Risk Of Diabetic Ketoacidosis After Initiation Of An Sglt2 Inhibitor

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Risk of Diabetic Ketoacidosis after Initiation of an SGLT2 Inhibitor Inhibitors of sodiumglucose cotransporter 2 (SGLT2) decrease plasma glucose by blocking the reabsorption of glucose at the proximal tubule.1,2 Case reports have suggested that SGLT2 inhibitors may be associated with an increased risk of diabetic ketoacidosis, which led to a warning from the Food and Drug Administration (FDA) in May 2015.3,4 The objective of our study was to assess the risk of diabetic ketoacidosis after the initiation of an SGLT2 inhibitor. https://www.youtube.com/channel/UCsqm...

Sodium-glucose Cotransporter-2 Inhibitors | Sglt2 Inhibitor Initiation Linked To Raised Diabetic Ketoacidosis Risk | Diabetes.medicinematters.com

SGLT2 inhibitor initiation linked to raised diabetic ketoacidosis risk medwireNews: Research findings indicate that patients with type 2 diabetes may have an increased risk for diabetic ketoacidosis when they begin treatment with a sodiumglucose cotransporter 2 (SGLT2) inhibitor. The risk was increased around twofold during the first 180days after initiating an SGLT2 inhibitor, relative to the same period after starting treatment with a dipeptidyl peptidase (DPP)-4 inhibitor. The absolute risk was very low, however, with just 55 of 38,045 patients in the SGLT2 inhibitor group experiencing this outcome. These patients were matched for the propensity to receive an SGLT2 inhibitor with 38,045 patients given a DPP-4 inhibitor, 26 of whom had diabetic ketoacidosis during the first 180days after they started treatment. The increased risk in the SGLT2 inhibitor group persisted when the analysis was restricted to patients not taking insulin. In a press statement, lead researcher Michael Fralick (Brigham and Womens Hospital, Boston, Massachusetts, USA) observed that diabetic ketoacidosis is usually associated with type 1 diabetes, rather than type 2, so doctors are not on the lookout for i Continue reading >>

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  1. Unregistered

    I know this fits into the "low carb fixes everything!!!" camp, but its true: ever since I went completely primal, without cheats, I rarely, if ever, have colds.
    Same here. I was just thinking last weekend when I went past the drug section of the grocery store that I don't go in that section to buy meds anymore. I can't think of anything in there that I needed since 2008.
    Things I had a lot of and dont even keep any more- aspirin or ibuprofen, nose spray, anti-biotic skin cream, toothache pain killer, eye drops, cough syrup, and cold meds. It's all gone.
    Hay fever goes around Memphis in March and it got everyone at work. It got me too for a couple of weeks, but I didn't use any meds except for a supplement I use that boosts immunity, plus a lot of vitamin D.

  2. Unregistered

    Good article.
    Here's another-
    I've been taking 10,000IU since 2007. Blood tests show its in range long term if I take that much. I'm also using a miatake mushroom SX fraction supplement that helps immunity-
    My collegue was really feeling the hay fever and I talked him into using my spare bottle of D3, 5,000 IU each.

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http://whataresideeffects.com/metopro... A review of metoprolol side effects, lisinopril side effects, and side effects of beta blockers to lower blood pressure. I hope you enjoy it and find it helpful.

Sglt2 Inhibitors Side Effects

Sodium-glucose cotransporter-2 (SGLT2) inhibitors are intended to treat Type 2 diabetes along with diet and exercise. They have also been prescribed for off-label, or unapproved, uses including weight loss. The active ingredients in the drugs are different gliflozin compounds. SGLT2 inhibitors approved for use in the U.S. include: In addition, some medications combine SGLT2 inhibitors with other diabetes drugs. These include: Metformin decreases glucose production in the liver while increasing the body’s ability to absorb glucose. It is often used in conjunction with insulin as well as SGLT2 inhibitors to treat Type 2 diabetes. It carries additional risks of side effects. Linagliptin works by regulating insulin levels after meals. When first approved, SGLT2 inhibitors took a revolutionary approach to controlling blood sugar in diabetic patients. The drugs cause the body to direct excess glucose to the kidneys. From there, it is expelled through a patient’s urine. SGLT2 Inhibitor Side Effects Range from Minor to Life-Threatening While the way SGLT2 drugs work is unique, this can also lead to unique side effects. For example, because the drugs cause excess sugar to escape the bod Continue reading >>

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  1. ashmashh

    I was curious how many people practice IF with keto. I started both at the beginning of June. I practice a 20:4 IF schedule and usually eat one meal and maybe a small snack before or after. My eating window is from 7pm-11pm so my SO and I can eat dinner together when he gets home from work around 8pm-9pm. I'm starting to wonder if IF is worth practicing anymore. I'm pretty adapted to this way of eating and don't usually get hungry until around 5pm-6pm, occasionally earlier. I also find it easier to hit my macros this way compared to trying to spread them out throughout the day. The health benefits seem worth it, I'm just not sure if I want to do IF anymore. Any and all feedback is appreciated.

  2. atxtraveler

    I went from 16:8 to 20:4 to OMAD pretty quickly. I like it, because I practice what my skinny 7 year old learned on his own... he just eats when he is hungry. Turns out I am only actually hungry once a day.
    Having said that, what has really worked for me is 20:4 or OMAD per day depending on whether I am working out, and then on weekends 16:8 if there are events I need to either be social at or avoid by eating before or after. Kids birthday parties at say 11am are killers for me because I am "just hungry enough" to make a bad decision, so I make a pound of bacon that morning before I go.

  3. skepticallypessimist

    I do this on days I work now, saves money, I only eat before and maybe after my big lifts. Helped me get past a plateau

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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.

Sglt2 Inhibitors And The Risk Of Diabetic Ketoacidosis| Dailyrounds

SGLT2 Inhibitors and the Risk of Diabetic Ketoacidosis SGLT2 Inhibitors and the Risk of Diabetic Ketoacidosis SGLT2 inhibitors decrease plasma glucose by blocking the reabsorption of glucose at the proximal tubule. Case reports have suggested that SGLT2 inhibitors may be associated with an increased risk of diabetic ketoacidosis, which led to a warning from the FDA in May 2015. The results of the largest study conducted to date to investigate the issue were published as a research letter in the June 8 issue of the New England Journal of Medicine. 1. The overall absolute risk is low. However, the risk of developing DKA among type 2 diabetes patients initiating a SGLT2 inhibitor is about double that seen among patients starting a dipeptidyl peptidase-4 (DPP-4) inhibitor. 2. An estimated 5 to 8 patients per 1000 initiating SGLT2 inhibitors will develop DKA. 3. Patients should be strictly monitored for signs of DKA after starting on SGLT2 inhibitors. Using a large claims database of commercially insured patients in the United States (Truven MarketScan), authors identified a cohort of adult patients (18 years of age) who had newly started treatment with either an SGLT2 inhibitor or a d Continue reading >>

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  1. uktay001

    Hi everyone i just found this interesting article about the difference between diabetic ketoacidosis with nutritional ketosis.
    Hope this helps someone or gives them an understanding how different they are.
    Is ketosis dangerous?

    You may have heard from your doctor that ketosis is a life-threatening condition. If so, your doctor is confusing diabetic ketoacidosis (DKA) with nutritional ketosis, or keto-adaptation. First, some semantics. Our body can produce, from fat and some amino acids, three ketone bodies (a “ketone” refers the chemical structure where oxygen is double-bonded to carbon sandwiched between at least 2 other carbons). These ketone bodies we produce are: acetone, acetoacetone, and beta-hydroxybutyrate (B-OHB). [For anyone who is interested, they are the 3 most right structures on the figure, below.]
    Why do we make ketones? For starters, it’s a vital evolutionary advantage. Our brain can only function with glucose and ketones. Since we can’t store more than about 24 hours worth of glucose, we would all die of hypoglycemia if ever forced to fast for more than 24 hours. Fortunately, our liver can take fat and select amino acids (the building blocks of proteins) and turn them into ketones, first and foremost to feed our brains. Hence, our body’s ability to produce ketones is required for basic survival.
    What is diabetic ketoacidosis? When a diabetic (usually a Type I diabetic, but sometimes this occurs in very late-stage, insulin-dependent, Type II diabetics) fails to receive enough insulin, they go into an effective state of starvation. While they may have all the glucose in the world in their bloodstream, without insulin, they can’t get any into their cells. Hence, they are effectively going into starvation. The body does what it would do in anyone – it starts to make ketones out of fat and proteins. Here’s the problem: the diabetic patient in this case can’t produce any insulin, so there is no feedback loop and they continue to produce more and more ketones without stopping. By the time ketone levels (specifically, beta-hydroxybutyrate) approach 15 to 25 mM, the resulting pH imbalance leads to profound metabolic derangement and the patient is critically ill.
    But this state of metabolic derangement is not actually possible in a person who can produce insulin, even in small amounts. The reason is that a feedback loop prevents the ketone level from getting high enough to cause the change in pH that leads to the cascade of bad problems. A person who is said to be “keto-adapted,” or in a state of nutritional ketosis, generally has beta-hydroxybutyrate levels between about 0.5 and 3.0 mM. This is far less than the levels required to cause harm through acid-base abnormalities.
    Keto-adaption is a state, achieved through significant reduction of carbohydrate intake (typically to less than 50 grams per day), where the body changes from relying on glycogen as its main source of energy to relying on fat. Specifically, the brain shifts from being primarily dependent on glucose, to being primarily dependent on beta-hydroxybutyrate. This has nothing to do with what a diabetic patient is experiencing in DKA, but does illustrate how poorly informed and quick to react the medical community is. DKA and nutritional ketosis (or keto-adaptation) have as much in common as a house fire and a fireplace.

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    The Question isn't CAN YOU? It's WILL YOU?
    Back again after a break took up running and kept at the same weight now going for 1 more stone.​

  2. uktay001

    Metabolism and ketosis
    The primary goal of our metabolic system is to provide fuels in the amounts needed at the times needed to keep us alive and functioning. As long as we’ve got plenty of food, the metabolic systems busies itself with allocating it to the right places and storing what’s left over. In a society such as ours, there is usually too much food so the metabolic system has to deal with it in amounts and configurations that it wasn’t really designed to handle, leading to all kinds of problems. But that’s a story for another day.
    If you read any medical school biochemistry textbook, you’ll find a section devoted to what happens metabolically during starvation. If you read these sections with a knowing eye, you’ll realize that everything discussed as happening during starvation happens during carbohydrate restriction as well. There have been a few papers published recently showing the same thing: the metabolism of carb restriction = the metabolism of starvation. I would maintain, however, based on my study of the Paleolithic diet, that starvation and carb restriction are simply the polar ends of a continuum, and that carb restriction was the norm for most of our existence as upright walking beings on this planet, making the metabolism of what biochemistry textbook authors call starvation the ‘normal’ metabolism.
    So, bearing in mind that carb restriction and starvation are opposite ends of the same stick and that what applies to one applies to the other, let’s look at how it all works. I’ll explain it from a starvation perspective, but all the mechanisms work the same for a carb-restricted diet.
    During starvation the primary goal of the metabolic system is to provide enough glucose to the brain and other tissues (the red blood cells, certain kidney cells, and others) that absolutely require glucose to function. Which makes sense if you think about it. You’re a Paleolithic man or woman, you’re starving, you’ve got to find food, you need a brain, red blood cells, etc. to do it. You’ve got to be alert, quick on your feet, and not focused on how hungry you are.
    If you’re not eating or if you’re on a low-carbohydrate diet, where does this glucose come from?
    If you’re starving, glucose comes mainly from one place, and that is from the body’s protein reservoir: muscle. A little can come from stored fat, but not from the fatty acids themselves. Although glucose can be converted to fat, the reaction can’t go the other way. Fat is stored as a triglyceride, which is three fatty acids hooked on to a glycerol molecule. The glycerol molecule is a three-carbon structure that, when freed from the attached fatty acids, can combine with another glycerol molecule to make glucose. Thus a starving person can get a little glucose from the fat that is released from the fat cells, but not nearly enough. The lion’s share has to come from muscle that breaks down into amino acids, several of which can be converted by the liver into glucose. (There are a few other minor sources of glucose conversion: the Cori cycle, for example, but these are not major sources, so we’ll leave them for another, more technical, discussion.)
    But the breakdown of muscle creates another problem, namely, that (in Paleolithic times and before) survival was dependent upon our being able to hunt down other animals and/or forage for plant foods. It makes it tough to do this if a lot of muscle is being converted into glucose and your muscle mass is dwindling.
    The metabolic system is then presented with two problems: 1) getting glucose for the glucose-dependent tissues; and 2) maintaining as much muscle mass as possible to allow hunting and foraging to continue.
    Early on, the metabolic system doesn’t know that the starvation is going to go on for a day or for a week or two weeks. At first it plunders the muscle to get its sugar. And remember from a past post that a normal blood sugar represents only about a teaspoon of sugar dissolved in the entire blood volume, so keeping the blood sugar normal for a day or so doesn’t require a whole lot of muscular sacrifice. If we figure that an average person requires about 200 grams of sugar per day to meet all the needs of the glucose-dependent tissues, we’re looking at maybe a third of a pound of muscle per day, which isn’t all that big a deal over the first day. But we wouldn’t want it to continue at that rate. If we could reduce that amount and allow our muscle mass to last as long as possible, it would be a big help.
    The metabolic system could solve its problem by a coming up with a way to reduce the glucose-dependent tissues’ need for glucose so that the protein could be spared as long as possible.
    Ketones to the rescue.
    The liver requires energy to convert the protein to glucose. The energy comes from fat. As the liver breaks down the fat to release its energy to power gluconeogenesis, the conversion of protein to sugar, it produces ketones as a byproduct. And what a byproduct they are. Ketones are basically water soluble (meaning they dissolve in blood) fats that are a source of energy for many tissues including the muscles, brain and heart. In fact, ketones act as a stand in for sugar in the brain. Although ketones can’t totally replace all the sugar required by the brain, they can replace a pretty good chunk of it. By reducing the body’s need for sugar, less protein is required, allowing the muscle mass (the protein reservoir) to last a lot longer before it is depleted. And ketones are the preferred fuel for the heart, making that organ operate at about 28 percent greater efficiency.
    Fat is the perfect fuel. Part of it provides energy to the liver so that the liver can convert protein to glucose. The unusable part of the fat then converts to ketones, which reduce the need for glucose and spare the muscle in the process.
    If, instead of starving, you’re following a low-carb diet, it gets even better. The protein you eat is converted to glucose instead of the protein in your muscles. If you keep the carbs low enough so that the liver still has to make some sugar, then you will be in fat-burning mode while maintaining your muscle mass, the best of all worlds. How low is low enough? Well, when the ketosis process is humming along nicely and the brain and other tissues have converted to ketones for fuel, the requirement for glucose drops to about 120-130 gm per day. If you keep your carbs below that at, say, 60 grams per day, you’re liver will have to produce at least 60-70 grams of glucose to make up the deficit, so you will generate ketones that entire time.
    So, on a low-carb diet you can feast and starve all at the same time. Is it any wonder it’s so effective for weight loss?

    The Question isn't CAN YOU? It's WILL YOU?
    Back again after a break took up running and kept at the same weight now going for 1 more stone.​

  3. mels72

    Wow thanks for those... It is useful to understand the mechanics and useful to be able to answer all the do gooders who tut at me and claim i am not doing my body any good oh and it is a lazy way of losing weight.... Lolz. Little do they know..

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