Читать книгу Clinical Obesity in Adults and Children - Группа авторов - Страница 108

Two decades ago, the World Health Organization declared the rising levels of obesity a “global epidemic.” No sophisticated epidemiological tools were needed to reach that diagnosis – it is probably the most abrupt morphological transition in the history of our species, if not any species. For researchers accustomed to studying the ecology and mechanisms of diet selection in simpler animals, such as insects, the scale, rapidity, and tenacity of the transition stood out as a biological enigma [1].

Many insect species studied to that point showed a remarkable ability to select food combinations and regulate the amounts of each eaten to compose a diet balanced in macronutrients. Some experiments simulated the essential properties of human obesogenic environments, involving unlimited access over prolonged periods to combinations of synthetic foods manufactured from refined ingredients, including at least one food high in palatable carbohydrate [2]. Yet, there was no obesity produced. This could not be explained by high levels of energy expenditure because even though the insects could move freely within the experimental boxes, they moved little. Rather, it was due to their ability to self‐compose a diet that defended a healthy body composition. Indeed, when the insects were experimentally induced into increased levels of physical activity, they changed their diet selection to compensate for the additional energetic costs [3]. More complex non‐human animals, such as rodents and chickens, likewise balance their macronutrient intake in this way, and change the selected diet to match changing nutritional requirements [3,4].

Why is it that our own species, with unprecedented privilege in terms of science and technology, fails in something so fundamental as eating a healthy diet, whereas species as simple as insects succeed using raw biology alone, even when surrounded by abundant palatable, calorie‐dense refined foods with no need for exercise? Were the psychological and biological capacities for diet selection by humans a casualty of 10,000 years of self‐domestication? Or was the problem in the environment? Or some combination of the two?

These questions are more than academic curiosities; they are central to framing obesity science and deeply entangled in the political issue of individual vs. societal responsibility [5–7]. They are pivotal for the management and prevention of obesity determining, inter‐alia, who bears the cost, the extent to which public resources are focussed on changing the behavior of individuals versus implementing public health policy [8], and indeed the severity and time course of the epidemic [9]. They also influence the quality of life for people with obesity through their role in generating blame and stigma [10] or normalizing a condition that can have serious health implications [11].

With the rise of obesity having continued unabated since it was first declared a global epidemic, to the point where the prevalence in several countries now exceeds 50% and others are fast approaching these levels [12], it is more urgent than ever to find fresh approaches to understand, prevent and manage the problem. In this chapter, we show how research, initially on insects and subsequently many other species (from single cellular slime molds to apes in the wild), has suggested a new ecologically inspired approach for understanding the roles of biology, environment, and their interactions in driving the obesity epidemic, and potentially identifying solutions [13]. We explain the theoretical foundations for the approach, illustrate its application to addressing relevant questions in some non‐human species, and show how it has been applied in studies of humans. The research suggests that humans are no different from other species in fundamental respects and that these similarities can provide a powerful guide for identifying relevant biological and environmental factors and examining how they interact to generate obesity.