Energy in, energy out and the fairies in the back of my garden

Science philosopher Karl Popper proposed that science is easily performed. A theory must be falsifiable and the role of science is to prove a theory wrong. On the other hand if a theory resists constant attempts of falsification the probability of it being true increases. This is a very satisfying, concrete and mechanistic view of science; it is also not how science actually works. As Paul “Anything goes” Feyerabend commented, theories often survive falsification through changing the interpretations of results and sometimes by simply disregarding the results. Science is often performed blindfolded.

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?

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:

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 

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. 

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.

For the most part the report bases its conclusions (also those about causation) on epidemiologic studies. To further show of their incompetence the authors of the WCRF report writes: “As stated, the physiological cause of weight gain, overweight, and obesity is the consumption of more energy from foods and drinks than is used.

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.


Most of this is based on the writings of Gary Taubes. If you haven’t already read his work, do it!

A tribute to the bloggers

During my student years I read the standard scientific method curriculum book, “The Structure of Scientific Revolutions” by Thomas S. Kuhn.

In it, Kuhn writes about scientific paradigms and paradigm shifts. Although he was criticized for using the word “paradigm” in a rather inconsistent manner, it was still marvelous reading. What I learned then was that there are rarely major shifts in the way a scientific community views its major hypotheses. Simply put, scientists rarely change their minds about the big important questions.

Paradigm shifts are most likely to happen when new hard undeniable data are acquired. The Large Hadron Collider could for example cause a paradigm shift in physics.

“The Structure of Scientific Revolutions” describes basic scientific principles, how failures of observations to fit with current theories (anomalies) accumulate. How the observations are often dismissed, but sometimes accumulate until old theories are forced to fall and new emerge.

Kuhn gives examples in his book illustrating how the purveyors of the scientific consensus, or those upholding the paradigm must leave the scientific community or, to be frank, die out in order to give rise to new hypotheses and major scientific change.

Greatly criticized as the book was, it was right in that scientists do not have a history of easily changing their mind. This is in many ways a good thing. Living in a world of constant conflicting results would easily make your head spin if you just tried to go with the flow. But still, scientists often don’t change their mind when in fact they should. This too can make them strange in the head as observed by a widespread cognitive dissonance.

The thing is, when I first read Kuhn I though science was as he described it. That, if leading scientists in their field wouldn’t accept new and better theories I would have to wait for them to croak before we would see some change. What I forgot about then was that the book I was reading was written in 1962. They didn’t have the internet.

Compared to the present day, 1962 was the stone age of science. Those days you would have to go to libraries to find the odd article or book. It took a lot of time and work to find literature and thus scientist would concentrate their efforts on finding only the most pressing. Articles were published in journals like today, but the journals were mostly read by the people in the specific scientific field the journal covered. There were limits to how many journals you could subscribe to.

And so every scientific community sat on their individual hill knowing little about what the other communities were doing or if their research was of any interest to their own community.

Those working with overweigh would not necessarily know much of the science being done in relation to underweight or eating disorders, although both communities could learn a lot from each other’s data.

But know things have changed. There is still the standard scientific way of doing things. Submitting articles to peer reviewed journals, sometimes waiting up to a couple of years before it is accepted and some more time before it is published. When it’s published other scientist can submit comments or feedback that also has to be subjected to reviewing. It is a slow and tedious process, but it’s the best we’ve got.

However, living a life of its own in parallel to the standard scientific way is the internet way. This is where the bloggers reside. 

The really interesting thing about blogs is that it has evolved into a natural peer reviewing process. A post is written and in an instant it is subjected to questions, comments, feedback and sometimes thrashed within a few moments by another blog which is also subjected to the same scrutiny. Not only is blogging, twittering and other interactive social media an incredibly effective and fast way of spreading and acquiring knowledge, it is also something that affects the scientists themselves (who are also often a part of the same cyber world).

I don’t think we have to wait for people to pass away before we can see major change in health science. I think it is happening right now. I think it is inevitable. And, I think the bloggers are an important part of it. They are constantly exposing the readers to old and new knowledge. A lot of people who have science degrees read blogs, and if they don’t they have friends or family or colleagues who do. Either way, blogging affects people.

So this is me saying “thank you” to everybody out there working the blogosphere, and remember, you don’ have to be right and we don’t have to agree about everything, because there is no bigger threat to the expanding human knowledge than consensus.

The death of a theory

If I haven’t seen further than others it’s because giants were standing on my shoulders« – Richard Feinman quoting Hal Abelson quoting his roommate. 

I’ve been reading a fantastic book lately. Lee Smolins “The trouble with physics – The Rise of String Theory, the Fall of a Science, and What Comes Next.” The book is exactly as great as the title sounds, although admittedly, I only understand a fraction of it. Lee Smolin discusses string theory, how is came to be the leading theory in theoretical physics and how it might prove to be one of the greatest dead ends in the history of science. I’m by no means qualified to discuss theoretical physics, but as always when reading science my head draws parallels to my own area of research. String theory, as the leading theory in theoretical physics, does have a lot in common with the leading theory in obesity treatment, the low fat theory.
There is little doubt that the “low fat diet for weight loss” theory is a theory that should have been rejected a long time ago. There are good reasons it should be rejected. It only indirectly addresses the physiological causes of excess fat storage. And because it only indirectly addresses the real problem, it only works temporarily.

«They will devise numerous articulations and ad hoc modifications of their theory in order to eliminate any apparent conflict.» – T. Kuhn

In the near future the low fat theory might be considered one of the greatest blunders in health science. At least, it has the potential to be considered as such. Some theories have been shown to be near immortal and this is definitely one of them.

It is easy to draw parallels between the low fat theory and string theory. String theory is an attempt to unite different aspects of physics, general relativity and quantum mechanics, into one great unifying theory, a complete theory of nature. It is based on simplicity and beauty, but what seems intuitively logic is not necessarily logic at all.

Before Keppler, the planetary orbits were thought to be circular. A circle is beautiful and symmetric and it seemed logic that this was how the planets moved. And yet, observations showed the planetary orbits to be elliptical. The low fat theory is also intuitively logic. Fat contains much more energy than other nutrients of the same weight and excess energy is stored as fat. Thus eating fat in excess makes the body store fat in excess. Fat from foods makes fat in the body. It is simple, beautiful, logic and wrong.

String theory, like the low fat theory, does not have a good track record as far as theories go. It started as a simple theory, and many people think that a theory that incorporates all of physics should be simple. But there were fundamental problems with string theory right from the start. In order to get it to work on paper a lot of dimensions had to be added (the 3 dimensions we are used to, were by far enough), new and unobserved particles were invented and the theory had to be background dependent to work when the whole point was that it should be background independent. It also made few predictions and proved close to impossible to falsify by experiment. A theory has to be falsifiable, because only by opposing repeated attempts of falsification does a theory evolve into truth.

«A nice adaptation of conditions will make almost any hypothesis agree with the phenomena. This will please the imagination, but does not advance our knowledge.» – J. Black

Still, string theory survived. It survived because it was constantly added ad hoc additions and because conditions were constantly changed. Now, this is a normal scientific process. Few theories are perfect when they emerge. The question is, how many conditions can be changed and alterations be made before the theory should be replaced by a new one?

Like the string theory, the low fat theory needs to rest on several assumptions in order to survive. The low fat theory is based on the belief that energy intake and energy expenditure are independent factors. Little scientific data support this, and it is not possible to consider the body to be a closed system. It is also based on the assumption that we can all control our energy intake and expenditure by will. Low fat diets don’t work in the long run. Upon discovering this we can change the theory or consider it faulty. Because it didn’t work, modifications were made; People are lazy, have poor self control, exercise too little and so on. None of these assumptions are justified. They are often not given directly, but disguised by the fact that they are logical consequences of the theory.

Both the low fat and string theory were the leading theories in their field for a long time and in many ways still are. Other theories, even better theories, has constantly been placed in the shadow and were given little financial support. People who worked on alternative theories to string theory were automatically outsiders, low in the field’s hierarchy, just like the researchers working on low carb diets was given less attention than they deserved.

This is painful for many who have invested years and even decades of their working lives in string theory. If it is painful for me, imagine how some of my friends who have staked their whole careers on string theory must feel. Still, even if it hurts like hell, acknowledging the reduction ad absurdum seems a rational and honest response to the situation. It is a response that few people I know have chosen. But it is not one that most string theorists choose.”  – Lee Smolin

Although there’s still some hope for string theory, there is none for the low fat theory. We’ve tried it. It didn’t work. We are getting fatter than ever. Often the scientific standards themselves are reduced in order to keep these gargantuan theories alive. Intentionally or not, the result of this is sometimes the death of science itself and the people considered scientists are no longer scientists in the true definition of the word. The death of a theory is replaced by the death of science.

It doesn’t take an expert
There are usually no sides in science. Sometimes people ask me; what do you believe in/ who do you believe to be right or what dietary method do you teach? The way I see it the only correct answer is that I don’t believe anything. I know what some of the facts are. I can make some calculated guesses on what is less certain, and there is a lot I don’t know. Of course, I cannot actually give this answer. People need substance, and as soon as I mention carbohydrates, I’m on the low carb side. But there are no sides. Science is not a battle between teams, it is a unified search for truth.

The reason that mathematics invented the idea of proof and made it the criterion for belief is that human intuition has so often proved faulty– Lee Smolin 
Basic scientific principles are not difficult to understand and they are independent of scientific subject. When scientific standards are reduced, any lay person can see the faulty logic. Tom Naughton is being accused of writing about things he does not have the authority to write about. But, he does know what he is talking about, much more so than many of the experts in the field. You do not have to be a nutritionist or even a scientist to address the core problems related to basic scientific principles. A beginners mind easily spots the obvious flaws. Diabetes means you can’t handle dietary carbohydrates, yet a doctor may easily tell you to cut fat from your diet after diagnosing you. The doctor’s mind is that of an expert, clouded by experience.

«…insist that we should change the rules of science just to save a theory that has failed to fulfill the expectations we originally had for it. – Lee Smolin

Why aren’t we all fat?

I have noticed that there is one argument used in the nutrition debate that is used by both the low carb and the low fat community (in this context, dividing it into two sides make perfect sense). The same argument keep flying back and forth but I feel it is rarely given the response it deserves.

It goes something like this; “If carbohydrates make us fat, why aren’t all the people of the world, like many Asian people, who live on high rice diets, fat?”

For the record, I am fully aware that the composition of a traditional Asian diets is debated and that a general shortage of food may protect against any harmful effects of a high carb diet. The above argument is a poor argument for another more important reason.

In the low carb world the same argument is used, often in a form resembling the following; “Eating fat cannot make us fat. Because, if fat made us fat, why aren’t all people who live on regular high fat diets, like the Inuit or the Masai fat?”

This argument (and all similar) is easily refuted. Part of the reason these arguments are fallacious is that they rely on an unstated assumption, an assumption we cannot make. A causal factor may affect us differently and may only end up in full blown disease in predisposed individuals. We are not genetic copies. If we were all clones, finding causal factors would be so much easier (there is a reason twins make for popular study subjects). But we’re not. We respond differently to the same stimuli and only by being clones would we all be able to react similarly.

Smokers have a greatly increased risk of lung cancer, yet many smokers smoke their way through long lives with no cancer.

Still, the causal factor is still the causal factor. Insulin and glucose drive fat storage in all of us. Some of us however have counter regulatory mechanisms that may overpower the fat storing effects causing us to remain lean. The above arguments rest on the assumption that we are genetic copies. We’re not.

Ok, I realize the clone analogy is stretching it a bit. After all, as members of the same species we are very similar and we may easily all respond similarly to the same stimuli. But the truth is that the arguments do rest on the assumption that we will respond in the same way and the danger is that the assumption will be used to discard a theory when responses differ.

In some studies of low carb diets the results have been less than expected. My experience is that many of these studies are also easily criticized, but that doesn’t really matter. It also doesn’t matter that studies using body weight may not detect large alterations in body composition. What matters is that the cause for a disease does not necessarily make everybody exposed to the causative agent, sick. Carbohydrates may easily be the main cause of excess fat accumulation in fat cells even if not everybody who eats great amounts of carbs gets fat. We cannot simply reject a theory that points to carbohydrates as the main cause of overweight just because there are people who don’t get fat in the face of plentiful carbohydrates.

«If any and every failure to fit were ground for theory rejection, all theories ought to be rejected at all times.» – T. Kuhn 

Imagine a disease spreading through society and everything points to a virus as a cause. Then some people argument that the virus cannot be the cause of the disease, simply because there are people being exposed that does not get sick. It makes no sense.

On a similar note, the fact that you can lose weight by starving yourself (eating less energy) does not in any way contradict a theory pointing to carbohydrate as the causative agent.

The simple and undeniable fact is that many high quality studies of low carb diets have illustrated the diets efficiency in reducing weight. It makes perfect physiological sense and even evolutionary perspectives support it. These results cannot be rejected simply because someone loses weight by eating less energy. The results still stand. Getting them to fit with results from energy restriction studies is a matter of physiology, not theoretical science.

So, although carbohydrate restriction does not always give the expected positive results, this is not ground for theory rejection. On the other hand, when low fat diets have never given the long term results the theory predicts, this is ground for rejection. Treating overweigh people with low fat diets is a prime example of treating a symptom, the fat stores, rather than treating the cause of the fat storage. Because this is a strategy focusing on a symptom is will not work long term. Science supports this. Low fat diets simply do not work long term. We must reject the theory and try something else.

Is there a chance that such observations have already been made but ignored because, if confirmed, they would be inconvenient for our theorizing?” – Lee Smolin

Intention to treat – what was the question again?

If you haven’t already heard there is a new low carb study out. It shows similar effects on weight compared to a low fat diet over 2 years, but better HDL results in the low carb arm. It’s a really interesting study, but I’ll leave it to others, like Jimmy to elaborate.

Once again this low carb study is from Gary Foster and colleagues. Foster has previously given us this one. Although containing a lot of interesting data the researchers once again insist on only presenting the data as intention to treat with missing data carried forward.

Statistics is definitely not my strong side, and if I’m way off on this one please show me why. And if there is a stat wiz out there who can tell me why this is the right way to present results, please do.

The researchers did do some sort of sensitivity analysis and tried to justify using the entire sample of 307 participants in the final analysis. But it still does not compare to actually giving us the data on the compliers vs. non compliers. A lot of people dropped out of the study. Of the 154 randomized to the low fat group, 49 was not assessed at 24 months. Of the 153 in the low carb group, 64 were not assessed at 24 months.

Now, intent to treat analysis is a perfectly fair method to use. But it means that the results cannot tell us which dietary approach is the more effective. If we want to know which diet causes the greatest weight loss we must look at the data from the participants that actually followed the diet, and only those. What the results of this recent study tells us, is the effect of being put on a diet as opposed to the effect of following one. Is it really so bloody impossible to include data on compliers vs non compliers? As interesting as it is to know the effect of being put on a diet I for one would also like to know the actual effect of following the diets.

Like many other studies using similar analyses, this one also show a regression to the mean, that is the results differ the most at 6 months and slowly merge into similarity as the low carbers eat more carbs, and the low fat group eat more total energy. Whether this is because of the type of analysis and the increasing number of participants discontinuing the treatment is beyond me.

The title of table 2 of the study says is all really, “Predicted Mean Changes…”. But what about the actual change and the actual effect of following the prescribed diet?

Richard Feinman has written this article, illustrating the trouble with using an intent to treat analysis.
Still, Foster has done a good job and provided interesting data. Looking forward to seeing how this study is going to be received.