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Ketoacidosis When Fasting

Short-term Fasting Is A Mechanism For The Development Of Euglycemic Ketoacidosis During Periods Of Insulin Deficiency.

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 >>

Incidence Of Diabetic Ketoacidosis During Ramadan Fasting In Benghazi-libya

Incidence Of Diabetic Ketoacidosis During Ramadan Fasting In Benghazi-libya

Go to: Introduction Ramadan is the ninth month on the lunar calendar and for Muslims it is a holy month during which all healthy (mentally and physically) adults must fast during day time. Fasting in Islam means absolute self-restraint from food, drink and sex from dawn to sunset which is not a very difficult duty for healthy subjects nevertheless, it might be difficult or impossible for sick people to cope with fasting, therefore by the mercy of Allah they were exempted from fasting Ramadan. However, people with chronic illnesses like diabetes mellitus (DM) find it psychologically unacceptable not to fast and they do not agree to be considered as ill people, therefore they usually attempt to fast and on most occassions they succeed, for instance in Epidimiology of Diabetes and Ramadhan (EPIDIAR) study, 43% of type-1 diabetics and 86% of type-2 patients managed to fast a mean of 23 and 27 days respectively.1 The risk of Diabetic Ketoacidosis (DKA) is thought to be higher during Ramadan (at least theoretically) as fasting will result in hypoinsulinemia and hyperglucagonemia, this hormonal disequilibrium favouring hyperglycemia, lipolysis and ketone body formation and eventually development of DKA.2 However, this remains just a speculation as there are no studies showing that the incidence of DKA is actually increased during Ramadan, as a matter of fact there are some evidence against this assumption. For instance, Kadiki reported that only 2.5% of Libyan diabetics in one study developed DKA during Ramadan fasting, similarly in another study; Abusreiwil reported that 1.8% of type-1 patients developed DKA during Ramadan fasting figures that are comparable with non fasting months.3,4 Frequency of different precipitating factors Precipitating factors Ramadan Other months p-v 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

Diabetic Ketoacidosis

The Facts Diabetic ketoacidosis (DKA) is a condition that may occur in people who have diabetes, most often in those who have type 1 (insulin-dependent) diabetes. It involves the buildup of toxic substances called ketones that make the blood too acidic. High ketone levels can be readily managed, but if they aren't detected and treated in time, a person can eventually slip into a fatal coma. DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. Although much less common, DKA can occasionally occur in people with type 2 diabetes under extreme physiologic stress. Causes With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body's cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can't get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn't available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body's metabolic processes aren't able 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 >>

The Effects Of Fasting Ketosis

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 >>

Fasting And Lipolysis – Part 4

Fasting And Lipolysis – Part 4

Insulin is the main driver of both obesity and type 2 diabetes. The key to reversing both conditions is therefore not “How do we reduce calories?”, but instead “How do we reduce Insulin?” There are almost no drugs that will do this. There is actually two classes of medications that consistently reduces insulin – one by a lot, one by a little. Not by co-incidence, they are the only drugs that consistently reduces weight. But the problem is that they are both expensive and have side effects. Short of drugs, we need an efficient, effective way to lower insulin if we are to be successful in losing weight. A diet low in refined carbs and sugar will certainly do the trick for some, but for others it is not enough. The answer, if you haven’t guessed yet, is fasting. The classic descriptions of fasting physiology were written by Dr. George Cahill. We reviewed this in a previous post, but here’s a pictorial version. Essentially, fasting is the gradual shift of burning glucose to burning fat. In stage 1, most of the body is using exogenous glucose. By stage 2 and 3, glycogen (stored sugar) provides much of the glucose needed. Most tissues are still using sugar, but the liver, muscle and fat cells have started to burn fat. By stage 4 and 5, glycogen stores have run out. Hepatic and renal (liver and kidney) gluconeogenesis is now providing all the glucose, but only the brain, red blood cells and the renal medulla (the inner part of the kidney) uses glucose. Everything else has shifted over to burning fat. By stage 5, the brain has mostly shifted to burning fat in the form of ketone bodies. Only a small amount of glucose is needed for red blood cells. You can see that the origin of the blood glucose gradually switches from exogenous (dietary) to gluconeogenesis made fr Continue reading >>

Diabetic, Alcoholic And Starvation Ketoacidosis

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 >>

Fasting Induces Ketoacidosis And Hypothermia In Pdhk2/pdhk4-double-knockout Mice

Fasting Induces Ketoacidosis And Hypothermia In Pdhk2/pdhk4-double-knockout Mice

Go to: Introduction The PDH complex (pyruvate dehydrogenase complex) plays a pivotal role in controlling the concentrations of glucose in the fed and fasted state [1]. In the well-fed state, the PDH complex is highly active, promoting glucose oxidation by generating acetyl-CoA, which can be oxidized by the citric acid cycle or used for fatty acid and cholesterol synthesis. In the fasted state, the PDH complex is inactivated by phosphorylation by PDHKs (pyruvate dehydrogenase kinases) to conserve three carbon compounds for the production of glucose [2]. The four PDHK isoenzymes responsible for phosphorylating the PDH complex are expressed in a tissue-specific manner [3–5]. Among the four, PDHK2 and PDHK4 are most abundantly expressed in the heart [5–7], skeletal muscle [5,8–10] and liver [5,11–14] of fasted mice. Of these two, PDHK2 is of interest because of its greater sensitivity to activation by acetyl-CoA and NADH and inhibition by pyruvate [15]. However, PDHK4 has received greater attention because its expression is increased in many tissues by fasting and diabetes [12] and transcription of its gene is regulated by insulin, glucocorticoids, thyroid hormone and fatty acids [16,17]. Inactivation of the PDH complex by phosphorylation helps to maintain euglycaemia during fasting, but contributes to hyperglycaemia in Type 2 diabetics. The increase in PDHK activity in diabetes raises the question of whether the PDHKs should be considered therapeutic targets for the treatment of diabetes [18]. Support for this possibility has been provided by the finding that mice lacking PDHK4 are euglycaemic in the fasted state and are more glucose tolerant than wild-type mice fed on a high-fat diet [19–21]. In the present study, PDHK2-KO (knockout) mice were produced to determ Continue reading >>

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

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 >>

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 >>

Ketosis Vs. Ketoacidosis: Understanding The Differences

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 >>

Incidence Of Diabetic Ketoacidosis During Ramadan Fasting In Benghazi, Libya

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 >>

Managing Diabetes During Ramadan Is All About Smart Management And Making Healthy Choices. Some Interesting Information To Note:

Managing Diabetes During Ramadan Is All About Smart Management And Making Healthy Choices. Some Interesting Information To Note:

If you are planning to fast and you have diabetes, it is important to speak to your diabetes healthcare team as early as possible before Ramadan begins. For some people with diabetes, fasting can be dangerous. Your diabetes team will be able to advise you on whether it is safe for you to fast. If you are able to fast, they will advise you on how to manage your condition throughout the fasting period. Possible Complications of Fasting during Ramadan Fasting among patients with type 1 diabetes, and among those with type 2 diabetes who have inadequately managed blood glucose levels, is associated with multiple risks. Some of the major potential diabetes-related complications of fasting include dangerously low blood glucose (hypoglycemia), excessively high blood glucose (hyperglycemia), diabetic ketoacidosis and thrombosis (blood clots). Hypoglycemia and Hyperglycemia Hypoglycemia is the fall of blood sugar under the normal levels (less than 70mg/dl – 3.9mmol/l). Hyperglycemia is the rise of blood sugar above normal levels (above 200 mg/dl – 11.1 mmol/l) which may lead to diabetic Ketoacidosis in type 1 diabetes patients. Diabetic Ketoacidosis When the body’s cells don’t get enough glucose, it starts to burn fat for energy. When the body burns fat instead of glucose it causes waste products called ketones. Ketones can make the blood acidic and this can be dangerous. The risk for diabetic ketoacidosis may be further increased due to excessive reduction of insulin – based on the assumption that food intake is reduced during the month. Patients with type 1 diabetes who choose to fast during Ramadan are at a higher risk of developing ketoacidosis, especially if they have been experiencing hyperglycemia frequently before Ramadan. Dehydration and Thrombosis Fasting duri Continue reading >>

In Defense Of Fasting: Common Misconceptions

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 >>

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