Excellent article. I’m an athlete and the phenomenon I am dealing with is normal fasting glucose(85) , low insulin (2.5), but high A1C (6.2). I’ve searched high and low to understand this and doctor says “I’m fine”…. Would love help in understanding why markers don’t always align.l and how this makes sense.
I look at Type 2 Diabetes as not a “sugar” problem but actually a chronic excess storage problem.
In reality glucose is the last “marker” to rise in a true type 2 diabetic. They have many other markers rise before glucose including fasting insulin, triglycerides, Leptin and organ markers (liver function tests). They also have decreasing Adiponectin over time.
So fasting glucose is a not so great marker to diagnose diabetes.
I still want a better explanation though of A1C rise in people without diabetes. Just healthier rbcs isn’t enough of an explanation.
Hey Dr Guess, really interesting topic! I recently got into endurance sports myself and I didn't realise the medical profession would classify me as an athlete (I train 10 hours a week). I associate athlete with elite performers which I guess is wrong!
I'd question that athletes have good diets. Male marathon runners have worse atherosclerosis than matched non athlete controls (https://pubmed.ncbi.nlm.nih.gov/30323509/). That signals a poor diet.
The big fashion in endurance sports is gels loaded with sugar/glucose/high GI carbs. Taking those on every session. Most recreational athletes also train at their lactate threshold (LT1 or LT2) which is stressful for the autonomic system. Stephen Seiler's done the research by looking at training diaries. They tend to have an average higher intensity per session (https://twitter.com/StephenSeiler/status/1019857874133180416) & do not train at a sufficiently low intensity to build their aerobic base which improves mitochondrial function and the ability to metabolise fatty acids.
This leads to them being "sugar burners" even gym rats and moderately healthy people. See San Milan's paper here on p5 for charts on fatox between elite athletes, weekend warriors and sedentary people (https://escholarship.org/content/qt5cz1v976/qt5cz1v976.pdf).
So I wonder if an athletic population that was eating well (little atherosclerosis, low sat fat, whole food/med diet) & had a better intensity distribution (80% of training before the first lactate turn point, 20% more intense) would be healthier.
Please keep the articles coming, loving reading insights from a "non influencer" and someone who practices!
It's true that one of the new focuses in endurance sports is taking in lots of carbs. Like over 60g of carbs per hour, every hour, up to 90 or perhaps more. However, those are targeted at long, intense training sessions or races. A lot of the cyclists I hang on forums with are resistant to those recommendations, saying that it's a huge amount of carbs. I would be surprised if it truly is a big fashion, as in the general population of endurance sports is taking in 60+g of carbs an hour.
As measured by a power meter, I can burn 800 or more calories in a 75-90 minute, intense interval session on the trainer, at the intensity levels where they recommend lots of carbs. I can burn 1500+ calories on a 3-hour group ride, where the intensity is generally lower than where you'd want a high carb intake.
(NB: technically power meters measure the power output at the bicycle's cranks, not the energy expended by the body to turn the bicycle's cranks. You do have to assume the body's gross mechanical efficiency to get from work done to calories burnt; this has been measured in trained cyclists, and it averages about 21% but I forget the standard deviation. So the calorie estimates should have a range around them, but it's more accurate than estimating calories from heart rate.)
Just some constructive feedback: while you explained why post prandial glucose is generally normal, it doesn’t appear that you clearly explained HOW/WHY a slightly elevated fasting glucose in athletes comes to be.
Additionally it would help extremely helpful to use both standard and metric units (mmol/L to mg/dL) for us Americans. I had a conversion calculator opened in a second tab while reading your article :)
I'm so glad I found your post! I'm in just the situation you describe, and I'm about to meet with my doctor to discuss these confusing results (slightly elevated fasting glucose and H1AC, low fasting insulin, and normal post-prandial glucose response). I was getting worried that maybe I was headed toward adult-onset Type 1 diabetes, but maybe it's just that I'm an athlete on a relatively low carbohydrate diet :)
Well trained athlete, 650-700 annual hours of exercise, 55 yo, ~40 min 10k runner.
You might want to have your athletic populations check their fasted glucose "out of bed" vs their lab values.
My last two lab tests were 103/104 mg/dL, fasted. My doc wasn't concerned for the reasons you outline in your article.
I do a lot of blood lactate testing and noticed it was rising when I woke up, even when I didn't eat. Because of the link between lactate and glucose, I was curious if my glucose was rising out of bed too.
So I tested glucose manually (not CGM) ten mornings in a row, right out of bed. Result was an average of 90.5 mg/dL.
Based on your article (thanks) I gave myself a glucose tolerance test. Results were 87/158/99 mg/dL at 0/60/120 minutes.
Main thing I wanted to pass along was something we've seen with athletes and lactate. Make sure baseline is baseline.
Thanks for all your articles, they've been informative and helpful.
I found your blog after hearing exactly what you are writing about. I’m 67 years old, do one SIT run session every five days and two 4x4 HIIT run sessions per week. Add to that biking and resistance training, slim body, and good diet. So my A1C came in at 5.9 and fasting glucose at 106. Three days prior I completed a 10K race and came in third in my age group. So, your blog was very reassuring. Thank you so much.
In regards to the reference to old school insulin levels in athletes, insulin and glucagon demonstrate a large first pass liver effect. Systemic levels of insulin are not representative of what the liver sees.
Thank you for your article. I am no elite athlete, but I did run a couple marathons in my 30’s and biked a couple of century rides over the years. I stay active, I don’t drink much alcohol, I have no weight to lose, I eat lots of fruits and vegetables. My only knock is I do eat my fair share of sugar. I thought it was a joke when my A1C came back at 6.1 last year. So I looked at my granola cereal which was surprisingly high in sugar(even higher than my Lucky Charms and Capt Crunch I ate until I was 50 when I decided I should change to an adult cereal). I changed to a lower sugar cereal and slowly weened myself off of the sweetened vanilla almond milk changing it to the unsweetened, but still ate my big bowl of ice cream every night. After all, this had to be wrong and I didn’t want to go overboard. Lo and behold, my A1C came in at 6.0 this year. Now that I know it is not a fluke, I have been trying to cut out most added sugars. I am not giving up my fruits and vegetables. I get too many good things from them. I read a theory somewhere that athletes train their bodies to not let out as much insulin. I am hoping by changing my diet for one year, my body will retrain itself. At least one blogger did that and it worked. If you know of anyone studying this phenomenon, I would be happy to participate. There seems like there is very little information out there.
I received a text from my GP surgery informing me that I was pre-diabetic after having some blood tests for an illness that's since cleared up. It was alarming as I'm definitely one of the 'athletes' described, cycling, running and strength training ~10 hours a week, 76kgs and lean with healthy diet. I read your article around the time I got the text which calmed me down. I have since tried a CGM as it was free, not even sure this was there right thing to do but it never got out of the green zone for the 4 days it managed to stick to my arm before falling off after a workout.
Interesting thoughts, I would like to comment on the following:
"According to common understanding (at least mine, ha ha) we would expect that any rise in glucose above ~5.5mmol/L would cause the pancreas to release just enough insulin to bring glucose down again. "
My trick question is " there are 4-6 hormones guarding the lower level of blood glucose; how many to watch for the upper level?"
My answer is zero. Increting effect tells us, that iv glucose has minimal effect to insulin secretion. It is all regulated via gut, gip and glp. Apart from the fact that free fatty acids do affect to insulin, basal, maybe in the context of background glucose. And what is insulin resistance? Uncontrolled release of free fatty acids to bloodstream. This way, chronic blood glucose excess becomes possible.
I like the comment of Dr. Horvitz. Glucose is the last red flag in the context of td2. It is too late, too far. I refuse ogtt if there is not insulin measured at the same time. Prediabetes= excess insulin can still hammer the glucose down to cells. So nothing to see here, even though your balance of energy flux is lost and needs repairing.
Have a read of this great paper: Relationships between insulin secretion after intravenous and oral glucose administration in subjects with glucose tolerance ranging from normal to overt diabetes - authors Mani & Ferrannini. They compare the insulin response to OGTT and IVGTT in people with NGT, IGT, and T2D. It's a phenomenal paper. Check out figure 1 and table 1 - and see just how much insulin goes up after an intravenous glucose infusion. (A LOT). If you're interested in reading hard data in this area - these authors (ralph de fronzo, andrea mari, e ferranni, Leigh Perreault, richard bergman, Kristine Faerch, muhammad abdul ghani, rita basu) are where you should start.
Located the study, thank you. Learnd something new as well.
My understanding of the incretin effect is that they mimic the glucose curve after ogtt. Here they have giant bolus, peaking at 17mmol glucose, when oggt results in 7mmol for normo-people. This is hardly physiological, they needed to "extinguish the fire " with iv insulin at 20 min. But point taken; this bolus does affect to the secretion of insulin.
They downplay incretins at discussion, I would not do that. Maybe the knowlegde has evolved since early 2000? The body handles things at arrival, the rate of disappearance takes care of glucose even for td1; slowly though. It is life threatening short term with low glucose, not so with high glucose.
Dr Guess, read this through again very closely. Is this a typo? “Conversely, isolated-IGT is characterised by marked muscle insulin sensitivity but minimal hepatic insulin resistance.”
Do you mean “marked muscle INsensitivity?”
The abstract in the link says “While subjects with IGT have marked muscle insulin resistance with only mild hepatic insulin resistance,” so I do believe you have a typo.
Very timely! I just got my hba1c results back: 5.7%.
I am 46, F, and of mixed British/Arab ancestry with a parent with diabetes. BUT I am physically active, pescatarian (after being vegan for 10 years). I was wondering whether you could advise as to whether I should do a GTT or just try and stay active and perhaps eat less biscuits and sugar..? Thanks.
Excellent article. I’m an athlete and the phenomenon I am dealing with is normal fasting glucose(85) , low insulin (2.5), but high A1C (6.2). I’ve searched high and low to understand this and doctor says “I’m fine”…. Would love help in understanding why markers don’t always align.l and how this makes sense.
Thank you. Well written and researched.
I look at Type 2 Diabetes as not a “sugar” problem but actually a chronic excess storage problem.
In reality glucose is the last “marker” to rise in a true type 2 diabetic. They have many other markers rise before glucose including fasting insulin, triglycerides, Leptin and organ markers (liver function tests). They also have decreasing Adiponectin over time.
So fasting glucose is a not so great marker to diagnose diabetes.
I still want a better explanation though of A1C rise in people without diabetes. Just healthier rbcs isn’t enough of an explanation.
Hey Dr Guess, really interesting topic! I recently got into endurance sports myself and I didn't realise the medical profession would classify me as an athlete (I train 10 hours a week). I associate athlete with elite performers which I guess is wrong!
I'd question that athletes have good diets. Male marathon runners have worse atherosclerosis than matched non athlete controls (https://pubmed.ncbi.nlm.nih.gov/30323509/). That signals a poor diet.
The big fashion in endurance sports is gels loaded with sugar/glucose/high GI carbs. Taking those on every session. Most recreational athletes also train at their lactate threshold (LT1 or LT2) which is stressful for the autonomic system. Stephen Seiler's done the research by looking at training diaries. They tend to have an average higher intensity per session (https://twitter.com/StephenSeiler/status/1019857874133180416) & do not train at a sufficiently low intensity to build their aerobic base which improves mitochondrial function and the ability to metabolise fatty acids.
This leads to them being "sugar burners" even gym rats and moderately healthy people. See San Milan's paper here on p5 for charts on fatox between elite athletes, weekend warriors and sedentary people (https://escholarship.org/content/qt5cz1v976/qt5cz1v976.pdf).
So I wonder if an athletic population that was eating well (little atherosclerosis, low sat fat, whole food/med diet) & had a better intensity distribution (80% of training before the first lactate turn point, 20% more intense) would be healthier.
Please keep the articles coming, loving reading insights from a "non influencer" and someone who practices!
It's true that one of the new focuses in endurance sports is taking in lots of carbs. Like over 60g of carbs per hour, every hour, up to 90 or perhaps more. However, those are targeted at long, intense training sessions or races. A lot of the cyclists I hang on forums with are resistant to those recommendations, saying that it's a huge amount of carbs. I would be surprised if it truly is a big fashion, as in the general population of endurance sports is taking in 60+g of carbs an hour.
As measured by a power meter, I can burn 800 or more calories in a 75-90 minute, intense interval session on the trainer, at the intensity levels where they recommend lots of carbs. I can burn 1500+ calories on a 3-hour group ride, where the intensity is generally lower than where you'd want a high carb intake.
(NB: technically power meters measure the power output at the bicycle's cranks, not the energy expended by the body to turn the bicycle's cranks. You do have to assume the body's gross mechanical efficiency to get from work done to calories burnt; this has been measured in trained cyclists, and it averages about 21% but I forget the standard deviation. So the calorie estimates should have a range around them, but it's more accurate than estimating calories from heart rate.)
Thanks for your helpful article.
Just some constructive feedback: while you explained why post prandial glucose is generally normal, it doesn’t appear that you clearly explained HOW/WHY a slightly elevated fasting glucose in athletes comes to be.
Additionally it would help extremely helpful to use both standard and metric units (mmol/L to mg/dL) for us Americans. I had a conversion calculator opened in a second tab while reading your article :)
Thanks!!
I'm so glad I found your post! I'm in just the situation you describe, and I'm about to meet with my doctor to discuss these confusing results (slightly elevated fasting glucose and H1AC, low fasting insulin, and normal post-prandial glucose response). I was getting worried that maybe I was headed toward adult-onset Type 1 diabetes, but maybe it's just that I'm an athlete on a relatively low carbohydrate diet :)
Well trained athlete, 650-700 annual hours of exercise, 55 yo, ~40 min 10k runner.
You might want to have your athletic populations check their fasted glucose "out of bed" vs their lab values.
My last two lab tests were 103/104 mg/dL, fasted. My doc wasn't concerned for the reasons you outline in your article.
I do a lot of blood lactate testing and noticed it was rising when I woke up, even when I didn't eat. Because of the link between lactate and glucose, I was curious if my glucose was rising out of bed too.
So I tested glucose manually (not CGM) ten mornings in a row, right out of bed. Result was an average of 90.5 mg/dL.
Based on your article (thanks) I gave myself a glucose tolerance test. Results were 87/158/99 mg/dL at 0/60/120 minutes.
Main thing I wanted to pass along was something we've seen with athletes and lactate. Make sure baseline is baseline.
Thanks for all your articles, they've been informative and helpful.
Gordo
I found your blog after hearing exactly what you are writing about. I’m 67 years old, do one SIT run session every five days and two 4x4 HIIT run sessions per week. Add to that biking and resistance training, slim body, and good diet. So my A1C came in at 5.9 and fasting glucose at 106. Three days prior I completed a 10K race and came in third in my age group. So, your blog was very reassuring. Thank you so much.
could you define better the volume/intensity that would qualify one as an athlete as the concept is used in this post?
Phenomenal! great info
Glad to discover another physician who is interested in this area. Here’s my article on the same subject:
Does the Prediabetic Cyclist Need to Worry?
https://usafmd.medium.com/does-the-prediabetic-cyclist-need-to-worry-f221388587c0
In regards to the reference to old school insulin levels in athletes, insulin and glucagon demonstrate a large first pass liver effect. Systemic levels of insulin are not representative of what the liver sees.
Thank you for your article. I am no elite athlete, but I did run a couple marathons in my 30’s and biked a couple of century rides over the years. I stay active, I don’t drink much alcohol, I have no weight to lose, I eat lots of fruits and vegetables. My only knock is I do eat my fair share of sugar. I thought it was a joke when my A1C came back at 6.1 last year. So I looked at my granola cereal which was surprisingly high in sugar(even higher than my Lucky Charms and Capt Crunch I ate until I was 50 when I decided I should change to an adult cereal). I changed to a lower sugar cereal and slowly weened myself off of the sweetened vanilla almond milk changing it to the unsweetened, but still ate my big bowl of ice cream every night. After all, this had to be wrong and I didn’t want to go overboard. Lo and behold, my A1C came in at 6.0 this year. Now that I know it is not a fluke, I have been trying to cut out most added sugars. I am not giving up my fruits and vegetables. I get too many good things from them. I read a theory somewhere that athletes train their bodies to not let out as much insulin. I am hoping by changing my diet for one year, my body will retrain itself. At least one blogger did that and it worked. If you know of anyone studying this phenomenon, I would be happy to participate. There seems like there is very little information out there.
I received a text from my GP surgery informing me that I was pre-diabetic after having some blood tests for an illness that's since cleared up. It was alarming as I'm definitely one of the 'athletes' described, cycling, running and strength training ~10 hours a week, 76kgs and lean with healthy diet. I read your article around the time I got the text which calmed me down. I have since tried a CGM as it was free, not even sure this was there right thing to do but it never got out of the green zone for the 4 days it managed to stick to my arm before falling off after a workout.
Interesting thoughts, I would like to comment on the following:
"According to common understanding (at least mine, ha ha) we would expect that any rise in glucose above ~5.5mmol/L would cause the pancreas to release just enough insulin to bring glucose down again. "
My trick question is " there are 4-6 hormones guarding the lower level of blood glucose; how many to watch for the upper level?"
My answer is zero. Increting effect tells us, that iv glucose has minimal effect to insulin secretion. It is all regulated via gut, gip and glp. Apart from the fact that free fatty acids do affect to insulin, basal, maybe in the context of background glucose. And what is insulin resistance? Uncontrolled release of free fatty acids to bloodstream. This way, chronic blood glucose excess becomes possible.
I like the comment of Dr. Horvitz. Glucose is the last red flag in the context of td2. It is too late, too far. I refuse ogtt if there is not insulin measured at the same time. Prediabetes= excess insulin can still hammer the glucose down to cells. So nothing to see here, even though your balance of energy flux is lost and needs repairing.
JR
Have a read of this great paper: Relationships between insulin secretion after intravenous and oral glucose administration in subjects with glucose tolerance ranging from normal to overt diabetes - authors Mani & Ferrannini. They compare the insulin response to OGTT and IVGTT in people with NGT, IGT, and T2D. It's a phenomenal paper. Check out figure 1 and table 1 - and see just how much insulin goes up after an intravenous glucose infusion. (A LOT). If you're interested in reading hard data in this area - these authors (ralph de fronzo, andrea mari, e ferranni, Leigh Perreault, richard bergman, Kristine Faerch, muhammad abdul ghani, rita basu) are where you should start.
Thanks for the reply, Dr Guess.
Located the study, thank you. Learnd something new as well.
My understanding of the incretin effect is that they mimic the glucose curve after ogtt. Here they have giant bolus, peaking at 17mmol glucose, when oggt results in 7mmol for normo-people. This is hardly physiological, they needed to "extinguish the fire " with iv insulin at 20 min. But point taken; this bolus does affect to the secretion of insulin.
They downplay incretins at discussion, I would not do that. Maybe the knowlegde has evolved since early 2000? The body handles things at arrival, the rate of disappearance takes care of glucose even for td1; slowly though. It is life threatening short term with low glucose, not so with high glucose.
JR
Dr Guess, read this through again very closely. Is this a typo? “Conversely, isolated-IGT is characterised by marked muscle insulin sensitivity but minimal hepatic insulin resistance.”
Do you mean “marked muscle INsensitivity?”
The abstract in the link says “While subjects with IGT have marked muscle insulin resistance with only mild hepatic insulin resistance,” so I do believe you have a typo.
Very timely! I just got my hba1c results back: 5.7%.
I am 46, F, and of mixed British/Arab ancestry with a parent with diabetes. BUT I am physically active, pescatarian (after being vegan for 10 years). I was wondering whether you could advise as to whether I should do a GTT or just try and stay active and perhaps eat less biscuits and sugar..? Thanks.