European Glut1 Conference Summary


Summary of the European Glut1 Conference held in Aschaffenburg, Germany on June 15-16, 2023
Written by Sandra Ojeda, PhD – Science Director for the Glut1 Deficiency Foundation

Day 1 European Glut1 conference

The conference began with a talk by Dr. Joerg Klepper “the Glut1DS story”. The talk summarized how the knowledge of the disease has changed since it was first described in 1991. 

Some open questions that were mentioned in the talk that are yet to be answered:

  • Is Glut1 involved in other tissues that are important in the disease?
  • Are proteins other than Glut1 involved in the disease?
  • What happens in the microbiome of Glut1 Deficiency patients?
  • Are there other genes involved in the disease?
  • What can we learn about speech impediments and how to help our patients?
  • What is the safety, stability, specificity and long-term effect of gene therapy?

The ketogenic diet (KD) treatment is the standard of care treatment for Glut1 Deficiency; however, it fails to help all patients and with all the symptoms. About 25% of patients do not respond to the diet, 55% do not respond to the diet for paroxysmal movements and about 70% do not benefit from the diet for speech. This data indicates that more needs to be done to find better treatments that will benefit all our patients.

Dr. Klepper also mentioned new concepts for treatment of Glut1 Deficiency. Among these are the increase of glucose. This is exemplified by the use of Diazoxide which blocks insulin release therefore allowing more glucose to be available in the blood. It has been successfully used in at least one Glut1 Deficiency patient. Another possible avenue discussed was the use of nanocarriers to deliver glucose to the brain.

Other possibilities mentioned were lactate, which is necessary for neurons to function properly and glycogen which is a polysaccharide of glucose which is used for energy storage.

This talk was a really important starting point for the conference because it summarized the history of Glut1, the symptoms, questions that would be important to answer but most importantly all the possibilities that can be explored for future treatments.

Session 1: Glut1 Research

Dr. Darryl De Vivo pre-recorded a message for the conference and he said a phrase that to me, is the take home message of the conference. Dr. De Vivo said “A future cure is now more realistic than ever”. That phrase helped us start the conference with a message of hope for everyone in the community.

The first talk of the session was by Dr. Jong Rho from the Rady’s Children Hospital in San Diego and the name of his talk was “How does the diet work? Ketogenic dietary effects and mechanisms in brain metabolism”.

Dr. Rho by explained why epileptic seizures occur – when there is hyperexcitability and hypersynchrony in the brain. Hyperexcitability means that when excitation exceeds inhibition, seizures occur, while hypersynchrony is a state where a group of neurons fire at the same time at a similar rate.

In general, anti-seizure drugs target the excitatory and/or the inhibitory events and the ketogenic diet is often used when these are not effective at treating seizures.

In epilepsy, many biochemical pathways are affected; there is energy deficit, abnormal energy function and lack of equilibrium. The ketogenic diet normalizes abnormal metabolism in the epileptic brain in areas such as inflammation, cell death, and others. The Ketogenic diet has been shown to improve energy, decreases inflammation, decreases oxidation. 

Dr. Pierre Magistretti from the King Abdullah University of Science and Technology gave a talk about lactate: “How to feed hungry neurons: The astrocyte-neuron lactate shuttle (ANLS)”.

Dr. Magistretti talked about astrocytes which are cells important for brain energy and metabolism. When glutamate, an excitatory neurotransmitter, is delivered during neuronal excitation it enters astrocytes and this uptake triggers glucose uptake by these cells which leads to the production of lactate. Lactate in then delivered to neurons for energy.

In his talk, Dr. Magistretti talked about some studies done with Glut1 deficient mice and he described how these mice have decreased glucose, glycogen and lactate. In addition, they studied the gene expression and found that the expression of different genes was altered in these mice. They decided to treat these mice with lactate for 10 weeks and they observed improvements in in their motor skills and coordination.

Dr. Magistretti is the founder and chairman of a company called GliaPharm. They have developed a compound which they have used to treat a Glut1 deficient mice and astrocytes derived from Glut1 deficient patient’s induced pluripotent stem cells (iPSC). The results have shown that this compound induces the increase of glucose and lactate uptake as well as increase on the expression of Glut1 protein in endothelial cells.

Their plan is to start a phase 1 clinical trial with this compound in 2024.

Session II: Novel Therapies for Glut1 Deficiency Syndrome

Dr. Sameer Zuberi from the University of Glasgow talked about his studies on “the genetics of Glut1 Deficiency Syndrome”. He and his team have done a study with Scottish patients with epilepsy and according to their results they suggest that the prevalence of Glut1 Deficiency could be 1 in 21,000. This means that just in the US only, there could be around 15,000 Glut1 Deficiency patients. These results suggest that more needs to be done regarding improvement of diagnosis for Glut1 Deficiency patients.

Dr. Helen Cross from the University College London talked about her studies on “C10 for Glut1 Deficiency”. C10 is a medium chain fatty acid that has been studied to treat epilepsy. C10 and C8 are the main components of a product called K. Vita that is sold in the UK only and that is used for patients who have drug resistant epilepsy. C10 and C8 are the number of carbons present in those medium chain fatty acids. Dr. Cross shared that the studies using K. Vita in patients with epilepsy including some Glut1 Deficient patients have shown that it decreases seizures, paroxysmal events and they have mild intestinal side effects.

Dr. Cross also explained that these medium chain fatty acids would work for Glut1 Deficiency because they can cross the blood brain barrier, produce ketones and can provide energy as an alternative fuel.

 Dr. Michel Willemsen from the Radboud University Medical Center gave a talk about “Lactate for Glut1 Deficiency”. He shared that studies have shown that lactate when it increases in blood during strenuous exercise in healthy individuals it protects the brain. Other studies have shown that insulin induced hypoglycemia increases blood lactate and that this has a protective effect in the brain. Literature review indicates that Glut1 Deficiency patients would benefit from lactate infusion. Therefore, Dr. Willemsen and his team conducted a pilot study as a proof of concept. Two patients were included in this study and have Glut1 deficiency; one had a variant on the SLC2A1 gene and the other did not, both had seizures. In addition, they did not respond to the ketogenic diet. Both patients were infused with lactate for 2 hours and only the patient with a variant showed increased levels of lactate in blood which had a positive effect on seizure control. 

Dr. Willemsen concluded that lactate can be used as an alternative fuel for the brain and that lactate infusion may have an anti-seizure effect on Glut1 Deficiency patients.

Dr. Juan Pascual from UT Southwestern gave his talk on “New mechanisms and potential treatments for Glut1 Deficiency: Studies in cells, mice, children and adults”. He summarized some of the results that he has shared in recent publications. One of them is the finding that Glut1 Deficiency patients show a significant decrease in inhibitory events in the thalamocortical somatosensory circuit in the brain. This decrease in inhibitory events upsets the delicate balance of inhibition and excitation and allows the excitatory events, seizures, to happen.

Dr. Pascual also shared that he and his team are developing a pig model of Glut1 Deficiency. The reason for this is that pig and human brains compare better than mice and human brains, therefore studies performed in pigs would be more meaningful and probably easier to extrapolate into humans.

Finally, he shared some results he has found in a Glut1 Deficiency patient donated brain, in which he has found that in a specific area of the brain called the superior frontal gyrus, there is an increase in the number of oligodendrocytes. The significance of this results is not clear yet, but these cells generate and maintain myelin in the central nervous system, which allows the fast and efficient transfer of neuronal communication. 

Some questions that I have are: 

  • How different are these cells in Glut1 deficiency patients compared to healthy individuals? 
  • Are they less effective or more effective at producing myelin in Glut1 deficiency patients vs. healthy individuals? 

I’m sure we will learn more about this and other projects from Dr. Pascual in future publications and conferences.

The next speaker was Dr. Umrao Monani from Columbia University. The title of his talk was “SLC2A1 gene induction for treatment of Glut 1 Deficiency”. He shared results from his studies on human fibroblasts, a type of cell found in skin. He and his team discovered a novel transcript or molecule called long non coding RNA (lncRNA) which seems to control the expression of the SLC2A1 gene, increasing or decreasing depending on the levels of this novel transcript. He found the same effects on brain endothelial cells. 

Dr. Monani and his team packaged this novel transcript in an Adeno-associated virus vector (AAV) designed by them that has specificity for brain endothelial cells, meaning it targets just those cells. The AAV vector containing the novel lncRNA transcript was injected into Glut1 Deficiency mice, and they observed that treated mice improved their motor performance, Glut1 expression increased in the brain endothelial cells, CSF glucose increased, and they observed some other positive effects on those mice.

Session III: Living with Glut1 Deficiency Syndrome and the ketogenic Dietary Therapies

Dr. Sara Olivotto from the Buzzi Children’s Hospital in Italy, talked about “Life quality in Glut1 Deficiency Syndrome”. She summarized the results of her 2022 paper on clinical phenotypes, intelligence and quality of life. She mentioned how seizures are the most prominent symptom in childhood while paroxysmal movements are more prominent during teen and adult years. She also added that the degrees of autonomy in Glut1 Deficiency patients vary and that overall, their quality of life is comparable to the healthy population.

There were two talks regarding speech in Glut1 Deficiency patients. The first one was by Dr. Valentina De Giorgis from the IRCCS National Neurological Institute C. Mondino in Italy. She 

Talked about the speech impairment in Glut1 Deficiency. Studies done by her and her team have shown that Glut1 deficiency is associated to different levels of speech and language impairment and 50% of the patients evaluated have problems with speech intelligibility or the measure of how comprehensible speech is in given conditions. Results also show that articulation, oral motor and phonological planning are impaired.

The second talk was done by Dr. Anne Jurkutat from The Julius-Maximilians-University in Germany. She talked about a study on speech in German Glut1 Deficiency patients. Dr. Jurkutat explained that language has two components: competence or mental knowledge and performance or articulation, realization of language. Her study included 28 patients but only data for 19 patients has been analyzed to date. Some of the assessments evaluated cognition and dysarthria. The test for dysarthria was designed in Germany for German speakers and evaluates different aspects such as pitch, respiration, voice quality, resonance and articulation rate. Their preliminary results indicate that articulation seems to be impaired in Glut1 Deficiency patients and about 50% of the participants have dysarthria. Finally, Dr. Jurkutat mentioned that she believes that when Glut1 Deficiency patients are evaluated for speech they should receive tests for receptive language and dysarthria because it will give a better idea of the state of their speech.

The next two speakers, Dr. Adella De la Marina and Dr. Johann Phillip from Germany, talked about the transition from pediatric neurology patients into adult neurology care. The recommendations made were to start planning the transition early during the teen years. They also recommended to look for movement disorder specialists as an option to transition into adult care. Another recommendation is to have a multidisciplinary care team that will include the pediatric neurologist and the adult neurologist. These specialists should talk to each other, parents, patients and the rest of the team to support the transition.

Finally, the last part of the first day had two round tables. The first one was for Glut1 Deficiency support groups, patient advocacy organizations from Europe and the US. The purpose was to share our experiences, mostly, the programs and projects each of the organizations have and how we can connect and support each other to provide better services to our Global Glut1 community. 

The moderators of this roundtable were Glenna Steele our Executive Director and Trudy Morgan our European Outreach Director and the Chair of Glut1 Deficiency UK. The participants were Maria Barthel from the Glut1 Deficiency organization in Germany, Heidi Junnila from the Finish Association for Rare Diseases, Alessandra Camerini from the Italian Glut1 Association, Stefanie Plomer from Glut1 Deficiency UK, Buliga Elena-Simona from the Glut1 Rebe&Luca Association in Romania, Cindy and Tim Oliver from Glut1 Deficiency Australia, Magali Sorret from the Association for Glut1 Deficiency in France and myself, Sandra Ojeda from the Glut1 Deficiency Foundation.

The second roundtable was focused on Glut1 Deficiency patients and their experiences. Dr. Jörg Klepper and Dr. Eric Kossoff were the moderators. The participants were three 17-year-old German patients, two girls and a boy. It was wonderful to hear them talk, to learn about their hopes and dreams for the future.

Day 2 European Glut1 Conference

Dr. Marisa Armeno from Hospital Garrahan in Argentina and Dr. Sabine Scholl from the Medical University of Innsbruck in Austria talked about the ketogenic diet and its implementation. They mentioned that one of the benefits of using MCT with the ketogenic diet is that it helps with constipation and other side effects of the KD. They also talked about C7 triheptanoin, and said that it has an anaplerotic function. Anaplerotic means that it can replenish molecules that are lost during the Tricarboxylic cycle (TCA), which is crucial for cells to breakdown molecules for fuel to get energy. They explained that ketone bodies are 4 carbon molecules andthat’s the reason why they cannot be used for the replenishment of the citrate cycle.

Another interesting topic they talked about was breast feeding while a patient is on the Ketogenic Diet. They shared some case reports and the conclusion was that it is possible to breastfeed a baby who is on the KD.

They also shared their experience of getting patients started on the ketogenic diet through telemedicine.  They said that it has been published that during the pandemic families initiated the KD. Patients started it slowly and doctors increased the ratio weekly instead of daily. Patients received remote support and educational materials. The study compared in person vs virtual KD initiation and there were no significant differences. 

Some questions answered from their talk:

Should MCT based fat be used? Yes
Is C7 beneficial? yes
Breastfeed while on the diet? yes
Can Glut1 patients use a Modified Atkins Diet? yes
Is virtual implementation of the diet possible? yes

Session IV: ketogenic dietary Therapies (KDT)

Dr. Eric Kossoff from John’s Hopkins Hospital talked about “KDT – where do we stand in 2023? Updates and challenges”He mentioned that the number of research publications on the KD have increased over the last years and it is widely available all over the world.

In 2022 the iInternational Neurological Ketogenic Society (INKS) was created and the 8th Global Keto Symposium hosted for the first time by INKS will take place in September 2023 in San Diego. The Glut1 Deficiency Foundation is partnering in this meeting.

There’s increased collaboration including with other groups beyond epilepsy. Cancer use of KD studies are now very prominent.

Dr. Kossoff summarized the current state of the KD: 

  • No need to fast before starting the diet
  • Ratio daily changed
  • No need to admit patient to start the diet
  • Telemedicine introduction of the KD is now possible

He also mentioned that there is still not a consensus on: 

  • how often and how to measure ketones
  • which supplements to use (some common ones are multivitamins, calcium, Vitamin D)
  • what is the true incidence of adverse effects
  • true impact of the KD not only in seizures but in quality of life and the KD in adults

Dr. Kossoff pointed out what do we know about KD in Glut1 Deficiency, this information comes from the Glut1 Deficiency consensus guidelines:

Duration: into adolescence/adulthood
Initiation: as early as possible
Ketosis: as high as tolerated
Blood ketones measured recommended
Carnitine recommended
Treatment of choice

  • Classic KD for infancy and childhood
  • MAD appropriate for adolescents and adults
  • Target blood ketones 2-5 

Finally, Dr. Kossoff gave a list of things that still need to be studied regarding the KD:

  • Important to find out about cardio vascular health
  • Long term risks of pregnancy
  • Are there risks to take a break from the KD (KD holiday)
  • Value of keto esters, salts, probiotics to boost the diet
  • What should be done when the KD fails to work?

The next speaker was Dr. Juan Pascual – and he talked about “Alternatives to the ketogenic diet”. First, he shared some information about C7 triheptanion, it makes ketones, glucose and is consumed by itself. It is a fuel for neurotransmitter synthesis. The maximum tolerable dose for C7 in Glut1 deficiency has been established.

From his studies on the compatibility between the KD and C7 he shared that C7 with the KD is not for every G1D patient. In some patients, ketosis goes down, therefore, the establishment of this supplementation should be individualized.

Regarding his studies with blood replacement in Glut1 Deficiency patients, he explained that for these studies blood from Glut1 Deficiency patients is replaced with blood of a healthy donor. The red blood cells (RBC) present in the donor have intact Glut1 protein. 40% of glucose in blood is inside the RBC, 60% is in plasma. Results from this study showed that the amount of Glucose present in the RBC post blood exchange increases and cognition improves. 

RBC stay for some days in the patient. It is not recommended to be used as a treatment at this moment.

Another study Dr. Pascual talked about was a study for Drug Discovery in Glut1 Deficiency. In the study they did a high throughput screening which tested more than 9,000 compounds. Some of those were approved drugs by FDA, some were new compounds. They found some compounds that are activators of Glut1 and some inhibitors, from these they decided to concentrate on 42 compounds. They are currently testing these 42 compounds in Glut1 Deficient mice to evaluate their behavior when treated with these compounds. They use a machine learning device to check the mice movement, velocity, oscillation and others. Their results show that 45 of these characteristics are different between Glut1 deficient mice and healthy mice.

One of the compounds they found which activates Glut1 is Acetazolamide. To further investigate, they surveyed Glut1 patients about the use and benefits of this drug. Their findings show that this drug has a positive effect in a large proportion of patients who have used this drug. 

The next speaker was Dr. Stephane Auvin from the Université Paris Citéhis talk was about “Use of IV KDT in the emergency setting”. Dr. Auvin pointed out how many ER professionals are not aware of the KD and how parents need to address that as soon as they arrive to the emergency room (ER).

He also talked about some of the risks for KD maintenance while in the ER are the administration of drug with carbohydrates, the inability of patients to eat their diet due to the procedure, fatigue, fever, trauma, respiratory issues.

Finally, he highlighted the importance of having an emergency plan. This plan should include a document for healthcare professionals, and a document for the family or caregiver. In France they have an emergency plan for caregivers and one for professionals that is provided for the patients to share in case of emergency.

Session V: Ketogenic Dietary Therapies (KDT) – Beyond Routine

The first speaker of the session was Dr. Sabine Scholl who gave a talk about “KD for inborn errors of metabolism”. She explained how the KD is used in disorders such as Glut1 Deficiency, mitochondrial disorders, Pyruvate dehydrogenase, Congenital Disorders of Glycosylation (CDG) syndromes and Gangliosidoses morbus Pompe, among others.

Dr. Scholl mentioned that some of the possible explanations for why the KD does not work for all the patients is because of decreased concentrations of gluconic + galactonic acid, xylose alpha 1 in the Cerebrospinal fluid (CSF). She concluded that understanding the pathophysiology of the disorder is key for managing the KD and that nutrition therapy team approach is best.

Prof. Anastasia Male-Dressler from the Medical University of Vienna in Austria talked about “KDT in infants”. Some of the facts she mentioned are that in infants between 0 to 12 months., the ratio of the KD should not go over 3:1, and there should not be fasting or fluid restriction during the initiation of the diet for this age group.

Regarding the effectiveness of the diet in infants she said that seizure reduction >50% in 50-80% patients and seizure freedom in 10-55% of patients, close to 20% seizure freedom. Additional results indicate that during the first year of life infants on the KD show no slow down in growth velocity or individual growth percentiles.

Another topic she discussed was “Human milk and breastfeeding on the KDT”. Dr Male-Dressler conducted a survey in 2021 and 2023 to moms breastfeeding infants on the KDT. They are preparing recommendations for the initiation and maintenance of KDT while including breast milk. They have seen that ketones go up in babies breastfed during KDT.

There are some reports about ketoacidosis in infants breastfed. It is not recommended right now. The ratio of KDT is modified and the mother’s milk is incorporated in the diet. Caregiver is given the exact amounts of breast milk that can be given to infant according to the ratio.

The next speaker in this session was Dr. Michel Willemsen from the Radboud University Medical Center in the Netherlands. Hi talk was entitled “The Failure of KDT in Glut1 Deficiency”.

Dr. Willemsen conducted a study on this topic. In that study, participants in from a previous study were reevaluated, some of them did not fit the Glut1 Deficiency parameters to have this disease while others did. Failure of the diet was reevaluated in those patients.

What they learned? Why does the diet fail? In one case the diet failed because a wrong diagnosis had been made. However, in other cases where patients had been correctly diagnosed the KD failed in patients due to intolerance.

He concluded that although failures may occur, the KD is the first line of treatment for Glut1 Deficiency. 

Some comments were that there might be good reasons at some point in time to stop the diet, not even start it or have a “KD holiday”, a break from the diet.

More research is needed to understand the road to success and the road to failure of the diet.

Finally, I’m quoting and important remark from Dr. Willemsen: “The diet should work for every patient if Glut1 Deficiency was just an energy failure disease, the disease is complex and more than just energy failure to the brain.”

The next talk in the session was “KDT in gut microbiome” by Dr. Jong Rho from Rady Children’s Hospital in San Diego. Dr. Rho explained that the gut microbiome is composed of trillions of microbes: bacteria, virus, bacteroides. It is a very diverse environment, just in the colon there are up to a 1,000 different species.

Gut microbiota changes over life and differs from patient to patient. Studies have shown that brain development and how the gut microbiome changes throughout life are related. In addition, there is some evidence that the gut microbiota is associated with human diseases such as Alzheimer’s, Parkinson and asthma.

Finally, in summary Dr. Rho mentioned that metabolism-based treatments for epilepsy have been increasingly validated over the past 15-20 years. There is growing evidence that changes in the gut microbiota are linked to seizure activity. 

Session VI: Dietary aspects of Ketogenic Dietary Therapies (KDT)

The first speaker of the session was DrElles Van der Louw and her talk was entitled: “KD during pregnancy”. She explained how maternal metabolism works.

  • Caloric need increases
  • During the 3rd trimester accelerated baby growth occurs-caloric demand increases
  • Increased lipolysis (fat breakdown) and ketone production is normal during pregnancy
  • When there’s illness in the pregnant woman they are more at risk for keto/metabolic acidosis

What’s the role of placenta? It produces hormones during the over-night fast which inhibit insulin and stimulate glucagon production. Glucagon is a hormone that promotes the breakdown of glycogen. Placenta also produces ketones.

Some important information Dr. Van der Louw shared is that maternal diabetic ketoacidosis is a severe medical condition associated with high rates of perinatal mortality and morbidity. Also, she mentioned that a study on pregnant women showed that women in a restricted carb diet during pregnancy were slightly likely to have children with neuronal tube defects.

Finally, she shared that published recommendation guidelines state that the KD is not recommended during pregnancy.

The next speaker of the session was Dr. Marisa Armeno. The title of her talk was “Chance or risk: what is the best lipid composition in KDT”. 

Why is fat composition important in KD? Fat composition can have profound implications in metabolism of patient. There are different types of fats:

Saturated: animal-based products, eggs, coconut
Trans fats: artificial, milk and meat can contain some of those
Monounsaturated: avocado, olive oil
Polyunsaturated: nuts and salmon

What’s the risk of a high fat diet? Dietary intake of fat can increase cholesterol and can lead to cardiovascular risks. 

What are the risks factors: Genetic, body weight, physical activity and even the medicines a person takes.

Dr. Armeno shared the results of a of 5-year study, a follow up of 58 patients. 29% of These patients had hypertriglyceridemia (too many triglycerides in the blood) before starting the KD. In addition, cholesterol increased in the first months of the KD but the value was within normal levels, same with triglycerides.

What happens in Glut1 patients?

A 10-year follow-up study from Germany found NO significant differences in weight and blood pressure, similar to a study in Italy of 15 children. Similar findings have been found in studies on adult patients.

Dr. Armeno shared some important suggestions when following the KD:

Do a pre-diet lipid profile, optimize the types of fats that are included in the diet to prevent the risk of high cholesterol and other molecules that increase cardiovascular problems. In clinical practice clinicians should adapt a more flexible, patient-tailored approach improving fat quality in the KD.


  • MCT does not affect total cholesterol, LDL or HDL.
  • Replace SFA with polyunsaturated fats
  • Replace a % fat with MCT oil
  • Supplement the diet with omega 3 and carnitine

The next speaker in this session was Dr. Mackenzie Cervenka and the title of her talk was “Pitfalls in KDT for adults”. Many Glut1 Deficient children that were diagnosed in 1990 are now adults and need transition to the adult neurology. In addition, some adult patients are diagnosed late and have children; only when their children get a Glut1 Deficiency diagnose, they get diagnosed and start a late treatment.

Dr Cervenka shared some of the pitfalls for adult Glut1 Deficiency patients regarding providers and the diet:

  • Getting a diagnosis and finding a provider
  • Currently there are not enough adult neurologists who know about Glut1 Deficiency or the Ketogenic diet 
  • More education is needed

She also shared the pitfalls and challenges during transition from pediatric to adult neurology for patients with Glut1 Deficiency on a KD:

  • Contraception
  • Symptoms during period
  • Pregnancy planning
  • Alcohol use, is it possible or recommended?
  • Delayed transition into adult neurology care

Some of the recommendations made by Dr. Cervenka were:

  • Involve the patient to plan transition from pediatric to adult care.
  • Plan the transition ahead of time, during early adolescence.
  • Share information with medical team.
  • Consider transitioning to a Modified Atkins Diet (MAD). It is Flexible and helps with independence for patients
  • Create a multidisciplinary team for care
  • Test annually for a complete blood count, comprehensive metabolic panel, fasting lipid panel, vitamin D3, zinc, selenium, free and total carnitine and urinalysis (urine analysis)

Resources: Hopkins has a Modified Atkins Diet (MAD) manual available for everyone who wants it. The International League Against Epilepsy has an International ketogenic diet centers list that has information about KD centers around the world.

Some of the Long -long-term side effects of the KD are:

  • Vitamin and mineral deficiencies
  • Selenium, zinc, vitamin D and carnitine deficiencies
  • Low bone mass
  • Kidney stones
  • Hyperlipidemia (abnormally high concentration of fats in the blood
  • Cardiovascular disease

A longitudinal study is being done on the long-term effect of the KD in patients

The last talk of the conference was about Vegan KDT by Dr. Susanne Baum from Germany.

Why to have a vegan KD? The number of plant-based diets like the vegan diet as well as the number of vegan consumers have increased in recent years.

What to consider? The vegan diet is a very low calorie diet.

It is a good source of phytate from cereals and legumes oil seeds and nuts. Phytate is the principal storage form of phosphorus in many plant tissues. Phytates can have positive and negative effects. The positives are that it may reduce the risk of cancer, may act as an antioxidant. The negatives are that it can decrease the absorption of iron, zinc, magnesium and calcium.

Dr. Baum mentioned that the vegan diet has been shown to be low on iron, calcium, vitamin D and B12. These deficiencies can be supplemented by taking iodine salt, soy products like tofu, green leaves vegetables, and vitamin D and B12 supplements.

The best Protein source in KD vegan is soy. Even for children as young as 6 months, almond or hazelnuts can be added to increase the protein and have a better protein quality. In addition, there is vegan fortified infant milk available.