Deficiencies, nutritional thiamine

Deficiencies of thiamine and B vitamins arising from poor nutrition and malabsorption are usually the basis for these neurological sequelae. 

The use of oral contraceptive agents (OCAs) is widespread and is being increasingly encouraged in developing countries. Their use has been associated with a number of side effects, in particular, a possible increased risk of thrombotic and embolic vascular disease. There is also evidence that OCAs may affect the metabolism of a number of vitamins. Evidence for deficiency of thiamine, riboflb vin, ascorbic acid, pyridoxine, folic acid, and vitamin B12, and for excess accumulation of vitamin A has been reported. This is of particular concern to populations in which vitamin nutrition may already be suboptimal and has been the subject of recent brief reviews (02, R4, Tl, W13). 

A varied diet should provide an adequate level of thiamine to prevent deficiency. The thiamine requirement of an individual is influenced by age, energy and carbohydrate intake, and body mass. On the basis of considerable evidence, the Food and Nutrition Board of the US Institute of Medicine recommends thiamine intake at a level of 0.5mg/1000kcal (4184KJ) (National... 

This ancient nutritional disease results from a severe deficiency of thiamin (vitamin B-1). It is usually found in areas of the world where diets are high in carbohydrate, but low... 

The biochemical changes that are present in the polyneuropathy which can result from a deficiency of thiamine in the diet have been well worked out in the years that have elapsed since 1885 when the Japanese naval surgeon, Takaki, first claimed that beri-beri is a nutritional disease resulting from the ingestion of excessive quantities of polished rice [2]. Eijkmann in 1897 [3] carried out a classical nutritional experiment when he showed for the first time that fowls fed on a diet of polished rice developed weakness of the legs and opisthotonus. As a result of his observations he was able to... 

The part of thiamin in the nutrition of propionic acid bacteria was further illmninated by Wood, Andersen, and Werkman (435) and by Silverman and Werkman (346) who found it possible to train certain strains, which ori ally required the addition of thiamin, to dispense with this substance and to give vigorous and continued growth on a basal medium not containing it. Serial transfer in a medium deficient in thiamin was the method... 

Thiamine deficiency results in early decreases in activity of the mitochondrial enzyme a-ketoglutarate dehydrogenase in brain. Wernicke s encephalopathy, also known as the Wernicke-Korsakoff syndrome is a neuropsychiatric disorder characterized by ophthalmoplegia, ataxia and memory loss. Wernicke s encephalopathy is encountered in chronic alcoholism, in patients with HIV-AIDS and in other disorders associated with grossly impaired nutritional status. The condition results from thiamine deficiency. 

Classic beri-beri, rarely seen in the United States and Europe, except in alcoholism (P4), is endemic in the Far East because of the prevalent diet of decorticated rice (F6). It occurs in two forms wet beri-beri, characterized by edema and cardiovascular symptoms (G6), and dry beri-beri with peripheral neuritis, paralysis, and atrophy of the muscles. Conditions which may predispose to deficiency by increasing thiamine requirements are pregnancy (see section 2.4), and lactation, hyperthyroidism, malignant disease, febrile conditions, increased muscular activity, high carbohydrate diets, and parenteral administration of glucose solutions. A constant supply of thiamine is required for optimal nutrition because storage in the liver and elsewhere is limited. Thiamine is synthesized by bacteria in the intestinal tract of various animals, but this is not a dependable source for man. 

A further assumption is also often made, namely, that even a mild thiamine deficiency, if it is a real deficiency, will make itself known by outward signs. This, in the author s opinion, is probably far from true. In animal experiments, for example, deficiencies require weeks to develop, and long before an animal shows overt symptoms of deficiency, an analysis of its tissues would show that deficiencies are present and metabolism is being impaired. The importance of considering other evidence about the nutritional state besides overt symptoms is stressed in a recent review by Lowry. 19... 

We know something about the factors that enter into making for the wisdom of the body of which we are speaking. Good nutrition itself is an important factor. We have said that one of the wisdoms of the body is the wisdom to eat. But if individuals are fed deficient diets (it is notably true in the case of thiamine-deficient diets), they lose this wisdom of the body. Anorexia develops, and they starve themselves. 

There was a time when students of nutrition were inclined to think that certain vitamins, e g., thiamine, vitamin A, and ascorbic acid, were the "important vitamins" and that others brought up the rear of the procession. From the standpoint of ease of discovery on the basis of deficiency disease, there is some justification in this view. 

Psychoneuroses involving depression, irritability, anxiety, increased sensitivity to noise and painful stimuli, and uncertainty of memory have been induced in human patients as a result of thiamine deficiency. 22 It seems probable that the Wernicke type syndrome, which is more severe, can likewise be caused by thiamine deficiency. In all cases the psychological symptoms are eliminated or prevented by the administration of adequate amounts of thiamine. Here again is a clear-cut case in which mental disease can be caused by a nutritional deficiency and cured by supplying adequate amounts of the missing nutritional factor. 

Nutritional Folate deficiency Iron deficiency Vitamin Bi (thiamine) deficiency Vitamin B2 (riboflavin) deficiency Vitamin Bg (pyridoxine) deficiency Vitamin B12 (cyanocobalamin) deficiency... 

Nutritional Deficiency-Related Dementias. We have already mentioned that chronic alcoholics are subject to thiamine deficiency that can cause dementia. It usually occurs only after heavy, prolonged abuse of alcohol. In developed countries, the other key nutritional concern is vitamin deficiency. Vitamin deficiency can surprisingly strike even those with a healthy diet. Such people are missing a vital protein, intrinsic factor, which would enable them to absorb it from their digestive tract. 

Thiamine deficiency Is often seen as a nutritional disease In populations whose sole food source Is polished rice, resulting In beriberi. 

Thiamine deficiency may also develop In alcoholics due to poor nutrition and poor absorption of thiamine In the gastrointestinal tract. 

Inadequate nutrition and conditions which are complicated by malabsorption may lead to thiamine deficiency. Beriberi, a diet-deficiency disease, is especially prevalent in those parts of the East where the diet consists mainly of polished rice. The disease is characterized by neuritis but may also lead to serious heart failure. Recovery is prompt when adequate amounts of vitamin B1 are restored to the diet. Severe deficiency as can occur in alcoholics may lead to Wernicke s encephalopathy, often accompanied by Korsakoff s syndrome. Care should be taken with intravenous substitution with thiamine in these cases to prevent serious complications like vascular collapse with hypotension, respiratory distress or an-gioedema. 

Answer The symptoms resemble those you remember from medical school for beriberi, but you fail to see the coimection. Then a light clicks on. If the patient were consuming most of his calories as alcohol, he may have a nutritional deficiency, a beriberi-Uke syndrome, as a result of insufficient intake of thiamine. You prescribe a daily vitamin tablet and admonish the patient to cut back on alcohol intake. At the next appointment, the edema is much better and the cardiac stress tests results are normal. He has joined Alcohohcs Anonymous and indicates that he is doing better. 

Thiamin was the first of the vitamins to be demonstrated to have a clearly defined metabolic function as a coenzyme indeed, the studies of Peters group in the 1920s and 1930s laid the foundations not only of nutritional biochemistry but also of modern metabolic biochemistry and neurochemistry. Despite this, the mechanism by which thiamin deficiency results in central and peripheral nervous system lesions remains unclear in addition to its established coenzyme role, thiamin regulates the activity of a chloride transporter in nerve cells. 

Table 6.1 Indices of Thiamin Nutritional Status Adequate Marginal Deficient...

McCandless DW, Hanson C, Speeg KV Jr, and Schenker S (1970) Cardiac metabolism in thiamin deficiency in mts. Journal of Nutrition 100, 991-1002. 

Page MG, Ankoma-Sey V, Coulson WF, and Bender DA (1989) Brain glutamate and gamma-amlnohutyrate (GABA) metaholism in thiamin-deficient rats. British Journal of Nutrition 62, 245-53. 

Pekovich SR, Martin PR and Singleton CK (1998) Thiamine deficiency decreases steady-state transketolase and pyruvate dehydrogenase but not alpha-ketoglutarate dehydrogenase mRNA levels in three human cell types. Journal of Nutrition 128, 683-7. 

Harata N, Iwasaki Y (1995) Evidence for early blood-brain btirrier breakdown in experimental thiamine deficiency in the mouse. Metab Brain Dis 10(2) 159-174 Harper CG (1983) The incidence of Wernicke s encephalopathy in Australia A neuropathological study of 131 cases. J Neurol Neurosurg Psychiatry 46 593-598 Harper CG, Butterworth RF (1997) Nutritional and metabolic disorders. In Graham DI, Lantos PL (eds) Greenfield s neuropathology. Arnold, London, pp 601-655 Hayton SM, Kriss T, Wase A, Muller DP (2006) Effects on neural function of repleting vitamin E-deflcient rats with alpha-tocopherol. J Neurophysiol 95(4) 2553-2559 Hayton SM, MuUer DP (2004) Vitamin E in neural and visual function. Ann N Y Acad Sd 1031 263-270... 

TanPhaichitr V (1985) Epidemiology and clinical assessment of vitamin deficiencies in Thai children. In Eeckels RE, Ransome-Kuti O, Kroonenberg CC (eds) Child health in the tropics. Martinus Nijhoff Publishers, Dordrecht, pp 157-166 TanPhaichitr V (1999) Thiamin. In Shils ME, Olsen JA, Shike M et al (eds) Modem nutrition in health and disease, 9th edn. Lippincott Willitims Wilkins, Baltimore, MD Todd KG, Butterworth RE (1999) Early microglitil response in experimental thiamine deficiency tm immunohistochemical analysis. Glia 25(2) 190-198 Torvik A (1985) Two types of brain lesions in Wernicke s encephalopathy. Neuropathol Appl Neutobiol 11(3) 179-190... 

---