Ketogenic diet and epilepsy pdf

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Skip to search form Skip to main content You are currently offline. Some features of the site may not work correctly. DOI: The Ketogenic Diet KD is a modality of treatment used since the s as a treatment for intractable epilepsy. It has been proposed as a dietary treatment that would produce similar benefits to fasting, which is already recorded in the Hippocratic collection.

History and Origin of the Ketogenic Diet

The Ketogenic Diet KD is a modality of treatment used since the s as a treatment for intractable epilepsy.

It has been proposed as a dietary treatment that would produce similar benefits to fasting, which is already recorded in the Hippocratic collection. Evidence shows that KD and its variants are a good alternative for non-surgical pharmacoresistant patients with epilepsy of any age, taking into account that the type of diet should be designed individually and that less-restrictive and more-palatable diets are usually better options for adults and adolescents.

Epilepsy is a disabling and common neurological disease, which can be controlled successfully in most patients with one or more antiepileptic drugs. Some of these patients are not surgery candidates, so it is necessary to search for alternative treatments for epilepsy such as palliative surgery, neuromodulation, and a ketogenic diet KD.

The classic ketogenic diet CKD consists of a high-fat and low-protein and carbohydrate diet, with restricted calories and fluids.

The diet mimics the fasting state, altering the metabolism to use fats as a primary fuel source; catabolism of fatty acids in the liver produces ketone bodies KB , which induces urinary ketosis Rho, Recent studies have found a significantly positive outcome with the use of the KD for treatment of refractory epilepsy in children and adults Barborka, ; Neal et al. Regardless of the efficacy of the KD, most patients discontinue the diet because of its unpalatable and restrictive features. In the last 20 years, new variants of the KD diet have emerged, including the Modified Atkins diet MAD , a low-glycemic-index diet, which although it has a high fat content, allows more protein and does not restrict calories and fluids.

As presently understood, the KD is involved in multiple mechanisms responsible for biochemical alterations, including cellular substrates and mediators responsible for neuronal hyperexcitability. However, it is not yet known with certainty whether the success of the KD is due to a single or several mechanisms Bough and Rho, ; Lutas and Yellen, ; Rho, ; Youngson et al.

Because epilepsy is a metabolic disease Clanton et al. This contribution reviews the use and effects of the KD and its variants for the treatment of adults and children with intractable epilepsy. Dietary treatments for diseases have probably been used for over years Yuen and Sander, Fasting is the only therapeutic measure against epilepsy recorded in the Hippocratic collection.

Two Parisian physicians, G Guelpa, and A Marie, recorded the first modern use of starvation as a treatment for epilepsy in Wheless, The modern use of this form of therapy began in the early s Lima et al. Stanley Cobb and W.

Lennox of Harvard at Harvard Medical School observed the effects of starvation as a treatment for epilepsy, noting that seizure improvement typically occurred after 2—3 days Wheless, In the same period, Dr. Russel M. Wilder a physician at the Mayo Clinic in Minnesota, suggested that a specific diet could produce similar benefits to fasting, and proposed a diet that produced ketonemia.

He studied a series of patients with epilepsy and demonstrated a result equivalent to fasting and that was maintained for a much longer period. In , Robert C. Atkins developed a weight-loss diet that restricted the intake of carbohydrates Sharma and Jain, , and this diet was later evaluated for seizure treatment.

The first patient was a 7-year-old girl with intractable epilepsy due to a left parietal cortical dysplasia, who used the Atkins diet for a week in order to acclimate to the CKD. After 3 days, her seizures stopped, and she remained seizure-free for 3 years with continued dietary treatment Kossoff et al. The MAD has three significant differences from the first version: the induction phase of limiting carbohydrates is maintained indefinitely; high-fat foods are not only allowed, but encouraged; and the primary goal of the diet is seizure control Atkins, ; Sharma and Jain, Interest in dietary therapy continues as a means of treatment for this group, even more with advances in knowledge regarding the association of gut microbiota and neurological diseases.

It is a rigid diet, mathematically and individually calculated, and medically monitored Armeno et al. It must also provide adequate vitamins and minerals. The shift in the energy metabolism from glycolytic energy production to energy generation through oxidative phosphorylation fatty acid b-oxidation and ketone-body production is part of the anticonvulsant mechanism of the KD Bough, ; Liu et al. This is discussed in more detail in the section on the mechanism of action.

The KD has also been used in other conditions with less evidence, but possible benefits Table 2 Kossoff et al. Additionally, the KD is an important alternative treatment for patients with refractory epilepsy Rho, that are not surgery candidates. Table 1.

Table 2. Kossoff et al. In contrast, some pathologies are considered contra-indicated for KD. Absolute contraindications have been described and summarized by Kossoff et al.

The surgical epilepsies, whenever the patient or caregivers are having difficulty maintaining compliance with the diet, are relative contra-indications for KD Table 4 Kossoff et al. Table 3. Table 4. To obtain the optimum engagement of the family and the patients, providing information and training is essential because the diet is difficult to maintain.

Counselors should talk with the family about their expectations and make clear the efficacy rate and adverse events AE , to reduce the abandonment of the diet. Websites, videos and publications, especially from support groups, can be very helpful and should be encouraged. It is also important to review the medications and change from oral solutions carbohydrate content to tablets Armeno et al. The KD counseling, evaluation and follow-up should be done by a multidisciplinary team.

A pediatric neurologist or neurologist and a nutritionist are the minimum team requirements. Before starting the diet, the patient should maintain a seizure diary to establish a frequency parameter. Also needed are a laboratory evaluation including selenium and carnitine levels Table 5 , electroencephalogram EEG , and a magnetic resonance image MRI of the brain.

A renal ultrasound should be done in case of kidney stones; an electrocardiogram and carotid ultrasound are considered optional Kossoff et al. The nutritional evaluation includes a nutritional anamnesis including a 3-day food report, food habits, allergies, aversions, and intolerances. Baseline weight, height, and the ideal weight for stature and body mass index BMI are needed to calculate the ketogenic ratio, calories, and fluid intake. In the former approach, the patient must be hospitalized for 12—48 h, or when ketones are present in the urine Rubenstein, , to prevent the development of hypoglycemia and dehydration.

This method tends to accelerate the development of ketosis although it can generate more stress on the patient Armeno et al. When ketosis is reached, the meals are calculated to maintain a constant KD ratio, while calories are added until full-calorie meals are tolerated Kossoff et al. The latter approach requires no hospitalization and the KD ratio increases weekly, from , and to Bergqvist et al. Most of the literature suggests that there is no significant difference between the two approaches in terms of the time needed to reach ketosis and the occurrence of hypoglycemia Kim et al.

Taking into account that the KD provides only small amounts of fruits, vegetables, grains, milk and cheese, supplementation is essential.

Low-carbohydrate multivitamin and mineral supplements should be taken daily. Patients on the KD should be seen regularly every 3 months, and the family should be able to easily contact the diet team to resolve possible doubts and discuss adverse effects.

It has been noted that it is possible to improve the cognitive development and behavior even without a change in the seizure frequency. Although some authors have reported no relationship between the efficacy and the level of ketosis, it is still recommended to measure the urine ketosis several times a week Kossoff et al. For efficacy, the KD requires a period of at least 3 months from the time that the patient reaches ketosis, so it is important to encourage the patient and the family to continue with the diet for this period without changing the medication.

Because KD is not a physiological diet, it is necessary to recognize and closely manage AE Kossoff et al. Acute AE include dehydration, hypoglycemia, lethargy, metabolic acidosis, and gastrointestinal symptoms. However, most of the side effects involve weight loss, high levels of low-density lipoprotein, and elevated total cholesterol Liu et al. Other important AE are gastrointestinal symptoms, which include constipation, diarrhea, vomiting, and abdominal pain.

The family should also be informed about how to recognize the symptoms of hypoglycemia and be advised to administer a small amount of juice or other forms of dextrose Kossoff et al.

Nephrolithiasis may also develop, and an abdominal ultrasonography should be requested. The understanding of the mechanisms of action of KD is incomplete; however, some theories have been advanced about how it modifies the neuronal metabolism and excitability in order to reduce the seizure frequency. Possibly, the real mechanism of reduction of cortical hyperexcitability involves multiple factors.

Some of the systems involved in seizure reduction are related to metabolic changes in the blood and cerebrospinal fluid CSF , including a decrease in glucose levels and an increase in KB. The mitochondria function and energy reserve may also play a role in the KD mechanisms, resulting in synapse stabilization and excitatory decrease.

There are many theories about the role of KB, but the existence of an anticonvulsant effect is controversial. Some authors have found no relationship between KB and synaptic transmission and seizure control. Experimental studies in an animal model showed that in rats exposed to KD there was no change in synaptic plasticity, using paired-pulse modulation and long-term potentiation Thio et al.

Similarly, Likhodii et al. In spontaneously epileptic Kcna1 -null mice, KB supplementation resulted in attenuation of electrographic seizure-like events Kim et al. These authors also observed an inhibitory effect of KB on mitochondrial permeability transition related to apoptotic and necrotic death. Moreover, in experimental models, acetoacetate exerted a broad-spectrum anticonvulsant effect Rho et al.

Similarly, to these studies, injection of KB led to the reduction of seizure susceptibility Gasior et al. Ma et al. In addition, KB can exert a direct inhibitory effect on the vesicular glutamate transport Juge et al. It is possible that these divergent results are related to the different concentrations of KB used in these studies and the diverse seizure thresholds of the animal models. These conflicting results can be also explained by differences in diet composition.

Another hypothesis regarding the function of the KD is related to changes in neuronal metabolism, mitochondrial function and energy reserve, and the environment. In normal conditions, the usual substrate for the neurons is glucose. To facilitate its diffusion through the brain-blood barrier, glucose transports are present in the brain capillary endothelial layer Greene et al. The glucose metabolism produces the rapidly available energy that is necessary for seizure activity.

Therefore, in patients on the KD, the blood glucose energy levels are low, and the brain begins to use KB for energy. This anaerobic metabolism slows the energy availability, which reduces seizures. The anticonvulsant propriety of a decrease in glucose metabolism has been shown in experimental models in which the administration of 2-Deoxy-D-glucose elevates the seizure threshold Garriga-Canut et al.

The anticonvulsant effect of the KD can be quickly reversed after glucose infusion Huttenlocher, Based on these data, we can postulate the influences not only of the KB, as discussed above, but also the reduction in glucose levels as a mechanism of action of the KD. Chronic ketosis may play a role in the KD anticonvulsant properties, since it has been shown that chronic ketosis elevates the brain energy reserve via stabilization and reduction of excitability of synapses Devivo et al.

The energy reserve is directly associated with mitochondria, which is an important element to consider in the antiepileptic effect of KD.

Ketogenic Diet and Epilepsy: What We Know So Far

With the rising demand for ketogenic diet therapy in adult epilepsy, there is a need for research describing the real-life effectiveness, retention, and safety of relevant services. Of the first referrals, 42 31 females, 11 males; mean age The most common reasons for discontinuing MKD were side effects and diet restrictiveness. The most common side effects were weight loss, gastrointestinal symptoms and low mood. This study demonstrates that MKD can be effective in adults, although, even with regular dietetic support, retention rates remain low, and periods of worsening seizure frequency are common. Approximately one third of adult epilepsy patients do not achieve seizure freedom with antiepileptic drugs AEDs [ 1 , 2 ]. These patients with drug-resistant epilepsy carry a significant disease burden [ 4 , 5 ].


The ketogenic diet (KD) was found to be effective in treatment of intractable seizures. The KD consists of a high fat, low carbohydrate and.


Ketogenic Diet and Epilepsy: What We Know So Far

The Ketogenic Diet KD is a modality of treatment used since the s as a treatment for intractable epilepsy. It has been proposed as a dietary treatment that would produce similar benefits to fasting, which is already recorded in the Hippocratic collection. Evidence shows that KD and its variants are a good alternative for non-surgical pharmacoresistant patients with epilepsy of any age, taking into account that the type of diet should be designed individually and that less-restrictive and more-palatable diets are usually better options for adults and adolescents. Epilepsy is a disabling and common neurological disease, which can be controlled successfully in most patients with one or more antiepileptic drugs.

From the Section on Pediatrics, Mayo Clinic. During the last two and one-half years, the ketogenic, or high fat, diet has been given a trial in the treatment of epilepsy in childhood. Thirty-seven patients with essential or idiopathic epilepsy, whose parents were able to comprehend and carry out the diet intelligently at home, have been observed over periods of from four months to two and one-half years. Twenty of the patients were boys and seventeen girls. Seven of the patients had grand mal convulsions, seventeen petit mal, and thirteen both grand and petit mal.

Ketogenic diets for drug-resistant epilepsy

Epilepsy and the Ketogenic Diet pp Cite as. However, fasting as a treatment for seizures was less recognized. Fasting is the only therapeutic measure against epilepsy recorded in the Hippocratic collection 1. In the fifth century BC, Hippocrates reported on a man who had been seized by epileptic convulsions after having anointed himself before the fire in a bath, in winter. Complete abstinence from food and drink was prescribed, and the cure was effective. Unable to display preview.

Citation Information : Journal of Epileptology. Finding an effective epilepsy treatment has been a challenge in medicine for centuries. This gives an incentive to search for therapies other than pharmacotherapy, e. The present review paper aims to present the current state of knowledge regarding the effectiveness of the KD, its mechanism of action, indications, method of treatment and potential adverse effects.


The Ketogenic Diet for Epilepsy — Learn About the Diet, the Medical Conditions It's The ketogenic diet (KD) is a high-fat, low-carbohydrate diet with adequate protein that's a friendsofhiddenriver.org Updated July 24, Accessed October 9, 40​.


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Metrics details. The incidence of epilepsy is greatest in the first 2 years of life, an age group where there is generally a poor prognosis for both seizure control and neurodevelopmental outcome. Early control of seizures can be associated with better developmental outcome but many of the epilepsies presenting in infancy are poorly responsive to antiepileptic medication. The ketogenic diet KD is a high-fat, low-carbohydrate diet designed to mimic the effects of starvation on the body. Dietary fat is converted into ketones in the body and used as an energy source by the brain. The KD has been shown to be successful in controlling seizures in many observational studies, and in two randomised controlled trials RCTs in older children. However, little evidence is available in the very young.

Соши смотрела на монитор и читала вслух: - В бомбе, сброшенной на Нагасаки, использовался не плутоний, а искусственно произведенный, обогащенный нейтронами изотоп урана с атомным весом 238. - Черт возьми! - выругался Бринкерхофф.  - В обеих бомбах уран. Элементы, ответственные за Хиросиму и Нагасаки, - оба являются ураном. Никакого различия.

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