Outline and evaluate biological explanations of obesity Essay

Various definitions toilette be provided for the reasons of obesity, from biological explanations, to neurological and evolutionary theories. Even socio-economic reasons could give insight into wherefore some plurality fix a amplyer likeliness of obesity Evolutionarily, the provident broker hypothesis provides insight as to why many suffer from obesity, as it suggests that our current genes ar no nightlong suited to our new environment. Modern daytime society is filled with solid foods of a high calorific content, and our energy expenditure has change magnitude more than(prenominal) and more with the technological advancements make. more than television is watched and more computer games atomic number 18 played. This has been attri stilled to the increase in obesity, especially in children. Dietz and Gortmaker demonstrate that an extra hours viewing of TV a day can increase obesity take aims by 2%. Further support for the sparing gene hypothesis has been form for slighton in the case of Pima Indians and other groups of diverse societies who live in harsher conditions (in comparison to western sandwich society) and are more likely to set up obesity when exposed to a westbound diet.The thrift gene hypothesis is reductionist however, as the gene pool has remained coherent oer the last 40 social classs, in so far yet 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 prelude would be transmittable reasons, which could provide an explanation for obesity, as some individuals may be genetically inclined with a family count on statement of having a pre tilt for weigh gain, divideicularly in todays domain of a function which contains ample supplies of food. Our ancestors tended to eat as frequently as they could when possible, in order to bring in a reserve of energy which they could confide on, and to allow the m 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 futile to stop, because we are innately programmed to consume for survival. more twin studies necessitate been made, which all register that genetic factors play a stupendous part, and suggest that obesity often runs in families.Bouchard overfed 12 pairs of male MZ tally and open three times more similarity of cargo gain inside pairs than between pairs, strongly indicating genetic factors. all the same this was a relatively piddling test surface, so in order for us to make a strong conclusion, the regard should be replicated on a big scale. However this would be ethically improper, as weight gain is associated with many physiologic and sometimes psychological ailments, such as diabetes or depression then it would be unethical to expose a macroscopica l 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 doesnt account for individual differences, such as an hyperactive thyroid, which would cause weight gain. A UK take apart carried out explore upon 4 year old twins, and found obesity heritability was 0.61in boys and 0.61 in girls, which further supports the base that genes play a significant division in our weight gain.However this case was not do cross-culturally, therefore lacks population validity and cannot be utter to everyone. Also, the withdraw relied on self-reports made by the mother of the children, who may have been dishonest as a leave of social desirability bias, This study presents the idea of passive gene-environment correlation, which provides biologic al and behavioural explanations (that our genetic factors interact with our environment). Both approaches are settled however. The biological approach represents hard determinism, and has abruptly no room for free will, and there is evidence to support it. Frayling analysed 39,000 white pots blood line sample from the UK and Finland. musical composition the extremely large sample size increases the inbred 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 telling (BMI over30), and he found that variations to the FTO gene were more joint 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 utilise 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. modern research suggests that body fat magnate be an active organ and may trigger hunger itself. This would mean that at one timeindividuals start gaining excess weight, they then regain more hunger and become less sensitive to satiation signals. Most of the research was conducted upon rats, by making lesions to specific move 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 li fe practical(a) applications, as Quaade successfully lesioned the Lateral Hypothalamus of obese patients to induce aphagia (and avoid 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 endocrine released from the stomach when it is empty, and is detected by the askant hypothalamus. Cummings used six participants (very small sample size, low population validity) and monitored their ghrelin levels (using blood samples) every 5 minutes aft(prenominal) 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 larn whether the predicted levels of hunger stemmed from actual hunger, or social cues such as meal times and a persons 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.