This one is a doozy! It turns out that prolonged fasting induces insulin resistance. This particular study takes a look at whether fasting induced insulin resistance differs from insulin resistance in Type II diabetics. Since Dr. Fung’s “The Obesity Code” was my first intro to insulin resistance, this study took a little while to wrap my head around…
Enjoy!
Anybody have any clue what the hell this study found or proved? The abstract and conclusion were clearly not written for laymen.
From a researchers’ standpoint I’m sure it’s well done. From a lifelong journalists’ view it is garbage.
It’s not bad news, I think, Ben. They note an important difference: “The underlying mechanism behind insulin resistance in obesity is thus not comparable to the physiological adaptations in skeletal muscle induced by prolonged fasting in lean participants.” There’s an acute response to 3 days of fasting in skeletal muscle, not the same as the chronic insulin resistance we find with obesity.
3 days of fasting - the body is mostly running on ketones, and that includes skeletal muscles. They found ketone levels 15 to 20 times as high in those muscles as when not fasting. The body has reduced glucose after the 3 days, and needs to save it for the relatively few parts of the body that do require it. So the muscle - which runs fine on ketones - gets more resistant to the effects of insulin, which would move glucose into the muscle tissue. Sounds okay and makes sense to me thus far.
What I don’t know is the role of insulin, if any, in moving ketones into muscle - this would obviously complicate things. Insulin directly works against ketone production, as well.
This is why when you say “insulin resistance”, you have to define what you mean. Obesity goes with whole-body insulin resistance, which is a complex amalgamation of fatty liver, fatty pancreas, and insulin resistance at the cellular level.
I don’t think it’s bad news either, although I’ll admit it goes a little over my head. Besides, the only bad news in science is orthodoxy. I agree with @OldDoug that it sounds like fasting elicits a different kind of insulin resistance than SAD. To wildly oversimply it, my take on the article is that SAD induces insulin resistance due to too much sugar and fasting induces insulin resistance because there is too little sugar. That doesn’t make fasting bad and it certainly doesn’t mean we shouldn’t do it, but it does call into question insulin’s role in the whole thing.
The Obesity Code made an interesting claim about insulin; that it was the primary driver in the retention of fat, because it inhibits lipolysis (fat burning). Here we have a study that reinforces prior studies in the fact that extended fasting induces insulin resistance. One of the symptoms of insulin resistance is rising serum insulin levels. How can fat burning hit it’s zenith as serum insulin levels are increasing if insulin is the key culprit? Something doesn’t totally add up. Here is a study of people water fasting for 21 days; note that the peak insulin level of 122 hits 18 days into the water fast!
My takeaway from this study is that there may be a chapter or two missing from the Obesity Code regarding insulin’s role in obesity. That’s not bad news, but I thought it was interesting enough to share.
BTW, I’ve bought 4 copies of The Obesity Code, I have it on my night stand, and I still think Dr. Jason Fung deserves a nobel prize for writing it. This study just raises interesting questions that might clarify insulins role in lipolysis, obesity, and fasting and it’s a little over my head. No offense is intended, and I’m not claiming that people shouldn’t fast. I do it 3 consecutive days every week and it’s changed my life.
The title of this thread is misleading. In this study, they were trying to compare what happens with obese versus lean individuals. What this means is that the obese (270 pounds on average) really have whole-body insulin resistance, whereas the lean individuals (154 pounds on average) likely do not. That’s the starting point. Then, they tried to determine what happens during long term fasting. They did use the hyperinsulinemic euglycemic clamp (HEC) technique, which is supposedly THE way to gauge insulin resistance.
Unfortunately, I can’t look at this now, but will try to look at this week sometime.
A quick note. This shows the “insulin resistance” went up (234 to 257) for lean people, but down (or stayed the same…305 to 299 doesn’t seem much of a difference) for obese:
Oh yeah, the way to read that table is that “- insulin” is basically fasting, and “+ insulin” is after the insulin clamp was performed.
Agreed, Bob - I came away feeling pretty good, i.e. the muscles were getting plenty of ketones, and wouldn’t miss a little insulin action as far as moving glucose in (if things are as simple as that).
Don, as I read through the study, one thing that struck me was that the lean people had what seemed like a better response, several times - reinforced my desire to be lean, not fat.
Precisely! Haven’t checked out the paper yet, but off the top of my head I suspect it’s about “physiological” insulin resistance, which is when fat adapted muscles refuse to take on glucose so as to spare it for the red blood cells and other organs that need it. (I like the term “adaptative glucose sparing,” which I learned from these forums, better.)
Peter at the Hyperlipid blog is a big fan of this type of insulin resistance. It’s a bit weird reading the phrase “insulin-resistance, which is a good thing,” out of context, however! 
Here’s his post on the topic, for those who might be interested:
Thanks for posting that. That blog is a gold mine! I’m changing the post title to “physiological insulin resistance”.
Two videos that look interesting since were on the subject:
@OldDoug and others ?
What do you think? Any opposing opinions?
Why Insulin Doesn’t Make Us Fat | MWM 2.26
Is Insulin Really a Response to Carbohydrate or Just a Gauge of Energy Status? | MWM 2.23
A lot of docs are using the “glucose sparing” to re-define and differentiate it, ‘resistance’ being to sharp a term?
“physiological insulin resistance (glucose sparing)”
Related:
Good thoughts, Paul. Like fat cells can become “resistant to insulin” when they get very full of fat - so full that they really don’t ‘want’ to take in more fat, even as insulin levels rise.
Bunny, wow - you better not leave the room when you’re listening to Chris Masterjohn - there is a LOT in there. Good mention on your part here. 
I don’t disagree with him. Toward the end of the first video he says that both insulin levels and energy balance have an effect; makes sense to me. If glucose is high enough, then insulin does drive it into muscle and fat cells - no argument from me.
He says that fasting level blood glucose goes through the blood, to give all cells and and tissue the glucose they need. He doesn’t address what happens when we’re using ketones for energy - I would think then that most cells and tissues don’t need glucose because they’re getting energy from ketones.
In the first video at 13:13 he makes a good argument for obese people being low-carb, and for exercise/work to get muscles into a low-energy state.
I need to watch these videos over and over and write stuff down and make diagrams - there is a ton of stuff to learn and internalize. 
I scanned the paper. It’s a small sampling of men (18) and I didn’t see anything about what type of diet the subjects were on. It seems to me that would have been taken into consideration here…,
