Oral B12 equivalent
to B12 injections
by T. Mitchell
For decades, people have been injecting themselves
with vitamin B12 because they thought oral supplements
were not adequately absorbed. New research indicates
that oral B12 supplements may be as good or better
Those who have low levels of vitamin B12 in the blood
have long resorted to injections of this essential
B vitamin, an uncomfortable delivery method at best.
New evidence suggests that oral B12 works as well
as injections, according to a study published in the
journal Blood -but high doses must be taken. This
verifies reports from Sweden dating from the 1970s
that pernicious anemia, a disease of B12 deficiency,
can be controlled with oral B12. Resolving the debate
over oral-versus-injections is very timely, given
that vitamin B12 is a homocysteine-lowering factor.
Homocysteine has emerged as a strong and independent
risk factor for heart disease and stroke, and is also
connected to chronic diseases such as arthritis, Alzheimer's
According to the recent data, 2,000 micrograms/day
of oral B12 cures the symptoms of B12 deficiency,
including elevated homocysteine, neurological problems,
and elevated methylmalonic acid (a marker of B12 deficiency).
The oral version works as well as injections, with
the added feature of maintaining high levels in the
blood over time. The study showed that after a month,
the blood levels of the vitamin in people receiving
injections dropped and stayed at a plateau, whereas
blood levels of those receiving oral B12 continued
B12 lowers homocysteine
Although oral B12 did not reduce homocysteine in
every case, when it did, the results were dramatic.
Some of the people in the study had homocysteine levels
as high as 175 micromoles per liter (the optimal safe
range for homocysteine is under 6). In the case of
one patient, 2,000 micrograms of oral B12 for four
months reduced their homocysteine from 113.4 micromoles
per liter to 8.2. Injected B12 also significantly
reduced homocysteine - the main difference being that
the injected version worked faster.
Interestingly, some of the patients did not respond
to supplemental vitamin B12. It was discovered that
they were also deficient in folate, and until folate
was replaced, their homocysteine remained elevated.
Vitamin B12 and folate work synergistically in
the chemical reactions that recycle homocysteine
back to methionine in the methylation cycle. It is
also interesting to note that participants in the
study with both B12 and folate deficiencies were depressed,
had anorexia, and addiction to alcohol. It is well-established
that folate or B12 deficiency causes psychiatric problems
ranging from loss of memory to insanity. This is probably
due to the vitamin's role in methylation - a biochemical
process crucial for the maintenance of brain chemistry
and nerves. B12 plays a role in the synthesis of serotonin,
dopamine and norepinephrine.
Intrinsic factor is secreted by the stomach to help
the body absorb B12. Older people produce less intrinsic
factor, and are thus more vulnerable to B12 deficiency.
In the study mentioned at the beginning of this article,
high-dose oral B12 was absorbed as well as injectable.
No supplemental intrinsic factor was given. Intrinsic
factor is usually associated with a chronic B12 deficiency
known as pernicious anemia. Patients with pernicious
anemia lack intrinsic factor usually because of insufficient
stomach acid. Others may have antibodies to the factor
- an inappropriate autoimmune response to one's own
proteins. Injected B12 has traditionally been used
for pernicious anemia because it bypasses the absorption
problem. However, doctors are beginning to realize
that pernicious anemia patients are not the only patients
they see with B12 deficiencies. Anyone with elevated
homocysteine, psychiatric disorders, eating disorders,
sleep disorders, or who is elderly is potentially
B12-deficient. These conditions are more likely caused
by diet-induced B12-deficiency than a lack of intrinsic
factor. All should respond to oral B12.
Different forms of vitamin B12
Cyanocobalamin is the usual form of B12 sold in this
country. Hydroxocobalamin and adenosylcobalamin are
two other forms. For the past 20 years English doctor
Anthony G. Freeman has been attempting to get the
cyano form of B12 removed from the market and replaced
with the hydroxocobalamin. He points out that the
cyano form is not effective for certain eye degenerations
caused by smoking and alcohol.
But another form, methylcobalamin, may be the best
of all. Research shows that this active form of B12
has the unique ability to provoke the regeneration
of nerves without adverse side effects. This is because
B12 facilitates methylation, the process that
creates and maintains nerves and brain chemicals.
Research shows that a lack of methylcobalamin causes
degeneration of the brain and spinal cord - a condition
known as subacute combined degeneration. In this disease,
nerves lose their insulation and begin to deteriorate.
This process, known as demyelination, occurs in other
neurological diseases such as multiple sclerosis and
chronic inflammatory demyelinating polyneuropathy.
High doses of methylcobalamin have been used to treat
degenerative neurological diseases in rodents and
humans. People with amyotrophic lateral sclerosis
(Lou Gehrig's disease) took 25 mg a day of methylcobalamin
for a month. In this disease, the neurons that control
muscle movements deteriorate. The double-blind, controlled
study showed that methylcobalamin improved muscle
response after a month of treatment.
Methylcobalamin has been given to mice with the mouse
version of muscular dystrophy. A remarkable reversal
of degenerating nerves occurred. Methylcobalamin did
not stop the disease, but it slowed it down.
It has been documented that the level of B12 decreases
every year with age. Age-related deficiency is associated
with hearing loss, memory impairment and psychiatric
disorders, along with heart disease and stroke. Alzheimer's
disease (AD) patients have less B12 in their spinal
fluid than people without the disease. They also have
less SAMe - the substance required to methylate cobalamin
(B12) to methylcobalamin, the active form. The failure
of B12 supplementation to improve AD patients in some
studies may be due to their inability to activate
B12 in the brain. Methylcobalamin is already methylated:
it doesn't require SAMe.
Another feature of aging is the increase of free
radicals. Free radicals are elevated in Parkinson's
disease (PD) and AD. In PD, a substance known as MAO-B
is also elevated. MAO-B creates free radicals, and
the MAO-B inhibitor, selegiline, is often given to
PD patients. MAO-B is linked to memory impairment.
In 1992 Italian researchers reported that elevated
MAO-B, dementia and B12 deficiency all go together.
B12 deficiency diseases
Diet, age and drugs are the prime culprits behind
B12 deficiency. Meat is the primary source of vitamin
B12. Strict vegetarians - people who eat no animal
products whatsoever are at risk for B12 deficiency.
(Vegetarians who eat eggs and fish will get B12 in
their diet. In addition, some seaweeds contain the
vitamin, and the gut may manufacture a certain amount.)
However, a meat diet doesn't guarantee that a person
won't be B12 deficient. Some elderly people, for example,
can eat high quantities of meat but still be B12 deficient
because they don't have enough hydrochloric acid in
their stomach to maintain intrinsic factor. Meat-eaters
taking certain drugs are also at risk for B12 deficiency.
Cimetidine (Tagamet), omeprazole (Prilosec), and other
drugs that inhibit gastric secretion can cause B12
deficiency. Anyone who chronically takes drugs for
stomach ulcers, "heartburn" or gastroesophageal
reflux may be creating B12 deficiency in themselves.
There appears to be something else causing B12 deficiency
in older people that researchers don't yet understand.
In a Dutch study, researchers found that about 25%
of the participants had low B12. But gut problems
only accounted for 28% of those cases. The cause in
the remaining 72% is a mystery. Researchers do know
that more people may be deficient than currently appreciated.
When researchers at the Veterans Administration Hospital
in Oklahoma used modified criteria for B12 deficiency
(elevations in homocysteine and methylmalonic acid,
plus serum B12 up to 300 pg/mL-the norm is usually
200), they uncovered twice as many people with B12
deficiency than would have been detected by serum
Elevated homocysteine is found in many chronic diseases
including arthritis and diabetes. Researchers in Japan
have discovered that noninsulin-dependent diabetes
patients with blood vessel problems have elevated
homocysteine. When treated with 1000 micrograms of
vitamin B12 (methylcobalamin) daily for three weeks,
homocysteine levels dropped significantly. Although
the study didn't follow the patients long enough to
see the effects of long-term treatment, the condition
of the patients' blood vessels
will likely improve as the levels of homocysteine
are reduced, as homocysteine is extremely toxic to
B12 and sleep
Those who can't get to sleep at night may need vitamin
B12. Studies show that B12 causes an earlier release
of melatonin at night which resets the sleep-wake
cycle. (Melatonin has been called "the sleep
hormone" because of its effects on sleep). B12
acts directly on the pineal gland to provoke a faster
release of melatonin. At the tail end, B12 causes
melatonin to drop off faster. B12 helps you get to
sleep earlier, and may help you wake up earlier if
you leave a curtain open to the morning sun. B12 sensitizes
you to morning light, which helps you wake up. Very
serious sleep-wake disorders have been successfully
treated with vitamin B12 in the methylcobalamin form,
although it may not work for everyone. Unfortunately,
the vitamin doesn't help people who want to cut down
on their sleep time altogether.
During the 1950s, B12 was frequently given to heart
patients. The vitamin fell out of vogue as drugs took
over the therapeutic picture. New findings on the
connection between homocysteine and vascular disease,
plus the failure of drugs to have an impact on the
number of heart attacks and strokes, have shifted
the focus back to B12 and other homocysteine-lowering
vitamins. The notion that B12 must be injected to
be effective has been disproven in recent studies.
Swedish experience shows that oral B12 is effective
for the treatment of pernicious anemia.
B12 has many benefits, including the reduction of
homocysteine, restoration of normal sleep patterns,
and mood effects. B12 deficiency is a fairly common
deficiency in elderly people who frequently have disrupted
digestion. It can cause symptoms that look
exactly like Alzheimer's disease, and it's crucial
for the retention of folate in cells.
Testing for B12 deficiency
There are several tests geared towards diagnosing
B12 deficiency. Homocysteine is an indirect test.
A more direct method is to measure methylmalonic acid
which becomes elevated in B12 deficiency. There are
other tests which measure gut secretions or antibodies
to gut secretions. The Schilling test can help ferret
out what is causing the deficiency, and a simple blood
test can show blood levels.
The dose of oral B12 supplements for sleep disorders
is 3000 mcg a day, while 2000 mcg a day has proven
useful in lowering homocysteine and correcting B12
deficiency. In published studies, it took four weeks
for the sleep effect, and four months for the homocysteine-lowering
effect-so be patient. People with degenerative diseases,
including Alzheimer's, should take very high doses
in the range of 3-4000 mg, supplemented with SAMe.
There is also the option of taking methylcobalamin,
which is the neurologically active form of B12. The
potential age-reversing benefits are well-worth the
modest price. Methylcobalamin is a form of B12 that
is sold as a drug in Japan. It is the methylcobalamin
form of B12 that has been used in most European and
Japanese studies showing efficacy against neurological
disease. The liver converts about 1% of ingested cyanocobalamin
into methylcobalamin, but it is far more efficient
to dissolve a good tasting methylcobalamin lozenge
in the mouth for immediately assimilation into the
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Neuropathy.org & Diabetic-Neuropathy.org