Someone shot a link to the blog about a guy who was taking Gary Taubes to task on various issues. Link to that here. Well…actually, that link is to the blog, not the specific post I wanted. Well, anyway, James’ original post had a list a greivances with Gary Taubes stuff, one of which was a statement that really left me scratching my head, that insulin was anorexic. James Kreiger said insulin reduces the sense of appetite! Now, this seemed both counter intuitive and completely against the research looking at insulin, leptin and hunger. High insulin seems to dysregulate appetite control mechanisms and it is what allows peopel to literally eat themselves to death. Mat Lalonde did soem poking around and just shot me this email:
Someone pointed you to some blog where someone was saying that insulin was a satiety hormone (made animals stop eating). This initially made no sense. I got the answer. Old school insulin research experiments involved injecting insulin into the brains of animals. They would inject one large dose of insulin and noticed that it made the animals stop eating. However, this is an acute response. Most hormones have acute and chronic responses. Acute exposure of the brain to insulin blunts hunger because it clears dopamine from the brain, which signals the end of a meal. The brain becomes insulin resistant upon chronic exposure to insulin. The chronically high levels of insulin that result interfere with the satiety hormone leptin, which makes the body think it is starving and causes the animal to eat more.
In Good Calories, Bad Calories Taubes pulls together two very interesting scenarios. One is calorie restricted in which individuals are at similar calorie intake as the Ansel Keys starvation studies, yet these individuals are NOT hungry. This is in stark contrast to the Ansel Keys folks. The difference? Taubes example was of calorie restriction plus low carb and therefore low insulin. The net result being low to no sense of hunger as compared to the literally starving Ansel Keys (calorie restricted, but high carb) group. Another interesting point by Taubes related the study of folks eating over 10,000 calories per day…folks who were sickened and distended from the amount of food they had to eat…yet were STILL HUNGRY! High insulin, even in a hyper caloric state, can bypass satiety centers in the brain.
This is nothing new. Hyperinsulinism causes some very odd things to happen. Cardiac enlargement is caused in part by elevated IGF (insulin like growth factor) due to a reduction in IGF binding protein under conditions of elevated insulin. This left ventricular enlargement can lead to congestive heart failure and interestingly, a situation of IGF RESISTANCE in the cardiac tissue which may be a precipitator to more advanced cardiac events.
Anyway, the self anointed “BS-Detective” cherry-picked this notion that insulin is anorexic, and then failed to look that the whole picture. When you look at his blog roll you see a list of characters who do not much like Taubes, paleo or anything they have not generated. BS detective? Hmmm…
That’s a pretty big “bullshit”. Great detective work gumshoe! ^_^ These questions really don’t get any easier do they? I figure as long as there’s shoddy work and false claims, you’ll always be in high demand.
This looks like a little guy trying to make a name for himself by going after the champ. He calls Taubes a BSer and then in the comments says he’s only attacking the Carbohydrate Hypothesis and not other things that Taubes says. Furthermore, I seem to remember that Taubes suggested that the hypothesis merited further study as opposed to being ignored by the nutrition establishment. I don’t remember him ever claiming it was the revealed truth.
Having said that, I do feel there could be some validity to a critique of the Carbohydrate Hypothesis. Namely, that there are a lot of confounding factors that accompany carbohydrates such as gluten and fructose that could be the primary actors in poor effects of a SAD diet. How do you tease that out?
The well worn counter example is of course the Kitavans – and I’m sorry I had to bring it up since everyone is sick of it. But they eat the carbs but not in a highly refined state or with gluten and fructose.
So is high-carb a cause of a poor diet or merely a correlate?
Matt-
It IS interesting stuff with the Kitavans. I forget if it was PA-NU or Heart Scan that made the point we might be witnessing “tolerance” in the Kitavans, not optimization but the reality of a 60% carb diet producing essentially NO metabolic derangement…that’s interesting stuff. Lectins, fructose…these items sure need closer study.
Here’s the specific post…http://www.thebsdetective.com/2009/10/bullshitter-of-day-oct-7th-gary-taubes.html#comments
Wow, that guy is really full of himself. I like that he lists his degrees as M.S., M.S., no B.S. Then gets things wrong that anyone boasting a bachelor of science should get right.
I’m surprised he got into UFlorida and Washington State’s Master’s programs without his BS.
(note sarcasm)
Dave-
So much BS it’s tough to decide where to start!!
This is just a gnat buzzing around the eye of a lion. This is just the type of attention he’s trying to draw to himself. Don’t participate!
Robb,
Since we are talking about hunger I have a quick question for ya. This came up in the CF boards nutrition area, a few people had the same question/issue. Lets assume I go out and eat a big steak dinner, 12-20oz of NY strip or some other moderately fatty cut, not a filet or a rib eye, something in the middle. Something large enough to fill me up and make me put my fork down, a good wack of protein and fat (no real carb load though, no sides just the steak) on the order of 800-1300 calories. Why then am I hungry about 30 minutes later? It’s not heavy hunger just enough to make me want to eat some more. If I push past this initial post eating hunger I’m good to go for a few more hours. Is if because the stomach has emptied but the lack of blood sugar rise has made my body think I didn’t eat anything? It’s very strange, I’m on the typical low carb paleo diet and it’s been great, but controlling hunger has been an issue for me. I’m 5’10” 177# 11%BF and currently eating about 2400kc/day
Mike-
You DO get some insulin release from protein, particularly beef. Could be from that…may need more fat to balance that out.
That blog is a joke. The guy uses the word bullshit so much it no longer has any meaning to me. I like how some people took him to task on his post and he couldn’t come up with any response.
Robb,
The post was by Kurt Harris of PaNu
http://www.paleonu.com/panu-weblog/2009/11/2/im-so-bored-with-the-kitavans.html
How did I forget that?! He had The Clash reference!!
Enlarged heart? I’d be curious to see the diets of all these young athletes, guys in the NFL, etc. that are dying of enlarged hearts. I’m curious to hear if you think there may be some kind of causal link.
Tim-
No, this type of hypertrophy is more from sedentism and bad diet. Se frank Booths paper on exercise and gene expression:
Mike D,
My guess is that you are hungry because you just aren’t eating enough. If you are doing any kind of serious workout such as Crossfit or Starting Strength that is just not enough calories. I’m bigger than you at 210#, but I am eating 3700-4000 cals a day. My BF is around 16%, but I’m also 41 yo and in spite of that level of eating my BF has gone down from about 19% when I started. I’m always battling overtraining. When I take an offload week my weight goes up and my BF goes down with the same food intake. I’m probably still not eating enough for best recovery!
Last Sunday I ate about 28oz of steak (porterhouse) two cups of creamed potatoes (I know, I know), a pile of brocolli, and two glasses of wine. Trust when I say I was full. I didn’t feel like eating again until lunchtime on Monday. Granted, that was a huge meal with a lot of fat.
If you’re active, you need to add about 1000 cal to your diet. That looks like a maintenance level of eating for a sedentary person to me. If I were you I would keep adding quality food until the BF% started to rise.
@Mike D: I know what you mean. The stomach muscles contract a while after the meal, pushing the food into the small intestine, and then there are “housekeeping waves” every so often – stomach contractions that make your stomach “growl”, that we interpret as signs of hunger. I think a lot of what we consider hunger is really just misinterpretation of those stomach contractions, and when combined with habit and desire, lead us to believe that we are hungry again when in fact we are not hungry, just emptying out.
Robb, thanks for digging deeper. It’s superficial thinking like his that cause so much unnecessary confusion and self-doubt.
Isn’t hunger also an acute response from low blood sugar which would occur after a big insulin spike? So not a direct acute response, but indirect, i.e. I feel sated after drinking a coke, but 15 minutes later I’m feeling much more hungry.
Jonathan-
Yep, exactly.
It’s true that the carbohydrate hypothesis as presented in Taubes’ book is simple and incomplete. As Taubes’ himself said, there just isn’t enough good research on the subject and more is needed.
But this Krieger guy is way out on a limb. His post is little more than a strawman argument designed to fool those who were originally fooled by the entire “fat is bad” dogma to begin with. And he does pretty poorly even at that, judging by the comments section.
The BS detective actually gets a few things right accidentally and helps to prove the carbohydrate hypothesis. He just has the science behind it wrong and follows blindly like most of mainstream medicine. He talks about low carb diets only working if they are less than 100 grams a day and that they do not work if greater than 35% of calories (is that low carb anymore?) He is looking for a linear relationship in a logarithmic system. He thinks in black and white about a subject that is very gray. I mean he quotes a study (for prediction 3) that uses 25% of caloric intake from either liquid fructose or liquid glucose, and both groups got fat. How does this discredit the carbohydrate hypothesis?
Loving the blog and podcasts. Looking forward to a New England seminar please…
P.S. Mike D should check out Lights Out. Does his hunger only happen after dinner like his scenario portrayed? Could be the excess light exposure?
Mathieu,
If you don’t mind me asking you a quick question here…How long after you started the ketogenic diet did you start feeling good? I mean, how long before you started seeing strength gains and started feeling your energy return? I am in week 3 and am ready for the good stuff to start happening:) Just curious about your experience. I know everyone is different. Thanks so much!
Thristy,
I started feeling better after three weeks but the real results came a little later for me. Things improved from week 4 to 6. I really started crushing things after week 6. Hang in there and let me know how it goes.
I have nothing useful to add to this discussion aside from the fact that the visual styling of the comments on the BS’rs blog seem to purposefully designed to be impossible to read or decipher.
I dig these green boxes.
Whoa, this guy’s got an MS in nutrition and an MS in exercise science. Are you sure you want to be messing with this guy Robb? He’ll eat you alive!
He just needs to get a masters in sociology as well and he’ll be unstoppable.
Seb-
Agreed. His Professional wrestling name would be “El Apocalypticao”!
Hey Mike D,
I am with you. After a steak I am hungry too, if I give in and eat something even small, I go from hungry to stuffed, weird. Last week I had a 16 oz striploin with 4 or 5 tbsp of bernaise sauce(straight butter), still hungry. Doesn’t happen with chicken and pork though. So I don’t think it has much to do with calories for me (that steak alone was almost 1000kcal), more likely to do with glucagon/insulin release from beef…I could be totally out to lunch though.
It’s not all that old-school, really. There are papers from just last year investigating this. Work in humans using intranasal insulin, too.
Hey Robb,
Off topic (sort of). Would you have any recommendations for paleo compliant dog food ??
Thanks !
EVO- by Enova. We use this for our cat and he does great on it.
Mathieu…Thank you!!! FGB this morning almost killed me, but going into week 4 now, so you have given me a light at the end of the tunnel! Thank you!!
Opps..that was me instead of Wes
Thanks Rob. Several people have said Evo is great. Evo it is !!!
Hey Mat,
Are you still sticking to under 50 grams of usable carbs/day?
Off topic, great source of pet food:
http://www.texasgrassfedbeef.com/id77.htm
Cook it or serve it raw. We use the “high organ” mix for our cats and Siberian Husky.
Hey Robb great stuff here! I have a blood sugar meter and strips from when my wife was prego and they “thought” she had gestational diabetes. Baby born 7 lbs10oz and officially the cutest baby ever!
Question: what kind of numbers make sense morning fasting and two hours post meal. I have been consistantly 115 or so post meal and over 100 but under 120 am fast. I suspect I am having some cortisol issues..would that morning number suggest that…sleeping more caffeinating less and eating as much good food as possible! Many Thanks Kind Sir
Fondly,
Listener 13 and devoted pseudoscientologist
Ryan-
Does seem a little high. It’s tough to overdo sleep!
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Anyway, the self anointed “BS-Detective” cherry-picked this notion that insulin is anorexic, and then failed to look that the whole picture.
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On the contrary, I have quite a strong comprehension of the “big picture” regarding insulin’s relationship to appetite and feeding.
It is true that *chronically* high insulin causes leptin resistance in the brain. However, it is incorrect to think that it is a diet high in carbohydrate that is causing the chronically high insulin levels.
Chronic hyperinsulinemia is the result of insulin resistance. It is a compensatory mechanism in response to insulin resistance. Many Taubes supporters have the entire concept backwards….that high insulin levels cause insulin resistance. This is not the case. Insulin fluctuates dramatically throughout the day. Unless you are continuously being infused with high levels of glucose, or are continuously feeding throughout the day, insulin cannot be “chronically high” because of a diet high in carbohydrate.
Higher-than-normal fasting and postprandial insulin levels are compensatory mechanisms in response to insulin resistance. When insulin “can’t do it’s job”, the body senses this and releases more insulin to try to do the same job. This leads to an elevation in both fasting and postprandial levels….hence “chronically” high insulin.
One must also consider the insulin resistance in the brain, which will also blunt insulins’ acute anorexigenic effects.
This brings the concept of what causes insulin resistance in the first place. There are numerous factors that play a role in insulin resistance, but a diet high in carbohydrate will not alone cause insulin resistance. Intramuscular fat deposition has been found to play a key role in interfering with insulin signaling and causing insulin resistance. This deposition, however, will not occur in conditions of energy balance or energy deficit….only in conditions of an energy surplus. Thus, it still comes down to energy balance.
The fact is, you can’t look at carbohydrate or fat metabolism in a vacuum as many Taubes supporters do….you have to look at the energy status of the body. A perfect example is fructose. Fructose causes de novo lipogenesis and insulin resistance when overfeeding and liver glycogen stores are full. However, it does not do this when liver glycogen stores are low and the body is in an energy deficit.
Now, I have no doubt that high sugar, high fat foods can disrupt appetite regulation, but it has little to do with the insulin surge caused by carbohydrate, and everything to do with other factors such as neuropeptide Y, agouti-related peptide, blunting of the brains’ response to CCK, as well as the opioid and dopamine systems which the hedonic response to these foods override natural appetite control mechanisms and reinforces the brain reward signals for eating these foods.
One must also consider the lack of protein intake that is generally involved with a high sugar, high fat diet. This is the other problem I have with Taubes supporters….their tendency to look at a macronutrient (carbohydrate) in isolation. However, you cannot change one macronutrient without changing another if you are keeping energy intake the same. Thus, one cannot consider the effects of reducing or increasing carbohydrate without considering the effects of reducing or increasing protein or fat. This is particularly problematic when one tries to blame carbohydrate and insulin for all sorts of ills. One has to consider that many diets high in carbohydrate are often low in protein, and it’s been well established that protein has powerful effects on satiety. In fact, there are many studies showing that high protein/moderate-high carb diets are very effective for weight loss, which completely blows apart the notion that insulin and carbohydrate are somehow the main problem when it comes to obesity.
James- I like the focus on protein and what is essentially the 3 body problem in physics…how does changing one variable in a complex system alter the other players? Also, we cannot overlook the insulin sensitizing action of glucagon itself. And…if we look at those pesky Kitavans we see a pretty good illustration of excellent insulin sensitivity throughout life despite a high carbohydrate diet. Well, until the consumption of Neolithic foods:
http://www.staffanlindeberg.com/TheKitavaStudy.html
http://www.staffanlindeberg.com/DiabetesStudy.html
So in our westernized terms we may be seeing low carb diets being more a protector from grain exposure than from carbohydrate intake.
Also, there is no doubt a consideration of energy expenditure via exercise is an important factor. Frank Booth’s work clearly illustrates the need for a basal activity level which mimics ancestral patterns for optimum health and hormonal response.
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Another interesting point by Taubes related the study of folks eating over 10,000 calories per day…folks who were sickened and distended from the amount of food they had to eat…yet were STILL HUNGRY!
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This is not the whole story in regards to the paper by Ethan Sims. First, his initial report only involved 5 subjects….hardly a strong sample to make strong conclusions.
Second, the subjects did not eat “over” 10,000 calories per day. They ate “up to” 9-10,000 per day. The mean intake was more along the lines of around 6000-7000 per day, although one subject did eat 10,200 for a period of time. What you are failing to mention is that the subjects developed an aversion to breakfast during the study….they didn’t want to eat it. They only experienced hunger later in the day (and that was only true in some of the subjects). You are also failing to mention that the subjects found it more and more difficult to overeat as the study progressed, with some dropping out of the study as they couldn’t handle eating the volumes of food they were eating.
Talk about “cherry picking”…..
James-
Going completely off memory on that, care to share that paper? Mike Eades seems to be in the same camp as myself on this:
http://www.proteinpower.com/drmike/metabolism/overfeeding-and-metabolic-advantage/
The irony here is that people were hungry AT ALL in a hyper caloric state. According to YOUR hypothesis this should not be happening. Also, there appeared to be a remarkable variety amongst those individuals as to HOW they responded to both the over feeding and subsequent fat loss, centered on hormonal response.
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When you look at his blog roll you see a list of characters who do not much like Taubes, paleo or anything they have not generated.
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When you look at your blog roll has a list of characters who do not much like anything that they have not generated. What does that matter?
And maybe these individuals don’t like Taubes et al. because they consider the weight of the evidence rather than developing stories around pet hypotheses?
James-
Wacky Pet Hypotheses like Evolutionary Medicine? If you are not couching all this in those terms, what exactly ARE you using as an evaluator for your ideas?
Fructose metabolism issues, grain intolerances and the fact food quality MATTERS are all borne out with an evolutionary view…what do you and Lyle have that even begins to touch on this?
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Then gets things wrong that anyone boasting a bachelor of science should get right.
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Care to share what I’ve gotten wrong, Dave?
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I like how some people took him to task on his post and he couldn’t come up with any response.
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Kellen, maybe I was slow to respond because I simply didn’t have the time to make an adequate response. You will see now that I’ve responded to many people’s comments in detail.
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He talks about low carb diets only working if they are less than 100 grams a day and that they do not work if greater than 35% of calories (is that low carb anymore?) He is looking for a linear relationship in a logarithmic system.
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Even if the system is logarithmic, you would still see an effect when comparing moderate carbohydrate intakes to very high carbohydrate intakes, if insulin is really the “bad guy” as everyone tries to make insulin out to be. But this is simply not observed.
It should also be noted that in my own study, energy intake was still one of the strongest predictors of weight loss. The effect of carbohydrate was certainly not enough to support the “carbohydrate hypothesis”. In addition, because of limitations of study design and including protein and carbohydrate simultaenously in the statistical model, it is difficult to know whether the observed effects were due to protein, carbohydrate, or both (as many studies low in carbohydrate are usually high in protein). Another limitation is the fact that I used self-report trials. Even though I tried to use trials where there was some sort of verification of food intake, the fact is that many were still self-report, and given the evidence that underreporting may vary depending upon macronutrient content of the diet, this is a serious confounder in my study design which limits the conclusions.
James-
I appreciate the clarification on that. I’d be disinclined to even call that a logarithmic system considering the confounders of sleep, hormone status etc. All that considered, I just can’t shake this hypnosis I’ve been under for over 10 years in which the folks who control insulin (both dietarily and via lifestyle means) get these remarkably consistent results.
Mike D hola..was going to say something then i saw Roberto’s little post(steady …steadeeee)
Thats a hunk of meat from an evolutionary standpoint so it makes ‘sense’ that as protein does cause some insulin you’d get the resultant hunger.
Why not go for smaller amounts of protein and bigger fat amounts..works for me.
Sorry the partial re-iteration.
Anyways listen to Wobert..as Jesus the Nazarene sayeth ‘He one smart fooker’
My goodness there is so much information floating around, commercials, tv, magazines, websites, blogs, and books. It can hard be separate fact and science based from sciencey smart sounding bs. Speaking of books does anyone know of a good book covering Intermittent Fasting, Fitness, & Paleolithic Nutrition? I heard there was supposed to be a really good one coming out in December but, I never saw one.
If some one would only write one or two even…
Dave-
DAMN YOU!! Book is due out…soon!
I can’t say I’m really surprised. We see all the time the effects of programs lacking chemistry/biochemistry education and the results are painfully obvious … or in this case, very painful. This sort of thing happens all the time with people who view the body as a human bomb calorimeter not a complex system driven by enzymatic reactions.
will-
Amen, on that. Even a simple exposure to some non-linear thinking and systems theory (non-math based of course…would not want to make anyone un-comfortable!!) would really help the critical thinking of some folks.
Robb,
I am absolutely STOKED to hear you’ll be covering Indian diets in your upcoming book! That is a fabulous idea. The more data we have the better as far as I’m concerned.
I don’t mean to bug you on this omega 3/grassfed beef stuff, but the numbers are just gnawing at me. Trust me, I don’t have any ties at all to any beef organizations. I’m just a server security analyst for Texas Tech University that took up diet-related reading as a hobby a few years back after a stroke-like episode.
I just don’t see how recommending grassfed or lean meat makes sense in light of the numbers below. I know I’m probably missing something glaring here and that’s why I’m emailing you.
Off Cordain’s numbers from his 2002 European Journal of Clinical Nutrition Article:
I may have gotten the numbers wrong, but I assumed a sample day in the life of a plains Indian eating nearly 100% animal kill. One meal was brain, one was marrow, and one was pure muscle meat (the least desired in non-lean times). Those three, again according to my very possibly messed up numbers, came out with the following total.
Plains Day:
16:0 14.7g
18:0 5.8g
18:2 2.8g
18:3 1.3g
20:4 2g
20:5 .6 (estimated)
22:6 1.4g (estimated)
Tot Sat 22.7g
Tot Mono 62.3g
Steffansson’s Day (3x 100g Grainfed Porterhouses):
16:0 15g
18:0 7.5g
18:2 1.8g
18:3 .7g
20:4 .09g
20:5 0
22:6 0
Tot Sat 25g
Tot Mono 27g
As you can see, it would be extremely hard to add up to the Total Fat eaten by the Indians if we ate the way Steffansson ate that one year. The main difference besides the mono to saturated ratio and the total fat differences between these two sample days is the fact that the stearic acid is in higher proportions in grainfed beef. It sure looks like to me that the plains Indians likely ate much more fat than we could even eat in three 100g porterhouses. Also, I didn’t even factor in Pemmican which would have added an even higher fat content (along with a higher stearic acid ratio as well assuming they used subcutaneous fat).
It’s difficult for me to see how recommending lean meat is called for here (or grassfed). If your thinking is to reduce AA (20:4), then the plains Indians were getting plenty with 2g in that sample day (way more than 3 porterhouses at .90). Also, the total omega 6’s were higher in the plains example (2.8 versus .8) even though the ratio was better. If the thinking is along the lines of Cordain (i.e. recommending lean meat because of the dangers of excess Saturated and Omega 6 fat), that doesn’t seem to add up either.
To me, it seems reasonable to allow for regular eggs, beef, and chicken and then make up the lost omega 3 and monounsaturated fat by taking some fish oil (~2-5g a day depending on how much n-6 for a given day) and eating an avocado.
Robb, what am I missing here? This mystery is killing me 🙂 Thanks for a great blog and radio podcasts!
John
John-
Really interesting stuff here…let me work on this. The work from cordain indicates much lower n-6 fats, and generally lower sat’d fats, specifically, Palmitic acid. Let me dig around on this and see if I can get some more perspective.
James said:
“it is incorrect to think that it is a diet high in carbohydrate that is causing the chronically high insulin levels.”
I have found no conclusive scientific evidence for you to be able to make that statement and have it be true. If you can produce a list of references for that conclusion, I would be interested to read them.
I do not believe that has been established conclusively either way. I
James then said…
“Unless you are continuously being infused with high levels of glucose, or are continuously feeding throughout the day, insulin cannot be ‘chronically high’ because of a diet high in carbohydrate.”
So here you are contradicting your above statement- allowing for the possibility that if one were continuously feeding on high levels of carbohydrate throughout the day (which MANY people with insulin resistance have been doing for years) that their insulin could be chronically high. How could this be if eating high levels of carbohydrate can not cause hyperinsulinemia?
You were taken to task because you wrote an article describing insulin as anorexigenic. That is still a claim that has not been supported adequately to be believed- if Mat ‘cherry-picked’ faults in your supporting study, then please show us definitive proof of your claim. It seems to me that saying insulin has an ‘acute anorexigenic effect’ is like saying cocaine has an acute positive psychological effect. Technically true but missing the point.
James,
Sometimes it is necessary to simplify complex systems when trying to explain them to the public. Often times, very complex systems need to be simplified so much that the descriptions are no longer accurate.
I am very well aware of the multivariate problem that is insulin resistance. When I wrote to Robb that “the brain becomes insulin resistant upon chronic exposure to insulin”, I assumed he knew I was simplifying things to the point of inaccuracy.
Know, however, that there is literature to support the notion that constant high levels of insulin causes insulin resistance. The studies are based on experiments that involved glucose overfeeding to human subjects.
See: (1) “Effect of Sustained Physiologic Hyperinsulinaemia and Hyperglycaemia on Insulin Secretion and Insulin Sensitivity in Man”, Del Prato, S.; Leonetti, F.; Simonson, D.C.; Sheelhan, P.; Matsuda, M.; DeFonzo, R.A.; Diabetologia, 1994, 37, 1025–1035. (2) “Production of Insulin Resistance by Hyperinsulinaemia in Man”, Rizza, R. A.; Mandarino, L. J.; Genest, J.; Baker, B. A.; Gerich, G. E.; Diabetologia, 1985, 28, 70–75. (3) “Regulation of the Insulin Receptor Kinase by Hyperinsulinism”, Treadway, J. L.; Whittaker, J.; Pessin, J. E.; The Journal of Biological Chemistry, 1989, 264, 15136–15143.
However, as I’m sure you know, the notion that glucose or high levels of insulin cause insulin resistance has been challenged. In 1980, a glucose and fructose overfeeding study indicated that “high-glucose feeding caused no significant changes in insulin binding or insulin sensitivity whereas high-fructose feeding was accompanied by a significant reduction both of insulin binding and insulin sensitivity” See:”Impaired Cellular Insulin Binding and Insulin Sensitivity Induced by High-Fructose Feeding in Normal Subjects”; Beck-Nielsen, H.; Pedersen, O.; Lindskov, H. O.; The American Journal of Clinical Nutrition, 1980, 33, 273–278.
More recently, it has been shown that fructose impairs leptin sensitivity and exacerbates weight gain. See: “Fructose-Induced Leptin Resistance Exacerbates Weight Gain in Response to Subsequent High-Fat Feeding”, Shapiro, A; Mu, W.; Roncal, C.; Cheng, K.-Y.; Johnson, R.J.; Scarpace, P. J.; Am. J. Physiol. Regul. integr. Comp. Physiol. 2008, 295, R1370–R1375.
Interestingly, the muscular fat deposits that you refer to as a cause for insulin resistance are thought to be the result of fructose metabolism. See: “Sugar: The bitter Truth” by Robetr Lustig, MD on Youtube
Fructose is a carbohydrate and telling people to avoid carbohydrates in general typically minimizes exposure to fructose. Sure, other factors such as lectins, gut health, lack of exercise, lack of fiber in the diet, etc…are involved. Nevertheless, the avoidance of carbohydrate, specifically fructose, does seem to help people. We now have anecdotal evidence that even excess fruit, even though it contains fiber that slows down fructose absorption, can mess up cholesterol profiles and biomarkers of health.
http://heartscanblog.blogspot.com/2010/02/diabetes-from-fruit.html
This is one reason why we tell people to eat low-carb. Interestingly enough, the Kitavans have little to no fructose or lectins in their diet given that the preponderance of carbohydrate originates from starchy tubers.
So did I write something that was false in order to quickly communicate a piece of information? Yes I did. Guilty as charged. But then again, you also made an error by neglecting to differentiate acute and chronic responses to insulin.
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All that considered, I just can’t shake this hypnosis I’ve been under for over 10 years in which the folks who control insulin (both dietarily and via lifestyle means) get these remarkably consistent results.
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Correlation does not equal causation. Remember, the dietary steps that people use to “control insulin” also involve reductions in energy intake, increases in protein intake (which improves satiety and also improves hepatic glucose regulation), increases in energy expenditure (activity improves insulin sensitivity and hepatic glucose regulation), etc. Thus, it is a mistake to assume that controlling insulin is the primary causative factor of success.
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Going completely off memory on that, care to share that paper?
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Here’s the reference for the original paper:
Sims et al. Experimental Obesity in Man. Trans Assoc Am Physicians. 1968; 81:153-170
A series of papers were published after that one. You can do a PubMed search for EA Sims.
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The irony here is that people were hungry AT ALL in a hyper caloric state. According to YOUR hypothesis this should not be happening.
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“My” hypothesis? What hypothesis? I never presented a hypothesis.
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Also, there appeared to be a remarkable variety amongst those individuals as to HOW they responded to both the over feeding and subsequent fat loss, centered on hormonal response.
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No, Robb, you are ASSUMING it is all centered on hormonal response.
You need to look at the growing body of studies on non-exercise activity thermogenesis (NEAT), which is basically spontaneous physical activity. There is strong evidence that NEAT has a strong genetic component. There is also strong evidence that NEAT explains a large portion of the variations in weight gain in response to overfeeding. In other words, some people, when they overfeed, spontaneously increase their physical activity (I don’t mean exercise….I mean overall activity which ranges from fidgeting to walking around), while others do not. The people who spontaneously increase their activity gain less weight than the people who don’t, and also lose the weight faster when the overfeeding is done. The fact is, some people’s bodies “sense” an energy surplus better than others, and their bodies respond accordingly….without even the person consciously thinking about it.
The factors regulating NEAT are still not well understood, but some factors that have been found to play a role include sympathetic nervous system activity as well as orexins.
James-
NEATO! I’d love to be in on the lab which studies fidgeting.
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So here you are contradicting your above statement- allowing for the possibility that if one were continuously feeding on high levels of carbohydrate throughout the day (which MANY people with insulin resistance have been doing for years) that their insulin could be chronically high. How could this be if eating high levels of carbohydrate can not cause hyperinsulinemia?
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Preston,
If someone is eating carbohydrates all day long, then they are overeating on calories….period. Of course that’s going to cause insulin resistance.
If you overeat on fat calories, you will also cause insulin resistance.
In either case, it is the insulin resistance that leads to hyperinsulinemia.
However, it’s not the insulin or carbohydrates themselves causing the insulin resistance. If my energy expenditure is 2000 calories per day and I consume 2000 calories of carbohydrate, I will not become insulin resistant (and thus will not have hyperinsulinemia). Now, if I consume 3000 calories per day of carbohydrate OR fat OR protein, then, yeah, I’m going to become insulin resistant. And it’s the insulin resistance that causes the hyperinsulinemia.
Hyperinsulinemia (defined as elevating fasting and postprandial insulin above normal levels) is a compensatory mechanism for insulin resistance….it is not a direct result of consuming carbohydrate.
Regarding insulin’s anorexigenic effects, there’s plenty of data on this:
http://www.ncbi.nlm.nih.gov/pubmed/19389827?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=14
http://www.ncbi.nlm.nih.gov/pubmed/18230654?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=45
http://www.ncbi.nlm.nih.gov/pubmed/17693022?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=50
http://www.ncbi.nlm.nih.gov/pubmed/17629654?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=52
http://www.ncbi.nlm.nih.gov/pubmed/16933179?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=66
http://www.ncbi.nlm.nih.gov/pubmed/16876161?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=72
http://www.ncbi.nlm.nih.gov/pubmed/16221860?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=88
http://www.ncbi.nlm.nih.gov/pubmed/15501491?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=111
There are many, many, many more papers on this…so one can hardly accuse me of cherry picking.
Matthew,
Here are my comments. First, in regards to the papers you cited:
“Effect of Sustained Physiologic Hyperinsulinaemia and Hyperglycaemia on Insulin Secretion and Insulin Sensitivity in Man”
In this paper, the model they used is simply not relevant to what happens in the human body. They used chronic insulin infusion, which does not mimic the natural swings in insulin that happens in someone eating food. They also used chronic glucose infusion, which again does not mimic the natural swings in blood glucose that happens when someone eats food.
The same holds true with the other papers you cited….chronic insulin infusion. Now, these models may be relevant to someone who already has insulin resistance (and hyperinsulinemia as a result)…..it can start a vicious cycle where the hyperinsulinemia exacerbates the insulin resistance futher, which exacerbates the hyperinsulinemia, and so on. But the papers you cite don’t support the concept that a high carbohydrate diet will cause hyperinsulinemia (unless the carbs are being consumed all day long, which in that case you’re simply overeating on calories).
And in regards to Robert Lustig, the problem with his lecture is that he doesn’t take into consideration dose or context. Alan Aragon does an excellent critique of Lustig’s lecture here:
http://www.alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/
I expanded on this in my most recent blog post:
http://www.thebsdetective.com/2010/02/partial-bullsht-of-day-fructose-makes.html
Robb,
I’ve actually know Jim Levine, the primary research guy on NEAT. He works out of the Mayo Clinic. He’s got some great review papers on it.
He’s also done some interesting studies where people had to wear a special underwear that could sense their movement and body position so that their NEAT could be tracked under free-living conditions.
James-
I want in on those skivies. GPS for my junk! I did a little poking around on NEAT and leptin… some interesting stuff there. Some folks show NEAT in hypercaloric situations, some do not…why the difference? I’m guessing some leptin/ghrelin issues…might even be an autoimmune linkage. Thoughts?
I’ve had the same perspective as James regarding insulin’s role in energy homeostasis. Thus, I was surprised to see Robb’s callout. I had a feeling James would come in here & straighten things out. Good discussion, guys.
Alan-
BIG fan of your work. Mat and I were just having a discussion about digging deeper on all this but it seems very circuitous to me at this point:
1-Calories matter.
2-So do macronutrients.
3-Especially when we consider the role of lectins on leptin and autoimmunity.
4-Brown adipose tissue appears to have a greater impact on RMR than NEAT if I recall…Also a quick google search of NEAT shows some interesting linkage to Leptin…
If I’ve taken anything from this it’s that we REALLY need to define our terms. Low carb may simply be protecting us from Leptin dysregulation via grain intolerance. there might also be some benefit to ketosis or a quasi-ketogenic environment via hormesis…
At the end of the day I am still looking for some way to improve my delivery to folks such that they see better performance and health. If James, you or anyone else has some suggestions on that, I’m all ears.
James,
I cited those studies to offer a plausible explanation for the origin of the “excess insulin causes insulin resistance” hypothesis. I did not cite them because I thought they were correct. I am very well aware that research has since established that high fasting insulin levels are the result, not the cause, of metabolic syndrome.
This blog post started because you also failed to take into account dose or context when you discussed the anorexigenic effects of insulin. This whole discussion is just a problem of working from different contexts and doses. You are working from a context of caloric deficit (or neutral) as well as acute and short-term exposure with moderate to low doses. Robb and I are working from the context of caloric surplus, as well as chronic and long-term exposure with high doses. We do so because it reflects the reality that we see in our gyms and practices. Clients that come into our gyms have metabolic syndrome, are eating too much, some of them have a really low tolerance to carbohydrate irrespective of the presence or absence of metabolic syndrome, inflammation is out of control. We teach them the importance of omega-6:omega-3 ratios, avoidance of grains and other prolamine proteins, avoidance of lectins and phytates and we get them to reduce their carbohydrate intake to become fat adapted. And it works really well. Telling them that insulin is anorexigenic, although scientifically accurate within specific contexts, doesn’t help.
Robb,
The factors regulating NEAT are still not well understood. One thing that is evident is that it’s partly genetic, and it’s known that levels of spontaneous physical activity tend to cluster in both animal and human families (you can actually breed mice to be wheel runners versus sedentary).
Orexins are one class of hormones known to play a role in NEAT regulation in animals. However, the extent to which they regulate NEAT in humans is still not well understood. But it’s a fascinating area of research.
I’m one of those people that everyone always accused of having a “fast metabolism”, but my RMR is actually 10% below predicted for my age, weight, and height. However, my NEAT is high….I’m the fidgeting, can’t-sit-still type, and everyone in my family is like that too. And I’ve had my daily energy expenditure estimated using the Sensewear armband and it consistently clocks in around 3200 – 3400 kcal/day, even on days where I don’t work out.
James-
Good stuff. I only did a prelim look at NEAT but I have a hunch some, possibly all of the variability is attributable to an autoimmune issue surrounding trans-glutaminase. As TG is involved postranscriptionaln modifications in virtually every tissue this explains the broad and highly variable nature of conditions ranging from narcolepsy to Huntingtons to Porphyria. There MUST be a mechanism which describes that NEAT variability. One I’m done with the book I will come back and take a bigger crack at this. Would love your thoughts on it.
Whoa what a fascinating discussion. Learned a whole lot about NEAT. Definitely going to do some looking into Sims and Levine.
Thanks guys 🙂