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Starvation Ketoacidosis Medscape

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Constipation : How To Relieve Constipation Naturally - VitaLife Show Episode 129 How to Cure Constipation using yoga facial acupressure exercises and remedies, constipation can be debilitating and cause a lot of health problems in both children and adult alike which can lead to irritable bowel syndrome, intestinal blockage, bowel obstruction and colon pain, etc. Children's constipation can start from infancy and can be a serious problem for both the infant and very stressful to the new mom, some children are born constipated. What is constipation? Constipation can be described as obstruction by fecal matter in the bowel creating irregular bowel movement and incomplete bowel evacuation that can lead to intestinal blockage causing serious bowel problems, health complications, chronic constipation, colon pains and abdominal pain. Causes of constipation, Constipation can be cause by eating diet with low fiber such found in most fast food which is present in most American diets , insufficient fluid intake and poor dieting. Many medications can also lead to constipation, this side effect is a common culprit most medication found in most pain killers, antidepressants, anticonvulsants and

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Author: James L Webb, MD (Internal Medicine, SAUSHEC, USAF) and Brit Long, MD (@long_brit) // Edited by: Erica Simon, DO, MHA (@E_M_Simon) & Alex Koyfman, MD (@EMHighAK) A 20 year-old female presents to the ED after a witnessed fall. According to bystanders, the young woman was walking towards a gym treadmill when she collapsed to the floor below, convulsing for approximately1-2 minutes. Upon EMS arrival VS were within normal limits, GCS was noted as 14 (confusion, orientation only to self), EKG revealed NSR, and accucheck demonstrated a blood glucose of 134. Intravenous access was obtained en route to your facility. As you interview and examine the patient, you note ABCs intact, a GCS of 15, an ample history remarkable only for report of a rising feeling in the abdomen prior to the event, and a secondary survey without obvious signs of trauma. ED evaluation, to include a CBC, CMP, EKG, and non-contrasted head CT are all within normal limits. Urine Hcg is negative. Was this a seizure? Whats the appropriate patient disposition? If youve got questions, weve got important details on seizures and their mimics. Current data indicate that nearly 2 million U.S. residents are affected by Continue reading >>

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Popular Questions

  1. taponte

    How to know if you are in ketosis.

    Well i am sure there is another post like this, because i read it before, but i dont remeber exactly what it said and I cant find it.
    The quesiton is just as the title says, how can i know if i am in ketosis or not?
    I have been reading and the people says that at the second day, or thirth day or X day they get in to ketosis, but how they know that?
    Thanks

  2. jumpingjupiter

    If you have never been in Ketosis buy some keto sticks. You can pick them up at most drug stores in the US and Canada. Ask the pharmisist if you can't find them on the shelf. Usually they will be with diabetic supplies. Lots of people will say not to waist your money but they are cheap and I get an instant gratification when I see the test strip turn color. Besides, it is always nice to see evidence that your effort is paying off.
    -odd metalic taste in your mouth and bad breath.
    -Odd smelling urine is another symptom.
    -You will pee like a race horse.
    - I also get cotton mouth (dry mouth and really foamy saliva). Not sure if anyone else gets this.

  3. Andypandy999

    Normally i pee like a race horse for 2 days after my carb up which means im back in ketosis, Breath smells like crap, my wee smells like meat, and i find i get really de-hydrated...

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Why Ditch The Infant Cereals?

nutritional philosophy, tradition has weight. After all, weve survived anywhere from 7,000 to 77,000 generations on this planet (depending on whose science you believe). If we didnt know how to adequately nourish our children all that time, how did we even get here? And guess what? Traditional cultures didnt (and dont) feed their young babies infant cereal. Among the few cultures who fed their babies a gruel of grains, their practice radically differed from what we do today. First, they only introduced the gruel after the baby was more than a year old. And second, they ensured that the gruel was mildly fermented by soaking the grains for 24 hours or more. In order to digest grains, your body needs to make use of an enzyme called amylase. Amylase is the enzyme responsible for splitting starches. And, guess what? Babies dont make amylase in large enough quantities to digest grains until after they are a year old at the earliest. Sometimes it can take up to two years. You see, newborns dont produce amylase at all. Salivary amylase makes a small appearance at about 6 months old, but pancreatic amylase (what you need to actually digest grains) is not produced until molar teeth are full Continue reading >>

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Popular Questions

  1. visvavasu

    Observation: My Blood Glucose levels in nutritional ketosis are markedly higher than normal. Following a meal, glucose levels rise higher, and take longer to come back to their equilibrium levels (which are higher). I have observed this myself (I'm not a diabetic, and yet when in keto FBG ~100 mg/dl, post prandial ~130 mg/dl for 4-8 hours), and so have others [1]
    Theory: This is termed 'physiological insulin resistance' by some sources [1] [2] [3]. I'd be grateful here if the experts here can verify if my articulation below is accurate, and help me with my questions.
    The only sources of blood glucose are ingested carbs and in-vivo production by glycogenolysis or gluconeogenesis. In ketosis, there is a scarcity of carbs. The presence of insulin would cause blood glucose to be absorbed by the three insulin-dependent glucose sinks (muscle, fat and liver tissue) [Q1]. Therefore, in order to sustain blood glucose levels in ketosis [Q2], circulating insulin levels are forced to be lower [Q3] AND the three insulin-dependent glucose sinks become insulin resistant [Q4].
    By the net effect of lower insulin AND lower effectiveness of that insulin, catabolic events dominate. Glycogen is broken down in the liver and muscles, and glycogen synthesis is retarded. Muscle tissue switches to using fatty acids and ketones for energy. Lipids are broken down, causing lipid levels in the blood to rise (leading to higher HDL, LDL and triglyceride levels in keto blood tests). The usual blood-glucose level dependent signalling for appetite is disrupted, as likely are the leptin/ghrelin equilibria. All effects of ketosis (weight loss, different energy levels, etc.) follow.
    But what happens to blood glucose levels? With a diminished role of insulin, the only sink for glucose levels are neurons, which are the only cells that can use glucose without insulin. A new equilibrium is reached between the sources glucose production (only in-vivo glycogenolysis or gluconeogenesis) and glucose consumption by the neurons. This equilibrium is higher than the equilibrium levels enforced by insulin [FBG 100 mg/dl vs 80 mg/dl normally] [Q5]. However, since the body is itself the source of the glucose, there is no cause for worry [Q6]
    What happens if one eats a cheat meal with lots of carbs? The body is not immediately ready to handle the ingested carbs. The diminished role of insulin will cause glucose levels to spike and stay high. At some point [Q7], the body starts producing more insulin in response [Q8]. This takes much longer when keto-adapted than otherwise, which is why it may take 10-12 hours to bring blood glucose down after a cheat meal. As a direct consequence of higher insulin, much of the conditions in ketosis are reversed and one is 'kicked out of keto': glycogen synthesis instead of glycogenolysis, shut down ketone production and gluconeogenesis, etc.
    Corollary 1: When in ketosis, it makes little sense to test glucose response of foods. Cookies, quest bars, etc. must be tested only outside of ketosis
    Corollary 2: When fully adjusted to keto, a cheat meal will cause blood glucose levels to be elevated for a long duration. Muscles/fat don't want glucose in keto, and the brain which does now has a surplus. Therefore cheat meals cause a significant loss of appetite for 10-12 hours following. I have observed this in myself, anybody else?
    Questions for experts
    [Q1] Are these the only insulin-dependent glucose sinks?
    [Q2] Why should blood glucose levels be sustained if ketones are available for use? What mandates a minimum glucose level?
    [Q3] Is this true? Is post-prandial insulin release really lower in ketosis? Both first pass as well as pulsatory?
    [Q4] Is this true? If so, do all 3 become insulin resistant? By what mechanism?
    [Q5] Why is the new equilibrium higher?
    [Q6] Is this true?
    [Q7] At what point?
    [Q8] Are there also changes to the insulin resistance asked in Q4?
    Broader questions
    [BQ1] Diabetic ketoacidosis has the exact same mechanism of ketone production as ketosis. Cells cannot use glucose, and so the liver starts producing ketones. What makes the former uncontrolled and dangerous, and the latter controlled and benign?
    [BQ2] Insulin resistance must necessarily lead to weight loss, never weight gain. Diabetes cannot lead to obesity, in fact diabetes must necessarily lead to weight loss. Is this true?
    [BQ3] A person in ketosis loses fat by the same mechanism as a diabetic loses weight. Far from being the "opposite" of diabetes, ketosis employs the same mechanisms to produce the same results. What makes the former safe and the latter dangerous?
    References
    [1] http://high-fat-nutrition.blogspot.com/2007/10/physiological-insulin-resistance.html
    [2] Resources referred to in http://ketopia.com/physiological-insulin-resistance/
    [3] http://ketopia.com/high-blood-sugar-in-ketogenic-dieters-plus-a-special-surprise-hint-genotypes-and-metabolism/

  2. anbeav

    For the most part, yes

    Other tissues use glucose like red blood cells, glucose acts in the bloo as an important molecule to regulate osmotic pressure

    It depends, everyone is different with varying insulin sensitivity

    Not everyone shows elevated fasting glucose

    Glucose is spared for tissues that need it
    BQ1. Without insulin you can't control the process. Ketones themselves feedback to reduce ketone produciton (high ketones stimulate insulin secretion as well as lipolysis. Insulin facilitates glucose uptake in to cells, without that you become hyperglycemic which has an osmotic effect and causes other issues in addition to acidosis. Without insulin, and without cellular utilization of glucose, counterregulatory hormones are activated like glucagon which increases lipolysis as well as gluconeogenesis both of which further increase ketones as well as blood glucose.
    BQ2. Why? That's completely untrue. Have you seen diabetic people recently most are overweight
    BQ3. Ketoacidosis is unregulated ketone production, so much so that you become acidotic, there's a huge difference between that and regulated nutritional ketosis

  3. visvavasu

    Thanks for the prompt reply.
    BQ1 ... Ketones themselves feedback to reduce ketone produciton (high ketones stimulate insulin secretion as well as lipolysis. Insulin facilitates glucose uptake in to cells, without that you become hyperglycemic which has an osmotic effect and causes other issues in addition to acidosis. ...
    Do ketones reduce ketone production via insulin?
    In essence, the concern in ketoacidosis is not the ketones but the hyperglycemia? i.e. the hyperglycemia causes dehydration, increasing the acidity of the blood. But this does not answer why the liver continues runaway production of ketones in ketoacidosis, and not in ketosis. Please help.
    BQ2: Yes, this is the contradiction I'm trying to resolve. Per the theory, a diabetic person's muscles/fat cannot utilize blood glucose due to insulin resistance. How can lipogenesis occur when insulin is ineffective?
    Of course, the reverse is easily understood: obesity can cause diabetes by the increased adipose tissue becoming resistant to insulin. Once they're resistant though, I can't understand how they can continue to grow.
    BQ3: Agree, but by what mechanism is nutritional ketosis regulated?

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Popular Questions

  1. manohman

    Why can't fat be converted into Glucose?

    So the reason cited is that beta oxidation/metabolism of fats leads to formation of acetyl coa, a 2 carbon molecule, and that because of that it cannot be converted back into glucose.
    Why exactly is that the case?
    If Glucogenic amino acids can be converted into citric acid cycle intermediates and then turn back into glucose via gluconeogensis, then why cant Fatty Acids which yield Acetyl Coa. Can't you just have Acetyl Coa enter the citric acid cycle and produce the same intermediates that the glucogenic amino acids creat?

  2. Czarcasm

    manohman said: ↑
    So the reason cited is that beta oxidation/metabolism of fats leads to formation of acetyl coa, a 2 carbon molecule, and that because of that it cannot be converted back into glucose.
    Why exactly is that the case?
    If Glucogenic amino acids can be converted into citric acid cycle intermediates and then turn back into glucose via gluconeogensis, then why cant Fatty Acids which yield Acetyl Coa. Can't you just have Acetyl Coa enter the citric acid cycle and produce the same intermediates that the glucogenic amino acids creat?
    Click to expand... Both glucose and fatty acids can be stored in the body as either glycogen for glucose (stored mainly in the liver or skeletal cells) or for FA's, as triacylglycerides (stored in adipose cells). We cannot store excess protein. It's either used to make other proteins, or flushed out of the body if in excess; that's generally the case but we try to make use of some of that energy instead of throwing it all away.
    When a person is deprived of nutrition for a period of time and glycogen stores are depleted, the body will immediately seek out alternative energy sources. Fats (stored for use) are the first priority over protein (which requires the breakdown of tissues such as muscle). We can mobilize these FA's to the liver and convert them to Acetyl-CoA to be used in the TCA cycle and generate much needed energy. On the contrary, when a person eats in excess (a fatty meal high in protein), it's more efficient to store fatty acids as TAG's over glycogen simply because glycogen is extremely hydrophilic and attracts excess water weight; fatty acids are largely stored anhydrously and so you essentially get more bang for your buck. This is evolutionary significant and why birds are able to stay light weight but fly for periods at a time, or why bears are able to hibernate for months at a time. Proteins on the other hand may be used anabolically to build up active tissues (such as when your working out those muscles), unless you live a sedentary lifestyle (less anabolism and therefore, less use of the proteins). As part of the excretion process, protein must be broken down to urea to avoid toxic ammonia and in doing so, the Liver can extract some of that usable energy for storage as glycogen.
    Also, it is worth noting that it is indeed possible to convert FA's to glucose but the pathway can be a little complex and so in terms of energy storage, is not very efficient. The process involves converting Acetyl-CoA to Acetone (transported out of mitochondria to cytosol) where it's converted to Pyruvate which can then be used in the Gluconeogenesis pathway to make Glucose and eventually stored as Glycogen. Have a look for yourself if your interested: http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1002116.g003/originalimage (and this excludes the whole glycogenesis pathway, which hasn't even begun yet).
    TLDR: it's because proteins have no ability to be stored in the body, but we can convert them to glycogen for storage during the breakdown process for excretion. Also, in terms of energy, it's a more efficient process than converting FA's to glycogen for storage.

  3. soccerman93

    This is where biochem comes in handy. Czarcasm gives a really good in depth answer, but a simpler approach is to count carbons. The first step of gluconeogenesis(formation of glucose) requires pyruvate, a 3 carbon molecule. Acetyl Co-A is a 2 carbon molecule, and most animals lack the enzymes (malate synthase and isocitrate lyase) required to convert acetyl co-A into a 3 carbon molecule suitable for the gluconeogenesis pathway. The ketogenic pathway is not efficient, as czarcasm pointed out. While acetyl co-A can indeed be used to form citric acid intermediates, these intermediates will be used in forming ATP, not glucose. Fatty acid oxidation does not yield suitable amounts of pyruvate, which is required for gluconeogenesis. This is part of why losing weight is fairly difficult for those that are overweight, we can't efficiently directly convert fat to glucose, which we need a fairly constant supply of. Sorry, that got a little long-winded

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