Colouring in dog food

There seems to be a lack of scientific research into the subject of food colouring, present in most commercial dog foods, and any link to unwanted canine behaviour. There are however anecdotal reports where removal of food additives have resulted in an improvement in a dog’s behaviour.

At a neurobiological level additives are broken down in the intestine and carried through the bloodstream to the brain, where they can affect brain chemistry in a variety of different ways. Brown (2003) suggests that in particular petroleum-based dyes, such as tartrazine and erythrosine can act within the brain just like neurotransmitters; these fake neurotransmitters bind to receptors within nerves and deliver what Brown terms as “a false signal” resulting in unwanted firing within these nerves, and potential issues such as overactivity, aggression, and issues such as poor coordination and poor impulse control. 

Ward’s (1997) findings that synthetic food colourings in particular lead to attention deficit hyperactive disorder (ADHD) in children through the mechanism that Brown suggests, further supports Brown’s argument for food colouring as a potential “false” neurotransmitter. Ward suggested the reason for increased ADHD in children was linked to Zinc and or Iron deficiency, and that this in turn leads to elevated levels of copper within the blood, which in humans has been linked to periods of violence, learning disability, depression and hyperactivity. Toren et al (1996) also point out that Zinc deficiency reduces the production of melatonin and serotonin and that this reduction “could plausibly contribute to the kinds of behavioural disturbances found in children with ADHD”. 

Both Brown and Ward suggest that because nerves (together with the endocrine system) control almost all bodily functions, then small disturbances in nerve transmissions can affect behaviour; there is however little evidence to show what is a safe level of artificial colouring.

Silbergeld’s (1982) research into artificial colourings and behavioural change found that erythrosin and tartrazine inhibited the uptake of neurotransmitters and precursors and in particular affected the levels of sodium, potassium and ATP in the brain, and that this reduction affected the ability of nerve terminals to take up and retain dopamine.

The European food safety authority conducted a study in 2011 looking at the safety of erythrosine, which is commonly used in cat and dog food, their findings show that erythrosine contains 56% iodine and that this high level of iodine can affect thyroid function, and in turn metabolism and behaviour, they also note that most commercial pet food manufacturers used up to 500 mg per kilogram (complete feed) and that this amount is excessive and should be reduced to no more than 18 mg per kilogram (complete feed) for dog and cat food; they note that research shows that excessive levels have led to allergy type symptoms, but they make no note of its effect on behaviour, other than to say that rats showed symptoms suggestive of an ADHD type disorder when fed the equivalent of 500 mg per kilogram.

So if artificial colours are so bad why are they in dog food? I believe there are several reasons, firstly while there is a substantial body of evidence that hyperactivity in children and ingesting food colourings are linked, not all authorities agree; and while veterinarians suggest they have seen “substantial rises in … behavioural issues linked to artificial additives” (Daily Mail 2008), artificial colouring (along with other artificial additives) remain legal and there is no empirical evidence to support their removal.  

Secondly as consumers, we feel a need to have enticing looking food, because as a species humans rely on the look of food to tell us whether it is appetizing, and we believe this applies to our dogs. Visual enhancement of dog food can be achieved by both natural and artificial colouring (we only have to look at the likes of Beneful www.beneful.com to see the visual effects of colouring); our dogs however have little interest in the colour of the food as they rely much more on olfactory and palatability factors than foods visual appearance (Lindsay 2000). 

And lastly the vast majority of research into commercial pet food is carried out by the pet food manufacturers, through its various worldwide pet food manufacturers associations. So we could argue there is a conflict of interest between profitability (through the sale of manufactured pet food) and the health of the animals concerned.  The Pet Food Manufacturers' Association suggests there is no evidence that additives in pet food cause behavioural problems in dogs. They state:

"The use of additives in pet food is strictly regulated by the EU, the authorisation process is rigorous and pet food additives are regularly reviewed to ensure safety… Consumers want reassurance on additives, but not full listing… There is no peer-reviewed scientific evidence currently available, or that we are aware of, to suggest a link between behavioural problems in pets and additives in pet food."  (PFMA 2014).

The debate on the use of food colourings is set to continue, and many colourings once deemed “safe” are now banned worldwide for human consumption, but a few still used for pet foods. A study being undertaken by veterinarians in the UK on the behavioural effect of food colouring using 300 dogs is underway and while this is only a small number of dogs it will hopefully set the benchmark for future studies, which may, or may not prove, that artificial food colourings in manufactured dog foods lead to problem behaviours. Until this study is completed it would seem reasonable that food colouring related behavioural issues affecting children, be used as a blueprint for the regulation of artificial colouring use in pet food.

 

References

Brown, L. (2003) Diet and Behaviour: first do no harm. Retrieved 22^nd of December 2013 from http://www.iwu,edu/-wellness/environment_folder/nehaviour_noharm.htm

Daily Mail (2008) Vet’s warning over additives in food which could put your pet at risk. Retrieved 22^nd of December 2013 from http://www.dailymail.co.uk/news/article-1051189/Vets-warning-additives-food-pets-risk.html

European food safety authority (2011). Scientific opinion on the safety and efficacy of erythrosine in feed for cats and dogs. Retrieved 3^rd of January 2014 from http://www.efsa.europa.eu/en/efsajournal/pub/2447.htm

Lindsay, S.R. (2000) Handbook of applied dog behaviour and training volume 1. Blackwell publishing. Iowa.

PFMA (2013). Prepared pet foods deliver optimum nutrition. Retrieved 12^th of December 2013 from http://www.pfma.org.uk/news/press-releases/prepared-pet-foods.cfm

Toren, P., Eldar, S., Sela, B.A., Wolmer, L., Weitz, R., Inbar, D., Koren, S., Reiss, A., Weizman, R., Laor, N. (1996) zinc deficiency in attention deficit hyperactivity disorder. Retrieved 10^th of December 2013 from http://www.fabresearch.org/423

Ward, N.I. (1997) Assessment of clinical factors in relation to child hyperactivity. Retrieved 22^nd of December 2013 from http://hriptc.org/zinc_defficiency.html

Canine Epilepsy

Canine epilepsy is a brain disorder that is manifested in the form of recurrent seizures, and is the most common chronic neurological disorder seen in dogs. The majority of dogs being diagnosed with idiopathic epilepsy, which is often described as having no underlying cause, though it is thought to have a genetic basis, are diagnosed between the age of 3 and 5 (Chandler 2011). Nearly all breeds of dogs have recorded incidents of idiopathic epilepsy and when we compare them with other domestic animals, the dog has the highest incidence of epilepsy, ranging from 0.5% to 4.1% dependent on breed. Seizures that occurred before or after this age range are more likely to be caused by infection, trauma, a metabolic disorder, or some other measurable disease process (Oberbauer, Grossman, Irion, Schaffer, Eggelston & Famula 2002). 

The University of Prince Edward Island (UPEI) (2014) have compiled a database of canine inherited disorders, in which they cite idiopathic epilepsy as a genetic disorder, and while the exact genetic make-up of this disorder is largely unknown, they suggest that more than one gene is involved. This is supported by Oberbauer et al (2002) who state that ‘there is a growing body of evidence that supports a hereditary basis for idiopathic epilepsy in the dog’, and by Rusbridge (2014) who describes a late onset form of epilepsy called Lafora’s disease (usually occuring in animals over seven years of age), which is found in the Miniature Wire-Haired Dachshund, Basset hound and Beagle, and suggests this disease is caused by an autosomal recessive inheritance, in which both parents will either carry or have the disease, with the Beagle showing a more severe form of the disease.

It is important to rule out one-off causes of a seizure such as heatstroke (which is not uncommon in puppies, just as febrile convulsions occur in humans), as a one-off episode of seizure shouldn’t be used as an indicator of a serious breed-related problem. In March 2014, the UK Kennel Club approved a DNA Lafora test which has been developed in Canada and the results are held in the Kennel Club database, through the dog’s registration details, and then published in the club’s breed supplement; through this process the Club states it aims that ‘responsible breeders can safely use all dogs not suffering from this condition, to eliminate this condition over time, to protect the diversity of the breed, without producing affected dogs’, but they do note that this is only a recommended test, and that the aim is only as good as the information they receive from responsible breeders (The Kennel Club 2014) 

Veterinarians rely heavily on the accounts of owners to reach their diagnosis, some of which may not know their dog has had a seizure, because while a major seizure that has the dog paddling on the ground with complete loss of motor control is easily comprehended, a minor seizure may appear as a slight loss of muscle control, or even just a loss of attention (called an absence); and often the episode is over by the time the vet is called, so the use of video is often recommended to confirm epilepsy and drive the correct treatment regime (Hahn 1997).

The first line of treatment for canine epilepsy is the use of barbiturates, such as phenobarbital, or potassium bromide (Compass 2014), both of which work to inhibit the nerve impulses (although by differing mechanisms). Munana (2009) suggests that only about 20 -30% of dogs achieve a good level of control without serious side effects, mainly sedation and vomiting, so often owners will reduce or stop medication to negate the side effects. Conversely owners may seek out excess medication, by exploiting the fact that Veterinarians rely on owner reporting of suspected seizures.

Dryden-Edwards (2014) suggests that a rise in the use of stimulating drugs, such as cocaine, and methamphetamine, has seen an increase use of barbiturates (downers) to counteract the ‘excitement’ phase of drug abuse, when the user needs to appear ‘normal’ with the resulting need to continue as the brain develops a dependence on the barbiturate, which causes withdrawal symptoms when the drug is withheld

Fremuth (2003), suggests, in her article for the Australian Shepherd Journal, that many of the above mentioned factors come into play when breeders are faced with a breeding dog with idiopathic epilepsy, she suggests that many breeders will not openly discuss if there is epilepsy in their breed and particularly in their stud, for fear of losing their status; also that just the suspicion of epilepsy in a breed can impact a breeder even if none of their dogs are affected; so the pressure to keep any hint of epilepsy ‘confidential’ is overwhelming.

Fermuth proposes the reasons that breeders would ‘hide’ whether their dog or dogs had epilepsy has many facets, the knowledge of seizures puts the breeder in a catch 22 position, if they mention seizures, to try to improve the line, then there is a reduction in the price they can achieve, but if they don’t mention it then they open themselves up to possible litigation. The fact that most idiopathic epilepsy begins in adulthood means that puppies are sold without any indication of whether they have the disease, and allows breeders to state ‘they had no idea’ when challenged. With the attitude that many breeders prefer not to know about epilepsy in their lines, it is difficult to make informed choices about appropriate matings. 

Budiansky (1999) suggests that one reason for the rise in inheritable diseases (which may or may not include idiopathic epilepsy) is that many breeds suffer from the ‘popular sire effect’ in that a successful champions is in great demand, commands high stud fees, and is likely to sire hundreds of litter, potentially swamping the gene pool with defective genes, often breeding out healthier ancestral lines.

Responsible breeders should be screening for inherited disorders, because it is the responsible thing to do, and it could be argued that these breeders will eventually be rewarded by producing health individuals that will command even higher prices, but there would need to be a change of emphasis from one of secrecy to one of openness, by making official test results public record, in order to reduce the production of epileptic individuals (Bell 2014).

References

Bell, J, S. (2014) Responsible Breeding Management of Genetic Disease, Retreived from http://www.tualatinkc.org/pdf/Responsible%20Breeding%20Management%20of%20Genetic%20Disease.pdf 25^th March 2014.

Budiansky, S. (1999), The Truth About Dogs, Retrieved from http://www.theatlantic.com/ideastour/animals/budiansky-full.html 26th March 2014

Chandler, K. (2011), treatment and monitoring of epilepsy in dogs, In Practice 2011;33:98-104

Compass (2014), [course notes], Module 4 Pharmacology.

Dryden-Edwards, R. (2014), Barbiturate Abuse Causes and Risks, Retrieved from http://www.emedicinehealth.com/drug-phenobarbital/page2_em.htm 26th March 2014

Fremuth, L.  (2003), The Epilepsy Underground, Australian Shepherd Journal, vol 13 (4). United States Australian Shepherd Association. Retrieved from http://www.dogstuff.info/epilepsy_underground_fremuth.html 26th March 2014

Hahn, J. (1997), When Epilepsy Strikes: Signs and Treatment for Dogs. Retrieved from http://vetmed.illinois.edu/petcolumns/petcols_article_page.php?PETCOLID=83&URL=0 26th March 2014

Munana, K. R. (2009), Newer Options for Medically Managing Refractory Canine Epilepsy, DVM 360. Retrieved from http://veterinarymedicine.dvm360.com/vetmed/Medicine/Newer-options-for-medically-managing-refractory-ca/ArticleStandard/Article/detail/608398 26th March 2014

The Kennel Club (2014), Kennel Club approves Lafora Test for Mini Wire Dachshunds, Retrieved from http://dachshundbreedcouncil.wordpress.com/2014/03/04/kennel-club-approves-lafora-test-for-mini-wire-dachshunds/ 8th april 2014

Oberbauer, A.M. Grossman, D.N. Irion, D.M. Schaffer, M.L. and Famula, T.R. (2002), The Genetics of Epilepsy in the Belgian Tervuren and Sheepdog. Retrieved from http://jhered.oxfordjournals.org/content/94/1/57.full 26th March 2014

Rusbridge, C. (2014) Lafora’s Disease. Retrieved from http://www.veterinary-neurologist.co.uk/lafora.htm March 2014. 26th March 2014

The University of Prince Edward Island (2014). Idiopathic epilepsy. Retrieved from http://ic.upei.ca/cidd/disorder/idiopathic-epilepsy