Vitamin B-12 is a water-soluble crystalline compound that contains
phosphorus, nitrogen, and cobalt. The latter gives it a rich red color.
It is heat stable in neutral solutions, but it is destroyed by heat in
both acid and alkaline mediums. It is also sensitive to light and is
destroyed by heavy metals and strong oxidizing and reducing agents.
Vitamin B-12 is the most complex compound of the vitamins. Its chemical
symbol is C63H90CON14O14P. It contains one cobalt atom that is similar
in structure to the position of iron in hemoglobin. B12 is the only
naturally occurring organic compound that contains cobalt. The
commercially available form of Vitamin B-12 is Cyanocobalamin.
It helps activate amino acids during protein formation and in the
anaerobic degradation of the amino acid lysine. The coenzyme of
cobalamin is a carrier of methyl groups and hydrogen, and is necessary
for carbohydrate, protein, and fat metabolism.
Cobalamin also provides important protection of the heart by way of its
methyl transfer role. It is active in the synthesis of the amino acid
methionine from its precursor, homocysteine. The synthesis occurs by
first removing a methyl group from methyl folate, a derivative of the
biologically active form of folic acid. This methyl group is then
transferred to homocysteine and methionine is formed. It has been
recently acknowledged that excess homocysteine in the blood is the
cause of heart disease, blood clots, stroke and gangrene. Therefore,
the understanding of this complementary action between B-12 and folic
acid is a significant addition to our arsenal of weapons for the fight
against heart disease. It is important to note that adequate amounts of
both vitamin B12 and folic acid are necessary for methionine synthesis
to take place. You can say keeping homocysteine levels low is a matter
of life and death.
Methionine is essential for choline synthesis; therefore, vitamin B12
plays a secondary role in this lipid pathway. A choline deficiency that
causes fatty liver can be prevented by cobalamin or the other methyl
donors (betaine, methionine, folic acid).
It has been observed that fatty acid synthesis is impaired when this B
vitamin is deficient. A lack of sufficient essential fatty acids
results in impairment of brain and nerve tissue. The myelin sheath (the
insulation around nerve cells) is malformed in a cobalamin deficiency
and contributes to faulty nerve transmission. A prolonged B12
deficiency will ultimately lead to neurological disturbances.
DNA replication is dependent on the function of coenzyme cobalamin as a
methyl group carrier. It is this role that explains why a deficiency of
B-12 leads to megaloblastic anemia. This disorder is characterized by
large immature blood cells and changes in bone marrow. Inadequate DNA
translation leading to improper cell replication results in the large
blood cells observed in this disorder. These large misshapen red blood
cells are unable to transport oxygen. This results in anemia,
leukopenia, thrombopenia and fewer, but larger and less mature, blood
cells. Poor cell division in the gastrointestinal tract and epithelial
tissues produces glossitis and megaloblastosis. Furthermore, general
growth and repair are likewise impaired.
The characteristic symptom of a severe deficiency of this B vitamin is
pernicious or megaloblastic anemia. This condition is most often caused
by either inadequate consumption of B-12 or by a reduced gastric
secretion of a mucoprotein called intrinsic factor. This intrinsic
factor is necessary for proper vitamin B12 absorption through the
intestinal tract. It is produced by the parietal cells of the stomach
and binds onto the vitamin to transport it into the small intestine. In
the presence of calcium, this transport mechanism attaches to the
intestinal wall, facilitating absorption of the vitamin.
Pernicious anemia can also result from several other conditions, including:
Gastrectomy (surgical removal of the stomach)
Surgical removal of the lower ileum (were B vitamins are absorbed)
Developing antibodies to intrinsic factor
Hereditary malabsorption
Strict vegetarianism (absence of animal products in diet)
Homocystinuria (characterized by large amounts of homocysteine in the urine)
We now know that a deficiency of B vitamins (B6, Folic Acid & B-12)
is the trigger for heart disease. This occurs when homocysteine levels
rise unchecked by sufficient blood levels of these three B vitamins.
There is good news in this message. Now, we know how to prevent heart
disease and have a longer healthier life.
Too much homocysteine in the blood damages arteries and blood vessels
causing the formation of arterial plaques. This results in
arteriosclerosis and heart disease.
Other deficiency symptoms include glossitis, degeneration of the spinal
cord, loss of appetite, gastrointestinal disturbances, fatigue, pallor,
dizziness, hypotension, disorientation, numbness, tingling, ataxia,
moodiness, confusion, agitation, dimmed vision, delusions,
hallucinations, and eventually, "megaloblastic madness" (psychosis).
A long-term marginal b-12 deficiency has been associated with increased
risk of Alzheimer's disease. It has been found that over 70% of older
persons having a B-12 deficiency also have Alzheimer's. Alzheimer's
patients also exhibit lower blood levels of this B vitamin than
patients who suffer from other brain or memory disorders. B-12 status
correlates with the severity of cognitive impairment in Alzheimer's
patients. It is presently unknown whether the deficiency is a cause or
result of the disease. However, cobalamin functions in numerous
metabolic processes that affect nerve tissue. These processes include
the synthesis of neurotransmitters and phospholipids which may explain
B-12's possible link with the development and progression of
Alzheimer's disease.
Symptoms of Vitamin B-12 deficiency are most commonly found in people
over the age of 40 with increasing occurrences as age increased and is
often a result of the reduced secretion of intrinsic factor. This
condition is corrected with B-12 injections. Patients suffering form
dementia often exhibit a deficiency of this B vitamin and
supplementation improves mental functioning in some of these cases.
Vitamin B-12 absorption can be inhibited by many gastrointestinal
disorders including, gluten-induced enteropathy, tropical sprue,
regional ileitis, malignancies, and granulomatous lesions in the small
intestine, tapeworm, bacteria associated with blind loop syndrome, and
other disorders that impair the proper intestinal function. The need
for B12 intake is increased by hyperthyroidism, parasitism and
pregnancy.
The only source of vitamin B-12 in nature is microbial synthesis.
Cobalamin is not found in plants, but is produced by bacteria in the
digestive tract of animals or by microbial fermentation of foods.
Sources containing more than 10mcg/100 grams are organ meats (liver,
kidney, heart), clams, and oysters. Good sources (3 to 10mcg/100 grams)
are nonfat dry milk, crab, salmon, sardines, and egg yolk. Moderate
amounts (1 to 3 mcg/100 grams) are meat, lobster, scallops, flounder,
swordfish, tuna and fermented cheese. Other sources are fermented
soybean products, poultry, and liquid milk products.
Because cobalamin is affected by temperatures above 100 degrees
Celsius, some or all of this B vitamin is lost when meat is cooked.
The minimum daily requirement for B12 can be exceeded by ten thousand
fold with no signs of toxicity. Excesses are excreted in the urine.
Many of the tests available to assess cobalamin deficiency have
limitations and can give false results. For example, the MCV test
(macrocytosis test) is not a sensitive test. Several conditions such as
folacin deficiency, vitamin C supplementation, and antibiotics can
result in high or low levels of B-12 being indicated in the essay. The
Schilling test can give both false abnormal and false normal readings.
Vitamin B-12 deficiency detection requires multiple testing methods and
the patient's symptoms being used in combination to diagnose.
References:
Garrison Jr., R.PH., Robert & Somer, M.A., R.D., Elizabeth, The
Nutrition Desk Reference, 3rd ed., New Canaan: Keats Publishing, 1999,
pp 124-128, 431, 434
McCully, M.D., Kilmer S. & McCully, Martha, The Heart Revolution, New York: Harper Perennial, 1999, pp 1-10
Article Source:
ArticleDepot.net
