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Appetite-related problems, such as
obesity, a state in which excess lipids accumulate in areas of the body (Tan et al., 2014), are common in
modern society. The prevalence of obesity is 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 (e.g. Lu & Loos, 2013), genetic influence alone has been found to only have
a small impact (Naukkarinen et al., 2010), 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
body mass index (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.

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            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). Further research has consolidated these previous findings (e.g. Peeters et al., 2008;
Andreasen et al., 2008) and
have shown that FTO is also associated with numerous obesity-related traits
such as fat mass (Frayling
et al., 2007; Peeters et al., 2008; Andreasen et al., 2008) and leptin levels (Andreasen et al., 2008), although not with lean mass or body
height (Frayling et
al., 2007; Peeters et al., 2008; Andreasen et al., 2008).

 

Although this is the case, the results do have
limitations as the majority of the studies used Caucasian populations and,
while studies do exist that have examined the relationship between genetics and
obesity in populations of other ethnic descent (Fernandez-Rhodes et al., 2017; Monda et al., 2013;
Wen et al., 2014; Tan et al., 2014), there are conflicting findings regarding its effect. Despite FTO being found to be replicated in almost
all populations, evidence suggests that there is an ethnic difference in terms
of its effect on obesity (Tan et al., 2014). This is important, particularly as evidence has
found that known single nucleotide peptides (SNP’s) associated with waist to
hip ratio do not account for the elevated risk of obesity in South Asian populations
compared to Europeans (Scott et al., 2016), thus suggesting
that perhaps it is instead due to the higher obesogenic environment in which
South Asians live (e.g. Fischbacher, Hunt &
Alexander, 2004; Donin et al., 2010).

 

Nevertheless, despite previous research (e.g. Frayling
et al., 2007), carrying the FTO
gene does not necessarily determine that an individual will be obese. While the
genes may predispose individuals to obesity, they are only activated if they
are in an environment that allows them to be (Weinsier,
Hunter, Heini, Goran & Sell, 1998). Research by Andreasen et al. (2008) found that
physical activity led to the suppression of genetic susceptibility of
individuals with two FTO risk alleles. Thus, individuals carrying two FTO risk
alleles who were also physically active were found to have the same BMI as
those without the gene, and were lighter than those carrying two risk alleles
who were also physically inactive. Therefore, this supports other evidence
stating that the amount of obesity caused solely by genetic factors is small,
as the 32 loci associated with BMI only explain 1.5% of the variance in BMI (Naukkarinen et al., 2010) and suggests that instead,
the aetiology of obesity is due to an interaction between the environment and
genetics, with the environment having the most dominant effect.

 

However, evidence exists to suggest that obesity
may not be due to an interaction between normal physiology and the pathological
environment and instead may be due to abnormal physiology. Research has shown
that there is an association between dopamine receptors in the brain and obesity
(e.g. Wang et al., 2001; Foltin,
Fischman & Nautiyal, 1990; Noble et al., 1994) due to the involvement of dopamine in food intake (Balcioglu & Wurtman, 1998) and reward (Martel
& Fantino, 1996). It has been found that obese individuals have a
lower dopamine D2 receptor availability in their striatum than that
of normal individuals and that levels of these D2 receptors in obese
individuals were negatively correlated with their BMI (Wang et al., 2001). Thus,
as eating increases extracellular dopamine concentration in the nucleus accumbens
(Bassareo & Di Chiara, 1999), obese individuals may overconsume in
order to compensate for their reward hyposensitivity (Wang et al., 2001; Wang, Volkow & Fowler, 2002). Research
suggests that this hyposensitivity may be due to obese individuals having at
least one A1 allele of the TaqIA1 dopamine D2 receptor gene which
has been found to be associated with 30-40% fewer D2 receptors than
those with the A2/A2 allele (e.g. Noble, 1991; Noble
et al., 1994) and results
in more reinforcement from snack foods (Epstein, Leddy, Temple & Faith, 2007). This
is a finding which is said to be robust, as the only study that did not find
the same result used a different technique known as SPECT (Laruelle & Gelernter, 1998), thus suggesting
that it may not be sensitive enough to detect the difference in the number of D2
receptors (Noble, 2003). Thus, whilst reward hyposensitivity
leads to overconsumption and obesity (Wang
et al., 2001), this
effect is likely to be amplified in an obesogenic environment where availability
of palatable foods that provide high levels of reward (REF) is
high.

 

            To conclude, extensive evidence exists
to suggest that obesity is caused by the interaction between normal physiology and
an obesogenic environment as the high availability of palatable, high fat foods
(Pollan, 2008) allows “obesity
genes” such as FTO to be activated, thus leading to an increase in BMI (Andreasen et al., 2008). On their own,
these genes have very little contribution to obesity (Naukkarinen et al., 2010).
However, it is
likely that abnormal physiology does play a role in obesity as reward hyposensitivity
caused by a lower dopamine D2 receptor availability leads to
overconsumption as a means of compensation for their lack of reward (Wang et al., 2001). Although this is
the case, it could be possible that rather than obesity being caused by fewer
dopamine D2 receptors, that in fact, the receptors may be
downregulated due to excessive dopamine increases caused by overconsumption (Wang et al., 2001). This therefore
suggests that whilst there are numerous contributors to the obesity pandemic,
the interaction between normal physiology and a pathological environment has
the most influence.

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