Why Did Energy Expenditure Differ Between Diets in the Recent Study by Dr. Ludwig's Group?

As discussed in the previous post, a recent study by Dr. David Ludwig's group suggested that during weight maintenance following fat loss, eating a very low carbohydrate (VLC) diet led to a higher metabolic rate (energy expenditure) than eating a low-fat (LF) diet, with a low glycemic index (LGI) diet falling in between the two (1).  The VLC diet was 30 percent protein, while the other two were 20 percent.  It's important to note that these were three dietary patterns that differed in many ways, and contrary to claims that are being made in the popular media, the study was not designed to isolate the specific influence of protein, carbohydrate or fat on energy expenditure in this context. 

Not only did the VLC diet lead to a higher total energy expenditure than the LF and LGI diets, the most remarkable finding is that it led to a higher resting energy expenditure.  Basically, people on the VLC diet woke up in the morning burning more energy than people on the LGI diet, and people on the LGI diet woke up burning more than people on the LF diet.  The VLC dieters burned 326 more calories than the LF dieters, and 200 more than the LGI dieters.

It's always tempting to view each new study in isolation, without considering the numerous studies that came before it, but in this case it's essential to see this study through a skeptical lens that places it into the proper scientific context.  Previous studies have suggested that:

1. The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure in people who are not trying to lose weight (2, 3).
2. The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure in people who are being experimentally overfed, and if anything carbohydrate increases energy expenditure more than fat (4, 5).
3. The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure during weight loss (6, 7, 8), and does not influence the rate of fat loss when calories are precisely controlled. 

This new study does not erase or invalidate any of these previous findings.  It fills a knowledge gap about the effect of diet composition on energy expenditure specifically in people who have lost weight and are trying to maintain the reduced weight.

With that, let's see what could have accounted for the differences observed in Dr. Ludwig's study.
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New Study: Is a Calorie a Calorie?

A new study in JAMA led by Dr. Cara B. Ebbeling and colleagues purports to challenge the idea that all calories are equally fattening (1).  Let's have a look.  When thinking about the role of calorie intake in body fatness, there are basically three camps:

1.    Calories don’t matter at all, only diet composition matters.
2.    Calories are the only thing that matters, and diet composition is irrelevant.
3.    Calories matter, but diet composition may also play a role.

The first one is an odd position that is not very well populated.  The second one has a lot of adherents in the research world, and there’s enough evidence to make a good case for it.  It’s represented by the phrase ‘a calorie is a calorie’, i.e. all calories are equally fattening.  #1 and #2 are both extreme positions, and as such they get a lot of attention.  But the third group, although less vocal, may be closest to the truth. 
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What Puts Fat Into Fat Cells, and What Takes it Out?

Body fatness at its most basic level is determined by the rate of fat going into vs. out of fat cells. This in/out cycle occurs regardless of conditions outside the cell, but the balance between in and out is influenced by a variety of external factors.  One of the arguments that has been made in the popular media about obesity goes something like this:  


A number of factors can promote the release of fat from fat cells, including:

Epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), glucagon, thyroid-stimulating hormone, melanocyte-stimulating hormone, vasopressin, and growth hormone

 But only two promote fat storage:

Insulin, and acylation-stimulating protein (ASP)*

Therefore if we want to understand body fat accumulation, we should focus on the latter category, because that's what puts fat inside fat cells.  Simple, right?

Can you spot the logical error in this argument?

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New Study Demonstrates that Sugar has to be Palatable to be Fattening in Mice

Dr. Anthony Sclafani's research group just published a study definitively demonstrating that high palatability, or pleasantness of taste, is required for sugar to be fattening in mice (1).  Dr. John Glendinning was lead author. Dr. Sclafani's group has done a lot of excellent research over the years.  Among other things, he's the person who invented the most fattening rodent diet in the world-- the 'cafeteria diet'-- composed of human junk food. 

Mice and rats love sweet food and drinks, just like humans.  If you give them a choice between plain water and sugar water, they'll overconsume the sugar water and become obese.  I have argued, based on a large body of evidence, that the reward value and palatability* of these solutions are important to this process (2, 3, 4).  This is really just common sense honestly, because by definition if the solution weren't rewarding the mice wouldn't go out of their way to drink it instead of water, the same way people wouldn't go out of their way to get soda if it weren't rewarding.  But it's always best to confirm common sense with research.
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Sugar Intake and Body Fatness in Non-industrial Cultures

Around the world, non-industrial cultures following an ancestral diet and lifestyle tend to be lean. When they transition a modern diet and lifestyle, they typically put on body fat and develop the classic "diseases of civilization" such as diabetes and cardiovascular disease.  If we can understand the reasons why this health transition occurs, we will understand why these problems afflict us today.  Research has already identified a number of important factors, but today I'm going to discuss one in particular that has received a lot of attention lately: sugar.

There's an idea currently circulating that sugar is the main reason why healthy traditional cultures end up obese and sick.  It’s easy to find non-industrial cultures that are lean and don’t eat much sugar, and it’s easy to find industrial cultures that are obese and eat a lot of it.  But many factors are changing simultaneously there.  We could use the same examples to demonstrate that blue jeans and hair gel cause obesity.  If sugar is truly the important factor, then cultures with a high sugar intake, but an otherwise ancestral diet and lifestyle, should also be overweight and sick.  Let’s see if that's true. 

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Calories Still Matter

The Centers for Disease Control's NHANES surveys documented a massive increase in obesity in the United States between the 1960-62 and 2007-2008 survey periods (1).  In 1960, 13 percent of US adults were obese, while in 2008 that number had risen to 34 percent.  The prevalence of extreme obesity increased from 0.9 to 6.0 percent over the same time period!

Something has changed, but what?  Well, the most parsimonious explanation is that we're simply eating more.  Here is a graph I created of our calorie intake (green) overlaid on a graph of obesity prevalence (blue) between 1970 and 2008:

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How Bad is Fructose? David Despain Interviews Dr. John Sievenpiper

In my article "Is Sugar Fattening?", I discussed a recent review paper on fructose, by Dr. John Sievenpiper and colleagues (1).  It was the most recent of several review papers to conclude that fructose is probably not inherently fattening in humans, but that it can be fattening if it's consumed to excess, due to the added calories.  Dr. Sievenpiper and colleagues have also written other papers addressing the metabolic effects of fructose, which appear to be fairly minor unless it's consumed to excess (2, 3, 4, 5).  The senior author on these studies is Dr. David Jenkins at McMaster University.  David Despain, a science and health writer who publishes a nice blog called Evolving Health, recently interviewed Dr. Sievenpiper about his work.

It's an interesting interview and very timely, due to the recent attention paid to fructose in the popular media. This has mostly been driven by a couple of high-profile individuals-- an issue they discuss in the interview.  The interview, recent papers, and sessions at scientific conferences are part of an effort by researchers to push back against some of the less well founded claims that have received widespread attention lately.

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Exercise and Food Intake

The New York Times just published an article reviewing some of the recent research on exercise, food intake and food reward, titled "Does Exercise Make You Overeat?".  I was planning to write about this at some point, but I don't know when I'd be able to get around to it, and the NYT article is a fair treatment of the subject, so I'll just point you to the article.

Basically, burning calories through exercise causes some people to eat more, but not everyone does, and a few people actually eat less.  Alex Hutchinson discussed this point recently on his blog (1).  Part of it depends on how much fat you carry-- if you're already lean, the body is more likely to increase hunger because it very much dislikes going too low in body fat.  Most overweight/obese people do not totally make up for the calories they burn through exercise by eating more, so they lose fat.  There is a lot of individual variability here.  The average obese person won't lose a substantial amount of fat through exercise alone.  However, everyone knows someone who lost 50+ pounds through exercise alone, and the controlled trials support that it happens in a minority of people.  On the other side of the spectrum, I have a friend who gained fat while training for a marathon, and lost it afterward. 

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Recent Media Appearances

Men's Health interviewed and quoted me in an article titled "Reprogram Your Metabolism", written by Lou Schuler.  Part of the article was related to the food reward concept.  I'm glad to see the idea gradually reaching the mainstream. 

Boing Boing recently covered an article by Dr. Hisham Ziauddeen and colleagues in Nature Reviews Neuroscience that questioned the idea that common obesity represents food addiction-- an idea that I often encounter in my reading.  Maggie Koerth-Baker asked me if I wanted to respond.  I sent her a response explaining that I agree with the authors' conclusions and I also doubt obesity is food addiction per se, as I have explained in the past, although a subset of obese people can be addicted to food.  I explained that the conclusions of the paper are consistent with the idea that food reward influences fat mass.  You can find my explanation here.

Food Reward: Approaching a Scientific Consensus

Review papers provide a bird's-eye view of a field from the perspective of experts.  Recent review papers show that many obesity researchers are converging on a model for the development of obesity that includes excessive food reward*, in addition to other factors such as physical inactivity, behavioral traits, and alterations in the function of the hypothalamus (a key brain region for the regulation of body fatness).  Take for example the four new review papers I posted recently by obesity and reward researchers:
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Qnexa, the Latest Obesity Drug

There are very few obesity drugs currently approved for use in the US-- not because effective drugs don't exist, but because the FDA has judged that the side effects of existing drugs are unacceptable. 

Although ultimately I believe the most satisfying resolution to the obesity epidemic will not come from drugs, drugs offer us a window into the biological processes that underlie obesity and fat loss.  Along those lines, here's a quote from a review paper on obesity drugs that I think is particularly enlightening (1):
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Boing!

I just had a featured article published on Boing Boing, "Seduced by Food: Obesity and the Human Brain".  Boing Boing is the most popular blog on the Internet, with over 5 million unique visitors per month, and it's also one of my favorite haunts, so it was really exciting for me to be invited to submit an article.  For comparison, Whole Health Source had about 72,000 unique visitors last month (200,000+ hits).

The article is a concise review of the food reward concept, and how it relates to the current obesity epidemic.  Concise compared to all the writing I've done on this blog, anyway.  I put a lot of work into making the article cohesive and understandable for a somewhat general audience, and I think it's much more effective at explaining the concept than the scattered blog posts I've published here.  I hope it will clear up some of the confusion about food reward.  I don't know what's up with the image they decided to use at the top. 

Many thanks to Mark Frauenfelder, Maggie Koerth-Baker, and Rob Beschizza for the opportunity to publish on Boing Boing, as well as their comments on the draft versions!

For those who have arrived at Whole Health Source for the first time via Boing Boing, welcome!   Have a look around.  The "labels" menu on the sidebar is a good place to start-- you can browse by topic.

Palatability, Satiety and Calorie Intake

WHS reader Paul Hagerty recently sent me a very interesting paper titled "A Satiety Index of Common Foods", by Dr. SHA Holt and colleagues (1).  This paper quantified how full we feel after eating specific foods.  I've been aware of it for a while, but hadn't read it until recently.  They fed volunteers a variety of commonly eaten foods, each in a 240 calorie portion, and measured how full each food made them feel, and how much they ate at a subsequent meal.  Using the results, they calculated a "satiety index", which represents the fullness per calorie of each food, normalized to white bread (white bread arbitrarily set to SI = 100).  So for example, popcorn has a satiety index of 154, meaning it's more filling than white bread per calorie. 

One of the most interesting aspects of the paper is that the investigators measured a variety of food properties (energy density, fat, starch, sugar, fiber, water content, palatability), and then determined which of them explained the SI values most completely.

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Soda-Free Sunday

Last Thursday, I received a message from a gentleman named Dorsol Plants about a public health campaign here in King County called Soda Free Sunday.  They're asking people to visit www.sodafreesundays.com and make a pledge to go soda-free for one day per week. 

Drinking sugar-sweetened beverages (SSBs), including soda, is one of the worst things you can do for your health.  SSB consumption is probably one of the major contributors to the modern epidemics of obesity and metabolic dysfunction.

I imagine that most WHS readers don't drink SSBs very often if at all, but I'm sure some do.  Whether you want to try drinking fewer SSBs, or just re-affirm an ongoing commitment to avoid them, I encourage you to visit www.sodafreesundays.com and make the pledge.  You can do so even if you're not a resident of King county.

Is Sugar Fattening?

Buckle your seat belts, ladies and gentlemen-- we're going on a long ride through the scientific literature on sugar and body fatness.  Some of the evidence will be surprising and challenging for many of you, as it was for me, but ultimately it paints a coherent and actionable picture.

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Cigarette Smoking-- Another Factor in the Obesity Epidemic

Obesity rates in the US have more than doubled in the last 30 years, and rates of childhood obesity and extreme adult obesity have tripled.  One third of US adults are considered obese, and another third overweight.  This is the "obesity epidemic".

The obesity epidemic has coincided with significant changes in the US diet, which are clearly involved.  However, there's another probable contributor that's often overlooked: declining smoking rates.  

Here's a graph of cigarette consumption over the last century in the US (1):
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Insulin and Obesity: Another Nail in the Coffin

There are several versions of the insulin hypothesis of obesity, but the versions that are most visible to the public generally state that elevated circulating insulin (whether acute or chronic) increases body fatness.  Some versions invoke insulin's effects on fat tissue, others its effects in the brain.  This idea has been used to explain why low-carbohydrate and low-glycemic-index diets can lead to weight loss (although frankly, glycemic index per se doesn't seem to have much if any impact on body weight in controlled trials). 

I have explained in various posts why this idea does not appear to be correct (1, 2, 3), and why, after extensive research, the insulin hypothesis of obesity lost steam by the late 1980s.  However, I recently came across two experiments that tested the hypothesis as directly as it can be tested-- by chronically increasing circulating insulin in animals and measuring food intake and body weight and/or body fatness.  If the hypothesis is correct, these animals should gain fat, and perhaps eat more as well. 

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What Causes Insulin Resistance? Part VII

In previous posts, I outlined the factors I'm aware of that can contribute to insulin resistance.  In this post, first I'll list the factors, then I'll provide my opinion of effective strategies for preventing and potentially reversing insulin resistance.

The factors

These are the factors I'm aware of that can contribute to insulin resistance, listed in approximate order of importance.  I could be quite wrong about the order-- this is just my best guess. Many of these factors are intertwined with one another. 
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New Obesity Review Paper by Yours Truly

The Journal of Clinical Endocrinology and Metabolism just published a clinical review paper written by myself and my mentor Dr. Mike Schwartz, titled "Regulation of Food Intake, Energy Balance, and Body Fat Mass: Implications for the Pathogenesis and Treatment of Obesity" (1).  JCEM is one of the most cited peer-reviewed journals in the fields of endocrinology, obesity and diabetes, and I'm very pleased that it spans the gap between scientists and physicians.  Our paper takes a fresh and up-to-date look at the mechanisms by which food intake and body fat mass are regulated by the body, and how these mechanisms are altered in obesity.  We explain the obesity epidemic in terms of the mismatch between our genes and our current environment, a theme that is frequently invoked in ancestral health circles.

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What Causes Insulin Resistance? Part I

Insulin is an ancient hormone that influences many processes in the body.  Its main role is to manage circulating concentrations of nutrients (principally glucose and fatty acids, the body's two main fuels), keeping them within a fairly narrow range*.  It does this by encouraging the transport of nutrients into cells from the circulation, and discouraging the export of nutrients out of storage sites, in response to an increase in circulating nutrients (glucose or fatty acids). It therefore operates a negative feedback loop that constrains circulating nutrient concentrations.  It also has many other functions that are tissue-specific.

Insulin resistance is a state in which cells lose sensitivity to the effects of insulin, eventually leading to a diminished ability to control circulating nutrients (glucose and fatty acids).  It is a major contributor to diabetes risk, and probably a contributor to the risk of cardiovascular disease, certain cancers and a number of other disorders. 

Why is it important to manage the concentration of circulating nutrients to keep them within a narrow range?  The answer to that question is the crux of this post. 

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