Friday, September 16, 2016

Do Blood Glucose Levels Affect Hunger and Satiety?

You've heard the story before: when you eat carbohydrate-rich foods that digest quickly, it sends your blood sugar and insulin levels soaring, then your blood sugar level comes crashing back down and you feel hungry and cranky.  You reach for more carbohydrate, perpetuating the cycle of crashes, overeating, and fat gain.

It sounds pretty reasonable-- in fact, so reasonable that it's commonly stated as fact in popular media and in casual conversation.  This idea is so deeply ingrained in the popular psyche that people often say "I have low blood sugar" instead of "I'm hungry" or "I'm tired".  But this hypothesis has a big problem: despite extensive research, it hasn't been clearly supported.  I've written about this issue before (1).

A new study offers a straightforward test of the hypothesis, and once again finds it lacking.

The study

Friday, July 22, 2016

The most slimming tortillas in the world

It's no secret that I'm an avid food gardener.  In the last two years, I've moved from exclusively growing vegetables to growing large quantities of staple calorie crops, such as potatoes, flour corn, and long-storing winter squash.

Why do I put so much effort into growing my own food, when I could buy it easily and cheaply at the grocery store?  There are a few reasons.  First and foremost, I enjoy it.  Second, it allows me to grow the healthiest and best-tasting ingredients possible (although I think you can compose a very healthy diet from grocery store foods).  Third, it saves a bit of money.  And fourth, it gives me a window into the world of my ancestors.

The fourth point is an important one for me, and it's why I can justify making tortillas the hard way.  What's the hard way, you ask?  Well, first you plant corn.  Then you water and weed it for several months.  Then you harvest the corn, shuck it and dry it on the cob.

Painted Mountain corn from my garden.

Wednesday, July 20, 2016

The Hungry Brain: Book Update

In January of this year, I handed in a complete manuscript draft of my first book, The Hungry Brain, to my editor at Flatiron Books.  This book represents more than two full-time years of my life, and I can't wait for it to hit shelves.  It's markedly different from any other book in its category, and believe it has the potential to substantially change the public conversation on eating behavior and obesity.

In the process of writing The Hungry Brain, I read countless papers and interviewed 36 leading researchers in the fields of neuroscience, obesity research, and anthropology.  I had my brain scanned in an fMRI machine while looking at junk food.  I commissioned and compiled 47 illustrations, schematics, and graphs, mostly by a skilled medical illustrator named Shizuka Aoki.  Yet the book will be accessible to anyone who loves science.

This book is not about me or my world views.  It's not a conspiracy story about how everything we've been told is actually wrong, nor is it a critique of existing ideas about eating behavior and obesity-- although I do correct some misconceptions along the way.  It's about the incredible and rapidly evolving world of research that has so much to teach us about ourselves, but rarely trickles down into the public sphere in a useful form.

In interviews this year, I said I thought the book would be out around September 2016.  That was based on a rough estimate my agent gave me last year.  Sadly, it won't be out until first quarter 2017-- the gears turn slowly in the publishing industry.  But the good news is that Flatiron Books is using this time to do a great job of copyediting, interior design, cover design, and marketing, to make sure this book is as good as it can be, and gets into as many hands as possible.  I'll provide a better date estimate when I have one.

In the meantime, enjoy this short description of the book:

From an obesity and neuroscience researcher with a knack for storytelling, The Hungry Brain uses cutting-edge science to answer the questions: why do we overeat, and what can we do about it?

No one wants to overeat. And certainly no one wants to overeat for years, become overweight, and end up with a high risk of diabetes or heart disease--yet two thirds of Americans do precisely that.  Even though we know better, we often eat too much. Why does our behavior betray our own intentions to be lean and healthy? The problem, argues obesity and neuroscience researcher Stephan J. Guyenet, is not necessarily a lack of willpower or an incorrect understanding of what to eat. Rather, our appetites and food choices are led astray by ancient, instinctive brain circuits that play by the rules of a survival game that no longer exists. And these circuits don’t care about how you look in a bathing suit next summer.

To make the case, The Hungry Brain takes readers on an eye-opening journey through cutting-edge neuroscience that has never before been available to a general audience. The Hungry Brain delivers profound insights into why the brain undermines our weight goals and transforms these insights into practical guidelines for eating well and staying slim. Along the way, it explores how the human brain works, revealing how this mysterious organ makes us who we are.

Wednesday, July 6, 2016

NuSI-funded Study Serves Up Disappointment for the Carbohydrate-insulin Hypothesis of Obesity

A new metabolic ward study tests the idea that lowering insulin via severe carbohydrate restriction increases metabolic rate and accelerates fat loss, independently of calorie intake.  Although carbohydrate restriction did modestly increase metabolic rate, it actually slowed fat loss.  One of the details that sets this study apart from previous studies is that it was funded by the Nutrition Science Initiative, an organization that was founded specifically to test the insulin hypothesis of obesity and related concepts.

Wednesday, June 29, 2016

Two huge new studies further undermine the "obesity paradox"

The "obesity paradox" is the observation that people with higher fat mass sometimes have better health outcomes than lean people, including a lower overall risk of death.  Evidence has been steadily mounting that this finding may be a misleading artifact of the methods used to observe it.  Two massive new studies add to this evidence.

Thursday, June 9, 2016

A Serious Challenge to the 2012 Low-carbohydrate "Metabolic Advantage" Study

Warning: this post will be a bit more wonkish than usual, because I need to get detailed to make my points.  To read a summary, skip to the end.

In 2012, David Ludwig's group published an interesting RCT that suggested a substantial "metabolic advantage" resulting from a high-protein, very-low-carbohydrate diet (VLC) (1).  In other words, this diet led to a higher energy expenditure relative to a normal-protein, low-fat diet (LF) over a one month period (a low-glycemic-load, normal-protein diet was in the middle and not significantly different from the other two).  Resting energy expenditure (REE) was slightly but significantly higher on the VLC diet, and total energy expenditure (TEE) was elevated by a whopping 300+ kcal/day!  I covered the study at the time, describing it as "fascinating" and "groundbreaking", and calling for the study to be replicated so we can be more confident in its unexpected result (2).

This finding has been used by Ludwig, Gary Taubes, and others to support the carbohydrate-insulin hypothesis of obesity, although there is no evidence that the effect was mediated by insulin, and also no evidence that it was mediated by reduced carbohydrate rather than increased protein (3).

Since I published that post, my confidence in the finding-- and particularly the common interpretation of it that reducing carbohydrate intake to a very low level increases REE and TEE-- has gradually been eroding.  This is partially because other studies have generally reported that the carbohydrate:fat ratio of the diet has little or no effect on REE, TEE, or fat storage (4, 5, 6, 7, 8, 9, 10).

Tuesday, May 10, 2016

Why some dogs (and humans) are born hungry

The brain is the central regulator of appetite and body fatness, and genetic variation that affects body fatness tends to act in the brain.  One important site of variation is the POMC gene, which codes for a signaling molecule that suppresses food intake.  A new study shows that Labrador retrievers often carry an inactive version of the POMC gene, causing them to be highly food motivated, obesity-prone-- and perhaps more easily trainable.