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Diet vs exercise for the prevention of pediatric obesity: the role of exercise


As pediatric obesity is commonly viewed as the result of an excessively positive energy balance, preventive efforts typically emphasize reduction of energy intake, with increases in physical activity (PA) having a supporting role. However, recent research that has focused on body composition rather than weight has found that PA stimulates development of lean tissue rather than fat tissue. Preventive interventions that emphasize vigorous PA rather than restriction of energy intake can help youths to develop lean bodies, at the same time that they ingest sufficient amounts of the energy and accompanying nutrients needed for healthy growth.


There are three features of this debate: 1 clarification of the exact debate issue; 2 analysis of the best and most current scientific evidence available; and 3 societal policies that are implied by this analysis.

Let us begin by clarifying that this debate concerns strategies for prevention of obesity, not treatment of people who are already obese, which may involve different strategies. Next we must focus on theory and research in growing youths, who are not simply small adults. The biological demands of growth require that we take a developmental approach in trying to understand why some youths become fatter than others.

The simple theory that currently guides our efforts is that some youths become fatter than others because of interactions between multiple genetic and environmental factors that influence energy intake or expenditure.1 This energy balance theory has generally led to interventions that have emphasized restriction of dietary energy intake, with increases in general physical activity (PA) having a supporting role. Although this theory is a useful guide for obese people who want to lose weight, it is not consistent with a growing body of emerging research on the relations among diet, PA and body fatness in the general population of youths. Therefore, it is a poor guide to the development of successful preventive interventions.

One way to examine this matter is by analyzing changes in diet, PA and body size over the last several decades to see whether diet or PA is more responsible for the growing obesity epidemic.2 Limitations to this approach include the uncertainty of the measurements of all the variables over the decades involved.

A different approach is to examine recent research that uses up-to-date scientific methods to determine why some youths become fatter than others. Contrary to what would be predicted from the energy balance theory, this research has surprisingly found that fatter youths generally ingest less dietary energy than their leaner peers. Thus, interventions that promote restriction of energy intake in youths may run up against the nutritional demands of growth.

Rather than focusing exclusively on the theory of energy balance, I suggest a different theory that takes a developmental rather than a metabolic approach to the matter. This theory posits that PA, especially vigorous PA, drives the system that influences the development of body composition in growing youths, with energy intake being a result, rather than a driver of the system. More specifically, vigorous PA stimulates stem cells to differentiate into bone and muscle cells rather than to fat cells; that is, the ingested energy and nutrients tend to be partitioned into lean tissue rather than into fat tissue. As lean tissue has a high metabolic rate, vigorously active youths tend to ingest relatively large amounts of energy, permitting them to obtain the nutrients needed for healthy growth. This theory suggests that we can help youths to develop healthy bodies if we focus more attention on promoting vigorous PA rather than restricting energy intake.

In weighing the available evidence in this complex matter, we must recognize that the limited accuracy in measurement of all the variables involved limits our ability to produce definitive results in favor of one theory or the other. Nevertheless, recent studies that have used objective accelerometry measurements of PA show that American youths generally do not meet public health recommendations for adequate PA, especially, as they grow into the adolescent years.3 We must also recognize that the biological mechanisms through which PA influences nutrient partitioning and body composition are still a ‘black box.’ Nevertheless, by testing the predictions of the theories in different types of research, we can determine which theory seems to be more valid.

Why should we focus on body composition rather than body weight?

Incorporating the concept of nutrient partitioning into our analysis requires that we go beyond the use of body weight as a surrogate index of fatness and focus instead on recent research that has measured body fatness.4 Although body mass index (BMI) is an effective surrogate index of fatness for epidemiological investigations, the numerator (weight) includes both fat mass and fat-free mass; this is a serious deficiency for several reasons. Most important is the fact that it is the fat tissue, not the lean tissue, which is deleterious to health, as illustrated in a study that showed weight loss to increase mortality rate, whereas fat loss decreased mortality rate.5 The use of BMI as an outcome metric in intervention studies is especially unwise, because a PA intervention might increase muscle and bone mass at the same time that it reduces fat mass, with the net result that BMI does not change significantly.6 Because fat is more calorically dense than muscle, a shift in energy stored from fat to muscle in a child might even result in an increase in BMI, even though fatness is reduced. Thus, this paper will focus on the increasing number of projects that have measured fatness rather than relying on older projects that report only weight indices such as BMI. Because of the importance of demographic factors to body composition, these new studies generally control for age, race and sex.

Why do some youths become fatter than other youths?

Let us first consider the energy balance theory. If this theory were correct, one prediction would be that fatter youths would be found to ingest more energy than their peers. Surprisingly, this prediction has not been confirmed. Indeed, recent projects that have measured body composition (rather than body weight) have generally found that fatter youths tend to ingest less energy than leaner youths.4, 7 One explanation for this counter-intuitive finding is that fatter youths under-report their energy intake more than leaner youths. This formulation requires that we assume that fatter youths eat more in the face of data that do not support the assumption, hardly an appropriate scientific attitude. Moreover, studies that have measured fatness rather than weight have failed to provide evidence that fatter youths under-report total energy intake to a greater degree than leaner youths.8 Thus, until more definitive results of reporting bias in youths are obtained, we cannot conclude that individual variability in fatness is explained by excessive energy intake.

If excess dietary energy intake is not the cause of individual differences in pediatric fatness, perhaps there are other aspects of diet that might be responsible, such as macronutrient distribution, energy density or specific categories of food. Unfortunately, studies that have measured fatness do not paint a clear and consistent picture of the influence of any aspect of diet.9, 10

In contrast to the counter-intuitive or inconclusive results of the diet studies, recent projects that have used accelerometry to obtain objective information about free-living PA have shown those youths who do more PA over a several year period become leaner than their less active peers.11, 12 This is consistent with the findings that fatter youths watch more TV, as a surrogate for sedentariness, than leaner youths.4

Especially noteworthy results have been obtained from recent studies that distinguished moderate PA (3–6 METS) from vigorous PA (>6 METS); the breakpoint between moderate and vigorous PA is approximately the difference between brisk walking and jogging-running.13, 14 These studies have shown that the amount of time spent in vigorous PA explained more of the variance in body fatness than did lower intensities of PA. Although beyond the scope of the current debate, it is worth noting that vigorous PA also explains a greater amount of the variance in aerobic fitness than does moderate PA15 and that higher fitness is associated with more favorable metabolic syndrome scores, regardless of obesity status.16 Thus, there seems to be something about vigorous PA that encourages ingested energy to be partitioned into lean tissue rather than fat.

Intervention trials that emphasized substantial doses of vigorous PA, without any attempt to restrict the energy intake of the youths, have found that youths who engaged in exercise sessions at least 2 days per week showed beneficial changes in total body fatness, visceral adiposity, bone mass and aerobic fitness. Moreover, the greatest impact on body composition and fitness were found in the youths who maintained the highest heart rates.17

The role of stem cell differentiation in the development of obesity

As studies of stem cell differentiation are quite new and the mechanisms complex, the role that it has in development of pediatric obesity is still unclear. There are reciprocal relationships in the processes through which stem cells differentiate into different tissues, such that mechanical signals that stimulate deposition of energy and nutrients into bone and muscle tend to direct them away from fat; moreover, the mechanical stimulation, which is effective in preventing the development of fatness, is not necessarily effective in reducing the fatness of already obese animals. This emphasizes the importance of focusing our efforts on prevention, rather than treatment, of obesity. Although these studies have generally been conducted in rodent models, some confirming human data are becoming available.18

The mechanical stimulation imparted by the vibrating platforms used in these studies has been of very low magnitude, which would seem to argue against the vigorous PA hypothesis. However, the frequency of the stimulation has been relatively high. In the human studies mentioned above, the dividing point between moderate and vigorous PA is walking vs running; that is, vigorous PA includes greater frequency of movement along with greater impact forces on the skeleton. Thus, it is reasonable to hypothesize that enhancing the mechanical signals applied to developing tissues by vigorous PA causes human stem cells to develop into muscle and bone rather than to fat. It will be interesting to learn the results of future studies that investigate the effect of different doses of mechanical stimulation on stem cell differentiation and body composition.

Implications for the prevention of pediatric obesity

The emerging evidence suggests that continuing to expend large amounts of our resources on interventions that emphasize dietary changes is unwise and wasteful. It is likely that we can improve the effectiveness of our preventive efforts by focusing on body composition rather than body weight, and by devoting more attention to PA, especially vigorous PA, rather than restriction of energy intake.19

In general, vigorous PA involves activities such as dancing, running, strength training and sports. In youths, such high-intensity activities generally involve both anaerobic and aerobic energy systems, but little information is available on the relative impact of these energy systems. To involve youths of varying fatness levels in the activities, it will be necessary to provide structured activities within regular physical education classes, as well as less-structured activities during non-school hours, weekends and vacations. Although providing the facilities and teachers needed so that every youth can be involved in these activities will be expensive for our societies, the resulting improvements in public health are likely to make it worthwhile. Moreover, funds will be saved by reducing what may be counter-productive efforts to prevent growing youths from eating as much as their biological needs incline them to eat.

It must be emphasized that a greater emphasis on vigorous PA does not imply a reduction in the importance of good nutrition for health; for example, it is certainly more healthful for youths to drink milk than sugared drinks. However, it is a mistake to assume that good nutrition involves restriction of energy intake—quite the opposite is true. Youths who engage in vigorous PA tend to have a high-energy throughput; that is, relatively high levels of both energy intake and expenditure. Such a high-energy lifestyle enables a youth to attain a healthy body composition while ingesting sufficient energy and accompanying nutrients needed for healthy growth. Moreover, the positive impact of vigorous PA on physical fitness is likely to have a positive influence on many other aspects of health as well.20


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Dr Gutin's work has been funded by the NIH. He thanks the journal editors, Richard Atkinson and Ian Macdonald, for their kind invitation to participate in this debate, and the journal reviewers for their helpful comments on an early draft.

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Correspondence to B Gutin.

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The author declares no conflict of interest.

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Submitted to the International Journal of Obesity, by invitation of the editors, April, 2010.

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Gutin, B. Diet vs exercise for the prevention of pediatric obesity: the role of exercise. Int J Obes 35, 29–32 (2011).

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  • body composition
  • youths
  • physical activity
  • exercise
  • diet
  • stem cell differentiation

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