Sunday, October 3, 2021

Ketogenic Diet – an alternative treatment for epilepsy

 

Epilepsy is a widely known disorder that is characterized by episodes of seizures. This disorder can either be inherited or be developed through life due to traumatic brain injuries. Epilepsy is caused by a change in the way neuronal messages fire. These neuronal messages are transmitted by electrical impulses called the Action Potential. Usually, the action potential reaches peak depolarization (+30 mv), followed by repolarization, and then returns to the resting state.  With epilepsy, there is either too much excitatory transmission, or not enough inhibitory transmission (Engelborghs et al., 2000). When either of these occur, they result in prolonged depolarization with continuous bursts of action potentials, which leads to hyperexcitability, resulting in a seizure.

The usual treatment for epilepsy is antiepileptic drugs (AED). AEDs have multiple modes of action that include membrane stabilizers, which include sodium and potassium channel blockers/inhibitors, decreasing neurotransmitter release, or GABAmimetics which alter the effects of GABA (Howard et al., 2011). There are constantly new AEDs being created, but despite advancements, “approximately 30% of children who develop epilepsy still experience uncontrolled seizures or intolerable side effects from AEDs.” (Sampaio, 2016). This has led to the use of alternative methods, one of them being the newly popularized Ketogenic diet (KD).

The KD includes a low-carbohydrate high-fat diet, in addition to a fair amount of meat for protein. It has become a mainstream dieting fad because of the fast results and lack of calorie counting. But alternatively, it can be used as a treatment for epilepsy. More specifically, the KD treatment for people who have not had success with AEDs. It is used when a patient has had no success and has a failed response to three different AEDs in the case of children and around five different AEDs for adults (Sampaio, 2016).

The KD has been used for centuries to treat epilepsy, but they didn’t truly understand the reason as to why it worked until the 1900’s, and even so, only theories exist to explain the phenomenon. There are two theories as to why the KD can be used as an alternative treatment for epilepsy. One of them involves glucose metabolism and how the KD greatly decreasing their glucose intake. Glucose produces the rapidly available energy that allows for seizure activity, so patients on the KD have low glucose energy levels. This causes the brain to use ketone bodies for energy instead which slows the energy availability, ultimately reducing seizure activity (D’Andrea et al., 2019). More recent studies have been exploring alterations of the KD such at the modified Atkins diet (MAD) which is a low glycemic index diet. Overall, these new modified KDs have shown great results in many cases, and if applied correctly, are a great alternative treatment for epilepsy.  

D'Andrea Meira, I., Romão, T. T., Pires do Prado, H. J., Krüger, L. T., Pires, M., & da Conceição, P. O. (2019). Ketogenic Diet and Epilepsy: What We Know So Far. Frontiers in neuroscience, 13, 5. https://doi.org/10.3389/fnins.2019.00005

Engelborghs, S., D'Hooge, R., & De Deyn, P. P. (2000). Pathophysiology of epilepsy. Acta neurologica Belgica, 100(4), 201–213.

Howard, P., Twycross, R., Shuster, J., Mihalyo, M., Rémi, J., & Wilcock, A. (2011). Anti-epileptic Drugs. Journal of Pain and Symptom Management, 42(5), 788–804. https://doi.org/10.1016/j.jpainsymman.2011.10.007

Sampaio, L. P. (2016). Ketogenic diet for epilepsy treatment. Arquivos De Neuro-Psiquiatria, 74(10), 842–848. https://doi.org/10.1590/0004-282x20160116


3 comments:

  1. So, I was able to find some recent research that corroborates your argument. In this specific article, “The Ketogenic and Modified Atkins Diet Therapy for Children with Refractory Epilepsy of Genetic Etiology,” the researchers were able to conclude that “the ketogenic diet is an effective treatment modality in children with refractory epilepsy of genetic etiology” (Jagadish et al., 2019). After multiple readings, however, I was unable to ascertain any specific parameters for what constitutes a “ketogenic diet” or a “modified Atkin’s diet.” This was strange to me, as the proportion of macronutrients alone can vary widely while still being defined as ketogenic, or rather there is immense variability within that single term. I am curious, then, if the anti-convulsant effects of the ketogenic and modified Atkin’s diet can be altered through manipulation of macronutrient ratios and their individual constituents (i.e. saturated fat versus unsaturated fat).

    Jagadish S, Payne ET, Wong-Kisiel L, Nickels KC, Eckert S, Wirrell EC. The Ketogenic and Modified Atkins Diet Therapy for Children with Refractory Epilepsy of Genetic Etiology. Pediatr Neurol. 2019 May; 94:32-37. doi: 10.1016/j.pediatrneurol.2018.12.012. Epub 2018 Dec 29. PMID: 30803845.

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  2. Hi Lixlia! I enjoyed reading your post about how the ketogenic diet can be used as an alternative treatment for epilepsy. I worked with a pharmacist who was on the ketogenic diet and she recommended I read the book, “The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally,” by Dr. Jason Fung. I did not get around to reading it, however, she explained the book essentially discusses, that the ketogenic diet along with intermittent fasting has been used as a way to treat type 2 diabetes and to reverse it. I found an article where Hussain et. al (2012) conducted a study to understand the effect of the low-calorie diet (LCD) versus low-carbohydrate ketogenic diet (LCKD). For the study, they recruited three hundred and sixty-three overweight and obese patients (and 102 of them had type 2 diabetes) for a 24-week diet intervention trial. The study found that both the LCD and LCKD had beneficial effects on changes in weight, body mass index, changes in waist circumference, blood glucose level, glycosylated hemoglobin, etc. However, interestingly, subjects who were on the LCKD showed results that the changes were more significant. It was also found that the dosage of anti-diabetic medications was decreased to half while some were discontinued in the subjects of the LCKD group. However, Hussain et. al (2012) also mentioned diabetic patients on the LCKD should be under strict medical supervision due to the LCKD potentially lowering the blood glucose levels to a dangerous level. Nevertheless, this study proposes that the ketogenic diet improves glycemic control and that this diet could potentially be used as an alternative treatment for other health conditions as well, such as type 2 diabetes.

    References:

    Hussain, T. A., Mathew, T. C., Dashti, A. A., Asfar, S., Al-Zaid, N., & Dashti, H. M. (2012).
    Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. Nutrition (Burbank, Los Angeles County, Calif.), 28(10), 1016–1021. https://doi.org/10.1016/j.nut.2012.01.016

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  3. Hi Lix,

    A lot of the refractory epilepsy patients I saw at Children’s for research were either on or had tried the keto diet before, and it’s a bit of a mixed bag. Like most epilepsy drugs, some patients respond well to it, and others not so much. Like you said, the underlying biological mechanism for how the keto diet works (and even how epilepsy works) isn’t entirely understood, so it’s difficult to know when exactly this treatment is indicated.

    I don’t think you mentioned this in your post, but another interesting theory that I have seen is that the ketogenic diet allows for more efficient conversion of glutamate to glutamine, which is a substrate for the inhibitory neurotransmitter, GABA. So basically it could have a dual effect by clearing glutamate from synapses and enhancing GABA release (Yudkoff et al., 2008). In reality, it’s probably a combination of all of these theories, so we may never be able to point to just one mechanism.

    References:
    Yudkoff, M., Daikhin, Y., Horyn, O., Nissim, I., & Nissim, I. (2008). Ketosis and brain handling of glutamate, glutamine, and GABA. Epilepsia, 49, 73–75. https://doi.org/10.1111/j.1528-1167.2008.01841.x

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