Overfeeding – Calories count, but don’t bother counting them

«The upper two sets of figures show Mr. A. Levanzin of Malta, Dr. Benedict’s celebrated subject, before and at the completion of his fast. ‘About two and a half years ago, while I was over-eating, obese, neurasthenic, pessimistic and with a shattered nervous system, I chanced to read. . . an article about fasting. It was a flash of light that struck me vividly. It indicated to rue the right path to health and happiness. . . Today is the 31st and last day of it. . . I am feeling very well, very uplifted, and. . . do not feel yet any trace of hunger. I did not feel the least uncomfortable sensation except the bad taste of my coated tongue. I hope that a great benefit to my health shall accrue from it’. The lower two sets of figures show Mr. Winston Morris, one of the subjects of the University of Vermont study of experimental obesity before and after gain in weight. For the initial 75 days his average calorie intake was 6,700 (5,400 kcal/70 kg body wt) and for the following 60 days 10,200 kcal (8,300 kcal/70 kg). During both periods the composition of the diet by weight was approximately: protein, 17%, fat, 28% and carbohydrate, 52%. In contrast to Mr. Levanzin, he does not recommend his regimen as the right path to health and happiness.» [1]

Even among individuals who appear to combine dietary and lifestyle habits believed to promote the development of obesity, weight gain over the years is much slower than one would expect considering the pleasure associated with eating, the loose regulation of daily food intake, and the great tolerance for excessive intakes. [2]

It is not strange that the matter of overfeeding has lodged itself at the core of many nutrition debates. Overfeeding address the very question of what makes us fat and how we fatten.

But overfeeding studies do not fit nicely into the «calories inn – calories out» dogma. In fact, the finding that overfeeding does not generally cause long term overweight, is used to argue that it is what we eat, as opposed to how much, that determines how much weight we gain. The logic is that what we eat affects how much we eat, how much we burn and how we feel and so on. If different types of food affect how energetic we feel, as we know they can, and this effect is independent of energy content, then calories do not seem worth counting.

Because changes in RMR and thermic effect of food were small, the resistance to weight and fat gain with overfeeding was attributed to changes in spontaneous physical activity… [3]

The whole subject of overfeeding is extremely interesting, but it requires some careful tongue in cheek navigation through a minefield of twisted logic and rhetoric traps. For example, is overfeeding even relevant to the normal physiology of overweight and obesity? And even if subjects in studies are not «force fed» but rather make a small effort to overeat, can it tell us what causes obesity? And if we accept that dietary composition matter in a normal diet, then composition matters in overfeeding as well. Do we then know what component of the diet is responsible for weight gain?

Body weight is definitely regulated, and as it seems, quite tightly so. Most people are relatively weight stable most of the time, despite large variations in day to day energy expenditure and energy intake. An age-related drift in body weight has been estimated to about half a pound per year. David Weigle calculates that if the cost of depositing this ½ pound is 1560 kcal and that the caloric intake of an average individual is approximately 900,000 kcal per year, this weight gain represents an excess energy consumption of less than 0.2% [4]. This number is simply too small to conclude that body weight is something we are in control of. Counting calories just does not make any sense, because our body is in charge, not our mind.

Individuals who gain the less body weight during overfeeding are those who experience a greater increase in total energy expenditure. [5]

But the fact that body weight is tightly regulated does not mean it is unchangeable. We know it’s not. Losing weight can be quite easy. This means that the mechanisms that regulate body weight (or rather fatness) are the very mechanisms we alter when we lose weight and so those mechanisms are easily manipulated.

Gaining weight, at least in a speed equaling the speed at which we can lose weight, is close to impossible. The main reason is that overfeeding makes us full. A near complete suppression of appetite has been observed in both human and animal subjects [1,4,6,7]. For example, in one study, normal weight men were overfed by 1000 kcal per day for 21 days. This produced a mean fat gain of 79 grams per day. The voluntary caloric intake over the first 10 days after the end of the overfeeding, was reduced by 476 kcal per day relative to baseline.

In one study where rats were overfed to achieve twice the body weight of control animals, two obese rats were kept at a temperature of 5 degrees Celsius (which is a temperature that requires the rats to burn more energy for heat production), and yet did not consume food for 11 and 16 days. The animals started eating again once they were down to their original weight.

This graph shows the feeding and weight response in three tube overfed macaques. Overfeeding is during the solid bar. Food intake goes down during overfeeding and increases once the animals approach baseline weight

Extra energy ingested during overfeeding does not simply become stored. That is, some does. But one common consequence of overfeeding is increased energy expenditure. In a study by Leibel and coworkers, both obese and lean subjects were overfed and kept at 10% increased bodyweight compared to normal. This caused an increase in energy expenditure of 9kcal per kilo fat free mass in the lean and 8kcal in the obese [8].

Hence, the hypothesis that higher food intake may be the cause rather than the consequence of higher 24-h carbohydrate oxidation rates cannot be positively ruled out. [9]

Because not all extra energy is stored, weight changes in response to overfeeding are generally small. Still, large individual variation is common [10-12] and this variation is important to consider. There are many proposed mechanisms for the individual variation, such as different mitochondrial efficiency, compliance to diet and differences in digestion. Of course, the amount of overfeeding is often calculated based on self-reported food intake prior to overfeeding. This may also be a source of error and underreporting may explain some of the individual differences. People with a family history of diabetes experience larger detrimental effects from overfeeding than people without [13], which illustrates how our genes determine our potential for disease and weight gain.

One of the more famous of overfeeding studies, which resulted in a pile of articles, was conducted by Claude Bouchard in 1990 [14]. To see if there really were differences in how individuals responded to overfeeding and to see if this difference was due to different genotypes, he used 12 pairs of monozygotic twins. They were overfed by 1000 kcal, six days a week for 84 days. On average this resulted in 8.1kg (2,7kg of which was lean body mass) gained weight. But the range was from 4,3kg to 13,3kg. The twins gained the same amount of weight, in the same way, and thus showed the importance of genes. But the large variation between twin pairs in response to overfeeding is interesting.

The Bouchard study also found that the twins with the most type 1 muscle fibers, the slow fat burning type, gained the least fat. It might seem that skeletal muscle oxidative capacity in part predicts weight gain [15]. 4 months after the overfeeding, the twins had lost 7 of the 8 kilos gained, but at a 5 year follow-up mean weight had increased by 5kg. This was however likely the result of the younger twins (youngest pairs were 19y) adding some normal late pubertal weight.

And, although Bouchard and coworkers seemed somewhat surprised by it, the study found that there was no correlation between the total energy ingested and weight gained.

No current treatment for obesity reliably sustains weight loss, perhaps because compensatory metabolic processes resist the maintenance of the altered body weight. [8]

Diet composition
In overfeeding, as in normal feeding, results depend on the type of nutrient consumed. Overfeeding on carbohydrate affects the body differently from overfeeding on fat and different fats and carbohydrates will, theoretically, affect us differently.

One of the most extreme overfeeding rituals is that of the Cameroonian Guru Walla. In the Guru Walla, young men consume a diet made of red sorghum and cow milk (makes up over 95% of calories). The young men isolate themselves in different houses with a female attendant devoted exclusively to the preparation of Guru Walla meals. The diet and exclusion is supposed to lead to a certain level of purity. The men eat every 3 hour for 60 days, during which time body-weight can increase by an average of 17kg [16]. The ritual food is truly a high carb diet, with 70% CHO, 15% fat and 15% protein. Despite their large weight gain, the excess weight is lost after the ritual ends.

Patrick Pasquet writes about the long term effects of the Guru Walla: «Thus, 2.5 y after cessation of fattening there was a spontaneous return to initial body weight and body composition of the overfed subjects.» Pasquet almost had his nice stats ruined by one Cameroonian getting married and not losing as much weight as the other subjects: «Eight of them did not change daily life patterns and food habits in relation to the pre overfeeding period. One subject got married in the meantime; interestingly, for this subject some persistent overweight was left (6.7 of a 19.7kg gain).» [17] Marriage is of course a common accelerator of weight gain.

In a crossover study from 1995, led by Tracy Horton [18], lean and obese subjects were overfed on either fat or carbohydrate for 2 weeks. All subjects gained a similar amount of weight on both overfeeding strategies, and post overfeeding body weight gradually came back to baseline in both groups. But measurements showed that energy expenditure was increased more with carbohydrates than fat. This is likely because the body tries to burn off as much glucose as possible to keep from getting dangerously high blood glucose, while increased fat intake is not as dangerous, and there is thus less need for increasing oxidation of it. There were also indications of more energy being stored with fat overfeeding than with carb overfeeding. Lean and obese subjects responded similarly to overfeeding, although not surprisingly, the obese had a higher proportional oxidization of carbohydrate on both strategies.

The obese are commonly recognized by the fact that they are carbohydrate burners rather than fat burners [19]. Although the researchers does not mention it, table 3 shows that carbohydrate overfeeding caused greatly increased fasting insulin concentration in both lean and obese subjects. But fat overfeeding halved insulin in the lean and doubled it in the obese. It is also strange that the lean subjects had much higher insulin before fat overfeeding than before carbohydrate overfeeding. As this was a crossover study the results should be interpreted with caution.

Danish researcher Ole Lammert, and colleagues, also compared carbohydrate and fat overfeeding [12]. No significant difference in carbohydrate (78% carbohydrates, 11% protein, 11% fat) and fat 58% fat, 11% protein, 31% carbohydrate) were found after 21 days overfeeding. Both groups gained 1,5kg of weight.

When we eat carbohydrates, much can be stored in muscles and liver as glycogen, but as soon as these stores are saturated, carbohydrate oxidation increases and de novo lipogenesis (conversion of carbohydrates to fat) increases [20]. In one study, extreme carbohydrate overfeeding caused subjects to burn 400g of carbs per day, without exercising. And resting energy expenditure increased by 35%. Fasting glucose levels did not increase, which shows the body’s great ability (in lean subjects) to convert glucose to fat so as to keep blood glucose low. In addition, the study showed that going from a low fat diet to eating a high carb (86%) overfeeding diet, can bring your triglycerides from 0,8 mmol/l to a whopping 8,6 mmol/l, which is an astonishing feat.

Body weight change in both lean and obese subjects in the Horton study. As usual, once overfeeding is finished, food intake and body weight goes down. You could theorize that the reduction in body weight post overfeeding is caused by the subjects wanting to lose the newly gained weight. But as the reaction is the same in many other animal species, it is likely a natural physiologic response.

Body composition
It is interesting that overfeeding also can cause quite an increase in lean body mass, sometimes half the weight gained [11,12]. Only 64-75% of the 17 kg weight gained during the Guru Walla is fat mass [16]. In the Vermont prison overfeeding study, inmates increased their body weight by 16,2kg of which 10.4kg was determined to be fat. This does not mean that overeating is a good or way to build muscles, but there is much indication that if you want optimal muscle growth, you shouldn’t hold back on food intake.

Weight gained as fat can be either hyperplasia (new cells) or hypertrophy (increased cell size). A 2010 study found that 8 weeks overfeeding in 28 healthy normal weight adults led to an obvious increase in fat cell size, but also an increase in fat cell number [21].

Weight gain from overfeeding is not large. In fact, we could say that overfeeding works about as well at increasing body weight as energy restriction works at decreasing it. People do gain weight by voluntary overfeeding themselves or being force fed, but as soon as subjects return to their regular diet, the newly gained weight is quickly lost. This finding is one important reason the set point hypothesis emerged. What part of the diet is mostly responsible for the weight gain is difficult to say, but it is not likely easy to overeat on a low carbohydrate diet. Overfeeding is not healthy, and one important reason for the observed increased energy expenditure, is likely the body desperately trying to keep blood glucose down.

Overfeeding pushes the body’s equilibrium towards increased fat storage, but in animals and humans alike, once normal feeding commences, the equilibrium is once again restored at the original body weight. It is also clear that although most of the surplus energy is stored, quite a large part is used to increase energy expenditure, and so it is difficult to calculate weight gain or fat gain from calories consumed as food. In other words, more energy (calories) increases body weight, but the processes of energy storage and expenditure are too complex for it to make any sense to count calories.


1. Sims EA, Danforth E Jr, Horton ES, Bray GA, Glennon JA, Salans LB: Endocrine and metabolic effects of experimental obesity in man. Recent Prog Horm Res 1973, 29: 457-496.

2. Flatt JP: Issues and misconceptions about obesity. Obesity (Silver Spring) 2011, 19: 676-686.

3. Galgani J, Ravussin E: Energy metabolism, fuel selection and body weight regulation. Int J Obes (Lond) 2008, 32 Suppl 7: S109-S119.

4. Weigle DS: Appetite and the regulation of body composition. FASEB J 1994, 8: 302-310.

5. Tappy L: Metabolic consequences of overfeeding in humans. Curr Opin Clin Nutr Metab Care 2004, 7: 623-628.

6. Roberts SB, Young VR, Fuss P, Fiatarone MA, Richard B, Rasmussen H, Wagner D, Joseph L, Holehouse E, Evans WJ: Energy expenditure and subsequent nutrient intakes in overfed young men. Am J Physiol 1990, 259: R461-R469.

7. Bessesen DH, Bull S, Cornier MA: Trafficking of dietary fat and resistance to obesity. Physiol Behav 2008, 94: 681-688.

8. Leibel RL, Rosenbaum M, Hirsch J: Changes in energy expenditure resulting from altered body weight. N Engl J Med 1995, 332: 621-628.

9. Pannacciulli N, Salbe AD, Ortega E, Venti CA, Bogardus C, Krakoff J: The 24-h carbohydrate oxidation rate in a human respiratory chamber predicts ad libitum food intake. Am J Clin Nutr 2007, 86: 625-632.

10. Stock MJ: Gluttony and thermogenesis revisited. Int J Obes Relat Metab Disord 1999, 23: 1105-1117.

11. Forbes GB, Brown MR, Welle SL, Lipinski BA: Deliberate overfeeding in women and men: energy cost and composition of the weight gain. Br J Nutr 1986, 56: 1-9.

12. Lammert O, Grunnet N, Faber P, Bjornsbo KS, Dich J, Larsen LO, Neese RA, Hellerstein MK, Quistorff B: Effects of isoenergetic overfeeding of either carbohydrate or fat in young men. Br J Nutr 2000, 84: 233-245.

13. Samocha-Bonet D, Campbell LV, Viardot A, Freund J, Tam CS, Greenfield JR, Heilbronn LK: A family history of type 2 diabetes increases risk factors associated with overfeeding. Diabetologia 2010, 53: 1700-1708.

14. Bouchard C, Tremblay A, Despres JP, Nadeau A, Lupien PJ, Theriault G, Dussault J, Moorjani S, Pinault S, Fournier G: The response to long-term overfeeding in identical twins. N Engl J Med 1990, 322: 1477-1482.

15. Sun G, Ukkola O, Rankinen T, Joanisse DR, Bouchard C: Skeletal muscle characteristics predict body fat gain in response to overfeeding in never-obese young men. Metabolism 2002, 51: 451-456.

16. Pasquet P, Brigant L, Froment A, Koppert GA, Bard D, de G, I, Apfelbaum M: Massive overfeeding and energy balance in men: the Guru Walla model. Am J Clin Nutr 1992, 56: 483-490.

17. Pasquet P, Apfelbaum M: Recovery of initial body weight and composition after long-term massive overfeeding in men. Am J Clin Nutr 1994, 60: 861-863.

18. Horton TJ, Drougas H, Brachey A, Reed GW, Peters JC, Hill JO: Fat and carbohydrate overfeeding in humans: different effects on energy storage. Am J Clin Nutr 1995, 62: 19-29.

19. Zurlo F, Lillioja S, Esposito-Del Puente A, Nyomba BL, Raz I, Saad MF, Swinburn BA, Knowler WC, Bogardus C, Ravussin E: Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ. Am J Physiol 1990, 259: E650-E657.

20. Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt JP, Jequier E: Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. Am J Clin Nutr 1988, 48: 240-247.

21. Tchoukalova YD, Votruba SB, Tchkonia T, Giorgadze N, Kirkland JL, Jensen MD: Regional differences in cellular mechanisms of adipose tissue gain with overfeeding. Proc Natl Acad Sci U S A 2010, 107: 18226-18231.

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!