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Starvation Ketoacidosis

Ketoacidosis Versus Ketosis

Ketoacidosis Versus Ketosis

Some medical professionals confuse ketoacidosis, an extremely abnormal form of ketosis, with the normal benign ketosis associated with ketogenic diets and fasting states in the body. They will then tell you that ketosis is dangerous. Testing Laboratory Microbiology - Air Quality - Mold Asbestos - Environmental - Lead emsl.com Ketosis is NOT Ketoacidosis The difference between the two conditions is a matter of volume and flow rate*: Benign nutritional ketosis is a controlled, insulin regulated process which results in a mild release of fatty acids and ketone body production in response to either a fast from food, or a reduction in carbohydrate intake. Ketoacidosis is driven by a lack of insulin in the body. Without insulin, blood sugar rises to high levels and stored fat streams from fat cells. This excess amount of fat metabolism results in the production of abnormal quantities of ketones. The combination of high blood sugar and high ketone levels can upset the normal acid/base balance in the blood and become dangerous. In order to reach a state of ketoacidosis, insulin levels must be so low that the regulation of blood sugar and fatty acid flow is impaired. *See this reference paper. Here's a table of the actual numbers to show the differences in magnitude: Body Condition Quantity of Ketones Being Produced After a meal: 0.1 mmol/L Overnight Fast: 0.3 mmol/L Ketogenic Diet (Nutritional ketosis): 1-8 mmol/L >20 Days Fasting: 10 mmol/L Uncontrolled Diabetes (Ketoacidosis): >20 mmol/L Here's a more detailed explanation: Fact 1: Every human body maintains the blood and cellular fluids within a very narrow range between being too acidic (low pH) and too basic (high pH). If the blood pH gets out of the normal range, either too low or too high, big problems happen. Fact 2: The Continue reading >>

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as "accelerated starvation." Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids. DOI: 10.1155/2014/906283 Continue reading >>

Starvation Ketoacidosis

Starvation Ketoacidosis

Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis. When insulin levels are low and glucagon levels are high (such as in a fasting state), long chain fatty acids and glycerol from triglycerides are released from peripheral fat stores and are transported to the liver. The fatty acids undergo beta-oxidation and generate acetyl-CoA. However, with excessive amounts of acetyl-CoA, the Krebs cycle may become oversaturated, and instead the acetyl-CoA enter the ketogenic pathway resulting in production of ketone bodies. Mild ketosis (1mmol/L) results after fasting for approximately 12 to 14 hours. However, the ketoacid concentration rises with continued fasting and will peak after 20 to 30 days (8-10mmol/L). Clinical Features Nausea and vomiting Abdominal pain Dehydration Altered mental status Fatigue Kussmaul breathing Differential Diagnosis Evaluation Serum chemistry (elevated anion gap) Glucose (usually euglycemic or hypoglycemic) Urinalysis (ketonuria) Serum beta-hydroxybutyrate Lactate Salicylate level (if overdose suspected) Serum osmolality (if toxic alcohol ingestion suspected) Management Dextrose and saline solutions Dextrose Will cause increase in insulin and decrease in glucagon secretion, which will reduce ketone production and increase ketone metabolism Beta-hydroxybutyrate and acetoacetate will regenerate bicarbonate, causing partial correction of metabolic acidosis Saline or lactated ringer Will provide volume resuscitation and will in turn reduce secretion of glucagon (which promotes ketogenesis) Considerations Rate of infusion dependent on volume status If hypokalemic, need to correct before administering glucose (as glucose stimulate Continue reading >>

Ketoacidosis

Ketoacidosis

GENERAL ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. a relative or absolute insulin deficiency is present in all cases. CAUSES The three major types of ketosis are: (i) Starvation ketosis (ii) Alcoholic ketoacidosis (iii) Diabetic ketoacidosis STARVATION KETOSIS when hepatic glycogen stores are exhausted (eg after 12-24 hours of total fasting), the liver produces ketones to provide an energy substrate for peripheral tissues. ketoacidosis can appear after an overnight fast but it typically requires 3 to 14 days of starvation to reach maximal severity. typical keto-anion levels are only 1 to 2 mmol/l and this will usually not alter the anion gap. the acidosis even with quite prolonged fasting is only ever of mild to moderate severity with keto-anion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. ketone bodies also stimulate some insulin release from the islets. patients are usually not diabetic. ALCOHOLIC KETOSIS Presentation a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake for a few days (ethanol and fasting) volume depletion is common and this can result in increased levels of counter regulatory hormones (eg glucagon) levels of free fatty acids (FFA) can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions GI symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena) acidaemia may be severe (eg pH down to 7.0) plasma glucose may be depressed or normal or Continue reading >>

“starvation Mode” And Muscle Wasting Myth On A Low Carbohydrate Diet

“starvation Mode” And Muscle Wasting Myth On A Low Carbohydrate Diet

Another one of the fallacies that seems to pervade is that a ketogenic diet is the same as being in starvation – whereby the body significantly reduces it’s metabolism and starts tapping into the muscles for energy. This is completely bogus and you’d be best off just ignoring the idea altogether. In light of restricted carbohydrates through either keto or starvation the body will focus on maintaining glucose homeostasis, ie constant blood-glucose level. It’s highest priority is to provide sufficient energy to the brain and other critical functions, and can do so with a mix of glucose and ketone bodies. The only real common ground is that ketone production is elevated in both a keto diet and in starvation due to reduced carbohydrate intake. Conflating keto with starvation is guilt by association – eg falling asleep makes you unconscious; being punched out also renders you unconscious and can cause serious injury; therefore falling asleep is dangerous like being punched out. Starvation is just that – severe restriction of calories over a long period, and “starvation mode” is what anti-low-carb people tend to call it as a scare tactic. After a few days of complete fasting the metabolic rate only drops 5-10% – sometimes increases – and even on an intake of half the amount of energy you’d normally consume for maintenance, you would be fine for months without too much of a drop. If you have a significant amount of fat to lose then your metabolism will barely drop at all, even on severe restriction your extra adipose stores will make up any energy requirements you have. A ketogenic diet stabilises glucose and maintains very low levels of circulating insulin, so access to liberating energy from your adipose stores is unhampered. A ketogenic diet is extreme Continue reading >>

Extreme Gestational Starvation Ketoacidosis: Case Report And Review Of Pathophysiology

Extreme Gestational Starvation Ketoacidosis: Case Report And Review Of Pathophysiology

Hypocalcemia: Sensipar® lowers serum calcium and can lead to hypocalcemia. Life threatening events and fatal outcomes associated with hypocalcemia have been reported in patients treated with Sensipar®, including pediatric patients. The safety and effectiveness of Sensipar® have not been established in pediatric patients. Decreases in serum calcium can prolong the QT interval, potentially resulting in ventricular arrhythmia. Cases of QT prolongation and ventricular arrhythmia have been reported in patients treated with Sensipar®. Patients with conditions that predispose to QT interval prolongation and ventricular arrhythmia may be at increased risk for QT interval prolongation and ventricular arrhythmias if they develop hypocalcemia due to Sensipar®. Closely monitor corrected serum calcium and QT interval in patients at risk receiving Sensipar®. Concurrent administration of Sensipar® with calcium-lowering drugs including other calcimimetics could result in severe hypocalcemia. Parsabiv™ (etelcalcetide) and Sensipar® should not be given together. Closely monitor serum calcium in patients receiving Sensipar® and concomitant therapies known to lower serum calcium levels. Serum calcium and serum phosphorus should be measured within 1 week and PTH should be measured 1 to 4 weeks after initiation or dose adjustment of Sensipar®. Once the maintenance dose has been established, serum calcium and serum phosphorus should be measured approximately monthly, and PTH every 1 to 3 months. Patients with risk factors for upper GI bleeding, such as known gastritis, esophagitis, ulcers or severe vomiting, may be at increased risk for GI bleeding with Sensipar®. Monitor patients for worsening of common Sensipar® GI adverse reactions and for signs and symptoms of GI bleeding an Continue reading >>

Case Of Nondiabetic Ketoacidosis In Third Term Twin Pregnancy | The Journal Of Clinical Endocrinology & Metabolism | Oxford Academic

Case Of Nondiabetic Ketoacidosis In Third Term Twin Pregnancy | The Journal Of Clinical Endocrinology & Metabolism | Oxford Academic

We provided appropriate management with fluid infusion after cesarean delivery. The patient and her two daughters survived, and no disabilities were foreseen. Alcohol, methanol, and lactic acid levels were normal. No signs of renal disease or diabetes were present. Pathological examination revealed no abnormalities of the placentae. Toxicological tests revealed a salicylate level of less than 5 mg/liter, an acetaminophen level of less than 1 mg/liter, and an acetone level of 300 mg/liter (reference, 520 mg/liter). We present a case of third term twin pregnancy with high anion gap metabolic acidosis due to (mild) starvation. Starvation, obesity, third term twin pregnancy, and perhaps a gastroenteritis were the ultimate provoking factors. In the light of the erroneous suspicion of sepsis and initial fluid therapy lacking glucose, one wonders whether, under a different fluid regime, cesarean section could have been avoided. Severe ketoacidosis in the pregnant woman is associated with impaired neurodevelopment. It therefore demands early recognition and immediate intervention. A 26-yr-old patient was admitted to our hospital complaining of rapid progressive dyspnea and abdominal discomfort. She was pregnant with dichorial, diamniotic twins for 35 wk and 4 d. Medical history showed that she was heterozygous for hemochromatosis. Two years before, she had given birth to a healthy girl of 3925 g by cesarean section, and 1 yr before, she had had a spontaneous abortion. Her preadmission outpatient surveillance revealed slightly elevated blood pressure varying from 132158 mm Hg systolic and 7995 mm Hg diastolic. Glucose and glycosylated hemoglobin were tested at 24 wk and were normal at 4.6 mmol/liter and 5.4% (36 mmol/mol), respectively. Urine analysis at the outpatient obstetri Continue reading >>

Fasting Ketosis And Alcoholic Ketoacidosis

Fasting Ketosis And Alcoholic Ketoacidosis

INTRODUCTION Ketoacidosis is the term used for metabolic acidoses associated with an accumulation of ketone bodies. The most common cause of ketoacidosis is diabetic ketoacidosis. Two other causes are fasting ketosis and alcoholic ketoacidosis. Fasting ketosis and alcoholic ketoacidosis will be reviewed here. Issues related to diabetic ketoacidosis are discussed in detail elsewhere. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment".) PHYSIOLOGY OF KETONE BODIES There are three major ketone bodies, with the interrelationships shown in the figure (figure 1): Acetoacetic acid is the only true ketoacid. The more dominant acid in patients with ketoacidosis is beta-hydroxybutyric acid, which results from the reduction of acetoacetic acid by NADH. Beta-hydroxybutyric acid is a hydroxyacid, not a true ketoacid. Continue reading >>

Ketosis

Ketosis

Not to be confused with Ketoacidosis. 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.[1][2] 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[3]). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate,[4] and the levels of ketone bodies are regulated mainly by insulin and glucagon.[5] 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.[6] 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.[5][7] For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.[8] 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 Continue reading >>

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Copyright © 2014 Nupur Sinha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as “accelerated starvation.” Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids. 1. Introduction A relative insulin deficient state has been well described in pregnancy. This is due to placentally derived hormones including glucagon, cortisol, and human placental lactogen which are increased in periods of stress [1]. The insulin resistance increases with gestational age Continue reading >>

Starvation Ketoacidosis In Pregnancy

Starvation Ketoacidosis In Pregnancy

Abstract Starvation ketosis outside pregnancy is rare and infrequently causes a severe acidosis. Placental production of hormones, including glucagon and human placental lactogen, leads to the insulin resistance that is seen in pregnancy, which in turn increases susceptibility to ketosis particularly in the third trimester. Starvation ketoacidosis in pregnancy has been reported and is usually precipitated by a period of severe vomiting. Ketoacidosis is likely to have important implications for fetal survival as ketoacidosis in women with type 1 diabetes mellitus is associated with intrauterine death. This article features four cases of women with vomiting in the third trimester of pregnancy associated with a severe metabolic acidosis. The mechanism underlying ketogenesis, the evidence for accelerated ketogenesis in pregnancy and other similar published cases are reviewed. A proposed strategy for management of these women is presented. Continue reading >>

Why Dka & Nutritional Ketosis Are Not The Same

Why Dka & Nutritional Ketosis Are Not The Same

There’s a very common misconception and general misunderstanding around ketones. Specifically, the misunderstandings lie in the areas of: ketones that are produced in low-carb diets of generally less than 50 grams of carbs per day, which is low enough to put a person in a state of “nutritional ketosis” ketones that are produced when a diabetic is in a state of “diabetic ketoacidosis” (DKA) and lastly, there are “starvation ketones” and “illness-induced ketones” The fact is they are very different. DKA is a dangerous state of ketosis that can easily land a diabetic in the hospital and is life-threatening. Meanwhile, “nutritional ketosis” is the result of a nutritional approach that both non-diabetics and diabetics can safely achieve through low-carb nutrition. Diabetic Ketoacidosis vs. Nutritional Ketosis Ryan Attar (soon to be Ryan Attar, ND) helps explain the science and actual human physiology behind these different types of ketone production. Ryan is currently studying to become a Doctor of Naturopathic Medicine in Connecticut and also pursuing a Masters Degree in Human Nutrition. He has interned under the supervision of the very well-known diabetes doc, Dr. Bernstein. Ryan explains: Diabetic Ketoacidosis: “Diabetic Ketoacidosis (DKA), is a very dangerous state where an individual with uncontrolled diabetes is effectively starving due to lack of insulin. Insulin brings glucose into our cells and without it the body switches to ketones. Our brain can function off either glucose or fat and ketones. Ketones are a breakdown of fat and amino acids that can travel through the blood to various tissues to be utilized for fuel.” “In normal individuals, or those with well controlled diabetes, insulin acts to cancel the feedback loop and slow and sto Continue reading >>

Ketoacidosis During A Low-carbohydrate Diet

Ketoacidosis During A Low-carbohydrate Diet

To the Editor: It is believed that low-carbohydrate diets work best in reducing weight when producing ketosis.1 We report on a 51-year-old white woman who does not have diabetes but had ketoacidosis while consuming a “no-carbohydrate” diet. There was no family history of diabetes, and she was not currently taking any medications. While adhering to a regimen of carbohydrate restriction, she reached a stable weight of 59.1 kg, a decrease from 72.7 kg. After several months of stable weight, she was admitted to the hospital four times with vomiting but without abdominal pain. On each occasion, she reported no alcohol use. Her body-mass index (the weight in kilograms divided by the square of the height in meters) was 26.7 before the weight loss and 21.7 afterward. Laboratory evaluation showed anion-gap acidosis, ketonuria, and elevated plasma glucose concentrations on three of the four occasions (Table 1). She had normal concentrations of plasma lactate and glycosylated hemoglobin. Screening for drugs, including ethyl alcohol and ethylene glycol, was negative. Abdominal ultrasonography showed hepatic steatosis. On each occasion, the patient recovered after administration of intravenous fluids and insulin, was prescribed insulin injections on discharge, and gradually reduced the use of insulin and then discontinued it while remaining euglycemic for six months or more between episodes. Testing for antibodies against glutamic acid decarboxylase and antinuclear antibodies was negative. Values on lipid studies were as follows: serum triglycerides, 102 mg per deciliter; high-density lipoprotein (HDL) cholesterol, 50 mg per deciliter; and calculated low-density lipoprotein (LDL) cholesterol, 189 mg per deciliter. The patient strictly adhered to a low-carbohydrate diet for four Continue reading >>

What Is Starvation Ketosis?

What Is Starvation Ketosis?

Starvation ketosis is a metabolic state in humans and many animals in which the body breaks down fat and produces acids known as ketones, then uses these as a primary energy source. The “starvation” part of the name owes to the fact that, in most cases, people only use ketones for energy when they aren’t getting adequate glucose from food. The body typically converts carbohydrates to glucose as a main source of energy, but once the liver has used all of its stored glucose it begins to metabolize fatty acids, forming ketone bodies. Malnutrition and fasting are two of the most common causes, but it can also be the result of conditions like diabetes, alcoholism, and a low carbohydrate diet. People sometimes intentionally trigger this state as a means of burning fat to lose weight, but whether this practice is safe or even advisable is widely disputed in the medical community. Ketones are capable of supplying energy to the body, but an abnormally high level can cause a number of problems, including organ damage, coma, and even death. Understanding Ketones The liver typically makes ketones in response to some sort of energy crisis in the body. People generally get the majority of their energy by synthesizing glucose, which is a sugar molecule found in carbohydrates like bread and grain products. When people aren’t getting enough glucose, the liver begins creating ketones that the body uses in combination with any fat stores it has on hand. Ketones in many ways prevent the body from robbing muscles of their core proteins. Starvation ketosis happens when these become the body’s primary source of energy. The condition can usually be identified by looking for excesses. The body gets rid of unneeded supplies by spilling them out through exhalations, urine, and sweat. Wh Continue reading >>

Starvation Ketoacidosis

Starvation Ketoacidosis

The definitions used in this glossary of terminology either have been provided by the authors of the articles, or have been extracted wholly or in part, or paraphrased from the following sources: The American Medical Association Encyclopedia of Medicine, Charles B. Clayman, MD, Medical Editor, Random House, New York, 1989; Biotechnology from A to Z, 2d Edition, William Bains, Oxford University Press, New York, New York, 2002; A Dictionary of Genetics, 6th Edition, Robert C. King and William D. Stansfield, Oxford University Press, New York, New York, 2002; Dorland's Illustrated Medical Dictionary, 29th and 30th Editions, W. B. Saunders Company, Philadelphia, 2000, 2003; Genes VII, Benjamin Lewin, Oxford University Press, New York, New York, 2000; The Gale Encyclopedia of Genetic Disorders, Volumes I and II, Stacey L. Blachford, Ed., Thomson Learning, New York, New York, 2002; The Merriam-Webster Dictionary, Merriam-Webster, Inc., Springfield, Massachusetts, 1997; Molecular Biology of the Cell, 3rd Edition, Bruce Alberts, et al., Garland Publishing, 1994; The Random House Dictionary of the English Language, Unabridged Edition, 1966; Webster's Ninth New Collegiate Dictionary, 1991. DEFINITION: Continue reading >>

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