Always Hungry? It's Probably Not Your Insulin.

David Ludwig, MD, recently published a new book titled Always Hungry? Conquer cravings, retrain your fat cells, and lose weight permanently.  The book is getting widespread media coverage.  Ludwig is a professor of pediatrics at the Harvard Medical School and a professor of nutrition at the Harvard School of Public Health.  He's a pediatric endocrinologist, but his primary focus is research, particularly the impact of nutrition on hunger, calorie expenditure, and body weight.  Although I sometimes disagree with how he interprets evidence, he has made significant and useful contributions to the scientific literature in these areas, and I also support his efforts to find policy solutions to curb the intake of sweetened beverages and other junk foods.  In the grand scheme of things, he's an ally in the fight to improve the American diet.

Ludwig has written several high-profile op-ed pieces in recent years, both in the popular press and in scientific journals (1, 2).  He argues that our understanding of eating behavior and obesity may be all wrong, and that our focus on calories may be leading us away from the true cause of obesity: hormonal imbalance.  And the primary culprit is insulin.  You might recognize this idea, because it's similar to the one that science journalist Gary Taubes developed in his book Good Calories, Bad Calories.

According to this view, overeating is irrelevant.  We gain fat because our insulin levels are too high, leading our fat tissue to take up too much fat, and other tissues to take up too much glucose, causing our blood energy levels to drop and resulting in fat gain, hunger, and fatigue.  The ultimate cause of the problem is the rapidly-digesting carbohydrate and sugar we eat.  This idea is encapsulated by Ludwig's quote, "Overeating doesn't make you fat.  The process of getting fat makes you overeat" (3).

Here are eleven facts that may make you question this line of reasoning:

How Much do You Know About Your Own Brain?

We tend to believe we're aware of what's happening in our own brains, and also in conscious control of our behavior.  But a growing body of neuroscience and psychology research demonstrates that most of what happens inside the brain-- including the processes that cause us to select and execute behaviors-- is beyond our conscious awareness.  This has important implications for our eating behavior, body weight, and health, as I explore in my upcoming book The Hungry Brain.

Let me give you a straightforward example that illustrates how little of our brain's activity we're aware of.  It focuses on information processing by the visual system, which is one of the best-understood systems of the brain.  I drew the basic facts of this example from a recent talk by the accomplished neuroscience researcher Marcus Raichle, who studies patterns of activity in the human brain.

Healing Back Pain

I've put off writing this post for many years because I know it will be controversial.  But we're a few days from Christmas, and I also know this post will be a wonderful gift for some people.

Chronic or intermittent pain, often located in the back, neck, and/or buttocks, is a major driver of personal suffering and reduced productivity in the US and other affluent nations.  While pain can obviously have a variety of structural causes, such as sprained ankles or bruising, garden-variety back pain usually doesn't.  I've come to believe that such pain is usually psychosomatic in nature-- in other words, caused by the brain but resulting in physical signs and symptoms in the body.  It's widely accepted that a person's mental state can affect pain perception, but this idea goes further.  Pain isn't just exacerbated by a person's mental state; it's often entirely caused by it.

New Evidence Strengthens the Link Between Hypothalamic Injury, Obesity, and Insulin Resistance

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

Fat, Added Fat, and Obesity in America

In the last post, we saw that carbohydrate and particularly sugar intake have been declining in the US since 1999, even as our obesity rate has continued to climb.

In this post, let's look at another putative driver of obesity: our fat intake, and especially our intake of added fats like seed oils, butter, and olive oil.  Like the graphs in the last post, the data underlying the following graphs come from USDA food disappearance records (not self-reported), and NHANES survey data (1, 2).  Also like the last post, the graph of total fat intake is not adjusted for waste (non-eaten food), while the graph of added fat intake is*.  As a consequence, the figures for total carbohydrate and total fat intake are higher than actual intakes, but still good for illustrating trends.

Here we go.  First, total fat:

Carbohydrate, Sugar, and Obesity in America

We like explanations that are simple, easy to understand, and explain everything.  One example of this is the idea that eating carbohydrate, or sugar, is the primary cause of obesity.  This lets us point our finger at something concrete and change our behavior accordingly.  And it's true enough that it has practical value.  But the world around us often turns out to be more complex than we'd like it to be.

The CDC recently released its latest data on the prevalence of obesity in the US, spanning the years 2013-2014 (1).  These data come from its periodic National Health and Nutrition Examination Surveys (NHANES).  Contrary to what many of us had hoped for after a slight decline in obesity in the last survey, the prevalence has once again increased.  Today, roughly 38 percent of US adults have obesity.  As a nation, we're continuing to gain fat, which is extremely concerning.

I decided to examine the relationship between obesity prevalence and our intake of carbohydrate and sugar over the years.  The food intake data come from the USDA's Economic Research Service (2).  For some reason, the data on carbohydrate don't extend beyond 2010.  This probably relates to funding cuts at the USDA*.

Let's have a look at the data for carbohydrate:

Food Reward Friday

This week's lucky "winner"... the Reese's PBC Burger!!

Image credit: The Works

Do Processed and Red Meat Cause Cancer?

Today, the World Health Organization's International Agency for Research on Cancer published a statement in The Lancet detailing its position on the carcinogenicity of processed and red meat (1).  The statement, resulting from a meeting of 22 scientists from 10 countries, concluded that processed meat is a group 1 carcinogen, meaning that it is "definitely carcinogenic to humans".  They also judged that red meat is a group 2A carcinogen, meaning that it probably causes cancer but the evidence isn't as strong.  They're mostly referring to the links between processed and red meat and digestive tract cancer, particularly cancers of the colon and rectum.

These statements were met with a media frenzy, and the expected furor from the meat industry.  The most surprising thing, for me, is that anyone would be surprised by the IARC's statement.

Why Do Girls and Boys Reach Puberty Younger Than They Used To?

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.

Will You Fill Out This Paleo Diet Survey?

This week, I received an e-mail from a graduate student at Humboldt State University named May Patiño.  She asked me to share her online research survey targeted to Paleo dieters.  Here are the goals of her research, in her words:

The main objective of my study is exploring how the Paleo diet is being implemented in practice.  I would like to assess the health outcomes of these practices, as well evaluate how closely they conform to, or deviate from ways this diet is being described in theoretical literature, and implemented in controlled diet trials. I also want to be able to use the data collected to help explain what is driving the popularity of the ancestral health movement. Ultimately, I would like this information to be used to better inform protocols for controlled diet trails.

The survey took me about 40 minutes to complete.  You're welcome to participate whether or not you're on the Paleo diet.  Please consider taking the survey, for the love of science!

Research Survey: The Paleo Diet in the US

That Time I Ate Most of a Large Pizza in One Sitting

Two weeks ago, I had a brush with Extreme Eating.  My experience illustrates some important principles of how the brain regulates appetite and body fatness-- and how it reacts to calorie-dense, highly rewarding foods.

Out for Two Weeks

I'll be out of town with limited internet until September 27th.  Feel free to leave comments, but I won't be able to moderate them until I return.  Sorry for the inconvenience!

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?

More Thoughts on the Recent Low-fat vs. Low-carb Metabolic Ward Study

The recent low-carb vs. low-fat study has provoked criticism from parts of the diet-health community.  Let's examine these objections and see how they hold up to scientific scrutiny.

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.

Refined Sugar Worsens Blood Lipid Markers of Cardiovascular Disease

Blood lipids such as LDL and HDL cholesterol are markers of the biological processes that impact cardiovascular disease, and they are commonly measured to assess cardiovascular risk.  When we think about the impact of food on blood lipids, dietary fat typically comes to mind.  Yet a new study shows that dietary carbohydrate, specifically high-fructose corn syrup, can have a large impact on blood lipid markers of cardiovascular disease risk.

Introduction

Dietary fats have well-established impacts on blood lipids.  For example, in short-term feeding trials, saturated fat tends to increase total cholesterol, increase LDL ("bad") cholesterol, and increase HDL ("good") cholesterol, while the omega-6 polyunsaturated fat linoleic acid decreases total cholesterol and decreases LDL cholesterol.  For this reason, dietary advice to reduce cardiovascular risk tends to focus on dietary fat.

The hypothesis that refined dietary sugar is harmful to the cardiovascular system isn't new.  In 1972, British physiologist and nutrition researcher John Yudkin published a classic book called Pure, White, and Deadly, which argued, among other things, that refined sugar is harmful to the cardiovascular system.  Yet at the time, the supporting data were weak, and the hypothesis was never taken very seriously by the scientific community.

Peter Havel and his group at UC Davis have begun to breathe new life into this hypothesis with their rigorous work on the cardiovascular effects of dietary sugars.

What Properties Make a Food "Addictive"?

Although the concept of food addiction remains controversial, there's no doubt that specific foods can provoke addiction-like behaviors in susceptible people.  Yet not all foods have this effect, suggesting that it's related to specific food properties.  A new study aims to identify the properties that make a food "addictive".

Introduction

Food Reward Friday

This week's luck winner... soy sauce!!

Food Reward Friday

This week's lucky winner... the Pizza Hut Hot Dog Bites pizza!!!

Insulin Resistance Predicts a Variety of Age-related Diseases

In the last post, I reviewed a study by Gerald Reaven's group showing that insulin resistance strongly predicts the risk of cardiovascular disease over a 5-year period.  In 2001, Reaven's group published an even more striking follow-up result from the same cohort (1).  This study shows that not only does insulin resistance predict cardiovascular disease risk, it also predicts a variety of age-related diseases, including hypertension, coronary heart disease, stroke, cancer, type 2 diabetes, and even overall mortality risk.