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EuRho vital multivitamin product contains B group vitamins and other elements that are important for human health

VITAMIN B12

Although the nutritional literature still uses the term vitamin B12, a more specific name for vitamin B12 is cobalamin. Vitamin B12 is the largest of the B complex vitamins, with a relative molecular mass of over 1000. the most important condition resulting in vitamin B12 malabsorption is the autoimmune disease called pernicious anaemia (PA). In most cases of PA, antibodies are produced against the parietal cells causing them to atrophy, and lose their ability to produce intrinsic factor and secrete hydrochloric acid. Historically, PA was considered to be the major cause of vitamin B12 deficiency, but it was a fairly rare condition, perhaps affecting between one and a few per cent of elderly populations. More recently, it has been suggested that a far more common problem is that of hypochlorhydria associated with atrophic gastritis, where there is a progressive reduction with age of the ability of the parietal cells to secrete hydrochloric acid.

One of the vitamin B12-dependent enzymes, methionine synthase, functions in one of the two folate cycles, namely, the methylation cycle . This cycle is necessary to maintain availability of the methyl donor, S-adenosylmethionine. Interruption of the cycle reduces the level of S adenosylmethionine. This occurs in PA and other causes of vitamin B12 deficiency, producing as a result demyelination of the peripheral nerves and the spinal column, giving rise to the clinical condition called subacute combined degeneration. This neuropathy is one of the main presenting conditions in PA. The other principal presenting condition in PA is a megaloblastic anaemia morphologically identical to that seen in folate deficiency. Disruption of the methylation cycle also causes a lack of DNA biosynthesis and anaemia. In humans, the vitamin B12-dependent enzyme methylmalonyl CoA mutase functions both in the metabolism of propionate and certain amino acids—converting them into succinyl CoA—and in the subsequent metabolism of these amino acids via the citric acid cycle. It is clear that in vitamin B12 deficiency the activity of the mutase is compromised, resulting in high plasma or urine concentrations of methylmalonic acid (MMA), a degradation product of methylmalonyl CoA mutase.

In adults, this mutase does not appear to have any vital function, but it clearly has an important role during embryonic life and in early development. Children deficient in this enzyme, through rare genetic mutations, suffer from mental retardation and other developmental defects.

THIAMINE (VITAMIN B1)

Thiamine functions as the coenzyme thiamine pyrophosphate (TPP) in the metabolism of carbohydrates and branched-chain amino acids. Specifically the Mg2+-coordinated TPP participates in the formation of a-ketols (e.g. among hexose and pentose phosphates) as catalysed by transketolase and in the oxidation of a-keto acids (e.g. pyruvate, a-ketoglutarate, and branchedchain a-keto acids) by dehydrogenase complexes .

Hence, when there is insufficient thiamine, the overall decrease in carbohydrate metabolism and its interconnection with amino acid metabolism has severe consequences, such as a decrease in the formation of acetylcholine for neural function. Thiamine (vitamin B1, aneurin) deficiency results in the disease called beriberi, which has been classically considered to exist in dry (paralytic) and wet (oede-matous) forms. Some cases of thiamine deficiency have been observed with patients who are hypermetabolic, are on parenteral nutrition, are undergoing chronic renal dialysis, or have undergone a gastrectomy. Because thiamine facilitates energy utilization, its requirements have traditionally been expressed on the basis of energy intake, which can vary depending on activity levels.

RIBOFLAVIN (VITAMIN B2)

Conversion of riboflavin to flavin mononucleotide (FMN) and then to the predominant flavin, flavin adenine dinucleotide (FAD), occurs before these flavins form complexes with numerous flavoprotein dehydrogenases and oxidases. The flavocoenzymes (FMN and FASD) participate in oxidation– reduction reactions in metabolic pathways and in energy production via the respiratory chain. Riboflavin (vitamin B2) deficiency results in the condition of hypo- or ariboflavinosis, with sore throat; hyperaemia; oedema of the pharyngeal and oral mucous membranes; cheilosis; angular stomatitis; glossitis; seborrheic dermatitis; and normochromic, normocytic anaemia associated with pure red cell cytoplasia of the bone marrow. As riboflavin deficiency almost invariably occurs in combination with a deficiency of other B-complex vitamins, some of the symptoms (e.g. glossitis and dermatitis) may result from other complicating deficiencies. The major cause of hyporiboflavinosis is inadequate dietary intake as a result of limited food supply, which is sometimes exacerbated by poor food storage or processing.

Children in developing countries will commonly demonstrate clinical signs of riboflavin deficiency during periods of the year when gastrointestinal infections are prevalent.

NIACIN

Niacin (nicotinic acid) deficiency classically results in pellagra, which is a chronic wasting disease associated with a characteristic erythematous dermatitis that is bilateral and symmetrical, a dementia after mental changes including insomnia and apathy preceding an overt encephalopathy, and diarrhea resulting from inflammation of the intestinal mucous surfaces. Niacin is chemically synonymous with nicotinic acid although the term is also used for its amide (nicotinamide). Nicotinamide is the other form of the vitamin; it does not have the pharmacologic action of the acid that is administered at high doses to lower blood lipids, but exists within the redox-active coenzymes, nicotinamide adenine dinucleotide (NAD) and its phosphate (NADP), which function in dehydrogenase–reductase systems requiring transfer of a hydride ion. NAD is also required for non-redox adenosine diphosphate–ribose transfer reactions involved in DNA repair and calcium mobilization. NAD functions in intracellular respiration and with enzymes involved in the oxidation of fuel substrates such as glyceraldehyde- 3-phosphate, lactate, alcohol, 3-hydroxybutyrate, and pyruvate. NADP functions in reductive biosyntheses such as fatty acid and steroid syntheses and in the oxidation of glucose-6-phosphate to ribose-5-phosphate in the pentose phosphate pathway.

VITAMIN B6

A deficiency of vitamin B6 alone is uncommon because it usually occurs in association with a deficit in other B-complex vitamins . Early biochemical changes include decreased levels of plasma pyridoxal 5¢-phosphate (PLP) and urinary 4-pyridoxic acid. These are followed by decreases in synthesis of transaminases (aminotransferases) and other enzymes of amino acid metabolism such that there is an increased presence of xanthurenate in the urine and a decreased glutamate conversion to the anti-neurotransmitter g-aminobutyrate. Infants are especially susceptible to insufficient intakes, which can lead to epileptiform convulsions. Skin changes include dermatitis with cheilosis and glossitis. Moreover, there is usually a decrease in circulating lymphocytes and sometimes a normocytic, microcytic, or sideroblastic anaemia as well.

 A decrease in the metabolism of glutamate in the brain, which is found in vitamin B6 insufficiency, reflects a nervous system dysfunction. As is the case with other micronutrient deficiencies, vitamin B6 deficiency results in an impairment of the immune system. Of current concern is the pandemic-like occurrence of low vitamin B6 intakes in many people who eat poorly. There are three natural vitamers (different forms of the vitamin) of vitamin B6, namely pyridoxine, pyridoxamine, and pyridoxal. All three must be phosphorylated and the 5¢-phosphates of the first two vitamers are oxidized to the functional PLP, which serves as a carbonyl-reactive coenzyme to a number of enzymes involved in the metabolism of amino acids. Such enzymes include aminotransferases, decarboxylases, and dehydratases; d-aminolevulinate synthase in haem biosynthesis; and phosphorylase in glycogen breakdown and sphingoid base biosynthesis.

PANTOTHENATE

Pantothenic acid is a component of CoA, a cofactor that carries acyl groups for many enzymatic processes, and of phosphopantetheine within acyl carrier proteins, a component of the fatty acid synthase complex .

The compounds containing pantothenate are most especially involved in fatty acid metabolism and the pantothenate-containing prosthetic group additionally facilitates binding with appropriate enzymes.

BIOTIN

Biotin deficiency in humans has been clearly documented with prolonged consumption of raw egg whites, which contain biotin-binding avidin. Biotin deficiency has also been observed in cases of parenteral nutrition with solutions lacking biotin given to patients with short-gut syndrome and other causes of malabsorption. Clinical signs of deficiency include dermatitis of an erythematous and seborrheic type; conjunctivitis; alopecia; and central nervous system abnormalities such as hypotonia, lethargy, and developmental delay in infants, and depression, hallucinations, and paresthesia of the extremities in adults. Biotin functions as a coenzyme within several carboxylases after its carboxyl functional group becomes amide linked to the e-amino of specific lysyl residues of the apoenzymes. In humans and other mammals, biotin operates within four carboxylases. Three of the four biotin-dependent carboxylases are mitochondrial (pyruvate carboxylase, methylcrotonyl-CoA carboxylase, and propionyl-CoA carboxylase) whereas the fourth (acetyl- CoA carboxylase) is found in both mitochondria and the cytosol. In all these cases, biotin serves as a carrier for the transfer of active bicarbonate into a substrate to generate a carboxyl product.

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