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1 1 Ketosis on the Epileptic Brain By Silas Aho I m sure some of you reading this paper may remember a diet in the early 2000 s called the Atkins diet that was based on eating a diet high in fats/proteins and low on carbohydrates. This diet worked by switching the main fuel your body used (carbohydrates) to a new fuel source (fats/proteins). What is amazing is that although this diet was part of large diet craze focused on weight loss it could be also used for treatment of epilepsy, a debilitating neurological disease. The success of this diet as an epilepsy treatment centers on one kind of main molecule: Ketones or specifically ketosis. Ketosis: what is it, why is it important, how does it work? From a biochemical viewpoint, ketosis is a metabolic state in which ketones derived from the fatty acid stores are used preferentially in place of glucose (American Heritage Medical Dictionary). Ok so that was pretty wordy, but what it means is that ketones are a part of the fat stored in your body. Usually when you run out of glucose (this comes from carbohydrates that you eat) your body begins to use the fats that you have been storing up. This really only happens naturally if you haven t eaten for a while, for instance, if you are stranded on an island for an extended period of time. Obviously there is a better way to induce the use of ketones over glucose than to strand a person on an island with no food, and that is what this paper will explain. This metabolic state (ketosis) was discovered to reduce the amount of seizure an epileptic person would have and has since been used clinically for decades and in some cases have led to patients who were seizure- free for over a year (Wibisono, 2014). This is why ketosis is so exciting; changing someone s diet can result in lasting treatment from a debilitating neurological disease. So how exactly does the ketogenic diet work? There are currently two main diets for inducing ketosis metabolism; the ketogenic diet (KD) and the modified Atkins diet (MAD). Both diets include a large proportion of protein/fat consumption coupled with a decreased carbohydrate consumption, 4:1

2 2 ratio of fats/proteins to carbs in KD and a more palatable 60% fat, 30% protein and 10% carb in MAD (Azevedo de Lima, 2014). To see if the patient is in ketosis their urine is check for excess amounts of ketones which signify that they are metabolizing fats. As is science, we are never quite sure how biological systems work, we may have a good guess of how a specific system works, up until a new discovery that makes your work redundant. Having said that three ways that ketosis may work to reduce the amounts of seizures a person has; carbohydrate reduction, adenosine triphosphate sensitive potassium channels, mitochondria metabolism and glutamatergic synaptic transmission (Danial, 2013). Don t get too worked up on the names I ll explain. Both the KD and MAD work on the principle of reducing carbohydrate consumption while increasing fat and proteins, but how much of a factor are carbohydrates on the onset of seizures? A clinical study by Dr. Nika Daniel and associates of John Hopkins University School of Medicine found that a patient with decreased seizure activity on a KD diet had recurring seizures within one hour of an intravenous infusion of glucose (the product formed from carbohydrate metabolism). This shows that carbohydrates play some kind of role in the prevalence of seizures and, possibly by the depletion of glucose, seizure activity went down (Danial, 2013). In order to show how Ketosis or more accurately the ketogenic diet reduces seizures it is important to define what a seizure is and how it happens. A seizure is an increase in excitability in neurons that interfere with each other. Neurons are always sending signals throughout the brain in fractions of a second, it only becomes a problem when those signals are not coordinated well. I like to think of it in terms of a telephone operator in the 30 s who had to manually plug cords from one area of a control board to another in order for people on both ends of the phone call to talk to each other. Now imagine that the cords are not placed in the right area and the signal doesn t go anywhere, what s worse is now that electrical signal begins messing with other signals around itself until the breaker blows (seizure). This increase in neuronal excitability can cause large amounts of neurons in a specific area of

3 3 the brain to begin messing with each other and cause what is called a depolarization or spike, this spike can then lead to a seizure (Kandel, 2013). The first possible pathway that ketosis reduces seizures is called Adenosine triphosphate (ATP) sensitive potassium channels. The excitability of neurons that lead to a seizure can be reduced by using potassium which makes the neurons that would send out signals that would interfere with other neurons close- by calm down reduce seizure activity. To make potassium more available to reduce the excitability potassium channels need to be open. In order to open the potassium channels ATP is used. This is how ATP sensitive potassium channels gets its name. Mitochondria metabolism is the second pathway and is related to the ATP sensitive potassium pathway. If enough ATP are available to open channels dedicated to potassium then hopefully a seizure can be stopped but where does the ATP come from? Ketosis has been shown to increase the production of ATP from the mitochondria by reducing reactive oxygen species (Danial, 2013). This means that with the increase of ketones in the blood, the mitochondria work more efficiently and produce enough ATP to allow the opening on potassium channels that, in turn, decrease the excitability of neurons and hopefully reduces the number of seizures a person has. The final possible pathway for the reduction of seizures via the ketogenic diet is glutamatergic synaptic transmission. Similar to ATP sensitive potassium channels and mitochondria metabolism, glutamatergic synaptic transmission focuses on reducing the excitability of cortical neurons in patients with histories of seizures. Again reducing excitability in neurons for patients with epilepsy is important because it decreases the interference of signals between neurons that could lead to a seizure. By the pathway in figure 1 below it shows that as ketones in the blood increase, the amount of GABA (major inhibitory neurotransmitter) hyperpolarizes target neurons, which in turn inhibits the release of glutamate, a major excitatory neurotransmitter

4 4 It was shown through clinical research that as rats were fed a diet high in fats and proteins in sufficient levels to induce ketosis, the levels of GABA increased, leading to the possibility of increased GABA levels contributing to reduce seizure activity via ketosis (Azevendo de Lima, 2014). The clinical use of the ketogenic diet has been common place for over a decade now, with the most common form being the KD, while the MAD is becoming more useful for patients who have trouble with the ridged structure of the KD. In a clinical study of ketosis on epilepsy 9 patients were administered a high fat/protein low carbohydrate diet in the form of KD or MAD. From the study 39% of participants became seizure free using the KD. This high percentage of patients who became seizure free while on the KD prompted the international Ketogenic Diet Working Group (KDWG) to support the KD as an effective treatment of epilepsy. MAD has also been known to be effective for treatment of epilepsy, but not to the extent of KD. From the same clinical study, patients who could not tolerate the KD were

5 5 moved to the MAD but did not see the same seizure reduction as the KD. On average, patients on the MAD who did see seizure freedom lasted months before using other treatments (Simard- Tremblay, 2015). There are, however, draw backs to the use of ketosis on the treatment of epilepsy, the least of which is the loss of interest in food specific for the KD, I mean who would want to eat nothing but steak for the rest of their lives? When the high fat/protein diet becomes unpalatable, the MAD is still an option but has shown decreased seizure fighting ability. For the most part patients who move from the KD to MAD also use some form of seizure medication to help with the increased seizure response after quitting the KD (Simard- Trembley, 2015). It has also been a concern that prolonged use of a high fat/protein diet such as the KD can lead to other side effects such as constipation, hypoglycemia, kidney stones acidosis and reduced vascular function via hardening of the carotid artery (Kossoff, 2014). A study by Kwiterovich and colleagues at Johns Hopkins Medical institute sought to see what lipid levels would be in children from 4 months to 20 years after being subjected to KD in response to hard to control seizures. What the researchers found was after 6 months of the KD cholesterol, triglyceride and HDL were far above the 95 th percentile of a healthy population. The researchers, however, found that 66% had a 50% improvement in seizure activity, 17 were seizure free and 39 patients were less than 50% seizure free (Kwiterovich, 2003). However, the use of multi- vitamins and calcium tablets, along with supervision from a doctor, have helped lessen some of the more major side effects such as heart attacks from reduced vascular function (Wibisono, 2014). The future of ketosis to fight epilepsy is now to find pharmaceutical interventions that target similar pathways as the KD (ATP sensitive potassium channels, mitochondria metabolism and glutamatergic synaptic transmission), but with reduced side effects. The pathways are still not fully understood and will take more research into the field but it is still very interesting that changing to a diet of high fat/protein can lead to alleviation from epilepsy.

6 6 References The American Heritage Medical Dictionary, Houghton Miffin Harcourt (2008): , Web, 2015 Azevedo de Lima, Patricia, Leticia Pereira de Brito Sampaio, Na gila Raquel Teixeira Damasceno, Neurobiochemical mechanisms of a ketogenic diet in refractory epilepsy, Clinics, 69(10) 2014: Web Danial, NN., Hartman, AL., Stafstrom, CE., Thio, LL., How does the ketogenic diet work? Four potential mechanisms, Journal of child neurology (8): Web Kandel, Eric., Schwartz, James., Jessell, Thomas., Siegelbaum, Steven., Hudspeth, A.J., Principles of Nueral Science 5 th edition McGraw Hill, 2013: Print. Kwiterovich, Peter., Vinning, Eileen., Pyzik, Paula., Skolasky, Richard., Freeman, John., Effects of a High- Fat diet on Plasma Levels of Lipids, Lipoprotiens, and Apolipoproteins in Children, The journal of the American Medical Association, 2003: 290(7): Web Simard- Tremblay, Elisabeth., Berry, Patricia, Owens, Aaron., Cook, William., Sittner, Haley., Mazzanti, Marta., Huber, Jennifer., Warner, Molly., Shurtleff, Hillary., Saneto, Russell., High- fat diets and seizure control in myoclonic- astatic epilepsy: A single center s experience, Seizure, 25: Web Wibisono, Cinthyia., Rowe, Natalie., Beavis, Erin., Kepreotes, Helen., Mackie, Fiona., Lawson, John., cardamone, Michael. Ten- Year Single- Center Experience of the Ketogenic Diet: Factors Influencing Efficacy, tolerability, and compliance, the Journal of Pediatrics, (018). Web

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