Assumptions are a major part of science. Sometimes they are confirmed other times they are disproven, and occasionally they form the foundation of an entire research area despite being completely wrong. The result is a branch of science where all results are interpreted in the light of its major underlying faulty theory. All results and assumptions that spring from such a major underlying theory are thus very likely to be wrong.
As far as I can tell, the whole “calories in, calories out” to lose or maintain body weight, is about as scientific as religion. I would like for nothing more than to be proven wrong on this. It would be great if someone would show up and say, “this is where you are wrong: you have forgotten to consider factor x.” I would like to be proven wrong on this, because I really don’t like the consequence of being right. The consequence is that a whole area of health science rests on a foundation of bollocks.
The correspondence between what is observed and what is stated
I know of a number of people who are and have always been lean, who have never bothered to keep a constant record of their energy intake and energy expenditure. Some of these people have taken educations in health, nutrition or some related subject and as a consequence they start caring about how much they eat and how much they exercise. After a short while these people are convinced that the reason they are lean is their strong will and ability to always mach their energy intake to their expenditure. It is a strange and a little frightening experience to observe this change in cognition.
I have always been thin. I have never bothered about how much energy I eat or how much I use. Yet somehow my weight stays the same. Some days I hardly eat, some days I feast, some days I spend being horizontal and some days I exercise at high intensities. The fact that my weight doesn’t change does not mean I have some superpower. It is simply the way we are as humans and as animals. Most people are relatively weight stable all the time despite large fluctuations in energy intake and energy expenditure. But how can this be?
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| Energyman! My superpower. I can eat as much as I want, without gaining weight. |
When an overweight person talks to his doctor he is instructed to count calories and make sure to expend a certain amount of energy every day to lose weight - perhaps start using the stairs instead of the elevator. But why does the overweight person need to be this obsessed with thermodynamics when most people do not?
Some clever scientist have tried to answer this question by creating an ad hoc hypothesis that states there must be a “set-point” hidden somewhere in the brain that determines our weight. The overweight have a set-point set to high. That is why they are overweight and why dieting, using a strategy based on energy reductions, don’t work. The set-point theory was invented much because dieting did not produce the results expected. It is an unproven theory and it will probably never be falsified, because it likely describes biological processes in equilibrium that appear to be a set point. The theory also has not gotten us any closer to understanding the problem that is overweight.
The rhetoric
If you are overweight it means you take in, or have at some point taken in, more energy than you expended and the excess energy is stored on your body. This is a statement of the obvious and health personnel and lay people alike often reduce it to: “Overeating causes overweight.” This statement however, makes as much sense as Willy Wonka. It is what is known as a tautology. It is a tautology because overeating means eating so much that you gain weight. The statement falls into the category of statement such as; free gift, added bonus, short summary and lying politician.
Similar to the above, it is stated that overweight is caused by to little physical activity. But the word overweight by definition means or implies that energy intake has exceeded energy expenditure. They are both very silly things to say. They make no sense and do not move the discussion forward.
Building on a tautology
You often hear well educated people say that the only thing that matters to people who wants to lose weight is to use more energy or consume less energy i.e. you must eat less than you expend. The statement rests on this equation:
This equation is a form of the first law of thermodynamics which states that energy can be transformed, but cannot be created or destroyed. The equation is sound. It is true and makes sense. What does not make sense is the way it is commonly used.
One very important thing to note about the equation is that it does not have an arrow of causation. That is, it is just as likely that you expend more energy because your energy stores are changing as it is that your energy stores are changing (losing weight) because you are expending energy. It is also just as likely that you eat more because you are gaining weight as it is that you are gaining weight because you eat more. I’ll give you some concrete examples of this in a bit.
Logic, as the equation is, it still does not tell us why energy expenditure might be less than energy intake, which is the only important question we want to answer.
What comes first
Gary Taubes uses the example of a child hitting puberty. When we reach puberty we start growing due to a change in the hormonal milieu. As a consequence, food intake also increases to support the increased growth. In this example, increased growth cause increased food intake. Is it thus likely that increased growth as seen in obesity may cause increased food intake and not the other way around? Yes it is, and here is why:
Many studies have been performed where scientists mess about with the brain of rodents. One strategy is to do a VentroMedial Hypothalamic lesion, (VMH lesions). These damages to a part of the hypothalamus cause a greatly increased food intake and the concomitant overweight in animals. This part of the brain is thought to control hunger and satiety. The increased food intake from VMH lesions was thus thought to be because of an increased hunger signaling from the brain. But the increase in hunger may not have been caused directly be the lesions. VMH lesions does cause increased food intake, but it also cause disruptions in the fat metabolism. It increases fat storage (for example by increasing insulin levels).
Hyperphagia (abnormal hunger and food intake) associated with the development of obesity is also accompanied by a metabolic state characterized by a large deposition of fat in fat tissues. This shift in fuel partitioning toward storage is independent of food intake and occurs before the change in food intake in most animal models studied.
People with the Prader-Willi syndrome are usually very overweight and are known for having a voracious appetite. The syndrome is due to a chromosomal error that affects the hypothalamus and the hunger is thought to be due to disruptions in the hunger center of the brain. But even the great hunger characteristic of this condition may be caused by excessive deposition of fat. When people with PWS are given a low carbohydrate ketogenic diet that makes the fat tissue release its energy rather than storing it, hunger decreases.
Some rodent models (ob/ob) produce little leptin and become very overweight. Both fa/fa rats and db/db rats have a leptin receptor defect which renders them very overweight. But their genetic defect is a defect that causes increased fat storage which makes them overweight even if calories are reduced. When obese Zucker rats (fa/fa) are put on low calorie diets their bodies respond as if it was starving. They lose muscle mass and their organs decrease in size, but their fat percentage remains the same. The increased fat storage cause increased hunger and reduced energy expenditure. In these rodents (as in many humans) low calorie diets does not make energy stored in the fat tissue available for use and so they simply starve.
If we reduce our carbohydrate intake we can lose weight without the hunger often observed in low calorie trials. Boden et al demonstrated that a 14 day low carbohydrate diet gave similar measurements of hunger compared to a regular diet, despite having 1000kcal less energy/day. In one trial the researchers put mice on a low carb ketogenic diet and observed the energy expenditure of the mice increasing (15% higher total heat output and 34% increased oxygen consumption). It seems that when insulin and glucose levels drop, the fat tissue pour out stored energy resulting in increased physical activity and heat production.
Phelan and coworkers compared people who had lost weight with low carb to people who had lost weight with low calorie. Those using low carb reported consuming more energy, expending fewer calories in weekly physical activity and reported much lower dietary restraint, yet regained the same amount of weight as low calorie.
Some clever scientist have tried to answer this question by creating an ad hoc hypothesis that states there must be a “set-point” hidden somewhere in the brain that determines our weight. The overweight have a set-point set to high. That is why they are overweight and why dieting, using a strategy based on energy reductions, don’t work. The set-point theory was invented much because dieting did not produce the results expected. It is an unproven theory and it will probably never be falsified, because it likely describes biological processes in equilibrium that appear to be a set point. The theory also has not gotten us any closer to understanding the problem that is overweight.
The rhetoric
If you are overweight it means you take in, or have at some point taken in, more energy than you expended and the excess energy is stored on your body. This is a statement of the obvious and health personnel and lay people alike often reduce it to: “Overeating causes overweight.” This statement however, makes as much sense as Willy Wonka. It is what is known as a tautology. It is a tautology because overeating means eating so much that you gain weight. The statement falls into the category of statement such as; free gift, added bonus, short summary and lying politician.
Similar to the above, it is stated that overweight is caused by to little physical activity. But the word overweight by definition means or implies that energy intake has exceeded energy expenditure. They are both very silly things to say. They make no sense and do not move the discussion forward.
Building on a tautology
You often hear well educated people say that the only thing that matters to people who wants to lose weight is to use more energy or consume less energy i.e. you must eat less than you expend. The statement rests on this equation:
Change in energy stores = energy intake – energy expenditure
This equation is a form of the first law of thermodynamics which states that energy can be transformed, but cannot be created or destroyed. The equation is sound. It is true and makes sense. What does not make sense is the way it is commonly used.
One very important thing to note about the equation is that it does not have an arrow of causation. That is, it is just as likely that you expend more energy because your energy stores are changing as it is that your energy stores are changing (losing weight) because you are expending energy. It is also just as likely that you eat more because you are gaining weight as it is that you are gaining weight because you eat more. I’ll give you some concrete examples of this in a bit.
Logic, as the equation is, it still does not tell us why energy expenditure might be less than energy intake, which is the only important question we want to answer.
What comes first
Gary Taubes uses the example of a child hitting puberty. When we reach puberty we start growing due to a change in the hormonal milieu. As a consequence, food intake also increases to support the increased growth. In this example, increased growth cause increased food intake. Is it thus likely that increased growth as seen in obesity may cause increased food intake and not the other way around? Yes it is, and here is why:
Many studies have been performed where scientists mess about with the brain of rodents. One strategy is to do a VentroMedial Hypothalamic lesion, (VMH lesions). These damages to a part of the hypothalamus cause a greatly increased food intake and the concomitant overweight in animals. This part of the brain is thought to control hunger and satiety. The increased food intake from VMH lesions was thus thought to be because of an increased hunger signaling from the brain. But the increase in hunger may not have been caused directly be the lesions. VMH lesions does cause increased food intake, but it also cause disruptions in the fat metabolism. It increases fat storage (for example by increasing insulin levels).
Hyperphagia (abnormal hunger and food intake) associated with the development of obesity is also accompanied by a metabolic state characterized by a large deposition of fat in fat tissues. This shift in fuel partitioning toward storage is independent of food intake and occurs before the change in food intake in most animal models studied.
People with the Prader-Willi syndrome are usually very overweight and are known for having a voracious appetite. The syndrome is due to a chromosomal error that affects the hypothalamus and the hunger is thought to be due to disruptions in the hunger center of the brain. But even the great hunger characteristic of this condition may be caused by excessive deposition of fat. When people with PWS are given a low carbohydrate ketogenic diet that makes the fat tissue release its energy rather than storing it, hunger decreases.
Some rodent models (ob/ob) produce little leptin and become very overweight. Both fa/fa rats and db/db rats have a leptin receptor defect which renders them very overweight. But their genetic defect is a defect that causes increased fat storage which makes them overweight even if calories are reduced. When obese Zucker rats (fa/fa) are put on low calorie diets their bodies respond as if it was starving. They lose muscle mass and their organs decrease in size, but their fat percentage remains the same. The increased fat storage cause increased hunger and reduced energy expenditure. In these rodents (as in many humans) low calorie diets does not make energy stored in the fat tissue available for use and so they simply starve.
If we reduce our carbohydrate intake we can lose weight without the hunger often observed in low calorie trials. Boden et al demonstrated that a 14 day low carbohydrate diet gave similar measurements of hunger compared to a regular diet, despite having 1000kcal less energy/day. In one trial the researchers put mice on a low carb ketogenic diet and observed the energy expenditure of the mice increasing (15% higher total heat output and 34% increased oxygen consumption). It seems that when insulin and glucose levels drop, the fat tissue pour out stored energy resulting in increased physical activity and heat production.
Phelan and coworkers compared people who had lost weight with low carb to people who had lost weight with low calorie. Those using low carb reported consuming more energy, expending fewer calories in weekly physical activity and reported much lower dietary restraint, yet regained the same amount of weight as low calorie.
This actually makes a lot of sense. Because our feelings of hunger and satiety are not determined by how much energy is available for the body, but how much energy is available to specific cells. It is an important distinction to make.
Why we are hungry
Why we are hungry
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| Recipe for disaster. istockphoto |
The cells that make up our body get the energy they need to maintain proper function from two sources; the food we eat and the energy stored in the body. When we eat we consume much more energy than is acutely needed and the extra energy is stored for later use. The cells that monitor the energy availability are situated in the liver. When they sense there is a lack of energy the body does several things. It increases our hunger to make us eat. It also makes us tiered and less energetic in order to conserve energy. If more energy is not supplied the body decides it is starving and starts shutting down energy consuming functions not needed for survival.
In the muscles the myostatin production may be increased by lack of energy. Muscle tissue is energy demanding tissue and not vital in large amounts. It thus breaks down when we starve independent of the size of our fat tissue.
In women, menstrual cycle disturbances can be a sign of insufficient energy availability to cells. Insulin injections can for example halt the reproductive function in animals and most likely in humans as well. This is how G.N. Wade put it 1996; “When food intake is limited or when an inordinate fraction of the available energy is diverted to other uses such as exercise or fattening[my bold], reproductive attempts are suspended in favor of processes necessary for individual survival.”
There is no direct correlation between the amount of energy stored in the fat cells and the amount of energy available for use. If the fat cells for some reason are reluctant to give out energy or the oxidation of fatty acids are hindered, the body often does not have enough energy to keep all systems functioning and tells our brain it is starving. That is why an overweight person can be in a catabolic state or simply being hungry despite the large amounts of energy stored.
If there was a direct correlation between the energy stored and how much was available for use we would expect overweight people to be more like a Duracell bunny and not being hungry. This is not the case.
As early as 1953 Albert Pennington wrote that; ”Energy expenditure is an index of calorie nutrition at a cellular level,” and thus hinted that increased energy expenditure may be caused by greater availability of oxidizable fuels, i.e. we run because we are losing weight.
Increased release of energy from fat tissue makes us sated and energetic. Increased fat storage makes us hungry and tiered. Inhibiting fatty acid release increases food intake while inhibiting the building of triglycerides reduce food intake. This holds true in several animal models and in humans. But data also show that a large lipolysis is not always enough to stimulate decreased food intake if the oxidation of fatty acids to ATP in the liver is somehow reduced. The satiety signal is then not created.
We eat because we are getting fat and we run because we are losing weight. Remember the nonexistent arrow of causation.
About counting calories
Here is small calculation stolen from a Gary Taubes lecture:
Let’s say there is a person whose caloric intake is 2700kcal per day, which is quite the likely number.
2700kcal/day makes a total of 1000000kcal per year. That’s 10 million kcal in a decade or roughly 12 tons of food.
For a person to keep his weight within 5kg in the course of a decade he must have an accuracy in controlling energy intake and expenditure of 0,4% or 11kcal/day.
Having this kind of accuracy is impossible. 11kcal is the equivalent of a medium sized fart. What this shows, is that it is highly unlikely that energy balance is matter of cognitive control. We cannot tell people to count calories because it rests on an assumption of an inhuman accuracy equivalent to that of a very, very accurate machine.
Energy intake and energy expenditure are not independent factors
There is a consequence of the reasoning that claims people must control of their energy intake and energy expenditure to not gain weight. The consequence is that all people who are overweight are so because they lack the willpower to be in energy equilibrium (gluttony and sloth). A second consequence of the theory is that everybody who’s lean is lean because they manage to control their expenditure and intake.
As illustrated, this is highly unlikely. And the fact that most people don’t care about energy inn vs. energy out, but still remain the same weight, should be enough to make the whole energy terror go away.
Also, if an overweight person is told that eating less or exercising more will make them lose weight, then the assumption is that energy expenditure and energy intake are independent factors. That is, that you can change one factor without the change affecting the other factor. The caveat is that this is not how the body actually works.
This is how Mark I. Friedman puts it; “Energy storage, expenditure, and intake can and do change and in doing so influence each other.”
In 1998 J.E. Blundell put it bluntly; “…there is a widely held belief that physical activity is a poor strategy for losing weight, since the energy expended drives up hunger and food intake to compensate for the energy deficit incurred.”
In 1977, when The National Institutes of Health hosted their second conference on obesity and weight control, they concluded that: “The importance of exercise in weight control is less than might be believed, because increases in energy expenditure due to exercise also tend to increase food consumption, and it is not possible to predict whether the increased caloric output will be outweighed by the greater food intake.”
In a 1995 meta-analysis, the effect of exercise on weight loss and conservation of fat free mass was determined. The authors concluded thusly: “Aerobic exercise causes a modest loss in weight without dieting. Exercise provides some conservation of FFM during weight loss by dieting, probably in part by maintaining glycogen and water.”
In a 1995 edition of The New England Journal of Medicine Jules Hirsch reported in collaboration with Leibel and Rosenbaum, that calorie restriction in overweight cause decreased energy expenditure and decreased metabolic activity adjusted for fat free mass. What they showed is that overweight people who are starved respond like thin people who are starved, by down regulating metabolism.
Jules Hirsch later said, in an interview with science journalist Gary Taubes:
“Of all the damn unsuccessful treatments, the treatment of weight reduction by diet for obese people just doesn´t seem to work.”
In the 1998 version of the Handbook of obesity, Bray, Bouchard and James describe countless of interventions based on calorie reduction to lose weight. Most of these failed at producing long term weight loss. The authors write that; “Energy intake is clearly elevated after significant loss of body mass. Furthermore, during weight gain, body weight does not increase monotonically but usually plateaus at higher levels.” The authors still sums it all up by recommending caloric restriction as the only sensible strategy to use.
In 2002, a Cochrane systematic review of low calorie and low fat diets for weight loss was published. The analysis showed that low fat diets were as effective as low calorie diets and that both diet strategies produced a weight loss that in the word of the authors was;”…so small as to be clinically insignificant.” The article is now, for some reason, withdrawn.
In 2000, Fogelholm and Kukkonen-Harjula concluded that everybody who lost weight with low calorie dieting eventually regained the lost weight. They also found that exercise could not prevent this weight regain. Their conclusion; ”...the role of prescribed physical activity in prevention of weight gain remains modest.”
There are numerous examples from the scientific literature illustrating clearly how energy intake and expenditure are highly dependent factors. Neither traditional dieting nor exercise actually works. The misinterpretation that led people to believe intake and expenditure are independent factors forms the basis of both dietary recommendations as well as many other aspects of our lives. It is the reason that the cardio machine at your local gym has a silly calorie counter on the panel, and it forms the basis of the long held belief that the more energy you burn during exercise the more weight you’ll lose.
In the muscles the myostatin production may be increased by lack of energy. Muscle tissue is energy demanding tissue and not vital in large amounts. It thus breaks down when we starve independent of the size of our fat tissue.
In women, menstrual cycle disturbances can be a sign of insufficient energy availability to cells. Insulin injections can for example halt the reproductive function in animals and most likely in humans as well. This is how G.N. Wade put it 1996; “When food intake is limited or when an inordinate fraction of the available energy is diverted to other uses such as exercise or fattening[my bold], reproductive attempts are suspended in favor of processes necessary for individual survival.”
There is no direct correlation between the amount of energy stored in the fat cells and the amount of energy available for use. If the fat cells for some reason are reluctant to give out energy or the oxidation of fatty acids are hindered, the body often does not have enough energy to keep all systems functioning and tells our brain it is starving. That is why an overweight person can be in a catabolic state or simply being hungry despite the large amounts of energy stored.
If there was a direct correlation between the energy stored and how much was available for use we would expect overweight people to be more like a Duracell bunny and not being hungry. This is not the case.
As early as 1953 Albert Pennington wrote that; ”Energy expenditure is an index of calorie nutrition at a cellular level,” and thus hinted that increased energy expenditure may be caused by greater availability of oxidizable fuels, i.e. we run because we are losing weight.
Increased release of energy from fat tissue makes us sated and energetic. Increased fat storage makes us hungry and tiered. Inhibiting fatty acid release increases food intake while inhibiting the building of triglycerides reduce food intake. This holds true in several animal models and in humans. But data also show that a large lipolysis is not always enough to stimulate decreased food intake if the oxidation of fatty acids to ATP in the liver is somehow reduced. The satiety signal is then not created.
We eat because we are getting fat and we run because we are losing weight. Remember the nonexistent arrow of causation.
About counting calories
Here is small calculation stolen from a Gary Taubes lecture:
Let’s say there is a person whose caloric intake is 2700kcal per day, which is quite the likely number.
2700kcal/day makes a total of 1000000kcal per year. That’s 10 million kcal in a decade or roughly 12 tons of food.
For a person to keep his weight within 5kg in the course of a decade he must have an accuracy in controlling energy intake and expenditure of 0,4% or 11kcal/day.
Having this kind of accuracy is impossible. 11kcal is the equivalent of a medium sized fart. What this shows, is that it is highly unlikely that energy balance is matter of cognitive control. We cannot tell people to count calories because it rests on an assumption of an inhuman accuracy equivalent to that of a very, very accurate machine.
There is a consequence of the reasoning that claims people must control of their energy intake and energy expenditure to not gain weight. The consequence is that all people who are overweight are so because they lack the willpower to be in energy equilibrium (gluttony and sloth). A second consequence of the theory is that everybody who’s lean is lean because they manage to control their expenditure and intake.
As illustrated, this is highly unlikely. And the fact that most people don’t care about energy inn vs. energy out, but still remain the same weight, should be enough to make the whole energy terror go away.
Also, if an overweight person is told that eating less or exercising more will make them lose weight, then the assumption is that energy expenditure and energy intake are independent factors. That is, that you can change one factor without the change affecting the other factor. The caveat is that this is not how the body actually works.
This is how Mark I. Friedman puts it; “Energy storage, expenditure, and intake can and do change and in doing so influence each other.”
In 1998 J.E. Blundell put it bluntly; “…there is a widely held belief that physical activity is a poor strategy for losing weight, since the energy expended drives up hunger and food intake to compensate for the energy deficit incurred.”
In 1977, when The National Institutes of Health hosted their second conference on obesity and weight control, they concluded that: “The importance of exercise in weight control is less than might be believed, because increases in energy expenditure due to exercise also tend to increase food consumption, and it is not possible to predict whether the increased caloric output will be outweighed by the greater food intake.”
In a 1995 meta-analysis, the effect of exercise on weight loss and conservation of fat free mass was determined. The authors concluded thusly: “Aerobic exercise causes a modest loss in weight without dieting. Exercise provides some conservation of FFM during weight loss by dieting, probably in part by maintaining glycogen and water.”
In a 1995 edition of The New England Journal of Medicine Jules Hirsch reported in collaboration with Leibel and Rosenbaum, that calorie restriction in overweight cause decreased energy expenditure and decreased metabolic activity adjusted for fat free mass. What they showed is that overweight people who are starved respond like thin people who are starved, by down regulating metabolism.
Jules Hirsch later said, in an interview with science journalist Gary Taubes:
“Of all the damn unsuccessful treatments, the treatment of weight reduction by diet for obese people just doesn´t seem to work.”
In the 1998 version of the Handbook of obesity, Bray, Bouchard and James describe countless of interventions based on calorie reduction to lose weight. Most of these failed at producing long term weight loss. The authors write that; “Energy intake is clearly elevated after significant loss of body mass. Furthermore, during weight gain, body weight does not increase monotonically but usually plateaus at higher levels.” The authors still sums it all up by recommending caloric restriction as the only sensible strategy to use.
In 2002, a Cochrane systematic review of low calorie and low fat diets for weight loss was published. The analysis showed that low fat diets were as effective as low calorie diets and that both diet strategies produced a weight loss that in the word of the authors was;”…so small as to be clinically insignificant.” The article is now, for some reason, withdrawn.
In 2000, Fogelholm and Kukkonen-Harjula concluded that everybody who lost weight with low calorie dieting eventually regained the lost weight. They also found that exercise could not prevent this weight regain. Their conclusion; ”...the role of prescribed physical activity in prevention of weight gain remains modest.”
There are numerous examples from the scientific literature illustrating clearly how energy intake and expenditure are highly dependent factors. Neither traditional dieting nor exercise actually works. The misinterpretation that led people to believe intake and expenditure are independent factors forms the basis of both dietary recommendations as well as many other aspects of our lives. It is the reason that the cardio machine at your local gym has a silly calorie counter on the panel, and it forms the basis of the long held belief that the more energy you burn during exercise the more weight you’ll lose.
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| What is the point of exercising if you can't count calories? |
The worst and most absurd recommendations are those claiming that if you take the stairs instead of the elevator you will expend a little more energy each day, that during the course of the year, results in x amount of kilos lost. It is as rational as the fairies in the back of my garden.
About exercise
If energy intake and expenditure are dependent factors, then we would not expect exercise to be a good weight loss method in itself. As illustrated from some of the quotes, exercise very often doesn’t make us thinner. It still can though. But it is important to remember that although exercise may make you lose weight, it is by no means obvious that the weight lost is because of the extra energy spent. It is in fact very unlikely that this is the mechanism.
The likely explanation for weight loss following increased exercise, is increased muscular insulin sensitivity accompanied by other factors that together cause a reduced fat storing, making fat reserves more available for use. And when a larger percentage of your body’s energy demand comes from your fat stores, you lose weight.
Contrary to popular belief, it is in fact likely that people who are lean are physically active because they are lean. Their bodies are often not very effective fat storers. Instead, their bodies supply a constant flow of energy producing a desire for or need to move about. The runner is running because he is lean, not necessarily the other way around.
And speaking of runners - in 1989 a group of Dutch scientists made 9 women and 18 men train for 18 months with the goal of running a marathon. During the 18 months the men lost 2,5kg of fat. The women didn’t lose any weight. The men increased their energy intake, the women didn’t. The women thus increased their energy expenditure without an obvious change in energy intake. However the women cut down on their fat intake and increased their intake of carbohydrates.
In a very recent report by Hopkins, King and Blundell, this is how they consider exercise for weight loss:
“Recent evidence indicates that longer term exercise is characterized by a highly variable response in eating behaviour. Individuals display susceptibility or resistance to exercise-induced weight loss, with changes in energy intake playing a key role in determining the degree of weight loss achieved."
There is no correlation between the energy expended during a bout of exercise and resulting weight loss. If our body was an isolated system, exercise could be considered the equivalent of opening a valve and letting some steam out. If a body was an isolated system such a correlation would be present, but the body is complex and not disconnected from its surroundings. The calorie hypothesis reduces it to the complexity of legos.
What we eat is more important than how much we eat. What we eat determines both what happens to the energy eaten and the energy stored in the body. You are not what you eat; you are what your body does with what you eat.
Speaking of fairies
The Norwegian dietary guidelines, as many other countries guidelines, are based largely on a document from the World Cancer Research Fund. It is a tome of a document that is held in high regard by many. Despite its size it is a horrible, unscientific document. It is not unlikely that a large enough group of blindfolded chimpanzees could have produced something of higher quality.
One way the WCRF document is flawed is in its use of the calorie hypothesis as a foundation for everything it has to say about overweight.
In chapter 8, p 322, “Determinants of weight gain, overweight, and obesity,” the WCRF has this to say:
“… a review of the epidemiological literature should be amplified by consideration of established knowledge on mechanisms, including basic thermodynamics and mechanisms of energy input, output, and balance.”
As I have already explained, this makes absolutely no sense at all. And yet, this is the basis of my governments' dietary recommendations.
To top it all of here is another memorable quote:
“The Panel has given special emphasis to the substantial body of robust experimental evidence, both in humans and in relevant animal models, underpinned by the principles of thermodynamics. To reach its conclusions, the Panel interpreted the epidemiological findings in the light of this experimental evidence. Thus, the Panel notes the associations between specific foods and food groups with weight gain, overweight, and obesity, and has interpreted them, in the light of the experimental evidence, as indicating a general effect of energy density [my bold] rather than as several different specific effects of particular foods and drinks.”
What does all this mean?
A number of studies have demonstrated that hunger occurs when fat storage is too high. Reducing fat storage reduce hunger. The best way to reduce fat storage is to reduce glucose and insulin levels. The best strategy to do this is to mind what you eat not how much. The body takes care of the how much part of its own. This is quite different from the conclusion reached from the calorie hypothesis which simply tells us to eat less.
If you want to lose weight it is implicit that you want to lose fat. To lose fat you need to mobilize the fat tissues e.g. make the fat tissue give out energy. This will make sure that a larger percentage of the energy you use comes from your own body stores. It will reduce the feeling of hunger while reducing your weight.
It is beyond human control to be in energy equilibrium. It is not how a body works.
As I said in the introduction to this piece of rambling, I would like for nothing more than to be shown that the calorie hypothesis is not flawed, as I argue it is. There is a comment section under the post. Consider this a plea rather than a challenge.
PS.
Most of this is based on the writings of Gary Taubes. If you haven’t already read his work, do it!
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