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Fasting Ketoacidosis Treatment

The Perks Of Fasting, With None Of The Work

The Perks Of Fasting, With None Of The Work

“If there’s a downside, it is kind of crazy tasting,” said Geoff Woo, the founder of HVMN, a Silicon Valley company that makes nootropics, or performance-enhancing supplements. We were in a conference room in The Atlantic’s office building, and he was bracing me for my trial run of his latest product. It was a small, clear vial labeled “Ketone,” a new type of energy drink his company is releasing this week. Its nutrition label says it contains 120 calories, but no carbs, no fat, and no protein. Instead, it’s all ketones, the chemical that Woo and his company are calling a “fourth food group.” He hopes the drink will allow people to reap the benefits of occasional fasting—high ketone levels inside the body—without actually having to not eat. I unscrewed the top and, college-days muscle memory kicking in, chugged it like a shot of Captain Morgan. It tasted like cough syrup that had been poured into a garbage bag and left in the sun. “Augh!” I cried. “I compare it to a combination of a liquor shot with nail-polish remover,” Woo said. Woo’s coworker, Brianna Stubbs, went to fetch me a glass of water. “We’ve done a lot of work to make it better,” she said. Within an hour, the drink was supposed to help improve my athletic performance by changing how my body burned energy during exercise. Some people also say it helps them feel more energetic and focused on their work. About 25 minutes after I drank Ketone, Woo and Stubbs pricked my finger to see if it was working. My blood sugar, which had verged on diabetic levels from some pineapple I had eaten that morning, was down to near-normal levels. Meanwhile, my ketones, which had been practically nonexistent before imbibing—measuring just 0.2 millimolar—had soared to 4.9. “It would have Continue reading >>

Metabolism And Ketosis

Metabolism And Ketosis

Dr. Eades, If the body tends to resort to gluconeogenesis for glucose during a short-term carbohydrate deficit, are those who inconsistently reduce carb intake only messing things up by not effecting full blown ketosis? If the body will still prefer glucose as main energy source unless forced otherwise for at least a few days, is it absolutely necessary to completely transform metabolism for minimal muscle loss? Also, if alcohol is broken down into ketones and acetaldehyde, technically couldn’t you continue to drink during your diet or would the resulting gluconeogenesis inhibition from alcohol lead to blood glucose problems on top of the ketotic metabolism? Would your liver ever just be overwhelmed by all that action? I’m still in high school so hypothetical, of course haha… Sorry, lots of questions but I’m always so curious. Thank you so much for taking the time to inform the public. You’re my hero! P.S. Random question…what’s the difference between beta and gamma hydroxybutyric acids? It’s crazy how simple orientation can be the difference between a ketone and date rape drug…biochem is so cool! P.P.S. You should definitely post the details of that inner mitochondrial membrane transport. I’m curious how much energy expenditure we’re talkin there.. Keep doin your thing! Your Fan, Trey No, I don’t think people are messing up if they don’t get into full-blown ketosis. For short term low-carb dieting, the body turns to glycogen. Gluconeogenesis kicks in fairly quickly, though, and uses dietary protein – assuming there is plenty – before turning to muscle tissue for glucose substrate. And you have the Cori cycle kicking in and all sorts of things to spare muscle, so I wouldn’t worry about it. And you can continue to drink while low-carbing. Continue reading >>

The Emedicinehealth Doctors Ask About Diabetic Ketoacidosis:

The Emedicinehealth Doctors Ask About Diabetic Ketoacidosis:

A A A Diabetic Ketoacidosis (cont.) A person developing diabetic ketoacidosis may have one or more of these symptoms: excessive thirst or drinking lots of fluid, frequent urination, general weakness, vomiting, loss of appetite, confusion, abdominal pain, shortness of breath, a generally ill appearance, increased heart rate, low blood pressure, increased rate of breathing, and a distinctive fruity odor on the breath. If you have any form of diabetes, contact your doctor when you have very high blood sugars (generally more than 350 mg) or moderate elevations that do not respond to home treatment. At initial diagnosis your doctor should have provided you with specific rules for dosing your medication(s) and for checking your urinary ketone level whenever you become ill. If not, ask your health care practitioner to provide such "sick day rules." If you have diabetes and start vomiting, seek immediate medical attention. If you have diabetes and develop a fever, contact your health care practitioner. If you feel sick, check your urinary ketone levels with home test strips. If your urinary ketones are moderate or higher, contact your health care practitioner. People with diabetes should be taken to a hospital's emergency department if they appear significantly ill, dehydrated, confused, or very weak. Other reasons to seek immediate medical treatment include shortness of breath, chest pain, severe abdominal pain with vomiting, or high fever (above 101 F or 38.3 C). Continue Reading A A A Diabetic Ketoacidosis (cont.) The diagnosis of diabetic ketoacidosis is typically made after the health care practitioner obtains a history, performs a physical examination, and reviews the laboratory tests. Blood tests will be ordered to document the levels of sugar, potassium, sodium, and oth Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>

Ketoacidosis: A Diabetes Complication

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 In A Non-diabetic Woman Who Was Fasting During Lactation

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 >>

Extreme Gestational Starvation Ketoacidosis: Case Report And Review Of Pathophysiology

Extreme Gestational Starvation Ketoacidosis: Case Report And Review Of Pathophysiology

A case of severe starvation ketoacidosis developing during pregnancy is presented. The insulinopenic/insulinresistant state found during fasting in late gestation predisposes to ketosis. Superimposition of stress hormones, which further augment lipolysis, exacerbates the degree of ketoacidosis. In our patient, gestational diabetes, twin pregnancies, preterm labor, and occult infection were factors that contributed to severe starvation ketoacidosis. Diagnosis was delayed because starvation ketosis is not generally considered to be a cause of severe acidosis, and because the anion gap was not elevated. Improved understanding of the complex fuel metabolism during pregnancy should aid in prevention, early recognition, and appropriate therapy of this condition. Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Prashanth Rawla1, Anantha R Vellipuram2, Sathyajit S Bandaru3 and Jeffrey Pradeep Raj4[1] Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA [2] Texas Tech University Health Sciences Center, El Paso, Texas, USA [3] Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA [4] Department of Pharmacology, St John’s Medical College, Bangalore, India Summary Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA. Euglycemic diabetic ketoacidosis is rare. Consider ketosis in patients with DKA even if their serum glucose levels are normal. High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma. Blood pH and blood or urine ketones should be checked in ill patients with diabetes regardless of blood glucose levels. Background Diabetic ket Continue reading >>

Fasting May Improve Cancer Treatment, But Needs Further Exploration

Fasting May Improve Cancer Treatment, But Needs Further Exploration

The gold standard treatment for cancer in the last few decades has been a combination of surgery – to remove tumours – and chemotherapy and radiotherapy – to kill cancer cells. With the progress of personalised medicine, where identifying specific mutations in the tumour guides treatment selection, there has been increasing success in survival rates. But there has been little improvement in reducing side effects on healthy cells caused by chemotherapy, which also limit the dosage that can be administered. Over the last two decades, research in animals has shown restricting calories - with alternating periods of fasting and feeding – promotes protection mechanisms for healthy cells, while increasing white blood cells that kill cancer cells. A 2008 study showed mice with neuroblastoma, a common childhood cancer, that had only water for two days before receiving a large dose of chemotherapy, experienced less or no side effects compared to mice fed normally. In another study, tumour cells were killed more efficiently in mice who weren’t fed than in those that were. Since then, further animal studies and early trials in humans confirmed short-term fasting prior to, and after, chemotherapy treatment reduced side effects. It also protected healthy cells from the toxicity of the drug, while killing cancerous ones. So does this mean we can use fasting to help with cancer treatment? Glucose and cancer Cancerous cells are known to rely on glucose, a type of sugar, for their energy metabolism, rapid growth, and resistance to chemotherapy. That cancer cells thrive on glucose was first shown by German physiologist Otto Warburg in the 1950s. He also showed they were unable to use fatty acids as efficiently for energy, or at all. This idea of cancer being a disease reliant on Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea 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 >>

3.1.4.5. Ketoacidosis

3.1.4.5. Ketoacidosis

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. The three major types of ketosis are: * Starvation ketosis * Alcoholic ketoacidosis * Diabetic ketoacidosis ==== 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 ketoanion levels are only 1 to 2 mmol/l and this will not much alter the anion gap. The acidosis even with quite prolonged fasting is only ever of mild to moderate severity with ketoanion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. This is probably due to the insulin level, which though lower, is still enough to keep the FFA levels less than 1mM. This limits substrate delivery to the liver restraining hepatic ketogenesis. Ketone bodies also stimulate some insulin release from the islets. The anion gap will usually not be much elevated. ==== Alcoholic ketoacidosis Typical Presentation This typical situation leading to alcoholic ketoacidosis is a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake. Food intake may be limited because of vomiting. The two key factors are the combination of ethanol and fasting. Presentation is typically a couple of days after the drinking binge has ceased. Pathophysiology The poor oral intake results in de Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com Continue reading >>

Ketosis: Symptoms, Signs & More

Ketosis: Symptoms, Signs & More

Every cell in your body needs energy to survive. Most of the time, you create energy from the sugar (glucose) in your bloodstream. Insulin helps regulate glucose levels in the blood and stimulate the absorption of glucose by the cells in your body. If you don’t have enough glucose or insufficient insulin to get the job done, your body will break down fat instead for energy. This supply of fat is an alternative energy source that keeps you from starvation. When you break down fat, you produce a compound called a ketone body. This process is called ketosis. Insulin is required by your cells in order to use the glucose in your blood, but ketones do not require insulin. The ketones that don’t get used for energy pass through your kidneys and out through your urine. Ketosis is most likely to occur in people who have diabetes, a condition in which the body produces little or no insulin. Ketosis and Ketoacidosis: What You Need To Know Ketosis simply means that your body is producing ketone bodies. You’re burning fat instead of glucose. Ketosis isn’t necessarily harmful to your health. If you don’t have diabetes and you maintain a healthy diet, it’s unlikely to be a problem. While ketosis itself isn’t particularly dangerous, it’s definitely something to keep an eye on, especially if you have diabetes. Ketosis can be a precursor to ketoacidosis, also known as diabetic ketoacidosis. Ketoacidosis is a condition in which you have both high glucose and high ketone levels. Having ketoacidosis results in your blood becoming too acidic. It’s more common for those with type 1 diabetes rather than type 2. Once symptoms of ketoacidosis begin, they can escalate very quickly. Symptoms include: breath that smells fruity or like nail polish or nail polish remover rapid breat Continue reading >>

Ketosis Explained – For Weight Loss, Health Or Performance

Ketosis Explained – For Weight Loss, Health Or Performance

Get Started Ketosis is a natural state for the body, when it is almost completely fueled by fat. This is normal during fasting, or when on a strict low-carb diet. Ketosis has many potential benefits, but there are also side effects. In type 1 diabetes and certain other rare situations excessive ketosis can even become dangerous. On this page you can learn all about how to harness the benefits of ketosis, while avoiding any problems. It all starts with understanding what ketosis is. Choose a section, or keep reading below for all of them. Ketosis ExplainedKetosis Explained BenefitsBenefits How to Get Into KetosisHow to Get Into Ketosis Ketosis ExplainedSymptoms & How to Know You’re In Ketosis Side Effects, Fears & Potential DangersSide Effects, Fears & Potential Dangers How to Reach Optimal KetosisHow to Reach Optimal Ketosis ketones Ketosis Explained The “keto” in the word ketosis comes from the fact that it makes the body produce small fuel molecules called “ketones”.1 This is an alternative fuel for the body, used when blood sugar (glucose) is in short supply. Ketones are produced if you eat very few carbs (that are broken down into blood sugar) and only moderate amounts of protein (excess protein can be converted to blood sugar). Ketones are produced in the liver, from fat. They are then consumed as fuel in the body, including by the brain. This is important as the brain is a hungry organ that consumes lots of energy every day,2 and it can’t run on fat directly. It can only run on glucose… or ketones. Maximizing fat burning On a ketogenic diet your entire body switches its fuel supply to run almost entirely on fat. Insulin levels become very low and fat burning increases dramatically. It becomes easy to access your fat stores to burn them off. This is o Continue reading >>

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