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The first step when you receive a diagnosis of multiple
sclerosis is to determine if you really have MS. A vitamin B-12 deficiency has
very similar symptoms and is frequently misdiagnosed as MS. The type of
anemia resulting from B-12 deficiency is called pernicious anemia.
|Hosp Pract (Off Ed) 1995 Jul 15;30(7):47-52; discussion 52,
Vitamin B12 deficiency: underdiagnosed, overtreated?
Schilling RF, Williams WJ
University of Wisconsin Medical School, Madison, USA.
Neurologic damage may become permanent when the disorder is mistaken for
multiple sclerosis or diabetic neuropathy--hence the need for prompt
parenteral B12 in patients with pernicious anemia. The need for B12
injections is questionable for patients with achlorhydria and for those with
a marginal or low serum B12 level but no signs or symptoms of deficiency.
PMID: 7601897, UI: 95325377
- There seems to be more than misdiagnosis when it comes to B-12.
Studies show that B-12 deficiency is very central to MS. As this study
states, "There is a significant association between MS and disturbed
vitamin B12 metabolism."
|Arch Neurol 1992 Jun;49(6):649-52
Vitamin B12 metabolism in multiple sclerosis.
Reynolds EH, Bottiglieri T, Laundy M, Crellin RF, Kirker SG
Department of Neurology, King's College Hospital, London, England.
We have previously described 10 patients with multiple sclerosis (MS) and
unusual vitamin B12 deficiency. We have therefore studied vitamin B12
metabolism in 29 consecutive cases of MS, 17 neurological controls, and 31
normal subjects. Patients with MS had significantly lower serum vitamin
B12 levels and significantly higher unsaturated R-binder capacities than
neurological and normal controls, and they were significantly macrocytic
compared with normal controls. Nine patients with MS had serum vitamin B12
levels less than 147 pmol/L and, in the absence of anemia, this subgroup was
significantly macrocytic and had significantly lower red blood cell folate
levels than neurological and normal controls. Nine patients with MS had
raised plasma unsaturated R-binder capacities, including three patients with
very high values. There is a significant association between MS and
disturbed vitamin B12 metabolism. Vitamin B12 deficiency should always
be looked for in patients with MS. The cause of the vitamin B12 disorder and
the nature of the overlap with MS deserve further investigation. Coexisting
vitamin B12 deficiency might aggravate MS or impair recovery from MS.
PMID: 1596201, UI: 92281466
Multiple sclerosis involves a deficiency in the production of the myelin
sheath that protects the nerves. The following study states "vitamin
B12 is required for the formation of myelin." This is pretty strong
evidence that MS is a disease caused by nutrient deficiencies including vitamin
|Int J Neurosci 1993 Jul-Aug;71(1-4):93-9
- Vitamin B12 and its relationship to age of onset of
Sandyk R, Awerbuch GI
NeuroCommunication Research Laboratories, Danbury, CT 06811.
Attention has been focused recently on the association between vitamin
B12 metabolism and the pathogenesis of multiple sclerosis (MS). Several
recent reports have documented vitamin B12 deficiency in patients with MS. The
etiology of this deficiency in MS is unknown. The majority of these patients
do not have pernicious anemia and serum levels of the vitamin are unrelated
to the course or chronicity of the disease. Moreover, vitamin B12 does not
reverse the associated macrocytic anemia nor are the neurological deficits
of MS improved following supplementation with vitamin B12. It has been
suggested that vitamin B12 deficiency may render the patient more vulnerable
to the putative viral and/or immunologic mechanisms widely suspected in MS.
In the present communication, we report that serum vitamin B12 levels in MS
patients are related to the age of onset of the disease. Specifically, we
found in 45 MS patients that vitamin B12 levels were significantly lower in
those who experienced the onset of first neurological symptoms prior to age
18 years (N = 10) compared to patients in whom the disease first manifested
after age 18 (N = 35). In contrast, serum folate levels were unrelated to
age of onset of the disease. As vitamin B12 levels were statistically
unrelated to chronicity of illness, these findings suggest a specific
association between the timing of onset of first neurological symptoms of MS
and vitamin B12 metabolism. In addition, since vitamin B12 is required
for the formation of myelin and for immune mechanisms, we propose that its
deficiency in MS is of critical pathogenetic significance.
PMID: 8407160, UI: 94011702
- The following three studies show that copper is low in multiple
|J Neurol Neurosurg Psychiatry 1982 Aug;45(8):691-8
Zinc and copper in multiple sclerosis.
Palm R, Hallmans G
The serum concentrations of zinc and copper were measured in 50 patients
with multiple sclerosis. Lower serum zinc levels were found compared to age-
and sex-matched controls. In younger patients low serum copper
concentrations were noted. Zinc concentrations in CSF were unchanged.
The possibility that malabsorption of the metals causes the low serum
concentrations is discussed.
PMID: 7130993, UI: 83032559
|Am J Clin Nutr 1989 Jul;50(1):136-40
Trace element status in multiple sclerosis.
Smith DK, Feldman EB, Feldman DS
Department of Medicine, Medical College of Georgia, Augusta 30912.
We compared trace element status in multiple sclerosis (MS) patients (n =
27) with and without treatment with corticosteroids and groups of healthy
subjects. Concentrations of plasma ceruloplasmin, selenium, and zinc and
erythrocyte (RBC) glutathione peroxidase, Se, and Zn were similar in all
groups. RBC copper concentrations were significantly lower in MS patients
than in control subjects (mean +/- SEM: 0.048 +/- 0.005 vs 0.060 +/-
0.002 mumol/g Hb) because of decreased RBC Cu with steroid therapy. RBC
Zn-Cu ratios were significantly higher (14.9 +/- 1.0 vs 10.1 +/- 0.3) in MS
patients than in control subjects, differing in both groups of MS patients.
In MS and control subjects, RBC Cu correlated significantly with RBC Zn (r =
0.56, 0.49). Disease acuity and disability had no effect on trace-mineral
status. These data suggest that in MS there is altered Cu and Zn homeostasis
that may cause or result from the disease and is influenced by
corticosteroid therapy. Systemic trace element alterations might provide
clinically useful markers of MS.
PMID: 2750686, UI: 89320353
|Acta Neurol Scand 1989 May;79(5):373-8
Zinc, copper and magnesium concentration in serum and CSF
of patients with neurological disorders.
Kapaki E, Segditsa J, Papageorgiou C
Department of Neurology, Aeginition University Hospital, Athens, Greece.
Zinc (Zn), copper (Cu) and magnesium (Mg) concentrations in cerebrospinal
fluid (CSF) and serum were determined with atomic absorption
spectrophotometry in 74 patients suffering from various neurological
diseases, and in 28 healthy controls. Increased CSF zinc levels were found
in the group of peripheral nervous system diseases (P less than 0.01) and in
the cases of different neurological syndromes with increased CSF protein
concentration (P less than 0.001). Increased CSF and serum copper levels
were found in the cases with increased CSF protein levels (P less than
0.05). It is probable that the damaged blood-brain-barrier (BBB) permits the
passage of the trace elements Zn, Cu and of Mg into the subarachnoid space.
Decreased serum Cu levels (P less than 0.01) were found in the group of
multiple sclerosis (MS). The findings are correlated to those of previous
PMID: 2545071, UI: 89300228
What causes the vitamin B-12 and copper deficiencies seen in multiple
sclerosis? Following is a study showing a cluster of MS in Ohio in
1982-1985. The conclusion of the study was that these cases were
related to the excess concentration of cadmium and chromium in sewage and
river water. We have seen that cadmium is a direct antagonist to
copper and this may be the mechanism by which copper is depleted in
MS. What remains to be determined is whether the vitamin B-12
deficiency is also a result of cadmium toxicity or an unrelated factor.
If cadmium toxicity and vitamin B-12 deficiency are causative factors in
MS, then a vegetarian diet (low in B-12) with a high intake of green leafy
vegetables and carrots (high in cadmium) might promote the development of MS.
|Am J Forensic Med Pathol 1989 Sep;10(3):213-5
Clustering of multiple sclerosis in Galion, Ohio,
School of Public Health, Boston University School of Medicine,
Epidemiologic evidence indicates that the outbreak of 30-40 cases of
multiple sclerosis and other demyelinating syndromes in Galion, Ohio, USA,
during 1982-1985 was related to an excess concentration of heavy-metal
wastes, especially of cadmium and chromium in sewage and river water. Both
multiple sclerosis and myasthenia gravis were diagnosed by board-certified
PMID: 2782299, UI: 89390412
Geotoxicology of multiple sclerosis: the Henribourg,
Saskatchewan, cluster focus. II. The soil.
Irvine DG, Schiefer HB, Hader WJ
Toxicology Research Centre, University of Saskatchewan, Saskatoon, Canada.
The childhood-related, geographically-linked factor which predisposes
towards (or protects against) multiple sclerosis (MS) could be one or more
chemicals in the environment. Chemical study of the environment or
"focus" of an MS cluster may maximize the chances of detecting
such an etiological link. The soil chemistry of an MS focus (Henribourg,
Saskatchewan) was compared with North American norms, and with the chemistry
of soil from a nearby control area with a near-zero incidence of MS and of
childhood homes of MS cases. A combination of our present results with those
reported in the literature suggests that an environment predisposing to MS
may have a number of the following chemical characteristics: Calcareous;
with soils (but not necessarily waters) generally low in copper, iron and
vanadium; with excess lead, nickel and zinc in the upper soil layer; with
waters relatively high in chloride, chromium, molybdenum, nitrate plus
nitrite, and zinc; but low in selenium and sulfate. One possible causal
pathway to explain the apparent link between the excess rate of MS and some
of the curious geochemical findings at Henribourg is presented. Many other
possible explanations could equally well be advanced, and methods for
testing such alternative hypotheses are proposed.
PMID: 3241961, UI: 89203241
|Clin Chem 1978 Nov;24(11):1996-2000
Trace elements in scalp-hair of persons with multiple
sclerosis and of normal individuals.
Ryan DE, Holzbecher J, Stuart DC
Scalp-hair samples from 40 multiple sclerosis patients and 42 controls were
analyzed by neutron activation analysis, with a SLOWPOKE reactor as the
neutron source. Ag, Al, As, Au, Ba, Br, Ca, Cl, Cu, l, K, Mg, Mn, Na, S, Sb,
Se, Sr, V, and Zn were determined in samples of about 0.1 g. Highly
significant differences (99% confidence) were observed between the two
groups in concentrations of Cu, l, Mn, S, Se, and V.
PMID: 709834, UI: 79044087
- The following study suggests that a selenium deficiency may be involved
|Acta Neurol Scand 1976 Sep;54(3):287-90
Selenium, vitamin E and copper in multiple sclerosis.
Wikstrom J, Westermarck T, Palo J
There has been accumulation of the nutritional muscular dystrophy of the
cattle in a certain western district of Finland where the prevalence of
multiple sclerosis (MS) is also highest. This animal disease is due to lack
of selenium (Se) and vitamin E. The Se content of whole blood was low (52.6
+/- 11.3 ng/ml) in MS patients from this high-risk area compared to the
controls (68.8 +/- 11.0). The data for serum failed to confirm this
tendency. All Se values appeared to be lower than international values
suggested. The values for both vitamin E and copper were within the
international normal range.
PMID: 961380, UI: 76274379
Following is a study showing that rubidium is low in the urine of MS
patients. The significance of this information is unclear.
excretion of lithium, sodium, potassium, rubidium, magnesium and
strontium in the urine of a multiple sclerosis patient.
- Schulten HR; Palavinskas R; Kriesten K
- Biomed Mass Spectrom, 10(3):192-6 1983 Mar
Field desorption mass spectrometry and stable isotope dilution have been used
for direct trace analysis of metals in urine. Samples were collected over 24 h
at 2 h intervals from a hospitalized multiple sclerosis patient. Quantitative
determinations of Li+, Rb+, Mg2+ and Sr2+ from individual samples have been made
and correlated with the amounts of urine excreted as well as with the time of
day. The concentrations of Na+ and K+ were determined by flame photometry. The
quantities of metals excreted in urine during the course of 24 h were 0.0129 mg
for lithium, 4700 mg for sodium, 2100 mg for potassium, 1.4 mg for rubidium,
78.8 mg for magnesium and 0.2356 mg for strontium. The maximal absolute
quantities excreted of all metals determined correspond with the largest volume
of urine. The highest amounts of potassium, rubidium and strontium
were found in urine during the daytime (8.00-20.00), whilst magnesium was
excreted increasingly during the night hours (20.00-8.00). The excretion of
lithium and sodium is fairly even over the entire 24 h period. It is noteworthy
that similarities in the excretion profile and the concentration course are
observed between Li+ and Na+ on one hand and between K+ and Rb+ on the other. Moreover,
the lower concentration of Rb+ ions in urine of multiple sclerosis patients, in
comparison to healthy individuals and clinical controls as reported previously,
|Med Hypotheses 1984 Jun;14(2):111-4
The increased prevalence of multiple sclerosis among
people who were born and bred in areas where goitre is endemic.
The adverse effects of feeding vitamin A deficient diets to newborn infants
are found to include an increased propensity for them to fall victim to
multiple sclerosis (MS) later in life. When they are artificially fed on
cow's milk, this deficiency is accentuated by a number of factors such as
the need to dilute the milk in view of its high protein content, births
occurring during the winter when the vitamin A content of the milk reaches
its lowest value, insufficient selenium (Se) in the cow's forage which is
otherwise required to safeguard the vitamin against peroxidation, and
finally a lack of iodine in the soil which deprives the cattle of the
thyroid hormone thyroxin necessary to effect the conversion of the carotene
in their diet to vitamin A. Whichever of these factors preponderates,
newborn infants who are fed on cow's milk for the normal period of
approximately six months are at risk of suffering from MS.
|Med Hypotheses 2000 Sep;55(3):239-241
The possible role of gradual accumulation of copper, cadmium, lead and
iron and gradual depletion of zinc, magnesium, selenium, vitamins B2, B6, D,
and E and essential fatty acids in multiple sclerosis.
Moses Lake, Washington, USA
[Record supplied by publisher]
Multiple sclerosis (MS) has a much higher incidence among caucasians that in
any other race. Furthermore: females are much more susceptible than males
and white females living in colder, wetter areas are much more susceptible
than those living in warmer areas. On the other hand, menstruating women
have increased copper (Cu) absorption and half-life, so they tend to
accumulate more Cu than males. Moreover, rapidly growing girls have an
increased demand for zinc (Zn), but their rapidly decreasing production of
melatonin results in impaired Zn absorption, which is exacerbated by the
high Cu levels. The low Zn levels result in deficient CuZnSuperoxide
dismutase (CuZnSOD), which in turn leads to increased levels of superoxide.
Menstruating females also often present with low magnesium (Mg) and vitamin
B6 levels. Vitamin B6 moderates intracellular nitric oxide (NO) production
and extracellular Mg is required for NO release from the cell, so that a
deficiency of these nutrients results in increased NO production in the cell
and reduced release from the cell. The trapped NO combines with superoxide
to form peroxinitrite, an extremely powerful free radical that leads to the
myelin damage of MS. Iron (Fe), molybdenum (Mo) and cadmium (Cd)
accumulation also increase superoxide production. Which explains MS in
males, who tend to accumulate Fe much faster and Cu much less rapidly than
females. Since vitamin D is paramount for Mg absorption, the much reduced
exposure to sunlight in the higher latitudes may account for the higher
incidence in these areas. Moreover, vitamin B2 is a cofactor for xanthine
oxidase, and its deficiency exacerbates the low levels of uric acid caused
by high Cu levels, resulting in myelin degeneration. Finally Selenium (Se)
and vitamin E prevent lipid peroxidation and EPA and DHA upregulate CuZnSOD.
Therefore, supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg
Zn and 400 IU vit D and E, 100 mug Se, 180 mg EPA and 120 mg DHA per day
between 14 and 16 years of age may prevent MS. Copyright 2000 Harcourt