CAPÍTULO V. ANÁLISIS INTERNO
8.2 Matriz de Ansoff
1.4.1 Early theories of homeostatic appetite control
EI is 100% behaviour; and in principal the amount of food and drink we consume is under our volitional control. Traditionally, the regulation of food intake has been viewed as a physiological system (Bernard, 1855, Cannon, 1932). Homeostatic control of feeding is concerned primarily with regulation of energy balance. Early theories of homeostatic appetite where based on signals arising from different body energy stores to relay information about the body’s energy stores to the central nervous system.
These included the aminostatic theory (Mellinkoff et al., 1956), the glucostatic theory (Mayer, 1953) and the lipostatic theory (Kennedy, 1953). The discovery of leptin provided support for the lipostatic theory (Zhang et al., 1994). Forty years prior to the discovery of leptin Kennedy described a circulating metabolite that acted on the hypothalamus to inhibit feeding and leptin provided support for this mechanism (Kennedy, 1953). However, the lipostatic theory cannot explain eating behaviours exhibited in the current obesogenic environment.
1.4.2 The Satiety Cascade
Whereas the theories above were related to an understanding of the total amount of energy consumed, the Satiety Cascade was developed to understand the pattern of eating throughout the day. Since the early theories of appetite control, a number of physiological and psychological processes have been identified that influence appetite control. The concept is that eating behaviour is stimulated and supressed by
physiological signals thereby producing an episodic pattern of eating occasions throughout the day. The homeostatic control of appetite can be conceptualized through a series of psychobiological processes that initiate and terminate feeding episodes (satiation), and those which suppress inter-meal hunger (satiety). Over 25 years ago Blundell et al. (1987) proposed the Satiety Cascade to help explain the underlying processes controlling food intake; for example, what initiates an eating episode and what determines its termination. The satiety cascade has been updated several times since it was first described in order to incorporate new developments in the field of appetite control (Figure 1.3). It describes the events that occur before, during and after the consumption of food which help to regulate EI. The satiety
cascade can be partitioned into two distinct processes; satiation and satiety. Satiation describes the processes that bring an eating episode to an end and therefore
determines meal size; along with the macronutrient composition of the food, these determine the amount of energy consumed. Satiation occurs when the stomach feels full or when the individual is satisfied with the amount of food consumed. Satiation can be measured by accurately measuring food consumption during meals. Satiety is defined as the inhibition of further eating together with the continued suppression of
hunger and increase in fullness that occurs once eating has ceased. The feeling of satiety lasts until the recovery of hunger and readiness for the next meal. Satiety can be measured by assessing changes in subjective appetite sensation such as hunger and fullness (using visual analogue scales) which provide valid markers of the intensity and rate of change of satiety (Flint et al., 2000).
Figure 1.3 The Satiety Cascade illustrates how the pattern of eating is influenced by psychological and physiological processes arising from food
consumption, source: Blundell (2010)
The processes of the satiety cascade are influenced by physiological actions of consumed foods in the stomach and the hormones released in the gastro-intestinal tract in response to the digestion and absorption of foods (Wang et al., 2008a). Neural and hormone signals communicate information to key regions of the brain (the
hypothalamus and brainstem) about the current state of energy balance to either stimulate or supress hunger and subsequent eating behaviour. These hormones can be categorised as either tonic, which are important for energy storage over the long term, or episodic, which are released in response to feeding (Blundell, 2006). The hormone leptin, discovered in 1994, can be considered a tonic hormone (Zhang et al., 1994). It is secreted by adipose tissue and signals to the brain the size of the adipose tissue store in order to inhibit hunger, however, most obese individuals have high
leptin levels suggesting a leptin resistance (Heymsfield et al., 1999). Episodic
hormones include ghrelin, peptide YY (PYY), cholecystokinin (CCK) and glucagon-like peptide 1 (GLP-1). Ghrelin, the only gut hormone known to enhance appetite, is an orexigenic (hunger) hormone thought to play a role in short-term meal initiation as circulating levels rise before a meal and decline once food has been consumed (Cummings et al., 2004). Ghrelin has been shown to increase with dietary-induced weight loss suggesting it may play a role in weight regain (Cummings et al., 2002).
Anorexigenic (satiety) hormones are released from the gut in response to food ingestion and play a role in early suppression of appetite. Hormones such as PYY, CCK and GLP-1 all increase in response to food consumption and are thought to inhibit food intake (Badman and Flier, 2005). Recent research has shown that despite similar levels of satiety and satiation following a high fat versus a high carbohydrate meal, the peptide response was markedly different. This indicates there is no single peptide or peptide profile that is solely responsible for satiety and different peptide profiles can confer the same degree of satiety (Gibbons et al., 2013). For a detailed review of the molecular mechanisms which regulate appetite see Schwartz et al.
(2000). It is important to note that the homeostatic mechanisms of appetite control described here may be modified at times by reward pathways relating to the pleasurable qualities of food and drink; a major concern in our obesogenic environment. Biological mechanisms which regulate appetite interact with
environmental, psychological and social factors to influence food intake (Berthoud, 2006). Non-homeostatic pathways involved in the control of food intake can override homeostatic signals promoting eating in the absence of physiological hunger
(Finlayson et al., 2007).
1.4.3 A new formulation of appetite control using an energy balance framework
The original lipostatic theory was only concerned with preventing excessive EI and fat gain and did not identify mechanisms driving ingestive behaviour to prevent loss of FM by maintaining a lower limit of EI. Recently, the role of FFM in appetite control has received attention. Accumulating evidence suggests FFM and RMR play an important role in the orexigenic drive to eat. Studies have demonstrated FFM and RMR are associated with hunger, self-selected meal size and EI (Blundell et al., 2012b, Caudwell et al., 2013a, Weise et al., 2014, Blundell et al., 2015a). RMR reflects the lower limit of the amount of energy required to maintain key biological and behavioural processes and it has been proposed that RMR produces a tonic drive to eat in order to maintain these processes (Blundell et al., 2012b). A new formulation of the major contributing factors to appetite control has been proposed in which both FM and FFM both influence eating behaviour (Hopkins and Blundell, 2016). This new formulation is depicted in Figure 1.4. Tonic signals (enduring, relatively stable over days) arise from
FM, FFM and metabolism. Signals arising from FM, such as leptin, inhibit EI whereas signals arising from FFM and RMR promote EI. The tonic appetite signals arising from FFM and RMR are, as yet, unidentified and represent a target for future research.
Episodic signals arise following food consumption as previously described. The overall strength of the orexigenic drive for food depends on the interplay between tonic
excitatory and inhibitory processes. There is evidence to suggest that the tonic inhibitory effect of adipose tissue becomes blunted as FM accumulates in the body due to leptin and insulin resistance. It follows that as people accumulate more FM, it becomes more difficult to control their appetite and further weight gain ensues.
Figure 1.4 Factors that influence appetite control within an energy balance framework, source: Blundell et al. (2012a)
The rising number of adults who are overweight and obese highlights how difficult it is to maintain energy homeostasis in the current obesogenic environment. Theoretically, maintaining a stable body mass, and even reducing body mass, should be straight forward; consume less energy than is expended. However, energy balance is affected by complex biological and behavioural mechanisms that operate asymmetrically to
defend against weight loss whilst permitting weight gain. A new formulation of appetite control provides insight into the underlying mechanisms controlling eating behaviour using an energy balance framework. This approach enables the investigation of factors influencing appetite control that would otherwise be examined in isolation.
Because this energy balance formulation provides a framework for considering the effect of PA and sedentary behaviour (SB) on appetite and body composition, it will be used as a framework for the studies in this thesis. It can be considered that exercise and PA could modify appetite directly (through a drive from EE) or indirectly by altering FM and FFM. This formulation therefore provides a way of linking PA, SB and appetite control within an energy balance framework.