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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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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By 2606, the US Diet will be 100 Percent Sugar

The US diet has changed dramatically in the last 200 years.  Many of these changes stem from a single factor: the industrialization and commercialization of the American food system.  We've outsourced most of our food preparation, placing it into the hands of professionals whose interests aren't always well aligned with ours.

It's hard to appreciate just how much things have changed, because none of us were alive 200 years ago.  To help illustrate some of these changes, I've been collecting statistics on US diet trends.  Since sugar is the most refined food we eat in quantity, and it's a good marker of processed food consumption, naturally I wanted to get my hands on sugar intake statistics-- but solid numbers going back to the early 19th century are hard to come by!  Of all the diet-related books I've read, I've never seen a graph of year-by-year sugar intake going back more than 100 years.

A gentleman by the name of Jeremy Landen and I eventually tracked down some outstanding statistics from old US Department of Commerce reports and the USDA: continuous yearly sweetener sales from 1822 to 2005, which have appeared in two of my talks but I have never seen graphed anywhere else*.  These numbers represent added sweeteners such as cane sugar, high-fructose corn syrup and maple syrup, but not naturally occurring sugars in fruit and vegetables.  Behold:

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My TEDx Talk, "The American Diet: a Historical Perspective"

On October 21st, I spoke at the Harvard Food Law Society's TEDx conference, Forum on Food Policy.  The conference kicked off with three talks on nutrition, by Drs. Walter Willett, David Ludwig and myself.  My talk is only 17 minutes long as per TED format, but it's packed with research on both quantitative and qualitative changes in the US diet over the last two centuries.  It contains surprises for almost anyone, and I can guarantee you've never learned this much about the history of the US diet in 17 minutes.  The talk was titled "The American Diet: a Historical Perspective"; you can access it by following that link.

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An Interview with Dr. C. Vicky Beer, Paleo-friendly MD

As I was preparing my recent article on the Paleo diet (1), I interviewed a local Paleo-friendly MD named C. Vicky Beer.  I was only able to include a snippet of the interview in the article, but I thought WHS readers would be interested to read the rest of the interview with Dr. Beer:

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Paleo Diet Article in Sound Consumer

I recently wrote an article for my local natural foods grocery store, PCC, about the "Paleolithic" diet.  You can read it online here.  I explain the basic rationale for Paleo diets, some of the scientific support behind it, and how it can be helpful for people with certain health problems.  I focused in particular on the research of Dr. Staffan Lindeberg at the University of Lund, who has studied non-industrial populations using modern medical techniques and also conducted clinical diet trials using the Paleo diet.
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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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What Causes Insulin Resistance? Part VI

In this post, I'll explore a few miscellaneous factors that can contribute to insulin resistance: smoking, glucocorticoids/stress, cooking temperature, age, genetics and low birth weight.

Smoking

Smoking tobacco acutely and chronically reduces insulin sensitivity (1, 2, 3), possibly via:

1. Increased inflammation
2. Increased circulating free fatty acids (4)

Paradoxically, since smoking also protects against fat gain, in the very long term it may not produce as much insulin resistance as one would otherwise expect.  Diabetes risk is greatly elevated in the three years following smoking cessation (5), and this is likely due to the fat gain that occurs.  This is not a good excuse to keep smoking, because smoking tobacco is one of the most unhealthy things you can possibly do.  But it is a good reason to tighten up your diet and lifestyle after quitting.

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What Causes Insulin Resistance? Part V

Previously in this series, we've discussed the role of cellular energy excess, inflammation, brain insulin resistance, and micronutrient status in insulin resistance.  In this post, I'll explore the role of macronutrients and sugar in insulin sensitivity.

Carbohydrate and Fat

There are a number of studies on the effect of carbohydrate:fat ratios on insulin sensitivity, but many of them are confounded by fat loss (e.g., low-carbohydrate and low-fat weight loss studies), which almost invariably improves insulin sensitivity.  What interests me the most is to understand what effect different carbohydrate:fat ratios have on insulin sensitivity in healthy, weight stable people.  This will get at what causes insulin resistance in someone who does not already have it.

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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 IV

So far, we've explored three interlinked causes of insulin resistance: cellular energy excess, inflammation, and insulin resistance in the brain.  In this post, I'll explore the effects on micronutrient status on insulin sensitivity.

Micronutrient Status

There is a large body of literature on the effects of nutrient intake/status on insulin action, and it's not my field, so I don't intend this to be a comprehensive post.  My intention is simply to demonstrate that it's important, and highlight a few major factors I'm aware of.

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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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High-Fat Diets, Obesity and Brain Damage

Many of you have probably heard the news this week:

High-fat diet may damage the brain
Eating a high-fat diet may rapidly injure brain cells
High fat diet injures the brain
Brain injury from high-fat foods

Your brain cells are exploding with every bite of butter!  Just kidding.  The study in question is titled "Obesity is Associated with Hypothalamic Injury in Rodents and Humans", by Dr. Josh Thaler and colleagues, with my mentor Dr. Mike Schwartz as senior author (1).  We collaborated with the labs of Drs. Tamas Horvath and Matthias Tschop.  I'm fourth author on the paper, so let me explain what we found and why it's important.  

The Questions

Among the many questions that interest obesity researchers, two stand out:

1. What causes obesity?
2. Once obesity is established, why is it so difficult to treat?

Our study expands on the efforts of many other labs to answer the first question, and takes a stab at the second one as well.  Dr. Licio Velloso and collaborators were the first to show in 2005 that inflammation in a part of the brain called the hypothalamus contributes to the development of obesity in rodents (2), and this has been independently confirmed several times since then.  The hypothalamus is an important brain region for the regulation of body fatness, and inflammation keeps it from doing its job correctly.

The Findings

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A Brief Response to Taubes's Food Reward Critique, and a Little Something Extra

It appears Gary Taubes has completed his series critiquing the food reward hypothesis of obesity (1).  I have to hand it to him, it takes some cojones to critique an entire field of research, particularly when you have no scientific background in it.

The food reward hypothesis of obesity states that the reward and palatability value of food influence body fatness, and excess reward/palatability can promote body fat accumulation.  If we want to test the hypothesis, the most direct way is to find experiments in which 1) the nutritional qualities of the experimental diet groups are kept the same or at least very similar, 2) some aspect of diet reward/palatability differs, and 3) changes in body fat/weight are measured (for example, 2, 3, 4, 5, 6, 7, 8, 9).  In these experiments the hypothesis has both arms and one leg tied behind its back, because the most potent reward factors (energy density, sugar, fat) have nutritional value and therefore experiments that modify these cannot be tightly controlled for nutritional differences.  Yet even with this severe disadvantage, the hypothesis is consistently supported by the scientific evidence.  Taubes repeatedly stated in his series that controlled studies like these have not been conducted, apparently basing this belief on a 22-year-old review paper by Dr. Israel Ramirez and colleagues that does not contain the word 'reward' (10). 

Another way to test the hypothesis is to see if people with higher food reward sensitivity (due to genetics or other factors) tend to gain more fat over time (for example, 11, 12, 13, 14, 15, 16).  In addition, studies that have examined the effect of palatability/reward on food intake in a controlled manner are relevant (17, 18, 19, 20, 21, 22), as are studies that have identified some of the mechanisms by which these effects occur (reviewed in 23).  Even if not all of the studies are perfect, at some point, one has to acknowledge that there are a lot of mutually buttressing lines of evidence here.  It is notable that virtually none of these studies appeared in Taubes's posts, and he appeared largely unaware of them. 
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Losing Fat With Simple Food-- Two Reader Anecdotes

Each week, I'm receiving more e-mails and comments from people who are successfully losing fat by eating simple (low reward) food, similar to what I described here.  In some cases, people are breaking through fat loss plateaus that they had reached on conventional low-carbohydrate, low-fat or paleo diets.  This concept can be applied to any type of diet, and I believe it is an important characteristic of ancestral food patterns.

At the Ancestral Health Symposium, I met two Whole Health Source readers, Aravind Balasubramanian and Kamal Patel, who were interested in trying a simple diet to lose fat and improve their health.  In addition, they wanted to break free of certain other high-reward activities in their lives that they felt were not constructive.  They recently embarked on an 8-week low-reward diet and lifestyle to test the effectiveness of the concepts.  Both of them had previously achieved a stable (in Aravind's case, reduced) weight on a paleo-ish diet prior to this experiment, but they still carried more fat than they wanted to.  They offered to write about their experience for WHS, and I thought other readers might find it informative.  Their story is below, followed by a few of my comments.

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The Case for the Food Reward Hypothesis of Obesity, Part II

In this post, I'll explore whether or not the scientific evidence is consistent with the predictions of the food reward hypothesis, as outlined in the last post.

Before diving in, I'd like to address the critique that the food reward concept is a tautology or relies on circular reasoning (or is not testable/falsifiable).  This critique has no logical basis.  The reward and palatability value of a food is not defined by its effect on energy intake or body fatness.  In the research setting, food reward is measured by the ability of food or food-related stimuli to reinforce or motivate behavior (e.g., 1).  In humans, palatability is measured by having a person taste a food and rate its pleasantness in a standardized, quantifiable manner, or sometimes by looking at brain activity by fMRI or related techniques (2).  In rodents, it is measured by observing stereotyped facial responses to palatable and unpalatable foods, which are similar to those seen in human infants.  It is not a tautology or circular reasoning to say that the reinforcing value or pleasantness of food influences food intake and body fatness. These are quantifiable concepts and as I will explain, their relationship with food intake and body fatness can be, and already has been, tested in a controlled manner. 

1.   Increasing the reward/palatability value of the diet should cause fat gain in animals and humans

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The Case for the Food Reward Hypothesis of Obesity, Part I

Introduction

When you want to investigate something using the scientific method, first you create a model that you hope describes a natural phenomenon-- this is called a hypothesis.  Then you go about testing that model against reality, under controlled conditions, to see if it has any predictive power.  There is rarely a single experiment, or single study, that can demonstrate that a hypothesis is correct.  Most important hypotheses require many mutually buttressing lines of evidence from multiple research groups before they're widely accepted.  Although it's not necessary, understanding the mechanism by which an effect occurs, and having that mechanism be consistent with the hypothesis, adds substantially to the case.

With that in mind, this post will go into greater detail on the evidence supporting food reward and palatability as major factors in the regulation of food intake and body fatness.  There is a large amount of supportive evidence at this point, which is rapidly expanding due to the efforts of many brilliant researchers, however for the sake of clarity and brevity, so far I've only given a "tip of the iceberg" view of it.  But there are two types of people who want more detail: (1) the skeptics, and (2) scientifically inclined people who want mechanism.  This post is for them.  It will get technical at times, as there is no other way to convey the material effectively.

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Humans on a Cafeteria Diet

In the 1970s, as the modern obesity epidemic was just getting started, investigators were searching for new animal models of diet-induced obesity.  They tried all sorts of things, from sugar to various types of fats, but none of them caused obesity as rapidly and reproducibly as desired*.  1976, Anthony Sclafani tried something new, and disarmingly simple, which he called the "supermarket diet": he gave his rats access to a variety of palatable human foods, in addition to standard rodent chow.  They immediately ignored the chow, instead gorging on the palatable food and rapidly becoming obese (1).  Later renamed the "cafeteria diet", it remains the most rapid and effective way of producing dietary obesity and metabolic syndrome in rodents using solid food (2).

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Hyperinsulinemia: Cause or Effect of Obesity?

Is Elevated Insulin the Cause or Effect of Obesity?

The carbohydrate hypothesis, in its most popular current incarnation, states that elevated insulin acts on fat cells to cause fat storage, leading to obesity.  This is due to its ability to increase the activity of lipoprotein lipase and decrease the activity of hormone-sensitive lipase, thus creating a net flux of fat into fat cells.  I'm still not sure why this would be the case, considering that fat tissue becomes more insulin resistant as body fat accumulates, therefore insulin action on it is not necessarily increased.  Total fat release from fat tissue increases with total fat mass (1), demonstrating that insulin is not able to do its job of suppressing fat release as effectively in people who carry excess fat.  But let's put that problem aside for the moment and keep trucking.

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