Vitamin B12 Deficiency...
Are You at Risk?
The impact vitamin B12 deficiency has in your life is far-reaching. Vitamin B12 is intimately involved with protein metabolism and DNA synthesis, two major biochemical processes controlling everything from heredity to metabolism. Consequently, the results of B12 deficiency are very serious...
Consequences of B12 Deficiency
Vitamin B12 Deficiency Puts The Brakes on DNA Synthesis and Protein Metabolism This Creates a Wide Spectrum of Dysfunction. For Example...
Deficiency of B12 Causes "Megaloblastic Anemia"
Megaloblastic Anemia is a Debilitating Condition Characterized by Fatigue, Lack of Energy, Diarrhea, Nausea, Decreased Appetite, Weak Muscles, Headaches, Tingling Sensations and Sore Tongue
Irreversible Degenerative Neuropathy is A Hallmark of B12 Deficiency
Deterioration of the Peripheral and Central Nervous System, Including Brain Occurs if Vitamin B12 Deficiency is not Ameliorated
Deficiency of Vitamin B12 Increases Levels of "Homocysteine"
Homocysteine is a Toxic Amino Acid Associated With Significant Cardiovascular Risk
Lack of B12 Traps Another Important B Vitamin Called Folate in a Metabolically Useless Form
In order to understand how vitamin B12 becomes deficient, first we must understand how vitamin B12 originates in your diet. Lets take a look at dietary sources of B12...
Your Dietary Sources of Vitamin B12
In sharp contrast to most vitamins which are synthesized by plants, vitamin B12 or cobalamin is unique... it is synthesized naturally by bacteria growing in soil, water and intestinal tract of animals. For this reason, the vast majority of plants don't contain vitamin B12 in their tissues, any trace of cobalamin in plants are due to microbial contamination from soil or manure.
Your best dietary sources of vitamin B12 are foods of animal origin, such as meats. Vitamin B12 originating in protein sources, like meats, are derived from the animals ingestion of cobalamin-containing animal tissues, in addition to endogenously synthesized vitamin B12 by bacteria within the animals own digestive tract.
Avoid Vitamin B12 Deficiency...
Learn How Your Body Absorbs Vitamin B12
Vitamin B12 ingested in protein-based foods such as meats, must be freed or released from the protein to be absorbed. Gastric acid and enzymes secreted within the stomach, breaks down protein-bound vitamin B12, releasing it into the stomach.
Two distinct cobalamin-binding proteins compete for free vitamin B12 released within the stomach:
1) "Haptocorrin" originating from the saliva
2) "Intrinsic factor" (IF) secreted by the parietal cells of the stomach
Normally, within the highly acidic environment of the stomach, haptocorrin binds free vitamin B12 with much greater affinity than intrinsic factor. Therefore, as cobalamin leaves the stomach and enters the small intestine, it is bound to haptocorrin and accompanied by free intrinsic factor.
Within the alkaline (or basic) environment of the small intestine , pancreatic enzymes degrade the haptocorrin-vitamin B12 complex, releasing free vitamin B12 again. Intrinsic factor is resistant to enzymatic degradation and must now bind to the freed vitamin B12 before it can be recognized and absorbed at the intestinal receptor.
The IF-B12 complex is absorbed at the intestinal wall by highly specialized receptors. Calcium ions and pH greater than 5.5 are required to induce appropriate configuration of the receptor for binding the IF-B12 complex
Now that we understand the way your body digests and absorbs food-bound vitamin B12, lets take a look at the many ways vitamin B12 deficiency can develop...
How does Vitamin B12 Deficiency Develop?
1) Auto-immune Disease
Normally our immune system protects our bodies against foreign invaders, killing bacteria and viruses to keep us healthy. But an auto-immune inflammation is a immune response turned against yourself! Your own antibodies are unable to distinguish "self" from "non-self" and literally attack and destroy your own living tissue .
If, for example, antibodies destroy your vitally important acid-secreting cells lining the stomach through auto-immune inflammation, less stomach acid is secreted and vitamin B12 deficiency is often the result. Here is why...
Lack of Stomach Acid
Traps Vitamin B12 in Food
Stomach acid is necessary for breakdown and solubilization of nutrients within food before intestinal absorption can begin.
"Any Food Remaining in the Solid or Undissolved State Simply Cannot be Absorbed and Utilized by Your Body."
If stomach acid is not secreted due to auto-immune inflammation of parietal cells lining the stomach, breakdown and solubilization of food is prevented. As a result, vitamin B12 is trapped within its food-bound protein matrix, unable to freely bind to haptocorrin and be absorbed.
Secondly, if autoantibodies are formed against intrinsic factor, they will bind intrinsic factor, preventing formation of the IF-B12 complex. Remember, binding of vitamin B12 to intrinsic factor within the intestine is absolutely essential before absorption can occur. The IF-B12 complex induces proper configuration of the intestinal receptor for binding and absorption.
Direct injection of B12 into the body, bypassing the dysfunctional digestive system or administration of high dose oral supplementation are general treatment options to ameliorate this form of vitamin B12 deficiency.
2) Atrophic Gastritis
About 10 - 30% of us older than 60 experience "atrophic gastritis", an inflammation of the stomach, usually linked to infection by the bacterium Helicobactor pylori. Helicobactor pylori infection induces chronic inflammation within the acid secreting cells lining the stomach, which may progress to peptic ulcer disease or gastric cancer. This chronic inflammation eventually reduces your stomachs acid-generating capability. And you know what happens next, right?
Vitamin B12 within food is trapped because stomach acid is no longer available to dissolve and release vitamin B12 from protein. Supplemental doses of B12 circumvent absorption problems because supplemental B12 is not bound to protein as it is in foods and intrinsic factor is still available for binding
3) Pancreatic Insufficiency
Normally, haptocorrin binds free vitamin B12 in the stomach before passage to the small intestine. As the haptocorrin-vitamin B12 complex travels from the stomach into the small intestine, pancreatic enzymes break down haptocorrin-vitamin B12 and releases free vitamin B12 into the intestinal lumen.
The release of vitamin B12 from haptocorrin is necessary so that free B12 may bind to intrinsic factor. If pancreatic enzymes are not released, the haptocorrin-vitamin B12 complex cannot be degraded and vitamin B12 will not bind to intrinsic factor.
Intrinsic factor (IF), which is resistant to proteolytic breakdown by pancreatic enzymes, binds vitamin B12 and the B12-IF complex, in the presence of calcium ( also secreted by the pancreas) and pH greater than 5.5, induces proper configuration of the intestinal receptor for binding and absorption.
Any form of pancreatic insufficiency such as lack of pancreatic enzymes, calcium, etc. inhibits absorption at the intestinal wall. If these conditions persist, vitamin B12 deficiency will develop.
4) Excessive Alcohol Intake
Alchohol reduces vitamin B12 absorption and at the same time increase clearance of vitamin B12 in the urine.
5)Strict Vegetarians (Vegans)
Plants don't contain vitamin B12 in their tissues. A strict plant-based diet (vegan) will therefore eventually cause vitamin B12 deficiency. However your body is extremely efficient conserving vitamin B12 and unlike other water-soluble vitamins, vitamin B12 is actually stored in the liver. This helps explain why vegans may take as long as 20 years to develop vitamin B12 deficiency symptoms.
In sharp contrast, people with absorptive malfunctions like atrophic gastritis, autoimmune inflammation or pancreatic insufficiency may develop vitamin B12 deficiency symptoms within 2-3 years.
Vital Roles of B12 in Your Body...
Consequence of Vitamin B12 deficiency
The metabolic chemistry of vitamin B12 and another B vitamin called folate are highly interrelated... deficiencies of either vitamin are grave threats to your good health. Here is why...
First, both vitamin B12 and folate are "carbon shuttles", shuttling simple carbon compounds from one molecule to another.
Why is this so important?
Life is based on carbon... carbon forms the "backbone" of biological molecules like proteins, DNA, lipids (fat), and carbohydrates. And by shuttling simple carbon compounds like "methyl" (1 carbon atom and 3 attached hydrogens-CH3) from 1 molecule to another, vitamin B12 and folate support 2 major pathways of life...
Pathways of Life Supported by
Vitamin B12 and Folate Carbon Shuttle
1) DNA Synthesis
2) Synthesis and Metabolism of Proteins
The shuttle of simple carbon compounds within your body into DNA synthesis or protein metabolism is called the "cycle of single carbon metabolism" and is vital to your wellbeing.
Vitamin B12 is also participates in the regeneration of a form of folate called "folic acid." Folic acid is the required form of folate for re-entry into the cycle of single carbon metabolism and continuous flow of carbon. If vitamin B12 deficiency is present, folate is trapped in a metabolically useless form, unable to re-enter the cycle.
This inter-dependent relationship between vitamin B12 and folic acid explains how deficiency of either vitamin shuts down the flow of carbon into the single carbon cycle, ultimately inhibiting the synthesis of DNA. The disease, megaloblastic anemia is usually the first clinical outcome of vitamin B12 inhibited DNA synthesis. Here is why...
Vitamin B12 Deficiency and Disease...
Growth and maintenance of healthy new tissue depends upon the division and multiplication of new cells (cell division). Before cells divide into new ones, DNA must be copied... the process of DNA synthesis and replication. This means, if DNA synthesis is inhibited due to vitamin B12 deficiency or folate deficiency, the process of growth and cell division is shut down or slows dramatically.
This affects the rapidly dividing cells like those within the bone marrow first, producing large, immature, hemoglobin-poor red blood cells that are unable to efficiently transport oxygen to your tissues. The resulting anemia, known as megaloblastic anemia a major symptom of vitamin B12 deficiency, is characterized by fatigue, lack of energy, diarrhea, nausea, decreased appetite, weak muscles, headaches, tingling sensations and sore tongue
Resupplying your body with adequate levels of vitamin B12 and folic acid restores vitamin B12 benefits and normalizes metabolic flow of carbon into both DNA and protein single carbon cycles, reversing megaloblastic anemia.
Vitamin B12 Deficiency and Disease...
Vitamin B12 also appears to be involved in the manufacture of lipid (fat) for the mylin sheath, the fatty, insulative layer surrounding individual nerve fibers. The mylin sheath insulates and protects nerve fibers, allowing fibers to conduct nerve impulses at rapid rate within your body without interference's.
Demylination or loss of mylin due to vitamin B12 deficiency essentially "short circuits" these fibers. Neuropathy begins with the peripheral nerves and progresses to the brain and spinal cord.
Initial neurological symptoms of vitamin B12 deficiency include, tingling, numbness and feeling of muscle weakness. If symptoms are not corrected, demylination progresses to the deep white matter of the cerebral hemispheres inducing neurological symptoms such as irritability, memory disturbances, mild depression, apathy and even dementia and psychosis
Treating Megaloblastic Anemia and
Remember, Vitamin B12 participates in the regeneration of folic acid, the required form of folate necessary for re-entry into the flow of single carbon metabolism for DNA synthesis. Dietary deficiency of either vitamin B12 or folic acid interrupts the flow of carbon and inhibits the synthesis of DNA.
Megaloblastic anemia, one of the first clinical symptoms of inhibited DNA synthesis, can therefore be the result of folic acid or vitamin B12 deficiency. Before treating megaloblastic anemia, it is important to understand if the anemia is actually caused by a deficiency of B12 or folic acid. Here is why...
If the megaloblastic anemia is due to a simple dietary deficiency of folic acid, supplemental folic acid should resolve the condition.
But if the megaloblastic anemia is actually due to a vitamin B12 deficiency, treating it with supplemental folic acid will provide enough folic acid to resolve the anemia, but will do nothing for the degenerative neurological symptoms also directly associated with vitamin B12 deficiency. In fact, the neurological symptoms are generally irreversible and will only worsen with time if vitamin B12 is not supplied.
Therefore, megaloblastic anemia should not be treated with folic acid until it is determined whether the deficiency is actually due to folic acid or vitamin B12 deficiency.
Avoid Vitamin B12 deficiency
Daily requirements of vitamin B12 for normal individuals is very small ( approximately 1 microgram per day), because the vitamin is extensively recycled and conserved within your body. The recommended daily allowance (RDA) is set higher at 2.6 ug / day to insure adequate blood serum concentrations and sufficient body stores.
During pregnancy, the human placenta concentrates vitamin B12 and newborns may have 2X the concentration of their mothers. Although maternal stores should be adequate, the RDA is increased to 2.6 ug /day during pregnancy and 2.8 ug / day during lactation. Women planing to become pregnant should consider a high quality multiple.
A varied and healthy diet should meet vitamin B12 dietary requirements for most adults with normal requirements. Specialized cases need further concern. For example, due to increased risk of food-bound vitamin B12 malabsorption as we age, the Food and Nutrition Board recommends adults over the age of 50 meet their vitamin B12 requirements with fortified foods or a high quality multivitamin.
In fact, many respected nutritionists suggest adults over the age of 65 supplement with 100 to 400 ug /day vitamin B12 due to the increased prevalence of vitamin B12 deficiency within this demographic.
Methyl cobalamin and deoxyadenosylcobalamin are the forms of vitamin B12 metabolically active in your body, however cyanocobalamin is more stable and since it is easily converted to these other forms, it is the form most widely used in supplements.