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Ketogenic Diet (KD)

Ketogenic Diet (KD). Arna Vanebo Sarah Tobin Heather Davis Selva Wohlgemuth. Ketogenic Diet: what is it?. High fat (85-90%) Low carbohydrate (2-4%) Adequate protein (6-8%) Used as a control method for intractable seizures (non-responsive to drug Tx )

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Ketogenic Diet (KD)

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  1. Ketogenic Diet (KD) ArnaVanebo Sarah Tobin Heather Davis Selva Wohlgemuth

  2. Ketogenic Diet: what is it? • High fat (85-90%) • Low carbohydrate (2-4%) • Adequate protein (6-8%) • Used as a control method for intractable seizures (non-responsive to drug Tx) • Diet begins under hospital supervision • Closely monitored with frequent follow-ups • Education • Ketosis vs. Ketoacidosis

  3. Types of Ketogenic Diets • Classic KD (most common) • MAD (modified Atkin’s Diet) • 60-70% fat, 25-30% protein, 5% carb • LGIT (low glycemic index treatment) • 60-70% fat, 20-30% protein, 10% carb • MCT (medium chain triglyceride) • A modification of Classic KD that allows for 19% carbs, 10% protein, 71% MCT

  4. Example Menu A typical day’s menu for a child on the standard 4:1 ratio diet, allowing 1500 calories per day: Breakfast: Egg with bacon, made with heavy cream and butter, plus an apple Snack: Peanut butter mixed with butter Lunch: Tuna salad made with celery, mayonnaise, and heavy cream, served with lettuce Snack: Ketoyogurt (made with heavy cream, sour cream, strawberries, and artificial sweetener) Dinner: Cheeseburger with lettuce and green beans Snack: Ketocustard (heavy cream, egg, and pure unsweetened vanilla flavoring)

  5. Metabolism of FA’s for energy

  6. Ketone Body Metabolism

  7. Hormonal Effects of KD • Blood sugar decreases after exhaustion of glycogen stores • Insulin levels decline • Increase in Glucagon & Norepinephrine • Serotonin levels decrease

  8. Treatment with KD • EPILEPSY • Exception is medically refractory epilepsy (responsive to anticonvulsive drug treatment) • GLUT 1 glucose transport deficiency • First line of therapy is KD • Pyruvate dehydrogenase complex deficiency • Phosphofructokinase deficiency

  9. Mechanisms • No definitive mechanism for epilepsy control by KD, but many hypotheses • Both elevated FA’s and reduced glucose levels are thought to be responsible for anticonvulsant effects • Ketone bodies • 4 mmol/L [BHB] • Increase [BHB + ACA] reduces spontaneous firing of GABAergicneruons • ACA decreases excitatory response of glutamate • Which is the most responsible?

  10. Mechanisms continued • GABAergic Inhibition • Increase glutamate to aspartate ratio • [BHB] and decrease degradation of GABA • Glucose Reduction • Increase extracellular ATP encourages opening of ATP K+ channels • Decrease phosphorylation of GABA receptors • Regulates neuronal genes • BDNF • NRSF

  11. Mechanisms continued • Polyunsaturated Fatty Acids • Regulate gene expression • Indirectly stimulate mitochondrial biogenesis in hippocampal tissue, increasing tissue resilience • Omega 3’s and sodium pump function • Norepinephrine • Levels inversely related to seizure activity

  12. Prognosis • Rates: • 3 months: 3% free from seizures, 30% had >90% reduction in seizure frequency, 26% had 50-90% reduction • After 12 months: moderate increase in number of patients free from seizures • Children between ages 1 and 10 are observed to benefit more than older individuals • Discontinuation of KD

  13. Possible Consequences • Suboptimal development • Increased Ca2+excretion • Nephrolithiasis • Decreased bone density • Vitamin and mineral deficiencies • Dehydration • Risk of ketoacidosis • Exercise intolerance • GI disturbances

  14. KD in a pill? • No single proposed mechanism of action is thought to be responsible for the success seen in KD, but rather the synergistic interplay among many mechanisms

  15. Share your thoughts… • Are there any differences in the Ketogenic Diet and the starved state, if so what are they??

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