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When your child’s seizures do not respond to medication, the search for answers can feel overwhelming. For many families, the ketogenic diet has become an important option worth exploring. This medically supervised, high-fat, low-carbohydrate diet has helped children with drug-resistant epilepsy for over a century, and published case reports and small cohort studies suggest it may also be worth exploring for children with SCN2A-related disorders. Whether your child has an SCN2A diagnosis or you are exploring dietary therapies for epilepsy more broadly, this guide will walk you through how the diet works, what the research shows, the different diet types available, and what to discuss with your medical team before starting.
The ketogenic diet for epilepsy is not the same as the popular weight-loss version of keto you may have seen in headlines. It is a precise, medically prescribed dietary therapy designed to fundamentally change how the brain gets its energy. First developed in the 1920s by physicians who observed that fasting reduced seizures, it remains one of the most studied non-drug treatments for drug-resistant epilepsy, defined by the International League Against Epilepsy (ILAE) as epilepsy in which sustained seizure freedom has not been achieved despite adequate trials of two tolerated, appropriately chosen, and appropriately used antiseizure medication schedules.
Under normal conditions, the body burns carbohydrates (glucose) for fuel. The ketogenic diet drastically reduces carbohydrate intake and replaces it with fat, forcing the body into a metabolic state called ketosis. In ketosis, the liver converts fats into molecules called ketone bodies, which the brain uses as an alternative energy source. Researchers are still studying exactly why this shift reduces seizures, and no single mechanism has been established. Current theories suggest several possible mechanisms working together. Ketone bodies may reduce abnormal neuron firing that contributes to seizures. Fatty acids appear to affect ion channels the tiny gates that control electrical signals in brain cells. The metabolic shift may also activate protective genes that may help shield brain cells from damage. Additionally, early research suggests the diet may alter the gut microbiome in ways that could influence neurotransmitter levels in the brain, though this area of study is still in its early stages. The result, for many children, is fewer and less severe seizures ,though the exact combination of mechanisms likely varies from person to person.
There is no single “keto diet” for epilepsy. Medical teams choose from several versions depending on your child’s age, needs, and tolerance.
The most restrictive and most studied version uses a 4:1 ratio of fat to combined protein and carbohydrates — meaning for every four grams of fat, a child eats just one gram of protein and carbohydrates combined. Roughly 90% of daily calories come from fat. A 3:1 ratio may be used for infants, adolescents, or children who need higher protein intake for growth, though the ratio is individualized based on each child’s clinical response, tolerance, and nutritional needs — not age alone. This diet requires careful weighing and measurement of every meal and snack. While the classic diet has traditionally been started during a short hospital stay, outpatient initiation is increasingly common and is now offered by many programs.
Less restrictive than the classic version, the modified Atkins diet limits carbohydrates but does not require precise fat-to-protein ratios. It allows more flexibility for families and is often easier for older children and adults to follow. Research suggests it can be effective for seizure reduction, though evidence in adults is more limited.
The MCT diet uses a specific type of fat — medium-chain triglycerides — that produces ketones more efficiently. Because MCT oil is more ketogenic per calorie, this diet allows slightly more carbohydrates and protein than the classic version, giving families more variety in meal planning.
The Low Glycemic Index Treatment focuses on carbohydrates that have a low glycemic index, meaning they raise blood sugar slowly. It is generally considered one of the less restrictive ketogenic options, though the choice of diet type depends on clinical judgment, not restrictiveness alone. Portion sizes are monitored but not weighed precisely.
The evidence base for ketogenic diets in epilepsy is substantial, though important limitations exist. A major Cochrane review analyzed 13 clinical trials with 932 total participants. Within the pediatric subset — four trials involving 385 children — those on ketogenic diets were approximately three times more likely to achieve complete seizure freedom and nearly six times more likely to experience at least a 50% reduction in seizures, compared to controls. However, the certainty of this evidence was rated “low to very low” due to small sample sizes and methodological limitations. Across published studies, approximately 40–50% of children with drug-resistant epilepsy who try the diet achieve at least a 50% reduction in seizures, and roughly 10–15% achieve complete seizure freedom.
The ketogenic diet is a first-choice treatment for GLUT-1 deficiency syndrome, a metabolic condition where the brain cannot properly use glucose, and for pyruvate dehydrogenase deficiency, where it provides an alternative fuel source that bypasses the metabolic block. It has also shown effectiveness for other conditions, including infantile spasms and Dravet syndrome. Adult outcomes have been less well-studied. In the adult trials included in the Cochrane review, no participants achieved complete seizure freedom, though some experienced seizure reduction with the modified Atkins diet. Some children respond within days to weeks, but three months is generally considered the minimum evaluation period before determining whether the diet is effective. The diet does not work for everyone.
For families navigating an SCN2A diagnosis, a natural question is whether the ketogenic diet might help. Published evidence includes both individual case reports and small retrospective cohort studies, though controlled SCN2A-specific trials do not yet exist. In one published case, an infant with a confirmed SCN2A mutation and early infantile DEE (historically called Ohtahara syndrome) achieved complete resolution of seizures and EEG abnormalities after starting the ketogenic diet at 39 days of age (Turkdogan et al., 2019). In another report, an infant with a de novo SCN2A mutation experiencing dozens of seizures per day saw a significant decrease in seizures after the ketogenic diet was added to ongoing antiseizure medications before two months of age (Tian et al., 2021). A third published case documented an infant with an SCN2A mutation and migrating focal seizures who responded to the ketogenic diet (Su et al., 2018). Beyond individual cases, a small retrospective cohort study of children with genetic mutations and drug-resistant developmental and epileptic encephalopathy found that all three SCN2A patients in the cohort achieved at least a 90% seizure reduction on the ketogenic diet (Ko et al., 2018). These reports are encouraging but have important limitations. Most involve infants who were receiving concurrent antiseizure medications, making it difficult to isolate the ketogenic diet as the sole cause of improvement. Sample sizes are small, and results may not generalize to all children with SCN2A mutations.
The ketogenic diet is not safe for everyone. Certain metabolic conditions are absolute contraindications, meaning the diet must not be used. These include fatty acid oxidation disorders, primary carnitine deficiency, pyruvate carboxylase deficiency, and porphyria. In these conditions, the body cannot safely process the high fat load the diet requires, and starting the diet could cause a life-threatening metabolic crisis. This is why a comprehensive baseline evaluation is essential before starting any ketogenic diet. International recommendations call for a medical, nutritional, and laboratory assessment before initiation, typically including blood counts, electrolytes and bicarbonate, calcium, liver and kidney function, fasting lipids, vitamin D, urinalysis, and in pediatric cases, a serum acylcarnitine profile, as recommended by the International Ketogenic Diet Study Group — along with any additional metabolic studies indicated by clinical judgment. Your medical team should evaluate your child for contraindicated conditions and establish baseline values for ongoing monitoring. It is important to distinguish pyruvate carboxylase deficiency (a contraindication) from pyruvate dehydrogenase deficiency (for which the ketogenic diet is a treatment of choice) — these are separate metabolic conditions with opposite implications for dietary therapy.
If you are considering the ketogenic diet for your child, preparation and ongoing support are essential.
The ketogenic diet must be initiated under medical supervision. Whether initiation takes place during a two- to three-day hospital stay or through an outpatient program depends on the diet type, your child’s age and clinical stability, center protocol, and family circumstances. Outpatient initiation is increasingly common and is now offered by many programs, particularly for the modified Atkins diet and LGIT. Routine fasting before initiation is no longer standard practice at most centers. Your medical team will likely include a neurologist and a registered dietitian with specialized experience in ketogenic dietary therapy. During initiation, the team will monitor your child’s blood sugar and ketone levels, watch for any adverse reactions, adjust the fat-to-combined-protein-and-carbohydrate ratio as needed, and train your family on how to weigh, measure, and prepare meals at home. This supervised start is essential — the diet involves a significant metabolic shift, and your child’s body needs to be monitored as it adjusts.
Daily life on the ketogenic diet requires commitment and consistency. For the classic ketogenic diet, every meal and snack must be precisely weighed and measured to meet specific macronutrient targets, and even small deviations can affect ketone levels and potentially seizure control. The modified Atkins diet and LGIT are generally less demanding — they limit carbohydrates but do not require the same level of precision with every meal. Many families find that batch cooking, meal planning, and preparing keto-friendly options in advance helps manage the daily workload. For families on the classic diet, a digital food scale becomes one of the most important tools in the kitchen. It is also important to coordinate with your child’s school, daycare, or other caregivers to ensure the diet is followed consistently outside the home. Connecting with other families who have navigated the diet can provide practical tips, recipes, and encouragement. You can explore our latest articles for insights from the rare disease community on managing complex treatment plans.
Like any medical treatment, the ketogenic diet carries potential side effects that require careful monitoring. Common short-term effects include vomiting, constipation, diarrhea, hypoglycemia (low blood sugar), dehydration, and metabolic acidosis, particularly during the initiation period. Excessive ketosis can also occur and requires prompt medical attention. Longer-term concerns may include kidney stones, elevated cholesterol, reduced bone density, slowed growth, bone fractures, nutritional deficiencies, and weight loss in children. Children taking carbonic anhydrase inhibitors such as topiramate or zonisamide alongside the ketogenic diet face an increased risk of metabolic acidosis and kidney stones, and this combination requires especially close monitoring. Families should work with their medical team to develop an individualized illness and emergency plan. This plan should address what to do in the event of prolonged vomiting, inability to maintain fluids, symptomatic hypoglycemia, severe lethargy, or excessive ketosis, situations that may require temporary diet modification or medical intervention. This is especially important for infants and young children, who are more vulnerable to these complications.
Regular monitoring by your medical team is critical. Most children on the diet require a carbohydrate-free multivitamin and mineral supplement along with calcium and vitamin D. Additional supplements such as B vitamins or selenium may be recommended based on your child’s individual needs and bloodwork results. Your dietitian will schedule regular appointments to track your child’s growth, bloodwork, and overall nutritional status. Kidney function and bone density may also need periodic monitoring, especially if your child remains on the diet for an extended period.
Before starting any dietary therapy, have a thorough conversation with your child’s neurologist. Consider asking these questions:
Is the ketogenic diet appropriate for my child’s specific type of epilepsy and mutation?
Which version of the ketogenic diet do you recommend, and why?
What is a realistic timeline for seeing results? How will we monitor for side effects?
What nutritional supplements will my child need?
Under what circumstances would we consider stopping the diet?
Are there any medications my child is currently taking that could interact with the diet?
Writing these questions down before your appointment can help ensure nothing is missed. Your neurologist and dietitian are your partners in this decision, and a thorough conversation upfront can set realistic expectations and help you feel confident in the path forward.
No family should have to navigate a complex diagnosis or treatment decision alone. The SCN2A Foundation connects families, caregivers, researchers, and clinicians who share a commitment to improving outcomes for children with SCN2A-related disorders. Whether you are just learning about the ketogenic diet or already managing it at home, being part of a community that understands your journey matters. You can join the SC2NA Worldmap to others with similar variants find support, or participate in our Contact Registry. Every family navigating an SCN2A diagnosis deserves answers, community, and hope. The work to find them depends on your support. Please consider making a donation to help fund the research and resources that move us all forward.
This content is provided for educational and informational purposes only and does not constitute medical advice. The information on this page is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the guidance of a qualified healthcare provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.
Martin-McGill, K.J., et al. (2020). Ketogenic diets for drug-resistant epilepsy. Cochrane Database of Systematic Reviews. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD001903.pub5/full
Epilepsy Foundation. Ketogenic Diet. https://www.epilepsy.com/treatment/dietary-therapies/ketogenic-diet
Cleveland Clinic. Ketogenic Diet (Keto Diet) for Epilepsy. https://my.clevelandclinic.org/health/treatments/7156-ketogenic-diet-keto-diet-for-epilepsy
CURE Epilepsy. Keto Diet for Epilepsy. https://www.cureepilepsy.org/understanding-epilepsy/treatments-and-therapies/keto-diet-for-epilepsy/
Turkdogan, D., et al. (2019). Ketogenic diet as a successful early treatment modality for SCN2A mutation. Brain and Development. https://pubmed.ncbi.nlm.nih.gov/30415926/
Tian, X., et al. (2021). Ketogenic diet in infants with early-onset epileptic encephalopathy and SCN2A mutation. Yonsei Medical Journal. https://pubmed.ncbi.nlm.nih.gov/33779092/
Su, D.J., et al. (2018). SCN2A mutation in an infant presenting with migrating focal seizures and infantile spasm responsive to a ketogenic diet. Brain and Development. https://pubmed.ncbi.nlm.nih.gov/29625812/
Kwan, P., et al. (2010). Definition of drug resistant epilepsy. Epilepsia. https://pubmed.ncbi.nlm.nih.gov/19889013/
Kossoff, E.H., et al. (2018). Optimal clinical management of children receiving dietary therapies for epilepsy: Updated recommendations of the International Ketogenic Diet Study Group. Epilepsia Open. https://discovery.ucl.ac.uk/id/eprint/10053983/
Ko, A., et al. (2018). The Efficacy of Ketogenic Diet for Specific Genetic Mutation in Developmental and Epileptic Encephalopathy. Frontiers in Neurology, 9, 530. https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2018.00530/full
American Epilepsy Society. (2026). Clinical Practice Guideline: Infantile Epilepsy. Epilepsy Currents. DOI: 10.1177/15357597261433266. https://aesnet.org/infantile-epilepsy-guidelines
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When your child’s seizures do not respond to medication, the search for answers can feel overwhelming. For many families, the ketogenic diet has become an important option worth exploring. This medically supervised, high-fat, low-carbohydrate diet has helped children with drug-resistant epilepsy for over a century, and published case reports and small cohort studies suggest it may also be worth exploring for children with SCN2A-related disorders. Whether your child has an SCN2A diagnosis or you are exploring dietary therapies for epilepsy more broadly, this guide will walk you through how the diet works, what the research shows, the different diet types available, and what to discuss with your medical team before starting.
The ketogenic diet for epilepsy is not the same as the popular weight-loss version of keto you may have seen in headlines. It is a precise, medically prescribed dietary therapy designed to fundamentally change how the brain gets its energy. First developed in the 1920s by physicians who observed that fasting reduced seizures, it remains one of the most studied non-drug treatments for drug-resistant epilepsy, defined by the International League Against Epilepsy (ILAE) as epilepsy in which sustained seizure freedom has not been achieved despite adequate trials of two tolerated, appropriately chosen, and appropriately used antiseizure medication schedules.
Under normal conditions, the body burns carbohydrates (glucose) for fuel. The ketogenic diet drastically reduces carbohydrate intake and replaces it with fat, forcing the body into a metabolic state called ketosis. In ketosis, the liver converts fats into molecules called ketone bodies, which the brain uses as an alternative energy source. Researchers are still studying exactly why this shift reduces seizures, and no single mechanism has been established. Current theories suggest several possible mechanisms working together. Ketone bodies may reduce abnormal neuron firing that contributes to seizures. Fatty acids appear to affect ion channels the tiny gates that control electrical signals in brain cells. The metabolic shift may also activate protective genes that may help shield brain cells from damage. Additionally, early research suggests the diet may alter the gut microbiome in ways that could influence neurotransmitter levels in the brain, though this area of study is still in its early stages. The result, for many children, is fewer and less severe seizures ,though the exact combination of mechanisms likely varies from person to person.
There is no single “keto diet” for epilepsy. Medical teams choose from several versions depending on your child’s age, needs, and tolerance.
The most restrictive and most studied version uses a 4:1 ratio of fat to combined protein and carbohydrates — meaning for every four grams of fat, a child eats just one gram of protein and carbohydrates combined. Roughly 90% of daily calories come from fat. A 3:1 ratio may be used for infants, adolescents, or children who need higher protein intake for growth, though the ratio is individualized based on each child’s clinical response, tolerance, and nutritional needs — not age alone. This diet requires careful weighing and measurement of every meal and snack. While the classic diet has traditionally been started during a short hospital stay, outpatient initiation is increasingly common and is now offered by many programs.
Less restrictive than the classic version, the modified Atkins diet limits carbohydrates but does not require precise fat-to-protein ratios. It allows more flexibility for families and is often easier for older children and adults to follow. Research suggests it can be effective for seizure reduction, though evidence in adults is more limited.
The MCT diet uses a specific type of fat — medium-chain triglycerides — that produces ketones more efficiently. Because MCT oil is more ketogenic per calorie, this diet allows slightly more carbohydrates and protein than the classic version, giving families more variety in meal planning.
The Low Glycemic Index Treatment focuses on carbohydrates that have a low glycemic index, meaning they raise blood sugar slowly. It is generally considered one of the less restrictive ketogenic options, though the choice of diet type depends on clinical judgment, not restrictiveness alone. Portion sizes are monitored but not weighed precisely.
The evidence base for ketogenic diets in epilepsy is substantial, though important limitations exist. A major Cochrane review analyzed 13 clinical trials with 932 total participants. Within the pediatric subset — four trials involving 385 children — those on ketogenic diets were approximately three times more likely to achieve complete seizure freedom and nearly six times more likely to experience at least a 50% reduction in seizures, compared to controls. However, the certainty of this evidence was rated “low to very low” due to small sample sizes and methodological limitations. Across published studies, approximately 40–50% of children with drug-resistant epilepsy who try the diet achieve at least a 50% reduction in seizures, and roughly 10–15% achieve complete seizure freedom.
The ketogenic diet is a first-choice treatment for GLUT-1 deficiency syndrome, a metabolic condition where the brain cannot properly use glucose, and for pyruvate dehydrogenase deficiency, where it provides an alternative fuel source that bypasses the metabolic block. It has also shown effectiveness for other conditions, including infantile spasms and Dravet syndrome. Adult outcomes have been less well-studied. In the adult trials included in the Cochrane review, no participants achieved complete seizure freedom, though some experienced seizure reduction with the modified Atkins diet. Some children respond within days to weeks, but three months is generally considered the minimum evaluation period before determining whether the diet is effective. The diet does not work for everyone.
For families navigating an SCN2A diagnosis, a natural question is whether the ketogenic diet might help. Published evidence includes both individual case reports and small retrospective cohort studies, though controlled SCN2A-specific trials do not yet exist. In one published case, an infant with a confirmed SCN2A mutation and early infantile DEE (historically called Ohtahara syndrome) achieved complete resolution of seizures and EEG abnormalities after starting the ketogenic diet at 39 days of age (Turkdogan et al., 2019). In another report, an infant with a de novo SCN2A mutation experiencing dozens of seizures per day saw a significant decrease in seizures after the ketogenic diet was added to ongoing antiseizure medications before two months of age (Tian et al., 2021). A third published case documented an infant with an SCN2A mutation and migrating focal seizures who responded to the ketogenic diet (Su et al., 2018). Beyond individual cases, a small retrospective cohort study of children with genetic mutations and drug-resistant developmental and epileptic encephalopathy found that all three SCN2A patients in the cohort achieved at least a 90% seizure reduction on the ketogenic diet (Ko et al., 2018). These reports are encouraging but have important limitations. Most involve infants who were receiving concurrent antiseizure medications, making it difficult to isolate the ketogenic diet as the sole cause of improvement. Sample sizes are small, and results may not generalize to all children with SCN2A mutations.
The ketogenic diet is not safe for everyone. Certain metabolic conditions are absolute contraindications, meaning the diet must not be used. These include fatty acid oxidation disorders, primary carnitine deficiency, pyruvate carboxylase deficiency, and porphyria. In these conditions, the body cannot safely process the high fat load the diet requires, and starting the diet could cause a life-threatening metabolic crisis. This is why a comprehensive baseline evaluation is essential before starting any ketogenic diet. International recommendations call for a medical, nutritional, and laboratory assessment before initiation, typically including blood counts, electrolytes and bicarbonate, calcium, liver and kidney function, fasting lipids, vitamin D, urinalysis, and in pediatric cases, a serum acylcarnitine profile, as recommended by the International Ketogenic Diet Study Group — along with any additional metabolic studies indicated by clinical judgment. Your medical team should evaluate your child for contraindicated conditions and establish baseline values for ongoing monitoring. It is important to distinguish pyruvate carboxylase deficiency (a contraindication) from pyruvate dehydrogenase deficiency (for which the ketogenic diet is a treatment of choice) — these are separate metabolic conditions with opposite implications for dietary therapy.
If you are considering the ketogenic diet for your child, preparation and ongoing support are essential.
The ketogenic diet must be initiated under medical supervision. Whether initiation takes place during a two- to three-day hospital stay or through an outpatient program depends on the diet type, your child’s age and clinical stability, center protocol, and family circumstances. Outpatient initiation is increasingly common and is now offered by many programs, particularly for the modified Atkins diet and LGIT. Routine fasting before initiation is no longer standard practice at most centers. Your medical team will likely include a neurologist and a registered dietitian with specialized experience in ketogenic dietary therapy. During initiation, the team will monitor your child’s blood sugar and ketone levels, watch for any adverse reactions, adjust the fat-to-combined-protein-and-carbohydrate ratio as needed, and train your family on how to weigh, measure, and prepare meals at home. This supervised start is essential — the diet involves a significant metabolic shift, and your child’s body needs to be monitored as it adjusts.
Daily life on the ketogenic diet requires commitment and consistency. For the classic ketogenic diet, every meal and snack must be precisely weighed and measured to meet specific macronutrient targets, and even small deviations can affect ketone levels and potentially seizure control. The modified Atkins diet and LGIT are generally less demanding — they limit carbohydrates but do not require the same level of precision with every meal. Many families find that batch cooking, meal planning, and preparing keto-friendly options in advance helps manage the daily workload. For families on the classic diet, a digital food scale becomes one of the most important tools in the kitchen. It is also important to coordinate with your child’s school, daycare, or other caregivers to ensure the diet is followed consistently outside the home. Connecting with other families who have navigated the diet can provide practical tips, recipes, and encouragement. You can explore our latest articles for insights from the rare disease community on managing complex treatment plans.
Like any medical treatment, the ketogenic diet carries potential side effects that require careful monitoring. Common short-term effects include vomiting, constipation, diarrhea, hypoglycemia (low blood sugar), dehydration, and metabolic acidosis, particularly during the initiation period. Excessive ketosis can also occur and requires prompt medical attention. Longer-term concerns may include kidney stones, elevated cholesterol, reduced bone density, slowed growth, bone fractures, nutritional deficiencies, and weight loss in children. Children taking carbonic anhydrase inhibitors such as topiramate or zonisamide alongside the ketogenic diet face an increased risk of metabolic acidosis and kidney stones, and this combination requires especially close monitoring. Families should work with their medical team to develop an individualized illness and emergency plan. This plan should address what to do in the event of prolonged vomiting, inability to maintain fluids, symptomatic hypoglycemia, severe lethargy, or excessive ketosis, situations that may require temporary diet modification or medical intervention. This is especially important for infants and young children, who are more vulnerable to these complications.
Regular monitoring by your medical team is critical. Most children on the diet require a carbohydrate-free multivitamin and mineral supplement along with calcium and vitamin D. Additional supplements such as B vitamins or selenium may be recommended based on your child’s individual needs and bloodwork results. Your dietitian will schedule regular appointments to track your child’s growth, bloodwork, and overall nutritional status. Kidney function and bone density may also need periodic monitoring, especially if your child remains on the diet for an extended period.
Before starting any dietary therapy, have a thorough conversation with your child’s neurologist. Consider asking these questions:
Is the ketogenic diet appropriate for my child’s specific type of epilepsy and mutation?
Which version of the ketogenic diet do you recommend, and why?
What is a realistic timeline for seeing results? How will we monitor for side effects?
What nutritional supplements will my child need?
Under what circumstances would we consider stopping the diet?
Are there any medications my child is currently taking that could interact with the diet?
Writing these questions down before your appointment can help ensure nothing is missed. Your neurologist and dietitian are your partners in this decision, and a thorough conversation upfront can set realistic expectations and help you feel confident in the path forward.
No family should have to navigate a complex diagnosis or treatment decision alone. The SCN2A Foundation connects families, caregivers, researchers, and clinicians who share a commitment to improving outcomes for children with SCN2A-related disorders. Whether you are just learning about the ketogenic diet or already managing it at home, being part of a community that understands your journey matters. You can join the SC2NA Worldmap to others with similar variants find support, or participate in our Contact Registry. Every family navigating an SCN2A diagnosis deserves answers, community, and hope. The work to find them depends on your support. Please consider making a donation to help fund the research and resources that move us all forward.
This content is provided for educational and informational purposes only and does not constitute medical advice. The information on this page is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the guidance of a qualified healthcare provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.
Martin-McGill, K.J., et al. (2020). Ketogenic diets for drug-resistant epilepsy. Cochrane Database of Systematic Reviews. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD001903.pub5/full
Epilepsy Foundation. Ketogenic Diet. https://www.epilepsy.com/treatment/dietary-therapies/ketogenic-diet
Cleveland Clinic. Ketogenic Diet (Keto Diet) for Epilepsy. https://my.clevelandclinic.org/health/treatments/7156-ketogenic-diet-keto-diet-for-epilepsy
CURE Epilepsy. Keto Diet for Epilepsy. https://www.cureepilepsy.org/understanding-epilepsy/treatments-and-therapies/keto-diet-for-epilepsy/
Turkdogan, D., et al. (2019). Ketogenic diet as a successful early treatment modality for SCN2A mutation. Brain and Development. https://pubmed.ncbi.nlm.nih.gov/30415926/
Tian, X., et al. (2021). Ketogenic diet in infants with early-onset epileptic encephalopathy and SCN2A mutation. Yonsei Medical Journal. https://pubmed.ncbi.nlm.nih.gov/33779092/
Su, D.J., et al. (2018). SCN2A mutation in an infant presenting with migrating focal seizures and infantile spasm responsive to a ketogenic diet. Brain and Development. https://pubmed.ncbi.nlm.nih.gov/29625812/
Kwan, P., et al. (2010). Definition of drug resistant epilepsy. Epilepsia. https://pubmed.ncbi.nlm.nih.gov/19889013/
Kossoff, E.H., et al. (2018). Optimal clinical management of children receiving dietary therapies for epilepsy: Updated recommendations of the International Ketogenic Diet Study Group. Epilepsia Open. https://discovery.ucl.ac.uk/id/eprint/10053983/
Ko, A., et al. (2018). The Efficacy of Ketogenic Diet for Specific Genetic Mutation in Developmental and Epileptic Encephalopathy. Frontiers in Neurology, 9, 530. https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2018.00530/full
American Epilepsy Society. (2026). Clinical Practice Guideline: Infantile Epilepsy. Epilepsy Currents. DOI: 10.1177/15357597261433266. https://aesnet.org/infantile-epilepsy-guidelines
Vlad Magdalin
Accelerating research and treatment for SCN2A-related disorders.
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