Thiamin, Riboflavin, Niacin, Vitamin B6, Pantothenic Acid and Biotin

Reference from the joint report of FAO/WHO expert consultation on Human Vitamins and Minerals verbatim. (Chapter 3)

The B-complex vitamins covered here are presented in Table 5 along with the biochemical and physiologic roles of the co-enzyme forms and a brief description of clinical deficiency symptoms. Rice and wheat are the staples for many populations of the world. Excessive refining and polishing of cereals removes considerable proportions of B vitamins contained in these cereals. Clinical manifestations of deficiency of some B vitamins – such as beri-beri (cardiac and dry), peripheral neuropathies, pellagra, and oral and genital lesions (related to riboflavin deficiency) – were once major public health problems in parts of the world.

These manifestations have now declined, the decline being brought about not through programmes, which distribute synthetic vitamins but through changes in the patterns of food availability and consequent changes in dietary practices of the populations. Although these clinical manifestations of B-vitamin deficiencies have decreased, there is evidence of widespread sub-clinical deficiency of these vitamins (especially of riboflavin and pyridoxine). These sub-clinical deficiencies, although less dramatic in their manifestations, exert deleterious metabolic effects.

1. United Nations Sub-Committee on Nutrition. 1988. Report on the Nutrition Situation of Refugees and Displaced Populations. No. 25; p.5., Geneva, Switzerland.

Despite the progress in reduction of large-scale deficiency in the world, there are periodic reports of outbreaks of B-complex deficiencies, which are linked to deficits of B vitamins in populations under various distress conditions. Refugee and displaced population groups (20 million people by current United Nations estimates) are at risk for B-complex deficiency because most cereal foods used under emergency situations are not fortified with micronutrients (1).

2. Sadun, J. Martone, R. Muci-Mendoza, L. Reyes, J. C. Silva & B. Caballero. 1994 Epidemic optic neuropathy in Cuba: eye findings. Arch. Ophthalmol., 112: 691-699.

3. O. Ordunez-Garcia, J. F. Nieto, A. D. Espinosa-Brito & B. Caballero. 1996. Cuban epidemic neuropathy, 1991-1994: history repeats itself a century after the "amblyopia of the blockade". Am. J. Public Health, 86 (5): 738-743.

4. R. Hedges, K. Tucker, M. Hirano & B. Caballero. 1997 Epidemic optic and peripheral neuropathy in Cuba: the unique geopolitical public health problem. Surveys Ophthalmol., 41: 341-353.

Recent reports have implicated the low B-complex content of diets as a factor in the outbreak of peripheral neuropathy and visual loss observed the adult population of Cuba (2-4). This deficiency in Cuba resulted from the consequences of an economic blockade (4).

5. FAO/WHO. 1974. Handbook on Human Nutritional Requirements, eds. Passmore R, Nicol BM, Rao M. Narayana, Beaton GH, de Mayer EM. FAO Nutritional Studies No.28; WHO Monograph Series No. 61, Rome, Italy. 

Because of the extensive literature pertaining to the study of the B-complex vitamins, the references cited here were selected from those published after the FAO/WHO handbook on human nutritional requirements was published in 1974 (5).

6. Food and Nutrition Board, Institute of Medicine/National Academy of Sciences- National Research Council. 1998. Dietary Reference Intake: Folate, Other B Vitamins, and Choline. Washington, D.C., National Academy Press.

Greater weight has been given to studies which used larger numbers of subjects over longer periods, more thoroughly assessed dietary intake, varied the level of the specific vitamin being investigated, and used multiple indicators, including those considered functional in the assessment of status. These indicators have been the main basis for ascertaining requirements. 

Although extensive, the bibliographic search of recently published reports presented in this chapter most likely underestimates the extent of B-complex deficiency considering that many cases are not reported in the medical literature. 

Moreover, outbreaks of vitamin deficiencies in populations are usually not publicised because governments may consider the existence of these conditions to be politically sensitive information. Additional references are listed in the publication by the Food and Nutrition Board of the Institute of Medicine of the US National Academy of Sciences (6).

Thiamin 

Background with requisite function in human metabolic processes

Deficiency

7. McCormick, D.B. Thiamin. 1988. In: Modern Nutrition in Health and Disease, 6th edition. Shils, M.E., Young V.R., eds. Philadelphia: Lea & Febiger, p. 355-61.

8. McCormick, D.B. 1997. Vitamin, Structure and Function of. In: Encyclopedia of Molecular Biology and Molecular Medicine, Vol. 6. Meyers, R.A., ed. Weinheim: VCH, p. 244-52.

Thiamin (vitamin B1, aneurin) deficiency results in the disease called beri-beri, which has been classically considered to exist in dry (paralytic) and wet (oedematous) forms (7, 8).

9. McCormick, D.B & Greene, H.L. 1994. Vitamins. In: Tietz Textbook of Clin Chem., 2nd edition. Burtis, V.A., Ashwood, E.R., eds. Philadelphia: W.B. Saunders, p. 1275-1316.

Beriberi occurs in human-milk-fed infants whose nursing mothers are deficient. It also occurs in adults with high carbohydrate intakes mainly from milled rice and with intakes of antithiamin factors. Beri-beri is still endemic in Asia. In relatively industrialized nations, the neurologic reflections of Wernicke-Korsakoff syndrome are frequently associated with chronic alcoholism with limited food consumption (9).

Some cases of thiamin deficiency have been observed with patients who are hypermetabolic, are on parenteral nutrition, are undergoing chronic renal dialysis, or have undergone a gastrectomy. Thiamin deficiency has also been observed in Nigerians who ate silk worms, Russian schoolchildren (in Moscow), Thai rural elderly, Cubans, Japanese elderly, Brazilian Xavante Indians, French Guyanense, Southeast Asian schoolchildren who were infected with hookworm, Malaysian detention inmates, and people with chronic alcoholism.

Toxicity

Toxicity is not a problem with thiamin because renal clearance of levels conceivably ingested is rapid.

Functions

10. McCormick, D.B. 1996. Co-enzymes, Biochemistry of. In: Encyclopedia of Molecular Biology and Molecular Medicine, Vol. 1. Meyers, R.A., ed. Weinheim: VCH, p. 396-406.

11. McCormick, D.B. 1997. Co-enzymes, Biochemistry. In: Encyclopedia of Human Biology 2nd edition. Dulbecco, R., ed.-in-chief. San Diego: Academic Press, p. 847-64.

Thiamin functions as the co-enzyme thiamin pyrophosphate (TPP) in the metabolism of carbohydrates and branched-chain amino acids. Specifically the Mg2+-coordinated TPP participates in the formation of α-ketols (e.g., among hexose and pentose phosphates) as catalysed by transketolase and in the oxidation of α-keto acids (e.g., pyruvate, α-ketoglutarate, and branched-chain α-keto acids) by dehydrogenase complexes (10, 11). 

Hence, when there is insufficient thiamin, the overall decrease in carbohydrate metabolism and its inter-connection with amino acid metabolism (via α-keto acids) have severe consequences, such as a decrease in the formation of acetylcholine for neural function.