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Exercise and Blood Sugar spike?

Discussion in 'Ketogenic diet forum' started by Debra67, May 8, 2019.

  1. Debra67

    Debra67 · Newbie

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    I have been on keto for the past 6 months my blood sugar as dropped and I average 5.4 but if I exercise and take it, it jumps high 7.1 _ 9. Is this normal?
     
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  2. Debra67

    Debra67 · Newbie

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    Thank you
     
  3. KenMacK

    KenMacK MODY · Member

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    For a diabetic this is normal or typical. A diabetic is insulin-deficient (including type-2), and hence the secondary hormones (e.g. adrenal) have a more powerful effect than in a non-diabetic.
    There is a large diurnal dependence. If you can, perform exercise in afternoon or evening, and avoid it in the morning. It is likely you may see no hyperglycemia if you can shift physical exercise to late in the day. Dr. Richard Bernstein often prescribes a rapid-acting beta blocker to prevent the hyperglycemic spike in diabetics during exercise -- this apparently is quite effective, if necessary. If you search on it you should be able to find the specific drug he uses -- I cannot recall off the top of head.
     
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  4. KenMacK

    KenMacK MODY · Member

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    P.S. Debra, I just listened to a 2016 interview with Bernstein. He mentions the rapid-acting beta blocker in it. You can find with a search including the following:
    *** diaVerge interview Dr. Bernstein Lisa ***
    I think you will find the mention of beta blockers in Part 2. Also, he has published a large series of video podcasts named "Diabetes University" on Youtube. He definitely mentions the beta blocker many times within these podcasts, but this runs to hundreds of hours of content. Well worth starting to listen to, though, in general.
    Beta blockers apparently inhibit epinephrine, which predominates the so-called "secondary response" (glucagon is primary) to signal the liver to raise BG. Bernstein uses these drugs not only for reducing or eliminating hyperglycemia in response to physical exercise, but also to other forms of stress to which the brain responds with stimulation of stress-hormone secretion. He does not appear to have included anything pertinent in my 2011 edition (apparently the latest) of his book "Diabetes Solution".
     
  5. bulkbiker

    bulkbiker Type 2 · Oracle

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    Not necessarily.. they can be overproducing insulin but resistant to it.
     
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  6. KenMacK

    KenMacK MODY · Member

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    P.S. In the diaVerge interview with Lisa, Bernstein tells a story about Elliott P. Joslin (after whom the Joslin Diabetes Center in Boston, Massachusetts is named) teaching that a diabetic should never run just one block to catch a bus, but should run a mile. Joslin used this quip to illustrate the point that a burst of stress will stimulate the adrenal response that raises blood sugar, but that this will be too brief to then significantly deplete blood sugar into skeletal muscle to compensate and lower BG back down.
     
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  7. Jim Lahey

    Jim Lahey I reversed my Type 2 · Well-Known Member

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    Sorry but this is erroneous information. A type 2 can become insulin deficient in time, but their condition at its core is not one of insulin deficiency.
     
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  8. KenMacK

    KenMacK MODY · Member

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    Sorry, the widespread myth that a T2D is not insulin deficient reflects the widespread misunderstanding of the hepatic-islets (i.e. portal) axis and its endocrinology, both in diabetes and in non-diabetes. This is WHY I emphasized that there is sustantial insulin deficiency in T2DM.
    The basics of the endocinological defects of T1DM, T2DM, and almost all forms of MODY (excepting MODY2 or the glucokinase monogenic form) are underpinned by an insulin-secretion deficiency. Regardless of the specific form of diabetes, which is very different at the endocrine-pancreatic/cellular level, diabetes will not be diagnosed by conventional medical practice and guidelines until the overall beta-cell function drops to 20% (a loss of 80% in the acquired forms, T1DM and T2DM). In my form of MODY there is never any loss -- there is an underexpression of many proteins underpinning insulin production/secretion in the beta cells due to inherited mutations in the HNF1-alpha homeobox gene (HNF stands for "Hepatic Nuclear Factor" -- the gene is expressed in endocrine pancreas, liver, small intestine and kidneys).
    In T1DM all of the loss of function is due to death/destruction of beta cells. The remaining beta cells are normal, but there are far too few present to balance the alpha cell population. In T2DM the loss of function comes from BOTH beta-cell apoptosis (i.e. death) and from beta-cell derangement (i.e. the remaining beta cells have abnormal and weak function, and are morphologically distorted and visibly inflamed).
    However, regardless of type, the clinical manifestation (i.e. diagnosis) of diabetes does not occur until beta-cell function drops to 20% of normal. This takes years in either T1DM or T2DM. When the 20% threshold is crossed there is loss of insulin granulation (i.e. storage) in beta cells, and this results in the classic clinical symptoms of polyuria and polydipsia. The sudden appearance of these symptoms only occurs once insulin granulation is lost. It is very rare that diabetes is diagnosed until these symptoms appear.
    IMO it is likely that a form of insulin resistance underpins T2DM (whereas this is not intrinsically true of T1DM or MODY), and that this insulin resistance is the earliest detectable defect of pre-diabetes, occuring in the alpha cells. Many independent diabetes basic research groups have detected the early defect in different ways, and it produces the hyperglucagonemia intrinsic to insulin deficiency of diabetes. However, at this early stage there is no insulin deficiency (yet) in animal models of T2DM. IR is one hypothesis that could explain the observed "early defect" of pre-diabetes (i.e. metabolic syndrome), but there are others and noone has yet been able to develop an experimental method to investigate the mechanism in alpha cells directly.
    In the endocrine pancreas, or islets, insulin is the primary regulator of glucagon secretion by alpha cells. Islet BG is the secondary regulator. Glucagon is stimulated inversely to insulin. This is why insulin-deficient response to portal nutrients (i.e. glucose and amino acids) results in hyperglucagonemia for the entire absorptive/prandial period after a meal. It is the hyperglucagonemia itself that is responsible, almost entirely, for the hyperglycemia of diabetes. The liver exhibits excessive HGO (hepatic glucose output), but is correctly and normally responding to the hypoinsulinemic/hyperglucagonemic portal signaling.
    This basic endocrinology has been verified by experiment continually since the 1970s. Roger Unger and colleagues did the original work, and Unger had to invent the first glucagon assay in order to accomplish this. I would recommend the work of Unger's current lab and also that of Alan Cherrington's lab for reference. And there are others that study the portal endocrinology in a quantitative fashion -- that is, they make measurements in vivo (usually in canine models).
    The simplistic, and completely incorrect, notion that T2DM is a disease of whole-body IR and does not include insulin-secretion deficiency, beta-cell apoptosis, beta-cell derangement and lipotoxicity, etc. is absolutely tragic, especially for T2Ds. One need only read the massive body of islets research, including direct imaging of in-vivo islets in T2DM as well as extensive analysis of endocrine pancreas in autopsy, to understand this. The massive loss of beta cells in an overt T2D is not really subject to question, nor is the insulin deficiency at this stage of the condition.
    Both pre-diabetics and overt T2Ds should practice strict ketogenic diets. These conditions are straightforwardly reversible, unlike other forms of diabetes, although full reversal and normalization of beta-cell population will take more than a decade for any overt T2D and is rarely accomplished. T2Ds should be using insulin to prevent the tissue death of diabetic complications that occur due to postprandial excursions. Other drugs such as metformin and GLP-1 agonists are simply impotent, especially during the most important hyperglycemic intervals of time following meals.
    The process of tissue death, especially in certain tissues that do not express insulin, over many years due to diabetic hyperglycemia is INSIDIOUS. Later in life overt diabetics (excepting MODY2, in which complications do not occur because there is no insulin secretion defect) who do not practice insulin therapy to (albeit crudely) compensate for hyperglucagonemia and excessive HGO are likely to regret it. The excessive HGO (via hepatic glycogenolysis) of the diabetic cannot be prevented by any yet-known technology. However, exogenously-administred subcutaneous insulin flux (into circulation) can drive the excess glucose into "clearance" tissues -- mainly muscle -- to prevent large hyperglycemic transients.
    Because a diabetic overproduces hepatic glycogen/glucose every day, and the substrates for this are gluconeogenic amino acids, the diabetic would be very wise to practice a diet rich in animal-source protein. So would the aging non-diabetic, for many reasons. But a diabetic definitely needs MORE high-quality protein on a daily basis due to the extra demand for hepatic gluconeogenic production.
     
    #8 KenMacK, May 16, 2019 at 1:28 PM
    Last edited: May 16, 2019
  9. KenMacK

    KenMacK MODY · Member

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    P.S. One of the many things that distinguishes T2DM from other insulin-deficient forms is that there is no measureable early loss of normal islets-hormonal response to AAs (amino acids). This is a HUGE advantage. Hence, a sufficiently low-carb diet will normalize BG during the first few years after conventional diagnosis (i.e. after loss of insulin granulation), and insulin therapy is NOT required to prevent diabetic complications in early T2DM. I should have mentioned this above, particulary for Debra's benefit if she has been only recently diagnosed. Once again, this has been well recognized since the 1970s, and back then it was actually studied by some researchers. Due to the insulin/glucose-centric myopia of later decades little has been done since -- evidently funding is not available, unsurprisingly.
    Once the T2D advances (in loss of beta-cell function) more toward insulin dependence the hyperglycemic response to AAs will appear.
    I would strongly recommend regular prolonged (e.g. five days) fasting -- no food, only water -- several times a year for a T2D seriously working upon beta-cell regeneration and reversal of the condition. This is, by far, the most potent stimulus for cellular repair and regeneration. Short of a full fast, there are some medically prescribed forms of very-low nutrient formulas now available, and these can achieve a close approximation of the fasted state for those who prefer to put something (however nutritionally insignificant) into their stomachs every day. ProLon (developed by Valter Longo) is one such.
    Adding some electrolytes, especially Na and K, to daily water is recommended for those who perform a conventional fast. One should probably consult an appropriate physician (if one can be found) in preparation, but IMO this is unnecessary unless there are complications of abnormal health. T2DM itself would not be such a complication. Anyone performing a fast should first be fully, long-term keto-adapted -- this is a must.
     
  10. KenMacK

    KenMacK MODY · Member

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    P.S. Outside of the researchers who perform portal hormone measurements, there seems to be little understanding of the non-diabetic and diabetic islet function.
    Hyperglycemia due to dietary carb's (i.e. portal/islet glucose) CANNOT be compensated for with sub-Q insulin. Even in the non-diabetic there is a hyperglycemic response to prandial glucose, but there is a strong acute insulin response and (hence) a total suppression of glucagon secretion. This is a negative feedback, and hence regulatory in nature.
    By contrast, in the diabetic there is a weak or absent GSIS (glucose stimulated insulin secretion) and an INCREASE in GSIG (glucagon secretion). This is a POSITIVE feedback, and fundamentally unstable in nature. Those who understand control/regulatory systems, either in engineering or in nature, should recognize that during the prandial or meal-absorptive interval this will induce an oscillatory and amplified hormone response that is unpredictable, capable of producing both hyperglycemia and hypoglycemia at different times if one attempts to compensate with exogenous insulin.
    This IS THE REASON that a diabetic (excepting MODY2) should eliminate carb's in the diet. It is not simply that carb's generate a stronger (gram for gram) acute insuin response than most AAs -- this reflects a very simplistic and incomplete understanding of the endocrinology.
    People who talk about rapidity of release of various forms of fast-acting manufactured insulins simply do not understand insulin therapy and what it does and does not do. All fast-acting forms of insulin (mimetics or analogs) are attempts to compensate for dietary carb's, and all cannot work (well or consistently and predictably, at least). There is no substitute, presently, for the elimination of significant amounts of carb's in meals. All meals should be AA-dominated, in terms of required compensatory insulin bolus.
    By contrast, the islet response to AAs is quite different. AASIS will be deficient in most diabetics (notably excepting early T2DM), and hence AASGS will be excessive. However, the excess of glucagon will be predictable and largely proportional to mass of animal-sourced protein (each individual AA has its own unique potency of AASGS, acting directly upon both alpha cells and beta cells, and so proportions matter) ingested during absorption. The feedback will never become positive -- it will remain negative albeit weak or deficient. This is WHY an insulin bolus will have a consistent and predictable compensatory effect to diabetic hyperglycemia from dietary protein.
    The definition of carb elimination, as a practical matter for the diabetic, is a meal composition that produces a protein-dominated requirement for insulin bolus quantity (i.e. number of units).
    The diabetic practicing a ketogenic diet MUST use only insulin Regular (e.g. Novolin R or Humilin R). This is the only form of insulin that has appropriate time-release/flux profile for absorption of protein from the small intestines. All other forms of insulin are inappropriate for bolus application. Fast-acting, intermediate-acting, and long-acting insulin analogs must be avoided in covering meals, and will result in both prandial hypoglyemia and prandial hyperglycemia in the best case.
    Diabetics should also be aware that there is a lag (typically about a half hour) between capillary blood glucose and serum BG. Not only do home meters/strips rely upon capillary/interstitial BG, but so do CGMs (all or most, I think, although I do not use one). For basal compensation (i.e. non-absorptive intervals) this is not a huge problem, although even in this state any stress-hormone induced hyperglycemia will not be compensated for properly. But for bolus compensation a CGM cannot fulfill the function of sensor (operating in paralle with endocrine pancreas).
    Furthermore, for correct bolus compensation and feedback (using a pump, for example) it is the ISLET blood that would have to be sensed. Not even portal blood would be adequately adequate, although this would be better than serum blood and serum blood is better than capillary blood. During the absorptive period the portal blood glucose can be up to 40 times that of peripheral blood and islet blood glucose can be up to 400 times that of peripheral blood! This is what the lab measurements illustrate. This is why quantitative analysis is essential.
    I cannot overemphasize how incorrect any whole-body IR model is. It is metaphorical at best, very misleading in general, and incorrect. IR is a measureable independent characteristic of each individual tissue in the body -- there is no such thing, physiologically, as whole-body IR. And there is no such thing as "hepatic IR", although one can find this term extensively used in the clinical research literature. It is just as much a mere metaphor as is whole-body IR. The liver is normal, without significant defect, in most diabetes. It is responding normally to an imbalance of portal hormones. The defect is at the level of the islets.
    For those who might mention fatty liver as an example of hepatic abnormality -- this is an effect, and not a cause, of T2DM and pre-diabetes (MetS) and generally not present at all in other forms of diabetes. It is a manifestation of disrupted fatty-acid metabolism in liver. In MetS ALL of the insulin-expressing tissues are similarly disrupted, and filled with ectopic FA intermediates (aka lipotoxicity). These include muscle, kidney, intestine, and adipose.
    NAFLD is not universally present in either pre-diabetes or in T2DM. It is not required, and is certainly not causal.
     
    #10 KenMacK, May 16, 2019 at 2:49 PM
    Last edited: May 16, 2019
  11. bulkbiker

    bulkbiker Type 2 · Oracle

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    Apart from those of us that have had our insulin tested you mean.. those mythical creatures? The one's that have "normal" insulin levels.
    You write very authoritatively however that doesn't mean you are correct. and walls of text don't make for easy reading...
     
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  12. TimJP

    TimJP · Newbie

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    Wow - I didn’t know that about time of day exercise. How much does AM (start of day) exercise impact a T2D?
     
  13. KenMacK

    KenMacK MODY · Member

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    Also, I might add or clarify, the condition of lipotoxicity (which I consider an effect rather than cause of degenerated organ function -- especially adipose de novo lipogenesis -- in MetS) is known to include a downregulation of glucose transport (via GLUT4) in insulin-sensitive tissues -- hence, these tissues, including fatty liver, are technically insulin-resistant to some quantifiable extent -- the primary consequent metabolic degeneration is of FA (fatty-acid) metabolism. This can drop to < 20% of normal. On the other hand, in the same tissues, glucose metabolism remains close to normal at >> 80%. In tissues evolved to rely upon FAs, such as muscle, there is a switch to reliance upon glucose for ATP production and this robs huge amounts of BG from the brain. Hence, constant brain fuel crises and carb craving to rapidly resupply the blood with glucose.
    With this minor qualification, I would challenge anyone to provide evidence to refute my claim that the diabetic liver is not significantly or meaningfully insulin resistant.
    On the other hand, it is catastrophic for the entire body to have a fatty liver, which means that the liver cannot engage properly in the normal FA metabolism of the fasted or semi-fasted states, including ketosis. Hence, the brain is not supplied with the appropriate alternative fuel of ketones and the liver cannot rapidly respond to the overdemand for blood glucose induced by lipotoxicity in major, high-mass high-energy tissues such as muscle without direct resupply of glucose portally (from meals).
     
  14. Jim Lahey

    Jim Lahey I reversed my Type 2 · Well-Known Member

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    If it is true that type 2 diabetes is a disease of insulin deficiency then why does it get worse when you add insulin?
     
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  15. catinahat

    catinahat Type 2 · Well-Known Member

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    Agree -- I need a lie down with a wet flannel on my head after reading that
     
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  16. Stephen Lewis

    Stephen Lewis Type 2 · Well-Known Member

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    To try and actually provide some short and hopefully helpful information, I go to the gym 4 or 5 times a week. I fast walk as warm up for about 10 minutes then heavy weight-lifting for another 30+ minutes. I go in the morning and in the afternoon. 8 months ago and nearly 30 lbs heavier with a lot of bad fat under the stomach muscles my bg levels would spike from about 6 to over 10 and the morning was always worse. Now, with the same exercise and much less fat (from a low carb diet) there is no significant spike. In fact I sometimes need to have a snack afterwards to bring my glucose levels back up. My understanding is that the liver stores and releases glucose when the pancreas sees a low level. I rarely get below 5.0 because this process works really well. The glucose in the liver has to be replenished from somewhere and if it is not available in the blood then the body burns fat to create energy with any surplus going to the liver for future use. (This is the KISS explanation that I need). We are all different and you may have a different reaction but spiking after exercise seems normal for many of us but I was able to control this through diet. Come back to the forum and read the information from how those of us with T2 deal with our condition. I suggest supposed scientific research has not found an answer for us in nearly 100 years and we probably know more about how our own body works and reacts.
     
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  17. Debra67

    Debra67 · Newbie

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    Thank you I'm doing keto still have a lot of weight to go and this was very helpfull
     
  18. sunspots

    sunspots Type 2 · Well-Known Member

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    Presumably during the fast medication would still be taken. What about those that rely on food for absorption or to minimise side-effects (e.g. ibuprofen)? It is best to consult a doctor if on other medication as a fast might interfere with treatment of unrelated disorders.
     
  19. Theroadlesstravelled

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