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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Zucchini: The Home Gardener's Worst Friend? With bonus garden-related rambling.

One of my main gardening goals has been to harvest more of something than I can eat, despite my limited gardening space here in the Emerald City.  I want the feeling of abundance that comes with having to preserve and give away food because I can't eat it all.

Enter zucchini.  My grandfather used to say that in New Jersey in summertime, you'd have to keep your car doors locked, otherwise the car would be full of zucchini the next time you got in!  In mid-May, I planted two starts from my local grocery store labeled "green zucchini", with no further information.  I put them in a bed that used to be a pile of composted horse manure, and that I had also cover cropped, mulched, fertilized, and loosened deeply with my broadfork.  They look pleased.

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Dietary Guidelines for Americans, My Way

I just saw this on BoingBoing.  Simple but true. 

This image was created by Adam Fields. 

The people who design government dietary guidelines are gagged by the fact that politics and business are so tightly intertwined in this country.  Their advice will never directly target the primary source of obesity and metabolic dysfunction-- industrially processed food-- because that would hurt corporate profits in one of the country's biggest economic sectors.  You can only squeeze so much profit out of a carrot, so food engineers design "value-added" ultrapalatable/rewarding foods with a larger profit margin.

We don't even have the political will to regulate food advertisements directed at defenseless children, which are systematically training them from an early age to prefer foods that are fattening and unhealthy.  This is supposedly out of a "free market" spirit, but that justification is hollow because processed food manufacturers benefit from tax loopholes and major government subsidies, including programs supporting grain production and the employment of disadvantaged citizens (see Fast Food Nation).

Interview on Super Human Radio

Today, I did an audio interview with Carl Lanore of Super Human Radio.  Carl seems like a sharp guy who focuses on physical fitness, nutrition, health and aging.  We talked mostly about food reward and body fatness-- I think it went well.  Carl went from obese to fit, and his fat loss experience lines up well with the food reward concept.  As he was losing fat rapidly, he told friends that he had "divorced from flavor", eating plain chicken, sweet potatoes and oatmeal, yet he grew to enjoy simple food over time.

The interview is here.  It also includes an interview of Dr. Matthew Andry about Dr. Loren Cordain's position on dairy; my interview starts at about 57 minutes.  Just to warn you, the website and podcast are both full of ads.

How Should Science be Done?

Lately I keep running into the idea that the proper way to do science is to continually strive to disprove a hypothesis, rather than support it*.  According to these writers, this is what scientists are supposed to aspire to, but I've never actually heard a scientist say this.  The latest example was recently published in the Wall Street Journal (1).  This evokes an image of the Super Scientist, one who is so skeptical that he never believes his own ideas and is constantly trying to tear them down.  I'm no philosopher of science, but this idea never sat well with me, and it's contrary to how science is practiced. 
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New Review Paper by Yours Truly: High-Fat Dairy, Obesity, Metabolic Health and Cardiovascular Disease

My colleagues Drs. Mario Kratz, Ton Baars, and I just published a paper in the European Journal of Nutrition titled "The Relationship Between High-Fat Dairy Consumption and Obesity, Cardiovascular, and Metabolic Disease".  Mario is a nutrition researcher at the Fred Hutchinson Cancer Research Center here in Seattle, and friend of mine.  He's doing some very interesting research on nutrition and health (with an interest in ancestral diets), and I'm confident that we'll be getting some major insights from his research group in the near future.  Mario specializes in tightly controlled human feeding trials.  Ton is an agricultural scientist at the University of Kassel in Germany, who specializes in the effect of animal husbandry practices (e.g., grass vs. grain feeding) on the nutritional composition of dairy.  None of us have any connection to the dairy industry or any other conflicts of interest.

The paper is organized into three sections:

1. A comprehensive review of the observational studies that have examined the relationship between high-fat dairy and/or dairy fat consumption and obesity, metabolic health, diabetes, and cardiovascular disease.
2. A discussion of the possible mechanisms that could underlie the observational findings.
3. Differences between pasture-fed and conventional dairy, and the potential health implications of these differences.

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Weight Gain and Weight Loss in a Traditional African Society

The Massas is an ethnic group in Northern Cameroon that subsists mostly on plain sorghum loaves and porridge, along with a small amount of milk, fish and vegetables (1, 2).  They have a peculiar tradition called Guru Walla that is only undertaken by men (2, 1):
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What Causes Type 2 Diabetes, and How Can it be Prevented?

In the comments of the last post, we've been discussing the relationship between body fatness and diabetes risk.  I think this is really worth understanding, because type 2 diabetes is one of the few lifestyle disorders where 1) the basic causes are fairly well understood, and 2) we have effective diet/lifestyle prevention strategies that have been clearly supported by multiple controlled trials.

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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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Return to the Source Parkour Camp

For those who are interested in natural movement training, this summer my friend Rafe Kelley will be hosting an interesting three-day event near Bellingham, WA called "Return to the Source".  Rafe is skilled in a variety of movement disciplines and is the co-founder of the Seattle parkour gym Parkour Visions.  Parkour is a very fun sport that hones our natural ability to skillfully navigate physical obstacles, but it's usually done in an urban context.

The camp will take place from August 23-25.  Here's a description from the Parkour Visions site:

"This summer, return to the source of human movement with Parkour Visions as we explore the natural environment in and around Bellingham, WA. Rafe Kelley will introduce you to the benefits of training and playing in nature. You will learn how to adapt your technique and movement to moving effectively through woods, over rocks, and in trees during this unique, 3-day experience."

Watch this video if you want to see what you're in for.

Knowing Rafe, it will be fun and productive.  You can sign up through this page.

Simple Food: Thoughts on Practicality

Some people have reacted negatively to the idea of a reduced-reward diet because it strikes them as difficult or unsustainable.  In this post, I'll discuss my thoughts on the practicality and sustainability of this way of eating.  I've also thrown in a few philosophical points about reward and the modern world.
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Interview with Aitor Calero of Directo al Paladar

Aitor Calero writes for the popular Spanish cooking and nutrition blog, Directo al Paladar ("straight to the palate").  We did a written interview a while back, and he agreed to let me post the English version on my blog.  The Spanish version is here and here.

Without further ado, here it is:

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How Does Gastric Bypass Surgery Cause Fat Loss?

Gastric bypass surgery is an operation that causes food to bypass part of the digestive tract.  In the most common surgery, Roux-en-Y bypass, stomach size is reduced and a portion of the upper small intestine is bypassed.  This means that food skips most of the stomach and the duodenum (upper small intestine), passing from the tiny stomach directly into the jejunum (a lower part of the upper small intestine)*.  It looks something like this:
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Liposuction and Fat Regain

If body fat really is actively regulated by the body, rather than just being a passive result of voluntary food intake and exercise behaviors, then liposuction shouldn't be very effective at reducing total fat mass in the long run.  People should return to their body fat "setpoint" rather than remaining at a lower fat mass. 

Teri L. Hernandez and colleagues recently performed the first ever randomized liposuction study to answer this question (1).  Participants were randomly selected to either receive liposuction, or not.  They were all instructed not to make any lifestyle changes for the duration of the study, and body fatness was measured at 6 weeks, 6 months and one year by DXA. 

At 6 weeks, the liposuction group was significantly leaner than the control group.  At 6 months, the difference between the two groups had decreased.  At one year, it had decreased further and the difference between the groups was no longer statistically significant.  Furthermore, the liposuction group regained fat disproportionately in the abdominal area (belly), which is more dangerous than where it was before. The investigators stated:

We conclude that [body fat] is not only restored to baseline levels in nonobese women after small-volume liposuction, but is redistributed abdominally.

This is consistent with animal studies showing that when you surgically remove fat, total fat mass "catches up" to animals that had no fat removed (2).  Fat mass is too important to be left up to chance.  That's why the body regulates it, and that's why any satisfying resolution of obesity must address that regulatory mechanism.

Food Reward: a Dominant Factor in Obesity, Part VIII

Further reading

I didn't come up with the idea that excessive food reward increases calorie intake and can lead to obesity, far from it.  The idea has been floating around the scientific literature for decades.  In 1976, after conducting an interesting diet study in humans, Dr. Michel Cabanac stated that the "palatability of the diet influences the set point of the ponderostat [system that regulates body fatness]" (1).  

Currently there is a growing consensus that food reward/palatability is a major contributor to obesity. This is reflected by the proliferation of review articles appearing in high-profile journals.  For the scientists in the audience who want more detail than I provide on my blog, here are some of the reviews I've read and enjoyed.  These were written by some of the leading scientists in the study of food reward and hedonics:

Palatability of food and the ponderostat.  Michel Cabanac, 1989.
Food reward, hyperphagia and obesity.  Hans-Rudolf Berthoud et al., 2015.
Reward mechanisms in obesity: new insights and future directions.  Paul J. Kenny, 2015.
Relation of obesity to consummatory and anticipatory food reward.  Eric Stice, 2009.
Hedonic and incentive signals for body weight control.  Emil Egecioglu et al., 2015.
Homeostatic and hedonic signals interact in the control of food intake.  Michael Lutter and Eric J. Nestler, 2009.
Opioids as agents of reward-related feeding: a consideration of the evidence.  Allen S. Levine and Charles J. Billington, 2004.
Central opioids and consumption of sweet tastants: when reward outweighs homeostasis.  Pawel K. Olszewski and Allen S. Levine, 2007.
Oral and postoral determinants of food reward.  Anthony Sclafani, 2004.
Reduced dopaminergic tone in hypothalamic neural circuits: expression of a "thrifty" genotype underlying the metabolic syndrome?  Hanno Pijl, 2003.

If you can read all these papers and still not believe in the food reward hypothesis... you deserve some kind of award.

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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Why Did Energy Expenditure Differ Between Diets in the Recent Study by Dr. Ludwig's Group?

As discussed in the previous post, a recent study by Dr. David Ludwig's group suggested that during weight maintenance following fat loss, eating a very low carbohydrate (VLC) diet led to a higher metabolic rate (energy expenditure) than eating a low-fat (LF) diet, with a low glycemic index (LGI) diet falling in between the two (1).  The VLC diet was 30 percent protein, while the other two were 20 percent.  It's important to note that these were three dietary patterns that differed in many ways, and contrary to claims that are being made in the popular media, the study was not designed to isolate the specific influence of protein, carbohydrate or fat on energy expenditure in this context. 

Not only did the VLC diet lead to a higher total energy expenditure than the LF and LGI diets, the most remarkable finding is that it led to a higher resting energy expenditure.  Basically, people on the VLC diet woke up in the morning burning more energy than people on the LGI diet, and people on the LGI diet woke up burning more than people on the LF diet.  The VLC dieters burned 326 more calories than the LF dieters, and 200 more than the LGI dieters.

It's always tempting to view each new study in isolation, without considering the numerous studies that came before it, but in this case it's essential to see this study through a skeptical lens that places it into the proper scientific context.  Previous studies have suggested that:

1. The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure in people who are not trying to lose weight (2, 3).
2. The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure in people who are being experimentally overfed, and if anything carbohydrate increases energy expenditure more than fat (4, 5).
3. The carbohydrate:fat ratio of the diet has little or no detectable impact on energy expenditure during weight loss (6, 7, 8), and does not influence the rate of fat loss when calories are precisely controlled. 

This new study does not erase or invalidate any of these previous findings.  It fills a knowledge gap about the effect of diet composition on energy expenditure specifically in people who have lost weight and are trying to maintain the reduced weight.

With that, let's see what could have accounted for the differences observed in Dr. Ludwig's study.
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