As you've gathered from my books, for various reasons I'm not a fan of excessive ketosis (at least to the point of obsessing over ketonuria). First of all I believe that staying in ketosis may have long-term adverse effects (such as dehydration of various tissues and possible deterioration of cartilage and connective tissues, especially those that are weight bearing such as the vertebral disks). Secondly being constantly in ketosis is catabolic and counter productive for keeping or enhancing muscle mass.
And thirdly I don't believe that achieving ketosis to the point of showing significant ketonuria is necessary for any of the beneficial effects of the Metabolic Diet on body composition. There are several reasons for my views and I'll try and outline them below. Keep in mind, however, that one of the more important ones is that the lack of the insulin-mediated anabolic effect. Insulin has been shown to both increase protein synthesis and decrease protein catabolism. In the Metabolic Diet, the anabolic effect of insulin (both direct and indirect - for example insulin in concert with GH leads to increases in muscle IGF-1 and subsequently to muscle hypertrophy) are harnessed while at the same time its lipogenic and anti-lipolytic effects are controlled. Purely ketogenic diets have other drawbacks as well. First of all staying in ketosis can lower metabolic rate and thyroid hormone levels and activity (specifically T3 levels). This can make it more difficult to increase protein synthesis and muscle hypertrophy. Also, as mentioned above, chronic ketogenic diets dehydrate the body and can have adverse effects on joint tissues, including spinal discs, and may result in increased injuries.
Those that argue that it's vital to show significant ketonuria, and that without it the protein sparing effect of the ketogenic diet is lost, are confusing the issues involved in switching the metabolism from a carb burning to a fat burning one. The point is that by titrating the Metabolic Diet to the lowest carb level that works for you, you're maximizing the fat loss, minimizing muscle catabolism, and more importantly using a macronutrient mix that is in tune to your genotypic and phenotypic makeup.
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As you know the Metabolic Diet is a cycling diet, not a strictly ketogenic diet. Unlike cycling ketogenic diets (CKDs) it's more dynamic in that it can be used to find the optimal level of carbs that matches any individuals metabolism and that will result in maximum results as far as altering body composition. This effect on body composition is helped by the weekly phase shift that results from the changes in macronutrient composition and the subsequent metabolic and hormonal environment.
Needless to say if you follow the strict part of the Metabolic Diet you will have significant degree of ketosis and variable levels of ketonuria. As you know ketones are formed all the time to some extent in everyone, just much more so as the dietary carb levels drop and fat intake increases. The amount of ketones that end up in the urine is a function of several factors including the amount formed secondary to carb availability, and insulin and glucagons levels, the extent to which they are able to be metabolized and used efficiently (a function of a person's genetic ability to oxidize fat and ketones efficiently and of time), and the efficiency of the gluconeogenic process and availability of gluconeogenic substrates thus decreasing the need for ketone formation.
Reaching ketosis, at least as far as being able to measure it using a ketostix, believe it or not, doesn't relate in the least to how well you do on the diet. Keep in mind that the depth of ketosis is NOT indicative of the degree of fat oxidation or lipolysis. I don't even suggest you check your urine for ketones never mind fussing over the degree of ketonuria.
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Studies have also shown that the phase shift that occurs every week for anywhere between 12 and 36 hours (although as per my book the shift can be very flexible depending on the individual person's metabolism and reaction to the diet) does not adversely affect the established fat burning mode and as such does not reverse the enzymatic changes that have been induced as a result of the prior lower carb, higher fat phase.
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