You’ll quickly find that salads are your friend when in ketosis, and for a good reason: they provide lots of food to fill you up, but they’re not going to bog you down. A bed of spinach with some red onion, bacon, a little tomato, and a hot sauce vinaigrette is quick and delicious. Add in some protein – perhaps that leftover salmon from day 1 – and you’ve got a complete, healthy lunch.
Keto for Epilepsy: The ketogenic diet originated in the 1920s as an effective treatment for children suffering from drug-resistant epilepsy. Since then, its highly successful applications have expanded to treat adult epileptic patients as well. This was an important progression in treatment because, despite the introduction of anticonvulsant drugs in the 1930s, at least one third of patients suffering from epileptic seizures are still fully resistant to anticonvulsant drug therapy.[26] Early studies found that, when placed on a ketogenic diet, 12% of children suffering from epileptic seizures experienced full remission and 42% saw a reduction in seizures.[27]
Rami co-founded Tasteaholics with Vicky at the start of 2015 to master the art of creating extremely delicious food while researching the truth behind nutrition, dieting and overall health. You can usually find him marketing, coding or coming up with the next crazy idea because he can’t sit still for too long. His favorite book is The 4-Hour Workweek and artist is Infected Mushroom.
This plan is very high on protein. I’ve learned that high healthy fat is what’s needed, not high protein.. as I am now kicked out of ketosis due to high protein intake (insulin’s fault). Given the fact i didn’t eat a bowl of salad per day (my tummy doesn’t digest salad well at all – i get bloated), but i do eat broccoli (i don’t get bloated from those strangely enough), cauliflower, asparagus, mushrooms… tomatoes (rarely, though). So, my question is… are you in ketosis following the menu you’ve presented? I’m 5 months into Keto and the last 3 weeks i am not in ketosis. My carb intake is 20-30g… but my protein is pretty high.
Because people with type 2 diabetes are at an increased risk for cardiovascular disease, there’s a specific concern that the saturated fat in the diet may drive up LDL, or “bad,” cholesterol levels, and further increase the odds of heart problems. If you have type 2 diabetes, talk to your doctor before attempting a ketogenic diet. They may recommend a different weight-loss diet for you, like a reduced-calorie diet, to manage diabetes. Those with epilepsy should also consult their doctor before using this as part of their treatment plan.

H. Guldbrand, B. Dizdar, B. Bunjaku, T. Lindström, M. Bachrach-Lindström, M. Fredrikson, C. J. Östgren, F. H. Nystrom, “In Type 2 Diabetes, Randomisation to Advice to Follow a Low-carbohydrate Diet Transiently Improves Glycaemic Control Compared with Advice to Follow a Low-fat Diet Producing a Similar Weight Loss,” Diabetologia (2012) 55: 2118. http://link.springer.com/article/10.1007/s00125-012-2567-4.
H. Guldbrand, B. Dizdar, B. Bunjaku, T. Lindström, M. Bachrach-Lindström, M. Fredrikson, C. J. Östgren, F. H. Nystrom, “In Type 2 Diabetes, Randomisation to Advice to Follow a Low-carbohydrate Diet Transiently Improves Glycaemic Control Compared with Advice to Follow a Low-fat Diet Producing a Similar Weight Loss,” Diabetologia (2012) 55: 2118. http://link.springer.com/article/10.1007/s00125-012-2567-4.
After about two to seven days of following the keto diet, you go into something called ketosis, or the state your body enters when it doesn't have enough carbs for your cells to use for energy. That's when you start making ketones, or organic compounds that your bod then uses in place of those missing carbs. At this point, your body also starts burning fat for more energy, says Beth Warren, RD, founder of Beth Warren Nutrition and author of Living A Real Life With Real Food.
There are many ways in which epilepsy occurs. Examples of pathological physiology include: unusual excitatory connections within the neuronal network of the brain; abnormal neuron structure leading to altered current flow; decreased inhibitory neurotransmitter synthesis; ineffective receptors for inhibitory neurotransmitters; insufficient breakdown of excitatory neurotransmitters leading to excess; immature synapse development; and impaired function of ionic channels.[7] 
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