How Much Does Sugar Contribute to Obesity?

Last week, the British Medical Journal published a review article titled "Dietary Sugars and Body Weight", concluding that "free sugars" and sugar-sweetened beverages contribute to weight gain. But what are "free sugars", and why does the scientific literature suggest that the relationship between sugar intake and body weight isn't as straightforward as it may initially appear?

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A New Human Trial Undermines the Carbohydrate-insulin Hypothesis of Obesity, Again

The carbohydrate-insulin hypothesis of obesity states that carbohydrates (particularly refined carbohydrates and sugar) are the primary cause of obesity due to their ability to increase circulating insulin, and that the solution to obesity is to restrict carbohydrate intake. Numerous studies have tested this hypothesis, more or less directly, in animals and humans. Despite the fact that many of these studies undermine the hypothesis, it remains extremely popular, both in the popular media and to a lesser extent among researchers. A new human trial by Kevin Hall's research team at the US National Institutes of Health offers very strong evidence that the carbohydrate-insulin hypothesis of obesity is incorrect. At the same time, it offers surprising and provocative results that challenge prevailing ideas about diet and weight loss.

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Obesity ? Diabetes

A new study adds to the evidence that the prevalence of type 2 diabetes is rapidly increasing in the US, and our national weight problem is largely to blame.

The Centers for Disease Control (CDC) currently estimates that a jaw-dropping 33 percent of US men, and 39 percent of US women, will develop diabetes at some point in their lives (1). Roughly one out of three people in this country will develop diabetes, and those who don't manage it effectively will suffer debilitating health consequences. Has the risk of developing diabetes always been so high, and if not, why is it increasing?

In the same issue of the Annals of Internal Medicine as the low-carb vs. low-fat study, appears another study that aims to partially address this question (2).

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My AHS14 Talk on Leptin Resistance is Posted

The Ancestral Health Society just posted a video of my recent talk "What Causes Leptin Resistance?"  Follow the link below to access it.  Enjoy!

What Causes Leptin Resistance?

What about the Other Weight Loss Diet Study??

The same day the low-fat vs low-carb study by Bazzano and colleagues was published, the Journal of the American Medical Association published a meta-analysis that compared the effectiveness of "named diet programs". Many people have interpreted this study as demonstrating that low-carbohydrate and low-fat diets are both effective for weight loss, and that we simply need to pick a diet and stick with it, but that's not really what the study showed. Let's take a closer look.

Johnston and colleagues sifted through PubMed for studies that evaluated "named diet programs", such as Ornish, Atkins, LEARN, Weight Watchers, etc (1). In addition, the methods state that they included any study as low-carbohydrate that recommended less than 40% of calories from carbohydrate, was funded by the Atkins foundation, or was "Atkins-like". These criteria weren't extended to the low-fat diet: only studies of name-brand low-fat diets like the Ornish diet were included, while the meta-analysis excluded low-fat diet studies whose guidelines were based on recommendations from government and academic sources, even though the latter group represents the majority of the evidence we have for low-fat diets. The inclusion criteria were therefore extremely asymmetrical in how they represented low-carb and low-fat diets. This fact explains the unusual findings of the paper.

The abstract immediately activated my skeptic alarm, because it states that at the one-year mark, low-carbohydrate diets and low-fat diets both led to a sustained weight loss of about 16 pounds (7.3 kg). Based on my understanding of the weight loss literature, that number seems far too high for the low-fat diet, and also too high for the low-carbohydrate diet.

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Low-carbohydrate vs. Low-fat diets for Weight Loss: New Evidence

A new high-profile study compared the weight loss and cardiovascular effects of a low-carbohydrate diet vs. a low-fat diet. Although many studies have done this before, this one is novel enough to add to our current understanding of diet and health. Unlike most other studies of this nature, diet adherence was fairly good, and carbohydrate restriction produced greater weight loss and cardiovascular risk factor improvements than fat restriction at the one-year mark. Yet like previous studies, neither diet produced very impressive results.

The Study

Lydia A. Bazzano and colleagues at Tulane University randomly assigned 148 obese men and women without cardiovascular disease into two groups (1):

1. Received instructions to eat less than 40 grams of carbohydrate per day, plus one low-carbohydrate meal replacement per day. No specific advice to alter calorie intake. Met regularly with dietitians to explain the dietary changes and maintain motivation.
2. Received instructions to eat less than 30 percent of calories from fat, less than 7 percent of calories as saturated fat, and 55 percent of calories from carbohydrate, plus one low-fat meal replacement per day. No specific advice to alter calorie intake. This is based on NCEP guidelines, which are actually designed for cardiovascular risk reduction and not weight loss. Met regularly with dietitians to explain the dietary changes and maintain motivation.

Participants were followed up for one year, with data reported for 3 month, 6 month, and 12 month timepoints. This study actually measured body fat percentage, but unfortunately did so using bioelectrical impedance (like on some bathroom scales), which is essentially meaningless in this context.

Results

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Fat and Carbohydrate: Clarifications and Details

The last two posts on fat and carbohydrate were written to answer a few important, but relatively narrow, questions that I feel are particularly pertinent at the moment:

• Was the US obesity epidemic caused by an increase in calorie intake?
• Could it have been caused by an increase in carbohydrate intake, independent of the increase in calorie intake?
• Does an unrestricted high-carbohydrate diet lead to a higher calorie intake and body fatness than an unrestricted high-fat diet, or vice versa?
• Could the US government's advice to eat a low-fat diet have caused the obesity epidemic by causing a dietary shift toward carbohydrate?

However, those posts left a few loose ends that I'd like to tie up in this post. Here, I'll lay out my opinions on the relationship between macronutrient intake and obesity in more detail. I'll give my opinions on the following questions:

• What dietary macronutrient composition is the least likely to cause obesity over a lifetime?
• What dietary macronutrient composition is best for a person who is already overweight or obese?
• Is fat inherently fattening and/or unhealthy?

From the beginning

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Has Obesity Research Failed?

I frequently encounter the argument that obesity research has failed because it hasn't stopped the global increase in obesity rates. According to this argument, we need to re-think our approach to obesity research because the current approach just isn't working.

Grant funding for obesity research keeps increasing in the US, and the prevalence of obesity also keeps increasing*. What gives? Maybe if we just scrapped the whole endeavor we'd be better off.

Let's take a closer look at this argument and see how it holds up.

Why Do Research?

There are two fundamental reasons why we do research:

1. To gather accurate information about the natural world. This information is intrinsically valuable because we like knowing how the world works, and it may eventually have practical value that's not immediately obvious.
2. Practical applications. We want to solve problems and improve our lives.

If we want to determine whether or not obesity research has failed, we should evaluate it using those two metrics.

Has Obesity Research Gathered Accurate Information?

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A New Understanding of an Old "Obesity Gene"

As you know if you've been following this blog for a while, obesity risk has a strong genetic component. Genome-wide association studies (GWAS) attempt to identify the specific locations of genetic differences (single-nucleotide polymorphisms or SNPs) that are associated with a particular trait. In the case of obesity, GWAS studies have had limited success in identifying obesity-associated genes. However, one cluster of SNPs consistently show up at the top of the list in these studies: those that are near the gene FTO.

As with many of the genes in our genome, different people carry different versions of FTO. People with two copies of the "fat" version of the FTO SNPs average about 7 pounds (3 kg) heavier than people with two copies of the "thin" version, and they also tend to eat more calories (1, 2).

Despite being the most consistent hit in these genetic studies, FTO has remained a mystery. As with most obesity-associated genes, it's expressed in the brain and it seems to respond somewhat to nutritional status. Yet its function is difficult to reconcile with a role in weight regulation:

• It's an enzyme that removes methyl groups from RNA, which doesn't immediately suggest a weight-specific function.
• It's not primarily expressed in the brain or in body fat, but in all tissues.
• Most importantly, as far as we know, the different versions of the gene do not result in different tissue levels of FTO, or different activity of the FTO enzyme, so it's hard to understand how they would impact anything at all.

An important thing to keep in mind is that GWAS studies don't usually pinpoint specific genes. Typically, they tell us that obesity risk is associated with variability in a particular region of the genome. If the region corresponds to the location of a single gene, it's a pretty good guess that the gene is the culprit. However, that's not always the case...

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Fat vs. Carbohydrate Overeating: Which Causes More Fat Gain?

Two human studies, published in 1995 and 2000, tested the effect of carbohydrate vs. fat overfeeding on body fat gain in humans. What did they find, and why is it important?

We know that daily calorie intake has increased the US, in parallel with the dramatic increase in body fatness. These excess calories appear to have come from fat, carbohydrate, and protein all at the same time (although carbohydrate increased the most). Since the increase in calories, carbohydrate, fat, and protein all happened at the same time, how do we know that the obesity epidemic was due to increased calorie intake and not just increased carbohydrate or fat intake? If our calorie intake had increased solely by the addition of carbohydrate or fat, would we be in the midst of an obesity epidemic?

The best way to answer this question is to examine the controlled studies that have compared carbohydrate and fat overfeeding in humans.

Horton et al.

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More Graphs of Calorie Intake vs. BMI

In the last post, a reader commented that the correlation would be more convincing if I graphed calories vs. average BMI rather than the prevalence of obesity.  It was a valid point, so I went searching for average BMI values from NHANES surveys.  I dug up a CDC document that contains data from surveys between 1960 and 2002 (1).  Because these data only cover five survey periods, we only get five data points to analyze, as opposed to the eight used in the last post.  The document contains BMI values for men and women separately, so I averaged the two to approximate average BMI in the general adult population.  It's also worth noting that I use the approximate midpoint of the survey period as the year.

First, a graph of average BMI over time.  It went up:

Now, let's see how well average BMI correlates with calorie intake:

The correlation between calorie intake and obesity prevalence was remarkable, but this correlation is simply incredible.  An R-squared value of 0.98 indicates that daily calorie intake and average BMI are almost perfectly correlated.

We can further deduce that each 100-calorie increase in daily food intake is associated with an 0.62-point increase in average BMI among US adults.  

Calorie Intake and the US Obesity Epidemic

Between 1960 and 2008, the prevalence of obesity in US adults increased from 13 to 34 percent, and the prevalence of extreme obesity increased from 0.9 to 6 percent (NHANES surveys). This major shift in population fatness is called the "obesity epidemic".

What caused the obesity epidemic? As I've noted in my writing and talks, the obesity epidemic was paralleled by an increase in daily calorie intake that was sufficiently large to fully account for it. There are two main sources of data for US calorie intake. The first is NHANES surveys conducted by the Centers for Disease Control. They periodically collect data on food intake using questionnaires, and these surveys confirm that calorie intake has increased. The problem with the NHANES food intake data is that they're self-reported and therefore subject to major reporting errors. However, NHANES surveys provide the best quality (objectively measured) data on obesity prevalence since 1960, which we'll be using in this post.

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Uncovering the True Health Costs of Excess Weight

Is excess weight hazardous to health, or can it actually be protective? This question has provoked intense debate in the academic community, in some cases even leading researchers to angrily denounce the work of others (1). There is good evidence to suggest that excess body fat increases the risk of specific diseases, including many of our major killers: diabetes, heart attack, stroke, heart failure, cancer, and kidney failure (2). Yet strangely, the studies relating excess weight to the total risk of dying-- an overall measure of health that's hard to argue with-- are inconsistent. Why?
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Why Do We Overeat? A Neurobiological Perspective

I just posted a narrated Powerpoint version of my talk "Why Do We Overeat? A Neurobiological Perspective" to YouTube.  Here's the abstract:

In the United States, the "obesity epidemic" has paralleled a gradual increase in daily calorie intake.  Why do we eat more than we used to, and more than we need to remain lean-- despite negative consequences?  This talk reviews the neurobiology of eating behavior, recent changes in the US food system, and why the brain's hardware may not be up to the task of constructively navigating the modern food environment.

This is the same talk I gave at the University of Virginia this January.  I had a number of people request it, so here it is:

 

Why Do We Overeat? A Neurobiological Perspective

 

This is one of my favorite talks, and it was very well received at UVA.  If you find it informative, please share it!

 

 

Mindless Eating

You think you're in control of your eating behavior-- but you aren't

In 2005, Brian Wansink's research group published a remarkable study that demonstrates the powerful unconscious influence of the food environment on our consumption (1).

Volunteers were invited to a test kitchen to eat bowls of tomato soup for lunch. Each person was given a bowl containing 18 ounces of soup-- but there was a catch. Half the volunteers were given custom-made soup bowls that partially refilled as they ate, such that the soup level dropped more slowly.

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5 Easy and Effective Ways to Eat Less

Why do we overeat?  Why is it hard to lose fat once we've gained it?  Is there a way to comfortably and sustainably eat less and lose fat? 

 

I recently did an interview with Armi Legge of Evidence Magazine that gives an overview of my thinking on these topics-- based on a large and compelling body of research that rarely reaches popular media sources in useful form. 

 

At the end of the interview, Armi asks me to list my top five tips for reducing calorie intake.  Enjoy!

 

5 Easy and Effective Ways to Eat Less

 

 

Mysteries of Energy Balance and Weight Loss

How to Lose Weight Effortlessly

You've probably seen this claim many times: a pound of fat contains 3,500 kilocalories (kcal). A slice of toast is 80 kcal. All you have to do is forego one slice of toast per day-- just a few percent of your total calorie intake-- and you will lose 8.3 lbs of fat per year. Fat loss is so easy!

This reasoning is extremely common both in the popular media and among researchers. Here's an example from the book Mindless Eating, by researcher Brian Wansink:

...the difference between 1,900 and 2,000 calories is one we cannot detect, nor can we detect the difference between 2,000 and 2,100 calories. But over the course of a year, this mindless margin would either cause us to lose ten pounds or to gain ten pounds. It takes 3,500 extra calories to equal one pound. It doesn't matter if we eat these extra 3,500 calories in one week or gradually over the entire year. They'll add up to one pound.

This is the danger of creeping calories. Just 10 extra calories a day-- one stick of Doublemint gum or three small Jelly Belly jelly beans-- will make you a pound more portly one year from today. Only three Jelly Bellys a day.

According to this reasoning, if I reduced my calorie intake by 80 kcal per day, I'd become skeletal in two years and vanish in a puff of smoke within 10 years*. All from a meager 3 percent reduction in calorie intake!

What's wrong here?

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Public Talk at the University of Virginia on Friday, January 17

This Friday, I'll be giving an invited lecture at the University of Virginia, my undergraduate alma mater.  I was kindly invited by a medical student named Robert Abbott, and it worked out well because I was already traveling to Charlottesville.

The talk will be titled "Why Do We Overeat?  A Neurobiological Perspective".  Here's the teaser:

Obesity is a leading cause of morbidity and mortality in industrialized nations, yet this is a relatively recent phenomenon.  In the United States, increasing obesity prevalence has paralleled a gradual increase of daily energy intake.  Why do most Americans eat more than we used to, and more than we need to maintain a lean state, despite negative consequences?  This presentation will touch on the neurobiology of action selection, the neurobiology of energy homeostasis, and why our central nervous system hardware may not be up to the task of constructively navigating the modern food environment.

The talk will be attended by medical students, but I also hope to have some doctors and researchers show up, as well as people from the broader Charlottesville community.  It will be a thought-provoking talk regardless of your background, and it will touch on some of my own work.

The talk will be held in the main medical school auditorium, MEB 3110, on Friday, January 17 at noon.  You can find driving directions and parking information by following this link.  You'll probably have to park in a parking garage, either the Lee Street or Central Grounds garage (directions in the link).

For a map of the UVA health system, follow this link.  The Medical Education Building is number 44 on the map, and the talk will be in room MEB 3110 on the 3rd floor of the building.

See you there!

Free e-Book and Ideal Weight Program 2.0 Announcement

I'm happy to announce that we're releasing a free e-book titled Why do We Gain Fat, and How do We Lose it? An Introduction to the Science of Body Fat, by Dan Pardi and myself. This is a slimmed-down version of the longer, fully referenced e-book we offer as part of the Ideal Weight Program. In it, we provide a succinct overview of the science of body fat gain and loss, and the evidence base for our program.  It also contains a schematic that ties together the various concepts in visual form. You can download it from the Dan�s Plan site by following this link to our program overview page.

Ideal Weight Program 2.0 Upgrades

Over the last year, Dan and I have been working hard to improve the Ideal Weight Program, both in response to user feedback and our own ideas for development.  Here are some of the new features we offer in 2014:

1. Four-week meal plans and shopping lists for the FLASH diet and the Simple Food Diet, as requested by Ideal Weight Program users.  This is in addition to the recipes and cooking guides we already provide.  
2. The Protein Unit system.  Research suggests there's an optimal amount of protein for appetite control and fat loss, depending on your height, weight, gender, and physical activity level.  Our fat loss diets are high in protein, but how do you know you're getting the right amount?  We've created a calculator that does it for you automatically, and explains how to apply your personalized Protein Unit value easily and intuitively using real food. 
3. Diet plates.  These are visual guides to following our diets, based loosely on the intuitive USDA MyPlate design.  
4. Cheat sheets.  Put these on your fridge to remind yourself of your diet and lifestyle guidelines, and daily protein unit goal.
5. Updated guidance.  We've refined a few things in the diet guidance documents. 

At a time of year when many people want to shed excess holiday pounds and start down a leaner, healthier path, we offer the Ideal Weight Program 2.0.  The program comes with a 30-day no-questions-asked refund policy so you can try it without risk.  We think you'll love this program, but if it doesn't work for you, we're happy to refund your purchase price. 

Financial disclosure: I receive a portion of the revenue from the sale of the Ideal Weight Program.  I do not receive revenue from the sale of other products associated with Dan's Plan or the Ideal Weight Program (such as the Fitbit, cooking tools, and other programs).

Does the Vitamin and Mineral Content of Food Influence Our Food Intake and Body Fatness?

The Claim: We Overeat Because Our Diet is Low in Vitamins and Minerals

We know that animals, including humans, seek certain properties of food. Humans are naturally attracted to food that's high in fat, sugar, starch, and protein, and tend to be less enthusiastic about low-calorie foods that don't have these properties, like vegetables (1). Think cookies vs. plain carrots.

In certain cases, the human body is able to detect a nutritional need and take steps to correct it. For example, people who are placed on a calorie-restricted diet become hungry and are motivated to make up for the calorie shortfall (2, 3). People who are placed on a low-protein diet crave protein and eat more of it after the restriction is lifted (4). Humans and many other animals also crave and seek salt, which supplies the essential minerals sodium and chlorine, although today most of us eat much more of it than we need to. At certain times, we may crave something sweet or acidic, and pregnant women are well known to have specific food cravings and aversions, although explanations for this remain speculative. Research suggests that certain animals have the ability to correct mineral deficiencies by selecting foods rich in the missing mineral (5).

These observations have led to a long-standing idea that the human body is able to detect vitamin and mineral (micronutrient) status and take steps to correct a deficit. This has led to the secondary idea that nutrient-poor food leads to overeating, as the body attempts to make up for low nutrient density by eating more food. In other words, we overeat because our food doesn't supply the micronutrients our bodies need, and eating a micronutrient-rich diet corrects this and allows us to eat less and lose body fat. These ideas are very intuitive, but intuition doesn't always get you very far in biology. Let's see how they hold up to scrutiny.

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