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Anti-Thiamine factors

aliml

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Joined
Apr 17, 2017
Messages
566
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

1636869707090.png

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.


 

Dr. B

Member
Joined
Mar 16, 2021
Messages
3,613
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

View attachment 30164

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.


what does the ascorbic acid do?
does USP caffeine contain caffeic acid or chlorogenic acid and how much... wiki says caffeic acid is actually in caffeine...
 

aliml

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what does the ascorbic acid do?
does USP caffeine contain caffeic acid or chlorogenic acid and how much... wiki says caffeic acid is actually in caffeine...
Caffeic acid/Chlorogenic acid is unrelated to caffeine.

Vitamin C neutralizes tannins so as not to interfere with the absorption of thiamine.


However, thiamine might also reduce the risk of renal oxalate crystallization by preventing the conversion of vitamin C into oxalate, which is a potential adverse effect of vitamin C administration
 

Perry Staltic

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5,403
One question of course is how potent the thiaminase is in each food. A takeaway from reading this is to supplement before eating so that thiamine gets absorbed, and then you can go on your merry way and eat whatever you want.
 

magnesiumania

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Jul 17, 2018
Messages
600
Thiamine HCL seem to give a mild but noticable effect when taken at the same time as having coffee. THis is 100mg and probably too much for anti-thiamine factors to break down.

Ive never felt ANYTHING from HCL form of thiamine before but after starting biotin i actually feel it. Probably from upregulation of transporters by vitamin B7 (biotin)
 

Dr. B

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Joined
Mar 16, 2021
Messages
3,613
Thiamine HCL seem to give a mild but noticable effect when taken at the same time as having coffee. THis is 100mg and probably too much for anti-thiamine factors to break down.

Ive never felt ANYTHING from HCL form of thiamine before but after starting biotin i actually feel it. Probably from upregulation of transporters by vitamin B7 (biotin)
what effect do you get with it after starting biotin
 

mostlylurking

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May 13, 2015
Messages
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Location
Texas
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

View attachment 30164

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.


Thanks for the link. Very good information!

Does anyone know who, when, and how the RDA for thiamine was determined? It seems to be woefully low. Since thiamine gets used up in the oxidative metabolism of glucose, it seems to me that the increased amount of sugar in the modern diet would overwhelm the paltry RDA for thiamine pretty quickly.

-edit-
I found the RDA information in the same article: Thiamine Deficiency and its Prevention and Control in Major Emergencies: RDA (Recommended Daily Allowance) for Thiamine: Calculating RDA for thiamine

Calculating RDA for thiamine​


Recommended daily allowances for thiamine have been based on the following:
• assessment of the effects of varying levels of dietary thiamine on the occurrence of clinical signs of deficiency;
• urinary excretion of thiamine;
• erythrocyte transketolase activity.​
Several studies were undertaken in the 1940s and 1950s to come up with the minimum levels of thiamine intakes to prevent clinical signs from appearing. Table C, Annex 3 shows the results of some experimental human thiamine deficiency studies.
Thiamine requirements are closely related to carbohydrate intake. In rice diets, 75% or more of the energy is provided by carbohydrate. Thiamine needs have usually been expressed as mg per 1000 kcal energy from carbohydrate intake. However, the error involved in relating the thiamine content of a diet to the total energy content of the diet rather than to the energy derived from carbohydrate alone is minimal.
Foltz and others (1944) reported that thiamine deficiency occurred within 8 weeks in the majority of humans kept on an intake of 0.20 mg thiamine/1000 kcal or less (total intakes of 0.6 mg thiamine or less daily). The minimum requirement was stated as ranging from 0.33 to 0.45 mg thiamine/1000 kcal (1.0 to 1.5 mg thiamine daily) which was necessary for maintenance and for well-being. Anderson and others (1986) recommended a minimum thiamine intake of 1.22 mg/day for men and 1.03 mg/day for women. Values for thiamine intake ranging between 0.2 and 0.5 mg per 1000 kcal have been reported as those needed to satisfy requirements. The large differences can be explained by differences in approach and in experimental procedures used to estimate thiamine requirements.
Anderson and others (1986) reported that restricting thiamine intake to 0.45 mg/day for up to 6 months caused anorexia and eventually progressive general impairment of mental and physical health that took three months to respond fully to oral thiamine replacement.
Based on the urinary excretion of thiamine, a critical intake appears to be approximately 0.2 mg thiamine/1000 kcal, below which urinary excretion is low (5 to 20 µg) and clinical signs of thiamine deficiency may appear. Studies suggest that the minimum requirement is 0.33 mg thiamine/1000 kcal, and that an intake of over 0.5 mg/1000 kcal is necessary for tissue saturation.
Normal red-cell transketolase activities have been observed in subjects consuming 0.4 mg/1000 kcal but at least 0.6 mg/1000 kcal of thiamine was necessary to obtain maximum activity (National Research Council [US], 1989).

-edit-
also this:

RDA for adults​

WHO (1967) states that the recommended intake for thiamine is 0.4 mg/1000 kcal. An adult man consuming 3200 kcal daily would therefore need a daily intake of 1.3 mg thiamine, whereas a woman consuming an average of 2300 kcal would require an intake of 0.9 mg thiamine daily. A thiamine allowance for adults of 0.5 mg/1000 kcal is recommended by the National Research Council [US] (1989) but they also recommend that the total daily intake should not be less than 1.0 mg even for those consuming less than 2000 kcal daily.
-end-
So it's that great trustworthy entity, the WHO....​
 
Last edited:

Ben.

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From the Wondro Thread, i found this to be super interesting:

"Pause for a moment and consider the effects of a commensal organism (Candida Albicans) capable of producing and releasing acetaldehyde into its environment, i.e. your body, on a daily basis...

The hazardous material data sheets for acetaldehyde drive home just how dangerous this stuff is. It ishighly flammable, reactive, and poses a health hazard in the industrial workplace unless utmostprecautions are exercised in its handling [1,2]. Acetaldehyde is so highly reactive that it is difficult to trace, especially in the body. However, in the presence of thiamine-pyrophosphate and acetyl-coenzyme A it reacts to form a stable metabolite called2,3-butanediol. 2,3-butanediol has been found in the urine of humans in "apparently unrelated diseasestates" [3]. It has also been found in the urine of premature babies indicative of "abnormal colonisation of neonates" [4].



So not only is sugar a factor directly related to thiamine and requires balance of the two, yeast or other organisms feeding off sugar and other food produce toxic byproducts binding to our precious thiamine-pyrophopsphate. Did i understand this correctly?
 

PolishSun

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That would explain why people with candida have symptoms of vitamin B1 deficiency.
 

dogtrainer

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From the Wondro Thread, i found this to be super interesting:

"Pause for a moment and consider the effects of a commensal organism (Candida Albicans) capable of producing and releasing acetaldehyde into its environment, i.e. your body, on a daily basis...

The hazardous material data sheets for acetaldehyde drive home just how dangerous this stuff is. It ishighly flammable, reactive, and poses a health hazard in the industrial workplace unless utmostprecautions are exercised in its handling [1,2]. Acetaldehyde is so highly reactive that it is difficult to trace, especially in the body. However, in the presence of thiamine-pyrophosphate and acetyl-coenzyme A it reacts to form a stable metabolite called2,3-butanediol. 2,3-butanediol has been found in the urine of humans in "apparently unrelated diseasestates" [3]. It has also been found in the urine of premature babies indicative of "abnormal colonisation of neonates" [4].



So not only is sugar a factor directly related to thiamine and requires balance of the two, yeast or other organisms feeding off sugar and other food produce toxic byproducts binding to our precious thiamine-pyrophopsphate. Did i understand this correctly?
From "Astrophysiology and Yeast:"


"Acetaldehyde stemming from yeast is a thiamine antagonist. It combines irreversibly with thiamine to form 2,3-butanediol, a stable adduct, that is excreted in the urine. The thiamine molecules thus imprisoned are no longer available for either aspect of the chi cycle. Thiamine is required for the liver energy requirements during the aldehyde dehydrogenase oxidation of acetaldehyde and for neutrophils that attempt to surround and destroy budding yeast as it shifts into its hyphal form. Responding to the metabolic impact of yeast in the system has increased the demand upon thiamine reserves already serving the energy requirements of every other active cell in the body's conglomeration of organs and tissues.

When all of these concurrent demands reach a critical threshold and the normal background chi pressure that keeps the body's chi spring wound up creates a sudden shift of thiamine out of the bloodstream, then normal chi pressure becomes excessive chi stress and body processes start to fail. The symptom first experienced might be a sudden headache, hot flash, night sweat, panic attack, fit of rage, dizzy spell, nausea, spike in blood pressure, or enervating fatigue that continues to worsen until the condition becomes chronic and internal organs begin to fail. When there is an overall insufficiency of thiamine in the system, so that both blood stream and chi field requirements cannot be adequately met, the body has slipped into a state of sub-clinical beri-beri, the thiamine deficiency disease."
 

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