Thiamine (vitamin B1) is a water-soluble vitamin required by mammals for energy metabolism.1 The presence of carbohydrates in the diet increases the need for thiamine. It is minimally stored in the body, and thus must be constantly supplied in the diet. Thiamine can be synthesised by bacteria in the lower intestine of carnivores, however this does not result in sufficient thiamine availability to prevent deficiency.2
Cats and dogs rely on dietary thiamine to stay healthy. This may be from high-thiamine foods (such as meat and organs), or supplementation. An uncorrected thiamine deficiency can be fatal.3
"(meat) normally contains thiamin adequate to meet requirements of dogs and cats. Lean pork and organ meats such as heart, brain, liver and kidney are especially good sources of thiamin.”1
“carnivores do not synthesise thiamine or store significant amounts in the body and therefore depend upon a regular dietary intake to maintain good health.”4
Currently there exists no reference range for healthy blood levels of thiamine in cats and dogs.2 Establishing reference ranges will be challenging due to the great variability in thiamine requirements for individual cats and dogs. Requirements are affected by multiple factors such as: age, reproduction, genetics, illness, diet, parasitism and stress.1,4
Thiamine deficiency can be caused by the following:
Cooking or processing raw ingredients can result in up to a 50% reduction of thiamine levels.1
Thiaminases are enzymes that split thiamine, thus inactivating it. They are found in some plants, some species of raw fish and shellfish; and can be produced by some bacteria.5,1
A case report6 describes a team of sled dogs that were fed exclusively on frozen carp (a high thiaminase fish) for six months prior to the onset of thiamine deficiency symptoms. In previous years, they had eaten the same diet, but supplemented with fresh horse organs, and no deficiency had resulted.6 Deficiency has also been seen in mink and foxes fed large amounts of raw fish over time.5
In some cases, a varied diet is enough to offset the inhibitory effects of thiaminase. Lichtenberger7 describes the effect of thiaminase on carnivorous fish species:
“predatory fishes maintain a kind of balance between those prey fish rich in thiaminase and those fish rich in vitamin Bl. As long as the predator has a reasonably varied diet, it should get enough vitamin B1 to stay healthy."7
Thiaminase will degrade thiamine present in frozen fish over time.7 The thiaminase in fish should not be a problem for dogs and cats as long as fish is not fed with every thiamine-containing meal.1
Not all fish contain thiaminase, and in those that do, the amount varies. Thiaminase data has been collected for many fish species, including:8
Contain thiaminase:
Do not contain thiaminase:
Nowadays it is common for cats, dogs and ruminant production animals (such as cows and sheep) to be fed a diet high in grains. This is because grains are a very cheap source of energy. High grain diets negatively affect the health of pets and production animals in a number of ways. One if these is the effect on thiamine.
In ruminants, high grain diets favour the growth of bacterial species that can produce thiaminases, resulting in thiamine deficiency.5
The high carbohydrate content of grain-based diets leads to an increased thiamine requirement for cats and dogs. A diet higher in protein and fat does not have the same detrimental effect on thiamine levels:
"Because thiamin is specifically involved in carbohydrate metabolism, the requirement is raised when the dietary carbohydrate is increased relative to other energy-supplying components. The thiamin-sparing effects of protein and fat has been recognised."1,2
Thiamine deficiency may cause serious acute illness, which is usually rapidly fatal if untreated; or it may have subclinical effects on heath.1
The time it takes for acute illness to develop is variable, and based on numerous factors (diet composition, time on diet, life stage of animal etc). If caught early, deficiency can be completely reversed with thiamine injections.4,2
The clinical signs displayed in acute deficiency are variable, which makes diagnosis challenging.2 Sufferers are unable to fully utilise energy in their diets, so they lose condition and become weak. They may also display neurological, and cardiac dysfunction.5
Clinical signs in dogs may include (chronologically): anorexia, vomiting, lethargy, CNS depression, paraparesis, ataxia, spasticity, convulsions, and death (in some cases from acute cardiac failure).4 Cats may present with convulsions, hyperaesthesia, dilated unresponsive pupils, and death.11,4
Taking a comprehensive diet history is a vital diagnostic tool:
"the key historical finding (in thiamine deficiency) is feeding 'pet mince', 'pet meat’ or 'unrefrigerated food rolls' especially when there is a relationship in time between the development of signs and a change in the composition of the diet”12
The following are cases studies of thiamine-deficiency in cats and dogs. All the diets in the case reports had sulphite preservative added.1
A cat was hospitalised and treated for allergic infected dermatitis. She was put on a novel protein diet consisting solely of kangaroo meat and calcium carbonate powder for 38 days before she became symptomatic. She died soon after.13
A number of cats at a shelter succumbed to thiamine deficiency when they were fed on a fresh pet meat diet (the preservative was not declared on the label), even though it was supplemented (50:50) with canned food, and brewer's yeast (a source of thiamine). The canned meat ought to have provided adequate thiamine to the cats, however it was found that, in mixing the canned and the fresh pet meat, the sulphites in the fresh pet meat destroyed much of the thiamine in the canned food, resulting in deficiency.1
A German Shepherd died of thiamine deficiency after six weeks on fresh pet mince.1
Two Springer Spaniels were successfully treated for thiamine deficiency. They had been on a diet of fresh pet meat plus added vegetables and table scraps for a long time, however they were fed fresh pet meat exclusively in the three weeks prior to becoming symptomatic.1
Six Bouvier dogs developed deficiency on a diet of preserved “knacker’s yard” horse meat plus cereal and some “rendering residue.”1
A Golden Retriever was fed on pet meat, vegetables, rice and some biscuits. Six weeks prior to becoming symptomatic, the brand of pet meat was changed, and it was fed almost to the exclusion of the other foods.2
Three seven week old American Staffordshire puppies developed deficiency after being weaned at 3-4 weeks of age onto kangaroo mince, brewer’s yeast, flaxseed oil and cod-liver oil.2
A Maltese Terrier became deficient on an exclusive diet of non-refrigerated, sulphite-preserved pet roll.2
Supplementing extra thiamine in the diet is not enough to overcome the effects of sulphite preservatives. A diet may contain ample thiamine, but if it is routinely fed simultaneously with a food containing sulphites, the dietary thiamine will be largely inactivated, and deficiency will ensue.3,13
Sulphite preservatives are added to meat products because they prolong shelf life by masking the signs of spoilage without actually preventing putrefaction.3,1 In preservative-free meat, a putrid odour occurs when bacterial counts reach about 100 million per gram. In meat preserved with sulphites, the odour is not detectable until counts reach about 500 million per gram, at which point it is still considerably weaker than its preserved counterpart.1
The World Health Organisation recommends that sulphite preservatives be avoided, particularly in meat “because they can lead to deception regarding freshness and possible injury from the consumption of tainted meat.”1
Sulphite preservatives are not permitted in meat products (except sausages) intended for human consumption. Recently, sixteen Auckland butchers were fined for adding sulphite preservatives to their meat products.9 The Ministry of Health has warned of the potential for “serious reaction” if the additives were surreptitiously used in meat products:
“foods containing sulphur dioxide/sulphites can provoke asthma attacks, severe allergic reactions or gastric irritation.”9
For at least the last two decades it has been known that sulphite preservatives cause thiamine deficiency by rendering the vitamin inactive – yet despite this, they continue to be added to pet foods.3,10
"In addition to their effects on thiamine, sulphites have been associated with the full range of food intolerance symptoms in people, including headaches, irritable bowel symptoms, behavioural disturbances and skin rashes. They are well known for their ability to exacerbate asthma in human patients, which might be a pertinent consideration when managing cats with 'asthma', or dogs with chronic bronchitis or atopic dermatitis."12
Preservatives in food contribute to chronic anti-oxidative stress. This results in the suppression of T helper type 1 (Th1) immune responses, in favour of Th2 activation. Th2 responses promote asthma, allergies and obesity. Behavioural symptoms have also been noted.14
Preservatives, such as sulphites, can suppress the release of leptin (an important regulator of appetite and energy homeostasis). This may be contributing to the rise in obesity.14
There are numerous other additives and preservatives of concern commonly present in pet foods.
It is highly likely that many diseases, including autoimmune conditions, are being caused or exacerbated by the presence of these food industry substances. An epithelial barrier lines the gastrointestinal tract. The barrier is meant to determine which substances are allowed to cross over into the circulation, and which substances warrant an immune response. The barrier is made up of cells with tiny gaps (tight junctions) between them. Increased epithelial 'tight junction’ permeability (this is when the tiny gaps widen and allow substances to cross over to the circulation that would not normally gain access, a condition otherwise known as 'leaky gut') is a key factor in the development of autoimmune diseases. A range of food industry additives (including glucose, salt, emulsifiers, organic solvents, gluten, microbial transglutamase, and nanoparticles) have been shown to increase epithelial permeability – thus playing a role in the increasing incidence of autoimmune disease.15
Nitrites are a preservative used in human and pet food for their effects on colour, flavour, oxidation, and bacterial (clostridium botulinum) growth.11 They can cause acute, potentially fatal, toxicity (methaemoglobinaemia) via a reduced oxygen supply to tissues. Methaemoglobinaemia has also been noted in children associated with ingestion of nitrite-preserved sausages, and baby formula made with nitrite-contaminated water.11
In New Zealand, nitrites are used in chilled pet rolls. There are reports in the literature of commercial pet foods with excessive nitrite levels leading to illness and fatalities in pets. A case study in New Zealand describes the death and illness of five animals (pet cats and dogs) fed on a commercial pet food containing 140 times the AAFCO-approved acceptable upper limit of nitrites.11
Despite the known effects of sulphites and preservatives and additives, significant numbers of pets are still being exposed to them. The New Zealand Pet Food Manufacturers Association sets its own voluntary code of practice.10
“In New Zealand, the use of meat by-products from abattoirs is controlled by the Meat Act 1981 but the Act does not provide for any control over the composition of manufactured pet food. The Stock Foods Act 1982 dictates that manufacturers must state only the level of fat, protein, ash and antioxidants in prepared food intended for animal consumption. Section 9 on the Act prohibits the sale, or offer for sale, of stock food containing any ingredient injurious to the health of the stock for which it was intended… there was no industry guidelines or legislation that prescribe maximum levels of chemical preservatives such as nitrite.”11
An Australian study revealed that 15 of 16 pet mince samples tested contained sulphites, and 10 had levels up to 8 times higher than the allowable level in meat for human consumption.1 Another study showed that almost all pet minces and pet rolls analysed contained sulphites – however most of the labels either: failed to declare the preservatives; declared them at greatly lower levels than were present; or declared that they were preservative-free.12
The consumer is largely kept in the dark on this issue:
“As well as masking the signs of spoilage and bacterial contamination, which misleads the purchaser and increases the risk of food poisoning, the destruction of thiamin by S02 leads to a serious, life threatening nutritional deficiency.”1
1) Butchers fined for using unsafe preservatives in meat; April 21 2015, http://www.stuff.co.nz/business/better4business/67921029/Butchers-fined-for-using-unsafe-preservatives-in-meat
2) Call for action on harmful preservatives in pet food; The University of Sydney News, 29 April 2014, http://sydney.edu.au/news/84htnnl?newsstoryid=13411
3) Changes in intestinal tight junction permeability associated with industrial food additives explain the rising in incidence of autoimmune disease; A. Lerner, T. Matthias, Autoimmune Reviews (2015), http://dx.doi.org/10.1016/j.autrev.2015.01.009
4) Nitrate poisoning in cats and dogs fed a commercial pet food; A.J. Worth, S.J. Ainsworth, P.J. Brocklehurst & M.G. Collet, New Zealand Veterinary Journal (1997) 45:5, 193195, 10.1080/00480169.1997.36025
5) Nutrient Requirements of Mink and Foxes, 2nd Revised Edition; National Research Council. The National Academies Press (1982)
6) Plants Poisonous to Livestock; Cornell University Department of Animal Science, http://www.ansci.cornell.edu/plants/toxicagents/thiaminase.html
7) Sulphite preservatives in pet meats; R. Baral, CVE Control & Therapy Series (2014) 275
8) The good and bad of antioxidant foods: An immunological perspective; J.M. Gostner, K. Becker, F. Ueberall, & D. Fuchs; Food and Chemical Toxicology (2015) 80:72-79; http://dx.doi.org/10.1016/j.fct.2015.02.012
9) Thiaminase and its role in predatory pet fish (and other piscivores) nutrition; M. Lichtenberger; http://www.wetwebmedia.com/ca/volume_6/volume_6_1/thiaminase.htm
10) Thiamine deficiency due to sulphur dioxide preservative in ‘pet meat’ – a case of déjà vu; R. Malik & D. Sibraa; Australian Veterinary Journal (2005) 83:7
11) Thiamine deficiency in a cat associated with the preservation of ‘pet meat/ with sulphur dioxide; R.J.S. Steel; Australian Veterinary Journal (1997) 75:10
12) Thiamine deficiency in a team of sled dogs; D.M. Houston & T.J. Hulland; Canadian Veterinary Journal (1988) 29
13) Thiamine deficiency in cats and dogs associated with feeding meat preserved with sulphur dioxide; V.P. Studdert & R.H. Labuc; Australian Veterinary Journal (1991) 86:2
14) Thiamine deficiency in dogs and cats; P. Staples; Surveillance 24(3) 1997
15) Thiamine deficiency in dogs due to the feeding of sulphite preserved meat; M. Singh, M. Thompson, N. Sullivan & G. Child; Australian Veterinary Journal (2005) 83:7