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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PMC said...

Great post Stephan. You finally decided to let people see that you are a BIOCHEMIST and neurobiologist!

Stephen said...

Here's a thought:

It seems that those populations that subsist on a high carb diet are always isolated and primitive; they don't live in suburban Los Angeles. These genes of these people may have evolved to tolerate such a diet. I've read that epigenetics would allow for such evolution.

Also, what would happen if a group of people in suburbia America adopted the same diet? Would they lose weight or gain it?

Any research dollars out there?

Melchior Meijer said...

Stephen,

Such studies have been done, albeit small ones. Here is one. Not low carb by any standard.

http://yaboga.com/paleo-metabolic.pdf

Beth@WeightMaven said...

Hmm. Why would the ideal macronutrient breakdown during infancy map to later in life?

Carnivore said...

To expand on my original post, I would like to make the following points:

I was never able to achieve a bodyfat of 8% by eating a calorie restricted high carb diet, the best I could do was get to around 13% when I had dropped my calories really low to about half of maintenance. So yes, calorie restriction does work to a certain degree.

When I switched to a calorie restricted low carb diet, I got down to 8%. It seems low carb is an easier and more effective tool for burning fat, especially when you want to get extremely lean. That's why it's used extensively by bodybuilders in their cutting cycle before a competition. Would I have been able to achieve the same bodyfat percentage eating high carb? Maybe, but it would have involved some severe caloric restriction and hunger, not to mention a loss of lean mass which I already started observing when my calories went too low on high carb.

Having reached my target, I am now maintaining my bodyfat percentage by eating around 3400 calories/day. My protein intake has stayed constant because I am into weight training and I try to get at least 1g of protein per pound of bodyweight, no matter whether I eat low or high carb. Eating high fat foods is infinitely more rewarding for me though. I don't believe a diet which isn't rewarding is sustainable, to be honest.

The conclusions which I can draw from my personal experience are that low carb diets work better for burning bodyfat, but you do need a restriction of calories to ensure continuous fat loss. With the same caloric restriction eating high carb, my rate of fat loss was slower and I felt hungrier throughout.

It is possible to eat more calories than you might need with low carb and not end up gaining bodyfat. Is the first law of thermodynamics not being obeyed? Of course not, but it seems eating more calories on low carb tends to increase calorie expenditure as well. How, I don't know. My activity level has stayed the same, in fact I recently took a couple of weeks off from the gym and went crazy on food just to see what would happen. On the other hand, overconsuming calories on high carb is easier but it just doesn't bring about the same adaptation of increased calorie expenditure. I believe this is what the Metabolic Advantage is all about, at least in my case.

David Pier said...

A suggestion for Stephan: At the end of a post like this, set an informal rule for the comments, a rule mandating that the comment indicate if the idea advocated applies to all people, or only to certain disordered metabolisms or other special cases. A lot of the confusion swirling around here is based on the lack of specificity.

Rebecca Latham said...

Frank said, "Rebecca, You might control very well for you caloric intake, but you have absolutly no way of knowing your daily energy expenditure, unless you're telling me you've spent some time in a metabolic chamber figuring out."

Frank, you are not carefully reading what I said. I do not disagree with what you are saying. What I said was that my calories out (CO) CHANGES based on the makeup and amount of my calories in (CI).

That is why I can eat only 1100 calories of low fat, high carb food to maintain my weight, but if I switch to high fat, low carb food, I can eat 1800 calories to maintain that same weight. Eat more without gaining weight, because the macros and amount of the food I am eating CHANGES how the food is utilized as fuel. Less incoming fuel stored as fat and more incoming fuel used as actual fuel.

Obviously, if I am maintaining my weight at 1100 calories on low fat, high carb, it means that I am also burning off 1100 calories.

But if I switch to 1800 calories of high fat, low carb food, and my weight is still maintained, do you see any scientific way that I am not NOW burning off 1800 calories?

I am not surprised by this.

Rebecca Latham said...

@Frank

"There are multiple studies totalising multiple subject readily available on pubmed showing that when substituing carbs for fat while keeping protein and calories constant, there is not effect on the rate/amount of fat loss."

And there are multiple studies that come to the exact opposite conclusion. You can't convince me that I am mistaken about what happens with my own body, all studies aside.

Rebecca Latham said...

@Dr. J

"I realize n=1 doesn't get a lot of respect, but I have seen the same results in so many others that I have few doubts as to the validity of my observations. I also find lots of supportive literature, especially the carefully executed studies by Jeff Volek et al. In my own research, I have seen remarkable results, unlike anything achieved through other diets or pharmacology.

On balance, I find the explanations put forward by Taubes and Lustig to explain these phenomena more compelling than anything else I have encountered, including the notion of palatability and reward."

My point exactly.

Rebecca Latham said...

@Carnivore

"It is possible to eat more calories than you might need with low carb and not end up gaining bodyfat. Is the first law of thermodynamics not being obeyed? Of course not, but it seems eating more calories on low carb tends to increase calorie expenditure as well. How, I don't know. My activity level has stayed the same, in fact I recently took a couple of weeks off from the gym and went crazy on food just to see what would happen. On the other hand, overconsuming calories on high carb is easier but it just doesn't bring about the same adaptation of increased calorie expenditure. I believe this is what the Metabolic Advantage is all about, at least in my case."

n=2

Anyone else out there who has found this to be true for them?

JimBob said...

Just something I'd like to through out there, for those many people in the comments who said they followed LC or VLC diets for a long time and whenever they started introducing more carbohydrate they began gaining weight, while keeping calorie intake the same.

Lets assume that the calories and energy expenditure were indeed the same (though that's questionable at best), there is still a very simple possible explanation for the weight gain. I may be wrong but my best guess is you folks added some starch and later that day, or in the next few days saw a peculiar increase in weight on the scale and freaked out, thinking back to your previous experiences with a crappy diet, a la SAD, that you would go back to your former self if you continued with this. So you ended little experiment in short notice, now completely confident that the evil carb is and always was the source of all your body comp and health related issues.

Thing is, after being, in a sense, deprived of carbohydrate for a relatively long time it's not much of a stretch to assume that the added weight very well may be increased muscle glycogen content and water retention. Both of which should normalize within a week at most and you probably wouldn't have seen any additional weight gain past the initial, scary, several pounds.

Just my 0.2$

chakaal said...

When looking at South Indians you may not see a lot of obesity but you will see a lot of heart disease. If you have not seen the Railway study, it shows a dramatic difference between north indian omnivores and south indian vegetarian railway workers.

Amber said...

Rebecca, of course there are. The are countless ranks of us. I don't even see it as controversial, though there are always people who think I must be mistaken about my intake even though I've measured it rigorously for long periods. Last time I checked I was eating about 2500-3000 calories a day. I'm not particularly active. I'm a 130 lb woman, 5'6, down from 185. I'm still losing. I eat pretty much only meat. I gain with even small amounts of carbohydrate.

I've talked with some seemingly bright people who simply cannot wrap their heads around the idea that just because energy balance can be calculated as CI-CO doesn't imply that it is a *function* of CI and CO.

I don't think the effectiveness of LC diets are in question at all. What's at stake is the mechanisms. Lot's of people have stated that they don't care, they only want to know how to eat, but from the perspective of science it's important, and it's especially important for the minority for whom LC doesn't work, who may benefit from further knowledge.

One mechanism I don't think is a candidate is the observation that LC dieters often spontaneously reduce calories. As you and Carnivore point out, that still doesn't explain that more calories are used on a LC diet, and fuel partitioning is affected, since body composition is affected: more fat is lost of the total lost weight the lower the carbs.

Dave said...

@Stephan,

Just to clarify (and apologies if already discussed, I haven't gone through all of the comments): what precisely is the "carbohydrate hypothesis" under discussion? Is it that carbohydrate is *necessary* for obesity, or *sufficient*? My reading of Taubes is the former, that you need carbohydrate to drive fat storage, but not that just eating carbohydrates will make you fat.

I don't find anything in what you presented which is inconsistent with that view, e.g. examples of lean cultures with traditionally high-carbohydrate diets may simply indicate that other factors are needed to drive obesity, and particularly metabolic syndrome. Are there any examples of obesity occurring in the absence of dietary carbohydrate?

Amber said...

JimBob, that's a valid point, but at least for me and some others I've talked with it's not just water weight, (which I'm well aware of, and don't "freak out" about), it's continuous gain of fat.

On the other hand, I also know of people who seem to have regained carb tolerance, so that does happen, too. But I don't think a formerly obese person can necessarily count on it.

And seeing as there are people for whom the metabolic disease pattern doesn't make them fat, increasing carbs just going on lack of weight gain might not be prudent.

Rebecca Latham said...

@Amber "Rebecca, of course there are. The are countless ranks of us. I don't even see it as controversial, though there are always people who think I must be mistaken about my intake even though I've measured it rigorously for long periods. Last time I checked I was eating about 2500-3000 calories a day. I'm not particularly active. I'm a 130 lb woman, 5'6, down from 185. I'm still losing. I eat pretty much only meat. I gain with even small amounts of carbohydrate.

I've talked with some seemingly bright people who simply cannot wrap their heads around the idea that just because energy balance can be calculated as CI-CO doesn't imply that it is a *function* of CI and CO.

I don't think the effectiveness of LC diets are in question at all. What's at stake is the mechanisms. Lot's of people have stated that they don't care, they only want to know how to eat, but from the perspective of science it's important, and it's especially important for the minority for whom LC doesn't work, who may benefit from further knowledge.

One mechanism I don't think is a candidate is the observation that LC dieters often spontaneously reduce calories. As you and Carnivore point out, that still doesn't explain that more calories are used on a LC diet, and fuel partitioning is affected, since body composition is affected: more fat is lost of the total lost weight the lower the carbs."

n=3 and counting. Thanks for your comment!

Andreas Eenfeldt said...

Melchior Meijer,
"An important hallmark of healthy (long lived) populations is excellent insulin sensitivity and glucose tolerance. I therefore think it would be wiser to follow Staffan Lindberg's model than let's say classical Atkins. I'm very interested in Andreas' thoughts on this."

Good question. I think the Lindeberg model has been proven to work great, with the result of long term health, at least in populations that are fairly physically active and healthy/slim to start with.

Regarding diets similar the Atkins diet, there is no population except perhaps Inuits and other smaller groups that have lived on it all their lives. They seem to have done fine too, but I guess it's not quite as certain.

I think the main strength of an Atkins (or LCHF) approach is in conditions like obesity, diabetes and metabolic syndrome. There we now have plenty of good quality research showing a good effect. Much more support (so far) than the Paleo approach has. Will Paleo eventually show equally good or better results for these disorders? Perhaps, perhaps not. We don't know yet.

Of course another strength of LCHF is that a lot of food taste pretty damn good fried in butter. :)

David Csonka said...

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

More correctly, it seems that evolution wants human babies to drink breast milk.

The act of inferring anything more from that is similar to the reason why Stephan wrote this article. Unsupportable extrapolations.

The nutritional needs of rapidly growing infants are very different from those of adult humans who are no longer growing.

JimBob said...

@Amber

You may be right but there is also a strong possiblity that a decent percentage of people who claim to suffer from metabolic syndrome and not handling carbs well simply aren't telling the truth, not intentionally of course, but for lack of better knowledge. Many of them were on a crappy, chronically hypercaloric diet, then switched to LC and felt much better. Not all of them felt better because carbs were the culprit for their problems, some simply went from a very poor diet to a very rich diet, strictly nutritionally speaking. Then they went on to rationalize why it is that they felt like crap before and now they feel awesome - so they self-diagnosed carb sensitivity. And that's the group of people I was aiming at with the first comment.

I cycle my carbohydrate intake as per Martin Berkhan's leangains and weight train intensely a couple of times a week. On the days that I don't train my diet would be considered LC or even VLC (<50g a day?), conversely, on training days it is extremely high in carbohydrate, to the point that I'll consume more than 400 grams of starch and sugar (plum jam = yum) in a single meal and often more than 600 for the day. This has increased muscle glycogen synthesis and water retention as a consequence. It's not uncommon for my weight to increase as much as 8 pounds in a relatively short time frame, like <8 hours. I'll also lose that extra weight and sometimes even more in the next few days, so it's the long term effect that matters. Keep in mind that I'm not eating low carb more than 3 days at a time, so I can only imagine how the body of someone who's been at it for years could react to reintroducing carbs. I realize it's not very applicable to someone who is or was very obese, but it's just here to illustrate the point of muscle glycogen and water content changes, which I feel doesn't get mentioned enough in the context of rebound weight gain. While this is common knowledge to scientists and many people who are into strength training and calorie/carb cycling, I'm guessing for the target audience of Gary Taubes' books it might not be the case. They'll go by what the scale says and automatically connect the dots in a fashion that probably isn't entirely true but it fits their picture so they go with it.

Just curious, for how many days at a time have you tried bringing carbs back and what quantities are we talking about here? Also, how do you know the weight gain was fat?

Dave Clary said...

I just want to clarify my earlier comment concerning removing my Primal Blueprint poster from the wall. I credit my change in lifestyle to Mark Sisson, and I believe in the vast majority of what he espouses. I'm just not convinced at this point that carb intake necessarily leads to problems.

Melchior Meijer said...

Thank you very much for your response, Andreas. I totally agree on the butter argument ;-). It's was really heart warming to read on your Swedish blog that you are enduring a serious butter shortage up north.

You are right, there is precious little data on paleo interventions in people with metabolic syndrome and/or NIDDM and/or CHD, but we do have the small trials done by Lindeberg and Frassetto. What striked me in these experiments was the improved insulin sensitivity and glucose tolerance in these folks, despite (or thanks to) the pretty high carb intake. This seems to indicate that other factors than carbs per se cause and perpetuate insulin resistance, hyperinsulinemia, etc. I am of course thinking NAD's as per Staffan Lindeberg, Robb Wolf et al. Pure low carb generally induces a plethora of improvements in unfit people, but increased insulin sensitivity/glucose tolerance is not one of them, if I am informed correctly. If anything, very low carb induces insulin resistance. Since there is evidence that the Inuit suffered osteoporosis (a clear disease of insulin resistance), and maybe even advanced atherosclerosis and CHD pre contact with Western food, I wonder if LCHF is the optimal way to achieve good health long term. I am convinced that advising (pre)diabetics to follow the official recommendations borders on criminal and that LCHF is improving and saving lifes. But I wonder if these victims would become even healthier if they were advised to eat a bit more carbs (sans the NAD's) in order to restore/sustain insulin sensitivity. Proper insulin signaling (low levels can do the job) just seems so important to me.

One more question if you don't mind. Were you totally fine (mentally) with the lingering 'high' blood sugar on that crappy lunch OGTT in Stockholm?

Dr J said...

There is paleological evidence that Inuit had CVD but they also had lung disease. I think it is more likely that indoor air pollution from the use of seal oil lamps is the cause.

Tracy said...

@Rebecca, I noticed the same thing: prior to changing my diet, I was struggling to lose and/or maintain my weight while eating between 1200-1400 cals of low fat, high carb. At the time, I was also exercising (cardio and strength training) 5x/week.

Low carb, I was eating substantially more, even though my appetite and desire to eat had lessened (1800-2500 cals), and was not exercising at all. Lost weight, have kept it off 6+ years.

HOWEVER - I also discovered I was gluten intolerant/celiac, and I went gluten-free at the same time. So if my overweight was linked to gluten/gut damage or carbs (or both), I can't say with certainty. What I can say though is that when I do increase the frequency by which I consume carby foods such as rice or potatoes, I do begin to gain weight... but that also tends to go along with a recurrence of gut issues.

As far as food reward goes, I'm still not sure about it. In the past, one of the most rewarding foods for me was plain French bread, as well as plain Melba toast and plain saltines (ie: with no salt. Salted ones were better, but I'd still sit with a whole package of unsalted ones and eat, and eat, and eat... ) Those were also the foods I would have insane cravings for - so bad that I'd literally have to leave the house after dinner to avoid bingeing on them. The effect they had on my brain was like a drug effect - perhaps food reward is different, or for my celiac brain that's how food reward worked?

malpaz said...

about breast milk and babies..

babies use energy different than grown humans. a newborns energy needs for the brain are consumed by 69% of calories thus more glucose(present in moters milk) would allow more energy for the baby brain, hence why babies sleep all the time. it is NOT an accurate depiction of what grown humans, who use about 20% of energy for brain activity, should eat

i dont have an opinion on carbohydrates, people have been eating them forever. someting to think about though. while i understand there are some wild tropical sweet fruits, roots/tuber and legumes cultures came across were eatten and the result was one thing, they wanted to grow them and find ways to produce them to be sweeter, bigger and more bang for the buck. original roots and tubers were bitter, it ONLY makes evolutionary sense that they wanted them sweeter, they desired their enjoyment. that same process has continued and continued sine day one of a human eating a roots/tuber/fruit. they wanted more, wanted sweeter and wanted more bang for the buck. they spent seasons cultivating what they had to work with to make it taste better. it IS HUMAN INSTINCT to do this.

the food reward stephens proposes follows evoltuion to a key, it is what humans are bred to do. as technology advanced, so did flavors and food combinations and sweetness, so did waist lines, so did food choices... IMO, obesity is the expected result of human evolution. our genetics are set up for us to desire finding ways to eat and sustain ample good tasting food

Stargazey said...

@Wati

If I'm reading the growth grid correctly, an average baby boy will gain 33% in length and 125% in weight in the first six months of life. With growth expectations like that, the composition of human breast milk seems entirely logical.

By and large, human adults do not expect to gain height and hope not to gain weight. Why would you expect that the composition of human breast milk would be optimal for them?

InNewOrleans said...

@Woo

I read this blog a lot and don't often comment, but I"m about to make up for it with a crazy long 2-part post. ;) As a woman who has also had personal experience with anorexia, mood disorders, and later PCOS, just as you have, I feel the need to chime in with my two cents. I think there is a lot in what Stephan is saying that can be reconciled with what you are saying.

When I ate too little and exercised too much as a teenager, participating in half-marathons and living on less than 600 calories a day sometimes, my body reacted in all sorts of bad ways, like low estrogen, amenorrhea, thinner hair, etc. It wrecked havoc with my HPA function, lowering it to the point that my basal body temperature was about 95 degrees.

At some point during college, when I no longer had the will to starve myself to the same extent, I was running about 20 miles per week and eating about 1500 calories per day and gaining weight at a very rapid pace, which I'm sure many readers won't believe but which is an energy-balance phenomenon I'm sure you are very familiar with. Some people's bodies can conserve energy to an almost unbelievable extreme. I began to have very painful periods. By the time I graduated, I had gained 60 pounds on a small frame (50% increase in body weight in about 2 years), was profoundly insulin resistant, and had anovulatory cycles and facial hair from PCOS. So I had completely swung in the other direction, and despite the weight gain my body temperature and HPA function were still lower than normal. Virtually everyone else in my family is obese, so this didn't really shock anyone. But I was unhappy, to say the least. PCOS can really mess with your psyche, especially if you are a woman with very light skin, and very thick, dark hair who starts to develop a beard. Not peach fuzz, but thick, dark hairs on your chin. Not fun. I got so much conflicting advice, and there were times I got very, very angry about the fact that my body seemed so out of control and no one, not even fancy doctors, seemed to have any good answers as to how to fix it.

PCOS starts with insulin resistance, and one of the pieces of advice I got was to cut out carbs. I did some reading on insulin resistance, and low-carb seemed to make perfect sense. I tried it and stuck with it for months. I did not gain more weight, but I did not lose weight and my quality of life did not improve. I know you put a lot of stock in your own personal experience, and I put a lot of stock in mine. My HPA function started decreasing again, I was constipated, my hair started thinning again, and none of my underlying symptoms really resolved. This was about 10 years ago. I didn't know at the time but suspect now that my leptin levels were decreasing. A low-carb diet treated the effect that I could no longer process carbs properly, but I was still miserable and still didn't really know why I could not process carbs normally. So I gave that up and decided to do some more reading on insulin resistance and try to find a different approach that would do more than paper over the problem. You said in your post:

"You are describing people who do not produce huge amounts of insulin to process trivial amounts of sugar."

Yes, but why are certain people producing so much insulin in response--and keeping it so high between meals? And should the primary goal be to bring insulin levels down? Or is it like heart disease, where people thought hight cholesterol caused heart disease until they realized the real problem is inflammation, and high cholesterol is the body's attempt to repair it?

InNewOrleans said...

"What occurs in (garden variety) obesity, instead, is that an excessive amount of insulin is produced in an attempt to reduce the blood glucose level."

Yes, exactly. Why do obese people produce so much insulin in response to a comparatively small amount of glucose? Because they are insulin resistant. And why are their cells insulin resistant? Because their cells don't want any more glucose. But the body needs some place to store the excess energy, so it produces more insulin so that it can stuff the glucose somewhere. In modern-day life, we don't have much occasion to decrease our glycogen stores. When we do, we immediately improve insulin sensitivity, because our muscles need to replenish the lost glycogen. There is a lot of genetic variation in this, and some people's muscles are much less prone to becoming insulin resistant than others. But the basic processing of glucose appears to be the same.

Even though in my heyday I was doing a ridiculous amount of cardio, cardio uses up shockingly little of our glycogen stores and puts a lot of stress on the body. I think this probably contributed to my HPA function decreasing, thus lowering metabolism and need for energy, thus even though I ate only a little, it was more than my body needed at my low metabolic rate. When base levels of insulin increase in order to keep glucose forced into cells and not floating around in the bloodstream, certain other hormones increase as well, especially estrogen, leading to all sorts of gynecological problems for women with high insulin, including fibroids, weird-feeling breast tissue, etc. But this has nothing to do with postprandial increases in insulin, which I would expect the body to be well adapted to.

I do believe it is possible that a low-carb diet can help some people who are insulin-resistance or T2 diabetic because with so few carbs coming in, those get used mostly by the brain, and even if we use very little of our glycogen stores in daily modern living, eventually we do use something, and that has to be replaced. So maybe that helps insulin levels go down over time. For me, for whatever reason, it did not work and was a miserable experience. What worked a thousand times better was a hardcore, glycogen-depleting workout every one-two weeks. I got a cheap home gym and would do reps of various exercises for about 20 minutes, which was the point at which I was basically sitting on the bench or at the leg press unable to move. When I was diagnosed with PCOS, I was told the syndrome was not reversible. For the past five years, I have had normal, ovulatory cycles and have maintained a healthy weight. A couple of years ago, I had laser hair removal on my chin, and the hair has not grown back, which is a good sign that the underlying hormonal imbalance has completely resolved. I don't attribute this 100% to the weight-bearing exercises. I'm not sure what all of the factors have been. But I do know the human body's metabolism is extraordinarily complex and difficult to forcefully manipulate without a lot of follow-on effects. I am glad people like Stephan are trying hard to learn more about it.

I think food reward is probably a piece of the puzzle, though in my opinion probably a minor one. But an honest and curious researcher like Stephan is likely to figure that out over time, and I don't think his current line of thinking/speculation is completely useless. I have a lot of family experience with addiction, and so have done a lot of layperson reading on the neurobiology of addiction. Who knows, but I would not be surprised to see that downregulation in the receptors of certain neurotransmitters play a key role in moving the set point up.

luckybastard said...

@inneworleans

thanks for sharing. during my weight loss, i also was doing heavy glycogen depleting workouts at least once, sometimes twice a week. in fact, when i started putting starch back into my diet after being vlc for several months, i initially would only do it shortly after one of these workouts. i used to describe this ritual as "teaching" my body how to use carbohydrates properly- something it never knew how to do even in childhood. i try not to be adamant about the fact that the vast majority of people should be able to tolerate safe starch once they're metabolically healed(whether they want to stay lc or vlc is up to them), however, i think of myself as insulin resistant as you can get and in my 30s i finally got around to correcting that situation.

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Frank said...

Hello Rebecca.

Stephan have provide you with 2 study already in this post, which shows that altering carbs/fat composition don't matter for weight loss, and I can provide a few more.

I'm very curious to know what are these multiple studies which found the oposite result, because i've never seems them.

Anthony Colpo reviewed all the revelant study few years back, and i've discussed the matter often enough to be very sure that people would have presented them to me already.

Obviously, we are talking about controlled, protein and calorie matched, metabolic ward study, and not self reported in free living subject.

Maybe you can show them to me?

bonnie said...

Where are the studies that look at relative insulin sensitivity and address how different people respond to different quantities of carbohydrate.

Research too often looks at a point of statistical significance without discussing the range. We end up treating to the mean. Not effective.

For those of us working in the trenches, there is not one right way to eat. The quandary cannot be reduced to a question of carbohydrates versus protein/fat. One fundamental factor in metabolism does concern what balance of carbohydrate, protein and fat works better for any one individual.

Until researchers design studies with far more sophistication and stop this silly polarizing argument the rest of us are left to figure it out on our own.

InNewOrleans said...

Thanks, luckybastard. Also, from what I remember of the reading I did, your muscles actually rebuild glycogen over the several days following a hard workout. So it might make sense to introduce a modest amount of plain starches in the meals after a glycogen-depleting workout, while your muscles are naturally less insulin-resistant.

Over time, I've noticed that the timing of eating carbs vs. when I workout doesn't matter much anymore so long as I do the workouts periodically and don't eat anything between meals. I'm not sure why, but for me eating anything at all between meals, even if it is a "healthy" snack, seems to rev up my insulin resistance. I know this is very new-agey and not scientific (until someone like Stephan explains it), but I think of it as sort of a natural flow and ebb. Eating another bit of food just two or three hours after a meal makes my body flow again just when it was getting ready to ebb. I think of snacking as the body being in a constant state of flow with no ebb, and fasting as constant ebbing with no flow. I think of the workouts similarly. Muscle cells were meant to periodically expend some of their glycogen stores, not to be in a constant state of fullness. A small bit of insulin resistance can have cascading effects and cause even more insulin resistance. You need some ebb (glycogen depletion) to get some flow (insulin sensitivity). And that sensitivity can have the same cascading effects in the other direction by lowering base levels of insulin, so long as you are not eating between meals.

On a somewhat related note, I think it would be interesting if Stephan considered his food reward ideas not only in terms of the absolute reward, but also in terms of the timing. I have a strong suspicion that most people respond better in terms of weight management and health to short bursts of relatively high reward (say, a very satisfying meal, but nothing over-the-top) than more continuous stimulus, even if the food eaten is of lower palatability.

bonnie said...

Research quoted leaves one to believe that all humans respond to carbohydrate in the same way. This is not true. I wonder about any of the other references that pretend there is only one way things happen.

Researchers need to take better care to address the range of physiological response, not just a point of statistical significance. By not addressing the range,we are left treating to the mean. Not efficient or effective.

There is not one right way to eat. Until researchers design far more sophisticated studies, we are left with a polarized and silly argument pitting carbohydrate against protein and/or fat. This is not the issue.

There is one question that needs to be asked. What balance of carbohydrate, protein and fat is best for any one individual? In a clinical setting our current research merely provides a point of reference.

paleotwopointoh said...

When I switched to lower carb eating, I also thought I was eating 2000+ calories a day, but I actually was not eating even close to that much.

I especially don't believe the reports of higher calorie intakes from people who claim to gain on the barest smidge of added carbohydrate from any source (starch, sugar, vegetable).

I don't think they are failing to count a meal or anything like that, but more that animal protein, especially meat seems to be overestimated in common listings of calories that regular people use.

Private said...

Your insights were shed a welcome light on the subject, but as a 42 year old female runner/mountaineer, I often point out to my (chubby) friends - I've never climbed a mountain and found a fat person at the summit cairn. Move. Eat. Move again. It's what we were designed to do. (and eat real food that comes from the earth, not manufactured crap.)

gunther gatherer said...
This comment has been removed by the author.
gunther gatherer said...

Hi Stephan, I'm interested in Dr. J's question too. If insulin has nothing to do with overall weight gain or loss, does it also not have anything to do with BP, HDL, LDL, inflammation and other health markers?

Taubes does mention the other health benefits of low carb diets aside from the fat loss issue in his book (according to him, the more fat you eat, the lower your trigs), and I haven't seen you address them yet. This is assuming we all agree that lipid scores even matter.

Carnivore said...

For the record, I make logs of whatever I eat. I did this when I was eating high carb and I do it now as well. Not everyday, but whenever I plan a change in menu, I calculate exactly how much macros I am getting. I am the sort of person who can alternate between one or two alternative menus for months on end and take a lot of pains to measure everything. So when I say I now eat around 3400 calories, you can take it as an accurate value. Could it be a few calories less or more? Sure.
It really isn't that unusual to eat this much on low carb and not gain weight. The bodybuilding forums I frequent are chock full of people who eat way more than their 'maintenance' calories and don't add bodyfat. Losing fat is different and I do believe you need to be in a deficit to achieve substantial fat loss.

If you know anything about bodybuilding, you would know that people who are into it can get pretty obsessed with whatever goes through their lips. I am no different.

If you don't find studies showing such results, it's probably because no one has tried to see what happens when people 'overconsume' calories on low carb. All studies I know of have been obsessed with finding out the results of obese people trying to lose weight on low carb/high carb diets. As far as I'm concerned, obese people tend to have great results following ANY diet if it is sufficiently calorie restricted (with results being slightly or significantly better for low carb even after taking into account water weight loss), so these studies don't really mean much to me. I was never obese, I was just carrying more bodyfat than I would like despite being meticulous with what I ate and also being fairly active.

In essence, I'm just saying that low carb works for me, not arguing how or why.

Jake Croker said...

An outstanding critique, I feel brighter for having read it.

"This is where he should have mentioned leptin signaling, which would have taken the book is a scientifically accurate direction." the second 'is' in the sentence should be an 'in'?

Elizabeth Miller said...

@ Grok
my money's on Taubes

Since we're trying to explain the uptick in obesity in the last thirty years it is clear to me from the food clearance data and other reports that the fraction in our food that has gone up is carbs. You can actually observe it all around you -- people are constantly snacking and it's usually carby, crunchy stuff - it's not steak. Protein and fat consumption have actually gone down. From my reading the most important variable might be the relative low amount of protein. I think a lot people in the US eat a nutrient poor diet devoid of sufficient protein -- and at the cellular level they are hungry and if there insulin is high they won't readily have access to their fat stores.

From "Insulin in health and disease" by Sonksen and Sonksen "Insulin simultaneously stimulates lipogenesis from glucose and inhibits lipolysis. Both mechanisms are mediated by the same receptor. The data illustrate what Schafer referred to as the the 'autocoid' (excitatory action, i.e. stimulation of lipogenesis, and the 'chalonic' (inhibitory) action, i.e. inhibition of lipolysis, both of which are integral to the hormone and medicated by the same receptor. It is the 'chalonic' action which has most relevance to human physiology and the use of insulin therapeutically." p.70

techn0scho0lbus said...

This post is unscientific and filled with generalizations. I laughed when he wrote without citation that insulin did not cause an increased appetite. Then he often uses just two studies to rest his arguments on. Or even worse, he uses only one, inconclusive study and claims it supports a middle ground instead of not supporting either hypothesis. This is just a basic misunderstanding of science and I'm disturbed at how many people think this post 'falsifies' the insulin hypothesis. As a side note, this author claims that all of science is behind him on this and that there is a lot of evidence, but he doesn't prove that, no statistical averages, no meta studies, nothing. His claim about science is as anecdotal as the stories from the many people who have lost weight on low-carb diets. On top of that, there actually is an avalanche of studies linking obesity with diabetes and insulin with fat storage. http://scholar.google.com/scholar?q=insulin+diabetes+fat+obesity&hl=en&btnG=Search&as_sdt=1%2C28&as_sdtp=on

Josh said...

I think we need to get this discussion moving in a forwards direction. So now that we have established once and for all that the effect of carbs on insulin does not lead to insulin resistance and obesity we can put this myth to rest and focus on what actually does cause insulin resistance. I'll get the ball rolling - fructose, nutrient deficiencies - vitamin d & magnesium, chronic cortisol elevation due to stress, low carb diets (increase insulin resistance but not obesity), poor sleep, omega6, oxidative stress .......................

Andreas Eenfeldt said...

Melchior Meijer,
"One more question if you don't mind. Were you totally fine (mentally) with the lingering 'high' blood sugar on that crappy lunch OGTT in Stockholm?"

Yes I felt fine. Only one thing: as the blood sugar peaked at 179 I may have felt some minor tingling in my body, but that may have been my imagination.

As I understand it on a very low carb diet your body is not prepared for a sudden OGTT. If you do a few days of eating more carbs before it, the OGTT should be much better.

Dr J said...

There are at least three mechanisms where a high carb intake can lead to hypertension.

The antinatriuretic effect of insulin is well documented, even within a normal physiological range. Fructose also causes sodium resorption in the distal tubule as well as generating uric acid which interferes with NO regulation of vascular tone.

Insulin also drives hepatic de novo lipogenesis which will raise triglyceride levels and shift the FA gradient at the surface of the adipocyte towards storage by upregulating LPL.

All of these problems correct when carbs are significantly restricted. Perhaps there is a similar benefit obtained from a paleo diet of carbs which are slower to raise insulin levels. However, depending on the severity of their insulin resistance, I think many people will still need to get their overall carb levels very low in order to normalize these things.

michael-ray said...

Thank you. Well done and needed.

Elizabeth Miller said...

@Bonnie

Absolutely,
From an article called the DNA diet:
“Each one of our genomes has been interacting with the environment for thousands of years,” he says. “This created an understanding between our genome and the environment. Imagine you take an orchid native to the tropics and move it to Toronto. It is the same if you take a Puerto Rican to Boston,” Ordovas says, pointing to big changes not only in climate, but in living conditions (close-packed, urban housing), work (indoor as opposed to outdoor) and what foods are available and affordable (processed rather than fresh). “The genome is not prepared for the environment. And this is why you have the increased morbidity.”

Many of the genetic markers associated with higher risk for heart disease, obesity and diabetes are more common in Hispanics. Ordovas theorizes that some of these markers might have worked well with a traditional Puerto Rican diet of rice, beans, fish and fruit, but the addition of starches and sugars—and a pattern of snacking common in the mainland U.S.—may overtax these same genes.

I've been reading lots of articles on uncoupling proteins -- they actually interact with the expression of insulin.

I know that a high carb diet (whole and complex and even when I added calorie restriction) was a disaster for me -- my northern European genome expects more fat and protein which appear to up-regulate UCPs 1 and 2. UCP 2 has been shown to decrease glucose stimulated insulin secretion. The plot thickens. The lynch-pin though still appears to be insulin.

I am not a Kitavan!

paleotwopointoh said...

Me: "Perhaps readily available animal protein estimates are overly high and this makes people think they are consuming more calories"

Carnivore and Rebecca Latham:"We log everything we eat using readily available animal protein estimates!"

Ok, we get it, you count every gram that passes your lips. But it's quite possible and in fact probable that your low carb calories are overestimated by the sources you rely upon. I am not suggesting you fail to count each morsel, but that the references you use might be flawed.

Actual controlled studies suggest lower consumption, so you both are probably not eating quite as much as you think, plus you are likely moving more on top of that, and the two confounds explain much of the difference simply and plausibly.

dextery said...

Dr Jack Kruse has entered the fray regarding the SG/GT smackdown with this posting about obesity with the introduction of the role of magnesium in insulin resistance.

http://jackkruse.com/gnolls-com-opens-the-door-to-obesity-fight/

Rebecca Latham said...

Frank, I suggest reading Volek et al in "The New Atkins For a New You" and "The Art and Science of Low Carbohydrate Living".

Joe Taylor said...

Perhaps our problem with obesity in today's world is not all about the calories in but more related to the calories out part of the equation. We live and work in climate controlled environments. My body probably expends significantly less energy over the course of a day regulating body temperature. We do not exert much energy sitting at a desk, typing on a keyboard etc. Have there been any studies that show any correlation between the expansion of technology and the expansion of our waistlines?

Frank said...

Rebecca

I'm asking for studies, not for books. Do you have those studies? You claim that such studies exist, surely you must know them and must have reviewed them yourself (at least looked at the result part)? Or are you blindly trusting someone selling a diet book that is confirming what you want to believe?

Here, I'll help you.

http://www.ncbi.nlm.nih.gov/pubmed/16685046

http://www.ncbi.nlm.nih.gov/pubmed/8561057

http://www.ncbi.nlm.nih.gov/pubmed/2058571

http://www.ncbi.nlm.nih.gov/pubmed/9497169

http://www.jci.org/articles/view/108519/pdf

http://www.sciencedirect.com/science/article/pii/0026049564900988

http://www.ncbi.nlm.nih.gov/pubmed/6020514

There is much more papers like this. How would you account for so many studies arguing agaisnt your hypothesis?

I'm gonna assume that Volek use the same kind of data that this review paper uses, which are useless, because they are from self-reported, are not protein matched (look at table 1, most of the study have double the amount of protein on the LC diet) and no metabolic chamber was used to measure the energy expenditure of the subjects. http://www.ajcn.org/content/79/5/899S.full.pdf+html

There are, to my knowledge, 2 studies which found greater WEIGHT (we don't know if it was fat or water and glycogen of muscle mass since the study did not measure body composition) loss on a LC diet, but these results have never been replicated by many following studies.

I'd like to add the general comments that some people are claiming that the higher energy consumption that has been happening in the past years is coming from carbs but Stephan has been posting data showing that everything macro is being more consumed, not just carbs. Here is another reference validating this

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm

psychic24 said...

@Joe Taylor
You think lumberjacking and sitting on a chair all day have the same effect on your appetite?

Dan said...

Maybe think a little harder about Taubes' advice about how to conduct good statistical science. Don't just be an anti-processed food activist. Come up with a testable hypothesis and a clear definition of "rewarding" or "overstimulating" food, and define it in a non-circular way (i.e. don't define "overstimulating" foods as all those foods that people eat prior to and subsequent to becoming obese). Then actually look and see if there are populations that get obese without these "overstimulating" diets. And if you have to continue refine what "overstimulating" is until it becomes "anything that people overeat until they become obese" then your theory has become useless. And if you ultimately come to the conclusion that otherwise healthy populations can't develop significant problems with obesity without wheat and/or sugar, then all you've done is refined the carbohydrate hypothesis and not really refuted it, even if the description of the mechanism is off. And if you look hard enough I can bet that you'll find people who thrive on these "overstimulating" diet that you tell us are necessary to avoid for optimal health.

Don't be so smug when people tell you how to conduct science and consider that maybe he has a point. I'm sure you're aware that an appeal to hypocrisy is not an argument in favor of your hypothesis. Maybe Gary assumed before that you respected him enough that you would have called him out when he made conclusion out of line with the evidence. He has always deserved to have any missteps pointed out, as do you.

Sam Knox said...

@Rebecca Latham

Thank you for pointing-out that combining calorie-restriction with carbohydrate-restriction sabotages weight-loss.

Paleo Garden said...

Stephan,
As Michael said... simply superb.

Cheers,
http://www.thepaleogarden.com/2011/08/13/slaughtering-sacred-cows/

Paleo Garden said...
This comment has been removed by the author.
M. said...

Dan said: “And if you ultimately come to the conclusion that otherwise healthy populations can't develop significant problems with obesity without wheat and/or sugar, then all you've done is refined the carbohydrate hypothesis and not really refuted it, even if the description of the mechanism is off”

Just about every health conscious person on the planet says that refined wheat flour and sugar is not so good for you. It is absurd to say that this just a refinement of the Carbohydrate Hypothesis. Just about everybody says these are not so good for you - Campbell, Ornish, Fuhrman, McDougal, the AHA, the Food Pyramid, and just about every diet book on the planet. Why does it validate Taubes and nobody else? Because Taubes is your personal guru.

The Carbohydrate Hypothesis says that refined wheat flour should be no worse than white rice. A billion or so people in Asia kind of shows that the Carbohydrate Hypothesis is crap. If people do fine on white rice, then switch to an industrial diet and encounter problems, the question should be what is wrong with the industrial diet. Do you not see the scientific absurdity of framing it around all around “carbs”? The only reason people do this is because they are stuck in a “carbs” paradigm.

This blog post was not about Food Reward vs Carbohydrate Hypothesis. It is about Carbohydrate Hypothesis being crap. Attacking Food Reward does not support the Carbohydrate Hypothesis. The Carbohydrate Hypothesis is scientifically dead. Unfortunately, the mythology lives on, and some low-carbers have decided to champion pseudoscience. It is T. Colin Campbell and The China Study all over again.

Nathan R. Hodges said...

Interesting write up. I reviewed the USDA statistics and didn't see the cumulative data you presented on protein/fat/carb percentages. Did you crunch those numbers yourself from the USDA data and if so what was your sorting/methodology? And how did you derive the data points since the USDA data was not presented in tabular form, just visual? Thanks!

Dr J said...

@ Frank - search PubMed for the Volek et al studies which are mainly published in Lipids. You will find that a low carb diet vs a eucaloric "prudent" diet resulted in significant differences in weight loss, fat loss and abdominal fat loss, all in favour of the LC diet.

mamaelvis said...

The one thing this article proves beyond a shadow of a doubt is:

Bullshit baffles brains.

ItsTheWooo2 said...

You are aware that milk is designed to promote rapid anabolism, right?

YOu are aware that our metabolic needs change throughout the life span, right?

You are aware that an newborn animal is growing far, far, far rapidly than you are, an adult, right?

Lord. My brain hurtz.

ItsTheWooo2 said...

@mamaelvis

"Bullshit baffles brains. "

Yes, this is exactly the conclusion I came to when I saw so many people shouting WELL DONE! Even though there were *numerous* factual errors easily recognized by anyone slightly medically trained/interested in obesity research.

ItsTheWooo2 said...

@Melchior

"However, the same improvements Dr J mentions are seen when people with metabolic syndrome and all the related (downstream?) pathology are put on an ad libitum 'paleo' diet, regardless of macronutrient composition."

As someone with a few of the condition's Dr J mentioned, I can assure you that a diet full of atkins bars and splenda and coffee will control my issues nicely. It's not the "paleo", its the presence of dietary fat a fuel , with the subtraction of dietary carbohydrate as fuel.

"Paleo" works because all paleo diets are low carb compared to the baseline diet, and many paleo diets are low carb by an absolute standard (e.g. 100 carbs or less per day).

"Paleo" works because it IS low carb, almost all the time.


But like I said, it's not the paleo, it's the carb thing. I can totally eat a boat load of atkins bars and cheese and creamy coffees + splenda, none of which is paleo, and I will not have a regression of obesity or PCOS.

If I try to eat a "whole foods" diet which is made up of fruit and sugar and starch, I will have problems.



is this fairly well established low carb induced 'physiological' insulin resistance a bad thing, or just a benign adaptation to very low carb?

It is the expected outcome of burning lots of fat for energy.

It is not a problem any more than insulin serving to usher glucose in cells is a problem. It is normal and the way things are engineered by evolution.

If you remove the high dietary fat by stopping the low carb eating, the glucose tolerance returns to baseline. Using fat for energy results in not using glucose for energy; removing the fat will result in glucose being used for energy again.


A temporary decrease in glucose tolerance due to eating fat is not the same thing as dead mitochondria and low dopaminergic tone, all of which shift the body away from being able to process glucose normally. It is not the same thing any more than wearing protective gloves to cover your hands is the same thing as being an amputee and not having hands. Not even a comparable situation.


The irony is that by eating low carb and removing pressure from a poor glucose metabolism will actually preserve mitochondria and in the long run improve glucose tolerance. It is documented that caloric restriction (which is synonymous with low carb dieting for anyone who is glucose intolerant) helps mitochondria stay healthy and increase in number.

Elizabeth Miller said...

Score one for Taubes and Lustisg:
I encouraging everyone reading this post to read this article (is it possible to attach a pdf?)

Obesity and energy balance: is the tail wagging
the dog?
JCK Wells1 and M Siervo2
1Childhood Nutrition Research Centre, UCL Institute of Child Health, London, UK and 2Human Physiology and Nutrition Unit,
Department of Neuroscience, Faculty of Medicine, University ‘Federico II’ of Naples, Naples, Italy
The scientific study of obesity has been dominated throughout the twentieth century by the concept of energy balance. This conceptual approach, based on fundamental thermodynamic principles, states that energy cannot be destroyed, and can only
be gained, lost or stored by an organism. Its application in obesity research has emphasised excessive appetite (gluttony), or insufficient physical activity (sloth), as the primary determinants of excess weight gain, reflected in current guidelines for obesity prevention and treatment. This model cannot explain why weight accumulates persistently rather than reaching a plateau, and underplays the effect of variability in dietary constituents on energy and intermediary metabolism. An alternative model
emphasises the capacity of fructose and fructose-derived sweeteners (sucrose, high-fructose corn syrup) to perturb cellular metabolism via modification of the adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio, activation of AMP kinase and compensatory mechanisms, which favour adipose tissue accretion and increased appetite while depressing physical
activity. This conceptual model implicates chronic hyperinsulinaemia in the presence of a paradoxical state of ‘cellular starvation’ as a key driver of the metabolic modifications inducing chronic weight gain. We combine evidence from in vitro and in vivo
experiments to formulate a perspective on obesity aetiology that emphasises metabolic flexibility and dietary composition rather than energy balance. Using this model, we question the direction of causation of reported associations between obesity and sleep duration or childhood growth. Our perspective generates new hypotheses, which can be tested to improve our understanding of the current obesity epidemic, and to identify novel strategies for prevention or treatment.
European Journal of Clinical Nutrition advance online publication, 20 July 2011; doi:10.1038/ejcn.2011.132

NICE!

PigeonOrStatue said...

LCHF diets work, even when consuming more calories. Regarding the mechanism, who knows, maybe peoples' engines do not burn fat as efficiently as a laboratory and so get lower mpg? As far as I am aware the 1st law does not apply in an open system. Just a thought.

Elizabeth Miller said...

Score one for Taubes and Lustsig:

Obesity and energy balance: is the tail wagging
the dog?
JCK Wells1 and M Siervo2
1Childhood Nutrition Research Centre, UCL Institute of Child Health, London, UK and 2Human Physiology and Nutrition Unit,
Department of Neuroscience, Faculty of Medicine, University ‘Federico II’ of Naples, Naples, Italy
The scientific study of obesity has been dominated throughout the twentieth century by the concept of energy balance. This
conceptual approach, based on fundamental thermodynamic principles, states that energy cannot be destroyed, and can only
be gained, lost or stored by an organism. Its application in obesity research has emphasised excessive appetite (gluttony), or
insufficient physical activity (sloth), as the primary determinants of excess weight gain, reflected in current guidelines for obesity
prevention and treatment. This model cannot explain why weight accumulates persistently rather than reaching a plateau, and
underplays the effect of variability in dietary constituents on energy and intermediary metabolism. An alternative model
emphasises the capacity of fructose and fructose-derived sweeteners (sucrose, high-fructose corn syrup) to perturb cellular
metabolism via modification of the adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio, activation of AMP
kinase and compensatory mechanisms, which favour adipose tissue accretion and increased appetite while depressing physical
activity. This conceptual model implicates chronic hyperinsulinaemia in the presence of a paradoxical state of ‘cellular starvation’
as a key driver of the metabolic modifications inducing chronic weight gain. We combine evidence from in vitro and in vivo
experiments to formulate a perspective on obesity aetiology that emphasises metabolic flexibility and dietary composition rather
than energy balance. Using this model, we question the direction of causation of reported associations between obesity and
sleep duration or childhood growth. Our perspective generates new hypotheses, which can be tested to improve our
understanding of the current obesity epidemic, and to identify novel strategies for prevention or treatment.
European Journal of Clinical Nutrition advance online publication, 20 July 2011; doi:10.1038/ejcn.2011.132

NICE

ItsTheWooo2 said...

@InNewOrleans

Your story is interesting and we share some commonalities.

Since I may have insight into what this is like as I myself have experienced it, do you think it is possible that your anorexia was an attempt to resolve your depression, which in turn was a result of your underlying glucose intolerance?

YOu seem to assume that anorexia is causing your later metabolic problems. I think it is far more likely that your genetic disorder (likely implicating inositol metabolism) is producing your mood disorders, glucose intolerance, and PCOS. Your self starvation is an attempt to normalize your mood and energy, which I can first hand tell you absolutely does help if you have PCOS and glucose intolerance.


The rapid weight gain you experienced after you stopped starving is probably a result of your underlying metabolic disorder, in the context of eating a high carbohydrate diet. Most anorexics are weight gain resistant and this is true even after they have severely starved themselves. Most anorexics are highly resistant to obesity, and this is why they are predisposed to self starvation. They are naturally very unrewarded by food - they have a central reward defect which may be related to excessive serotonin. This is the stereotypical RESTRICTIVE ANOREXIC.

In your case, it sounds like you are not a classic anorexic. Most likely you're more like me - you restrict because it helps your depression which in turn is a result of glucose intolerance / PCOS.

ItsTheWooo2 said...

(continued)

There is no relationship between self starvation and "causing" PCOS. There is a relationship, however, between PCOS and mental illness and glucose intolerance... the combination of which can make a person more likely to not eat to feel better, as eating will only exacerbate the disorders.

It is impossible to "cause" PCOS, if you already did not have the genetics to allow for it. The only way to "cause" PCOS is to take a drug that disrupts inositol metabolism, such as depakote. If you had taken depakote or any other b vitamin depleteing drug for your mood disorders, then you might want to consider this drug is the reason you developed PCOS.

PCOS is a polygenetic disorder, and the crux of the issue is a problem in synthesizing d-chiro-inositol. A woman can be a million pounds with an insulin level through the roof... she won't get PCOS if she makes INOSITOL well.

Mood disorders are very common in PCOS, probably because inositol also regulates serotonin function, and an inability to make enough inositol to cover a high carb diet will lead to inositol deficiency thus PCOS and depression/anxiety. Your self starvation is a way of keeping your inositol adequate.

"Yes, but why are certain people producing so much insulin in response--and keeping it so high between meals? And should the primary goal be to bring insulin levels down?"

Some people do this because some people have genetic quirks and/or aquired damage to how they process glucose. It is a safe bet that you, and I, do not make enough inositol at baseline probably because of novel genetic mutations OR because of evolutionarily conserved traits (I inherited it from my maternal grandmother who was living in an isolated tribe - this may have been an advantage in that environment, who knows). There are other factors too I am sure.


It seems like you are stuck on the assumption that your anorexia CAUSED your obesity and your PCOS. I think it is far more likely that your glucose disorder CAUSED your pcos, your depression, your obesity, as well as your anorexia. If you have a family full of fat people it is very likely you have glucose tolerance problems by genetics.


It's extremely rare that PCOS would vanish simply by exercising. I am suspecting you may have taken DEPAKOTE or another inositol disrupting psychiatric med for your depression, or some other type of medication. It seems, more than anything, you just got better with time.

That is not how PCOS usually plays out. Usually the woman with PCOS is always in "balance" with it, doing her interventions to control the problem, with flare ups and remissions depending on how well she is controlling her glucose. Speaking personally, I still go through phases where my hormones are "off" and this is marked by an increase flare of acne, with a bit of thickening facial hair, etc. These "phases" are always associated with eating carbs for a long time, in excess. When I am diligent about glucose control I do not have acne or any hair growth problems.

It is almost impossible to control PCOS without at least, at a minimum, low carbing. That is like, intervention #1, and everything else is just extra.

ItsTheWooo2 said...

@Private

I have never seen a sane person in a mental institution, either.

Fat people don't climb mountains because fat people are tired because they have metabolic disorders.

Lack of climbing mountains or other vigorous activities do not make people fat - but rather, people who have very high insulin and very poor glucose tolerance find that it is too hard to even stand up, never mind CLIMB A MOUNTAIN.

Melchior Meijer said...

Andreas,

Thanks again. I didn't express myself clearly. What I mean is that I myself would be uneasy with the idea of being pretty glucose intolerant (even if only relatively little glucose is coming in). It's very possible that I'm chasing a ghost. I agree that the LCHF-induced insulin resistance is a normal, even necessary physiological adaptation, which will reverse itself upon introducing more carbs. Again, my concern is if this state is optimal.

Dr J.

Thanks! I've read that too and it is plausible. Exposure to fine particles is causally related to metabolic syndrome and CHD. But then, the Kitavans smoke like chimneys. And why had the Inuits such a high prevalence of osteoporosis? We don't buy the 'high protein is leaching calcium from the bones' model, do we (this is by no means meant sarcastically, I just assume you don't buy that either)? My speculative theory is that insulin signaling eventually can become too low on severe LCHF. Too weak insulin signaling at the level of bone tissue causes osteoporosis in the long run.

Isthewoo,

Thanks. Your contributions always make a lot of sense and give us a lot to ponder over. You make a few assumptions I don't immediately agree with. You say the 'paleo' interventions I linked to were low carb, but they were not. They excluded grains, legumes, concentrated sucrose, (vegetable oils in one study) and dairy, but included fruits, honey and tubers. You say ad libitum LCHF is physiologically comparable to calorie restriction. But ad lib LCHF makes you insulin resistant, calorie restriction makes you - up to a certain point, I'm not talking total starvation - more insulin sensitive.

As you might have noticed ;-), my main concern is prolonged physiological insulin resistance. You call it perfectly benign and I hope you are right. I'm not yet convinced though.

And just to be clear: 'paleo' is not some definitive list of foods, it's just a rude compass that might us some clues. Modern analysis of items that are suspect when looking through a paleo lens, strengthen the likelihood that gluten, concentrated n-6, concentrated fructose, lactose and casein are less than optimal.

Andreas Eenfeldt said...

Frank,
"There are, to my knowledge, 2 studies which found greater WEIGHT (we don't know if it was fat or water and glycogen of muscle mass since the study did not measure body composition) loss on a LC diet, but these results have never been replicated by many following studies. "

No? Please let me update your list. Here are not two, not three, but fourteen studies of the highest quality (RCTs), all showing statistically more weight loss on low carb diets. All of them published since 2003:

http://www.dietdoctor.com/weight-loss-time-to-stop-denying-the-science

Actually there may even be two more, meaning sixteen studies. I'll update the list later.

On the other hand I do not know of a single study showing statistically significantly less weigh loss on low carb. If anyone knows of any such study please let me know.

To his credit, even Stephan Guyenet acknowledges that low carb usually is effective for losing weight.

Andreas Eenfeldt said...

Dan
"Come up with a testable hypothesis and a clear definition of "rewarding" or "overstimulating" food, and define it in a non-circular way (i.e. don't define "overstimulating" foods as all those foods that people eat prior to and subsequent to becoming obese)... And if you have to continue refine what "overstimulating" is until it becomes "anything that people overeat until they become obese" then your theory has become useless."

Spot on. This kind of circular thinking (and premature "falsification" of other potentially important theories) may be why obesity researchers so far has failed to come up with anything useful for actually curing obesity.

It's just as circular as "you must eat too many calories to get fat, thus the cause of obesity is eating too many calories".

It's mindboggling how many obviously smart people actually think like that.

Mirrorball said...

@Andreas Eenfeldt

I haven't checked every reference in your list, but I hope you realize that free-living studies that didn't control calories are useless as evidence for the carbohydrate hypothesis. Some didn't differentiate between water loss and fat loss. It is a well-accepted fact that people eat less on low-carb diets, which neither confirms nor denies the carbohydrate or the food reward hypotheses.

Hornet0123 said...

To all defending Taubes:
You can give 15,000 instances of his hypothesis being right, and if I give just one negating it, than in the scientific world it's falsified.
I really don't see how anyone can truly believe all carbs cause weight gain when there are are several BILLION contradictions walking the earth right now.
Check out the 30 bananas crowd sometime. Those people may not be the perfect vision of health, but they ain't fat!

Frank said...

Hi Andreas

I think you miss the ''protein matched'' and ''metabolic chamber '' studies part.

So far none of your references are like that, they are all the same kind of data used in the review paper ''is a calorie a calorie'' which i've already stated that are useless = free living subject, ad libidum studies, not protein matched. In most of your studies, the diet is not even controlled, subject are only told to restrain themselves to a number of grams of carbs a day. Far from proving anything.

I'm looking for metabolic chamber, diet, protein, and calorie matched and controlled study.


This is the kind of study that I have posted and they do not support the hypothesis that at the same number of calorie, changing the ratio fat/carbs affect fat loss.

Razwell said...

Obesity CAN and HAS been induced WITH NO CHANGE AT ALL in food intake or activity in individuals who were previously slim all of their lives .

The endocrinologist Dr. Friedman has seen this more times than you might think during his career as a doctor.

http://www.youtube.com/watch?v=vxSAhLyKVqw


Obesity's heritablity is almost that of height.


10 % of morbidy obese people have a single gene defect that is responsible, and Dr. Jeffrey Friedman thinks there is reason to believe that number is significantly higher.

The caloric hypothesis is DEAD. There is much about obesity which has NOTHING to do with behavior at all. The insulin hypothesis is ALSO too simplistic.

People such as Manuel Uribe are in a DISEASE STATE where their fat cell sare in HOARD MODE and become extremely disregulated. Hormones gone haywire.

Kindke said...

so did anyone find a study showing rapid onset of morbid obesity after adoption of a strict ketogenic diet yet?

From all i've seen, under voluntary circumstances people always choose carbs over fat. Make no mistake, Carbs are addictive.

Razwell said...

We ALL need to DROP this whole irrelevant high carb debate, low carb and REALIZE:


*that studies using international samples of Monozygotic twins reared apart SOUNDLY DEMONSTRATE that obesity's genetic component is EXTREMELY GREAT.


Obesity is more heritable than ANY OTHER CONDITION with the POSSIBLE exception of height ALONE- and possibly equalling height.


Dr. Jeffrey Friedman is a world class scientist and pioneer and above ALL of us here by far in obesity knowledge , myself included.

I am just a layman - but a very knowledgeable layman.

The FUTURE will deal with GENETIC research to help morbidly obese people. Perhaps we will actually have an EFFECTIVE treatment for once.

Friedman or his colleagues are the guys to do it, not the ramblings of the latest Internet gurus.




CarbSane, Anthony Colpo, James Krieger, Lyle McDonald - ALL SALESMAN- NOT VALID sources of obesity information at all



NONE of them are HIGHLY QUALIFIED like Dr. Friedman is.



Sorry, but a simple Google search is NOT a replacement for highly qaulified , world renowned scientists to access the relevant data, and relay ACCURATE obesity information.

Beth@WeightMaven said...

Timely comment from Seth Roberts today (emphasis mine):

"One problem with a low-carb high-meat diet: bad metabolites. This is why it is a good idea to find out what causes obesity rather than simply lose weight with something that works (such as a low-carb diet)."

The researchers studied two lower-carb diets with ~140g protein, one that was really Zone-like (P/F/C: 28/37/36 % respectively) and LCHF (P/F/C: 28/67/5), and found:

"weight-loss diets that were high in protein but reduced in total carbohydrates and fiber resulted in a significant decrease in fecal cancer-protective metabolites and increased concentrations of hazardous metabolites. Long-term adherence to such diets may increase risk of colonic disease."

Brad Marshall said...

Just wanted to throw a personal anecdote into the ring. I've been on a low carb diet for the better part of a year. So far I've lost 40 pounds with 20 to go.

The other night my wife and I were celebrating a special occasion and I ordered a cheeseburger with fries. Not what I normally eat these days, but it was a special occasion. A year ago I would've ordered a large appetizer, packed away the cheeseburger and all of the fries and then went looking for more food.

This weekend I was barely able to finish the cheeseburger. I ate maybe a third of the fries. I was so satiated that when my wife asked if I wanted any of hers I literally had zero interest. This feeling of satiation is a new thing for me. Rarely in my life have I felt truly satiated.

I think this anecdote has all sorts of ramifications, though:

1) Something about a low carb diet has restored my satiation pathways. Maybe I have higher leptin sensitivity. Maybe my stomach has shrunk. Who knows?

2) Despite the fact that a cheeseburger and fries are highly "rewarding" I had zero interest in overeating. I hadn't eaten much that day (almost nothing, actually) - it was a good sized cheeseburger but certainly didn't bring my daily caloric intake past what it should be.

3) If I was living on pizza and cheeseburgers I know from past experience I would have polished away twice as much food in that meal. So maybe food reward is more important in the long term than the short term (if at all. I remain sceptical.)

Any thoughts?

Beth@WeightMaven said...

Kindke writes: "Make no mistake, Carbs are addictive."

I don't know that "carbs" are addictive, but suspect that there are substances in some carbs (such as opiod peptides in wheat and dairy) that are very likely to be problematic.

BTW, Denise Minger makes a great argument (IMO) that the success of seemingly opposite diets (e.g. Ornish and paleo) comes from eliminating these more problematic substances.

Carnivore said...

@paleotwopointoh: If anything, I underestimate the amount of calories I get from animal protein sources. I eat about 600g of beef everyday and use the USDA values for 90% lean beef whereas the beef I get from my butcher usually has more fat than this. In other words, I underestimate the fat content, if anything, while slightly overestimating protein; the net result being that I underestimate calories. Plus, my major source of fat calories is not animal protein, it is butter, coconut oil, olive oil, almonds, etc. There is just no way that anyone can explain my consuming in excess of 3400 calories per day of low carb and not gaining bodyfat, unless you agree that such a diet increases calorie expenditure as well. It should be noted that I would start to gain bodyfat by eating anywhere close to 2800 calories when I used to eat high-carb. My activity level has stayed the same throughout: weight training 5 times a week.

I really don't see the big deal with this since it is a common occurrence, especially in low carb bodybuilding circles.

Also, I don't see how people think that Taubes' hypothesis is falsified by the existence of people and cultures who are lean eating high carb diets. First of all, I am an Asian and from one of these cultures myself and I can tell you we are not very lean in general. Yes, we are not usually obese, but we just tend to have smaller frames than Europeans and don't have much lean mass either. Anyway, this 'lean' look tends to go away when we enter our thirties or forties, depending on the individual person. Middle-aged people in my country almost always have pot bellies or wide hips despite not being obsese according to the BMI. They have the classic 'skinny fat' look.

Regardless, the existence of lean people who eat high carb does not disprove Taubes' theory. Taubes has said that carbohydrates are necessarry for obesity, not that everyone who eats carbohydrates is necessarily obese. To disprove him, someone needs to find a group of people who are obese in the absence of carbs in their diet, or in the presence of very few carbs. I would be interested to see if there are such examples.

Sam Knox said...

@Frank

I take it that the studies you cite show that there is no difference in the rate or amount of fat loss when the amounts of carbohydrate and fat in the diet are varied but protein and total calories are held constant.

Is that correct?

If so, they would not appear to be a refutation of the carbohydrate theory. They only show that in a laboratory, when the subjects are forced to eat the same number of calories, the effect on fat-loss is the same regardless of the macronutrient composition of the diet.

This is nothing more than what anyone would expect: The rate and amount of fat-loss is determined by the total calories in the diet.

The carbohydrate theory of obesity predicts that, in the wild, restricting carbohydrates results in a spontaneous reduction of total calories, and this appears to be the case, based on the studies cited by Andreas.

M. said...

Carnivore said: “Also, I don't see how people think that Taubes' hypothesis is falsified by the existence of people and cultures who are lean eating high carb diets.”

I think the issue is that the people and cultures that seem to have not too many problems with white rice, THEN they experience a problem after the introduction of an industrial diet. The industrial diet seems to be the problem, not the “carbs”.

You can argue about falsification, but the demonization of entire class of macronutrients does not appear to be the way forward.

If you have to quibble over the difference between this “carb” and that “carb”, maybe the “carb” paradigm should be abandoned.

Moose said...

Excellent ... until the end.

"These people ate XYZ for a million years and were healthy, but when they started eating LMN, they developed health problems."

The problem with this argument is that it fails to take into account that all humans are not identical and alike clones. If a group of relatively isolated people have been eating the same foods for hundreds and hundreds of years, that's what their metabolism is used to. By changing the foods they eat you are introducing a change into their metabolism. An over-exaggerated example of this would be pouring diesel fuel into a gasoline engine. It might run for a short period but then major problems will happen. Yet, both are combustible fuels.

Blaming the foods themselves is a failure of correlation. Were you to find people who had been living for hundreds of years solely on meats and were suddenly given nothing but carbs, I suspect you'd find the same health failings. (I've yet to find any studies looking at any such thing, were it possible.)

I've also long suspected that this is why low-carb diets only work for some people, and low-fat diets work for another group, etc. We are not made from cookie cutters, and when science forgets that it's a problem, because then you get sweeping conclusions of "X means Y", when X doesn't always apply to everyone.

Sisyphus Jones said...

A lot to think about here, thank you.

I have just one minor quibble.
"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. "

To my eye and long experience, these are all refined carbs.
Your body sees little to know difference between a bowl of sugar and a bowl of Cheerios, or between doughnuts and bread.
An unrefined carb would be something that hasn't gone through a machine before you ate it.
E.g. leafy greens, nuts.

While I agree that it's more than possible to stay lean on a high carb diet, I wonder about the effects of a high-carb diet that's essentially all sucrose and fructose. = the Western diet, cf. Weston Price.

Frank said...

Hi Sam Knox

Absolutly correct. No one is arguing about the effectiveness of LC diet for weight-loss. Stephan made that clear at the beggining of the post.

My concern is to know if this is optimal and necessary, given that there can be some downside to LC that might be avoided if LC is not necessary in the first place.

We're arguing about the mecanisms.

We're having two opposing view : At the same number of calories, if you restrict carbs and eat more fat, you shall lose more fat/weight (could be true short-term if we take account of water and glycogen loss). Or some people say that if you're very low-carb, you can overfeed fat and not get fat. Here some hormones, mainly insulin, is though to play the biggest role in the regulation of body fat.

On the other side, regardeless of macro composition of the diet (to some extent, because we know that protein are beneficial in regard to body composition) it is the total amount of energy provided by the diet, regarless of the macro source, that is the major determinant of fat/weight loss/gain. Here hormones obviously play a role, but they won't make you starve on a high-carb diet low-calorie if you're insulin resistant, eating away your muscle and not using your fat store. If you create a caloric deficit, you'll lose the same amount of weight if you play around with carbs/fat. I'm not aware of any overfeeding fat study on a very low carb diet, so there seem only to be n=1 at this point on this.

malpaz said...

itsthewoo:The rapid weight gain you experienced after you stopped starving is probably a result of your underlying metabolic disorder, in the context of eating a high carbohydrate diet. Most anorexics are weight gain resistant and this is true even after they have severely starved themselves. Most anorexics are highly resistant to obesity, and this is why they are predisposed to self starvation. They are naturally very unrewarded by food - they have a central reward defect which may be related to excessive serotonin. This is the stereotypical RESTRICTIVE ANOREXIC.


i so absolutely DISAGREE with this statement, as my personal experience almost MIRRORS neworleans experience. NOT to mention OVER 1/3 or anorexics become binge eaters post recovery and over 70% go on to maintain a HIGH than 'normal' BMI. check out ANY recovery discussion on anorexia and it is more full of binge eaters who are post anorexics. its almost as bad as this back and forth carb war.

i do however, agree with what you said. but i also agree with new orleans, a weekly depletion of my glucose seems to work well in my ability to maintain some sort of tolerance.

and odd you mention genetics, my family IS CHOCK FULL of fat people and diabetics and ladies withh PCOS.

razwell presents a very good arguement but leaves fixing it out of our hands which is something most people are unwilling to accept. our genetics are making us fat, no doubt, and i personally think it is the result of a malfunctioning and mal-forming brain. food per sae doesnt have anything to do with it

Chris said...

Oh no, Razwell has joined in.

mem said...

Any doubt that marketers are deadly seriously after your brain and deftly manipulating it?

http://www.neurofocus.com/

Carnivore said...

To be clear, I'm not for demonizing carbs. I myself eat a moderately low carb diet: around 100g of non-fiber carbs per day which consist mostly of vegetables, starch and some dairy. Since I workout, I feel that I need this amount to maintain my muscle glycogen. I do try to minimise fructose and sugar intake though. From previous experience, I know I was gaining bodyfat when I reached an intake of 2800 calories while eating around 400g of carbs from the same healthy sources.

Even while aggressively cutting fat with a calorie deficit, eating low or moderately low carb makes it easier to lose fat continuously when you get to a fairly low bodyfat percentage. High carb just makes it more difficult, regardless of the fact that the same calorie deficit is employed.

Stargazey said...

@Carnivore

To disprove him, someone needs to find a group of people who are obese in the absence of carbs in their diet, or in the presence of very few carbs. I would be interested to see if there are such examples.

I can't cite a group of people, but there is one notable example: Jimmy Moore.

Keith Grimaldi said...

Do you think that you need to do a bit more analysis before saying that hypothesis #3 is falsified? I'm not a Taubes supporter but in fairness he, and others, do implicate refined carbs and sugars rather than carbs as a class. I would expect that the high carbs content of the early 1900's would have been much lower in these types - is that correct?

Stan (Heretic) said...

Dr.J wrote: My main issue with this debate is that LC works so brilliantly, a virtual magic bullet, for the conditions associated with insulin resistance. Not just overweight, but lipids, BP, PCOS, GERD, etc etc along with a host of inflammatory conditions, too. There is more to this than insulin, LPL and adipocytes. Way more.

Exactly! This was my main reason too behind my decision to post my (mild) criticism of Stephen's article.

We understand now (though not 100% sure) that the highly processed junk food with both junk carbs and junk fats (transfats and veg oils) is most likely behind the obesity and diabetes epidemics in the Western world. I think that some mass conditioning using taste enhancers by food producers etc played a prominent role so Lyle's and Stephen's idea of pleasure traps/food rewarding may have some validity too. We agree that a diet high in unprocessed vegetables and fruit can be quite healthy too but presenting it as _equally_ healthy as a high fat low carb diet
based on natural unprocessed fat, meat fish etc, is like claiming that a bike is as good as a car.

We agree with Stephan that not all carbs are unhealthy but it does not invalidate many links and connections between excessive consumption of carbohydrates, hyperinsulinemia and the ensuing diseases.

No such links have been found (trust me, there were "scientists" who tried _really_ hard...) with the high consumption of animal fat and diseases, even as high as 80% fat as in Kwasniewski's Optimal Diet. I can say it from my experience since I am on it since 1999 (in Poland it was known and used since 1980-ties!) and have studied it extensively ever since.

Lucas,

Breast milk has higher carb contents than that of the Optimal Diet. Optimal Diet is not strictly speaking based on breast milk idea, rather on an initial observation by dr. Kwasniewski that a diet with 35-45% of fat contents is the most fattening and deleterious of all, of the same caloric contents. Thus advice to go higher (or lower) than that.

manthy said...

Nice Stephan, I must say I am in 100% agreement,I think you hit a home run with this.
I love your blog,it is awesome. I have added it to my bookmarks and I will be back and often.
If you want to follow me back you can find me here
http://ismanthyhere.blogspot.com

Paulo said...

Stephan, great great great post!


@Jeff Consiglio


"Most of the bodybuilders I know, who I would consider to often be of much lower IQ's than the erudite commenters found on this blog, are MUCH leaner than most of you."

"They simply RESTRICT CALORIE INTAKE. Some use an LC diet as an "automatic" way to do so. Some use a low fat diet to do it. Others simply count calories."

]

I don't believe CALORIE RESTRICTION is necessary for weight loss. I also don't think OVEREATING will necessarily make someone gain fat (and it may even makes one loses fat)

MY PERSONAL EXPERIENCE:

I've never been fat in my whole life but I lost so much fat by limiting my fructose intake. Before the fructose restriction, my body fat percentage was around 18%. It is now less than 10% (even though I'm not exercising properly due to my crazy work schedule).

I DO NOT LIMIT CALORIES, CARBS AND FATS. I just eat all the REAL FOOD I want and I avoid PUFA's and fructose (maybe a piece of fruit a day, if any). I can see myself easily eating in one sitting almost 2 pounds of mashed potatoes with a whole stick of butter plus a steak. If I don't add that stick of butter to my mashed potatoes, I get sleepy after the meal (not to mention that I like'em together).

Crazy? No! Delicious!

What happens next when I overeat: I feel great, my body temperature goes up and I notice more "poop coming out". That's all. No weight gain whatsoever.


OK OK OK. MY BACKGROUND HELPS ME A LOT.

As a kid, I wouldn't stuff myself with crappy junk food. I don't like sugar (and never did), although I used to have some chocolate and "liquid sugars" (fruit juices and sodas) plus some fruits. That was all the sugar I could stand.

Besides, real food has always been the core of my diet. As a Brazilian, my whole life I've been eating white rice, beans, vegetables and some animal protein for lunch and dinner. For breakfast: eggs, milk and "pão-de-queijo" (traditional Brazilian cheese bread made out of cassava starch - thus gluten free).

Thanks to my mom, butter, lard and palm oil have always been the cooking fats used home.

The changes in my diet: less fruits and no more white sugar, pufa's and gluten (their previous consumption was already minimal).


Any thoughts???

Dan said...

M,

My point is this: "Don't eat carbs" is just a paradigm. "Don't eat refined carbs" is a little better. "Don't eat palatable foods" is another. I've never thought Gary Taubes was right about everything. Hell, I haven't even read the second half of his book.

Sugar and wheat are carbohydrates. If you can't find significant obesity problems without sugar and wheat, and plenty of populations have stayed healthy despite eating plenty of tasty "processed" food (you know, like cheese, pepperoni, bacon, sausage, etc.) then the "low carb" paradigm is more useful than the "low fat" paradigm or the "if it tastes good, spit it out" paradigm. None of them are perfect. But hey, I'm all about redeeming foods that our found to be not inherently bad.

I appreciated the work of Taubes and others because it let me know that I'm not fat because I like beef, and that I can enjoy beef.

If I can enjoy potatoes and rice without regaining significant weight, all the better, especially if I go broke again, it will be nice to have something cheap to eat that I don't feel is killing me. No more ramen noodles.

Taubes was wrong. His hypothesis went beyond what the evidence showed. Big deal. There's little need to make it personal just because he criticized Stephan's hypothesis. Stephan should have been posting this stuff all along.

I think demonizing any hormone in our body is probably a bad thing, since obviously they each serve some useful purpose. I do find it a bit absurd to believe that insulin would make you crave more insulin-stimulating foods and thus would perpetuate its own feedback loop to make you fat, but that doesn't mean that overstimulating insulin over and over every day doesn't lead to insulin resistance or that it's dependent on daily calorie consumption. It just means that insulin doesn't cause you to overstimulate insulin, and that carbohydrates aren't the only foods that stimulate insulin to begin with.

Stuart in Austin said...

Marie Curious ask early in the thread whether it is possible to be lean, muscular, and insulin resistant. I can assure her from my personal experience that the answer is yes.

In my thirties, 20 years before I was diagnosed with diabetes, I ran 1600 miles a year and my BMI was 22.5 but my blood pressure was high, my triglycerides were over 250, and my HDL was 26. These are the symptoms of hepatic insulin resistance. I have always been one of those skinny people who ate more than any of the fat people that I knew.

Paulo said...

Stephan, great great great post!


@Jeff Consiglio


"Most of the bodybuilders I know, who I would consider to often be of much lower IQ's than the erudite commenters found on this blog, are MUCH leaner than most of you."

"They simply RESTRICT CALORIE INTAKE. Some use an LC diet as an "automatic" way to do so. Some use a low fat diet to do it. Others simply count calories."

]

I don't believe CALORIE RESTRICTION is necessary for weight loss. I also don't think OVEREATING will necessarily make someone gain fat (and it may even makes one loses fat)

MY PERSONAL EXPERIENCE:

I've never been fat in my whole life but I lost so much fat by limiting my fructose intake. Before the fructose restriction, my body fat percentage was around 18%. It is now less than 10% (even though I'm not exercising properly due to my crazy work schedule).

I DO NOT LIMIT CALORIES, CARBS AND FATS. I just eat all the REAL FOOD I want and I avoid PUFA's and fructose (maybe a piece of fruit a day, if any). I can see myself easily eating in one sitting almost 2 pounds of mashed potatoes with a whole stick of butter plus a steak. If I don't add that stick of butter to my mashed potatoes, I get sleepy after the meal (not to mention that I like'em together).

Crazy? No! Delicious!

What happens next when I overeat: I feel great, my body temperature goes up and I notice more "poop coming out". That's all. No weight gain whatsoever.


OK OK OK. MY BACKGROUND HELPS ME A LOT.

As a kid, I wouldn't stuff myself with crappy junk food. I don't like sugar (and never did), although I used to have some chocolate and "liquid sugars" (fruit juices and sodas) plus some fruits. That was all the sugar I could stand.

Besides, real food has always been the core of my diet. As a Brazilian, my whole life I've been eating white rice, beans, vegetables and some animal protein for lunch and dinner. For breakfast: eggs, milk and "pão-de-queijo" (traditional Brazilian cheese bread made out of cassava starch - thus gluten free).

Thanks to my mom, butter, lard and palm oil have always been the cooking fats used home.

The changes in my diet: less fruits and no more white sugar, pufa's and gluten (their previous consumption was already minimal).


Any thoughts???

Thomas said...

"I think the best model macronutrients to follow for a healthy human diet is human breast milk."

Consider that there is no "best" macronutrient model for human adults. And, yes, breast milk is best for babies but can this really be extrapolated to adults?

Consider that if there is a best macronutrient ratio then it maybe an individual matter (what makes you feel better). Certainly in the past it was based on food availability.

These days, for healthy people, intake moderation is THE most important factor across all macro ratios IMO (assuming relatively nutritious food is being eaten).

Mark said...

Stephan,

Can we please get away from comparing the diets of sedentary Americans with that of an African tribesman who probably expends more energy exercising in one hour than an American does in a day (or a week)? These are poor comparisons. Exercise affects insulin sensitivity levels. I don't understand why this is ignored on every "paleo" blog (except Health Correlator).

Rebecca Latham said...

"Ok, we get it, you count every gram that passes your lips. But it's quite possible and in fact probable that your low carb calories are overestimated by the sources you rely upon. I am not suggesting you fail to count each morsel, but that the references you use might be flawed."

Fine. In your opinion, I'm either not black, or I'm not a swan.

If there are people who lose weight on low carb and do not on high carb, it disproves any research that's out there, and I understand it completely that you do not want to accept that.

You are forgetting that I am using the same sources for macro counts when I was eating high fat, low carb as when eating low fat, high carb. The numbers are not off, and even if they were slightly off, they are not off with any significance.

Carnivore said...

I am not very familiar with Jimmy Moore but I believe he claims to have lost 'triple digit weight' on low carb. That implies he was probably obese at some time but I'm pretty sure he didn't get that way by eating low carb. If he's experienced some weight gain now, that's a different issue. A previously damaged metabolism, excessive overconsumption of calories coupled with an inactive lifestyle, it could be anything. I'm overconsuming myself by eating 3400 calories/day and it's very much possible that if I somehow manage to increase them to say 4000, that my body will not be able to ramp up my metabolism to match this crazy intake and that I do eventually start to put on some bodyfat. I do believe that there is a limit to which you can 'overeat' and not gain weight, even on low carb, but it would be very difficult for someone to breach this limit under normal circumstances.
I haven't yet come across any example of people actually getting obese without consuming significant amounts of carbohydrates. Already obese people struggling to lose weight after a certain point, that's a different matter.

Rebecca Latham said...

"Fat people don't climb mountains because fat people are tired because they have metabolic disorders.

Lack of climbing mountains or other vigorous activities do not make people fat - but rather, people who have very high insulin and very poor glucose tolerance find that it is too hard to even stand up, never mind CLIMB A MOUNTAIN."

Agree. To paraphrase Taubes, "You are not thin because you climb mountains, you climb mountains because you are thin."

Rebecca Latham said...

@Mirrorball

"It is a well-accepted fact that people eat less on low-carb diets, which neither confirms nor denies the carbohydrate or the food reward hypotheses."

Saying "Everyone know this!" does not make it true.

For the record, I eat more on low carb than I ever did on high carb.

Rebecca Latham said...

@Hornet

"
To all defending Taubes:
You can give 15,000 instances of his hypothesis being right, and if I give just one negating it, than in the scientific world it's falsified.
I really don't see how anyone can truly believe all carbs cause weight gain when there are are several BILLION contradictions walking the earth right now.
Check out the 30 bananas crowd sometime. Those people may not be the perfect vision of health, but they ain't fat!"

If that is true, I am the one case that disproves the theory. If I eat a lot of carbs, I gain weight, which does not happen if I eat low carb.

All that is being proven here is that different people react to carbs in different ways. I'm not claiming that no one is able to lose weight eating lots of carbs - why do you have to claim that the opposite is true?

Saying that everyone who eats high carb will gain weight is uninformed.

Saying that no one loses better on low carb than high carb is also uninformed.

Why is there so much time spent here trying to prove that low carb is not different for some people that high carb, and visa versa.

Taking a stand and saying that all people react to carbs in the same way is uninformed.

Sam Knox said...

This discussion makes me think of Green Day.

They started selling a lot of records and, all of a sudden, they weren't "punk" anymore.

Dr J said...

@ Rebecca - I like the way you think. I can be found if you search My Big Fat Diet.

karl 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

Well duh - someone that is obese has to expend more energy to move and has more muscles to move - more muscles means higher resting metabolism.

I don't recall Taubes ever saying that carbs-vs-fat had to do with lower expenditure - it was starvation diets.

I think you present this as a false dilemma - Just because leptin has a profound effect does not mean that insulin is not involved. It could be that elevated insulin levels at times of leptin resistance has a different effect.

I don't think you have convinced me that insulin is not involved with fat storage.

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)

There is a constant flux of fatty acid in and out of fat cells - obesity means a larger flux. It is the net movement over time that counts.

It is obvious that when given the choice of two food products, the public chooses the one with more sugar to buy. That sugar provides a special food reward via spiking seritonin is not questioned. But I also think that insulin is used to protect the body from excess BG - and the way it does that is, in part, to increase the amount of fat stored.

Rebecca Latham said...

Dr. J

Thanks! You mean the movie My Big Fat Diet? What is your connection with that?

Rebecca Latham said...

@Dr. J

I found your blog. I will read it with interest. Thanks!

karl said...

Perhaps insulin act as a leptin cofactor?


My experience with low carb was weight loss - that stopped at about 18% bodyfat. I ate high gluten/lowcarb wheat products. I easily maintained this weight for 3 years.

When I stopped wheat and maintained teh same carb intake, my body fat went to 15% AND is stable over a years time.

Increasing carbs causes increases in oxLDL - the (only?) type of LDL that causes CAD. One can test oxLDL with a inexpensive blood test.

Postprandial BG is elevated from eating carbs - and it is elevated longer when those carbs are complex and mixed with fiber - and then the insulin stays higher for longer. If I combine this with your claims - one should only eat refined carbs so as to limit the exposure of insulin over the course of a day.. I don't think that is a good idea..

Dave Tate said...

@Mark,

That's a really fascinating question. I don't know the answer but I'd find that sort of study very interesting. Taubes does mention physical activity in GC, BC but is dismissive of the concept of physical activity having any benefit at all, at least according to my recollection. There have been studies that suggest physical activity (I think the studies were focused on resistance training) increases insulin sensitivity.

Rebecca Latham said...

@Dave

To summarize Taubes' view on exercise (and I'm sure I'm oversimplifying here), he says that the number of "calories burned" are insignificant, so that people should not approach exercise in a "I'm going to burn off those extra calories I just ate" way.

But exercise has other benefits and should be used by people. On significant benefit would be an increase in insulin sensitivity, which would be an indirect way of losing weight.

One of his main statements about exercise is that it increases appetite and drives the person to eat enough to "make up for" the energy expended through that exercise.

I have always found this to be true of steady state cardio (which I no longer bother with) but not with lifting weights (which I do hard once per week).

All cardio ever did was make me ravenous, and then I would eat more than I would have had I not done the cardio.

It makes sense - if a body is intent on holding onto its fat stores, trying to burn some of that off would just make the body try to get you to replenish them.

Wolfstriked said...

For me the reason for the obesity epidemic is very VERY easy to understand.You can throw all the science talk into it you want but all of it points to the same theory.We eat too much.....

Why is obesity prevalent now more than in past human civilizations is so easy to understand its silly.How people can take all the Kitavans and Eskimos and whatnot and forget one major factor into their leaness??? These people have to hunt and gather their food everyday.They do not have a choice of....should I eat a Mcdonalds Big Breakfast today or some Dunkin Donuts and a coffee with cream and sugar.Just look at the French who eat a very rich diet in both sugar and fat and stay lean.Why is that.....does anyone here know why?

And you have to ask again why people overlook the reason of why we overeat.How much potatoes can you eat?How much seal can you eat?Not much as body has mechanism for food intake.

But add into the mix the abundance of delicious variety we moderns have.How much cake/pie/pizza/tacos/meat/burgers/chicken nuggets/egg rolls/lo mein/fried rice/chips/soda/nachos etc can you eat?Then think of all the varieties of each foods mentioned out there....my mouth is watering now just thinking about it....and I live above a 7eleven that has killer nachos;)

Wolfstriked said...

Oh and I forgot t post here that we all have various amounts of pleasure to eating and same with sex.My ex GF would always ask me not to moan when I would eat as it irritated her.But food like sex is one super enjoyable aspect of life and a HUGE reason as to why I became obese at 306 pounds.

All these skinny people that eat whatever and stay skinny......jeeez they do not eat much.Just watch one for a few weeks.My workplace is interesting in that the heavy people are always eating and I rarely spot the skinny people eat.

Dave Tate said...

@Rebecca,

Thanks for confirming what I thought I'd read regarding exercise and insulin sensitivity. I recall Taubes looking at the calories in, calories out aspect of exercise and found it wanting.

Rebecca Latham said...

@Wolf,

I did not gain weight from overeating. I ate less and less and got heavier and heavier. That commonly happens to people in middle age, and I am no exception.

Now I eat more. Cutting out the carbs was the way to lose weight without starving to death. I could also lose some weight eating low fat and high carb, but could only eat 1000 calories per day, and it was just not sustainable. Eating 1800 calories a day of high fat and low carb will maintain my weight.

I eating more and not starving.

Rebecca Latham said...

@Wolf

There are many people (mostly male and young) who can eat overeat great quantities of food and not gain weight.

mem said...

Very interestingly, something I have never seen remarked on, much less examined, is the fact that 70% of the Kitavans were SMOKERS.

Now, I have seen this remarked on in another, different vein in the paleo-sphere...that of an insinuation that optimal, healthy, non-industrialized diet might be so powerful that significantly high intake of other known toxins, ie., tobacco and alcohol, might really not matter.

I find it very interesting that the smoking of 70% of Kitavans, in a population that is decidedly not oeverwieght as a whole, but not denied having *some* overweight members, ins't examined in light of what we know about the effects of smoking tobacco.

It is my experience that smokers who quit gain a non-trivial amount of weight. This would be consistent with what we know about nicotine - speeds up metabolism (and apparently this can be markedly greater in those who are non sedentary while smoking )reduces appetite and as Stephan has stated previously in the blog, he believes promotes fat burning.

From a study on smoking cessation:

"Nearly everyone, including the smokers, had gained some weight over the eight years, but those who had succeeded in quitting smoking put on significantly more. Just a quarter of them were at a healthy weight for their height, the researchers found.

Those who had abstained since the original patch trial gained an average of about 8.8 kilograms (nearly 20 pounds), while the current smokers gained just 2.2 kilograms (about five pounds). The relapsed smokers gained 3.3 kilograms (around 7 pounds), and late abstainers who had quit sometime after the original trial put on 8.3 kilograms (18 pounds).

But among abstainers, there were also big differences in weight gain depending on the subjects' original BMIs. Both abstainers who started out underweight and those who were overweight (with average BMIs of 18 and 29, respectively) gained about 10 kilograms, or 22 pounds. Normal-weight people with BMIs of 23 gained slightly less, averaging 7.8 kilograms (17 pounds). But individuals who started out severely obese (BMI of 36) gained 19.4 kilograms, or more than 40 pounds.

For smokers, weight gain went in the opposite direction, with underweight people gaining the most (3.8 kilograms, or 8.5 pounds) and the heaviest people actually losing a bit of weight over time (0.8 kilograms, or about 2 pounds)."

So, those who had abstained since the original patch trail for the entire time, had gained an average of 20lbs. (And you can read the rest for yourself.)

http://www.reuters.com/article/2010/10/21/us-fatter-smokers-idUSTRE69K3SR20101021

I think the follwoing is further interesting as given the cultural differences of Kitavan lifestyle, I think there is an excellent chance that Kitavans are smoking alot while they are non-sedentary, whihc can mean just moving around.

"Smoking while active led to significantly greater increases in energy consumption than did smoking while resting, the researchers found. Smoking increased energy consumption by 6.3 percent when the men were physically active, but by just 3.6 percent when they remained at rest. "

http://www.quitsmokingsupport.com/clearreasons.htm

So here's the obvious question. If the 70% of smoking Kitavans quit, how would that change things?

Might we be seeing a 17 to 20 or more lb weight gain? Where would that place them then on measures of weight and other measures? And if this had been lifelong...Interesting to ponder.

Note: I have pored over the study. I am making an assumption that they are smoking *tobacco* as it is not specified otherwise.

mem said...

Correction: In the previous post I wrote: "I have pored over the study." I meant to write: " I have NOT pored over the study."

Wolfstriked said...

@Rebecca,I agree with you that our metabolisms drop as we age.From loss of muscle mass to a dropping of hormones we are destined to have to eat less and less foods.I also agree that VLC is healthy and great way to have little hunger but also feel its a great way to control calories.

When you drop one macronutrient down your calories drop also.Yes "we" VLC eaters add in alot of fat but we are not matching what we ate before calorie wise.I eat 1600 and lose weight with VLC.Never hungry either.But just look at what 1600cal is in a Burger King meal.My normal BK meal was a DBL whopper medium size at 1600cal.If I was to eat 3 meals a day at BK I would have to eat this.

Meal one....value meal sized fries and a Whopper JR.

This is doable and how the French stay slim but for me it just feels so small and I cant follow it.VLC works for me allowing lower calories with little craving.

Frank said...

Oh well.

It's pointless to argue with someone who use how he feels/ what he thinks/ what he believes/ what he did as evidence of what is probably ''true'', for not having a better word. Especially when we have controlled trial showing what they claim to be true is not replicated in controlled setting.

Could someone adress the studies that i've posted a few comments back and tell me how it's still possible to claim that one can lose more weight if you restrict carbs, irrespective of the calorie deficit, after reading the result of these papers?

Rebecca Latham said...

@Wolf,

In my case, I DID increase my total calories when eating low carb. I did not just drop carbs lower. I increased fat so that now I can eat almost double the amount of total calories than when I was on high carb low fat.

That may not be true for all, but it is true for me and for many other people on the Atkins Community Forum.

Yep. Eating more and losing weight. It does happen. :)

Rebecca Latham said...

"It's pointless to argue with someone who use how he feels/ what he thinks/ what he believes/ what he did as evidence of what is probably ''true'', for not having a better word. Especially when we have controlled trial showing what they claim to be true is not replicated in controlled setting."

My personal experience disproves those studies.

And I agree with you about the pointlessness of arguing about it. You will continue to say "What about the research" and I will continue to say "I disprove that research, and I am not the only one."

We are at a stalemate.da

karl said...

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 do not cause fat accumulation.

Where is the citation for this?

This also misses that not all tissue is equally insulin resistant..

I would love to hear/read this fully debated between Taubes and Stephan.

Rebecca Latham said...

An interesting quote from Dr. J's blog on the subject of exercise while losing weight:

"This is where CBC redeems themselves by reporting on the amazing work of a young South African doctor, Stefan Du Toit, who has been getting people to lose weight in Valemount, BC. Stefan lost about 40 lbs using a very low calorie, low-fat, low-carb diet before moving to Valemount from South Africa a couple of years ago. When staff in his clinic learned of this they asked him to put them on the same diet. It worked so well that patients began asking for it, too. Stefan now has treated over 100 people with this diet approach and has had amazing results. Their total weight loss is over 3000 lbs! The really interesting thing about this, when compared to the approach used in Taylor, is that Stefan expressly forbids his patients to exercise until they have reached their goal weight. He says, accurately in my opinion, that exercising makes dieting more difficult because it stimulates your appetite."

Wolfstriked said...

My original point got lost in the mix.The kitavans eat high carb and are thin.I saw a video once yrs back that showed what a modern dat hunter gatherer group ate.Then men came back with one monkey for the 12 people in the tribe.The women gathered starchy tubers and spent the day preparing them....all 12 of them.

I just feel that many people overlook calories.Jimmy Moore is perfect example f a guy who says he eats this much and then loses weight by "cutting the carbs to zero".I went and added up all his foods for a month while he was gaining and while losing on the egg fest and the calories were perfectly in tune with the weightloss.Yes metabolism slows when you cut calories and his weightloss went from 5 to 1 pound per week.This is where I believe you went wrong with the high carb diet.If you ate half of what you eat now thats 900cal and a severe drop to your metabolism definitely happened.

Dave Tate said...

@mem,

Yes! Everyone mentions the Kitavans as a population that eats a high carb diet yet has little in the way of obesity or CHD. I am not sure if anyone has really investigated the smoking angle. Not to get all Mick Jagger but perhaps they don't smoke the same cigatettes that the tobacco companies in the U.S. sell to Americans? It could be yet another version of the reward theory. Don't the big tobacco companies add ingredients to make their product more addictive?

Dave Tate said...

@Rebecca,

"It worked so well that patients began asking for it, too. Stefan now has treated over 100 people with this diet approach and has had amazing results."

Yeah I remember a doctor that Taubes spoke to that said he had great success with an Atkins like high fat, low carb diet. He said it was so successful they couldn't drive people away with a bat!

Does fat consumption generate as much of an insulin response as protein and carbohydrate?

Kindke said...

@mem

As it would happen this recent study shows that smoking ( nicotine )does infact tickle your POMC neurons,

Tickling your POMC neurons induces sensation of satiety, and according to the study has downstream effects of increased melanocortin 4 receptor signalling.

Have a look here to see what happens if your MC4R signalling completely fails, you become as big as a bus REGARDLESS of "calories in calories out."

Rebecca Latham said...

Evidently, fat does not promote an insulin response. Carbs and protein do.

karl said...

Re: Rebecca Latham

Evidently, fat does not promote an insulin response. Carbs and protein do.

Not quite true - they both can increase insulin - but carbs do much more. Carbs also spike trygly - and that is thought to cause leptin resistance.

Carbs also increase average BG which increases many cancers and oxLDL.

Stephan claims - but offers no citation:

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 do not cause fat accumulation.


I don't think this is true. My hunch is that leptin and insulin are cofactors.

karl said...

Argh - did Stephan read this one of his Citations?

http://www.ncbi.nlm.nih.gov/pubmed/12609497

And the insulin injection study was into the brain - I don't think insulin creates hunger in the brain - it is the effect of lowered BG that makes people hungry.

http://www.ncbi.nlm.nih.gov/pubmed/116135

Some of the other studies he sites have been debunked elsewhere. The meta studies are worthless. and many of these are based on a single meal.

That Leptin is involved does not mean that insulin is not involved. I saw no referenced study that shows that the change in insulin response from low carb diets fails to produce weight lose.

There are two cases two consider: one is average insulin - does it matter (long term of course). No citation supports Stephans claim.

The second case is insulin response - low carb reduces insulin resistance - more glucose is taken up by muscles rather than fat.

This is a long term effect that a single meal study is not going to reveal.

Re: genetics - It can't be all genetics - look at class pictures from the '40s and '50s - same genetic stock was slim.

Stephan - you can do better than this.

maurile said...

Here is the article Lustig cited on his slide stating that hyperinsulinaemia may cause leptin resistance.

http://www.ncbi.nlm.nih.gov/pubmed/11596667

Any comments?

Frank said...

Indeed Rebecca, we should also start prescribing drugs base on anecdocte, do brain chirurgy on how we feel about it, and actually we should stop using science altogheter since what we do is so much more revelant.

Medecine books should be based on what people did to heal themselves, not on our scientific understanding of human physio-pathology.

From now on, anecdocte shall be the ultimate evidence.

Rebecca, i'm eating McDonald twice a week since the beggining of the summer; my diet is highly high-carb, i'm drinkin soda lately because I feel like it. My diet is very crappy since a few month actually.

Yet, since i'm having access to a DXA at our research center and that I take my body composition every month or so, I know that 2 weeks ago I was at 6.7% fat. I was at 7.8% 2 months ago, when my diet was actually better (less refined crap).

All of that is true. And that mean that my situation disprove your hypothesis that carbs makes one fat, since anecdote are the ultimate evidence.

karl said...

maurile -

Interesting paper - pretty much refutes Stephans thesis that insulin is not involved with appetite.

He also mentions 'amylin' but blurs the idea that amylin is a cofactor of leptin AND insulin. I can't find the half life of amylin - but insulin is short and leptin is long. That carbohydrates stimulate appetite 6 -8 hours latter might be explained by this.

Both insulin and leptin control the net flux going into adipose tissue .. this is more complication by amylin that seems to be a leptin co-factor that is secreted with insulin. Amylin also contributes to BG control - and BG also effects appetite.

Stephan has to show a lot more to take insulin out of the appetite picture.

Rebecca Latham said...

"I do not believe that obesity is caused by gluttony or sloth, but I do believe it results predominantly from food choices, which do eventually lead to energy imbalance due to alterations in the homeostatic mechanism." Stephan Guyenet

For all those who are saying that they believe Stephan, they should consider this quote from him when they say that all people have to do is cut down the amount of food they eat and they will lose weight, that is, unless they want to disobey the Laws of Thermodynamics.

Rebecca Latham said...

Frank,

I have been civil and factual about my experiences in everything I have said. To put ridiculous words in my mouth that I have not said or implied is the height of immaturity. In the childish department, you just won.

InNewOrleans said...

@Woo,

Thank you for replying, but I feel like your response to my post twisted a few things and made some assumptions in order for you to make the point you wanted to make.

I never said that I thought calorie restriction or anorexia caused PCOS. I was clear in my post that insulin resistance causes PCOS, and that I do believe there is a great deal of genetic variation in the tendency to develop insulin resistance. Not all women who are insulin resistance will develop PCOS, as you point out, but all women who develop PCOS do so because of insulin resistance. We both agree on this. Many, many women who develop PCOS have a history of dieting and calorie restriction in an attempt to control their spiralling weight. This was the case for me. So there is correlation between the two, but that doesn't mean causation.

You responded, "It's extremely rare that PCOS would vanish simply by exercising." As I said in my post, I don't know that it was the only factor. I strongly feel that it contributed, and I tried to describe why I think it contributed. If the underlying cause of PCOS is insulin resistance, and if the insulin resistance is reversed, it is absolutely possible for PCOS to vanish. It took years for me, but it did resolve.

Also, I've never taken depakote. I've taken very few prescription medications ever in my life other than BCP for the first few years after being diagnosed with PCOS. I go back and forth on whether I think it helped balance things out or just prolonged the imbalance. I took ortho-triclen, which had more binding globulin. I think this is a bigger factor in improving symptoms for women with PCOS than the type of progesterone. The FDA should not allow products like Yasmin and the newer Yaz to be promoted as being good for PCOS. My doctor switched me to Yasmin back in the day based on the marketing pitch from the pharmaceutical rep. It was horrible. Ortho Tricyclen may have been a factor in controlling the excess hormone levels, thereby helping me improve the underlying insulin resistance. As you know, the higher hormones lead to more insulin resistance, which leads to more hormones, etc. I don't discount the possibility of other factors, as well.

The one and only point I was trying to make with my post is that people like you and Stephan, who obviously both know a great deal about nutrition/obesity and tend to lack perspective exactly where the other doesn't, can and should be collaborating. There is a lot in your points of view that is reconcilable. The statement "insulin resistance is very bad for you and leads to obesity," a point on which we both agree, does not logically lead to the conclusion that the solution for obesity is to eliminate carbs or to the conclusion that insulin resistance could not be reversed. There are a lot of logical steps in between that have not been sufficiently studied. Insulin resistance is an adaptive response to something. What? Who knows. The body is very good at regulating pathways up and down in response to various stimuli. Maybe, per the Dr. Kruse article someone posted earlier, it is all about Mg. I am skeptical. But that is something worth looking into. I can wrap my head around the idea that it is simply a matter of genetically being "broken" and unable to process carbs for a very small percentage of the population. But when considering the growing obesity problems in the developed world, the growing number of women with PCOS, etc., I simply do not buy that low-carb is the end solution. It is a temporary solution at best.

InNewOrleans said...

Aso, it is interesting that you mention inositol. I supplemented with choline/inositol for several years and then with DCI when it became available. But I have not supplemented for over a year now with no noticeable effect on my carb tolerance. I think the shortage of inositol is not genetic in at least some women who develop PCOS. I think it is possibly just one more example of the body producing too much of this, too little of that when things are out of balance.

As for mental issues, HPA dysfunction is strongly correlated with calorie restriction. I was not depressed before I started dieting in an attempt to escape the family obesity curse and have not been depressed since my HPA function improved.

Mark said...

Rebecca Latham wrote:

"This is where CBC redeems themselves by reporting on the amazing work of a young South African doctor, Stefan Du Toit, who has been getting people to lose weight in Valemount, BC. Stefan lost about 40 lbs using a very low calorie, low-fat, low-carb diet before moving to Valemount from South Africa a couple of years ago."

Well, yes, I have no doubts this worked. Just as I'm sure that the diet the camp guards devised at Auschwitz caused weight loss independent of the prisoner's physical activity. Both were starvation diets.

I've been reading this blog and every other paleo blog for the past (jeez...has it been 4 years?) and I have come to believe that the "paleo" blogs are ignoring some "unpleasant truths" that must be confronted before we can move forward to understande the obesity epidemic:

1) Exercise more likely than not assists with weight loss. I agree with Taubes that it can stimulate appetite. I agree that it goes beyond calories-in/calories-out. But *something* beneficial happens from exercise. I find walking and weight training helps me lose weight the most. Running just makes me hungry. Perhaps one needs to exercise but keep cortisol in check. Perhaps running pumps up cortisol too much.

2) In the history of the world, most people went hungry. My grandmother often spoke of going to bed hungry during the Depression. That wasn't that long ago. The farm had no food that day, guess what? You starved. She spoke about it all the time. Today we believe food comes from Safeway and Whole Foods.

3) 50 years ago most Americans did manual labor for a living. My grandfather built houses for a living. He did it with one other man. It was exhausting. Today I push a mouse around on a computer. The idea that our respective occupations doesn't affect the fact that he looked like he was carved out of wood and me out of cookie dough is flat out delusion.

4) Exercise does affect insulin sensitivy. Carbs *can* be a problem if you don't exercise.

http://www.sciencedaily.com/releases/2009/09/090901082406.htm

http://www.medscape.org/viewarticle/438372

5) We can't compare macronutrient consumption of today vs. 100 years ago. Older generations ate *far* more vegetables than we do. If I had to guess, Generation X and beyond consumes FAR more high-carbohydrate foods than older generations. We wolf down granola, cereal, pasta, rice, and bread with glee. check out what thin old people eat: veggies, cheese, meat, and more potatoes than cereals. Non-processed, lower in carbs. Ever see a 20 year old order a grilled cheese and a black coffee at a diner? No, exactly. But that's what my grandparents would order. Perhaps light up a cigarette afterwards. (Not healthy, true. But they were thin.)

6) Fat is more likely than not more easily converted into body fat.

7) Fat is the most satiating macronutrient.

8) Most people can't get their heads around the ideas expressed in 6 & 7 and why eating a little more fat probably helps with weight loss.

Simple Mama said...

Any thoughts on this recent study
http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.2414.html

I don't have access, and I'm assuming the fats used are junk...my husband forwarded the link to me.

Rob said...

Hey Mark,

Protein is actually the most satiating.

http://www.ncbi.nlm.nih.gov/pubmed/18469287

Paul Jaminet wrote a good post about it.

http://perfecthealthdiet.com/?p=2046

karl said...

Simple Mama -
I think you are correct - the so-called hi-fat diet they use in these mouse studies have used crisco (read transfat made from vegetable oil - no problem for Nature (do not trust Nature papers)).

Anyway - mice are herbivores - they normally eat a very low fat diet - even the standard mouse diet is not normal for them - it contains too much fat and refined sugar.

How much of the mouse science is invalid due to the weird diets they feed them is anyones guess.

Stan (Heretic) said...

M. wrote: A billion or so people in Asia kind of shows that the Carbohydrate Hypothesis is crap. If people do fine on white rice, then switch to an industrial diet and encounter problems, the question should be what is wrong with the industrial diet. Do you not see the scientific absurdity of framing it around all around "carbs"? The only reason people do this is because they are stuck in a “carbs” paradigm.

Absolutely not!

Billions of people in Asia remain lean eating rice because rice is relatively low caloric density (~20% carbs, boiled rice) and thus harder to overeat. Much lower glycemic load than the Western staple wheat product: bread (70% carbs). Asians do not overeat rice, also due to traditiona: rice is served there typically in a small dessert-size bowls as an add-on rather than the main dish; they generally do not overeat it. What happens when they do overeat it consuming thousands of calories per day out of rice, can be seen in this picture.

Lack of problems with certain low caloric high carb diets in some populations does not automatically falsify the carb hypothesis as per Taubes' book. For the same reason that the Chinese Study showing tobacco smokers being healthier than non-smokers does not falsify the theory that smoking is a health hazard.

If Stephan wanted to falsify Taubes by proving that the carbs are not the main cause, then he ought to show counter-examples among populations consuming HIGH (not low) caloric high carbohydrate diets and compare them against age and income matched populations on HIGH (equal) caloric medium carbohydrate or HIGH (equal) caloric low carbohydrate diets.

Stephan, I think you should seriously consider Dan's advise regarding forming first some logically consistent definitions of the "food rewarding" property, if this research is going to carry any weight.

Stan (Heretic)

mem said...

Dave Tate,
The additives in cigarettes do things like make the cigarettes burn faster (so you'll smoke more and buy more!) and there are flavorings and other stuff in othe ones that haven't removed them. But the NICOTINE is what acts on the brain to induce the eating related effects and lipolysis. Nicotine is what is always studied in research. It is acknowleged that it isn't the nicotine that is so health hazardous but the soup of other chemicals and tars that are inhaled.

mem said...

Kindke,

Thanks for the great and very recent research link. I really like the detail and the specific breakdown that my link gave as well.

The other link was so very sad. I hope that they will be able to help her.

M. said...

Stan,

Like I said, it is not that they are lean on white rice; it is that they are “carb-adjusted” but still have problems when industrial diet is introduced. The “insulin spike” from white rice isn’t much different than the “insulin spike” from wheat. They can handle “insulin spikes” from white rice, but apparently not from wheat or whatever comes with an Industrial / Western diet. Whether “carb-adjusted” or not, introduction of an Industrial/Western diet seems to destroy health.

“Carbs” and “insulin spikes” does not seem to be the right direction, and Taubes’ Carbohydrate Hypothesis does not seem to be at work. It seems like Industrial Diet or Western Diet or Refined Wheat and Sugar or "whatever" might be the issue instead of “carbs” and “insulin spikes”. It might not be falsification of Taubes’ hypothesis, but it seems to be strong indication that something else is going on.

When you have to start talking about “this carb” (white rice) doing this and “that carb” (wheat) doing that, why bother speaking in terms of “carbs”? Speaking in terms of the negative aspects of modern diet (NADs for example) seems more precise.

There might be something to the idea of “Glycemic Load,” but it seems to have a lot of confounders. You yourself were speaking about caloric density and overeating, but that is not very Taubesian. Many modern foods with high glycemic load are manufactured for food reward and include NADs. Glycemic load would also depend on meals, not individual food items. Bread is dry, so people drink more water while they eat it or butter it up or both.

I think “carbs”, especially in terms of Taubes’ Carohydrate Hypothesis, is just not very accurate or precise way to be looking at the problems of modern diets.

ItsTheWooo2 said...

@malpaz:
and odd you mention genetics, my family IS CHOCK FULL of fat people and diabetics and ladies withh PCOS.

As I said to INOrleans, it's highly likely, malpaz, that your glucose disorder and PCOS is not caused by your anorexia, but rather, your underlying metabolic issues are behind everything else (your PCOS, your weight troubles, your proneness to starvation, your mood troubles). If your family is full of obese women with PCOS, then if you also find you are obese with PCOS, what makes you think your anorexia caused it? Much more likely that your anorexia is probably a result of having an underlying metabolic disorder which causes mood/motivational disturbances resulting in anorexia.

If you don't process glucose normally, if a "normal" carb diet causes depression and listlessness, if starving makes you feel better, it is only logical that a person will starve themselves. However, you can't starve forever. When eating "normally" the person finds they develop weight and endocrine disorders.

Most research seems to suggests that restrictive type anorexia nervosa is related to excessive serotonin activity in a brain, with a perturbation of reward feedback from food, even normal hunger. I have spoken with many anorexic people online, the overwhelming majority of restrictive anorexics never are overweight, and have difficulty gaining weight.

With binge / purge anorexia, or anorexia where there is a problem with binging, or when there is a history of weight gain, then the reverse is true and it is quite common for there to be glucose problems.


PCOS is a genetic disorder, in its pure form. There is no way to "cause" PCOS, no matter how stressed or fat or glucose intolerant a woman is, she will never have PCOS if she does not have the genes for it. The only way to cause PCOS in a person who does not have the genes for it, is to take medications which mimic the genetic defects that cause PCOS... for example, depakote will cause PCOS in normal healthy women because depakote disrupts inostiol synthesis, and a lack of inositol is at the heart of PCOS.

ItsTheWooo2 said...

@Stargazey

Jimmy Moore is by far thinner after adopting a very low carb diet. Just because JImmy Moore has not been able to completely cure his obesity - none of us really can, actually - does not mean that the low carb diet causes obesity.

If Jimmy Moore was given leptin at a replacement dose I highly suspect he would instantly lose his body fat and eat far fewer calories. His muscle mass would increase, his body fat layer would thin, his mood would improve and he would lose his cravings for junk food.

It's too bad we have idiots spreading the idea that leptin is bad for fat people, and that they are "leptin resistant", so poor jimmy will never see this medication in his lifetime. He will keep struggling with hunger , food obsession, and a high body fat level in spite of diligent attempts to be good. His leptin level is probably quite low relative to his body fat.

Sudarsan said...

Stephan,

In one of your previous articles you mentioned about fasting insulin and said that having a low fasting insulin between 2 to 6 is good for fat loss.. You also mentioned about the non industrialized cultures having low fasting insulin even at higher age groups
I am just curious to know how that article fits with what you mentioned in this?.

Thanks

stereodemon said...

Sweet potatos boiled are GI of: 44

Potatos with skin boiled GI of: 67

http://www.glycemicindex.com/

shortrib said...

This all reminds me of talking to overweight people about diets. They will drone on about complex carbs, low-fat, moderation, vegetarianism, breakfast-is-the-most-important-meal-of-the-day, high fiber, whole foods, low sodium, evil red meat, angelic boneless chicken breasts, emotional eating, and how a low-carb diet doesn't work. Meanwhile, the healthy-weight, low-carber is there, right in front of them, evidence they choose to ignore.

No wonder Gary Taubes was cranky. It's just more of the same kind of thinking that got us into the obesity crisis in the first place.

Reijo said...

This port was needed, thank you!

Complex carbs are less fattening partly because they contain substantial amount "low digestable carbohydrates". These include:
-resistant starch (RS)
-fructans (ie. inulin etc)
-polyols (sorbitol, xylitol etc.)
-galactans
-fructose (almost 50 % of population are fructose intolerant)

Energy value of RS, polyols, fructans etc. is 1,5 -2,5 kcal/g, NOT 4 kcal/g as for sugar or "normal" starch As these carbs are fermented in colon, they also induce SCFA production, which improves satiety.

Apart from leptin and insulin, grehlin, PPY and GLP-1 are very important determinant of satiety and can be manipulated by nutrients, like protein and carbs.

Dan said...
This comment has been removed by the author.
ItsTheWooo2 said...

@Melchior
We can eat fruits tubers and honey, and still maintain a low carb level.
Anytime I have ever seen a paleo diet used, the end macronutrient ratios are low carb. Paleo diets emphasize meat, nuts, and green veggies, with some fruit and tubers. Tubers, by the way, are relatively low in starch assuming they are not processed.
I have never seen a paleo diet where the ratios for carb/fat/protein were *anything* like a modern diet or even a mediterranean diet.
I have decided a paleo diet is basically a more politically correct word for a low carb diet. When you are too afraid to admit you low carb, call it paleo and suddenly its medically respectable, and no one is going to lecture you about how you need to eat carbs to feed your brainz or your kidneys will asplode.

If you are a glucose intolerant person who adopts an ad lib low carb diet, there will always be a spontaneous reduction in calories due to the lack of insulin to stimulate fat gain and feeding. Not all low carb diets are CR, but almost always is there a relative reduction in calories for people who are glucose intolerant, and those are the very people who are at risk for progressive worsening of glucose intolerance.

HEY KIDS, want to grow new mitochondria and avoid insulin resistance therebywhich? Want to know how? EAT LESS. Glucose and fat damage mitochondria; the less you subject your cells to this, the better your energy generating potential and thus insulin sensitivity.
This is why it is often observed that extended time on a LC diet results in improved carb tolerance, not worsening carb tolerance.


That low carb diets cause permanently reduced carb tolerance is pure hearsay and myth.

ItsTheWooo2 said...

@InNewOrleans


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

That would be like if I had type I diabetes and I was arguing that I was cured by bananas... but oh wait I did use insulin for like, 2 years.

DCI and choline/inositol will absolutely help if not cure PCOS. THe cure rate has been as high as 90 something percent when using DCI in studies. It's pretty clear cut that the heart of PCOS is a lack of DCI, although a whole lot more trigger/exacerbate it.


I find it hard to believe your mental state was totally normal while developing anorexia. Yes, as a depressive, I can affirm that being entrenched in starvation and hyperactive HPA will worsen and trigger bad depressions... but I've never met a totally mentally normal person who suddenly randomly developed an eating disorder like anorexia. There was almost always some kind of anxiety, OCD, depression type issue going on before, or at least a strong vulnerability to it.

James Kimbell said...

Rebecca,

You can tell us your experience, and we can quibble about whether the caloric estimates are right. (I have no idea, but it's possible that the commonly consulted sources are off in some way.)

But let's assume you are eating exactly as many calories as you calculate. That still doesn't reach across time and space and invalidate a study - which is, surely, even more accurate in its calculations. It may be that those people got one result and you get another result, and the reasons for that may be interesting, but don't say that your result "disproves" theirs. It might "disprove" their conclusion if their conclusion was too broad of a generalization, but come on.

Paolo said...

I can't believe how much energy and intelligence is spent on this discussion. The truth is that low carb diet are great to lose weight but are not necessary NOT to gain it. And everybody should it what they like (avoiding agents of disease of course) and not rely on scientific studies.

Rebecca Latham said...

@Stan

"Billions of people in Asia remain lean eating rice because rice is relatively low caloric density (~20% carbs, boiled rice) and thus harder to overeat. Much lower glycemic load than the Western staple wheat product: bread (70% carbs). Asians do not overeat rice, also due to traditiona: rice is served there typically in a small dessert-size bowls as an add-on rather than the main dish; they generally do not overeat it. What happens when they do overeat it consuming thousands of calories per day out of rice, can be seen in this picture.

Lack of problems with certain low caloric high carb diets in some populations does not automatically falsify the carb hypothesis as per Taubes' book. For the same reason that the Chinese Study showing tobacco smokers being healthier than non-smokers does not falsify the theory that smoking is a health hazard."

Excellent point.

CarbSane said...

@ItsTheWooo2: Rather than calling people who deal with leptin resistance "idiots" and presuming Jimmy Moore has low leptin and feeling sorry for his predicament, why not write him and ask if he's ever had his leptin levels measured.

In January of this year JM re-lost a lot of weight by cutting all frankenfoods from his diet and eating just beef, CO and eggs. He even continued to lose weight when he added in some sf dark chocolate. He was reporting no cravings or hunger despite eating WAY less than he usually does. Why he started in on the Atkins bars, eating small amounts of veggies drowned in butter or dressing, futzing with bread&butter and sweet potato fries to test "adding in carbs" on top of his increased LC intake can hardly be pinned on leptin.

@Paolo: LC does not work for everyone, and it works to a limited extent for many (one might even say most) over the long term. It is important to dispel myths that keep folks from banging their heads against the wall doing the same thing and expecting a different result because they think eating rice is going to make them fat and diabetic.

Rebecca Latham said...

@ItsTheWooo2

"If Jimmy Moore was given leptin at a replacement dose I highly suspect he would instantly lose his body fat and eat far fewer calories. His muscle mass would increase, his body fat layer would thin, his mood would improve and he would lose his cravings for junk food.

It's too bad we have idiots spreading the idea that leptin is bad for fat people, and that they are "leptin resistant", so poor jimmy will never see this medication in his lifetime. He will keep struggling with hunger , food obsession, and a high body fat level in spite of diligent attempts to be good. His leptin level is probably quite low relative to his body fat."

I'm just starting to learn about leptin. I know there is a blood test that will show if you are low or high leptin. If Jimmy had that test, and it showed that he was already high leptin, would that not show that he does NOT need more, but is leptin resistant? If so, giving him more leptin would not be a solution for him.

On the other hand, if the test showed he was low, then supplementing leptin would help, I would think.

Please explain... Am I missing something? Thanks!

Rebecca Latham said...

@Dan

"Frank,

You know that Rebecca knows what her energy output is because she knows her energy input, right? Does it just fly right past you that if you are maintaining weight that energy out = energy in? So, the question is, why is she able to output so much more energy on low carb?

N=1 experimentation proves that your advice for the population doesn't apply to that one person, and you can't put your fingers in your ears and pretend that there's no difference in isocaloric diets."

The voice of reason. Thanks, Dan!

Rebecca Latham said...

@James Kimbell

"You can tell us your experience, and we can quibble about whether the caloric estimates are right. (I have no idea, but it's possible that the commonly consulted sources are off in some way.)

But let's assume you are eating exactly as many calories as you calculate. That still doesn't reach across time and space and invalidate a study - which is, surely, even more accurate in its calculations. It may be that those people got one result and you get another result, and the reasons for that may be interesting, but don't say that your result "disproves" theirs. It might "disprove" their conclusion if their conclusion was too broad of a generalization, but come on."

Then let me rephrase: If there is a study out there that says that, given the same amount of calories, either high carb low fat or low carb high fat, will cause identical weight loss, gain or maintenance in the same person, and in EVERY person, then my experience disproves that theory.

On your other point about my accuracy, if I was saying that I changed my macros and calories by a small degree, I could see where someone could say that I was just miscalculating my intake.

But my numbers are so greatly different that my results cannot be chalked up to miscalculating fractions.

On the Zone (before going low carb), here is what I, a 5'3" woman, ate:

1000 calories
33.3g fat (30%)
75g protein (30%)
100g carbs (40%)

If I maintained my weight on that, then it stands to reason that if I increased my calories by 180%, I should gain weight, right?

1800 calories
140g fat (70%)
100g protein (22.2%)
35g carbs (7.8%)

I achieved "energy balance" eating both of these ways at the same body weight. If all calories are equal, when I switched to high fat low carb, I should have gained 1.6 pounds per week, every week. If that were true, I would now weigh just over 200 pounds. My weight this morning is 144 pounds, within a pound or two of what it was when I was doing "The Zone".

If I used too broad of terms, I apologize for that. But there are people here who are saying that my results are not scientifically possible, and that's just plain silly.

I OBVIOUSLY "burn" more calories when doing low carb high fat than when I do high carb low fat. There is a metabolic advantage to eating this way, at least for me, and any research that says that this is impossible has reached a faulty conclusion.

Rebecca Latham said...

@ Paolo

"The truth is that low carb diet are great to lose weight but are not necessary NOT to gain it. And everybody should it what they like (avoiding agents of disease of course) and not rely on scientific studies."

Exactly. I'm not a scientist or even a researcher, but I know what is happening to my body, and for someone to say "That's not happening to you!" is just plain silly.

At the end of the day, all scientific studies aside, we have to take responsibility for our own health and eat the way we believe we should, and hopefully, that will help us achieve a normal body composition and a disease-free state. If I eat the way I think I should and I achieve my goals, for someone to say that it is "off" in some way because it disagrees with some study somewhere, is just, well, what would be a good word for that? Oh, yeah. Silly.

I think my approach is balanced. I can agree that for some people, calories matter. For some people, they don't. For some people, they can lose weight on an isocaloric diet, regardless of the macro makeup. For some people, it needs to be low carb for it to work, and for some people, it may be low fat.

Where I have a problem is the dogmatism that says that we are all the same and what works for someone else must work for me, and if it doesn't, it means I am either lying or deluding myself.

Here's where I say, "Come on!"

gunther gatherer said...

I'd just like to know what DOES cause diseases of civilization if it isn't carbs.

I'll take a stab at what Stephan might say: Is it mineral deficiency?

Melchior Meijer said...

Gunther,

FWIW, I bet on too much energy in. Full circle round. Calorie intake seems to be the greatest confounder in all the confusing and 'contradicting' observations. The old Luigi Carnaro was right ;-).

NAD's seem to somehow mess with our appetite regulation, therefore a 'paleo' diet (and to a certain extend LCHF) makes 'calorie restriction' (and thus becoming healthier) easier.

Beth@WeightMaven said...

Nice comment from Matt Stone on this:

"Obesity is caused by a large combination of things. The typical obese person did not become obese by eating to appetite of a diet of boiled potatoes, fruits, and lentils. Nor did they do it eating a boring diet of hard-boiled eggs, bacon, cheddar cheese, and steak. The trigger of obesity is highly individual and extraordinarily complex – even multi-generational. Hopefully this will help to end the foolish bun vs. burger game. The only way to win that game is not to play."

Read the whole post for the rest.

Dr. N said...

I find discussions of this sort lead to confusion when the discussion is not restricted to a specific patient (i.e., individuals eating historically native foods, recent Americans without evidence of insulin resistance, obese indivduals, lean individuals with evidence of insulin resistance).

For example, I don't find any discussion about Katavians (who have been eating a native diet) particularly useful when I am dealing with my T2DM patients.

The scienctific studies/explanations for one population is not necessarily applicable to others when some are healthy and others are not.

In my pratcial experience, carbohydrate restriction is critical in the management of T2DM. But this does not mean that excess carbohydrates were the cause of the T2DM in formerly healthy individuals.

Long discussions such as this one only serve to further confusion the topic without the discussion being more restrictive and focused in nature.

Evan said...

Stephan, very interesting post, but to all the back-slappers and coffin-nailers: really?really? One blog post (from a very sharp and well-informed fellow) takes down 500 pages and 10 years of research? Stephan has presented an hypothesis, just as Taubes has presented one, so let's test them (I believe I have heard GT outline a clinical study to test his hypothesis and has said that he would admit that he has misinterpreted the literature if the results suggested that).

karl said...

OK it appears that this blog is really about this:

http://www.dietdoctor.com/ahs-showdown-gary-taubes-vs-stephan-guyenet

Taubes came on to strong - Stephan got hurt and is now gunning for Taubes

Stephan - this does not help further the science. I think you have hurt yourself with this blog.

Food reward is obviously involved (why else is sugar now in every box food ?).

But appetite is a learned behavior that involves many things - including insulin.

James Kimbell said...

Rebecca,

If I held a heavy object in one hand and lighter object (of the same size and shape) in my other hand, I would think that the heavy object falls faster. Even if I dropped them and watched, I would probably think that.

And even if I heard of controlled studies that showed the opposite, I still might think the objects fall differently.

But I'd be wrong, and I couldn't expect people to believe me when I said my experience disproved those studies.

I'm not trying to be snarky, or to say you're crazy, or even to say you're wrong. I actually think you are right in a general sense - that calories from one diet are used differently than calories from another, and that some would be stored as fat and some would be used in other ways.

But that's not the point. The point is that one person's experience doesn't trump a study - which is, after all, just lots of people's experiences, controlled and compiled and measured. Maybe your diet has a different number of calories than you think. Maybe it doesn't. Maybe your body temperature is higher now than it was on the other diet. Maybe it's not. Maybe carbs are the difference. Maybe they're not. Maybe - in fact, probably - there are important factors we haven't thought of. We don't know, and if all we do is stick with our own experiences, we'll never know.

Wolfstriked said...

Someone posted about people who were lean in the 40s and 50s and being the same genetic stock as us.I feel the reason is the amount of foods we eat nowadays.Back then you ate breakfast lunch and dinner and kids would buy candy with what little money they could beg.Nowadays we have stores filled to the rim with high calorie foods that are cheap and large portioned to boot.I mean look at cola consumption in the 50s to today.I remember when the cups started getting larger and larger until we hit the motherlode MEGA BIG GULP at like a gallon of soda for 2 bucks.Since I wasn't around in that time I am just guessing here but people who were can fill in the info.

And I do believe that the lower the insulin the better the fatburning of the body.I see it in my own body very well.Calories count but so does insulin.It amazes me that doctors in this top notch country do not test insulin levels.Hyperinsulemia is a great test to show how bad/good your body will be at burning fat.If someone shows up as very hyperinsulemic then I would suggest the very high fat diet with carbs and protein both at 40 to 60gms per day.If you do not show bad then I would suggest a normal diet and if your slightly hyperinsulemic then I would suggest regular low carb with as much meats as needed for satiety.But alas I am not a doc.;)

ItsTheWooo2 said...

@Rebecca
If Jimmy were to have a blood test which came back showing that his leptin was high (I seriously doubt this, unless he was actively gaining body fat due to unbalanced blood sugar and high insulin)... that may indicate he had leptin resistance. Or, more likely, it would just indicate that when he had his leptin measured, his insulin was high and his glucose was not well controlled due to eating a lot of carbs that his glucose intolerance renders him unable to process.

When fat people are found to have very high leptin, combined with very high body fat, the scientific community makes a massive leap of logic and states, without much evidence, that they are leptin resistant. However, what they fail to realize is that leptin has nothing to do with glucose intolerance, hyperinsulinemic obesity. THe high leptin found in obesity is just a passive sign that they are disturbed and have a gross imbalance of fat metabolism - far too much in, not enough out. The very high leptin found in obese individuals only shows that their fat cells are in a positive balance (duh) and it shows that their insulin levels are very high (duh) and it also shows that their fat cells are both numerous and large (duh again). Nothing else at ALL can be inferred by the finding of hyperleptinemia in obesity.

There is no direction of causation when observing that a fat person has very high leptin. It is a flight of fancy to assume the high leptin, and high body fat, is a resistance to leptin.

This is also how people make the mistake of assuming that a high metabolic rate protects against obesity. Stephan pointed out, above, that fatties have high resting metabolic rates, at least in garden variety obesity. This is true, but there is no relationship between body fat growth and high or low metabolism. Body fat growth occurs independently of metabolic rate, although in normal physiology body fat growth will INDUCE a higher metabolic rate. Why is that? Because insulin upregulates thyroid activity, so does leptin. So a fat person who is actively growing fatter due to uncontrolled metabolic disease will find their fat tissue is expanding, but their T3 levels are also very high. This is why fat people so often appear hyperthyroid - sweating alot, anxious, uncomfortable, complaining of being hot all the time, high BP. Their very high insulin jacks up their thyroid hormone and their sympathetic nervous system. However, their very high insulin also makes body fat grow pretty well.

There are obesities found with a low metabolic rate (e.g. primary hypothyroidism) but the common person who is obese will observe higher T3 levels and complaints of hypermetabolism along with growing body fat. These are not mutually exclusive and it is a cavernous leap of logic to assume that having more T3 will automatically lower body fat, without being combined with an insulin control/glucose control diet or medication.

M. said...

Evan said: “really?really? One blog post (from a very sharp and well-informed fellow) takes down 500 pages and 10 years of research?”

You sound just like a vegan defending The China Study…

Asim said...

Hey all,

I'm not a scientist, but most people seem to be neglecting a pretty-well established fact in regards to obesity, especially as it relates to insulin resistance.

Thos that are obese have a higher state of INFLAMMATION, because of the presence of macrophages within the fatty tissue. In fact, according to what I have read, this presence makes up a significant portion of the weight. At the same time, evidence is clearly mounting with respect to the relationship between the immune system and endocrine functions, such as insulin.

http://www.scientificamerican.com/article.cfm?id=inflammatory-clues

The reality is that in over-eating of any kind, when fatty cells grow to big because of EXCESS energy intake, they eventually saturate and die. Macrophages then come to the site to clean it up. In a person that is particular obese, the problem compounds leading to malfucntioning of the overall system, whether leptin or insuling signalling. CRP inhibits leptin signalling.

http://www.genego.com/map_718.php

There are other ways in which inflammation may be created, amongst them, as pointed out by Dr. Ayers, is superxide production. This would increase the overall state of inflammation.

It is this inflammation that scientists posit as the basis of many if the metabolic disorders that one is seeing as prevalent.

IMO, traditional societies, no matter what they ate, their overall approach was generally sound in not the macronutrients approach, but the overall life style. They would have eaten foods that incorporated a diverse gut flora, the implication being the impact of a particular type of food on their immune system as it releates to the gut flora, would develop more properly. It is precisely this gut flora that allows for the DIVERSITY IN TEH HUMAN DIET. The traditional cultures also ate whole foods, meaning their body wasn't submerged in the excess calories, which is a commen feature of the modern civilization.

I don't think any discussion on food today can be made without a thorough discussion on inflammation.

That is my two cents...

paleotwopointoh said...

huh, the USDA nutritional database doesn't account for shape variation, heat loss or seasonal variation, among other factors. it is not bad, but for things that are assumed to have a lot of calories, it's not exactly optimal and relies on broad assumptions that can add up to dozens of calories' difference per item.

which is itself interesting.

rebecca, unless you have a sample menu, a macronutrient breakdown doesn't say much. also, you upped your protein by 33%, which probably had some positive effects with fat loss.

also, you are aware that your n=1 shows you gain or struggle to maintain on 'low carb', right?

100g of carbs is low-carb. anything under 200g/day is low-carb and anything under 50g/day is 'very low-carb'.

anyway, it's certainly possible that people feel so happy eating lower carb that they spontaneously bounce about more and increase incidental activity, increasing their NEAT, without there being thermogenic 'metabolic advantage'.

Jason said...

It's interesting how being challenged causes some people to rise to the occasion; huzzah for competition and the free market system of ideas. I for one am glad that Gary Taubes was being a jerk during that exchange. Had he not, you would not have written this beautifully put, concise elaboration of the facts - which is much clearer than anything you've done in the past. Now, a bone to pick. If fat diets cause weight loss in most people then how does that square with food reward theory? After all no one could say that a nice steak or eggs with cheese are bland tasting foods. Also why have you seemingly neglected the nutrient density of foods (especially after having written about it in the past)? As you correctly state, fat accumulation is complicated; thus why only look at one angle. Perhaps it is the combination of nutrient density and food reward. Perhaps low nutrient and low fiber dense foods are more palatable. This would make sense since there's more room for better taste when there's less fiber or bad tasting nutrients getting in the way. Anyways, thank you for your blog; all the best and God bless you.

psychic24 said...

Being a bit introspective I have tried narrowing down what exactly elicits satiety for me....

High protein

high calorie

Feeling terrible (inordinate amounts of sugar in one sitting, for instance)

To Muse a bit further I would say that a high protein meal is brought about through eating whole foods or eating enough "pure" protein to make you sick

A high calorie meal obviously represents our homeostatic mechanism within the body...and the more broken the metabolism the more calories needed to activate the satiety

And the final aspect of feeling terrible I think makes great sense of the pathological tendencies, if any, of the macronutrient rationing of the SAD. Being raised on toxin ridden food, we exhibit varying degrees of glucose intolerance; meaning we can't eat a diet of 60%+ carbohydrates without feeling terrible. This, as many of you probably experience, can be ameliorated by adding in fat calories...making an otherwise lethargy inducing (sugar coma-esque) meal, perfectly harmless. It is in this manner that we can maintain eating in a hypercaloric manner and furthering our metabolic dysfunction

It is for this reasoning that Stephan's graph representing an increased fat intake in americans over the years is merely symptomatic of increased glucose intolerance while maintaing a metabolism that is heavily carbohydrate geared. (As many on the SAD will go through withdrawal, low carb flu..etc when adapting a higher fat diet--indicating their inefficiency metabolizing fats.)

DOn't know if this has any validity...feedback is appreciated =)

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

Rebecca

Sorry for being rude and childish. I’ll have to admit though that as someone who is actually studying nutrition SCIENCE, I’m getting quite pissed by people who are not taking a scientific approach to a science.

You probably know what a confounder variable is? And why we call it a ‘’controlled’’ study? It is because there can be a lot of factor that can affect a given result, and even if you think that you have simply change your caloric intake, there might be a lot of other factors that have changed at the same time and that are influencing your results. Without some sort of control, how can we know? And really, why would I believe an anonymous woman over the internet when I’ve got study showing me different results of what you are claiming to get, especially when you’re result don’t fit with our knowledge of metabolism and physiology. You could be lying. How can I know? What are happening to those 800 calories more that you’ve got on the LC diet? Maybe you have a fat malabsorption issue? Maybe you have something that you’re not even aware of that makes it possible for you?

Shall we remember that nutrition is a science please, not a religion?

It’s not about what you see,
believe or feel; it’s about objective and measurable data that we gather in experimental trial using a define scientific method.

So far, studies are not supported what you are claiming to be possible, and you won’t convince any scientific oriented individual by telling him ‘’yes but it worked for me!’’

Edit:

As I’ve said already, I’m eating a shit load of refined crap lately (soft drink, McDo, white bread, candies) and I’m leaner than 2 months ago. If i’m using the n=1 logic, everybody should be eating refined craps to get leaner. That would invalidate anyone saying that carbs make one fat. The guy on the twinkie diet lost weight and his biomarkers improved; that would invalidate all the study saying that you need to eat healthy to improve your biomarkers. Now, we know this is not true, because there are confounding variable. But I guess that you see how that kind of reasoning is leading us nowhere?

Tony C. said...

The science is mostly over head, and I have never been more than a few pounds overweight. But from my observations, this, from Sam, is the key point:

"We understand now (though not 100% sure) that the highly processed junk food with both junk carbs and junk fats (transfats and veg oils) is most likely behind the obesity and diabetes epidemics in the Western world."

I say that in part because I was shocked to find, on a recent trip to Buenos Aires, how few people were significantly overweight. We're talking about a major city, in a country where huge amounts of meat are eaten, carbs and sugar are also quite popular, and dinner is eaten very late at night.

The only possible explanation, to my mind, is that very little processed food is consumed vis-a-vis the U.S.

Chris McEliece said...

I'm totally shocked that Tim Ferriss' Slow Carb Diet has not come up in this discussion. (Disclaimer, I haven't read ALL of the posts, but I did ctrl-F for any relevant terms).

I lost 30 lbs in 10 weeks using his method:
-No white carbs. Wheat, rice, potatoes, etc.
-Increased protein intake to 1g/lbs of lean body mass
-Eat breakfast (high protein!) within 30 minutes of waking
-No fruit, minimize sugar intake to the bare minimum.
-1 day per week, eat anything and everything you want to avoid ketosis. Generally this translates into eating a whole large pizza.
-2 glasses red wine per day are OK, as is 16 oz of diet soda (I drank the wine but not the diet soda, I don't understand why anyone drinks that sh&t)

The replacement is to eat a lot of legumes- beans, lentils, etc. Tim mentions insulin regularly in his book, but honestly I didn't read it deeply. I was just looking for the method.

During the summer of 2010, I trained and climbed Mt. Rainier, equivalent to 25-30 hours of physical training per week for 6 months. I gained weight, and gained fat. I crested over 300 lbs. I'm 6'5", so that's not obese but is certainly overweight. When I started the Slow Carb Diet, I lost 20 lbs in 5 weeks, and another 10 lbs in the second 5 weeks. I would have lost another 15, but this summer has been full of weddings w/ cake and BBQ's with burgers. I have NOT gained back any weight, I'm still basically at my low.

Anyway, I wanted to know how this information about carbs relates to the slow carb diet? Anyone with some bright ideas?

Harry said...

To those that think carbs cause obesity (either by promoting over-eating or by 'trapping' energy in the fat cells), please answer this:

Given the rapid rise in North american obesity since 1980 -

If carbs causes obesity, then people post-1980 started to eat more carbs than people pre-1980.

So, what caused people to start eating more carbs at around the 1980 mark? And why were carb-eaters pre-1980 not getting fat from eating carbs while carb-eaters post-1980 were getting fat?

It wasn't the 'availability' or 'cost' of carbs themselves, as they have always been plentiful and cheap, relative to fat and protein.

Neither can we say that the mere fact that people were eating carbs caused them to eat more, as this doesn't explain why people spontaneously starting eating more of them since 1980.

Moreover, the proliferation of societies and individuals that do not get fat eating carbs demonstrates that the mere presence of carbs in the diet does not, of itself, initiate fat gain.

So, any takers?

Note: The food reward hypothesis answers all of these questions perfectly; the rise in obesity post-1980 reflects the increasing prevalence and cost-effectiveness of hyper-palatable fast food, convenience food, and junk food.

Dr J said...

@ Frank - I gather you haven't looked at the Volek et al papers in Lipids where he clearly showed greater weight loss, fat loss and abd fat loss on eucaloric LC vs LF diets.

@ Harry - the rise in CHO in the food supply starting in the late 70's reflected the addition of HFCS to the food supply. Pretty much all of the subsequent increase can be attributed to caloric sweeteners and probably fruit juice, too.

jlglex said...

Do you have an opinion on the effect of green tea consumption? Do the anti-oxidants in green tea really have protective effects?

Stephan Guyenet said...

Hi Harry,

Well said!

Hi ItsTheWoo2,

You've again proven yourself incapable of making your point without insulting me and other commenters. I've been extremely patient with you, given you multiple warnings, but my patience has run out. I'll be deleting your comments from now on.

Rebecca Latham said...

@ItsTheWooo2

Thanks you for sharing your understanding of leptin.

Rebecca Latham said...

@paleotwopointoh

We're going to have to agree to disagree, because I am growing weary of explaining what is going on with me and have you keep saying, "No, it isn't."

Let's just stop this part of the discussion

Stacy said...

@Stephan re: itsthewoo2 delete = YAHOO!

Rebecca Latham said...

@Frank

"So far, studies are not supported what you are claiming to be possible, and you won’t convince any scientific oriented individual by telling him ‘’yes but it worked for me!’’"

You are ignoring all of Volek's research that shows that I am not the only person who it "works for."

As I mentioned in my last post, I'm just tired of talking about this and coming under attack for reporting what is happening to me.

My point: I can eat more calories if I eat low carb high fat than if I eat high carb low fat.

Your point: Studies prove that you cannot.

Let's just drop it.

maurile said...

@Harry, I think the rise to prominence of the low-fat mantra is a possible explanation for increased carb consumption around 1980.

Dave Tate said...

@Harry,

One of the factors Taubes mentions is sugar consumption, along with the huge increase in high fructose corn syrup. I don't have GC, BC in front of me but I do remember sugar consumption being presented as being tied to the outbreak of diseases of civilization/western diseases. As far as fast food is concerned Taubes mentioned that McDonalds has been around long before the 1980s. Perhaps the fast food restaurants changed their recipes to make their food more palatable/rewarding, I don't know but I'm pretty sure they've been around since the 50s. Maybe frying their food in omega 6 rich vegetable oil rather than beef tallow is part of the problem?

Harry said...

@ Dr J

Yes, HFCS is a potential factor. But, it's not chemically all that different from sucrose (table sugar), and since sucrose has been part of the food supply pre-1980, I'd call it a long shot in terms of explaining the precipitous rise in obesity.

And, of course, it's not consistent with the general "all carbs > insulin > obesity" paradigm.

@ maurile

Assuming a significant portion of people actually followed the low-fat advice, and then subsequently got fat as a consequence - then yes...it may have played a part. But that's a pretty dubious assumption to make I think...most post-1980 fat people I know (including my previous self and my clients) got fat by eating the plain ol' SAD...and that includes plenty of fat! The NHANES data shows that, while people moderately increased their carbs (by 4% as a proportion of total calories) between 1971-2006, their total calorie intake want up massively (completely in line with actual fat gains)...so this backs up the notion that the "low fat message" got lost in translation and got implemented as "eat a touch less fat, a touch more carbs, and a whole lot more of everything".

@ Dave Tate

Sugar was around pre-1980...why didn't it cause the obesity rise that we see post-1980. Besides, if you finger sugar as the culprit, the whole "insulin causes obesity" theory goes out the window, since glucose from starches raises insulin as much as table sugar.

The Omega 6 oils - well, they may play a part too. But they're not carbs.

So again...are there any other takers as to how the "insulin > obesity" theory explains the lack of pre-1980 obesity versus the proliferation of post-1980 obesity (remember, insulin wasn't an innovation of the 80s !).

Dr J said...

@ Harry - yes, HFCS is about equivalent to sugar, hence the reference to caloric sweeteners. If you look at USDA food disappearance data, the only macronutrient to rise at the time of the onset of the obesity epidemic is CHO. Caloric sweetener pretty much accounts for that rise. Yes, sugar is less glycemic than some sources of starch. Perhaps it was the increase in fructose load that reached a tipping point. And, perhaps the addition of omega-6 oils to the food supply also played a part. In either case, the cure is CHO reduction. For those affected, it pretty reliably reverses the problems of obesity, metabolic syndrome and type 2 diabetes.

said...

Folks, I just hope you all realize that you don't need insulin to store fat.

Look up "acylation stimulating protein", a very important but somewhat recent discovery.

Fat will be stored as bodyfat without an insulin response.

Harry said...

@ woo2

Ok, so your candidates are sugar (due to cheapness) and sugary cereals (due to women's work patterns).

Again, both of these food stuffs were well entrenched in the SAD prior to 1980 (and again, these are NOT consistent with the general "insulin hypothesis of obesity", as they are a small sub-set of carbs; and in the case of HFCS, they are LESS insulinemic than many starches).

While sugar and sugary cereals can be obesogenic for sure, they cannot explain why people spontaneously started eating more and more of them at 1980, since they were freely and cheaply available prior to that time (and while manufacturers may have improved profits by replacing sugar with HFCS, sugary confections and table sugar have always been cheap at the retail level).

Further, if the death of slow cooking and the rise of convenience food changed us from carb-eating slim people to carb-eating fat people, this suggests again that carbs do not cause obesity, but rather, that obesity is multi-factorial! That is not consistent with the "all carbs > insulin > obesity" reductivism.

Chris said...

@woo: "Fast food and sugary junk food for breakfast became more common as less women had the time to prepare real meals. "

You meant fewer, not less.

James Kimbell said...

Rebecca,

Sorry to keep on the same point, and I'll be done after this post, but I just want to correct one thing, so you can see it and so people reading this can see it, too.

You said:

"My point: I can eat more calories if I eat low carb high fat than if I eat high carb low fat.

Your point: Studies prove that you cannot."

That's just not a fair summary of the argument people are using against you. (Hint: You are the only person using "prove.") A fair summary would be this:

"My point: I can eat more calories if I eat low carb high fat than if I eat high carb low fat.

Your point: When one person (i.e. you) looks at the question, you get one answer. But when lots of people, professionally organized and orchestrated and measured, (i.e. researchers) look at the question, they get a different answer. It's unlikely that they, with all their advantages, managed to the wrong answer while you got the right one. Therefore either there are complications we need to find out, or you are measuring something wrong, or something else. The metabolic chamber studies don't 'prove' anything for sure, but they do throw a large kink in your assertion, which you would do well to acknowledge."

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