Saturday, July 9, 2011

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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Tuesday, July 5, 2011

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.

Saturday, July 2, 2011

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., 2011.
Reward mechanisms in obesity: new insights and future directions.  Paul J. Kenny, 2011.
Relation of obesity to consummatory and anticipatory food reward.  Eric Stice, 2009.
Hedonic and incentive signals for body weight control.  Emil Egecioglu et al., 2011.
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.

Tuesday, June 28, 2011

Food Reward: a Dominant Factor in Obesity, Part VII

Now that I've explained the importance of food reward to obesity, and you're tired of reading about it, it's time to share my ideas on how to prevent and perhaps reverse fat gain.  First, I want to point out that although food reward is important, it's not the only factor.  Heritable factors (genetics and epigenetics), developmental factors (uterine environment, childhood diet), lifestyle factors (exercise, sleep, stress) and dietary factors besides reward also play a role.  That's why I called this series "a dominant factor in obesity", rather than "the dominant factor in obesity".
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Thursday, June 23, 2011

Drug Cessation and Weight Gain

Commenter "mem", who has been practicing healthcare for 30+ years, made an interesting remark that I think is relevant to this discussion:
Recovering substance dependent people often put on lots of weight and it is not uncommon for them to become obese or morbidly obese.
This relates to the question that commenter "Gunther Gatherer" and I have been pondering in the comments: can stimulating reward pathways through non-food stimuli influence body fatness?  

It's clear that smoking cigarettes, taking cocaine and certain other pleasure drugs suppress appetite and can prevent weight gain.  These drugs all activate dopamine-dependent reward centers, which is why they're addictive.  Cocaine in particular directly inhibits dopamine clearance from the synapse (neuron-neuron junction), increasing its availability for signaling.
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Saturday, June 18, 2011

Food Reward: a Dominant Factor in Obesity, Part VI

Reward Centers can Modify the Body Fat Setpoint

Dopamine is a neurotransmitter (chemical that signals between neurons) that is a central mediator of reward and motivation in the brain.  It has been known for decades that dopamine injections into the brain suppress food intake, and that this is due primarily to its action in the hypothalamus, which is the main region that regulates body fatness (1).  Dopamine-producing neurons from reward centers contact neurons in the hypothalamus that regulate body fatness (2).  I recently came across a paper by a researcher named Dr. Hanno Pijl, from Leiden University in the Netherlands (3).  The paper is a nice overview of the evidence linking dopamine signaling with body fatness via its effects on the hypothalamus, and I recommend it to any scientists out there who want to read more about the concept.
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Thursday, June 2, 2011

Food Reward: a Dominant Factor in Obesity, Part V

Non-industrial diets from a food reward perspective

In 21st century affluent nations, we have unprecedented control over what food crosses our lips.  We can buy nearly any fruit or vegetable in any season, and a massive processed food industry has sprung up to satisfy (or manufacture) our every craving.  Most people can afford exotic spices and herbs from around the world-- consider that only a hundred years ago, black pepper was a luxury item.  But our degree of control goes even deeper: over the last century, kitchen technology such as electric/gas stoves, refrigerators, microwaves and a variety of other now-indispensable devices have changed the way we prepare food at home (Megan J. Elias.  Food in the United States, 1890-1945). 

To help calibrate our thinking about the role of food reward (and food palatability) in human evolutionary history, I offer a few brief descriptions of contemporary hunter-gatherer and non-industrial agriculturalist diets.  What did they eat, and how did they prepare it? 
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