The beriberi weight loss diet; fortification for the "fattening carbohydrate" theory of obesity.
The obesity epidemic is more advanced in wheat-eating countries and countries with a high intake of processed carbohydrates, and less advanced in countries with a high intake of carbohydrate from polished rice.
It has been noticed for more than a hundred and fifty years that animals accumulate fat on a low-fat, high-carbohydrate diet. Metabolism favours lipogenosis; the steady state (isocaloric) metabolic flux is carbohydrate => fatty acids => CO2 + H2O.
There are exceptions to this rule; lipogenesis is decreased to 5% of normal when caloric intake is inadequate to maintain weight. And lipogenesis is decreased when the B vitamin thiamine is deficient in the diet.
The metabolism of carbohydrate greatly increases the requirement for thiamine (anuerine, vitamin B1). Thiamine is the required co-enzyme for the first step in the conversion of pyruvate to acetyl-CoA, which is how energy from glucose enters the Citric Acid, Krebs, or TCA cycle.
http://en.wikipedia.org/wiki/Pyruvate_dehydrogenase
http://en.wikipedia.org/wiki/Pyruvate_dehydrogenase
Conversion of pyruvate to acetyl-CoA is required for conversion of glucose to ATP and also for conversion of excess glucose to fatty acids (which requires ATP).
Thiamine is one of the B vitamins and plays an important role in energy metabolism and tissue building. It combines with phosphate to form the coenzyme thiamine pyrophosphate (TPP), which is essential in reactions that produce energy from glucose or that convert glucose to fat for storage in the tissues. When there is not enough thiamine in the diet, these basic energy functions are disturbed, leading to problems throughout the body.
http://medical-dictionary.thefreedictionary.com/Thiamine+deficiency
Thiamine is one of the B vitamins and plays an important role in energy metabolism and tissue building. It combines with phosphate to form the coenzyme thiamine pyrophosphate (TPP), which is essential in reactions that produce energy from glucose or that convert glucose to fat for storage in the tissues. When there is not enough thiamine in the diet, these basic energy functions are disturbed, leading to problems throughout the body.
http://medical-dictionary.thefreedictionary.com/Thiamine+deficiency
In a situation where the ability to convert pyruvate to acetyl-CoA is not restricted by the availability of thiamine, some individuals will experience increased appetite and fat storage. This is a normal adaptation to store energy against future lean periods (fat being the body’s default fuel).
When thiamine is severely depleted, as in alcoholism, energy cannot be stored as fat and even the normal fat deposits of lean individuals shrink.
The exception is beer drinkers, who can gain fat (”beer belly"). Beer is a better source of thiamine than other alcoholic drinks.
In most western countries white flour is fortified with vitamins including thiamine. In America, white rice is also fortified. 75% of white bread was fortified by 1942 in the USA. Since then fortification and supplementation has spread through the food supply. Vitamins are popular and thiamine is known to be non-toxic.
The thiamine content of a modern multivitamin is about 10 times the amount issued to prevent beri beri in troops serving in WW2.
This is the oldest formulation I can find data on:
Vitamin waters and energy drinks are popular sources of extra thiamine (and carbohydrate). In New Zealand thiamine is added to breakfast cereals, yeast extract spreads, Milo and other popular chocolate drinks; fortification is pervasive in the food supply.
What happens if thiamine intake is marginal on a high-carbohydrate diet? Surely the conversion of carbohydrate for immediate energy needs would be favoured, and the consumption of extra carbohydrate to be stored as fat would be suppressed. And we do in fact find that deficiency of thiamine causes anorexia. Imagine a diet where carbohydrate is not fortified, and thiamine comes from pork, fish, dairy etc. eaten with polished grains (these foods are of course also eaten in the USA and Europe with fortified grains), or with root vegetables which supply more thiamine than polished grains but less than fortified foods.
Thiamine on such a diet would be adequate for good health but would not favour extreme accumulation of fat; accumulation of pyruvate would work to suppress appetite if excess carbohydrate was consumed.
The non-glucose related TPP-dependent enzyme, branched-chain ketoacid dehydrogenase, catalyses the production of acyl-CoA derivatives from branched-chain amino acids in liver and muscle.
Professor Bruce Ames has published a number of reviews on the Micronutrient Triage theory; that micronutrients are apportioned differently when scarce. Mild deficiency of selenium, for example, spares the systems affected by severe deficiency. Short-term survival takes precedence over long-term survival. In the case of thiamine, fat storage is a long-term survival project.
The non-glucose related TPP-dependent enzyme, branched-chain ketoacid dehydrogenase, catalyses the production of acyl-CoA derivatives from branched-chain amino acids in liver and muscle.
Professor Bruce Ames has published a number of reviews on the Micronutrient Triage theory; that micronutrients are apportioned differently when scarce. Mild deficiency of selenium, for example, spares the systems affected by severe deficiency. Short-term survival takes precedence over long-term survival. In the case of thiamine, fat storage is a long-term survival project.
In a country such as New Zealand, with a large impoverished underclass (“let them eat carbs!”), and a high rate of alcoholism due in part to tradition, in part to pro-alcohol governments washing their hands of responsibility for issues of pricing and availability, thiamine over-abundance undoubtedly prevents much harm. We are not discussing a toxic effect of thiamine, nor a benefit from deficiency, but the likelihood that marginal thiamine status, and the metabolic adjustments this requires on a high-carbohydrate diet, was preventive of obesity in past populations eating white bread, white sugar, polished rice, boiled potato, and so on.
This is not meant to imply that these populations were healthy as a result.
The association between vitamin fortification and obesity has been well studied. There is indeed a strong association (with a 10-year delay). http://www.ncbi.nlm.nih.gov/pubmed/21126339
In this paper, obese individuals store and recycle thiamine more than controls.http://www.ncbi.nlm.nih.gov/pubmed/15098017
The bottom line: even if this hypothesis is correct, no responsible person would advocate thiamine restriction as a response to the obesity epidemic or a treatment for obesity. Thiamine-replete populations are healthier, even if they are fatter, and the fat storage process that thiamine catalyses is not pathological in itself. Carbohydrate restriction, on the other hand, is a practical way out of any dilemma, as it reduces the requirement for thiamine at the same time as exposure to fortified foods and fattening carbohydrates is reduced.
In fact, high-fat diets can be used to prevent thiamine deficiency: http://www.jbc.org/content/206/2/725.full.pdf
In fact, high-fat diets can be used to prevent thiamine deficiency: http://www.jbc.org/content/206/2/725.full.pdf
Thiamine is also essential for production of acetylcholine and GABA. These are vital neurotransmitters and deficiency of thiamine causes severe neurological and psychological symptoms and, if prolonged, nerve and brain damage, due in part to disordered glutamate and GABA signalling and oxidative stress. In alcoholism or severe malnutrition this is called Korsakoff’s syndrome.
http://pubs.niaaa.nih.gov/publications/arh27-2/134-142.htm
![pentose phosphate pathway]()
http://pubs.niaaa.nih.gov/publications/arh27-2/134-142.htm
A classic symptom of early thiamine deficiency is a “sense of impending doom”. This is like something from the weird tales of H. P. Lovecraft. You feel in your soul that your doom is near; exactly when, how, or why you have no idea. This literally dreadful sensation might be familiar to anyone with experience of amphetamine or cocaine abuse. It is probably related to low GABA status.
Raw fish can contain a thiamine-destroying enzyme, thiaminase. Perhaps this also helps to explain the popularity of sushi among dieters, and the low incidence of obesity in high-carb cultures like Japan and Okinawa.
Thiaminase can also be produced by some gut bacteria, perhaps as a way of competing with other commensal species for carbohydrate released from resistant starch.
Thiamine is released by the action of phosphatase and pyrophosphatase in the upper small intestine. At low concentrations, the process is carrier-mediated, and, at higher concentrations, absorption occurs via passive diffusion. Active transport is greatest in the jejunum and ileum (it is inhibited by alcohol consumption and by folic deficiency). Decline in thiamine absorption occurs at intakes above 5 mg. _ Wikipedia
The presence of anti-thiamin factors (ATF) in foods also contributes to the risk of thiamin deficiency. Certain plants contain ATF, which react with thiamin to form an oxidized, inactive product. Consuming large amounts of tea and coffee (including decaffeinated), as well as chewing tea leaves and betel nuts, have been associated with thiamin depletion in humans due to the presence of ATF. Thiaminases are enzymes that break down thiamin in food. Individuals who habitually eat certain raw freshwater fish, raw shellfish, and ferns are at higher risk of thiamin deficiency because these foods contain thiaminase that normally is inactivated by heat in cooking.
http://lpi.oregonstate.edu/infocenter/vitamins/thiamin/Thiaminase can also be produced by some gut bacteria, perhaps as a way of competing with other commensal species for carbohydrate released from resistant starch.
Thiamine is released by the action of phosphatase and pyrophosphatase in the upper small intestine. At low concentrations, the process is carrier-mediated, and, at higher concentrations, absorption occurs via passive diffusion. Active transport is greatest in the jejunum and ileum (it is inhibited by alcohol consumption and by folic deficiency). Decline in thiamine absorption occurs at intakes above 5 mg. _ Wikipedia
The presence of anti-thiamin factors (ATF) in foods also contributes to the risk of thiamin deficiency. Certain plants contain ATF, which react with thiamin to form an oxidized, inactive product. Consuming large amounts of tea and coffee (including decaffeinated), as well as chewing tea leaves and betel nuts, have been associated with thiamin depletion in humans due to the presence of ATF. Thiaminases are enzymes that break down thiamin in food. Individuals who habitually eat certain raw freshwater fish, raw shellfish, and ferns are at higher risk of thiamin deficiency because these foods contain thiaminase that normally is inactivated by heat in cooking.
In fact, it looks as though anti-thiamine factors of all classes might be prevalent in precisely those diets most often called in evidence to falsify the carbohydrate-insulin hypothesis of obesity: for example,
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.
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).
http://helid.digicollection.org/en/d/Js2900e/8.2.html
