my article

Obesity involves changes in the function of brain regions that regulate body fatness and blood glucose, particularly a region called the hypothalamus.  My colleagues and I previously showed that obesity is associated with inflammation and injury of the hypothalamus in rodent models, and we also presented preliminary evidence that the same might be true in humans.  In our latest paper, we confirm this association, and show that hypothalamic injury is also associated with a marker of insulin resistance, independently of BMI. Introduction Read more »

Girls, and probably boys, are reaching puberty years younger than they did in our great-grandparents' generation.  Why?  There's no shortage of explanations, but the primary reason is probably quite simple. Read more »

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? Read more »

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. Read more »

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 ). Read more »

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?

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 ...

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 ): 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. Received instructions to eat less than...

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 macro...

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: 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. 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 i...

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...

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. Read more »

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-squa...

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 u...

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? Read more »

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. Read more »

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    

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 otherwise excellent 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...

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 a...

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: 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...