iThyroid.com

MULTIPLE SCLEROSIS

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, 54

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 B-12.

Int J Neurosci 1993 Jul-Aug;71(1-4):93-9

Vitamin B12 and its relationship to age of onset of multiple sclerosis.

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 sclerosis patients.

 

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 communications.

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

t

Clustering of multiple sclerosis in Galion, Ohio, 1982-1985.

Ingalls TH

School of Public Health, Boston University School of Medicine, Massachusetts.

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 neurologists.

PMID: 2782299, UI: 89390412

 

Sci Total Environ 1988 Dec;77(2-3):175-88

Related Articles, Books, LinkOut

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 in MS.

 

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.

Title
            Time-dependent excretion of lithium, sodium, potassium, rubidium, magnesium and strontium in the urine of a multiple sclerosis patient.

Author

Schulten HR; Palavinskas R; Kriesten K

Source

Biomed Mass Spectrom, 10(3):192-6 1983 Mar

Abstract

 

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.

Warren TR

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

s

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.

Johnson S

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 Publishers Ltd.