No weight-loss program that relies on decreased caloric intake and increased caloric expenditure has proven to be effective in the long term. It was a difficult journey for me to come to understand that calories-in versus calories-out is meaningless. But, alas, the truth is the truth. I know your defenses are up. They should be. Just hear me out. If we define "works" by long-term sustained results, you'll see that this is incontestable. I'm going to show you negative calorie balance plans can't work beyond a few years. In fact, even in meta-analyses aimed at showing the long-term benefit of hypocaloric diets, the absolute best results are an average loss of 15 pounds with only 7 gained in the following years [1]. This of course includes no data about body composition, only weight. Therefore, these already bleak stats, which are amusingly heralded as proof of success, could (and most likely do) represent a net loss of 20lbs of bone tissue and 12lbs gained in fat tissue. For most people, being down in weight most often means getting fatter, not leaner. For the uninitiated this may seem surprising. But veterans in the fitness community know what I'm talking about when I say I have taken skinfold caliper readings of 35% bodyfat (obese) on 95lb people and 4% bodyfat on 220lb people.
It's hard to know where to begin with this topic. It took me over thirty years, fifteen in the fitness industry, 100 hour work weeks, thousands of client hours, over ten thousand consults, thousands upon thousands of research hours to get to where I am. So I get it. I'm not going to change the world with one article. Just stay mindful that American fitness hasn't progressed a nanometer coming from the paradigm of the last sixty years: cut calories; eat whole grains; cut fats out; avoid saturated fat; do lots of cardio; get a diet plan, fully customized, etc. And every person out there who has failed to reach an easy maintenance program after year two or five is more evidence that we're doing the wrong things. So, maybe... just maybe, you're willing to listen to this without ridicule and without dismissing it.
Whatever you're gathering up inside yourself in order to reject this article's angle, I've been there and heard it. One day, when working with a cardiologist, I began to explain the reasons why one should consider avoiding gluten. The cardiologist, without even hearing one word, cut in and said, "let's sit down and I'll explain." I was his guest at the hospital so I diplomatically obliged to give him the floor. He proceeded to put forth an anecdote he'd heard of some guy who put himself on a super-low calorie diet of only candy. "And," the cardiologist gleefully sniped, "the guy lost weight; ergo, PROOF that the only thing that matters is calories-in versus calories-out." This is the type of sentiment I know I'm up against when writing this.
Not only was it preposterous that a one-person population study, in anecdote fashion, be touted as proof of anything, especially without reference to what the "weight" was comprised of, long term impact and the like. But then, the greatest offense was the contrast of storyteller and audience. At the time I had recently cut down to about 8% bodyfat with a decent six pack by doing no more than 4 hours of intense activity per week and my calories were VERY high, in the 6000+ range. The lecturing cardiologist, on the other hand, had about 80lbs of visceral belly fat, even though he worked up to 12 hour days with 40lbs of lead vest sitting on his shoulders, and never eating anywhere near a much as I did.
So where are we going with all this? Firstly, let me make the distinction between energy balance and energy distribution. Energy balance tells us nothing and gives us no tools. To clarify, I think Gary Taubes, author of "Good Calories, Bad Calories," gives one of the best illustrations: it's like trying to explain why so many people are in a room by saying, "well, you see, more people entered the room than left" - that isn't an explanation; it's a description. Likewise, saying that you grew fat tissue because you took in more calories isn't an explanation. Actually, it's not even a description. It's nonsense.
All weight-loss and all weight-gain can be explained by calorie or energy distribution, not by calorie or energy balance. Think of a 250lb lean bodybuilder. How did he net a result of increased muscle weight and decreased fat weight? Was it by a means of calorie balance or calorie distribution? Did he eat more calories than he burned in order to gain 100lbs of muscle, or did he eat fewer calories than he burned to lose so much fat? People say, "he's got good genes" or "steroids," as their usual retort. But how does that change anything? I thought calories-in versus calories-out was the explanation we were relying on. Now we're invoking genes and steroids?
I first became aware that something was amiss with the calorie balance paradigm when I was a kid. I was a heavier kid who later got skinny in high school. I couldn't seem to figure out how to get heavier AND leaner. I was either moderately lean and very light or fatter and more muscular. The energy balance equation wasn't netting me a great physique. Fast forward from there about a decade and I was performing metabolic testing as a young trainer at Bally Total Fitness. To make a long story short, I found that people who ate a lot had high metabolisms; and people who dieted hard and did a lot of cardio had very low metabolisms. Later I would put the pieces together on hormone balance, hypothyroidism and the like.
Fast forward almost fifteen more years and here we are. Though what I'm saying at first seems very controversial, it really isn't. Energy distribution is all that matters. And we all instinctively know this. That's why we make appeals to heredity or hormones when confronted with examples which challenge the standard paradigm. We know that calories-in versus calories-out doesn't tell us anything. When we eat a thousand extra calories, some people allocate it toward increased bone density, some toward increased mitochondrial output, some toward increased thyroid output, some toward lean mass synthesis, some toward cancer cell growth, and most toward adipose anabolism (fat gain). The thousand extra calories does not matter. All that matters is how you distribute it.
In fact, let us take a step back. In the previous paragraph I used the terminology "extra calories" and you just accepted it without scrutiny. I tricked you. There's no such thing as excess calories. Energy gets used toward something. Thus, the very concept of too many calories is defunct.
If you're sharp, you're already thinking, "so what determines distribution?" The answer is complex and includes a lot of our intuited response: genetics, hormones, activity and nutrition. Just none of them play the role you may be thinking.
First on the chopping block is genetics. Your genes aren't fixed. This had been supposed for a long time. Then, in 2008, researchers at Johns Hopkins confirmed it. It's given rise to a whole new area of interest within the study of epigenetics. Consider this: every moment of your day you transcribe DNA. Throughout your life you execute this process sometimes at a rate of 2800 nucleotides per minute. Every 1/43rd of a second you choose which piece of data you will encode, keep around, pass on, etc. That means that you can and do change your DNA within the span of your life. In fact, you already do this every time you subject yourself to a stress, with every chemical to which you do or do not subject yourself, with every food choice and every lifestyle decision. This may mean that someone is lean because they're genetically lean and someone is fat because they're genetically fat; but if we accept the premise, then the good news is that you can stop encoding for fatness and begin encoding for leanness. There are some limits (i.e. - eye color), but very few. You can encode for intelligence and less for stupidity. I don't want to get too controversial with this; but you can start to imagine some of the ramifications toward psychology, addiction, identity and so on. It's just going to take some work to change. How exactly do you change your genes? We'll get to that in a coming article.
Second on the chopping block is hormones, obviously intertwined with genetics. They aren't fixed. Not even close. Intra-daily fluctuations can be drastic. Lifestyle will tell your body to create hormones that make you fatter or hormones that make you leaner. Concerning metabolic rate, blood serum levels of thyroid hormone increase with more calories and decrease with fewer. This is actually one of several reasons why standard dieting is a perpetually disempowering proposition. As you create a "caloric deficit," you suppress your thyroid, sometimes irreparably. Interestingly enough, even the American Medical Association , although late to the party by about 70 years, is coming along for the ride. In 2012 a very well-conducted study, accepted for publication in JAMA, demonstrated that as fat intake decreases so does metabolic rate [2]. It also showed that even with compensatory increases in carbohydrate intake the net impact to metabolism was not good: proof positive that mere calories are simply an incomplete picture.
We're starting to really get into the nitty gritty. However, I'm going to have to sacrifice a lot of details for the sake of brevity and impact. Your mind is hopefully swimming with a lot of new ideas and new questions; and one article won't address them all. But, what we can do is begin to clear up fat growth versus non-fat energy distribution. On to activity and nutrition.
A simplified primer on preferential lean mass caloric distribution:
Let us look first at activity. Keep in mind that muscle cells have receptors that take up energy and fat cells have receptors that take up energy. As you challenge muscles in specific ways you increase the hormones that make you leaner [3] while up-regulating and growing more receptors in muscle cells that are going to demand energy that might otherwise go toward fat tissue. Although some people can try to stimulate these pathways through varieties of activity, only heavy resistance training is unequivocally good at it for all people.
Conversely, long bouts of cardiovascular activity send the communication to your body that it needs to store energy for long bouts of exertion. Therefore, surprise surprise, it's best at up-regulating and growing more receptors in fat tissue. You read that right. Extended bouts of cardio grow fat cells, which, if you pause and consider what is happening under the surface, makes this an obvious and scientific fact. Think about it from a survival perspective. As you log hours of moderately intense activity, your body's need to hold onto stored energy (i.e. - fat) increases, so it's going to downregulate the capacity of ALL other (including cardiac and brain) tissue to take up energy while increasing fat's ability to do so. A major function of the fat cell is to store energy for the long haul. So when you do the long haul, don't be surprised at fat growth after the long haul. That's just your body preparing for the next long haul. This response is so strong that standard weight loss program subjects have higher concentrations of LPL for years after the program than they did before starting the program [4]. LPL in its feedback loop makes it possible for circulating triglycerides to get deposited or redeposited into the fat cell.
And at long last, let us look at nutrition. Some foods instigate the hormones that grow fat. Some foods instigate the hormones that break down fat. We can't cover them all here. We'll just stick to two hormones: insulin and cortisol. I chose perhaps the most complicated ones, since insulin can grow all tissue and cortisol can break down all tissue. But they explain a lot.
How do we make cortisol break down only fat? Restore optimal adrenal function (yeah I know this is a huge subject in and of itself). Afterwards, increase cortisol in the absence of blood sugar. Cortisol is trying to help you cope. If your blood sugar is low, it will help you cope by breaking down fat to unlock energy that can be used in the addressing of whatever needs your attention.
How do we prevent insulin from growing fat? Keep blood sugar low. If blood sugar is high, insulin is high for the most part. Insulin is going to knock on the doors of transport molecules in all tissue, but mostly fat, especially if you've already been priming the fat cells with your long bouts of moderately intense activity. Perhaps you're seeing a theme: elevated blood sugar prevents cortisol from breaking down fat; elevated blood sugar ensures insulin primarily grows fat. Where does elevated blood sugar come from? Carbohydrates and too much stress. So guess what happens with persistently elevated carbohydrate intake and stress? Yeah, you're figuring it out.
To wrap this up, let me paint two pictures of weight loss for you:
Imagine one person, Ms. Jones, whose primary method of weight loss is based on calorie balance. She cuts her calories and fat low; and she takes her activity sky high. As a result, her blood sugar plummets, so her insulin drops and her capacity to make fat decreases. Her long bouts of exercise stimulate her adrenal cortex to pump out cortisol, so she breaks down fat. Pounds melt away. After several weeks the lack of dietary fat intake suppresses her capacity to make all hormones, including cortisol, sex hormones and thyroid hormones. She uses all of the nutrients that should be supporting cell integrity instead toward barely supporting her high activity. Lean mass wastes. Metabolic hormones crash. Gut health suffers. Progress grinds to a halt. Cravings to restore stasis begin with a vengeance. Fat cells are upregulated in their capacity to take in energy. All other cells are turned off. Ms. Jones' motivation wanes because she's no longer making the hormones that keep her mind engaged and driven. She's hungry. She's seeing results slow or stop. Then, one week, she decides it isn't worth all this work and she eats a little more and works out a little less. But remember, her fat cells are the only tissue that can take in energy at this moment. So every resource goes toward growing fat, especially because her cravings are for sweets and that's what she eats, just a little, because "life is about moderation." Then one week turns to two. The forty pounds she lost in the prior four months has all returned, except now she has less muscle/bone and more fat than when she started. Oh yeah, and her hormones are shot and her metabolism is garbage. Next time she joins a gym, 60lbs heavier, she tells the story of her great success of 40lbs lost, and she knows what to do, she just has to apply herself with discipline. Did I mention that the second time she tries this method the metabolic outcome is two orders worse?
Now imagine yourself. You lift weights. Lean tissue upregulates. Muscles arrogantly steal calories from the dinner table. Fat cells starve and shrink. You cut carbs from the front of your day when cortisol is highest, so you burn fat for hours by simply existing. You eat more fat. As a result, your body learns to rely on body fat for fueling everything it does. Also, high dietary fat ensures you have plenty of raw material to make hormones. So, you can make cortisol when needed to break down fat. Mental clarity sharpens. Drive increases. Thyroid output goes up healthily. Hunger goes down. You can make melatonin to sleep, regulate serotonin to enjoy, maintain sufficient mucosal barrier to never have bad gut health. Cravings disappear. Willpower attains a lifelong peak. Then, imagine a major disruption to your life occurs. Oh wait, you weren't relying on long bouts of exercise anyway. Your weight stays exactly the same. The stress was doable. The motivation to reach your goal weight intensifies. You never burn out. This just becomes who you are. It's not a diet or a "plan".
It's just changing your genes.
[1] january 25, 2001 American Society for Clinical Nutrition
Long-term weight-loss maintenance: a meta-analysis of US studies1,2,3
James W Anderson, Elizabeth C Konz, Robert C Frederich, and Constance L Wood
+ Author Affiliations
1From the VA Medical Center, Graduate Center for Nutritional Sciences, University of Kentucky Health Management Resources Weight Management Program, Lexington, and the Departments of Internal Medicine and Biostatistics, University of Kentucky, Lexington.
[2] < Previous ArticleNext Article >
Preliminary Communication | June 27, 2012
Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance FREE
Cara B. Ebbeling, PhD; Janis F. Swain, MS, RD; Henry A. Feldman, PhD; William W. Wong, PhD; David L. Hachey, PhD; Erica Garcia-Lago, BA; David S. Ludwig, MD, PhD
[+] Author Affiliations
JAMA. 2012;307(24):2627-2634. doi:10.1001/jama.2012.6607.
[3] Med Hypotheses. 2013 Mar 12. pii: S0306-9877(13)00085-6. doi: 10.1016/j.mehy.2013.02.013. [Epub ahead of print]
Resistance exercise: A non-pharmacological strategy to minimize or reverse sleep deprivation-induced muscle atrophy.
Mônico-Neto M, Antunes HK, Dattilo M, Medeiros A, Souza HS, Lee KS, de Melo CM, Tufik S, de Mello MT.
[4] J Clin Invest. 1981 May; 67(5): 1425–1430.
doi: 10.1172/JCI110171
PMCID: PMC370709
Increase of adipose tissue lipoprotein lipase activity with weight loss.
R S Schwartz and J D Brunzell
Copyright and License information ►
This article has been cited by other articles in PMC.
It's hard to know where to begin with this topic. It took me over thirty years, fifteen in the fitness industry, 100 hour work weeks, thousands of client hours, over ten thousand consults, thousands upon thousands of research hours to get to where I am. So I get it. I'm not going to change the world with one article. Just stay mindful that American fitness hasn't progressed a nanometer coming from the paradigm of the last sixty years: cut calories; eat whole grains; cut fats out; avoid saturated fat; do lots of cardio; get a diet plan, fully customized, etc. And every person out there who has failed to reach an easy maintenance program after year two or five is more evidence that we're doing the wrong things. So, maybe... just maybe, you're willing to listen to this without ridicule and without dismissing it.
Whatever you're gathering up inside yourself in order to reject this article's angle, I've been there and heard it. One day, when working with a cardiologist, I began to explain the reasons why one should consider avoiding gluten. The cardiologist, without even hearing one word, cut in and said, "let's sit down and I'll explain." I was his guest at the hospital so I diplomatically obliged to give him the floor. He proceeded to put forth an anecdote he'd heard of some guy who put himself on a super-low calorie diet of only candy. "And," the cardiologist gleefully sniped, "the guy lost weight; ergo, PROOF that the only thing that matters is calories-in versus calories-out." This is the type of sentiment I know I'm up against when writing this.
Not only was it preposterous that a one-person population study, in anecdote fashion, be touted as proof of anything, especially without reference to what the "weight" was comprised of, long term impact and the like. But then, the greatest offense was the contrast of storyteller and audience. At the time I had recently cut down to about 8% bodyfat with a decent six pack by doing no more than 4 hours of intense activity per week and my calories were VERY high, in the 6000+ range. The lecturing cardiologist, on the other hand, had about 80lbs of visceral belly fat, even though he worked up to 12 hour days with 40lbs of lead vest sitting on his shoulders, and never eating anywhere near a much as I did.
So where are we going with all this? Firstly, let me make the distinction between energy balance and energy distribution. Energy balance tells us nothing and gives us no tools. To clarify, I think Gary Taubes, author of "Good Calories, Bad Calories," gives one of the best illustrations: it's like trying to explain why so many people are in a room by saying, "well, you see, more people entered the room than left" - that isn't an explanation; it's a description. Likewise, saying that you grew fat tissue because you took in more calories isn't an explanation. Actually, it's not even a description. It's nonsense.
All weight-loss and all weight-gain can be explained by calorie or energy distribution, not by calorie or energy balance. Think of a 250lb lean bodybuilder. How did he net a result of increased muscle weight and decreased fat weight? Was it by a means of calorie balance or calorie distribution? Did he eat more calories than he burned in order to gain 100lbs of muscle, or did he eat fewer calories than he burned to lose so much fat? People say, "he's got good genes" or "steroids," as their usual retort. But how does that change anything? I thought calories-in versus calories-out was the explanation we were relying on. Now we're invoking genes and steroids?
I first became aware that something was amiss with the calorie balance paradigm when I was a kid. I was a heavier kid who later got skinny in high school. I couldn't seem to figure out how to get heavier AND leaner. I was either moderately lean and very light or fatter and more muscular. The energy balance equation wasn't netting me a great physique. Fast forward from there about a decade and I was performing metabolic testing as a young trainer at Bally Total Fitness. To make a long story short, I found that people who ate a lot had high metabolisms; and people who dieted hard and did a lot of cardio had very low metabolisms. Later I would put the pieces together on hormone balance, hypothyroidism and the like.
Fast forward almost fifteen more years and here we are. Though what I'm saying at first seems very controversial, it really isn't. Energy distribution is all that matters. And we all instinctively know this. That's why we make appeals to heredity or hormones when confronted with examples which challenge the standard paradigm. We know that calories-in versus calories-out doesn't tell us anything. When we eat a thousand extra calories, some people allocate it toward increased bone density, some toward increased mitochondrial output, some toward increased thyroid output, some toward lean mass synthesis, some toward cancer cell growth, and most toward adipose anabolism (fat gain). The thousand extra calories does not matter. All that matters is how you distribute it.
In fact, let us take a step back. In the previous paragraph I used the terminology "extra calories" and you just accepted it without scrutiny. I tricked you. There's no such thing as excess calories. Energy gets used toward something. Thus, the very concept of too many calories is defunct.
If you're sharp, you're already thinking, "so what determines distribution?" The answer is complex and includes a lot of our intuited response: genetics, hormones, activity and nutrition. Just none of them play the role you may be thinking.
First on the chopping block is genetics. Your genes aren't fixed. This had been supposed for a long time. Then, in 2008, researchers at Johns Hopkins confirmed it. It's given rise to a whole new area of interest within the study of epigenetics. Consider this: every moment of your day you transcribe DNA. Throughout your life you execute this process sometimes at a rate of 2800 nucleotides per minute. Every 1/43rd of a second you choose which piece of data you will encode, keep around, pass on, etc. That means that you can and do change your DNA within the span of your life. In fact, you already do this every time you subject yourself to a stress, with every chemical to which you do or do not subject yourself, with every food choice and every lifestyle decision. This may mean that someone is lean because they're genetically lean and someone is fat because they're genetically fat; but if we accept the premise, then the good news is that you can stop encoding for fatness and begin encoding for leanness. There are some limits (i.e. - eye color), but very few. You can encode for intelligence and less for stupidity. I don't want to get too controversial with this; but you can start to imagine some of the ramifications toward psychology, addiction, identity and so on. It's just going to take some work to change. How exactly do you change your genes? We'll get to that in a coming article.
Second on the chopping block is hormones, obviously intertwined with genetics. They aren't fixed. Not even close. Intra-daily fluctuations can be drastic. Lifestyle will tell your body to create hormones that make you fatter or hormones that make you leaner. Concerning metabolic rate, blood serum levels of thyroid hormone increase with more calories and decrease with fewer. This is actually one of several reasons why standard dieting is a perpetually disempowering proposition. As you create a "caloric deficit," you suppress your thyroid, sometimes irreparably. Interestingly enough, even the American Medical Association , although late to the party by about 70 years, is coming along for the ride. In 2012 a very well-conducted study, accepted for publication in JAMA, demonstrated that as fat intake decreases so does metabolic rate [2]. It also showed that even with compensatory increases in carbohydrate intake the net impact to metabolism was not good: proof positive that mere calories are simply an incomplete picture.
We're starting to really get into the nitty gritty. However, I'm going to have to sacrifice a lot of details for the sake of brevity and impact. Your mind is hopefully swimming with a lot of new ideas and new questions; and one article won't address them all. But, what we can do is begin to clear up fat growth versus non-fat energy distribution. On to activity and nutrition.
A simplified primer on preferential lean mass caloric distribution:
Let us look first at activity. Keep in mind that muscle cells have receptors that take up energy and fat cells have receptors that take up energy. As you challenge muscles in specific ways you increase the hormones that make you leaner [3] while up-regulating and growing more receptors in muscle cells that are going to demand energy that might otherwise go toward fat tissue. Although some people can try to stimulate these pathways through varieties of activity, only heavy resistance training is unequivocally good at it for all people.
Conversely, long bouts of cardiovascular activity send the communication to your body that it needs to store energy for long bouts of exertion. Therefore, surprise surprise, it's best at up-regulating and growing more receptors in fat tissue. You read that right. Extended bouts of cardio grow fat cells, which, if you pause and consider what is happening under the surface, makes this an obvious and scientific fact. Think about it from a survival perspective. As you log hours of moderately intense activity, your body's need to hold onto stored energy (i.e. - fat) increases, so it's going to downregulate the capacity of ALL other (including cardiac and brain) tissue to take up energy while increasing fat's ability to do so. A major function of the fat cell is to store energy for the long haul. So when you do the long haul, don't be surprised at fat growth after the long haul. That's just your body preparing for the next long haul. This response is so strong that standard weight loss program subjects have higher concentrations of LPL for years after the program than they did before starting the program [4]. LPL in its feedback loop makes it possible for circulating triglycerides to get deposited or redeposited into the fat cell.
And at long last, let us look at nutrition. Some foods instigate the hormones that grow fat. Some foods instigate the hormones that break down fat. We can't cover them all here. We'll just stick to two hormones: insulin and cortisol. I chose perhaps the most complicated ones, since insulin can grow all tissue and cortisol can break down all tissue. But they explain a lot.
How do we make cortisol break down only fat? Restore optimal adrenal function (yeah I know this is a huge subject in and of itself). Afterwards, increase cortisol in the absence of blood sugar. Cortisol is trying to help you cope. If your blood sugar is low, it will help you cope by breaking down fat to unlock energy that can be used in the addressing of whatever needs your attention.
How do we prevent insulin from growing fat? Keep blood sugar low. If blood sugar is high, insulin is high for the most part. Insulin is going to knock on the doors of transport molecules in all tissue, but mostly fat, especially if you've already been priming the fat cells with your long bouts of moderately intense activity. Perhaps you're seeing a theme: elevated blood sugar prevents cortisol from breaking down fat; elevated blood sugar ensures insulin primarily grows fat. Where does elevated blood sugar come from? Carbohydrates and too much stress. So guess what happens with persistently elevated carbohydrate intake and stress? Yeah, you're figuring it out.
To wrap this up, let me paint two pictures of weight loss for you:
Imagine one person, Ms. Jones, whose primary method of weight loss is based on calorie balance. She cuts her calories and fat low; and she takes her activity sky high. As a result, her blood sugar plummets, so her insulin drops and her capacity to make fat decreases. Her long bouts of exercise stimulate her adrenal cortex to pump out cortisol, so she breaks down fat. Pounds melt away. After several weeks the lack of dietary fat intake suppresses her capacity to make all hormones, including cortisol, sex hormones and thyroid hormones. She uses all of the nutrients that should be supporting cell integrity instead toward barely supporting her high activity. Lean mass wastes. Metabolic hormones crash. Gut health suffers. Progress grinds to a halt. Cravings to restore stasis begin with a vengeance. Fat cells are upregulated in their capacity to take in energy. All other cells are turned off. Ms. Jones' motivation wanes because she's no longer making the hormones that keep her mind engaged and driven. She's hungry. She's seeing results slow or stop. Then, one week, she decides it isn't worth all this work and she eats a little more and works out a little less. But remember, her fat cells are the only tissue that can take in energy at this moment. So every resource goes toward growing fat, especially because her cravings are for sweets and that's what she eats, just a little, because "life is about moderation." Then one week turns to two. The forty pounds she lost in the prior four months has all returned, except now she has less muscle/bone and more fat than when she started. Oh yeah, and her hormones are shot and her metabolism is garbage. Next time she joins a gym, 60lbs heavier, she tells the story of her great success of 40lbs lost, and she knows what to do, she just has to apply herself with discipline. Did I mention that the second time she tries this method the metabolic outcome is two orders worse?
Now imagine yourself. You lift weights. Lean tissue upregulates. Muscles arrogantly steal calories from the dinner table. Fat cells starve and shrink. You cut carbs from the front of your day when cortisol is highest, so you burn fat for hours by simply existing. You eat more fat. As a result, your body learns to rely on body fat for fueling everything it does. Also, high dietary fat ensures you have plenty of raw material to make hormones. So, you can make cortisol when needed to break down fat. Mental clarity sharpens. Drive increases. Thyroid output goes up healthily. Hunger goes down. You can make melatonin to sleep, regulate serotonin to enjoy, maintain sufficient mucosal barrier to never have bad gut health. Cravings disappear. Willpower attains a lifelong peak. Then, imagine a major disruption to your life occurs. Oh wait, you weren't relying on long bouts of exercise anyway. Your weight stays exactly the same. The stress was doable. The motivation to reach your goal weight intensifies. You never burn out. This just becomes who you are. It's not a diet or a "plan".
It's just changing your genes.
[1] january 25, 2001 American Society for Clinical Nutrition
Long-term weight-loss maintenance: a meta-analysis of US studies1,2,3
James W Anderson, Elizabeth C Konz, Robert C Frederich, and Constance L Wood
+ Author Affiliations
1From the VA Medical Center, Graduate Center for Nutritional Sciences, University of Kentucky Health Management Resources Weight Management Program, Lexington, and the Departments of Internal Medicine and Biostatistics, University of Kentucky, Lexington.
[2] < Previous ArticleNext Article >
Preliminary Communication | June 27, 2012
Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance FREE
Cara B. Ebbeling, PhD; Janis F. Swain, MS, RD; Henry A. Feldman, PhD; William W. Wong, PhD; David L. Hachey, PhD; Erica Garcia-Lago, BA; David S. Ludwig, MD, PhD
[+] Author Affiliations
JAMA. 2012;307(24):2627-2634. doi:10.1001/jama.2012.6607.
[3] Med Hypotheses. 2013 Mar 12. pii: S0306-9877(13)00085-6. doi: 10.1016/j.mehy.2013.02.013. [Epub ahead of print]
Resistance exercise: A non-pharmacological strategy to minimize or reverse sleep deprivation-induced muscle atrophy.
Mônico-Neto M, Antunes HK, Dattilo M, Medeiros A, Souza HS, Lee KS, de Melo CM, Tufik S, de Mello MT.
[4] J Clin Invest. 1981 May; 67(5): 1425–1430.
doi: 10.1172/JCI110171
PMCID: PMC370709
Increase of adipose tissue lipoprotein lipase activity with weight loss.
R S Schwartz and J D Brunzell
Copyright and License information ►
This article has been cited by other articles in PMC.