Appetite-related problems are common in modern society, with the prevalence of obesity steadily increasing in developed countries (Dixon, 2010), and, as they become more westernised, in developing countries (Haidar & Cosman, 2011), due to readily available food sources and the promotion of sedentary behaviours creating what is known as an ‘obesogenic environment’ or pathological environment (REF). The obesogenicity of the environment is said to be “the sum of influences that the surroundings, opportunities, or conditions of life have on promoting obesity in individuals or populations” (Swinburn & Egger, 2002). Increasing obesity is a particular problem as it is known to be associated with type 2 diabetes, cardiovascular disease and cancer (REF) and thus puts substantial pressure on public healthcare services and resources, costing a country approximately 0.7-2.8% of its total healthcare costs (Withrow & Alter, 2011). Therefore, it is important to understand the causes of appetite-related problems such as obesity, allowing interventions to be implemented that may lead to reductions in the prevalence of the issue, and allow treatments to be developed for those who are already obese. Research has been conducted to help to explain the obesity pandemic and while genes have been identified that may contribute to the problem (REF), genetic influence alone has been found to only have a small impact (REF), and thus obesity is instead said to be due to the complex relationship between genes and the environment (Farias, Cuevas and Rodriguez, 2011). Therefore, this essay will look at the extent to which appetite related problems, such as obesity, are caused by the interaction between a normal physiology, in this instance defined as the healthy functioning of the appetite system (REF), and the obesogenic environment.
It has been argued that as genes have not been altered, then the increasing obesity pandemic must be due to environmental changes (Wardle, Carnell, Haworth and Plomin, 2008) namely, the development of the obesogenic environment (Hill & Peters, 1998). Increased portion sizes of inexpensive, palatable and high-calorie foods associated with the obesogenic environment (Pollan, 2008) cause individuals to overconsume (REF). This can be said to be due to the ‘thrifty gene’ hypothesis proposed by Neel (1962) which suggests that individuals carry genes that, in early history, would have provided an evolutionary advantage by allowing efficient fat deposition in times of famine. However, in modern society these same genes are disadvantageous as they encourage fat deposition in the obesogenic environment and lead to overconsumption and thus obesity (Speakman, 2008). Evidence exists for this hypothesis, as it has been found that the C230 allele has been found in the majority of Native American groups, but not in individuals from European, Asian or African groups and therefore may explain why in the current westernised environment, Native American populations are found to have a higher BMI (Acuña-Alonzo et al., 2010). This is further supported by research from migrant studies that show that there is a marked change in BMI when individuals move to an area where there are differences in their diet and lifestyle (James, 1996). For example, Pima Indians living in the United States with access to readily available high-fat foods have been found to be approximately 25kg heavier than those living in Mexico where they follow a lower-fat diet (Ravussin, 1995). Not only that but, those living in the United States have an obesity rate that is more than double the national United States average (REF) thus suggesting that obesity is caused by an interaction between an individual’s normal physiology and the obesogenic environment in which they live.
Although this is the case, not all individuals living in an obesogenic environment are obese (Llewellyn & Wardle, 2015), thus leading to questions regarding the accuracy of the thrifty gene hypothesis (e.g. Speakman, 2008). It has been argued that if the hypothesis is correct, then all individuals will by now have inherited these thrifty genes and thus, everyone would be obese (Speakman, 2008). This however, is not the case, as while obesity is steadily increasing, only an estimated 37.9% of adults in the United States are obese, thus resulting in a large proportion of the population not suffering from obesity (Fryar, Carroll & Ogden, 2016). This therefore suggests that while thrifty genes could be a possible explanation as to why some individuals are obese, other factors play a role in its prevalence.
Previous research suggests that there is a further role of genetics in controlling the variability in body weight, with evidence from twin-studies showing that there is a high heritability of BMI with genes accounting for over 50% (Elks et al., 2012). Interestingly, twin-data has also found that shared environment only has a small effect on childhood weight and that this influence diminishes by adolescence (Silventoinen, Rokholm, Kaprio & Rasmussen, 2007) thus suggesting that perhaps genetic influence has a greater impact on body weight regardless of the environment. This therefore has led to genome-wide association studies (GWAS) attempting to identify specific genes that may predispose individuals to obesity. From these, 58 genetic loci have been found to be associated with obesity (Lu & Loos, 2013), of which fat mass and obesity associated gene (FTO) (Frayling et al., 2007; Scuteri et al., 2007) was found to be the most significant and has been found to be replicated in almost all populations (Tan et al., 2014).
Originally published 15.10.2019