Biologically Occurring Ketone Bodies.

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Ketogenic Diet Does Not “beat Chemo For Almost All Cancers”

One of the difficult things about science-based medicine is determining what is and isn’t quackery. While it is quite obvious that modalities such as homeopathy, acupuncture, reflexology, craniosacral therapy, Hulda Clark’s “zapper,” the Gerson therapy and Gonzalez protocol for cancer, and reiki (not to mention every other “energy healing” therapy) are the rankest quackery, there are lots of treatments that are harder to classify. Much of the time, these treatments that seemingly fall into a “gray area” are treatments that have shown promise in animals but have never been tested rigorously in humans or are based on scientific principles that sound reasonable but, again, have never been tested rigorously in humans. (Are you sensing a pattern here yet?) Often these therapies are promoted by true believers whose enthusiasm greatly outstrips the evidence base for their preferred treatment. Lately, I’ve been seeing just such a therapy being promoted around the usual social media sources, such as Facebook, Twitter, and the like. I’ve been meaning to write about it for a bit, but, as is so often the case with my Dug the Dog nature—squirrel!—other topics caught my a Continue reading >>

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  1. jayhiller21

    Anyone understand ketone bodies utilization?

    From what I can gather, ketone bodies are created during times of prolonged starvation, when OAA is diverted to gluconeogenesis. When OAA gets too low, the krebs cycle cannot continue so the accumulation of acetyl CoA is used to create ketone bodies. Here's what I don't get: Supposedly these ketone bodies are then transferred from the liver to the tissues, where it is turned back into acetyl co A to enter the krebs cycle.
    TLDR, I have one main question. 1) How is acetyl CoA that is made from ketone bodies able to enter the krebs cycle if there supposedly a lack of OAA (b/c of increased gluconeogenesis)?
    Is it that once the body resorts to forming ketone bodies, gluconeogenesis activity has declined, enabling krebs to continue?
    Clarification would be much appreciated!

  2. ryansmith1235515

    I think this answers your question... gluconeogensis occurs mainly in the LIVER. As a result it is true that there is less OAA in the liver now slowing down entry of acetyl coA (made from fatty acid oxidation) in the Krebs cycle. But, Ketone bodies can move in the bloodstream to other tissues where gluconeogensis is not occuring, therefore plenty of OAA to proceed through the Krebs Cycle.
    This is how the liver can use fats to make more energy by breaking down those fats and putting the byproducts (glycerol + fatty acid chains) into the metabolic cycles. I think you can view ketones as a vehicle in which the liver "shares" the breaking down of fats so all tissues in the body can use the energy.
    During long-term starvation, you're body is adapted to stop using as much gluconeogensis and increase ketogensis. The reason is gluconeogensis uses amino acids which requires the breakdown of proteins. You're body would rather breakdown fat than protein so it is advantageous to use fat as a fuel source rather than muscle.
    Let me know what you guys think about these explanations, I'm not 100% sure myself. Metabolism is such a tricky subject!

  3. jayhiller21

    This clears things up, thanks! Ketone bodies acting as an acetyl coa transporter are kind of analogous to how malate transports nadh into the mitochondria...

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