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close this bookThiamine Deficiency and its Prevention and Control in Major Emergencies (WHO; 1999; 62 pages)
View the documentAcknowledgements
View the documentThiamine deficiency: Definition
open this folder and view contentsIntroduction
open this folder and view contentsThiamine deficiency
open this folder and view contentsThiamine, the vitamin
open this folder and view contentsRDA (Recommended Daily Allowance) for Thiamine
open this folder and view contentsSources of thiamine
close this folderFactors influencing content and utilization of thiamine in foods
open this folder and view contentsStability in foods
View the documentAnti-thiamine factors
open this folder and view contentsStrategies to prevent thiamine deficiency in large populations affected by emergencies
open this folder and view contentsConclusions and recommendations
View the documentReferences
View the documentAnnex 1: Summary of major symptoms of thiamine deficiency in adults, adolescents and older children
View the documentAnnex 2: Summary of major symptoms of thiamine deficiency in infants
open this folder and view contentsAnnex 3: Tables
View the documentBack cover
 

Anti-thiamine factors

Thiamine in foods can be destroyed by anti-thiamine compounds that occur naturally in food or are produced in food as a result of microbial or other action. Dietary analyses may indicate adequate intakes of thiamine, but do not take into consideration the influence of anti-thiamine factors in the diet that may affect the requirement of the vitamin. Studies indicate that situations may exist where such factors may influence the availability of the thiamine present in the food.

An early documented case of thiamine deficiency resulting from the ingestion of food containing such thiamine antagonists was that seen on a fox farm owned by Mr. Chastak in the 1940's. The neurological disorder in the commercially raised foxes fed a diet containing about 10% raw carp was referred to as 'Chastak paralysis'. The condition was brought on by a thiamine-degrading enzyme (thiaminase) present in fish gut tissue. Cooking the fish prior to feeding them to the foxes prevented occurrence of the syndrome, apparently by heat-denaturation of the thiaminase. Thiaminases are present in the raw tissues of many fishes, chiefly fresh water fishes but also in Atlantic herring. These are heat labile and can be effective antagonists of the vitamin when consumed without heat treatment (Combs, 1992).

In the Philippines, the Tagalog word for beriberi is 'bangungut' which means nightmare and classically death occurs in sleep after a heavy meal consisting of rice and fish (Lonsdale, 1990). The thiaminase in the fish may compound an initial marginal dietary thiamine deficiency and can be fatal.

Probably the first description of thiaminase poisoning in humans was documented in the diaries of explorers in 1860-61 in Australia (Steinhart et al,1995). An Australian fern (Marsilea drummondii) with high levels of thiaminase was the cause of the death of the explorers. Aboriginal people in Australia prepared the fern sporocarps by grinding them with water to make a flour paste which could then be made into bread or eaten in a soup. However, the expedition members failed to realize the importance of this method of preparation and did not leach out or inactivate the thiaminase in the fern before consumption. The expedition members became progressively weaker, developed muscle wasting and eventually died of beriberi.

Heat-stable thiamine antagonists occur in several plants; ferns, tea, betel nut. They include polyphenols; these and related compounds are found in blueberries, red currants, red beets, brussel sprouts, red cabbage, betel nuts, coffee and tea (Hilker and Somogyi, 1982). They react with thiamine to yield the non-absorbable thiamine disulfide. In addition, some flavonoids have been reported to antagonize thiamine as well as haemin in animal tissues. (See Table 15).

Some bacteria (e.g. Bacillus thiamineolyticus) are also capable of destroying thiamine. It has been reported that 3% of Japanese show a thiamine deficiency due to this cause. Thiaminase bacteria have been frequently isolated from human stools in Japan and it was reported that the thiamine levels in the blood of these patients was low in spite of adequate intake largely due to the destruction of thiamine in the intestines (Bhuvaneswaran and Sreenivasan, 1962).

In Thailand, biochemical thiamine deficiency was reported to be common in the northern and north eastern provinces. Approximately 25% of the subjects studied were found to be deficient, i.e. TPP effect > 20% (Vimokesant et al,1975) and showed signs of extremity numbness, anorexia, weakness and aching of calf muscles. In the northern provinces about 80% of the adults chewed fermented tea leaves as a stimulant while betel nut chewing was common in other areas. In the north eastern provinces, fermented fish was eaten daily. A study undertaken by Vimokesant and others (1975) showed that the abstention from both betel nut chewing and raw fermented fish consumption resulted in a significant reduction of the TPP effect. The TPP effect again increased significantly when the subjects resumed their chewing habits. Cooking of fermented fish destroyed thiaminase and resulted in a significant decrease of the TPP effect. Thiamine supplementation (10 mg/day) further decreased the TPP effect and could counteract the effect of raw fermented fish consumption but was not sufficient to neutralize the effect of betel nut chewing. The habitual diet of the people studied provided for the RDA for thiamine (1.0 mg/day) thus suggesting that the regular consumption of natural anti-thiamine substances can lead to a biochemical thiamine deficiency even in the presence of adequate dietary thiamine intakes.

Table 15. Types of anti-thiamine factors and their actions

Anti-thiamine factor

Mechanism

Source

Thiaminase 1

Type I

alters the structure of thiamine

raw or fermented fish, shellfish, ferns, some bacteria

Type II

reduces biological activity of thiamine

certain bacteria

Thiamine antagonists 2

polyphenols (e.g. caffeic acid, chlorogenic acid, tannic acid)

interferes with absorption or digestion of thiamine

tea, coffee, betel nuts, red cabbage, blueberries, red currants, red beets, also in cereals, pulses, oilseeds

flavonoids (e.g. quercetin, rutin)

interferes with absorption or digestion of thiamine

widely distributed in edible fruits and vegetables, buckwheat plants

haemin

interferes with absorption or digestion of thiamine

animal tissues

1 heat labile enzyme
2 heat stable non-enzymatic factors

Another cause of thiamine deficiency in Thailand was reported to be tea drinking and chewing of fermented tea leaves; tannins being the major component having anti-thiamine activity (Hilker et al,1971). A study by Kositawattanakul and colleagues (1977) found that ascorbic acid (vitamin C) protected the modification of thiamine by tea extract, not only at acidic pH, but also at neutral pH. High concentrations of Ca 2+ and Mg 2+ present in water were also reported by Vimokesant and others (1982) to augment the precipitation of thiamine by tannins. The precipitate formation makes thiamine less available for absorption by the intestine. Again, ascorbic acid, tartaric acid, and citric acid, all present in many vegetables and fruits, are said to lower such precipitation and increase thiamine bioavailability.

The following recommendations were made to decrease the influence of anti-thiamine factors in reducing thiamine absorption (Vimokesant et al, (1982):

• delay the consumption of tea or other tannin-containing products after a meal;
• consume foods high in ascorbic acid along with the meals;
• heat products containing thiaminase before consumption.

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