Various explanations can be provided for the reasons of obesity, from biological explanations, to neurological and evolutionary theories. Even socio-economic reasons could give insight into why some people have a higher likeliness of obesity Evolutionarily, the thrifty gene hypothesis provides insight as to why many suffer from obesity, as it suggests that our current genes are no longer suited to our new environment. Modern day society is filled with foods of a high calorific content, and our energy expenditure has decreased more and more with the technological advancements made. More television is watched and more computer games are played. This has been attributed to the increase in obesity, especially in children. Dietz and Gortmaker found that an extra hour’s viewing of TV a day can increase obesity levels by 2%. Further support for the thrifty gene hypothesis has been found for example in the case of Pima Indians and other groups of different societies who live in harsher conditions (in comparison to Western society) and are more likely to develop obesity when exposed to a Western diet.
The thrift gene hypothesis is reductionist however, as the gene pool has remained consistent over the last 40 years, yet only now are levels of obesity rapidly increasing, which suggests that other factors, such as biological and behavioural reasons are more significant. An example of a biological approach would be genetic reasons, which could provide an explanation for obesity, as some individuals may be genetically inclined with a family history of having a predisposition for weigh gain, particularly in today’s world which contains ample supplies of food. Our ancestors tended to eat as much as they could when possible, in order to create a reserve of energy which they could rely on, and to allow them to survive when no food was available. Our systems which control our satiety are not very sensitive to knowing when to stop, as they are programmed to find food when we are hungry, so now, we continue to overeat, are unable to stop, because we are innately programmed to consume for survival. Many twin studies have been made, which all indicate that genetic factors play a large part, and suggest that obesity often runs in families.
Bouchard overfed 12 pairs of male MZ twins and found three times more similarity of weight gain within pairs than between pairs, strongly indicating genetic factors. However this was a relatively small sample size, so in order for us to make a strong conclusion, the study should be replicated on a larger scale. However this would be ethically improper, as weight gain is associated with many physiological and sometimes psychological ailments, such as diabetes or depression; therefore it would be unethical to expose a large number of participants to weight gain. This was supported by Stunkard who examined the BMI of 93 pairs of MZ twins reared apart and found that genetic factors accounted for 66-70% of variance in body weight. However to assume that we inherit our BMI disposition from our parents would be reductionist, as it doesn’t account for individual differences, such as an overactive thyroid, which would cause weight gain. A UK study carried out research upon 4 year old twins, and found obesity heritability was 0.61in boys and 0.61 in girls, which further supports the idea that genes play a significant role in our weight gain.
However this study was not done cross-culturally, therefore lacks population validity and cannot be generalised to everyone. Also, the study relied on self-reports made by the mother of the children, who may have been dishonest as a result of social desirability bias, This study presents the idea of passive gene-environment correlation, which provides biological and behavioural explanations (that our genetic factors interact with our environment). Both approaches are deterministic however. The biological approach represents hard determinism, and has absolutely no room for free will, and there is evidence to support it. Frayling analysed 39,000 white people’s blood sample from the UK and Finland. While the extremely large sample size increases the internal validity of the study, using only white Finnish and British participants is ethnocentric, therefore the results cannot be generalised to others. In his study, 25% of participants were clinically obese (BMI over30), and he found that variations to the FTO gene were more common amongst obese participants.
In fact, those with the altered gene were on average, 3 kgs heavier than those with the usual chromosome 16. Whilst this cannot be used to explain all cases of obesity, as there are many individuals without a mutated chromosome 16 who are still obese, but it does explain why some people struggle more than others to lose weight (due to their unchangeable genes). Possible neurochemical imbalances cause overeating. Recent research suggests that body fat might be an active organ and may trigger hunger itself. This would mean that once individuals start gaining excess weight, they then feel more hunger and become less sensitive to satiation signals. Most of the research was conducted upon rats, by making lesions to specific parts of their hypothalamus which we assume play a role in our eating behaviour. It was found by Hetherington and Ranson that rats with lesions to the ventromedial hypothalamus would overeat until they became obese. However rats are not humans, therefore the finding cannot be generalised from one to the other.
Also, this study breaks various ethical boundaries, as the effects of the lesions were irreversible and would have resulted in the suffering, and eventual deaths of the rats. Fortunately this study did have real life practical applications, as Quaade successfully lesioned the Lateral Hypothalamus of obese patients to induce aphagia (and reduce their eating). Other neurological pathways also play a part in our eating behaviour, as found by Cummings, who investigated the changes in blood ghrelin levels over time between meals. Ghrelin is a hormone released from the stomach when it is empty, and is detected by the lateral hypothalamus. Cummings used six participants (very small sample size, low population validity) and monitored their ghrelin levels (using blood samples) every 5 minutes after they had eaten their lunch.
Participants were asked to assess their levels of hunger every 30 minutes, and it was shown that 5 out of the 6 participants used, showed that their ghrelin levels were closely correlated with degree of reported hunger. This was a lab study, with a high level of control, and easily replicable, so has high internal validity and reliability. However it is hard to determine whether the predicted levels of hunger stemmed from actual hunger, or social cues such as meal times and a person’s learnt expectancy of when they should next eat. However this study has real life practical applications, as gastric bands can be used to treat obesity, as they have been shown to reduce ghrelin secretion.