Signs of ketosis in diet

One of the questions people who are new to the LCHF (keto/ketogenic/low carb) diet frequently ask me is: how do I know if I’m in ketosis? What are the main signs of ketosis?

Everyone’s different and while some may experience all of the symptoms of ketosis, some might only feel a couple of them. Some feel none at all. There are basic signs and symptoms that indicate that you’re in ketosis. But please note that I’m differentiating between the signs of keto flu (covered in the post I’m linking to) that many experience in the first days of a ketogenic diet, and the feeling of being in ketosis when the flu has subsided:

  • Dry mouth (eat more salt and drink more water to alleviate this). See my keto breath article here.
  • Weight loss. Yay!
  • Metallic taste in your mouth or a strange taste in the back of your throat. Some describe it as fruity or a little sweet.
  • A kind of “buzzing” feeling that’s hard to describe. Almost euphoric at times.
  • Different kind of urine smell, stronger too!
  • “Ketosis breath” – It can range from being a little sweet to being almost like you’ve had a drink of alcohol.
  • Less appetite. You can go for hours without eating and don’t feel very hungry.
  • Increased energy. If you don’t experience it try to eat more fat. Also, drink more water and watch your electrolytes.
  • A ketone strip you pee on shows a positive result. There are also blood ketone meters, or the popular ketone breath test, that give a more specific result. (Pro-tip: If you get the pee strips, cut them in half 😉 ) But do note that even with a positive pee strip it’s not 100% certain that you’re in ketosis. A very dark positive result may only indicate that you’re dehydrated.

For me personally, the main signs of ketosis are hard to miss. I just feel different! It’s hard to describe. Fortunately I don’t get ketosis breath, but I do have a different taste in my mouth. I also get that buzzing feeling, dry mouth (when I forget to drink enough), less appetite and increased energy. That is, unless I forget to eat. However, my husband had a different experience and I’ve heard many versions and stories of people’s experiences with ketosis. So keep in mind that everyone’s different and even if you don’t have the signs of ketosis I describe in this post it doesn’t mean that you’re not 😉

If you’re eating low carb, lost some water weight already or went through the dreaded keto flu I’ll bet at least a few $$ that you’re in ketosis.

One of the main goals of starting the ketogenic diet is to get your body into a metabolic state known as ketosis.

Note: If you don’t know what the ketogenic is all about then check out the Ketogenic Diet: Beginner’s Guide to Keto and Weight Loss.

This is when your body starts to produce a lot of ketones to supply energy for your body.

Why is this good? Because it means your body has converted from a sugar-burner to a fat-burner.

If your body is burning fat for energy then something amazing starts to happen. The fat on your body starts to disappear.

But how do you know when you’re in ketosis? Besides using test strips or an instrument there are some signs that your body will give.

7 Signs You Might Be in Ketosis

These don’t 100% guarantee that your body is in ketosis but if it is in ketosis then these signs will appear.

1. Weight Loss

One of the obvious signs of ketosis is weight loss but this can also be pretty deceptive because many people don’t experience the kind of weight loss that they expect.

This can happen for a variety of reasons but when you get close to entering ketosis or do enter ketosis you’ll find that you lose a healthy amount of weight quickly.

For example, when you switch to low carbs you usually experience significant weight loss in the first week. In fact, my wife lost 12 lbs in the first 28 days of Keto and I lost 13.

This isn’t your body burning fat but finally being able to release the water that was being held by the fat cells.

If your fat cells don’t release this water then they can’t flow through the bloodstream to be used as fuel so losing water weight is a good thing.

After the initial rapid drop in water weight, you should continue to lose body fat consistently if you are able to stick with the low-carb aspects of the diet and keep your body in a caloric deficit.

2. Loss of Appetite

Something strange happens when you leave the world of carbs behind.

You don’t get as hungry.

You still get hungry but your stomach won’t do earth shattering rumblings that make you think you need to clear out the buffet.

Instead, you will find that you eat only what is necessary and continue on with your day.

The reason for this is because your body does a better job of regulating the hormones that trigger your brain to let you know that you need to eat.

When you overeat enough with carbs your brain starts to ignore the hormone. This is why you can sometimes eat so much you feel like you are going to explode.

3. Increased Focus and Energy

A personal favorite when it comes to ketosis.

If you are the type of person that is used to your body crashing in the afternoon then ketosis might seem like a miracle diet.

When people talk about no longer being tired in the afternoon it’s just a small difference that produces huge results.

In ketosis, your body does a great job of producing ketones (it’s good at what it does) so you almost have an endless supply of fuel for your brain.

When your brain has the fuel it allows you to stay focused instead of wandering off envisioning the cupcakes in the break room.

4. Short-Term Fatigue

Wait, what?

We just talked about increased energy and now we are talking about fatigue.

The problem with switching over to the ketogenic diet is that your body has to completely transition over.

During this transition, your body is looking for glucose and when it doesn’t have it, it isn’t quite ready yet to produce enough ketones to sustain you.

Your body is also releasing a lot of electrolytes through urine that you aren’t used to replacing. Hint: If you aren’t in ketosis yet it might be because you aren’t drinking enough water.

To fight the short-term fatigue and get over this initial hump simply make sure that you are replacing all of the electrolytes that your body is losing.

You can do this with specialized drinks and supplements or make sure you get them in the foods that you eat.

If you go the supplement route be sure that you are taking 2,000 – 4,000 mg of sodium, 1,000 mg of potassium and 300 mg of magnesium.

What we like to do is mix Mio Electrolytes Berry Blast with our water. It’s a great way to replenish your electrolytes, is easy to carry around and it tastes great.

You never had to worry about these things before because the bad foods with carbs also pack these minerals in as well.

5. Toilet Issues

No, your toilet won’t be broken but you might find that your normal toilet routine isn’t the same.

Your body can go one of three ways here:

  1. Constipation. Some people go days without using the bathroom. In these cases, you might need to add more fiber or magnesium to your diet.
  2. Diarrhea. When you’re adding more fat than your body is used to it’s a huge shift to your body. Eventually, it will get used to it but if you want to make the transition quicker then take a fiber supplement.
  3. Nothing. Some people don’t experience any change. Things just continue on as normal. They are the lucky ones.

6. Bad Breath

Halitosis is one of the side effects that I do not like with the ketogenic diet.

It’s no fun waking up and wondering what died in your mouth.

It’s probably not as bad as I made it sound but you will experience bad breath.

The reason for this is because your body is producing more acetone which exits your body through your urine and breath.

It doesn’t carry on throughout the day, just when you wake up so make sure you brush your teeth.

You can also chew on sugar-free gum throughout the day if you are afraid of it appearing with your noticing.

For most people, the bad breath usually goes away after a certain amount of time.

7. Increased Ketones

Obviously, if you are in ketosis your body is producing more ketones.

If you really want to check your ketone levels then the best route to go is to use a Glucose Meter.

A cheaper alternative, although a bit harder to read, is test strips.

Everybody Is Different

One of the toughest things about the ketogenic diet that many people struggle with is that all of our bodies are different and therefore our bodies will react differently when on the diet.

You might read how someone was able to lose 10 lbs in 1 week and got into ketosis after just 3 days while you’ve been struggling for 3+ weeks to make the pee strip turn darker.

There is no step-by-step formula to get into ketosis that can apply to everybody.

Some people need to eat fewer carbs than others while some might need to incorporate exercise into their daily routine sooner.

The point is that when you get rid of sugars and lower the number of carbs you consume you are doing a great thing for your body anyways. If you can focus on those things and let everything else happen naturally you’ll find yourself in a much better state of mind.

If you’re interested in getting more guidance with regards to the Ketogenic Diet then check out our program Keto Dash. We help walk you through the Ketogenic Diet and provide you with all of the information that you need to succeed.

If you are considering the ketogenic diet or have already started down this carb-free road, you may wonder what you can expect. Here’s the thing. Ketosis looks different for everyone, but I will share many of the most common symptoms with you today. If something other than what’s listed here is happening to you, just do a quick Google search for that symptom and keto. You should be able to find what you’re looking for!

The Early Signs:

The early signs of ketosis vary from person to person. The biggest impact on how quickly you notice the symptoms of ketosis will have a lot to do with how you ate before you started the diet. If your diet was very high carb, you might get hit pretty quickly and furiously with what we like to call the “Keto Flu.” This can last anywhere from 3 days to a week or more. Once your body has adapted to burning ketones for energy instead of glucose, you’ll be golden so don’t give up!

Here’s what you can expect within the first 2-3 days of starting the Ketogenic Diet:

Fatigue & Weakness (lack of concentration)
Metallic taste or sweet taste in your mouth (I experienced this, and it tasted like blood in my mouth)
Lightheaded / Dizzy upon standing
Heightened Thirst
Hunger / Sweet or Carb Cravings
Dry Mouth possibly paired with “Keto Breath.”
Stomach Discomfort / Mild Nausea / Cramping
Trouble Sleeping or Staying Asleep (early waking)
Water weight loss (perhaps an excessive loss of weight within the first two weeks)
Frequent Urination
Allergies or cold like symptoms may flair up

For the ladies: 
Period issues: You may experience a longer, shorter, earlier, later period because of Keto. Seriously it causes all of that. Each woman is different, and I have experienced every one of those issues with my period since starting keto. Don’t worry you will get back to normal but be prepared at all times, just in case!

Hair loss/growth: This one is a weird one, but I have seen it on both sides. When I first started keto I could have sworn the white peach fuzz hair on my face was getting longer (maybe I was paranoid) but I was also losing so much hair from my head that it was starting to worry me. Thankfully that usually stops after a few weeks so don’t be too worried if your hair starts acting wonky. This diet and our diets, in general, are greatly linked to our hormones, metabolism, and everything else going on inside our bodies so if you’re dealing with any female issues you should find that being in Ketosis is like medication for all that ails you! Before keto, I would break out every month with hormonal acne, get ridiculously bloated and feel like total crap. Now my shark weeks are 100 times better, and I can’t imagine going back to that. Yay for no acne!!

I personally didn’t eat a ton of carbs before starting keto and when I knew I was going to start I stopped eating bread a few days before to prepare. For those reasons my initial induction into ketosis were pretty painless. I did have a mild headache and was tired for 2-3 days but after that I was good to go. I also deal with the occasional light-headedness even now, but I attribute that to not drinking enough water (which I still struggle with).

After Your Body Adapts To Ketosis:

Once your body adapts to running on ketones you can expect to experience any of the following:

Increased awareness/concentration
More energy
Better more even sleep cycles
Possible Euphoria (This was the most fabulous part of ketosis for me)
Fat Loss (you’ll start to notice the number on the scale drop along with the inches)
Reduced Appetite

Dealing with the Symptoms of Ketosis:

Anything worth doing hurts (at least a little). Please whatever you do, don’t give up or give in. You can do this. Here are some tips that helped me get by when I was dealing with the early stages of ketosis.

Drink lots and lots and lots of water. Don’t be crazy about it, but drink at least 100oz a day. This will help with the headaches, fatigue, and even the keto breath.

Remember why you’re doing this. This is a forever change. Yes the diet will change as you make progress but you’re changing your life forever and a few days are totally worth forever right?

Exercise helps too. I know you’re tired but even spend 10 minutes a day working on those abs will be enough to motivate you to keep going. One healthy thing leads to another and the next thing you know you’ve reached your goal and are inspiring others to do the same.

Get some keto strips and test yourself daily. Now these strips don’t always work but early on you should be fine. You may notice trace amounts of ketones in your urine within three days. Trust me that will keep you motivated!

Start keto with a friend or join a group on Facebook. Having support is so important and finding like-minded people to help you when you have questions or push you when you need motivation is paramount!

Start by eating smaller meals more often. Be sure to track everything and stay within your ranges, but eating a little throughout the day can be very helpful when you’re first starting out.

A word of caution here. Be careful who you tell about your new lifestyle and make sure you fully understand how this diet works and why you are changing your lifestyle. You may experience some push back from close friends and even family because everyone is skeptical when they hear the word diet, especially when it comes to low carb diets. Also, know that some may misunderstand Ketosis and compare it to Ketoacidosis which is completely different and very dangerous. So know your terminology and teach them a thing or two!

My experience going into ketosis is documented week by week here on the blog along with the foods I ate during the week. You can check those posts out here:

Keto Week 1

Keto Week 2 Keto Week 3

If you ever have any questions about what you’re going through, please don’t hesitate to reach out to me. If I don’t know the answer, I can help you find it. Also, (I have to say this) please talk to your doctor before starting any diet or exercise program. I am not a doctor nor am I a scientist (that would be so rad) so I can only tell you what I have learned and have experienced myself.

Ketosis is a metabolic state in which some of the body’s energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis in which blood glucose provides energy. Ketosis is a result of metabolizing fat to provide energy.

Ketosis is a nutritional process characterised by serum concentrations of ketone bodies over 0.5 mM, with low and stable levels of insulin and blood glucose. It is almost always generalized with hyperketonemia, that is, an elevated level of ketone bodies in the blood throughout the body. Ketone bodies are formed by ketogenesis when liver glycogen stores are depleted (or from metabolising medium-chain triglycerides). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate, and the levels of ketone bodies are regulated mainly by insulin and glucagon. Most cells in the body can use both glucose and ketone bodies for fuel, and during ketosis, free fatty acids and glucose synthesis (gluconeogenesis) fuel the remainder.

Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet (ketogenic diet), and deliberately induced ketosis serves as a medical intervention for various conditions, such as intractable epilepsy, and the various types of diabetes. In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed. For this reason, ketosis is sometimes referred to as the body’s “fat burning” mode.

Ketosis and ketoacidosis are similar, but ketoacidosis is an acute life-threatening state requiring prompt medical intervention while ketosis can be physiological. However, there are situations (such as treatment-resistant epilepsy) where ketosis can be rather beneficial to health.



Ketone bodies are acidic, but acid-base homeostasis in the blood is normally maintained through bicarbonate buffering, respiratory compensation to vary the amount of CO2 in the bloodstream, hydrogen ion absorption by tissue proteins and bone, and renal compensation through increased excretion of dihydrogen phosphate and ammonium ions. Prolonged excess of ketone bodies can overwhelm normal compensatory mechanisms, defined as acidosis if blood pH falls below 7.35.

There are two major causes of ketoacidosis:

  • Most commonly, ketoacidosis is diabetic ketoacidosis (DKA), resulting from increased fat metabolism due to a shortage of insulin. It is associated primarily with type I diabetes, and may result in a diabetic coma if left untreated.
  • Alcoholic ketoacidosis (AKA) presents infrequently, but can occur with acute alcohol intoxication, most often following a binge in alcoholics with acute or chronic liver or pancreatic disorders. Alcoholic ketoacidosis occurs more frequently following methanol or ethylene glycol intoxication than following intoxication with uncontaminated ethanol.

A mild acidosis may result from prolonged fasting or when following a ketogenic diet or a very low calorie diet.


Ketosis is deliberately induced by use of a ketogenic diet as a medical intervention in cases of intractable epilepsy. Other uses of low-carbohydrate diets remain controversial. Carbohydrate deprivation to the point of ketosis has been argued to have both negative and positive effects on health.


The two sources of ketone bodies in the body are fatty acids in adipose tissue and ketogenic amino acids. The main formation of ketone bodies is through ketogenesis.

Adipose tissue can be used to store fatty acids for regulating temperature and energy. These fatty acids can be released by adipokine signaling of high glucagon and epinephrine levels, which inversely corresponds to low insulin levels. High glucagon and low insulin correspond to times of fasting or to times when blood glucose levels are low. Fatty acids must be metabolized in mitochondria, so coenzyme A is bound to the fatty acid to produce acyl-CoA. The acyl-CoA are able to enter the mitochondria. These fatty acids are used as fuel in cells through β-oxidation, which gives a large energy payout per acyl-CoA molecule that is formed from the β-oxidation of a fatty acid.

As β-oxidation begins, FAD dehydrogenates acyl-CoA to form trans-Δ2-enoyl-CoA and FADH2. Acyl-CoA Dehydrogenase catalyses a double bond in this step. Next, trans-Δ2-enoyl-CoA is hydrogenated by enoyl CoA hydratase to form L-β-hydroxyacyl CoA. NAD+ and the enzyme 3-hydroxyacyl-CoA dehydrogenase oxidize L-β-hydroxyacyl CoA to form β-ketoacyl CoA and NADH. Lastly, the β-ketoacyl CoA is cleaved by a thiol group in CoA to form another acyl-CoA and an acetyl-CoA. This reaction is catalyzed by thiolase. The acyl-CoA is two carbons shorter than before, so it enters β-oxidation again until it all converts into acetyl-CoA.

The acetyl-CoA enters the citric acid cycle and undergoes an aldol condensation with oxaloacetate to form citrate. The citric acid cycle is a key pathway for metabolism. It provides precursors for many amino acids as steps in the cycle. It also allows high energy molecules to form; 3x NADH, FADH2, and GTP/ATP are all produced by one iteration of the cycle. This is equivalent to 10 ATP. Acetyl-CoA undergoes this process in any cell, while liver cells can also undergo a different process: ketogenesis.

In the liver, acetyl-CoA can undergo ketogenesis to form ketone bodies. They are produced in mitochondria, and usually occur in response to low blood glucose levels. In the mitochondria, the acetyl-CoA does not enter the citric acid cycle when the amount of acetyl-CoA widely exceeds that of oxaloacetate, as the first step cannot proceed. Along with the fatty acids, deaminated ketogenic amino acids can be converted into intermediates in the citric acid cycle and produce ketone bodies.

Ketogenesis produces one ketone body per two acetyl-CoA. Two acetyl-CoA 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 forms acetoacetate via HMG-CoA lyase. Acetoacetate can then reversibly convert to D-β-hydroxybutyrate via D–β-hydroxybutyrate dehydrogenase. Another option here is acetoacetate can spontaneously degrade to acetone and carbon dioxide. From here, all three ketone bodies (acetoacetate, D–β-hydroxybutyrate, and acetone) have been formed, but acetoacetate and D–β-hydroxybutyrate are in much greater concentrations.


Whether ketosis is taking place can be checked by using special urine test strips such as Ketostix. The strips have a small pad on the end, which the user dips in a fresh urine specimen. Within seconds, the strip changes color to indicate the level of acetoacetate ketone bodies, which reflects the degree of ketonuria, which, in turn, gives a rough estimate of the level of hyperketonemia in the body (see table below). Alternatively, some products targeted to diabetics such as the Abbott Precision Xtra or the Nova Max can be used to take a blood sample and measure the β-hydroxybutyrate ketone levels directly. Normal serum reference ranges for ketone bodies are 0.5–3.0 mg/dL, equivalent to 0.05–0.29 mmol/L.

Also, when the body is in ketosis, one’s breath may smell of acetone. This is due to the breakdown of acetoacetic acid into acetone and carbon dioxide exhaled through the lungs. Acetone is the chemical responsible for the smell of nail polish remover and some paint thinners.


The concentration of ketone bodies may vary depending on diet, exercise, degree of metabolic adaptation and genetic factors. Ketosis can be induced when a ketogenic diet is followed for more than 3 days. This induced ketosis is sometimes called nutritional ketosis. This table shows the concentrations typically seen under different conditions

< 0.2 not in ketosis
0.2 – 0.5 slight/mild ketosis
0.5 – 3.0 induced/nutritional ketosis
2.5 – 3.5 post-exercise ketosis
3.0 – 6.0 starvation ketosis
15 – 25 ketoacidosis

Note that urine measurements may not reflect blood concentrations. Urine concentrations are lower with greater hydration, and after adaptation to a ketogenic diet the amount lost in the urine may drop while the metabolism remains ketotic. Most urine strips only measure acetoacetate, while when ketosis is more severe the predominant ketone body is β-hydroxybutyrate. Unlike glucose, ketones are excreted into urine at any blood level. Ketoacidosis is a metabolic derangement that cannot occur in a healthy individual who can produce insulin, and should not be confused with physiologic ketosis.


Some clinicians regard eliminating carbohydrates as unhealthy and dangerous. However, it is not necessary to eliminate carbohydrates from the diet completely to achieve ketosis. Other clinicians regard ketosis as a safe biochemical process that occurs during the fat-burning state. Ketosis, which is accompanied by gluconeogenesis (the creation of glucose de novo from pyruvate), is the specific state that concerns some clinicians. However, it is unlikely for a normally functioning person to reach life-threatening levels of ketosis, defined as serum beta-hydroxybutyrate (B-OHB) levels above 15 millimolar (mM) compared to ketogenic diets among non diabetics, which “rarely run serum B-OHB levels above 3 mM.” This is avoided with proper basal secretion of pancreatic insulin. People who are unable to secrete basal insulin, such as type 1 diabetics and long-term type II diabetics, are liable to enter an unsafe level of ketosis, eventually resulting in a coma that requires emergency medical treatment. The anti-ketosis conclusions have been challenged by a number of doctors and advocates of low-carbohydrate diets, who dispute assertions that the body has a preference for glucose and that there are dangers associated with ketosis.

Inuit people

The Inuit are often cited as an example of a culture that has lived for hundreds of years on a low-carbohydrate diet. However, in multiple studies the traditional Inuit diet has not been shown to be a ketogenic diet. Not only have multiple researchers been unable to detect any evidence of ketosis resulting from the traditional Inuit diet, but the ratios of fatty-acid to glucose were observed at well below the generally accepted level of ketogenesis. Furthermore, studies investigating the fat yields from fully dressed wild ungulates, and the dietary habits of the cultures who rely on them, suggest that they are too lean to support a ketogenic diet. With limited access to fat and carbohydrates, cultures such as the Nunamiut Eskimos—who relied heavily on caribou for subsistence—annually traded for fat and seaweed with coastal-dwelling Taremiut.

Some Inuit consume as much as 15–20% of their calories from carbohydrates, largely from the glycogen found in raw meats. Furthermore, the blubber, organs, muscle and skin of the diving marine mammals that the Inuit eat have significant glycogen stores that are able to delay postmortem degradation, particularly in cold weather.

Moreover, recent studies show that the Inuit have evolved a number of rare genetic adaptations that make them especially well suited to eat large amounts of omega-3 fat. And earlier studies showed that the Inuit have a very high frequency—68% to 81% in certain arctic coastal populations—of an extremely rare autosomal recessive mutation of the CPT1A gene—a key regulator of mitochondrial long-chain fatty-acid oxidation—which results in a rare metabolic disorder known as carnitine palmitoyltransferase 1A (CPT1A) deficiency and promotes hypoketotic hypoglycemia—low levels of ketones and low blood sugar. The condition presents symptoms of a fatty acid and ketogenesis disorder. However, it appears highly beneficial to the Inuit as it shunts free fatty acids away from liver cells to brown fat, for thermogenesis. Thus the mutation may help the Inuit stay warm by preferentially burning fatty acids for heat in brown fat cells. In addition to promoting low ketone levels, this disorder also typically results in hepatic encephalopathy (enlarged liver) and high infant mortality. Inuit have been observed to have enlarged livers with an increased capacity for gluconeogenesis, and have greater capacity for excreting urea to remove ammonia, a toxic byproduct of protein breakdown. Ethnographic texts have documented the Inuit’s customary habit of snacking frequently and this may well be a direct consequence of their high prevalence of the CPT1A mutation as fasting, even for several hours, can be deleterious for individuals with that allele, particularly during strenuous exercise. The high frequency of the CPT1A mutation in the Inuit therefore suggests that it is an important adaptation to their low carbohydrate diet and their extreme environment.

In addition to the seaweed and glycogen carbohydrates mentioned above, the Inuit can access many plant sources. The stomach contents of caribou contain a large quantity of partially digested lichens and plants, which the Inuit once considered a delicacy. They also harvested reindeer moss and other lichens directly. The extended daylight of the arctic summer led to a profusion of plant life, and they harvested plant parts including berries, roots and stems, as well as mushrooms. They preserved some gathered plant life to eat during winter, often by dipping it in seal fat.


While it is believed that carbohydrate intake after exercise is the most effective way of replacing depleted glycogen stores, studies have shown that, after a period of 2–4 weeks of adaptation, physical endurance (as opposed to physical intensity) is unaffected by ketosis, as long as the diet contains high amounts of fat, relative to carbohydrates. Some clinicians refer to this period of keto-adaptation as the “Schwatka imperative” after Frederick Schwatka, the explorer who first identified the transition period from glucose-adaptation to keto-adaptation.

Veterinary medicine

In dairy cattle, ketosis is a common ailment that usually occurs during the first weeks after giving birth to a calf. Ketosis is in these cases sometimes referred to as acetonemia. A study from 2011 revealed that whether ketosis is developed or not depends on the lipids a cow uses to create butterfat. Animals prone to ketosis mobilize fatty acids from adipose tissue, while robust animals create fatty acids from blood phosphatidylcholine (lecithin). Healthy animals can be recognized by high levels of milk glycerophosphocholine and low levels of milk phosphocholine. Point of care diagnostic tests are available and are reasonably useful.

In sheep, ketosis, evidenced by hyperketonemia with beta-hydroxybutyrate in blood over 0.7 mmol/L, occurs in pregnancy toxemia. This may develop in late pregnancy in ewes bearing multiple fetuses, and is associated with the considerable glucose demands of the conceptuses. In ruminants, because most glucose in the digestive tract is metabolized by rumen organisms, glucose must be supplied by gluconeogenesis, for which propionate (produced by rumen bacteria and absorbed across the rumen wall) is normally the principal substrate in sheep, with other gluconeogenic substrates increasing in importance when glucose demand is high or propionate is limited. Pregnancy toxemia is most likely to occur in late pregnancy because most fetal growth (and hence most glucose demand) occurs in the final weeks of gestation; it may be triggered by insufficient feed energy intake (anorexia due to weather conditions, stress or other causes), necessitating reliance on hydrolysis of stored triglyceride, with the glycerol moiety being used in gluconeogenesis and the fatty acid moieties being subject to oxidation, producing ketone bodies. Among ewes with pregnancy toxemia, beta-hydroxybutyrate in blood tends to be higher in those that die than in survivors. 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 ovine ketosis.

See also

  • Bioenergetics
  • Ketoacidosis
  • Ketogenic diet
  • Ketonuria
  • Low-carbohydrate diet
  • Fasting
  • Ketogenesis
  • Spontaneous human combustion, for which acetone produced by ketosis has been suggested as a cause.
  • Very-low-calorie diet
  • Gluconeogenesis


  1. ^ a b Volek & Phinney, page 91.
  2. ^ citing:
    • The American Heritage® Medical Dictionary Copyright © 2007
    • Mosby’s Medical Dictionary, 8th edition. © 2009
    • Dorland’s Medical Dictionary for Health Consumers. © 2007
  3. ^ Bach, A; Schirardin, H; Weryha, A; Bauer, M (1977). “Ketogenic response to medium-chain triglyceride load in the rat”. J. Nutr. (10): 1863–70. PMID 903830. 
  4. ^ Champe, Pamela C.; Harvey, Richard A. Lippincott’s Illustrated Reviews: Biochemistry. Lippincott Williams & Wilkins. 
  5. ^ a b Johnston, DG; Pernet, A; McCulloch, A; Blesa-Malpica, G; Burrin, JM; Alberti, KG (1982). “Some hormonal influences on glucose and ketone body metabolism in normal human subjects”. Ciba Foundation symposium. Novartis Foundation Symposia. : 168–91. doi:10.1002/9780470720691.ch10. ISBN 9780470720691. PMID 6122546. 
  6. ^ Kossoff, Eric H.; Freeman, John M.; Turner, Zahava; Rubenstein, James E. (2011). Ketogenic Diets: Treatments for Epilepsy and Other Diseases. Demos Health. 
  7. ^ Manninen, Anssi H (2004). “Metabolic Effects of the Very-Low-Carbohydrate Diets: Misunderstood “Villains” of Human Metabolism”. J Int Soc Sports Nutr. (2): 7–11. doi:10.1186/1550-2783-1-2-7. PMC 2129159 . PMID 18500949. 
  8. ^ Paoli, A; Rubini, A; Volek, J S; Grimaldi, K A (2013). “Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets”. European Journal of Clinical Nutrition. (8): 789–796. doi:10.1038/ejcn.2013.116. PMC 3826507 . PMID 23801097. 
  9. ^ Marshall, William J.; Bangert, Stephen K. (2008). Clinical biochemistry: metabolic and clinical aspects. Elsevier Health Sciences. pp. 67–80. ISBN 978-0-443-10186-1. 
  10. ^ Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA (December 2006). “Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association”. Diabetes Care. (12): 2739–48. doi:10.2337/dc06-9916. PMID 17130218. 
  11. ^ Kraut JA, Kurtz I (January 2008). “Toxic alcohol ingestions: clinical features, diagnosis, and management”. Clinical Journal of the American Society of Nephrology. (1): 208–25. doi:10.2215/CJN.03220807. PMID 18045860. 
  12. ^ a b Hartman AL, Vining EP (January 2007). “Clinical aspects of the ketogenic diet”. Epilepsia. (1): 31–42. doi:10.1111/j.1528-1167.2007.00914.x. PMID 17241206. 
  13. ^ Delbridge E, Proietto J (2006). “State of the science: VLED (Very Low Energy Diet) for obesity”. Asia Pac J Clin Nutr. : 49–54. PMID 16928661. 
  14. ^ Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S (May 2003). “A randomized trial of a low-carbohydrate diet for obesity”. N. Engl. J. Med. (21): 2082–90. doi:10.1056/NEJMoa022207. PMID 12761365. 
  15. ^ Bravata DM, Sanders L, Huang J, Krumholz HM, Olkin I, Gardner CD, Bravata DM (April 2003). “Efficacy and safety of low-carbohydrate diets: a systematic review”. JAMA. (14): 1837–50. doi:10.1001/jama.289.14.1837. PMID 12684364. 
  16. ^ Plaskett, L. G. (September 2003). “On the Essentiality of Dietary Carbohydrate”. Journal of Nutritional & Environmental Medicine. (3): 161–168. doi:10.1080/13590840310001619405. 
  17. ^ Pérez-Guisado, J (2008). “Ketogenic diets: Additional benefits to the weight loss and unfounded secondary effects”. Archivos latinoamericanos de nutricion. (4): 323–9. PMID 19368291. 
  18. ^ Westman, EC; Yancy Jr, WS; Mavropoulos, JC; Marquart, M; McDuffie, JR (2008). “The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus”. Nutrition & metabolism. : 36. doi:10.1186/1743-7075-5-36. PMC 2633336 . PMID 19099589. 
  19. ^ a b Coelho, Marisa; Oliveira, Teresa; Fernandes, Ruben (2013-04-20). “Biochemistry of adipose tissue: an endocrine organ”. Archives of Medical Science : AMS. (2): 191–200. doi:10.5114/aoms.2013.33181. ISSN 1734-1922. PMC 3648822 . PMID 23671428. 
  20. ^ a b Martin,, Kohlmeier,. Nutrient metabolism : structures, functions, and genes. ISBN 9780123877840. OCLC 913852019. 
  21. ^ Owen, Oliver E. (2005-07-01). “Ketone bodies as a fuel for the brain during starvation”. Biochemistry and Molecular Biology Education. (4): 246–251. doi:10.1002/bmb.2005.49403304246. ISSN 1539-3429. 
  22. ^ Cahill, George F.; Veech, Richard L. (2003-01-01). “Ketoacids? Good medicine?”. Transactions of the American Clinical and Climatological Association. : 149–163. ISSN 0065-7778. PMC 2194504 . PMID 12813917. 
  23. ^ Stryer, Lubert (1995). Biochemistry (Fourth ed.). New York: W.H. Freeman and Company. pp. 510–515, 581–613, 775–778. ISBN 0 7167 2009 4. 
  24. ^ Oxidation of fatty acids
  25. ^ Laffel, Lori (1999-11-01). “Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes”. Diabetes/Metabolism Research and Reviews. (6): 412–426. doi:10.1002/(SICI)1520-7560(199911/12)15:63.0.CO;2-8. ISSN 1520-7560. 
  26. ^ Fukao, Toshiyuki; Mitchell, Grant; Sass, Jörn Oliver; Hori, Tomohiro; Orii, Kenji; Aoyama, Yuka (2014-07-01). “Ketone body metabolism and its defects”. Journal of Inherited Metabolic Disease. (4): 541–551. doi:10.1007/s10545-014-9704-9. ISSN 0141-8955. PMID 24706027. 
  27. ^ a b c PTS PANELS™ Ketone Test Strips Information paper PS-002588E Rev. 2 10/05 by Polymer Technology Systems
  28. ^ a b c Converted from molar values, using average of 10.3 g/mol as used in: PTS PANELS™ Ketone Test Strips Information paper PS-002588E Rev. 2 10/05 by Polymer Technology Systems, and subsequently rounded to same number of significant figures as molar value
  29. ^ a b c Taboulet P, Deconinck N, Thurel A, Haas L, Manamani J, Porcher R, Schmit C, Fontaine JP, Gautier JF (2007). “Correlation between urine ketones (acetoacetate) and capillary blood ketones (3-beta-hydroxybutyrate) in hyperglycaemic patients”. Diabetes & Metabolism. (2): 135–139. doi:10.1016/j.diabet.2006.11.006. PMID 17320448. 
  30. ^ Sekizawa A, Sugito Y, Iwasaki M, Watanabe A, Jimbo M, Hoshi S, Saito H, Okai T (2001). “Cell-free fetal DNA is increased in plasma of women with hyperemesis gravidarum”. Clinical Chemistry. (12): 2164–5. PMID 11719487. 
  31. ^ Burbos N, Shiner AM, Morris E (2008). “Severe metabolic acidosis as a consequence of acute starvation in pregnancy”. Archives of Gynecology and Obstetrics. (3): 399–400. doi:10.1007/s00404-008-0715-3. PMID 18592261. 
  32. ^ a b Volek & Phinney, page 302.
  33. ^ Galvin, R. Dennis; Harris, Janet A.; Johnson, Robert E. (1968). “Urinary Excretion of Beta-Hydroxybutyrate and Acetoacetate during Experimental Ketosis”. Experimental Physiology. (2): 181–193. doi:10.1113/expphysiol.1968.sp001958. 
  34. ^ McDougall, John (July 9, 2012). “The Paleo Diet Is Uncivilized (And Unhealthy and Untrue)”. Forks over Knives
  35. ^ Karra, Cindy: Shape Up America! Reveals The Truth About Dieters, Shape Up America! (by former U.S. Surgeon General C. Everett Koop), 29 December 2003
  36. ^ Volek and Phinney, p. 4
  37. ^ Eaton SB, Konner M (1985). “Paleolithic Nutrition”. New England Journal of Medicine. (5): 283–289. doi:10.1056/NEJM198501313120505. PMID 2981409. 
  38. ^ Yancy WS, Foy M, Chalecki AM, Vernon MC, Westman EC (2005). “A low-carbohydrate, ketogenic diet to treat type 2 diabetes”. Journal of Nutrition and Metabolism. : 34. doi:10.1186/1743-7075-2-34. PMC 1325029 . PMID 16318637. 
  39. ^ Michael R. Eades; Mary Dan Eades (21 October 2009). Protein Power: The High-Protein/Low-Carbohydrate Way to Lose Weight, Feel Fit, and Boost Your Health—in Just Weeks!. Random House Publishing Group. pp. 135–. ISBN 978-0-307-57380-3. 
  40. ^ a b Krogh, August; Krogh, Marie (1915). “A Study of The Diet And Metabolism of Eskimos Undertaken In 1908 On An Expedition To Greenland”. Meddelelser om Grønland. (1). Retrieved 2015-12-19. 
  41. ^ a b c Peter Heinbecker (1928). “Studies on the Metabolism of Eskimos” (PDF). J. Biol. Chem. : 461–475. Retrieved 2014-04-07. 
  42. ^ a b c Ho KJ, Mikkelson B, Lewis LA, Feldman SA, Taylor CB (1972). “Alaskan Arctic Eskimo: responses to a customary high fat diet” (PDF). Am. J. Clin. Nutr. (8): 737–45. PMID 5046723. 
  43. ^ a b Sinclair, H. M. (1953). “The Diet of Canadian Indians and Eskimos” (PDF). Proceedings of the Nutrition Society. (1): 69–82. doi:10.1079/PNS19530016. ISSN 0029-6651. It is, however, worth noting that according to the customary convention (Woodyatt, 1921 ; Shaffer, 1921) this diet is not ketogenic since the ratio of ketogenic(FA) to ketolytic (G) aliments is 1.09. Indeed, the content of fat would have to exactly double (324 g daily) to make the diet ketogenic (FA/G>1–5). 
  44. ^ a b Corcoran AC, Rabinowitch IM (1937). “A study of the blood lipids and blood protein in Canadian Eastern Arctic Eskimos”. Biochem. J. (3): 343–8. PMC 1266943 . PMID 16746345. 
  45. ^ a b Speth, John D; Spielmann, Katherine A (1983). “Energy source, protein metabolism, and hunter-gatherer subsistence strategies” (PDF). Journal of Anthropological Archaeology. (1): 1–31. doi:10.1016/0278-4165(83)90006-5. ISSN 0278-4165. 
  46. ^ Ringberg, Tata M.; White, Robert G.; Holleman, Dan F.; Luick, Jack R. (1981). “Body growth and carcass composition of lean reindeer (Rangifer tarandus tarandusL.) from birth to sexual maturity” (PDF). Canadian Journal of Zoology. (6): 1040–1044. doi:10.1139/z81-145. ISSN 0008-4301. Body growth and carcass composition were measured in lean reindeer during the juvenile growth period between birth and 3 years of age. Mean carcass weight in these lean reindeer was 56 ± 4% of body weight and the deposition of body muscle and bone mass was linearly correlated with body weight after the 1st month of age. The weight of the brain relative to body weight and carcass weight declined, while the relative changes in heart, liver, kidneys, parotid glands, and tissues of the gastrointestinal tract were small after the neonatal period. The extractable fat content in carcasses increased from 4.4 to 11.4% of wet weight or approximately 100 g fat at birth and 3.5 kg fat in adult reindeer. Fat-free dry matter represented a constant percentage (18–20%) of wet carcass weight independent of body weight after the neonatal period, while a significant inverse relationship between carcass fat and body water was found. 
  47. ^ Yiu H. Hui (February 1985). Principles and issues in nutrition. Wadsworth Health Sciences Division. p. 91. Retrieved 2014-05-19. Eskimos actually consume more carbohydrates than most nutritionists have assumed. Because Eskimos frequently eat their meat raw and frozen, they take in more glycogen than a person purchasing meat with a lower glycogen content in a grocery store. The Eskimo practice of preserving a whole seal or bird carcass under an intact whole skin with a thick layer of blubber also permits some proteins to ferment into carbohydrates. 
  48. ^ Pfeiffer, Carl J. (1997). “Renal cellular and tissue specializations in the bottlenose dolphin (Tursiops truncatus) and beluga whale (Delphinapterus leucas)” (PDF). Aquatic Mammals. (2): 75–84. Retrieved 2014-04-25. 
  49. ^ Lockyer, Christina (1991). “Body composition of the sperm whale, Physeter cation, with special reference to the possible functions of fat depots” (PDF). Journal of the Marine Research Institute. (2). ISSN 0484-9019. Retrieved 2014-04-25. The significant levels of carbohydrate, probably mostly in the form of glycogen, in both blubber and muscle, may represent an instant form of energy for diving via anaerobic glycolysis. 
  50. ^ Hochachka, P.; Storey, K. (1975). “Metabolic consequences of diving in animals and man”. Science. (4177): 613–621. Bibcode:1975Sci…187..613H. doi:10.1126/science.163485. ISSN 0036-8075. PMID 163485. In the terminal stages of prolonged diving, however, even these organs must tolerate anoxia for surprisingly long times, and they typically store unusually large amounts of glycogen for this purpose. 
  51. ^ Lawrie 2014, pp. 92-. “A much delayed onset of rigor mortis has been observed in the muscle of the whale (Marsh, 1952b). The ATP level and the pH may remain at their high in vivo values for as much as 24h at 37ºC. No adequate explanation of this phenomenon has yet been given; but the low basal metabolic rate of whale muscle (Benedict, 1958), in combination with the high content of oxymyoglobin in vivo (cf 4.3.1), may permit aerobic metabolism to continue slowly for some time after the death of the animal, whereby ATP levels can be maintained sufficiently to delay the union of actin and myosin in rigor mortis.”
  52. ^ Peter J. Bechtel; UNKNOWN. AUTHOR (2 December 2012). Muscle as Food. Elsevier Science. pp. 171–. ISBN 978-0-323-13953-3. Retrieved 19 May 2014. Freezing does stop the postmortem metabolism but only at about −18ºC and lower temperatures. Above −18ºC increasing temperatures of storage cause an increasing rate of ATP breakdown and glycolysis that is higher in the comminuted meat than in the intact tissue (Fisher et al., 1980b). If the ATP concentration in the frozen tissue falls below ~ 1 µmol/g no contraction or rigor can occur because they are prevented by the rigid matrix of ice. 
  53. ^ Lawrie 2014, p. 298.
  54. ^ a b c d Hardy, Karen; Brand-Miller, Jennie; Brown, Katherine D.; Thomas, Mark G.; Copeland, Les (2015). “The Importance of Dietary Carbohydrate in Human Evolution”. The Quarterly Review of Biology. (3): 251–268. doi:10.1086/682587. ISSN 0033-5770. PMID 26591850. 
  55. ^ Fumagalli, M.; Moltke, I.; Grarup, N.; Racimo, F.; Bjerregaard, P.; Jorgensen, M. E.; Korneliussen, T. S.; Gerbault, P.; Skotte, L.; Linneberg, A.; Christensen, C.; Brandslund, I.; Jorgensen, T.; Huerta-Sanchez, E.; Schmidt, E. B.; Pedersen, O.; Hansen, T.; Albrechtsen, A.; Nielsen, R. (2015). “Greenlandic Inuit show genetic signatures of diet and climate adaptation”. Science. (6254): 1343–1347. Bibcode:2015Sci…349.1343F. doi:10.1126/science.aab2319. hdl:10044/1/43212. ISSN 0036-8075. PMID 26383953. 
  56. ^ Zimmer, Carl (2015-09-17). “Inuit Study Adds Twist to Omega-3 Fatty Acids’ Health Story”. The New York Times. New York. Retrieved 2015-12-03. 
  57. ^ a b c Clemente, Florian J.; Cardona, Alexia; Inchley, Charlotte E.; Peter, Benjamin M.; Jacobs, Guy; Pagani, Luca; Lawson, Daniel J.; Antão, Tiago; Vicente, Mário; Mitt, Mario; DeGiorgio, Michael; Faltyskova, Zuzana; Xue, Yali; Ayub, Qasim; Szpak, Michal; Mägi, Reedik; Eriksson, Anders; Manica, Andrea; Raghavan, Maanasa; Rasmussen, Morten; Rasmussen, Simon; Willerslev, Eske; Vidal-Puig, Antonio; Tyler-Smith, Chris; Villems, Richard; Nielsen, Rasmus; Metspalu, Mait; Malyarchuk, Boris; Derenko, Miroslava; Kivisild, Toomas (2014). “A Selective Sweep on a Deleterious Mutation in CPT1A in Arctic Populations”. The American Journal of Human Genetics. (5): 584–589. doi:10.1016/j.ajhg.2014.09.016. ISSN 0002-9297. PMC 4225582 . PMID 25449608. 
  58. ^ Greenberg, Cheryl; al., et. (2009-04-09). “The paradox of the carnitine palmitoyltransferase type Ia P479L variant in Canadian Aboriginal populations”. Mol. Genet. Metab. Molecular Genetics and Metabolism. (4): 201–7. doi:10.1016/j.ymgme.2008.12.018. PMID 19217814. 
  59. ^ a b Bennett, Michael; Stanley, Charles (2011-03-01). “Carnitine palmitoyl transferase 1A deficiency”. Orphanet. Retrieved 2014-12-04. 
  60. ^ Lee, Jieun; Ellis, Jessica M.; Wolfgang, Michael J. (2015). “Adipose Fatty Acid Oxidation Is Required for Thermogenesis and Potentiates Oxidative Stress-Induced Inflammation”. Cell Reports. (2): 266–279. doi:10.1016/j.celrep.2014.12.023. ISSN 2211-1247. PMC 4359063 . PMID 25578732. 
  61. ^ a b Kayser, Manfred; Cardona, Alexia; Pagani, Luca; Antao, Tiago; Lawson, Daniel J.; Eichstaedt, Christina A.; Yngvadottir, Bryndis; Shwe, Ma Than Than; Wee, Joseph; Romero, Irene Gallego; Raj, Srilakshmi; Metspalu, Mait; Villems, Richard; Willerslev, Eske; Tyler-Smith, Chris; Malyarchuk, Boris A.; Derenko, Miroslava V.; Kivisild, Toomas (2014). “Genome-Wide Analysis of Cold Adaptation in Indigenous Siberian Populations”. PLoS ONE. (5): e98076. Bibcode:2014PLoSO…998076C. doi:10.1371/journal.pone.0098076. ISSN 1932-6203. PMC 4029955 . PMID 24847810. 
  62. ^ Dykema, Deanna M. (2012). “Carnitine Palmitoyltransferase-1A Deficiency”. Advances in Neonatal Care. (1): 23–27. doi:10.1097/ANC.0b013e318242df6d. ISSN 1536-0903. PMID 22301540. 
  63. ^ Draper, H. H. (1977). “The Aboriginal Eskimo Diet in Modern Perspective”. American Anthropologist. (2): 309–316. doi:10.1525/aa.1977.79.2.02a00070. ISSN 0002-7294. 
  64. ^ Gadsby, Patricia (October 1, 2004). “The Inuit Paradox”. Discover Magazine. p. 2. Retrieved 18 December 2015. 
  65. ^ Hubert Carey Trowell (1 January 1981). Western Diseases, Their Emergence and Prevention. Harvard University Press. pp. 114–115. ISBN 978-0-674-95020-7. 
  66. ^ Klutschak, Heinrich. Overland to Starvation Cove. Trans. and Ed. William Barr. Canada: Univ. of Toronto Press, 1987.
  67. ^ a b c Rosen, Yereth (2014-11-29). “Clues emerging about Arctic gene, diet and health”. Arctic Newswire. Alaska Dispatch News. Retrieved 2015-12-03. 
  68. ^ “Traditional Plant Foods of canadian indigenous peoples, Nutrition, Botany and Use”. Retrieved 2015-10-06. 
  69. ^ Ivy JL (Jun 19, 1998). “Glycogen Resynthesis After Exercise: Effect of Carbohydrate Intake”. Int J Sports Med. : S142–5. doi:10.1055/s-2007-971981. PMID 9694422. 
  70. ^ Burke LM, Collier GR, Hargreaves M (August 1993). “Muscle glycogen storage after prolonged exercise: effect of the glycemic index of carbohydrate feedings”. Journal of Applied Physiology. 2. (2): 1019–1023. PMID 8226443. 
  71. ^ Phinney SD (2004). “Ketogenic diets and physical performance”. Nutrition & Metabolism. (1): 2. doi:10.1186/1743-7075-1-2. PMC 524027 . PMID 15507148. 
  72. ^ Volek and Phinney, p. 237.
  73. ^ Klein MS, Buttchereit N, Miemczyk SP, Immervoll AK, Louis C, Wiedemann S, Junge W, Thaller G, Oefner PJ, Gronwald W (February 2012). “NMR metabolomic analysis of dairy cows reveals milk glycerophosphocholine to phosphocholine ratio as prognostic biomarker for risk of ketosis”. J. Proteome Res. (2): 1373–81. doi:10.1021/pr201017n. PMID 22098372. 
  74. ^ Tatone, EH; Gordon, JL; Hubbs, J; LeBlanc, SJ; DeVries, TJ; Duffield, TF (1 August 2016). “A systematic review and meta-analysis of the diagnostic accuracy of point-of-care tests for the detection of hyperketonemia in dairy cows”. Preventive veterinary medicine. : 18–32. doi:10.1016/j.prevetmed.2016.06.002. PMID 27435643. 
  75. ^ a b c Pugh, D. G. 2002. Sheep and goat medicine. Saunders, Philadelphia. 468 pp.
  76. ^ a b c Kimberling, C. V. 1988. Jensen and Swift’s diseases of sheep. 3rd Ed. Lea & Febiger, Philadelphia. 394 pp.
  77. ^ Marteniuk J. V.; Herdt T. H. (1988). “Pregnancy toxemia and ketosis of ewes and does”. Vet. Clin. North Am. Food Anim. Pract. : 307–315. doi:10.1016/s0749-0720(15)31050-1. PMID 3264753. 
  78. ^ Reid R. L. (1960). “Studies on the carbohydrate metabolism of sheep. IX. Metabolic effects of glucose and glycerol in undernourished pregnant ewes and in ewes with pregnancy toxaemia”. Aust. J. Agr. Res. : 42–47. doi:10.1071/ar9600042. 
  79. ^ Van Soest, P. J. 1994. Nutritional ecology of the ruminant. 2nd Ed. Cornell Univ. Press. 476 pp.
  80. ^ Overton TR, Drackley JK, Ottemann-Abbamonte CJ, Beaulieu AD, Emmert LS, Clark JH (1999). “Substrate utilization for hepatic gluconeogenesis is altered by increased glucose demand in ruminants”. J. Anim. Sci. (7): 1940–51. PMID 10438042. 
  81. ^ Sasaki S.; Ambo K.; Muramatsu M.; Tsuda T. (1975). “Gluconeogenesis in the kidney-cortex slices of normal fed and starved sheep”. Tohoku J. Agr. Res. : 20–29. 
  82. ^ Henze P, Bickhardt K, Fuhrmann H, Sallmann HP (1998). “Spontaneous pregnancy toxaemia (ketosis) in sheep and the role of insulin”. Zentralbl Veterinarmed A. (5): 255–66. doi:10.1111/j.1439-0442.1998.tb00825.x. PMID 9719756. 
  83. ^ Kahn, C. M., ed. (2005). Merck Veterinary Manual (9th ed.). Whitehouse Station: Merck & Co. 


  • Lawrie, R. A.; Ledward, David (23 January 2014). Lawrie’s Meat Science. Elsevier Science. ISBN 978-1-84569-161-5. 
  • Volek, Jeff S.; Phinney, Stephen D. (2012). The Art and Science of Low Carbohydrate Performance. Beyond Obesity. p. 91. ISBN 978-0983490715. 

External links

  • Diabetic Ketoacidosis at eMedicine
  • NHS Direct: Ketosis
  • The Merck Manual —
    • Diabetic Ketoacidosis
    • Alcoholic Ketoacidosis

Leave a Reply

Your email address will not be published. Required fields are marked *