Human Obesity is not Caused Merely by a Weak Will Essay

Human Obesity is not Caused Merely by a Weak Will - Essay Example The UK government in its Foresight programme (2007) recorded a rapid rise in the number of overweight and obese people in Britain, and at an average estimate predicted that by 2050 more than 50% of the UK adult population would become overweight or obese (Foresight, 2007, 5). The recent spurt in global obesity has led to the derivation of a number of factors related to environmental determinants of this epidemic, amongst which eating habits driven by food marketing and reduction in physical activities due to technological advancement, are considered the two major causes (the ‘Big Two’). Despite the popularity amongst of these two factors, it is necessary that other causal factors of obesity are also identified, since an overall understanding of all probable factors are necessary, in order to control this global health hazard.   Discussion Mechanisms that control human appetite or regulates feeding pattern For appropriate regulation of body weight, there must be a good coordination between intake of food and energy output. The current global epidemic of overweight and obesity is owing to the fact that energy requirements of a human are very near to his/her BMI, thus, allowing it to be easily crossed, making it necessary to focus on appetite control. This function of controlling feeding or appetite is performed by hypothalamus, located between pituitary and thalamus in the brain (Legg and Booth, 1994). Neuron clusters are present within the hypothalamus and one such cluster (arcuate nucleus), forms to be the appetite centre. The arcuate nucleus controls the hormones and metabolites through the vagus nerve, while regulating metabolism through the coordination of adipose tissue, intestines, kidneys, and liver activities. Hypothalamus, which controls feeding while coordinating it with appropriate amount of energy expenditure by the body is, therefore, indirectly responsible for maintaining body weight, by balancing physical activities with the amount the food to be eaten (Logue, 2004). Appetite centre is comprised of primary neurons (that control hormonal and metabolite levels), and secondary neurons that after receiving information from the primary neurons, regulate body functions. The primary neurons have cells that can stimulate hunger via production of agouti-related peptide or AgRP and neuropeptide or NPY. It is also comprised of cells that can supress hunger by production of proopiomelanocortin or POMC. Therefore, either activation of AgRP or NPY or stopping the production of POMC can bring about a feeling of hunger (Smith, 1998). Various hormones play major roles in control feeding via the appetite centre. One such hormone is ghrelin, which activates NPY/AgRP and stimulates hunger. The arcuate nucleus also reacts to the hormones leptin and insulin, and here it is seen that insulin suppresses appetite by stopping AgRP or NPY producing neurons and by activating POMC producing neurons. Leptin levels respond to the levels of body fat, and observations reveal that there is an increase in circulating levels of leptin within obese individuals (Schwartz and Morton, 2002). Leptin may suppress appetite by activating inhibitory neurons; however, the arcuate nucleus may also become leptin-resistant. Individuals who are overweight or obese are often seen to possess high levels of leptin, but arcuate nucleus often fails to respond to such high levels. Aberration in the