Food Reward Friday

This week's lucky winner... Cheesecake Factory carrot cake!!

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Food Reward Friday

This week's lucky "winner"... Pumpkin pie!!

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Food Reward Friday

This week's lucky "winner"... Pizza Hut Doritos Crunchy Crust Pizza!

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Recent Interviews

For those who don't follow my Twitter account (@whsource), here are links to my two most recent interviews.

Smash the Fat with Sam Feltham.  We discuss the eternally controversial question, "is a calorie a calorie"?  Like many other advocates of the low-carbohydrate diet, Feltham believes that the metabolic effects of food (particularly on insulin), rather than calorie intake per se, are the primary determinants of body fatness.  I explain the perspective that my field of research has provided on this question.  We also discussed why some lean people become diabetic.  Feltham was a gracious host.

Nourish, Balance, Thrive with Christopher Kelly.  Kelly is also an advocate of the low-carbohydrate diet for fat loss.  This interview covered a lot of ground, including the insulin-obesity hypothesis, regulation of body fatness by the leptin-brain axis, how food reward works to increase calorie intake, and the impact of the food environment on food intake.  I explain why I think proponents of the insulin-obesity hypothesis have mistaken association for causation, and what I believe the true relationship is between insulin biology and obesity.  Kelly was also a gracious host.  He provides a transcript if you'd rather read the interview in text form.

Food Reward Friday

This week's lucky "winner"... the pumpkin spice latte!!

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Obesity → Diabetes

A new study adds to the evidence that the prevalence of type 2 diabetes is rapidly increasing in the US, and our national weight problem is largely to blame.

The Centers for Disease Control (CDC) currently estimates that a jaw-dropping 33 percent of US men, and 39 percent of US women, will develop diabetes at some point in their lives (1).  Roughly one out of three people in this country will develop diabetes, and those who don't manage it effectively will suffer debilitating health consequences.  Has the risk of developing diabetes always been so high, and if not, why is it increasing?

In the same issue of the Annals of Internal Medicine as the low-carb vs. low-fat study, appears another study that aims to partially address this question (2).

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Food Reward Friday

This week's lucky "winner"... profiteroles!!

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Metabolic Effects of a Traditional Asian High-carbohydrate Diet

A recent study supports the notion that an 'ancestral diet' focused around high-starch agricultural foods can cultivate leanness and metabolic health.

John McDougall gave Christopher Gardner a hard time at the McDougall Advanced Study Weekend.  Dr. Gardner conducts high-profile randomized controlled trials (RCTs) at Stanford to compare the effectiveness of a variety of diets for weight loss, cardiovascular and metabolic health.  The "A to Z Study", in which Atkins, Zone, Ornish, and LEARN diets were pitted against one another for one year, is one of his best-known trials (1).

Dr. McDougall asked a simple question: why haven't these trials evaluated the diet that has sustained the large majority of the world's population for the last several thousand years?  This is an agriculturalist or horticulturalist diet based around starchy foods such as grains, tubers, legumes, and plantains, and containing little fat or animal foods.  Researchers have studied a number of cultures eating this way, and have usually found them to be lean, with good cardiovascular and metabolic health.  Why not devote resources to studying this time-tested ancestral diet?  I think it's a fair question.

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Help Advance Diabetes Research

A University of Virginia researcher named Hannah Menefee contacted me recently to ask for our help.  She and her colleagues are conducting a study on how people with type 2 diabetes use Facebook to manage their health, and how that technology can be leveraged to support effective health communication.

If you have type 2 diabetes, and you'd like to participate in the study, please join their Diabetes Management Study Facebook group.  There, you'll receive more information about the study, you'll receive a short survey, and you may be invited into one of the study phases.

Food Reward Friday

Today's lucky "winner"... waffles!!!

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My AHS14 Talk on Leptin Resistance is Posted

The Ancestral Health Society just posted a video of my recent talk "What Causes Leptin Resistance?"  Follow the link below to access it.  Enjoy!

What Causes Leptin Resistance?

Thoughts on the McDougall Advanced Study Weekend

For those of you who aren't familiar with him, Dr. John McDougall is a doctor and diet/health advocate who recommends a very low fat, high starch, whole food vegan diet to control weight and avoid chronic disease.  He's been at it for a long time, and he's a major figure in the "plant-based diet" community (i.e., a diet including little or no animal foods).

Dr. McDougall invited me to participate in his 3-day Advanced Study Weekend retreat in Santa Rosa, CA.  My job was to give my talk on insulin and obesity, and participate in a panel discussion/debate with Dr. McDougall in which we sorted through issues related to low-carb, Paleo, and the health implications of eating animal foods.  I was glad to receive the invitation, because I don't see myself as a diet partisan, and I believe that my evidence-based information is applicable to a variety of diet styles.  I saw the Weekend as an opportunity to extend my thoughts to a new community, challenge myself, and maybe even learn a thing or two.  It was particularly interesting to compare and contrast the Advanced Study Weekend with the Ancestral Health Symposium, which is more Paleo- and low-carb-friendly.

General Observations

The attendees were a lot older than AHS attendees.  I estimate that most of them were in their 60s, although there were some young people in attendance.

I don't place too much emphasis on peoples' personal appearance at conferences like this.  You don't know what a person's background, genetics, or personal struggles may be, you don't know how closely they adhere to the program, and you don't know to what degree a group of people might be self-selected for particular traits*.  But I will note that Dr. McDougall, his family, and many of the other starch-based/plant-based diet advocates tended to be extremely lean with low fat and muscle mass.  They also tended to have a healthy and energetic appearance and demeanor.  As I would expect, decades of exceptionally high starch intake hasn't made them obese or obviously ill.

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What about the Other Weight Loss Diet Study??

The same day the low-fat vs low-carb study by Bazzano and colleagues was published, the Journal of the American Medical Association published a meta-analysis that compared the effectiveness of "named diet programs".  Many people have interpreted this study as demonstrating that low-carbohydrate and low-fat diets are both effective for weight loss, and that we simply need to pick a diet and stick with it, but that's not really what the study showed.  Let's take a closer look.

Johnston and colleagues sifted through PubMed for studies that evaluated "named diet programs", such as Ornish, Atkins, LEARN, Weight Watchers, etc (1).  In addition, the methods state that they included any study as low-carbohydrate that recommended less than 40% of calories from carbohydrate, was funded by the Atkins foundation, or was "Atkins-like".  These criteria weren't extended to the low-fat diet: only studies of name-brand low-fat diets like the Ornish diet were included, while the meta-analysis excluded low-fat diet studies whose guidelines were based on recommendations from government and academic sources, even though the latter group represents the majority of the evidence we have for low-fat diets.  The inclusion criteria were therefore extremely asymmetrical in how they represented low-carb and low-fat diets.  This fact explains the unusual findings of the paper.

The abstract immediately activated my skeptic alarm, because it states that at the one-year mark, low-carbohydrate diets and low-fat diets both led to a sustained weight loss of about 16 pounds (7.3 kg).  Based on my understanding of the weight loss literature, that number seems far too high for the low-fat diet, and also too high for the low-carbohydrate diet.

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Low-carbohydrate vs. Low-fat diets for Weight Loss: New Evidence

A new high-profile study compared the weight loss and cardiovascular effects of a low-carbohydrate diet vs. a low-fat diet.  Although many studies have done this before, this one is novel enough to add to our current understanding of diet and health.  Unlike most other studies of this nature, diet adherence was fairly good, and carbohydrate restriction produced greater weight loss and cardiovascular risk factor improvements than fat restriction at the one-year mark.  Yet like previous studies, neither diet produced very impressive results.

The Study

Lydia A. Bazzano and colleagues at Tulane University randomly assigned 148 obese men and women without cardiovascular disease into two groups (1):

1. Received instructions to eat less than 40 grams of carbohydrate per day, plus one low-carbohydrate meal replacement per day.  No specific advice to alter calorie intake.  Met regularly with dietitians to explain the dietary changes and maintain motivation.
2. Received instructions to eat less than 30 percent of calories from fat, less than 7 percent of calories as saturated fat, and 55 percent of calories from carbohydrate, plus one low-fat meal replacement per day.  No specific advice to alter calorie intake.  This is based on NCEP guidelines, which are actually designed for cardiovascular risk reduction and not weight loss.  Met regularly with dietitians to explain the dietary changes and maintain motivation.

Participants were followed up for one year, with data reported for 3 month, 6 month, and 12 month timepoints.  This study actually measured body fat percentage, but unfortunately did so using bioelectrical impedance (like on some bathroom scales), which is essentially meaningless in this context.

Results

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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!

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

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Food Reward Friday

This week's lucky "winner"...  Cheesecake Factory Bruleed French Toast!

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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.

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:

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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.

Food Reward Friday

This week's lucky "winner"... kettle corn!

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Has Obesity Research Failed?

I frequently encounter the argument that obesity research has failed because it hasn't stopped the global increase in obesity rates.  According to this argument, we need to re-think our approach to obesity research because the current approach just isn't working.

Grant funding for obesity research keeps increasing in the US, and the prevalence of obesity also keeps increasing*.  What gives?  Maybe if we just scrapped the whole endeavor we'd be better off.

Let's take a closer look at this argument and see how it holds up.

Why Do Research?

There are two fundamental reasons why we do research:

1. To gather accurate information about the natural world.  This information is intrinsically valuable because we like knowing how the world works, and it may eventually have practical value that's not immediately obvious.
2. Practical applications.  We want to solve problems and improve our lives.

If we want to determine whether or not obesity research has failed, we should evaluate it using those two metrics.

Has Obesity Research Gathered Accurate Information?

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Food Reward Friday

This week's lucky "winner"... Lay's milk chocolate-dipped potato chips!!

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A New Understanding of an Old "Obesity Gene"

As you know if you've been following this blog for a while, obesity risk has a strong genetic component.  Genome-wide association studies (GWAS) attempt to identify the specific locations of genetic differences (single-nucleotide polymorphisms or SNPs) that are associated with a particular trait.  In the case of obesity, GWAS studies have had limited success in identifying obesity-associated genes.  However, one cluster of SNPs consistently show up at the top of the list in these studies: those that are near the gene FTO.

As with many of the genes in our genome, different people carry different versions of FTO.  People with two copies of the "fat" version of the FTO SNPs average about 7 pounds (3 kg) heavier than people with two copies of the "thin" version, and they also tend to eat more calories (1, 2).  

Despite being the most consistent hit in these genetic studies, FTO has remained a mystery.  As with most obesity-associated genes, it's expressed in the brain and it seems to respond somewhat to nutritional status.  Yet its function is difficult to reconcile with a role in weight regulation: 

• It's an enzyme that removes methyl groups from RNA, which doesn't immediately suggest a weight-specific function.
• It's not primarily expressed in the brain or in body fat, but in all tissues.
• Most importantly, as far as we know, the different versions of the gene do not result in different tissue levels of FTO, or different activity of the FTO enzyme, so it's hard to understand how they would impact anything at all.  

An important thing to keep in mind is that GWAS studies don't usually pinpoint specific genes.  Typically, they tell us that obesity risk is associated with variability in a particular region of the genome.  If the region corresponds to the location of a single gene, it's a pretty good guess that the gene is the culprit.  However, that's not always the case...

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Fat vs. Carbohydrate Overeating: Which Causes More Fat Gain?

Two human studies, published in 1995 and 2000, tested the effect of carbohydrate vs. fat overfeeding on body fat gain in humans.  What did they find, and why is it important?

We know that daily calorie intake has increased the US, in parallel with the dramatic increase in body fatness.  These excess calories appear to have come from fat, carbohydrate, and protein all at the same time (although carbohydrate increased the most).  Since the increase in calories, carbohydrate, fat, and protein all happened at the same time, how do we know that the obesity epidemic was due to increased calorie intake and not just increased carbohydrate or fat intake?  If our calorie intake had increased solely by the addition of carbohydrate or fat, would we be in the midst of an obesity epidemic?

The best way to answer this question is to examine the controlled studies that have compared carbohydrate and fat overfeeding in humans.

Horton et al.

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Garden Update: A Banner Year

Things are warming up here in Seattle and the flowers are blooming.  I just planted my first crops of the year-- potatoes and strawberries.

2013 was a banner year for my 500-square-foot urban vegetable garden, including my first experience growing and processing a grain.  I never got around to posting about it last year-- so here it is.

Interbay mulch technique

The bed on the right has been mulched with leaves, spent coffee
grounds, and burlap sacks ($1/sack at the local hardware store).
The beds on the left were planted with a rye-clover-vetch-pea
cover crop.  Paths are mulched with wood chips.

In the fall of 2012, I tried a new technique for improving the soil called "Interbay mulching".  This is a variation on sheet mulching, which involves placing uncomposted organic matter directly onto the garden soil in fall and letting it compost until the next growing season.  To Interbay mulch, you simply cover your sheet mulch with burlap.  This keeps everything moist, protects earthworms from bird predation so they can munch freely, and suppresses weeds.  I used leaves (carbon) and spent coffee grounds from a local coffee shop (nitrogen) for my organic matter.

When I pulled back the burlap last spring, I was initially disappointed.  The coffee grounds had disappeared completely, but there was still a lot of leaf matter left on the soil, indicating that it had only partially composted.  However, I later decided that it had worked well, because the soil structure underneath was improved and it seemed to be enriched with significant organic matter as well as a large population of fat earthworms.  The mulch suppressed weeds remarkably well, and the beds remained mostly clean for the rest of the season.

Those observations, combined with huge yields from the mulched beds, convinced me that it was worthwhile.

New tools
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More Graphs of Calorie Intake vs. BMI

In the last post, a reader commented that the correlation would be more convincing if I graphed calories vs. average BMI rather than the prevalence of obesity.  It was a valid point, so I went searching for average BMI values from NHANES surveys.  I dug up a CDC document that contains data from surveys between 1960 and 2002 (1).  Because these data only cover five survey periods, we only get five data points to analyze, as opposed to the eight used in the last post.  The document contains BMI values for men and women separately, so I averaged the two to approximate average BMI in the general adult population.  It's also worth noting that I use the approximate midpoint of the survey period as the year.

First, a graph of average BMI over time.  It went up:

Now, let's see how well average BMI correlates with calorie intake:

The correlation between calorie intake and obesity prevalence was remarkable, but this correlation is simply incredible.  An R-squared value of 0.98 indicates that daily calorie intake and average BMI are almost perfectly correlated.

We can further deduce that each 100-calorie increase in daily food intake is associated with an 0.62-point increase in average BMI among US adults.  

Calorie Intake and the US Obesity Epidemic

Between 1960 and 2008, the prevalence of obesity in US adults increased from 13 to 34 percent, and the prevalence of extreme obesity increased from 0.9 to 6 percent (NHANES surveys).  This major shift in population fatness is called the "obesity epidemic".

What caused the obesity epidemic?  As I've noted in my writing and talks, the obesity epidemic was paralleled by an increase in daily calorie intake that was sufficiently large to fully account for it.  There are two main sources of data for US calorie intake.  The first is NHANES surveys conducted by the Centers for Disease Control.  They periodically collect data on food intake using questionnaires, and these surveys confirm that calorie intake has increased.  The problem with the NHANES food intake data is that they're self-reported and therefore subject to major reporting errors.  However, NHANES surveys provide the best quality (objectively measured) data on obesity prevalence since 1960, which we'll be using in this post.

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Uncovering the True Health Costs of Excess Weight

Is excess weight hazardous to health, or can it actually be protective?  This question has provoked intense debate in the academic community, in some cases even leading researchers to angrily denounce the work of others (1).  There is good evidence to suggest that excess body fat increases the risk of specific diseases, including many of our major killers: diabetes, heart attack, stroke, heart failure, cancer, and kidney failure (2).  Yet strangely, the studies relating excess weight to the total risk of dying-- an overall measure of health that's hard to argue with-- are inconsistent.  Why?
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Corrections to the New Review Paper on Dietary Fat and Cardiovascular Risk

The meta-analysis by Chowdhury et al. raised quite a furor from certain segments of researchers and the popular media.  I find this reaction interesting.  I usually write about obesity, which is a topic of great interest to people, but my post about the review paper received more than twice my usual traffic.  People whose findings or opinions are questioned by the paper are aggressively denouncing it in the media, even calling for retraction (1).  This resembles what happens every time a high-profile review paper is published that doesn't support the conventional stance on fatty acids and health (e.g., Siri-Tarino et al. [2], which despite much gnashing of teeth is still standing*).  I'm not sure why this issue in particular arouses such excitement, but I find it amusing and disturbing at the same time.  This kind of reaction would be totally out of place in most other fields of science, where aggressive public media outbursts by researchers are usually frowned upon.

As it turns out, the critics have a point this time.  Significant errors were uncovered in the original version of the meta-analysis, which have been corrected in the current version (3).  These include the following two errors, one of which alters the conclusion somewhat:

• The outcome of one observational study on omega-3 fatty acids was reported as slightly negative, when it was actually strongly positive.  This changes the conclusion of the meta-analysis, making it somewhat more favorable to omega-3 consumption for cardiovascular protection.
• The authors left out two studies on omega-6 fatty acids.  These didn't change the overall conclusions on omega-6.

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New Review Paper on Dietary Fat and Heart Disease Risk

A new review paper on dietary fatty acids and heart disease risk was just published by Dr. Rajiv Chowdhury and colleagues in the Annals of Internal Medicine-- one of the top medical journals (1).  The goal of the paper is to comprehensively review the studies evaluating the effect of dietary fatty acids on heart (coronary) disease.  The review covers observational and intervention studies pertaining to saturated, monounsaturated, trans, omega-6 polyunsaturated, and omega-3 polyunsaturated fats.  The paper is notable for its comprehensiveness (inclusion criteria were very lax).

Here is a summary of the results:

• In observational studies that measured diet, only trans fat was related to cardiovascular risk.  Saturated, monounsaturated, and polyunsaturated fats were unrelated to risk.
• In observational studies that measured circulating concentrations of fatty acids, long-chain polyunsaturated fatty acids (DHA, DPA, EPA, AA) were associated with lower risk.  The dairy-fat-derived margaric acid (17:0) was also associated with lower risk.  No other fatty acids were related to risk, including trans fatty acids.
• In controlled trials, supplementation with omega-3 or omega-6 fatty acids did not alter risk.

The authors conclude:

In conclusion, the pattern of findings from this analysis did not yield clearly supportive evidence for current cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of saturated fats.  Nutritional guidelines on fatty acids and cardiovascular guidelines may require reappraisal to reflect the current evidence.

My view

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Food Reward Friday

This week's lucky "winner"...  the Taco Bell waffle taco!!

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The Ultimate Detox: Your Kidneys

The specter of unseen, unspecified toxins eroding our health is worth many millions of dollars in the United States and abroad.  Companies offer "detox" supplements, beverages, and creams that supposedly rid us of supposed toxins, despite a complete lack of evidence that these products do anything at all*.  This comes from an industry that excels at creating boogeymen and offering costly solutions for them.

If your wallet needs to lose weight, then these products are highly effective, otherwise it's probably best to save your money.  Here's why.

The body is equipped with an extremely advanced system for excreting toxins.  The kidneys are part of this system, and their design is genius.  The basic functional unit of the kidney is the nephron, and the average kidney contains about a million of them.  Nephrons have two major parts: a renal corpuscle and a renal tubule. 

A nephron.  In this image, the Bowman's capsule and glomerulus make up the renal corpuscle, and the proximal/distal tubules and the loop of Henle (#1-3) make up the renal tubule.  Note the network of blood vessels (capillaries) that allow the transfer of water and other goodies from the tubule back into the blood.  Image source.

The renal corpuscle is the interface between the blood and the fluid that will eventually become urine.  Blood is filtered by a fine "sieve" of cells that prevents everything larger than a small protein from passing into the renal tubule.  Red blood cells, platelets, and most proteins stay on the blood side, while small proteins such as albumin, minerals, urea, glucose, water, and almost anything that would be considered a toxin** are allowed through into the renal tubule.

The renal tubule is a long tube that re-absorbs everything in this filtered blood that the body wants to keep.  Water, minerals, albumin, glucose, amino acids, and other useful molecules are re-absorbed.  Everything else ends up as urine and is excreted. 

Can you see the genius of this design?  Urine is blood, minus all the good stuff.  Everything that isn't specifically recognized by the body as useful is excreted by default, no matter what it is.  The body doesn't have to recognize each of the thousands of foreign compounds that make their way into our circulation each day.  These substances are all out the door, by default.

Are you impressed by your kidneys yet?  If not, consider this.  Your kidneys filter your entire blood volume roughly 70 times per day.  The reason you don't have to pee a liter a minute is that urine volume is reduced by 99 percent due to water reabsorption in the renal tubules.

This is why most drugs have to be taken on a regular basis, often several times per day.  In concert with the detoxification enzymes of the liver, which tend to make drugs easier for the kidneys to excrete, the kidneys rapidly reduce the circulating concentration of drugs simply by excreting everything they don't recognize as useful.

Can a detox product improve upon 500 million years of kidney evolution***?  I have my doubts.


* Exception: chelation therapy offered by a licensed medical practitioner for actual, diagnosed heavy metal poisoning.  Second exception: strategies that use the word "detox" loosely to refer to removing unhealthy foods from the diet.

** Toxins tend to be very small-- either small organic molecules or minerals such as arsenic.  Larger toxins such as proteins are uncommon in the circulation because proteins are generally not absorbed by the digestive tract.  Toxic proteins have to be injected or otherwise directly introduced into the circulation, e.g. by a snake bite or a bacterial infection.  But if you're bitten by a rattlesnake, I hope your first line of treatment won't be a detox kit from your local supplement store.

*** Kidneys are present in hagfish and lampreys, the most "primitive" living vertebrates.

Food Reward Friday

This week's lucky "winner"...  Kirkland Signature Cashew Clusters!!

 

 



WHS reader Brad Dieter mentioned these on Facebook the other day:

Nutrition tip of the day. Do not buy Cashew Clusters from Costco. You will eat an entire bag in one fell swoop. Sweet, salty, crunchy, and calorie dense, the perfect storm in Stephan Guyenet's model of overeating. I have n=1 data as proof.

n=1 quickly turned into n=6 as other people chimed in, including myself.  I can attest to the fact that Cashew Clusters are like crack.  Here's more evidence from their Amazon reviews:

"Addiction with less guilt!"  These things are SO freaking good!!!... I'm eating some right now and I am having trouble keeping my hand out of the bag long enough to write this review!

"Delicious".  I gave this as a gift to my girl friend... She loved it ! Heard there wasn't much sugar either. Seems the nuts were crispy and the clusters were very addicting, in a nice way. It lasted only for 6 days. [SG- each bag contains 4,800 calories]

"Buy these and you will be hooked for life!"  One word "NUMMY!"...  Very addicting.

Cashew Clusters are only about 11 percent sugar by calories, with the other 89 percent of calories coming from whole nuts and seeds.  They're probably a healthy snack if you can eat them in moderation.  Can you?



Snacktime in My Kitchen

Here is a photo of all visible food in my kitchen:

 

 

Along the back wall, we have glass containers of raw nuts, unsalted roasted nuts, grains, and legumes.  It's easy and attractive to organize your dry foods using inexpensive 2 quart Ball jars.  They also have the advantage of being moth-proof.  On the left, we have fresh fruit and a few onions.  On the far left in the background is our hand-cranked conical burr grinder, for occasional coffee (Skerton).

 

If I walk into my kitchen between meals, the only food available to eat without doing any cooking or reheating is unsalted nuts and fresh fruit.  There is no other snack food in the kitchen.  No chips, cookies, bars, popcorn, snack mix, candy, or anything else that's tempting and easy to grab and devour. 

 

When it's mealtime, we eat good home-cooked food.  When it isn't mealtime, we don't have anything available that we would eat without feeling genuinely hungry.  If we do feel genuinely hungry, fresh fruit and unsalted nuts make a satisfying snack.

This is the way of my people. 

What's the point?  Eliminating tempting food cues from our surroundings and creating small barriers to food consumption decreases the quantity of food we eat while increasing the quality.  Engineering a food environment that discourages eating for reasons other than hunger helps match food intake to the body's true energy needs, favoring leanness and health.

 

Why Do We Overeat? A Neurobiological Perspective

I just posted a narrated Powerpoint version of my talk "Why Do We Overeat? A Neurobiological Perspective" to YouTube.  Here's the abstract:

In the United States, the "obesity epidemic" has paralleled a gradual increase in daily calorie intake.  Why do we eat more than we used to, and more than we need to remain lean-- despite negative consequences?  This talk reviews the neurobiology of eating behavior, recent changes in the US food system, and why the brain's hardware may not be up to the task of constructively navigating the modern food environment.

This is the same talk I gave at the University of Virginia this January.  I had a number of people request it, so here it is:

 

Why Do We Overeat? A Neurobiological Perspective

 

This is one of my favorite talks, and it was very well received at UVA.  If you find it informative, please share it!

 

 

5 Easy and Effective Ways to Eat Less

Why do we overeat?  Why is it hard to lose fat once we've gained it?  Is there a way to comfortably and sustainably eat less and lose fat? 

 

I recently did an interview with Armi Legge of Evidence Magazine that gives an overview of my thinking on these topics-- based on a large and compelling body of research that rarely reaches popular media sources in useful form. 

 

At the end of the interview, Armi asks me to list my top five tips for reducing calorie intake.  Enjoy!

 

5 Easy and Effective Ways to Eat Less

 

 

Mysteries of Energy Balance and Weight Loss

How to Lose Weight Effortlessly

 

You've probably seen this claim many times: a pound of fat contains 3,500 kilocalories (kcal).  A slice of toast is 80 kcal.  All you have to do is forego one slice of toast per day-- just a few percent of your total calorie intake-- and you will lose 8.3 lbs of fat per year.  Fat loss is so easy!

 

This reasoning is extremely common both in the popular media and among researchers.  Here's an example from the otherwise excellent book Mindless Eating, by researcher Brian Wansink:

...the difference between 1,900 and 2,000 calories is one we cannot detect, nor can we detect the difference between 2,000 and 2,100 calories.  But over the course of a year, this mindless margin would either cause us to lose ten pounds or to gain ten pounds.  It takes 3,500 extra calories to equal one pound.  It doesn't matter if we eat these extra 3,500 calories in one week or gradually over the entire year.  They'll add up to one pound.

This is the danger of creeping calories.  Just 10 extra calories a day-- one stick of Doublemint gum or three small Jelly Belly jelly beans-- will make you a pound more portly one year from today.  Only three Jelly Bellys a day.

According to this reasoning, if I reduced my calorie intake by 80 kcal per day, I'd become skeletal in two years and vanish in a puff of smoke within 10 years*.  All from a meager 3 percent reduction in calorie intake! 

 

What's wrong here?

Read more »

NutriScience Seminar in Lisbon with Lindeberg, Fontes, and Bastos

My friend Pedro Bastos has asked me to spread the word about a seminar he's organizing in Lisbon titled "Evidence and Evolution-based Nutrition".  It will include Staffan Lindeberg, Maelan Fontes, and Pedro Bastos-- three quality researchers in the area of evolutionary health-- I'm sure it will be interesting.  Here's the flier:

 

 

Public Talk at the University of Virginia on Friday, January 17

This Friday, I'll be giving an invited lecture at the University of Virginia, my undergraduate alma mater.  I was kindly invited by a medical student named Robert Abbott, and it worked out well because I was already traveling to Charlottesville.

The talk will be titled "Why Do We Overeat?  A Neurobiological Perspective".  Here's the teaser:

Obesity is a leading cause of morbidity and mortality in industrialized nations, yet this is a relatively recent phenomenon.  In the United States, increasing obesity prevalence has paralleled a gradual increase of daily energy intake.  Why do most Americans eat more than we used to, and more than we need to maintain a lean state, despite negative consequences?  This presentation will touch on the neurobiology of action selection, the neurobiology of energy homeostasis, and why our central nervous system hardware may not be up to the task of constructively navigating the modern food environment.

The talk will be attended by medical students, but I also hope to have some doctors and researchers show up, as well as people from the broader Charlottesville community.  It will be a thought-provoking talk regardless of your background, and it will touch on some of my own work.

The talk will be held in the main medical school auditorium, MEB 3110, on Friday, January 17 at noon.  You can find driving directions and parking information by following this link.  You'll probably have to park in a parking garage, either the Lee Street or Central Grounds garage (directions in the link).

For a map of the UVA health system, follow this link.  The Medical Education Building is number 44 on the map, and the talk will be in room MEB 3110 on the 3rd floor of the building.

See you there!

Free e-Book and Ideal Weight Program 2.0 Announcement

I'm happy to announce that we're releasing a free e-book titled Why do We Gain Fat, and How do We Lose it? An Introduction to the Science of Body Fat, by Dan Pardi and myself. This is a slimmed-down version of the longer, fully referenced e-book we offer as part of the Ideal Weight Program. In it, we provide a succinct overview of the science of body fat gain and loss, and the evidence base for our program.  It also contains a schematic that ties together the various concepts in visual form. You can download it from the Dan’s Plan site by following this link to our program overview page.

Ideal Weight Program 2.0 Upgrades

Over the last year, Dan and I have been working hard to improve the Ideal Weight Program, both in response to user feedback and our own ideas for development.  Here are some of the new features we offer in 2014:

1. Four-week meal plans and shopping lists for the FLASH diet and the Simple Food Diet, as requested by Ideal Weight Program users.  This is in addition to the recipes and cooking guides we already provide.  
2. The Protein Unit system.  Research suggests there's an optimal amount of protein for appetite control and fat loss, depending on your height, weight, gender, and physical activity level.  Our fat loss diets are high in protein, but how do you know you're getting the right amount?  We've created a calculator that does it for you automatically, and explains how to apply your personalized Protein Unit value easily and intuitively using real food. 
3. Diet plates.  These are visual guides to following our diets, based loosely on the intuitive USDA MyPlate design.  
4. Cheat sheets.  Put these on your fridge to remind yourself of your diet and lifestyle guidelines, and daily protein unit goal.
5. Updated guidance.  We've refined a few things in the diet guidance documents. 

At a time of year when many people want to shed excess holiday pounds and start down a leaner, healthier path, we offer the Ideal Weight Program 2.0.  The program comes with a 30-day no-questions-asked refund policy so you can try it without risk.  We think you'll love this program, but if it doesn't work for you, we're happy to refund your purchase price. 

Financial disclosure: I receive a portion of the revenue from the sale of the Ideal Weight Program.  I do not receive revenue from the sale of other products associated with Dan's Plan or the Ideal Weight Program (such as the Fitbit, cooking tools, and other programs).