Brain Conditions


Idiopathic epilepsy (IE) is the most common cause of chronic seizures in dogs and can have numerous adverse effects on dogs and owners. Disruptions in brain glucose metabolism can contribute to seizure frequency. Anti-epileptic drugs used to reduce or eliminate seizures commonly cause side effects which must be balanced with the benefits of reduced seizure frequency. 

Research by Purina  in partnership with the Royal Veterinary College of London showed that dietary supplementation - as an adjunct to treatment with anti-epilepsy medications - with nutrients including medium-chain triglycerides (MCTs) significantly reduced seizure frequency in more than two-thirds of the dogs, and reduced seizure frequency by at least 50% in almost half of the dogs studied.1

Adverse effects of canine epilepsy

IE can reduce the quality of the dog’s life as well as their lifespan. The impact of caring for a dog with IE may afect the owner’s quality of life and subsequent treatment decisions. In addition to seizures, canine IE also impairs dogs’ cognition.

An electroencephalogram (EEG) is a non-invasive procedure that displays the electrical activity generated by nerve impulses in the brain. Although not a tool typically available in private practice, dogs with epilepsy will have an abnormal EEG.


A study showed that the salivary cortisol level, a measure of stress, increases significantly after a seizure in both dogs and owners.2 In one study, increased seizure frequency was shown to be associated with significantly decreased quality of life for dogs as perceived by owners, as well as a concern for owners.3

Dogs with IE may show lower trainability, as shown by difficulty obeying a sit command, being slower to learn new tricks, and showing decreased attention spans; common anti-epileptic drugs may also worsen these behaviors.4 Dogs with epilepsy may also have difficulty finding dropped food, wander without purpose, and be less likely to recognize familiar people.5 This is even true for dogs under 4 years of age.

Finally, dogs with IE have also been shown to struggle with spatial memory tasks compared with controls, indicating that they have more difficulty navigating their environment or remembering the location of an item.6 Dogs with IE are more likely to develop cognitive dysfunction later in life.5

Brain glucose metabolism and seizures

In dogs and humans with epilepsy, there is a disruption in brain glucose metabolism. This may predispose them to subsequent seizures as well as cellular damage that can lead to neurodegeneration and cognitive impairment. Although it’s not possible to entirely replace glucose as an energy source, ketone bodies can provide an alternative. 

Dietary MCTs are a source of ketones, mitigating the metabolic consequences of epilepsy. MCTs are fats found in botanical oils. Octanoic acid, a medium-chain fatty acid derived from MCTs, can also be metabolized by the brain for energy.

presynaptic neuron, mcfas block ampa receptor, postsynaptic neuron

Research has shown that ketones and medium-chain fatty acids derived from MCTs have anti-seizure efects beyond their roles as energy sources.⁷–⁹ The mediumchain fatty acids also help restore mitochondrial function. Decanoic acid, one of the medium-chain fatty acids from MCTs, helps break the cycle of abnormal electrical activity by blocking the AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor on neurons.

Ketogenic diets have been used successfully in conjunction with medical therapy for many years to manage epilepsy in humans.¹⁰

Purina's research

Purina has investigated the role of MCTs in managing idiopathic epilepsy.

A double-blinded, crossover, clinical trial conducted by the Royal Veterinary College (London) evaluated MCT supplementation in dogs with IE. Dogs with refractory IE were fed either a control diet or a diet supplemented with MCTs for 3 months, then switched to the other diet for 3 months. Their medications were not changed.

With the MCT diet, 48% of the dogs that were previously refractory became treatment successes (achieved 50% or greater reduction in seizure frequency), and this included 14% that became completely seizure-free. Overall, 71% of the dogs significantly improved on the MCT diet.

A diet supplemented with MCTs also significantly improved two of four attention deficit/hyperactivity disorder (ADHD)-related behaviors and increased trainability, suggesting potential anxiety-reducing effects of MCT ketogenic diets.¹¹

Watch this video

to find out more about nutritional innovation to manage canine epilepsy.


Epilepsy can affect any dog

a helpful infographic on canine epilepsy

Key things to remember

  • When used as an adjunct to medical therapy in canine epilepsy, ketones and medium-chain fatty acids derived from MCTs provide alternative energy sources for the brain.
  • The ketones and medium-chain fatty acids resulting from MCT metabolism can have anti-seizure effects, which complement anti-epileptic medications.
  • Purina research showed that more than two-thirds of dogs with refractory epilepsy fed a diet supplemented with MCTs showed a reduction in seizures, and 14% of dogs became seizure-free.
  • Idiopatic epilepsy is associated with ADHD-related behaviors and reduced trainability, and MCT supplementation may improve some of these behaviors.

Find out more

1. Law, T. H., Davies, E. S., Pan, Y., Zanghi, B., Want, E., Volk, H. A. (2016). A randomised trial of a medium-chain TAG diet as treatment for dogs with idiopathic epilepsy. British Journal of Nutrition, 114, 1438–1447. Erratum in: British Journal of Nutrition, 2016; 115:1696

2. Packer, R. M. A., Volk, H. A., & Fowkes, R. C. (2017). Physiological reactivity to spontaneously occurring seizure activity in dogs with epilepsy and their carers. Physiology & Behavior, 177, 27–33. doi: 10.1016/j.physbeh.2017.04.008               

3. Chang, Y., Mellor, D. J., & Anderson, T. J. (2006). Idiopathic epilepsy in dogs: owners’ perspectives on management with phenobarbitone and/or potassium bromide. Journal of Small Animal Practice, 47, 574–581

4. Packer, R. M. A., McGreevy, P. D., Pergande, A., & Volk, H. A. (2018). Negative effects of epilepsy and antiepileptic drugs on the trainability of dogs with naturally occurring idiopathic epilepsy. Applied Animal Behaviour Science, 200, 106–113. doi: 10.1016/j.applanim.2017.11.008 

5. Packer, R. M. A., McGreevy, P. D., Salvin, H. E., Valenzuela, M. J., Chaplin, C. M., & Volk, H. A. (2018). Cognitive dysfunction in naturally occurring canine idiopathic epilepsy. PLOS One. doi: 10.1371/journal.pone.0192182

6. Winter, J., Packer, R. M. A., Volk, H.A. (2018c). Preliminary assessment of cognitive impairments in canine idiopathic epilepsy. Veterinary Record. 182(22), 663. doi: 10.1136/vr.104603

7. Kim, D. Y., Simeone, K. A., Simeone, T. A., Pandya, J. D., Wilke, J. C., Ahn, Y., Geddes, J. W., Sullivan, P. G., Rho, J. M. (2015). Ketone bodies mediate antiseizure effects through mitochondrial permeability transition. Annals of Neurology 78, 77–87. doi: 10.1002/ana.24424

8. Masino, S. A., Li, T., Theofilas, P., Sandau, U. S., Ruskin, D. N., Fredholm, B. B., Geiger, J. D., Aronica, E., Boison, D. (2011). A ketogenic diet suppresses seizures in mice through adenosine A₁ receptors. Journal of Clinical Investigation 121, 2679–2683. doi: 10.1172/JCI57813

9. Wlaź, P., Socała, K., Nieoczym, D., Łuszczki, J. J., Zarnowska, I., Zarnowski, T., Czuczwar, S. J., Gasior, M. (2012). Anticonvulsant profile of caprylic acid, a main constituent of the medium-chain triglyceride (MCT) ketogenic diet, in mice. Neuropharmacology 62, 1882–1889. doi: 10.1016/j.neuropharm.2011

10. Neal, E. G., Chaffe, H., Schwartz, R. H., Lawson, M. S., Edwards, N., Fitzsimmons, G. Cross, J. H. (2009). A randomized trial of classical and medium-chain triglyceride ketogenic diets in the treatment of childhood epilepsy. Epilepsia 50, 1109–1117. doi: 10.1111/j.1528-1167.2008.01870.x

11. Packer, R. M. A., Law, T. H., Davies, E., Zanghi, B., Pan, Y., & Volk, H. A. (2016). Effects of a ketogenic diet on ADHD-like behavior in dogs with idiopathic epilepsy. Epilepsy & Behavior, 55, 62–68. doi: 10.1016/j.yebeh.2015.11.014