I have chosen a ketogenic low carbohydrate high fat (KLCHF) diet to improve the management of my type 1 diabetes (T1D). In addition to being easier and safer (less hypoglycemia) to manage blood glucose, I think it will maximize my chance of avoiding both microvascular and macrovascular diabetic complications. The simple fact is that diabetes is a state of carbohydrate intolerance. The more dietary carbohydrate one consumes, the more difficult it is to manage diabetes despite any number of medications. This is my opinion based on both my reading of the medical literature and my direct experience using the KLCHF diet since Feb. 8, 2012. The purpose of this blog post is to describe the ketogenic aspect of the KLCHF diet especially in the context of managing diabetes since many people including some physicians confuse nutritional ketosis with diabetic ketoacidosis (DKA). Because of this confusion, many persons with diabetes may be afraid to consider this approach or be warned by their diabetes care team to avoid it. As often happens in medicine and science, new ideas are usually rejected out of hand without taking careful consideration first. Interestingly, the KLCHF diet is not new, but just rediscovered since 1972 when Robert C. Atkins, MD published “Dr. Atkins’ Diet Revolution.” Turns out the KLCHF diet appears in the medical textbook “Principles and Practice of Medicine” by Sir William Osler, MD in the early 1920’s as a treatment for diabetes before the discovery of insulin. Dr. Osler credited Elliot P. Joslin, MD (the first diabetes specialist in the US) with the diet. Once insulin was discovered and production ramped up by Eli Lilly and Company, the KLCHF diet was essentially abandoned as insulin was considered the “cure” so why should diabetics be expected to eat differently than everyone else.
What Are Ketones and When Do We Make Them?
Ketones are water soluble molecules made from fat to provide our large brains with energy when dietary sources of glucose (carbohydrates) are scarce.
The chemical formulas for the three ketones: acetoacetate, beta-hydroxybutyrate, and acetone are shown above. Note both acetoacetate and beta-hydroxybutyrate each have 4 carbon (C) atoms. Fat is stored as triglycerides in adipose tissue. The figure below shows a triglyceride with three fatty acids labeled 1, 2, and 3. The red circle surrounds fatty acid #1, palmitic acid with 16 carbon atoms. The blue circle surrounds glycerol with 3 carbon atoms. The name triglyceride should now make sense. The liver and kidney can make glucose, a 6 carbon molecule, using two glycerols, as well as from amino acids (from protein), lactate, pyruvate, and acetone in a process called gluconeogenesis. Just to be clear, glucose is vital for our existence, but we are well equipped to make it from five different sources and thus we do not need to consume dietary carbohydrate to make glucose. There will not be a quiz at the end, but I am simply trying to demystify the clever biochemistry that allows for human existence.
The figure below shows a medium-chain fatty acid, capric acid, with 10 carbon atoms and two red ovals around 4 carbon portions of the fatty acid from which ketones can be made.
Acetoacetate and beta-hydroxybutyrate are made by the liver under the signal of low insulin levels when dietary carbohydrates are either low or absent. Most of the acetoacetate is converted to beta-hydroxybutyrate in the liver. Once released into the blood, the concentration of beta-hydroxybutyrate is about three times that of acetoacetate. When these two ketones arrive to the tissues that can use them (principally brain, heart, kidney, and muscle) beta-hydroxybutyrate is converted back to acetoacetate in the mitochondria for oxidization to form ATP, the universal cellular energy. Up to one third of acetoacetate can be converted to acetone and anywhere from one fourth to two thirds of acetone can be converted to glucose.
Why Do We Make Ketones And What If We Couldn’t Make Them?
Let’s say our hunter gatherer ancestors have difficulty locating edible plants or animals for several weeks. Would the human race become extinct for a temporary lack of food? The human body does have fuel reserves for times like this as shown in Table 1 below.
Table 1 from Starvation, by George F. Cahill, Jr.
As you can see, the vast majority of our energy reserves are stored in fat. Our liver and muscles store a limited supply (1-2 days) of glucose in the form of glycogen. As mentioned above, our liver has the ability to make glucose from amino acids from the normal breakdown of protein in muscle. But humans and animals do not appear to store protein in muscle or in any other organ for storage’s sake alone. Thus if amino acids were the major source of glucose and we could not make ketones, we would be forced to cannibalize our muscle and organ proteins to make glucose. This would limit our ability to survive to at most a few weeks. Contrast that with our ability to utilize fat which is in greater quantity and is expendable without dire consequences. But there’s one problem; whereas most tissues can adapt to using fatty acids as their sole source of energy, the majority of fatty acids are too large to cross the blood-brain barrier to supply our brain. Our large brain which consumes about 600 kcal/day would be entirely dependent on glucose and thus ultimately we would be forced to cannibalize our vital proteins. This is where ketones come to the rescue. Ketones can be made in abundance from our expendable fat, are small enough to cross the blood-brain barrier, and are readily used as energy by the brain. Ketones thus spare the need to cannibalize our vital organ proteins to make glucose and extend our ability to survive without food for several months, not weeks. Keep in mind that the details of ketone metabolism was discovered by studying obese persons undergoing therapeutic fasting conducted by George Cahill, Jr. and his many talented colleagues (e.g. Oliver E. Owen) in the early 1960’s at Harvard Medical School. The figure below shows urinary nitrogen excretion in a 49 yo male who fasted for 39 days.
Ketone Bodies as a Fuel for the Brain during Starvation
Urinary nitrogen excretion on Day 1 of the fast was 16.2 grams (equivalent to 102 grams of protein loss/day), but it steadily decreases during the fast due to the increase in ketone production which replaces glucose as a fuel. By Day 39 of the fast, urinary nitrogen excretion had fallen and leveled off at 4 grams/day (equivalent to 25 grams of protein loss/day). Thus during each day of a fast vital organ proteins are lost, but ketone production from fat extends survival from 2-3 weeks to about 2 months in lean persons, or longer in obese persons. Interestingly, the reduction in urinary urea and increase in urinary ammonia was due to the increasing contribution of gluconeogenesis by the kidney. By the end of the fast, 55% of glucose was produced by the liver whereas 45% of glucose from amino acids (mainly alanine & glutamine), lactate, pyruvate, glycerol, and acetone (study here).
Therapeutic Fasting as a Therapy for Diabetes & Obesity
Since I’ve noticed that fasting has become “in vogue” on the internet lately and I have just reviewed the physiologic adaptations in response to starvation above, I thought I should take this opportunity to caution my readers about prolonged fasting.
‘‘Therapeutic fasting’’ in humans first appeared for the treatment of diabetes and was used from 1913 until the first use of insulin in 1922. Prolonged fasting became a therapy for obesity in the 1960’s, but it was later recognized to result in some unexpected deaths. In a review published in 2012 titled “A History of Modern Research into Fasting, Starvation, and Inanition,” the authors note that “Spencer (1968) also reported the deaths of two patients due to heart failure while they were undergoing therapeutic starvation at 3 and 8 weeks of total starvation, respectively.” Other causes of death included lactic acidosis, cardiac arrhythmias with prolonged QT syndrome, small bowel obstruction with complications, renal failure, and the refeeding syndrome. Non-fatal complications included electrolyte abnormalities, severe orthostatic hypotension, severe anemia, gouty arthritis, kidney stones, amenorrhea, alopecia, parotitis, polyneuritis, and vitamin deficiency. “These observed deaths occurred despite patients having huge fat stores at the time of their deaths. Therapeutic starvation was finally stigmatized as an unsafe procedure exposing the patient to an undue risk of physical danger.”
In a future blog post, I’ll review other fasting regimens e.g. alternate day fasting, one week fasts several times a year, The 5:2 Fast Diet, and others regarding their safety and efficacy for the treatment of diabetes and obesity. Until then I would caution anyone taking diabetic medications or insulin to discuss any fasting plans with their physician before starting a fast. I think fasting is not necessary to control diabetes and/or to lose excess body fat. Anyone choosing to fast should be aware of the consequences and risks of doing so.
How Does The KLCHF Diet Work For Diabetes & Obesity?
You don’t need to fast or starve to make ketones, control diabetes, or lose excess body fat. Ketones are normally produced by the liver anytime dietary intake of carbohydrates are restricted and is referred to as ketogenesis. Ketosis due to a KLCHF diet is called nutritional ketosis, a term coined by Dr. Stephen Phinney (others sometimes call it dietary ketosis). A low level of insulin is required to enhance ketone production and fat & ketone burning (oxidation). Because dietary carbohydrate is the strongest stimulus of insulin secretion, a low dietary carbohydrate intake results in a low level of insulin. Dietary protein stimulates insulin secretion as well, but to a lesser extent (and dietary fat even less), thus a moderate dietary protein intake combined with a low carbohydrate intake will facilitate low insulin levels and thus nutritional ketosis. Also, keep in mind that the body has zero requirement for dietary carbohydrate, but dietary protein and fat are essential for life. Thus the KLCHF diet minimizes, but does not totally eliminate, the non-essential dietary carbohydrate to which the person with diabetes is intolerant. Adequate dietary protein and energy intake maintains vital organ and muscle proteins. The KLCHF diet also reduces appetite in most which naturally allows energy intake to be appropriate to shed any excess body fat. To put it another way, high insulin levels are a signal to store fat while low insulin levels lead to appropriate fat storage after meals and fat release after meals. Even when dietary carbohydrate is low, dietary protein adequate, and nutritional ketosis is achieved, eating excess dietary fat beyond appetite can prevent weight loss in overweight/obese persons.
How about the person with type 1 diabetes (T1D) who does not make insulin? They need to inject insulin to “cover” dietary carbohydrate (and protein). It takes a lot more insulin to “cover” dietary carbohydrate (which we don’t need in our diet) than to “cover” dietary protein (which we can’t live without). Thus, the person with T1D who adopts the KLCHF diet will need to lower their insulin doses (and possibly other medications, e.g. those for high blood pressure) and this will result in the same signal to the liver to make ketones and burn fat and ketones. The same cautions would apply to persons with type 2 diabetes (T2D). So speak with your physician before making any changes. I’ll be doing a future blog post on DKA, but for now know that a well-formulated KLCHF diet will not cause DKA. DKA is caused by a lack of insulin, not a lack of dietary carbohydrates.
As explained in my blog post #3, reducing dietary carbohydrate and insulin greatly improves blood glucose variability and thus facilitates lowering blood glucose toward normal. Also explained in that post is the fact that exercise improves insulin sensitivity and allows for a further reduction in insulin doses and/or non-insulin medications in T1D & T2D. Another potential benefit of nutritional ketosis is a reduction in symptoms of hypoglycemia due to brain ketone utilization. As explained in my blog post #7, there is no way to distinguish whether lack of symptoms of hypoglycemia is due to brain ketone utilization versus hypoglycemia unawareness which is potentially dangerous. Thus, care must be taken to avoid hypoglycemia. I’ll be doing a future blog post on hypoglycemia to explore this topic further.
Nutritional Ketosis & The Well-Formulated KLCHF Diet
Nutritional ketosis results from following a well-formulated KLCHF diet usually containing less than 50 grams of total carbohydrate per day. Some athletes (me included) will be able to eat more than 50 grams/day particularly if most of those 50 grams come from non-starchy vegetables, low sugar fruit (berries), and nut & seeds with a high fiber content. What are some of the features of a well-formulated KLCHF diet? Focusing on whole nutrient-dense unprocessed foods is the most important in my opinion. By doing this, one avoids the most offensive processed foods: grains, sugars, and vegetable (seed) oils the later of which are high in polyunsaturated fats. Although a small amount of polyunsaturated fats are essential, most of the fats on a KLCHF diet should be both saturated and mono-unsaturated coming from animal fats, nuts & seeds, avocados, and olive & coconut oils primarily. A source of omega-3 fatty acids (EPA and DHA) & vitamin D is important as well. For me, salmon and grass-fed beef heart, liver, and kidney meet my needs, but there are other sources as well. In general, too little dietary protein leads to vital organ and muscle protein loss while excessive dietary protein can prevent ketone formation. Too much dietary carbohydrate will also prevent nutritional ketosis. There is no such thing as too little dietary carbohydrate. Sometimes it needs to be severely restricted due to severe insulin resistance more commonly in T2D. In insulin sensitive T1D, the dietary carbohydrate in non-starchy vegetables, nuts & seeds, low sugar fruit, avocado, usually does not interfere with blood glucose management and these foods provide beneficial micronutrients, protein, fat, fiber, and anti-oxidants. Dietary fat is adjusted up or down to achieve the desired body composition (degree of leanness) and has little effect on insulin doses.
Because low insulin levels tell the kidneys to excrete more salt and water, a well-formulated KLCHF diet must have adequate salt and likely more water than most are accustomed to drinking. These few stipulations will address the most common symptoms (constipation, headache, dizziness on standing, muscle cramps) that result from a less than well-formulated KLCHF diet.
Diet Terminology
For those familiar with Richard K. Bernstein, MD, a pioneer in the use of the low carbohydrate diet for diabetes, he recommends a low carbohydrate high protein diet. In chapter 11 of his book “Dr. Berstein’s Diabetes Solution,” (see the Book page above for a link) in the section titled “Protein,” he states “In order to maintain muscle mass, most people should consume at least 1-1.2 grams of protein per kilogram of ideal body weight. Athletes will require considerably more, as will growing children.”
As I stated in my blog post #9, I consume 1.4 grams protein/kg body weight/day and yet I call my diet a ketogenic low carbohydrate high fat (KLCHF) diet. I do this simply because the majority of my caloric intake comes from fat (75%), the least amount from carbohydrate (8%), and protein intake (17%) falls in the middle.
Drs. Phinney and Volek in their book “The Art and Science of Low Carbohydrate Living” (see the Book page above for a link) recommend 1.5-2.0 grams protein/kg body weight/day, although I have heard them say 1-1.5 g/kg/d during lectures and interviews, but either way, they call their protein recommendation “moderate.” So what’s the difference? I think it is just semantics. The words low, moderate, and high are just not specific enough and different people will assign different meanings to them.
It’s probably best to use the numbers as a starting place and then adjust to accomplish your goals.
Ketones Can Be Measured At Home
As an aside, all three ketones can be measured at home if needed: acetoacetate in the urine, beta-hydroxybutyrate in the blood, and acetone in the breath. Urine acetoacetate can be measured inexpensively using Ketostix. In some individuals, their kidneys become better at reabsorbing acetoacetate such that the urine test strip reading can be low or negative even when the person is in nutritional ketosis (called a false negative test result). Blood ketones can be measured using home meters as well, Precision Xtra by Abbott and Nova Max Plus by Nova Diabetes Care. Both meters measure beta-hydroxybutyrate (BHB) in millimoles per liter or mM which stands for millimolar. I used the Precision Xtra for all of my measurements in blog post #6. According to Drs. Stephen Phinney and Jeff Volek, in “The Art and Science of Low Carbohydrate Living,” blood BHB levels generally fall in the range of 0.5 to 3 mM during nutritional ketosis. The strips are fairly expensive; the best price I found was at Universal Drug Store. Finally, breath acetone can be measured with a reusable device called Ketonix. The Ketonix device was developed by an engineer, Michel Lundell, who uses the KLCHF diet to control his epilepsy. As way of disclosure, I met Michel on the 2015 Low Carb Cruise and he kindly gave all of the speakers on the cruise one of his Ketonix devices. He has not paid me to advertise his device. I have used the Ketonix breath acetone device many times, most days of the week, since June 2, 2015 mainly because I have it. In blog post #6, I showed by blood beta-hydroxybutyrate (BHB) results and concluded that measuring blood ketones was not helpful to me. The Ketonix device is easy to use. Michel told me he purchases the acetone detector from another company. Hopefully they have verified its accuracy. As far as I know, Michel did not independently test the Ketonix device for accuracy against known samples containing acetone, but I could be wrong about that. I can tell you that it is precise. Accurate and precise are different measures. Precise means I get almost the exact same readings if I test repeatedly several minutes apart (allowing it to equilibrate). Michel also told me that Ketonix will detect methane and alcohol. For me, these are not a problem since I don’t consume beans, grains, or alcohol. Here are my Ketonix reading since June 2, 2015.
This study did show a good correlation between blood BHB and breath acetone. The authors used a very accurate measure of breath acetone called gas chromatography-mass spectrometry. The results are shown below.
I understand that other companies are developing breath acetone devices and will be seeking FDA approval.
Whether or not ketones in any form need to be measured depends on the reason for adopting a ketogenic diet. Certainly, if you think you need to be on a KLCHF diet, knowing that you are generating ketones can be reassuring.
Will The KLCHF Diet Become Standard of Care for Diabetes?
There are definite signs that the low carbohydrate approach is taking hold and I feel that eventually it will become the standard of care for diabetes. Read this blog post titled “Nutrition Revolution: The End of the High Carbohydrates Era for Type 2 Diabetes Prevention and Management” by Osama Hamdy, MD, Medical Director, Obesity Clinical Program, Director of Inpatient Diabetes Management at Joslin Diabetes Center. Admittedly, the Joslin Clinic is not specifically recommending the very low carbohydrate intake that constitutes the KLCHF diet. According to Dr. Hamdy, “Since 2005, the Joslin Clinic has been recommending a reduction of carbohydrate intake to 40-45% of the total daily calories and avoidance of food that rank high on the glycemic index of carbohydrates.” He poignantly states that, “It is now clear that a major mistake was made in the 1970’s in recommending an increase in carbohydrates to >40% of the total daily calories. This era should come to an end if we seriously want to reduce the obesity and type 2 diabetes epidemics.”
My Blood Glucose and Insulin Dose Results including Last 30 Days
My Blood Glucose Variability including Last 30 Days
My Blood Glucose and Insulin Doses Last 30 Days
That is all for today.
Ketogenic Diabetic Athlete 
Dr. Runyan very interesting!
Do you know if these dangers of “deaths of two patients due to heart failure while they were undergoing therapeutic starvation at 3 and 8 weeks of total starvation, respectively.” Other causes of death included lactic acidosis, cardiac arrhythmias with prolonged QT syndrome, small bowel obstruction with complications, renal failure, and the refeeding syndrome. Non-fatal complications included electrolyte abnormalities, severe orthostatic hypotension, severe anemia, gouty arthritis, kidney stones, amenorrhea, alopecia, parotitis, polyneuritis, and vitamin deficiency” are more dangerous than those associated with i) medication ii) bariatric surgery or and are more common than those associated with iii) a VLCHF diet combined with Intermittent Fasting and/or iv) the Standardard American diet. Do you expect to make that comparison in a future post.
Thank you!
Sylvain M
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Yes, I was planning to address those issues in the fasting blog post. My main point was that I have read others boasting the benefits of fasting, but not mentioning that there are risks, some fatal, and that protein loss does occur especially at the beginning of a fast. There just needs to be a balanced presentation of fasting. Yes, weight loss medications, bariatric surgery, or continuing the same old Standard American Diet have risks too and I am no fan of those either. As with all medical therapies, persons need to understand the benefits and risks to make an informed decision.
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Interesting read. Lots of information to digest. (FYI it’s actually spelled “lose” excess fat, not loose.. ie., “if I lose fat my clothes will get loose”.)
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Thanks for proofreading, fixed two occurrences.
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Just wondering if your approach applies to very young infants , toddlers and young developing children up till the age of twelve years?..
Would like your views on his please.
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I have no experience with it, but my understanding is that yes it works for children as well. The neurologists at Johns Hopkins, Eric Kosoff, MD, http://www.hopkinschildrens.org/eric-kossoff-md.aspx
use a much stricter version of the ketogenic diet for seizures (90% fat, 8% protein) in small children, so a ketogenic diet for diabetes would be doable. Don’t know where to refer you to in Australia, but I bet there are neurology clinics that use the ketogenic diet who might be able to help.
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Nice post, thanks!
Just a small comment so far regarding picture #4 and the corresponding text: As far as I remember, ketogenesis starts with acetyl groups coming from beta oxidation, i.e. 2 carbon pieces glued together to form ketone bodies. So they are not directly chopped off as 4-C molecules from fatty acids. In fact Ac-CoA level plays a very important rate setting role in both ketogenesis and gluconeogenesis.
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You’re right. The corresponding text was “4 carbon portions of the fatty acid from which ketones can be made.” That was not meant to mean “directly chopped off.” There are quite a few steps in the biochemistry, but most people are not interested in each step so I was trying to summarize and mainly demystify the process. The main point was to show that ketone production and utilization are not abnormal and/or dangerous processes. In fact, it has a lot to do with why humans have survived for as long as we have.
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Very interesting, but there is something that I do not get. Why at time of diagnosis of T1D the doctors consider a “bad/dangerous” thing to have ketones in the urine or blood. And if i understand correctly your whole diet is based on creating ketones from fat, which is encouraged here. Thanks, Svet.
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Svet, at the time of diagnosis of T1D, the patient is insulin deficit. A low insulin level is a stimulus for ketone production by the liver. In untreated T1D, the insulin level can be so low that ketone production far exceeds ketone utilization resulting in ketoacidosis (ketones are organic acids). It is the ketoacidosis that is “bad/dangerous.” During ketoacidosis, blood ketones levels are in the range of 15-25 mM whereas in nutritional ketosis they range from 0.5-3 mM. The ketogenic diet works for T1D by limiting the dietary carbohydrates that are non-essential, lead to wide fluctuations in blood glucose, and requires additional injected insulin which also adds to blood glucose variability. In addition, the blood ketones during nutritional ketosis may, in my opinion, partially protect the brain during hypoglycemia. The difference between “good” ketones and “bad/dangerous” ketones is really a matter of the quantity of ketones and the cause of the ketosis, nutritional = “good” vs insulin deficiency = “bad/dangerous.” I hope that clarifies it for you.
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Dr. Runyan,
Thank you for your extremely informative blog posts. As a newly diagnosed T1D patient (March 2015), and one who is very interested in keeping and increasing physical performance in physical activity, this site has been invaluable. Over the past week I had a run in with what I thought at the time was mild DKA. However, my blood ketone meter told me I was between 1.2-1.5 mM, which is not a completely abnormal number for me since I began a ketogenic diet in September 2015. I essentially did a VERY strenuous workout (deadlifts w/high volume of accessory exercises) while in a mostly fasted state (~13 or 14 hours). I had about 250 calories post-workout, with some dextrose and whey protein. I went home and began feeling very weak, tingly legs/toes, and felt somewhat nauseated. I ended up vomiting and having abdominal pain very severely, but upon vomiting began to tolerate fluids and some glucose tablets. My blood sugar was a very dynamic for the next 16+ hours (very high – very low), and I saw that my blood ketone levels were dropping to near 0.1 mM. I’m curious to know whether or not you would think DKA or hyperkalemia in this moment? I should also state that I am a physician assistant student currently, and we’re going over this in our clinical science class coming up in the summer, and I’d like to have a better understanding of what happened during this time, and any input would be appreciated. I’ve had bouts like this in the past (before being diagnosed T1D), and am hoping if I can understand the physiology better, I can better take care of myself before and after heavy training sessions.
Thanks again for the great learning material! I’m doing my best to put it to good use.
– Luke
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Luke, obviously I can’t make a diagnosis here, the best I could do is make a guess. My guess is you had neither DKA nor hyperkalemia, but more likely you developed hypoglycemia during the VERY intense workout while fasting. The post-workout dextrose and whey protein was appropriate but just not enough to correct the hypoglycemia since your muscles were trying to replenish their glucose/glycogen supply. The hyperglycemia/hypoglycemia over the next 16 hours was just the usual problem of diabetes of not getting the exact insulin need correct. The low blood ketone (0.1 mM) was due to the insulin and dextrose you were taking for the hyperglycemia/hypoglycemia, i.e. the dextrose requires more insulin to bring the blood glucose down and insulin inhibits ketone production. So what to do? I think fasted workouts are not a good idea for persons with type 1 diabetes (T1D). If you are following a ketogenic diet there is no reason to fast or to exercise in a fasted state. The ketogenic diet will result in a fat-adapted state which is the purpose of a fasted workout. Persons with T1D should try to avoid exercising right after a meal as well. They should wait until the mealtime insulin has finished working and measure the blood glucose before exercising. Although it is difficult for motivated people to take it easy, you should more gradually increase your exercise intensity. That gives your body a chance to adapt to the stress you asking your body to tolerate. That way you will find that your body can use fat for energy more so than glucose and thus your blood glucose will not tank during your workout. I realize I’m old (55 yo), but I only increase my maximum weight by 5 lb. at a time. I will use that max weight for at least the next several days until it doesn’t tax me very much before increasing it. Maybe if your young you could use 10 lb. or 5 kg, but you get the idea. Also, check your blood glucose at the end of the workout or sooner if you are not feeling right so that you can learn how that workout affects your blood glucose. Hope that helps.
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Dr. Runyan, thanks so much for the reply. I realize a diagnosis is completely out of the question, of course, but that was helpful information. What troubles me is the high BG during the workout (around 185) and then never really went down until (it seemed) like a larger than normal amount of insulin was used. I think you’re very right about the fasting. If ketogenic diets, when properly implemented, increased fat adaptation then why fast on prior to a workout? I do find fasting to be particularly helpful on non-workout days, but now that I think about it it’s never given me any increase in performance or fat utilization on workout days. I will be reading and re-reading your blog for any nuggets of information I’ve missed. I really can’t stress enough how amazing your input into this diet has been for me, and likely many others.
Take care!
– Luke
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With the additional information you are now adding that you actually had hyperglycemia during the intense resistance exercise particularly if that fasted workout was in the morning, it makes sense. Intense exercise causes stress hormone release including glucagon, cortisol, epinephrine, and growth hormone. Normally, insulin is released to counteract those hormones, but in insulin-requiring diabetes it does not happen until after the fact with exogenous insulin. If the workout was in the morning, you also have cortisol related to the dawn phenomenon added to the effects of the exercise. When you started treating the hyperglycemia with insulin and didn’t get the response you expected, I presume you took additional insulin until you ended up with hypoglycemia. By eating breakfast and taking mealtime insulin, that insulin will reverse the dawn phenomenon and at least you will start off with a normal blood glucose. Lesson learned.
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Dr. Runyan, I think you just nailed down the reasoning for me. I’ve read briefly about the dawn phenomenon, and notice my body loves to increase BG in the early morning hours. I’ve decided I’m going to stop the fasting (i.e. 16/8 Leangains type fasting) for the foreseeable future and make sure to have adequate nutrition (and insulin) in the mornings prior to training. Thank you again for the information and thoughtful responses. It is so very rare to find that these days. You seem like the type of physician I’d like to work with/for post-PA school.
– Luke
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Thanks Dr. Runyan – very informative post presented in a very readable form. I am obese, but have been on KLCHF for 18 months and lost/used about 60% of my fat. I have just acquired a Ketonix, inspired by Alison Gannett’s comment about her discovery about how Coconut oil does not work too well for her. My wife, who has T2D, also saw different responses in her BG to different foods, so I am trying to determine which foods work for me and which do not (the “everybody is different” theme repeated by Phinney/Volek/Noakes etc). Do you have any observations about how different foods might affect different people ??
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In general, foods can and do affect different people differently. Food allergies and intolerances are common examples. I think that refined carbohydrates, sugar, and vegetable oils commonly found in processed foods are probably not good for anyone and are especially problematic for those with insulin resistance and type 2 diabetes. Many but not all of those with obesity are insulin resistant. Blog post #22: Prevention of Prediabetes & Type 2 Diabetes covers how to diagnose and treat insulin resistance. Using a meter to determine which foods raise blood glucose is a good start, but many foods (mainly refined carbohydrates and sugar) can raise insulin but the blood glucose is still kept in check. The resulting hyperinsulinemia then further contributes to insulin resistance and obesity. So a blood glucose meter is helpful if the blood glucose rises excessively, but can’t tell you about the insulin response. Measuring ketones helps people understand if they are following a ketogenic diet well enough to have ketone production. But being in nutritional ketosis does not guarantee excess body fat loss. Even though many in the low carb community do not like to admit it, it is possible to not loose excess body fat or to gain excess body fat while still having positive blood ketones or breath acetone. That can come from eating too much carbs, protein, or fat. The main advantage of the ketogenic diet from my point of view is that appetite is much reduced (in most) and this leads to reduced food consumption as well as to reduced insulin resistance and insulin levels which assists in mobilizing excess body fat as long as there is a caloric deficit. If you are continuing to lose excess body fat with nutrient dense whole foods, then you are eating the right foods. If your excess body fat loss stalls, then you need to reexamine the foods and the amount you are eating and make a change. Smaller bodies need less food and the need to eat less than that to which one has become habituated is sometimes hard to accept. Hope that helps.
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Thank you Dr. Runyan – yes that certainly helps. I have been measuring BG and certainly identified milk as one substance that definitely impacts my BG (but not Cream 🙂 ). I do follow Tim Noakes’ advice to eat whole real food, so I do avoid as much as humanly possible modern processed food. I have recently reduced my eating volume and eating speed (boarding school and 10 years military) along with some High Intensity gym work to burn off glycogen, so I think I am back on track!
Thanks again for a grand place of really useful information
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