Carbs Too Low = Insulin Resistance? - Paul Jaminet : Low-carb War Zone Forum : Active Low-carber Forums
Carbs Too Low = Insulin Resistance? - Paul Jaminet Carbs Too Low = Insulin Resistance? - Paul Jaminet I've just started reading Paul Jaminet's book "Perfect Health Diet".........He is generally low carb (with "safe" starches), but the statement he made that really caught my attention (below) "You might think that the answer is to consume very few carbs. But this would be naive! It turns out that on low-carb diets, much of the body becomes insulin resistant meaning that it doesnt respond to insulin signals and so doesnt take in glucose after meals. This happens so that glucose will be directed to the liver, where it can be stored in glycogen and released later for use by the brain. This physiological insulin resistance is a protective response of the body that assures that the brain gets the benefit of a limited supply of glucose. But it has a paradoxical effect: because the rest of the body is refusing to take up glucose and the liver takes it up slowly, a meal of carbohydrates is followed by higher postprandial blood glucose levels in low-carb dieters than in high-carb dieters. In short, low-carb dieting can increase the risk of postprandial hyper -glycemia." Jaminet, Paul; Jaminet, Shou-Ching (2012-12-11). Perfect Health Diet: Regain Health and Lose Weight by Eating the Way You Were Meant to Eat (Kindle Locations 1659-1666). Scribner. Kindle Edition. Can somebody please explain this! I am keeping my carbs VERY low (under 10 grams a day)..........Is this possibly too low? Is there indeed a benefit to increasing them a bit? Can lowering them too much backfire? Well, what he says is very much in line with what Jenny Ruhl writes about in her book about low carb diets, Diet 101. She goes into why you need to re-carb for several days before an insulin resistance test in or Continue reading >>
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 >>
Steve Phinney Low-carb Preserves Glycogen Better Than High Carb
I can ride continuously for three hours and go 60 miles without any hunger or food cravings or drop off in performance. And I ride as well in the last 20 miles coming home as I do going out. Steve Phinney, can you tell us who you are? Im a medical doctor and have my training in internal medicine. Early in my career developed an interest in nutrition and got a PhD in nutritional biochemistry. That was 30 odd years ago, and since then my primary interests have been in weight management, ie, obesity, exercise and the human economy of the various fats we either put in our mouths or make in our bodies. Youre a star in a Canadian documentary called My Big Fat Diet, because you helped a whole group change their eating habits to reduce insulin resistance and lose a lot of weight. youre the co-author of a book about the Atkins Diet thats been updated by you and two other clinician scientists. Partially correct. I had a bit part in My Big Fat Diet. The star is Dr. James Wortman, a Canadian physician. And yes, Im a coauthor of the updated, new Atkins book which came out last March. Youre also in the process of creating a new book thats more technical about high fat diets. Thats correct. Dr. Volek, whos one of the coauthors on the Atkins book felt, like me, that we needed to offer more information for people who are interested in the medical side of low-carb diets, with a more detailed explanation of the workings of the human body when carbohydrates are restricted. Its readable by both a health care professional and an interested, educated lay person. Im physically active. Though after high school, Ive not been involved in competition athletics. I stay between 25 and 50 grams of carbohydrate a day. I eat a moderate amount of protein. Its not a high-protein diet. I eat 2800 calorie Continue reading >>
Beyond Weight Loss: A Review Of The Therapeutic Uses Of Very-low-carbohydrate (ketogenic) Diets
European Journal of Clinical Nutrition volume 67, pages 789796 (2013) Very-low-carbohydrate diets or ketogenic diets have been in use since the 1920s as a therapy for epilepsy and can, in some cases, completely remove the need for medication. From the 1960s onwards they have become widely known as one of the most common methods for obesity treatment. Recent work over the last decade or so has provided evidence of the therapeutic potential of ketogenic diets in many pathological conditions, such as diabetes, polycystic ovary syndrome, acne, neurological diseases, cancer and the amelioration of respiratory and cardiovascular disease risk factors. The possibility that modifying food intake can be useful for reducing or eliminating pharmaceutical methods of treatment, which are often lifelong with significant side effects, calls for serious investigation. This review revisits the meaning of physiological ketosis in the light of this evidence and considers possible mechanisms for the therapeutic actions of the ketogenic diet on different diseases. The present review also questions whether there are still some preconceived ideas about ketogenic diets, which may be presenting unnecessary barriers to their use as therapeutic tools in the physicians hand. During recent years, an increasing amount of evidence has accumulated in the literature, suggesting that very-low-carbohydrate ketogenic diets (VLCKD) could have a therapeutic role in numerous diseases. The use of VLCKD in treating epilepsy has been well established for many decades and these diets have become even more widely known, as they became popular in the 1970s for weight lossespecially as the Atkins Diet. 1 More recently, the therapeutic use of ketogenic diets in other diseases has been studied with positive resultsit Continue reading >>
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 >>
Mark Sisson: Fat Adaptation Is The Normal Metabolic State
Fitness Disclaimer: The information contained in this site is for educational purposes only. Vigorous high-intensity exercise is not safe or suitable for everyone. You should consult a physician before beginning a new diet or exercise program and discontinue exercise immediately and consult your physician if you experience pain, dizziness, or discomfort. The results, if any, from the exercises may vary from person-to-person. Engaging in any exercise or fitness program involves the risk of injury. Mercola.com or our panel of fitness experts shall not be liable for any claims for injuries or damages resulting from or connected with the use of this site. Specific questions about your fitness condition cannot be answered without first establishing a trainer-client relationship. Fat-adaptation is the normal, preferred metabolic state of the human body. Sugar-dependency is an abnormal metabolic state that inevitably leads to insulin resistance and chronic disease Once you are fat-adapted, your body can effectively burn stored fat for energy throughout the day, and can effectively oxidize dietary fat for energy. Hence less fat will be stored in adipose tissue Fat adapted people essentially reprogram their bodies, allowing genes associated with lipid metabolism to be upregulated If you can handle exercising without having to carb-load, youre probably fat-adapted. If you can work out effectively in a fasted state, youre definitely fat-adapted When describing someone that has successfully made the transition to the Primal way of eating I often refer to them as "fat-adapted" or as "fat-burning beasts". But what exactly does it mean to be "fat-adapted"? How can you tell if you're fat-adapted or still a "sugar-burner"? I get these and related questions fairly often, so I thought I' Continue reading >>
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 >>
Protein Over-consumption In Ketogenic Diets Explained
Protein over-consumption is one of the main issues discussed at the Ketogains Group everyday. People are always reading, hearing and/or misunderstanding that eating protein will cause gluconeogenesis and kick you out of ketosis. Tyler Cartwright splendidly refuted the claim that protein supply activates GNG in this post, I recommend you check it out. So, if protein consumption doesn’t massively increase gluconeogenesis, then two questions remain: Why doesn’t ketogains recommend you eat tons of protein? Why does protein over-consumption lower ketones? Ketogains Protein Recommendation Of these questions, the first is easier to answer. The reason we don’t advocate the consumption of tons of protein is because beyond a certain point -arguably somewhere between .8g and 1.2g per pound of lean mass(lbm)- there’s just no benefit. Protein also carries a couple of minor inconveniences: It tends to be expensive and it can cause indigestion. If there were no other reason not to over-consume protein, this would simply be enough. There is also a minor debate over whether or not protein over-consumption prolongs the adaptation phase (irrelevant if you are already adapted). Also some people argue that it may be sub-optimal for performance, but these are secondary to the previous points: It’s unnecessary to eat more, so there’s no reason to recommend over-consumption. Protein and lower ketones The second gets a bit more complicated, and touches on something that Tyler just hinted at in his article. My soapbox is diabetes, and to a lesser extent, obesity… Diabetes has a lot to tell us about blood sugar control and precisely how and why certain food items impact blood glucose. In type one diabetes, the population of beta cells in the pancreas mostly dies, leaving the alpha c Continue reading >>
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
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 >>
Does Your Thyroid Need Dietary Carbohydrates?
Thyroid hormones have an important role in regulating metabolic rate, and that’s why they have emerged front and center as a common concern associated with nutritional ketosis among some internet bloggers. There’s no question that when some people adopt a low-carbohydrate lifestyle, their thyroid hormone levels may change. Several factors may contribute to the thyroid response. For example, eating fewer calories than you expend, causing weight loss, prompts the body to reduce thyroid function to slow its metabolism. That’s because the body interprets any form of energy restriction from any cause as a sign of famine, leading it to reduce metabolism by 5-15% to conserve energy stores. Second, even when energy is not restricted, a ketogenic diet is associated with sharply reduced blood levels of active thyroid hormone. In this case, even when energy is plentiful and body weight stable, either the low intake of carbs or the presence of ketones reduces circulating concentrations of active thyroid hormone. To the casual observer, this reduction in active thyroid hormone (called T3) has been taken as evidence that carbohydrate restriction impairs thyroid function. Some have opined that carb restriction should never be maintained below 100 grams per day in order to prevent this effect. Others advocate that people on a low-carbohydrate, high fat (LCHF) diet take intermittent “holidays” from carb restriction to boost thyroid function back up to “normal.” An alternative explanation for these changes in thyroid hormones when one is weight stable on a LCHF diet is that the body becomes more responsive to these hormones due to beneficial changes in cell structure and function when in nutritional ketosis. As a result, it can function normally at lower T3 levels. Put anot Continue reading >>
Increased Insulin Resistance With A Low Carb Diet?
Diabetes Forum The Global Diabetes Community Find support, ask questions and share your experiences. Join the community Increased Insulin Resistance with a low carb diet? Bebo321 Family member Well-Known Member @azure @Brunneria @tim2000s , I would be interested to hear your thoughts on an observation of increased insulin resistance with a very low carb/keto diet. I was discussing this topic recently with somebody with T1D (we tried a food fast together over a number of days) They noticed that coming back out of the fast, their insulin requirements had increased fairly significantly in order to manage any carb they ate (the increased requirements only lasted a few days). Interestingly, their basal had remained exactly the same throughout the fast however and blood glucose levels had remained level. This would suggest that their 'insulin resistance' hadn't actually changed at all. What we considered had perhaps happened was that the body had become so effective at burning ketones and generating its own glucose requirements (gluconeogenesis), that once carbs were re-introduced, the body was fairly 'ambivalent' to it - after all, it had everything it needed to fuel itself perfectly well up until that point. Without cells calling out for a top up of glucose, more insulin would be required in order to be effective at taking the glucose out of the bloodstream. This was a temporary effect and therefore perhaps different to insulin resistance created through the build up of fat deposits. Anyway, I thought I would relay this to you (and anyone who might have their own experience to add). Perhaps it is misleading to think of the body's adaptation to a low carb diet as becoming 'insulin resistant' and it might be better instead to think of it becoming 'fat complient' It's referre Continue reading >>
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 >>
Insulin Sensitivity And Glucose Tolerance Are Altered By Maintenance On A Ketogenic Diet
The ketogenic diet (KD) is a low-carbohydrate, high-fat diet that is used for a variety of health-related effects. This type of diet is effective at suppressing seizure activity in children with refractory epilepsy (1) and has perhaps more commonly been implemented as a dietary strategy by which weight maintenance or weight loss is the desired outcome. It has been demonstrated that restriction of dietary carbohydrates results in positive effects on cardiovascular parameters. Consuming this type of diet favorably affects body adiposity and improves features of metabolic syndrome in humans (2,3,4,5,6). Although studies evaluating the efficacy and metabolic effects of KDs have increased in recent years, the effects of macronutrient-controlled diets remain controversial in the literature. Insulin has potent short-term and long-term effects on energy intake and glucose homeostasis. In the short term, insulin release is cephalic; the brain initiates insulin secretion by directing messages through the vagus nerves to the pancreas as opposed to direct pancreatic stimulation of insulin-secreting cells. Cephalic insulin is most readily observed at the onset of a meal and consists of a short burst of insulin that is preabsorptive with regard to the ingested food. After consumption of a meal, insulin secretion increases and is sustained, because one of insulin’s roles is to prepare the body for the increase in glucose that accompanies food intake and to control the increased levels and use of glucose (7). In the long term, insulin’s role as an adiposity signal is well known, with increased plasma insulin levels resulting from increased body weight. Together, the short- and long-term effects of insulin allow for proper glucose homeostasis and assist in the regulation of body wei Continue reading >>
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 >>