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 >>
Rare Presentations Of Ketoacidosis: Diabetic Ketoalkalosis And Ketoacidosis Secondary To Fasting And Muscular Dystrophy
Presentation 1 A 42-year-old man with known alcohol abuse and type 1 diabetes resulting from pancreatitis was brought to the hospital with vomiting, coughing, and general weakness. Before hospitalization, he had not taken any alkaline medicine or diuretics. His status at arrival and his blood test results are shown in Table 1. He had high 3-hydroxybutyrate (3-OHB), low potassium, and an anion gap >12 mEq/L. His condition was furthermore complicated by pneumonia. He was moved to the intensive care unit (ICU), where treatment with antibiotics, insulin, glucose, and potassium was initiated, and he recovered. Presentation 2 A 28-year-old woman with type 1 diabetes was hospitalized. She had multiple complications, including nephropathy, retinopathy, peripheral neuropathy, gastroparesis treated with gastric electric stimulation (GES), and impaired urinary bladder function. On admission, she had symptoms of urinary tract infection (UTI) and reported having undergone eye surgery with local anesthesia the day before. She reported abdominal discomfort and vomiting. Blood test results (Table 1) showed hyperglycemia, high 3-OHB, pH of 7.47 indicating alkalosis, and low levels of bicarbonate compensated by hyperventilation. She was treated with insulin, glucose, and potassium and recovered fully. Presentation 3 A 38-year-old woman with type 1 diabetes, nephropathy, incipient retinopathy, and gastroparesis treated with GES was hospitalized with lower stomach pain, signs of a UTI, and vomiting. She had a metabolic alkalosis and high 3-OHB (Table 1). Serum chloride was not measured. The infection and DKA were successfully treated with antibiotics, insulin, glucose, and potassium. Presentation 4 A healthy 50-year-old man was brought to the hospital with nausea and abdominal pain. He had Continue reading >>
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 >>
Ketoacidosis In A Non-diabetic Woman Who Was Fasting During Lactation
Abstract Ketoacidosis is a potential complication of type 1 diabetes. Severe ketoacidosis with a blood pH below 7.0 is only rarely seen in other diseases. Three weeks after delivery, a young woman was admitted because of tachypnoe and tachycardia. Blood gas analysis showed a severe metabolic acidosis with a high anion gap. Further workup revealed the presence of ketone bodies in the urine with normal blood glucose and no history of diabetes. The patient reported that she had not eaten for days because of abdominal pain. After initial treatment in the ICU and immediate re-feeding, the patient’s condition rapidly improved. While under normal circumstances fasting causes at most only mild acidosis, it can be dangerous during lactation. Prolonged fasting in combination with different forms of stress puts breast feeding women at risk for starvation ketoacidosis and should therefore be avoided. Background Severe acidosis is a potentially life-threatening condition. In case of metabolic acidosis, determination of the serum anion gap helps to narrow down the differential diagnosis. An increased anion gap indicates the presence of an unusual amount of an acid that is most commonly found in ketoacidosis, lactic acidosis, renal insufficiency, and intoxications while other causes are rare. Ketoacidosis is a potential complication of type 1 diabetes while severe ketoacidosis with a blood pH below 7.0 is only rarely seen in other diseases. In diabetic ketoacidosis, glucose is not properly taken up into tissue due to an absolute insulin deficiency that is mainly found in type 1 diabetes. In parallel, glucagon release is not suppressed leading to hyperglucagonemia. Subsequently the body activates stress hormones, which worsen hyperglycemia by promoting gluconeogenesis (and also ketog Continue reading >>
Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression
Go to: A 34-year-old man with a 19-year history of type 1 diabetes presented as an emergency with a 4-day history of nausea, vomiting, and flu-like symptoms. He was on a basal bolus insulin regime comprising 8 units of bolus insulin lispro injected at mealtimes and 12 units of basal isophane insulin at bedtime, but did not monitor capillary blood glucose levels. He did however empirically increase his insulin doses during times of illness and had increased his isophane insulin to 15 units during the 3 days prior to presentation. He had only one prior hospital admission, which occurred 6 years previously and was due to an episode of DKA precipitated by gastroenteritis. He was single, unemployed, did not drink alcohol, had no previous psychiatric history, no family history of diabetes or other medical conditions, and lived in a hostel. He had a record of poor clinic attendances and a history of long-term cannabis use. He denied any salicylate consumption, but admitted to some weight loss; however, he was unable to quantify this. His body mass index (BMI) was 19 kg/m2, and he looked unkempt. Physical examination revealed a temperature of 36.4°C (97.5°F), heart rate of 106 beats per minute, supine blood pressure of 131/85 mmHg, and sitting blood pressure of 122/80 mmHg. He had a respiratory rate of 30 breaths per minute, and his oxygen saturation using a pulsoximeter was 99% on room air. He appeared clinically dehydrated with dry oral mucosa, but cardiovascular, respiratory, abdominal, and neurological examinations were otherwise normal. Diabetic ketoacidosis (DKA) was suspected; metabolic acidosis was confirmed with a pH of 7.3, bicarbonate concentration of 10 mEq/l, and an elevated anion gap of 29 mEq/l [sodium = 134 mEq/l, potassium = 5.7 mEq/l, chloride = 101 mEq/l, b Continue reading >>
Differential Effects Of Fasting And Dehydration In The Pathogenesis Of Diabetic Ketoacidosis
Abstract Glycemia varies widely in patients with diabetic ketoacidosis (DKA), with plasma glucose concentrations between 10 to 50 mmol/L commonly encountered. The mechanism of this glycemic variability is uncertain. Our study examined the differential effects of fasting and dehydration on hyperglycemia induced by withdrawal of insulin in type 1 diabetes. To evaluate the respective roles of dehydration and fasting in the pathogenesis of DKA, 25 subjects with type 1 diabetes were studied during 5 hours of insulin withdrawal before (control) and after either 32 hours of fasting (n = 10) or dehydration of 4.1% ± 2.0% of baseline body weight (n = 15). Samples were obtained every 30 minutes during insulin withdrawal for substrate and counterregulatory hormone levels and rates of glucose production and disposal. Fasting resulted in reduced plasma glucose concentrations compared with the control study, while dehydration resulted in increased plasma glucose concentrations compared with the control study (P < .001). Glucose production and disposal were decreased during the fasting study and increased during the dehydration study compared with the control study. Glucagon concentrations and rates of development of ketosis and metabolic acidosis were increased during both fasting and dehydration compared with control. These data suggest that fasting and dehydration have differential effects on glycemia during insulin deficiency, with dehydration favoring the development of hyperglycemia and fasting resulting in reduced glucose concentrations. This finding is probably attributable to the differing effect of these conditions on endogenous glucose production, as well as to differences in substrate availability and counterregulatory hormone concentrations. The severity of pre-existing Continue reading >>
Ketoacidosis
Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate. Ketoacidosis is a pathological metabolic state marked by extreme and uncontrolled ketosis. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased. In extreme cases ketoacidosis can be fatal.[1] Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct by-product of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover.[2] Ketosis may also give off an odor, but the odor is usually more subtle due to lower concentrations of acetone. Treatment consists most simply of correcting blood sugar and insulin levels, which will halt ketone production. If the severity of the case warrants more aggressive measures, intravenous sodium bicarbonate infusion can be given to raise blood pH back to an acceptable range. However, serious caution must be exercised with IV sodium bicarbonate to avoid the risk of equally life-threatening hypernatremia. Cause[edit] Three common causes of ketoacidosis are alcohol, starvation, and diabetes, resulting in alcoholic ketoacidosis, starvation ketoacidosis, and diabetic ketoacidosis respectively.[3] In diabetic ketoacidosis, a high concentration of ketone bodies is usually accomp Continue reading >>
The Effects Of Fasting Ketosis
Understanding ketosis and muscle loss during fasting. The process of ketosis is one of the physiological effects of fasting in which the brain (and some other bodily processes) uses ketones produced from fatty tissues as a fuel instead of the usual glucose. This is called "muscle sparing". When glucose isn't readily available via the diet (in the form of carbohydrates) and the glycogen stores in the liver become depleted, the body could break down muscle to get it. But ketosis is an adaptation that will spare muscle during times of shortage by instead breaking down fat stores and manufacturing ketones for brain fuel. It is said this state is attained at approximately 48 hours of a water fast for women and closer to 72 hours for men. The effects of fasting ketosis have become a more popular and controversial subject in recent years due to low-carb, high-protein dieters relying on it long-term to "burn the fat". Where ketosis was once considered a "crisis response" of the body and fine only for short durations, there are some doctors who now contend ketones are an acceptable alternative fuel, produced and used by the body any time glucose is scarce, which can happen even in non-fasting, non-dieting individuals, such as during intense exercise or during sleep. They are considering it a natural metabolic process where ketone production and use fluctuates constantly in response to the body's needs. What is so controversial about the low-carbers use of ketosis is the long term, artificially produced, use of it. Over long periods of time, their high-protein diet produces excess protein by-products that become a strain on the kidneys to eliminate. Ketosis also creates a mild acidosis of the blood, which, over a long period of time is considered detrimental to our health. One ef Continue reading >>
Short-term Fasting Is A Mechanism For The Development Of Euglycemic Ketoacidosis During Periods Of Insulin Deficiency.
To determine the etiology of euglycemic ketoacidosis, the effect of a 32-h fast on the rate of metabolic deterioration was examined in a group of 10 healthy subjects with type I diabetes mellitus. Patients were studied during 5 h of insulin withdrawal after 8 h (postprandial) and 32 h (fasted) of food deprivation. Study parameters included substrate levels, electrolytes, counterregulatory hormone levels, and rates of glucose and glycerol turnover. In the fasted state, mean peak plasma glucose concentrations were significantly lower than those in the 8-h postprandial state (13.3 +/- 1.6 vs. 17.4 +/- 1.4 mmol/L, respectively; P < 0.05), and mean rates of glucose production were also significantly lower at all time points in the fasting state. The rate of development of ketosis was significantly more rapid during insulin deficiency after a fast (8.82 +/- 0.63 vs. 6.23 +/- 0.30 micro/L.min; P < 0.05), while plasma nonesterified fatty acids and glycerol turnover showed a biphasic response to insulin withdrawal, which was also more robust after a fast. Metabolic acidosis, as reflected in the rate of decrease in serum bicarbonate concentration, was more severe after 32 h of fasting than in the postprandial state (mean nadir, 15.4 +/- 0.9 vs. 18.6 +/- 0.5 mmol/L; P < 0.001). In contrast to values in the postprandial state, serum glucagon levels rose during insulin withdrawal in the fasting state, and plasma norepinephrine levels also correlated positively with the ongoing metabolic decompensation. Other counterregulatory hormones did not differ significantly in the fasted vs. postprandial states in these short term metabolic studies. We conclude that a fast of moderate duration, such as might be expected to occur during the development of diabetic ketoacidosis, predisposes pati Continue reading >>
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Ketoacidosis: A Diabetes Complication
Ketoacidosis can affect both type 1 diabetes and type 2 diabetes patients. It's a possible short-term complication of diabetes, one caused by hyperglycemia—and one that can be avoided. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two of the most serious complications of diabetes. These hyperglycemic emergencies continue to be important causes of mortality among persons with diabetes in spite of all of the advances in understanding diabetes. The annual incidence rate of DKA estimated from population-based studies ranges from 4.8 to 8 episodes per 1,000 patients with diabetes. Unfortunately, in the US, incidents of hospitalization due to DKA have increased. Currently, 4% to 9% of all hospital discharge summaries among patients with diabetes include DKA. The incidence of HHS is more difficult to determine because of lack of population studies but it is still high at around 15%. The prognosis of both conditions is substantially worsened at the extremes of age, and in the presence of coma and hypertension. Why and How Does Ketoacidosis Occur? The pathogenesis of DKA is more understood than HHS but both relate to the basic underlying reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counter regulatory hormones such as glucagons, catecholamines, cortisol, and growth hormone. These hormonal alterations in both DKA and HHS lead to increased hepatic and renal glucose production and impaired use of glucose in peripheral tissues, which results in hyperglycemia and parallel changes in osmolality in extracellular space. This same combination also leads to release of free fatty acids into the circulation from adipose tissue and to unrestrained hepatic fatty acid oxidation to ketone bodies. Some drugs ca Continue reading >>
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 >>
Incidence Of Diabetic Ketoacidosis During Ramadan Fasting In Benghazi, Libya
Background: Ramadan is the ninth month on the lunar calendar and for over a billion Muslims it is a holy month during which all healthy adults must observe absolute fasting from dawn to sunset. The risk of diabetic ketoacidosis is thought to be higher during Ramadan fasting due to hormonal disequilibrium. Aim and objectives: The aim of this study was to examine the hypothesis that diabetic ketoacidosis is more frequent during Ramadan fasting. Patients and methods: A retrospective analysis of the records of all patients admitted with DKA to all Benghazi hospitals during the lunar year 1428 Hijri (January 2007 to January 2008). Results: Fifteen episodes occurred during Ramadan (4.6 episode/10 000 diabetic) as compare to 19.45 episodes/month (6 episode/10 000 diabetic/month) during the other lunar months (P=0.000), there was no significant difference in the patients’ mean age (37.6±10 vs 38.3±19, P=0.8), or mortality rate (13.3 vs 14.4%, P=0.9) during Ramadan and other months. The commonest precipitating factor of diabetic ketoacidosis during Ramadan was infection (46.6%), followed by miss dosing (33.3%). Conclusion: There is no increase in the incidence and mortality from DKA during Ramadan which might indicate that Ramadan fasting is not a significant risk factor for diabetic ketoacidosis. ApoB plays a central role in lipoprotein metabolism through regulation of total cholesterol and LDL-cholesterol (LDL-C) concentrations in plasma. Two restriction fragment length polymorphisms (ECoRI and XbaI) represent single base alterations in the coding region of ApoB gene. ECoRI polymorphic region of ApoB gene is due to on an amino acid change (Glu→Lys). The XbaI polymorphic region of ApoB gene results from a substitution of (A→T) in the threonine codon and does not change Continue reading >>
In Defense Of Fasting: Common Misconceptions
Clearing misconceptions For those of you wondering, the tone of this article has been highly edited from my anger-rant earlier. I used my blog as catharsis, but now it’s back to business. I get a message across better being polite anyway. Fasting is a fairly unique diet technique. It’s at a crossroads (more like highway junction) of efficacy, health, social perception, eating disorders, and overall safety. It’s not bad given you avoid a few pitfalls and don’t blatantly starve yourself, but some people are still caught up in the midst of all this confusion, not knowing whether not eating for a single day will hurt them or help them. This article is subject to editing in the future. I am using this to keep tabs on the current science of fasting, both good and bad. It might be nice to keep it bookmarked and come back to it from time to time. I also suspect some time in the future it might become Tl;Dr, but a valuable tool nonetheless. This can be used in drug testing also and because of this some people have found a way to access synthetic urine. One of the most popular sites is Since fasting is put on ‘trail’ a lot, I figured I might bring up the common arguments like a court case. Just for kicks. Exhibit A: Ketosis and Ketoacidosis First, definitions: Ketosis is the state of an organism characterized by elevated serum levels of ketones Ketoacidosis is a metabolic state characterized by uncontrolled production of ketone bodies and decreased serum pH Ketosis is the presence of ketones, ketoacidosis is the presence of ketones combined with a drop in pH. The drop in pH is due in part to overproduction of ketones (which are acidic in nature) and a failure of the body/diet to buffer said acidity. So from this, we can preliminarily conclude that ketoacidosis will ki Continue reading >>
Diabetic, Alcoholic And Starvation Ketoacidosis
Copious amounts of ketones which are generated in insulin-deficient or insulin-unresponsive patients will give rise to a high anion gap metabolic acidosis. Ketones are anions, and they form the high anion gap. Management of DKA and HONK is discussed elsewhere. Meet the ketones Chemically speaking, a ketone is anything with a carbonyl group between a bunch of other carbon atoms. The above are your three typical ketoacidosis-associated ketone bodies. The biochemistry nerds among us will hasten to add that the beta-hydroxybutyrate is in fact not a ketone but a carboxylic acid, but - because it is associated with ketoacidosis, we will continue to refer to it as a ketone for the remainder of this chapter, in the spirit of convention. In the same spirit, we can suspend our objections to acetone being included in a discussion of ketoacidosis, which (though a true ketone) is in fact not acidic or basic, as it does not ionise at physiological pH (its pKa is 20 or so). So really, the only serious ketone acid is acetoacetate, which has a pKa of 3.77. However, beta-hydroxybutyrate is the prevalent ketone in ketoacidosis; the normal ratio of beta-hydroxybutyrate and acetoacetate is 3:1, and it can rise to 10:1 in diabetic ketoacidosis. Acetone is the least abundant. The metabolic origin of ketones The generation of ketones is a normal response to fasting, which follows the depletion of hepatic glycogen stores. Let us discuss normal physiology for a change. You, a healthy adult without serious alcohol problems, are fasting from midnight for a routine elective hernia repair. You will go to be after dinner with a few nice lumps of undigested food in your intestine, as well as about 75g of hepatic glycogen. As you sleep, you gradually digest the food and dip into the glycogen store. At Continue reading >>
Ketosis Vs. Ketoacidosis: Understanding The Differences
Introduction to Ketosis vs Ketoacidosis Historically, ketosis has been one of the most vaguely defined and poorly understood concepts of the last century. There are different scenarios in which are body can be in a state of ketosis (including ketoacidosis). The most basic definition of ketosis is a general increase in blood levels of ketone bodies to 0.5 mmol or above. However, the reasons for the development of ketosis, the resultant levels of blood ketones, and the associated outcomes (health versus possible death) differ drastically between different situations of ketosis. Failure to understand the differences between various incidents of ketosis has led to the common misconceptions we have today that ultimately has made educating the masses on the ketogenic diet difficult. The single most important take home from this article should be that diabetic ketoacidosis is not the same as the ketosis experienced from a ketogenic diet. Diabetic Ketoacidosis Whenever I speak about ketogenic dieting, almost inevitably I am asked the question: “But shouldn’t you be worried about going into a state of ketoacidosis?” Ketoacidosis occurs when the formation ketone bodies are uncontrolled (15-25 mmol) and acidity in the blood increases (1). It is important to understand that our body regulates blood acid concentrations tightly. We typically measure blood acidity vs. alkalinity using the pH scale. If your blood’s pH is less than 7 it is acidic, and if greater it is basic, or alkaline. Our blood is usually slightly alkaline with a pH ranging from 7.35 to 7.45. Any deviation up or down from the norm by even the smallest amount can prove fatal! The most common form of ketoacidosis to occur is known as diabetic ketoacidosis. This usually occurs in type I diabetics but can also oc Continue reading >>
