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Reverse Physiological Insulin Resistance

Low Carbing And Physiological Insulin Resistance

Low Carbing And Physiological Insulin Resistance

Diabetes Forum The Global Diabetes Community Find support, ask questions and share your experiences. Join the community Low Carbing and Physiological Insulin Resistance On a T1 thread ( ), @azure , in past #35, you post: "I agree @Garr Eating a moderate level of carbs can give you a great HbA1C as long as you apply yourself. That way you also avoid the physiological insulin resistance that so,often comes with cutting out carbs and ketosis. You also usually don't need to bolus for protein when you have carbs with it. It's a total fallacy to say that LCHF is the only way to get good results. Controlling carbs, yes, but that doesn't mean you have to cut them out completely." I would be interested to learn what percentage of low carbers you believe develop physiological insulin resistance (PIR), as a result of the LC approach, and at what point they develop it? I started a new thread to prevent derailing the source thread, and think others could be interested too. For those reading who are T2 (or other non-insulin dependant members) who have not fully read the source thread, please note it is a T1 thread, so please do not post on there, unless you have something both relevant and on-topic. I would hate to be stimulating content at risk of editing or deletion. Edited to add that I have deliberately posted in this section for those of us who consider food to be our medicine' How do you know you have no physiological insulin resistance, unless you stuff your face full of carbs? Then, assuming you do go on the odd bender, and so prove you don't have physiological insulin resistance, you are an addict, and then it's a play on alcoholics anonymous. Well, my diet and blood numbers have pretty consistent, and (albeit badly) illustrated by my HbA1c. I have also used several Libre s Continue reading >>

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Is "fat-induced" Muscle Insulin Resistance Rapidly Reversible?

Am J Physiol Endocrinol Metab. 2009 Jul;297(1):E236-41. doi: 10.1152/ajpendo.00244.2009. Epub 2009 May 12. Is "fat-induced" muscle insulin resistance rapidly reversible? Department of Internal Medicine, Washington University School of Medicine, 4566 Scott Ave., Campus Box 8113, St. Louis, MO 63110, USA. [email protected] Elevated plasma free fatty acids (FFA) cause insulin resistance and are thought to play a key role in mediating insulin resistance in patients with the metabolic syndrome (MTS) and type 2 diabetes mellitus (DM). Two experimental models used to study the mechanisms responsible for insulin resistance in patients are high-fat diet-fed rodents and administration of triglycerides and heparin to raise plasma FFA. As evidence that insulin resistance in high-fat diet-fed rats is due to high FFA, it has been reported that the insulin resistance is rapidly reversed by an overnight fast, a high-glucose meal, and an exercise bout. If true, these findings would invalidate the high-fat diet-fed rodent as a model for MTS or type 2 DM, because insulin resistance is not rapidly reversed by these treatments in patients. The purpose of this study was to determine whether diet-induced insulin resistance is, in fact, rapidly reversible. Incubation of muscles in vitro rapidly reversed insulin resistance induced by administration of triglycerides and heparin, but not by a high-fat diet. An overnight fast and a high-glucose meal were followed by a large increase in insulin-stimulated muscle glucose transport. However, these are adaptive responses, rather than reversals of insulin resistance, because they also occurred in muscles of insulin-sensitive, chow-fed control rats. Our results show that insulin resistance induced by high FFA, i.e., Randle glucose-fatty acid cycle, is Continue reading >>

Insulin And Insulin Resistance - The Ultimate Guide

Insulin And Insulin Resistance - The Ultimate Guide

Insulin is an important hormone that controls many processes in the body. However, problems with this hormone are at the heart of many modern health conditions. Sometimes our cells stop responding to insulin like they are supposed to. This condition is termed insulin resistance, and is incredibly common. In fact, a 2002 study showed that 32.2% of the US population may be insulin resistant (1). This number may rise to 70% in obese adult women and over 80% in some patient groups (2, 3). About a third of obese children and teenagers may also have insulin resistance (4). These numbers are scary, but the good news is that insulin resistance can be dramatically improved with simple lifestyle measures. This article explains what insulin resistance is, why you should care and how you can overcome it. Insulin is a hormone secreted by an organ called the pancreas. Its main role is to regulate the amount of nutrients circulating in the bloodstream. Although insulin is mostly implicated in blood sugar management, it also affects fat and protein metabolism. When we eat a meal that contains carbohydrates, the amount of blood sugar in the bloodstream increases. This is sensed by the cells in the pancreas, which then release insulin into the blood. Then insulin travels around the bloodstream, telling the body's cells that they should pick up sugar from the blood. This leads to reduced amounts of sugar in the blood, and puts it where it is intended to go, into the cells for use or storage. This is important, because high amounts of sugar in the blood can have toxic effects, causing severe harm and potentially leading to death if untreated. However, due to various reasons (discussed below), sometimes the cells stop responding to the insulin like they are supposed to. In other words, they 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 >>

A New Paradigm Of

A New Paradigm Of

What exactly is insulin resistance? One of insulin’s jobs is to help move glucose from the blood into the cells for energy. When blood glucose remains elevated despite normal or high levels of insulin, this is called insulin resistance. The cells are resisting insulin’s pleas to take up glucose. But why is this happening? What causes insulin resistance? The current paradigm of understanding insulin resistance is the ‘lock and key’ model. The hormone insulin acts upon a cell surface receptor to do its job. The insulin receptor is like a lock keeping the gates to the cell closed. Insulin is like the proper key. When inserted, the gate opens to let glucose from the blood inside the cell for energy. Once you remove the key (insulin), the gate closes back up and blood glucose can no longer enter the cell. During the phenomenon of insulin resistance, we imagine that the lock and key no longer fit together very well. The key (insulin) only partially opens the lock (receptor) and not very easily. Glucose cannot pass through the gate normally, and as a result, less gets into the cell. The blood glucose piles up outside the gate, becoming detectable as the clinical diagnosis of type 2 diabetes is made. Because the cell has less glucose inside, this has been described as a state of ‘internal starvation’. The body’s knee-jerk reaction is to increase insulin production. Since each key works efficiently, the body compensates by producing more keys than usual. This hyperinsulinemia ensures that enough glucose gets into the cells to meet its energy requirement. A nice, neat theory. Too bad it has no basis in reality. The problems with the ‘lock and key’ model First, is the problem the key (insulin), or the lock (insulin receptor)? It’s quite easy these days to deter 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 >>

Need Help With Insulin Resistance As A Result Of My Low Carb/vlc Diet. Anything Current?

Need Help With Insulin Resistance As A Result Of My Low Carb/vlc Diet. Anything Current?

I know there are other threads on this topic and I have read a lot of them. I just wonder if there is anything more current than this article from 2007 to help me understand this. Perhaps its still current and valid. Im unclear what to do exactly to reverse this, or do I even need to if its not "pathological". Summary: I am 5-8 pounds over-fat. 10-15 years of labs have all been good/very good for fasting Bg and insulin, until this recent one (the only one when I was low carb/vlc). My insulin was high at 9.00 on last fasting blood draw. Bg was 98 I have been eating high protein, high healthy fat, low carb or vlc. My current labs showed "pre-diabetes" 3 Foods to Remove from - The Fridge Forever Cut a bit of belly bloat each day, by avoiding these 3 foods nucific.com I got an at home glucometer. My Bg never goes too high but it doesn't recover either. Its stays around 100-111 after peaking at 123 or so. Oddly too is that every test is higher at 2 hours and even three than at one hour. Can somebody recommend one or two good resources for this issue. The frustration I'm having is that everything I read about insulin resistance says to "lower carb intake". That is what caused this issue it seems. Thank you. Edited to add: My A1C was not tested this time (arggg) although it was not optimal at all a year ago when it was tested and when my Fbg and insulin were way lower. A1C was 5.7 then. Thanks 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 >>

Carb Reloading

Carb Reloading

Id like to share with you my recent journey out of the low carb maze, which Ive been more or less stuck in since 2010. My initial launch into Paleo started off like most peoples as a 30 day reset 4 years ago. I fell for Robbs used car salesman pitch and gave it a shot. I felt so great and I liked it so much that its still going on today and now I even work for the guy! Imagine that! When I started this whole thing, I consciously decided that I wanted to try no starches or fruit for the 30 days, really only because I found it interesting (thanks Vilhjamur Stefansson) and wanted to see what would happen. Im curious that way. I was having amazing results at 30 days, so I extended it to 60. Then I planned on reintroducing starches and fruit, and including them regularly from then on forward. I tried but it didnt go so well. I was a little surprised. (I wish I was smart enough to turn that and then I got high song into something that would cleverly explain what I was going through every time I tried to bring the carbs back in, but I know my talents and rappin aint one.) Basically, trying to eat modest, normal amounts of fruits and starches sucked for me. It seemed to reverse all of the joy and warm fuzzy feelings from my initial Paleo high. Id experience a whole grab bag of symptoms: joint inflammation (I have some creaky worn out business from all the ballet and hypermobility plus carpal tunnel), 5lbs of instant water retention, wicked PMS and I mean every symptom there was, aaand weight gain- which was always hard to gauge with the stupid water retention, but when Id return to low carb and shed the water there was some undeniable extra weight. I wasnt in freak out mode about it I just thought, Boy, carbs Fing suck! At the time, it was still cool to think carbs Fing suck b Continue reading >>

Dear Mark: Does Eating A Low Carb Diet Cause Insulin Resistance?

Dear Mark: Does Eating A Low Carb Diet Cause Insulin Resistance?

157 Comments Despite all the success you might have had with the Primal way of life, doubts can still nag at you. Maybe it’s something you read, or something someone said to you, or a disapproving glance or offhand comment from a person you otherwise respect, but it’s pretty common when you’re doing something, like giving up grains, avoiding processed food, or eating animal fat, that challenges deeply-and-widely held beliefs about health and wellness. It doesn’t really even matter that you’re losing weight or seem to be thriving; you may still have questions. That’s healthy and smart, and it’s totally natural. A question I’ve been getting of late is the effect of reducing carb intake on insulin sensitivity. It’s often bandied about that going low carb is good for folks with insulin resistance, but it’s also said that low carb can worsen insulin resistance. Are both true and, if so, how do they all jibe together? That’s what the reader was wondering with this week’s question: Hi Mark, I’ve been Primal for a few months now and love it. Lowering my carbs and upping my animal fat helped me lose weight and gain tons of energy (not too shabby for a middle-aged guy!). However, I’m a little worried. I’ve heard that low carb diets can increase insulin resistance. Even though I’ve done well and feel great, should I be worried about insulin resistance? Do I need to increase my carb intake? I always thought low carb Primal was supposed to improve insulin function. Vince Going Primal usually does improve insulin sensitivity, both directly and in a roundabout way. It improves directly because you lose weight, you reduce your intake of inflammatory foods, you lower systemic inflammation (by getting some sun, smart exercise, omega-3s, and reducing or dea Continue reading >>

The Ketogenic Diet And Insulin Resistance

The Ketogenic Diet And Insulin Resistance

We recently touched on how you can use the ketogenic diet to control symptoms of diabetes such as elevated glucose and triglycerides. In this article, we examine research showing the impact that the ketogenic diet has on levels of the hormone insulin, a key regulator of blood sugar in the body. What is Insulin’s Role in the Body? Before we look at the research, we need to know our main players. Insulin is a protein-based hormone produced by beta-cells located in the pancreas. The pancreas, which is located under the stomach, also produces enzymes that aid with digestion. Insulin’s primary purpose is to regulate the metabolism of fats and carbohydrates. The digestive system breaks down carbohydrates, such as sugars and starches, into a molecule called glucose. This compound can be used by cells to produce energy through a process called cellular respiration. Insulin allows cells in the body absorb glucose, ultimately lowering levels of glucose in the blood stream. After a meal is consumed, blood glucose levels increase and the pancreas responds by releasing insulin into the blood. Insulin assists fat, liver, and muscle cells absorb glucose from the blood, resulting in lower levels of blood glucose. Insulin stimulates liver and muscle tissues to store excess glucose as a molecule called glycogen and also reduces glucose production by the liver. When blood sugar is low, the hormone glucagon (produced by alpha-cells in the pancreas) stimulate cells to break down glycogen into glucose that is subsequently released into the blood stream. In healthy people who do not have type II diabetes, these functions allow levels of blood glucose and insulin to stay in a normal range. What Is Insulin Resistance and Why Is It a Problem? Unfortunately, for many Americans and other peopl Continue reading >>

Physiologic Insulin Resistance

Physiologic Insulin Resistance

I'm hoping you can give me a simple response to a mess I'veapparently created in my own body. I've queried Petro Dobromylskyj,because it was his blog entry of October 2007 ( )that began to explain to me what was happening to my metabolism. Icontacted Dawn Tasher ( www.peelingbacktheonionlayers.com )because she was a strongly recommended nutritionist, and shesuggested I get in touch with Paul Jaminet, whose work I'd seen onthe internet. I've also had no response from him. My own doctor(s)don't seem to have answers. Like Peter, I am a veterinarian so amused to creative problem solving, often making difficult diagnoseson patients who are incapable of giving any history whatsoever ontheir health condition. So here's my story. I have been a lacto-vegetarian for 45 years.Added in eggs about ten years ago. About 13 years ago, my husbandembarked on the classic Atkins diet - as a vegetarian - to try tolose weight. After two days of eating extremely low carbs, he saidhe didn't care if he never lost an ounce on the diet because hefelt ten years younger and was dedicating himself to living a lowcarb lifestyle forever. (He did end up losing 35 pounds and keepingit off). "Ten years younger" sounded great to me so I did myhomework and joined in. I never needed to lose weight - at 5'4", myweight has fluctuated between 108 and 114 pounds since high school.So - I've been eating VERY low carb (probably less than 40 gramsper day), with adequate calories, largely from fats, to maintain myweight for about thirteen years, feeling great, and enjoying what Ieat. BUT - my fasting blood sugars have been consistently high(103-107 range) for the past several years when I've had my annualmedical check-up. My A1c has always been OK, so my doc alwaysshrugged her shoulders and we both casually figured Continue reading >>

Insulin Resistance Is Good? – T2d 7

Insulin Resistance Is Good? – T2d 7

Everybody says that insulin resistance is bad. Very bad. It’s the root cause of type 2 diabetes (T2D), and metabolic syndrome, isn’t it? So, if it is so bad, why do we all develop it in the first place? What’s the root cause? My friend Dr. Gary Fettke from Tasmania wrote an illuminating book called ‘Inversion’ where he describes how you can learn a lot from looking at things from another perspective. Invert (turn upside down) your perspective, and see how your horizons are immensely broadened. So let’s look at why we develop insulin resistance. Why is it good? Root Cause Analysis What is the root cause of insulin resistance? Some people say inflammation or oxidative stress or free radicals causes insulin resistance. Those are total cop-out answers. Inflammation is the body’s non-specific response to injury. But what causes the injury in the first place? That’s the real problem. The inflammation is only the body’s response to whatever is causing the injury. Think about it this way. Suppose we are battlefield surgeons. After decades on the job, we decide that blood is bad. After all, every time we see blood, bad things are happening. When we don’t see blood, bad things are not happening. It must be the blood that is dangerous. So, deciding that blood is what is killing people, we invent a machine to suction all the blood of people. Genius! The problem, of course, is what’s causing the bleeding, rather than the blood itself. Look for the root cause. Bleeding’s only the response, not the cause. Bleeding is a marker for disease. So is inflammation. Something causes bleeding, the body’s non specific response. Something causes inflammation, the body’s non specific response. Gunshots cause bleeding, knife wounds cause bleeding, and shrapnel causes bl Continue reading >>

Ketoadaptation And Physiological Insulin Resistance

Ketoadaptation And Physiological Insulin Resistance

This is where the magic happens. Rat pups, fed a flaxseed oil-based ketogenic diet from weaning onward – note the drop-off in ketones after 2 weeks (Likhodii et al., 2002): Patient history: these rats have been “low carb” their whole lives. Side note: flaxseed oil is very ketogenic! (Likhodii et al., 2000): Flaxseed oil-based ketogenic diet produced higher ketones than 48h fasting; the same can’t be said for butter or lard. PUFAs in general are more ketogenic than saturated fats in humans, too (eg, Fuehrlein et al., 2004): Crisco keto (adult rats) (Rho et al., 1999): At this point, please just note the stunning consistency in the drop-off of ketones. Experiment 1 & 2 (above) are adult rats; they went through a period of high carb chow dieting, unlike experiment 3 and the rats in the first study, who were weaned onto ketogenic diets. Still same phenomenon: ~few weeks after initiation of ketogenic diet = breakpoint; ketones decline. Ketoadaptation: why do ketone levels decline? This happened in both rat studies above, Phinney 1983, and in many “n=1” practitioners. Possible explanation 1 (ketoadaptation): rat milk is kind of like a low carb diet; high in fat, but not low enough in other stuff to be ketogenic. -Hooded seal milk is practically heavy cream: imagine the amount of suction pups must need to apply. Poor mom, that’s gotta hurt; fortunately, lactation only lasts 4 days. -Rat milk is super-high protein. Therefore, weaning to the flaxseed oil-based keto diet is what really initiates ketoadaptation… which seems to take 2-3 weeks (judging by the decline in ketones [this is explained further below]). Possible explanation 2 (physiological insulin resistance): free fatty acids released faster then they’re burned, accumulate in skeletal muscle, induce mil Continue reading >>

Does Long Term Ketosis Cause Insulin Resistance?

Does Long Term Ketosis Cause Insulin Resistance?

“It’s a snake.” “It’s a wall.” “It’s a rope.” “It’s a fan.” “It’s a tree.” “It’s insulin resistance.” I’ve always been fascinated by those describing a “new finding” in medicine. I am reminded of the story of 5 men who, never having seen an elephant before, were blindfolded and asked to describe what he discovered. However, each man was introduced to a different part of the elephant. Each of them had a dramatically different description of the elephant and each made a conclusion that was very different from the others. What is fascinating, is that we usually make our “blindfolded comparisons” to those things we have seen or about which we have some descriptive understanding. Observing and describing human physiology is much like examining an elephant while blindfolded for the first time. This week’s “blind-folded finding” is what has been interpreted by some as “insulin resistance” made worse by a ketogenic diet. Really? This perked my curiosity, because I’ve personally been following a low-carbohydrate/ketogenic diet for 10 years and have thousands of patients doing the same. To this day, I’ve never seen insulin resistance “get worse.” In fact, it gets better. Clinically, it seems to take about 18-24 months to improve, but, it usually gets better. THE QUESTION – I’ve had three people from around the world contact me this week and ask why, after being on a ketogenic diet and “in ketosis,” they suddenly get a notably large blood glucose spike when they cheat. By notably large, I mean that their blood sugars rise to over 200 mg/dl within 2 hours of a carbohydrate containing meal. Now, they admit to rapid glucose recovery within an hour or two, and their hemoglobin A1c levels are subjectively normal (l Continue reading >>

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