An “ecological” approach to the obesity pandemicBMJ 1997; 315 doi: https://doi.org/10.1136/bmj.315.7106.477 (Published 23 August 1997) Cite this as: BMJ 1997;315:477
- a School of Human Movement, Deakin University, Melbourne, Australia
- b Department of Community Health, University of Auckland, Auckland, New Zealand
- Correspondence to: Garry Egger Centre for Health Promotion and Research, PO Box 313, Balgowlah, NSW 2093, Australia
- Accepted 17 February 1997
The increasing prevalence of obesity in many countries means that it should now be considered a pandemic.1 One estimate from Australia suggests that over the past decade the average adult has been adding 1 gram a day to body weight.2 This has occurred in the face of increasing knowledge, awareness, and education about obesity, nutrition, and exercise. It has been suggested that a paradigm shift is necessary if future progress is to be made.3
Traditionally, weight gain was thought of as caused by eating too much or exercising too little, or both (changes in weight=energy intake-energy expenditure). This led to the search for small deficiencies in energy metabolism such as a reduced thermic effect of food to explain obesity.4 Treatment was dominated by calorie counting, and public health messages extolled people to balance their intake and output. This paradigm has changed with the increasing understanding of the dynamic relations between energy stores, appetite mechanisms, and energy metabolism and of the wider recognition of nutrient partitioning.5 6 From studies which have shown that fat balance is equivalent to energy balance,7 the fat balance equation was developed (rate of change of fat stores=rate of fat intake-rate of fat oxidation).5 This equation is more dynamic than the original static equation and reflects energy balance under normal conditions of free access to foods. Because fat intake and oxidation are not closely balanced,8 this approach does not need metabolic abnormalities or genetic mutations to explain weight gain. Indeed, the differences in body fat between people living in the same environment could be better described as normal physiological variation. This paradigm is more helpful in explaining changes in body fat within an individual over time, but it does not account for the wider influences within and around individuals on obesity.
An ecological model
The model presented in figure 1) proposes three main influences on equilibrium levels of body fat—biological, behavioural, and environmental—mediated through energy intake or energy expenditure, or both, but moderated by physiological adjustments during periods of energy imbalance. The level of body fat is seen not as a “set point” like a thermostat fixed on an exact temperature but as a “settling point” that depends on the net effects of the other components of the model and that changes as they change. This places obesity in an ecological context which calls for more than simple education about risk factors and needs a collaborative strategy with the multiple sectors which impact on the problem.9
Current strategies are not containing the obesity pandemic
A shift is needed away from the traditional view of obesity as a personal disorder that requires treatment
An ecological approach regards obesity as a normal response to an abnormal environment, rather than vice versa
This approach resembles the classical epidemiological triad used in successfully controlling other epidemics
Understanding, measuring, and altering the “obesogenic” environment is critical to success
The ecological model uses total energy as mediator; for most conditions of human living it is interchangeable with fat energy. Fat intake is an important determinant of total energy intake, and for output, total energy expenditure is a major determinant of fat oxidation.
Energy intake—Dietary fat is very energy dense and has a limited effect on suppressing appetite and enhancing fat oxidation.10 This makes reducing dietary fat an obvious choice for reducing total energy to treat or prevent obesity. A reduction in dietary fat with an otherwise free choice of food promotes a modest weight loss which is initially less than that from a conventional low energy diet.11 However, the longer term results are similar,12 and the reduced fat regimen seems easier to maintain.13 All weight loss programmes suffer from rebound weight gain, probably partly because of physiological defences against weight loss,14 but ultimately weight loss is limited by the high settling point of fat stores for people living in an environment that promotes obesity. To keep fat stores below this point often requires considerable effort, which is difficult to maintain in an unsupportive “obesogenic” environment.
At a population level, it seems that dietary fat and energy intake have not fallen as fast as energy output.15 The result is a large energy imbalance, leading to obesity. On the input side of the equation, the strategy of reducing dietary fat within the diet (that is, changing the foods eaten and the composition of meals) seems a more realistic approach than reducing total energy (decreasing the size and frequency of meals). Large reductions in the fat content of the modern diet seem unlikely, and they may not be necessary for a population based approach, as small changes made by a large percentage of the population often show up as greater improvements in a population's disease index than do large shifts made by only a few people.16
Energy expenditure—The intensity of physical activity required for optimal oxidation of fat is controversial. Relative fat utilisation is higher during activity of moderate intensity such as walking, but absolute energy use is higher during vigorous exercise such as running. It has thus been suggested that vigorous exercise results in greater absolute fat oxidation.17 This may be true for aerobically fit people, but unfit people tend to oxidise less fat at all levels of intensity. Hence, vigorous exercise—even if it could be carried out—is not likely to result in as much fat oxidation in unfit people as activity of more moderate intensity which can be comfortably sustained for longer periods. Obese people are usually unfit, and so moderately intense physical activity should be recommended for them.
As with fat intake, population benefits are more likely to come from modest increases in activity of low or moderate intensity in many people than from increases in high intensity exercise in a few. Indeed, part of the secular increase in obesity is probably attributable to modest, population-wide reductions in physical activity of low to moderate intensity or to reduction in “incidental movement” due to the introduction of labour saving technology.18
Physiological adjustment refers to the metabolic and, in some cases, behavioural changes that follow a disequilibrium in energy balance and that minimise large fluctuations in body weight. For example, in response to a negative energy balance, initially appetite may increase or physical activity may decrease14; then, with weight loss, fat oxidation and resting metabolic rate may decline until a new energy balance is achieved.19 Physiological adjustment may be more vigorous in some people, as a result of biological factors such as sex, age, or genetic makeup.20
One implication of this is that frequent plateaus, or slowing of weight losses over time, are a normal physiological response to energy disequilibrium.14 Adjustments seem to be more vigorous in response to weight loss than weight gain, especially in lean individuals,21 and they may also be more vigorous after rapid, rather than slow, changes. Hence the need to concentrate on long term loss of fat rather than short term, and usually temporary, loss of weight. This questions the ethics of programmes that advertise large weight losses in short periods.
Biological influences—Biological factors known to influence body fat levels include age, sex, hormonal factors, and genetics,22 all of which have been considered to be unalterable. The identification of the ob gene and its product leptin in 1994 caused widespread optimism about unlocking the cause of obesity and developing successful treatments.23 A greater understanding of appetite control will undoubtedly come from research on leptin, but no major effect of single gene defects has yet been identified, and it is likely that the genetic influences on body fat levels are polygenic.
There are also important sex differences in fat storage.24 The differences between the sexes are apparent early in life, become greatest with the onset of menses, then tend to decrease with the changes in hormone status in postmenopausal women.25 Fat loss and maintenance of lower equilibrium fat stores also becomes more difficult with age.26 Finally, there is increasing evidence of racial influences on energy balance.27 These biological influences explain much of the variance in body fat in individuals within a given environment, but they do not explain the large population increases which represent the epidemic itself.
Behavioural influences—Behavioural factors typically thought to influence obesity are “sloth” and “gluttony,” which imply a potential for willful control over the forces affecting body weight. Behaviours are the result of complex psychological factors, including habits, emotions, attitudes, beliefs, and cognitions developed through a background of learning history. Biological and environmental influences also affect behaviour, and, in turn, energy balance. Cognitive factors (willpower based on knowledge, for example) may have only a minor effect on eventual behaviour, and this explains the limitations of education in the treatment and prevention of obesity. However, the causes and effects of behavioural factors do have to be considered,28 and interventions to deal with these should be a part of any overall strategy.
Environmental influences—Environment can be broadly categorised into “macro” (of the wider population) and “micro” (with close proximity to the individual). In general, the macro-environment determines the prevalence of obesity in a population and the micro-environment, along with biological and behavioural influences, determines whether an individual is obese. The environmental influences on the amount and type of food eaten and the amount and type of physical activity taken are vast and underrated; table 1) shows some examples. A close examination of specific macro-environmental sectors (such as the fitness industry or the food service industry) or micro-environmental settings (such as the local gym or the workplace) will reveal many more interconnecting environmental influences than those listed. For example, food safety regulations, policies of food manufacturers, costs of cooking oils, and the availability of training programmes for food caterers can affect the choice, price, and quality of food at the work canteen.
Environmental influences represent the public health arm of the obesity problem. If the macro-environment is obesogenic, obesity will become more prevalent and programmes aimed at influencing individual behaviour can be expected to have only a limited effect. Historically, epidemics have been controlled only after environmental factors have been modified. Similarly, reductions in population levels of obesity seem unlikely until the environments which facilitate its development are modified. Yet this is often neglected in obesity management (as it was initially with tobacco control). Environmental change, such as regulation of the food industry or changes in building design, is likely to be unpopular. Although some changes may be overt, others—such as reductions of fat in the meat supply—may be more surreptitious.
Epidemiology of an ecological model
The model proposed in figure 1 bears a resemblance to the epidemiological triad (fig 3) which has proved to be a robust model with epidemics such as infectious diseases, smoking, coronary heart disease, and, more recently, injuries.29 For obesity, “host” encompasses the biological and behavioural influences, plus physiological adjustment. “Environment” is similar in the two models, and “vehicle” is represented by energy intake (food) and energy expenditure (physical activity). Preventive interventions are superimposed on components of the triad in figure 3. These provide some options for a wider approach to obesity.
Recent advances in obesity research (especially in molecular biology) may have an impact on treatment at the individual level. It is clear, however, that there is a major deficiency in research into the “obesogenic” environment and potential interventions. Without a supportive environment, treatment programmes are likely to be ineffectual and preventive programs will be restricted to mass education strategies.
Obesity presents us with two challenges: to treat people who are currently obese and to prevent obesity in people who are still lean. Neither of these challenges is currently being met; hence it is important to re-examine the paradigms on which treatment and prevention programmes are based. The model presented here suggests that the driving force for the increasing prevalence of obesity in populations is the increasingly obesogenic environment rather than any “pathology” in metabolic defects or genetic mutations within individuals. A paradigm shift to understanding obesity as “normal physiology within a pathological environment” signposts the directions for a wider public health approach to the obesity pandemic.