Nutrition is a multifaceted field of study which plays an integral role in determining a person’s health. Arguably, it is nigh impossible to cover everything that falls under its umbrella. Therefore, it is perhaps only practical to focus on an individual topic, in this case obesity. In order to understand obesity we must first understand nutrition. Black’s Medical Dictionary (2005) states that nutrition is the absorption of food in order to produce energy. This food comes in the form of six nutrients, protein, fats, carbohydrates, fibres, vitamins and minerals, and water (Johnson, 2008).
What and how much we eat impacts heavily upon our bodies and lifestyles. Too little and we become malnourished and in extreme cases vulnerable to cardiac arrest and hypokalemia (Garner et al, 1985). Too much and we risk coronary heart disease and cancer (Webb, 2008). The causes of obesity are varied and controversial. They include genetics, psychological factors, lifestyle, lack of exercise and diet. Although genetic factors are certainly prevalent, obesity is, according to Caterson (2004), strongly linked to the over consumption of food and moreover certain types of food.
It is the academic controversy surrounding what nutrients in the diet cause obesity and the consequences thereof on the adult population of the United Kingdom (UK) that will be focused on here in more depth. Defining obesity is not straightforward. As Webb (2008) infers body fat is troublesome to measure accurately. It is for this reason, he claims, that the Body Mass Index (BMI) is the most accepted determiner of obesity. The BMI takes into account not only a person’s weight but also their height.
Williams (2001) states that obesity in the medical sense is a clinical term for excess fat accumulation commonly applied to persons who are at least 20% above a desired weight for their stature. The World Health Organisation (WHO) goes on to define the clinical obese as having a BMI of 30 kg/m2 and over (Webb, 2008). Williams (2001) points out that obesity is not simply a matter of being overweight but instead is far more specific and refers to the degree of body mass pertaining to an individual. It takes its name from the Latin root obdere, meaning to devour.
It is therefore by no means a new phenomenon peculiar only to the 21st century. It does however remains a contemporary condition with far reaching consequences for our health today. If defining obesity is somewhat difficult then determining which nutrients cause obesity and thus are detrimental to our health is equally problematic. Indeed, it is the cause of much heated debate within medical circles. Ostensibly, argument arises not from micronutrient intake (vitamins and minerals) but from our macronutrient intake.
Namely, the debate arises from whether it is carbohydrates or fats that are the main instigators of weight gain and obesity. Astrup et al (2008) fall into the latter school of thought believing a high fat diet to be the main determiner of the obese. They point to the ever increasing use of fast food chains with their ‘… industrially produced trans fatty acids… ‘ as a significant cause of obesity and its associated illnesses (Astrup et al, 2008, p. 48). Astrup et al (2008) state that type 2 diabetes and cardiovascular disease would be greatly reduced if low fat, carbohydrate dense diets replaced it.
Webb (2008) reiterates the latter and states furthermore that that those who exercise are able to tolerate a higher intake of fat than those whose exercise is restricted. From his viewpoint a low fat diet with a high intake of carbohydrates should be combined with exercise for optimum results. Thus we can ascertain from this school of thought that overeating and specifically overeating fats whilst living a sedentary lifestyle is a primary cause of obesity driven illnesses. However Taubes’ (2002) work offers a very contrasting opinion to the above.
In his volume Good Calories, Bad Calories (2002) he claims that obesity is not the consequence of high fat intake, overeating and sedentary behaviour but solely the responsibility of carbohydrates and moreover the insulin secreted from these carbohydrates. He argues that the more refined the carbohydrates, starches and sugars we eat the worse the effect on our health. Taubes (2002) points to sugar as being particularly harmful. For example, he states that, the combination of glucose and fructose raises the insulin levels and the liver becomes overloaded with carbohydrates.
This overload causes a rapid rise in blood glucose level. Insulin is then produced to counter this rise and it does so by storing the excess carbohydrate as fat in the adipose. Therefore, Taubes (2002) argues, the more insulin is stimulated (a direct result of carbohydrate consumption) the more body mass we will inevitably accumulate. This in turn, he argues, causes diabetes as well as coronary heart disease, Alzheimer’s and cancer. Nevertheless, the strength of the correlation between carbohydrates and weight gain is vehemently criticised by others in the medical sphere.
Certainly Bray (2008) is one such adversary. In his direct address of Taubes’ (2002) work he accuses him of vast oversimplification. Bray (2008) acknowledges that some diets can be too carbohydrate laden, especially with refined carbohydrate. However he argues that other body types undoubtedly suffer from obesity as an exact consequence of high fat diets. He believes there is no overwhelming evidence that carbohydrates are directly causing the diseases Taubes articulates. Indeed, Bray (2008) argues that fat is indisputably associated with diabetes and heart disease.
Bray (2009) also argues that insulin secretion has only a marginal effect on weight gain. He states that Taubes’ view is too ‘insulin centric’ (Bray, 2009, p. 99). Taubes (2002) argues that insulin is the principle cause of obesity. However Bray (2009) disputes this claim arguing that insulin when elevated has an unexceptional effect on weight. He also states that Taubes’ work fails to acknowledge the discovery of leptin. Leptin, as discovered by Zhang et al (Webb, 2008), is now known as the obese gene and is believed to work on satiety areas in the brain (Webb, 2009).
For example, it informs the brain when the stomach is full and regulates meal portions. Those deficient in this gene, Bray (2009) argues, are directly predisposed to becoming obese. Bray (2009) contends that such a discovery cannot be ignored. Nonetheless, Bray’s critique and emphasis on leptin have been dismissed by others. Webb (2008) states that only a small minority of people have been diagnosed as leptin deficient. Moreover, he argues that very few obese people have been found with low lepton levels.
This back and forth debating on the causes of obesity continues ad infinitum and is of course vital in the successful treatment of obesity through diet. Undoubtedly the treatment of obesity much like the causes once again ignites heated and varying responses. However, within the scope of this assignment it is perhaps enough to conclude that being obese undoubtedly has a calamitous impact upon our health. Undeniably, the catalogue of illnesses attributed to obesity are extensive and escalating (Williams, 2001).
Mann and Truswell (2000) believe these illnesses fall into four main categories, metabolic, cardiovascular, mechanical and social. They state that metabolic illnesses can include dyslipidaemia (a prolonged elevation of insulin) and metabolic syndrome which can in extreme cases lead to infertility in women. Cardiovascular illnesses, they claim, include hypertension and coronary heart disease and mechanical illnesses can comprise of spinal problems and osteoarthritis.
In addition are the psychological consequences on the health caused by society’s judgement of obesity. The Department of Health (2007) writes in some detail about this and argues that societal pressure regarding body shape can lead to living with a constant low self esteem and under society’s ongoing judgement. Both pressures can in turn, they argue, cause a detrimental psychological effect on the health of an individual. Arguably such illnesses affect not only the individual but the welfare system as a whole.
Indeed, the responsibility on the NHS to treat such a plethora of obesity driven illness is onerous and has been aptly demonstrated of late through such television documentaries as The Hospital (2009) ‘The burden of obesity on the NHS’ The Department of Health (2007) estimate that the cost to the NHS of obesity could be as much as 1 billion per annum. Indeed, a report by Wanless predicts that if this trend continues the cost to the economy by 2010 could be as much as i?? 3. 6 billion per year (Department of Health, 2007). It is therefore abundantly clear that obesity is and should be an area of fundamental concern.
Although much of the latter provides only a mere snapshot into the causes and consequences arising from obesity it does highlight the breadth of the problem. Obesity concerns not only a person’s health but places a tremendous economic strain on the NHS, the government and ultimately the tax payer. Therefore despite diverging opinions regarding the causes of obesity it is clearly essential to persevere in the research of why we become overweight. For only in doing so can we hope to alleviate the burden of obesity on the individual and on society as a whole.