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Vitamin B Nutritional Disorders

Definition

Most nutritional disorders with deleterious effects on the central and peripheral nervous system are secondary to vitamin deficiencies, particularly those of the B group. Many of these disorders occur in the setting of malnutrition associated with alcoholism.

A detailed discussion of all vitamin B deficiencies is beyond the scope of this article. However, four of the more common vitamin B deficiencies—thiamine (B1), cobalamin (B12), niacin (B3), and folate (B9)—are reviewed.

Thiamine (vitamin B1)

Thiamine is a water-soluble vitamin required for carbohydrate metabolism. Thiamine diphosphate, the biologically active form of thiamine, is a required cofactor for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, two important enzymes in the Krebs cycle, and for transketolase, a key enzyme involved in the pentose phosphate pathway. Thiamine deficiency results in impaired carbohydrate and lipid metabolism, altered mitochondrial activity, decreased energy stores, reduced neurotransmitter synthesis, and altered cellular membrane functions.

Thiamine deficiency can result in disorders that affect both the central and peripheral nervous systems. Wernicke encephalopathy (WE) is an acute, life-threatening but potentially reversible central nervous system disorder. If WE is not treated, the condition progresses to Korsakoff syndrome (KS), with resulting permanent brain damage. Wernicke-Korsakoff syndrome (KWS) has been used to describe the spectrum of clinical and pathologic changes associated with thiamine deficiency.

Thiamine deficiency can also cause beriberi. Dry beriberi is a peripheral nervous system disorder associated with peripheral neuropathy. Wet beriberi is a cardiovascular disorder associated with cardiac manifestations and edema secondary to congestive heart failure.
 Infantile beriberi can occur in breastfed infants secondary to inadequate thiamine levels in the mother’s breast milk.

Cobalamin (vitamin B12)

Cobalamin is found exclusively in animal products. It is required cofactor for two enzymatic reactions in humans. Methylcobalamin is required for methionine synthase, which converts homocysteine to methionine while simultaneously transforming 5’-methyltetrahydrofolate (5-MTHF) to tetrahydrofolate (THF). Adenosylcobalamin is necessary for methylmalonyl-CoA mutase, which converts methylmalonyl-CoA to succinyl-CoA within mitochondria.

Cobalamin deficiency leads to reduced DNA synthesis, altered cell metabolism, and impaired myelin maintenance. Clinical features of cobalamin deficiency include myelopathy, peripheral neuropathy, optic neuropathy, glossitis, neuropsychiatric changes, and hematologic manifestations including megaloblastic anemia.

Niacin (vitamin B3, nicotinic acid)

Niacin is a water-soluble vitamin and an essential component of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), coenzymes required for oxidation-reduction reactions.
Niacin can be found in the diet or can be synthesized during tryptophan metabolism. Niacin deficiency results in pellagra, a condition characterized by diarrhea, dermatitis, dementia and, eventually, death.

Folate (vitamin B9)

Folate is a water-soluble essential vitamin found in green leafy vegetables and the liver. Folate is converted into THF, the active form involved in single-carbon transfers in a variety of metabolic reactions.
THF is required for the conversion of homocysteine to methionine (which also requires cobalamine), the synthesis of thymine and purine bases, and the metabolism of serine and glycine.

Folate deficiency is most commonly associated with megaloblastic anemia. Pregnant women with low folate intake have an increased risk of neural tube defects (NTDs); folic acid supplementation reduces the risk of NTDs.
 In rare cases, folate deficiency may be associated with subacute combined degeneration of the spinal cord.

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