• Cheilanthes sieberi (Rock fern) [Mccleary, 1977]
  • Equisetum arvense [Cornell]
  • Pteridum aquilinum - Bracken [Cornell][Mccleary, 1977]
  • Marsilea drummondii - Nardoo [Cornell][Mccleary, 1977]
  • Marsilea augustifoliia and M. mutica[Mccleary, 1977]
  • Nephrolepis exaltata [Mehltreter FE]
  • Raw flesh and viscera of certain fish and shellfish [Cornell]
  • Scolopendrium vulgare - Hartstongue [PDR]
  • Bacteria: Bacillus thiaminolyticus, Clostridium sporogenes [Mccleary, 1977]
  • Veksunio ambiguus(Freshwater mussel) [Mccleary, 1977]
  • "Found in raw fish or polyhydroxyphenols found in certain food and beverages; for example, coffee, tea, blueberries, redcabbage and brussel sprouts (Groff&Gropper2000)" [HNS Cohen]


Thiaminases are enzmyes found in a few plants and the raw flesh and viscera of certain fish and shellfish. When ingested these enzymes split thiamin (Vitamin B1), an important compound in energy metabolism, and render it inactive.[Cornell]


"Thiaminases are enzymes that cleave the thiamin molecule and render it biologically inactive. Generally there are two types of thiaminases: "
Type I - "Thiatninase I occurs in a wide range of fiih, shellfish, ferns and bacteria" [Mccleary, 1977] "It acts by displacing the pyrimidine methylene group with a nitrogenous base or SH-compound to eliminate the thiazole ring. "
Type II - "thiaminase II has so far been obtained only from culture fluids of various bacteria and yeastlike fungi" "...this type acts through the hydrolytic cleavage of the methylene-thiazole-N bond to yield pyrimidine and thiamin moieties."
"Both types of thiaminase require a cosubstrate - usually an amine or sulfahydryl-containing compound such as proline or cysteine. Once the thiamin molecule is cleaved by a thiaminase the body is incapable of restoring it. Thus, the ingestion of significant amounts of thiaminases can induce thiamin deficiency even though there may be a sufficient amount of thiamin in the diet." [Cornell]


"There are two sources of thiamine: dietary and a bacterial source where by it is synthesised by the normal intestinal microflora. Thiamine is absorbed from the small intestine by a saturable rate-limiting transport mechanism. The absorption of thiamine in the gastrointestinal tract can be impaired by the presence of naturally occurring thiaminases..." [HNS Cohen]

"Brewer’s yeast, lean meat and legumes are considered the richest sources of thiamine.... it is possible to lose up to 85% of the thiamine content in meat through cooking and canning, and up to 60% from cooking vegetables (Tanphaichitr1999). There is also loss through refining of grains and in some countries the fortification of wheat flour with B vitamins is mandatory to compensate for this loss" [HNS Cohen]

"The body only stores a small amount of thiamine and signs of deficiency tend to develop within 15–18 days of restricted intake" [HNS Cohen]

"Two mechanisms for the enzymatic fission of thiamine have been reported. The first involves the enzyme thiaminase I...) which catalyses the decomposition of thiamine by a base exchange reaction involving a nucleophilic displacement on the methylene group of the pyrimidine moiety [1].The second mechanism is a hydrolytic fission of thiamine involving the enzyme thiaminase II ...."

Many thiaminases are denatured by heat, but apparently vary in their heat stability.[Cornell] "The temperature for 50% denaturation is 60-65o" [Mccleary, 1977]

Subjecting thiaminases found in some types of raw fish and fish entrails to cooking or other heat treatment will render those thiaminases inactive enough to prevent thiamin deficiency in carnivores. The original inhabitants of Australia soaked thiaminase-rich nardoo in water for a time and cooked them into bread and soup before ingesting them, thus avoiding the thiamin deficiency symptoms presented by people who eat nardoo raw. Fern thiaminases may not be completely destroyed by cooking, so until it is clearly established which combinations of cooking time, cooking pressure and cooking temperature is needed to eliminate pteridophyte thaminase, caution should be exercised in consuming ferns as human food. [Cornell] "thiaminase is highly heat-resistant" [Cheryll Williams]

Signs of Thiamine Deficiency in Humans

In humans thiamin deficiency leads to a disease termed "beri-beri". Symptoms of beri-beri are basically the same as thiamin deficiency in other non-ruminants - anorexia, cardiac enlargement, and muscular weakness leading to ataxia. However, the disease has been divided into the following two forms:

1.Dry beri-beri - usually without cardiac involvement, this form of the disease is typified by atrophy of the legs and peripheral neuritis. It occurs mainly in adults.
2.Wet beri-beri - the primary sign of this form of the disease is cardiac enlargement and edema. [Cornell]

"thiaminase... causes polioencephalomalacia." [Riet-Correa PPMRT]

Signs of Thiamine Deficiency in Ruminants

Thiamin deficiency in ruminants manifests itself as polioencephalomalacia. Signs of polioencephalomalacia include disorientation and wandering, blindness and opishotonus or retraction of the head. The brain of infected animals becomes inflamed and edematous. Ruminants will also show symptoms as seen in other animals - anorexia, poor feed utilization and weakness. [Cornell]

Normally ruminants are fairly resistant to thiamin deficiency since rumen microbes provide the animal with sufficient amounts of thiamin. However, the ingestion of thiaminases will lead to polioencephalomalacia. Additionally, young growing ruminants, especially cattle and sheep, fed high-grain diets are especially susceptable. Diets high in grains can encourage the growth of certain thiaminase-producing bacteria in the rumen. These bacteria, including Clostridium sporogenes and a few species of Bascillus can produce enough thiaminases to induce thiamin deficiency.[Cornell]

"Induced thiamine deficiency, which causes a nervous condition especially in monogastric animals such as pigs and horses, but has been induced experimentally in sheep (Evans et al. 1975).This is caused by a Type 1 thiaminase (Evans 1976b). In cattle ingestion of an amount (greenordry)equal to the animal's weight over 3-4 months results in overt symptoms followed by death in 1-4 days;" [Marrs&Watt, 2006] "Bracken fern causes a nervous condition in animals.... Its earliest signs consist of anorexia and ataxia but these may proceed to opisthotonus, convulsions and death with irreversible lesions of polioencephalomalacia present in the brain. The early signs respond well to thiamine administration." [Acamovie PPRT] "Feeding a diet of 15–30% rhizome mixed with green grass to sheep produced thiamine deficiency within a month (Meyer 1989)." [Fernandez WWF]


"Bracken fern, rock fern and mussel enzymes were partially purified to final sp acts of 0.30,0.25 and 0.10 pkat/m protein, respectively." [Mccleary,1977]

Bracken Fern (Pteridum aquilinum)

Bracken fern is widespread in humid temperate areas including the North American West Coast, Europe, Japan, Australia, and New Zealand. The highest thiaminase activity is in the rhizomes, but all areas of the plant contain some thiaminase and show seasonal variability..." [Cornell] "Activity in lush bracken fronds did not exceed a value of 4 mg thiamine hydrolysed/hr/g dry wt." [Mccleary,1977] "The thiaminase activity of bracken is highest in rhizomes, especially in the summer, and in the croziers but declines with maturation of the plant." [Acamovie PPRT]

"The most active co-substrates found in bracken fern extracts by Watkin et al. [19] were proline and hydroxyproline. These two and adenine are good co substrates for the thiaminase I from nardoo." [Mccleary,1977]


Non-ruminants consuming significant amounts of bracken fern in their diet will exhibit signs of thiamin deficiency. Horses fed hay with greater than twenty percent bracken fern will begin to be symptomatic within a month.[Cornell]

Horsetails (Equisetum arvense)

Horsetails are widespread in moist areas of the United States and Canada and contian significant thiamin activity. The most common instance of thiamase poisoning resulting from horsetails is the contamination of hay with horsetails. A horse consuming hay containing twenty percent or more of horsetail plants will show signs of thiamin deficiency in two to five weeks.[Cornell] "Thiaminase, which causes this [thiamine (vitamin B1) deficiency], is destroyed by heat, so is not present in a horsetail tea or syrup." [BackMed]

"Despite reported benefits of silicon, it seems prudent that infants, young children, and pregnant women not ingest horsetail for extended periods, unless its thiaminase enzyme has been deactivated (Reichert, 1994)." [HMH Duke]


"Lush nardoo fronds contain much higher levels of activity than any of the other species investigated-5 times that of rock fern and mussel and 100 times that of bracken. " [Mccleary,1977]

"Fronds of nardoo contain extremely high levels of thiaminase I enzyme. Activity appears to be related to lushness of growth of the plant.... High activities,relative to those in bracken fern, were found all year round. However, highest values appear to be associated with the initial surge of growth following heavy rainfall and flooding....In June, 1976,even though the fronds still appeared quite lush and there was still an ample supply of water, activity values had decreased by about 5 fold. Hot dry weather... also resulted in a rapid decrease in activity." [Mccleary,1977]

Historical Perspectives

The story of Australian explorers, or why you should cook your ferns.

Okay, so legend has it, and so does Moorehead's book Cooper's Creek (1963), that a couple of Australian explorers, Robert Burke and Willliam Wills, died in 1861 from thiaminase poisoning. They were wandering around the Australian continent, doing what explorers do, and their supply of pork, which was their main source of thiamin, ran out. So what did these guys start feasting on? Nardoo, of course. Now, if they had watched the Aborigines they would have known that one does not eat nardoo without cooking it first. But, being typical explorers, and thus thinking that they were smarter than the indigenous people that had lived on the continent for thousands of years, Burke and Wills ate their nardoo raw. They began complaining in their journals of increasing weakness and starvation, but "not so much from absulute want of food" because, Wills wrote, "I have a good appetite and relish the nardoo much but it seems to give us no nutriment." What they were suffering from then, was thiamin deficiency. Coupling a low-thiamin diet with a large intake of thiaminases from the nardoo, Burke and Wills developed beri-beri. They complained not only of weakness, but of edema too, and sensitivity to cold. They died. [Cornell]

Ataxia from Silkworm Larvae

"In the early 1990s it was noticed that a form of ataxia occurred on a seasonal basis in southwest Nigeria. Ataxia is a neurological disorder that results in muscular incoordination, which can be particularly evident with walking. A dietary link was suspected, which was later confrmed, when heat-stable thiaminase was found in the larvae of Anaphe venata, a butterfly that utilises Triplochiton scleroxylon as its food plant. Te larvae, which provide a seasonal harvest in poor areas, have a food value similar to eggs – although the thiaminase activity is equivalent to that of Nardoo. Cooking the larvae does not detoxify the heat-resistant enzyme. The end result, in combination with a monotonous carbohydrate diet lacking B vitamins, is thiamine defciency." [Cheryll Williams]

"The edible larva of the Japanese Silkworm (Bombyx mori) also contains thiaminase, although the activity was less than one-third of that of Anaphe. Silkworms are less likely to be problematic because they are not usually incorporated into a thiamine-defcient diet". [Cheryll Williams]


  1. [Cornell] THIAMINASES, , Updated 05/22/2014, Accessed Feb 13, 2015,
  2. Marrs&Watt, 2006 - Biological Flora of the British Isles: Pteridium aquilinum (L.) Kuhn, R. H. Marrs and A. S. Watt, Journal of Ecology, Vol. 94, No. 6 (Nov., 2006), pp. 1272-1321