Thursday, August 11, 2011

The Carbohydrate Hypothesis of Obesity: a Critical Examination

Introduction

I'd like to begin by emphasizing that carbohydrate restriction has helped many people lose body fat and improve their metabolic health.  Although it doesn't work for everyone, there is no doubt that carbohydrate restriction causes fat loss in many, perhaps even most obese people.  For a subset of people, the results can be very impressive.  I consider that to be a fact at this point, but that's not what I'll be discussing here. 

What I want to discuss is a hypothesis.  It's the idea, championed by Gary Taubes, that carbohydrate (particularly refined carbohydrate) is the primary cause of common obesity due to its ability to elevate insulin, thereby causing increased fat storage in fat cells.  To demonstrate that I'm representing this hypothesis accurately, here is a quote from his book Good Calories, Bad Calories:

This alternative hypothesis of obesity constitutes three distinct propositions.  First, as I've said, is the basic proposition that obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of energy intake and expenditure.  The second is that insulin plays a primary role in this fattening process, and the compensatory behaviors of hunger and lethargy.  The third is that carbohydrates, and particularly refined carbohydrates-- and perhaps the fructose content as well, and thus perhaps the amount of sugars consumed-- are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity. 
There are three parts to this idea.  I'll discuss them each separately. 

Part I: A Defect of Fat Metabolism?

The first part of this hypothesis states that energy balance is not the ultimate cause of fat gain, it's the proximal cause.  That is, Taubes is not disagreeing with the first law of thermodynamics: he understands that fat accumulation depends on how much energy is entering the body vs. leaving it.  However, he feels that the entire industrialized world didn't just wake up one morning and decide to eat more calories, therefore something must be driving the increased calorie consumption.

He cited the research of Drs. Jules Hirsch and Rudy Leibel, various underfeeding and overfeeding studies, lipectomy studies, and evidence from genetically obese rodents, to demonstrate that body fatness is biologically regulated rather than being the passive result of voluntary food intake and exercise behaviors.  He then advances the idea that it's an alteration in this body fat regulatory system that is behind obesity.  This may sound familiar because I've written about it several times.  So far, so good.

This is where he should have mentioned leptin signaling, and the circuits in the brain that regulate body fat mass, which would have taken the book in a more compelling direction.  According to literally thousands of publications spanning nearly two centuries, the brain is the only organ that is known to regulate body fat mass in humans and other animals-- neither fat tissue itself, nor the insulin-secreting pancreas have the ability to regulate body fat mass as far as we currently know.  Leptin is the system that Drs. Jules Hirsch and Rudy Leibel have shown in carefully controlled human studies is responsible for the metabolic defect Taubes alluded to (1).  It's also the system that is mutated in the genetically obese rodents he discusses (2, 3).  Yet it receives no mention in the book.  This is a fork in the road, where Taubes discards a solid hypothesis in favor of a shaky one.

Part II: The Role of Insulin in Body Fatness

Insulin has many functions throughout the body.  The primary role of insulin is to manage circulating concentrations of nutrients (principally glucose, amino acids, and fatty acids, the body's three main fuels), keeping them within an optimal range, and coordinating the shift between metabolic fuels that is required when a person consumes more of one or the other.  Any time insulin suppresses fat burning, it increases carbohydrate and/or protein burning by an equivalent amount.  That is what insulin does. 

Insulin has a number of actions on fat and lean tissues that favor fat storage and suppress fat burning, and this is the crux of Taubes's basic argument in support of the idea that insulin causes fat accumulation.  Some of these actions  have been recognized for many decades.  Taubes's idea is so simple, you might think someone had already thought of it.  In fact, the idea has been around for a long time, but it has very little traction among obesity researchers today because it doesn't fit with a variety of basic observations, as I will explain. 

The reason insulin suppresses fat burning is because it's a signal of glucose abundance.  It's telling tissues to stop burning fat because carbohydrate is the available fuel.  If you eat a meal of 500 calories of carbohydrate, you will burn that carbohydrate under the direction of insulin, which will also make sure body fat mostly stays inside your fat cells during the process.  If you eat a meal of 500 calories of fat, you will burn fat instead of carbohydrate, but since you just ate fat, you aren't dipping into your body fat stores any more than you were when you ate carbohydrate.  So even though insulin temporarily suppresses fat burning and the release of fat from fat cells when you eat carbohydrate, at the end of the day if you ate the same number of calories you end up with the same amount of fat in your fat cells either way.  You now know more about insulin than many popular diet gurus.

As we are all on the same page (I hope) that the first law of thermodynamics applies to humans, for insulin to cause fat gain, it must either increase energy intake, decrease energy expenditure, or both.  Let's see if that's true.

Let's look at the effect of insulin on food intake.  To keep it as realistic as possible, let's compare satiety and subsequent food intake among foods that raise insulin to varying degrees.  If calories and protein are kept the same, high-carbohydrate meals cause equal or greater satiety than high-fat meals, and equal or less subsequent food intake, despite a much larger insulin response (4, 5, 6, 7).  Due to the insulin-stimulating effect of protein, low-carbohydrate high-protein meals can sometimes stimulate insulin to an equal or greater degree than high-carbohydrate meals, yet even in these cases higher insulin release is associated with increased satiety (8).  Experiments in which investigators feed volunteers protein foods that stimulate insulin to different degrees show that the amount of satiety is positively correlated with the degree of insulin release (9), which is not consistent with the idea that insulin stimulates food intake.  In the long term, low-carbohydrate diets suppress appetite in many overweight/obese people, however this is unlikely to be related to insulin. 

If elevated insulin leads to increased fat storage and increased food intake, then experimentally elevating insulin in animals should replicate this (since insulin acts on fat cells in the same manner in humans and non-human mammals).  However, this is not observed.  Insulin injections at a dose that does not cause frank hypoglycemia do not increase food intake, and in some cases they even reduce it (48).  Chronically increasing circulating insulin without causing hypoglycemia reduces food intake and body weight in non-diabetic animals, without causing illness, contrary to what this idea would predict (49, 50).  If anything, insulin constrains food intake and body fatness, and research indicates that this action occurs via the brain.  Insulin infused into the brains of baboons causes a suppression of appetite and fat loss, which is consistent with the fact that insulin and leptin have overlapping functions in the brain (10, 11).  Knocking out insulin receptors in the brain leads to increased fat mass in rodents, suggesting that its normal function involves constraining fat mass (12).  Insulin is also co-secreted with amylin, which suppresses food intake and body weight (13).  This is why insulin is viewed by some obesity researchers as an anti-obesity hormone. 

Now let's look at energy expenditure.  If insulin is increasing fat accumulation due to a decrease in energy expenditure (presumably because elevated insulin is locking fat away inside fat cells), then people with higher fasting insulin should have lower resting energy expenditure.  Lucky for us, that hypothesis has been tested.  At least two studies have shown that higher fasting insulin is associated with a higher resting energy expenditure, independent of body fatness, not a lower expenditure (14, 15).  If anything, this is the opposite of what the hypothesis would predict.  How about post-meal insulin spikes due to eating carbohydrate?  A number of studies have consistently shown that under isocaloric controlled conditions, substantially different carbohydrate:fat ratios do not influence energy expenditure in any measurable way, even over long periods of time (16, 17).

Therefore, if insulin doesn't increase energy intake (if anything, the combination of insulin and amylin that the pancreas releases in response to carbohydrate decreases it), and doesn't decrease energy expenditure, then how exactly is it supposed to cause energy accumulation in the body as fat?  There is no energy fairy.  Obese people are obese despite having higher fasting insulin, not because of it.  The fact is, insulin spikes after meals temporarily decrease fat release from fat cells, but if you look at total 24 hour energy balance, insulin spikes, in conjunction with all the other hormones that are released in response to food ingestion, do not cause fat accumulation.  This is exactly how you would expect the system to work if it were designed to constructively handle a wide variety of macronutrient ratios, which it is.  Just as cholesterol did not evolve to give us heart attacks, insulin did not evolve to make us fat.

Now let's address the common sense arguments that are used to support the insulin hypothesis of obesity.  These include:
  1. Type I diabetics, who don't produce enough insulin, lose fat.
  2. Animals lacking insulin receptors on fat cells are resistant to fat gain.
  3. Insulin therapy often causes fat gain in diabetics.
  4. Repeated insulin injection into the same site causes fat accumulation at that site (lipoma).
  5. Two drugs that suppress insulin secretion, diazoxide and octreotide, sometimes cause weight loss in controlled trials.
These observations are all accurate, and at a glance, they seem to support the hypothesis.  Manipulating insulin signaling can change fat mass, and obese people have higher insulin, so it must be involved in obesity, right?  Unfortunately these arguments fall apart upon closer scrutiny, not because they're based on inaccurate observations, but because they're irrelevant to common obesity.  In obesity as in most other conditions where insulin is high, elevated insulin is a symptom of insulin resistance, and the two occur in parallel.  The pancreas secretes more insulin because the tissues can't "hear" it as well, so they need more of it to do the job.  The more insulin resistance, the more insulin.  The key point here is that elevated insulin in obesity is a compensatory response to insulin resistance, i.e. a reduced insulin signal.  The cells are not seeing more insulin signaling, because they're insulin resistant, so it makes no sense to invoke increased insulin action to explain common obesity. 

Arguments 1-5 listed above are cases where insulin levels and/or insulin sensitivity are changing independently of one another, either through a pathological process (islet autoimmunity), genetic manipulation (fat cell insulin receptor knockout), or through drugs.  This is why they're irrelevant to common obesity, where insulin levels and insulin resistance rise in parallel, such that total insulin action is either maintained or diminished.  If we want to do an experiment that's actually relevant to the question, we can use animal models that are genetically manipulated to maintain insulin sensitivity in response to fattening diets, which as expected eliminates the increase in insulin that is typically observed on these diets.  These experiments show that fat mass accumulation does not consistently differ between animals that experience an increase in insulin, and those that don't-- they all get fat at approximately the same rate (17a, 17b, 17c).

In addition to what I just explained, both diazoxide and octreotide (argument #5) are extremely nonspecific drugs that have actions in the hypothalamus (brain) that would be expected to influence fat mass, so we actually have no idea if they act by reducing circulating insulin levels or through some other mechanism.

The idea of fat gain in insulin-treated diabetics (argument #3) is not as airtight as it might at first seem.  On average, diabetics do gain fat when they initiate insulin therapy using short-acting insulins.  This is partially because insulin keeps them from peeing out glucose (glycosuria) to the tune of a couple hundred calories a day.  It's also because there isn't enough insulin around to restrain the release of fat from fat cells (lipolysis), which is one of insulin's jobs, as described above.  When you correct this insulin deficiency (absolute or relative), obviously a diabetic person will typically gain weight.  In addition, short-acting insulins are hard to control, and often create episodes where glucose drops too low (hypoglycemia), which is a potent trigger for food intake and fat gain.

So what happens when you administer insulin to less severe diabetics that don't have much glycosuria, and you use a type of insulin that is more stable in the bloodstream and so causes fewer hypoglycemic episodes?  This was recently addressed by the massive ORIGIN trial (17d).  Investigators randomized 12,537 diabetic or pre-diabetic people to insulin therapy or treatment as usual, and followed them for 6 years.  The insulin group received insulin glargine, a form of long-acting "basal" insulin that elevates baseline insulin throughout the day and night.  In this study, insulin treatment brought fasting glucose from 125 to 93 mg/dL on average, so it was clearly a high enough dosage to have meaningful biological effects.  After 6 years of divergent insulin levels, the difference in body weight was only 4.6 lbs (2.1 kg), which is at least partially explained by the fact that the insulin group had more hypoglycemic episodes, and took less metformin (a diabetes drug that causes fat loss).  A previous study found that three different kinds of long-acting insulin actually caused a slight weight loss over three months (17e).  This is rather difficult to reconcile with the idea that elevated fasting insulin is as fattening as claimed.

In obesity, fat tissue is insulin resistant.  The fat tissue of obese people doesn't suppress fatty acid release in response to experimentally elevated insulin or mixed meals as effectively as the fat tissue of a lean individual (18, 19).  In fact, obese people release an equal or larger amount of fatty acids from their fat tissue than lean people under basal conditions as well (20, 21).  If this is true, then why do they remain obese?  It's simple: the long-term rate of fat entering the fat cells is equal to the rate exiting, or higher.  There is no defect in the ability of fat cells to release fat in obesity, the problem is that the fat that is released is not being oxidized (burned) at a rate that exceeds what is coming in from the diet, therefore it all ends up back in the fat tissue. 

While we're on the subject, let's address the idea of "internal starvation".  Taubes suggests that people overeat because they can't access their fat stores due to elevated insulin. However, obese people have normal or elevated levels of circulating fat (22, 23), so how is that possible?  The internal starvation model was interesting, if speculative, at the time it was proposed, however the evidence for it has simply failed to materialize.  If anything, obesity is a condition of "internal excess". 

Let's also address the claim that obese people don't necessarily eat more than lean people.  Food records are notoriously inaccurate, however there is at least one way to measure total energy intake in a precise and unbiased manner.  It is called the "doubly labeled water method" (DLW).  DLW studies have shown that after controlling for confounding factors (gender, age, physical activity), obese people almost invariably expend more, and consume more calories than lean people (24, 25).  Weight stable obese people have a higher energy flux out of fat cells, and a higher metabolic rate, but it is not enough to overcome the higher calorie intake that is also observed (26, 27).  That has been repeatedly confirmed and it is simply a fact at this point.

If elevated insulin leads to fat gain, then this should be scientifically observable.  All we have to do is look for people with different levels of circulating insulin (controlling for baseline fat mass), and see if it predicts fat gain over time.  Fortunately for us, this has been studied many times.  In most studies, insulin levels are unrelated to future fat gain, or people with higher fasting insulin at baseline actually gain less fat over time that people with lower fasting insulin (27a).  In the most recent study, higher insulin (and insulin resistance) at baseline was associated with less fat gain over time, but this relationship was eliminated by adjusting for baseline fat mass, leaving no relationship between insulin and fat gain after adjustment (27b).  Again, I don't see how this can be reconciled with the idea that elevated fasting insulin is the cause of common obesity.

Therefore, the insulin hypothesis is not consistent with basic thermodynamics, it's not consistent with research on the biological functions of insulin, and it's not consistent with observational studies.  Obese people do not have a defect in the ability to release fat from fat cells and burn it, to the contrary.  They release more fat from fat cells than lean people, and burn more of it.  However, this is compensated for by a higher energy intake, and a higher rate of fat incorporation into fat cells that counterbalances the increased expenditure.  This shows that insulin does not cause obesity by acting directly on fat cells to cause fat storage. To understand obesity, we have to understand what causes increased food intake, and that factor is not insulin.

Part IIB: Insights From Human Genetics

Genetic studies can give us important clues to the biological processes underlying common diseases.  For example, common genetic variants associated with type 2 diabetes risk tend to be in genes that regulate the insulin-secreting pancreas (38).  This tells us, as one would expect, that pancreatic function is important in diabetes.  What does genetics tell us about the mechanisms of obesity?

There are a handful of rare single-gene mutations in humans that lead to severe obesity.   Every single one that has been discovered to date that does not also result in deformity (nondysmorphic monogenic obesity) is in the leptin signaling pathway (39), and even those that do result in deformity all influence how the brain regulates body fatness, suggesting that body fatness is normally regulated by the brain, not by fat tissue.  From a 2009 review paper (40):
There are now at least 20 single gene disorders that clearly result in an autosomal form of human obesity. Notably, so far all these disorders affect the central [i.e., brain] sensing and control of energy balance.
Genome-wide association studies (GWAS) give us a different perspective-- they look for common genetic variants that associate with higher or lower body mass index (BMI) in the general population.  These are not mutations that make genes non-functional, they are simply common differences between genes that in some cases subtly influence their activity.  Of the numerous common gene variants that have been found to associate with BMI variability, and whose function is known, the large majority are expressed in the brain, particularly the hypothalamus, and some are in the leptin signaling pathway (41, 42).  That's why these papers often make statements like this (43):
...when we look at the information gleaned from the past 15 years of molecular genetic activity we cannot avoid concluding that, as much as type 2 diabetes is clearly a disease in which pancreatic beta-cell dysfunction is a critical element, obesity is a condition in which inherent genetic predisposition is dominated by the brain.
 And this (44):
Many of our associated loci highlight genes that are highly expressed in the brain (and several particularly so in the hypothalamus), consistent with an important role for CNS [central nervous system] processes in weight regulation.
If insulin action on fat cells is a dominant factor in obesity, why don't genes linked to insulin signaling show up at the top of the list in these studies?  There are enough proteins that regulate insulin secretion in the pancreas and insulin signaling in fat cells that one would expect genetic variability in these genes to turn up frequently if they were important regulators of fat mass, but instead the list is dominated by genes that relate to the brain, and leptin signaling in particular.  This is consistent with a huge body of literature implicating the brain in body fat mass regulation and the development of obesity.

Part III: Carbohydrate, Particularly Refined Carbohydrate and Sugar, Cause Fat Accumulation by Increasing Insulin?

I've already demonstrated that it makes no sense to invoke insulin as a mechanism between carbohydrate consumption and body fatness.  Another problem with the hypothesis is a thing called the insulinogenic index (II).  The II is simply a measure of how much eating a food increases insulin, per unit calorie (28).  It turns out, it doesn't correspond with the carbohydrate content of a food very well.  In particular, protein-rich foods such as beef can increase insulin secretion as much as certain starch foods such as pasta, or more.  High-protein diets, as many of you know, aid with weight loss.  Some have suggested that this is because of glucagon release by the pancreas in response to protein.  That may well play a role, but if we are going to invoke glucagon, then aren't we acknowledging that other signals besides insulin play an important role in this process?  That's the larger point I'm trying to make here-- you can't just look at insulin, you have to consider amylin, glucagon, GLP-1, ghrelin, leptin, stomach distension, and all of the other short- and long-term signals that are activated in response to nutrient ingestion and changes in body fat mass.  These collectively regulate food intake and long-term body fatness via the brain.

The other problem is that refined and unrefined carbohydrates often have a similar II.  Pasta made from white and whole-grain wheat have the same II, and the same goes for white and whole-grain bread (29).   Doughnuts and cookies are on par with whole grain bread.  So post-meal insulin is not a compelling explanation for the potentially different effects of protein, unrefined carbohydrate, refined carbohydrate and sugar on body fatness. 

I think it's likely that refined carbohydrate and sugar can contribute to obesity, but by what mechanism?  Insulin is not a compelling explanation.

But let's forget about insulin for a minute.  Without worrying about the mechanism, let's simply consider the hypothesis that carbohydrate consumption per se causes body fat accumulation. At this point, I know some people will be insisting that Taubes is talking specifically about refined carbohydrate, not carbohydrate in general.  Taubes does repeatedly suggest in GCBC that all carbohydrate is fattening, although refined carbohydrate is more fattening.  Otherwise, why would he write "...carbohydrates, and particularly refined carbohydrates... are the ultimate cause of common obesity", rather than simply stating "...refined carbohydrates... are the ultimate cause of common obesity"?  This wording, used throughout CGBC, implies that all carbohydrate is fattening to some degree.  There is also the example in GCBC of the Massas tribe fattening on unrefined sorghum, described below.  If Taubes doesn't think unrefined carbohydrate is fattening, then why does he recommend a low-carbohydrate diet rather that suggesting that people replace refined carbohydrate with unrefined carbohydrate?

To address this hypothesis, first let's find some cultures that have a very high carbohydrate intake and see how fat they are. Let's start with a culture that eats more carbohydrate than any other I know: the New Guinea highland tribe at Tukisenta that was studied extensively in the 1960s and 70s.  They ate 94 percent of their calories as carbohydrate, mostly from sweet potatoes, for a total calorie intake of 2,300 kcal/day in men and 1,770 kcal/day in women.  Investigators found them to be fit, lean and muscular, with no sign of protein deficiency (Trowell and Burkitt. Western Diseases. 1981).

West Nile district, Uganda, 1940s.  The diet consisted of millet, cassava, corn, lentils, peanuts, bananas and vegetables (Trowell and Burkitt. Western Diseases. 1981).  Despite food abundance, "in the 1940s it was quite unusual to see a stout man or woman."  "In recent years, however, a fair number of upper-class middle-aged West Nile women have begun to look rather stout, and some men have become very obese, especially those who hold lucrative posts and can purchase whatever food they like."  This corresponded with an increase in "sugar, cooking oils, milk, fish and meat" and a corresponding decrease in "home-grown starchy staple foods."  This same scenario has happened to hundreds, if not thousands of African communities whose traditional diets are very high in carbohydrate.

Northern Cameroon, 1980s.  The Massas tribe (also spelled Massa) is known for its overfeeding ritual called Guru Walla, which Taubes describes in GCBC:
The Massa tribe of northern Cameroon fattens their males using both milk and a porridge made from sorghum, a corn-like grain that provides sweet syrup from the stalk. One man gained seventy-five pounds on a ceremonial binge. The average weight gain tends to be fifteen to twenty pounds using milk and porridge.  The Massa are cattle herders and their staple diet is primarily milk. This fattening comes about by the addition of carbohydrates (sorghum) almost exclusively.
Taubes states here that the typical diet is "primarily milk", therefore by inference, low in carbohydrate.  Let's follow his reference and see what it says.  It leads to a freely accessible paper by Drs. Igor de Garine and Georgius J.A. Koppert titled "Guru Fattening Sessions Among the Massa" (30).  The Massas indeed herd cattle, but "their main use is not as food."  The typical diet (not during overfeeding) is described as containing 516 grams of carbohydrate per day, and only 32 grams of fat (Table VIII).  The typical diet is 81% carbohydrate, and primarily based on sorghum, according to his reference.  This account is consistent with other freely accessible references in respected peer-reviewed journals (31).  These people are lean on their typical high-carbohydrate fare until they deliberately overconsume a mixture of sorghum and milk.

Most of Asia, 20th century.  Many Asian countries, including China, Japan, Taiwan and India, have a traditional diet that is very high in carbohydrate.  In many cases, the dominant carbohydrate was white rice, a refined carbohydrate.  Yet traditional Japanese, Chinese and Southern Indians eating mostly white rice were renowned for their leanness. Any plausible hypothesis of obesity needs to account for these observations.

Kitava, 1990s.  Dr. Staffan Lindeberg showed that the Kitavan diet is 69% carbohydrate, mostly from taro, breadfruit, sweet potatoes and cassava (32).  Thus, their diet would have had a high glycemic load and high II.  They also obtain 50 g/day of carbohydrate from fruit, most of which would presumably been sugar (unrefined).  Yet there was no obesity on the island, and only a few individuals that were slightly overweight (33). Fasting serum insulin was low, consistent with other high-carbohydrate cultures.  Dietary carbohydrate does not cause insulin resistance. 

Pima, 20th century.  The Pima of New Mexico currently have one of the highest obesity rates in the world, on par with Nauru.  It is rather ironic that Taubes uses them as an example in GCBC, when they are at odds with his hypothesis.  The Pima were first contacted in 1539 by the Spanish, who apparently found them to be lean and healthy.  At the time, they were eating a high-carbohydrate, low-fat diet based on corn, beans, starchy squash, and a modest amount of gathered animal and plant foods from the forest and rivers in the area.  In 1869, the Gila river went dry for the first time, and 1886 was the last year water flowed onto their land, due to upstream river diversion by settlers.  They suffered famine, and were rescued by government rations consisting of white flour, sugar, lard, canned meats, salt and other canned and processed goods.  They subsequently became obese and have remained that way ever since.  Their diet consisted mostly of bread cooked in lard, sweetened beverages and canned goods, and they also received salt. More recently, their diet has modernized but still relies heavily on processed food (34, 35).

Finally, let's take a look at my country, the United States of America.  Total calorie intake has increased since the 1970s, and the excess calories came mostly from carbohydrate (primarily refined), and also from fat and protein to a lesser extent.  But what happens if we go back further, to the turn of the 20th century?  Here's our per capita macronutrient consumption in calories per day from 1909 to 2006, according to USDA data*:


If we take the long view, the only thing that has consistently increased is fat, not carbohydrate.  The prevalence of obesity was very low at the turn of the century (36), yet our diet was 57% carbohydrate by calories, much of which came from white flour.  These USDA figures account for food produced and consumed on farms and in home gardens, in addition to what passed through commercial sales (37).  Why would carbohydrate promote obesity today when it didn't 100 years ago, and it continues not to in numerous high-carbohydrate cultures around the world? 

Conclusion

I hope you can see by now that the carbohydrate hypothesis of obesity is not only incorrect on a number of levels, but it may even be backward.  The reason why obesity and metabolism researchers don't typically subscribe to this idea is that it is contradicted by a large body of evidence from multiple fields.  I understand that people like ideas that "challenge conventional wisdom", but the fact is that obesity is a complex state and it will not be shoehorned into simplistic hypotheses.

Carbohydrate consumption per se is not behind the obesity epidemic.  However, once overweight or obesity is established, carbohydrate restriction can aid fat loss in some people.  The mechanism by which this occurs is not totally clear, but there is no evidence that insulin plays a causal role in this process.  Carbohydrate restriction spontaneously reduces calorie intake (as does fat restriction to a lesser extent), suggesting the possibility that it alters body fat homeostasis, but there is no compelling evidence that this happens due to a hormonal influence on fat tissue itself.  The brain is the primary homeostatic regulator of fat mass, just as it homeostatically regulates blood pressure, breathing rate, and body temperature.  This has been suspected since the early brain lesion studies of the 1940s (47) and even before, and the discovery of leptin in 1994 cemented leptin's role as the main player in body fat homeostasis.  In some cases, the setpoint around which the body defends these variables can be changed (e.g., hypertension, fever, and obesity).  Research is ongoing to understand how this process works.


* I've adjusted these data for loss, using the standard USDA adjustment of 28.8 percent, to get a more accurate picture of actual consumption rather than sales.  I've also adjusted for an artifact in the fat data in 2000, where there was a big spike due to a change in the assessment method.

563 comments:

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Asim said...

The idea of trying to trace the rise in obesity to the latter half of the 20th century based upon things like over-stimulation of the senses or sugar or carbohydrates or salt intake for that matter is rather strange and a rather simple picture, considering the following:

1. Frosted Flakes was introduced in 1952, and Fruit Loops in 1960.
2. As somebody pointed out, though in the context of Taubes, McDonalds also originated way before the 80s. So did Kentucky Fried Chicken.
3. Certain traditional societies did have a wide range of food choices, the Indians amongst them, whose use of a wide variety of spices goes back thousands of years.
4. Salt is mentioned in the OT as a flavoring of food, meaning it's usage goes way back. It holds a symbolic status in many of the major religions, including among the oldest, Hinduism. Greeks and Romans offered it to the gods.
5. Carbohydrate usage goes back to traditional societies as well.

It's like nutritionism has become a new religion, with certain macronutrients being demonized as a whole.

Asim said...

Again, without taking into account the gut flora in the context of obesity and terms like bod set-point, one is doing injustice. As Dr. Ayers points out, mice studies have clearly shown that replacing the gut flora of obese mice with lean mice gut flora, and vice verse, has been well-documented to change the 'set-point' of the mice, meaning obese mice become lean and lean mice become obese.

http://coolinginflammation.blogspot.com/2010/01/constipation-gut-flora-and-health.html

Chris Masterjohn has alos pointed this out here especially relevant in the context of LEPTIN, although I am not sure about his conlusions regarding the study he references:

http://blog.cholesterol-and-health.com/2011/04/new-genetics-part-v-is-intestinal.html

Masterjohn states:

"While these genetically defective mice eat more and weigh more than genetically normal mice, there was one runted mouse in the study with defective leptin signaling that actually ate less and weighed less than the genetically normal mice, but it's microbial profile was similar to the other mice with defective leptin signaling. While we would want to see a larger study to confirm this, the observation suggests that leptin-induced changes in intestinal flora are not a result of increased food intake.

Remarkably, Ley's group later showed that if they transferred the intestinal flora from ob/ob mice to germ-free lean mice without any leptin defects, the mice gained twice as much weight and 50 percent more fat over two weeks compared to mice receiving intestinal flora from normal mice, despite no difference in food intake.

There is an abundant amount of evidence showing that leptin prevents obesity by decreasing food intake and increasing metabolism through direct effects on the central nervous system and other body systems. These results suggest, however, that leptin also prevents obesity in part by maintaining the proper balance of intestinal flora."

Looking at the summary of the study by Ley, it seems the point Ley was making was simply that the gut flora induced the changes, not that hormones like Leptin regulated the gut flora population. Although I don't have the study, this can be inferred by the high-lgihted portion of above. If leptin was the major culprit, than the obese gut flora, when transferred to the non-defective (in respect to the leptin signalling genes) mice should have adjusted, but the mice themselves became more obese than the obese mice who took the lean gut flora, despite no change in food intake.

This would also lend evidence to the fact that the endocrine system is dependent pretty significantly upon what type of gut flora a person has. This would essentially provide a huge answer to why people have different experiences on particular diets and why the effects of a diet may just be temporary, because the gut flora has not really changed, only the 'ratios' did as a result of the type of feeding. This is why fecal transplats would most likely alter the set-point of many people complaining about their inability to lose certain amount of weight on a particular diet.

Asim said...

And one more thing:

Traditional socieities were not overly hygienic, meaning they often ate food simply by brushing off the dirt of a food item.

I am quite sure that studies that track a transition of a person from a traditional way of living to a modern one, if they checked the gut flora before and after, would see stark differences, as well as a change in their "hormone responses"...

http://www.medpagetoday.com/MeetingCoverage/EASD/22352

Frank said...

Dr J.

I know these studies, but i've said that they are not as good as the one i've posted.

Take, for example this one

http://www.ncbi.nlm.nih.gov/pubmed/15533250

1. protein are not matched ( it's 20% of energy for LF agaisnt 30% of energy for LC)

2. The diet is not control by the researchers. Subject are given instruction on what to eat, and we are left to believe that they did not cheat and that they followed the plan perfectly.

3. REE was measured only at the beggining and at the end of the study.

It's also curious, if you look at fig. 1, to see how much lean tissue men lost on LC, althought it appears the result are not signifiant.

Now, in comparison, I've posted study where

1. Protein were matched.

2. Subjects were in a metabolic chamber for the whole study duration and the food was provided by the researchers.

3. REE was measured troughout the study. (There are factors that can affect REE on a daily basis such as sleep deprivation and probably others)

How do you account for these studies, Dr. J? Which by anyone standard would be consider to have a stronger design. Why when you control protein and the diet you no longer get the the same results?

Self-reporting is one very well known innacurate way of making a nutrition study. In the Volek study, people had to write what they ate in a journal and then give that to the researchers. In Men case, they reported 21 days out of 50, and for women, 21 days out of 30. How much more innacurate can this get? What happened to they other 30 days that men did not report?

I'm not aware that Volek did any metabolic chamber, iso-caloric iso-protein study. Did he?

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Carnivore said...

I am not aware of any studies which have tried to ascertain the effect of overconsuming on low carb and high carb diets. Let me explain what maybe Rebecca, me and others have experienced:

I can start to put on bodyfat at around 2800 calories per day on high carb. When I low carb, I can eat over 3400 and not gain bodyfat.

This is a very simple observation which happens to be common among people who eat low carb. You can quibble all you want about the references for calorie counts not being reliable, but 600 calories is a significant difference and I for one always tend to underestimate my calorie consumption from meat.

Metabolic chamber studies tend to get obese people to eat LC and HC while creating a ridiculously huge calorie deficit, with the result that their bodies adapt to the reduced intake by slowing down their metabolism substantially. These studies typically show significant weight loss initially and a tapering few weeks later, depending on the excess weight individuals are carrying.
HC and LC are expected to perform similarly when calories are reduced so significantly. At such low intake, the body's response to slow down it's metabolism is quite independent of the macros.

The whole point of low carb is to NOT create a huge calorie deficit and still lose weight. The sort of study which needs to happen is one where people are randomized to low or high carb with protein and calories kept constant and a reasonable calorie deficit of, say 750, being employed. This sort of study should then go on long term, not a few weeks and then assess the body composition of the subjects. And somebody tell the people who conduct these trials that a liquid diet with corn oil or the like as the primary fat source really doesn't simulate real world situations.

Last I checked, thinking scientifically doesn't mean you have to disregard the observations of a significant number of people, it means you come up with explanations for them.

As a sidenote, check out this link:

The purpose of this experiment was to see the effect of the consumption of 100g/day of SFA on lipids. However, this guy actually lost a small amount of weight (maybe just water) while overconsuming calories on low carb. His average intake for 15 days was 3112 calories/day, while his maintenance level was 2800 calories. He provides a link to his daily food menu and maybe if someone is interested, they could get in touch with him to get more details about his experiment. Of course, he wasn't in a metabolic chamber, so don't bother looking if that's the only thing that can convince you.

By the way, I want to volunteer next time someone plans a metabolic ward study. I don't mind free food.

Ross said...

Asim, regarding your points #1 and #2, it's not important so much when frosted flakes & co. were introduced, as when their popularity took off.

In the 1950s, the average american on average ate 109.6 pounds of caloric sweeteners. In the year 2000, that number was 152.4.

www.usda.gov/factbook/chapter2.pdf (Table 2-6)

Carnivore said...

Missed the link:

http://comprehensivefitness.blogspot.com/2011/08/effects-of-15-days-of-100-grams-of.html?spref=fb

montediaz said...

@Ross

Lets look at the exponential increase in refined sugar consumption in a much larger context; pre-industrial revolution and post-industrial revolution.

http://www.indiana.edu/~oso/Fructose/sugar-consumption-graph.jpg

I don't know why we are so caught up in data that is only 100 years old. By that time we were already consuming several dozen pounds of refined sugar per day. Far more than our ancestral...or even pre-industrial diets.

Given what we know about epigenetics so far, this should be telling.

Carnivore said...

The link between carbohydrate consumption and obesity does not cease to exist just because there are people who can eat carbs/refined carbs and not get fat. I am one of those too, as long as I watch my overall intake, I can pretty much eat as much sugar and bread as I please. If I'm clear about what Taubes says, carbs are not a sufficient condition for obesity, but they are necessary.

The fact remains that unless a population or group of people can be shown to have become obese without consuming a significant amount of carbs, the carbohydrate hypothesis cannot be debunked. Yes, the mechanism may need to be refined, but that's another story.

Sue said...

Rebecca Latham, you write that you can eat more calories on low carb and lose weight compared to high carb.
I note that you had to lower calories on Atkins because you were not losing. Also you think low carb is affecting your thyroid so you are increasing carbs. Right now you are on about 1400 cals to try and get some more fat loss.

Beth@WeightMaven said...

Carnivore, but why isn't the flip true as well? I.e., if a population or group of people can be shown to remain slim while consuming a significant amount of carbs, the carbohydrate hypothesis cannot be true.

As I think someone else commented here, the fact that reducing carbs helps people lose weight does not necessarily mean that eating carbs caused them to gain weight ... or that reducing carbs is the best or only weight loss mechanism.

Sue said...

If carbohydrates lead to obesity shouldn't everyone become obese?

Carnivore said...

I don't believe the Carbohydrate Hypothesis can be extrapolated to mean that everyone who eats carbohydrates is bound to be obese. It's the other way round, everyone who is obese is bound to have been eating carbohydrates. I really haven't seen an example to the contrary and would reconsider if provided with it.

It makes sense that indigenous populations who are fairly active eat carbohydrates and don't get fat. Activity cannot be detached from the equation, especially because the purpose of carbs is to provide energy. They tend to utilise that energy better than the average Joe munching on crisps watching a baseball game.

Sue said...

So those that are obese from carbohydrates became so from lack of activity whilst over-consuming carbs.

Carnivore said...

If you ask my opinion, it's because carbs, especially refined carbs are easier to overconsume because they produce little satiety. This is where Stephan's FRT comes in; rewarding food with little satiety almost always involves refined carbs. I personally find a steak more rewarding, but it's reward-to-satiety ratio is much better, i.e. I will struggle to overconsume it enough to get fat. This coupled with the fact that overconsuming on low carb doesn't seem to have the same deleterious effects as overconsuming on high carb (personal experience) pretty much explains (to me) why people get obese eating high carb foods.
Whether you can actually overconsume rice or potatoes is still up for discussion but I personally see my own family members eating a huge mountain of rice with every main meal. I can only venture a guess that that's partly why we have a strong family history of diabetes.

Personally, I do eat carbs and I feel they have a place in the human diet. Potatoes or rice in small servings, sure. The problem occurs when you base the entire diet on carbs AND have a sedentary lifestlyle. Kitavans probably are not the people we ought to compare ourselves with when we try to ascertain what constitutes a healthy diet.

Frank said...
This comment has been removed by the author.
Frank said...

@Carnivore

I'm not sure i'm following you as to why on a larger caloric deficit isocaloric diet would bring the same weight loss, but on a smaller caloric deficit it would not. What is suppose to happen in the latter case that don't happen in the former one?

Also, REE don't decrease in anyone on a diet. Some individual actually see an increase of REE while dieting.

See this : http://www.ncbi.nlm.nih.gov/pubmed/19846179

Also, as pointed out, why do we need a fat population eating no carbs, when we have lean population eating carbs? Asian individual have been eating a lot of rice in the past years, even when physical activity decreased, and yet they remained slim. Also, you say that one can eat carbs if exercising. Now, that would mean there could be 2 hypothesis : either obesity is cause by carbs, or either it's cause by a lack of physical activity. How can we know?

I personnally know individual who could put on weight (muscle and fat) while being ketogenic diet. I did the metabolic diet ( a cycled ketogenic diet) for 8 months 3 years ago and I was much fatter than I am right now (around 8-9% fat whereas right now i'm under 7%).

Also, one last thing but, Eades in an old post was speaking about a 100-300 calorie difference for the metabolic advantage, if it exists.

Why do you believe that it can get as high as 600 calories when no one, not even people claiming that MA exist, ever acknowledge that this could be?

Asim said...

Ross,

I agree that sugar consumption has gone up and that is problem.

My only point is that people make irresponsible correlations, when they actually have no real meaning in determining what the actual issue is. I could argue that metabolic issues we are seeing is a result of the lack of vitamin D because of the rise on sun-screen the last 20 years, as opposed to the rise in sugar by that token that HFCS consumption has increased dramatically during this time-frame. Who is right based upon the observations?

There are a whole series of factors that lead to weight gain and which may impact eating habits. It is well-documented in cachexia, that the matebolic syndrome of muscle wasting is a result of inflammation, not starvation as previously thought. This clearly shows that metabolic adaptations are also tied to the immune system. Macrophages are present in the fatty tissue of obese people as well, which contributes to a cycle of hormone disruption. Inflammation also leads to depression, which is often tied to obesity and eating habits as well. This would provide some evidence that weight is tied to the immune system response as well.

Body set-point is also tied in to gut flora pretty much without a doubt, and transferrence of a lean mices gut flora to an obese mice changes the body set-point in experiments. Some evidence indicates it being more of significant than the hormone signalling in certain cases, including mroe than leptin. This gut flora is precisely the reason one may see difference in results of diets for particular people.

We often here about control groups, but one control that is often left out of these studies is the gut flora. This gut flora explains why a person may eat purely potatoes and not get fat, while another may get fat in a matter of days.

M. said...

Carnivore,

Activity levels, overconsumption, satiety – talk like that is not really supporting Taubes’ theory.

Taubes believes the thermodynamic direction of causality is reversed – carbs make you fat, then you eat extra to replace all the carbs/calories being sequestered in fat.

It looks like what is happening is that people see negative aspects of certain foods, they label these foods as refined carbs or sugary drinks or whatever, and they build up the idea in their head that this anti-carb guy Taubes must be on to something.

Your idea that refined carbs produce less satiety and this leads to overconsumption which leads to fat gain is not part of Taubes' theory or argument.

Carnivore said...

@Frank: Not necessarily the same fat loss, but similar enough to not be statistically different in the short term, which is how all these studies are designed. My point is that a massive calorie deficit tends to make the body fight back hard by slowing down metabolism. That's why successful dieters know not to create too big a deficit initially when they want to lose fat. Try going on a 800 calorie diet; sure you'll lose weight fast initially but a few weeks later, weight loss will slow down or completely cease because the body has adapted to the decreased energy intake. You'd have lost a fair bit of lean mass too but your weight wouldn't have decreased enough to warrant an 800 calorie maintenance level, yet you will be in energy balance eating 800 calories.

If you eat 1600 calories instead, you will find weight loss to be slower initially, but it will last longer and you'll end up losing more bodyfat than lean mass compared to an 800 calorie diet. Eventually, the body will adapt and you will stop losing weight, that's when you could increase the deficit by another 200 calories, for example. Such diets can be carried out over a longer term and lead to more fat loss, moreso when the diet is LC. With HC, the plateau tends to come earlier and calories need to be restricted further to continue progress. This is personal experience of course, so take it with a grain of salt if you wish.

@M: To make it clear, I'm not trying to defend Taubes or his theory as it stands today. I just don't think that the link between carbohydrate consumption and obesity should be dismissed so easily.

I am South Asian myself and I can tell you first hand that we aren't as naturally lean as people make us out to be. We just have smaller frames and less lean mass; our BMIs tell us that we aren't obese, but we tend to develop pot bellies, wide hips, skinny arms and narrow shoulders, i.e. the classic skinny fat look unless we exercise. The lean people you talk about are poor people who work on farms the whole day and cannot afford to overconsume food. The people working office jobs who have easy access to food and don't get much exercise are far from lean. The regular consumption of 'chapatis' and rice takes it's toll slowly, so you're much more likely to see an unfit 35 or 40 year old than a 20 year old. And by unfit I don't mean grossly obese, more like 20-30% bodyfat males, 30-40% bodyfat females.

I think carbohydrates are one link in the chain of obesity, but a link without which the chain cannot be completed. I am not denying the existence of other factors like activity level, malnutrition (see Paul Jaminet's view), etc. To me, this is why you can have people living primarily on carbs and being lean. The chain isn't completed.

Frank said...

@Carnivore

Your point might not be always valid. Did you look at the study I posted? Some ppl REE increase on a low-calorie diet.

Also, take a look at this link : http://www.thepermanentejournal.org/issues/2010/spr/or/132-obesity-problem-solution-or-both.html

They have used a fasting protocol supplemented with multi-vitamin for weight loss.

From the article :

''Given that the average weight loss of someone completing our 20-week program is 62 lb (28 kg) and that approximately 5000 patients each have lost more than 100 lb (45 kg), we realize we have challenged the belief systems of some who assume either that such weight loss cannot commonly be achieved or that the process of supplemented absolute fasting must be dangerous.''

How would that be possible if metabolic slowdown would impair weight loss? These ppl were not even getting 500 calories a day.

I also think that obesity is multifactorials, and I think carbs really are not so much of a big player in the whole picture - relatively to all the other factors.

Carnivore said...

Putting on weight on the metabolic diet isn't surprising. The carb refeeds can do that, as can excessive overconsumption of calories in general. Bear in mind that putting on a few pounds of muscle and fat is not the equivalent of becoming obese, especially when you are maintaining single digit bodyfat. Plus, the metabolic diet tends to have a lot of protein which can get converted to glucose via gluconeogenesis. Still, obesity resulting from ketogenic dieting is something I haven't heard of.

I missed the metabolic advantage part. I believe Dr. Eades has said that this varies from person to person and is hard to quantify. Also, he talks about it in the context of losing weight as he treats patients who are obese and have already damaged metabolisms. It is entirely possible that a healthy 27 year old can overconsume by more than 200 calories and not gain fat. I don't believe Dr. Eades has ever talked about the metabolic advantage in terms of overconsumption.
There are mechanisms by which the body can deal with the excess energy: raised body temperature for example. It's not as utterly impossible as it may seem.

Carnivore said...

Yes, I did look at that study. I was going to say that their subjects were obese, post-menopausal women and as such, their results were highly individual so I don't think we can derive a general rule from that study.

Again, damaged metabolisms may respond differently, but among people with normal weight, trying to lose the last few pounds of fat is a bitch precisely because your body tends to adapt quickly to the low intake.

I'm not denying the possibility of people continually losing weight on an extremely low calorie diet, especially if they have a huge amount of fat to lose. When the body has to tap into lean tissue, the natural defence mechanism is to adapt to surviving on fewer calories by lowering metabolism. Would it happen at the same time for everyone? Probably not.

Carnivore said...

As an example, an obese 350 lb guy is likely to be consuming in excess of 5000-6000 calories to maintain his weight. If he goes down to 500 calories, that's a deficit big enough to feed two people. It's not surprising he can lose a 100 lbs before his metabolism slows down enough to be in energy balance at 500 calories. (The numbers are just random, not calculated).

Frank said...

@Carnivore

Ok but where are we going with this?

I told you isocaloric diet bring the same weight loss.

You say that studies use a too big caloric deficit which slow down metabolism and make the weight loss be the same.

Then we agree that REE can either decrease or increase depending on the individual and you tell me that obese individual won't see a decrease of REE on a big caloric deficit before a long time, because they have a lot of fat mass.

Most LC diet study that I know and most dieter that I know are obese individual, hence, do you still stand by the fact that study use too much of a huge caloric deficit?

It should not matter if they do, if we agree that obese individual can do fairly well on a big caloric deficit and will still lose weight, not plateau very fast as you first claimed.

Why would a 1000 calorie deficit on varying macro distribution bring the same weight loss, and not a 500 calorie deficit if we agree that obese ppl won't see a big decrease in REE?

STG said...

Stephan said:

"HiItsTheWoo2,

You've again proven yourself incapapble of making your point without insulting me and other commentors. . . .I'll be deleting your comments for now on."

I am trying to understand why you are censoring ItsTheWoo2, but not other people who post on your blog who "insult" you and/or other people?

Dan questioned you? Is this an "insult":

"Maybe think a little harder about Taubes' advice about how to conduct good statistical science."
". . . .Don't be so smug when people tell you how to conduct science."

So is Dan going to be deleted?

Frank said:

". . . as someone who is studying nutrition SCIENCE, I'm getting quite pissed by people who are not taking a scientific approach to science."

Isn't this comment directed at someone and couldn't it be construed as insulting?

". . . I'm eating a shit load of refined crap lately. . . ."

So is using profanity (pissed, crap and shit) acceptable on your blog?

Stacy said:

"@Stephan:isTheWoo2delete=YAHOO."

So it is not ok for TheWoo2 to "insult" others, but its ok for other people to insult her and they won't have their remarks deleted?

said...

hmm, new study out - "How Fatty Diets Causes Diabetes"

http://www.sciencedaily.com/releases/2011/08/110814141432.htm

Jack said...

STG - "I am trying to understand why you are censoring ItsTheWoo2, but not other people who post on your blog who "insult" you and/or other people?"

If you want to really understand, you're gonna need to wade through dozens and dozens of previous articles that Stephan has written, and then search for Wooo's comments. Compile them all up and read through them. You'll probably die at 99 years old before you get through them. In other words, there's a history here that you obvsiouly don't know about. She's been warned before.

Stephan Guyenet said...

Hi STG,

As Jack said, ItsTheWoo2 has a long history of insulting me and other commenters, monopolizing the comments section and going on very long, multi-comment unreferenced rants. Her behavior in this post was simply the straw that broke the camel's back.

I understand that this is the internet, and things can get heated sometimes. That's fine. I warned her to be more respectful on several occasions. I gave ItsTheWoo2 a choice to play nice or leave, and she made her choice. I have no regrets about that.

Harry said...

I noticed a few comments regarding the nature of the 'causal' role carbs play in obesity...

Are carbs a 'necessary' condition for obesity, a 'sufficient' condition, or something else (say, a contributory cause)?

Firstly, we need to realise that science does not define casuality in these terms (these are philosophical taxonomies based on deductive and inductive logic, harking back to J.S. Mill et al).

Science generally operates on a statistical and empirical model, not a logical model. To wit, a 'cause' in science is some factor that has been shown to be statistically associated with some other factor, and which has a causal mechanism that can be explicated and duplicated.

So, when we say that "smoking causes lung cancer", we don't mean that smoking is necessary to develop lung cancer, nor do we mean that it is sufficient to cause lung cancer. We simply mean that there is a significant statistical correlation between smoking a getting lung cancer, and that there are explicable and testable mechanisms that explain the correlation...(yes, this a crude oversimplification of the scientific method).

So, according to the logical model, I think it's pretty uncontroversial that carbs do not cause obesity; they are not a 'necessary' condition for obesity (see Jimmy Moore), nor are they a 'sufficient' condition (see Kitivans et al).

Now, according to the statistical and empirical models, that's more of an open question. Statistically, some studies show some form of correlation, some clearly don't. And as for the mechanism...well, there clearly isn't a well-defined account of how carbs cause obesity (despite Taubes' insistence that insulin secretion causes obesity). If some such mechanism is out there, it is yet to be explicated.

Helen said...

Holy cow! Now that's a lot of comments!

Dan said...

How does Food Reward explain obesity? Food Reward is just self-evident because it says we're obese because we eat too much and we eat too much because eating too much is positively reinforced in some way. That is self-evident. It's just CICO dressed up.

One day Stephan is explaining that the brain regulates body fat set point in response to the foods we eat, the next day he's saying that people who gain weight invariably eat more than people who don't, seemingly contradicting himself just to spite Gary Taubes, when in fact the conclusion he quoted didn't negate what Gary Taubes was saying, anyhow.

What happened to the Massas, who "appeared to have mounted a compensatory response aimed at countering fat gain" and gained substantially less weight than their caloric intake suggested? So, is it not clear then that when people are GAINING weight, that they are not necessarily eating more than people who are NOT GAINING weight?

Stephan Guyenet said...

Hi Dan,

You need to understand the thermodynamics of the human body. That changes in the amount of energy stored inside the human body (primarily as fat) depends on the balance of energy entering vs energy leaving is a physical fact. Taubes and I both agree on that.

The problem is that both calories in and calories out depend on other factors, including one another. In the case of the Massas, the reason they didn't gain as much weight as expected is that their energy expenditure increased in response to the overfeeding. There is no contradiction there.

To explain fat accumulation, we need to explain why energy intake has increased by 250-570 calories per day in the US. That's where food reward/palatability comes in.

Dan said...

Stephan, you are ignoring my point.

You acknowledge that calories in and calories out depend on a lot of other factors, and have shown that overfeeding doesn't necessarily lead to the expected amount of weight gain.

So, does this not contradict your "refutation" of Gary Taubes' statement that people who weigh more or who are gaining weight don't necessarily weigh more than people who are not?

It seems to me to be a contradiction of yourself to spite Gary Taubes.

You seemed a little indignant that he referred to Food Reward as YOUR theory, when it predates you. Then you want to make it personal against him rather than against his ideas, and because of this, you have tried to refute an unremarkable statement of his that is in line with your own writing about bodyfat setpoint increasing or decreasing based on the types of foods you eat, and not strictly based on the quantity. It just seems petty to me.

Furthermore, I don't know what I need to understand about the thermodynamics of the human body to make my point. I don't make specific criticisms of science that I haven't read or don't fully understand, but I'm well qualified to criticize reasoning and to recognize passive aggressive behavior.

As far as Food Reward explaining the obesity epidemic, I would like to see some distinction between the psychological aspects of food reward -- which are self-evident (i.e. of course we eat more because eating more has been positively reinforced), and palatability. Refine the hypothesis with clearly defined terms instead of using the self-evident concept of positive reinforcement to fill in the gaps left by palatability.

Yeah, I'll probably eat more potatoes if they're whipped than if they're baked, but I don't think it's possible for me to accidentally overeat steak - my favorite food (even if it's spiced!).

And if your food reward theory says "If you think you will be able to find a way to lose fat and remain in long-term health while eating mostly commercially processed food (including restaurant food), you are fooling yourself" then maybe you need to cool down with the dogma a little bit.

Most modern foods aren't excessively rewarding if you aren't talking about sweets. Refined sugar, white flour, and vegetable oil are bad even if they aren't baked into a twinkie. Restaurant food typically isn't bad as long as it isn't served on a bun or fried in vegetable oil. Traditional processing is about preservation, just like modern processing. Other than the sweets, there's nothing else that is excessively rewarding. I'm certainly not addicted to processed meats, because they are too rich to overeat, anyhow. So why demonize all "commercially processed" food and restaurant food?

I gave up anti-carb dogma a good while ago; I'm not going to trade it for anti-"process" dogma. If you are going to get indignant with Taubes over not distinguishing between carbohydrates, then you need to be more careful about making distinctions with your theory that "commercially processed" foods are the culprit. I don't think that's a testable hypothesis.

Asim said...

Just want to point out that the following study sheds some light on the relationship between leptin and gut flora:

http://www.ncbi.nlm.nih.gov/pubmed/17183312

Per Chris Masterjohn, who sumamrize the article, mice that had leptin defects, when their gut flora was shifted to lean mice, the latter gained 50 percent more fat and twice the weight gain than the defective mice who received intestinal flora from the normal mice, despite no difference in food intake.

In this particular case, the gut flora had "more influence" on weight gain than the leptin signaling.

I think the fundamental problem we are seeing is that we tend to view the human body as an isolated phenomenon, without taking into account the symbiotic relationship that exists with our own microbiome.

The principle is clear that enery in = energy out, but the human being isn't metabolizing all the energy he/she is eating. He/she is sharing it with his/her own microbiome.

David Pier said...

Asim,
In that study, the obese mice were only 2% more efficient in harvesting energy from food than the lean mice. There was a dramatic difference between germ-free mice and mice with any type of intestinal flora, but none of us have germ free intestines. Not that the whole gut biome thing isn't fascinating. I'm sure it plays some role in obesity, as well as immunity.

blogblog said...
This comment has been removed by the author.
blogblog said...

There are two reasons why people are thin on these traditional high carbohydrate diets:

a) because food is available in adequate but not excessive quantities.

b) physical activity cannot be further minimised.

There is very little risk of overeating on these high carbohydrate diets. In fact people typically force themselves to eat vast amounts (2-3kg each day) just to maintain their weight.

If you make the high carbohydrate food available in unlimited quantities and take away the physical activity you have obesity.

M. said...

Blogblog,

You are basically saying “eat less, move more” (not very Taubesian). If you don’t buy Taubes’ reverse direction of thermodynamic causality, is there any point in speaking in terms of “carbs” instead of FOOD. It would seem that “carbs” are heavily confounded by calories in “eat less, move more”.

Asim said...

david,

Are we referring to the same study? I am conly going by the summary and what Chris Masterjon referenced here:

http://blog.cholesterol-and-health.com/2011/04/new-genetics-part-v-is-intestinal.html

The reason I am asking is the following:

1. This comparison that is noted in the sumamry, as well as Chris' reading, is that it was a comparison between obese and lean mice that were NOT free of gut-flora, meaning the issue of being germ-free doesn't enter the picture. Further, they don't even mention germ-free mice.

2. The difference mentioned by Chris is 50 percent fat gain and twice the weight gain. If it was a 2 percent difference in energy uefficiency as you say with the mice, than this too me raises more of a paradox, because how does one account for such a monumental change in the body composition with only a 2 percent increase in efficiency, when the food intake is the same?

Asim said...

One more thing Dan:

http://www.sciencedaily.com/releases/2010/03/100304142232.htm

The article essentially affirms the position that "intestinal bacteria contribute to changes in appetite and metabolism."

This artilce also mentions Ley, the reseracher in the previous study I mentioned, meaning we may be referring to two different studies.

David Pier said...

Asim:
quote from the study (the study you posted the PubMed link for):
"Strikingly, mice colonized with an ob/ob microbiota exhibited a significantly greater percentage increase in body fat over two weeks than mice colonized with a +/+ microbiota (Fig. 3c; 47 plusminus 8.3 versus 27 plusminus 3.6 percentage increase or 1.3 plusminus 0.2 versus 0.86 plusminus 0.1 g fat (dual-energy X-ray absorptiometry): at 9.3 kcal g-1 fat, this corresponds to a difference of 4 kcal or 2% of total calories consumed)."

It doesn't take much of a difference over time, and it was just the body fat, not body weight that increased that much. The most interesting thing is that the mice didn't adjust their caloric intake down to compensate for the greater efficiency. Also relevant here, Stephan's post about gastric bypass and the comments there about capsaicin disruption of the vagus nerve. Very significant effects on the amount of energy used in thermogenesis...

Stephan Guyenet said...

Hi Dan,

Let me explain briefly how the ideas fit together so you can see that there is no contradiction.

In summary, something is increasing the body fat setpoint. That requires a change in energy balance, that's simple thermodynamics. Once body weight is elevated, it requires more energy to maintain. Therefore, one would expect that obese people eat more calories than the lean, which is the case once you control for other things like height, gender and activity level. It turns out that they also expend more energy, so they have a higher energy "flux".

The question is, what increased the body fat setpoint, which in turn raised calorie intake to maintain it? Another related way of asking this question is "what caused an increased calorie intake"?

That's where food reward comes in, because it can change the setpoint. However, a change int he setpoint requires a change in energy balance. Again, that's just physics. If there is no change in energy balance, there can be no change in the amount of energy stored in the body as fat.

I'm sorry to disappoint you, but I didn't write this post out of spite. I did it because I knew many people would find it useful, which was the case.

Asim said...

Hey David,

I don't see where the connection to gastric bypass is made in relation to this situation.

In the case of the gut flora of BOTH the obese and lean mice, the duodendum remains intact, meaning the interaction between the small intestine and the brain is still there, the only difference being the gut-flora. Further, the quality of the food was the same in this case, i.e. they were fed the same things meaning 'taste' should not have been an issue.

Yet, we have clear cases of mice putting on significantly more fat based upon the gut flora, even if we discount the total 'calories' being 2%.

I'm not denying that 'food reward' has it's place, but again, this seems to be a case of the microbiome.

Dan said...

I think we're arguing two separate things. I acknowledge that heavier people require more energy to maintain weight. I would also like to see the make-up of the diet controlled for, as well. I don't believe that energy balance is simply determined by macronutrients and movement. Weight alters total energy expenditure upwards. I think everyone accepts that. But is it true when you change the make-up of the diet? I will peruse the studies when I have some time and see how they corrected the data, but I admit that I'm not a statistics guy, just a straight math guy.

Does someone who is gaining weight invariably eat more than someone at the same weight who is not gaining weight? I doubt it.

Could someone have gained more weight than the Massas did eating a diet of processed foods with less than 8000 calories per day? What do you think? I'm genuinely curious.

Though, of course, I don't have the Taubes quote to determine whether he was talking about weight-stable obese people or people who were gaining weight. So perhaps we are discussing two different things, though I think they are essentially the same. But even if Taubes literally said that weight-stable obese people don't necessarily eat more than lean people, "not necessarily" and "almost invariably" are not mutually exclusive. I don't think you can use "almost invariably" to tell a single person like Rebecca that she must be mistaken about her singular experience because a study found something that is "almost invariably" true.

As for your motivations, I'm only criticizing bits and pieces, while on the whole I think the information is valuable and something you should have written up a long time ago if you've just been sitting on this information. Regardless, I'll not escalate further on this issue, as I do not question the validity of the vast majority of the information presented.

Sue said...

Where's Taubes???

Carl said...

Thanks Stephan.
N=1 ......When I quit smoking, I gained 20 pounds. Didn't change my diet but the food was more rewarding.

InNewOrleans said...

@ Woo

"SO you used a nutrient factor well described to resolve PCOS, and yet for some reason you think it was exercise?"

This is a ridiculous statement. Inositol has been shown to result in marginal improvement of symptoms in some women, if they are also managing their insulin resistance. Most women I know who take it notice no benefits at all. Let's be real.

My last post was actually the second part of a two-part post. The first part must not have gone through, and I didn't check back until now. No matter. It seems your mind is made up. You will believe what you want to believe and are completely closed to all other points of view, to the extreme of making incredible assumptions and leaps of logic in your response to my original post. I must have been on depakote? Is this the rationalization that was necessary to fit your preconceived notions? You are too smart to be so closed-minded.

Grok said...

@Elizabeth Miller, you will lose. Put yourself on a mono diet of rice cakes and see what happens.

Richard said...

So, in the end, this is a discussion of set-point. Which is to say that the food itself is not making anyone fat, but rather that the body (brain) has chosen, with some help, to decide how much fat it needs to store. Something has changed the set-point, and after some examination, it turns out to be food that is "rewarding" a term which is not the same as good tasting, but rather suggesting an almost unnatural urge to eat it.

I have to go along with Carnivore and a few others that these problems can be solved, and maybe can only be solved, with a diet that eliminates dependence on carbohydrates as the major food source.

I would propose based on what I have read, and experienced, that although the set-point and food reward proposal may explain the problem in one sense, what it fails to provide is an explanation of why the body reacts that way. My proposal is that the body recognizes the lack of saturated fat in the diet and then the individual eats a lot more carbs than necessary to make up for that missing fat. The body and brain are fooled by the sugar and PUFA to some extent (which of course adds to the caloric excess and makes more fat), and also by the substituted satiety caused by carbs as opposed to fat. With Carbs you eat until your stomach is about to burst. With fats you stop eating a lot sooner.

In the end with a low carb diet, which is to say carb calories mainly replaced by fat calories, you will get weight loss, because the body is getting the fat calories it wants.

As I see this, a carb heavy diet is telling the body to store fat, because a poor hunting time is upon it. I do not go along with the idea that somehow storing fat is anomalous or strange. It can't be, if it happens to almost everyone. And obesity is natural, to the extent that if you feed someone too many carbs this is the result you get.

There is an evolutionary reason for the body storing the fat. It is not some cruel trick.

As I have read Stephan's posts and posts from others I respect, what seems clear is that a diet that does not over-do on carbs is the only successful approach. And although a maintenance diet may include more carbs, an initial approach has to be more heavily focused on fat consumption to the point of minimizing carbs.

Ultimately for me, the idea is that humans are omnivores, and that carbs are part of the diet. That's fine until carbs become the mainstay of the diet. At that point the body has to be convinced that it is back in a good hunting area, one with all the fat wild creatures it could dream of eating. In other words, eating fatty meat is not just the cure for the problem. The lack of proper fats and meat is the problem.

blogblog said...

M. said...

Blogblog,

You are basically saying “eat less, move more” (not very Taubesian). If you don’t buy Taubes’ reverse direction of thermodynamic causality, is there any point in speaking in terms of “carbs” instead of FOOD. It would seem that “carbs” are heavily confounded by calories in “eat less, move more”.



I'm not saying "eat less move more" at all. I am saying that high carbohydrate diet may work in a situation of caloric restriction and high levels of physical activity. However in the modern western context this situation is basically confined to athletes.

There is also the totally false assumption that East Asians, South Asian. Okinawans etc were extremely healthy on these high carbohydrate diets. In reality these people were generally very short with small frames, very little skeletal muscle and and realtively high body fat.

The Kitivans actually have very poor physiques (from the photos I've seen) compared with many other pre-industrial societies such as the Masai or even their more carnivorous Melanesian relatives.

M. said...

Blogblog said: “I'm not saying "eat less move more" at all. I am saying that high carbohydrate diet may work in a situation of caloric restriction and high levels of physical activity. However in the modern western context this situation is basically confined to athletes.”

It does really kind of sound like you are saying that “Gluttony and Sloth” is the problem with modern western diet and lifestyle. The “Gluttony and Sloth” argument would seem to emphasize calories over “carbs”. I think Taubes would consider “Gluttony and Sloth” the antithesis of his argument.

Many of these cultures don’t really start experiencing the so-called diseases of civilization until they begin adopting a western diet and lifestyle. Whether they are used to eating high carb, high glycemic or not, the problem seems to come with western diet and lifestyle. It looks like this should be the area of interest – not “carbs” or “insulin spikes”.

poe said...

I'm obese and not very active (I walk to work, which is about 4 miles a day, but the rest of my time is mostly spent sitting in front of a computer). I'm on a high carb high fiber diet (approx. 65% calories from carbs, that is, about 55 g fiber per day). I chose this diet not because I know anything about nutrition, but because I'm a vegetarian, and this suits my lifestyle the best.

I eat about 1700 calories a day, and lose about 2 pounds per week. I eat lots of soups, stews, fresh veg and fruit, moderate amounts of whole grains, very little dairy and almost no bread or pasta and stuff like that. I've eliminated all the high rewarding foods that I used to indulge in, and the diet works great.

I've been on it for over three months; the first month was a pain in the neck as it took some time to get used to a new regime and stop missing all the bread and pasta and sweets I used to eat, but now I find it easy to stick to. It's great because when you eat a variety of fruit and veg – lots and lots of veg :) – your meals are rarely monotonous.

I'd recommend this diet to anyone who may have a problem with low carb diets, or are vegetarian, etc.

poe said...

*I walk to work, which is about 4 miles a day

D'oh, I meant to say 4 kilometers, not miles :)

blogblog said...

Blogger M. said...

It does really kind of sound like you are saying that “Gluttony and Sloth” is the problem with modern western diet and lifestyle. The “Gluttony and Sloth” argument would seem to emphasize calories over “carbs”. I think Taubes would consider “Gluttony and Sloth” the antithesis of his argument.

Did you even bother to read my comment?

I actually said that carbohydrates are BAD. However physically activity and calorie restriction can mitigate thye worst effects.

I even consider humans to be obligate carnivores not omnivores. I consider any diet containing over 20g/day to be high carbohdrate.

The Okinawans or Kitivans etc can only be considered "healthy" in comparison to the abysmal standards of the unhealthiest modern westerners. By hunter-gather standards they are physically pathetic examples of humanity.

blogblog said...

Virtually all mammals on a natural diet derive almost all their nutrition from fatty acids and protein. This occurs via direct consumption of meat or via gut fermentations.

Cows fed on natural pastures get approximately (via fermentation) 80% of their energy from volatile fatty acids, 18% from protein and only 2% from carbohydrates.[In fact ketosis is very common in lactating cows.] This nutritional ratio is virtually identical to the diet of domestic cats the which are the most strictly carnivorous mammal.

Animal nutritionists know that the only practical way to produce very rapid weight gain and high fat levels in poultry and livestock is to a) use a diet high in refined carbohydrates and b) minimise physical activity.

Simply offering unlimited natural food and allowing normal physical activity will rarely cause overeating or excessive weight. This is because activity will alter to match caloric intake.

It should be noted that laboratory dietary experiments on rats and mice are totally unrealistic. This is because rats mice are naturally hyper-athletic. They normally run at high speed for several hours each day. This level of physical activity never occurs in the confines of a laboratory cage.

M. said...

Blogblog said: “I even consider humans to be obligate carnivores not omnivores. I consider any diet containing over 20g/day to be high carbohdrate.”

Alrighty then…mythology FTW.

Asim said...
This comment has been removed by the author.
Asim said...

Hey Richard,

"As I see this, a carb heavy diet is telling the body to store fat, because a poor hunting time is upon it. I do not go along with the idea that somehow storing fat is anomalous or strange. It can't be, if it happens to almost everyone. And obesity is natural, to the extent that if you feed someone too many carbs this is the result you get.

There is an evolutionary reason for the body storing the fat. It is not some cruel trick."

Bears and others animals do hibernate in the winter, and they prepare for it by seeking out and gorging on fruits, honey and berries to get fat, as mentioned by Mark Sisson. Also, fat provides a 'protective element' against the cold weather, not just starvation. I would guess there is a reason most animals of the arctic or plump and 'fatty' as a general rule.

Asim said...

blogblog,

"Animal nutritionists know that the only practical way to produce very rapid weight gain and high fat levels in poultry and livestock is to a) use a diet high in refined carbohydrates and b) minimise physical activity."

Not necessarily true, thus the introduction of antibiotics on a mass scale for the purpose of fattening the animals.

blogblog said...
This comment has been removed by the author.
blogblog said...

Blogger Asim said...

blogblog,

"Animal nutritionists know that the only practical way to produce very rapid weight gain and high fat levels in poultry and livestock is to a) use a diet high in refined carbohydrates and b) minimise physical activity."

Not necessarily true, thus the introduction of antibiotics on a mass scale for the purpose of fattening the animals.

Antibiotics don't increase weight directly. They reduce the level of infectious diseases which cause weight loss. These diseases are a result of intensive farming practices such as feedlots.

blogblog said...

Blogger Asim said..


Bears and others animals do hibernate in the winter, and they prepare for it by seeking out and gorging on fruits, honey and berries to get fat, as mentioned by Mark Sisson. Also, fat provides a 'protective element' against the cold weather, not just starvation. I would guess there is a reason most animals of the arctic or plump and 'fatty' as a general rule.

There is a tendency for Europeans and North Americans who live in cold climates to naturally assume that humans have evolved to fatten up for the winter.

However humans evolved in a high altitude tropical grasslands where wild fruit is both relatively rare and low in sugars and winter is non-existent.

The vast majority of humans still live in tropical and subtropical environments where winters are very mild.

blogblog said...

M. said...

Blogblog said: “I even consider humans to be obligate carnivores not omnivores. I consider any diet containing over 20g/day to be high carbohdrate.”

Alrighty then…mythology FTW.

An interesting fact... Diets with <20g/day carbohydrate are a 100% effective means of eliminating gastresophageal reflux disease.

I suggest you read some actual science before being so dismissive. For example:

a) Humans have amongst the lowest efficiency of carotene to vitamin A conversion of any mammal species.

b) We have very limited (nil in some individuals) ability to convert short chain omega-3 fatty acids found in plants to long chain omega-3 acids.

c) Fructose malabsorption is very common.

d) No functional cecum.

e) Thin dental enamel and reduced molars.

These are all characteristics of carnivores such as dogs and cats not omnivores.

If you do some reading you might also discover that mammals on natural diets typically get <2% of their calories directly from carbohydrates. Carbohydrates found in unprocessed wild foods eaten by herbivores are typically converted to fatty acids and protein via gut fermentations rather than directly absorbed.

Even strict herbivores such as cattle obtain around 80% of the calories from volatile fatty acids and about 18% from amino acids via gut fermentation. Ketosis is relatively common in grass fed dairy cows.

Melchior Meijer said...

Hi Blogblog,

You sound a bit grumpy, but I take the chance. Why do humans have high amylase activity, much higher than chimps? Just some strange relict? Or could it be that we are adapted to digging up and cooking starchy tubers? Could it be that we are omnivores, able to exploit practically every ecological niche on earth? Could it be that we (well some of us) evolved our relatively huge brains thanks to energy and nutrient dense foods, including marine foods (coastal dwellers, 'Survival of the fattest, the key to human brain evolution', Stephen Cunnane, all folks with a slight interest in this topic should read it), but also including those much maligned tubers, fruits, and anything we could hit, steal, dig, pick, regardless of macro nutrient ratio? Or do you dismiss that possibility as a preposterous idea, which could only pop up in a hopelesly glycated, ketone depleted brain?

Little Black Car said...

Jason sandeman:
That doesn't mean that carbohydrates are causing obesity.

You know who else gains weight on insulin? Diabetic cats. If you put an underweight diabetic cat on insulin and feed in straight meat, it will gain weight.

We're not cats, of course, but that still at least suggests that carbohydrates are not the specific cause.

Swede said...

I think Blogblog used to post on here as Bris, about 2 or so years ago. His statements on Hyperlipid have the same language and tone.

Staphan banned him because, much like itsthewoo, he was a royal pain in the ass.

Melchior Meijer said...

Blogblog says:

"The Okinawans or Kitivans etc can only be considered "healthy" in comparison to the abysmal standards of the unhealthiest modern westerners. By hunter-gather standards they are physically pathetic examples of humanity."

Wow. This is cognitive dissonance operating at full force. Please go see Mat Lalondes' talk (AHS). Lesson 1: Never make bold claims (like this) among hard core scientists. You will be grilled and they'll order a taxi for you. I'm no scientist, but this is utter bullshit. Many Okinawans are extremely healthy, by any medical standard. Mail Staffan Lindeberg and tell him his Kitavans clearly were in sub optimal health because of their high carbd intake. Only if they had eaten a 90 percent fat diet they would have had a chance to improve that crippled insulin sensitivity of them... O, did they have excellent insulin sensitivity? Eating all these tubers? Tralalala, I have my fingers in my ears, so I don't hear you...

Monica said...

I'll add my personal experience to the others who have commented here on their own experiences with food reward.

I did a low carb diet for several years and stuck with it because of the convincing nature of Taubes' arguments. While I felt fine on the diet, and did initially lose about 15 lbs, I gained it back. This is consistent with what is observed for most diets, including low carb. Perhaps what is happening is that the brain "re-assesses" food reward and beings to "assign" a higher reward to foods with fat. What I found was that small amounts of fatty foods were enough at first, but as I continued with a low carb diet it was easier to eat more and more of those foods.

I strongly believe now that some of us tend to eat out of habit when we are not really hungry. I could eat a pound of bacon right now if someone put a plate in front of me, but I'm not hungry right now.

I challenge anyone to try eating the same amount of a steak that is cooked gently in water until it is grey vs. salted, spiced, and then grilled/fried. In my experience, it's almost impossible.

A few months ago I began experimenting with Seth Roberts' oil protocol and Stephan's ideas about bland food. I haven't tracked calories faithfully, but I do find that in general I eat about 400 calories less daily on a bland diet. Also, eating bland food my macronutrient ratios are about 1/3 from carbs, 1/3 from protein and 1/3 from fat. Yesterday I ate 1000 calories, 70% carbohydrate and lost 2 lbs overnight. I've maintained an 8 lbs. weight loss doing bland food that has a moderate amount of all macronutrients. For the past several weeks, I've had relatives visiting and have alternated between bland and "tasty" and haven't lost or gained anything, but now I'm going back on the bland food protocol.

This is also roughly consistent with my attempts to lose weight in the past on Weight Watchers. Many people gravitate toward the prepared meals and snacks on weight watchers, but I did not. I stuck to real foods and I remember my macronutrient caloric ratios being about 1/3 from each macronutrient.

Recently I have lost weight eating an amount of fruit that most low carbers would consider heresy.

I wholeheartedly acknowledge that low carb helps many people lose weight. Perhaps it does that through lowering food reward. But some of us, perhaps it is a minority, do require different strategies.

Stephan Guyenet said...

Hi Monica,

Thanks for relating your story, very interesting.

M C Lewis said...

This is a fantastic piece of analysis for which Stephan should be commended. As a dedicated low-carber myself, I was surprised at how much new information I was able to glean. However, I wonder if the evidence which Stephan presents still lends validity to much of what Gary Taubes proposes.

To summarise Stephan's high-level points:

• There is no correlation between insulin levels and satiety. In fact, high levels of insulin tend to produce higher levels of satiety.
• Insulin levels are actually higher in meals which consist of both carbohydrate and protein compared to carbohydrate alone.
• High insulin levels positively correlate to an increased metabolic rate.
• The insulin spikes experienced after a meal is temporarily and not sufficient to promote fat accumulation.
• Taubes’ internal starvation theory cannot be valid because obese people aren't that insulin insensitive yet exhibit high levels of free fatty acids.

Based on this evidence (for which Stephan supports with several references) let's consider the case of an individual who is significantly overweight, but not obese (so is not insulin insensitive), and look at the insulin response to 2 different meals:

(A) carbohydrates 60%, proteins 30%, fat 10%
(B) carbohydrates 10%, protein 40%, fat 50%

While Stefan points out that both carbohydrates and protein are capable of elevating insulin, fat does not. As a result, I would suggest that meal (B), with almost half the combined amount of carbohydrates and protein, would produce a substantially lower insulin response. Stephan posits that consuming a meal like (A) only produces a temporary insulin spike, but three of these meals each day, along with one or two snacks, will surely turn these temporary insulin spikes into an overall state of insulin elevation.

Stephan accepts that insulin promotes fat storage while at the same time promoting glucose oxidation. Therefore, the diet (B) will encourage a greater level of fat metabolism.

Adhering to a low carb diet like meal (B) will likely push the individual into a state of ketosis, where fat is used as a primary energy source and is converted by the liver into ketone bodies to provide fuel for the brain and central nervous system. The body has the ability to expel unused ketone bodies in a number of ways, including in the breath (producing the characteristic ketogenic bad breath) and in the urine. By comparison, the body does not expel unused glucose, and simply converts them into fat or glycogen for storage.

Considering these factors, I therefore wonder if there is still some validity to Taubes’ theory. It might help to look at Taubes’ concept of internal starvation as something which is not an absolute, but perhaps relative - relative in the way the body responds to a diet like meal (A) versus meal (B). If we keep calories the same, my feeling is that the human body is more forgiving of a low carb diet like (B) - forgiving in the sense that excess calories are less likely to be deposited as fat. I realise this statement will have thermodynamicists out there howling, but the conversion of any fuel into energy can be subjected to inefficiencies and is a fundamental aspect of thermodynamics. Expulsion of ketone bodies in the urine could be one such example of fat metabolism being less efficient than glucose metabolism.

Carnivore said...

@Frank: I don't know where we're going, I'm just along for the ride! :D

Yes, most studies use too big a calorie deficit and my point is that this deficit renders any two diets virtually the same in the short term as far as weight loss is concerned. There may be a difference in favour of low carb but it wouldn't be statistically significant. A deficit of say 2000 calories is going to render the effect of a metabolic advantage for low carb (which is highly individual) quite unnoticeable over a few weeks. Plus, the bigger the deficit, the quicker the body adjusts to slow down it's metabolism.

Note that I never said REE shall not decrease for obese individuals, my point is that the huge calorie deficit means that obese people will continue losing weight for a long time under severe caloric restriction, despite decrease in REE. No one loses weight forever eating a fixed amount of calories and it isn't only because the new weight equates to less caloric needs, it's also because the body adapts to the lower intake.

People in these studies show different changes in REE, probably because they were obese to different extents and the calories they were consuming on the study diets could have been less or more than what they were consuming prior. I am familiar with obese people who are on a diet all year long and if such people enroll for these studies, they could be consuming more or less than what they were before. It probably isn't very helpful to draw general conclusions in REE change from such studies.

On whether LC diets for obese people should have big calorie deficits or not, I'd say it depends on what the study wants to show. For the sake of the obese people though, it would make sense to start off with a reasonable calorie deficit and increase it gradually as weight loss tapers off. This makes the diet more sustainable and would most likely lead to a more positive effect on body composition in the long run (less starvation = less lean mass loss).

Finally, for those pointing out Jimmy Moore or other examples of obese people yo-yoing on low carb diets, consider the fact that these people have already damaged metabolisms. None of them got obese eating low carb in the first place, so citing such examples does not in any way invalidate carbohydrates as a 'necessary' factor for obesity.

You're obese, you start eating low carb and lose some weight (or a lot). You start to want to make your meals more tasty (food reward?) and add more sauces, have more fried stuff which basically all adds up to more calories. For a metabolically damaged individual, eating beyond satiety on low carb can take him/her beyond the maximum calories which would maintain weight (metabolic advantage included), so the individual can start to gain. Not to mention that people increasing carbs after reaching a certain 'desirable' weight can lead to the same result.

Ellen said...

I was with you until you wrote this: " However, this system is not activated except in severe hypoglycemia, which is rare except in diabetics, thus it is not relevant to common obesity."

This is incorrect, and a sand castle under the rest of your argument on this hypothesis. Severe hypoglycemia is NOT rare, as most overweight people experience severe episodes of the reactive type when first cutting back on carbohydrate consumption.

Hunger IS tied to carb consumption, and I can tell you that in my n=1 experience, I eat way more if I eat a high carb diet. I am constantly hungry, no matter how much I eat. The opposite is true when I eat low carb.

I would imagine most of the low carbers I know would agree.

Alan said...

>> In other words, it seems that evolution wants human to eat carbs.

Change "humans" to "human un-weaned juveniles", and we will all agree with you.

By the way, "evolution wants" you to teach your children to hunt; will you do that?

"Evolution wants" your children to experience being a small "band of brothers" that are driven by small-unit cohesion; will you send your children to Singapore National Service like Israeli expats do send their kids back home to serve?

Alex said...

@Ellen

My experience matches yours: carbs drive hunger and overeating. For me, it does seem to be more a problem with starch than sugar. I can eat quite a lot of fruit and not gain weight, but eating starchy foods on a regular basis upregulates my appetite and drives me to eat more.

Paleo Phil said...

Alex said... "I can eat quite a lot of fruit and not gain weight, but eating starchy foods on a regular basis upregulates my appetite and drives me to eat more."

Raw fruit or cooked fruit? Raw starches or cooked starches? Do you eat any fat, salt or spice with the starches? What about with the fruits?

Robert Miles said...

Much of what I've seen on the internet about human metabolism says that most of the human body (including much, but not all of the brain) can switch back and forth between using glucose and ketones as their source of energy, but cannot use both at once. Also, the liver can convert proteins into glucose more than fast enough to supply those portions of the body that cannot use ketones instead. Fat metabolism uses an extra step - the liver converts the fatty acids portion into ketones and waste products.

Ketones have gotten a bad reputation due to some forms of diabetes causing the liver to produce an oversupply in response to the body signalling that it does not have enough glucose inside cells to use it instead - but only such an oversupply has noticeable bad effects.

Both low-carb diets and low-fat diets have been shown to produce weight loss is some people. Low-calorie diets tend to slow the metabolism, and therefore require more of a reduction in calories than expected to produce a weight loss.

Therefore, an idea to consider (although not adequately tested yet): Many of the prehistoric humans switched back and forth between low-fat diets for some parts of the year, and low-carb diets for other parts of the year, but seldom were able to consume diets high in both fats and carbs at once. Therefore, the dietary problems for recent decades could easily be due to having too much access to both carbs and fats at the same time. Diets high in both carbs and fats tend to cause weight gains. Switching from using carbs to using fats tends to be somewhat slow and uncomfortable, but once the switch is made, the appetite tends to decrease. Switching from using fats to using carbs goes much faster, so rapidly switching back and forth is not a very good idea.

This would imply that low-fat and low-carb are not adequate descriptions of the best diets for weight loss, so they do not mention what was used to replace whatever was lowered.

Most of the human body cannot use fructose. It stimulates an appetite for carbs in the brain, and the liver can convert it into cholesterol and saturated fats; but there is little other use for it. A few other simple sugars exist, but I've seen little on their effects on the metabolism.

Someone mentioned leptin tests. They may be easily available in your area, but I've seen no sign that this applies to most of the US, or that most doctors in the US would know what to do with the results of such tests.

What I've seen on PCOS and diabetes suggests that PCOS often causes diabetes, but diabetes does not cause PCOS.

On meats: Farmers often feed animals intended to become meat a diet high in grains to make them gain weight, instead of their natural diets, so they can earn a higher price for them. Do you expect that to make the resulting meat healthier for you? I suspect it makes it worse for you instead, by altering the balance of nutrients in that meat.

On fish: Many of the fish now available were farmed on diets low in the omega-3 type of PUFA fats easily available from their natural diets. Do you expect that to make them as healthy as the same species of fish caught wild? Some of what I've seen shows that they often aren't.

Robert Miles said...

On fats: What I've found on fat metabolism indicates that we need to aim at separate levels of control on the various types of fats. For example, the liver can convert excess carbohydrates into saturated fats, so saturated fats aren't an essential part of the diet. I've seen mixed reports on monounsaturated fats; they appear to improve the health somewhat but aren't essential either. There are two main types of polyunsaturated fats - the omega-3 type and the omega-6 type. Both are essential; they human body requires both of them and cannot make either of them, although it can do some conversion between the various omega-3 types and between the various omega-6 types. Many of the vegetable oil processors partially hydrogenate the oils - ignoring the fact that this preferentially removes the omega-3 type, and often converts them into transfats. Omega-3 fats tend to go rancid the fastest; one reason for this. Transfats are a type seldom found in nature; therefore I would not expect human metabolism to be able to make much use of them; except for the CLA type found in breast milk, and the ability to use that type could easily not last into adulthood. The human metabolism appears to be able to store most transfats in the fatty tissues, but not to be able to use them afterwards. As a result, the movement toward low-fat diets, with special attention to reducing saturated fats, has made deficiencies in omega-3 rather common.

On complex carbohydrates: Most of the articles I've seen that mention the nutritional effects of complex carbohydrates appear to be based on research that accepted the obsolete idea that all complex carbohydrate digest much slower than sugars, and therefore have much less of an effect on the blood glucose levels. Part of this appears to be from the ADA believing that no research to check the digestion speeds was worthwhile, and therefore not providing any more research funds to researchers showing any signs of wanting to check. Well. guess what - the research was finally done anyway, and it showed a wide range in how fast the complex carbohydrate digest. Some of the common white starchy foods, such as white bread, rice, corn, and Irish potatoes digest about as fast as table sugar (sucrose) and into similar mixes of simple sugars - and therefore have similar effects of the blood glucose levels. Whole wheat bread varies in how fast it digests; this depends partly on how small the wheat grains were ground and whether molasses residue was added to produce part of the color. Sweet potatoes and cooked dried beans contain carbohydrates that actually digest slower, and are therefore better for those with diabetes. There are some types of complex carbohydrates that humans can't digest well enough to get much nutrition from them directly; those are now usually known as fibers. The bacteria in the large intestine then gets a chance to digest those, and can produce intestinal gas and diarrhea if they get too much as once. There are some fibers they can't digest either, such as the cellulose common in wood.

On lc weight losses: Tends to be fast at first, when the reduction of carb stores in the body releases the water attracted to those carb stores. Then usually slows down, as slower methods of weight reduction take over, such as using the fat stores for energy.

On why I've gathered this data: I was diagnosed with type 2 diabetes about 9.5 years ago, along with a disability that has kept me from going back to work since then. Since then, I've been especially interested in web I could find on the internet that's related to diabetes, carbohydrate metabolism, weight loss, and more.

Robert Miles said...

On HCFS: Already converted to simple sugars (glucose and fructose) during production and therefor likely to be absorbed faster and produce higher levels of those blood sugars for some time.

Also, heating high-fructose mixtures such as HCFS has been shown to combine pairs of the fructose molecules into a larger molecule toxic to honeybees. HCFS is often overheated during manufacture. Although that larger molecule appears to be much less toxic to humans, do you want to bet your health on assuming that it is not toxic to humans at all? I've seen little sign that much research has been done on whether it is or not.

Robert Miles said...

On the glycerol portion of fats: I've seen a variety of opinions on whether the liver can convert it to glucose, and whether it is efficient enough at this for it to matter. I consider all of these opinions unproven for now.

Monica said...

" Alex said... "I can eat quite a lot of fruit and not gain weight, but eating starchy foods on a regular basis upregulates my appetite and drives me to eat more."

Raw fruit or cooked fruit? Raw starches or cooked starches? Do you eat any fat, salt or spice with the starches? What about with the fruits?
"

Great point, Paleo Phil. I am currently eating a bland diet moderate to high in carbohydrate (raw fruits, cooked tubers) and I don't feel driven to eat more than 1000-1200 calories daily most days. I am sure if I was eating bread I would feel driven to eat more, though.

Dave Asprey said...

Great thinking!

But no matter how many papers it cites, it's easy to verify by using yourself as a guinea pig.

Case in point: me. (I run an anti-aging nonprofit and have my first nutrition book being published by Wiley soon.) 15 years ago, I weighed 300lbs. 210 is ideal for my height.

In an experiment, I ate 4500 calories per day of this diet http://www.bulletproofexec.com/the-complete-illustrated-one-page-bulletproof-diet/ (which evolved over time based on > 1,000 references and lots of anti-aging researchers...) that consisted of 60% plus calories from mostly saturated fats. I also stopped sleeping more than 5 hours a night. And I stopped exercising. For two years.

The results? I'm leaner and more muscular now. Blood chemistry is awesome...triglycerides are 47. I eat a stick of grass-fed butter every day. I drink coffee with 80 grams of butter in it for breakfast. My brain and body work better now, and I measure those too.

If everything in Steven's analysis was true, I'd weigh something like 500 lbs or be dead, yet every measure I can find says I'm better than I was - lower cortisol, better ANS function than people my age in 24 hour heart monitoring, everything.

2 weeks ago I added more carbs to my diet - mostly rice and sweet potatoes, no grain at all - and now I'm 5 lbs heavier, and it's around my middle.

Another MAJOR criticism of both Taubes and Guyunet is that they ignore the very strong role that mycotoxins and xenoestrogens play in obesity in their research. I'm still trying to get Gary (a friend I owe a great debt of gratitude to) to try my low mycotoxin, high sat fat Bulletproof Diet...

My blog is www.bulletproofexec.com and my upcoming book is www.betterbabybook.com

Thanks again Steven for this post. The world needs more thinkers like you!

Alex said...

@Paleo Phil

"Raw fruit or cooked fruit? Raw starches or cooked starches? Do you eat any fat, salt or spice with the starches? What about with the fruits?"

Raw fruit, generally eaten by itself, with the exception of a piece of cheese eaten with a single apple. The starches are cooked. My most recent experiment with adding back starch was eating a small sweetpotato with my steak breakfast (yes, with fat, salt, and spices) on workout days. The result was three weeks of two pounds per week weight gain. The overall dietary context is low-ish carb paleo with some dairy.

Years ago, when I still believed all the bollocks about the dietary idealness of whole grains and beans, my diet was predominantly vegetarian and largely starched based. As I hit my late 30s, I started getting fat. Often, I'd have to take an afternoon nap, after which, I'd get up and inhale a bag of dried dates or a box of Newman-O's cookies. It was a blood sugar roller coaster. In 2003, when I cut out almost all the starch, I dropped thirty pounds in five months. The weight loss was spontaneous and completely effortless. With so much less carbohydrate in my diet, I was simply not as hungry, and I ate less. When I did experience hunger, it was only the gentlest of hunger impulses. By contrast, post-starch hunger is gnawing and voracious.

For me, low-carb is all about satiety and regulation of hunger, with no need for ketosis or being as low-carb as the Atkins induction phase.

Asim said...

blogblog

"Antibiotics don't increase weight directly. They reduce the level of infectious diseases which cause weight loss. These diseases are a result of intensive farming practices such as feedlots."

Your argument is predicated on the fact that farmers give animals anti-biotics when they are sick, which is not true by a long shot. Even those that claim it is for general health argue it is to prevent illnesses from occurring. Giving antiobiotics is standard practice in the meat industry.

Antiobtiocs kills the gut flora, meaning the imapcts on weight gain are direct.

http://www.ucsusa.org/food_and_agriculture/science_and_impacts/impacts_industrial_agriculture/prescription-for-trouble.html

"While some uses of antibiotics in livestock operations are a matter of animal health, other uses have an economic motive. Especially troubling is their use not to cure sick animals but to promote "feed efficiency," that is, to increase the animal's weight gain per unit of feed. These drugs are also regularly added to the feed and water of animals that are not sick in order to prevent diseases caused by overcrowded and unsanitary CAFO conditions. These nontherapeutic uses translate into relatively cheap meat prices at the grocery store."

In fact, the weight gain is the primary use.

Asim said...

"However humans evolved in a high altitude tropical grasslands where wild fruit is both relatively rare and low in sugars and winter is non-existent."

Huh? They have fossil records of 'humans' going well back to around 2 million years in China, i.e. homo erectus as well as the country of Georgia. There are 'plenty' European fossil records between 1 and 3 million years, not to speak of many records in South Africa, which surely isn't tropical. While it is true, there are more records in the tropics, this in now way an accurate picture of human beings.
The idea that our 'ancestors' did not 'evolve' under winter conditions is pretty much wrong.

But this has little relevance to the mechanisms of fat as it relates to winter.

Asim said...
This comment has been removed by the author.
Asim said...
This comment has been removed by the author.
Asim said...

blogblog,

"Antibiotics don't increase weight directly. They reduce the level of infectious diseases which cause weight loss. These diseases are a result of intensive farming practices such as feedlots."

This is incorrect.

It is well known that antiobiotics are given to healthy cattle, meaning those that have not contracted any illness, meaning the curing of infectious disease that allegedly causes the weight loss is not relevant. The point is the healthy cattle get fatter because of anti-biotics.

http://www.ucsusa.org/food_and_agriculture/science_and_impacts/impacts_industrial_agriculture/prescription-for-trouble.html

"While some uses of antibiotics in livestock operations are a matter of animal health, other uses have an economic motive. Especially troubling is their use not to cure sick animals but to promote "feed efficiency," that is, to increase the animal's weight gain per unit of feed."

This is all because of the killing off of the gut flora.

Razwell said...

Dr. Jeffrey Friedman has said "it is time to move on from "eat less, move more".

You could not be more qualified to talk about obesity than he is. There are probably only a handful of scientists in the world on his level about the subject of obesity.

Razwell said...

Die is only one factor in the etiology of obesity among lietarlly dozens ,upon dozens, upon dozens.

No one ever mentioned MEDICATIONS people take, disease states, in utero nutrient exposure, why fat cells are in hoard mode, and he growing research on unfortunate gut microbiota, and MOST importantly GENETICS.


(Our GENES , as well as the hormone leptin determine a lot about our feeding ,our inclination to move etc.

Lastly, obesity is almost as heritable as height, possibly equalling it.

shaun said...

Finally, a voice of reason amongst the craziness. Thank you for this well-written post.

Paleo Phil said...

@Monica: thanks for the compliment and for sharing your experience.

Alex wrote: "Raw fruit, generally eaten by itself, with the exception of a piece of cheese eaten with a single apple. The starches are cooked. My most recent experiment with adding back starch was eating a small sweetpotato with my steak breakfast (yes, with fat, salt, and spices) on workout days. The result was three weeks of two pounds per week weight gain."

Thanks for the reply, Alex. Your report includes several known food reward elements that Stephan identified--cooking, mixing carbs with fat, and adding salt and spices. So there are more variables at play here than just fruit sugars vs. starches.

"I'd get up and inhale a bag of dried dates or a box of Newman-O's cookies. It was a blood sugar roller coaster."

No surprise there and again, there are more variables than just blood sugar. My guess is that cookies and dried dates are regarded as even higher-reward foods than cooked sweet potatoes. I find dried dates even more addictive when I mix them with nuts (and mixing of foods and macronutrients is yet another food reward element).

I do well on a VLC diet myself, but I don't think that macronutrients are the only important variable in diets, obesity or health and your experience (as well as Monica's) jibes with Stephan's points on food reward.

In addition to Stephan's excellent posts on food reward, I recommend checking out J. Stanton's posts that touch on the subject, such as this one: http://www.gnolls.org/2074/why-snack-food-is-addictive-the-grand-unified-theory-of-snack-appeal/. I agree with J.S., and I think Stephan may as well, that food reward seems to be a mostly beneficial signal in the context of a wild, ancestral diet of raw and/or traditionally-cooked/fermented foods and only seems to become a problem in the context of modern processing and cooking techniques and other factors. Unfortunately, most Westerners follow diets high in foods that are processed, cooked, spiced, additive-ridden, or have other pathological food reward triggering elements. On the bright side, my guess is that many people who read this blog have already cut out many pathological food reward elements from their diet.

Alex said...

@Paleo Phil

Well, as I wrote on Stephan's most recent post, "The only paleo food I will eat addictively to excess is nuts. Otherwise, the primary palatability offenders are fatty starches, like potato chips, tortilla chips, French fries, buttery croissants, crusty French or Italian white bread slathered with butter, puff pastry, etc."

Even Dr. Michael Eades has commented on oil and carbs being a particularly effective weapon of hypercaloric delivery: "The combination of oil and carbohydrate is deadly only in that it has a taste and mouth feel that humans love, and, consequently, are driven to eat too much of it. No one binges on butter (an oil) all by itself, but add some sugar to it, and you’ve got frosting, which everyone loves and eats to excess."

But, even in the absence of fat, starch can cause problems for me. My blood sugar can crash after eating too much rice in a very low-fat Japanese meal. Usually I order a big sashimi platter and maybe a couple rolls; but, if the sashimi platter comes with a bowl of rice, and I eat it, I'll be fast asleep an hour or two later.

I'm not arguing that Taubes is right. I honestly don't have much of a grasp of his perspective. I bought 'Good Calories, Bad Calories' but it was so dry and boring that I couldn't even wade through the first chapter. From my perspective, it doesn't matter one iota if Gary or Stephan is right, because as long as I restrict carbs, not a damn thing either one of them says has any relevance to me at all.

M. said...

Alex said: “From my perspective, it doesn't matter one iota if Gary or Stephan is right, because as long as I restrict carbs, not a damn thing either one of them says has any relevance to me at all.”

I understand your point, but there are two other possible issues to think about (at least two anyways):

1. If you can figure out “why” you personally need to restrict carbs, maybe you could derive a solution and have a healthier life. Taubes is telling you why he thinks you need to restrict carbs, but it is probably not the answer. I believe Colpo has argued about blood iron levels being a factor. Whatever the answer is, it is beneficial to reject the wrong answers so you can move on to better theories.

2. Think about the children! Seriously, though, at my children’s daycare they get 3 snacks a day in addition to breakfast and lunch. Often “whole-grain” snack foods. Because that is the current “conventional wisdom”. Maybe the more discussion about the science, maybe the more chance that conventional wisdom will be changed. Not only do none of the scientists take Taubes seriously, but most of the bloggers in the ancestral blogosphere say he is wrong about his insulin theory. Taubes and his insulin mythology are not going change conventional wisdom if he cannot even convince such a receptive audience as ancestral bloggers.

Olga said...

Interesting study.

"Individuals with Laron syndrome who carry mutations in the growth hormone receptor (GHR) gene that lead to severe congenital IGF-1 deficiency with decreased insulin/IGF-1 signaling (IIS) exhibit reduced prevalence rates of acne, diabetes and cancer."

http://www.nutritionandmetabolism.com/content/8/1/41

Alex said...

@M "If you can figure out “why” you personally need to restrict carbs, maybe you could derive a solution and have a healthier life."

To me, that's a very odd perspective. I don't regard the limitations of having a food sensitivity as signifying a lesser state of health. That the percentage of carbohydrate in my diet maxes out at ~30% instead of CW's recommended 65% doesn't mean I'm unhealthy. Today, for lunch, I had a grilled eel sushi roll, and I'm fine. It's not going to kill me that I'm better off not not eating half a dozen sushi rolls.

Dr. Curmudgeon Gee said...

thanks for the article.
but i'm so confused now.

I know quite a few people who are quite thin & seemed healthy enough (no diabetics nor prediabetics or apparent ailment); they need to eat every 2 hours! otherwise, they get hungry/weak/headache.

are they hypoglycemic?

regards,

shortrib said...

M said:

"Not only do none of the scientists take Taubes seriously, but most of the bloggers in the ancestral blogosphere say he is wrong about his insulin theory. Taubes and his insulin mythology are not going change conventional wisdom if he cannot even convince such a receptive audience as ancestral bloggers."

What scientists are you referring to?

A "blogosphere" (about any topic) that does not agree with a hypothesis isn't exactly a good reason to discount the hypothesis.

Markusn said...

Somehow I think it would be great if everybody commenting on this article would state their current personal weight: I would love to understand who is commenting with "oh, I'm alright but I love to dive into nutritional theory and this is brilliant somehow" versus "I'm affected, I'm desperate and now I know less than before". But that's just a casual thought :)
Stephan, the difference between you and Taubes is that he offers a path forward for those affected, while you start out strong and end somewhat vague in that respect. In the beginning, you state that a low-carb diet change helped a lot of people, you end with "might have helped some". That's a world of a difference for those reading your post not just for scientific pleasure, but because they seek answers to an immediate problem.
Reading between the lines I would interpret your statements as if you'd still suggest to an obese friend to give a low-carb approach a try, as even if not fully understood it has helped a lot of people who stagnated with everything else. If that's the case, I'd love to see that clarified somewhere at the end, for the sake of helping those who don't want or can't wait until the scientific world finally settled (as if that ever happened). If not, what would you recommend to a friend right now?
Also, I wanted to ask if satiety is the same as cravings. When I go low-carb, my cravings go from really strong to barely notable and that in itself changes my dietary behavior. A lot, actually.
Personally, I was frightened to keep that going for too long even when it showed good results, because it had that idea of malnutrition attached. Something that Taubes really cleans up with (and you are not contradicting that either), so I'm encouraged to give it a longer try. Let me know if you disagree with that or if you are really all for it, but wanted to clarify certain aspects and drive the discussion further.
Note I'm not criticizing your work at all, on the contrary, just wondering on the impact it has on the many who just got introduced to Taubes these days and the idea of low-carb being not so evil after all, searching the net for discussion. It is too easy, especially when obese, to dismiss an idea that would work, just because it might not and I'm not sure that's what you intended. Thanks for good work!!

Robert Miles said...

@Dr. Curmudgeon Gee -

That looks like a possible symptom of hypoglycemia. Could you either loan them a blood glucose meter or persuade them to get their own so that they can test for hypoglycemia any time they feel that way?

Also, hypoglycemia often leads to diabetes later, so they may want to occasionally check for that as well.

Dr. Curmudgeon Gee said...

@Robert Miles,

you're being kind. but the problem is i'm not an MD, nor do i want to be a "food nazi"

i did politely suggest a colleague who is "somewhat" prediabetic to get a glucose meter; he told me it is stupid to stick one's all the time.

now he's going raw vegan & live on mostly raw nuts & berries.

oh, well, i've tried!

regards,

Fred Hahn said...

"Another problem with the hypothesis is a thing called the insulinogenic index (II). The II is simply a measure of how much eating a food increases insulin, per unit calorie (28). It turns out, it doesn't correspond with the carbohydrate content of the food very well. In particular, protein-rich foods such as beef can increase insulin secretion as much as certain starch foods such as pasta, or more."

Stephan - Can you elaborate and include the role of glucagon in this process? Thank you.

Stephan Guyenet said...

Hi Fred,

I think your point is that insulin doesn't act in a vacuum-- there are other factors that change at the same time. I agree. That's one of my points as well-- you can't just look at insulin.

The gut and pancreas secrete dozens of bioactive peptides in response to food ingestion (in addition to sending signals via vagal and spinal sensory nerves), some of which are specific to protein, some of which are specific to carbohydrate, and some of which are specific to fat.

Protein causes a spike in insulin and glucagon, among other factors, which attempts to maintain blood glucose by glycogenolysis. Carbohydrate releases insulin, amylin, and several incretins, which coordinate the metabolic and satiety response to glucose.

The human body is complex, and that's why it's important to consider the basic empirical evidence first, rather than trying to deduce physiological outcomes from mechanism. In that regard, I think the controlled trials that manipulated macronutrient ratios and looked at satiety, body weight, energy expenditure and metabolic variables are very important.

Fredrik Gyllensten said...

Great article!

Paleo Phil said...

Alex wrote: "But, even in the absence of fat, starch can cause problems for me. My blood sugar can crash after eating too much rice in a very low-fat Japanese meal. Usually I order a big sashimi platter and maybe a couple rolls; but, if the sashimi platter comes with a bowl of rice, and I eat it, I'll be fast asleep an hour or two later."

Your experience sounds a lot like mine. I don't fare well on cooked starches either and if you can handle a couple of rolls, then your tolerance may be better than mine (though gluten may be the main problem there for me). How well do you handle carb-containing veggies that are edible raw, which I've noticed that I handle better, like carrots (89% carbs raw, 90% boiled per Nutritiondata), parsnips (93% carbs raw, 91% boiled), cabbage (85% carbs raw) and sauerkraut (80% carbs canned)? I don't think my problem with the cooked starches is due to food reward, I suspect that it's due to getting too large a dose of carbs at once, and I suspect that that's a problem for me due to gut dysbiosis, given my medical history, though I'm not sure. Interestingly, raw fermented honey (it's honey, NOT mead) seems to be slowly improving my tolerance for carbs, though it's a bit early to tell for sure.

Alex said...

@Paleo Phil "How well do you handle carb-containing veggies that are edible raw, which I've noticed that I handle better, like carrots (89% carbs raw, 90% boiled per Nutritiondata), parsnips (93% carbs raw, 91% boiled), cabbage (85% carbs raw) and sauerkraut (80% carbs canned)?"

I handle them no prob. I go through food phases, and when I'm in a carrot phase, I'll eat as many as ten per day, usually raw. I don't notice any difference with cooked carrots vs. raw.

studentoflife said...

foot note number "8" states in the study:

The HP/LC breakfast induced higher levels of satiety and specific parameters of postprandial wellness (satisfaction, pleasantness and the pleasantness of these feelings) than the LP/HC breakfast at 3 or 4h after consumption. The corresponding higher CCK and lower ghrelin concentrations at these time points supported these subject reported changes. These results indicate that meal composition influences some parameters of postprandial wellness in line with physiological responses.

doesn't this contradict the first part of that paragraph?

In one of the studies they used "whey" as a carbohydrate. I don't think there is any carbohydrate in whey.

leading said...

Hi Good morning i was looking for health tips and got this qoutation. i like it and sharing for you here.
I heard a definition once: Happiness is health and a short memory! I wish I'd invented it, because it is very true.
(Audrey Hepburn )

thanks loss weight quick

twilight2281 said...
This comment has been removed by the author.
twilight2281 said...

Hi,

Someone here noted that human breast milk is highest in fat followed by carbs then low amounts of protein. Can someone please post a link to that info as the only websites on the subject I can find show that human breast milk is highest in carbs followed by fat and again low in protein. I have been curious about this for a long time now so I would like to get the true nutrition facts. Thank you so much guys!


Take care!
Jennifer

Luming said...

@studentoflife

Protein stimulates insulin production, and insulin blunts appetite.

Eggs are extremely satiating beacuse it stimulates insulin so much.

Paleo Phil said...

Alex said...
"I handle [carb-containing veggies that are edible raw] no prob. I go through food phases, and when I'm in a carrot phase, I'll eat as many as ten per day, usually raw. I don't notice any difference with cooked carrots vs. raw."
August 22, 2011 6:44 PM

Same here. I can eat a pound of raw carrots in one sitting (if they are particuarly sweet and tasty ones) with no noticeable problems other than maybe a throat that's slightly itchy. Carby plants that [i]require[/i] cooking or fermenting to be edible are a different story for me. I get problems even from boiled, baked or steamed potatoes, sweet potatoes and rice. So regardless of whether humans are fully adapted to cooking or not, I get better results when I eat [i]as if[/i] humans weren't fully adapted to cooking. Most of the bloggers seem to attribute such problems to gut issues, which I do have, so perhaps that's the main cause, I don't know.

If so, that still leaves me wondering why I handle roots and veggies that are edible raw (whether eaten raw or cooked), raw fermented honey, and berries (particularly wild berries) better than cooked tubers, most other fruits (even avocadoes, surprisingly) or standard raw honey. There are multiple variables involved with cooked tubers--high starch levels, antinutrients, potential effects from the products of cooking, and who knows what--so it's difficult to know what exactly is causing what, though it's clear that I appear to be more negatively affected by them than most.

Pekka Pessi said...

Interesting entry, Stephan.

If you want to understand how insulin works perhaps it best to start with liver. Carbohydrates and proteins may have similar insulin response but the effect of that insulin in liver is markedly different for obvious reasons.

Gordon (1960) mentions an interesting phenomena regarding gluconeogenesis and subsequent ketogenesis. I wonder if there has been some further work on the matter. Why the liver does not start to generate ketone bodies when obese people fast?

I don't know how nervous system and liver communicate so perhaps the liver is not interesting in your field of study. But obviously liver and the effect of insulin to it seems to be the central piece in development of obesity. My first bet would be sugar (saccharose) and fructose.

Pekka Pessi said...

Jennifer,

USDA probably does give you similar information:

http://www.fineli.fi/food.php?foodid=603&lang=en

Energy content is 55/37/8 fat/CH₂O/protein, but dry mass content is 4.5/6.5/1.5 respectively because fat is more energy-dense.

Ken said...

I don't think you've successfully
refuted any element of Taubes' (and many, many others') hypothesis.

As I would guess you are aware, Taubes' argument about leptin resistance is that it is a "downstream" effect of insulin resistance and not really necessary to explain the fundamentals of chronic obesity. I don't think you have offered any counter to this (in Part 1).

In your Part 2A I'd agree with most, but not quite all, of your statements about the physiology. Mostly, your logic and hence your conclusions are wrong. Obesity results in a proportional SMALL increase in plasma FFA/NEFA levels that is reflective of a small increase in adipose IR. I have read a lot of the most recent research on pre-diabetes and T2DM, and this is a good place to go to get an idea of the quantitative magnitude of the adipose tissue IR in overweight, but non-diabetic subjects. By contrast, only with the onset of T2DM (if it occurs) do most people develop a "primary defect" of adipose tissue IR (and consequent several-fold increase in endogenous glucose production) that is large in magnitude. Otherwise they DO NOT -- the fat tissue remains quite insulin-sensitive in relative comparison to that of the skeletal muscle and hence the ability to increase overall triglyceride storage over time IS PRESERVED while the ability to burn triglycerides is degraded. Reference Ethan Sims' famous experiment from the 1960s and much else detailed in GCBC.

You are correct that the bottleneck that gradually drives up overweight is an inability to burn (oxidize) fatty acids. But the bottleneck is in the skeletal muscle and it is a fundamental characteristic of whole-body IR -- generally called "lipotoxicity" (re Unger et al). If the adipose tissue IR were the problem, then people WOULDN'T become fatter over time. In fact, a minority of pre-diabetics (who later develop T2DM) are lean (i.e not overweight by BMI, etc.) and have early-stage large adipose IR, but this is not common or typical at all in the general population.

See Taubes' Science article "Prosperity's Plague" (on molecular-biological research of insulin resistance), which I recommend to you and your readers, for a relevant discussion not covered in GCBC.

The known characteristics of typical IR in skeletal muscle have been in the relevant textbooks for years. FA oxidation is radically degraded (almost eliminated) whereas glucose oxidation is only mildly degraded. This situation creates the dependency on dietary carbohydrates -- i.e. the chronic cell starvation -- that ensues. FAs cannot be burned and glucose can, but (blood) glucose is only available for a short time after a meal and needs to be continually replenished with dietary carb's. The overconsumption of dietary carb's also leads to de novo lipogenesis in the liver (only a fraction is burned and the rest is stored as fat), and hence often a gradual increase in overweight follows.

I think all of this is pretty basic and well-known, and Taubes certainly understands it. I am a layman and I have easily picked it up by reading the mainstream medical literature. The mainstream medical researchers don't like to draw the final conclusions (it's not PC), but they are pretty obvious.

IR -> obesity (not vice versa), by this mechanism -- it's a vicious cycle of cellular starvation.

Modern, high-carb diet -> hyperinsulinemia -> IR and lipotoxicity, and so on. I can explain the Kitavans too, but I'll need another post.

Ravi said...

i hope i'm not too dense for this conversation - but no matter where i look i see CICO constantly bantered about with the most glaring missing component - high school science is enough to know that to get an accurate measure of a system, you need to know all sources and expenditures/loss of energy - every time someone counts calories - even in a metabolic chamber - they are assuming a flat rate of absorptive efficiency - a little googling will quickly show that the caloric content in poop - the relative efficiency of everyone's bowels, intestinal flora etc etc - this varies dramatically -

why - in the calorie counting game being constantly bantered about - would not the unabsorbed/undigested caloric content of our excrement be absolutely critical in evaluating?

just the different combination of foods can substantially alter the absorption of this or that and completely toss any accurate measure of caloric values--

just saying...

Jim said...

Just for completeness, these three options:

As we are all on the same page (I hope) that the first law of thermodynamics applies to humans, for insulin to cause fat gain, it must either 1) increase energy intake, 2) decrease energy expenditure, or 3) both.

should have a fourth appended:

. . . or 4) causes a repartitioning of fuel that leads to a substitution of fat for lean tissue.

Personally I don't think #4 can account for the obesity epidemic, but it does form part of Taubes's position, and should probably be addressed along with the other three.

Wanna Be Mother said...

Logically, if you concede that low carb works for losing weight for obese people, would it not also help people prone to obesity to prevent weight gain in the first place? Do you agree with that? In that case, couldn't you then say that, were that same person to continue eating carbs and gain weight, becoming obese, that the carbs contributed to their obesity? Fundamentally, I think there is a logical fallacy to say that low carb diets work work yet high carb diets (including lots of sugar and refined carbs) won't cause people PRONE TO OBESITY to become obese, when they could have avoided getting obese by following that low carb diet that you freely admit would rid them of excess body fat once they are obese.

I personally don't think it is insulin alone that is the problem, as the human body is really complicated and I'm sure there are many contributing factors. But I know that I and others who eat low carb now have a much easier time limiting our food intake on low carb. If that is the only reason low carb works, whether that is because of insulin regulation or some other hormone or brain thing (leptin), I'm just happy I can easily maintain my weight! I don't really miss the carbs though, since I used to get more ravenously hungry and moody when hungry and I don't anymore :)

Also, do you agree with what Gary says about blood lipids, ie, that eating a high carb diet makes your blood lipid profile more negative, ie, more likely to have problems, whereas fewer carbs make your blood lipid profile better? Because then, even if you disagree that carbs make us fat, don't carbs make us sick in other ways, ie, heart disease?

Iain said...

To Grok's comments. The real problem with these discussions is that science isn't about winners and losers. When the discussion devolves into winners and losers it's politics.

Don said...

Interesting . . . However I find the fawning accolades a bit over the top!!!

dreambake said...

It is very convincingly that insulin is not the mechanism that leads to changes in weight with a diet low in carbohydrates, but do not seem to explain the loss of weight or the elimination of hunger as a result of some of the people of the deal. He convinced me to investigate leptin.

hmmm said...

"At least two studies have shown that higher fasting insulin is associated with a higher resting energy expenditure, independent of body fatness, not a lower expenditure (14, 15)." this presupposes the energy expenditure cited is responsible for weight loss; it goes back to caloric balance being paramount with regard to obesity--taubes does not accept that premise, while this rebuttal takes it for granted. there is a disconnect here.

Kyle said...

I thought quality of the carbohydrate was the key thing.

Are you not working under the assumption that 30g of carbohydrates from one source has the same insulin response as 30g of carbohydrates from a different source e.g., a pile of vegetables versus a can of coke?

This makes the graph of total macro intakes totally useless.

Junie said...

Your chart cannot be in grams per day...... please check and correct.

Stephan Guyenet said...

Hi Junie,

Actually, it is in grams per day. The reason the numbers are high is that they are not corrected for waste. The numbers serve to illustrate trends but are ~50% higher than actual consumption. You can find the data on the USDA ERS website if you'd like to see for yourself.

Unknown said...

Stephan Guyenet said:

"At least two studies have shown that higher fasting insulin is associated with a higher resting energy expenditure, independent of body fatness, not a lower expenditure (14, 15). If anything, this is the opposite of what the hypothesis would predict."

Your reference #14 examines Pima Indians, who are prone to developing type 2 diabetes. It describes not only an association between higher fasting insulin and an increased resting metabolic rate (RMR), but also an association between higher fasting insulin and a decreased insulin-induced thermogenesis (IIT). For readers unfamiliar, IIT reflects energy dissipated by the body as heat in response to insulin.

The full paper is here:

http://diabetes.diabetesjournals.org/content/48/8/1607.full.pdf

RMR increased by a lesser percentage (6.8%) than IIT decreased (19%) as patients progressed over time from normal glucose tolerance (NGT) to impaired glucose tolerance (IGT) to type 2 diabetes:

"Longitudinally, RMR ... increased progressively in 17 subjects in whom glucose tolerance deteriorated from NGT [normal glucose tolerance] to IGT [impaired glucose tolerance] (+4.2%) to diabetes (+2.6%) over 5.1 +/- 1.4 years (P < 0.05 for trend).

"In parallel, IIT (% increase in metabolic rate during an insulin/glucose infusion) decreased during the transition from NGT (11.7%) to IGT (7.3%) to diabetes (6.5%) (P < 0.05 for trend)."

The decrease in IIT fully offset the increase in RMR in patients with IGT, such that 24-hour energy expenditure (24-EE) was unchanged. On the other hand, 24-EE "was slightly increased in people with diabetes."

So the article indicates:

1) high fasting insulin is NOT associated with any increase in energy expenditure in patients with IGT compared to NGT; and

2) high fasting insulin IS associated with a slight increase in energy expenditure in patients with Type 2 diabetes compared to NGT.

Quote:

"The clinical significance of increased RMR and decreased IIT in type 2 diabetes is a matter of debate. Some authors have proposed that reduced glucose-induced thermogenesis contributes to the development of obesity and the propensity for relapse after weight loss, while others argue that in individuals with diabetes, this defect may be compensated for by the simultaneous increase in RMR. In support of the latter argument, 24-EE was only slightly increased in people with diabetes and not increased in those with IGT. Our findings of increasing RMR during the development of diabetes may thus be primarily of pathophysiological interest. However, we have previously shown that even a small difference in RMR (70 kcal/d) can have a significant impact on long-term
body-weight regulation, and it is possible that even a slight increase in RMR contributes to a limitation of further weight gain after the onset of IGT and diabetes."

RedCairo said...

I am incredibly grateful to Taubes for the work he put into looking into the topic and for publishing on it. I'm not at all surprised that he is not entirely right given it's a very complex subject, but I think the book got a ton of people to simply THINK. I'm delighted that it led to a lot of debate and eventually to posts like this. Taubes's greatest achievement in this field is as a "catalyst."

RedCairo said...

Once I got a glucose monitor I found that I had pretty regular and severe hypoglycemia. I'm a little confused by your comment about that being very rare. It's certainly not rare for me.

I did some testing and discovered that eating essentially nothing, my blood sugar zooms way up high, and insanely low, back and forth like a mountain range, for two days. Food doesn't even need to be involved. Apparently the body's reaction, adrenaline, whatever else, can do that.

(I'm severely obese, although VLC took a lot off me -- not remotely enough before it ceased to have any weight effect and my body didn't want to enter serious ketosis at all anymore, just got a 'crisis' reaction instead. An extended period of massive supplementation didn't solve that but did help it some.)

As for the food 'reward' system, living on things that bore and revile you doesn't seem like too workable a solution for the majority population to get on board with. My favorite tasting foods (e.g. beef and cheese) have no discernible effect on my intake then or later. But if I eat more than ~25 carbs esp. in the morning I'll be wanting to nosh all day, and if I eat gluten grains (or the killer combo: gluten grains + dairy), I'm fighting the see-food diet all day. Reward in this case would have to be measured by "invisible neural reactions" to food, not by taste buds... I find the confusion between those concepts/terms doesn't help discussion of it.

It seems to me that we have a lot of efforts into saying, "Well if X is bad, why is selected population Y not (skinny, fat, whatever)?!" but there is clearly more involved than JUST some micronutrient or macronutrient. That doesn't mean that some things (like deficiency in magnesium and choline and chronic over- consumption of carbs) can't cause problems. And it's certainly possible that different composition of carbs (e.g. rice and sweet potatoes on one side, vs. wheat on another) could have a fairly profound effect. Seems like there is more study to be done on these things before anything is sure.

Fred Hahn said...

Stephen -

What is Gary wrong about specifically. And what resources are you using to support yourself?

I personally don't think you are clear on Gary or Mike Eades position on this subject.

Please tell me how one could become obese on a low carb diet. Let's start there.

John M said...

I'm less concerned about the science of a low carb regimes than about its effectiveness; in my case extremely effective,both in weight loss and gain in key lipid indicators.

I am surprised that neither party seems to have heard that a high protein regime induces a higher release of peptide YY, a hormone that reduces hunger. Is this another claim that we should expect to be refuted?

Chris said...

Fred

1 - It is STEPHAN not Stephen

2 - Stephan has made his criticisms pretty clear in this and other posts.

Naxossa said...

@Melchior :"..containing the usual processed crab)... crab ? crap ? or carb (s)? The first being low carb, the last high carb most likely while the middle one could be any and all. But to stay on topic, none of all the distinguished commentators nor the blogger himself has given me enough arguments to change my present, quite satisfying low carb, virtually no-wheat diet back to the old high to regular carb diet. Fewer migraine headaches, no weight problems (while eating to my heart's content, fewer allergies, more energy,better quality of life. And of course I should mention, complete disappearance of angina chest pains. I do not believe that Gary has an angle on the truth, but neither has Stephan. It has been mentioned before but I too miss any reference to glucagon, neither is there any mentioning of the relationship between the triglycerides and the VLDL and ensuing inflammation in the overload (with carbs). Too glib and too theoretical and sounds more like a kid playing with Lego blocks. It does fit, because that what the blocks are for. But there is a lot that does not fit, because they are not Lego .

montmorency said...

Stephan wrote:
"Carbohydrate consumption per se is not behind the obesity epidemic. However, once overweight or obesity is established, carbohydrate restriction can aid fat loss in some people. The mechanism by which this occurs is not totally clear, but it has nothing to do with removing the supposed suppressive effect of insulin on fat release from fat cells. Carbohydrate restriction spontaneously reduces calorie intake (as does fat restriction),"



Let us suppose for a moment that your assertion that carbohydrate restriction works by restricting calories, and has nothing to do with the "supposed suppressive effect of insulin on fat release from fat cells." is true.

How then do you explain the experience of many low-carbers (including myself) who experience no hunger in between meals (even without any snacks whatever), whereas with a simple calorie restriction of the same amount compared to our former intake, we would undoubtedly experience hunger?

You do not think that it is the free fatty acids which are now allowed to be released from the adipocytes which is adding to our now-reduced external calorie intake, and making up the calorie deficit?

If not, then how do you explain the lack of hunger?

montmorency said...

I believe that one of the points that is sometimes made about HFCS (not saying I necessarily agree with it), is not that it is worse than plain old sucrose, but that, partly because it was very cheap, and partly because it was not called "sugar", it started getting added to a whole lot of products where sugar might not have been before (or not in such large quantities).

And a lot of people (understandably), for a long time, didn't realise that it was functionally identical to "sugar", and probably thought they were getting something healthier than "sugar".


I believe that is part of the story, anyway.


That having been said, while a lot of people no doubt got overweight and obese mainly due to (added) sugar and HFCS, I don't think everyone who got overweight and obese, did so because of (added) sugar and HFCS.

wayward foodie said...

thank you

Mikal said...

Very useful: there's too much idle dismissal of Taubes' ideas out there, with little serious grappling with his arguments.

Stephan, at one point you had a transcript of your debate with Gary, didn't you? I can't seem to find it any more; would you give me a pointer?

Thanks!

robrob said...

not being insulin sensitive enough would explain my relentless hunger. seems I am eating all the time even tho it is mostly lower carb stuff. I take gtf, and just started pure cod liver oil for the vita d, e, omegas. I still have not lost a pound, been following a lower carb diet for over a year now. making sure to get plenty of vita d, and calcium from dairy and other saturated fats like coconut oil.

my hubby lost alot of weight without trying by simply taking omega 3, and lowering his simple sugars found in pop and cakes and cookies not that he ate alot of cookies. he still drank apple cider vinegar and raw honey together for energy while driving truck.

he wasnt trying to lose weight just lower his cholesterol he lost 50 pounds in a little over a year it was so subtle i hardly noticed until he came home for the doctors and told me.all his eating stayed the same.

I am trying all kinds of stuff to become fully insulin sensitive again, there is improvements but the results are slow and for all appearances sake dismal.

jenny you might be right about the low blood sugar thing (my sugars are in normal range when I get a glucose tolerance test), it being the rate of fall not the amount, I suffer middle of the night jitteries tension and after about 20 minutes or so extreme hunger. that is after sleeping for about 6 hours. I attribute to possibility of sleep apnea which would cause stress and release of cortisol which lowers your sugars right?

not sure, it is funny last summer and fall as I ate most of my carbs as fruit and drank my milk and ate lots of veggeies as I was hungry for it, and did alot of juicing of veggies forcing it down, and taking gtf I started to get improvments in my sleep. sleeping longer and feeling a bit more refreshed and for the life of me I can't figure out what changed.

maybe juicing veggies again (those I can't eat yuck) might be the trick don't know. I plan on doing that again. everything is about the same. I eat my fruits not alot some days I hunger for it others I don't. I am not sure what exactly changed, maybe less sun bathing?

rose

Brendan said...

Brilliant work. Chapeau!

Anand Teke said...

Outstanding write-up. I tend to agree that obesity is a complex phenomenon and cannot be reduced to simplistic cause-effect relationships.

As you say, everything happens through brain; is there any study to examine effectiveness of mental techniques such as neurolinguistic programming to controll obesity?

Adam St.Pierre said...

I'm a little late to the party for commenting... My personal take is that obesity is not about carbohydrate in general, rather it is largely caused by overconsumption of nutrient poor carbohydrate calories (alhtough I blame inactivity even more than diet). The calories in refined carbohydrate don't pack a large nutritional punch (aren't dense with vitamins, minerals, etc.), therefore you must consume more calories to meet nutritional demands.

Ben said...

I was interested in the studies that show high carb intakes don't increase hunger or energy intake. I did notice that all of the cited studies were on lean, healthy people. I wonder if overweight/obese subjects would produce the same results. I have also seen one study that came to the opposite conclusion, on a mixed group of preadolescent children. A high-GI breakfast resulted in a higher energy intake at lunch by 147 calories.

http://www.ncbi.nlm.nih.gov/pubmed/14595085

How would you reconcile this finding? It's not the only one, either. Here's a study showing that a 4-week low-carb diet reduced ad-libitum food intake more than a high-carb diet:

http://www.ncbi.nlm.nih.gov/pubmed/18175736

And what about this 2007 review that found similar studies supporting the idea that low-GI eating reduces food intake?

http://www.ncbi.nlm.nih.gov/pubmed/17610996

TB said...

I think the main issue of High fructose corn syrup and other sugars and the exposion of obesity is that they are added into a ton of foods.

Some of the comments on here make me think many people dont really cook for themselves, and by that Im not referring to making your self canned soup or boiling pasta, but actually making your sauces etc from scratch.

For example if I make pasta sauce from scratch I will often add a bit of sugar to help soften the acidity and also bring out the flavour.

Now take your average processed sauce/food which has the lesser quality ingredients (tomatoes not fit for produce stands etc) and to make them taste good and consistent a number of things are added.

No doubt people are eating more carbs now than before and often unintentionally.

I can see the low carb diets working because it has for me in the past (15 years ago) Although I was on the specific carb diet by Elaine Gotschall for non-weight loss reasons, I had some changes in my digestive tract after drinking tap water in mexico.

I spent 2 or so months on it and lost about 25 pounds or 11 kilos.

I was not exercising anymore but I just dropped weight.

This was facinating to me and a real eye opener, into diet.

Robert said...

Is there a graph of consumption of consumption of sugars, refined carbohydrates and other carbs over the same time period?

George Henderson said...

There are two graphs on one of R D Feinman's posts on his blog.

Rations of sugar, starch, protein and fat in the USA haven't changed much in recent decades.
Calories eaten by men, on average haven't increased.
Calories eaten by women have increased during the period.
There is one difference between the two charts;
women (not men) are now eating more of their fat as PUFA, less as SFA; and this increase is parallel to the increase in calories consumed...

Robert Miles said...

Note that two kinds of PUFA has been found to be essential to human health - the omega-3 kind and the omega-6 kind, and the proper ratio between the two is needed. There is also an omega-9 kind, not essential. Partial hydrogenation (to preserve fats) tends to destroy the omega-3 kind, and upset the ratio between omega-3 and omega-6. Also, the omega-3 kind needs to be split up even more, since human bodies are very inefficient at converting the ALA variety into the DHA and EPA varieties it has more need for (under 1% gets converted). SFA is not essential - the liver can make it from the carbohydrates in the diet. MUFA is not essential, but I haven't found the way the body can make it.

IanD said...

Stephen - its seems your fundamental objection to Taubes is in this para:
"The reason insulin suppresses fat burning is because it's a signal of glucose abundance. It's telling tissues to stop burning fat because carbohydrate is the available fuel. If you eat a meal of 500 calories of carbohydrate, you will burn that carbohydrate under the direction of insulin, which will also make sure body fat mostly stays inside your fat cells during the process. If you eat a meal of 500 calories of fat, you will burn fat instead of carbohydrate, but since you just ate fat, you aren't dipping into your body fat stores any more than you were when you ate carbohydrate. So even though insulin temporarily suppresses fat burning and the release of fat from fat cells when you eat carbohydrate, at the end of the day if you ate the same number of calories you end up with the same amount of fat in your fat cells either way. You now know more about insulin than many popular diet gurus."

The assumption is that we are using all the energy we eat. We do convert all the carb energy which is rapidly metabolised. Fat is much more slowly metabolised so we do not overeat.

Exp results:
500 kcals cereal b'fast - B gluc
1 hour 14, 2 hours 5.1 3 hours 4.1 - HUNGRY again.
370 kcals Nut porridge
1 hour 7.4, 2 hours 5.5, 3 hours 5.7.

Cab calories are fully used, fat cals are sustaining.

I'm T2 diabetic for 12 years. 7-8 years on a low fat, complex carb diet caused crippling complications. 3 months on a low carb diet restored my health.

John said...

Excellent article, rite up in McDougall Diet territroy. But too much is being made of food, and not enuf of ACTIVITY. I didn't write "excercise", I wrote :activity". It's what you do ALL DAY LONG., not for an hour ina gym. Food and activity, in nature, are one and the same, despite that there are more than a few ways to obtain burnable energy from foods. There is one activity humans have evolved to do, and from it all other activity stems--WALKING. When this is factored into the erudite--I mean that, erudite--equations offered here, the "answer" to fatness will be clear.

marcus volke said...

There is another palusible hypothesis which seems obvious to me and so i'm surprised no one has venture to posit it yet.
The contradictory results in clinical studies in response to high carb vs high fat diets (specifically, the tendency for one to induce insulin/leptin resistance and/or metabolic syndrome in some people but to have a favourable result in others, might more easily be explained by metabolic individuality.
Isn't it possible, even likely that each person's metabolic response to different macronutrient ratios is unique, and this the optimum ratio might not be universally applied?
This is exactly what metabolic typing proposes, and it explains a whole lot of incongruous studies and anecdotal experiences.

marcus volke said...

This was an interesting critique that raised some difficult questions. Overall I did not find it very convincing because Dr.Guyenet failed to address some key points raised in Good calories Bad calories:

Raising insulin only improves insulin sensitivity short term in the same way that opium improves opioid sensitivity short term by increasing the size and number of protein receptors for that chemical on the cell membrane. Long term use of opium will eventually cause the protein receptors to shrink and die off, leading to opioid resistance. That is why drug addicts continually need a higher dose to get the same ‘high’ that they used to get at a lower dose.
The same thing happens with insulin – in the short term raising insulin improves insulin sensitivity. However long term exposure to chronically raised insulin levels eventually leads to insulin resistance. Here is the proof -

Raising glucose, raises insulin, increases insulin resistance…
Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study.
Diabetologia (2004) 47:31–39
“Conclusion/interpretation. When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in “normal” glucose tolerant individuals.”

Barbara B. Kahn and Jeffrey S. Flier, Harvard Medical School
The Journal of Clinical Investigation, August 2000 | Volume 106
“Hyperinsulinemia per se can cause insulin resistance by downregulating insulin receptors and desensitizing postreceptor pathways, as was confirmed by overexpression of insulin in livers of otherwise normal transgenic mice. This transgene resulted in an age-related reduction in insulin receptor expression, glucose intolerance, and hyperlipidemia without any primary genetic defect in insulin action or secretion.”
And again…
Alternative Approach to Treating Diabetes Tested
ScienceDaily (June 10, 2011)
From; Deletion of Insulin-Degrading Enzyme Elicits Antipodal, Age-Dependent Effects on Glucose and Insulin Tolerance.
Plos One June 2011 | Volume 6 | Issue 6
“It’s an example of too much of a good thing [insulin] becoming bad for you…chronic hyperinsulinemia seemed to actually cause diabetes. As they aged, the mice appeared to adapt to the chronically high insulin levels, for example, by reducing the number of receptors for insulin in their tissues. These adaptations make the mice less sensitive to insulin, which is the exact cause of type 2 diabetes.”
And again…
Insulin: In need of some restraint? Salk Institute
Proceedings of the National Academy of Sciences,March 07, 2007
“the study reveals the “dark side” of high insulin production, the kind that results from over eating and obesity. “Insulin is very effective at lowering blood sugar, and promotes fat storage, preparing the animal for times when food may not be available,” he says. “But when the hormone [insulin] is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organ.”

marcus volke said...

There are other limitations -
1:
in GCBC, gary taubes cites numerous examples of people on bland high carbohydrate semi starvation diets. Invariably the people on these diets remained ‘ravenously hungry’ throughout the experiment and developed severe physical/psychological symptoms (including self-mutilation and suicide threats).
For example, in 1944 Ancel keys and his colleagues replicated benedict’s experiment on semi starvation diets. The subjects ate 1570 calories a day consisting mostly of whole wheat bread, potatoes, cereals, turnips and cabbage. This diet would hardly evoke the food-reward feedback loop that Stephan claims is the cause of overeating...so why were they still so ‘ravenously hungry’?

2:
By contrast Gary refers to various experiments were subjects are placed on comparably low calorie low carbohydrate diets and the results are contra positive – the subjects are satiated on the sparse caloric diet and exhibit no symptoms of malnutrition or hunger.
For example, Ohlsen tested Pennington’s low carb low calorie diet a number of times and even though the subjects were restricted to eating 1400-1500 calories a day they reported feeling satisfied. Arguably eating meat and fatty foods are going to be more rewarding than eating potatoes and turnips, so again this contradicts Dr.Guyenet’s assertion that food-reward dominates hunger and calorie intake.

3:
This critique does not explain why some researchers have been able to produce weight loss in subjects on high calorie low carbohydrate diets, again gary taubes cites copious examples in his book.
One such case was the DuPont experience published in the journal ‘industrial medicine’ authored by pennington in june 1949. Subjects ate a minimum of 2400 calories a day and averaged 3000 calories a day yet still lost between 9 and 54 pounds averaging 2 pounds a week.

marcus volke said...

4:
Dr.Guyenet does not explain why some groups and subcultures have become obese on low calorie semi-starvation diets in which the predominant food was simple sugars. For example, in Trinidad a team of nutritionists from the United States reported in 1966 that one third of the women were obese and that they achieved this condition eating fewer than 2000 calories a day.
By 1973 in Jamaica 10% of adult men were obese and nearly two thirds of the women were obese in a society in which “malnutrition in infancy and early childhood remains one of the most important disorders contributing to childhood mortality”. Presumably, if the kids are starving, the adults are probably not eating many calories either.

5:
Since Dr.Guyenet maintains that weight gain and loss is determined solely by calories consumed vs. calories burnt one would expect that force feeding high calorie diets would produce marked and significant increases in adipose if combined with a sedentary lifestyle.
IN GCBC, there are a number of studies that contradict this assumption, for example a study conducted in the late 1960s by endocrinologist Ethan Sims at the University of Vermont.
In this study he used convicts at the Vermont state prison, who raised their food consumption to 4000 calories a day. They gained a few pounds but then their weight stabilized. So they ate 5000 calories a day, then 7000, then 10,000, while remaining sedentary.
Of his 8 subjects that went 200 days on this regimen, two gained weight easily and six did not. One convict managed to gain less than 10 pounds after 30 weeks of this forced gluttony. One would expect that should all be obese if calories and not a metabolic defect was the critical element in obesity.


6:
Dr.Guyenet admits that chronic inflammation contributes to leptin resistance, which in turn contributes to obesity; but neglects to mention that carbohydrates and particularly refined sugars create reactive oxygen species and raise HBA1C, a measure of glycation – all of which contributes to chronic inflammation.

marcus volke said...

Raising insulin only improves insulin sensitivity short term in the same way that opium improves opioid sensitivity short term by increasing the size and number of protein receptors for that chemical on the cell membrane. Long term use of opium will eventually cause the protein receptors to shrink and die off, leading to opioid resistance. That is why drug addicts continually need a higher dose to get the same ‘high’ that they used to get at a lower dose.
The same thing happens with insulin – in the short term raising insulin improves insulin sensitivity. However long term exposure to chronically raised insulin levels eventually leads to insulin resistance. Here is the proof -

Raising glucose, raises insulin, increases insulin resistance…
Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study.
Diabetologia (2004) 47:31–39
“Conclusion/interpretation. When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in “normal” glucose tolerant individuals.”

Barbara B. Kahn and Jeffrey S. Flier, Harvard Medical School
The Journal of Clinical Investigation, August 2000 | Volume 106
“Hyperinsulinemia per se can cause insulin resistance by downregulating insulin receptors and desensitizing postreceptor pathways, as was confirmed by overexpression of insulin in livers of otherwise normal transgenic mice. This transgene resulted in an age-related reduction in insulin receptor expression, glucose intolerance, and hyperlipidemia without any primary genetic defect in insulin action or secretion.”
And again…
Alternative Approach to Treating Diabetes Tested
ScienceDaily (June 10, 2011)
From; Deletion of Insulin-Degrading Enzyme Elicits Antipodal, Age-Dependent Effects on Glucose and Insulin Tolerance.
Plos One June 2011 | Volume 6 | Issue 6
“It’s an example of too much of a good thing [insulin] becoming bad for you…chronic hyperinsulinemia seemed to actually cause diabetes. As they aged, the mice appeared to adapt to the chronically high insulin levels, for example, by reducing the number of receptors for insulin in their tissues. These adaptations make the mice less sensitive to insulin, which is the exact cause of type 2 diabetes.”
And again…
Insulin: In need of some restraint? Salk Institute
Proceedings of the National Academy of Sciences,March 07, 2007
“the study reveals the “dark side” of high insulin production, the kind that results from over eating and obesity. “Insulin is very effective at lowering blood sugar, and promotes fat storage, preparing the animal for times when food may not be available,” he says. “But when the hormone [insulin] is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organ.”

And of course insulin resistance goes hand in hand with leptin resistance. Gary taubes’ preoccupation with insulin was a tad myopic, and apparently he did not know how it interrelated with leptin resistance.
But his conclusions were still probably sound; I see nothing in this critique to refute that.

Homer Greens said...

"Carbohydrate restriction spontaneously reduces calorie intake."

Now that is a real knee slapper!

I am never trying to lose weight, but when I reduce carb intake without reducing overall calorie intake I always lose weight.

yanks1mig said...

Having recently completed my master's degree in human nutrition, I can say that everything in your post is spot on and scientifically accurate. This was a thoroughly enjoyable read - we need better advocates out there to get the right message to both healthy and overweight individuals.

Dark Unicorn said...

" Carbohydrate restriction spontaneously reduces calorie intake (as does fat restriction to a lesser extent), suggesting the possibility that it alters body fat homeostasis, but there is no compelling evidence that that happens due to a hormonal influence on fat tissue itself."

If you reduce carb intake and replace it with fat, how does that reduce calorie intake?

Most people who are succesful with low carb diets, replace the carbs with fat, they are not losing weight just because they took their usual diet and just reduced carbs.


If it's true that there are around 9 calories per gram of fat, and around 4 per gram of carbohydrate, wouldn't it make more sense that if you replace cabs with fats, that you should significantly increase your overal calorie intake? If so, then why are people so successful with this way of living (low carb high fat)?

Just asking questions, I might have misunderstood something!

Inese Poga said...

Many interesting thoughts. It's just so that neither one of these theories answers some very crucial questions: why has obesity become epidemic only by now and it was not a problem about hundred years ago? Why we are seeing most extreme obesity issues only in the countries which belong to so called "highly developed countries"? There are still lots of countries which do not have obesity problem at all. This all makes one think that the answer is not within leptin-insulin-glucose interaction. Secondly, all these theories and trials treat carbohydrates as simply carbohydrates of any type (with high glycemic index, low glycemic index, fast action, slow acting, so on), but there are huge differences, "fats" are also assumed to be simply "fats", and not fats from different sources, natural fats or chemically produced substitutes. Most likely, not carbs themselves, but chemically modified carbs, chemically modified proteins, chemically processed foods with high content of huge numbers of substances which were never assumed to be proper for human consumption cause interactions which do not exist in natural food chains with the same values of natural carbohydrates, fats and other nutrients.
I am more than sure that obesity is caused by overexposure to chemical substances over prolonged periods of time, and the interactions of these substances have resulted in destruction of normal metabolism, normal insulin and pancreatic enzyme functions. I am originally from Latvia, and I was recently there visiting. It was not open for any processed foods until 90s of the last century. Obese people were big rarity there, but with more processed foods on the market, increase in consumption of chemically produced soft drinks, more obese people have started to appear there, as well. The answer to North American obesity is within chemically enhanced foods, drinks, fast food chains. There is a big difference in metabolism and absorption of foods from natural source (normally grown vegetables, fruits, berries, grains, real meat, fish, etc.) and those which have been exposed to long-processing procedures and reactions, and have additives in form of all kinds of enhancers and supplements. Extreme obesity started in North America and is spreading out since US manufacturers export lots of their poisonous stuff.

Fred Hahn said...

Inese - if obesity is caused by overexposure to chemicals, then why is it so easy to cure with a well formulated low cab/sugar diet?

Christian Rafael Resener said...

And what about this study showing the relation about insulin/obesity?

http://www.medicalnewstoday.com/articles/253713.php

Alan2102 said...

A comment here from the very beginning (within the first 10 comments or so), which seemed to have been neglected. Too bad, because the point is critical.

Begin quote:

"Marie Curious said...
Terrific explanation of otherwise difficult-to-follow interactions, but I'm confused on one point. How can we draw useful conclusions about the effects of serum glucose or insulin from 'traditional' tribes and cultures, which have constant activity all day long? Similarly, Americans were a majority of manual laborers earlier in the last century. Is the effect of a high carbohydrate diet or of chronically elevated insulin the same in active and sedentary individuals? Do our hormones work the same way irrespective of muscle mass and activity level? For that matter, do we know if muscular, lean, active people ever become 'insulin resistant'?"

Haha! Excellent!

The whole discussion is hopelessly crippled and nearly meaningless unless activity (and to a lesser extent, as she says, muscle mass) is accounted for. It is possible to eat a moderately high-carb diet and stay in ketosis, if you're performing extreme physical work. Correspondingly, for couch potatoes, and particularly for ones with already-damaged metabolisms, even small amounts of carb can screw everything up. Taubes may not be wrong, but his view needs this vital context, and is lost without it. It is not (and cannot be) carbs *per se*, but rather carbs in relation to activity or lack thereof. And Stephan's analysis is similarly lost without it.

earthgirl said...

Taking this particular 'fact' as a given, I question and caution the use of such a statistic to promote a perspective if it itself has not been examined for consistency. e.g. I am referring to:
..taking a long view.. "per capita macronutrient consumption in calories per day from 1909 to 2006, according to USDA data*:"

This is just a fact with no mention made of contributing or ameliorating factors and certainly is not derived by controls or double blinds. It therefore may be a skewed fact when interpreted through the above. And this I suspect it has.

S Guyenet puts a convincing case above, however that statement serves it no good at all. CHO per se seems ill attacked, but there is another case to be made that specific carbs - sugars specifically fructose and inflammatory proteins contained within carbs (such as gluten) may have a greater contribution to obesity and that they have risen as the intake of specific manufactured products containing CHO have risen predominately in the past 40 years. To include these in such a longitude study is obviously minimising their influence within CHO versus fats etc.

VS Rao said...

Thanks so much for so much of information in one post. While it took just over 30 minutes to read this, it probably would have taken months for you to compile this and we, fitness conscious folks from around the world, owe you a lot for this wonderful exposition. Very scientific with ample reference to genuine research. Probably what I gained from reading this would not even be possible even if I did a specialized course. You have answered so many of questions in the blog that I always was trying to find an answer and what a way to find answers for all questions at one single place.

You are the man...! Please continue to enlighten the human kind with more such scholarly blogs. God bless you!

Trond Hagen said...

It would be interesting to see the macronutrient graph in the article with carbs divided into refined cars and unrefined. Does anyone know where to find an overview of the rise in refined carbs?

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