scholarly journals Is Modified Atkins Diet Therapy Applicable for Adults with Intractable Epilepsy Patients? - A Short Trial in Adult Volunteers

2011 ◽  
Vol 4 (1) ◽  
pp. 7-14
Author(s):  
Miyako Oguni ◽  
Noriyo Inoue ◽  
Kyoya Takahata ◽  
Masamichi Koseki
2019 ◽  
Vol 94 ◽  
pp. 32-37 ◽  
Author(s):  
Spoorthi Jagadish ◽  
Eric T. Payne ◽  
Lily Wong-Kisiel ◽  
Katherine C. Nickels ◽  
Susan Eckert ◽  
...  

Seizure ◽  
2011 ◽  
Vol 20 (2) ◽  
pp. 151-155 ◽  
Author(s):  
Maria J. Miranda ◽  
Mette Mortensen ◽  
Jane H. Povlsen ◽  
Helle Nielsen ◽  
Sándor Beniczky

Author(s):  
Luisa A. Diaz-Arias ◽  
Bobbie J. Henry-Barron ◽  
Alison Buchholz ◽  
Mackenzie C. Cervenka

Glucose is the primary energy fuel used by the brain and is transported across the blood-brain barrier (BBB) by the glucose transporter type 1 and 2.[1] A GLUT1 genetic defect is responsible for glucose transporter type 1 deficiency syndrome (GLUT1DS). Patients with GLUT1DS may present with pharmaco-resistant epilepsy, developmental delay, microcephaly, and/or abnormal movements, with tremendous phenotypic variability. Diagnosis is made by the presence of specific clinical features, hypoglycorrhachia and an SLC2A1 gene mutation. Treatment with a ketogenic diet therapy (KDT) is the standard of care as it results in production of ketone bodies which can readily cross the BBB and provide an alternate energy source to the brain in the absence of glucose. KDTs have been shown to reduce seizures and abnormal movements in children diagnosed with GLUT1DS. However, little is known about the impact of KDT on cognitive function, seizures and movement disorders in adults newly diagnosed with GLUT1DS and started on a KDT in adulthood, or the appropriate ketogenic diet therapy to administer. This case report demonstrates the potential benefits of using a modified Atkins diet (MAD), a less restrictive ketogenic diet therapy on cognition, seizure control and motor function in an adult with newly-diagnosed GLUT1SD.


2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Maryam Salaudeen ◽  
Mohammed Magaji ◽  
Abdulkadir Zezi

2009 ◽  
Vol 13 ◽  
pp. S79
Author(s):  
M.J. Miranda ◽  
M. Mortensen ◽  
J.H. Povlsen ◽  
H. Nielsen ◽  
S. Beniczky

2013 ◽  
Vol 128 (6) ◽  
pp. 402-408 ◽  
Author(s):  
O. F. El-Rashidy ◽  
M. F. Nassar ◽  
I. A. Abdel-Hamid ◽  
R. H. Shatla ◽  
M. H. Abdel-Hamid ◽  
...  

Seizure ◽  
2009 ◽  
Vol 18 (4) ◽  
pp. 237-240 ◽  
Author(s):  
Susanne Weber ◽  
Christian Mølgaard ◽  
KarenTaudorf ◽  
Peter Uldall

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1139-1139
Author(s):  
Shahabeddin Rezaei ◽  
Mona Kavoosi ◽  
Reza Shervin Badv ◽  
Mahmoud Mohammadi ◽  
Gholam Reza Zamani ◽  
...  

Abstract Objectives This study aimed to shed light on the differences between the effect of classical ketogenic diet (KD) and modified Atkins diet (MAD) on lipid profile in children and adolescents with intractable epilepsy. Methods The study was a non-randomized controlled clinical trial, conducted in the period of 2015 to 2017 (ClinicalTrials.gov, NCT03014752). Inclusion criteria included patients aged 1–18 years old, resistance to at least two antiepileptic drugs and no history of metabolic diseases that KD is contraindicated. The exclusion criteria included the occurrence of serious adverse effects and reluctance to adhere to the diet. Patients received the interventions for three months. Classical KD was initiated with 4:1 ketogenic ratio. MAD was initiated with a ketogenic ratio of 1:1 to 2:1 according to the John Hopkins protocol. The blood sample was obtained for measurement of the lipid profile, including triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL) and high-density lipoprotein (HDL). A repeated measures ANOVA was performed to compare the differences between groups. Results Twenty-six patients were allocated to classical KD and 26 were allocated to MAD. Fourteen patients remained at the end of the study in each group. In the classical KD group, the serum levels of TC, TG and LDL increased significantly before and after three months. In the MAD group, the serum levels of TC and LDL increased significantly before and after the study. After three months, there was a significant difference in the serum levels of TG and LDL between classical KD and MAD groups (P < 0.05); however, no significant difference was observed in the serum levels of TC and HDL in both groups (P > 0.05). Conclusions Patients who were on the MAD had significantly higher levels of TG and LDL than those who were on classical KD. Funding Sources Tehran University of Medical Sciences.


2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi23-vi23
Author(s):  
Karisa Schreck ◽  
Fang-Chi Hsu ◽  
Adam Berrington ◽  
Bobbie J Henry-Barron ◽  
Lindsay Blair ◽  
...  

Abstract INTRODUCTION Exploiting metabolic vulnerabilities via ketosis is a promising approach for gliomas. The modified Atkins diet is a ketogenic diet therapy efficacious in adults with refractory epilepsy. We evaluated the feasibility, pharmacokinetics/pharmacodynamics(PK/PD), and cerebral activity of this dietary intervention intended to induce ketosis. METHODS 25 patients with biopsy-confirmed WHO Grade 2–4 astrocytoma with stable disease after adjuvant chemotherapy were enrolled in an 8-week GLioma Atkins-based Diet (GLAD). GLAD consisted of 2 ‘intermittent fasting’ days(IF; calories < 20% of recommended daily allowance) interleaved between 5 modified-Atkins diet days(MAD; carbohydrates < 20 gm/day) each week. The primary outcome was dietary compliance. Secondary outcomes were PK assessed by urine ketones post-FAST and post-MAD, PD assessed by serum insulin and IGF-1, and cerebral activity measured by MR spectroscopy at baseline and week 8. RESULTS Grade 2(n=2;8%), Grade 3(n=11;44%) and GBMs(n=12;48%) were enrolled. While only 48% of participants satisfied pre-defined compliance criteria, overall compliance with MAD(80%) was higher than IF(72%). Weight loss was observed (-4.8 + 2.2kg,p< 0.0001) consisting primarily of decreased fat mass (-2.5 + 3.1%,p< 0.0001), with increased lean body mass (2.4 + 3.2%,p< 0.0001), stable nutritional status (phase angle, -0.26 + 0.94%,p=0.22), and normalization of BMI. Urine acetoacetate significantly increased with 55% achieving moderate ketosis at week 8 (p=0.0005). Serum insulin and IGF-1 significantly decreased indicating systemic dietary response and were associated with higher ketones post-IF, but not post-MAD. MRS demonstrated cerebral activity with increased ketones in lesional (0.06±0.03- >0.27±0.06i.u,p=0.005) and contralateral brain at week 8 (0.041±0.01- >0.16±0.04i.u.,p=0.004). Higher cerebral acetone correlated with higher urine ketones (r >0.75,p< 0.02) and lower fasting glucose (r >-0.74,p< 0.05). CONCLUSIONS The GLAD diet was challenging to maintain but demonstrated quantifiable biologic effects systemically and intratumorally. MAD was more feasible than IF, but changes in PD markers correlated most strongly with IF. The role of ketogenic diet therapy for preventing glioma growth remains uncertain.


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