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There are many misconceptions about ketosis. The most common is mixing it up with ketoacidosis – a rare and dangerous medical condition that mostly happen to people with type 1 diabetes if they don’t take insulin. Even some health care professionals tend to mix up these two situations somewhat, perhaps due to the similar names and a lack of knowledge about the distinct differences.
Ketosis is an option for many people with type 2 diabetes because they still produce insulin, which helps their body maintain a safe level of ketones in the blood. If you’re considering trying ketosis or the ketogenic diet with type 2 diabetes, be sure to consult your healthcare provider first to ensure it’s safe for you. This eating approach may interfere with some types of diabetes medication or be inappropriate for you if you have certain diabetes complications, such as kidney damage.
For patients who benefit, half achieve a seizure reduction within five days (if the diet starts with an initial fast of one to two days), three-quarters achieve a reduction within two weeks, and 90% achieve a reduction within 23 days. If the diet does not begin with a fast, the time for half of the patients to achieve an improvement is longer (two weeks), but the long-term seizure reduction rates are unaffected.[44] Parents are encouraged to persist with the diet for at least three months before any final consideration is made regarding efficacy.[9]
A ketogenic diet helps control blood sugar levels. It is excellent for managing type 2 diabetes, sometimes even leading to complete reversal of the disease. This has been proven in studies. It makes perfect sense since keto lowers blood-sugar levels, reduces the need of medications and reduces the potentially negative impact of high insulin levels.
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).
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