View source for Ketosis

{{Short description|Using body fats as fuel instead of carbohydrates}}
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{{distinguish|Ketoacidosis}}
{{Infobox medical condition (new)
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| synonyms        = Ketonemia
| image           = Ketone bodies.png
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| caption         = [[Ketone bodies]]: acetone, acetoacetic acid, and beta-hydroxybutyric acid
| field           = [[Endocrinology]]
| pronounce       = {{IPAc-en|k|ᵻ|ˈ|t|oʊ|s|ᵻ|s}}
| symptoms        = 
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| risks           = 
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}}

'''Ketosis''' is a metabolic state characterized by elevated levels of [[ketone bodies]] in the blood or urine. Physiological ketosis is a normal response to low [[glucose]] availability. In physiological ketosis, ketones in the blood are elevated above baseline levels, but the body's [[acid–base homeostasis]] is maintained. This contrasts with [[ketoacidosis]], an uncontrolled production of ketones that occurs in pathologic states and causes a [[metabolic acidosis]], which is a medical emergency. Ketoacidosis is most commonly the result of complete [[insulin]] deficiency in [[type 1 diabetes]] or late-stage [[type 2 diabetes]]. Ketone levels can be measured in blood, urine or breath and are generally between 0.5 and 3.0 [[Molar concentration|millimolar]] (mM) in physiological ketosis, while ketoacidosis may cause blood concentrations greater than 10 mM.<ref name=":6" />

Trace levels of ketones are always present in the blood and increase when blood glucose reserves are low and the [[liver]] shifts from primarily metabolizing carbohydrates to metabolizing fatty acids.<ref name=":4">{{cite journal|url=https://www.diapedia.org/metabolism-and-hormones/51040851169/ketone-body-metabolism|title=Ketone Body Metabolism|last1=Ward|first1=Colin |website=Diapedia|doi=10.14496/dia.51040851169.29|url-status=dead|archive-url=https://web.archive.org/web/20181111193826/https://www.diapedia.org/metabolism-and-hormones/51040851169/ketone-body-metabolism|archive-date=2018-11-11|access-date=30 September 2019|year=2015|doi-broken-date=12 July 2025 |url-access=subscription}}{{self-published inline|date=March 2022}}</ref> This occurs during states of increased fatty acid oxidation such as fasting, carbohydrate restriction, or prolonged exercise. When the liver rapidly metabolizes [[fatty acids]] into [[acetyl-CoA]], some acetyl-CoA molecules can then be converted into ketone bodies: [[pyruvate]], [[acetoacetate]], [[beta-hydroxybutyrate]], and [[acetone]].<ref name=":6" /><ref name=":4" /> These ketone bodies can function as an energy source as well as signalling molecules.<ref name=":12">{{cite journal | vauthors = Mattson MP, Moehl K, Ghena N, Schmaedick M, Cheng A | title = Intermittent metabolic switching, neuroplasticity and brain health | journal = Nature Reviews. Neuroscience | volume = 19 | issue = 2 | pages = 63–80 | date = 2018 | pmid = 29321682 | pmc = 5913738 | doi = 10.1038/nrn.2017.156}}</ref> The liver itself cannot utilize these molecules for energy, so the ketone bodies are released into the blood for use by peripheral tissues including the brain.<ref name=":4" />

When ketosis is induced by carbohydrate restriction, it is sometimes called ''nutritional ketosis''.  This may be done intentionally, as a [[Low-carbohydrate diet#Ketogenic diet|low-carbohydrate diet for weight loss or lifestyle reasons]].  It may also be done medically, such as the [[ketogenic diet]] for refractory [[epilepsy in children]] or for treating [[type 2 diabetes]].<ref>{{cite journal |last1=Westman |first1=Eric C. |last2=Tondt |first2=Justin |last3=Maguire |first3=Emily |last4=Yancy |first4=William S. |title=Implementing a low-carbohydrate, ketogenic diet to manage type 2 diabetes mellitus |journal=Expert Review of Endocrinology & Metabolism |date=15 September 2018 |volume=13 |issue=5 |pages=263–272 |doi=10.1080/17446651.2018.1523713 |pmid=30289048 |s2cid=52920398 }}</ref>

==Definitions==

Normal serum levels of ketone bodies are less than 0.5 mM. ''Hyperketonemia'' is conventionally defined as levels in excess of 1&nbsp;mM.<ref name=":6" />

=== Physiological ketosis ===
Physiological ketosis is the non-pathological (normal functioning) elevation of ketone bodies that can result from any state of increased [[fatty acid oxidation]] including fasting, prolonged exercise, or very low-carbohydrate diets such as the [[ketogenic diet|medical ketogenic diet]] or the [[Low-carbohydrate diet#Ketogenic diet|lifestyle "keto" diet]].<ref name=":5">{{cite journal | vauthors = Cahill GF | title = Fuel metabolism in starvation |journal = Annual Review of Nutrition | volume = 26 | pages = 1–22 | date = 2006 | pmid = 16848698 | doi = 10.1146/annurev.nutr.26.061505.111258}}</ref> In physiological ketosis, serum ketone levels generally remain below 3 mM.<ref name=":6" /> 

===Ketoacidosis===
[[Ketoacidosis]] is a pathological state of uncontrolled production of ketones that results in a [[metabolic acidosis]], with serum ketone levels typically in excess of 3&nbsp;mM. Ketoacidosis is most commonly caused by a deficiency of insulin in type 1 diabetes or late stage type 2 diabetes but can also be the result of chronic heavy alcohol use, [[salicylate poisoning]], or isopropyl alcohol ingestion.<ref name=":6" /><ref name=":4" /> Ketoacidosis causes significant metabolic derangements and is a life-threatening medical emergency.<ref name=":4" /> Ketoacidosis is distinct from physiological ketosis as it requires failure of the normal regulation of ketone body production.<ref name=":9">{{cite journal |last1=Krebs |first1=H.A. |title=The regulation of the release of ketone bodies by the liver |journal=Advances in Enzyme Regulation |date=January 1966 |volume=4 |pages=339–353 |doi=10.1016/0065-2571(66)90027-6 |pmid=4865971 }}</ref><ref name=":5" />

==Causes==
Elevated blood ketone levels are most often caused by accelerated ketone production but may also be caused by consumption of exogenous ketones or precursors.

When [[glycogen]] and blood glucose reserves are low, a metabolic shift occurs in order to save glucose for the brain which is unable to use [[fatty acid]]s for energy. This shift involves increasing fatty acid oxidation and production of ketones in the liver as an alternate energy source for the brain as well as the skeletal muscles, heart, and kidney.<ref name=":4" /><ref name=":12" /> Low levels of ketones are always present in the blood and increase under circumstances of low glucose availability. For example, after an overnight fast, 2–6% of energy comes from ketones and this increases to 30–40% after a 3-day fast.<ref name=":6" /><ref name=":4" />

The amount of carbohydrate restriction required to induce a state of ketosis is variable and depends on activity level, [[insulin sensitivity]], genetics, age and other factors, but ketosis will usually occur when consuming less than 50 grams of carbohydrates per day for at least three days.<ref name=":7">{{cite journal | vauthors = Paoli A, Rubini A, Volek JS, Grimaldi KA |title=Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets | journal = European Journal of Clinical Nutrition | volume = 67 | issue = 8 | pages = 789–96 | date = 2013 | pmid = 23801097 | pmc = 3826507 | doi = 10.1038/ejcn.2013.116}}</ref><ref name=":13">{{cite journal | vauthors = Veech RL | title = The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism | journal = Prostaglandins, Leukotrienes, and Essential Fatty Acids | volume = 70 | issue = 3 | pages = 309–19 | date = 2004 | pmid = 14769489 | doi = 10.1016/j.plefa.2003.09.007}}</ref>

Neonates, pregnant women and lactating women are populations that develop physiological ketosis especially rapidly in response to energetic challenges such as fasting or illness. This can progress to ketoacidosis in the setting of illness, although it occurs rarely. Propensity for ketone production in neonates is caused by their high-fat breast milk diet, disproportionately large central nervous system and limited liver glycogen.<ref name=":6" /><ref>{{cite journal |vauthors=Fukao T, Mitchell G, Sass JO, Hori T, Orii K, Aoyama Y | title = Ketone body metabolism and its defects | journal = Journal of Inherited Metabolic Disease | volume = 37 | issue = 4 | pages = 541–51 | date = 2014 | pmid = 24706027 | doi = 10.1007/s10545-014-9704-9| s2cid = 21840932 }}</ref>

==Biochemistry==
The precursors of ketone bodies include fatty acids from [[adipose tissue]] or the diet and [[ketogenic amino acids]].<ref name=":0">{{cite journal | vauthors = Coelho M, Oliveira T, Fernandes R | title = Biochemistry of adipose tissue: an endocrine organ | journal = Archives of Medical Science | volume = 9 | issue = 2 | pages = 191–200 | date = 2013 | pmid = 23671428 | pmc = 3648822 | doi = 10.5114/aoms.2013.33181}}</ref><ref name=":1">{{Cite book|title=Nutrient metabolism : structures, functions, and genes|last=Kohlmeier|first=Martin|isbn=978-0-12-387784-0|oclc=913852019|date = 2015-05-22|publisher=Elsevier Science }}</ref> The formation of ketone bodies occurs via [[ketogenesis]] in the [[Mitochondrion|mitochondrial]] matrix of liver cells.

Fatty acids can be released from adipose tissue by [[adipokine]] signaling of high [[glucagon]] and [[epinephrine]] levels and low insulin levels. High glucagon and low insulin correspond to times of low glucose availability such as fasting.<ref>{{cite journal |last1=Owen |first1=Oliver E. |title=Ketone bodies as a fuel for the brain during starvation |journal=Biochemistry and Molecular Biology Education |date=July 2005 |volume=33 |issue=4 |pages=246–251 |doi=10.1002/bmb.2005.49403304246 |s2cid=11278861 |doi-access=free }}</ref> Fatty acids bound to [[coenzyme A]] allow penetration into mitochondria. Once inside the mitochondrion, the bound fatty acids are used as fuel in cells predominantly through [[beta oxidation]], which cleaves two carbons from the acyl-CoA molecule in every cycle to form [[acetyl-CoA]]. Acetyl-CoA enters the [[citric acid cycle]], where it undergoes an [[aldol condensation]] with [[Oxaloacetic acid|oxaloacetate]] to form [[citric acid]]; citric acid then enters the [[tricarboxylic acid cycle]] (TCA), which harvests a very high energy yield per carbon in the original fatty acid.<ref name="stryer32">{{cite book |title=Biochemistry |publisher=W.H. Freeman and Company |isbn=0-7167-2009-4 |edition=Fourth |location=New York|date=1995|pages=510–515, 581–613, 775–778 |last1=Stryer |first1=Lubert }}</ref>
[[File:Ketones.svg|right|frameless|420x420px|Biochemical pathway of ketone synthesis in the liver and utilization by organs]]
Acetyl-CoA can be metabolized through the TCA cycle in any cell, but it can also undergo ketogenesis in the mitochondria of liver cells.<ref name=":6">{{cite journal |last1=Laffel |first1=Lori |title=Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes |journal=Diabetes/Metabolism Research and Reviews |date=November 1999 |volume=15 |issue=6 |pages=412–426 |doi=10.1002/(SICI)1520-7560(199911/12)15:6<412::AID-DMRR72>3.0.CO;2-8 |pmid=10634967 |doi-access=free }}</ref> When glucose availability is low, oxaloacetate is diverted away from the TCA cycle and is instead used to produce glucose via [[gluconeogenesis]]. This utilization of oxaloacetate in gluconeogenesis can make it unavailable to condense with acetyl-CoA, preventing entrance into the TCA cycle. In this scenario, energy can be harvested from acetyl-CoA through ketone production.

In ketogenesis, two acetyl-CoA molecules condense to form [[acetoacetyl-CoA]] via [[thiolase]]. Acetoacetyl-CoA briefly combines with another acetyl-CoA via [[Hydroxymethylglutaryl-CoA synthase|HMG-CoA synthase]] to form [[HMG-CoA|hydroxy-β-methylglutaryl-CoA]]. Hydroxy-β-methylglutaryl-CoA form the ketone body acetoacetate via [[3-hydroxy-3-methylglutaryl-CoA lyase|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]], which generates much greater concentrations of acetoacetate and D-β-hydroxybutyrate. The resulting ketone bodies cannot be used for energy by the liver so are exported from the liver to supply energy to the brain and peripheral tissues.

In addition to fatty acids, deaminated [[ketogenic amino acids]] can also be converted into intermediates in the citric acid cycle and produce ketone bodies.<ref name=":1" />

==Measurement==
Ketone levels can be measured by testing urine, blood or breath. There are limitations in directly comparing these methods as they measure different ketone bodies.

===Urine testing===
[[File:Ketonuria.jpg|thumb|upright|Test for ketonuria using Bayer Ketostix reagent strips]]
Urine testing is the most common method of testing for ketones. Urine test strips utilize a [[nitroprusside]] reaction with acetoacetate to give a semi-quantitative measure based on color change of the strip. Although beta-hydroxybutyrate is the predominant circulating ketone, urine test strips only measure acetoacetate. Urinary ketones often correlate poorly with serum levels because of variability in excretion of ketones by the kidney, influence of hydration status, and renal function.<ref name=":6" /><ref name=":13" />

===Serum testing===
Finger-stick ketone meters allow instant testing of beta-hydroxybutyrate levels in the blood, similar to [[glucometers]]. Beta-hydroxybutrate levels in blood can also be measured in a laboratory.<ref name=":6" />

==Medical uses==
{{Coatrack section|date=May 2020}}

===Epilepsy===

Ketosis induced by a ketogenic diet is a long-accepted treatment for refractory [[epilepsy]].<ref name="Hartman2007">{{cite journal | vauthors = Hartman AL, Vining EP | title = Clinical aspects of the ketogenic diet | journal = Epilepsia | volume = 48 | issue = 1 | pages = 31–42 | date = 2007 | pmid = 17241206 | doi = 10.1111/j.1528-1167.2007.00914.x| doi-access =  }}</ref>

===Obesity and metabolic syndrome===

Ketosis can improve markers of [[metabolic syndrome]] through reduction in serum [[triglyceride]]s, elevation in [[high-density lipoprotein]] (HDL) as well as increased size and volume of [[low-density lipoprotein]] (LDL) particles. These changes are consistent with an improved lipid profile despite potential increases in [[Cholesterol|total cholesterol]] level.<ref name=":7" /><ref name="Gershuni Yan Medici 2018">{{cite journal |vauthors=Gershuni VM, Yan SL, Medici V | title = Nutritional Ketosis for Weight Management and Reversal of Metabolic Syndrome | journal = Current Nutrition Reports | volume = 7 | issue = 3 | pages = 97–106 | date = 2018 | pmid = 30128963 | pmc = 6472268 | doi = 10.1007/s13668-018-0235-0}}</ref>

==Safety==
The safety of ketosis from [[Low-carbohydrate diet|low-carbohydrate diets]] is often called into question by clinicians, researchers and the media.<ref>{{Cite web|url=https://news.usc.edu/154342/is-the-keto-diet-safe-usc-experts-have-some-serious-concerns/|title=Is the keto diet safe? USC experts have some serious concerns |date=2019-02-19 |website=USC News |language=en-US |access-date=2019-10-03}}</ref><ref>{{cite web|url=https://www.health.com/weight-loss/keto-diet-side-effects|title=7 Dangers of Going Keto |website=Health.com|language=en |access-date=2019-10-03}}</ref><ref name=Plaskett2003>{{cite journal |vauthors =Plaskett LG |title=On the Essentiality of Dietary Carbohydrate |journal=Journal of Nutritional & Environmental Medicine |date=September 2003 |volume=13 |issue=3 |pages=161–168 |doi=10.1080/13590840310001619405 }}</ref> A common safety concern stems from the misunderstanding of the difference between physiological ketosis and pathologic ketoacidosis.<ref name=":9" /><ref name=":7" /> There is also continued debate whether chronic ketosis is a healthy state or a stressor to be avoided. Some argue that humans evolved to avoid ketosis and should not be in ketosis long-term.<ref name=Plaskett2003/> The counter-argument is that there is no physiological requirement for dietary carbohydrates, as adequate energy can be made via gluconeogenesis and ketogenesis indefinitely.<ref name=":8">{{cite journal | vauthors = Manninen AH | title = Metabolic effects of the very-low-carbohydrate diets: misunderstood 'villains' of human metabolism | journal = Journal of the International Society of Sports Nutrition | volume = 1 | issue = 2 | pages = 7–11 | date = 2004 | pmid = 18500949 | pmc = 2129159 | doi = 10.1186/1550-2783-1-2-7 | doi-access = free }}</ref> Alternatively, the switching between a ketotic and fed state has been proposed to have beneficial effects on metabolic and neurologic health.<ref name=":12" /> The effects of sustaining ketosis for up to two years are known from studies of people following a strict ketogenic diet for epilepsy or type 2 diabetes; these include short-term adverse effects leading to potential long-term ones.<ref name=":11">{{cite book |vauthors=Masood W, Uppaluri KR |chapter=Ketogenic Diet |date=2019 |pmid=29763005 |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK499830/ |access-date=2019-10-03 |publisher=StatPearls Publishing |title=StatPearls}}</ref> However, literature on longer term effects of intermittent ketosis is lacking.<ref name=":11" />

=== Medication considerations ===
Some medications require attention when in a state of ketosis, especially several classes of diabetes medication. [[SGLT2 inhibitor]] medications have been associated with cases of [[Diabetic ketoacidosis|euglycemic ketoacidosis]] – a rare state of high ketones causing a metabolic acidosis with normal blood glucose levels. This usually occurs with missed insulin doses, illness, dehydration or adherence to a low-carbohydrate diet while taking the medication.<ref>{{cite journal | vauthors = Goldenberg RM, Berard LD, Cheng AY, Gilbert JD, Verma S, Woo VC, Yale JF | title = SGLT2 Inhibitor-associated Diabetic Ketoacidosis: Clinical Review and Recommendations for Prevention and Diagnosis | journal = Clinical Therapeutics | volume = 38 | issue = 12 | pages = 2654–2664.e1 | date = 2016 | pmid = 28003053 | doi = 10.1016/j.clinthera.2016.11.002}}</ref> Additionally, medications used to directly lower blood glucose including insulin and [[sulfonylurea]]s may cause hypoglycemia if they are not titrated prior to starting a diet that results in ketosis.<ref name=":11" />

=== Adverse effects ===
There may be side effects when changing over from glucose metabolism to fat metabolism.<ref>{{Cite web |last=Roberts |first=Vanessa |date=6 March 2017 |title=Side effects of a ketogenic diet |url=https://planketogenic.pro/en/keto-diet-guide#side-effects-of-a-ketogenic-diet |website=PlanKetogenic.pro}}</ref> These may include headache, fatigue, dizziness, insomnia, difficulty in exercise tolerance, constipation, and nausea, especially in the first days and weeks after starting a ketogenic diet.<ref name=":11" /> Breath may develop a sweet, fruity flavor via production of acetone that is exhaled because of its high volatility.<ref name=":7" />

Most adverse effects of long-term ketosis are reported among children because of its longstanding acceptance as a treatment for pediatric epilepsy. These include compromised bone health, stunted growth, [[hyperlipidemia]], and [[Kidney stone disease|kidney stones]].<ref>{{cite journal | vauthors = Kossoff EH, Zupec-Kania BA, Rho JM | title = Ketogenic diets: an update for child neurologists | journal = Journal of Child Neurology | volume = 24 | issue = 8 | pages = 979–88 | date = 2009 | pmid = 19535814 | doi = 10.1177/0883073809337162| s2cid = 11618891 }}</ref>

=== Contraindications ===
Ketosis induced by a ketogenic diet should not be pursued by people with [[pancreatitis]] because of the high dietary fat content. Ketosis is also contraindicated in [[pyruvate carboxylase deficiency]], [[porphyria]], and other rare [[Inborn errors of lipid metabolism|genetic disorders of fat metabolism]].<ref>{{cite journal | vauthors = Kossoff EH, Zupec-Kania BA, Amark PE, Ballaban-Gil KR, Christina Bergqvist AG, Blackford R, Buchhalter JR, Caraballo RH, Helen Cross J, Dahlin MG, Donner EJ, Klepper J, Jehle RS, Kim HD, Christiana Liu YM, Nation J, Nordli DR, Pfeifer HH, Rho JM, Stafstrom CE, Thiele EA, Turner Z, Wirrell EC, Wheless JW, Veggiotti P, Vining EP | title = Optimal clinical management of children receiving the ketogenic diet: recommendations of the International Ketogenic Diet Study Group | journal = Epilepsia | volume = 50 | issue = 2 | pages = 304–317 | date = 2009 | pmid = 18823325 | doi = 10.1111/j.1528-1167.2008.01765.x| doi-access = free }}</ref>

==Veterinary medicine==
===Cattle===
In [[dairy cattle]], ketosis commonly occurs during the first weeks after giving birth to a calf and is sometimes referred to as ''acetonemia''. This is most likely the result of an energy deficit when intake is inadequate to compensate for the increased metabolic demand of lactating.<ref>{{cite web |last1=McArt |first1=Jessica |title=Hyperketonemia in Cattle |url=https://www.merckvetmanual.com/metabolic-disorders/hyperketonemia-in-cattle/hyperketonemia-in-cattle |website=Merck Manual |access-date=2 October 2025}}</ref> The elevated β-hydroxybutyrate concentrations can depress gluconeogenesis, feed intake and the immune system, as well as have an impact on milk composition.<ref>{{cite journal | vauthors = Gross JJ, Bruckmaier RM | title = Review: Metabolic challenges in lactating dairy cows and their assessment via established and novel indicators in milk | journal = Animal | volume = 13 | issue = S1 | pages = s75–s81 | date = 2019 | pmid = 31280745 | doi = 10.1017/S175173111800349X| doi-access = free | bibcode = 2019Anim...13..s75G }}</ref> Point of care diagnostic tests can be useful to screen for ketosis in cattle.<ref>{{cite journal | vauthors = Tatone EH, Gordon JL, Hubbs J, LeBlanc SJ, DeVries TJ, Duffield TF | title = A systematic review and meta-analysis of the diagnostic accuracy of point-of-care tests for the detection of hyperketonemia in dairy cows | journal = Preventive Veterinary Medicine | volume = 130 | pages = 18–32 | date = 2016 | pmid = 27435643 | doi = 10.1016/j.prevetmed.2016.06.002}}</ref>
===Sheep===
In [[sheep]], ketosis, evidenced by hyperketonemia with [[beta-hydroxybutyrate]] in blood over 0.7&nbsp;mmol/L, is referred to as ''pregnancy toxemia''.<ref name=Pugh2002>Pugh, D. G. 2002. Sheep and goat medicine. Saunders, Philadelphia. 468 pp.</ref><ref name=Kimberling1988>Kimberling, C. V. 1988. Jensen and Swift's diseases of sheep. 3rd Ed. Lea & Febiger, Philadelphia. 394 pp.</ref> This may develop in late pregnancy in ewes bearing multiple fetuses and is associated with the considerable metabolic demands of the pregnancy.<ref>{{cite journal |vauthors=Marteniuk JV, Herdt TH |title=Pregnancy toxemia and ketosis of ewes and does |journal=The Veterinary Clinics of North America. Food Animal Practice |volume=4 |issue=2 |pages=307–15 |date=1988 |pmid=3264753 |doi=10.1016/s0749-0720(15)31050-1}}</ref><ref>{{cite journal |vauthors=Reid RL |year=1960 |title=Studies on the carbohydrate metabolism of sheep. IX. Metabolic effects of glucose and glycerol in undernourished pregnant ewes and in ewes with pregnancy toxaemia |journal=Australian Journal of Agricultural Research |volume=11 |pages=42–47 |doi=10.1071/ar9600042}}</ref> In ruminants, because most glucose in the digestive tract is metabolized by [[rumen]] organisms, glucose must be supplied by [[gluconeogenesis]].<ref>Van Soest, P. J. 1994. Nutritional ecology of the ruminant. 2nd Ed. Cornell Univ. Press. 476 pp.</ref> Pregnancy toxemia is most likely to occur in late pregnancy due to metabolic demand from rapid fetal growth and may be triggered by insufficient feed energy intake due to weather conditions, stress or other causes.<ref name=Kimberling1988 /> Prompt recovery may occur with natural parturition, Caesarean section or induced abortion. Prevention through appropriate feeding and other management is more effective than treatment of advanced stages of pregnancy toxemia.<ref>{{cite book |editor-last=Kahn |editor-first=C. M. |year=2005 |title=Merck Veterinary Manual |edition=9th |publisher=[[Merck & Co.]] |location=Whitehouse Station |title-link=Merck Veterinary Manual}}</ref>

== See also ==
{{col div|colwidth=30em}}
*[[Bioenergetics]]
*[[Ketonuria]]
*[[Ketogenic diet]]
*[[Very-low-calorie diet]]
*[[Inuit cuisine]]

{{colend}}

== References ==
{{reflist}}

== Further reading ==
{{refbegin}}
* {{cite book|first1=R. A. |last1=Lawrie |first2=David |last2=Ledward|title=Lawrie's Meat Science |url=https://books.google.com/books?id=b7xQAwAAQBAJ&pg=PA92|date=2014|publisher=Elsevier Science |isbn=978-1-84569-161-5}}
* {{cite book |last1=Volek |first1=Jeff S. |last2=Phinney |first2=Stephen D. |year=2012 |title=The Art and Science of Low Carbohydrate Performance |page=91 |publisher=Beyond Obesity |isbn=978-0-9834907-1-5}}
* {{cite book |last1=Lowery |first1=Ryan |last2=Wilson |first2=Jacob |year=2017 |title=The Ketogenic Bible: The Authoritative Guide to Ketosis |publisher=Victory Belt |isbn=978-1-62860-104-6}}
{{refend}}

== External links ==
{{Medical resources
| DiseasesDB      = 29485
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| ICD9            = {{ICD9|276.2}}
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| MeshID          = D007662
| SNOMED CT       = 2538008
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{{Wiktionary}}
*{{EMedicine|emerg|135|Diabetic Ketoacidosis}}
*[http://www.nhs.uk/conditions/ketosis/Pages/Introduction.aspx NHS Direct: Ketosis] {{Webarchive|url=https://web.archive.org/web/20120424095855/http://www.nhs.uk/conditions/Ketosis/Pages/Introduction.aspx |date=2012-04-24 }}
* The Merck Manual —
**[http://www.merckmanuals.com/professional/sec13/ch169/ch169b.html Diabetic Ketoacidosis]
**[http://www.merckmanuals.com/professional/sec13/ch169/ch169d.html Alcoholic Ketoacidosis]

{{Lipid metabolism}}

[[Category:Metabolism]]