Along with the development of the obesity epidemic, the prevalence of type 2 diabetes is also rising to epidemic levels and may be expected to rise further, although with some delay relative to the obesity epidemic (2). In view of the clinical burden of type 2 diabetes itself and of the associated greatly increased risk of microvascular and general cardiovascular complications, we must realize that we are approaching a severe global public health problem (2,3).

Obesity has a fairly strong, though yet insufficiently specified, genetic background (5), but the development of the epidemics, of course, must have been caused by changes in some environmental risk factors (2,5). The prevailing contention is that these environmental risk factors are the aspects of the "modern" lifestyle that are influencing energy balance—namely increased food intake (especially fat intake) and decreased energy expenditure by voluntary physical activity (2,6). This article critically discusses this contention.

The key question is what is disturbing the energy balance? The energy balance equation is as follows: energy intake minus energy expenditure equals change in energy stores. In most people, this balance is very finely regulated over longer time periods, i.e., weeks or months, or even years, resulting in almost stable individual body weight.

When obesity develops, it usually takes place over a long time period, i.e., several years (7). Because the caloric value of the accumulated fat is known and the approximate size of the fat stores is measurable, the degree of disturbance of the energy balance preceding the development of obesity can be easily calculated. It shows considerable interindividual differences but proves to amount to tiny proportions, only and not more than ~3% of the total energy turnover (e.g., if 10 kg of fat is accumulated over 5 years, then this corresponds to ~215 KJ/day, which is 2.5% of a daily turnover of 8.5 MJ/day). This means that the "overeating" is <3% of the total amount eaten every day by those who develop obesity.

Food intake is regulated by appetite, satiety signals, and behavior, be it deliberate or not. Energy expenditure is regulated by a complex series of physiological mechanisms and behavioral influences—particularly deliberate physical activity. The many complex processes involved in this homeostatic regulation obviously closely interact (8). In spite of relatively great short-term fluctuations in both intake and expenditure, homeostatic mechanisms are able to keep body weight stable in the long term under normal living conditions. Therefore, primarily increased intake or primarily decreased expenditure can be the cause of obesity only if the fine homeostatic regulation is either forced beyond the control limits or is slightly out of control.

Observation of energy intake or expenditure in those who have already developed obesity is not helpful in assessing whether these causes of disturbed energy balance are operating. The reason for this is that the development of obesity itself results in increased expenditure due to the growth of metabolically active fat tissue as well as the accompanying growth of lean body mass. Moreover, owing to the greater body weight, any movements of the body require more energy than in nonobese individuals. To satisfy the needs of energy, obese individuals have to eat relatively more than nonobese individuals. On the other hand, obese individuals usually are less physically active than nonobese individuals because of a variety of minor symptoms provoked by physical activity, such as dyspnea, joint pains, sweating tendency, etc.

This possibility is overlooked and needs much more attention along with the growing understanding of the regulation of the adipocyte fat balance. It has for many years been assumed that fat storage is a passive process that just picks up the superfluous energy from a positive energy balance. However, the recent years' rapid development of the knowledge about the fat cell, its development, and its hormonal regulation has shown that the idea of the fat tissue as a store room is a great oversimplification. There is now plenty of room for hypotheses about primary disturbances of the adipocyte fat balance as the cause of obesity.

Unfortunately, there is no similar global time trend study of the prevalence available. However, in most populations assessed by comparable surveys at different times, there is an increasing trend in higher body weights and prevalence of obesity (1,2). As with the regional variation in prevalence, there is also a considerable variation in the rates of changes in prevalence (Table 1). However, the prevalence of obesity is escalating so fast in so many places in the world that the phrase "global epidemic of obesity" is justified.

Table 1 shows the prevalence of obesity at two time points in men and women in selected North American and European countries and in countries in the Far East (2). In the U.S., England, and former East Germany, and in Finnish men, there is a considerable increase, whereas there is no increase in the Netherlands and Sweden and in Finnish women. All countries in the Far East group, barring Japan, show clear increases, with the most dramatic increases occurring in the Samoa Islands in the Pacific Ocean.

The magnitude of the obesity epidemic may be underestimated. It may be questioned if the usually shy severely obese people who are ashamed of their body image turn up at the health examination surveys. We have had the opportunity to investigate the relationship between degree of obesity at the mandatory draft board examination of Danish young men and the response rate many years later to an invitation to a health examination (13). The nonresponse rate increased as BMI increased, rising from ~20% in the leanest to ~45% in the most obese individuals. Valid studies of the detailed description of the obesity epidemic must therefore either assume that the nonresponder bias is equal across time and place or obtain data without this bias.

The link to the birth cohorts of the boys and young men indicates that the cause of the obesity epidemic in this population is an increasing environmental influence operating at an early age and resulting in a persistently increasing risk of developing obesity. The selective rise of prevalence of obesity during the first phase suggests that there is either a selective environmental exposure or greater susceptibility (possibly genetic) to a general increase in environmental exposure (16,19), whereas the combined effects on both prevalence of obesity and the median suggest a different or stronger exposure. The specific nature of these influences is still unknown.

An analysis of the changes in prevalence of obesity in relation to the changes in energy and fat intake during the period 1950–1990 in the U.K. did not show any relationship (20). In contrast, there was a parallel increase in the number of cars per household and the number of hours per week spent viewing television. On the other hand, in Denmark, the relative fat content of the diet seemed to increase a few years before the first phase in the rise in prevalence of obesity among the young men examined at the draft board examination (21).

In addition to the methodological problems in surveying dietary and physical activity habits, there is also the possibility that the effects of these influences depend on the susceptibility of the subjects to such influences, possibly, but necessarily, based on the genetic predisposition (22). Furthermore, the effect may be dependent on the combined exposure to both the high energy or fat intake and physical inactivity (23).