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Euglycemic Ketoacidosis Causes

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Susan Cornell, PharmD, CDE, FAPhA, FAADE, describes the risks for ketoacidosis and serious urinary tract infection associated with use of SGLT2 inhibitors. This video was recorded at APhA's 2016 Annual Meeting and Exposition in Baltimore, Maryland.

Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, And Preventable Safety Concern With Sglt2 Inhibitors

The Case At Hand Recently, the U.S. Food and Drug Administration (FDA) issued a Drug Safety Communication that warns of an increased risk of diabetic ketoacidosis (DKA) with uncharacteristically mild to moderate glucose elevations (euglycemic DKA [euDKA]) associated with the use of all the approved sodium–glucose cotransporter 2 (SGLT2) inhibitors (1). This Communication was based on 20 clinical cases requiring hospitalization captured between March 2013 and June 2014 in the FDA Adverse Event Reporting System database. The scarce clinical data provided suggested that most of the DKA cases were reported in patients with type 2 diabetes (T2D), for whom this class of agents is indicated; most likely, however, they were insulin-treated patients, some with type 1 diabetes (T1D). The FDA also identified potential triggering factors such as intercurrent illness, reduced food and fluid intake, reduced insulin doses, and history of alcohol intake. The following month, at the request of the European Commission, the European Medicines Agency (EMA) announced on 12 June 2015 that the Pharmacovigilance Risk Assessment Committee has started a review of all of the three approved SGLT2 inhibitors Continue reading >>

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  1. BobbyW

    Keto Sticks - Walgreens USA

    For those that want a good bargain and feel that you need them, todays Sunday (11-Jan-2004) Walgreens flyer has "Thinz Metabo Stix" 25 count for $9.99usd "Sale Priced"
    Walgreens Find a Store Near You link
    -BobbyW

  2. LeddySS98

    not too rain on your parade or anything, but I got mine from Rite Aid 100 sticks for $15

  3. reuabledats

    What kind did you get at Rite Aide, Bayer?

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What is DIABETIC KETOACIDOSIS? What does DIABETIC KETOACIDOSIS mean? DIABETIC KETOACIDOSIS meaning - DIABETIC KETOACIDOSIS definition - DIABETIC KETOACIDOSIS explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6Uu... Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes. DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine. The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. About 4% of people with type 1 diabetes in United Kingdom develop DKA a year, while in Malaysia the condition affects about 25% a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost universally fatal. The risk of death with adequate and timely treatment is currently around 1–4%. Up to 1% of children with DKA develop a complication known as cerebral edema. The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels). In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as "Kussmaul respiration"). The abdomen may be tender to the point that an acute abdomen may be suspected, such as acute pancreatitis, appendicitis or gastrointestinal perforation. Coffee ground vomiting (vomiting of altered blood) occurs in a minority of people; this tends to originate from erosion of the esophagus. In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness). On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, tachycardia (a fast heart rate) and low blood pressure may be observed. Often, a "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. If Kussmaul respiration is present, this is reflected in an increased respiratory rate.....

Euglycemic Diabetic Ketoacidosis, A Misleading Presentation Of Diabetic Ketoacidosis

Go to: Introduction Hyperglycemia and ketosis in diabetic ketoacidosis (DKA) are the result of insulin deficiency and an increase in the counterregulatory hormones glucagon, catecholamines, cortisol, and growth hormone. Three processes are mainly responsible for hyperglycemia: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues. This might also be augmented by transient insulin resistance due to hormone imbalance, as well as elevated free fatty acids.[1] DKA is most commonly precipitated by infections. Other factors include discontinuation of or inadequate insulin therapy, pancreatitis, myocardial infarction, cerebrovascular accident, and illicit drug use. The diagnostic criteria of DKA, established by the American Diabetic Association, consists of a plasma glucose of >250 mg/dL, positive urinary or serum ketones, arterial pH of <7.3, serum bicarbonate <18 mEq/L, and a high anion gap. The key diagnostic feature of DKA is elevated circulating total blood ketone concentration. Hyperglycemia is also a key diagnostic criterion of DKA; however, a wide range of plasma glucose levels can be present on admission. Continue reading >>

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  1. RawNut

    Humans are unique in their remarkable ability to enter ketosis. They’re also situated near the top of the food chain. Coincidence?
    During starvation, humans rapidly enter ketosis; they do this better than king penguins, and bears don’t do it at all.
    Starvation ketosis
    Humans maintain a high level of functionality during starvation. We can still hunt & plan; some would even argue it’s a more finely tuned state, cognitively. And that’s important, because if we became progressively weaker and slower, chances of acquiring food would rapidly decline.
    Perhaps this is why fasting bears just sleep most of the time: no ketones = no bueno..?
    Observation: chronic ketosis is relatively rare in nature. Angelo Coppola interpreted that to mean animals may have evolved a protective mechanism against ketosis (if you were following along, please let me know if this is a misrepresentation).
    But I think that is misguided. Animals with a low brain/carcass weight ratio (ie, small brain) don’t need it. Babies and children have a higher brain/carcass weight ratio, so they develop ketosis more rapidly than adults. Is this a harmful process? No! It’s an evolutionary adaptation which supports the brain.
    The brain of newborn babies consumes a huge amount of total daily energy, and nearly half comes from ketones. A week or so later, even after the carbohydrate content of breast milk increases, they still don’t get “kicked out of ketosis” (Bourneres et al., 1986). If this were a harmful state, why would Nature have done this? …and all those anecdotes, like babies learn at incredibly rapid rates… coincidence? Maybe they’re myths. Maybe not.
    Ketosis in the animal kingdom
    Imagine a hibernating bear: huge adipose tissue but small brain fuel requirement relative to body size and total energy expenditure. No ketosis, because brain accounts for less than 5% of total metabolism. In adult humans, this is around 19-23%, and babies are much higher (eg, Cahill and Veech, 2003 & Hayes et al., 2012).
    A possible exception to this is ruminant ketosis, but that’s for a different reason. They become ketotic because: 1) their gut turns much of what they eat into a ketogenic diet; and 2) this frequently happens during lactation, which combines very high energy expenditure and an enhanced draw on the oxaloacetate pool to make lactose.
    Whales? Nope. Despite eating for like, 1 month out of the year, they don’t develop ketosis.
    Snakes will enter ketosis, not due to high brain needs per se, but likely because even though small brain, total energy expenditure is so low that brain metabolism easily surpasses the [theoretical] 5% threshold (McCue 2006):
    Fasting baby elephant seals get ketotic, because their babies (Castellini and Costa, 1990):
    Hypercarnivores (eg, cats) don’t develop ketosis on very low carb diets, like humans would, which seems to be due to their inability to down regulate protein catabolism (urea cycle takes care of the nitrogen; gluconeogenesis the carbon)… but they will do so readily during starvation because of relatively big brains (Blanchard et al., 2002):
    Similar to cats, dolphins are carnivorous and also exhibit what appears to be a pathological inability to reduce protein catabolism when necessary. However, unlike cats, dolphins fail to develop ketosis of any sort, whether it’s on their typical low carb diet of fatty fish, or even complete starvation!
    Dolphins are the exception to a lot of rules. I don’t know why. Most animals with big brains have the ability to enter ketosis, but none do it as well as humans.
    Historically, while intermittent or cyclical ketosis was likely more common than nutritional [chronic] ketosis in humans, this doesn’t mean one form is better than another. Common =/= optimal.
    Starvation ketosis isn’t nutritional ketosis, but much of what we know about the latter stems from our understanding of the former… this is getting better, with more and more studies of longer and longer durations being published regularly. And hint: chronic ketosis doesn’t dissolve bones, deteriorate cognitive function, or break your metabolism.
    Are ketones the brain’s preferred fuel?
    Well, let’s just say this: when there are more ketones than glucose, brain uses more ketones than glucose. This happens in both starvation and nutritional ketosis.
    Ketosis proportionately spares glucose utilization in the brain (Zhang et al., 2013)
    If ketones were harmful, Nature would’ve surely devised a way to protect the brain!
    Disclosure: I’m not keto, not even very low carb in the summer really, so this obviously isn’t some sort of confirmation bias or logic fail or whatever you call it. I don’t practice what I preach. Sue me.
    Most of the time, I advocate a plant-based low-carb Paleo-like diet for health; keto if obese insulin resistant. High[ish] protein for all (ymmv). Seasonal when possible.
    Impact of ketones on cognition
    Would our ability to plan and set traps to acquire food, or quickly devise a strategy to escape predation have been negatively impacted during periods of intermittent or cyclical ketosis? I think not; more likely the opposite. And while I [still] believe the physical feats required to do these is not hindered after ketoadaptation, I also [still] believe it’s because we *out-smarted* them, not out-ran them. Compared to many other species, humans suck at speed.
    Some evidence:
    1. acute: in patients with moderate cognitive impairment or Alzheimer’s disease, given 40 mL MCTs to bolster ketoneshttp://ir-na.amazon-adsystem.com/e/...=1&a=B0019LRY8A: cognitive performance improved roughly in parallel with increasing ketones (Reger et al., 2004).
    2. chronic: 20 grams of Axona (purified MCTs) daily for 90 days improved cognition in people with age-associated memory impairment (Constantini et al., 2008).
    3. cruel and unusual: expose a group of type 1 diabetic patients to experimental hypoglycemia and give half 40 grams of coconut oilhttp://ir-na.amazon-adsystem.com/e/...=1&a=B003OGKCDC (which is like a longer-chained version of MCTs) (Page et al., 2009). Result? Hypoglycemia impairs cognition; however, this is largely offset by increasing ketones with coconut oil. This group experienced improved: 1) verbal memory; 2) delayed verbal memory; and 3) verbal memory recognition.
    4. nutritional ketosis: 6 weeks of a bona fide ketogenic diet in patients with mild cognitive impairment = improved verbal memory performance, and this positively correlated with ketones (Krikorian et al., 2012).
    Optimal, harmful, or somewhere in between? You decide (but if you choose harmful, please provide a link! or at least explain why, very clearly…)
    Hint: nutritional ketosis isn’t harmful. FOR. FIVE. YEARS… 1) that’s not cyclical or intermittent ketosis; and 2) five years is probably much longer than the diet you’re following has been tested for “safety.”
    Ketones in evolution
    Without our ability to rapidly enter a robust state of ketosis, we wouldn’t be here, or we’d be some weaker subhuman species. But ketones have been around for a while… some bacteria store energy in the form of poly-beta-hydroxybutyrate. Some prokaryotes use ketones instead of triacylglycerols. Archaea also use ketones; and they’ve been around for billions of years… it’s estimated that we’ve been doing it for quite a long time, too (from evidence on when our brain would’ve surpassed the [theoretical] threshold). I’d cite a study by George Cahill here, and maybe you’d read it. But you should really read all of the studies by George Cahill (it’s not a-whole-lot). Sorry, I know that sounds ‘preachy.’
    Would ketosis have hindered our ability to hunt prey and avoid predation? My thoughts on our ability to perform high intensity physical activity after ketoadaptation have been thoroughly expressed in the past. And ketosis clearly doesn’t hinder cognitive functioning.
    So, from both a mental and physical perspective, ketosis, chronic or otherwise, did not stop us from becoming who we are. Indeed, it probably contributed to how we did so. Well, that and seafood.
    http://caloriesproper.com/?p=5078

  2. keith v

    Wow thanks Rawnut, that was very interesting.
    It especially makes mouse studies suspect due to the mouses small brain

  3. teaser

    An aspect to this that I find interesting is the idea that ketones spare fat. An animal like an elephant seal with its relatively smaller brain and larger fat mass can afford to fuel its glucose cycle from glycerol almost exclusively. If we wanted to do the same trick, and needed 100-125 grams of glucose a day to fuel our brains--at around ten percent of triglyceride calories as glycerol, we'd have to burn through 4000-5000 calories of fat a day during complete starvation, obviously not a good strategy for a person with what used to be "normal" fat stores.

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Euglycemic Diabetic Ketoacidosis Sometimes Seen With Sglt2 Inhibitors

Euglycemic Diabetic Ketoacidosis Sometimes Seen with SGLT2 Inhibitors Diabetic ketoacidosis (DKA) in patients with presenting serum blood glucose <200 mg/dL isnt common. More often, its seen in patients with type 1 diabetes in conjunction with starvation and acute illness.1 Its difficult to determine an incidence of euglycemic DKA (euDKA) among all DKA cases in the literature, given the migration of the serum glucose cutoff from 300 mg/dL to 200 mg/dL. The best estimation based on an analysis of case reports suggests an incidence anywhere between 0.8% and 7.5%.1 However, the sodium-glucose cotransporter-2 (SGLT2) inhibitors canagliflozin, dapagliflozin, and empagliflozin can apparently induce this once-rare form of DKA.2,3 SGLT2 inhibitors are a class of oral hypoglycemic drugs indicated only for type 2 diabetes. Their novel mechanism of action prevents glucose reabsorption from the proximal renal tubules, resulting in increased glucosuria and decreasing plasma glucose. SGLT2 inhibitors lower serum glucose and HBA1C levels, and even produce weight loss. However, the increased glucose concentration in the bladder is a terrific incubation environment for fungi and bacteria, so much Continue reading >>

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  1. Import

    Is Ketosis really worth it?

    I'm doing a dedicated, strict cutting phase for summer (aren't we all?) and I'm using Fat Fast foods on a CKD schedule like Lyle M's book outlines. Since a calorie is a calorie, will I somehow actually lose more fat, or spare muscle better, by eating at a 500-700 calorie deficit during ketosis, VERSUS eating the same 500-700 deficit on a diet that still includes healthy veggies, juices, etc. without ketosis? In other words, all other things being equal--high protein, EFAs, responsible training--will the presence or absence of ketosis provide a benefit I won't otherwise have, if I were to eat at the same deficit anyway without going ketogenic?

  2. Bodybuilding

    Trying to Remember the Name of a 1980’s Bodybuilder

  3. Bodybuilding

    10 Weeks Out. Need Help Losing Weight

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