I talk about that quite a bit here :https://bengreenfieldfitness.com/2015/09/things-your-pee-can-tell-you-about-your-body/
The diet is extremely regimented and very difficult to stick to, as just one baked potato and one slice of bread could hold an entire day’s worth of carbohydrates. While this is a deterrent for many, Christy Brissette, RD, a private-practice dietitian in Chicago, notes that many of her patients like the diet because of its strictness. “Some of my clients feel that the keto diet works for them because it doesn't involve any calorie counting and the rules are simple to understand,” she says. “They feel they have strict parameters that can take the guesswork out of dieting.”
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 study with an intent-to-treat prospective design was published in 1998 by a team from the Johns Hopkins Hospital[20] and followed-up by a report published in 2001.[21] As with most studies of the ketogenic diet, no control group (patients who did not receive the treatment) was used. The study enrolled 150 children. After three months, 83% of them were still on the diet, 26% had experienced a good reduction in seizures, 31% had had an excellent reduction, and 3% were seizure-free.[Note 7] At 12 months, 55% were still on the diet, 23% had a good response, 20% had an excellent response, and 7% were seizure-free. Those who had discontinued the diet by this stage did so because it was ineffective, too restrictive, or due to illness, and most of those who remained were benefiting from it. The percentage of those still on the diet at two, three, and four years was 39%, 20%, and 12%, respectively. During this period, the most common reason for discontinuing the diet was because the children had become seizure-free or significantly better. At four years, 16% of the original 150 children had a good reduction in seizure frequency, 14% had an excellent reduction, and 13% were seizure-free, though these figures include many who were no longer on the diet. Those remaining on the diet after this duration were typically not seizure-free, but had had an excellent response.[21][22]
In ketogenesis, two acetyl-CoA molecules instead condense to form acetoacetyl-CoA via thiolase. Acetoacetyl-CoA momentarily combines with another acetyl-CoA via HMG-CoA synthase to form hydroxy-β-methylglutaryl-CoA. Hydroxy-β-methylglutaryl-CoA form the ketone body acetoacetate via HMG-CoA lyase. Acetoacetate can then reversibly convert to another ketone body—D-β-hydroxybutyrate—via D-β-hydroxybutyrate dehydrogenase. Alternatively, acetoacetate can spontaneously degrade to a third ketone body (acetone) and carbon dioxide, although the process generates much greater concentrations of acetoacetate and D-β-hydroxybutyrate. When blood glucose levels are low, ketone bodies can be exported from the liver to supply crucial energy to the brain.[28]
You said you saw Dr. Jeff Volek at UCONN. I am interested in ketosis to help me with my M.S. I still have questions related to M.S. and not so much as it effects on athletes. I do live in CT, but was unable to locate Dr. Volek at either the Storres or Farmington campus. Would you be able to give me either his e-mail address or telephone number so that I can contact him directly? Your help would be greatly appreciated.
^ Jump up to: a b c Clemente FJ, Cardona A, Inchley CE, Peter BM, Jacobs G, Pagani L, Lawson DJ, Antão T, Vicente M, Mitt M, DeGiorgio M, Faltyskova Z, Xue Y, Ayub Q, Szpak M, Mägi R, Eriksson A, Manica A, Raghavan M, Rasmussen M, Rasmussen S, Willerslev E, Vidal-Puig A, Tyler-Smith C, Villems R, Nielsen R, Metspalu M, Malyarchuk B, Derenko M, Kivisild T (October 2014). "A Selective Sweep on a Deleterious Mutation in CPT1A in Arctic Populations". American Journal of Human Genetics. 95 (5): 584–589. doi:10.1016/j.ajhg.2014.09.016. PMC 4225582. PMID 25449608.
The ketogenic diet is not a benign, holistic, or natural treatment for epilepsy; as with any serious medical therapy, complications may result.[28] These are generally less severe and less frequent than with anticonvulsant medication or surgery.[28] Common but easily treatable short-term side effects include constipation, low-grade acidosis, and hypoglycaemia if an initial fast is undertaken. Raised levels of lipids in the blood affect up to 60% of children[38] and cholesterol levels may increase by around 30%.[28] This can be treated by changes to the fat content of the diet, such as from saturated fats towards polyunsaturated fats, and if persistent, by lowering the ketogenic ratio.[38] Supplements are necessary to counter the dietary deficiency of many micronutrients.[18]
As insulin levels plummet from carb-cutting, more water is flushed out, along with excess sodium (in contrast, excess insulin from carbs causes sodium and water retention).4 In some people, dehydration contributes to constipation, which can also result from avoiding fiber-rich carbohydrate foods. While less common, diarrhea or loose bowels can be triggered by a number of factors including too much or too little fat, dairy intolerance, or changes in gut flora. 
Diabetic ketoacidosis occurs when ketone levels become too high, due to a lack of insulin, and poison the body. This condition can happen to anyone with diabetes, but it is more common in people with type 1 diabetes because their bodies don’t make insulin. In the event that their ketone level rises, their bodies are unable to produce insulin to slow down this production. If left untreated, this condition can lead to a diabetic coma or death.
Fascinating stuff and I am quite curious how we know for certain one is actually in ketosis i.e. using ketones as primary fuel source BECAUSE we do know that glucose has a shorter metabolic pathway to burn and under most conditions, given the presence of glucose, that is what the body will default to which is why high fat and high sugar together in diet is so detrimental. So if we use one or more of the above “boosters” and show high levels of blood ketones but also highish levels of glucose (during initial transition) will be mostly burning ketones or still defaulting to glucose?