Prevalence of Obesity - Essay Example

Running Head: EVOLUTIONARY PERSPECTIVE; ADAPTIVE VIEWPOINT Evolutionary Perspective; Adaptive Viewpoint Name: Institution: Introduction Obesity is a chronic disorder that is growing rapidly worldwide raising a concern on health and yet its causes is not fully understood. Obesity epidemic has hugely been manifested in industrialized societies but currently, the epidemic has spread and is still spreading widely worldwide. This is mainly attributed by the interaction between human culture and human biology over the long period of human beings evolution. Through studies, the etiology of the obesity epidemic is greatly influenced by our own understanding of the evolutionary roots of metabolic control (Lev-Ran, 2001). The high prevalence of this chronic disorder in our societies has two major contributing factors, i.e. genetic predisposition originating in human evolutionary history and secondly, environmental change that has occurred in historical times. Obesity has affected not only the aged but also the underage although the most affected lot is the aged bracket where the disorder predisposes them to many other chronic diseases such as heart attack. In his publication of 1998, Lean states that; “nearly, all obese individuals begins manifesting signs and symptoms of chronic diseases mainly at the age of 40’s (forty’s) and in such situations, many of them will need medical intervention for obesity-related diseases before they are 60 years of age. It is worth noting that obesity in our modern society represents the most crucial threat to the cardiovascular health of mainly the technologically advanced and advancing nations in the twenty first century and like many other risk factors for disease, obesity mainly results from human behavior and manifests a social gradient (Prentice, 2006). Evolutionary Perspective; Adaptive Viewpoint Based on evolutionary viewpoint, we derive three varied explanations explaining how evolution has resulted to obesity that is a modern chronic disorder affecting millions of people across the world more so in the developed/industrialized countries (Karelis, 2008). The first explanation is that obesity was at one time adaptive and thus enabled human beings to survive or rather sustain fecundity through times of famine. The second explanation states that obesity is not adaptive, i.e. it is maladaptive in nature and may never have existed at any time in our evolutionary past but as a result of some selective positive traits; an example suggesting that obesity results from variations in brown adipose tissue thermogenesis. Thirdly, the final explanation states that most mutation of the genes that predisposes human beings to obesity are neutral and have, with time been drifting over the period of evolution i.e. what is referred to as drifty genes thus making some people to be prone to obesity and others resistant to obesity (Neel, 1999). This research paper mainly focuses on the adaptive perspective as a factor contributing to the obesity more so in the modern world where the cases have been on rise. In 1962, James Neel, who was a geneticist by then introduced the first ever major evolution based explanation for the modern obesity chronic based disorder. His evolution explanation focused on giving an explanation on the unusually high prevalence of diabetes in some human beings but was letter revised putting into consideration obesity and many other components of metabolic syndrome. In his argument, Neel states that the tendency to become obese is an adaptive characteristic that for sure, has become incompatible with modern lifestyles. His evolution based explanation referred to as Thrift Gene Hypothesis (TGH) is based on the assumption that in the period of evolution, human beings were regularly subjected to periods of famine and feast. During the periods of famine, people who had more fat for energy store were more probably to survive and consequently produce more offspring unlike those who had low fat deposit as energy storage. In this case, evolution acted to select for genes that made those who possess high effective fat storage during periods of plenty. In the industrialized and modernized societies, which are characterized with frequent feasts and rare famines, this evolution adaptation becomes maladaptive. This therefore presents a mismatch between the environment in which human beings evolve and the living environment (Lean, 1998). The so called thrifty genes in some people enabled effective storage of fats which produced energy during the harsh periods mainly characterized with famines, this offered a bit of advantage to them. In the modern word, and more so in the industrialized countries where technology has taken center stage, the people who have inherited these genes deposit fat in preparation for a famine that never come to be witnessed and the end result is widespread obesity. This method has received lot of criticism from different scholars who argue that the problem with this approach is to understand the reason; if obesity was historical so advantageous, many individuals never inherited these thrifty genes and yet in the modernized societies, these individuals are able to remain slim despite the change in the environment which favor storage of fat in their bodies (Lev-Ran, 2001). The thrift gene hypothesis presents a simpler and well-designed explanation for obesity as a chronic modern epidemic and was with no hesitation embraced by scientists. In fact, this hypothesis has so far received support from a number of evidences. However, the hypothesis comes with a number of implications; importantly, the identifiable genetic polymorphisms that explains “thrifty” phenotype need to exist. Scientifically, obesity has been identified to possess a strong genetic component and many genetic polymorphism have been identified that predispose people to obesity and therefore submitting potential components of the thrifty genotype. In addition, SNPs (Single Nucleotide Polymorphisms) which are linked with increased risk of obesity have so far been recognized via GWA (Genome Wide Association) research although each has considerable little effect (Neel, 1999). However, this perspective has received criticism from different quarters. One criticism is that the hypothesis is not able to give a precise explanation of the heterogeneity of obesity within and between the populations. This raises a question; if the cycles of the famine and the feast was a crucial driving factor all through all of human beings evolution, why is it that not all human beings are obese? It is worth noting that scientifically, human beings manifest great variations in their susceptibility to obesity. In addition, looking at even the population living within the same environment, there are many people who mainly seem to be resistant to being overweight. More so, we see that famine is being used as a selective pressure all through human evolution and therefore, there is a high possibility that there has been no enough time for the thrifty genes to reach fixation. For instance, in the case of hunters and gatherers; they mainly never experience famine purposely because their nature of flexibility and mobility permits them to move or utilize other alternative sources of food mainly when they encounter environmental hardship (Barsh, Farooqi and O’Rahilly, 2000). In contrary, agriculturalists venture into considerably few stable crops and have less flexibility to counter draughts and other related calamities. This therefore connotes that the famine/feast cycle may have opted for thrifty genes solely in societies engaged in agriculture and therefore, this could clearly explain the reason as to why not all human beings become overweight and the reason as to why there are differences between populations. In this case, some populations could have probably encountered regular famines and/or periods of scarcity in food all through their life history and therefore having more pressure to advance a thrifty genotype. TGH presents many testable predictions and in this case, if we assume the post agricultural model, the genetic loci linked with obesity should manifest trait signs of a recent positive selection. However, in a recent study testing thirteen obesity linked genetic variants, gave little evidence for recent positive selection. The research established only a single risk loci mutation in the obesity linked FTO gene, manifesting evidence for recent positive selection. This therefore appears to be primarily as an evidence against the TGH. However, the study relied on SNP (Single Nucleotide Polymorphism) data and therefore, these loci may solely be associative rather than functional. Therefore, the refinement of risk of obesity should give a more informative tests for selection purposes (Caballero, 2007). Secondly, another prediction of post-agricultural TGH states that populations that have in history experienced more food scarcity and famine should be more prone to obesity the moment such a population is exposed to an obesogenic environment. However, there are varied evidences for this prediction so far. For instance, some hunter-gatherer populations, mainly those whom famine could have historically uncommon, appear to manifest some resistance to obesity that is induced by diet as compared to a agriculture population historically, which is steady with the TGH’s predictions. However, this model further offers a prediction that colder climates agricultural societies would particularly experience a firm selective pressures based on genetic thriftiness and therefore mainly prone to overweight. Europe is a good example, where they practice agriculture and their historical records on famine and war is so extensive and yet they exhibit a lower rate of obesity compared to many other populations. In contrary, Pacific Islanders exhibits a high rate of obesity and yet they live in tropical climate characterized with very little history of famine (Lev-Ran, 2001). Some studies have explained these discrepancies arguing that other than the recent selection for the thrifty genes, it is indeed genes conferring resistance to becoming overweight as well as other metabolic disorders that comprise a modern adaptation. This altered TGH postulates that thriftiness adaptations are ancient though populations that have opted for richer food sources following the introduction of agriculture have obtained some adaptations to avert metabolic disorders. Studies posit that European having adapted to their own diet, introduction of these diets to other populations that are mainly not used to it for instance the Pacific Islanders and Native Americans brings about mismatch between the diet that they have evolved with and the modern diet and thus resulting to metabolic dysfunction. This therefore gives a clear and precise explanation; the reason of the dramatic increase in obesity cases to these populations. In addition, studies further recommends that loss of thriftiness is a recent adaptation resulting to variations in the occurrence and prevalence of metabolic related diseases between populations. Other than looking for disease risk genes conferring susceptibility to metabolic related diseases, we should put our focus on establishing genetic variants which confer resistance to these disorders. A research by Southam et al. identified evidences of recent positive selection on one allele which is defensive against obesity and therefore, many researches in search of signs of recent positive selection on obesity resisting allele could probably be successful to put this hypothesis into test (Cannon and Nedergaard, 2009). Conclusion As earlier stated, obesity is a chronic disorder and a public health crisis and causing an enormous burden of mortality and morbidity resulting in huge social, economic and human costs. Owing to this, control measures are of great important in our societies; ensuring that we maintain a healthy population, society and the world in general. The background of evolution perspective of the obesity is a bit complex because in the three advanced models, none has been able to give a definite result. For instance, the adaptive perspective; despite the wide range of information that has been advanced providing arguments and counterarguments, there is no consensus so far on this model as explaining evolutionary context of the obesity epidemic on adaptive perspective. From the research, the balance of the evidence so far presented by various researchers based on the three evolutionary perspective, the evidence for and against the above three different scenarios posits that the thrifty gene idea/hypothesis is really untenable though the other two hypothesis may finally present a convincing and persuasive explanation of the phenomenon of modern obesity currently witnessed and affecting millions of people across the world (Caballero, 2007). For instance, the modern genetic technique permits a direct estimation of whether or not a certain gene have been under recent strong selection via exploration of the association disequilibrium patterns mainly adjacent to target polymorphism. If the genotypes that have been identified to be under recent selection, this is probably going to disprove the drift hypothesis and thus presenting a strong support for the thrifty gene hypothesis idea. Equally, if the aforementioned genes have not been under strong selection, this would probably be incompatible with the thrifty gene idea References Prentice AM (2006): The emerging epidemic of obesity in developing countries. Int J Epidemiol; 35(1):93–99. Karelis AD. (2008): Metabolically healthy but obese individuals.Lancet372:1281–83 Lev-Ran A. (2001): Human obesity: an evolutionary approach to understanding our bulging waistline. Obesity Metab. Res. Rev.17:347–62 Neel JV (1999): The “thrifty genotype” in 1998. Nutria Rev; 57(5 Pt 2):S2–S9. Neel JV (1992): Diabetes Mellitus: A “Thrifty” Genotype Rendered Detrimental by “Progress”? Am J Hum Genet; 14:353–362. Lean, M. E. (1998). "Obesity-what are the current treatment options? “Exp Clin Endocrinol Diabetes106 Suppl 2: 22-6. Barsh GS, Farooqi IS, O’Rahilly S. (2000): Genetics of body-weight regulation. Nature404:644–51 Cannon B, Nedergaard J (2009): Thermogenesis challenges the adipostat hypothesis for body-weight control. Proc. Nutria. Soc.68:401–7 Caballero B (2007): The Global Epidemic of Obesity: An Overview. Epidemiol Rev; 29:1–5. Read More