Is Refined Carbohydrate Addictive?

Recently, a new study was published that triggered an avalanche of media reports suggesting that refined carbohydrate may be addictive:

Refined Carbs May Trigger Food Addiction
Refined Carbs May Trigger Food Addictions
Can You be Addicted to Carbs?
etc.

This makes for attention-grabbing headlines, but in fact the study had virtually nothing to do with food addiction. The study made no attempt to measure addictive behavior related to refined carbohydrate or any other food, nor did it aim to do so.

So what did the study actually find, why is it being extrapolated to food addiction, and is this a reasonable extrapolation? Answering these questions dredges up a number of interesting scientific points, some of which undermine popular notions of what determines eating behavior.

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More Thoughts on Cold Training: Biology Chimes In

Now that the concept of cold training for cold adaptation and fat loss has received scientific support, I've been thinking more about how to apply it. A number of people have been practicing cold training for a long time, using various methods, most of which haven't been scientifically validated. That doesn't mean the methods don't work (some of them probably do), but I don't know how far we can generalize individual results prior to seeing controlled studies.

The studies that were published two weeks ago used prolonged, mild cold exposure (60-63 F air) to achieve cold adaptation and fat loss (1, 2). We still don't know whether or not we would see the same outcome from short, intense cold exposure such as a cold shower or brief cold water plunge. Also, the fat loss that occurred was modest (5%), and the subjects started off lean rather than overweight. Normally, overweight people lose more fat than lean people given the same fat loss intervention, but this possibility remains untested. So the current research leaves a lot of stones unturned, some of which are directly relevant to popular cold training concepts.

In my last post on brown fat, I mentioned that we already know a lot about how brown fat activity is regulated, and I touched briefly on a few key points. As is often the case, understanding the underlying biology provides clues that may help us train more effectively. Let's see what the biology has to say.

Biology of Temperature Regulation

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AHS Talk This Saturday

For those who are attending the Ancestral Health Symposium this year, my talk will be at 9:00 AM on Saturday.  The title is "Insulin and Obesity: Reconciling Conflicting Evidence", and it will focus on the following two questions:

1. Does elevated insulin cause obesity; does obesity cause elevated insulin; or both?
2. Is there a unifying hypothesis that's able to explain all of the seemingly conflicting evidence cited by each side of the debate?

I'll approach the matter in true scientific fashion: stating hypotheses, making rational predictions based on those hypotheses, and seeing how well the evidence matches the predictions.  I'll explore the evidence in a way that has never been done before (to my knowledge), even on this blog.

Why am I giving this talk?  Two reasons.  First, it's an important question that has implications for the prevention and treatment of obesity, and it has received a lot of interest in the ancestral health community and to some extent among obesity researchers.  Second, I study the mechanisms of obesity professionally, I'm wrapping up a postdoc in a lab that has focused on the role of insulin in body fatness (lab of Dr. Michael W. Schwartz), and I've thought about this question a lot over the years-- so I'm in a good position to speak about it.

The talk will be accessible and informative to almost all knowledge levels, including researchers, physicians, and anyone who knows a little bit about insulin.  I'll cover most of the basics as we go.  I guarantee you'll learn something, whatever your knowledge level.

Brown Fat: It's a Big Deal

Non-shivering thermogenesis is the process by which the body generates extra heat without shivering. Shivering is a way for the body to use muscular contractions to generate heat, but non-shivering thermogenesis uses a completely different mechanism to accomplish the same goal: a specialized fat-burning tissue called brown fat. Brown fat is brown rather than white because it's packed with mitochondria, the power plants of the cell. Under cold conditions, these mitochondria are activated, using a specialized molecular mechanism called uncoupling* to generate heat.

The mechanism of brown fat activation has been worked out fairly well in rodents, which rely heavily on non-shivering thermogenesis due to their small body size. Specialized areas of the hypothalamus in the brain sense body temperature (through sensors in the brain and body), body energy status (by measuring leptin and satiety signals), stress level, and probably other factors, and integrate this information to set brown fat activity. The hypothalamus does this by acting through the sympathetic nervous system, which heavily innervates brown fat. As an aside, this process works basically the same in humans, as far as we currently know. Those who claim that rodent models are irrelevant to humans are completely full of hot air**, as the high degree of conservation of the hypothalamus over 75 million years of evolution demonstrates.

Two new studies concurrently published in the Journal of Clinical Investigation last week demonstrate what I've suspected for a long time: brown fat can be 'trained' by cold exposure to be more active, and its activation by cold can reduce body fatness.

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The Genetics of Obesity, Part III

Genetics Loads the Gun, Environment Pulls the Trigger

Thanks to a WHS reader* for reminding me of the above quote by Dr. Francis Collins, director of the US National Institutes of Health**. This is a concept that helps reconcile the following two seemingly contradictory observations:

1. Roughly 70 percent of obesity risk is genetically inherited, leaving only 30 percent of risk to environmental factors such as diet and lifestyle.
2. Diet and lifestyle have a large impact on obesity risk. The prevalence of obesity has tripled in the last 30 years, and the prevalence of extreme obesity has increased by almost 10-fold. This is presumably not enough time for genetic changes to account for it.

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The Genetics of Obesity, Part II

Rodents Lead the Way

The study of obesity genetics dates back more than half a century. In 1949, researchers at the Jackson Laboratories identified a remarkably fat mouse, which they determined carried a spontaneous mutation in an unidentified gene. They named this the "obese" (ob/ob) mouse. Over the next few decades, researchers identified several other genetically obese mice with spontaneous mutations, including diabetic (db/db) mice, "agouti" (Avy) mice, and "Zucker" (fa/fa) rats.

At the time of discovery, no one knew where the mutations resided in the genome. All they knew is that the mutations were in single genes, and they resulted in extreme obesity. Researchers recognized this as a huge opportunity to learn something important about the regulation of body fatness in an unbiased way. Unbiased because these mutations could be identified with no prior knowledge about their function, therefore the investigators' pre-existing beliefs about the mechanisms of body fat regulation could have no impact on what they learned. Many different research groups tried to pin down the underlying source of dysfunction: some thought it was elevated insulin and changes in adipose tissue metabolism, others thought it was elevated cortisol, and a variety of other hypotheses.

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The Genetics of Obesity, Part I

Choosing the Right Parents: the Best Way to Stay Lean?

In 1990, Dr. Claude Bouchard and colleagues published a simple but fascinating study demonstrating the importance of genetics in body fatness (1). They took advantage of one of the most useful tools in human genetics: identical twins. This is what happens when a single fertilized egg generates two embryos in utero and two genetically identical humans are born from the same womb. By comparing identical twins to other people who are not genetically identical (e.g., non-identical twins), we can quantify the impact of genes vs. environment on individual characteristics (2).

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The Neurobiology of the Obesity Epidemic

I recently read an interesting review paper by Dr. Edmund T. Rolls titled "Taste, olfactory and food texture reward processing in the brain and the control of appetite" that I'll discuss in this post (1). Dr. Rolls is a prolific neuroscience researcher at Oxford who focuses on "the brain mechanisms of perception, memory, emotion and feeding, and thus of perceptual, memory, emotional and appetite disorders." His website is here.

The first half of the paper is technical and discusses some of Dr. Rolls' findings on how specific brain areas process sensory and reward information, and how individual neurons can integrate multiple sensory signals during this process. I recommend reading it if you have the background and interest, but I'm not going to cover it here. The second half of the paper is an attempt to explain the obesity epidemic based on what he knows about the brain and other aspects of human biology.

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Speaking at AHS13

The 2013 Ancestral Health Symposium will be held in Atlanta, GA, August 14-17.  Last year was a great conference, and I look forward to more informative talks and networking.  Tickets go fast, so reserve yours now if you plan to attend!

This year, I'll be speaking on insulin and obesity.  My talk will be titled "Insulin and Obesity: Reconciling Conflicting Evidence".  In this talk, I'll present the evidence for and against the idea that elevated insulin contributes to the development of obesity.  One hypothesis states that elevated insulin contributes to obesity, while the other states that elevated insulin is caused by obesity and does not contribute to it.  Both sides of the debate present evidence that appears compelling, and it often seems like each side is talking past the other rather than trying to incorporate all of the evidence into a larger, more powerful model.

There's a lot evidence that can be brought to bear on this question, but much of it hasn't reached the public yet.  I'll explore a broad swath of evidence from clinical case studies, observational studies, controlled trials, animal research, physiology, and cell biology to test the two competing hypotheses and outline a model that can explain all of the seemingly conflicting data.  Much of this information hasn't appeared on this blog.  My goal is to put together a talk that will be informative to a researcher but also accessible to an informed layperson.

On a separate note, my AHS12 talk "Digestive Health, Inflammation and the Metabolic Syndrome" has not been posted online because the video recording of my talk has mysteriously disappeared.  I think many WHS readers would be interested in the talk, since it covers research on the important and interdependent influence of gut health, inflammation, and psychological stress on the metabolic syndrome (the quintessential modern metabolic disorder).  I'm going to try to find time to make a narrated slideshow so I can post it on YouTube.

Food Variety, Calorie Intake, and Weight Gain

Let's kick off this post with a quote from a 2001 review paper (1):

Increased variety in the food supply may contribute to the development and maintenance of obesity. Thirty-nine studies examining dietary variety, energy intake, and body composition are reviewed. Animal and human studies show that food consumption increases when there is more variety in a meal or diet and that greater dietary variety is associated with increased body weight and fat.

This may seem counterintuitive, since variety in the diet is generally seen as a good thing. In some ways, it is a good thing, however in this post we'll see that it can have a downside.
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Book Review: Salt, Sugar, Fat

Michael Moss is a Pulitzer prize-winning journalist who has made a career writing about the US food system. In his latest book, Salt, Sugar, Fat: How the Food Giants Hooked Us, he attempts to explain how the processed food industry has been so successful at increasing its control over US "stomach share". Although the book doesn't focus on the obesity epidemic, the relevance is obvious. Salt, Sugar, Fat is required reading for anyone who wants to understand why obesity is becoming more common in the US and throughout the world.

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Glucagon, Dietary Protein, and Low-Carbohydrate Diets

Glucagon is a hormone that plays an important role in blood glucose control. Like insulin, it's secreted by the pancreas, though it's secreted by a different cell population than insulin (alpha vs. beta cells). In some ways, glucagon opposes insulin. However, the role of glucagon in metabolism is frequently misunderstood in diet-health circles.

The liver normally stores glucose in the form of glycogen and releases it into the bloodstream as needed. It can also manufacture glucose from glycerol, lactate, and certain amino acids. Glucagon's main job is to keep blood glucose from dipping too low by making sure the liver releases enough glucose. There are a few situations where this is particularly important:

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Neuronal Control of Appetite, Metabolism and Weight

Last week, I attended a Keystone conference, "Neuronal Control of Appetite, Metabolism and Weight", in Banff. Keystone conferences are small, focused meetings that tend to attract high quality science. This particular conference centered around my own professional research interests, and it was incredibly informative. This post is a summary of some of the most salient points.

Rapid Pace of Scientific Progress

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Body Fatness and Cardiovascular Risk Factors

I recently revisited a really cool paper published in the Lancet in 2009 on body fatness, biomarkers, health, and mortality (1). It's a meta-analysis that compiled body mass index (BMI) data from nearly 900,000 individual people, and related it to circulating lipids and various health outcomes. This is one of the most authoritative papers on the subject.

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Why Do We Eat? A Neurobiological Perspective. Part VIII

In the (probably) last post of this series, I'll take the pieces that I've gradually outlined in previous posts, and put them together into a big-picture, common-sense framework for thinking about human eating behavior, and why we eat more today than ever before.

Why is Eating Behavior Regulated?

Let's start at the most fundamental level. To be competitive in a natural environment, organisms must find rational ways of interacting with their surroundings to promote survival and reproduction. One of the most important elements of survival is the acquisition of energy and chemical building blocks, either by photosynthesis, or (in the case of animals) eating other organisms. This imperative drove the evolution of rational food seeking behaviors long before the emergence of humans, mammals, reptiles, amphibians, fish, worms, and even eukaryotes (organisms with nuclei).

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Why Do We Eat? A Neurobiological Perspective. Part VI

In previous posts in this series, I explained that the brain (primarily the mesolimbic system) integrates various factors to decide whether or not to drive food seeking and consumption behaviors. These include homeostatic factors such as hunger, and non-homeostatic factors such as palatability and the social environment.

In this post, I'll examine the reward system more closely. This is the system that governs the motivation for food, and behavioral reinforcement (a form of learning). It does this by receiving information from other parts of the brain that it uses to determine if it's appropriate to drive (motivate) food seeking behavior. I covered its role in motivation in the first post of the series, so in this post I'll address reinforcement.

Behavioral Reinforcement

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Why Do We Eat? A Neurobiological Perspective. Part IV

In this post, I'll follow up on the last post with a discussion two more important factors that can affect energy homeostasis and therefore our food intake and propensity to gain fat: age and menopause.

Age

Although it often isn't the case in non-industrial cultures, in affluent nations most people gain fat with age. This fat gain continues until old age, when many people once again lose fat. This is probably related to a number of factors, three of which I'll discuss. The first is that we tend to become less physically active with age. The second, related factor is that we lose lean mass with age, and so energy expenditure declines.

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Why Do We Eat? A Neurobiological Perspective. Part III

In the first post, I explained that all voluntary actions are driven by a central action selection system in the mesolimbic area (the reward system). This is the part of you that makes the decision to act, or not to act. This system determines your overall motivation to obtain food, based on a variety of internal and external factors, for example hunger, the effort required to obtain food, and the sensory qualities of food/drink. These factors are recognized and processed by a number of specialized 'modules' in the brain, and forwarded to the reward system where the decision to eat, or not to eat, is made. Researchers divide food intake into two categories: 1) eating from a true energy need by the body (homeostatic eating), e.g. hunger, and 2) eating for other reasons (non-homeostatic eating), e.g. eating for social reasons or because the food tastes really good.

In the second post of the series, we explored how the brain regulates food intake on a meal-to meal basis based on feedback from the digestive system, and how food properties can influence this process. The integrated gut-brain system that accomplishes this can be called the satiety system.

In this post, we'll explore the energy homeostasis system, which regulates energy balance (energy in vs. energy out) and body fatness on a long term basis.

The Energy Homeostasis System

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Why Do We Eat? A Neurobiological Perspective. Part II

In the last post, I explained that eating behavior is determined by a variety of factors, including hunger and a number of others that I'll gradually explore as we make our way through the series. These factors are recognized by specialized brain 'modules' and forwarded to a central action selection system in the mesolimbic area (the reward system), which determines if they are collectively sufficient cause for action. If so, they're forwarded to brain systems that directly drive the physical movements involved in seeking and consuming food (motor systems).

The term 'homeostasis' is important in biology. Homeostasis is a process that attempts to keep a particular factor within a certain stable range. The thermostat in your house is an example of a homeostatic system. It reacts to upward or downward changes in a manner that keeps temperature in a comfortable range. The human body also contains a thermostat that keeps internal temperature close to 98.6 F. Many things are homeostatically regulated by the body, and one of them is energy status (how much energy the body has available for use). Homeostasis of large-scale processes in the body is typically regulated by the brain.

We can divide the factors that determine feeding behavior into two categories, homeostatic and non-homeostatic. Homeostatic eating is when food intake is driven by a true energy need, as perceived by the brain. For the most part, this is eating in response to hunger. Non-homeostatic eating is when food intake is driven by factors other than energy need, such as palatability, habitual meal time, and food cues (e.g. you just walked by a vending machine full of Flamin' Hot Cheetos).

We can divide energy homeostasis into two sub-categories: 1) the system that regulates short-term, meal-to-meal calorie intake, and 2) the system that regulates fat mass, the long-term energy reserve of the human body. In this post, I'll give an overview of the process that regulates energy homeostasis on a short-term, meal-to-meal basis.

The Satiety System (Short-Term Energy Homeostasis)


The stomach of an adult human has a capacity of 2-4 liters. In practice, people rarely eat that volume of food. In fact, most of us feel completely stuffed long before we've reached full stomach capacity. Why?

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Why Do We Eat? A Neurobiological Perspective. Part I

As with all voluntary movements, eating food is an expression of activity in the brain. The brain integrates various inputs from around the body, and outside the body, and decides whether or not to execute the goal-directed behaviors of food seeking and consumption. Research has uncovered a lot about how this process works, and in this series I'll give a simplified overview of what scientists have learned about how, and why, the brain decides to eat.

The Gatekeeper of Voluntary Behaviors

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