these differences are not genetic, then what might be the basis for the increased susceptibility to abdominal obesity and diabetes? Barker et al. [44], in his original study, claimed that lower birth weight in babies of pre‐Second World War women in England seemed to determine an increased propensity of the offspring to develop the metabolic syndrome and diabetes 64 years later. The conditions amongst the working class in England at that time had already been documented as nutritionally totally inadequate [45], so Barker ascribes the propensity to metabolic syndrome and diabetes as reflecting the impact of maternal malnutrition with induced poor fetal growth. Yajnik in Pune, India, then showed with Barker startling differences between the offspring of mothers in Pune and those of now well‐fed mothers in Southampton, England [46]. The Indian children were smaller, with less lean tissue, and relatively fatter with distortions of the organ sizes which already related to increased insulin resistance in the newborn Indian babies. This seemed to be proportional to the degree of vitamin B12 deficiency and the discordant folate/B12 nutritional status of the mother [47], which has been shown to influence fetal growth. These vegetarian women were often being given inappropriately high doses of folic acid without any B12 and most likely would have been eating very modest amounts of food providing nucleic acids. Thus the generation of nucleotides in the crucial phase of early fetal development would have been compromised due to the lack of vitamin B12 required to generate methyl groups through folate remethylation.
These early nutritional effects relating to organ metabolism are probably amplified if there is some subsequent childhood malnutrition, because although they can recover their intestinal absorptive capacity on refeeding, their ability to mobilize insulin after a standard glucose test remains markedly reduced despite being extremely well‐fed for months and with body weights that had returned to the normal weight for their heights [48]. Further analyses have shown that this effect is long‐standing because adults in Jamaica who had been malnourished as children had a persisting impairment of insulin secretion [49], and this defect was also seen in survivors of early fetal deprivation during the Dutch famine [50].
The Millennium report for the United Nations on the global prevalence of persisting childhood malnutrition [51] highlighted the fact that almost all non‐Western countries after the Second World War had high prevalences of childhood malnutrition leading to long‐standing global, intergenerational malnutrition, which persisted throughout life. So a lifespan approach [52] to considering the problem of adult obesity begins with the nutritional state of the mothers before and during pregnancy with all its pathological and epigenetic implications for the offspring. We already know that the increase in body weight in previously malnourished women as they enter pregnancy leads to a much greater propensity to gestational diabetes [53], and they are then more likely to develop diabetes later themselves as well as having bigger and fatter children.
These global states of malnutrition almost certainly have lasted for millennia, so the early descriptions of obesity associated with ill health described by Bray are in line with the observed debilitating disease such as diabetes resulting from the impact of excess weight gain in people with lifelong malnutrition. In contrast, the Roman description of relatively healthy obese may then have reflected the better overall nutrition of the Romans in their Mediterranean environment.
Historical analyses of contributors to obesity
Weight gain leading to obesity occurs when energy intake from food exceeds energy expenditure from physical activity and metabolic processes over a considerable period. There has been much speculation as to the main driver of the global obesity epidemic, and this has often led to intense debate (see the analysis by Swinburn et al. [54] and the responses this generated). A complex and diverse range of factors can give rise to a positive energy balance, but it is the interaction between a number of these influences, rather than any single factor acting alone, that is thought to be responsible. The genesis of obesity at an individual level often focuses on a lack of cognitive control over personal behaviors that directly influence energy intake and ignores the critical role of physiological processes in driving or attenuating these behaviors. In addition, it is now recognized that powerful societal and environmental forces influence energy intake and expenditure through effects on dietary factors and physical activity patterns and may overwhelm the physiological control of body weight. It is the emergence of these environmental forces and the adjustments brought about by rapid changes in society which are the focus of most attempts to explain the emergence of the global obesity epidemic. The key elements of this transition and the emergence of our understanding around them are now set out below.
Marked declines in society’s physical activity
Given how sudden the development of obesity has been on a population basis, one has to ask what happened in the early 1980s to make such a difference to the prevalence of obesity in our environment? One clear societal change is the introduction of computers for a myriad of tasks in the early 1980s but in particular a complete transformation of many people’s office hours so now they spend their time sitting while working on their computers for hours on end. Even in such physically active jobs as construction or repairs, the introduction of a myriad of mechanical aids has also drastically reduced the need for sheer physical effort. The major development of the internet has also brought multiple opportunities for home entertainment and thus sedentary leisure time and reduced the need to leave home for entertainment. Life at home has also been transformed by new approaches to food preparation with microwaves, dishwashers, washing machines, etc. becoming a routine addition to kitchen hardware. It is regularly noted that with supermarkets providing ready‐to‐cook meals, the preparation time for meals has reduced from 2 to 3 hours to as little as 20 minutes.
Given all these changes, it is clear that the demand for energy expenditure has dropped dramatically on a secular basis since the early 1980s. Estimating the extent of this change in energetic terms is difficult in the absence of detailed sequential D2O18 data on energy expenditure. However, calculations can be made using the latest analyses of energy requirements by WHO [55] based on the original James and Schofield methodology [56]. Thus if a population of young men in their twenties weighing 70 kg was previously moderately active, i.e. with a physical activity level (PAL) of around 1.76 and a similar group are now sedentary (PAL 1.53), then men of this age would have reduced their average energy requirements by 400 kcal/day. Similarly, young women weighing 57 kg and moving from moderate to sedentary activity with PAL changes similar to men would reduce expenditure by 305 kcal/day (see examples in Table 5.1 of the UNU/WHO/FAO 2001 energy requirements report [55]). This would require a substantial and sustained reduction in food intake to match the lower energy expenditure. Originally when assessing UK household intakes in different decades, James estimated that from the 1950s to modern times there might on average have been an average reduction of energy demand for physical activity of about 700 kcal/day on the basis of a marked reduction in the proportion of adults engaged in very active jobs where PALs were 2.0 or more. The overall effects are illustrated in Figure 1.4.
Obtaining independent analyses of secular changes in energy expenditure is not easy, and if one simply relies on questionnaires, then sometimes total physical activity does not seem to have changed over time, e.g. in Finland [58]; but in China, there has been a marked decrease in physical activity [59], and the overall conclusions are that there has been a substantial decline in physical activity demands [60]. Secular studies in Norwegian children studied with accelerometer readings in 2005 and then again up to 2012 showed there was a consistent reduction in more intense physical activity even within this short time interval. In addition, there was an age‐related decline in physical expenditure as children became adolescents [61].
Figure 1.4 An illustration of the principal factors leading to the obesity epidemic.
