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Vitamin B12 / Cyanocobalamin
10 years ago
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Excerpt from and my appreciation to:
The Columbia Encyclopedia, Sixth Edition.  2001.
http://www.bartleby.com/65/vi/vitamin.html*
*If viewed at above web-page linked above, scroll down to section #16 to see Vitamin B12 ...

"Vitamin:  A group of organic substances that are required in the diet of humans and animals for normal growth, maintenance of life, and normal reproduction..."


16
Vitamin B12
The molecular structure of vitamin B12 vitamin. B12 (cobalamin), the most complex of all known vitamins, was announced in 1955 by several scientists, including British biochemists A. R. Todd and Dorothy Hodgkin. In 1973 the vitamin was reported to have been synthesized by organic chemists. Vitamin B12 and closely related cobalamins are necessary for folic acid to fulfill its role; both are involved in the synthesis of proteins. American physicians G. R. Minot and W. P. Murphy in 1926 fed large amounts of liver to patients with pernicious anemia and cured them; the curative substance in this case was probably vitamin B12. However, pernicious anemia in humans is caused not by a vitamin B12 deficiency in the diet but rather the absence of a substance called the intrinsic factor, ordinarily secreted by the stomach and responsible for facilitating the absorption of B12 from the intestine. When a person's body cannot produce the intrinsic factor, the standard treatment today is to inject vitamin B12 directly into the bloodstream. Minot and Murphy’s therapy worked because the liver they fed their patients contained such large quantities of B12 that sufficient amounts of the vitamin were absorbed without the assistance of the intrinsic factor. Inadequate absorption of B12 causes pernicious anemia, nervous system degeneration, and amenorrhea. The only site of cobalamin synthesis in nature appears to be in microorganisms*; neither animals nor higher plants are capable of making these vitamin B12 derivatives. Nevertheless, such animal tissues as the liver, kidney, and heart of ruminants contain relatively large quantities of vitamin B12; the vitamin stored in these organs was originally produced by the (Cyano-) bacteria (and is absorbed) in the ruminant gut. Bivalves (clams or oysters), which siphon microorganisms* from the sea, are also good sources. Plants, on the other hand, are poor sources of (concentrated)** vitamin B12. The recommended daily dietary allowance for adults is 3 micrograms (3 micrograms? - see all that is written below).


My notes and added information for understanding the statement of facts above:

microorganisms*
* Cyanocobalamin - Vitamin B12 producing bacteria are in the Cyanobacterium (algae, moses) family. This class of microorganisms are the bacteria that generally require and live in the sunlight and/or oxygenated environment of the plant surfaces, roots, upper soils and in the waters (near surface). They do not survive in the black dark anaerobic environment of interior animal tissues -- though their exo- and endo-compounds (metabolic excretions), including the vitamin B12 compound group, do remain viable and is accumulated and concentrated in the herbivorous (plant material consuming) animals (in fecal material, intestines, hence is delivered into all body tissues, blood, muscles, entrails, esp. liver and kidneys) and is also expressed, i.e. transported out (to manage internal tissue levels) through and in body fluids (milk, mucus, urine) or ova (eggs). 

There is some presumptions of data that pro ports they (Cyanocobalamin bacteria) have some survival and production activity in the (dissolved oxygen and plant nutrient available) gut (primarily gullet and lower intestine) of herbivores / ruminants (e.g. cow, goat, horse, etc.) animals.  But it is well understood that the critically important source of B12 in livestock (gen. ruminant) production is in their feeds (unwashed, untreated) silage (corn, grains, beet pulp, ferments) along with alfalfa and hay -- where these plant loving cyano-bacteria flourish, then enter into the consuming animal!

continues from the previous page
10 years ago

(concentrated**) -- my insertion to the Columbia Encyclopedia's text, 2nd to last line above.
God and nature has made no mistakes in providing sufficient Vitamin B12 to billions of herbivorous animals over millions of millennia - including the vegetarian primates (our biologically nearest creational equivalents) and man! -- if he (man) makes the right dietary choices and nourishes himself the way he was originally designed! -- That is: In and from the garden! -- the perfect home of pure, uncontaminated, light, oxygen and vegetation loving Cyanocobalamin, in correct bounty, in low concentrations, but sufficient for our needs!-- Not extorted from defiled, destroyed, killed, disease hosting, disease transmitting and B12 hyper-concentrating animals -- especially carnivorous animals (as poultry, pork, fish, etc.), which accumulate and concentrate even more B12 in their tissue, fluids and ova at levels above and higher than the herbivorous animals and/or the insects which they consume. Hence carnivores (including man when he chooses to be such) do ultra-concentrate B12 in their tissues! 

Hence in carnivorous man, a falsely high mean standard of B12 levels is accumulated and is consequently measured high in phlebotomy data; so it is accepted as the human norm! -- Not good or honest science!!! 

And that false high standard (as has been accepted by most all of medicine) precipitates wrong diagnosis! that is, lower test values of accumulatedserum*** B12 levels -- which are naturally (and correctly) less in non-carnivorous (vegetarian) humans and their dependent nursing infants! Those presumed "deficient" patients are then endangered with the unnecessary administrations of (the sewage and/or animal harvested and unnaturally formulated) B12 injections and/or tablets, with their plethora of contraindications (side affects) possible in many recipient patients or wrongly treated victims!

*** serum (blood stream) levels of B12 is not always a good indication of true internal, intra-/inter-cellular, metabolic, B12 functional levels. It is also (now) known that the cells are ultra conservative with B12; i.e. keeping appropriate stores of it within the cells themselves, recycling it within the intra-cellular (inside) chemistry and allowing only that which is absolutely necessary in inter-cellular (between cells) chemistry to be exported, hence not requiring (as was previously presumed) high levels of B12 to be carried in consumption, digestion, absorption and blood flow to replenish it.  -- tlr 7/3/03

Standard medicine has seriously erred in the violation of honored Koch postulates and true scientific method, by producing unnatural high average blood level standards for B12, and assuming them as the correct human  mean or standard  -- based upon hematological data accumulated and calculated in the cross-section of primarily heavily carnivorous USA/Industrial world humans! -- not a true or honest measure for serum B12 levels for all of humanity, nor for creation's biologically intended, apparent and correct human nutrition, chemistry and physiology! 

continues
10 years ago

The original concern over Vitamin B12 deficiency (based on research started more than three quarters of a century ago and completed over a half century ago) was a perceived relationship in poor health conditions called "pernicious anima" (and other closely related neurological and physiological malfunctions). It now has been established that the true cause of this group of maladies is a  failure in the bodies own ability to produce its own correct "intrinsic factor", a compound associated with B12's intra/intercellular transport and use -- which is ill-formed  in a hydrochloric acid and a bile abused (a condition specifically triggered by the corrosive digestion requirements for complex, high molecular weight, dense animal fats and proteins within a) malnourished, malfunctioning, or chemically damaged (or more rarely, genetically flawed) intestinal tract -- rather than the old belief that the cause was (as presumed) a Vitamin B12 intake or (a test determined*) serum level deficiency! 
*Remember, these test protocols and standards were determined over a half century year ago, and also were based on generally highly carnivorous, western human models.

 -- This error in perception, diagnoses and treatment does persist, even to date among too many non-current or incompletely educated health practitioners, their older peers,  administrations and dependent government health and welfare agencies! -- tlr 7/2/03


Personal references: Veterinary & Human Biology & Pathology education and reference books / personal Human, Animal, Livestock and Marine (algae) research and experience -- and personally required knowledge for good livestock production and profit -- in my past.

I will try to improve upon and expand this page later as my resources/time allow. In the meantime, you may see a reference to intestinal (microvilli) repair at LDSVeg.org/Raw.htm#microvilli, and other intestine and whole body healing and nutritional information on LifeSave.orgVeganCowboy.org, WaterAndLife.org and our other subject specific sites (listed on Lifesave.org and VeganCowboy.org)
TLR. 7/1/03

10 years ago

http://www.lifesave.org/VitaminB12.htm (for prev. page)

Vitamin B12 / Cyanocobalamin -- Continued (page 2)
(Internal B12 Activity)

A letter , which I received today from a Doctor in India after his reading my first page on Vitamin B12 and looking for answers to his own health challenges , provoked me to expand on my writing, Vitamin B12 page 1, started 2 months ago on the ignorant and eternal "Vitamin B12 supply-and-deficiencies" debate. So here is this second page on the internal B12 metabolic challenges -- The Real B12 "Deficiency" Issues!


    Sadly, much is still not widely understood or openly taught on this subject. 
    But worse, there is unbelievable bias and pathetic falsehoods abounding among too many so-called "Professionals", and even I certainly still don't know as much as I could or would like. But what I have known about B12 for more than four decades exceeds that which is proverbed among my peers -- but how does the voice of one nondescript fellow get heard in a crowd of flashy peers or medical egotists. So, to now defend an accused Vegan family and its medical fraud and state removed child, I am forced to disturb more convention and upset many peers and so-called friends and their too often repeatedly published, mindlessly accepted and parroted flawed beliefs, so I must continue writing this critical correction on Vitamin B12.

     You should consider the following conclusions based upon my extended education, sense, life experience and many reviews of good (but individually never completely perfect) research literature. That research literature should also be available to you or your doctor (on the web or in a good medical university's library).

    Also understand that in many so-called, even best-intended scientific writings, one prejudiced or flawed idea, perception or premise or even just a single erred word can and often does invalidate an entire thesis -- and all other thesis's or volumes based upon the flawed first!

 -- I will add as much here in time as I can. tlr/LSI 9/19/03

http://www.lifesave.org/VitaminB12Continued.htm

Real B12 "Deficiency" Issues!
10 years ago
The Real B12 "Deficiency" Issues!B12 Uptake:
     You have already seen my limited first page defining VitaminB12 and its source.
  -- So you should already understand that: 

  -- since cyano-bacterially produced cobalamin is ubiquitous in the environment, it appears that true B12 intake deficiencies, beyond that of severe starvation or malnutrition, are now understood to be reasonably rare!
  -- and that the now more apparent problem is the consuming human's failed pancreas, fundus and intrinsic factor production, internal binding, absorption, transport, use, and/or waste dysfunctions!
 

B12 absorption, impairment and loses:
   Clear physiology, simple logic and research literature indicates three important conditions --  besides insufficient uptake of B12 (which is truly rare in most all natural conditions or diets) --  that contribute to low serum or interstitial, or malfunctional B12.

1.  Damage to pancreas, fundus and/or intrinsic factor (ileum) production tissues by:
       a. Digestive (auto-)corrosion -- caused by acidic (hydrochloric acid) and caustic (bile) conditions -- which is triggered or precipitated and generally required only by dairy, cheese, egg, meat, fish, fowl, (insect,) industrially hardened fats, all animal fat, and animal protein (lipoprotein) consumption.
       b. Microbial / viral overgrowths: Pancreatitis and/or infections of fundus and/or infections or microbial overgrowths of the intrinsic factor producing (ileum located) cells  -- infections associated again with barehanded handling (butchering, preparing) and consumption of non sterile (not fully boiled) dairy, cheeses, and all incompletely sterilized (not fully cooked) animal tissues as food.
       c. Drugs and Chemical offenses: Environmentally or pharmaceutically ingested, tactile, or respiratory organic and inorganic poisonings (including low level but chronic respiratory exposures e.g. formaldehyde, CL, CO, SOx, NOx, restricted oxygen, petrochemicals, tobacco, etc.) can set up low B12 intrinsic factor production, failed binding, transport or function anywhere in the B12 absorption / intrinsic factor chemistry, including its more evident hemoglobin catalyzation, myelinzation, and critical neuro-function paths.
       d. Autoimmine attack against pancreas and/or fundus enzyme and R-Binding secretion (parietal) cells and/or intrinsic factor (ileum) production cells -- potentially triggered (if or while concurrent liver shunting or bypass error is extant) by the ingestion (or direct injection) of equivalent (antigenic) animal tissues, especially visceral animal products -- those made with pancreas, intestine and /or liver tissues (as cheeses made with "rennet" i.e. pancreatin, frankfurters, sausages, cold cuts or "pot" meats). Milk and eggs with their broadly inclusive base protein equivalents (i.e.. multitude of antigens or antibody triggers) have potential to also trigger pancreatic, fundus, or intrinsic factor production (ileum) cell antibodies .
       e. Intestinal surgeries or accidents which cause visceral structural or mechanical trauma (to pancreas, fundus, intestines, specifically ileum, and /or liver).
       f. Genetic factors - rare, but occasionally occurring recombination errors or radiation effected nucleic flaws regulating any B12 involved tissues and chemistry.

2.  Bacterial and parasitic competition for dietary B12 (AKA: "Blind Loop" losses):
       a.  Many animal dependent pathogenic microbes and parasites (again associated with non-sterile dairy, fish, insect and all animal consumption) as well as abnormal overgrowths of so-called "friendly" flora compete for and can steal most all ingested B12 from the host human's nutrient / fecal flow.

(continues)

10 years ago

3. Bile wasting of liver stores of B12:
       a. Bile production is the only true wasting transport and exit vehicle of body (liver) stores of B12, i.e. real losses. Urine only transports (or "spills" as a "safety valve") at threshold exceeded B12 serum levels. No other significant loss or export of B12 exists!-- except in placental transfer to fetus and in the milk of lactating females. So excessive bile production -- hence B12 wasting (via bile-bearing excrement) -- is only realized and is (again only truly) associated with dairy, egg, insect, industrially hardened fats, all animal fats and all animal protein (lipoprotein) consumption. 
       So to appropriately conserve uptake B12 liver, serum and interstitial stores -- and to minimize bile-waste losses -- a none-bile digestion requiring, solely vegetation based, nourishment regimen is indicated.


      All three main B12 defect producing conditions listed (with sublistings) above do generally exist, at varying "subclinical" levels in all persons eating some form of the "Western-like" dairy, fish, fowl and cattle meat (animal tissues centered) carnivorous diets.
      But since the first tiered, ie. herbivorous animals, like cattle (which are consumed directly by humans), or second tiered, carnivorous animals, like fish, fowl, swine (also consumed by humans), are very efficient collectors and concentrators of (vegetation decomposition sourced -- cyano-bactria produced) B12 within their body tissues (as would also, or does occur in totally herbivorous humans) -- the consequent "super-doping" or high intake of B12 by meat-eating humans generally compensates (often overcompensates) for the same animal-ingestion-caused impaired absorption, etc. (listed above) and so does mask those subclinical damages naturally inherent with dairy, egg and all animal (and insect) tissues consumption.
  --  That masking is generally successful! -- until the damage rates overtake and exceed the super-doping B12 compensation rates that the animal tissues also provide! 

    (The subtle but ultimate occurrence, over time, of animal tissue triggered B12 absorption breakdown may well be simply deemed, written off, or accepted as part of "normal" aging! -- or as a undetected factor in a host of other psychological, neurological, physiological, genetic and geriatric diseases, and dying or death, and "diagnosed" through many different nomen, up to and including "natural causes"!) 
 

   

10 years ago
Conversely, the highly efficient absorption of environmentally available (trace, but ever present, "botanical") dietary B12, along with efficient enzyme (pancreas), R-binding (fundus) and intrinsic factor (ileum) production, efficient binding of B12 with intrinsic factor, and efficient micro-villi transport (into the portal blood flow into an efficient Liver) -- is found associated and enhanced by and in a non-corrosive neutral intestinal pH nutrient (fecal) flow. 
  -- That healthy neutral pH condition is only realizedwithin a (non-hydrochloric acid, non-bile demanding) totally vegetation provident (herbivorous) dietary regimen and its resultant efficient liver storage and effecient conservation of B12 in the non-wasting conditions, maintained by a non-bile demanding, simple fats, simple proteins (and simple sugars), intestinal nutrient / fecal flow.
tlr/LSI - 9/19/03


My Cows are smarter than Scientists!
So now, my Vitamin B-12 metabolism wiser friends:

How can you best obtain a natural - antigen and disease free - source of Vitamin B-12?
(Not the Commercially provided, animal liver, animal tissues, slaughterhouse blood and trimmings waste,
feces or sewage harvested supplements!)
Everywhere in the Garden!!!
However, since B-12 producing Cyanocobalamin bacteria love light and air, and they flourish on the surfaces of all plant matter, the more surface of a plant food you can consume, the more B-12 you will obtain. In scientific terms: the higher the surface ratio to consumed end-product volume, the higher the Vitamin B-12. 

That means that the greens, that generally grow with large surface areas in relation to weight of consumed product, will carry in the most B-12. 

Items that can provide excellent boost to your B-12 stores are juiced greens, with the highest surface to volume ratio.  So the richest supplies of B-12 generally is in the grasses: wheat grass juice or Barley grass juice or other juicable grasses, then parsley, or similar thin leafed greens (or finely flowered greens like broccoli) - which concentrate even more available B-12 by juicing! 

 -- Remember that the favored food of my old cows is the grasses and any leafy silage -- 800 pounds of it to make 1 pound of finished cow! -- That's why my dumb colleagues think nature's supply is those animals! -- They don't understand or haven't figured how the cow truly came by so much vitamin B-12. -- So it is obvious that sometimes those "highly educated" "scientific" wives-tail finding (and actually self believing) human scientist fellows are not as smart as they think themselves to be! -- Sorry but my old cows are smarter! -- My old cows eat grass -- not another cow, some other critter, some liver, slaugtherhouse wastes or sewage to get their Vitamin B-12!!!

Also Cyanocobalamin bacteria (like my old cows) do well on the soil-oxygen supplied surfaces of tubers (potatoes, carrots, beets, etc.) - so the skins and sub skins are a good supply of B-12 and should not be discarded where possible. (My old cows love those tuber's skins.)

Also Cyanocobalamin bacteria do well on fomenting vegetation or on saprophytes, like yeast! Both are excellent in nutrients and rich with B-12! (Cows love them too!)

Also like all micro-biota, Cyanocobalamin bacteria are impaired or killed by pesticides, so you should try to choose organic or pesticide free produced foods wherever possible. But if organic is not available, at least consume plenty of greens. (You can spout and grow your own grasses or greens at home even on a window sill and the wind blown air-carried Cyanocobalamin bacteria will land and multiply on them.)

tlr/LSI 01/03/04

Important Note: 
Carbon Monoxide inhibits uptake of B-12 by preventing binding chemistry to complete!
Two classes of bacteria exist
10 years ago
Just so you are clear on bacteria (and not fearful of all):
Two classes of bacteria exist:

Animal bacterial pathogens (and symbiotes) -- the ones that can cause disease in you and in the animals -- are  darkness requiring (light and cosmic energy sensitive) and do not tolerate much "free" oxygen, if any at all (anaerobic). They do not survive well or for very long (only minutes) outside the protective and nutrient provident animal's (or human's) tissues and fluids (blood, eggs, lymphus, milk).

Plant pathogens and flora-symbiotic bacteria, all the "Cyano" bacteria, which includes the Vitamin B-12 producing Cyanocobalamin Bacteria; on the other hand, prefer light and require abundant free oxygen (aerobic) -- so they cannot survive in you or in any animal and cannot cause you or any animal disease. But they "happily" live everywhere else in the environment, even blowing in the wind as they are whisped from (and to) the leaves and surfaces of every tree and foliage on the Planet. It is their metabolic end-product (waste) which is consumed, collected and conservatively used by my old cows and by your body as Vitamin B-12.

Thanks to the plants and their special symbiotic kind-to-plant kind-to-animal kind-to-humanity bacteria! 
We should learn some divine good from then both! -- Let Live! Then We Can Live! 
tlr/LSI 01/06/04

10 years ago
Footnotes with precise references will be added as soon as is possible.
But in the mean time this is what I have available in rough:
1. VitaminB12Pathophysiology194-196
2. VitaminB12Pathophysiology215-216
3. VitaminB12Pathophysiology470-472
Remember some error is already introduced in these 3 citations above by several contributors - based on their compartmentalized education, misconceptions or traditional belief in their base error that useful cobalamin, B12, is provided only by animals! So ferreting truth from the empirical data and redrawing correct conclusions has always been required of me in formulating best understanding -- and is also required of you for yours!tlr/LSI - 9/19/03

Other References: Veterinary & Human Biology & Pathology education and reference books / personal Human, Animal, Livestock and Marine (algae) research and experience -- and required knowledge for good livestock production and profit -- in my past.

I will try to improve upon and expand this page later as my resources/time allow. In the meantime, you may see a reference to intestinal (microvilli) repair at LDSVeg.org/Raw.htm#microvilli, and other intestine and whole body healing and nutritional information on LifeSave.orgVeganCowboy.org, WaterAndLife.org and our other subject specific sites (listed on Lifesave.org and VeganCowboy.org)
T L R. 9/19/03

(Questions? - call me. 801-298-9095, active Caller ID required, displayed and recorded, or Email LifeSaveIn@aol.com or mail PO Box 304 Bountiful Utah 84011-0304)

Back to Vitamin B12 (page one). To Pathophysiology Text pages 194-196

Vitamin B12 / Pathophysiology Text Pages 194 - 196
10 years ago

http://www.lifesave.org/VitaminB12Pathophysiology194-196.htm

Second Edition

PATHOPHYSIOLOGY
The Biological Principles of Disease

LLOYD H. SMITH, Jr., M.D.
Professor of Medicine; Associate Dean, University of California, San Francisco, School of Medicine, San Francisco. California

SAMUEL 0. THIER, M.D.
Sterling Professor and Chairman, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut

1985

W B. SAUNDERS COMPANY
Philadelphia, London, Toronto, Mexico City, Rio de Janeiro, Sydney, Tokyo, Hong Kong


INTERNATIONAL TEXTBOOK OF MEDICINE
General Editors

A. H. SAMIY, M.D.
Professor of Clinical Medicine and Chief of
Division of Medicine, New York Hospital, Cornell Medical Center
New York, New York

LLOYD H. SMITH, JR., M.D.
Professor of Medicine; Associate Dean,
University of California, San Francisco, School of Medicine,
San Francisco, California

JAMES B. WYNGAARDEN, M.D.
Director, National Institutes of Health,
Bethesda, Maryland

VOLUME I
PATHOPHYSlOLOGY
The Biological Principles of Disease

VOLUME II
MEDICAL MICROBIOLOGY AND INFECTIOUS DISEASES

Volumes I and II of the International Textbook of Medicine
have been conceived and written to follow a logical pedagogical approach and can readily be used in conjunction with the
CECIL TEXTBOOK OF MEDICINE.

From Pages 194 - 196  PATHOPHYSIOLOGY / Chapter V - BLOOD AND BLOOD FORMING ORGANS

Page 194

    Vitamin B12. In 1926, Minot and Murphy observed that it was possible to treat pernicious anemia by feeding raw liver. In 1929, Castle discovered that the intestinal absorption of the anti-pernicious-anemia principle of liver, which he called extrinsic factor (vitamin B12), depended on its first being bound to a factor secreted by the gastric mucosa, which he called intrinsic factor. Further developments included the identification of the chemical structure of vitamin B12 and the elucidation of its mechanism of action.
    Vitamin B12 is synthesized only in certain microorganisms. Animals depend on microbial synthesis for their vitamin B12 supply. Human foods that contain [high levels of] the vitamin are of animal origin (meat, liver, fish, eggs, and milk). The average daily diet in Western countries contains 5 to 30 ~g of vitamin B12, of which 1 to 5 ~g is absorbed. The total body stores of the vitamin in adults range from 2 to 5 mg, of which approximately 1 mg is found in the liver. The daily dietary requirement is about 2 to 3 p.g. Hence, after stopping intake of vitamin B12, or after total gastrectomy, it takes several years to deplete the body stores and for the symptoms of vitamin B12 deficiency to develop.
    The structure of vitamin B12, or cyanocobalamin, was elucidated in 1955 by the x-ray crystallographic analysis of Dorothy Hodgkin. The vitamin B12 molecule (Fig. 16) consists of two main parts: (1) a planar group, a ring structure surrounding the cobalt atom, that resembles the porphyrin ring of heme except for a bond linking two pyrrole rings directly together instead of through a bridging carbon atom-this structure is called a corrin ring; and (2) a nucleotide group containing the base 5,6 dimethylbenzimidazolyl and phos­phorylated ribose esterified with 1 amino, 2 propranol. Finally, a cyanide group is carried by the trivalent cobalt atom, which is also linked to the benzimidazole base. The term vitamin B,2 may be used to describe cyanocobalamin, although it is often used to include other forms of the vitamin in which the -ON is replaced by another side group. In nature, vitamin B12 exists largely as the two forms, methylcobalamin and 5’deoxyadenosylcobalamin. These are labile [easily changed] and are converted to a fourth form of vitamin B12, hydroxyco­balamin. Both cyanocobalamin and hydroxycobalamin are used therapeutically.

*0.5 mg/dl bloodI24 hours.


   

10 years ago
Page 195

    Dietary vitamin B12 is released from protein and peptide complexes in the stomach, where it attaches to both intrinsic factor and a second vitamin B12 binding protein called R-binder. Intrinsic factor is a glycopro­tein that contains 15 per cent carbohydrate and is secreted by the parietal cells of the body and the fundus of the stomach. One molecule of intrinsic factor binds to one molecule of vitamin B12 in the region of the edge of the corrin ring. The R-protein is degraded by pancreatic secretions and the vitamin B12 released binds to further intrinsic factor. This step is impaired in patients with pancreatic disease, leading to reduced vitamin B12 absorption. The normal site of absorption appears to be the distal ileum. It is possible to absorb up to 1.5 pg of vitamin B12 from a single oral dose of intrinsic factor-vitamin B12 complex. Following absorption, the ileum is reffactory [resistant] to further vitamin B12 absorption for several hours. At a neutral pH and in the presence of talcium ions, intrinsic factor-vitamin B12 complex passively attaches to receptor sites on the brush borders of the ileal mucosa. It then enters the mucosal cell, where it is found in the cytosol. After exit from the ileal enterocyte, vitamin B12 is attached to a second major vitamin B12 transport protein (trans­cobalamin II, see below) which is synthesized in the ileal cells. Thereafter, the vitamin is transferred to the portal blood, the peak blood level being reached only 8 to 12 hours after an oral dose. Intrinsic factor does not enter the portal blood and its fate is not absolutely clear. Only about 1 per cent of an oral dose of the order of 30 to 300 p.g of vitamin B12 is absorbed in the absence of intrinsic factor. This form of absorption occurs throughout the gut by simple passive means.
    Vitamin B12 is transported on specific binding proteins called transcobalamins (TC), of which three forms, TOI, II, and III, have been isolated. TOII is the main delivery protein that transports cobalamins to tissues such as marrow and in the nervous system. It is synthesized by a variety of cells, including macro­phages, ileal enterocytes, and the liver. The TOIl­vitamin B12 complex attaches to a receptor site on the surface of various target cells and is internalized by pinocytosis. TOII is essential for vitamin uptake by cells, and in its absence a severe vitamin B12 deficiency state develops. The functions of TO’s I and III, which


Page 196

are probably produced by leukocytes, are unknown. The TO levels vary in a variety of disease states. As might be expected, TOI levels rise markedly in various forms of granulocytic leukemia and other myeloprolif­erative diseases and also during the leukocytosis of infection. Increased TOII levels are observed in liver disease and pregnancy.
     The metabolic functions of vitamin B12 are only understood in three well-defined reactions. One is the conversion of homocysteine to methionine, as shown in Figure 17. The enzyme involved is homocysteine­methionine methyl transferase, and the reaction requires 5-methyl tetrahydrofolate as a methyl donor, S. adenosylmethionine, and the reducing agent (FADH2) as well as methyl-B12 as a coenzyme. Vitamin B12-dependent methionine synthesis is important in the regeneration of tetrahydrofolate from methyltetrahy­drofolate. The second reaction involving vitamin B12, as deoxyadenosylcobalamin, is the conversion of pro­prionate to succinate, as shown in Figure 18. This reaction is part of the route by which cholesterol and odd-chain fatty acids as well as a number of amino acids and thymine are used for energy requirements via the Krebs cycle. Patients with vitamin B12 deficiency may excrete excess methylmalonic acid. Finally, vitamin B22 is involved in the i~omerization of j3-leucine to ct-leucine; in vitamin B12 deficiency 13-leucine accumulates while ct-leucine is decreased. The inter­relationships between vitamin B12 and folate metabolism in the synthesis of DNA are considered later-it is this function of vitamin B12 that undoubtedly accounts for the megaloblastic erythropoiesis and related phenomenon of abnormal DNA synthesis found in vitamin B12 deficiency states. Vitamin B12 is also essential for the function of metabolic pathways in the central nervous system.

VITAMIN B12 DEFICIENCY
10 years ago
From Pages 215 - 216   PATHOPHYSIOLOGY /Chapter V - THE BLOOD AND BLOOD-FORMING ORGAN

Page 215

VITAMIN B12 DEFICIENCY

      Pathogenesis. The most common cause of vitamin B12. deficiency is a deficiency of gastric intrinsic factor, which causes the clinical picture of pernicious anemia. A more complete classification of the causes of vitamin B12, deficiency is shown in Table 20. Like most vitamin deficiency states, they can be classified into those caused by defective intake, defective absorption, and defective utilization.
      Inadequate dietary intake of vitamin B12 is rare, accept in populations that for religious or other reasons where to a very strict vegetarian diet. It may [?] also occur in total vegetarians, called vegans. The commonest cause of intrinsic factor deficiency is gastric atrophy, which is the basic underlying pathology of pernicious anemia. There is a rare congenital form of pernicious anemia that behaves as an autosomal recessive in which there is failure of intrinsic factor production. Total gastrectomy predictably leads to negaloblastic anemia after about two to six years, but vitamin B12 deficiency occurs only rarely after partial gastrectomy, unless there has been an extensive resection of the intrinsic-factor producing area. Since vitamin B12 is absorbed in the ileum, disease of this area causes vitamin B12 deficiency. Examples include surgical resection or involvement with regional ileitis, lymphoma, or tuberculosis of the ileum. Extensive disease of the small bowel, as occurs with tropical sprue or adult celiac disease, may occasionally cause vitamin B12 deficiency. There is a rare abnormality of the terminal ileum that causes a megaloblastic anemia in childhood and is usually associated with proteinuria; this is known as Imerslund’s syndrome. Certain structural disorders of the small bowel reduce the availability of vitamin B12. Any anatomic lesion that causes stasis and pooling of the lumenal contents with proliferation of bacteria may cause a situation in which vitamin B12 is taken up in the stagnant area and utilized by the bacteria. Such “blind loop” syndromes are caused by strictures of the small bowel, fistulas, and large diverticulae. A similar mechanism explains the megaloblastic anemia associated with the fish tapeworm (Diphyllobothrium latum).
      Acquired intrinsic factor deficiency is by far the commonest cause of vitamin B12 deficiency, and the associated clinical disorder is known as pernicious anemia. It was first described in 1885 at Guy’s Hospital, London, by Thomas Addison, and is sometimes known as Addisonian pernicious anemia. The basic defect is atrophy of the gastric mucosa, which results in an intrinsic factor deficiency. The etiology of the gastric atrophy is still far from certain. It seems likely that both genetic and autoimmune factors are involved. A genetic basis is suggested by the high incidence in certain races, such as Scandinavians, and by its association with blood group A. Furthermore, there is an increased incidence of the disorder among sibships and a markedly increased incidence of latent pernicious anemia within families. Latent pernicious anemia is characterized by lack of gastric acidity [caused by, yet necessary for meat and animal fat digestion] and decreased vitamin B12 absorption without the full hematologic features of pernicious anemia.
     The atrophic gastritis of pernicious anemia is characterized by lack of normal gastric mucosa with a striking lymphocytic infiltration and an absence of gastric acid and pepsin production even after full stimulation with histamine or with pentagastrin. The serum gastrin level is raised. An autoimmine basis for this pathology has been suggested by the finding of autoantibodies against the cytoplasm of the gastric parietal cell in the serum of 90 per cent of patients with pernicious anemia. It should be noted, however, that individuals who do not have the disorder may have the same antibody. This includes 60 per cent of all individuals with atrophic gastritis, 30 per cent of relatives of patients with pernicious anemia, and about 10 per cent of the normal adult population. Patients with pernicious anemia frequently have antibodies directed against parenchymal tissue of endocrine glands, most commonly the acinar glands of the thyroid. On the other hand, patients with primary myxedema, or Hashimoto’s thyroiditis, have a 30 per cent incidence of parietal cell antibodies and a 12 per cent incidence of coexisting pernicious anemia. Of more direct interest, however, is the finding that in about 57 per cent of patients with pernicious anemia there are anti-intrinsic factor antibodies in the serum, saliva, and gastric juice. These antibodies are polyclonal and may be IgG or IgA. It appears that they react to two different sites on the intrinsic factor molecule; there are blocking antibodies preventing the binding of vitamin B12 to intrinsic factor and binding antibodies that do not interfere with the attachment but impede absorption in the ileum. Intrinsic factor antibodies are found much less frequently than parietal cell antibodies in the general population and seem to be more specifically associated with pernicious anemia.
     It appears, therefore, that individuals with a genetic predisposition toward pernicious anemia may develop autoimmune damage to the gastric mucosa and anti­bodies to intrinsic factor. It is unclear, however, whether the production of autoantibodies is a primary event or is secondary to whatever causes damage to the gastric mucosa.
     http://www.lifesave.org/VitaminB12Pathophysiology215-216.htm

10 years ago
Tissue and Neurologic Changes. There is a specific neurologic syndrome of vitamin B12 deficiency that is called subacute combined degeneration of the spinal cord. The pathologic changes are characterized by degenerative lesions in the dorsal and lateral columns. Early changes include swelling of individual myelinated nerve fibers and these lesions later coalesce into large foci involving many fiber systems. Similarly


Page 216 I V—THE BLOOD AND BLOOD-FORMING ORGAN

patchy degeneration occurs in the white matter of the brain. This produces a variety of clinical pictures, including cerebral manifestations (“megaloblastic madness”), perversions of taste and smell, defects in vision with central scotomata and optic atrophy, ataxia due to reduced dorsal column function, peripheral neuropathy, and, in some cases, a spastic paraplegia or quadriplegia when the lateral columns are involved.
     In addition to the symptoms and signs of anemia and neurologic damage, patients with pernicious anemia have a lemon-yellow color due to slightly elevated unconjugated bilirubin, and about a third of them have palpable enlarged spleens.
     Diagnosis of Vitamin B12 Deficiency. The laboratory investigation of vitamin B12 deficiency is based on an understanding of its pathophysiology. The finding of a macrocytic peripheral blood picture with a megaloblastic bone marrow usually indicates either vitamin B12 deficiency or float deficiency. With vitamin B12 deficiency, the serum vitamin B12 level, as assayed micro biologically with Lactobacillus leishmanii or Euglena gracilis, or by isotope dilution, is reduced. In true pernicious anemia there is a histamine or penta­gastrmn-fast achiorhydria. Radioactive vitamin B12 absorption can be assayed by the Schilling test, in which a dose of 58Co- or 57Co-labeled cyanocobalamin is given by mouth at the same time as an intramuscular “flushing” dose of non radioactive cyanocobalamin, and the amount of radioactivity in the urine is measured. The reason for giving the intramuscular dose of vitamin B12 is that normally when the vitamin is taken by mouth, it enters the liver, and only after a large dose given by injection to preload the liver does sufficient orally administered B12 appear in the urine to be easily measured. In the absence of intrinsic factor reduced amounts of radioactivity appear in the urine. The second part of the Schilling test consists of giving radioactive vitamin B12 together with intrinsic factor, after which a considerable portion of the radioactivity appears in the urine if the patient has genuine intrinsic factor deficiency. If vitamin B12 is due to small bowel disease, absorption is not corrected by intrinsic factor. Absorption can also be measured by monitoring the patient in a whole-body counter. In cases in which a blind loop is suspected, vitamin B12 absorption can be measured before and after giving a course of broad-spectrum antibiotics, which destroy the bacteria in the stagnant loop. Structural disease of the small bowel requires radiologic investigation and jejunal biopsy. Another test for vitamin B12 deficiency is the measurement of methylmalonic acid in the urine, which is elevated if there is a vitamin B12 deficiency (see pp. 194 to 195).

COBAIAMINS (VITAMIN B12)
10 years ago

From pages 470 - 472   PATHOPHYSIOLOGY / Chapter VII - PATHOPHYSIOLOGIC  PRINCIPLES OF NUTRITION http://www.lifesave.org/VitaminB12Pathophysiology470-472.htm

Page 470

COBAIAMINS (VITAMIN B12)

    More than 150 years ago, Combe and Addison described an anemia associated with gastric and neurologic disorders, with death usually occurring two to five years after onset. Successful treatment of perni­cious anemia was not achieved until 1926, when Minot and Murphy showed the effectiveness of feeding whole liver (Nobel Prize, 1934). Shortly thereafter, Castle demonstrated the need for both an extrinsic, dietary factor and an intrinsic, gastric factor. The structure of isolated, crystallized vitamin B12 was determined by Dorothy Hodgkins using x-ray diffraction (Nobel Prize, 1964).
    Chemistry. The stable pharmaceutical form of vi­tamin B12, and the form first isolated, is cyanocoba­lamin. It is not the natural form of the vitamin, however. The molecule consists of two major parta, a corrin nucleus similar to heme and a nucleotide, 5,6-dimethylbenzimidazole (Fig. 10). At the center of the corrin nucleus is an atom of cobalt. The major parts of the molec~ile are linked by a bridge consisting of D-1-aniino-2-propanol and a bond between cobalt and one of the nitrogens of the nucleotide. Also attached to the cobalt atom is one of several anionic CR—) groups that distinguish the various congeners. Cobalamin is the term used to describe the molecule in the absence of an R — group. In its presence, the name of the partic­ular R — group is prefixed to cobalamin.


Page 471

    Distribution and Bioavailability The sole source of vitamin B12 in nature is synthesis by microorga­nisms. Plants are totally devoid of the vitamin unless contaminated by microorganisms. The usual dietary sources are the organs of domestic animals, which absorb the vitamin produced by microorganisms in the gastrointestinal tract. Vitamin B12 is also synthesized in the colon of humans, but it is not absorbed. Prime dietary sources include beef liver, kidney, whole milk, eggs, oysters, fresh shrimp, pork, and chicken. The average American diet supplies 7 to 30 ug of the vitamin per day.
 Absorption. Vitamin B12 is absorbed by two mech­anisms. Pharmacologically, 1 per cent of any dose of the free vitamin is absorbed by diffusion along the entire small intestine. Physiologically, a maximum of 1.5 to 3 ug of the vitamin is absorbed. The vitamin in food is released from its polypeptide linkage by gastric and intestinal enzymes and combines with the gastric intrinsic factor. Dimerization occurs, and a complex is formed consisting of two molecules of intrinsic factor and two molecules of vitamin B12. The complex subse­quently attaches to the brush border of the ileum. In the presence of calcium ions and a pH greater than 6.0, the complex enters the mucosa cell and B12 is released. It then enters the bloodstream, where it is bound by vitamin B12—binding proteins.
    Transport and Storage. The normal plasma con­centration of vitamin B12 is 200 to 900 pg/ml. The vitamin is bound by three proteins in plasma, trans­cobalamin (TC) I, II, and III. Most of the B12 in plasma is bound to TC I, but it appears to be nonfunctional. Transcobalamins I and Ill are glycoproteins synthe­sized primarily by granulocytes and appear to serve a storage function. They are referred to collectively as cobalophilins. Unlike the cobalophilins, transcoba­lamin II is the vitamin B12 transport protein. It is a beta-globulin synthesized by the liver, and it delivers B12 to liver, bone marrow, lymphoblasts, fibroblasts, and tumor cells. It has a molecular weight of 38,000 compared with 60,000 for the cobalophilins, and it is not a glycoprotein.
The body stores of B12 range from 1 to 10 mg, 90 per cent of which is stored in the liver. Virtually the only
loss is through excretion into bile.  B12 is excreted into the bile and is reabsorbed in the ileum with an entero­hepatic circulation of 3 to 8 ug/day. The stored form of B12 is deoxyadenosylcobalamin, and the plasma form is methylcobalamin. Because of the efficiency of the enterohepatic circulation, B12 stores are not totally depleted until five to six years after cessation of intake or absorption.
    Transformation and Function. In the body, vita­min B12 is reduced and converted to two active coen­zyme forms, deoxyadenosylcobalamin and methylco­balamin. Only two metabolic pathways are known to require this cofactor.

    1. 5-Deoxyadenosylcobalamin is required for hydro­gen transfer and isomerization of methylmalonyl CoA to succinyl CoA. This reaction is involved in both fat and carbohydrate metabolism and may be related 

10 years ago
Page 472

to the abnormality of the lipid portion of the myelin sheath seen in B12 deficiency.
    2. Methylcobalamin acts as coenzyme in synthesis of methionine from homocysteine (Fig. 1). This reaction also regenerates tetrahydrofolate. In the absence of B12, the body becomes functionally folate deficient be­cause folate is trapped as methyl THF.

    Excretion. Vitamin B12 is not further metabolized in the body, and the major route of excretion is into bile. Losses at this step depend on the efficiency of reabsorption in the ileum. The vitamin is not excreated into urine until the renal tubular reabsorptive capacity has been exceeded.
    Requirement. Only small amounts of vitamin B12 are required by the body. The MDR is 1 ug/day, and 1 to 1.5 ug is absorbed from the 3 ug/day RDA. With the exception of vegetarian diets without supplements, most deficiencies do not result from inadequate intake but from a defect in absorption. Absorption can be impaired in two ways: (1) failure to produce the gly­copirotein gastric intrinsic factor and (2) interference with the absorption of the intrinsic factor—vitamin B12 complex, as in loss of the terminal ileum or intralum­inal catabolism of B12 by overgrowth of bacteria in intestinal stasis.
    Deficiency State. Deficiency is clinically manifest both hematopoietically and in the nervous system. Hematopoietic damage is caused by an inadequate amount of the vitamin to promote demethylation of N­methyltetrahydrofolate to THF, which is required for the synthesis of thymidine (and therefore of DNA). The sensitivity of the red blood cell to vitamin B12 deficiency is due to its rapid turnover rate. Vitamin B12 deficiency is suggested by large red blood cells (mean corpuscular volume> 95 fi) and is highly likely if the mean erythrocyte volume is> 110 fi and abnor­mally large numbers of segments (> 6) exist in nuclei of neutrophils. Deficiency in the nervous system can cause irreparable damage. Demyelination, cell death, and swelling of myelinated neurons are often seen.
    Deficiency may be determined in several ways: (1) determination of plasma concentration of B12 (2) gas­tric function tests; (3) excretion of methylmalonate; and (4) demonstration of reticulocytosis after a therapeutic dose of vitamin B12. The simplest screening test is the serum B12 level, usually by a radioimmunoassay which unfortunately has a decreasing accuracy at low levels of serum B12.
    The Schillings test is more sensitive for conditions that prevent proper cyanocobalamin absorption. It has four parts, of which only the first two are usually necessary: (1) The subject is given a known amount of radiolabeled vitamin B12 by mouth and a parenteral dose of 1 mg nonlabeled B12. This saturates vitamin B12—binding proteins and facilitates maximal urinary excretion of absorbed radioactive B12. More than 7 per cent of the ingested radioactive cobalt should be re­covered in the urine if normal absorption occurs. (2) The Schilling test is similarly repeated but with the ingested radiolabeled vitamin B12 attached to intrinsic factor. A normal result this time, after an abnormal result from the first part, confirms the presence of a gastric disorder causing insufficient production of in­trinsic factor.
    Parts three and four of the Schilling test involve treatment with antibiotics and pancreatic enzymes, respectively, and can be used with patients in whom small bowel bacterial overgrowth or pancreatic insuf­ficiency is a possible cause of vitamin B12 malabsorp­tion.
    Methylmalonicaciduria is a chemical sign of vitamin B12 deficiency because of the vitamin’s role as cofactor in the conversion of methylmalonate to succinate. Homocystinuria is also present, since the demethyla­tion of methyl THF, which normally converts homocysteine to methionine, is impaired.
    Therapeutic trials of B12 can be misleading, since large doses of B12 can partially correct a folate deficiency, thereby masking the true cause of the macrocytic anemia. Parenteral administration of’ 1 to 10 big/day of B12 should be followed by reticulocytosis in three to five days.
    Toxicity. Vitamin B12 is nontoxic in humans even at 10,000 times the minimum daily requirement. Excess amounts are excreted into the urine.

The Sabbath & Vitamin B-12 (Part 1)
10 years ago

The Sabbath & Vitamin B-12 (Part 1)

In the King James version of the Holy Bible (Exodus 20:8), the Fourth of Ten Commandments instructs us to:

"Remember the Sabbath day, to keep it holy."

Many people do so by reading the Bible for its wisdom and guidance, and I would like to take this opportunity to merge science, religion, and good
health into one very inspirational and instructional column based upon another chapter in the Good Book.

Got Vitamin B-12? If the Song of Solomon inspires you, then you will most certainly be in good hands.

From the Song of Solomon:
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
"Thy plants are an orchard of pomegranates, with pleasant fruits; camphor, with spikenard, spikenard and saffron; calamus and cinnamon, with all trees of frankincense; myrrh and aloes, with all the chief spices...A fountain of gardens, a well of living waters, and streams from Lebanon. Awake, north wind; and come, thou south; blow upon my garden, that the spices thereof may flow out. Let my beloved come into his garden, and eat his pleasant fruits. Open to me, my love, my dove, my undefiled: for my head is filled with dew, and my locks with the drops of the night.

His cheeks are as a bed of spices, as sweet flowers: his lips like lilies, dropping sweet smelling myrrh. His mouth is most sweet: yea, he is altogether lovely. This is my beloved, and this is my friend, O daughters of Jerusalem. My beloved is gone down into his garden, to the beds of spices, to feed in the gardens, and to gather lilies. I am my beloved's, and my beloved is mine: he feedeth among the lilies.

I went down into the garden of nuts to see the fruits of the valley, and to see whether the vine flourished and the pomegranates budded. How fair and how pleasant art thou, O love, for delights! And the roof of thy mouth like the best wine for my beloved, that goeth down sweetly, causing the lips of those that are asleep to speak. I am my beloved's, and his desire is toward me.

Let us get up early to the vineyards; let us see if the vine flourish, whether the tender grape appear, and the pomegranates bud forth: there will I give thee my love.

I would cause thee to drink of spiced wine of the juice of my pomegranate."
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
May God bless those wise prophets who without microscopes or chemical laboratories were divinely inspired to write about nature's most sensual source of Vitamin B-12.

If the Song of Solomon does not do for you what it does for me, then consider this information, when pondering the Vitamin B-12 controversy. In 1996, Victor Herbert determined that Vitamin B-12 deficiency is rare among vegans, even though most do not take supplemental B-12. His landmark work was published in the American Journal of Clinical Nutrition, vol. 59(suppl), pp. 1213S-1222S. Herbert wrote:

"To a great extent, B-12 is recycled from liver bile in the digestive system...The enterohepatic circulation of vitamin B-12 is very important in vitamin B-12 economy and homeostasis...bodies reabsorb 3-5 mcg of bile vitamin B-12. Because of this, an efficient enterohepatic circulation
keeps the adult vegan, who eats very little vitamin B-12,from developing B-12 deficiency disease..."

Shabbat Shalom!

Robert Cohen

http://www.notmilk.com
9 years ago

Red Star Nutritional Yeast 

**Now available in economical bulk pails!**

Not all nutritional yeast is created equal – Red Star's formula is made specifically for supporting the needs of vegans and vegetarians with added vitamins and minerals you won't find in other brands (it is a great natural source of all B vitamins, especially B-12). Handy 5 oz. shaker bottle makes it easy to use as much or as little as you'd like, so no more big bags to mess with. Use it in soups, salads, casseroles and gravies, or sprinkle it on popcorn for a delicious and nutritious cheesy taste. There are many, many uses for it, so be sure to take a look at Joanne Stepaniak's Nutritional Yeast Cookbook (see information at bottom of page.) $4.79 per bottle. Also available in 6 lb bulk pail of flakes for $39.95, and 10 lb pail of mini-flakes for $69.95.

Ingredients: Inactive Dry Yeast, Niacin (vitamin B3), Thiamin (vitamin B1), Riboflavin (vitamin B2), pyridoxine hydrochloride (vitamin B6), vitamin B12

Vitamin profile:

Thiamin - 640% RDA, Niacin – 280% RDA, Folic Acid – 60% RDA, Selenium – 32% RDA, Iron – 4% RDA, Riboflavin – 565% RDA, Vitamin B6 – 480% RDA, Vitamin B12 – 133% RDA, Zinc – 21% RDA

Nutritional Information:
Serving size – 1 ½ tablespoons
Servings per container – 9
Calories – 60
Total fat – 1g (0g saturated)
Sodium – 5mg
Total carbohydrate – 7g (4g dietary fiber)
Protein – 8g

Highly Recommended!!!!
From Dorine of Halifax, Nova Scotia on 4/7/2005.

This is simply the best nutritional yeast to use. It has a mild cheesy flavour.

The Nutritional Yeast Cookbook

 

By Joanne Stepaniak

Nutritional yeast is oftentimes the vegan's answer to getting extra Vitamin B-12 in their diet, and if you've looking for delicious recipe ideas then this book is for you. You'll find everything from breakfast favorites such as Eggless cheese omelets to delicious cheese-flavored sauces to tempting dinner entrées such as Crispy Tofu Sticks with Dijon Apricot Sauce. With over 100 recipes ranging from quick to extravagant, you'll have dozens of ideas how to incorporate healthy nutritional yeast into your meals. 143 pages. $9.95 per copy.

The Nutritional Yeast Cookbook

https://secure1.nexternal.com/shared/StoreFront/default.asp?CS=vegane&BusType=BtoC&Count1=354168117&Count2=271308541&Target=products%2Easp&ProductID=734

9 years ago
Vitamin B-12 is everywhere in the GARDEN!!! May 10, 2005 11:20 PM
Cows are smarter than Scientists!
So now, my Vitamin B-12 metabolism wiser friends:

How can you best obtain a natural - antigen and disease free - source of Vitamin B-12?

(Not the Commercially provided, animal liver, animal tissues, slaughterhouse blood and trimmings waste, feces or sewage harvested supplements!)
Everywhere in the Garden!!!
However, since B-12 producing Cyanocobalamin bacteria love light and air, and they flourish on the surfaces of all plant matter, the more surface of a plant food you can consume, the more B-12 you will obtain. In scientific terms: the higher the surface ratio to consumed end-product volume, the higher the Vitamin B-12. 

That means that the greens, that generally grow with large surface areas in relation to weight of consumed product, will carry in the most B-12. 

Items that can provide excellent boost to your B-12 stores are juiced greens, with the highest surface to volume ratio.  So the richest supplies of B-12 generally is in the grasses: wheat grass juice or Barley grass juice or other juicable grasses, then parsley, or similar thin leafed greens (or finely flowered greens like broccoli) - which concentrate even more available B-12 by juicing! 

 -- Remember that the favored food of my old cows is the grasses and any leafy silage -- 800 pounds of it to make 1 pound of finished cow! -- That's why my dumb colleagues think nature's supply is those animals! -- They don't understand or haven't figured how the cow truly came by so much vitamin B-12. -- So it is obvious that sometimes those "highly educated" "scientific" wives-tail finding (and actually self believing) human scientist fellows are not as smart as they think themselves to be! -- Sorry but my old cows are smarter! -- My old cows eat grass -- not another cow, some other critter, some liver, slaugtherhouse wastes or sewage to get their Vitamin B-12!!!

Also Cyanocobalamin bacteria (like my old cows) do well on the soil-oxygen supplied surfaces of tubers (potatoes, carrots, beets, etc.) - so the skins and sub skins are a good supply of B-12 and should not be discarded where possible. (My old cows love those tuber's skins.)

Also Cyanocobalamin bacteria do well on fomenting vegetation or on saprophytes, like yeast! Both are excellent in nutrients and rich with B-12! (Cows love them too!)

Also like all micro-biota, Cyanocobalamin bacteria are impaired or killed by pesticides, so you should try to choose organic or pesticide free produced foods wherever possible. But if organic is not available, at least consume plenty of greens. (You can spout and grow your own grasses or greens at home even on a window sill and the wind blown air-carried Cyanocobalamin bacteria will land and multiply on them.)

9 years ago
B12 absorption, impairment and loses May 10, 2005 11:45 PM

I am having problem with the format here.  Let me try it one more time.

DIGESTIVE (AUTO-)CORROSION
Caused by acidic (hydrochloric acid) and caustic (bile) conditions -- which is triggered or precipitated and generally required only by dairy, cheese, egg, meat, fish, fowl, (insect,) industrially hardened fats, all animal fat, and animal protein (lipoprotein) consumption.

MICROBIAL / VIRAL OVERGROWTHS
Pancreatitis and/or infections of fundus and/or infections or microbial overgrowths of the intrinsic factor producing (ileum located) cells -- infections associated again with barehanded handling (butchering, preparing) and consumption of non sterile (not fully boiled) dairy, cheeses, and all incompletely sterilized (not fully cooked) animal tissues as food.

DRUGS AND CHEMICAL OFFENSES
Environmentally or pharmaceutically ingested, tactile, or respiratory organic and inorganic poisonings (including low level but chronic respiratory exposures e.g. formaldehyde, CL, CO, SOx, NOx, restricted oxygen, petrochemicals, tobacco, etc.) can set up low B12 intrinsic factor production, failed binding, transport or function anywhere in the B12 absorption / intrinsic factor chemistry, including its more evident hemoglobin catalyzation, myelinzation, and critical neuro-function paths.

AUTOIMMINE ATTACK
against pancreas and/or fundus enzyme and R-Binding secretion (parietal) cells and/or intrinsic factor (ileum) production cells -- potentially triggered (if or while concurrent liver shunting or bypass error is extant) by the ingestion (or direct injection) of equivalent (antigenic) animal tissues, especially visceral animal products -- those made with pancreas, intestine and /or liver tissues (as cheeses made with "rennet" i.e. pancreatin, frankfurters, sausages, cold cuts or "pot" meats). Milk and eggs with their broadly inclusive base protein equivalents (i.e.. multitude of antigens or antibody triggers) have potential to also trigger pancreatic, fundus, or intrinsic factor production (ileum) cell antibodies .

INTESTINAL SURGERIES OR ACCIDENTS which cause visceral structural or mechanical trauma (to pancreas, fundus, intestines, specifically ileum, and /or liver).

GENETIC FACTORS rare, but occasionally occurring recombination errors or radiation effected nucleic flaws regulating any B12 involved tissues and chemistry.

BACTERIAL AND PARASITIC COMPETITION for dietary B12 (AKA: "Blind Loop" losses):
Many animal dependent pathogenic microbes and parasites (again associated with non-sterile dairy, fish, insect and all animal consumption) as well as abnormal overgrowths of so-called "friendly" flora compete for and can steal most all ingested B12 from the host human's nutrient / fecal flow.


BILE WASTING OF LIVER STORES OF B12
BILE PRODUCTION is the only true wasting transport and exit vehicle of body (liver) stores of B12, i.e. real losses. Urine only transports (or "spills" as a "safety valve") at threshold exceeded B12 serum levels. No other significant loss or export of B12 exists!-- except in placental transfer to fetus and in the milk of lactating females. So excessive bile production -- hence B12 wasting (via bile-bearing excrement) -- is only realized and is (again only truly) associated with dairy, egg, insect, industrially hardened fats, all animal fats and all animal protein (lipoprotein) consumption.

So to appropriately conserve uptake B12 liver, serum and interstitial stores -- and to minimize bile-waste losses -- a none-bile digestion requiring, solely vegetation based, nourishment regimen is indicated.  

9 years ago
Vegan Nutrition with Dina Aronson, M.S. R.D.

Vitamin B12 is produced by bacteria, fungi, and algae. Neither plants nor animals can synthesize the vitamin. Thus, it is not found in plant products naturally (there might be trace amounts in plant foods contaminated with B12-producing microorganisms, but we should not depend on contaminated food).

We vegans need to get B12 from supplements and/or fortified foods. The B12 added to foods and supplements are synthetically produced in a laboratory from bacteria, not animal sources. Here are some other foods that typically are B12-fortified. Make sure you read the food label! B12 is also called cobalamin.

  • Red Star Vegetarian Support Formula Nutritional Yeast*
  • Fortified breakfast cereals
  • Fortified soy milk
  • Fortified vegetarian meat analogs
  • Fortified energy or snack bars, such as Luna Bars
  • Fortified soy powders or other beverage mixes

*Nutritional yeast adds a cheesy flavor to foods; my favorite way to use it is in tofu scrambles.

By the way, the lack of vitamin B12 in plant foods has led many to question how "natural" a vegan diet is. After all, if an essential nutrient is lacking from a 100% plant-based diet, how can such a diet be good for you? This is a very good question. Remember, B12 is produced only by microorganisms. Consider the sanitary modern world: only in the last several decades have we had the luxury of treated water, power-washed produce, and machine-sanitized packaged foods. Before these conveniences, people (vegans and non-vegans) ate locally-grown fruits and vegetables and drank water from the well or public water supply, all of which were rich in vitamin B12 due to bacterial contamination. In those times, vitamin B12-producing microorganisms contaminated the entire food supply, not just animal products. The need of a modern-day vegan to supplement the diet with B12 is not because the vegan diet is inferior to a diet with animal products; it is the result of modern sanitary conditions.

Visit this page to see how much vitamin B12 you and your family need each day.

The Recommended Dietary Allowances for vitamin B12 are (numbers are in micrograms):

Infants
0-6 months 0.4
7-12 months 0.5

Children
1-3 years 0.9
4-8 years 1.2

Males and Females
9-13 years 1.8
14-18 years 2.4
19-30 years 2.4
31-50 years 2.4
51-70 years 2.4
> 70 years 2.4

Pregnancy
All ages 2.6

Lactation
All ages 2.8

As you can see, the recommended vitamin B12 intakes are 2-3 micrograms per day for most people. But these are not necessarily the numbers we should strive for! These numbers represent amounts that are enough to ensure that we do not become deficient in vitamin B12. However, cutting-edge research has shown that optimal intakes of vitamin B12 are actually higher--more in the range of 5-10 micrograms per day. Therefore, to ensure not only adequate but optimal intake of vitamin B12, vegans should strive for:

3 micrograms per day from fortified foods in 2 or more meals
or
10 mcg per day from supplements
or
2000 mcg per week from supplements
http://www.vegfamily.com/dietician/0504a.htm

B12 Methylcobalamin vs. Cyanocobalamin
7 years ago
I've heard that Methylcobalamin is better at setting circadian rhythms early in the day.  Does anyone know the difference b/t Methyl and Cyan?
peer review and bio active b12
6 years ago

Nice article and a lot of time put into this. I am a vegan in debate with a meat eating scientist-like person who has peer reviewed data which contradicts this article; specifically stating that b12 not found in animal products is not bio active.

Is there anyway I can get a peer reviewed article that supports these claims in favor of vegan b12 being Bio Active?

Just so you understand me regarding bio active, it has to do with the b12 molecule having the correct physical shape to be absorbed, similar to a lock and key. A key can't fit into a lock unless it is the right shape, and vegan b12 not being bio active won't either.

Any evidence so I can take to my debate in support of vegan b12 will be helpful.

Daniel

6 years ago

Welcome to the group, Andie & Daniel.  Sorry I haven’t read this sooner.  But I will do my search and respond to you accordingly.