This is interesting. Lists compounds that affect thiamine in food and supplements. There are a lot of things on that list that we eat! Might explain why the thiamine requirement is so high.
helid.digicollection.org/en...
"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."
One of the things on the list is quercetin so I was wondering whether it would be best not to take it, but then I read this about how it stops mercury by binding to it so now i think it needs to stay, although it also binds to other minerals so might deplete them:
Why You May Need Magnesium To Get The Most Out Of Thiamine
Thiamine and Dr Costantini, what we know and don't know
THIAMINE, another view
[The role of thiamine in neurodegenerative diseases] [Article in Polish] Irena Bubko et al. Postepy Hig Med Dosw (Online). 2015
