I have read Good Calories Bad Calories. At just under a kilogram there are minor points within it with which I disagree. But, for the majority of the people who have read it, it is basically correct.
One of the most recent critical appraisals of the carbohydrate hypothesis of obesity was posted by Stephan over at Whole Health Source. Obviously, I disagree with Stephan's appraisal. That's fine, to disagree is perfectly OK. We'd get nowhere if we all sang from the same hymn sheet. This post is basically my take on the evidence used to destroy the carbohydrate hypothesis. It's depressing to have to do this but reassuring at the same time.
So why do I cling to this apparently incorrect and outdated hypothesis? Let's look at the points in approximate order as taken by Stephan.
A defect of fat metabolism?
Taubes ignored leptin to concentrate on insulin; this appears to be the main conclusion in this section. Stephan cites a neat paper by Leibel et al which demonstrated that in four healthy, never-obese humans the fall in metabolic rate induced by 10% weight loss could be reversed by physiological leptin replacement. That's cool if you want to be a young, fit, healthy, never-obese experimental volunteer desperate to live comfortably at 10% below your normal, slim weight.
If you are currently morbidly obese it may be of some comfort to know that leptin might be able to help you correct your hypometabolism should you manage to lose some weight.
If you are ex-morbidly obese and have managed to lose a few hundred pounds of fat you will still own a set of injured adipocytes. These injured adipocytes refuse to produce physiologically appropriate levels of leptin for their fat stores. Now THERE is a role for leptin. It might even reverse the persistent hyperinsulinaemia present even during starvation in the morbidly obese...
If you are currently morbidly obese and think leptin will help you lose weight, think again.
So do I think leptin is unimportant? Of course not. Does this invalidate the carbohydrate hypothesis? Shrug.
What about the morbidly obese ob/ob mouse, which cannot make leptin? There are a handful of human families on the whole of the earth with this problem. They need leptin and it will work for them.
The population of the USA is around 300 million. Of the adults in this population, as of 2008, 34.2% are overweight, 33.8% are obese and 5.7% are morbidly obese. They are not going to benefit from leptin supplementation to lose weight.
According to Stephan many, if not most, of these few million people will benefit, for reasons which are not entirely clear, from carbohydrate restriction. But it's not due to lowered insulin levels... Fascinating conclusion.
How can anyone be so sure that it is not from a reduction in insulin levels?
Here's why, watch very carefully:
You may think you have seen this clip before but no, although the child is the same the chocolate is different. This is 90% cocoa chocolate, none of your boring 74% sugary stuff...
If your baby is going to self feed chocolate you are going have to bath her. Bathing babies is dangerous. We also have one of these:
I always try not to throw out the baby with the bathwater. You can't be too careful...
The big problem with insulin, as any obesity researcher will tell you, is that it is a satiety hormone. I've said it before, all you have to do is have it injected in to your brain and you won't feel like eating a steak for the next few hours. Let's get a nice juicy quote from this paper by Velloso and Schwartz, hot off the press in 2011:
"A major and persisting source of confusion surrounding the hypothesis that insulin action in the brain reduces food intake and body weight while also lowering hepatic glucose production and increasing thermogenesis stems from evidence that following systemic insulin administration, the subsequent fall in glucose levels potently increases food intake while also increasing liver glucose production and reducing sympathetically driven thermogenesis. Thus, insulin-induced hypoglycemia potently overrides virtually all of insulin’s central effects, an observation that for many years has confounded research in this field."
Did you see the baby go? Here it is again:
"Thus, insulin-induced hypoglycemia potently overrides virtually all of insulin’s central effects".
That's it: Baby, bathwater, gone. How can anyone be so careless? Oh, did you miss it?
The baby is the peripheral effect of insulin on lipolysis, which is discarded without mention. Because hypoglycaemia in your brain (a central effect) makes you hungry, the fact that hypoglycaemia can steamroller insulin's central effects appears to have allowed the discard of insulin's peripheral adipocyte effects. Insulin's inhibition of lipolysis, in a normal human being, occurs at concentrations which do not even budge muscle glucose uptake. Infuse it directly in to the arterial supply to the fore arm and the systemic hypoglycaemic effect is lost. All you get at low infusion rates is inhibited lipolysis. This is the baby in the bathwater. Up the rate a bit and potassium uptake is increased. Bugger glucose uptake, this needs far more insulin that inhibition of lipolysis or promotion of potassium translocation. To summarise, if abnormally high insulin levels are needed to deal with unwanted hyperglycaemia then lipolysis will be inhibited until such a time as fat cells become so distended they refuse to listen to this excessive insulin, ie when they have become insulin resistant.
There are certain other spectacularly obvious problems with this accidental baby loss. Once we have all accepted that insulin is a satiety hormone it becomes perfectly obvious that people on low carbohydrate diets, with their chronically reduced insulin levels, should be hungry. After all, I have seen it suggested by Stephan that insulin might assist weight loss. I'm still trying to get my head around that one, while eating low carb and trying to remember what it felt like to be hungry. Trouble is it's all so many years ago... Of course, as Stephan points out, hypoglycaemia is a potent appetite stimulant. Again LC eaters, with their chronically low blood glucose levels, should be ravenous. I'm also trying to get my head round that one too. Reality occasionally gets in the way of great theories. Sigh.
I'm not quite sure where to put in the neuronal insulin receptor knock-out mouse. It's fat, so the conclusion appears to be that brain insulin receptors are important to satiety. I'm sure they are. However, these fat mice are also hyperinsulinaemic and will be lipolytically challenged. I love these particular KO-mice... They do not have me mainlining insulin as a weight loss drug. I love the impaired spermatogenesis and ovarian follicular maturation too. I still would not decry leptin here but these hyperleptinaemic mice don't do reproduction terribly well. Dare I use the I-word when talking about fertility?
Insulin inhibits lipolysis. Don't forget that when we come to talk about the Pima.
Before we move on let's look at the satiating effects of foods. Stephan's refs 4, 5, 6 and 7 suggest no macronutrient matters much and ref 8 shows protein is more satiating than carbohydrate. But reference number 9 is the absolute beauty.
Satiety is proportional to the insulin response to protein. Wow! Must be the anorexic effect of insulin.
But there are problems, wouldn't you guess. I don't have the insulin/glucose data following ingestion of any of the proteins mentioned in the abstract but let's look at the effect of casein, which I do have data for. The principle is identical.
Casein raises blood insulin level from 39pmol to over 100pmol and it's still at 90pmol by the three hour mark when sampling stopped.
Amen, RIP the insulin hypothesis.
But just a minute.... There is no sugar in casein, any more than there is sugar in beef. If we took these same seven volunteers and, without feeding them, injected them with enough exogenous insulin to raise blood level to 100pmol and peg it there while simultaneously locking the canteen door, they would die in hypoglycaemic seizures somewhere around the 10 minute mark. We could even throw in a little amylin (which obese people happen overproduce, odd that) to stop them being hungry as they die.
But elevating insulin to lethal levels using glucose-free casein, beef, whey, eggs etc all produce acute, severe, unremitting, paradoxical normoglycaemia.
I can't blame Stephan for not mentioning glucagon as it doesn't help destroy the carbohydrate hypothesis. Explaining the physiology seems to be my problem.
In healthy people eating neat protein there is a rise in glucagon which slightly under compensates for, as far as blood glucose is concerned, the rise in insulin. There is normally a slight fall in blood glucose.
Does glucagon increase lipolysis? It certainly does in pharmacological doses, as any physiology text will explain. In real life people seem rather unwilling to publish the data. You would have thought that 30 seconds on pubmed would have shelled out the effect of isolated protein on lipolysis but there you go, the insulin hypothesis, while defunct, discourages dabbling...
In this study they fed children consistent meals of mixed formula for a couple of weeks, then they switched them to a split meal protocol with most of the carbohydrate in the morning meal and all of the protein in the afternoon meal, fat being held constant for both meals.
The morning high carbohydrate meal suppressed FFAs as you would expect because insulin inhibits lipolysis. The afternoon meal of reduced carbohydrate, high protein content spiked insulin all right, but also increased FFAs. As dietary fat was held constant those FFAs almost certainly came from lipolysis. The group didn't measure glucagon but normoglycaeimia in the presence of insulin smells of glucagon to me.
Whenever someone does a hatchet job on the carbohydrate hypothesis using the insulinogenic index of beef without mentioning glucagon I am left wondering why they were carrying an axe in the first place. I find this thought very uncomfortable.
As a complete aside, people may enjoy this snippet on glucagon receptor deficient mice. You can eliminate the diabetic phenotype induced by massive streptozotocin overdose so long as glucagon cannot act. Interesting stuff but off topic really. But you cannot have death by lipolysis under hypoinsulinaemia without the lipolytic action of glucagon...
We next have two excellent studies correctly showing that resting energy expenditure is higher in both Pima Indians and schizophrenics in direct proportion to their hyperinsulinaemia. Oddly enough they don't simply melt away to size zero supermodels under the anorexic effect of insulin because their post prandial thermogenesis is depressed to almost exactly the same amount as REE is increased. Neat huh? Did you realise when you read the citation?
There comes a point at which fat cells become sufficiently insulin resistant that they cannot hang on to the their fat content. You can still put fat in there with minimal insulin and minimal insulin sensitivity. Once adipocytes are sufficiently insulin resistant and they are leaking sufficient free fatty acids to match input, obviously weight gain stops. The inappropriate spilling of FFAs causes palmitate deriviatives to be produced which worsen insulin resistance, whole body, and obesity flips in to diabetes.
I am in complete agreement with Stephan here. What I object to is citing a situation where insulin is failing to progress obesity, when it is doing its best to, as evidence it did not cause it in the first place. Insulin is trying and FAILING to make the adipocytes fatter. The more impossible the task, the more insulin is produced.
So we have a muscle cell, for example, which is wondering what the hell is going on as it sits in a sea of glucose and free fatty acids which is physiologically completely inappropriate. As we have been told by Stephan:
"Let me explain what the primary role of insulin is. It is to coordinate the metabolic shift between burning primarily fat, to burning primarily carbohydrate. Any time insulin suppresses fat oxidation, it increases carbohydrate oxidation by an equivalent amount. That is what it is designed to do."
In morbidly obese people, as they flip in to diabetes, this is EXACTLY what insulin is NOT doing. If you make fat cells more insulin sensitive (or generate some new, insulin-sensitive adipocytes), say with with PPAR alpha agonists, you will correct the elevated FFAs as insulin starts working on fat cells again and diabetes will abate slightly until the ability to store fat under the influence of chronic hyperinsulinaemia is once again lost, but at a higher fat mass.
I dunno, maybe PPAR gamma agonists simply increase food reward??????????????
Why is resting energy expenditure high in the obese? The body hates hyperglycaemia and wants to burn glucose whenever it's high. FFAs are a supply led system. Failure of adipocytes to respond to insulin increases supply. You then have excess glucose from the diet and excess FFAs from leaky adipocytes. You have to do something with the calories.
So does this destroy the "insulin locks fat away and decreases the metabolic rate of hyperinsulinaemic people" hypothesis? This has particular relevance to the multiple observations of utterly impoverished communities were adult obesity co exists with infant malnutrition. I would stress that this does not reflect the situation in the Pima community as studied in the 1990s, where childhood obesity has certainly been an issue and calorie malnutrition is not. Everyone has enough junk food to eat. Everyone can be obese, everyone can have enough calories to run a high REE, keep total caloric output down by decreased post prandial thermogenesis and still manage to gain a few grams of adipose tissue a day until diabetes sets in.
If there is enough obesogenic food for all, a mother will be hypermetabolic at rest and her kids will be fat. The insulin hypothesis predicts that if there is a restricted supply of hyperinsulinaemic food the mother will remain fat due to her hyperinsulinaemia, while the child will remain emaciated while ever she maintains some degree of insulin sensitivity.
Let's do reductio ad absurdum: Mother and daughter have 8000kcal of hyperinsulinaemia generating food available. Mother eats 4500kcal, becomes as fat as her adipocytes will allow her to, then she leaks FFAs from her adipocytes to become diabetic. Daughter eats 3500kcal and does the same. Both are hypermetabolic at rest, the mother more so as she is not growing. Both become obese.
Now lets say mother and daughter have 2000kcal between them. Mother eats 1100kcal, moves as little as she can, drops her metabolic rate, is hungry all the time but stays fat. Daughter eats 900kcal and is malnourished, becomes emaciated.
This is an aspect of the insulin hypothesis which has not been tested for obvious reasons. It will be correct, in my opinion. I am unaware of any evidence base for this.
As I understand the reward hypothesis, the mother and daughter eat a high reward diet, hit their dopamine system, desensitise it by over rewarding and this ups the hypothalamic fat set-point. Mother increases her calorie intake to maintain her set point level of fatness and eats her starving daughter's food to stay there. Fascinating.
The dietary practices of the Pima under severe calorie restriction are a complete unknown to me but I have serious problems with the reductio ad absurdum example I've just discussed. I've never met a mother who appears to behave that way, but maybe I've never met anyone with adipose depots far enough below their bodyfat set-point to behave this way...... Even folks on WeightWatchers seem mostly human.
So looking at modern Pima Indians or schizophrenics fed to satiety in no way tests the insulin hypothesis of restricted metabolism under conditions where insulin remains elevated and people are hungry. In fact Stephan's neat leptin reference suggests if we went in and injected the hungry, obese mother with leptin twice a day we would reverse her hypothyroid state, fire up a few uncoupling proteins and stop her being hungry. We might even drop her chronically elevated insulin levels. She would lose a ton of weight, give all of her food to her daughter and die of a starvation related illness herself. Injectable altruism...
Looking at multiple studies where adipocyte insulin resistance has occurred under ad libitum conditions certainly demonstrates how metabolism breaks under free access to insulogenic calories. I can't see how it refutes the role of insulin in obesity. It utterly destroys a straw man, but you have to actually do some thinking to understand what is going on.
It's all genetic:
Twenty monogenetic obesity syndromes! All in leptin signalling! Unfortunately a) That hasn't given us 20 solutions to help the 200 million overweight and obese people in the USA. and b) In the last 30 years fat people must have instigated a covert "fatties only" breeding program. Think of orgies where skinny people get castrated by fatties as part of BDSM games. We all know it's happening and there is a government cover up. From about the 1970s onwards.
Ultimately life is genetic and if there wasn't variation in response to insult there would be limited ability to select for surviving that insult.
If you want to REALLY look at what a blind alley the genetics of obesity are leading you up just try ref 35 from Stephan. Same genes in Mexican Pima and USA Pima. Only the USA Pima are fed on "D12451" and look like ob/ob mice. Mexican Pima eat Mexican food and blend in to the population. I looks like my BDSM hypothesis on generation of the obesity epidemic might be incorrect. Ah well, back to the drawing board.
Let's look at the natives:
Starch based diets are not associated with obesity. They do not cause hyperinsulinaemia, post prandial or fasting. They do not cause insulin resistance. You can, with significant effort, become obese on starch but only if you force yourself to do so.
I agree with this, in unacculturated people.
I think it might even have applied to people in the USA of 1900.
I disagree with this if applied to the current industrialised world, especially anyone who has become obese. Why should this be?
Obesity was present at a low level in the USA of the 1900s. Rumour, without hard data that I can locate, suggests it affected less than 1% of the population. It increased slowly until the 1970s by which time it was present in around 15% of the population. From 1970 to 2000 it doubled to 30%.
There's a graph on wiki here.
We know form Stephan's neat graph that this gradual rise in obesity between 1900 and 1970 was associated with a fall in carbohydrate consumption and that the rise in obesity after 1970 was associated with a rise in simple sugar consumption.
If you were to include a separate line to show sucrose (plus, as it became available, HFCS) it would rather neatly parallel the obesity curve. Obviously no one wishing to discredit Gary Taubes would do this but, if you are interested in hyperinsulinaemia as a cause rather than a consequence of obesity, I would suggest that you might be rather interested in this line. Once you are insulin resistant carbohydrates become spontaneously fattening. No ritual needed, it happens very much against your will.
The body uses fructose to replenish liver glycogen. There, I said it. The occasional bit of fruit will not make you obese. You only convert fructose in to a fatty liver through denovo lipogenesis when intake is in excess of what humans are remotely able to make use of. Elite athletes consume rather a lot of fructose. It helps them win races. Try breaking your leg by falling off your pushbike and then still keep up the cola consumption needed to keep you in the yellow jersey... You may just develop a fatty liver. OK, you will.
With a sucrose content in the diet averaging 64 lb/year very few people would start on that journey to hepatic denovo lipogenesis in the USA of 1900. At 120 lb/y over a third of the population will go that route. Once you have accepted that dietary fat causes obesity you are then going to eat the replacement carbohydrate which will dial up your fasting insulin and hunger. Official fat phobia kicked in during the 1970s...
Oops, I forgot that insulin is a satiety hormone and facilitates weight loss and a low insulin level will make you hungry. That good old low carbohydrate paradox.
There is a rather stupid saying that "you are what you eat". It is slightly better phrased as "you are what you do with what you eat". You could go so far as to say "You are what your food does to you". I won't go in to epigenetics except to say that you can think about the phrase "You are what the food eaten by your mother and granny did to you". Certainly to your X chromosome(s) and your mitochondria.
In 1900 very few people had grannies who consumed even 64 lb/year of sucrose. More likely less than 30 lb/year. I remember dipping white bread toast spread with margarine and marmalade in to tea sweetened with three heaped spoonfuls of sugar at my granny's house in Bargeddie on the outskirts of Glasgow. And being amazed at how she could actually bring herself to inject her own leg every day with insulin. This was back in the 1960s, I'd have been about 5 years old.
If you are overweight and try going on a starch based spontaneously hypocaloric diet you may as well sign up for Barndard's disastrous diabetes diet. If you are far enough in to metabolic syndrome to find the label "diabetic" has been applied to yourself, going to a high carbohydrate diet will ruin you blood glucose control as soon as you stop losing weight. No one can lose weight for ever.
I was going to say that no one is going back to Kitava from modern Texas but this clearly depends on how permanent the damage done to you metabolism is. The more damaged you are, the more carbohydrate restriction is likely to benefit you long term.
As I read through this post there are two things which come to mind. First is that elevated insulin is core to weight gain. Second is that we have to be very careful about exactly what, under which circumstances, elevates insulin. Discarding insulin as a factor in obesity because there are circumstances in which starch does nor invariably elevate insulin is a serious case of throwing the baby out with the bath water. There are circumstances in which carbohydrate does not elevate insulin. Most of us don't live there, we can tell by our waist lines.
This post has been a long time coming. I've not particularly enjoyed writing it. But I have an insulocentric bias about obesity and its host of associated medical problems. Insulin provides a framework which, so far, paints a consistent picture of the way life works. It has served me pretty well.
Time to hit "post"
Sunday, August 28, 2011
Should we abandon the carbohydrate hypothesis of obesity?
Posted by Peter at Sunday, August 28, 2011
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Thanks Peter. I'll have to read it again to really understand, but I appreciate you taking this on.
Stephan wrote in his anti-Taubes/CH creed: "...but the fact is that obesity is a complex problem and it will not be shoehorned into simplistic hypotheses."
That's your problem, Peter, you are one of those damned shoehorners. I always suspected you of being a crypto-shoehorner, but now I have conclusive proof!
I think this back-and-forth, with smart people not being afraid to state strongly-held decisions strongly is...science!
Now the trick is to not confuse the person with the opinion. Everyone is providing great value.
I object to the "crypto".
Excellent post, Peter. Gotta read it a 2nd time later.
Gulp. You are one smart cookie. I mean, pork rind. I mean...never mind. Thanks for writing this. I am really enjoying the discussion.
"Insulin provides a framework which, so far, paints a consistent picture of the way life works. It has served me pretty well."
As an internal medicine doc who treats diabetes, obesity, gout, high blood pressure and hypertriglyceridemia everyday, it serves my patients and I very well and often with spectacular results.
As far as I'm concerned, the proof is in the (low carb) pudding.
This is a very good post Peter and agree particularly about low carb being a no-brainer as a method to lose weight for people coming from a standard american diet. my question is, we hear people talk about damaged metabolisms all the time and i use the phrase alot also. while reading your last couple of paragraphs it kind made me question if the "damage" that's happened to our metabolic system really irreversible?
i've been able to go from obese(~350lbs at my peak) to a person with normal bf%. i used a LC approach to get the train out of the station but along the way somewhere something healed and i've been able to tolerate starch very well. i had been obese since childhood so im pretty sure i was very damaged.
any thoughts on healing the pathways to the point of people being able to eat starch again?
I think this post really points out the differences between how we get fat and why we stay fat, and that the cause may not be the same.
Consider yourself grabbed, hugged and kissed ! And I will be reading it many, many times over.
For me, Stephan's theory continues to be quite valid and could be enormously helpful if applied via population based public health intervention, as well as taught very specifically to new mothers and families, for instance. If stated in people-ese, people can get that from a very young age we are shaping response to food and can choose to provide or not provide a food environment in the home and out which is obesogenic, a la food reward theory. I believe Stephan's theory can also be well used by those who have lost an appreciable amount of weight via low carb or other modifications, and are plateauing, or simply ready to consider more loss and in the long run, the possibility of a reduced "set-point" battle after that weight is lost.By modifying the complexity and stimulating effects of their food, via ingredient reduction and cooking method, they can also move food to a different place in their consciousness, all without resorting to "bland" really unpalatable food. Food can effectively be taken several steps down on the hyperpalatability scale without diminishing enjoyment if this is done thoughtfully when the person is ready. This also can provide a greatly reduced amount of time and thought in daily life which is spent with food, all of which can comfortably move food more toward the "fuel" side, on the "food is fabulous" vs food is fuel" continuuum.
I agree with Dr. N that, "the proof is in the pudding." Even if we knew nothing about the effects of food and hormones we would be able to use our eyes and see the results the bodybuilders get everyday.
Every single bodybuilder in the world uses a low carb diet to get contest ready and they are the leanest people in the world. Do people honestly think this is an accident? The analogy, if you wanted financial advice you wouldn't ask a bum holds equally true here.
If you wanted to get lean and I mean super lean, just look at what bodybuilders do everyday.
I'm not saying that they are the healthiest people in the world longer term or anything, only that when they make up their mind to get lean, they can and do very easily by eliminating carbs.
Sorry to disagree Dr. N because if it were all about insulin we would have cured diabetes and we have not. The reason is simple. It is a brain problem and always has been. The confounding insulin injection and leptin in the brain is not so confounding when you understand the central signaling and pathways in the brain. The details are being worked out now but it is already pretty clear from my readings as I blogged about everyone eventually will realize the problem is in hypothalamus at the hypocretin neurons. Obesity is a brain disorder and has little to do with macronutirents. Great post Peter.
Dr. Jack Kruse
Thank you for your most thoughtful post. Reminds me why I have been following your blog through the years.
An entertaining, thoughtful critique and analysis. Peter, thank you for the investment of your time!
"You then have excess glucose from the diet and excess FFAs from leaky adipocytes. You have to do something with the calories. "
This is suggestive that post prandial thermogenesis should be increased, yet you say in obese subjects it's decreased...
"All you get at low infusion rates is inhibited lipolysis."
I'm pretty sure it depends on the degree of insulin resistance of your fat cells.
"To summarise, if abnormally high insulin levels are needed to deal with unwanted hyperglycaemia then lipolysis will be inhibited until such a time as fat cells become so distended they refuse to listen to this excessive insulin, ie when they have become insulin resistant. "
You're making this seem like the more insulin resistant a person is, the longer lipolysis is inhibited; when in fact it's all relative...the more insulin resistance person will allow lipolysis at a higher insulin concentration than a non insulin resistance person.
"Now lets say mother and daughter have 2000kcal between them. Mother eats 1100kcal, moves as little as she can, drops her metabolic rate, is hungry all the time but stays fat. "
This is the mother you're saying will stay fat because she's still hyperinsulinaemic. Doesn't that mean she's still leaking ffa's....doesn't that mean she's losing fat. Maybe that should be a new post, "When staying fat means losing fat" (to keep with the satiric spirit).
reading this is like watching mike tyson boxing. you wonder what were the opponents thinking in the first place when they got up there. life is unfair!
peter, can I ask you a question on your hotmail account?
The only reason 68% of Americans are "overweight or obese" is because the BMI is such a stupid measure.
Height-weight charts were originally designed to classify 19th century European soldiers. "Overweight" simply meant too heavy to ride a horse (cavalry/mounted infantry). It had nothing to do with health.
In the Australian army it is now uncommon to see an infantry soldier who weighs less than about 90kg. This is because the massive weights (40-60kg) carried by modern infantry require considerable upper body strength.
The reality is that the optimum BMI for males is around 25-35 (females ~22-28) not 18-25. When you consider this it become obvious that only 5-10% of Americans are actually excessively heavy.
The reality is that our parents and grandparents were probably too thin not that we are too fat.
The evidence supporting "healthy" low body fat is essentially non-existent. The ideal for male health is around 15% body fat (25% for females) not the 8% (15% females) favoured by modern fashion.
None of the faculty members when I studied exercise science were thin. Most of the males had a BMI of at least 28 (the highest was about 36)
I will have to read it again, but I think one of your points was that multi-generational exposure to large amounts of sugar first damages the metabolism, then later leads to difficulty with all carbs. I don’t think that was the exact version of the “Carbohydrate Hypothesis” that Stephan was critiquing.
I think all this debate is great, but I think “Carbohydrate Hypothesis” has become rather nebulous in meaning. Some people for example are saying that Glycemic Load is the difference between Western style diets and pre-industrial type diets. I don’t know if these are all the same “Carbohydrate Hypothesis” so I wonder if this terminology is inhibiting better debate.
Chris Masterjohn has posted some fascinating stuff about the effects of choline deficiency on the development of fatty liver disease. Basically that in choline-deficient lab animals (mice? rats? don't remember), it was very easy to induce fatty liver disease but in animals that got enough choline it was pretty difficult to do.
I'm reminded of the last 30-40 years of people being told not to eat liver and egg yolks because they contain cholesterol and saturated fat. The two best dietary sources of that nutrient.
Yeah, I forget to be hungry if I keep my carbs low enough, too. It's actually a problem for me because still being obese, the less I eat, the less weight I lose. I'm guessing I'm not getting enough of some micronutrient or another and it's slowing down my metabolism as a result. I feel like telling people, either go low-calorie or go low-carb but don't try to do both. Well, I'm not trying, but you know what I mean.
Let's not forget, either, that lots of people get metabolic syndrome or go type 2 diabetic who never really got fat. We focus so hard on the fat people but at the end of the day, lots of people are sick. An ex of mine apparently lives on Mountain Dew and peanut butter and jelly sandwiches much of the time. He's skinny as a rail and tells himself he's OK because he's physically active, but he also has high blood pressure, which he has decided is hereditary. And I don't even wanna know what his LDL and triglyceride levels are.
In the end, that's one thing the fat-acceptance people are right about, besides it not being nice or useful to be mean to fat people: it's about the health, ultimately, not the number on the scale. Take care of the health and oftentimes the weight will change for the better.
Liver becomes insulin resistant first, muscles second, adipocyres last. Insulin levels in the obese remain about 10 times those of a normal person even under complete starvation. I would expect that feeding restricted amounts of white bread bread fried in lard and spread with jam would maintain significant levels of insulin in order to get glucose in to muscles. Under free caloric intake there will be excess FFAs available, as soon as caloric intake drops to force some weight loss adipocytes will decrease FFA spillage. Then what happens when you have a choice as to what you do with those 2000kcal between two people?
Everyone loses weight under restricted calories. My interest is in how easily this happens. I find Stephan's posts on drinking Nutribal fascinating.
One of the things I wish to look at is metabolic flexibility, your ability to switch between burning fat or glucose. Poor metabolic flexibility appears to be present early in life before obesity develops.
That's what it's there for.
Yes, the brain controls everything, as best it can. But we can undoubtedly influence it by what we eat...
A close family member lost a ton of weight when he lost his sense of smell due to taking griseofulvin, staring from a very lean baseline. He was pretty depressed too. I have all of these things to consider (and used), they're not to be ignored.
Not really, there's a lot of anecdote out there about a few years, as you know. I would want to know what will happen 10 years down the road with added starch. How healed is healed? I'm VERY dubious of "cures" for type 2 diabetes claims.
I would agree that BMI somewhere around 27 looks to be best on an all cause mortality basis, on the SAD. I think the 5.7% of morbidly obese USA citizens are in trouble. At BMI of 20 I'm probably in trouble...
"Insulin levels in the obese remain about 10 times those of a normal person even under complete starvation."
Hi Peter, I had my fasting glucose levels tested as part of a weight loss program (Yoni Freedhoff's), and my levels were very good, even though at the time my BMI was 38. All the other markers were very good too - blood pressure, cholesterol. Of course, I don't suppose that actually tell me what my insulin level was? Just wondering. It seems that just by looking at my blood, you would never know I was fat. What about that phenomenon? There are people out there who are fat, but don't appear to have metabolic syndrome.
You (along with Stephan and Kurt Harris) have been the guru of nutritional knowledge for me. I know, "no gurus", but oh well. Having said that, with all due respect -
Stephan stated that Food Reward was not THE factor, but A factor. Yes, he used the word DOMINANT. In hindsight a/the word that has created much of the contention and a regrettably poor choice IMO. However the carbohydrate theory as espoused by Gary Taubes indicts carbohydrates as THE factor. More to follow on this point...
Secondly, that low carb remediates metabolic derangement ONCE IT HAS HAPPENED seems quite solid. But what CAUSED it in the first place? In this post you cite what is applicable to natives may not be applicable to the current industrialized world. Moreover we "are what the foods eaten by granny did to" us. I whole heartedly agree, but does this not only suggest that carbohydrates are not the SINGULAR cause of our collective industrialized derangement. Excess vegetable oils, fructose (not glucose), gluten, other neolithic agents of disease??? In other words, excess carbohydrates alone are not sufficient to cause obesity and the indictment of an entire class of macronutrients seems as absurd as the vilification of saturated fat 50 years ago.
You wrote your Chris Voight post which I found fascinating (http://high-fat-nutrition.blogspot.com/2011/03/potatoes-and-weight-loss-1.html). Many great quotes there, but here's one that I like - "Ultimately the ability to live on varied macronutrient ratios comes down to how broken you are, especially your liver. Why a broken liver requires low carbohydrate eating is another post."
Again, I completely agree!!! But the starting point here is how broken we are. What broke us in the first place??? I know I am sound like an broken record and perhaps demonstrating some level of ignorance (which I'm ok with), but the fundamental problem I see in these recent debates is conflating causation with remediation.
My 2 cents/pence-
1) Do low carb diets work, whatever "works" means? YES
2) Do low carb diets avoid potential future metabolic derangements by side stepping many issues and thereby allow one to remain resilient to what granny did? YES
3) Can you lose weight on high carb diet and maintain satiety YES (see potato post)
4) Is there a singular cause of metabolic derangement - NO...I cannot accept YES
Finally, to state the obvious, proving the Carbohydrate Theory does not disprove the Reward Theory or vice versa. Many in the blogosphere/Internet forums (not saying you) seem to be faced with a "one or the other" choice. I am struggling with why anyone feels this is a choice to be made. And to be clear, I am not referring to the biochemical mechanisms which people like you and Stephan will/need-to work out, but the practical implications to the layperson trying to be healthy.
Reward does not equal palatability. Reward Theory does not exclude Low Carb as a strategy for metabolic healing. Again, more of the obvious.
The dialog between Stephan and Taubes has clearly degraded. What really excites me is that you and Stephan are respectful of one another, at least enough to engage in a constructive debate so we all improve as a result. I cling to this wishful thinking that the two of you will collaborate and cooperate. And maybe even Kurt Harris awakens from hibernation. Don't pinch me, I'm dreaming :-)
With the utmost of respect,
(I try to write ironic, I hope you are not offended)
We (and the obese) don't eat carbohydrates (and fat and proteins), we eat food. Food that is made out of different things. For example, food rich in carbohydrates is usually made out of grains or potatoes. These are plants. Plants contain all kinds of substances. Substances they (the plants) need for their survival. Some of these plant substances are very good at negatively impacting other living creatures that try to digest these said plants.
So, to put it short, I think it is the anti-nutrients. Plus an overabundance of plant oil rich in omega-6 fatty acids. And some of the nasty "artificial"" substances like trans-fatty-acids (or modern cured meat).
And as a bonus, can I can imagine a mechanism similar to the (suspected) type 1 diabetes: Infection with an enterovirus, but directed at other hormone producing cells.
I have never laughed so hard at science in my life! Beautiful piece of work.
And I adored the babee :)
I was getting confused and wondering if all I'd been told about insulin was wrong but now it all seems clear again so I shall carry on with my LC tendencies. Thanks Peter...
@Aravind about KH awakening from hibernation, on his latest post Taubes has a comment saying he "spent two hours on the phone" with Dr. Harris, and we know (or is it just my impression) he (KH) is also a friend of Stephan, so there seems to be some effort to mend any burned bridges. Unless of course he resurfaces with yet another competing theory, wouldn't that be fun
I wonder why the pharmacological interests aren't all over the insulin hypothesis? An insulin inhibition drug could parallel the "success" of statins! :)
Thank you for writing on this, Peter. I greatly appreciate your viewpoint.
"One of the things I wish to look at is metabolic flexibility, your ability to switch between burning fat or glucose. Poor metabolic flexibility appears to be present early in life before obesity develops."
I explore this subject at length here:
When Satiety Fails
and there is much more to say about it. The references on impaired mitochondrial function are worth reading, particularly Rogge's research review.
Also, for some reason this article showed up as being ~5 days old in everyone's blogroll when it was brand new...I know a lot of people who skipped over it because of that. Perhaps you could republish, or publish a new article that links to this one?
For many years I have felt that being fat is not a problem per se, provided both glucose and insulin are normalised. Actually losing weight is less important, though it should happen automatically. The elevated fasting insulin and the automatic increase in fasting insulin in proportion to carbohydrate intake are hallmarks of the obese which worry me far more nowadays. This does not happen in normal physiology. Chronic normoglycaemia will address some problems but chronically elevated insulin despite normoglycaemia is of some concern/interest.
As I mentioned, my hill walking friend became anosmic on griseofulvin and lost a ton of weight, very much against his wishes. And became depressed. I would certainly not decry the hyperpalatability concept completely.
I felt compelled to put up this post as I was very surprised at the remarkably poor arguments used to write off the hypothesis of obesity which, at the moment, supplies the only solution to the problem which actually involves eating something resembling food. It's not perfect but it's effective for most (not all) people provided they stick to it.
I watched the debacle between Colpo and Eades and stood back as there is no fundamental difference in their approaches, despite the rich Colpoesque rhetoric. Both are fundamentally correct. But Stephan's post was a complete destruction of the importance of insulin as well as of carbohydrate.
I'm pleased Stephan has down graded the importance of the hyperpalatability concept. It's a start.
As to what initiates the cascade I notice Stephan has commented that sugar is of interest. That's a start too.
Out of time now, JS thank you for putting up the link. I think you have pointed me in this direction before and, as always, there was no time. Nowadays it's worse but I will get there!
Thank you very much, Peter, for this great post.
In my view it is simply so, that starch and sugars are no longer tolerated after beeing fat for over 40 years: since I switched my WOE to LowCarbHighFat last year my healt is 100% up and my weight is 45 pounds down - and I feel great. But every tiny bit of starchy food or sweet fruit makes me sick for days.
Perhaps it is not fully understood how it works metabolically but I will stick to it.
Thanks Peter for stepping into the ring on this issue.
Both arguments are well-reasoned and instructive for the obese, but for many readers like me, the concern is not obesity or even weight loss. It is health.
If you are lean, not leading a stressful lifestyle, get all your vitamins/minerals in and avoid the SAD, do you think it matters to long-term health if one eats 80% starch or 80% fat/protein? If post-prandial insulin spikes aren't an issue for you (aka: not broken), is everything ok?
I remember the first time my 2 year old asked for some of my Lindts 85%. I told her, "you won't like it, it's strong chocolate." She told me that she wanted some. So I gave her a chunk and off she went. A few minutes later she came back asking for more of that "strong chocolate." She wasn't as messy as your toddler, but she's just as cute.
If there's anything else to this post, I'm sure it was good too. ;-)
"The proof is in the (low carb) pudding!"
Although carbohydrate restriction may not "cure" diabetes, it has the ability to dramatically improve blood glucose levels, blood pressure, decrease triglyceride levels, reverse autonomic dysfunction (eliminates sleep apnea, heartburn, migrane headaches, urinary frequency, lightheadedness and fatigue) and improves chronic kidney disease vastily beyond that of any medication. Patients almost universally begin to spontaneously lose weight to boot.
Does every diabetic revert to "normal" with a ketogenic diet? Absolutely not. Some are broken more than others (epigenomics, pancreatic burn out, oxidative stress). But I believe every pre-diabetic will go into remission (not cure).
Every single one of my patients who have been able to significantly reduce their carbohydrate intake have experienced vast improvements in their health and often a substantial reduction in the number of medications required.
There are many details that science will need to better understand what triggered this massive wave of disease the U.S. and other countries are experiencing. But after 4-5 years of utilizing carbohydrate restriction as a medical tool, one thing is for certain in my mind, the carbohydrate-insulin theory is one of the most powerful theories I've ever encountered.
inhibiting glucagon secretion reduces appetite?!
that's certainly an... interesting... interpretation of that study
I really don't know on this one. My gut feeling is that all macronutrient ratios are acceptable if hardcore limited to Food in unbroken people. We should watch the WAP members here, though many will be carrying epigenetic damage. However there has got to be some variation along the lines of your question. Here we seem to have to go to basic molecular biology and end up looking a C elegans worms and sugar and insulin like peptides and reproduction in yeasts. These tend to point me in the fat direction.
But I am undoubtedly broken myself and have spent years losing my evenings to the soporific effect on insulin on tryptophan and serotonin levels. So I'm not really in a position to judge.
If you are unbroken your 24h AUC for insulin on a HC diet will be quite low cf to an inujured person. But I would expect a healthy person on LC to have a lower AUC than one on HC yet with both within physiological limits. You are then in to subtleties for which I do not think we have any answers.
notrace, people are looking at diazoxide, it works well in ob/ob mice but the human studies are not particularly well performed or convincing. Though I quite like some of them.
psychic24, I've not read the fine print but my initial impression is that GLP-1 inhibits appetite and that GLP-1 lowers glucagon... It's a stretch to say lowering the glucagon is the cause of the lowered appetite.
Awesome post! The fact that the increase in obesity parallels the increase in sugar consumption and decrease in fat consumption after fat phobia set in is key. No hypothesis that doesn't explain that and the lack of insulin resistance and obesity in some cultures that do consume a relatively high level of carbohydrates isn't worth testing. You said it and so did Taubes. Carbohydrates aren't inherently fattening, but they become fattening once the metabolism is damaged. How the metabolism gets damaged is what we need to focus on if we are going to do anything about the growing epidemic of T2 diabetes, heart disease, and obesity, and I find it difficult to believe that it could all be in the brain and have nothing to do with the hyperinsulinaemia that results from excess consumption of sugar. The brain has amazing powers, but...
Poorly worded on my part, Peter. But yes, i guess my interpretation is super interesting, Chris.
"The main actions of GLP-1 are to stimulate insulin secretion (i.e., to act as an incretin hormone) and to inhibit glucagon secretion, thereby contributing to limit postprandial glucose excursions. It also inhibits gastrointestinal motility and secretion and thus acts as an enterogastrone and part of the "ileal brake" mechanism. GLP-1 also appears to be a physiological regulator of appetite and food intake. "
interesting part to be taken from this is the fact that GLP-1 seems to be a physiological regulator of appetite and food intake, obviously in the manner of suppressing it. Now what's even more interesting is that it also stimulates insulin and inhibits glucagon secretion...yet it still appears to reduce food intake.
I guess a better way of putting my prior statement: "stimulating insulin while inhibiting glucagon (high insulin/low glucagon)secretion has either no effect on appetite or an effect that favors suppressed food intake"--in direct contradiction the high insulin/high glucagon reaction to protein that was used to justify reduced food intake.
psychic24, yes, the system should integrate. Eat Food. The brain knows this first (unless it is fooled appearences and gets food-product or the menu instead). Next is the gut. If the gut sees enough Food arriving it needs to send a message to the brain to say stop eating. It sends a message to the pancreas to say store food, ie increase insulin, and it sends another message to the pancreas to say stop elevating blood glucose and free fatty acids (via glucagon suppression acting on the liver and adipocytes). This certainly applies to starch.
If insulin is needed but there is no challenge to normoglycaemia there would have to be a differential action on glucagon or catastrophic hypoglycaemia would occur. A hyperinsulinaemic euglycaemic clamp is looking at the effect of a spud only rather than a steak only.
In real life they would integrate smoothly unless your ability to mainatin normoglycaemia is damaged due to the failure of insulin's action on the liver and muscles to do this with physiological concentrations.
My type 1 diabetic patients certainly become acutely hyperglycaemic after a meat only meal. A glucagon spike without a necessary insulin spike elevates blood glucose.
Hi again psychic24, probably still at crossed purposes here.
I would go a step back and argue that protein allows the satiating effect of acute post pranial insulin (and GLP-1) without the inibited lipolysis effect as this is maintained by glucagon after protein but not starch.
Protein allows the intracerebral effects of insulogenic food without any nasty intracranial injection and with minimally inhibited lipolysis...
I have no problem with this. No one is arguing against the fact that insulin is a satiety hormone. My problem is when people argue that it's antilipolytic effect is unimportant.
You read right past the part where GLP-1 "inhibits gastrointestinal mobility and secretion ... In T1DM, gastric emptying, food intake, and appetite were reduced equally during low GLP-1"
A full stomach is a satiation signal. Nutrients entering the bloodstream is a satiety signal. Spreading these signals out over a longer period of time produces reduced appetite.
This is not controversial.
Therefore, your insistence that the appetite-suppressing effects of GLP-1 are due to glucagon is...strange.
Peter you are fabulous.
You have it more correct than anyone else, your reasoning is air tight and completely matches with all the available evidence... not fragments of the evidence, like Stephan and others would cherry pick to suit their novel chances at fame.
Furthermore you are far more intelligent and humorous / entertaining to read than almost any other health/nutrition/weight blogger so I can't seem to understand how this blog remains a hidden gem on the interwebz. Stephan's posts are always filled with mindless sycophants ... I DUNNA GET IT, you need more cred.
I guess it's because Stephan is always promising definitive answers, and dumb people want answers. Your blog leads to more questions, and dumb people hate more questions.
"I dunno, maybe PPAR alpha agonists simply increase food reward??????????????"
Oh noes...Zing. Hee heee.
Excellent post, Peter. Gotta read it a 2nd time later. Awesome work.
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I just found this interesting paper from describing traditional life on the Trobriand Islands which include Kitiva.
The most interesting fact IMHO is that Trobriand Islanders eat only one meal per day in the evening. This explains clearly why Kitivans can eat so much carbohydrate and still be healthy. They have only one insulin spike per day and rely on stored fat as an energy source for the other 80-90% of the time.
The diet also appears to be far more varied over the long term and higher in fat and protein than suggested by Lindeberg.
It seems that there is absolutely no Kitiva Paradox at all.
Before going VLC I used to have one massive high carbohydrate meal each evening, no breakfast and little or no lunch. Like the Kitivans I also had no obvious symptoms of metabolic disease that would show in a basic medical exam. It doesn't mean I was healthy just that I wasn't obviously unhealthy.
Reminder to self:
Place Kitiva Study in the junk epidemiology pile along with the Seven Countries Study.
but it's more than just the kitavans, you have okinawans who subsist on mostly starch. you also have other asians who maintain leanness with a diet comprising mostly from starch. pacific islanders. all it takes is one black swan. it's lazy thinking to try to destroy one study when there are other examples out there that point out the same issues as the so-called discredited one. it's a case of letting your bias dictate the science instead of just letting the science lead you to a more defensible conclusion.
btw, i'm in agreement that starch is probably not a good idea for the damaged. but for those undamaged or "healed"(i consider myself amongst the latter) it is tolerated pretty well. the baby and bathwater analogy goes both ways.
Peter - do you have any revisions to your Potato post based on this current dialog - http://high-fat-nutrition.blogspot.com/2011/03/potatoes-and-weight-loss-1.html
You wrote - So you have to ask whether an almost all potato diet genuinely leads low fasting insulin and subsequent weight loss. For my perspective the answer is yes. The precedent for this has to the Kitavans with fasting insulin levels of 4.0microIU/ml.
Perhaps another way of asking the question - Do you agree with blogblog re: the Kitavans. I do not agree unless some babies are more convenient to throw out than others.
I have a really hard time discerning when Peter is writing tongue-in-cheek and when he is making a straightforward statement. I know many readers appreciate that style, but for me, it only serves to confuse an already extremely confusing subject. The baby and bathwater analogies lost me entirely...
I will clarify it for you.
Stephan has dancing around proclaiming to have "destroyed" the insulin/carb hypothesis of obesity via lab studies where experimental subjects have their ventricles filled with a direct infusion of insulin, while maintaining blood glucose to normal levels. That means to say, in a lab, where everything is controlled, higher insulin in your brain makes you super not hungry. Which can be filed under D for Duh.
However, further even slightly curious investigation reveals the fact that any slight change from this perfect lab condition, i.e. relative hypoglycemia, a fall in blood glucose, quickly mitigates and undoes any appetite suppression or other benefit of high insulin.
Peter then goes on to describe a myriad of insulin linked abnormalities present in fat and diabetic people... and how things do NOT work like a direct brain infusion of insulin.
In other words, when Stephan conveniently dismisses the carb hypothesis as invalid based on a few isolated, irrelevant studies where cerebral infusions of insulin suppress appetite, but IGNORES the much more vast pile of evidence that high insulin and glucose metabolism dysfunction is at the heart of obesity, he is "throwing the baby out with the bathwater".
Which is truthfully too kind, IMO, because the phrase assumes his motivation is innocent but overzealous and misguided.
I personally just think he is a liar looking for fame and attention and doing what he can do to get it, because there is no way anyone this intelligent can be this illogical, assuming his investigations are honest and his questions are genuine. No, he's just trying to promote an idea and be somebody, truth or not.
Since such a huge proportion of the human population displays some degree of insulin-resistance, why do we continue to consider those of us with insulin-resistance to have "broken" metabolisms? It has occurred to me recently that I do not have a defect at all (I am extremely carbohydrate intolerant and so is everyone in my family, which points to a genetic trait), but I am actually quite normal. I am of the opinion that it is not insulin-resistance that is abnormal, but the modern, grain and sugar-based diet that is abnormal and that 75% of us (a number that I found in the recent Volek/Phinney book) have simply not evolved to handle the carbohydrate load it delivers. The pancreas keeps pumping out more and more insulin to try to force all that glucose into cells that genetically can't take it in. Those who can handle a carb-based diet (I keep seeing arguments for plant-based diets that cite the Kitavans) apparently are members of ethnic groups that have evolved selectively to thrive on the diet that is suitable to their environment. Those of us who are of African-American, Native-American, and northern European stock are still hunger-gatherers genetically. So, I refuse to consider myself to be "defective, but normal and my health is spectacular as long as I consume the diet that is appropriate for my genetics, which happens to be very low-carb and high fat. I thrive on ketones, and can bike for hours and hours at a pretty good clip. At age 59, that might be considered to be abnormal. :)
Wonderful post! All I know is that I've been vegetarian, & vegan, & done SAD, but only have lost weight and felt good, can sleep through the night, and have good blood work numbers on a low carb primal diet.
I see no explanation in this post for how short term insulin spikes result in hyperinsulinemia. No proposed mechanism, no evidence, etc.
I also see no explanation for the existence of people who are overweight/obese but not insulin resistant or hyperinsulinemic, of which there are many.
The negative feedback loop between adipocyes and the hypothalamus is pretty well established in the literature, and nothing I have read here really discredits it. I think that a lot of your assertions are attempts to discredit the position that insulin is totally meaningless, but that is not what we are saying. We are saying that insulin is a slave hormone to the master hormone leptin. It's still important, but its action occurs downstream of leptin.
@Peter - Looks like a virus has infiltrated your blog because some comments aren't getting through.
@Woo - you are a joke. You provide references for nothing, hijack other bloggers' comments, and then have the audacity to call people liars and repeatedly insult them simply because the individual has a position that is different than yours. Reasonable people can disagree. You are anything but. Perhaps you should replace your Leptin injections with some Prozac, or just develop some class and dignity. Not likely.
Is there a particular reason you're censoring Stephan (i.e., not posting his response)?
Comment moderation is not enabled on this blog. Rumors to the contrary have proven unfounded.
i know that Stephan has responded in the comments section and whether it's on his end or some type of unknown moderation feature on this site, his response wasn't posted.
Hi Stephan, your comment came through on another post for some reason, here it is copy pasted:
If we're discussing glucoagon, why not discuss amylin, which is a more potent satiety peptide (that has actually been shown to cause fat loss and is currently in clinical weight loss trials) released by the pancreas in response to carbohydrate ingestion? I think you forgot to mention that one.
The larger point is that insulin cannot be viewed in isolation. You can't say "carbs increase insulin, which decreases lipolysis, therefore fat accumulates". The body mounts a complex response to any meal that includes dozens of peptide and nerve signals, one of which is insulin. These are designed to steward the constructive use of nutrients. But it makes the system very complex, and one cannot extrapolate anything from observing insulin's anti-lipolytic action in isolation.
The only way to determine if carbs cause fat gain is by testing it directly. It has been tested, many times, in lean, overweight and obese people, and they don't. If carb-induced insulin suppressed lipolysis and that were relevant for fat balance, you would see that in metabolic ward studies where volunteers eat isocaloric diets of different macronutrient composition. Fat would be trapped in fat cells in the carb group, their energy expenditure would decrease and they would accumulate fat. However, all available evidence (and there is a lot of it) suggests that isocaloric diets have the same effect on body fatness, regardless of carb:fat ratio, regardless of whether they are designed for weight loss or weight maintenance, and regardless of whether they are conducted in lean, overweight or obese people.
I have seen no evidence whatsoever to support the claim that insulin is a physiologically relevant regulator of fat storage under normal conditions. That hypothesis has been around for a long time, but obesity and metabolism researchers considered it rejected by the mid 1980s if not earlier:
I also have seen no evidence to support your statement that "Once you are insulin resistant carbohydrates become spontaneously fattening".
Low-carb diets are not the miracle cure for obesity that you might expect them to be if carb-insulin were a dominant factor. If you look at long-term outcomes, they cause on average 2-6 kg of weight loss at one year, similar to higher-carb diets such as the Mediterranean diet:
LC is no cure for the obesity epidemic. Some individuals have very good success with LC, while others gain weight, but there is no indication that has anything to do with insulin.
I know it is convenient to reject the evidence from genetics offhand, but researchers find this evidence to be informative, particularly because it is consistent with the rest of the literature on how body fatness is regulated.
"Discarding insulin as a factor in obesity because there are circumstances in which starch does nor invariably elevate insulin is a serious case of throwing the baby out with the bath water." There was never any baby here Peter. The carb-insulin-obesity hypothesis never had any serious traction except in the lay press. If it were that simple, obesity would be a thing of the past and we'd be singing kumbaya by now.
Please don't jump on the bashing Woo bandwagon. You always post intelligent, thoughful comments. I look forward to your posts and hope you will continue to focus on content not personalities.
I have had similar thoughts but I don't think I could have expressed it as clearly as you have!
How does prediabetes, diabetes, insulin resistance. . . fit in with your hypothesis? What would your dietary advise be to individuals that have these conditions?
@STG - I will attempt to walk the straight and narrow. But I never claimed to be an honorable man and wear hypocrisy like a badge of honor.
I don't agree with everything Stephan writes. But liar, idiot...completely unacceptable IMO. Sometimes two wrongs make a right, right???
Thanks Peter. I'm sure we're all looking forward to Stephan's apology for accusing you of censorship. :-)
"The reality is that the optimum BMI for males is around 25-35 (females ~22-28) not 18-25."
to which Peter responded:
"would agree that BMI somewhere around 27 looks to be best on an all cause mortality basis, on the SAD. I"
I know that some studies correlating all-cause mortality rates with BMI have tried to account for the wasting effect of cancer, but I wonder how accurate that is, for doesn't weight loss start to occur long before diagnosis? The late Patrick Swayze wrote about how he had already lost weight before other symptoms clued in him that something was very wrong.
I am in good health in my mid-40s and thinking ahead about how to stay that way as long as possible. I observe among female colleagues in their 50s and 60s that mobility issues involving joints used in walking tend to afflict those who are overweight, and this includes women who are mildly overweight and not "fat." The healthiest older women at my school appear lean, except for a bit of post-menopausal widening around the midsection. These women do not all exercise, either. My observations are anecdotes, not science, I know, but human beings are wired to learn through observation and experience.
Peter - it must be a difficult post thanks for writing it. Like you I'm still fairly insulo-centric (nice term!) perhaps until better argument and data come along.
Regarding Velloso & Schwartz and the confusing role of insulin I would like to point out:
a) "the relationship between the concentrations of human insulin in brain and blood was nonlinear" (PMID: 9396070) and
b) "CNS insulin increases glucose and inhibits feeding, whereas serum insulin decreases glucose and increases feeding" (PMID: 1905822).
The error is in assuming that CNS insulin and serum insulin are playing the same role.
When adapting a Kitavan-like diet one should also account for the parasite load on their nutrition and metabolism and whether thermogenesis is desirable.
Thanks for also mentioning C.elegans and insulin. I think what constitutes a better diet would be clearer when the discussion moves away from obesity toward health and longevity and what fuel our pet mitochondria really prefer (hint: it's not carb).
I get what your saying. As an older adult, I like to b.... about the lack of civility in the country where I live (usa). I try to be civil in the public arena but my husband knows that I sometimes lack civility in our interactions!
Stephan said, "...If it were that simple, obesity would be a thing of the past and we'd be singing kumbaya by now."
I don't understand why Stephan is saying something like this (which he did also in his now-removed post), somewhat implying that because something isn't popular, it is incorrect. Nutritionists demonize saturated fat and cholesterol and praise polyunsaturated fat: by the above logic they would be right after all these years of research--does he now agree with them on this front? Also, does this mean Weston A Price's work is a bunch of crap because it hasn't caught on?...Most MDs and nutritionists haven't even heard of Weston A Price.
John N said, "...I think what constitutes a better diet would be clearer when the discussion moves away from obesity toward health and longevity..."
Hi Peter and Stephan,
What are your opinions on ChREBP? Do you think is important?
Respectfully, you are taking the criticisms of your work far too personally. Perhaps this is a function of your age/experience? This shows through in your responses to both Peter and Taubes. I'm not judging you, I am simply stating.
"The larger point is that insulin cannot be viewed in isolation."
The point of every study is to isolate a variable. An analysis of many studies may provide some evidence to base tentative conclusions on. Since every single scientific study seeks to isolate one variable, how can anything not be viewed in some isolation without some subjectivity creeping in during the larger analysis?
"If you look at long-term outcomes, they cause on average 2-6 kg of weight loss at one year, similar to higher-carb diets such as the Mediterranean diet:"
Here is where us current and ex-fatties take an offense to researchers who have never been fat. Seriously? Are your eyes so close to the pages of studies that you miss actual anecdotes and observations from the population? Even if half of all the individuals who ever went on a low-carb diet gained 10 lbs and kept them on, we would still clearly have a collective body weight deficit of more than 5-13 lbs per year.
This, I think, is where n=1 is truly dominant (I'm a health educator). What fattie cares whether it is insulin, leptin, fructose metabolism, or food reward - if eating steaks and broccoli drops 60 lbs off this next year - it works!
What we need is a working practical program, applicable to most, and individualized for the rest; and I think we have this in low-carb eating. The science behind it will always be up for grabs, and I truly appreciate the work that you and your colleagues produce (as well as everyone else), but sometimes when I read some of the content of your comments, I think to myself, this dude may be too smart for his own good.
Don't ever quit Stephan, however - just don't take the criticisms so obviously personal.
This notion that has been popping up...
"Here is where us current and ex-fatties take an offense to researchers who have never been fat."
...is nuts! Researchers research. People who lose lots of weight lose lots of weight, in thousands of different ways.
If there were not a quadrillion peer reviewed articles on obesity, it would be prudent to take advice from the person who is best at losing weight. Fortunately, that is not the case.
""Here is where us current and ex-fatties take an offense to researchers who have never been fat."
I call this the "male obstetricians are incompetent to deliver babies" argument.
"People who lose lots of weight lose lots of weight, in thousands of different ways."
That's why can't use your personal weight loss experience and apply it to everyone else as people lose weight a thousand different ways as you said. That's why can't say carbohydrates cause obesity so carbohydrate restriction only way to lose weight.
Have you ever read Lyle McDonald's stuff, or perhaps ordered his "The Protein Book"? The truth on how much protein you need to become scary to women everywhere lays within. There are actually some studies out on pubmed that are on honest-to-goodness bodybuilders.
That being said, eating 1-2 grams of protein per pound of bodyweight to get big appears to be a myth for the average lifter. This is actually a good example of a pervasive rule-of-thumb that does not make sense, and trickled down from the bodybuilders in Venice Beach decades ago.
Aravind has been attacking me since he started responding to me, he is an abusive, irrelevant coward with nothing interesting or stimulating to contribute to this discussion/debate and I have no interest in even communicating with him. He replies consist of him just basically insulting me as a person. He's pretty pathetic actually. I don't read anything he writes, it has no substance at all. It's like "your mother is a whore and you need to kill yourself". Ok? Thanks? The ironic thing is all of his responses are calling me this bad mean aggressive person, meanwhile I've never said anything to him but he has been tearing me apart for a few days now. Kinda funny. I think he needs some real life friends or hugs or something it'sl ike he gets off on attacking me on the computer.
I would also wonder why aravind has this creepy, unsettling reverence for stephen guyenet, as if he were a personal relation? I think someone needs to work on their boundaries. If I accuse stephan of possibly lying, or willfully misrepresenting information, how does that affect you personally? Why do you care?
DUe to the influx of stephan's weirdo, manson family-like abnormally emotionally dedicated sycophants I suspect this discussion is going to nose dive like a terrorist hijacked plane. It's a shame, it might have been a good discussion.
@It's the Woo
You're in luck. I saw Aravind get way too many hugs from beautiful women at the Ancestral Health Symposium.
Also, have you considered chillaxing a bit? I do enjoy reading some of your posts, but some of them seem a tad too personal. Some traditional cultures use kava kava to relax :)
OK, so what do you do if you are morbidly obese and had some good results with low carb at first, was kinda bad and went back and forth on it, and then now find lowcarb doesn't work anymore. You eat low carb, then your blood sugar crashes to dangerous low levels after every meal (hypoglycemia). Blood sugar is never too high, just too low after eating low carb meals, unless you eat some carb. Overall, you are not hungry much, especially on lowcarb, and can easily forget to eat all day, yet you can't lose weight. Sounds like some kind of hyper insulin problem but what to do about it? What diet to try if eating low carb causes hypoglycemia and the body has reached a point where it apparently almost refuses to go into fat burning mode at all. Part is genetic tendencies as older generations gain weight easily as well and many have become diabetic instead of becoming hypoglycemic. Yes, evil SAD got her there but then what kind of diet might help her? Doctors just tell her to 'eat less' but since she is already barely eating, that is not helpful. Doctors tend to assume that if you are fat, you MUST be eating a lot. But she is anexoric and has to be sometimes reminded or cajoled into eating. What can you do once metabolic derangement puts you into such a state? Any suggestions as to what to look into next would be appreciated.
You're too educated and thoughtful to think that these two examples are even the same ballpark. Babies deliver themselves, unless of course there is a problem, and in that case of an emergency I can't see how being male or female would preclude the attending physicians care.
The point I am making is that there is something different about those of us who have lived through it, and pondered on it from those who merely ponder on it. It doesn't necessarily make those who were never fat incorrect, or even without passion - it simply causes their focus to be more easily displaced - relying on research without any insider's viewpoint. Certainly, you can understand this.
Don't take my words out of context from that paragraph and ignore the foundation they laid upon - you also know that this is closer to the truth than what Stephan wrote about.
I respect your work, Dr. so don't get me wrong, but you can tend to be a bit deity-like, if not just narcissistic. You've acted like I took a shot at the whole community of research, when in fact, I've pointed out one idea about one particular researcher.
But I forgive you - I'm easy like that.
Your referring to "peer reviewed" as if it was the word handed down to us is the main reason to simply disregard anything that you have to say. Peer reviewed ain't what you think it is, buddy - mostly politics and little to do with precision.
Good timing! I just peer-reviewed my very first article this year, for the American Journal of Clinical Nutrition (I work in the evidence-based medicine field). I totally agree with you, peer-review is a bit of a joke with respect to article selection, but it can be very rigorous statistically/methodologically.
But why be nasty? My point was that there is a wealth of literature out there to be examined. By literature, I mean articles in journals and not on random websites, hence using the term "peer-reviewed". You can still disregard anything I have to say, but pick a different reason!
Actually I did not read your comment, and still haven't. My one-liner was responding to kamal. So you can't assume I think anything at all about your post.
Being fat gives you no more insight into obesity than being diabetic does into the science behind it.
Unless you are merely talking about the subjective experience of being fat, and not mechanism based on science.
I stick by my analogy. And it's obvious you've not delivered many babies if you think obstetrics and midwifery are superfluous.
And WTF is with discourse on the internet these days - a personal insult in every comment.
Did I address you by name? No, I did not even read your post.
Did I call you a name? No.
But I am the deity-like narcissist?
One more thing. If we're getting all semantic up this piece, you're using the term "precision" wrong in your commentary here:
"Peer reviewed ain't what you think it is, buddy - mostly politics and little to do with precision."
Precision refers to reproducability, while accuracy refers to veracity/truthiness. Journal research tends to be precise but not accurate. See the famous article by John Ionnidis in The Atlantic. Publication bias allows most any big cohort with p<0.05 for "fat=bad" and the like to be published. Hence, there is a large cluster of articles that have similar, confirmatory results (reinforcing the previously known "prior probability"), but are not at all accurate because of cohort study design.
So you should have said "Peer review has a lot to do with precision, and little to do with accuracy."
You're right about possibly not quoting me directly, though it was my quote and you left it address-less so what was I to think? In light of your stated position, I stand corrected, and apologize.
You weren't making a distinction between midwifery and obstetrics, you made a distinction between male and female physicians - unless I read too much into this statement as well.
I do apologize, sometimes we don't have the time to completely explain ourselves in the Inet, and get taken out of context regardless. I understand, and again, I apologize.
But you are a bit narcissistic, no? That's not an insult or a judgement, just an observation. I guess we all are to some extent.
Where do I go here? First let me apologize. Second, of course you're one of the gatekeeper's, now it makes sense as why you would refer to it as passionately as you did.
Precision is a measure against a standard; accuracy is a measure against another measure - unless I completely forgot my physics. Journal research tends to be precise (i recant my last post), exactly for this reason, but only in one variable (if it was designed correctly). It is the analysis of many such research pieces in order to bring together a dominating story - to come to conclusions, that I have a problem with. This is not only no longer precision, but, in most cases, a lack of accuracy as well.
What works on paper doesn't necessarily work in the real world.
No worries - were all trying to work it out. Again, my apologies, its late here and I've been hitting it.
I don't understand how you read narcissism into Dr. Harris's post, and neither do I understand how you read me to be passionately defending peer-reviewed research. I'm not even sure why I'm responding, to be honest.
Did you see that Dr. Harris was simply throwing out a zinger? And also how I referred to peer-review article selection as a joke? I'd obviously rather read some hyperlipid/guyenet/harris then the latest "insight" from the nutritional epidemiologists at Harvard.
All I'm saying is that reading comprehension is important, even in the labyrinthine world of blog comments. And it is rarely beneficial to thrown around veiled insults.
I keep seeing these metabolic ward studies being brandished about as if they are the end all of this or that debate. This is kinda curious to someone who designs clinical trials for a living (it would be nice if a statistician could chime in too about this). Just like Stephan's current "study" to test the food reward theory, all metabolic ward studies are underpowered and too short in duration to impart anything concrete about the diets being tested. Basically, the authors are gambling that they will get the results desired despite the low predictive power. We occasionally do this in the pharmaceutical industry (targeting the producer's risk side of the equation as opposed to the consumer risk). And when we do, the FDA or EMA or TGA, etc, usually take a big chunk of flesh out of our gluts. Unfortunately, this level of scrutiny doesn't seem to have infiltrated the peer review process of journals (the good ole boy’s club, as some like to call it). IMO, metabolic ward studies--all of them--are badly designed. For example, a fatal flaw I’ve noticed in all those I’ve peruse is the absence of a run-in period (sort of like a washout period for pharmacokinetic studies) before and after switching from one diet to the other (for crossover designs). This is absolutely crucial when you consider there might be an metabolic adaptation from burning predominantly carbs or fat. It's not done because the researchers aren't very good designers of clinical studies. Run-ins also increase the expense quite a bit. There are many other factors relating to the standardization of these type of studies that make them not as deity-like as Dr. Harris. Just my 2 cents (may become drachmas soon).
Excellent points! I can give a brief personal perspective, although I'm not as versed in study design as you. At our work, we do systematic reviews for the government. During this process, we have to decide if it's possible to do a meta-analysis of the data. Often, it is not, because of heterogeneity in populations and interventions. We usually have large trials too, not the small ones you mention.
In these tiny metabolic studies, the authors will often say something like this in the discussion "One limitation of our study is the small number of participants...our results suggest that a larger study should be done." The problem is that larger studies are often not done. And when the original studies are vastly under-powered, you get a random slice of possible outcomes. In these studies' favor, however, is the fact that they are often more highly controlled than intervention trials that involve more vague diet prescriptions, or use a food-frequency questionnaire to link diet with outcomes. Statistical power and significance are used similarly through different types of studies (alpha 0.05, power 0.8) without consideration of what is being studied.
Which all brings up an interesting point...what is the threshold for believing evidence and extrapolating it to ourselves? One of the uses of evidence-based methodology research is to make these thresholds. But the field has not been around long enough, and certainly does not systematically review paleo topics. There are so many issues, some of which you mentioned (lack of run-in period). Ideally, small studies would influence larger trials, and these could lead into even bigger multi-center trials so that even subgroups would be powered enough to draw conclusions.
But until then, we have the Paleo Blog Wars of 2011!
Peter, thanks for this post. Seems like the central actions of insulin are pretty ambiguous in the ocean of hunger-appetite-satiety-satiation-etc mechanisms we barely know about whereas the peripheral actions of insulin are pretty unambiguous in relation to bodyfat gain and retention. When Taubes says in his latest blog that he is arguing for the carb/insulin hypothesis "or something like it," he seems to be indicating the general argument is that the primary cause of obesity is to be physiologically found in adipose biology (e.g. lipid oxidation, peripheral insulin) influenced by diet and fetal environment as opposed to psychology or neurobiology (e.g. dopamine signaling, central leptin). Anyone else see the blog debate this way? High dietary sugar and/or refined carbs trigger the adipose biology problems a la Taubes. I thought he made this abundantly clear in WWGF?
Kamal, that's only what "precision" means within the terminology of academic statistics... in our natural language games outside stats, however, accuracy and precision are often synonyms as indicated by common lexicographical sources. Just sayin.
ItsTheWooo2, I think I agree with many of your positions on obesity etc, but I appreciate your comments for reasons completely unrelated to the substance of those issues. They funny.
KurtHarrisMD, what happened to you? You used to seem so on-point and conceptually clear. You had evidently absorbed insights from Taubes, Wittgenstein, and Rothbard. Rare. Now you're about attacking a strawman all-carbs-are-equally-necessarily-fattening hypothesis and proffering "multifactorial reward dysregulating our brains" as a causal behavioral CICO hypothesis. sigh. Sounds like you could seriously use some Wittgensteinian philosophy of neuroscience.
Kamal, as you point out, all studies have their limitations. The larger ones are tougher to standardize, etc. But as we like to say, correctly or not, “there is strength in numbers” (which may be why meta-analysis is booming right now). That’s why it’s important to have a good sample size estimation prior to conducting a study—it fixes the effect of these limitations as best as they can be fixed. There are also secondary markers which can be looked at to assess compliance (triglycerides for carb intake and ketones for fat intake, plus several others), and some obesity researchers are catching on to this (just to corroborate the food questionaire mumbo jumbo stuff). This is why I think the Shai et al trial is a Cadillac of sorts, if you will (not a Ferrari, but a good car nonetheless). The secondary markers are there and you can clearly see that as long as the subjects are compliant, the low carb branch loses at about twice the rate as the low fat side—that’s head to head (Stephan dismisses the results of this study because he’s got other studies that show the same weight loss with low fat as occurred with the low carb branch of the Shai et al study. He completely misses the point that his comparison—across two different studies—is infinitesimally weaker than the comparison within the same trial. There’s a low fat branch in the Shai et al trial that is conducted under the same study conditions--why not use that one? But he chooses to ignore this for reasons only he knows. Of mice and men, I guess). I’ve said enough. Signing out.
but it's more than just the kitavans, you have okinawans who subsist on mostly starch. you also have other asians who maintain leanness with a diet comprising mostly from starch. pacific islanders. all it takes is one black swan.
Okinawans, Kitivans and Pacific Islanders are all Austronesians with a common genetic heritage. eg The entire Maori population of New Zealand is descended from a mere 42 females.
All Austronesians have all hundreds of generations eating a high carbohydrate diet.
Obesity and diabetes is rampant throughout the Pacific. It is also possible that that physical activity and limited food supplies in the past were the real reasons why these people were healthy rather than any adapatations to a high carbohydrate diet.
Okinawans actually have amongst the lowest life expectancy in Japaan. The apparent extreme longevity of the Japanese is almost a certainly a product of rampant social security fraud involving pensions being paid to deceased individuals.
Gary Taubes has explained in detail how hard work and chronic food shortages kept Asians slender.
AFAIK every claim of an "exceptionally healthy" vegetarian society has been completely discredited when studied extensively.
Anthroplogists have known for decades that "primitive peoples" are notorious for deliberately decieving any scientists studying them. They tend to massively exaggerate their age, health status, sexual prowess etc.
I second Lucas Tafur's comment on the potential explanatory importance of the transcription factor ChREBP wrt sugar/carbs>metsyn>obesity. His summary of the current literature on the matter is informative and available here: http://www.ketotic.org/2011/08/chrebp-forgotten-factor.html. Seems interesting.
Stephan and Gary are giving some kind of (half assed) input there... eat bland food . eat low carb. sugar is bad. flavor is bad. etc. both are (lol) wrong.
How exactly and why precisely are they wrong?
heres is my: don't eat. but dont feel hungry.
Fascinating, Pablo. Please share more of your wisdom.
If you are crashing after low carb meals, I bet you are not sticking to low carb LONG ENOUGH to get your insulin levels low and fully adapt to a fat based metabolism. Yea, if you do low carb meals for like 2 days you may be hypoing constantly... if you stick it out for a week I would be surprised if you still continued to hypo after proper low carb meals.
If you are continuing to hypo after a week or more and you are sure you are eating a ketogenic macronutrient ratio, I would consider going to a doctor and getting ruled out for an insulinoma or some other issue like this - sometimes, morbidly obese people are only morbidly obese because of an undiagnosed insulinoma or some other issue with abnormal insulin secretion. It's happened before and no doctor suspects it because people assume fat is caused by gluttony and sloth. This would also be consistent with abnormally low appetite.
The analogy is false because obstericians are trained in the conditions and complications surrounding childbirth - a field where the science is well understood. APGAR scores and magnesium drips and tocometer readings and such - we know a TON about normal labor and delivery, and we know a TON about complications, and we have treatments that work. It's not hypothetical really.
An obstetrician, whether male or female, is a knowledgeable expert who typically knows a lot more than your average pregnant woman.
At this point in medical science, labor, delivery, antenatal care is extremely advanced and we know a lot, and our clinicians who went to medical schools learn this.
Now, on the other hand, with OBESITY? We know jack + crap, and agree upon little other than the fact that you can't get fat if you are starving, and fat people are storing more energy than they are expending in heat or metabolic activities. Which is to pretty much state the obvious.
There is no such thing, at all, as an obesity doctor who is proficient at making fat people thin. At this point in time, there is NO DOCTOR who can do for fat people what an obstetrician can do for pregnant people. Even the best diet doctors don't have very good long term success rates, suggesting our understanding and/or treatment of obesity sucks in some area of care (pre, interim , or post obesity... or, how about the fact that most doctors don't even consider care for obesity may be different depending on current state of adiposity? Because most researchers have such a poor, piss poor understanding of obesity, which truthfully is probably the result of insufficient real world experiments with real world obese people in various stages of fatness and dieting).
We know basics. Then there are the foundation building blocks - type 1 diabetics used to emaciate and develop severe acid base imbalances and die, until we discovered insulin. When we injected insulin into diabetic animals they gained fat. When the diabetic animals didn't have insulin, they rapidly lost fat, fat can not stay in the fat cell without insulin. We learned insulin controls fat cell balance.
But other than this (which some people, such as stephan guyenet, attempt to confuse for whatever reason by presenting the argument that insulin makes us thin, an absurd statement)... we don't know a lot.
You've got people who are like ITS ALL LEPTIN RESISTANCE but you know what, that has never been proven or even demonstrated to be relevant to most obese people. Speaking as a formerly obese person, I am clearly very leptin sensitive, based on a very good response to a low dose leptin replacement. Now what? I DONE SMASHED UP YOUR HYPOTHE-SEEZ BY EXISTING.
Given that, at this point in time, our understanding of obesity is pretty craptastic in terms of mainstream medicine and science, I think perhaps laypeople with experience in successful dieting or even regular obese people who have never lost weight may have some insight that can help further knowledge. If the latest uber hypothesis is going in one direction, but the majority of fat people are like "um no I can't say that this is relevant for me" perhaps that hypothesis is wrong? Hardly scientific, but it is a clue, maybe you need to ask different questions and think of different ideas and examine a different avenue.
It would be like if obstetric care was where obesity care is ... and obstetricians presently were entertaining the crazy shot in the dark hypothesis that uterine contractions were controlled by the amount of pastry products consumed the day before labor, based on evidence that pregnant women seem to enjoy eating a lot of calories from starchy fatty foods. Meanwhile, 15 of 20 pregnant women said they ate no bread before the onset of labor. Perhaps the obsetetric research squad should consider that their pastry products as a controller for contractions is wrong or ask new, different questions, look at things a little differently.
Sorta kinda like that.
@Woo - We can agree to disagree and end this ridiculousness, which is clearly counterproductive.
The writings of Peter and Stephan, along with some off blog exchanges, have been very instrumental in my own personal health transformation. I have a lot of gratitude for the wealth of information they provide and generosity with their time, even when at times I disagree with them. It is out my sense of gratitude and loyalty that I have reacted to your comments. I would do the same for Peter and Kurt Harris BTW. If this makes me a sycopant, so be it.
One final thing - I actually think you have a lot of interesting input based on your unique experiences. I wish you could purge the vitriolic comments at times which distract from the message you are trying to deliver.
My 2 cents...
the Kitivans have just one daily meal. It is eaten as quickly as possible in solitude. They get a 400g bolus of starch, a quick insulin spike and then go back to burning fat for the next 22 or so hours.
In contrast a typical westerner has a constant supply of carbohydrate with only 8-10 hours a day of fasting at night. The body never adapts properly fat burning and has little opportunity to repair itself.
A decade ago I had a very high carbohydrate diet with plenty of sugar. However my blood glucose was just as low as the Kitivans and my blood pressure etc was normal.However I can assure you my metabolism was well and truly broken.
Like the Kitivans I usually only ate one large evening meal per day.
My old and wise GP was sure I was developing Type II diabetes (polydipsia, polyuria) just that he couldn't prove it.
Stephan said: "That hypothesis has been around for a long time, but obesity and metabolism researchers considered it rejected by the mid 1980s if not earlier:
It's curious that you would link SP Grossman from 1986 to make this claim, since he spent the subsequent years of his career analyzing the effects of insulin on weight gain and saying things like: These data support the conclusion that IH insulin infusion alters food intake and body weight through a specific effect on a neural system that regulates food intake and body weight, and not by altering circadian rhythms. So it would seem to appear that he didn't totally dismiss the role of insulin in fatting people up. Or maybe he just enjoyed wasting his time. Who knows?
Thanks for making those points about metabolic ward studies.
Yes, I read it despite disagreeing often with him [Lyle]. Siff used to say the same thing about protein, as do many others. I know what the literature says, but I know too many athletes who can't eat low protein including myself. Maybe it has to do with my natural body type, maybe not. Remember too there's a big difference between someone deadlifting 2x bodyweight & running 11.5s 100m and someone approaching 4x & 10s.
@blog^2 - Thanks for that. So what made you so certain that you were still metabolically broken? Other biometrics like HbA1C, HS CRP? Other symptoms?
I am genuinely curious because I eat a pretty high carb diet currently, but am very careful to avoid neolithic toxins - excess fructose, gluten, vegetable oils, soy, etc. However tubers and white rice are staples for me. My biometrics are trending pretty well and in spite of being at 60-70% carb intake, I am down 22 lbs this year simply by toxin and reward avoidance.
However weight loss is only an ancillary benefit since health and longevitiy are the primary goals. Appreciate your thoughts.
More from Dr. Pablo please. It was time we had an injection of comic relief.
Ok, I'll come out and say it here then: I've gone much higher carb for the last 4 months in order to explore food reward. I'm a VLC traitor!
Well it's mainly a test. I haven't noticed any ill effects from eating high starch. I haven't gained any weight at all and in fact noticed my body has tightened up considerably. But I was never fat to begin with and now I assume I was never broken either. I never intentionally fast and I exercise almost infrequently enough to say I never exercise.
I thought it was VLC that originally helped me recover from so many ailments I was suffering from on the SAD, but maybe LCHF is right for the wrong reasons. Maybe it just happens to coincide with improved health because one cuts out all the NADs along with the carbs.
Let me go on the record by stating that none of this makes food reward theory incompatible with HFLC. Just try eating animal fat (not cream, I mean lard and tallow) with no salt or sugar and I'm sure you won't be hungry ever. It sucks!
kinda interested to hear Peter's response to Stephan...
I feel like these discussions between clashing bloggers (in a purely scientific manner) are very important and often neglected. I'd settle for less 7page-esque passion posts and more 1-2 page responses in the comment sections =)
"KurtHarrisMD, what happened to you? You used to seem so on-point and conceptually clear. You had evidently absorbed insights from Taubes, Wittgenstein, and Rothbard. Rare. Now you're about attacking a strawman all-carbs-are-equally-necessarily-fattening hypothesis and proffering "multifactorial reward dysregulating our brains" as a causal behavioral CICO hypothesis. sigh. Sounds like you could seriously use some Wittgensteinian philosophy of neuroscience."
If there is anything a student of Wittgenstein should take away from his thought -- besides, apparently, the overused (and largely misused) "language games" concept -- is that he was unsystematic and philosophically antitheoretical. He drastically shifted his position over the course of his career in pursuit of what he perceived to be the heart of the matter. (It's also important to remember that nearly everyone gets Wittgenstein wrong, including his devotees.)
So, it's worth considering that maybe "what happened" to Dr. Harris is that he has begun to question yet another dogmatic hypothesis and has yet to proffer a totalizing theory to replace it. That should be fine with us, as we are in search of truth. Indeed, that's what is also compelling about Peter's blog at its best -- he is willing to consider, reconsider and problematize. Arrogance is of no use here.
Hi, Peter. 1st, I suggest a minor correction -- I think that you meant to write "PPAR-gamma" agonists rather than PPAR-alpha (as in the TZDs).
Knocking down a "straw man" -- amen.
One thing I never see mentioned by those in the "low-carb" camp is skeletal-muscle lipotoxicity, which is associated with IR. This is literally from the textbooks, from what I have read. This lipotoxicity typically reduces fat-burning efficiency to levels as low as 10% or 20%, while simultaneously only slightly degrading glucose-burning efficiency (to maybe 80%).
This sets up, it seems to me, a good hypothesis for the cause of developing obesity. IR -> obesity (not vice versa). As the textbooks typically explain, the (classical/original) Randle cycle doesn't work under the chronic-disease conditions of IR.
The longstanding mainstream research only omits the obvious (to me, at least) final conclusion that IR -> obesity. Another clue is that the diabetes research consistently shows IR developing early in life, before any sign of hyperglycemia and often before overweight as well.
Thoughts? Is there a known problem with the idea that whole-body (i.e. skeletal-muscle) IR/lipotoxicity might be expected to slowly induce obesity over time? Taubes writes about IR/lipotoxicity/inflammation in "Prosperity's Plague", but not in GCBC. Too technical a subject for the latter?
By the way, Taubes quotes John Ziman:
regarding textbooks vs. journals. Rings true to me. Further reason for my questions.
Point taken. The wine may have got to my head quicker than I thought.
And I'm not too proud to announce that my insult to Dr. Harris was probably passive-aggressive behavior brought out by a private email between us a couple years ago.
I formally apologize for the insult Dr. Harris; and to both of you for missing the intentions of the earlier posts, and then erroneously commenting on them.
Very cool of you! Let's be paleoblog comment friends.
"Don't get involved in partial problems, but always take flight to where there is a free view over the whole single great problem, even if this view is still not a clear one."
That can't happen until you call me Al.
"I never intentionally fast and I exercise almost infrequently"
great, no that's terrible. stop eating and try to mover your ass more ( that is if you want to stay young) so you "feel great". great. how yrs digestion? sleeping? stamina? how do you look? ( also great?) and how is your health? great? whats your faster blood sugar after waking up? like a number. mine 70mg/dL
( rigth now) usually is a lil lower 63mg/dL . regarding fasting: absolutely no willpower required at all. no "intention" no thinking required. when you get there you'll know. example? just woke up ( overslept, 9 hours) btw im doing my lazy bodyWeight training right now (also every single day)and im not hungry / thisrthy nothing. 26hrs without food btw. in a few ours im could eat whatever the hell i want. (not going to do that) im going to eat the same meal i did yesterday, and the day, before, and before since like 6 months now.( Stephan is right on that one) the thing this meal is 1) super high reward, super high fat, high in sugar(chocolate, full fat chocolate milk, sucrose) and super insulin spiking. so excuse me if i then to lol at all this BS.
Hi All thanks for comments, I'll do my best to get to the important ones.
@eva, hyperinsulinaemic hypoglycaemia is now a well recognised response to bariatric surgery, estimated at 1% or so of victims.
I've not followed this up but I've seen it mentioned elsewhere without taking much note of where it was and you are the first person to mention it on blog.
The question is interesting as to whether it is a surgically induced GLP-1 problem or a result of effects of the intense carbohydrate restriction produced by bariatric surgery (or both), ie can it occur with LC alone as you discuss...
I've not been through the literature to see where a sensible approach might be, and I can't see that changing in the near future, but it is very real.
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Could you describe the meal you've been eating for the last 6 months?
I'm trying to go from eating 3 times, to 2, and maybe 1, but can use a little help.
I started LC for two reasons - weight-loss and migraines. I had several migraine triggers - stress, the end of menstrual cycle, blood sugar drop if I didn't eat in time after my previous meal. Unfortunately, back then I didn't measure my BS and I think I experienced BS drops based on symptoms - being light-headed, shaky feeling, you know.Ketogenic diet helped a lot diminishing significance of the stress and the end of month triggers, but Intermittent Fasting made my BS level really stable and eliminated completely the hunger trigger. However, each time when I increased interval between meals by 1 hour(after 5 hours it stopped), it caused me a migraine.The proses of retraining my body to tolerate hunger took approximately 3 months. It is possible that my experience is unrelated to you because you BS drops not from hunger but from LC.However, I find out that
IF stabilizes BS and somebody's body may be retrained. I eat now mostly 2 times a day during 6 hours window, also, I practice 20 and 24 hours fasts 2 times a week. If I eat LC, my BS never drops below 95 and stays around 100 if I didn't eat carbs. If I eat something sugary, BS will shot up to around 170 then drop to 65.May be some people decide it is too high. I am aware of physiological IR, but right now I am choosing to do what keeps me more functional.
"Thoughts? Is there a known problem with the idea that whole-body (i.e. skeletal-muscle) IR/lipotoxicity might be expected to slowly induce obesity over time? Taubes writes about IR/lipotoxicity/inflammation in "Prosperity's Plague", but not in GCBC. Too technical a subject for the latter?"
Other than the origins of IR being lipotoxicity (which is novel), it is generally accepted among low carb proponents that abnormal insulin signalling - skeletal muscle resistence, with fat cell sensitivity - mediates the development of obesity.
The development of diabetes occurs when the fat cells also become resistant, and that usually happens later in life, after obesity begins to slow or even regress.
Diabetes is all about fat cells not listening to insulin (and, also, the liver). If you suck out your fat cells with a catheter or develop an autoimmune disease which destroys your white fat, you will end up very very diabetic with triglycerides in the thousands, with a liver that is enormous with fat, with refractory diabetes, with a liver that can't stop making sugar even with a high insulin dose.
Look at anyone with lipodystrophy - congenital, or aquired via HIV meds. They are "metabolically obese" in spite of no body fat. Actually, it's not in SPITE of the lack of fat, it is precisely because of the fat. Nothing exists to listen to insulin and process nutrients.
The phrase "metabolically obese" is actually quite ironic and a misnomer, as obese people are protected from developing diabetes as long as they are capable of having working, expanding, growing, replicating, tumor-like fat tissue. Most diabetics do not have the fat cell genetics to grow to be hugely fat, and it's a shame, because if they did they probably wouldn't have serious diabetes. They would probably be diagnosed as a "metabolically healthy obese person", haha.
The obesity associated with metabolic disease is merely a sign that things are breaking down, much in the way flood water rising in your basement is a sign your house gonna done near float away if the rain doesn't stop.
If you circumvent the flood basement protection and just destroy ALL fat tissue, boom you're done, serious metabolic illness that cannot be controlled.
This is why experiments where scientists suck out or destroy white fat cells of obese people lead to a rapid worsening of metabolic syndrome (fat being gained in viscera and liver). Every fattie needs every single fat cell he or she has, as long as she is continuing to take back pepsi and massive sized sickeningly sweet pastry products and healthy whole grain granola products, and other metabolic disease causing foods.
Exercise is a modern invention, which correlates with the "fat is bad" movement in the 70s, and it, like fat restriction, has more to do with morality than scientific reality.
Physical stress is good for the soul! Fat and animal products are corrupting! - Cacophony of religious psychotic morons. Sorry not interested in your crazy emotional ideas about health.
I mean if you like exercise, have fun, but it's kinda like drinking beer: it makes you feel good, but years of it isn't exactly healthy.
Take a trip to a physical therapists waiting room or an orthopedic surgeon's client log to find out about the long term effects of abnormal physical stress and atheltic activity.
Nuttin there but old ppl who ruined their joints due to age, and exercise psychos who ruined them from exercise addiction.
Oh and I'll see how well you tolerate your "one daily meal of junkfood" at 30 or 40 years old. Fact: most young men can eat WHATEVER THEY WANT and feel energetic and be thin. See you early-late mid life, when your mitochondria start closing up shop, how well that's working out for you.
People like me are lucky in an ironic way; I never had a youthful metabolism, I was born with the metabolism of a 45 year old. So, this kinda gives me a head start in learning how not to age poorly because I had to figure it out before twenty.
I missed the part where Eva said she had bariatric surgery... but if she did have it, then absolutely it may be true that she is developing neisidioblastosis from excessive GLP-1 levels. I assumed she never had such a surgery, in which case the most likely cause for this novel hypoglycemia even on a low carb diet would be an insulinoma... which is, actually, sometimes a cause of morbid obesity and is rarely diagnosed because everyone assumes fatties are just gluttonous and slothful.
In a previous discussion on WHS I know I was pointing out that the development of neisidioblastosis after bariatric surgery is evidence that a deficiency of GLP-1 is not necessarily causative - and augment not necessarily theraputic - for obesity (if it was, GLP-1 augmentation would not result in this rare form of pancreatic islet hyperplasia typically only found in preterm infants).
Preterm infants have numerous gastrointestinal disorders which is a direct result of the preterm infant being unprepared to eat.
A common one is necrotising enterocolitis, large intestine rots and dies, not colonized and not prepared for nutrition which is already being poorly absorbed in the small intestine.
I suspect that what happens in bariatric surgery is that the small intestine is paralyzed and mutilated, so nutrients sit there unabsorbed, resulting in inappropriate GLP-1 levels and enhanced satiety , even when eating sugar and starch.
This is also what happens in preterm infants when we ask them to use their gastric anatomy before they are prepared to do so...
The trick with bariatric surgery though is that no one tells them that obese people have a blunted GLP-1 release to sugar and starch only but a totally normal and in tact one to dietary fat, which I suspect is yet another symptom of the genetic phenotype to transiently fatten on seasonal carbohydrate excesses (much in the way the obese also downregulate their dopamine receptors to a high glucose diet, and rapidly upregulate them when food/glucose is restricted).
So they get this surgery, most of the long term effect is in GLP-1 / forced bulimia, but if they adhered to a very low carb high fat diet they get that same benefit without attending risks complications and costs of surgery.
Funny, except not funny.
"I was pointing out that the development of neisidioblastosis after bariatric surgery is evidence that a deficiency of GLP-1 is not necessarily causative - and augment not necessarily theraputic - for obesity"
Im not sure so Woo, have you seen this study?
Reversal of obesity and insulin resistance by a non-peptidic glucagon-like peptide-1 receptor agonist in diet-induced obese mice.
obviously a drug is not the same as endogenous glp-1, but anyway, do you think it is convincing?
I didn't write anything implying that lipotoxicity->IR. I would assume the opposite causation, with IR in turn being caused by a combination of tissue aging and inappropriate diet -- usually (i.e. for most people) too much carb (to greatly simplify).
Also, T2DM is (usually) way down the road relative to Guyenet's (and Taubes') topic of obesity. And more than half the population is basically genetically immune. I wasn't implying anything at all about T2DM either, although the severe lipotoxicity numbers I cited might be more typical of overt diabetes rather than just non-diabetic overweight.
My point is, (I think) lipotoxicity provides a possible model for a gradual gain of adipose tissue. It is characterized by a relative lack of ability to use fat as fuel relative to sugar. This might explain other common characteristics of a high-carb diet, such as a typical need to eat frequently. Fatty acids are always AVAILABLE, but glucose has only small tissue stores (i.e. glycogen) and is more quickly exhausted from the blood (where its concentration is normally regulated), requiring resupply via diet, and so on.
I am just proposing that with IR there is lipotoxicity, hence causing abnormally low fatty acid oxidation and consequently also abnormally high glucose oxidation.
I think that this possible causation of obesity has been intentionally ignored by the mainstream research community, because they don't like the implications (for their grant-money sources, etc.). They'll talk about lipotoxicity in the context of diabetes, CVD, and so forth -- but NOT obesity, which they conveniently insist causes IR (and lipotoxicity itself, by implication)! Hogwash, I say (as does Taubes).
I have no doubt glp-1 helps people lose weight, amphetamines and dopamine agonists also help people lose weight.
I was arguing that a defect in glp-1 is probably not the reason people are fat, just as a lack of amphetamine or other dopaminergic/norepinephrine boosting stimulants are also not a reason people are fat.
If something helps a person lose weight does not necessarily mean that a lack of that thing is the reason they are fat. Evidence is the fact that abnormal GLP-1 levels after bariatric surgery lead to neisidioblastosis, previously only found in pre-term infants (who develop numerous gastrointestinal disorders due to being tube fed before their intestines are working properly).
I don't much put stock into diet induced obese mice. I do not think they have much in common with human obesity anyway.
The diet induced obese mouse is a model of human obesity, which is largely mythical and made up to satisfy the convention "Everyone knows" - that humans become fat because they eat too much fat. This is how the DIO mouse becomes fat, except for the fact its fatness doesn't really look like human obesity. For example, it has beta cell dysfunction, producing insufficient insulin after it becomes obese, which is the polar opposite of your average fat human.
Beta cell failure is a known consequence of insufficient GLP-1, so it may be possible in this particular mouse, its GLP-1 is insufficient after fat feeding.
Most humans do not find dietary fat obesigenic; most obese humans show a far more normal metabolic processing of fat than carbohydrate, therefore teh DIO mouse isn't much relevant to human obesity, it's sort of a "wishful thinking" that it is. The idea that fat makes humans fat is old and outdated, and this genetic freak mouse needs to go out of fashion. A mouse that fattens on carbohydrate would be a better approximation of most human obesities, lol (and even that mouse wouldn';t have much relevance to human obesity as it would probably be one or two irrelevent genetic defects in the mouse which have no relevance to any form of human obesity).
Fat people, again, have been studied and shown to have a normal glp-1 release when eating a high fat food; the GLP1 is only blunted when eating carbohydrate, which again, may be a functional trait to grow fatter on seasonal carbohydrate excesses, much like the d2 receptor downregulation in response to high glucose diet.
I was unaware that amylin facilitated an increase in free fatty acids in the same way as glucagon does, which was my point here. Of course, in the same manner as gastric banding, because amylin physically limits food intake by its effect on the gut, who is to say it does not limit carbohydrate intake. At least they won't be hungry compared to bariatric surgery.
I'm sure the role of insulin was abandoned 30 years ago. A pity, as other approaches do not seem to have been terribly successful. Or successful at all. Perhaps we all just need amylin injections.
Quote from http://jama.ama-assn.org/content/293/1/43.long
"we asked participants to follow their dietary assignment to the best of their ability until their 2-month assessment, after which time we encouraged them to follow their assigned diet according to their own self-determined interest level."
I'm not sure that this is actually a study comparing diets, more one looking at the individual participant's level of interest in the study diets. I could spend a lot of time taking this study to pieces. It would be fun. But figure 4 shows that fasting insulin correlates quite well with weight loss. I am still interested in why Chris Voight lost weight so easily while eating in a way similar to the Ornish diet here, which certainly worked no worse than the other non-diets not-used here, but I'm still looking at insulin levels. I have to accept that there is more than one way to lower insulin levels.
Some quotes from the http://www.ncbi.nlm.nih.gov/pubmed/18635428 study:
Low fat diet:
"We aimed at an energy intake of 1500 kcal per day for women and 1800 kcal per day for men"
"We restricted energy intake to 1500 kcal per day for women and 1800 kcal per day for men"
Low carbohydrate diet:
"The intakes of TOTAL CALORIES, protein, and fat were NOT limited"
Hmmm, now what would an unlimited calorie Mediterranean diet have done? Hint, not a lot.
Next quote is the advice to LC dieters to increase the carbohydrate content of their unrestricted calorie diet:
"20 g of carbohydrates per day for the 2-month induction phase and immediately after religious holidays, with a gradual increase to a maximum of 120 g per day to maintain the weight loss"
This increase partially reversed the weight loss of the first 6 months as carbohydrate was progressively (and deliberately) increased. It would have been interesting to see the effect of specifying progressive (and deliberate) increases in total calories of the two calorie restricted diets. Very, very interesting. And amusing.
End result was not a lot of difference in weight by two years, which could be anticipated if you were told in advance that there would not be a lot of difference in insulin levels at two years.
But look at the effects of the 20g/d period, the first two months. Sort of scary to think what the outcome might have been if they has stuck with 20g/d. And amusing.
Do you have any better studies from outside of metabolic wards?
pablo, take your lithium, man.
it is very easy for males your age to be lean and healthy.
You will probably be as fat and unhealthy as Diego Maradona when you are 50.
Shock! Horror! Mice get fat when fed a high fat diet!
A natural wild mouse diet is <5% fat, 80% carbohydrate and 15% protein. This is less than half the fat levels of even the ultra low fat Pritikin Diet.
yea how about no. (lol, never even smoked, used drugs, alcohol, not even coffee in my life) Anyway, i wish you no harm... Give fasting a try at least once a week and see how it goes.bah, why do i even, do whatever the hell you want.
Peter, I wouldn't expect a response from Stephan.
He made some snarky and paranoid comments about you on Carb(In)Sane's blog a few days ago, among which was a statement that the discussion with you was over:
I have no idea what the hell happened to him. A pity, really.
Glad I'm not the only one who has noticed Stephan's change of personality lately. It is indeed a real shame.
Stephan has also taken a body blow with regard to his proposed food-reward study. Apparently he was not aware of the implications of Institutional Review Boards (IRBs) and informed consents.
I have no idea what the hell happened to him. A pity, really.
He's in the establishment now...
Hello Peter, Really a great post. Gary will be happy with you :-).
One remark: "Don't overdo it with dark chocolate in small children. The theobromine can be very dangerous as you know"
One question: "Do you think very low carb or zero carb can automatically lead to starvation in certain individuals?"
Woo I understand what your saying, just because X cures Y, doesnt necessarily mean lack of X caused Y.
Thats fair enough.
Im slightly biased towards the incretin effect though because its basically the first way that your body hormonally reacts to the food you eat. Every other hormonal reaction your body has afterwards should just be downstream of the incretin effect. So if the incretin effect is messed up, the other hormonal responses should probably also be screwed up.
Thats my thinking anyway.
Stephan's "snarky and paranoid" comments include this, what I think to be a perfectly reasonable bit of criticism (with a touch of self-analysis):
"These last few years have been full of scientific growing pains for me, as I have realized that some of the people I respected have built their houses on sand and are irremediably wedded to their ideas."
The sentiment is right, after all, as anyone that read GCBC or has any involvement with the scientific (dis)establishment well knows. Stephan didn't specify at whom he was directing his attention. But it seems perfectly plausible that the statement could've easily been written to or BY Taubes, Peter, Harris, or any number of other bloggers with respect to any of the same.
The most frustrating part of the comment series from which the above was extracted is the ongoing bitter exchange between Harris and Evelyn/Carbsane. At this point, petty quibbles have begun to (apparently) "irremediably" cloud the potential for productive debate and discourse, increasingly undermining the usefulness of the scientific vantages being offered up. The same is true here and there in the blogosphere -- Stephan vs Peter, Stephan vs Taubes, Woo vs everybody, Taubes vs The Unreflecting Status Quo, etc etc etc. Admittedly, vigorous debate can be useful, but ad hominem is never useful and seems to be employed with increasing frequency. And, if not ad hominem, a basic unwillingness to take a step back or to reassess has become the mark of the upper hand. Condescending, sarcastic comments grace EVERYONE'S posts at this point. Consistency in analytical deftness is one thing, consistency in ideology (or even emotionality)is another.
From a purely selfish point of view, I feel as though I'm watching the clarity of the picture recede, but rather than being stimulated by the newly emergent possibilities, I'm being mired in a lot of smart folks' dirty laundry. About the only unembattled blogger I regularly read at this point is Art Ayers, but surely I won't have to reduce my range of perspectives simply because it's hard to trust that emotional intensities aren't confusing scientific rigor?
Thanks for the heads up, there's nothing much more needs to be said about Stephan's comment anyway and CarbSane is not a blog I read, oddly enough. I'm not starting now.
The only light relief in this whole episode (pax Gunther) is having had Stephan post his comment, presumably by accident, on the Mice and Breast Cancer post and then to find myself accused of having censored his reply.
I know I have a warped sense of humour but I found that very, very funny.
Is Stephan perhaps a 12-year-old girl merely posing as a 30-something science blogger on the internets? Sure seems out of character to make a silly comment like that. Maybe he's just trying to endear himself to carbsane by mimicking her batty personal attacks.
I wasn't implying that HarrisMD or anyone else shouldn't change their mind based on new evidence or whatever, but pointing to a conceptual problem in the "obesity is caused by 'food reward' dysregulating our brains and thus making us consume more calories" thing. Positing normal neurobiological as the relevant cause of behavior is problematic.
As Bennett and Hacker summarized:
If you look from one domain of cognitive neuroscience to another you will find that the operations of the brain thus conceived are being advanced as explanations for human behaviour, for our thinking, believing, seeing, hoping and fearing. That’s wrong, because it’s no explanation. If someone wants to know why poor old Snodgrass, as the result of some lesion, can’t do something that normal people can do, and you say that his brain can’t do it, you haven’t advanced any explanation at all. One cannot explain why someone cannot see by saying that his brain cannot see. One cannot explain why someone behaves in a certain way by suggesting that his brain tells him to. Cognitive defects can indeed sometimes be explained by reference to damage to the brain – but not by reference to cognitive deficiencies of the brain, since the brain has no cognitive powers at all. There is no such thing as a brain’s thinking, wanting, reasoning, believing or hypothesizing.
see the book or e.g. the review I cited here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1389787/.
Or as an excellent neuroscientist blogger recently put it:
The human brain is plastic and interacts with the environment. Indeed, this is how we are able to learn and adapt to anything. Were our brains entirely unresponsive to what happens to them we would have no memory and probably no behaviour at all. ... Because the brain is where behaviour happens, any change in behaviour must be accompanied by a change in the brain. By talking about how behaviour changes, we will, implicitly, also be discussing the brain. However it doesn't work in reverse. Changes in the brain can't be assumed to mean changes in behaviour.
We could go much farther down this neuroscience rabbit hole, but that should be enough to understand why I think that particular articulation of a food reward hypothesis is problematic.
You're wrong about Wittgenstein (his central points about natural language<>logic<>human thought stay substantively same from TLP all the way through CV and he goes to great lengths to make himself abundantly clear on those points, etc.) and claiming without relevant argument that "most people get him wrong" is rather a useless thing to say... but I don't want to get into a debate on Wittgenstein in this comments section and I mention him because he was correct and famous on the point relevant to neuroscience, not because I'm a devotee.
That doesn't necessarily mean that obesity hasn't in fact risen because more palatable food is more available so people eat more calories, or whatever psychological thing, it just means that the neuroscience doesn't necessarily add anything to that argument.
Oh lolz... whoever posted that link to carbsane's blog, OH MAH GAWD.
To think these people were criticizing me and the tone I write and post? LOL!
I couldn't even bring myself to read it. It wasn't even biting, sarcastic, humorous, it was screeching hysterical and nagging in quality. It gave me a headache after 60 seconds of attempting.
Then the comments were even better. All the usual suspects.
Thanks for posting the link, I truly do feel better about myself now though.
The one time I read a deconstruction of a study by carbsane, it was so illogical and full of holes, I can only imagine all of her writing is that bad... it was just as bad as Stephan. Yet we are the zealots, we are the biased, we are the dogmatic.
FACT: JUST BECAUSE MAINSTREAM OPINION IS ON YOUR SIDE, DOES NOT MEAN YOU ARE FAIR/BALANCED. It does not mean you are right, either. Strongly disagreeing and being fixed in an unpopular, opposite position does not equate to zealotry. The popularity of an opinion is not the barometer of reason, you dummies.
I strongly suspect few of these people are lean/fit. We have quite a few posters who have become quite lean from an obese state utilizing insulin control (high fat low carb eating). Do we have A SINGLE ONE who can say that eating a high carb, "low palatability/reward" diet has accomplished for them, what low carb has accomplished for me?
Can carbsane say that her clothing is 00, 0, xs, s? Probably not.
Stephan's mistake seems to be that he is incapable of understanding he might be very wrong.
The carb-insulin hypothesis/low carb camp's unwillingness to entertain him is not a sign that they are dogmatic , zealots, wedded to their ideas. It means he is wrong, and they do not agree for that reason.
The funny thing is, if Stephan dialed back his enthusiasm for this food reward thing a bit and didn't try to have it "compete with" or "replace" the insulin hypothesis of obesity, it wouldn't come accross so wrong and so ridiculous. When someone makes a statement like "HIGH INSULIN PROTECTS AGAINST OBESITY", that person has painted themselves with a big scarlet R for ridiculous. This is NON SENS-I-CAL. Insulin is the key that unlocks the fat cell. Insulin is REQUIRED for fat storage. You can NOT store fat without insulin. Excessive insulin levels, presuming skeletal muscle resistance but in tact fat cell sensitivity, will typically lead to obesity. This is not a debate. At the very least it must be said that insulin is required to become obese - to say that it is protective is absurd to insanity.
So, when Taubes, or Eades, or Peter or any other low carb proponent refuses to entertain an enthusiastic, up and coming young man who wants a name for himself, when this young man says he discovered the real cause of obesity and all those who think it's about insulin are wrong... don't be surprised when they are like "um, no, you haven't."
It does not mean Taubes and others are "wedded to their ideas" merely because they tell you that you're wrong when you say low carb only works for people because it lowers food reward. Food reward does not make a reactive hypoglycemic shaky and ravenous 1 hr after eating. Insulin from high carbohydrate food does, you dummy.
Maybe if you worked with real live fat people, you would realize, "holy crap, these people don't feel full and satisfied after a potato dinner the way I do, funny that". Yea, thin people feel stuffed and satisfied on carbs, that's because they are thin and do not overproduce insulin.
It is so obvious, so many of these theories are purely from reading too much and not interacting enough with real obese patients.
Any medical practitioner can tell you, whether it be nursing or medicine or therapy, that you learn like , only a FRACTION of what you need to know via text books. The real education is from working with real patients, that gives you insight into signs and symptoms and what is really up.
I have no idea at all why people think obesity is different, but for some reason they do.
But anyway, that's a tangent.
My point otherwise is that just because Stephan is meeting resistance doesn't mean the opposition is dogmatic. It just might mean he is quite wrong, and people don't agree for valid reasons.
I would also point out that I am not against "everybody", just quacks. I am also not a prominent blogger/speaker/icon so I really don't count. I am an anonymous internet ranter.
Peter has maintained tact throughout this debacle, which is admirable and very typical of him.
"But you are a bit narcissistic, no? That's not an insult or a judgement, just an observation."
You expect my assent to a repeated insult offered as an "apology" when I never addressed you in the first place?
Only on the internet can one encounter such insanity emanating from an apparent social retard.
"I wasn't implying that HarrisMD or anyone else shouldn't change their mind based on new evidence or whatever, but pointing to a conceptual problem in the "obesity is caused by 'food reward' dysregulating our brains and thus making us consume more calories" thing."
I have not once stated that I thought FR is primarily or even partially responsible for obesity, only that it might be plausible and requires consideration.
Rejection of the GCBC CH has nothing whatever to do with whether FR has merit.
I wanna know why, after it being stated that we're all different, and no one diet plan (in its exactness) fits all, we are not using the scientific studies geared towards nutrition more effectively. Instead of disregarding studies that have varied results (one might favor one variation, a different study another...), we could see them as an instance of variability in nutrition and record traits and parameters that respond more favorably to one element and vice versa--to create another aspect of nutrition that actually factors individuality into the picture, instead of just giving it a touch of mention when one long held theory turns to shit...
Dr. Harris, your comments on Stephan's CH critique:
Simply a tour de force.
And no succor either for the nutritional nihilists who think we get fat by accidently neglecting to count, weigh and measure:
"The brain is the primary homeostatic regulator of fat mass, just as it homeostatically regulates blood pressure, breathing rate, and body temperature..."
So onward in exploring what agents - whether nutritional, environmental or cultural - are causing the dysregulation of our brains.
These are food reward related weight loss tips.They are highly effective if you need to lose weight.
And the adipostat post:
People in our culture of continuous serial entertainment hate the idea that food be demoted from entertainment to the moderate pleasure of satisfaction of hunger and refueling....
They LIKE thinking about food all the time.
Food Reward theory is really a much more deeply subversive idea idea than either carbohydrate or fat as the black monolith of obesity and disease
I can at least be forgiven for getting the distinct impression from this that you thought food reward (or the "dysregulation of our brains" in some way) primarily or partially responsible for obesity and furthermore that you thought the neuro explanations of causality sensical.
I would be quite happy to hear I was completely wrong.
Indeed both FR and CH can be wrong... and the wrongess of one doesn't necessarily imply the rightness of the other. However they are largely competing hypotheses and posit completely different primary causes of obesity in mutually exclusive frameworks. Taubes point in his question and explicitly in his latest blog is that he is advocating the CH "or something like it" in opposition to the mainstream eating behavior --> CI>CO model of which FR theories make a subset.
Based on your comments, I think you're shortchanging Taubes and giving Guyenet undue credit.
I would expect nothing from Internet websites that are free of charge; and I would expect even less (save for predictability) from a narcissist.
Whatever lack of respect I had for Kurt has been reduced to zero. He seems awfully prickly, and yes, narcissistic, to be one of the stone heads on Mt. Carbmore. But I suppose a big ego is to be expected of any "great leader".
And as for Stephan, he's gone completely coocoo. Maybe it's the lack of food reward. Maybe he needs to meditate.
Now now Pete, n=2 does not make it fact.
Thank you for an excellent post.
Few questions though.
You explain that glucagon helps to prevent hypoglycemia (by insulin from protein).
Glucagon works by causing the liver to release stored glycogen. On the other hand, depleting the liver glycogen is the prerequisite for ketosis.
Q1: Does glucagon work while on ketosis?
Q2: Why glucagon and other hormones that prevent hypoglycemia does not work when same situation is induced by carbs?
I mean... the elegant explanation of regulation could be used for carbs too, so that you would never become hypoglycemic and hungry because your body would not let the the blood sugar drop too much.
Re. moderation of comments, I tried posting one on Carbsane's comment thread, providing a link to thread on this blog where Stephan's comment "mysteriously" appeared, and it hasn't been published yet. My comment on Peter's blog, however, appeared instantly. And Carbsane actually has to gall to ridicule other bloggers for moderating.
Your "warped sense of humor" keeps all of us coming back to your blog. Don't ever lose it!
I also checked out the link to CarbeSane's blog. Some interesting concepts discussed but mostly they were drowned out by the hostile comments and rants. The general tone was rather depressing to read. I was thinking about Chris Masterjohn's blog (The Daily Lipid). Chris is incredibly gracious and thoughful in his response to people (Peter too). Why do people personalize these discussions about diet? Its just food? So much anger can't be good for ones health.
The ad hominem nature of some of these critiques does not surprise me. You can add diet to the race, religion and politics list of topics not to bring up in mixed company. Have you ever debated diet with a vegan? Its like a Catholic debating Biblical interpretation with a Jehovah's Witness. Your not going to change many minds.
Peter, reading your lectures about physiology/nutrition reminds me of my husband's lectures about physics. I keep feeling like I should understand it, but I really don't. Perhaps reading this another couple of times will allow it to sink in.
However, I would like to mention something, mostly because I have not seen you mention it. I thought of it while watching that beautiful rug-rat munching away at the chocolate. Chocolate, unsweetened chocolate, has fructose in it. It isn't free-floating fructose, which is why unsweetened chocolate is not as pleasant as the sweetened type. The fructose is bound up in fructans, which are huge molecules composed of a lot of fructose molecules. I suppose this is partly why chocolate seems to be somewhat addictive, because it is a backdoor mechanism for getting fructose into our bodies.
Anyway, since I hadn't seen this on your site, I thought I would mention it.
You did it now, Dr. Harris. Of COURSE you're free to change your mind - as long as, of course, you stay more or less on the same side as other members of the LC cult - er, community! At any rate, the Taubesians will be out with their pitchforks now. Judging from a few of these comments I'd say they already are.
@pete (and all),
Oddly enough your current comment appeared in the spam folder and I had to tell the blogger software to go ahead and publish (there will have been a delay this time). I think the spam detection finds a certain combination of letters beginning with "C" as objectionable as I do! It has sent a fair number of her comments in the past in to the spam folder. From where I have retrieved them and published them of course (eventually, I wasn't checking every day, the spam software is quite functional).
I think Stephan made a genuine mistake with his posting on the wrong thread, although quite how he managed to do it I'm not sure. I just wonder how carbohydrate tolerant he really is. I guess he'll find out one day.
I'll have to put up another brief post on where my thinking is trending from here when I get the chance but JS has gotten me back to the mitochondrial thoughts which have been dormant for some time, but have always seemed very important.
even the 85% chocolate is heavily sweetened (15% added sugar).
Unsweetened chocolate is dry, hard and extremely bitter [imagine cocoa and candle wax mixed together]. It contains only ~1% carbohydrates and has a very unpleasant taste and texture. I can assure you no baby or adult would willingly eat it.
For the record, I have not deleted any comments (except spam). Perhaps Pete couldn't pass the word filter or something.
Stephan may be screening comments after they're posted. Last night I read a long one by Rap about IRB approval, and when I went back to re-read it, it had disappeared. Not "This post has been removed by the author." Disappeared. It is still missing as of this morning. Odd.
I have pounds of unsweetened chocolate, so that my husband (who is diabetic) can mix his own sugar substitute with it to make an acceptable candy. I used to eat it, without sugar (melted into half-and-half), until I realized it was making me sick. That is when I researched it, and found out about the fructan content (about 9.4%). So there are some dysfunctional adults who will willingly eat unsweetened chocolate. It is merely my body reacting against fructose that prevents me from indulging. Ah, the unfairness of it.
It's easy to ferment chocolate to make a sort of fluffy spread(on tapioca pancakes for me :D). Just melt/boil it to complete liquid with cream or coconut milk. Then leave in a warm place and should be ready in a week. Even quicker - add some yogurt or a tsp of krout juice after it cools off. When it's ready, the mixture should be full of holes and bubbles where the bacteria ate everything. Then off to the fridge. Very delectable. I add a little dextrose to sweeten. The soured taste works surprisingly well.
I too think that managing insulin is more important than eating bland food. Hehe, I can get a Pima to 10% bodyfat on a high carb diet if they eat real food and do enough pushups. Bland food may play a role for extreme leanness(I had to go through a little hunger to get there), but for the average person to have abdominals and defined musculature it's simply unnecessary.
i like (100% unsweeatened) dry roasted cacao (nibs or beans). i like it crunchy & bitter.
but i agree with you, no one else likes it. (no sugar).
Peter and Stephan are owed a debt of gratitude from all of us who learn from them. The fact that they take the time to share their analyses is of huge public benefit. And they do it for free. I find it disturbing that some posters would engage in vitriol and ad hominem attack just because they eithet disagree or don't understand.
Hi, Peter. This is unrelated, but I found this article in an old 1941 Portuguese magazine, and thought you might find it interesting, seeing as you're a veterinarian and also interested in nutrition:
"The turtle, as it is known, buries its eggs in the sand and it is the sun that incubates them.
Now, there are two kinds of turtle's eggs. One kind is perfect, destined for eclosion; the other kind contains no yolk or embryo, it's filled with an oily liquid.
The animal, when it lays its eggs, is perfectly aware of which is which, and with mathematical precision lays one oily egg for each three perfect eggs. The oily one is laid in the middle of the cavity, surrounded by the other ones. The aim of this solicitous precaution is to provide food to the little ones as soon as they hatch. They will feed on this liquid until they're strong enough to erupt through the sand layer that covers the nest. This demonstrates that turtles can count. Without an arithmetic notion they would not be able to spread throughout the viable eggs those that are merely a nourishing source."
I thought it was cute. :) As always, thanks for your great blog.
@Dr. Curmudgeon Gee
My husband and I both like unsweetened 100% raw cacao chocolate in moderation and in any form we find it so I disagree that "no one else likes it". We have found that when you don't eat sugar in any form, the strangest things taste sweet or at least not unsweetened.
I was talking to a friend of mine last week. She completed a dietetics degree (4 year Australian undergraduate) last year and has decided not to work in the field. In her opinion the theoretical background was totally inadequate (I would fully concur) and that far too much reliance was placed on computerised software to treat patients.
If I were a young postdoctoral nutrition researcher I wouldn't waste my time on the blogosphere. I would be working frantically on my research to get enough publications to get a tenured teaching position ASAP. In 20 years time if I had a high enough academic standing to give me credibility I might give a few interviews for radio and TV (if they're still around). I would also very seriously consider going to medical school because clinicians usually have far more influence in medical research than scientists.
haha, i should say "no one else (around me)" likes it.
(i was refering to friends & colleagues).
The resources you posted are interesting, thanks.
Re Wittgenstein: yes, "drastically" (my word) is too strong. I'll leave it at that, as I agree the other points you make.
Perhaps it was only annoyance with a general tone of arrogance (not just in your post) that prompted me to speak in misguided irritation.
I just remembered why I thought your position was that 'food reward dysregulating our brains' was indeed "a primary or partial cause of obesity." You told me you did on paleohacks:
"Food reward is the fourth horseman [of neolithic disease] ... If we are talking about causes - plural - of diseases of civilization I think the entire cultural milieu of food - how it is mixed, cooked, prepared, combined and processed and even literally the mental space it occupies is likely to be an independent contributor to DOC via excess caloric intake and to obesity via setpoint dysregulation."
I realize you may have forgotten you said this, but it contradicts your reply to me above:
"I have not once stated that I thought FR is primarily or even partially responsible for obesity, only that it might be plausible and requires consideration."
Could not the same thing be said about the CH/insulin hypothesis, i.e. ppl supporting it are not capable of seeing that they are wrong, and many people disagree with it for valid reasons? Because, you've got to admit, there are a LOT of people disagreeing with it (and not just a bunch of ignorant nutritionist enthousiast).
Also I don't think Stephan is trying to replace the CH hypothesis with the food reward one. As far as I know, he said that food reward was one factor, and that the CH hypothesis is wrong. He never said FR is right hence CH is wrong.
You say that it's not even to debate that ''fat cannot be store without insulin'' but what about ASP and Fat-specific protein 27, which both play a role in fat storage?
Have you ever consider that you might be too much focus yourself on insulin to realize that it might be wrong and/or strongly incomplete?
There are certainly valid disagreements regarding individuals who believe that carbs and insulin mediate obesity. For example, some individuals are under the impression that ONLY carbohydrate affects insulin levels, therefore only carbohydrate mediates obesity, which is clearly false. Even basic, trivial research quickly disproves the notion that carbs = insulin, and nothing else does. This is the problem with Taubes/GCBC... so much of it is written to give the reader the impression that if you go carb free it is impossible to have hyperinsulinemia, or excessive insulin action on fat cells, which is clearly very false. I have to assume Taubes wrote in this way just for simplicity sake: he was mainly trying to convince people that carbs are the most important dietary factor, and making the book too complicated would obsfucate his message. In that regard I can see why Taubes wrote his book the way he did... the problem, however, is for people already very familiar with everything he wrote (e.g. myself), then the book appears misleading and overly simplistic and untrue. I mean, this is just ONE of the many faults I have with what Taubes says.
We are not a hydra; we believe different things. I don't agree with a lot of what Taubes seems to believe and I think Taubes is looking at just a small piece of the big picture.
Ultimately I support taubes because he has things far more correct than anyone else, and that is important. Obesity absolutely is a disorder of fat accumulation, and obesity absolutely is mediated by excessive insulin action on fat cells with an imbalance of influx/efflux mediated thereby.
THis really isn't even controversial - the most basic, trivial examination of medical therapies which manipulate insulin levels (e.g. glucocorticoids for autoimmunity, t1 diabetes, t2 diabetes) will easily show that fat gain increases or decreases when peripheral insulin does. We very well understand the cell level reasons why. We've known for DECADES. It's only controversial because a lot of people want it to be... and because knowing this really doesnt get us closer to making a magic pill which allows fatso's to eat like fatso's and stay thin, which is what all the big pharma giants and their research teams are waiting for.
There are many valid disagreements of individual points made by the CH/insulin hypothesis people.
However, that insulin increases fat gain is not a valid disagreement. This is thumbing your nose at established medical facts. This is being an ignorant moron or a crazy crackpot, either or.
Regarding stephan and his idiotic FR hypothesis (really it isn't even his, however he is doing a fine job of copywriting it, making his intentions obvious)... Stephan is the one continuously blogging in a way which suggests he is looking to get on the next magic bullet diet craze. He always juxtaposes (badly interpreted/ cherry picked) "CR is wrong" bloggings with (equally badly interpreted/cherry picked) "FR is right" bloggings.
It's almost as if he is trying to MARKET this thing to the crowd, his readers, most of whom he knows previously may have been partial to the "carbs make you obese" line of thinking. So much of his crowd is paleo, and the paleo diet is almost always also a LC diet.
Reading his blog has come to feel like going to a nissan dealership, when they know you are a loyal toyota customer. "Well you know, nissan offers 0% interest for 2years, not like toyota, who are overpriced and quality of which is exaggerated by popular opinion".
Saying that stephan merely supports FR, and independently also does not support CH, is kind of like saying a charming narcissistic psychopath merely wants to take you to paris and sweep you off your feet, and also incidentally opens numerous credit lines with your social security number. You would have to be an alien, robot, or an autistic to be ignorant of the connection between these two activities and how they relate to each other.
Re: ASP, again I don't know much about it but I'm fairly certain it is insulin dependent, it seems to be an insulinotropic factor. Meaning to say, all the ASP in the world won't make you fat, if you don't have insulin.
It is a medically indisputed fact that insulin deficiency or insufficiency leads to body fat atrophy. Every single type 1 diabetic will die without treatment, but before they die, you can bet 10 years of pay that they will be hemorrhaging body fat from adipocytes... And feeling starving and peeing along the way.
The sort of classic diabetes (type 1) we thought of when we thought of diabetes before corn syrup in the 70s made us obese and diabetic was alerted by the three Ps...polyuria, polyphagia, polydispia. You pee because without insulin your glucose is crazy high and you urinate frequently; lack of insulin also causes electrolyte and kidney changes that lead to an inability to retain water (note: this is why fat people bloat and people complain of a bloated water retained feeling after eating excessively).
This also leads to being very thirsty.
You are always hungry because your cells are starving and no insulin = no leptin = hungry time. No insulin in your brain = hungry time as well.
Meanwhile, your body fat is shedding like snake skin.
The inability for your fat cells to keep in fat leads to acid base imbalances, known as ketoacidosis. Dietary ketosis is a controlled process - the ketotic dieter makes insulin, therefore can never develop acidosis. It is impossible, via diet, to develop such an extreme rate of fat breakdown, as normal basal insulin will prevent this.
However, in insulin DEFICIENCY, the fat can not stop elaving the fat cells, it is totally disregulated, and the person develops an acid base imbalance, alerted by kussmauls breathing. This is a reflexive attempt to release carbon dioxide (which is acidic.) The body is desperately trying to maintain the pH. Potassium levels also go to crap, due to the compensatory switching of H ions for intracellular potassium - another desperate attempt for the blood to avoid turning into battery acid in response to RAMPANT HYPOINSULINEMIC LIPOLYSIS.
This is another major risk in diabetes - yer heart gonna done stop, halp potassium through the roof.
I have to assume, so many of these dumbass theorists, are not drawing on prior medical knowledge, or alternately they have none.
The fact that the clinical picture of total insulin deficiency - type 1 diabetes - shows that body fat loss is impossible to stop, to the point of fatal metabolic acidosis, tells us all we need to know about ASP. IT tells us that ASP must be insulin dependent, or else total insulin deficiency would not always lead to uncontrolled lipolysis and attending metabolic acidosis.
I suppose ASP is only news for people who think only carbs can make you fat, but that is a small fringe group of nutters - most people who are actually reading and thinking realize that insulin/glucose disorder/obesity is waaay more than just "carbs make you fat".
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Carbohydrates appear in two forms, circuitous and simple. Simple carbs such as glucose are basal sugars and accommodate a fast activity accumulation in the anatomy of ATP, the body's accustomed activity supply. Circuitous carbohydrates such as those begin in breads and rice yield best to breach down, and accord a added abiding absolution of energy.
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"I have no idea what the hell happened to him. A pity, really.
He's in the establishment now... "
Actually I think he's discovered where research grants come from.
No doubt he, and his colleagues, are genuinely interested in benefitting all of humanity. However they study what they get grants for.
Assume Stephan discovers how food reward works. The Foodlike Substance Manufacturing Industry has first dibs on his findings and will be using them to generate even MORE addictive foods from wheat, sugar/HFCS, industrial Omega 6 seed oils and byproducts of the petrochemical industry.
They couldn't do this with research into reducing carbs and insulin. So the likes of Westman, Volek and even Krauss are funded by Atkins Foundation, the Dairy Council etc. and although they may well be correct their research is denigrated because they are not financed by the Usual Suspects.
I finally got around to reading Taubes. I was put off by the size (haven't been in Long Document Mode for a while now) and the fact someone whose views I normally trust called it "turgid". Actually once I started I found it quite unputdownable.
Got back from my holiday and self-imposed exile from t'interweb and TV to find all hell had broken loose in the Blogosphere, and I've been desperately trying to catch up ever since.
Thsi includes re-reading your blog among others, and revisiting a lot of the original "evidence".
OK so carbs/insulin/IR may only be one part of obesity but they are crucial to metabolic derangement in general and also insulin levels are comparatively easy to modulate through diet. How do you modulate leptin? Change insulin levels and wait?
Some of my food is so rewarding that I feel no desire to eat again for 8 - 9 hours, until it has all been metabolised. Oh hang on, that's not "rewarding", that's "satiating", so "reward" = "unsatiating". Hmmmm . . .
Could iodine be part of the reason some primitive societies tolerate carbohydrates so well? All the societies mentioned by Stephan Guyenet who eat primarily carbohydrates successfully live near the ocean. The Kitavan's, the Tokelauan's, the Okinawa. Perhpas they can eat carbohydrates, because they have healthy thyroids over their life times. The average Japanese consume about 12 mg of iodine per day. Far more than the RDI of 150 ug. It has been argued that 150 ug is merely the amount of iodine required to prevent goitre and that our actual needs are far greater for optimal health.
Is it possible that the reason some people claim to experience a decrease in thyroid function when on a low carb diet, is because a low carb diet unmasks an iodine deficiency?
Agreed. I'm typing on my ipad so forgive misspellings and the short response. I am disheartened by the pseudo trench warfare now present in regards to what actually make people fat or how they lose weight. Genetic variation in response to environmental variables makes such extreme stances unfounded. At the same time people are ignoring basic science (insulin makes people fat) ignore differences in individuals (people both secrete and and react to insulin in different ways) and basically just ignore anything not adhereing to the rules set forth in their cherry patch.
Thanks for this post, it saved my sanity.
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