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[[File:Ketones.png|right|thumb|500px|The three Ketones are interrelated. The body can convert between AcAc and BOHB, but AcAc spontaneously decomposes into Acetone.]]
The [[Ketogenic Diet]] produces three types of Ketone. (Add diagram of the ketones and their relationships.)
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There are three important ketones involved in [[Ketogenic Diet]]s.
* '''Acetoacetic acid (AcAc)'''. AcAc is the ketone that is produced by the liver from fats and can be metabolized to provide energy. It could be considered the most directly useful of these ketones to the human body. However, AcAc lowers the blood pH, causing potential acidosis. AcAC spontaneously decomposes into Acetone (the half-life is 11.7 hours at 27c<ref name="HayBond1967"/>).* '''Acetone'''. Generally is often believed to be a waste product, but it has now shown to be metabolically active<ref name="Reichard-1979"/><ref name="Kalapos-1999"/>. It is excreted through the breath and urine, which can sometimes be detected as a fruity smell. Radio-tagged Acetone has been shown to be converted to glucose, fats and protein, but not other Ketones<ref name="Reichard-1979"/>. Acetone levels are one possible [Ketogenic Mechanism of Action| mechanism of action]] behind the success of the [[Ketogenic Diets for Epilepsy]]<ref name="Kalapos-2007"/>. * '''Beta-hydroxybutyrate (BOHB)'''. Unlike AcAc, BOHB is stable and does not change blood pH. AcAc is converted to and from BOHB in the liver and muscles. (Technically BOHB is not a Ketone. =Relative Ketone Levels=* The ratio between AcAc and Acetone appears reasonably constant, and is based on the spontaneous, but it's normally considered one way decomposition of AcAc into Acetone. * The ratio of AcAc to BOHB is rather more varied and may change with [[Ketoadaptation]].)From "Physiological roles of ketone bodies as substrates and signals in mammalian tissues"<ref name="Robinson-1980"/>:{| class="wikitable"! Situation! Ketone Levels (Blood levels of AcAc + BOHB)|-| Fed| ~0.1|-| Fasted 12-24 Hours| Up to 0.3|-| Fasted 48-72 Hours| 2-3|-| Fasted 5-6 weeks (plateau)| ~8|-| Post exercise| Up to 2|-| Late Pregnancy| Up to 1|-| Late Pregnancy, fasted 48 hours| 4-6|-| Neonatal| 0.5-1.0|-| Hypoglycemia| 1-5|-| Controlled diabetes| Up to 25|} Ketone Metabolism=* [[Ketones]] are used by most tissues in the body with the exception of those cells that have few or no mitochondriawhich are dependent on glucose<ref name="Westman-2003"/>. (more at A review of low-carbohydrate ketogenic diets)* Cells with no mitochondria include erythrocytes, cornea, lens, and retina.* Cells with few mitochondria include renal medulla, testis, and leukocytes.* These cells are dependent on Glucose.=See Also={{KetoSeeAlsoKetoList}}=References=
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<ref name="Reichard-1979"> GA. Reichard, AC. Haff, CL. Skutches, P. Paul, CP. Holroyde, OE. Owen, Plasma acetone metabolism in the fasting human., J Clin Invest, volume 63, issue 4, pages 619-26, Apr 1979, doi [http://dx.doi.org/10.1172/JCI109344 10.1172/JCI109344], PMID [http://www.ncbi.nlm.nih.gov/pubmed/438326 438326]</ref>
<ref name="Westman-2003">Westman, Eric C., John Mavropoulos, and William S. Yancy Jr. "A review of low-carbohydrate ketogenic diets." Current atherosclerosis reports 5.6 (2003): 476-483.</ref>
<ref name="HayBond1967">RW Hay, MA Bond, Kinetics of the Decarboxylation of Acetoacetic acid, Australian Journal of Chemistry, volume 20, issue 9, 1967, pages 1823, ISSN [http://www.worldcat.org/issn/0004-9425 0004-9425], doi [http://dx.doi.org/10.1071/CH9671823 10.1071/CH9671823]</ref>
<ref name="Robinson-1980"> AM. Robinson, DH. Williamson, Physiological roles of ketone bodies as substrates and signals in mammalian tissues., Physiol Rev, volume 60, issue 1, pages 143-87, Jan 1980, PMID [http://www.ncbi.nlm.nih.gov/pubmed/6986618 6986618]</ref>
<ref name="Kalapos-2007"> MP. Kalapos, Possible mechanism for the effect of ketogenic diet in cases of uncontrolled seizures. The reconsideration of acetone theory., Med Hypotheses, volume 68, issue 6, pages 1382-8, 2007, doi [http://dx.doi.org/10.1016/j.mehy.2006.10.041 10.1016/j.mehy.2006.10.041], PMID [http://www.ncbi.nlm.nih.gov/pubmed/17166670 17166670]</ref>
<ref name="Kalapos-1999"> MP. Kalapos, Possible physiological roles of acetone metabolism in humans., Med Hypotheses, volume 53, issue 3, pages 236-42, Sep 1999, doi [http://dx.doi.org/10.1054/mehy.1998.0752 10.1054/mehy.1998.0752], PMID [http://www.ncbi.nlm.nih.gov/pubmed/10580530 10580530]</ref>
</references>