Physiological Insulin Resistance = Low Carbohydrate Diet Induced Insulin Resistance
I’ll admit to breathing a sigh of relief back in October of 2007, when Peter at Hyperlipid posted about “Physiological insulin resistance.” Curiously, looking at the post again, I note that he didn’t capitalize the second two words—as though it’s not a proper name for a specific condition.
Back in mid summer 2007 there was this thread on the Bernstein forum. Mark, posting as iwilsmar, asked about his gradual yet progressively rising fasting blood glucose (FBG) level over a 10 year period of paleolithic LC eating. Always eating less than 30g carbohydrate per day. Initially on LC his blood glucose was 83mg/dl but it has crept up, year by year, until now his FBG is up to 115mg/dl. Post prandial values are normal.
He wanted to know if he was developing diabetes. […]
What is happening? Well, the first thing is that LC eating rapidly induces insulin resistance. This is a completely and utterly normal physiological response to carbohydrate restriction. Carbohydrate restriction drops insulin levels. Low insulin levels activate hormone sensitive lipase. Fatty tissue breaks down and releases non esterified fatty acids. These are mostly taken up by muscle cells as fuel and automatically induce insulin resistance in those muscles.
Whew! Now I had something to tell my dad and others who’d been faithfully doing LC and became horrified, then scared, at fasting blood glucose measurements (which is primarily how the health community screens people for diabetes). I really didn’t concern myself with it again—for all these last almost 7 years. OK, so long as post-prandial is fine (caveat: AFTER AN LC MEAL!), nothing to worry about; and combined with good HbA1c, and the fact that so far as we know, this condition will reverse in normal people after a few days of carbage, then just relax.
…That was until earlier this year when one of my collaborators, “Duck Dodgers,” clued me into something. What if there are no populations on earth that we know of where you can observe the long-term effects of “physiological insulin resistance?” I mean, Kitavan vs. Inuit was always a kind of implicit A-OK. ‘Ok, so the Kitavans do fine on an 80% carb paleo diet. But they’ve never eaten SAD. Moreover, the Inuit are healthy too. And they’re always in a state of deep ketosis, ‘keto adapted,’ other buzzwords, etc. They eat almost no carbs, etc., etc.’
…Uh, then you would expect them to feature “physiological” insulin resistance—just like the thousands of LCers in various forums, my blog comments, and in my dad—right?
…Uh, but you don’t observe it. They don’t even feature elevated ketones.
To Reiterate, Just In Case You Missed It: No Elevated Ketone Levels in the Inuit
Since this post the other day and subsequent exchanging of some emails and comments here & there with those I’d generally consider advocates of very low carb dieting—to include those advocating near perpetual states of ketosis—I’ve been met with surprise bordering on disbelief that indeed no, the Inuit are no more a “ketogenic society” than anyone else across the planet Earth.
And if not, then there is literally not a shred of any basis that chronic ketosis is a healthy state to be in (and so sorry, but I’m just guessing it’s not “nutritional,” either).
Let’s dive into the three old papers cited in that other post: 1928, 1936, and 1972, all with identical findings.
Yea, so in 1928 and 1936 it was urinalysis, and in 1972, blood on test strips.
- All studies separated by 44 years achieved the same result in terms of no elevated ketones.
- All studies separated by 44 years demonstrated that Inuit on their normal diets could pass a typical glucose tolerance test (bolus dose of pure glucose, BG elevates to about 140, then comes down over a few hours).
- All studies separated by 44 years demonstrated that Inuit put into unequivocal ketosis via and 80 hr. fast failed glucose tolerance tests miserably, with elevations in BG as high as 400, some still over 300, 2 hrs. later.
First, this confirms to us what Peter was saying back in 2007 when everyone was ignorant of this research and alarmed at their physiological insulin resistance (PIR). All of that is our physiologic response; not evidence, per se, that extended ketosis or sufficient LC dieting to induce PIR is a very bad thing. In other words, it all makes perfect sense. There is no surprise. I believe this is what Peter was saying originally, and his ‘failure’ to capitalize two words in a title signals to me that this was where his mind was at: ‘Don’t really know for sure if it’s good or bad; but makes perfect sense as a normal physiological response to input stimuli.’ Correct, Peter?
But why? How come the Inuit—the Gold Standard of We Can Do This!—were not in perpetual ketosis and could take a bolus dose of glucose and display Physiological insulin sensitivity?
Here’s two clues as to why.
- Disrupting Paleo: Inuit and Masai Ate Carbs and Prebiotics, Part 1
- Disrupting Paleo: Inuit and Masai Ate Carbs and Prebiotics, Part 2
…Turns out they actually ate a lot more carbs than anyone ever thought. Mostly, by eating kills raw, fresh, or frozen, preserving muscle and liver glycogen—as well as nose-to-tail, with lots of bits that gut bugs feed on, just like plant fibers (‘animal fiber’). Moreover, they partake of a very unique niche, where the demands of diving sea mammals means that they store lots of carbohydrate in what’s supposedly just fat. Perhaps that’s why they call it blubber, not fat?
What Did Indigenous People Inhabiting the Coldest Places on Earth Really Eat?
From: Lawrie’s Meat Science by R. A. Lawrie, David Ledward, p 92, (23 Jan 2014) A much delayed onset of rigor mortis has been observed in the muscle of the whale (Marsh, 1952b). The ATP level and the pH may remain at their high in vivo values for as much as 24h at 37ºC. No adequate explanation of this phenomenon has yet been given; but the low basal metabolic rate of whale muscle (Benedict, 1958), in combination with the high content of oxymyoglobin in vivo (cf 4.3.1), may permit aerobic metabolism to continue slowly for some time after the death of the animal, whereby ATP levels can be maintained sufficiently to delay the union of actin and myosin in rigor mortis.
One Thousand Nails in the Coffin of Arctic Explorer Vilhjálmur Stefansson, and His Spawn
It turns out that marine mammals that spend a good deal of their time diving to great depths have significant glycogen stores. Sperm whales make routine dives to 400 meters for 40 minutes and can reach a maximum depth of 2000 meters (6,560 feet, or 1.25 miles). Narwhals make some of the deepest dives recorded for a marine mammal, diving to at least 800 meters (2,600 feet) 18 and 25 times per day every day for 6 months, with many dives reaching 1,500 meters (4,900 feet). Narwhals have been recorded diving to as deep as 1,800 meters (5,900 ft, over one mile). In addition to making remarkably deep dives, narwhals also spend more than 3 hours per day below 800 meters—this is an incredible amount of time at a depth where the pressure can exceed 2200 PSI (150 atmospheres).
[Editor’s note: most of your grilled Paleo land food lives its entire life at about 1 atmosphere.]
During their deep dives these marine mammals run out of oxygen and switch to their unique glycogen-based energy stores. They store large quantities of glycogen in very odd places, but it typically gets concentrated in the skin and organs. Researchers have discovered significant “glycogen pools” in the narwhal’s arterial thoracic retia. Ringed seals have “large quantities of glycogen” in a gelatinous material near their sinuses. A sperm whale’s blubber ranges from 8—30% carbohydrates, mostly believed to be glycogen. The hearts and brains of weddel seals have concentrations of glycogen that are two to three times that of land mammals. Furthermore; in marine mammals, these organs tend to be larger in proportion to the total body weight than in land-based mammals.
In 1973, George and Ronald wrote about the harp seal, “All the fiber types contained considerable amounts of glycogen…it is postulated that the seal muscle is basically geared for anaerobic use of carbohydrate as an adaptation for the animal’s diving habit.”
Let’s continue with the delicious iconoclasm, shall we?
…What Stefansson and Anderson set out to do in their Belleview experiment by modeling an “Inuit diet” for a year is, if you integrate all the foregoing: non sequitur (a conclusion that does not logically follow). They merely demonstrated that chronic ketosis was survivable for a year. It does not logically follow that the Inuit are a model for a chronic, ketogenic diet; because, they were not that and ironically, Stefansson and Anderson showed that. Stefansson and Anderson had vastly different outcomes than the Inuit, upon scientific scrutiny (as opposed to folklore).
Why? Because, unlike the Inuit in 3 studies over 44 years, they could not pass a glucose tolerance test on the diet they were eating, when tested at the very end of it. Why? Because, as I said, it was very far from an Inuit diet; thus non sequitur; and literally, NOBODY has made this connection but for Duck, to me, to promote to the unwashed.
More Uncovering of the Inuit Myth: Stefansson and Anderson Belleview Experiement; Compromised Glucose Tolerance
From that link, here’s Stefansson’s glucose tolerance at the conclusion of his Belleview experiment. (Anderson’s was worse.)
Stefansson – Solid line after 1-yr LCHF, dotted after 3-4 weeks normal carb
Need I remind you of how the Inuit test subjects faired in three separate studies separated by 44 years after not just a year, but a lifetime of eating their traditional diet? Occam’s Razor: were Stefansson and Anderson just way different than Inuit physiologically, after a year in a metabolic ward, or did they simply not eat a real Inuit Diet?
Normal glucose tolerance with adults receiving about 120 grams 12 hrs after last meal
Oh, yea, I know: Inuit are “Keto adapted,” according to Dr. Michael Eades. Way to “explain” away a Black Hole, Mike. …Of course, the New York Times obituary for Stefansson didn’t call anything into question, so that’s evidence of absence.
…Alright, let’s wrap up this pagan, heretical infidelity in clashing icons. This post was motivated by a comment a few days ago.
“I have an approach to life. I resist insulin. Running on the edge of ketosis, with a major preponderance of long chain saturated fatty acids as metabolic substrate, I expect to be insulin resistant. I am. It is pure physiology.”
Oh, that’s Peter, again. Didn’t we see him earlier? In the same post of May, last in 2014, he also wrote:
I like to have uncoupled mitochondria running with a relatively low delta psi, high oxygen consumption and low free radical leakage. On isolated occasions, a few times a week, my parsnip chips will spike my blood glucose and delta psi for an hour or so and generate a few extra superoxide/H2O2 molecules above basal levels. I hope that’s enough for generating a decent number of healthy mitochondria. I don’t know if I am correct.
Do you know what made me love Peter from day one in 2007? His sidebar. It reads differently now; but back then, it said he was a veterinary doc. Said he was practicing a high fat Optimal Diet a-la the Polish guy, which whom I’m not going to take the time to Google, to get the spelling right. Starts with a Kw. Very, very most notable: he had up there words to the effect that he doesn’t know if he’s right, but he keeps checking PubMed.
I read everything he posted and I told people routinely: “don’t go to an MD, go to a veterinarian. They’re species agnostic. They understand all about mammalian, even reptilian physiology, and dismiss doG and his meaningless distinctions.”
Later, Peter helped me greatly extend the life of our beloved rat terrier Rotor (about 3 years) when he developed EPI. I even got an email or two from Peter after the initial barrage: “how’s Rotor?” Beatrice thinks Peter is a doG.
…I wonder if Peter would enjoy so many folks out there saying “well, it’s physiological,” as though to say it’s necessarily ok, or even correct and right. I’m not getting that from the originator himself.
- I just cut off my finger. Shit, it’s way bleeding and hurts like hell. No worries. It’s physiological.
- My teenage daughter just got pregnant. She has a 16 yo boyfriend. No sweat. It’s physiological. It’s…”Physiological teenage pregnancy.”
Get the idea?
I think Peter never meant to convey the idea that because something makes perfect logical sense in terms of what we know about the physiology of organisms (remember, he’s species agnostic), that’ it’s right, wrong, or indifferent. It just is, and:
You’re still on your own. PubMed.
So, how about: Low Carbohydrate Diet Induced Insulin Resistance? And now, onus is on all y’all to demonstrate how that’s the optimal place to be for life, given that even the Inuit don’t demonstrate it.
Best of luck.
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Man I love your heresy. Looking forward to “safe sugar” being the next. One year ago when still LC I tried having some oatmeal porridge for breakfast just for kicks and I got massive confirmation it was The Poison by feeling like crap and of course ridiculously hungry again half an hour later. Now enjoying that same porridge with butter, eggs and some OJ every morning and barely hungry for lunch. Not to mention taters. Lots of taters. HA!
Btw Duck, your Stefansson bashing has made it into the LCHF Magasinet in Sweden, the main publication on LC, thanks to Per Wikholm who’s been featured on this blog earlier this year.
It was also endorsed by the high priest of LCHF in Sweden, DietDoctor Andreas Eenfeldt. Nice to see he’s still open to science as opposed to Mr Eades.
Have fun with the swedish 😛
Per had given me heads up about that article a couple of months ago but swore me to secrecy because of the “political” sensitivities involved. Glad he got it done.
Are there English translations by any chance, or do we get to laf at Google translate?
Haven’t read the actual article butjudging by Per’s blog post with the relevant links it seems to be material well known to readers of FTA, the inuit diet being too high in protein for them to be in ketosis, the tests showing they weren’t in ketosis on their natural diet etc. Don’t know if he mentions the high glycogen in marine mammals or not but perhaps he will be willing to provide a translation… At least he managed to piss some people off!
“At least he managed to piss some people off!”
That’s your best metric for knowing you’re doing good, on the right track.
Thanks for mentioning it, Nürnberg. As I pointed out in the comment above, I didn’t come up with any of this, it was just in the scientific literature all along. Nobody ever bothered to look it up until recently—or perhaps it just wasn’t easily accessible prior to the Internet libraries that make reading the literature so easy now. Either way, I was just the messenger.
I think Dr. Eades owes me an apology.
Love when you connect shit!
Personal “AHA” & “dot-connector” moment after reading Duck D’s post a few weeks/month ago and as you pointed out here again.
” Turns out they actually ate a lot more carbs than anyone ever thought. Mostly, by eating kills raw, fresh, or frozen, preserving muscle and liver glycogen—as well as nose-to-tail, with lots of bits that gut bugs feed on, just like plant fibers (‘animal fiber’). ”
Years ago (90, 91, 92) when there were still some really good sushi places around that served fresh WILD FISH, not rice and mayo as most do now…
I always had this strange experience. I would be EXTREMELY energized after the meal and never slept well. (I would eat A LOT of raw fish)
When I read Duck’s posts it dawned on me that I always blamed the “clean & quality protein” for that surge of energy. In hindsight… I now understand it was a “sugar/glycogen buzz”. 🙂
Probably the protein as fish have a lot less glycogen than mammals.
I think MikeT is probably right. It was only the air-breathing diving marine mammals that had large glycogen stores. They needed the glycogen to remain underwater, at insanely deep levels, for such prolonged periods. It was like an emergency fuel for them that the accessed when their air ran out (and they were built to hold their breath for a very long time).
I have no idea where Hyperlipid stands on ketosis. His comments run the gamut. He has said in the past that he (1) religiously avoids it, (2) runs on the edge of it, (3) or is in mild ketosis all the time.
“When I say I avoid ketosis because Kwasniewski says avoid ketosis, that’s religion.”
” I resist insulin. Running on the edge of ketosis…”
“I’ve never been zero carb though I am very low carb and I run in mild ketosis pretty much all of the time nowadays.”
Sounds like intermittent fasting to me.
“Sounds like intermittent fasting to me.”
He could be eating no carb… every 3-4hrs. That wouldn’t be fasting at all. Hell, he could be snacking no-carb every hour.
Keto =/= intermittent fasting.
(unless he he said as much on his site? I aint bothered to read it)
Cycling in and out mild ketosis is metabolically similar to intermittent fasting.
For example, if your daily eating pattern is an 8 hour feeding window followed by a 16 hour fast, your body will likely be in mild ketosis at the end of the fast and but not in ketosis during the feeding window. Implementing this daily will cause you to cycle in and out of ketosis which is probably how your body evolved.
When I was eating paleo it never occurred to me that I was low carb as I didn’t intend to be. It was only when Tim reviewed what I ate that he indicated that it was. I could have no doubt run it through some online calculator but it never occurred to me that it was a problem. However my health was suffering and I was looking for answers other than what mainstream medicine was offering. I was getting massive hot flushes, night sweats and terrible adrenaline surges that were not quite panic attacks but there was no stress nor emotional precipitating factors for panic. I was also getting more and more gluten insensitive. The writings here and on links provided me with information that was a missing link in my understanding of health. So many thanks.
After three months adding resistant starch – mostly potato starch to start with – I lost the adrenal surges and 90 per cent of my hot flushes and life became a lot more pleasant from a general well being perspective. I added in the recommended soil based organisms and by 6 months I had lost the acute gluten sensitivity. I can eat porridge/home made muesli two days in a row without a problem or indulge in some of my home made bread based chicken stuffing though I have breaks inbetween my indulgences. It is lovely to be able to increase my range of foods rather than cut them out.
The other thing to report is that if you find that you have prodigious farts with beans you must try lupin flour – they become spectacular. I have to be careful of the socialising I’m going to do when I eat it. I compromise by having very small quantities daily in the hope I adapt.
Okay, this helps explain something for me. I have yearly health tests through my work. We fast and then blood is drawn and several factors are measured. When I was new to LC/paleo eating my fasting blood glucose was 72. For the next four years it was 95. I was also having trouble w/weight loss and not feeling that good kind of full after eating a diet with carbs in it. Wow, I hope I can reverse it!
I have a question about the Kitavans. They eat roughly 80% carbs in sweet potatoes, yams, taro but not legumes, white potatoes, or rice. Is the starch/carbs in those things they eat good enough to count as good sources of starch or even resistant starch? It would seem their gut aren’t deranged.
It’s just one population, cited mostly because it’s high carb, and it’s Paleo high carb. But there’s lots of “blue zones” in stellar health and longevity that eat those other things.
For more context still, see http://high-fat-nutrition.blogspot.com/2008/08/physiological-insulin-resistance.html — starting at “OK, here we go,” I found Peter’s comparison of two people with high FBG (LC and SAD eater) interesting. The language suggests he finds LC-flavor PIR pretty functional.
For the record, I should clarify that the Inuit’s carbohydrate intake from glycogen and their high protein intake conversion to carbohydrates was never my theory. It’s just what the scientific literature said all along. Here are relevant quotes from the scientific literature explaining that.
The first statistical survey of foods eaten by Greenland Eskimos was by Dr. Hinrich Johannes Rink in 1855. Even by that point in history, the Eskimos already had access to minimal amounts of bread and sugar that was imported by visiting Europeans. These new foods were included in Rink’s figures and were later used by Krogh & Krogh (1914) and H. M. Sinclair (1953) many decades later.
Glycogen had barely even been discovered when Rink made his analysis in the 19th century, so Rink’s data of 54g of carbohydrate intake, which had been originally been attributed to small amounts of bread and sugar, was later adjusted for dietary glycogen by the 20th century scientists. At any rate, dietary glycogen has been supported in the scientific literature ever since. (Interestingly, it wasn’t until the 1970s and 1980s that researchers began to discover that marine mammals had even larger glycogen stores than what had been previously thought).
Anyhow, here is Heinbecker in 1928 saying that the Eskimos consumed dietary glycogen:
For the record, it was later pointed out by Sinclair (1953) that the calculated individual intake from Rink’s statistical survey was an underestimate, since their caloric requirements would have been much higher, particularly in such an extreme environment.
Next, in 1936, Rabinowitch also mentioned the Inuit’s dietary glycogen intake, but more importantly, he showed that much of the Inuit’s carbohydrate came from protein.
Other scientists concurred with Rabinowitch’s analysis:
And, Tolstoi found that Stefansson and Anderson were unable to reproduce the results from Heinbecker’s Eskimos—concluding with Rabinowitch that the Inuit were obtaining sufficient carbohydrates from high levels of protein and some dietary glycogen.
Hugh MacDonald Sinclair, a professor at Oxford University reviewed all of the available literature on the Inuit that had been published up until 1953 and concluded:
The idea that Inuit obtained dietary glycogen was still evident in the literature in 1972:
In 1985, Yiu H. Hui, Ph. D., a food scientist who published a long list of books for the food industry, wrote:
In 2003, seemingly unaware of the significant glycogen stores found in diving marine mammals (since they only refer to human glycogen values), VanItallie & Nufert wrote:
Of course, everyone thinks every Eskimo had an oversupply of fat. However, the literature suggests that most Inuit had to conserve their fat, because they needed to burn it in their oil lamps, for fuel. People seem to forget that it’s dark 24/7 during the winter, and if you run out of fuel, you’re cold, miserable, and risk death. So, they preferred to save their fats for the lamp.
By 1887, there had been at least two sensationalist accounts (namely isolated reports from Hall and Schwatka) of a few Eskimos drinking from an overabundance of oil, but it was considered to be an exception and was never observed during the Winter. One early rumor was that the Eskimos drank “train oil.” Unsurprisingly, it seemed that explorers loved to embellish to gain attention.
In 1953, Sinclair had clarified that the large yields of blubber were mainly reserved for fuel (unaware that in 1991, even day-old blubber would be shown to contain between 8—30% carbohydrates):
By conserving their fuel, what the Inuit were attempting to avoid was this (documented in the report from Stefansson’s controversial expedition when he lost the Karluk)…
Those in the interior, without access to seal oil had it even tougher according to the report.
This was echoed in an 1898 book detailing the importance of their oil lamps.
As you can see from all the quotes above, the idea that the Inuit were consuming sufficient carbohydrates—from either glycogen or excess protein—was well accepted in the scientific literature. And it was further compounded by the observation that they needed to curb their fat intake in order to preserve their fuel.
As far as I can tell, very few explorers ever claimed excessive fat intake. Stefansson certainly made that claim in his books, but he seems to justify it based on his measurements at Bellevue, believing that his Western interpretation of the Inuit diet was accurate—despite Heinbecker and Tolstoi proving otherwise with their blood tests. Hall and Schwatka both referenced isolated incidences of high fat consumption, during the summer and autumn, but those accounts were considered to be surprising and out of the ordinary.
At any rate, the point of these quotes is mainly to show that the Inuit’s consumption of glyocgen wasn’t some theory that I came up with. It’s just what was mentioned in every scientific paper on the Inuit published during the 20th century. No scientists ever found any evidence of ketosis, and every published study concluded that the Inuit didn’t eat enough fat to be in ketosis.
If you put “physiological” in front of something than it makes it ok.
I once googled “physiological insulin resistance” and the only thing that came up were low carb blogs.
Maybe we should also start calling atherosclerosis “Physiological heart disease”.
Saying something is predictable and understandable is not the same as saying it’s beneficial.
I’m loving this blog. Haha. It’s all starting to fall into place for me. As I mentioned in another comment regarding LCHF diets, my boyfriend and I have/had been LC for over a year and a half now. Recently I had some wellness blood screening done and his first question when he saw my results was, “Why is your fasting glucose so high? It should be low!” *DING* Now a lightbulb appears over my head.
In other news, I’ve been having RS in the mornings for the past week (about 3 Tbs) and I just started on the SBO probiotics recommended here. I’m happy to note that I’m no longer freezing all the time… I think I can feel my toes for the first time in a year. My hair has stopped falling out… maybe related to my thyroid not being so happy when I was doing keto?
Anyway, glad I found this information. Keep it coming.
Fascinating, but we also need well done HbA1c studies in LC/ketos. Increasing fasting glucose levels theoretically should lead eventually to increased HbA1c levels over appropriate time periods. But can we assume that? We need some data.
@Dwayne Lunsford — good point . I wonder though how such studies could be conducted when there is the confounding factor that HbA1c levels tend to rise with age — even in nondiabetics. I’m also curious as to why some long term low carbers such as myself do not see the rather significant fasting glucose increases some have reported here.
I have recently rediscovered this blog just in time for this awesome RS progress in ancestral/paleo world. This is my first comment.
Thank you Richard and Duck Dodger.
I’ve been gluten free most of the last ten years, about 90% whole unprocessed foods. Doing fairly well, except some persistent adrenal and low progesterone issues that required supplementation with adrenal cortex, progesterone cream, and about 6 to 8 evening primrose oil capsules PER DAY to keep PMS inflammation under control. Supplementing with fish oil didn’t do the trick.
A few years ago, after being guilt-tripped by some gym buddies into eating conventional low carb Paleo, my health quickly turned to shit. I was hungry and grumpy and tired, my skin broke out, my cycles were fucked, my adrenals tanked, and I gained 10 pounds. I had to quit the gym for six full months. I fell apart. I showed all signs of insulin resistance and I felt like a big fat failure for having the opposite results that most people have “going paleo.” When you walk by the rotisserie chickens at the grocery store, and an entire chicken looks like a “portion,” something is grotesquely off.
“Paleo” made me fat. (Not fat by most North Americans’ standards, but “fat” like “OMG did these jeans shrink?” fat.)
I gradually healed by letting myself have more carbs and not tearing through the Costco family pack of meat. My “rules” were my old rules – whole and fresh, no gluten and watch the portions. I rediscovered what foods actually made me feel good and which ones did not make me feel full and satisfied. Oddly, some of the most satisfying were the paleo-no-no foods (like roasted purple and red potatoes, eaten cold the next day), grits, and lentils. I eat a lot of cold leftovers and couldn’t explain why I liked them.
I just figured I was some kind of anomaly, that I did better on certain neolithic foods than I did eating big steaks all the time. I looked for a “scientific” reason that this must be true. I just decided, like if you’re going to decide whether you’re going to be a Democrat or a Republican when you grow up, that I was more of a “Weston A. Price follower” than a “Paleo adherent.” Because having an explanation made me feel better for being the one person in the world who got fat (and tired) on Paleo. But really, it is only starting to make sense now with these RS posts, and I hope that the humble potato will lead to world peace in the food internets.
My adrenals were still fucked no matter how well I ate. I thought, I eat no gluten, no fast food or junk, make bone broth and tons of yogurt, so what could be wrong? In search of some new information and inspiration I found my way back here. I now think my problems started when I was on constant antibiotics for about 2 years when I was 10-12 years old, and I never completely healed my gut.
Short story long, I have made only one change to my diet recently, and that is a prebiotic smoothie similar to the recipe Richard posted here (without the banana or plantain flours, because it was easier to just start without them). It has been two days. For the first time since adolescence, I have not felt hungry at 10 am two hours after breakfast, I have been able to go all the way to a feeling of true hunger at lunch, and I have had a little digestive cleansing effect but nothing severe. I have not had to use so much willpower to eat well. I think I am onto something here that is not just throwing another supplement at the problem. Oh, and I am having weird dreams, but sleeping well enough.
I will keep reading here.
Here’s an interesting study… While small and short, the study raises important questions:
So, if going LCHF for just three days causes one’s blood glucose to spike “significantly” with a carb refeeding, I would think that doesn’t bode well for cyclical ketogenic dieters who may think they are getting the best of both worlds.
Additionally, it sounds like it would cause someone to continually remain in that false-diabetic state that Tolstoi observed with Stefansson and Anderson after their year of ketosis.
Would welcome anyone to comment or correct my assumption on the study since I only glanced at the abstract and don’t have access to the full study.
I frankly don’t give a shit about the Inuit. I know what works for me and that’s low-carb. I can tolerate carbs blood-sugar-wise but I’ve always had trouble controlling myself. I can crush 1250 calories of a “high carb, low fat” meal in one sitting no problem but eating 1250 calories of low carb, high fat in one sitting is a task in and of itself.
Interestingly enough, I haven’t experienced this Physiological Insulin Resistance at all…and I’ve chronically low-carb for 16 months. My BG is normal 24/7. Even when I carb out for the fuck of it, it spikes normally then returns back down to the 80’s within an hour or two.
Being a Type 2 diabetic, I guess the importance I see in all this is that the Inuits did eat low carbs ( I saw 30-40 grams re the snip it of Rabinowitch scientific literature presented by Duck Dodger) which is 5-6% of the carbohydrate portion of daily calorie consumption. IF this is so, I feel confident they were indeed insulin resistant and would fail an OGTT. I don’t see where this is proving anything detrimental about low carb, it just debunks the “they ate no carbs” myth. What does anything in any of the “scientific literature” say about them having diabetes or CVD? Did they have any deficiencies due to, I assume, a very low level of resistant starch in their diet?
Collin, I’m with ya on low carb, but I crush 1250 LCHF calories in just my 2 cups of BP coffee every morning then add 3egg&cheese omelet and bacon for breakfast on top of that.
Not saying LCHF is for everybody, obviously it is not. I know the ADA recommended diet is not for me. I do know that I tolerate retrograded starch in Anasazi beans and resistant starch in BRM’s unmodified potato starch and wanting to know more about it.
“IF this is so, I feel confident they were indeed insulin resistant and would fail an OGTT”
In 1929, Tolstoi showed that the Inuit passed their glucose tolerance tests, while in a fed state from their native diets. Their high protein diet was a source of carbohydrates for them. It wasn’t until they fasted for many hours that they then failed their tests.
Whoops.. Correction. It was Heinbecker that showed it. Tolstoi just provided the explanation.
Looking at the Tolstoi paper, it seems to me that both subjects went up in the 200+ mg/dL range within 1/2 hour and still there at 1 hour. One was barely under 200 at 2 hours and the other was at his highest reading at 3 hours. First OGTT is described as both getting into hyperglycemia and one even showing glycosuria. After the 2 or 4 weeks of being back on normal diet OGTT was repeated and both appear to have normal reaction. I’m not sure if these test subjects were Eskimos that had only been eating this diet for life or two healthy men grabbed off the street that were put on this diet for a year and then tested. I am assuming it is the latter. And it seems to me it proves insulin resistance while low carbing and Tolstoi’s comments indicate it too.
But, not my main interest, which was my questions about did they find diabetes or CVD in the subjects in any of this literature and were their any deficiencies due to the lack of carbs or resistant starch? I am also assuming that if these were Eskimos in the test, the description of “healthy” means if n=2 proves anything, they had no diabetes or CVDs.
Heh… well that’s what’s so interesting about the Tolstoi paper. The two subjects he was testing were Stefansson and Anderson—the two white Arctic explorers who ate a ketogenic diet in New York City, for a year.
It was Heinbecker who tested actual Eskimos, on their native diet, and showed that they passed their tolerance tests when fed their native diet. This basically showed that Stefansson and Anderson were not able to reproduce the Eskimo diet with Western cuts of fatty meat.
Any takers on my questions?
“did they find diabetes or CVD in the subjects in any of this literature and were their any deficiencies due to the lack of carbs or resistant starch?”
I believe the incidence of diabetes was extremely low before 1940.
The Inuit were originally believed (by Bang & Dyerberg) to be protected to CVD, but a recent review has shown that they have had a similar prevalence of coronary artery disease as non-Inuit populations and they have excessive mortality due to cerebrovascular strokes. So, not the healthiest indigenous culture according to the literature. And it’s unclear if high PUFA intake could have something to do with it.
“Fishing” for the origins of the “Eskimos and heart disease” story. Facts or wishful thinking? A review
Slate: “The Fishy Origins of the Fish Oil Craze”
Familial Aggregation of Intracranial Aneurysms in an Inuit Patient Population in Kalaallit Nunaat (Greenland)
I believe Stefansson also noted that the Inuit appeared to age rapidly. It’s a bit of a mystery, but there may be some speculation that this may have had to do with low insulin and high metabolism of free fatty acids, which might lead to an excessive level of highly reactive dicarbonyls (or something along those lines). But again, it’s all rather speculative.
Thanks Duck Dodgers, now I get to do some more reading.
Has anyone gone from a long-term low-carb diet, experienced signs of physiological insulin resistance, and recovered after adding carbs back in? If so, how long did it take and what did your numbers look like?
I’m concerned, because I’ve been low-carb for more than a year and my FBG is 105-115. My typical post prandial 1h = 140 and 2h = 100 or below. I’ve been eating lots of carbs for the past 2.5 weeks (250g+ on non-training days, 400+ on training days), and the numbers haven’t budged.
I’m going to see an endocrinologist in a few weeks, and am concerned she’ll conclude it’s pre-diabetes. Yet, I am extremely fit (8% bf, 180lbs on 5’10 frame), eat “clean”, and have no familial history.
One thing I will note is that I don’t have a keen sense of hunger anymore. I don’t crave food or feel hungry very much, but find that I can continue eating, even if not “hungry”, and even after taking in 4,000+ cals. I also have restless sleep (onset is immediate, but I toss and turn starting at hour 3). Maybe I’m not eating enough and my blood glucose is reflecting that? It’s just hard to believe, considering how many calories I can scarf down, with seemingly no impact on my sleep or blood glucose. Low-carb, moderate carb and high carb don’t change my numbers, either (though, low-carb makes sleep even worse).
Thanks for helping me make sense of all of this!
That’s a symptom of cortisol dysregulation. If you wrecked your cortisol because of VLCing, your BG won’t recover after you start consuming normal levels of carbs. Just google hypercortisolemia. Happens a lot in the VLC community and it’s probably what Jimmy has. Cordain used to warn about this.
There is a threshold level of carbs you must eat to maintain proper cortisol functioning. Otherwise, your urinary cortisol output declines. It’s not something you can detect by taking “salivary cortisol” tests, which Paleo natruopaths have been recommending in lieu of serum cortisol. It’s not the pattern but the excretion of cortisol and you’ll need something like 24hr urinary test which most insurance won’t cover. Lesson: just assume you have dysregulated cortisol. Add back carbs and resistant starch. That hunger and wolfing down meals is another symptom. Check dry skin, slow wound healing, hair loss, etc. Hormonal dysfunctions usually involve not just cortisol but other hormones and they all have immune consequences. Check your WBCs and Globulin.
I’d love to hear more on this. I have exactly this issue but although I think it was triggered by too little carbs on a ketogenic diet, I have found that adding carbs back in leads to reactive hypoglycaemia and makes matters worst. It’s a lose lose situation…
For how long?
If a couch potato suddenly starts running up lots of stairs, his heart races to extremes. He cuts back to moderate exercise and builds tolerance to more over time.
Legumes might be a good choice for a period of time in modeation, since the fiber has a BG blunting effect, so less insulin, less crash.
Yes, I think this is a fair suggestion. Chickpeas seem to have an extremely low GI. Lentils too, i suppose. But those nasty lectins and phyta… “must resist deeply engrained paleo dogma”. Even so though, the question remains, if adrenal function is compromised, will blood sugar regulation ever normalise with the reintroduction of carbs – even if the elimination of said macronutrient catalysed the problem in the first instance.
Dayum this human body is a bastard!
Thing is, Josh, it’s all in your hands and dose is entirely up to you.
You could easily make a tasty garbanzo bean salad, the cold one with the onion in it, olive oil dressing. Plenty of recipes on line. Then you can just test. Start with a TBS, then two, so forth. Or a cup.
Also, are you measuring how low BG goes? I don’t think it’s entirely abnormal to be a little tired after a meal. Comatose, no, but I often think that’s partly to do with quantity as well.
After a quick trip to the supermarket I have some Garbanzo beans soaking, ready for tomorrow morning.
As for measuring how low blood glucose goes, as far as I can tell, not that low. Of course it is hard to tell whether you have caught a snapshot of BG at it’s lowest but I have never caught mine below 80. I claim reactive hypoglycaemia because my BG generally hits the 80-85 mark after 3-3.5 hours and then shoots up on its own, sometimes to 100+ numbers. This makes me think low cortisol being compensated by adrenaline but, hey, I’m open to suggestions.
I should also add that as a 23 year old guy, my caloric intake is pretty large. So whilst some days I might get 100-150 grams carbs this might still only be 10-15% of calories. Coupled with large amounts of saturated fat = physiological insulin resistance? who knows…
Fascinating. Thanks for this. I went from relatively low carb to a keto experiment (measuring glucose and ketone levels daily) and after leas than a week had increasingly high fasting levels.
I found it pretty scary and gave up after about two weeks and have gone back to moderate carbs. I need to measure where in at now but have lost my glucose meter.
I emailed/got in touch with lots of ‘experts’ at the time and got all sorts of answers, none of them great. This blog makes a lot of sense. Keep it up
“after leas than a week had increasingly high fasting levels”
Yea, it’s just “physiological,” euphemism for don’t worry about it, so long as you’re keeping to the Catechism, you’re right with doG, so no worries.
“got all sorts of answers”
Yea, you just didn’t do it right.
An interesting question is one that Joseph raises … does this revert back to ‘normal’ by then eating a moderate to high carb diet. I guess define that how you want but 150g + is the number that seems to get quoted related to ‘passing’ OGTT after LC i.e. how do you normalise yourself.
Joseph, where did you get to with this?
My son has basically doubled his insulin needs for carbs twice. Once at about a month after we went under 30% carbs, and again about 6 months after that. I am scared giving him so much. His patterns are difficult to interpret. For example, he can look like he is going low 2.5 hours after lunch but rise up in the next hour because the high fat meals take so long to digest. He is at about 25% carbs (110 grams a day). His doses for carbs are very very high for a kid his age and size, but he is not resistant to correction insulin and his total daily insulin is within normal amounts for type 1 diabetes. I thought that using lower carbs would keep him more insulin sensitive and so he would need less insulin, but it did the opposite. The fat seems to have made him resistant because his muscles seem to run on fat, and not let carbs “in the door”. It does help prevent low blood sugar because he has the fat IN the muscle cells for energy rather than having to mobilize them against the action of insulin to get them to the muscles. I would honestly rather have him with average blood sugars of 140 and peaks of 220 than having his average at 115 with peaks around 160, because he will look (on a continuous glucose monitor) like he is heading low, say into the 80s 3 hours after lunch but still come back up 50 points because I think that the fat in his diet causes delayed insulin resistance (3-5 hours) after the meal and since he injects long acting basal insulin he may not have enough during those periods. Because I watch his cgm by remote access over my I-phone, I can see the patterns but someone without a cgm would never be able to sort out the low to high pattern. I know that Dr. Bernstein says that a unit of insulin covers about 8 grams of carbs, and that you also need insulin to cover protein (about half as much per gram) when you go VERY low carb, but there is a difference with very low carb and with 20-30%. I wish now that I had stayed about 40% carb with him because I think that would have prevented the need for so much insulin per gram of carbs.
I was hoping someone here could guide me. My son is 9 years old and was dx’d with type 1 diabetes a year ago. I tried to control his carbs (about 100 grams a day, 25% of total calories) and give him a diet based on fat, mostly olive oil, high oleic safflower and sunflower and butter fat (reduced carb whole fat milk) and beef. It worked great for a year as he had 4 consecutive A1Cs of under 6.0. The last one was 5.8. His blood sugar peaks were phenomenal for a 50 pound kid with T1D, BUT as I increased the fat in his diet to 50 and then 60% he started needing dramatically more insulin to cover a given amount of carbs. This was even if he ate carbs alone without fat in the meal. I assume now that he has developed physiolgical insulin resistance. His doses for a given amount of carbs are 2-3x the normal rate. Now the high fat makes his spikes very very slow (he even can go low from insulin in the first hour or two and then rise later). Also, even though he needs the large dose to cover carbs even without fat in the meal, his basal insulin needs are fairly low and a unit of insulin will lower his blood sugar pretty fast if it is not around a meal time. So I need to know, how long, and what does it take to reverse the physiological insulin resistance if I decide to do that. There are advantages. His muscles are apparently loaded with fat so he has energy “on board” to prevent most activity related low blood sugar (the main cause of lows in T1D is that fatty acids don’t get mobilized to suppliment muscle energy due to high insulin levels.) Anyway, if I take him from say 25% to 40% carbs can that reverse the insulin resistance? Can activity like swimming help to burn out the intermuscular fat and get the muscle to start storing more glycogen again? Again not sure if I want to do this, but his doses per unit of carbs are very high and he CAN go low before he rises especially at dinner. It also seems that his peaks come later and later after each meal of the day.
Do you have an MD following him up closely ? You did not mention what the doc says about your tweaks.
They tend to recommend the standard American diet (15-20% protein, 20-35% fat for kids and about 50% carb). They do not tell people that they have to eat that way though. He is seen every 3 months but the endo’s are not concerned about a kid with a 5.9 HbA1C, with no dangerous lows and without very high blood sugar excursions. My son is between 70-180 well over 90% of the time.
The problem is that he has such very very late peaks that I can’t tell if he is going low. Almost all T1Ds are concerned about preventing that blood sugar spike in the first 90 minutes or so, but for breakfast today he did not even start to RISE until the 2 hour mark, and he peaked at past 3.5 hours! He was basically around 100 for the first 2 hours after eating breakfast. There is just no explanation for the late late rise in blood sugar. The endo is not concerned about “patterns” when a kid is not going low or high, but he can’t ride his bike after dinner without going low because his insulin is so much faster than his food absorption.
The doc doesn’t like a high fat (especially saturated fat diet) because she believes it causes heart disease (which I don’t) but the issue may be that the high fat is causing the physiological insulin resistance-the muscles loading on fat instead of carbs.
I seem to remember reading that eating digestible carbs + fats at the same time will increase insulin secretion. If your son is T1D, his insulin requirements will be increased if the meal is rich in fat and carbs.
See for example http://care.diabetesjournals.org/content/36/4/810.full
From the study I linked;
“Our findings are consistent with those of previous studies indicating that higher-fat pizza meals cause late postprandial hyperglycemia necessitating increased insulin doses. The time course of the increase in the glucose concentrations after the higher-fat dinner meal is in keeping with clamp studies in nondiabetic humans indicating that physiological FFA elevations lead to insulin resistance within several hours”
Yes I think that is part of the issue. Except that he now has the same carb ratios even if he eats just a banana or a low fat snack. I think that a YEAR of a 25% carb diet has basically fat loaded his muscles so that they have developed a resistance to meal time insulin. In other words, physiological insulin resistance is basically similar to having eating a high fat meal recently. The real problem is not just that the insulin requirements increase, but that the rise is so slow that his insulin will make him low before rising. It makes it hard to be active. Most “expert” higher fat T1Ds will use a pump and extend their insulin out for several hours with a high fat meal. If he just needed more insulin that would be fine, but its the fact that the insulin is so much faster than the meal time rise.
I read all about Type 1 diabetic adults going paleo, but none of them mention the problem of increased insulin need to cover fat, or of lows before highs.
I reduced my son’s fat intake from 60% to 35% and raised his carbs from 25 to 45 and whoa his insulin needs have been cut dramatically, down to 75% of where they were despite about 50% more carbs per day. This is in a span of 5 days. I had to cut his basal 3 times because he was going low at night on a basal that was having him rise through the night last week. Unfortunately he has dangerous patterns following meals and it is similar to what is seen with insulin resistance. He will get enough insulin to keep his blood sugar from rising for 2-3 hours, but then bam, 3 hours out he will rise 30-70 points. Not horrible numbers but dangerous because he is hanging in the 70-90 range for 3 hours after lunch and then ending up at 150. I believe that the low carbs have just made his muscle into poor glucose disposing machines. I never thought he would be so much more sensitive to insulin though with less fat and more carbs and require less total insulin. His ratios have gone from 8:1 to 16:1 but not just from the composition of the meal, but each day I have had to use less insulin (or add more carbs) to keep his blood sugar from going low. He has gone from 9:1 at dinner to about 19:1 (a little but each day). The patterns are still problematic.
I was diagnosed nearly twenty years ago as pre-diabetic in pharmacy school.
At the time I was eating the standard American fare and watching my waistline expand accordingly.
I did nothing for years until I began getting constantly sick – especially with sinus infections and what was later self-diagnosed as self-induced urticaria (numerous trips to allergists were no help).
Long story short, I cut out all processed foods and started on my journey. The sinus infections, rashes and ‘pre-diabetes’ diagnosis went the way of the Dodo bird.
As time went along I began to experiment with lowER carb (under 150 grams or so) and the weight really started coming off.
Like so many other people I figured that if dropping the carbs were that effective then REALLY cutting them back would be kick ass, right?
So I’ve been low carbish pushing 10 years. But, I was at a ‘set weight’ for most of that time and couldn’t seem to drop any lower than 18-20% body fat. The last six months were spent experimenting with ketosis in an effort to drop the weight.
By mere coincidence I had my labs drawn recently. Interestingly, my FBG and A1C are now in the pre-diabetes range again.
It came as a huge shock – and ego blow – to me because I thought low carb was the answer. How in the hell am I back with insulin/glucose issues again?
I guess my reason for commenting is to say – Yes, this low carb stuff is OK – to a point. But your body reacts and adjusts.
Worse, most MD’s are woefully ignorant about things like Physiological Insulin Resistance. I’ll push back on my doc but it wouldn’t surprise me if he suggested starting metformin or some such.
I’m slowly reintroducing carbs, feeling slightly better and getting better results in the gym. I plan on getting my labs re-drawn in a couple of months and will report back on my response.
The bottom line for me is eat natural foods in sensible amounts and avoid extremes. Listen to your body and adjust rather than drinking the Koolaid.
thanks for sharing–that helps. i’m now experimenting with adding carbs back, hoping to bring insulin and leptin levels back to normal.