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How To Induce Ketoacidosis

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>

Would You Recommend The Ketogenic Diet To An 18 Year Old Girl For Weight Loss?

Would You Recommend The Ketogenic Diet To An 18 Year Old Girl For Weight Loss?

I’ve been on the diet for about 6 months. I am now 18 years old. The thing about Keto is that it’s a difficult diet and requires dedication, but the results are admirable. I’ve lost about 40 pounds over the course of the first 4 months and am now at 132 pounds, exercising once a week for an hour at best. I’ll give you the info you actually need to know, and then the rest will be my response to Sally’s post :) Also, remember that most people who give advice about weight loss have never been obese or overweight to a significant degree. Weight loss is a struggle and a battle, and you cannot rely on people who only criticize from afar. Would a soldier take advice on how to shoot a rifle from a civilian who has played Call of Duty? No? Thought not. Pros: Most people on keto do not need to consciously restrict food intake, you should never feel hungry. Generally preserves muscle mass and maximizes fat loss. You can eat fat again! Do not be afraid of fat. The fattiest animals, ruminants, consume low fat, grain based diets high in fiber. In contrast, every carnivore preferentially eats the fattiest part of the animal, yet they are lean. Why in the world would we assume that humans would get fat off of fat, when we have hundreds of contradictory examples in nature? Lots of natural substitutes for carb based foods available now, Low Carb Tortillas, Ice Creams, you name it. Watch for artificial sweeteners though. Not wholly reliant on exercise for weight loss, but it’s good for personal sanity to do so. Frees you from sugar addiction Cons: No carbs. It’s for life, you don’t “leave it.” It is not a “fad diet” that you do for 2 months and stop, it’s a lifestyle change and an approach to appreciate food. Don’t think of it as a thing that you can have cheat Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci Continue reading >>

Diabetic Ketoacidosis Inducing Myocardial Infarction Secondary To Treatment With Dapagliflozin: A Case Report

Diabetic Ketoacidosis Inducing Myocardial Infarction Secondary To Treatment With Dapagliflozin: A Case Report

Go to: Case Report A 58‐year‐old male with dyslipidemia, an eight‐year history of T2DM, a family history, his mother, of T2DM, with no known micro‐ or macrovascular complications, was admitted to the emergency department for malaise, epigastric pain, polyuria, and progressive dyspnea which had begun 10 h ago. He had experienced a 2‐kg weight loss over the last few days. His usual medications included aspirin 100 mg q24 h, atorvastatin 40 mg q24 h, and metformin 850 mg q8 h, which had been switched to dapagliflozin 20 days before, due to poor glycemic control, with HbA1c 12% (108 mmol/mol). His vital signs included a heart rate of 122 bpm, respiratory rate 33 rpm, blood pressure 142/70 mmHg, temperature 36.1°C, and body mass index 22.5 kg/m2. On physical examination, somnolence, dry skin and mucous membranes, a Kussmaul breathing pattern, and a capillary refill of 3 sec were observed. Blood tests revealed hemoglobin 17.1 g/dL (13.5–18), leukocytes 19.5 × 103 (4–10 × 103), platelets 296 × 103 (150–450 × 103), glucose 248 mg/dL (60–100), creatinine 0.97 mg/dL (0.67–1.17), sodium 136 mmol/L (135–145), potassium 4.7 mmol/L (3.5–5.5), chloride 101 mmol/L (95–112), phosphate 4.9 mg/dL (2.5–4.5), amylase 70 U/L (10–115), lipase 28 U/L (1–67), pH 6.95 (7.35–7.45), pCO2 23 mmHg (35–45), HCO3 5 mmol/L (22–26), lactate 1.8 mmol/L (0–1.5), urine ketone bodies >150 mg/dL (0–0), CK 112 U/L (1–190), CK‐MB 7.3 ng/mL (0.1–5), and troponin I 0.07 ng/mL (0.001–0.05). The electrocardiogram (EKG) showed sinus rhythm with right bundle branch block, and nonspecific repolarization abnormalities. Because of the right bundle branch block was not previously known, a new troponin test was performed six hours later with a peak value of 4.28 ng/m Continue reading >>

A Case Of Clozapine-induced Diabetic Ketoacidosis

A Case Of Clozapine-induced Diabetic Ketoacidosis

A 29-year-old male of Yemeni descent detained in a medium secure unit was commenced on clozapine; after 4 weeks of treatment he was taking a total of 275 mg in divided doses. He developed nausea and vomiting which progressed over 36 hours to a point where he needed to be urgently transferred to the local accident and emergency unit. At assessment he was experiencing breathing problems, vomiting and he was incontinent of urine; he had a Glasgow Coma Scale score of five. He was immediately transferred to the intensive care unit. The differential diagnoses included drug overdose, alcohol intoxication and clozapine-induced hyperglycaemia. His blood chemistry showed evidence of diabetic ketoacidosis; his blood glucose level was grossly elevated. The clozapine was stopped and the patient was given appropriate treatment with glycaemic agents. In summary, the patient had become seriously unwell over a period of 36 hours. Apart from having a slightly raised body mass index, he was fit and well and had no family history of diabetes. His pre-treatment blood glucose had been normal. Diabetic ketoacidosis is over ten times more common in patients treated with atypical antipsychotics than in the general population,1 although the evidence is largely restricted to case reports and series.2 Clozapine has a higher risk of ketoacidosis than other oral antipsychotics3 and it tends to develop after a shorter duration of treatment, with a high proportion of patients developing it within 3-6 months. Low doses, being a young male and having a negative family history seem to be significant risk factors.4 There is also significant mortality.5 The unusual aspect of this case (although not unknown) was the occurrence of diabetic ketoacidosis during the titration phase of treatment. Continue reading >>

What Is The Difference Between Ketogenic Diet And Starvation?

What Is The Difference Between Ketogenic Diet And Starvation?

I really must track down how the unscientific drivel that the ketogenic diet is some sort of a starvation response got started. The only link between starvation and the ketogenic diet is the production of ketones in the body. I know certain Quora gurus posit such crap repeatedly but it’s not true. Ketones as a natural process in the body The body produces ketones naturally. It’s likely a protective mechanism due to the evolutionary instability of the food supply. Most of the time ketone levels are quite low. However, anytime the food supply gets interrupted, even short times like at night during sleep, the body starts to produce ketones. Ketones and fat metabolism Ketones are made in the liver from fat. One of the reasons people measure ketone levels in the body is that they are a marker for increased fat utilization in the body. There are two fuel partitioning schemes in the human body. The body can utilize glucose and glycogen or the body can utilize fats (dietary and body) and ketones. There are some overlaps in the utilization of these schemes but when foods that are easily broken down into glucose are withdrawn the body will start to burn fats and ketones as sources of energy. Ketones and starvation The similarity between starvation and the ketogenic diet is that both involve higher levels of circulating ketones in the body. This makes sense since in both situations foods that are easily broken down into glucose have been withdrawn. In both situations, levels of blood glucose and glycogen stores are lower and the body must fuel with other substances. Some tissues in the body are perfectly happy (and in many ways) prefer utilizing fats as fuels. However, some tissues need levels of glucose. These tissues when faced with lower glucose intake in the diet must rely Continue reading >>

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

Steroid-induced Diabetic Ketoacidosis.

Steroid-induced Diabetic Ketoacidosis.

This content is PDF only. Please click on the PDF icon to access. Abstract Although diabetes mellitus is not uncommon in patients on highdose steroid treatment, ketoacidosis is distinctly rare. Indeed only a few patients have been reported, and the ketoacidosis was so mild that none required insulin. We have studied four patients with systemic lupus erythematosus (SLE) who developed diabetic ketoacidosis after treatment with large doses of steroids. All received at least 60 mg of prednisone for 2 to 8 months. In addition, two had been maintained on small doses for 1 and 10 years. Family history of diabetes mellitus was present in two. One patient was on chlorothiazide diuretic for several months, Continue reading >>

Ketosis Vs. Ketoacidosis: What You Should Know

Ketosis Vs. Ketoacidosis: What You Should Know

Despite the similarity in name, ketosis and ketoacidosis are two different things. Ketoacidosis refers to diabetic ketoacidosis (DKA) and is a complication of type 1 diabetes mellitus. It’s a life-threatening condition resulting from dangerously high levels of ketones and blood sugar. This combination makes your blood too acidic, which can change the normal functioning of internal organs like your liver and kidneys. It’s critical that you get prompt treatment. DKA can occur very quickly. It may develop in less than 24 hours. It mostly occurs in people with type 1 diabetes whose bodies do not produce any insulin. Several things can lead to DKA, including illness, improper diet, or not taking an adequate dose of insulin. DKA can also occur in individuals with type 2 diabetes who have little or no insulin production. Ketosis is the presence of ketones. It’s not harmful. You can be in ketosis if you’re on a low-carbohydrate diet or fasting, or if you’ve consumed too much alcohol. If you have ketosis, you have a higher than usual level of ketones in your blood or urine, but not high enough to cause acidosis. Ketones are a chemical your body produces when it burns stored fat. Some people choose a low-carb diet to help with weight loss. While there is some controversy over their safety, low-carb diets are generally fine. Talk to your doctor before beginning any extreme diet plan. DKA is the leading cause of death in people under 24 years old who have diabetes. The overall death rate for ketoacidosis is 2 to 5 percent. People under the age of 30 make up 36 percent of DKA cases. Twenty-seven percent of people with DKA are between the ages of 30 and 50, 23 percent are between the ages of 51 and 70, and 14 percent are over the age of 70. Ketosis may cause bad breath. Ket Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Ketosis: Fear, Uncertainty And Doubt

Ketosis: Fear, Uncertainty And Doubt

Perhaps nothing is more damaging to the new low-carber than the intentional spread of fear, uncertainty and doubt regarding the state of ketosis compared to the dangerous state of ketoacidosis. The former is a natural and healthy state of existence, the latter is a condition that threatens the life of type 1 diabetics and type 2 diabetics whose disease has progressed to the point where their pancreatic beta cells can no longer produce insulin (ketoacidosis is also a risk for alcoholics). So if you’re not an alcoholic, a type 1 diabetic or a late-stage type 2 diabetic, fear of ketosis is misdirected. You should regard with suspicion anyone who confuses the two and warns you against a low-carb diet because they cannot tell the difference. The confusion between ketosis and ketoacidosis is a sign of a grave misunderstanding of basic biology (if not a complete lack of critical faculty). So too is the assumption that ketosis is the “early stage” of ketoacidosis or that “ketosis leads to ketoacidosis” in a person whose pancreas is still able to produce insulin. If you don’t trust me (and why should you), you should consider listening to some people who know a lot more about this than either you or I ever will: Nutritional ketosis is by definition a benign metabolic state… by contrast, ‘diabetic ketoacidosis’ is an unstable and dangerous condition that occurs when there is inadequate pancreatic insulin response to regulate serum B-OHB. This occurs only in type-1 diabetics or in late stage type-2 diabetics with advanced pancreatic burnout. (Dr. Phinney & Dr. Volek, The Art and Science of Low Carbohydrate Living, p.4) Later in the book (p.80), Phinney and Volek explain further: [Type-1 diabetics] need insulin injections not just to control blood glucose levels, Continue reading >>

Canagliflozin-induced Diabetic Ketoacidosis

Canagliflozin-induced Diabetic Ketoacidosis

Go to: Case Report A 62-year-old woman with type 2 diabetes mellitus, hypertension, gastroesophageal reflux disease, and depression presented with 4 days of nausea, vomiting, and generalized weakness. Her symptoms became progressively worse such that by the day of admission she had decreased appetite, polydipsia, polyuria, and could not walk. The patient denied fever, chills, abdominal pain, diarrhea, or sick contacts. Home medications were atorvastatin, metformin, sucralfate, pioglitazone, canagliflozin, exenatide, omeprazole, fluoxetine, ranitidine, lisinopril, and alprazolam. On physical examination, the patient’s vital signs included a temperature of 38.3°C, blood pressure 134/61, heart rate 107, respiratory rate 24, and oxygen saturation of 100% on 2 liters nasal cannula oxygen. The patient appeared ill and distressed. She had dry mucous membranes, clear lung sounds bilaterally, and her heart was regular without murmurs, gallops, or rubs. Her abdomen was soft and nontender with present bowel sounds. Extremities showed no edema, and she had no focal neurological findings. Laboratory revealed a metabolic acidosis with a pH of 7.08 and anion gap >17. Chemistry panel indicated sodium 134 mEq/L, potassium 5.2 mEq/L, chloride 112 mEq/L, CO2 <5 mEq/L, blood urea nitrogen 22 mg/dL, and creatinine 1.3 mg/dL. Blood glucose was 213 mg/dL, and urinalysis revealed glucose 2+ and ketones 3+. Serum ketones were present at 1:8 dilution, with a lactic acid of 0.8 mmol/L. The patient’s hemoglobin A1C (HbA1c) was 11.1. The patient was admitted to the intensive care unit for severe metabolic acidosis secondary to DKA. Aggressive fluid resuscitation was undertaken and an insulin drip initiated. Within 6 hours, the anion gap metabolic acidosis improved. On further review of her med Continue reading >>

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Laboratory tests, including blood and urine tests, are used to confirm a diagnosis of diabetic ketoacidosis. Tests for ketones are available for home use. Keep some test strips nearby in case your blood sugar level becomes high. When ketoacidosis is severe, it must be treated in the hospital, often in an intensive care unit. Treatment involves giving insulin and fluids through your vein and closely watching certain chemicals in your blood (electrolyt Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

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