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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Wednesday, July 13, 2011
Monday, July 11, 2011
Fasting for 24 hours and ending up with a bigger waist!? This may be a sign that you are losing abdominal fat
This is such a common phenomenon that you’d expect to see it discussed more often – people fasting for a non-negligible number of hours and ending up with a bigger waist. However, it is very difficult to find anything published on it. (Lyle McDonald discussed a related phenomenon on this post on whooshes and squishy fat.) I am not talking about only a perceived bigger waist; I am talking about measurably bigger. This frequently happens with folks who were obese, lost a lot of body fat, and are trying to get rid of the stubborn lower abdominal fat.
Fasting and ending up with a bigger waist; how is that possible?
Contrary to popular belief, this is very unlikely to be due to the body turning muscle protein into glucose, and then converting that glucose into fat for storage in fat cells around the waist. When you are fasting, one factor strongly opposes that transformation. The body is in net body fat release mode, due in part to low circulating insulin, and thus body fat cells are essentially rejecting glucose. Blood glucose levels are maintained, to feed the brain, but uptake by adipocytes via GLUT4 isn’t happening.
So where does the bigger waist come from?
When people fast they typically drink water, quite often lots of it. A reasonable explanation for the bigger waist is that body fat cells store water in place of fat, as fat becomes energy. Since water is denser than fat, the stronger gravitational pull will lead to a larger bulge around the lower abdominal area, increasing waist circumference at the point it is widest. The amount of fat mass, however, is going down due to fasting.
In the obese, body fat cells generally become insulin resistant, even though many people believe the opposite to be true. This leads to the creation of new body fat cells (hyperplasia) to store the extra fat. If body fat loss is maintained over time, I’d expect the body to get rid of those fat cells that were created through hyperplasia during the obese period. The literature, however, seems to suggest that the number of body fat cells is set before adulthood, and does not change afterwards. I am skeptical, as the body seems to be very good at getting rid of cells and tissues that are not used.
The loss of those extra body fat cells may bring the number of adipocytes to pre-obesity levels, but for many people quite some time is needed for that to happen. Often in the order of months; maintaining reasonably low body fat levels.
So don’t despair if you end up with a bigger waist around noon after skipping breakfast, or before dinner after fasting the whole day. That may be a good sign; a sign that you are actually losing abdominal fat.
(Source [ironically]: Gograins.com.au)
Fasting and ending up with a bigger waist; how is that possible?
Contrary to popular belief, this is very unlikely to be due to the body turning muscle protein into glucose, and then converting that glucose into fat for storage in fat cells around the waist. When you are fasting, one factor strongly opposes that transformation. The body is in net body fat release mode, due in part to low circulating insulin, and thus body fat cells are essentially rejecting glucose. Blood glucose levels are maintained, to feed the brain, but uptake by adipocytes via GLUT4 isn’t happening.
So where does the bigger waist come from?
When people fast they typically drink water, quite often lots of it. A reasonable explanation for the bigger waist is that body fat cells store water in place of fat, as fat becomes energy. Since water is denser than fat, the stronger gravitational pull will lead to a larger bulge around the lower abdominal area, increasing waist circumference at the point it is widest. The amount of fat mass, however, is going down due to fasting.
In the obese, body fat cells generally become insulin resistant, even though many people believe the opposite to be true. This leads to the creation of new body fat cells (hyperplasia) to store the extra fat. If body fat loss is maintained over time, I’d expect the body to get rid of those fat cells that were created through hyperplasia during the obese period. The literature, however, seems to suggest that the number of body fat cells is set before adulthood, and does not change afterwards. I am skeptical, as the body seems to be very good at getting rid of cells and tissues that are not used.
The loss of those extra body fat cells may bring the number of adipocytes to pre-obesity levels, but for many people quite some time is needed for that to happen. Often in the order of months; maintaining reasonably low body fat levels.
So don’t despair if you end up with a bigger waist around noon after skipping breakfast, or before dinner after fasting the whole day. That may be a good sign; a sign that you are actually losing abdominal fat.
Labels:
body fat,
fasting,
fat loss,
waist circumference
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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Labels:
diabetes,
Food reward,
overweight
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:
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.
Labels:
overweight
Monday, July 4, 2011
Liver and meatballs separated by a wall of sweet potatoes
A commenter wrote here some time ago that she liked to eat rice because rice can be easily used to separate food items on a plate. One can just as easily use sweet potatoes to do that; preparing the sweet potatoes in much less time than the rice. This post explains how, with a simple recipe.
- Cut up half of a sweet potato as shown on the first photo below, adding coconut oil or butter to prevent the pieces from sticking to a microwave-safe saucepan.
- Microwave the sweet potato pieces in high heat for about 5 minutes.
- Use the sweet potatoes to separate food items as in the second photo below, showing beef liver and meatballs with their respective sauces.
- Cover the dish with a wet paper towel to prevent spilling, and microwave it for as long as needed to heat up the meats. In this case, 2 minutes in high heat was enough. That will further cook the sweet potato, but not to the point of burning it.
The above assumes that the beef liver and meatballs are leftovers that had been cooked before. In this example, we have about ½ lb of meat and ½ of a sweet potato. As far as plant foods are concerned, sweet potatoes are at the very high end of the nutrition density scale. This is a very nutritious and satiating meal (for me) with over 55 g of protein, as well as a great mix of macro- and micro-nutrients.
- Cut up half of a sweet potato as shown on the first photo below, adding coconut oil or butter to prevent the pieces from sticking to a microwave-safe saucepan.
- Microwave the sweet potato pieces in high heat for about 5 minutes.
- Use the sweet potatoes to separate food items as in the second photo below, showing beef liver and meatballs with their respective sauces.
- Cover the dish with a wet paper towel to prevent spilling, and microwave it for as long as needed to heat up the meats. In this case, 2 minutes in high heat was enough. That will further cook the sweet potato, but not to the point of burning it.
The above assumes that the beef liver and meatballs are leftovers that had been cooked before. In this example, we have about ½ lb of meat and ½ of a sweet potato. As far as plant foods are concerned, sweet potatoes are at the very high end of the nutrition density scale. This is a very nutritious and satiating meal (for me) with over 55 g of protein, as well as a great mix of macro- and micro-nutrients.
Labels:
beef liver,
meatballs,
microwave oven,
recipe,
sweet potato
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.
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.
Labels:
diet,
Food reward,
hyperphagia,
overweight
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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Labels:
diet,
Food reward,
hyperphagia,
overweight,
real food,
superstimuli
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