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Hyperlipid Physiological Insulin Resistance

Physiological Ir. | Diabetes Forum The Global Diabetes Community

Physiological Ir. | Diabetes Forum The Global Diabetes Community

Diabetes Forum The Global Diabetes Community Find support, ask questions and share your experiences. Join the community Can members tell me the difference between Physiological IR and Diabetic IR, please? TIA not sure I can explain this really well, but I will try. (Mind you I am just a lay person, so can't guarantee I understood this correctly.) Physiological insulin resistance occurs due to a low-carb diet. On a low-carb diet the body scales back the use of glucose for some of your body's functions and uses ketones instead (e.g. brain, muscles). Glucose is thus conserved for the most essential functions (such as producing red blood cells). This is why some people also refer to physiological insulin resistance as adaptive glucose sparing. Physiological insulin resistance can be reversed when we start eating a lot of carbs again. Diabetic insulin resistance, also known as pathological insulin resistance, occurs when insulin is ineffective or not fully effective at getting glucose into your cells. (Sometimes a lock and key analogy is used meaning that insulin is the key to get glucose into the cell, but it no longer fits the lock). So, cells actually are starving because they lack glucose as fuel and cannot use ketones instead because they are not fat adapted. Thus glucose stays in the blood, but also very often your blood insulin levels will be high (at least as long as your pancreas tries to produce more insulin to force the blood sugar into the cells). Why insulin is ineffective at trying to push blood sugar into cells is, to my knowledge, not really known. There is probably some genetic component, but some also argue that this happens when there is too much fat in the cells and thus these cells refuse to take on any additional fuel. Can pathological insulin resistan Continue reading >>

Physiological Insulin Resistance

Physiological Insulin Resistance

I’ve been meaning to do a deep dive into physiological insulin resistance for quite a while now, but the universe keeps conspiring to take my time. Because I haven’t had time to read, learn more and write about it, I thought I’d share the links I have accumulated thus far. Mostly because I’ve now been asked a variant of the following multiple times, or have seen the following posted on various forums for discussing nutrition, health, and low carbohydrate diets: “Why has my blood glucose gone up on a low carb diet?” Typically this is accompanied by a good deal of anxiety and fretting over glucometers. I should know, I watched my blood glucose increase by a few points as I’ve sustained my low carb diet. My understanding is that this is a known adaptation completely unrelated to the insulin resistance concomitant with diabetes. While I’m not the person you should ask about anything health related, I’ve wanted an answer to this question myself. The explanation I’ve read is that after going low carb, your muscle tissue becomes insulin resistant in order to preserve serum glucose availability for the brain. If your muscle tissue did not do this, reduced availability of glucose in the serum could (theoretically) put you in dire straights if your brain can’t meet minimal demand for glucose. (Mind you, even on a zero carb diet you can meet all your glucose requirements via gluconeogenesis. The point is, your body needs a way to tell your muscle mass to stop taking all the glucose it makes. This is that way.) Because of this physiological insulin resistance (which I should mention is a benign state that is not making your diabetic insulin resistance worse) you wouldn’t want to take an oral glucose tolerance test while you are low carbing. If you took a glu Continue reading >>

Physiological Insulin Resistance: The Devil In The Prada.

Physiological Insulin Resistance: The Devil In The Prada.

On the surfing trip to Devon we watched The Devil Wears Prada on DVD. The best line for me was the fashion waif screaming at the heroine, with the deepest insulting angst: "and you eat CARBS" Well, it made me laugh. What made me think a little more was the same character talking about her latest diet, I paraphrase only slightly: "My new diet doesn't of course include any food. I simply don't eat until I am about to pass out from hypoglycaemia and then swallow a small cube of cheese" This was used to maintain the skeletal look so prized in the world of high fashion. Assuming the whole of the film is utterly true to life (except perhaps the too good then fashion corrupted heroine), I started to think about the physiology here, and about the physiology of that life threatening illness, anorexia nervosa. Now, anyone of us relatively normal people on a lowish carb diet will never become hypoglycaemic. If we don't eat we just convert the stored triglycerides in our adipose tissue to non esterified fatty acids in our blood stream and use these to fuel our muscles. The glycerol from the triglycerides is half a glucose molecule, we can join two of them together to make glucose. Filling muscles with palmitic or stearic acid makes them insulin resistant enough to spare glucose and so maintain an adequate plasma glucose concentration to keep our brains working. Brain tissue cannot suck glucose out of plasma. It gets it by diffusion down a concentration gradient. You need at least 3.0mmol/l in your plasma unless you are in deep ketosis, when you can get by on a shade less. But fashion waifs clearly can get hypoglycaemic if the script of the film is true. They are comparable to, or thinner than, anorexic patients. Here are the patient details of a group of ten anorexic patients. Note Continue reading >>

What Does Fasting Do To Insulin?

What Does Fasting Do To Insulin?

A common thread among many dietary plans is compressing eating times. On the one hand, some plans narrow periods to two to three meals per day, with substantial time gaps in between (i.e. time-restricted feeding). Variation include other strategies that suggest eating normally for a few days, then avoiding food entirely for a few days (i.e. intermittent fasting). On the other hand, some diet plans encourage eating several meals throughout the day (i.e, “grazing”; 6-8 small meals per day). Because elevated insulin is one of the most, if not the most, relevant factor in developing insulin resistance, a highly rational strategy is to follow a dietary plan that incorporates periods of time throughout the day wherein insulin is low. This philosophy immediately suggests that frequent eating is less effective than less frequent eating—indeed, three meals per day is better than six [1]—but are fewer than three meals best of all? Maybe. Fasting’s Effectiveness Partially Depends on How It’s Done Time-restricted feeding and intermittent fasting strategically include periods of deliberate food avoidance. The evidence regarding its efficacy in improving insulin sensitivity is valid, though it partially depends on how it’s done. Two studies used this idea by having study subjects eat normally one day (i.e. unrestricted) and essentially fast the entire second day (i.e., alternate-day fasting), repeated seven times over a two-week period and found conflicting results—one reporting an improvement in insulin sensitivity [2], while the other observed no benefit [3]. An alternative strategy, wherein the person confines eating to a specific window of time each day (e.g., eating breakfast and dinner only [4], or lunch and dinner only [5]) yielded robust improvements in insuli Continue reading >>

Insulin Resistance? - Low Carb Friends

Insulin Resistance? - Low Carb Friends

. I used to be insulin resistant before I started low carbing. I have a question. What has become of this condition? Is it reduced at all? Thanks guys im really concerned about this. Start Date: 01/2011, got lazy/married, rebooting FOR REAL 2014 When I first started, I had dark, velvety skin (Acanthosis nigricans) around my neck, between my breasts, and under my armpits, which was one of the signs of insulin resistance. I lost weight, and the dark skin went away completely. So yes, I'd say my condition was reduced. When I first started, I had dark, velvety skin (Acanthosis nigricans) around my neck, between my breasts, and under my armpits, which was one of the signs of insulin resistance. I lost weight, and the dark skin went away completely. So yes, I'd say my condition was reduced. I have this and never knew what it was till I looked up "dark skin under arms" on the net. I noticed it went away the first time I did Atkins (about 10 years ago), the second I stopped low carb and started chowing down on wheat again it came back. I love what Atkins does for my body even though I very rarely lose weight (my hair grows in nicely and my dark skin patches go away), unfortunatly I turn into super grump, my mood turns bad bad bad when doing strict low carb. I'm doing JUDDD with a low glycemic emphasis (just started the low glycemic) hopefully the marks will go away but havn't so far and have been doing JUDDD for 3 months, I have been eating very high carb though. If you are looking for a way to track this, have you had a doctor check you fasting insulin levels? That can give you a rough idea of your resistance. You could also ask your doc to provide a HOMA (homeostatic model assessment, which uses your fasting glucose and fasting insulin levels in a mathematical formula) or a Continue reading >>

Paleo Diet For Insulin Resistance

Paleo Diet For Insulin Resistance

Success stories and experiences on how the Paleo Diet has helped with Insulin Resistance. Has the Paleo Diet helped you with Insulin Resistance? Sign In , Sign Up , or What Causes Insulin Resistance? Part I. Whole Health Source November 11, 2011 Adipocyte insulin resistance. Hyperlipid (cites 4 articles) October 6, 2011 Insulin Resistance and PI3K. NephroPal October 2, 2009 Hepatic insulin resistance. Hyperlipid (cites 4 articles) September 15, 2009 Physiological insulin resistance. Hyperlipid (cites 5 articles) October 23, 2007 Real Resistance Stretching. Matt Metzgar July 27, 2010 Leptin Resistance and Sugar. Whole Health Source (cites 5 articles) December 26, 2008 Always Hungry? It's Probably Not Your Insulin.. Whole Health Source (cites 1 article) January 9, 2016 Insulin detemir (3). Hyperlipid (cites 2 articles) March 15, 2015 Insulin detemir (2). Hyperlipid (cites 4 articles) March 4, 2015 Insulin, are you hungry?. Hyperlipid June 19, 2012 Insulin secretagogue. The Heart Scan Blog March 14, 2011 Insulin secretagogue. The Heart Scan Blog (cites 1 article) March 14, 2011 Butter and insulin. The Heart Scan Blog (cites 1 article) March 19, 2010 Continue reading >>

It Always Bring My Blood Sugar Down!

It Always Bring My Blood Sugar Down!

There has been pretty good discussion going on here. I know I have expanded my knowledge a bit. One thing that to keep in mind as we have these discussion is respect for each other. The electronic medium can be difficult at times and sometimes what we are thinking we are getting across is not what is actually coming across. Lots of good discussion but there please try to refrain from getting personal or ridiculing someone for their belief or experiences. We have all heard the acronym YMMV. It applies and is true in every sense of the words! Lantus, Novolog, Metformin XR, Lipitor, Lopid, Lovaza, Topiramate, Lisinopril, and Zyrtec A1C: Feb '12: 6.2; Aug '12: 5.7; Nov '12: 5.9 Do you have an "old faithful" food or habit you can rely on to bring your high blood sugar down? Thank you for posting the foods and actions that have helped you bring your high blood sugar down. These are what you have found to be effective: Last edited by silverthaw; 11/27/12 at 09:49 AM. Interesting. I bet that scientific evidence is powerful. Which on a ketogenic diet - or I should say after effective keto-adaptation which could take longer than a few weeks - would be completely irrelevant. In this state, there is no dependence on insulin sensitivity in order to purge glucose. In fact, there is high insulin resistance which is INTENTIONAL and is a direct result of keto-adaptation. It is not a "maladay" like the original insulin resistance we found on diagnosis day but a normal and positive state which is an essential part of keto-adaptation. So, if something which increased insulin resistance causes a rise in BG, that proves that keto-adaptation has not been achieved. This article is a little hard to get through, but will shed some light on the subject, as well as some very interesting informati Continue reading >>

Physiological Insulin Resistance

Physiological Insulin Resistance

I have been trying to find an answer to why my FBG levels have been increasing over the last couple of weeks. It is very frustrating and as a diabetic trying to reverse the disease it is scary (will this WOE work? Are the consequences of out of control diabetes, I am trying to escape, going to happen anyways?). I ran across a blog post that seems to describe what may be happening in my case. It is a possible phenomenon called Physiological Insulin Resistance. The High Blood Glucose Dilemma on Low Carb (LC) Diets If you are on a ketogenic or very low carb (VLC) diet (e.g. with 50-100gr carb/day and/or eating ketone producing MCT oils such as coconut oil), you m Low insulin levels activate hormone sensitive lipase. Fatty tissue breaks down and releases non-esterified fatty acids (NEFA). These are mostly taken up by muscle cells as fuel and automatically induce insulin resistance in those muscles. Palmitic acid is the primary NEFA released from human adipose tissue during fasting. Think of palmitic as a signal molecule to tell the muscles that inhibition of glucose uptake is needed and to tell the liver that increased gluconeogenesis is required because there is no food coming in. This in turns increases the blood sugar. One of the supporting blog post to the one posted above spoke of person experience.The author, like me, gets a consistent mild ketosis readings. Using Ketostix I am getting a consistent 15 dl reading and at high BG. You need to get calories from somewhere, should it be from carbohydrate or fat? I am going to continue reading/researching down this path to determine the implications. The author of the blogs conclusion was as long as his HbA1c is 4.4% he does not care about the high blood sugar readings. This is one voice so I want to learn more. Has anyone Continue reading >>

Physiological Insulin Resistance

Physiological Insulin Resistance

Back in mid summer 2007 there was this thread on the Bernstein forum. Mark, posting as iwilsmar, asked about his gradual yet progressively rising fasting blood glucose (FBG) level over a 10 year period of paleolithic LC eating. Always eating less than 30g carbohydrate per day. Initially on LC his blood glucose was 83mg/dl but it has crept up, year by year, until now his FBG is up to 115mg/dl. Post prandial values are normal. He wanted to know if he was developing diabetes. I've been thinking about this for some time as my own FBG is usually five point something mmol/l whole blood. Converting my whole blood values to Mark's USA plasma values, this works out at about 100-120mg/dl. Normal to prediabetic in modern parlance. However my HbA1c is only 4.4%, well toward the lower end of normality and healthy. That's always assuming that I don't have some horrible problem resulting in very rapid red blood cell turnover. I don't think so... I spend rather a lot of my life in mild ketosis, despite the 50g of carbs I eat per day. So I can run a moderate ketonuric urine sample with a random post-chocolate blood glucose value of 6.5mmol/l. What is happening? Well, the first thing is that LC eating rapidly induces insulin resistance. This is a completely and utterly normal physiological response to carbohydrate restriction. Carbohydrate restriction drops insulin levels. Low insulin levels activate hormone sensitive lipase. Fatty tissue breaks down and releases non esterified fatty acids. These are mostly taken up by muscle cells as fuel and automatically induce insulin resistance in those muscles. There are a couple of nice summaries by Brand Miller (from back in the days when she used her brain for thinking) here and here and Wolever has some grasp of the problem too. This is patentl Continue reading >>

Hyperlipid: Physiological Insulin Resistance Again

Hyperlipid: Physiological Insulin Resistance Again

You need to get calories from somewhere, should it be from carbohydrate or fat? I started the Protons thread with the simple question: What is the difference, from the metabolic point of view, between the energy supplied by fat vs that supplied by glucose derivatives. This gives a simple picture of insulin resistance as a metabolic technique to limit caloric entry in to an individual cell under conditions of excess availability. NADH, tending to come from glucose, drives complex I to generate a decent inner mitochondrial membrane potential (delta psi). Feeding substrate in at other access points to the electron transport chain's CoQ couple, be that electron transporting flavoprotein dehydrogenase, mtG3Pdehydrogease, NADPH dehydrogenase or others, reduces that CoQ couple and promotes reverse electron flow through complex I, superoxide generation and insulin resistance. This is the insulin resistance seen so clearly when you pay folks to over-eat, assuming you feed them crapinabag. The exact mechanism of this failure of insulin to act is not clear, but large amounts of H2O2 act at several points to inhibit the activation pathway. Of course an intramitochondrial mechanism would be really neat, or some sort of complexing of the insulin/receptor with ETC proteins. Hard to say what we will find here in future, but an interesting area. What about the insulin resistance of starvation? Do we have the same phenomenon of reverse electron flow through complex I as the mechanism? So now we have to think about ketones with normolglycaemia. Back in my early days of looking at mitochondria I spent many hours with Veech's seminal paper on mechanical work generated by isolated rat hearts, pumping fat-free fluids spiked with glucose, ketones, glucose/insulin or glucose/insulin/ketones. K Continue reading >>

Hyperlipid: Physiological Insulin Resistance; Dawn Phenomenon

Hyperlipid: Physiological Insulin Resistance; Dawn Phenomenon

Physiological insulin resistance; Dawn Phenomenon What is the Dawn Phenomenon (DP)? A nice simple definition is available from here : "The dawn phenomenon is a term used to describe hyperglycemia or an increase in the amount of insulin needed to maintain normoglycemia, occurring in the absence of antecedent hypoglycemia or waning insulin levels, during the early morning hours. To be clinically relevant, the magnitude of the dawn increase in blood glucose level should be more than 10 mg/dL or the increase in insulin requirement should be at least 20% from the overnight nadir. Controversy exists regarding the frequency, reproducibility, and pathogenesis of the dawn phenomenon. Approximately 54% of patients with type 1 diabetes and 55% of patients with type 2 diabetes experience the dawn phenomenon when the foregoing quantitative definition is used" If you go back to 1988 this group seemed to think that the Dawn Phenomenon was pretty straight forward and amenable to pharmacological management. In the early hours of the morning humans have a growth hormone (GH) surge. GH causes lipolysis, lipolysis releases free fatty acids. No muscle wants glucose when it has access to free fatty acids. Muscle thus becomes insulin resistant and blood glucose rises. They studied type one diabetics as doing this eliminates all of those messy insulin responses to glucose that normal people produce. Give an anticholinergic, block the GH surge and you block the DP. All nice and simple. Then this group , in 1992, went out to check if this was true and gave a bolus of GH, again to some type one diabetics. Any old time of day as far as I can tell. As expected GH caused a rise in FFAs but no insulin resistance in this paper! Quite how they managed this is a bit beyond me. FFAs should produce insul Continue reading >>

Physiological Insulin Resistance = Low Carbohydrate Diet Induced Insulin Resistance

Physiological Insulin Resistance = Low Carbohydrate Diet Induced Insulin Resistance

I’ll admit to breathing a sigh of relief back in October of 2007, when Peter at Hyperlipid posted about “Physiological insulin resistance.” Curiously, looking at the post again, I note that he didn’t capitalize the second two words—as though it’s not a proper name for a specific condition. Back in mid summer 2007 there was this thread on the Bernstein forum. Mark, posting as iwilsmar, asked about his gradual yet progressively rising fasting blood glucose (FBG) level over a 10 year period of paleolithic LC eating. Always eating less than 30g carbohydrate per day. Initially on LC his blood glucose was 83mg/dl but it has crept up, year by year, until now his FBG is up to 115mg/dl. Post prandial values are normal. He wanted to know if he was developing diabetes. […] What is happening? Well, the first thing is that LC eating rapidly induces insulin resistance. This is a completely and utterly normal physiological response to carbohydrate restriction. Carbohydrate restriction drops insulin levels. Low insulin levels activate hormone sensitive lipase. Fatty tissue breaks down and releases non esterified fatty acids. These are mostly taken up by muscle cells as fuel and automatically induce insulin resistance in those muscles. Whew! Now I had something to tell my dad and others who’d been faithfully doing LC and became horrified, then scared, at fasting blood glucose measurements (which is primarily how the health community screens people for diabetes). I really didn’t concern myself with it again—for all these last almost 7 years. OK, so long as post-prandial is fine (caveat: AFTER AN LC MEAL!), nothing to worry about; and combined with good HbA1c, and the fact that so far as we know, this condition will reverse in normal people after a few days of carbage, Continue reading >>

Hyperlipid: Physiological Insulin Resistance: Clarification Of Fbg

Hyperlipid: Physiological Insulin Resistance: Clarification Of Fbg

A LC eater has a FBG of 5.5mmol/l, technically pre diabetic, but blood insulin is 3.5 IU/ml. This is VERY low. Glucose is in very short supply but blood glucose is maintained by physiological insulin resistance, ie the muscles are full of triglycerides assembled from free fatty acids (NEFA) from lipolysis. The LC eater has breakfast, with enough protein from his eggs or particularly casein from his yoghurt to raise insulin from 3.5 IU/ml to 5.0IU/ml. This inhibits lipolysis enough to reduce NEFA in the bloodstream, intramuscular triglycerides fall and muscle insulin sensitivity returns. There's minimal glucose coming from the gut and so plasma glucose drops to between 4.0 and 5.0mmol/l, probably nearer 4.0mmol/l. It fluctuates between 4.0 and 5.0 after and between each LC meal. In the early hours of the morning there is a growth hormone surge and NEFA from lipolysis peak early morning to give insulin resistant muscles and an elevated FBG. MEAN glucose over 24h will be in 4 point somethingish, HbA1c will be between 4 and 5%. INSULIN will probably average out around 5-10 IU/ml, averaged out over 24h. A SAD eater has a FBG of 5.5, prediabetic, because he is prediabetic. His muscles and liver are permanently and pathologically insulin resistant. His pancreas is cranking out 50 IU/ml of insulin to just keep that FBG in the 5.5mmol/l range. He eats bagels, jam and a large mocha for breakfast and his blood glucose hits 15mmol/l. His pancreas ups the insulin output as high as it can get it, perhaps to 150 IU/ml and just manages to to get blood glucose back down to 5.5mmol/l before lunch. Lunch is pasta and the cycle repeats. Mean glucose over 24 hours will be between 7 and 12mmol/l. HbA1c might just hover around 7%. INSULIN will average 100 IU/ml over the 24 hours. Helicobacte Continue reading >>

Hyperlipid: Protons: Physiological Insulin Resistance Addendum

Hyperlipid: Protons: Physiological Insulin Resistance Addendum

You need to get calories from somewhere, should it be from carbohydrate or fat? Protons: Physiological insulin resistance addendum Edward sent me this paper . I think I did already have a copy on my hard drive but you can't really start to make head nor tail of what is really going on until you have a handle on F:N ratio and the physiological role for superoxide. I'd completely forgotten about the paper. For those people who think humans are in some way different from rats, here's Fig 1 from the paper on humans eating either a saturated fat ketogenic diet or a polyunsaturated fat ketogenic diet, just for 5 days: Look at the glucose, lowest in the PUFA group, look at the ketones, highest in the PUFA group, look at the insulin sensitivity, waaaay higher in the PUFA group. Rat or human, makes no odds. PUFA fail to generate superoxide in mitochondria. Is this good or bad? The whole point of a ketogenic diet (epilepsy excepted) is to induce starvation-appropriate physiological insulin resistance. What is the point of setting up a ketogenic diet which does not have the ability to convert from running on glucose to running on fat? Aside: Why might anyone want to run their metabolism on FFAs? Superoxide. I want more mitochondria to supply spare ETC capacity, to minimise the sort of levels of free radicals which wipe out mitochondria when the pressure is on. Physiological superoxide signals for mitochondrial biogenesis, without all of that tedious exercise to do the same job on a mixed diet. End aside. Now it is just possible to argue that chronically reduced insulin may render adipocytes immune to the insulin sensitising effects of PUFA. Maybe. The obese mice of the next Protons post are on a mixed PUFA-carb diet to assist their "ballooning" experience. High insulin plus insul Continue reading >>

Hyperlipid: Physiological Insulin Resistance (low-carb Diets Induce Physiological Insulin Resistance) | Diabetes And Prediabetes | Pinterest | Insulin Resistan

Hyperlipid: Physiological Insulin Resistance (low-carb Diets Induce Physiological Insulin Resistance) | Diabetes And Prediabetes | Pinterest | Insulin Resistan

Hyperlipid: Physiological insulin resistance (Low-Carb Diets Induce Physiological Insulin Resistance) 12 Proven Foods Essential For Every Type 2 Diabetes Diet Focus is always on what to remove from your diet, and its incredibly frustrating. What about what you can eat? What about the foods you should be adding to a type 2 diabetes diet the foods that can actually improve blood sugar control? Low glycemic index foods Glycemic Index and Load Chart Infographic "The Truth about the Glycemic Load Tells You How Much Carb (Sugar) Your Food Actually Contains (Whereas the Glycemic Index Only Measures the Effect of Glucose on You Low carb for diabetes - learn how to stabilise your blood sugars today Low carb for diabetes - Read the full article which explains insulin resistance The 3 Week Diet - The Prediabetes Diet Plan: How to Reverse Prediabetes and Prevent Diabetes through Healthy Eating and Exercise - THE 3 WEEK DIET is a revolutionary new diet system that not only guarantees to help you lose weight 10 Foods That Lower Blood Sugars In Diabetics Maintaining low blood sugar levels can be difficult for diabetic patients. While a low carb diet appears to be useful on the whole, there are also many foods shown to help. Either by lowering blood sugars and/or improving insulin sensitivity. For more inf 11 Effective Diet Tips For People Suffering With Insulin Resistance Insulin resistance is a health disorder that is mainly caused from inactive lifestyle. Here are effective insulin resistance diet changes you should make in you The Big Diabetes Lie- Recipes-Diet - Top 21 Superfoods for Diabetics 2 Doctors at the International Council for Truth in Medicine are revealing the truth about diabetes that has been suppressed for over 21 years. A Definite and Effective Diet Plan to Overcom Continue reading >>

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