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Nutritional Ketoacidosis

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What Is Renal Failure: In this video, We will share information about what is renal failure - how to identify renal failure - symptoms of renal failure. Subscribe to our channel for more videos. Watch: (https://www.youtube.com/watch?v=ivQE7...) How to Identify Renal Failure Renal failure, also known as kidney failure, is a condition that can take two different forms: acute, when it presents itself very suddenly, and chronic, when it develops slowly over at least three months. Acute kidney failure has the potential to lead to chronic renal failure. During both types of renal failure your kidneys arent able to perform the necessary functions your body needs to stay healthy. Despite this similarity between types, the causes, symptoms, and treatments for the two kinds of renal failure vary significantly. Learning about the symptoms and causes of this disease and being able to differentiate between the two forms can be beneficial if you or a loved one have been diagnosed with renal failure. Thanks for watching what is renal failure - how to identify renal failure - symptoms of renal failure video and don't forget to like, comment and share. Related Searches: acute renal failure dr najeeb, acute renal failure explained clearly, acute renal failure kaplan, acute renal failure khan academy, acute renal failure lecture, acute renal failure management, acute renal failure medcram, acute renal failure nursing, acute renal failure treatment, acute renal failure usmle, chronic renal failure explained clearly, chronic renal failure khan academy, chronic renal failure lecture, chronic renal failure nursing, chronic renal failure treatment, chronic renal failure usmle, end stage renal failure, michael linares renal failure, pathophysiology of renal failure, renal failure, renal failure and abgs, renal failure and bone health, renal failure and dialysis, renal failure and electrolyte imbalances, renal failure and hyperkalemia, renal failure and hypocalcemia, renal failure and massage, renal failure and phosphorus, renal failure anemia, renal failure animation, renal failure bolin, renal failure calcium, renal failure care plan, renal failure case study presentation, renal failure cat, renal failure catheter, renal failure causes, renal failure causes hyperkalemia, renal failure chronic, renal failure concept map, renal failure cure, renal failure definition, renal failure diagnosis, renal failure diet, renal failure diet for humans, renal failure diet therapy, renal failure disease, renal failure dog, renal failure dr najeeb, renal failure due to ace inhibitor, renal failure electrolyte imbalance, renal failure examination, renal failure explained, renal failure fluid retention, renal failure for dummies, renal failure for nursing students, renal failure from ace inhibitor, renal failure funny, renal failure grinding, renal failure home remedy, renal failure homeopathic treatment, renal failure humans, renal failure hyperkalemia pathophysiology, renal failure icd 10, renal failure in cats, renal failure in children, renal failure in dogs, renal failure in hindi, renal failure in malayalam, renal failure in neonates, renal failure in sepsis, renal failure in the emergency department, renal failure in urdu, renal failure khan, renal failure khan academy, renal failure lab values, renal failure lecture, renal failure loss of appetite, renal failure made easy, renal failure malayalam, renal failure management, renal failure meaning in urdu, renal failure medcram, renal failure medications, renal failure metabolic acidosis, renal failure natural remedies, renal failure natural treatment, renal failure nclex, renal failure nclex questions, renal failure nucleus, renal failure nursing, renal failure nursing care plan, renal failure on dialysis, renal failure osce station, renal failure osmosis, renal failure pathology, renal failure pathophysiology, renal failure pathophysiology animation, renal failure patient, renal failure pbds, renal failure pharmacology, renal failure phases, renal failure physiology, renal failure prerenal intrarenal postrenal, renal failure pronunciation, renal failure quiz, renal failure registered nurse rn, renal failure shaking, renal failure skin itching, renal failure stage 3, renal failure stages, renal failure stories, renal failure support groups, renal failure swollen feet, renal failure symptoms, renal failure symptoms in cats, renal failure transplant, renal failure treatment, renal failure treatment in ayurveda, renal failure treatment in homeopathy, renal failure ultrasound, renal failure urine, renal failure usmle, renal failure vascular calcification, renal failure video, renal failure volume overload, renal failure vs ckd, renal failure youtube, renal kidney failure, stages of renal failure, symptoms of renal failure, types of renal failure, what is renal failure

I’ll See Your Ketoacidosis And Raise You A Renal Failure

A while back I posted on a paper that appeared in The Lancet about an obese woman who came to the emergency room with gastroenteritis and was misdiagnosed as being in diabetic ketoacidosis (a life-threatening disorder). She was misdiagnosed because the pinheads covering the ER couldn’t get past the fact that she had been on a low-carb diet. At the time I posted on this travesty I noted that this Lancet paper would from here on out be waved in the face of anyone who was following or advocated a low-carb diet as proof that such a diet is dangerous and can cause diabetic ketoacidosis (DKA). Well, now we’ve got an answer. Next time someone tells you that it has been proven that low-carb diets are dangerous and can cause ketoacidosis, you can resort to poker terminology and reply that you’ll see their ketoacidosis and raise them a renal failure. A few days ago I got wind of a paper published a few years ago that can be used as a counterpoint to the above mentioned idiotic paper in The Lancet that has given low-carbers such a bad time. This paper, published in the journal Renal Failure in 1998, is, like the other paper, a case report. The short version is as follows: An obese young Continue reading >>

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  1. Yai

    To start with, I apologise for my ignorance, however Forum members have been so helpful, I wish to ask another question please:
    I have read many threads saying how successful people have been in lowering their blood glucose and losing weight by drastically cutting their intake of carbohydrates. I believe that fewer than 30g of carbohydrates a day is classed as a ketogenic diet. As a type 2 diabetic of many years, I am worried to try lowering my carbohydrates so much in case I make myself ill. Can anyone offer any comfort please, or have I got my proverbials in a twist?

  2. BrianTheElder

    Yai said: ↑
    To start with, I apologise for my ignorance, however Forum members have been so helpful, I wish to ask another question please:
    I have read many threads saying how successful people have been in lowering their blood glucose and losing weight by drastically cutting their intake of carbohydrates. I believe that fewer than 30g of carbohydrates a day is classed as a ketogenic diet. As a type 2 diabetic of many years, I am worried to try lowering my carbohydrates so much in case I make myself ill. Can anyone offer any comfort please, or have I got my proverbials in a twist? Hi
    @Yai Ketosis is the state in which your body burns ketones instead of glucose for fuel.
    Normally carbs supply glucose and insulin is produced by your body when it detects glucose so that the glucose can cross cell membranes and enter the system. Unfortunately, excessive carbs can lead to excess insulin and your body becomes insulin resistant, which is the start of T2D. One of the functions of insulin is to store fat, so this is a direct side effect.
    An alternative, which was common in the diet in pre-modern times, was to eat more meat and fat (especially) rather than carbs. Without carbs your body produces ketones as fuel as a direct replacement for glucose, ie ketosis replaces glycolysis.
    Ketosis is a natural state and not to be confused with ketoacidosis, which is a serious condition in T1D when the ketones are an order of magnitude higher.
    Generally to achieve ketosis, you should eat less than 20g of carbs/day. You should also eat moderate protein, about 0.8g/kg of body weight. The rest of your diet is fat and you can eat what you like as fat is filling and you will reach satiety before you exceed any calorie limit.

  3. Resurgam

    As you are diabetic lowering your carbs should make you better - but it isn't a one size fits all level of carbs - I used to lose weight easily on 80 gm of carb a day and had to go up higher to stop it - on 20 gm a day I was in a state of collapse and could not walk up stairs, but crawled up on all fours.
    When diagnosed diabetic I went to low carbing to control it, but did not try to get down to what for me are low levels, just went back to normal for me eating - and that seems to have fixed things, though I will be adding in more exercise as the weather improves.

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Ketosis – What Is That All About?

What’s it all about? Is it good for you? Is it bad for you? What’s it like? How do I ‘do’ ketosis? How do I know I’m in ketosis? The questions everyone who’s Banting wants the answers to. Ketosis, in chef speak, is quite simply a state your body enters once it has been deprived of glucose. Your body switches to burning fat for energy (stored fat or fat that you have eaten) instead of glucose. A side-effect of that process is the release of ketone bodies into the blood stream. When you’re starved of glucose, your body has no choice but to burn fat for fuel, so it needs little explanation as to why ketosis works at melting fat like a blow heater on an ice sculpture. Ketosis comes with some added extras, namely a commonly noted sense of euphoria or lucidity and increased energy levels. A downside includes toothbrush-proof halitosis, which stems from the secretion of ammonia through the lungs as a side effect of burning all that fat. Some people on low-carb diets have reported kidney stones, gallstones and a number of other ailments. Scientific research on both sides of this debate is being done all the time, but in our experience from talking to the members of our commun Continue reading >>

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  1. Ash Simmonds

    This topic is actually much simpler than it's made out to be, that being it is merely a question of quantity of ketone production, and is only an issue in an individual who is unable to produce insulin.
    Unfortunately this is often glossed over even in medical texts, so it's not uncommon for even doctors and nurses to misunderstand the simple yet crucial difference, not to mention nutritionists.
    In the end it's all a matter of volume. Kind of like the difference between a sip, a gulp, and drowning.
    A moderate carbohydrate diet will often result in occasional trace amounts of ketone levels in the blood, typically after a fast (first thing in the morning) or after a decent exercise session. A very low carbohydrate diet is ketogenic by nature due to both low levels of carbohydrates in circulation/storage and ingestion of high levels of fat, and will result in moderate levels of ketone bodies circulating, usually around quarter-to-half the concentration of blood glucose, but occasionally reaching or even exceeding parity.
    Proper starvation - as in complete caloric avoidance for a week or two - can result in ketone bodies up to double or even triple circulating glucose levels, but even then the body has plenty of feedback loops to maintain ketone levels that are still well within safe parameters, you'll do organ damage from other stressors before ketones become a problem. There is of course something called alcoholic ketoacidosis, but this requires extensive periods of time where near 100% of your calories are derived from ethanol.
    Point being, this has nothing to do with nutritional ketosis. If you are capable of producing insulin then there is no danger of acidosis, which is actually ridiculously elevated ketones AND glucose levels.
    Serum ketone body levels typically look like this:
    Normal diet: 0-0.1 mmol/L
    Normal diet overnight fasted: 0.1-0.5 mmol/L
    Ketogenic Diet: 0.6-3.0 mmol/L
    1-4 weeks starvation: 6-10 mmol/L
    Diabetic insulin deficiency: >20 mmol/L

  2. Ketoacidosis

    http://caloriesproper.com/?p=4192
    Quote
    Ketoacidosis
    Nutritional ketosis is a normal, physiological response to carbohydrate and energy restriction. A ketogenic diet is an effective weight loss strategy for many. Ketoacidosis, on the other hand, is a pathological condition caused by insulin deficiency. The common theme is low insulin; however, in ketoacidosis, blood glucose levels are very high. Ketone levels are elevated in both states, although are 10-20x higher in ketoacidosis (~0.5-2 vs. > 20 mM). Nutritional ketosis and ketoacidosis should not be confused with one another, and a ketogenic diet doesn't cause ketoacidosis.
    ...
    In people on a ketogenic diet, blood glucose levels are not increased. This is an important aspect differentiating nutritional ketosis from ketoacidosis.
    ...
    Ketogenic dieting is safe, and can be beneficial. Ketoacidosis is pathological, and can be fatal.

  3. Ash Simmonds

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/
    Quote
    Metabolic Effects of the Very-Low-Carbohydrate Diets: Misunderstood "Villains" of Human Metabolism
    ...
    Diabetic Ketoacidosis vs. Dietary Ketosis
    Diabetic patients know that the detection in their urine of the ketone bodies is a danger signal that their diabetes is poorly controlled. Indeed, in severely uncontrolled diabetes, if the ketone bodies are produced in massive supranormal quantities, they are associated with ketoacidosis.
    ...
    However, during very low carbohydrate intake, the regulated and controlled production of ketone bodies causes a harmless physiological state known as dietary ketosis.

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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.....

Management Of Feline Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a complication of diabetes mellitus with concurrent and often severe metabolic derangements associated with hyperglycaemia, glucosuria, metabolic acidosis, ketonaemia +/- ketonuria. Patients with ketonaemia/ketosis are usually still bright, eating and maintaining their hydration. Those with ketoacidosis are dehydrated, clinically unwell (e.g., anorexia, vomiting, lethargy) and typically require hospitalisation and intensive management. DKA is distinguished from uncomplicated diabetes mellitus (DM) by a relative insulin lack and increased counter-regulatory hormones. The latter are thought to occur secondary to intercurrent disease. Concurrent disease has been documented in approximately 90% of cats with DKA, with the most common being hepatic lipidosis, chronic kidney disease, acute pancreatitis, bacterial or viral infections and neoplasia (Bruskiewicz et al. 1997). Heinz bodies, neutrophilia with a left shift, increased ALT and azotaemia is common. Most cats presenting with DKA are newly diagnosed diabetics or recently diagnosed but poorly controlled diabetics. Diagnosis Hyperglycaemia, Glucosuria, Metabolic Acidosis Plus Ketones in Plasma and/or Uri 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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  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?
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  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..
    Mels

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