Aside from the short answer "we don't really know," the longer answer to the question of how the ketogenic diet functions is that there may be a combination of factors at work:
- KETONE BODIES come in many chemical forms and are a result of the incomplete burning of fats in the body. Ketone bodies have a sedative effect and an appetite-suppressing effect. Some popular weight-reduction diets with very low calorie levels and low carbohydrates produce ketosis. The appetite-suppressing effect of ketosis explains why these diets can be followed without the dieter's feeling too hungry. Ketone bodies also have an anticonvulsant effect. However, ketones by themselves do not adequately explain the effectiveness of the ketogenic diet. For example, when a child whose seizures are well controlled on the diet eats a cookie, seizures may occur even if urinary ketones are not clearly affected. While their concentration in the blood is perhaps more important, we measure ketones in the urine for convenience. If there are no ketones in the urine, the diet is not going to work. Ketones in the blood and in the urine are necessary for the diet to be effective, but the presence of ketones alone is not sufficient.
- ACIDOSIS means an increased amount of acid in the blood. Ketone bodies are acids and therefore cause acidosis. There are several other chemical mechanisms by which the human body produces acidosis, and many ways in which the body compensates for ketones to maintain normal pH balance. Acidosis influences the threshold for seizures. This is why the ingestion of acids or acid-forming salts, or breathing a mixture high in carbon dioxide, can reduce seizures temporarily, just as hyperventilating, which reduces acidosis, can bring out seizures. Acidosis may be one of the participants facilitating seizure control in the ketogenic diet, but since the body quickly compensates for the acidosis to readjust its pH balance, acidosis cannot be the major determinant of the diet's success.
- DEHYDRATION was part of the original water diet used by McFadden that ultimately led to the development of the ketogenic diet. While fluids are traditionally limited during the diet, the role, if any, of dehydration in seizure control is unclear. It is known that administering excess water can provoke seizures, probably due to acute dilution of the body's sodium level. Indeed, this was one of the methods used by physicians to provoke seizures for observation. However, this in no way indicates that dehydration would prevent seizures by raising the body's sodium level. Normal kidneys do an excellent job of maintaining the body's chemical balance. Another misconception about fluid intake is that fluid dilutes the ketones, thereby negating the effects of the ketogenic diet. Increased water intake certainly results in urine that is more dilute. If the body's production and excretion of ketones is constant, the concentration of ketones in the urine (and therefore the strength of the urinary ketone test) will depend on the child's water intake. This does not, however, necessarily reflect the level of ketones in the blood and brain, which may be higher.
None of the individual mechanisms discussed here will in isolation lead to seizure control, since the body can compensate for each of them. Acidosis corrects itself in one to two weeks, and the pH of the blood will then remain normal throughout the remainder of the diet. Changes in the water and electrolyte content of the brain are rapidly compensated for by the rest of the body.
The real effectiveness of the diet probably lies in other influences on metabolism. For example, while the brains of infants, children and adults burn glucose almost exclusively, the foetus and newborn are able to exist on the metabolism of fats. Does the ketogenic diet enable the brain to revert to a more primitive form of metabolism? Is the reason that the ketogenic diet is more effective in children than in adults based on the younger brain's capability to metabolise fats? There is also some suggestion that a diet high in certain fats, particularly B-hydroxybuterate, may alter the chemistry of brain cell membranes and thereby the sensitivity of certain transmitter sites. Clearly, more research is needed to explore the mechanisms by which the ketogenic diet achieves its dramatic results.
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