiency) as well as its intracellular metabolism affecting adenosylcobalamin synthesis (cblA and cblB), methionine synthase function (cblE and cblG) or both (cblC, cblD and cblF). Inborn errors of folate metabolism include congenital folate malabsorption, severe methylenetetrahydrofolate reductase deficiency and formiminotransferase deficiency. The identification of disease-causing mutations in specific genes has improved our ability to diagnose many of these conditions, both before and after birth.http://www.ncbi.nlm.nih.gov/pubmed/1...gdbfrom=pubmed Cobalamins are essential biological compounds structurally related to haemoglobin and the cytochromes. Although the basic cobalamin molecule is only synthesized by micro-organisms, all mammalian cells can convert this into the coenzymes adenosylcobalamin (AdoCbl) and methylcobalamin (MeCbl). AdoCbl is the major form in cellular tissues, where it is retained in the mitochondria. MeCbl predominates in blood plasma and certain other body fluids such as breast milk; in cells MeCbl is found in the cytosol. Inherited disorders of cobalamin metabolism are single gene defects, transmitted as recessive traits. They affect absorption, transport or intracellular metabolism of cobalamin. At least 12 different mutations are known, including defects or deficiencies of IF, IF-receptor and TCII, MM-CoA mutase and of the various reductases and synthases required for synthesis of AdoCbl and MeCbl. These have been designated cblA to cblG. Abnormalities are detectable by urine and plasma assays of methylmalonic acid and homocysteine, and plasma and erythrocyte analysis of cobalamin coenzymes, which can reveal deficiencies of MeCbl or AdoCbl. Fibroblast studies discriminate between closely similar defects. In man, AdoCbl is required in only two reactions: the catabolic isomerization of MM-CoA to succinyl-CoA and interconversion of alpha- and beta-leucine. MeCbl is required in the anabolic transmethylation of homocysteine to methionine. Intestinal absorption of cobalamin requires the glycoproteins TCI and IF from the stomach and IF-cobalamin receptors in the ileum. Cobalamin is transported to cells bound to a polypeptide, TCII, is captured by surface receptors and absorbed by endocytosis. The complex is then split in the lysosomes, cobalamin is released and the coenzymes are synthesized. In plasma, 80-90% of the cobalamin is bound to TCI, whose function is uncertain. Megaloblastic anaemia at birth or in the first few weeks of life is a rare but serious event. Myelopathy and developmental delay, with or without seizures may also occur without anaemia. If urine and light-protected blood samples are collected and sent to an appropriate metabolic unit, an inborn error of cobalamin metabolism, including TCII deficiency in which the serum B12 may be normal, can quickly be diagnosed. IF deficiency or Imerslund-Gräsbeck disease usually presents with signs of cobalamin deficiency within the first year of life and can be diagnosed by absorption studies. Current treatment involves dietary protein restriction and/or parenteral OHCbl and the prognosis is very variable. Since lack of MeCbl leads to depressed DNA synthesis affecting rapidly dividing cells in the brain and elsewhere, treatment with this coenzyme should be considered at the earliest stage in appropriate cases.(ABSTRACT TRUNCATED AT 400 WORDS) http://www.ncbi.nlm.nih.gov/pubmed/8...gdbfrom=pubmed
    Freddd 3,576 Replies
    • August 15, 2009
    • 05:49 PM
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  • And vitamin e and fatty acids play a part. Excretion of methylmalonic acid by vitamin E-deficient patients and decreased labeling of adenosylcobalamin (AdoCbl) from cyanocobalamin in vitamin E-deficient rats suggest an interaction of vitamins E and B-12. We studied this interaction in two human cell culture systems: foreskin fibroblasts and a hepatoma cell line (HepG2). We measured radiolabeling of AdoCbl and methylcobalamin from hydroxycobalamin for 6 d in the presence and absence of linoleate (an oxidative stressor) and alpha-tocopherol. In both cell types, labeling of AdoCbl was lower in the presence of linoleate unless alpha-tocopherol was present. The decrease was accentuated by peroxidized linoleic acid; AdoCbl synthetic rate was inversely associated with thiobarbituric acid-reactive compound concentration. Subcellular partitioning of labeled cobalamin revealed less in mitochondria in the linoleate-stressed cells that were not treated with alpha-tocopherol. We conclude that lipoperoxidation reduces mitochondrial AdoCbl formation and that alpha-tocopherol exerts a protective effect in oxidatively stressed cells. We suggest that this subcellular deficiency in AdoCbl may be one mechanism by which vitamin E deficiency leads to neurologic injury. The mechanism seems primarily to involve an alteration in intracellular cobalamin distribution with perhaps a minor effect upon enzymes of AdoCbl synthesis. http://grande.nal.usda.gov/ibids/ind...s&therow=74607 __________________
    Freddd 3,576 Replies
    • August 15, 2009
    • 06:32 PM
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  • This article emphasizes the need, at any age, for extensive investigation of the vitamin B12 status in patients with neurological symptoms whose clinical picture is consistent with vitamin B12 deficiency and in whom the serum vitamin B12 level is normal. This article is a must read. It is free.Fred's last comment is to an article on "CblC disease." In the group of articles, however, there is one that stresses that mothers with folate deficiencies give birth to children with Neural Tube Defects (NTDs) and to resulting *normal b12* levels, yet abnormal synthesis of mb12 and adb12.I had passed over this information because it seemed to me that its appearance in the "short list" had eliminated some (necessary) introductory material.If there is more information, either prior to this post from Freddd, or in general on NTDs and b12 deficiencies, I would appreciate hearing about it. Also, if anybody on the list has been discovered to have an NTD (spina bifida occulta is mine), please post about it or give a reference to your initial post. I am going to start the protocols, even though it may mess up blood testing for MMA metabolism and the rest. That is partly because the information on CblC indicates that remediation (with hydroxocobalamin, though) does not change the clinical and laboratory picture immediately.NOTE: One statistic I saw (reference lost) said that perhaps 24% (1 in 4) people have a silent spina bifida occulta (place where the spine is open, rather than closed). That would mean, if you are older than a certain age (born before approximately 1980), that your mother may not have had enough folate/folic acid in her prenatal regimen, and, as a result, your spinal column did not close completely. You may have escaped most of the consequences, except for the b12 (mb12 and adb12) metabolism error -- that produces *normal* b12 levels.It all falls into place. I'll post again on my own symptom picture, with an unknown about whether I have the metabolic error.
    soycoffee 208 Replies
    • October 13, 2009
    • 08:01 PM
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  • Hi, I am new to this group and am really not sure how to post a new message. Sorry, if I am doing it wrong. Maybe someone could explain how to navigate this website. I was referred to this group for a possible B12 deficiency. My labs are: 11/17/09 Glucose 78 (65-99)Sodium 138 (135-145)Calcium 9.3 (8.5-10.6)Potassium 3.7 (3.5-5.2)MCV 98 (80-98)Hemoglobin 13.7 (11.5-15.0)Iron Bind Cap 320 (250-450) (was 301 before supplementing two months ago)UIBC 193 (150-375) (was 212)Iron Serum 127 (35-155) (was 89)Iron Saturation 40 (15-55) (was 30) Free T4 1.32 (.82-1.77)Free T3 3.3 (2.0-4.4)TSH .018 (.45-4.50) Vitamin D 74.2 (32-100) - supplementing daily Estradiol 88.5 (I am postmenapausal on estrogen/progesterone) Follicular 12.5-166.0 Ovulation 85.8-498.0 Luteal 43.8-211.0 Postmenapausal 20 (>5.4)Ferritin 30 (10-291) TSI Antibodies 168 (0-139)TPO Antibodies 90 (0-34) I have felt anemic for a few months now. My thyroid levels had been much much lower due to a suppressed TSH but I am now getting more thyroid hormone. Previously, my Ft3 2.3 and Ft4 .72 (both too low). My MCV was 92 this time last year. Can somone explain the low MCV with high B12? I do take Vitamin B complex with 600mcg daily and have for over a year and half. Do I need B12 or is it really iron or something else I need?
    DAB427 10 Replies
    • December 2, 2009
    • 03:33 AM
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