Apparently, there's no "physiological insulin resistance" in the context of a keto diet according to Dr. Bikman

(Bob M) #1

He says (about 3 minutes in, it’s only 3:39 long) that if you ever hear someone say there is physiological insulin resistance in the context of a keto diet, you’re supposed to laugh in their face. He thinks this only happens in pregnancy or when you’re a teen.

I guess morning blood sugar rise is “glucose sparing” then?

Personally, I’ve given up using the term “insulin resistant”. I no longer know what it means. I have too many questions.

For instance, I get that there can be a whole-body “insulin resistance” in the sense that your body has to produce more insulin for the same effect as before there was “insulin resistance”, but I’m making an effort to say this is a whole-body insulin resistance. But trying to drill down deeper than this, and the term “insulin resistance” seems to lose meaning. Exactly what is insulin resistant? Fat cells? Muscle cells? Both?

And there could be times when “insulin resistance” is GOOD. For example, the idea behind the theory that saturated fat causes you to not be hungry is because fat cells become – insulin resistant – due to saturated fat intake, thereby throwing up a signal indicating “I’m full.”

And I’m sure muscle cells become more insulin sensitive after working out. See here, for instance:

But this seems to be a transitory effect.

And I wonder why some people can get back to their teenage or near teenage level of fat, whereas some of (like me) can’t. Are our fat cells so insulin resistant, still after 9 years keto? Or is there some other reason?

Anyway, I thought this presentation by Dr. Bikman was interesting. As always, though, I have more questions than answers.

(Bob M) #2

Interesting. The link is a Facebook link. Not sure why it’s not showing up. I’ll try again:

www. facebook. com/BenjaminBikmanPhD/videos/insulin-resistance-physiological-vs-pathological-there-is-so-much-confusion-over/289668596409019/

You’ll have to add https:// and remove the dashes.


if you google ‘varying reasons and degrees of insulin resistance’ you find easily there is no one size fits all.

key being exercise, life stress, what you truly do eat, then put in ‘one’s actual physicology of their metabolism’ and ‘their current real diagnosed medical issues and ages’ and a crap ton more…yes insulin resistance is a real thing but the varying shades of gray that come after are so widely varied thru genetics and life environment and more we can’t ever blank statement anything on this ever.

how I see it all, just my personal chat on it :slight_smile: when one takes steps to correct health one drops big sugar, big processed/manufactured and goes more ‘healthy eating’ and more toward ‘ketogenic life’ in which the body burns ketones only! and not glucose as its prime source and then we got ‘who are we against insulin resistance’ being a ‘real deal ketone burning body’ only?

I think one can’t narrow down this chat too much in the bitter end of it all as some line liner sentence…nope.

who here HAS ever found a one liner sentence to be the end all and perfect life movement forward for them? No one HAHA

(Doug) #4

Bob, I’d say there is a difference between the baseline state of the body, and what the body may be experiencing at a given time. A few years back, I fasted for 5 days and checked my blood sugar. 90 mg/dl or 5 mmol/L. I was disappointed that it was still so high, but 90, per se, isn’t really “bad” - it’s not like at that point I had dangerously high blood sugar. That, of course, doesn’t necessarily mean that I don’t have a problem with high blood sugar overall.

Likewise - and I see Bikman’s point here - somebody on a strict enough keto diet usually isn’t going to need much insulin. It’s not that they have high blood sugar due to their diet at that time, and that they have to secret extra insulin. They’re not experiencing bad effects from insulin resistance, again - at that time.

For “physiological insulin resistance,” I think the best example is our fat cells. They’re rather like balloons. When they get very full, stretched tight, then they don’t ‘want’ to take in as much additional fat, or any at all - this prompts the body to make more fat cells.

The number of receptors on a cell that respond to hormones can change. Our really-full fat cell is going to cut the number of receptors - this is down-regulation - and that cell is then less sensitive to insulin. It’s going to be taking in less fat. The cell is physically full, and is resistant to the effects of insulin.

Bikman’s video was short, and I disagree with him, at least as far as semantics. “In the context of a keto diet” - probably not suffering from high blood sugar/high insulin, at least not as high as that person would have if on a carb-heavy diet. But the background overall state of the body hasn’t gone away.

If the body’s fat cells are full-up with fat, and the person is on a keto diet, hey - the cells are still full (at least for a while) and that physiological insulin resistance is definitely there.

Pathological insulin resistance - the keto diet is likely helping, but again, the background condition isn’t immediately reversed; it’s not like the body is reset to decades earlier, instantly cured, made new again, etc.

If that person eats a bunch of carbs over the next week, they’re not going to handle the carbs as well as if they weren’t insulin-resistant. Lowered insulin or not on a keto diet, hey - they’re still insulin-resistant.

Even if there is no pathological or physiological insulin resistance present, we tend to become more insulin-resistant as we age. There too, I’d say that “insulin resistance is there.”

(Bacon is a many-splendoured thing) #5

Bikman has a serious point. The phenomenon known as “physiological insulin resistance,” is actually better called “adaptative glucose and ketone sparing,” since fat-adapted skeletal muscles prefer to metabolise intact fatty acids over incomplete fats (i.e., ketones) or glucose.

True insulin resistance, the downregulating of insulin receptors, is also possible in varying degrees in different organs, apparently. But Bikman claims that real insulin resistance is always accompanied by hyperinsulinaemia, that one is not possible without the other.


Thanks for the link. For me the main takeaway is that both physiological and pathological ‘insulin resistance’ are caused by elevated insulin. Since a ketogenic diet keeps glucose low - and it’s glucose above ‘baseline’ that elevates insulin - a ketogenic diet also keeps insulin low. Therefore, Bikman’s ‘laugh in their face’ quip. Insulin is not elevated by eating a ketogenic diet. Just the opposite.

PS: @ctviggen @OldDoug I think Bikman is addressing the accusation that keto causes and/or exacerbates insulin resistance. He says this is false and folks who claim so are wrong. The problem is/was caused by elevated glucose. On the other hand, if one already suffers from pathological insulin resistant prior to commencing keto the damage won’t be healed overnight - as noted. But remaining consistently in ketosis is the best/only way to heal as much as can be healed.

PPS: I gained some excess weight during the decade of my 60s and I think it was partially due to insulin resistance developed over decades eating SAD finally overtaking my body’s ability to cope with elevated glucose. After 6 years in ketosis, my total weight and body comp are nearly identical to what they were when I was 18-20 years old. I interpret that as evidence that any ‘insulin resistance’ of any type I may have suffered previously has been healed. I’m nearly 78 years old now and in nearly as good or better physical condition and health as at any time during my adult life. I have a couple of age-related ‘wear/tear’ issues, but everything related to dietary and overall metabolic health is AOK. I work a full-time job with many others roughly in my age cohort and a decade or so younger and I’m in better health and physical condition than most of them. Most are overweight and diabetic.

(Doug) #7

Paul, perhaps there are shades of meaning here, and it matters exactly what we mean…? My opinion - if insulin resistance was there before, then going on a keto diet doesn’t make it disappear. The effects may be tempered, but circulating blood sugar and insulin are probably higher than what they would be were no insulin resistance present.

(Bacon is a many-splendoured thing) #8

Actually, “physiological insulin resistance” occurs in fat-adapted skeletal muscles, and fat-adaptation requires the lowering of insulin.

An insulin level of just under 25 μU/mL is the threshold. Below, the body shifts from metabolising glucose to metabolising fatty acids, above, the reverse occurs. Physiological insulin resistance is a state in which the skeletal muscle pass up both glucose and ketone bodies in favour of fatty acids. Above the insulin threshold mentioned, the muscle are required to metabolise glucose, so physiological insulin resistance is impossible.

(Bacon is a many-splendoured thing) #9

I don’t know. Hallberg’s study makes it sound as though insulin resistance is reversed after time on a ketogenic diet. But of course, insulin resistance can recur. Similarly, one can recover from arsenic poisoning, but returning to an arsenic-laden diet is likely to bring on symptoms again. Or as Dr. Andreas Eenfeldt has put it: “Keto is like showering. With both of them, if you stop doing them, you lose the benefits. Life is unfair like that.”

(Doug) #10

That would make sense, Matt. The one thing I can think of there is what PaulL has mentioned several times in other threads - that when eating ketogenically, the body often doesn’t keep as much insulin on hand, because it hasn’t needed much for a while. If, from that state, one eats a bunch of carbs, then at first the body acts like it’s insulin resistant, because it takes it a while to produce enough insulin - the expected results (lowering increased blood sugar) don’t appear as fast. After a day or two this resolves, the body ‘gets used’ to carbs again, and insulin resistance isn’t as bad as one might have first thought.

Bikman doesn’t talk about the notion of keto causing insulin resistance in the short video from Bob’s first post, but I’ve seen people make the claim. At the very end of the video, Bikman says, (without high insulin) “then the body is not experiencing insulin resistance.” Okay, yes - not experiencing it - but the given person may still be insulin-resistant.

(Doug) #11

I’m sure it partially reverses, more and more over time. If one was 10 to 20 years old, then maybe a true and total reversal could happen; just thinking out loud there. But for an old bloke like me I don’t think there is any real ‘going back.’ :smile:

Sounds exactly right to me.

(Bob M) #12

I’m pretty much in agreement with this, and I wonder if the more “damaged” you are, the longer reversal will take or the less likely you will be to return to the (fat) level you were when younger? I see people who get back to the weight they weighed when they were, say, 18, and I don’t have hope of getting there. Maybe I’m too damaged and/or old?

Whereas people like @MattWisti can get back there? (Congrats, by the way.)

It’s hard to know.

But the “physiological insulin resistance” in the morning as a cause of higher blood sugar made some sense: cells were supposedly more insulin resistant then, so blood sugar was higher. I can see @PaulL’s point about fat/muscle cells preferring instead to metabolize fatty acids, though, and therefore there’s more blood sugar in the blood.

And I’ve taken a Kraft test and had a pretty normal result, meaning by that metric, I’m not “insulin resistant”. (Though other metrics still peg me as “insulin resistant”.) So, what keeps the fat around my belly there? It’s always the first to grow when something happens (like The Croissant Diet), and the last to come off. Why?

And why do I still have belly fat (but fat basically no where else), yet others can lose it? Super insulin resistant fat cells? Genetics? Something else?

Too bad we can’t ask Dr. Bikman some questions. Like, “I’ve reversed all indications of being ‘insulin resistant’, yet I still have belly fat/am ‘overweight’. Why?”

(Bacon is a many-splendoured thing) #13

Fifty years of fat-shaming have taught us that obesity equals disease. According to statistics quoted by Dr. Robert Lustig in several of his lectures (near as I can tell, it’s NHANES data from 2014), only 80% of obese people are metabolically dysfunctional, the remaining 20% are simply fat. And thinness is no guarantee of metabolic health, either; that’s why the term “TOFI” was coined, after all. (In fact, if I remember correctly, there were five or six million more TOFI’s than metabolically dysfunctional obese people in the U.S. that year.)

So why some of us can’t take the pounds off past a certain point is a mystery. But on one of the Dudes’ podcasts, Dr. Phinney says that he and Prof. Volek typically see a fat loss equivalent to 20% of starting weight. I remember, because Richard said he took off 25%. I did about the same. But to look at Richard, Carl, and me (I feel funny putting myself in their company), you’d never guess how much weight we’ve lost, you’d only see how fat we still look. And Tom Seest lost an enormous amount of weight and he’s still bigger than the rest of us (or was, last time I saw him).

In my own case, my primary reason for going keto was to reverse my pre-diabetes, and I successfully did that. Sure, I’d love to lose a lot more fat, but I’m not going to jump through hoops to make it happen. Dr. Phinney also says that, after two or three years, he sometimes sees patients’ weight loss start up again. But it’s already been five years for me, so I ain’t gonna hold my breath for that one, lol!

(Doug) #14

Indeed, very hard to know, ahead of time. Even if one would be just as insulin sensitive as they were at a younger age, then there’s stuff like the ‘setpoint theory,’ etc. - maybe the body “wants” to weigh more when we’re older, and there isn’t any total reset of the entire endocrine system.


This link works:

PS: I just sent the following to Dr Bikman’s BYU email account:



I thank my ancestors daily. I spent 7 decades eating SAD with minimal metabolic damage and I am convinced genetics is probably about 99% of why. Although I have siblings who haven’t been as fortunate. Genetics is complicated.


In my case, I stay fat as I overeat on every woe… This simple.
Of course, it’s not that simple actually as the new question comes, WHY do I overeat? (Carbs was a good answer back then, even on keto but on carnivore or super close to it as I only can do that, it’s not anymore.)
I don’t really know the answer for my current situation. It’s probably a bit complex as human body is like that and I have a mind too. And circumstances.

I am very much aware that I have the “power” to slim down. My body obviously could become even too thin, just not by my own will. How healthy it would be to force things even to a healthy slim level is another matter, of course. But there must be a way to do it right and I don’t give up working on it. I have been basically stalling since, like, what, 12 years? I am only 46, I WILL slim down eventually. Maybe I get muscular first as I am unable to eat little (like keeping my protein and fat intake below 200g, it’s super hard these days, I fail a lot) so I need that kind of help, maybe I need to get used to long cycle tours as well… It wouldn’t help without eating little enough, of course but my allowance would grow and that should be enough if I do everything right. Almost. I never will do it perfectly and it’s fine, I am a human.

Genetics surely matter a lot and health and who knows what. But I focus on the part where I have some slim chance to make a change.

I think so too… Especially if you really did it the wrong way. I am not completely sure what people think when they say SAD, we obviously all have our own diet (and I never did “SAD”, I did my very own HFHC, similar to many Hungarians just with almost to really no meat. but I probably didn’t eat similarly to vegetarians at all, I ate huge amounts of fatty animal protein and probably most of them don’t do that). I always had some low-key health-consciousness and I loved all food groups so my diet was quite nutritious and it doesn’t seem to be the case for many people…
I even can imagine that some people have good instincts to eat healthier even on a basically wrong diet. I mean, high-carb diets are vastly different. Now that I am a veteran low-carber and body isn’t shy to scream its problems, a normal high-carb diet would cause a severe sugar poisoning (I mean, belly ache) but I could eat a high-carb diet what would feel okay-ish for longer term. Not ideal but still, way better than in the “normal” case.


… Backed by years of research, Dr. Bikman’s mission is to help the world appreciate the prevalence and relevance of insulin resistance.

Prof. Timothy Noakes:

Part 1: It’s the Insulin Resistance, Stupid

Part 2: Gerald Reaven Sets Out To Discover What Insulin Resistance Syndrome (IRS) Is

Part3: It’s the Insulin Resistance, Stupid

Part 4: Dr. Gerald Reaven Begins a Potentially Career-ending Journey

Part 5: President Eisenhower Prescribed Experimental, Untested Low-fat, Low-cholesterol Diet

Part 6: It’s the Insulin Resistance, Stupid

Part 7: Keys Argues Dietary Fat Consumption Causes Coronary Heart Disease (CHD) Epidemic in U.S.

Part 8: The Seven Countries Study (SCS)

Part 9: The Framingham Heart Study Inconveniently Fails To Support Keyss’ Hypotheses

Part 10: Keys’ Road of Discovery, from Minneapolis-St. Paul to Oxford to Pioppi

Part 11: It’s the Insulin Resistance, Stupid

(Alec) #18

I am very attracted to the way Bart Kay thinks of insulin resistance: he keeps saying “it’s a construct”, which it is, but the main thing he calls out is that it is not a disease, it is exactly the way the body is supposed to work: it is being protective of the cells that do not want or need any more glucose.

He has a very simple solution for the world to solve the issue being described as “insulin resistance” that costs absolutely nothing and will start working the moment you start executing it: stop pouring carbohydrates down your neck!


Yep! As I just said here: