Early studies reported high success rates; in one study in 1925, 60% of patients became seizure-free, and another 35% of patients had a 50% reduction in seizure frequency. These studies generally examined a cohort of patients recently treated by the physician (a retrospective study) and selected patients who had successfully maintained the dietary restrictions. However, these studies are difficult to compare to modern trials. One reason is that these older trials suffered from selection bias, as they excluded patients who were unable to start or maintain the diet and thereby selected from patients who would generate better results. In an attempt to control for this bias, modern study design prefers a prospective cohort (the patients in the study are chosen before therapy begins) in which the results are presented for all patients regardless of whether they started or completed the treatment (known as intent-to-treat analysis).
The presence of abnormally high levels of KETONES in the blood. These are produced when fats are used as fuel in the absence of carbohydrate or available protein as in DIABETES or starvation. Ketosis is dangerous because high levels make the blood abnormally acid and there is loss of water, sodium and potassium and a major biochemical upset with nausea, vomiting, abdominal pain, confusion, and, if the condition is not rapidly treated, coma and death. Mild ketosis also occurs in cases of excessive morning sickness in pregnancy.
These affect your brain and spine, as well as the nerves that link them together. Epilepsy is one, but others may be helped by a ketogenic diet as well, including Alzheimer’s disease, Parkinson’s disease, and sleep disorders. Scientists aren’t sure why, but it may be that the ketones your body makes when it breaks down fat for energy help protect your brain cells from damage.
Peak fat oxidation was 2.3-fold higher in the LC group (1.54 ± 0.18 vs 0.67 ± 0.14 g/min; P = 0.000) and it occurred at a higher percentage of VO2max (70.3 ± 6.3 vs 54.9 ± 7.8%; P = 0.000). Mean fat oxidation during submaximal exercise was 59% higher in the LC group (1.21 ± 0.02 vs 0.76 ± 0.11 g/min; P = 0.000) corresponding to a greater relative contribution of fat (88 ± 2 vs 56 ± 8%; P = 0.000). Despite these marked differences in fuel use between LC and HC athletes, there were no significant differences in resting muscle glycogen and the level of depletion after 180 min of running (−64% from pre-exercise) and 120 min of recovery (−36% from pre-exercise).