Monday, August 18, 2014

Science of Nutrition Podcast

I recently did an interview with Seth Yoder, who has a master's degree in nutrition science and writes the blog The Science of Nutrition.  Seth caught my attention recently with his withering review of The Big Fat Surprise, the latest book to claim that ideological/incompetent scientists and public policy makers got the science of nutrition backward and we should all be eating low-carb, high-fat, high-meat diets.  I was impressed by how deeply Seth dug into the reference list, and how well he picked up on subtle but troubling misrepresentations of the evidence.

Last week, Seth and I got together at a local brewpub to do an interview.  We were joined by Carrie Dennett, an MPH/RDN who has a nutrition blog and writes for the Seattle Times.  I'd probably do a lot more interviews if I could ride my bike to them and have my interviewer buy me a drink.

Speaking of drinks, by the end of the interview I had a little buzz-- you might hear it in my voice if you listen closely.  As usual, I had plenty to say about body fat regulation, food reward, and other topics, with plenty of side trips to discuss particularly fascinating studies.  Also, the word of the day was 'compelling'.

Enjoy the interview!

Tuesday, August 5, 2014

Can Hypothalamic Inflammation and Leptin Resistance be Reversed?

A new study by yours truly begins to address the key question: can hypothalamic inflammation and leptin resistance be reversed?

Leptin is the primary hormonal regulator of body fatness in the human body (1).  Secreted by fat tissue, it acts in many places in the body, but its most important effects on body weight occur via the brain, and particularly a brain region called the hypothalamus.  The hypothalamus is responsible for keeping certain physiological variables within the optimal range, including blood pressure, body temperature, and body fatness.

In obesity, the brain loses its sensitivity to leptin, and this causes the body to begin 'defending' a higher level of body fatness, analogous to how a person with a fever 'defends' a higher body temperature (1).  Once a person has become obese, it's difficult to return to true leanness because this system vigorously opposes major fat loss.  Leptin resistance makes fat loss more difficult.

In rodent models, leptin resistance is caused at least in part by inflammatory signaling in the hypothalamus.  We can observe this in multiple ways, but one common way is to look at the appearance of specific cells in the brain that change number, size, and shape when inflammation is present (2).  These cells are called microglia and astrocytes.  In addition to the work in rodents, we've published preliminary evidence that these same inflammatory changes occur in the hypothalamus of obese humans (2).

A key question is whether or not these inflammatory changes can be reversed.  Is a person with leptin resistance doomed to have it forever, undermining fat loss efforts for the rest of his or her life?  Or can it be corrected, possibly allowing easier and more sustainable fat loss?  We just published a study in Endocrinology that begins to answer this question, using a mouse model of dietary obesity (3).  I'm co-first author of this study along with my colleague Kathryn Berkseth, MD.  My former mentor Mike Schwartz, MD is senior author.

The Study

Friday, August 1, 2014

Wednesday, July 23, 2014

Help Fund High-Quality Research on Diet and Health

University of California, San Francisco researcher Dr. Ashley Mason has asked me to spread the word about a diet-health study she's preparing to conduct in collaboration with Dr. Lynda Frassetto.  Dr. Frassetto is a widely recognized expert on mineral metabolism and bone health, and also one of the few researchers who has managed to wrangle funding to study the health impacts of a Paleolithic-style diet.  Her findings have been quite provocative.  

Together with their collaborators, Drs. Mason and Frassetto are preparing another diet-health trial to study the impact of two different diets on polycystic ovary syndrome, or PCOS.  PCOS is a common hormonal disorder among reproductive-age women, and its signs and symptoms include ovarian cysts, excess hair growth, menstrual irregularity or absence, infertility, and obesity.  Its causes are unknown, but insulin resistance is a core characteristic of it and is thought to play an important role.  PCOS is thought to be influenced by diet and lifestyle. 


A research team including Drs. Frassetto and Mason, as well as Drs. Umesh Masharani, Heather Huddleston, and Michael Cohn will test a Paleolithic-style diet and an American Diabetes Asssociation diet to see if either or both improves insulin resistance and menstrual cycle regularity for women with PCOS.  Each diet will likely have beneficial effects, however it remains unknown which will be more effective at treating PCOS.

Currently, it's exceedingly difficult for researchers to land funding from the National Institutes of Health (NIH) to do nutrition-related research in the context of disease treatment or management, particularly if it involves a Paleo diet. Recognizing the important potential of fleshing out the relationship between diet and health, researchers are looking for other ways to fund their work.  This study will give them the early data they need to start large, truly definitive studies of the links between diet and insulin resistance, and you can help make it happen.

Please check out their crowdfunding website to learn more about the study, the researchers, and make tax-deductible donations to support their work. And, if you're attending the Ancestral Health Symposium, one of the "backer" rewards is having lunch with the researchers.

Click here to see their crowdfunding site! 



This post was prepared in part using content provided by Dr. Mason.

Monday, July 14, 2014

Instant Pot Electronic Pressure Cooker: Two Years Later

I've had several people tell me that the Whole Health Source post that changed their lives the most was one I published in 2012-- about a pressure cooker.

In 2012, I first reviewed the Instant Pot-- a "pressure cooker for the 21st century" that also doubles as a slow cooker and rice cooker (1).  Since then, we've used it more than 400 times, and it has saved us countless hours of kitchen drudgery.  It's indispensable for my current cooking style, and a major time saver for anyone who leads a busy life but still wants to cook wholesome food at home.  It's extremely satisfying to be able to put your ingredients into the Instant Pot, push a couple of buttons, do something else until it beeps, and then eat a healthy, inexpensive, and delicious meal.

Pressure cookers are one of the most time- and energy-efficient cooking tools, but electronic versions are even more efficient than traditional stovetop pressure cookers.  They're more time-efficient because you don't have to fiddle with them-- for example, adjusting the heat.  They're more energy-efficient because 1) they stop heating when the interior has reached the appropriate pressure, meaning that they're only using energy for part of the cooking process and they hardly vent any energy-wasting steam, and 2) they're insulated well enough that the sides never get hot.

I've used my Instant Pot for a wide variety of cooking tasks, and this is what it does best:

Thursday, July 10, 2014

Upcoming Talks

I have two talks planned over the next two months.  Hope to see you there!

Ancestral Health Symposium 2014: UC Berkeley, August 7-9

If you want to understand the most rigorous science available on leptin resistance-- a key mechanism of obesity and a major barrier to fat loss-- this talk is for you.  This is my primary area of professional expertise; I have years of firsthand research experience on the subject and I've published a number of related papers in peer-reviewed journals.  The talk will be accessible to nearly all levels of expertise.  AHS14 tickets are available here.  I've pasted the talk's abstract below.

What Causes Leptin Resistance?

Leptin is the primary hormonal regulator of body fatness.  Obese people exhibit a resistance to leptin’s effects in the brain, causing the brain to oppose fat loss by multiple mechanisms.  Research in animal models suggests that leptin resistance may be required for obesity to develop.  How does leptin resistance occur, and what causes it?  Research has not yet provided us with definitive answers, but several plausible possibilities have emerged.  This talk will review what is known about leptin resistance and its causes.

McDougall Advanced Study Weekend: Santa Rosa, CA, September 5-7

Dr. John McDougall invited me to speak at his yearly symposium after viewing my TEDx talk "The American Diet: a Historical Perspective".  I look forward to sharing my thoughts and interacting with a different audience than I'm used to.  The talk will be an expanded version of the one I presented at AHS13.  Tickets are available here.  I've pasted a modified version of my AHS13 abstract below.

Insulin and Obesity: Reconciling Conflicting Evidence

The pancreatic hormone insulin regulates the trafficking and metabolism of carbohydrate and fat, and its secretion is particularly stimulated by carbohydrate and protein.  Since circulating insulin is elevated in common obesity, and insulin influences fatty acid flux into and out of fat tissue, this has raised the possibility that elevated insulin causes common obesity, and that dietary carbohydrate is particularly fattening.  A large amount of evidence appears to support the hypothesis that insulin causes obesity, and a large amount of evidence appears to falsify it.  This presentation will outline a framework capable of reconciling this seemingly conflicting evidence.

Wednesday, June 25, 2014

Fat and Carbohydrate: Clarifications and Details

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 macronutrient composition is best for a person who is already overweight or obese?
  • Is fat inherently fattening and/or unhealthy?
From the beginning