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The critical role of vitamin B12.

ARTICLE in THE PHYSICIAN AND SPORTSMEDICINE DECEMBER 2008
Impact Factor: 1.49 DOI: 10.3810/psm.2008.12.9 Source: PubMed

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CLINICAL FOCUS: NUTRITION

The Critical Role of Vitamin B12

Ilia Volkov, MD

Abstract: Vitamin B12 affects the peripheral and central nervous systems, bone marrow, skin and mucous membranes, bones, and
vessels, as well as the normal development of children. Although there is undoubtedly an association between vitamin B12 and homocysteinemia, their relative influence on cardiovascular events is controversial.
Some large studies confirm that a supplementation with group B vitamins did not reduce the risk of major cardiovascular events
or all-cause mortality in patients with vascular disease. The outcomes of these and similar trials could have been different had the
researchers considered the following points: Using vitamin B12 or B-complex as secondary prevention of cardiovascular events for
patients with irreversible changes of blood vessels is probably in error. Rather, vitamin B12 or B-complex should be used as primary
prevention. Also, using high doses of vitamin B12 will probably be more effective than using low doses of group B vitamins.
The effect of vitamin B12 on the proliferation of malignant cells has been examined in vivo and in vitro in numerous studies. Their
results indicate that methylcobalamin inhibits the proliferation of malignant cells and propose the possibility of methylcobalamin as
a candidate of potentially useful agents for the treatment for some malignant tumors.
There are many articles indicating the increasing prevalence of low vitamin B12 level in different segments of general population.
In order to prevent serious health problems, vitamin B12 routine fortification should be seriously considered and discussed.
Keywords: vitamin B12; homocysteine; malignancy; vitamin B12 routine fortification; recurrent aphthous stomatitis
Ilia Volkov, MD 1
1

Department of Family Medicine,

Faculty of Health Sciences,
Ben-Gurion University of the
Negev, Beer-Sheva, Israel

Introduction
Vitamin B12 plays a functional role in a growing list of various organs and body systems. Vitamin B12
deficiency is a common problem. Early detection of vitamin B12 deficiency is essential in order to
prescribe opportune treatment, and there is evidence that such deficiency occurs more frequently than
expected. Vitamin B12 deficiency can occur in individuals with dietary patterns that exclude animal food
products and patients who are unable to absorb vitamin B12. Vitamin B12 deficiency has many causes, and
pernicious anemia has been described as a widespread cause of vitamin B12 deficiency. Current studies
on vitamin B12 deficiency, including more precise definitions and the description of new etiologies of
vitamin B12 deficiency, such as insufficient dietary intake,1 food-vitamin B12 malabsorption syndrome,27
and hereditary vitamin B12 metabolism diseases, such as Imerslund-Grasbeck syndrome,8 show that
hematological abnormalities are generally incomplete, as compared with historical descriptions.
Persons with B12 deficiency may be asymptomatic, but in patients presenting with myelopathy,
cognitive decline, neuropathy, psychiatric disturbances, or specific hematological signs and symptoms,
vitamin B12 deficiency should be suspected.
The author will demonstrate the critical roles of vitamin B12 by surveying and analyzing available
reports, as well as reporting personal clinical experience.

Vitamin B12 and Development

Correspondence:
Ilia Volkov, MD
Hogla Street 6,
Lehavim, 85338, Israel
Tel: 972-8-6431530
Fax: 972-8-6413135
E-mail: r0019@zahav.net.il
Conflict of Interest Statement:
Ilia Volkov, MD
discloses no conflicts of interest.

Many research studies emphasize the health complications of nutritional vitamin B12 deficiency and
a necessity of clinical, biochemical, and metabolic monitoring in infants born to mothers with a vitamin B12 deficiency. Dietary deficiencies of vitamin B12 during pregnancy and lactation may result in
health problems in exclusively breastfed infants. Physical examinations of these children often reveal
psychomotor retardation, apathy, muscular hypotonia, irritability, anorexia, abnormal movements, and
failure to thrive. Laboratory analyses show hematological abnormalities, such as a megaloblastic anemia,
low levels of vitamin B12, high levels of homocysteine and methylmalonic acid, and methylmalonic
aciduria. Magnetic resonance imaging (MRI) of the brain reveals diffuse frontotemporoparietal

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CLINICAL FOCUS: NUTRITION

Ilia Volkov

atrophy and retardation of myelination.9 Some studies have

shown a relationship between maternal vitamin B12 status and
birth weight. One extends those findings directly in terms
of neonatal vitamin B12 status and birth weight. VitaminB12
status in the mother was related to neonatal vitamin B12
status as measured by cord serum vitamin B12 concentration. In addition, low neonatal vitamin B12 concentrations
were adversely associated with low birth weights.10 Marginal
maternal vitamin B12 status increases the risk of an offspring
with spina bifida.11
Children have specific and increased nutritional requirements in comparison with adults. Rapid growth and enhanced
energy expenditure explain these differences. Any diet deviation will increase exposure to the risk of nutritional deficiency
along with corresponding health consequences. Whenever a
diet restriction for children is required for medical reasons,
particular attention must be paid to the food regimen in order
to avoid any health problems, especially growth retardation.12

Vitamin B12-Responsive
Neuropsychological Conditions
The only function that has been indicated as unique for
vitamin B12 is the synthesis of myelin, a component of the
sheaths that protect nerve fibers. Vitamin B12 deficiency can
cause peripheral neuropathy and combined system diseases
involving demyelination of the dorsal columns and the
corticospinal tract. A wide variety of neuropsychological
symptoms and signs have been encountered, such as ataxia,
loss of cutaneous sensation, muscle weakness, diminished or
hyperactive reflexes, spasticity, urinary or fecal incontinence,
orthostatic hypotension, loss of vision, dementia, psychoses,
and disturbances of mood. Multiple neurological syndromes
were often seen in a single patient. Severity of neurological
dysfunction before treatment is clearly related to the duration
of symptoms prior to diagnosis.13
Multiple sclerosis (MS) and vitamin B12 deficiency share
common inflammatory and neurodegenerative pathophysiological characteristics. Due to similarities in the clinical
presentations and MRI findings, the differential diagnosis
between vitamin B12 deficiency and MS may be difficult.
Additionally, low or decreased levels of vitamin B12 have been
demonstrated in MS patients. Moreover, recent studies suggest that vitamin B12, in addition to its known role as a cofactor in myelin formation, has important immunomodulatory
and neurotrophic effects. These observations raise questions

of possible causal relationship between the two disorders,

and suggest further studies of the need to closely monitor
vitaminB12 levels in MS patients, as well as possibly requiring
supplementation of vitamin B12 alone or in combination with
the immunotherapies.14 Interferon-beta is a mainstay therapy
of demyelinating diseases, but it has only a partial effect on MS
in humans and in several animal models of the disease. In a
recent report, the author demonstrated a dramatic improvement in the clinical, histological, and laboratory parameters
of disease in in vivo mouse models of demyelinating disease.
This was seen following combination therapy with interferon (IFN)-beta and vitaminB12 cyanocobalamin (B12CN)
in nonautoimmune primary demyelinating ND4 (DM20)
transgenic mice and in acute and chronic experimental autoimmune encephalomyelitis in mice. Clinical improvement,
manifested as near normal motor function, was associated
with reduced astrocytosis and demyelination. Interferonbeta-B12CN combination therapy may be promising for the
treatment of MS.15
The association of vitamin B12 deficiency with psychiatric
illness has been studied and debated since the vitamin was first
discovered in the 1940s. The clinical relevance of this deficiency
remains the subject of investigation and academic discussion.
Vitamin B12 has fundamental roles in brain function. Intracellular vitamin B12 is converted to adenosylcobalamin, coenzyme
for methylmalonyl-CoA mutase and to methylcobalamin,
coenzyme for methionine synthase, which mediates conversion of homocysteine to methionine. Consequently, there is an
increase in the level of homocysteine (Hcy) in B12 deficiency.
Homocysteine has been implicated as a risk factor for vascular
disease, as well as brain atrophy. There is evidence to implicate
Hcy in increased oxidative stress, DNA damage, and the
triggering of apoptosis and excitotoxicity, all of which are
important mechanisms in neurodegeneration. Homocysteine
is also prothrombotic and proatherogenic, causes damage to
the vessel wall, and is related to brain atrophy and possibly to
white matter hyperintensities in the brain. Epidemiological
evidence and longitudinal data support the finding that Hcy
is a risk factor for cognitive impairment and Alzheimers disease. 1618 This may be due to cerebrovascular as well as direct
neurotoxic mechanisms.
As well as cognitive impairment, the common psychiatric
symptoms of vitamin B12 deficiency are continuous depression,19
psychotic symptoms,20 mania, and obsessive compulsive
disorder. The neuropsychiatric severity of vitamin B12 deficiency

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Critical Role of Vitamin B12

and the therapeutic efficacy depends on the duration of signs

and symptoms. Therefore, the consideration of vitaminB12
deficiency and testing for serum B12 levels is recommended in
all patients with organic brain syndrome, atypical psychiatric
symptoms, and fluctuation of symptomatology.

Relationship of Vitamin B12

and Homocysteine: Is Their Function
in Cardiovascular Events Obvious?
Vitamin B12 deficiency and homocysteinemia are undoubtedly related,21,22 but their synergistic or separate role in the
development of atherosclerosis and influence on cardiovascular events is nevertheless controversial. In observational
studies, elevated plasma total homocysteine levels have been
positively associated with ischemic stroke risk.2325 Numerous retrospective and prospective studies have revealed a
consistent, independent relationship between mild hyperhomocysteinemia and cardiovascular disease or all-cause
mortality. Starting at a plasma homocysteine concentration
of approximately 10 mmol/L, the risk increase follows a
linear dose-response relationship with no specific threshold
level. Hyperhomocysteinemia, as an independent risk factor for cardiovascular disease, is thought to be responsible
for approximately 10% of the total risk. Elevated plasma
homocysteine levels ( 12 mmol/L; moderate hyperhomocysteinemia) are considered cytotoxic and are found in 5% to
10% of the general population and in up to 40% of patients
with vascular disease. Based on various calculation models,
reduction of elevated plasma homocysteine concentrations
may theoretically prevent up to 25% of cardiovascular events.
Treatment of hyperhomocysteinemia is recommended for the
apparently healthy general population.26 Some large studies
confirm that a supplementation with group B vitamins did
not reduce the risk of major cardiovascular events or all-cause
mortality in patients with vascular disease.27,28 The outcomes
of these and similar trials could have been different if the
researches had used vitamin B12 or B-complex for primary
prevention of cardiovascular events for patients with high
risk of developing atherosclerosis. Also, using high doses of
vitamin B12 will probably be more effective than using group
B vitamins as a rule presented by a set of various vitamins of
this group in low doses. For example, using folic acid alone
for prevention of cardiovascular diseases has been proven to
be ineffective,29 while very high doses of vitamin B12 (60 mg

every day for 6 months) has been used effectively without any
toxic side effects for the treatment of other diseases.30

What about Hematological Abnormalities?

Hemopoesis is the process in which new blood cells are
produced and in which vitamin B12, folate, and iron have fundamental roles. New erythrocytes replace the oldest erythrocytes
(normally about 1%) that are phagocytosed and destroyed
each day. Erythroblasts require folate and vitaminB12 for
proliferation during their differentiation. Deficiency of folate
or vitamin B12 inhibits purine and thymidylate syntheses,
impairs DNA synthesis, and causes erythroblast apoptosis,
resulting in megaloblastic anemia from ineffective erythropoiesis. The presence of macro-ovalocytes having a high
mean corpuscular value (MCV), anisocytosis, poikilocytosis
and hypersegmented neutrophils, anemia, leukopenia, and
thrombocytopenia or pancytopenia suggests a megaloblastic
disorder associated with a nutritional deficiency, ie, vitamin
B12. The usual presentation accompanies symptoms of anemia.
Asymptomatic patients can be identified by routine hematologic investigations. Vitamin B12 deficiency produces the
classic picture of macrocytic anemia, with a MCV 100 fL.
The MCV correlates with estimated vitamin B12 level: MCV of
80 to 100 fL indicates25% probability of vitamin B12 deficiency; MCV of 115 to 129fL indicates a 50% probability; MCV
130 indicates 100% probability.31 It is a classic textbook
picture of vitamin B12 deficiency, but usually the clinical picture
looks different. Hematological abnormalities, such as anemia
or macrocytosis, may be absent at the time of neurological
presentation.32 It is well known that vitamin B12 deficiency
may be accompanied by iron deficiency, and this association can mask the macrocytosis.33,34 There are no generally
accepted guidelines for the definition, diagnosis, treatment,
and follow-up of patients with vitaminB12 deficiency. Total
serum vitaminB12 may not reliably indicate vitamin B12 status.
Probability of functional vitamin B12 deficiency decreases
upon increasing the blood level of vitamin B12. To increase
specificity and sensitivity in diagnosing vitaminB12 deficiency,
the concept of measuring Hcy, methylmalonic acid (MMA) is
intended. Lately, for the solution of this problem, an evaluation
of holotranscobalaminII has aroused great interest.35
Vitamin B12 deficiency may also influence the granulocyte
and platelet lines and may be mistaken for leukemia.36 in all
cases, the important practical indicator is positive response to
vitamin B12 treatment.

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Ilia Volkov

Known Cutaneous and Mucous

Manifestations of Vitamin B12 Deficiency
and the Novel Use of Vitamin B12
in Dermatology
The characteristic dermatological sign of vitamin B12 deficiency
is cutaneous pigmentation,3740 which can be reversed by administration of vitamin B12. Increased cutaneous pigmentation is
especially accentuated in palmar creases, on the dorsa of hands
and feet, in intertriginous areas, on oral mucosa, and in recent
scars. The mechanism of hyperpigmentation is unexplained.
Histology shows an increase of melanin in the basal layer.
In an electron microscopic study, many melanosomes were
observed in melanocytes and surrounding keratinocytes. There
is supposition that the dominant mechanism of hyperpigmentation due to vitamin B12 deficiency is not a defect in melanin
transport, but is rather an increase in melanin synthesis.
The author investigated and reported a case of the
paradoxical disappearance of chronic erythema nodosum,41
which had persisted for more than 6 months in spite of a
prolonged treatment with nonsteroidal anti-inflammatory
drugs. When the patient complained of paresthesias, a blood
test for vitamin B12 was performed and a prominent vitaminB12
deficiency was discovered. Since treatment was initiated with
intramuscular vitamin B12 injections, not only did the paresthesias disappear, but the erythema nodosum did as well.
The patient continued to receive maintenance therapy with
vitaminB12 without recurrence of erythema nodosum.

Recurrent aphthous stomatitis (RAS) is one of the most

common oral mucosa lesions seen in primary care. Most
treatments given to patients suffering from RAS achieve shortterm therapeutic goals, such as alleviation of pain, reduction
of ulcer duration, and recovery of normal oral function. Just a
few reported treatments have achieved long-term therapeutic
goals, such as reduction of the frequency and severity of RAS
and maintenance of remission. Although the precise role of
vitaminB12 deficiency in the pathogenesis of RAS is unclear,
suppression of cell-mediated immunity and changes in the cells
of the tongue and buccal mucosa have been reported.42,43 We have
reported previously the successful treatment with vitamin B12 of
RAS patients (Figure 1).44,45 According to the authors 6 years of
clinical experience, vitamin B12 treatment achieves long-term
therapeutic goals and can be effective for patients suffering from
RAS, regardless of their serum vitamin B12 level. The author
and his colleagues have finished a randomized, double-placebo,
controlled clinical trial, and received results to confirm their
previous clinical observations.

Potential Role and Uses of Vitamin B12

in Previously Uncommon Areas
A possible correlation between vitamin B12 and fertility
problems, which indicates vitamin B12 deficiency as one of
cause of recurrent abortions and the use of vitamin B12 in
initial treatments in order to prevent these conditions, has
been debated for a long time.4648 In a statistical meta-analysis

Figure 1. Frequency of recurrent aphthous stomatitis (RAS) episodes prior to and during vitamin B12 treatment (episodes per month).

1.8
1.6

1.5

1.4
1.2
1

Prior to treatment

0.8

During treatment

0.6
0.4

0.13

0.2
0

Treatment status

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Critical Role of Vitamin B12

performed on 5 studies in which serum B12 was assayed in

women suffering from early recurrent abortions (ERA), a
significant relationship was found between ERA and vitamin
B12 deficiency.49 No difference was noticed between cases and
controls for folate. Vitamin B12 evaluation should be considered
in women with ERA regardless of whether or not hematological
or neurological abnormalities are present.
Osteoporosis is a widespread problem, which frequently has
devastating health consequences because of its association with
fragility fractures. The total number of fractures, and hence the
cost to society, will increase dramatically over the next 50 years
as a result of demographic changes in the number of elderly
people. Thus, prevention of osteoporosis by identifying risk
factors or risk indicators, as well as developing new treatment
strategies, is a major health issue. Recent data suggest that
vitamin B12 affects bone metabolism, bone quality, and fracture
risk in humans.50 Strokes increase the risk of subsequent hip
fracture by 2 to 4times. Hyperhomocysteinemia is a risk
factor for both ischemic stroke and osteoporotic fractures in
elderly men and women. In a population with a high baseline
fracture risk, combined treatment with folate and vitamin B12
has been shown to be safe and effective in reducing the risk
of a hip fracture in elderly patients following stroke.51 The
relationship of Hcy and vitamin B12 with bone turnover markers, broadband ultrasound attenuation (BUA), and fracture
incidence in healthy elderly people was studied by researchers
who found that high homocysteine and low vitamin B12 concentrations were significantly associated with low BUA, high
markers of bone turnover, and increased fracture risk.52 A
preventive vitamin B12 supplementation for healthy people
with mandatory risk factors for osteoporosis and a treatment
with vitamin B12 of patients suffering from osteoporosis could
be a promising treatment for this serious problem. Controlled
clinical trials should be conducted to confirm the safety and
effectiveness of vitamin B12 therapy for osteoporosis.
Vitamin B12 carrier proteins, the transcobalamins (TC), are
elevated during trauma, infections, and chronic inflammatory
conditions. This remains unexplained. It is proposed that
such TC elevations signal a need for vitamin B12 central to
the resolution of inflammation.53 Vitamin B12 is an effective
scavenger of nitric oxide (NO).54 Septic shock has an extremely
high mortality rate, with approximately 200000 people dying
from sepsis annually in the US. The high mortality results
partially from severe hypotension secondary to high serum
NO concentrations. Reducing NO levels should be beneficial

in sepsis; a possible approach in reducing NO levels in sepsis is

the use of an NO scavenger, which would leave sufficient free
NO for normal physiological functions. Animal and human
clinical data suggest that high-dose vitamin B12 may prove a
promising approach to systemic inflammatory response syndrome (SIRS), sepsis, and septic and traumatic shock.
Drugs which directly counteract NO, such as endothelial
receptor blockers, NO-synthase inhibitors, and NO-scavengers,
not only may be effective in the acute treatment of migraine,
but also are likely to be effective in migraine prophylaxis.
The first prospective, open study indicated that intranasal hydroxocobalamin may have a prophylactic effect in
migraine.55
A number of studies have demonstrated that vitamin B12
is important in maintaining differentiation, proliferation,
and metabolic status of cells. Nitric oxide can cause both
apoptosis and necrosis, making it a good candidate for antitumor therapy. Initially, vitamin B12 was proposed for use as a
scavenger and cytoprotective agent to bind and inactivate NO.
The use of vitamin B12 as a carrier to deliver NO into tumor
cells is novel. One investigational study showed that complex
NO-vitamin B12 inhibited tumor growth in vivo and in vitro
by activating the extrinsic apoptotic pathway.
Researchers have attempted to correlate vitamin B12 with
malignancy ever since the multifunctional role of vitaminB12
has begun to be understood. There are many hypotheses about
the role of vitamin B12 in growth of malignancy. What is the
explanation for elevation of vitamin B12 level in oncological
patients? Is it a marker of malignancy? Elevated levels of serum
vitamin B12 may be a sign of a serious, even life-threatening,
disease. Hematologic disorders, like chronic myelogeneous
leukemia, promyelocytic leukemia, polycythemia vera, and
hypereosinophilic syndrome can result in elevated levels
of vitamin B12. Not surprisingly, a rise of the vitamin B12
concentration in serum is one of the diagnostic criteria
for the latter two diseases. Several liver diseases, like acute
hepatitis, cirrhosis, hepatocellular carcinoma, and metastatic liver disease, can also be accompanied by an increase
in circulating vitamin B 12. This phenomenon is caused
predominantly by vitamin B12 release during hepatic cytolysis
and/or decreased vitamin B12 clearance by the affected liver.
Altogether, it can be concluded that an observed elevation of
vitamin B12 in blood merits a full diagnostic examination to
assess the presence of disease.56

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Ilia Volkov

Maybe an elevated level of vitamin B12 is a sign that the

body is fighting disease and that, as result of this battle, there
is a mobilization of resources and an attempt to compensate
by activating biologically active substances for repair of
defects.
Carmel etal (1977) studied 139 patients with
non-hematologic malignancy in order to define the incidence
of vitamin B12-related abnormalities and correlate them with
clinical findings. A high serum vitamin B12 level usually implied
a poor prognosis in a patient with cancer. However, while
most such patients had hepatic and other metastases, hepatic
involvement was not universal nor did most of the patients
with hepatic disease have high vitamin B12 levels.57
The relationship between vitamin B12 levels and survival
was studied in a group of 161 terminally ill cancer patients.
Their average age was 74.7 years. The length of survival
decreased with the increase in serum vitamin B12 levels. In
multivariate analyses, C-reactive protein (CRP) was the most
important prognostic factor in this population, and vitamin
B12 provided information independent of CRP in predicting
survival. These data indicate that an elevated serum vitamin
B12 level is a predictive factor for mortality in patients with
cancer, independent of CRP or other factors.58
The effect of vitamin B12 on the proliferation of malignant
cells has been examined in vivo and in vitro in numerous
studies.5961 Methylcobalamin inhibited the proliferation of
androgen-sensitive SC-3 cells (a cloned cell line from Shionogi
mouse mammary tumor, SC115) in culture at the concentration
of 100 to 300 g/mL. An inhibitory activity of methylcobalamin
on the proliferation was also observed in other cell lines
(estrogen-sensitive B-1F cells from mouse Leydig cell tumor and
MCF-7 cells from human mammary tumor) at the concentration
of 500 g/mL. Moreover, large doses of methylcobalamin
injected intraperitoneally (100 mg/kg body weight/day) were
nontoxic and suppressed the tumor growth of SC115 and B-1F
cells in mice fed a vitamin B12-deficient diet. These results
indicate that methylcobalamin inhibits the proliferation of
malignant cells in culture and in vivo and propose the possibility
of methylcobalamin as a candidate of potentially useful agents
for the treatment for some malignant tumors.59
Every system in mechanics and nature seeks some sort
of balance. The human body is no exception. Upon an
imbalance or disease, the organism tries to compensate by
the mobilization of its inner resources. There is an ongoing
process of accumulation of biologically active substances

to fight disease. Unfortunately, this battle for balance is not

always successful. Being stressed, the organism shows us signs
of distress and calls for help.
The author proposes that a high level of vitamin B12 in
oncological diseases is such a sign.62 The basis for such a
proposal can be summarized as follows:
1. The well-known fact that a high level of vitamin B12 is
present in different kinds of malignancy.
2. There is a positive correlation between level of vitaminB12
and the severity of the disease; the more severe the
disease, the higher the level of vitamin B12.
3. A number of the experimental laboratory studies indicate an inhibition in the growth of malignant cells upon
use of vitamin B12.
4. There are no experimental results indicating that
vitamin B12 stimulates growth of malignant cells.
5. There is no data about toxic effect of vitamin B12 in the
treatment of various diseases. Sometimes it is necessary
to use very high doses to achieve therapeutic effect.30
Vitamin B12 is the only known vitamin that does not
have any toxic effect.
The author has not yet been able to find another explanation
for high levels of vitamin B12 in oncology patients other than
that it is a compensatory mechanism.

Necessity of New Approach

to the Problem of Vitamin B12

We know that not only can individuals with special problems and vegetarians suffer from vitamin B12 deficiency, but
also patients with low meat intake. There are many articles
indicating the increasing prevalence of low vitamin B12 levels
in different segments of general population.6368 In the past
decade, it has become evident that vitamin B12 deficiency
occurs commonly in industrial countries at different levels of
economic and social status. A high prevalence of symptomatic
vitamin B12 deficiency was discovered in a pre-urban Bedouin
area in Southern Israel due to low intake of animal products.63
Dietary vitamin B12 deficiency is a severe problem in India,
Mexico, Central and South America,64 and selected areas
in Africa.65 For example, at least 40% of the population in
Central and South America has deficient or marginal plasma
vitamin B12 concentrations in almost all areas and in all age
groups.66 As a rule, it appears to be prevalent in 30% to 40%
of those in the lower socioeconomic levels. The authors
clinic serves middle to upper-middle class populations, and,

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Critical Role of Vitamin B12

according to data received in that clinics study,69 frequency

of deficient or marginal vitamin B12 level ( 250pg/mL)
was about 35%. The author cannot extrapolate the finding to
general population in this area, because the study population
is a selected sample, but a prevalence of low level of vitaminB12 in the overall population may be similar. Today
there is a tendency in modern society to change habits, for
example cessation of smoking, fighting with obesity, accentuating physical exercise, and adopting correct eating habits.
The author concludes that as a result of media information
disseminating the relationship between meat and cholesterol/
cardiovascular diseases, consumption of meatparticularly
beefhas decreased. The author hypothesizes that the decrease
of level of vitamin B12 in the population with higher educational
level is caused by a premeditated decrease in consumption of
animal products. Also, in modern society, there is a tendency
for ideological motives, particularly among the younger
generation, to be vegans. Changes in lifestyle among segments
of the population with high socioeconomic level on one hand,
and the existence of poverty on the other, are two main factors
in the decreasing consumption of animal products (particularly
red meat). This causes a decrease in the level of vitamin B12
in general population; as a consequence, this will increase
pathology due to vitamin B12 deficiency (such as neurological
and hematological disorders). As mentioned, vitamin B12 deficiency has various and serious health effects. In lieu of these
possible developments and in order to prevent serious health
problems, vitamin B12 routine fortification should be seriously
considered and discussed.

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