So, after a four day fast, I am reading on the BS monitor, between 100 mg/dL and 122 mg/dL when that hasn’t been the case… after a year and a half, how damn long should I expect my damn body to push out that damn sugar in my damn blood? Damn, I was such an idiot to eat the way I ate for so long. My patience is going to have to grow to make it through this journey. Any thoughts, Extended Fasting folks? Or shut up, fast and feast and deal?
I don’t have an answer for you but will be monitoring your replies. I too, am curious just how long it takes to heal from a lifetime of poor choices. Another lifetime? Hope not…
Dr. Fung’s answer - “ This is a normal process. When you fast, insulin levels start to drop and this triggers a surge of counter-regulatory hormones, including noradrenalin and growth hormone. This is normal, and meant to pull some of the stored sugar from the liver into the blood. If your liver is full of sugar, it may release lots of sugar into the blood, causing the blood sugar to rise.
So, yes, blood sugar may rise during fasting. The most important question to consider, though, is where this sugar came from. If you are not eating, the rise in blood sugar may only come from your own body. You are simply moving sugar from the liver to the blood. It means that there is too much sugar stored inside your body and you need to empty it out, either with LCHF diet or intermittent fasting”
I don’t have an answer either and when I question it I remind myself that there are no better options available for something quicker and I just KCKO.
Truth. It’s not like eating will make it better!!!
My problem is that I started longer term fasting after I’d already been keto for a long while, 1.5-2 years. So, when I fasted, my blood sugar always went down.
I do note that I’m about 6.5 years into low carb/keto, and I found some blood sugar testing strips (gave up testing some time last year). I have been testing my morning blood sugar. My morning blood sugar is now in the mid to upper 90s. It’s always been 100+ in the mornings. I have 4+ years of data that show this.
I’m not sure what to make of that. Maybe I’m still getting better over time?
I do want to caution that the error on pin prick blood sugar meters is allowed to be plus or minus 15 % of the real value, and most meters don’t even meet that. So, don’t get too excited if you have one high reading.
I also found in years of testing that I had to wash my hands before pricking my finger because residues from surrounding skin infected the blood in that split second and give me bogus readings. Try it, test your blood, wash your hands and test again back to back and compare readings.
I have been using a continuous glucose monitor, provided by insurance, and I don’t have to prick the finger any more! Yay! I am just not sure what to expect and I guess that is the frustrating thing. Where the hell does all this sugar in my blood stream come from? How long does it take? Gluconeogensis? Predictions about what the damn health will look like? Can I avoid glucose induced Alzheimer’s? Gah!
Part of this is that I am not a patient person, but after a year and a half, I ought to settle in and see what happens. I am getting close to 100 lbs lost, and if nothing else, at least the blood sugar isn’t in 200 or 300 mg/dL!!! I tend to be whiny so thanks for the support offered here!
Your kidneys (esp. after prolonged fasting store and secrete glucose, the second epicenter), intestines (esp. when fasting) also produce glucose besides the liver, so you will never escape producing glucose or your liver and kidneys from storing it and producing it from high cortisol.
Glucose is not the problem; it is your ability to produce insulin to clear it from the blood stream or store it as fat because maybe your fat cells are full is the real problem, so it just floats around in your blood stream fasting or not?
That is what kind of seems to make sense in my head, but damn, how much did I pack in there? A bunch, I think!!!
Glucose measurements aside, are you making fat loss progress?
Maybe your generating more insulin b cell islets or larger islets? More insulin, lower blood sugars?
Spiking insulin is not the same as chronically elevated insulin?
 “…Amino acids can, under appropriate conditions, enhance insulin secretion from primary islet cells and β-cell lines (1–5). …” …More
Last time I checked, I was right at 90 in the evening, after 5+ days of fasting. Substantially disappointed, but for many of us that’s just the way insulin resistance is - it can take a long time to fix it, if a true ‘fix’ is possible.
We’re heavily running on ketones when eating really low carb and/or fasting (for sure after 2+ days, I’d say) and the liver doesn’t have to make all that much glucose for the relatively few parts of the body that do really need it. Yet even with the greatly reduced sugar usage, insulin resistance means it’s still harder for it to get out of the blood and into the cells, so the blood level stays higher than what would be normal for perfect metabolic health.
It’s common on extremely long fasts to have much lower blood sugar levels - some people get into the 50s, 40s, even below that. Not advocating going exceedingly long; my own longest is a comparatively puny 12 days. But I do think that eventually the blood sugar is going to go down for almost everybody.
Chris, I hear you on patience, but you’ve already made it close to a 100 lb weight loss, and you are truly doing something very good for yourself, even with the ups and downs and blood sugar that can tend to hang up there… Keep on, man.
That is the most important point is the amount of circulating endogenous glucose when fasting compared to exogenous glucose and insulin elevation. A question I have in my head are we talking about a different kind and amount of glucose? What’s the difference between alpha and beta glucose?
The kidneys are the most important ones that need glucose or they would cease to function.
 In the mid 1970s, several gut hormones were identified. One of these, an incretin hormone, glucagon-like peptide-1 (GLP-1), was recognized as another important contributor to the maintenance of glucose homeostasis.9,10 Based on current understanding, glucose homeostasis is governed by the interplay of insulin, glucagon, amylin, and incretin hormones.
 “…Batman has Robin. The Lone Ranger has Tonto. And insulin has its own tough little partner: a hormone called amylin. …” …More
 “…In the fasting condition, plasma glucose concentrations are relatively stable, which indicates that rates of glucose production and utilization are equal. They average 2.2 mg·kg−1·min−1 (range: 1.8 to 2.6 mg·kg−1·min−1) in healthy adults after an overnight fast (1). After a meal, glucose absorption results in rates of exogenous glucose delivery into the circulation that can be more than twice the rate of postabsorptive endogenous glucose production, depending on the carbohydrate content of the meal and the rate and degree of glucose absorption. As glucose is adsorbed, endogenous glucose production is suppressed, and glucose utilization by liver, muscle, and fat accelerates (2). Thus, exogenous glucose is assimilated, and the plasma glucose concentration returns to approximately the fasting state.
“…Insulin is the dominant glucoregulatory hormone. In the fasting state, it regulates the plasma glucose concentration primarily by restraining hepatic glucose production; higher concentrations, such as those found after meals, are required to stimulate glucose utilization (3). Glucagon is a potent hyperglycemic hormone that acts almost exclusively on the liver to increase hepatic glucose production within minutes. Ingestion of carbohydrate elicits a prompt rise in insulin concentration and a decrease in glucagon concentration. The increase in insulin concentrations, which occurs before the rise in arterial glucose concentrations, is thought to be mediated largely via hormonal signals arising in the gastrointestinal tract (incretion effect) (4). The early insulin release allows increased glucose disposal during absorption and prevents hyperglycemia. If the rise in insulin concentration occurred only after glucose entered the circulation, much higher concentrations of the hormone would be required to correct the large change in glucose concentration that would result if absorption were unaccompanied by an early increase in utilization.
Islet dysfunction and peripheral insulin resistance are both present in type 2 diabetes and are both necessary for the development of hyperglycemia. Consequent to insulin deficiency (secretion or action), glucagon concentrations rise. A fall in the insulin-to-glucagon ratio causes increased production of glucose by the liver (basal hyperglycemia), whereas the absolute decrease in plasma insulin concentration or action reduces glucose utilization in peripheral tissues (postprandial hyperglycemia).*•
The profile of postprandial hyperglycemia is determined by many factors, including the timing, quantity, and composition of the meal; the carbohydrate content of the meal; and the resulting secretion of insulin and inhibition of glucagon secretion. Because the absorption of food continues for 5 to 6 h after a meal in persons with and without diabetes, the optimal time to measure postprandial blood glucose concentrations remains an open question. Postchallenge hyperglycemia refers to the glucose peak after a predefined load of glucose, ie, during an oral glucose tolerance test (OGTT). The 75-g OGTT was standardized by the World Health Organization (5) and is now the reference test for categorizing glucose tolerance. The relation between values of postprandial and postchallenge hyperglycemia is poorly understood, and differences depend in part on the ability of mixed meals containing amino acids to provoke greater insulin secretion than glucose alone. In one study, glycemia at 2 h after an OGTT was closely related to 2-h glycemia after a standardized meal (6), which suggests that subjects with high concentrations of postchallenge glycemia are also likely to have exaggerated glucose peaks after a normal meal in daily life. …” …More
While elevated serum glucose seems counterintuitive on a ketogenic diet, everyone’s normal range is different. The sorts of questions I would be asking are what your HbA1C, CRP, WBC, and ferritin levels are doing, what your triglyceride/HDL ratio is, etc. If markers of glycation and inflammation are normal, I’d not be so worried about serum glucose. I believe you stated that the readings are from a continuous glucose monitor, so what is the pattern of the readings over twenty-four hours? Do you notice that the reading is higher at certain times of day, or after certain activities?
As for possible sources of the glucose, do you have reason to believe that your liver was so enlarged that a year and a half of low carbohydrate hasn’t yet cleaned it out of glycogen? Unlike muscles, which cannot release glycogen once they’ve formed it, the liver can easily release its glycogen store into the bloodstream for use by any cell that wants it. Fat-adapted muscles tend to refuse this glycogen (“physiological insulin resistance” or “adaptative glucose-sparing”), which can lead to higher serum glucose readings, but as long as HbA1C and inflammatory markers remain low, these higher levels don’t seem to be any problem.
Another cause of elevated serum glucose is stress, so the question is whether and how you might be stressing your body as you fast. Stress comes in two kinds, however, and acute stress (such as exercise) is generally not a problem; the dangerous stress is the chronic kind.
It would be nice to know what glucagon and insulin are doing in your body when your glucose is high, but alas, home monitors for these hormones are not yet developed.
I am not a doctor or even super educated. But something I wondered about… how’s your A1C? Any numbers on how that may be looking over the time you’ve been losing that 100 pounds? Has that number been coming down into a more normal range? I know people can get hung up on glucose numbers and ignore the longer term view an A1C can offer. Hey, if it’s moving in the right direction, even slowly, that would be a point of encouragement!
Just a thought.
Truth, the A1C is 4.3, but due to COVID-19 I have not been back to the lab to get blood drawn to check it again. I have only gotten better and more consistent with keto as well as extended fasting, so I hope it to be the same or a bit lower.
Wow, a lot to digest there. Thank you it is very informative and helpful. Appreciate the time it took to share that!
You’re doing the low-carb stuff very well.
I am terrified of diabetes induced memory loss, to be perfectly honest. Trying to do all I can to reverse this at 43 because I was an idiot for a lot of years.