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?

Energy
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].

Conclusion
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.

References

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.

What drives me to move

’I can’t tell you how wonderful it was’, she told me. ‘I walked into this room, and it was full of people like me. People who couldn’t sit still. People who had to move to think.’

Ken Robinson, The Element 

I do some temp work at a local school. Noticed a boy in the top of a school yard tree the other day. I know he is one of those 14 year old boys who are completely unable to sit still for an entire class. That day, the first thing he did during break was to climb a tree. Because the tree was there.

If you place a running wheel in a rodent cage the animals will run. They will expend more energy and of course increase their food intake. But there is no need for rewards or incentives to get them to run. They thoroughly enjoy it. There is an inherent drive to run. It is in their nature.

A good fat metabolism will most likely make you active. Some people just can’t sit still. They are fat driven machines. If they can’t run they radiate heat and fidget non stop. These people are usually lean, which is the reason they can’t sit still.

Adam Kennedy and colleagues put mice on a ketogenic diet, a common obesogenic high-fat, high-sucrose diet, a 66% caloric restriction diet or control chow.

Mice on the ketogenic diet ate the same amount of calories as both the mice on control diet and the high fat/high sugar diet, but their weight dropped and stabilized at 85% of initial weight.

Analysis of energy expenditure in the high fat/high sugar and the ketogenic groups revealed an increase in energy expenditure in ketogenic diet animals. Total heat output was 15% higher in the ketogenic group.

Some nice quotes from the study authors.

Somewhat reduced exploratory activity was seen in HF [High Fat] animals compared with C-fed [chow] animals. 

The somewhat surprising preservation of fat mass in calorie-restricted animals has been described previously. 

Thus, although severe caloric restriction is known to cause fat mass loss in rodents, metabolic adaptations prevent fat mass loss during moderate CR in mice and even permit a small weight gain… 

Insulin levels were somewhat reduced in calorie-restricted animals compared with the chow-fed group, whereas insulin levels in ketogenic diet-fed animals were dramatically lower to a level that was only 10% of that seen in the calorie-restricted group. 

Give rats sugar, and they become passive, give them fat and they radiate heat. I am not sure if Kennedys rats had access to a wheel, but it would have been interesting to also have measured voluntary wheel running, which is easier to measure than exploratory activity.

You can breed mice to become wheel runners. These are so called “High Runner lines.” It is probably much worse for these mice to be deprived of their wheel than it is for other mice. It is also much worse to ask a human with an effective fat metabolism to sit still, than one operating on a lower gear.

In a somewhat interesting article entitled, The biological control of voluntary exercise, spontaneous physical activity and daily energy expenditure in relation to obesity: human and rodent perspectives, the authors note that:

…food consumption increases in the presence of wheels, at least in rodents. 

I do not get leaner and leaner the more I exercise, and this seems to be quite a universal human trait. This means that there must be a compensatory mechanism, and this mechanism has to be increased food intake or decreased non exercise energy expenditure.

In studies of human subjects confined within metabolic chambers for 24h, Ravussin et al. found that SPA [Spontaneous Physical Activity] varied widely and was a rather strong positive predictor of DEE [Daily Energy Expenditure] (Ravussin et al., 1986). They commented (p. 1577) that: “Because the subjects were not allowed to carry out physical exercise such as isometric exercises or calisthenics, it is possible that such activity represents an unconscious need to be active.” The implication is that forced reduction in voluntary exercise may lead to an increase in other types of physical activity. 

We move to little and this is making us fat. At least this is what those less informed are trying to convince us.

Westerterp and Speakman provide evidence that physical AEE [Activity Energy Expenditure] has not declined over the same period that obesity rates have increased, and argue that it is unlikely that decreased DEE has been a major contributor to the human obesity epidemic. 

Garland et al 2011

Even though obesity rates seem to increase universally, reduced physical activity do not seem to be a universal phenomenon. In Canada and Finland physical activity trends seem to be increasing while USA has hit a plateau. England and Australia though seem to have decreasing physical activity trends.

Based on this retrospective application of the energy balance equation, many investigators and public health officials have used the same energy balance equation in a prospective manner to predict that the obesity epidemic can be addressed by initiating changes in energy expenditure or energy intake as small as 25–50 kcal/day. From the energy expenditure side of the equation, 25–50 kcal/day can be spent by walking an additional 750–1500 steps per day. From the energy intake side of the equation, energy intake can be reduced by 25–50 kcal/day or by eating one less cookie, or forkful of food each day. Although this use of a valid retrospective application of the energy balance equation to a prospective prediction appears quite valid, it is not an equivalent situation. The prospective application of the energy balance equation for a single change in energy intake assumes that energy expenditure will not change in response and that a simple change in energy expenditure assumes that energy intake will not change in response. Evidence, however, does not support this assumption. 

The world is a funny place, but exercise will not make a fat person lean and simply eating less is a poor weight loss strategy. This, at least, we know.

You want cognitive dissonance? I’ll give you cognitive dissonance!

The latest issue of Obesity offers both welcome rationality, important discussions and good chances of some decent hair pulling.

It features an editorial by Jean-Pierre Flatt from the Department of Biochemistry and Molecular Biology, University of Massachusetts.

Flatt gives us an insight into some important misconceptions about obesity. He even made us a list of contents:

1. Problems in applying the energy balance concept  

2. Problems with the metabolic efficiency concept 

3. The misleading emphasis on the importance of low resting metabolic rates 

4. Misleading expectations about the importance of adaptive thermogenesis 

5. Problem in judging the importance of de novo lipogenesis and of its metabolic cost 

6. The irrelevance of the “nutrient partitioning” concept 

7. Failure to recognize the greater impact of energy intake than energy expenditure 

8. Difficulties in understanding food intake regulation 

9. Conditions for body weight stability: settling point vs. set point 

10. Problems with the application of the RQ/FQ concept 

11. The “defense of body weight” concept 

12. The different roles played by CHO and fat in energy metabolism 

13. Food intake regulation and carbohydrate balance 

14. The difficulty in obtaining experimental evidence about the role of carbohydrate balance in food intake regulation 

15. The need to distinguish between the role of carbohydrate balance in food intake regulation and the role of habitual glycogen levels in body weight regulation 

16. Understanding the recent increases in the preponderance of obesity 

17. Why don’t people eat even more? 

18. Confusion about the leverage of exercise on body weight 

19. Is dietary fat or is dietary CHO the major culprit in causing weight gain? 

20. How can inherited traits influence body weight regulation? 

21. The leverage of inherited vs. noninherited factors 

22. BMI vs. % ideal body weight 

Lots of interesting stuff right? Right. There is lots of interesting food for thought in the editorial and much is welcome food. For instance the problems with the energy balance concept, and:

The use of settling point rather than set point:

This corresponds to a “settling point” (20). Such a view accommodates the fact that circumstances cause weight stability to occur for various degrees of adiposity. Thus it seems to fit reality much better than the concept of a «set point» or «ponderostat». 

It has sometimes been considered that “set-points” are reset for different conditions, but in effect this argument reduces the set-point phenomenon to a settling point. 

I agree with him that saying the body is «defending» itself against body weight change is not a very helpful thing to say:

The common tendency of individual body weights to return to their original value after a weight-changing intervention is often explained as the manifestation of a mechanism tending to “defend” a particular body composition. The problem with this concept is that it appears to imply that mechanisms exist to actively drive the fat mass to a particular level, much as one would expect if a set-point mechanism existed (21). It fails to take into consideration that before the intervention, body composition for a given individual had already evolved until a steady state of weight maintenance had become established. 

He even mentions Mark Friedmans work on how liver substrate oxidation rates affect hunger, work I have previously written about on this blog. 

And he even acknowledges that exercise reduces weight by glycogen depletion and increased fat oxidation rather than by acutely increased energy expenditure.

But most of all, he talks about the importance of glycogen storage in obesity.

Thus, the role which increased habitual glycogen levels will play in promoting obesity in humans needs to be recognized! 

And the dissonance?

After elaborating thoroughly on the importance of glycogen stores:

“In view of the considerations made above, it is not surprising that a high incidence of obesity is typically encountered in sedentary populations consuming diets providing substantial amounts of fat.” (my bold) 

You can pull your hair now. It never seizes to surprise me how so much smart and something so incredibly stupid can be crammed into the same text.

Heres another brainmusher for you:

Thus the answer to the question asked above is that the major culprit is the unrestricted and ubiquitous availability of a mixed diet, offering numerous appetizing foods, often in large portions, in which sugar, and to an even greater extent fat, contribute to raise the energy density.

What is the best exercise for fat loss? Part II

Energy expenditure – does it count?

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

Leibel, Rosenbaum and Hirsch 1995 [1]
The energy

For some background reading on energy, this might be of interest.

Most endurance exercise apparatus found in a gym are equipped with a calorie counter. By inputting your weight and height and measuring your heart rate the display will tell you how many calories (kilocalories) you’ve burned (Calorie is a measure of energy. The international standard is Joule, but this is largely ignored.). You can literally count the fat loss while exercising. Or can you?

Robert W. Jeffery and coworkers randomized 202 obese men and women to standard behavioral therapy with the goal of either expending 1000kcal/week of exercise or 2500kcal/week, for 18 weeks. The actual reported energy expenditure for kilocalories per week at 18 months was 1629 and 2317 for the 1000- and 2500-kcal/week groups, respectively. At 6 months, there were no differences for weight loss between the groups, despite a reported difference in weekly energy expenditure of 562kcal. Reported energy intake was similar between groups. At 18 months the high PA (physical activity) group showed significantly more weight loss than the low PA group, 8.8kg vs 6.7kg. Now that’s a lot of extra exercise for a mere 2kg extra weight lost over 18 months [2].

All participants in the Jeffery study were instructed to reduce daily energy intake to 1000–1500 cal depending on initial body weight and to consume less than 20% of energy as fat. In addition they attended weekly group sessions for 6 months and one session per month thereafter. That is a lot of effort, exercise and starvation for 7-9kg of weight loss in 1.5years. It should also be mentioned that unlike the low PA group the high PA group were instructed weekly by trained exercise coaches and the participants in the high PA group were given 3$ for each week that they achieved or exceeded the energy expenditure goal of 2500 kcal/wk during the last 6 months of active intervention. Imagine the cost of treating overweight this way.

The authors of course concluded that when it comes to weight loss, more exercise is better and Donnelly [3] uses the study to conclude similarly – more is indeed better. However the study shows how there is little association between the amount of energy spent and consequent weight loss.

Many studies have showed that adding exercise to an energy restricted diet does not cause a greater weight loss [4-6] . If you are still a believer in the energy in energy out dogma this should have you worried. The truth is that expending more energy often does not lead to greater weight loss.

Leanne M. Redman [7] reported that one study [8] showed an 80% increased weight loss with exercise. Participants in the study were put on a National Cholesterol Education Program (NCEP) diet or the same diet with exercise (brisk walking or jogging 3 times a week). What Redman forgot to mention was that the exercise group also reported a 550 kJ/day smaller energy intake compared to the diet group.

McTiernan and co workers [9] randomized 202 men and women (sedentary/unfit persons, 40 to 75 years old) to control or an exercise intervention for 12 months. The exercise intervention was facility- and home-based moderate-to-vigorous intensity aerobic activity, 60 min per day, 6 days per week. Mean exercise time was 370 min per week for men and 295min per week for women. At 12 months exercise had resulted in 1.9kg and 3kg reduction in fat mass in women and men respectively. As mentioned in my previous post, it is difficult to account for all the variables in a study. Although the participants were asked not to change their diet, the researcher has only poor data on the participants’ diet.

You might argue that the above study shows positive results, showing how exercise effectively reduces weight and hinders weight gain. However, exercising for 60min per day for an entire year only to lose 3kg of fat, do not strike me as great results. Clearly the energy expended through exercise should have resulted in a larger weight loss according to the leading energy in – energy out dogma.

Joseph A. Houmard [10] and colleagues randomized 154 sedentary, overweight/obese subjects to either control or an exercise group for 6 months: 1) low-volume/moderate intensity group [~12 miles walking/week at 40–55% peak O2 consumption], 2) low-volume/high-intensity group (~12 miles jogging/week at 65–80% VO2 peak), and 3) high-volume/high-intensity group (~20 miles jogging/wk at 65–80% VO2 peak). At six months the low-volume/moderate intensity group had lost 0.8kg of body mass. The low-volume/high-intensity group lost 0,6kg of body mass, while the high-volume/high-intensity group which expended the most energy exercising, lost a whopping 1,8kg of body mass.

The fairies in the back of my garden were thrilled.

Back to Leanne M. Redman at Pennington Biomedical Research Center. Although she is convinced that the human body can be considered equal to a closed system where energy in and energy out is easy to measure and control and is the only thing worth measuring, she has done some very fine research. With her colleagues she did a study where 36 overweight, but otherwise healthy people were randomized to either control (healthy weight maintenance diet), caloric restriction (25% reduction in energy intake), or calorie restriction plus exercise (12.5% reduction in energy intake and 12.5% increase in exercise energy expenditure) for 6 months. After three months weight had declined by 7.4% for calorie restriction only and 5.8% for calorie restriction plus exercise. At six months the numbers were 10.4% and 10.1%, respectively. So the weight loss was equal using two different strategies and calculated energy deficit was equal. However, for men in the diet group fat loss accounted for roughly 64% of the weight lost and 68% in the exercise group. For women, fat loss accounted for 75% of total weight lost in the diet group and 85% in the exercise group.

There was a substantial loss of non fat tissue regardless of method, but the loss of different tissues also indicates different amounts of energy lost.

In 2002, Jeff Volek and co workers [11] put 12 overweight women and 10 overweight men on a low fat/low calorie diet and made them exercise four to five times a week. The goal was to reduce weight by 5kg in eight weeks. The women in the trial lost 4.3+3.4kg. But only 58% of this was fat mass. Percentage body fat went from 44.2 to 43.2. After eight weeks the women were just as fat. Had all the weight lost been fat, body fat percentage would have dropped to 41.8 – a much more reasonable drop. Imagine these women losing weight like this outside of a study setting, eating less and exercising – perhaps watching the calorie counter on the treadmill. They would probably have been thrilled to lose 0.5kg of weight each week.

Robert Ross [12] randomized 52 obese men to control, weight loss by diet alone, weight loss by exercise alone or exercise with stable body weight. Participants in the diet-induced weight loss group were asked to reduce daily intake by 700kcal during the treatment period to achieve a weekly weight loss of approximately 0.6kg. To lose the same amount of weight, participants in the exercise-induced weight loss group were asked to maintain a pre study isocaloric diet for the duration of the treatment period and to perform exercise that expended 700 kcal/d. Participants assigned to exercise without weight loss were asked to maintain body weight and to consume enough calories to compensate for the 700 kcal of energy expended during the daily exercise sessions.

The average weight loss was similar for both the diet-induced weight loss group (7.4 kg) and the exercise-induced weight loss group (7.6 kg). And the caveat? Calculated daily energy deficit (Doubly Labeled Water 14 Days during Weeks 6 to 7) was -663kcal in the diet group and -1039kcal in the exercise group. And although the participants in the exercise group were to not change their diet, they were instructed to follow official dietary guidelines. In addition the total fat loss in the diet group was 4.8kg and 6.1kg in the exercise group.

I could go on showing exercise studies that does not support the view that energy expenditure and intake is something we can control and should base exercise on – that we can calculate fat lost by exercise. Weight loss is vastly different between studies that are aiming for similar energy deficits. It is likely that the type of exercise is a confounding factor, as well as individual differences and lots of other hard to control for variables. My point is, if researchers struggle this hard to calculate fat loss and to use energy expenditure and intake as guidelines in weight loss, how is regular Joe to cope with the same task?

In “Exercise for overweight or obesity”, a Cochrane Database Systematic Review from 2006, the authors found that “When compared with no treatment, exercise resulted in small weight losses across studies.” The actual mean weight lost with exercise was 0.5 to 4.0kg. In the conclusion come the rather sad statements: 

The results of this review support the use of exercise as a weight loss intervention, particularly when combined with dietary change. Exercise is associated with improved cardiovascular disease risk factors even if no weight is lost.” 

Meaning that, exercise is good for you, even though you probably won’t lose any weight.   
In “A dose-response relation between aerobic exercise and visceral fat reduction: systematic review of clinical trials,” Ohkawara [13] and co workers found that there is a correlation between visceral fat loss and amount of energy expended exercising. But, the correlation was only present in subgroup analyses and nonexistent if people with metabolic-related disorders were included. Once again those with metabolic dysfunction ruin the perfect stats, and once again it seems that in those that need it the most, exercise don’t yield the expected results.

Robert Ross also did a dose-response review, in 2001. He found a dose response relationship between exercise and weight loss only in short term studies (less than 26 weeks), and not in long term studies [14].

Although there is a positive dose response correlation between exercise and weight loss (fat loss) in subgroups of people we still cannot assume that the correlation exists because more energy expended causes more weight loss. Exercise may cause a shift in the metabolism that make us less hungry and make us compensate less for the energy expended. The effect may also be unrelated to the amount of energy expended. As mentioned, there are a lot of variables at play here. Often when energy expenditure is upped it is through higher intensity exercise. Any difference between low and high energy expenditure might just as well be because of different intensities.

You will have a difficult time finding solid data showing a strong correlation between energy expended during exercise and consequent fat loss. More exercise and more energy demanding exercise does not necessarily give better long term results. (it often does not) Because of this, when we want to find the exercise type that is best for weight loss, we should base our decision on factors other than energy expenditure.

The question is what factors?

I’ll let Katarina Melzer at Geneva University Hospital have the last word on this subject:

Increased energy expenditure due to short-term PA is not immediately compensated for by changes in energy intake. Once moderate to intense PA is performed regularly and on the long-term basis, however, a distinction has to be drawn between lean and obese subjects. While the lean show a tendency to balance the extra PA energy expenditure by adapting their energy intake accordingly within a period, of about 3 days, the obese, probably due to their excess energy storage, do not show such a compensatory mechanisms.” [15]

Next: Exercise intensity

References

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2. Jeffery RW, Wing RR, Sherwood NE, Tate DF: Physical activity and weight loss: does prescribing higher physical activity goals improve outcome? Am J Clin Nutr 2003, 78: 684-689.

3. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK: American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2009, 41: 459-471.

4. Nieman DC, Brock DW, Butterworth D, Utter AC, Nieman CC: Reducing diet and/or exercise training decreases the lipid and lipoprotein risk factors of moderately obese women. J Am Coll Nutr 2002, 21: 344-350.

5. Cox KL, Burke V, Morton AR, Beilin LJ, Puddey IB: The independent and combined effects of 16 weeks of vigorous exercise and energy restriction on body mass and composition in free-living overweight men–a randomized controlled trial. Metabolism 2003, 52: 107-115.

6. Dengel DR, Galecki AT, Hagberg JM, Pratley RE: The independent and combined effects of weight loss and aerobic exercise on blood pressure and oral glucose tolerance in older men. Am J Hypertens 1998, 11: 1405-1412.

7. Redman LM, Heilbronn LK, Martin CK, Alfonso A, Smith SR, Ravussin E: Effect of calorie restriction with or without exercise on body composition and fat distribution. J Clin Endocrinol Metab 2007, 92: 865-872.

8. Wood PD, Stefanick ML, Williams PT, Haskell WL: The effects on plasma lipoproteins of a prudent weight-reducing diet, with or without exercise, in overweight men and women. N Engl J Med 1991, 325: 461-466.

9. McTiernan A, Sorensen B, Irwin ML, Morgan A, Yasui Y, Rudolph RE, Surawicz C, Lampe JW, Lampe PD, Ayub K, Potter JD: Exercise effect on weight and body fat in men and women. Obesity (Silver Spring) 2007, 15: 1496-1512.

10. Houmard JA, Tanner CJ, Slentz CA, Duscha BD, McCartney JS, Kraus WE: Effect of the volume and intensity of exercise training on insulin sensitivity. J Appl Physiol 2004, 96: 101-106.

11. Volek JS, Gomez AL, Love DM, Weyers AM, Hesslink R, Jr., Wise JA, Kraemer WJ: Effects of an 8-week weight-loss program on cardiovascular disease risk factors and regional body composition. Eur J Clin Nutr 2002, 56: 585-592.

12. Ross R, Dagnone D, Jones PJ, Smith H, Paddags A, Hudson R, Janssen I: Reduction in obesity and related comorbid conditions after diet-induced weight loss or exercise-induced weight loss in men. A randomized, controlled trial. Ann Intern Med 2000, 133: 92-103.

13. Ohkawara K, Tanaka S, Miyachi M, Ishikawa-Takata K, Tabata I: A dose-response relation between aerobic exercise and visceral fat reduction: systematic review of clinical trials. Int J Obes (Lond) 2007, 31: 1786-1797.

14. Ross R, Janssen I: Physical activity, total and regional obesity: dose-response considerations. Med Sci Sports Exerc 2001, 33: S521-S527.

15. Melzer K, Kayser B, Saris WH, Pichard C: Effects of physical activity on food intake. Clin Nutr 2005, 24: 885-895.