Acetyl-CoA can be metabolized through the TCA in any cell, but it can also undergo a different process in liver cells: ketogenesis, which produces ketone bodies.[27] Ketone bodies are also produced in mitochondria, and usually occur in response to low blood glucose levels.[28] When glucose levels are low, oxaloacetate is diverted away from the TCA cycle and is instead used to produce glucose de novo (gluconeogenesis). But when oxaloacetate is unavailable to condense with acetyl-CoA, acetyl-CoA cannot enter the cycle, and so the body has evolved an alternative way to harvest energy from it.

I see a lot of people say that ketosis is great for insulin sensitivity. BUT, in my experience ketosis causes physiological insulin resistance whereby the muscles and liver are sparing glucose for the brain. Hence, glucose tolerance actually goes down during ketosis. As such, is it possible that post workout carbs could do a lot more damage than they would on a non-ketogenic diet? Or maybe, as Kiefer suggests, glucose uptake post workout is not moderated by insulin at all i.e. muscles soak up glucose regardless of their insulin sensitivity? Or maybe cyclical ketosis doesn’t allow liver glycogen to get low enough to trigger physiological insulin resistance?
It also means that if you’re a very active athlete or exercise enthusiast and you’re following “trickle-down” advice from the sedentary or less active ketosis experts to eat less than 40g of carbs per day, you’re making a big mistake when it comes to your hormonal balance, and you need to up your carbohydrate intake to 100-200g of carbs per day. You’d be surprised at how easy it is (if you’re a very active person) to stay in ketosis on this level of carbohydrate intake. Go ahead. Do Ketonix breath testing to prove me wrong. You can eat boatloads of carbohydrates at night and be back in ketosis within just two to three hours. When you combine that with the cutting-edge tricks you’re about to learn, you’ll find that you can toss hormonal issues out the window, get into ketosis, have your cake, and eat it too. Literally.
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]
The addition of MCT powder to ketones serves the purpose of maintaining endogenous production of ketone bodies by stimulating fatty acid oxidation in the liver, which then causes the production of even more ketone bodies. In this transcript from a podcast with Dr. Dom D’Agostino it is mentioned that MCT’s cross the blood-brain barrier straight to the brain. So not only are the ketones being used by the brain as an alternative fuel but so are MCT’s.
Long-term use of the ketogenic diet in children increases the risk of slowed or stunted growth, bone fractures, and kidney stones.[18] The diet reduces levels of insulin-like growth factor 1, which is important for childhood growth. Like many anticonvulsant drugs, the ketogenic diet has an adverse effect on bone health. Many factors may be involved such as acidosis and suppressed growth hormone.[38] About one in 20 children on the ketogenic diet develop kidney stones (compared with one in several thousand for the general population). A class of anticonvulsants known as carbonic anhydrase inhibitors (topiramate, zonisamide) are known to increase the risk of kidney stones, but the combination of these anticonvulsants and the ketogenic diet does not appear to elevate the risk above that of the diet alone.[39] The stones are treatable and do not justify discontinuation of the diet.[39] Johns Hopkins Hospital now gives oral potassium citrate supplements to all ketogenic diet patients, resulting in one-seventh of the incidence of kidney stones.[40] However, this empiric usage has not been tested in a prospective controlled trial.[9] Kidney stone formation (nephrolithiasis) is associated with the diet for four reasons:[39]

1. If a set number ketones in the blood is an indicator that my body has transitioned to ketosis and not necessarily the cause (the cause being limited access to glycogen because of limited carb intake) then how does using exogenous ketones put me in ketosis as opposed to mimic being in ketosis (because when measuring blood ketones suddenly there are more because I put them there, I didn’t create them)?

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