Synthesis Of Obesity

Genetic research of obesity was partly successful in establishing obesity in model organisms – rodents where obesity occurs spontaneously together with other pathological aspects (insulin resistance, …). The main cause of monogenic obesity in these model organisms are common mutations always present in only one gene. Results of research on model organisms allowed us to understand biological mechanisms of calorie intake and regulation and maintenance of body weight. The most important insight into obesity was achieved in 1994 after discovery of ob gene encoding for leptin. In two years period, using screening method, candidate homologous genes, selected on genetic study basis on mice, another five genes were identified. Mutations on these genes were found to be the cause of autosomal recessive or dominant monogenic obesity. Products of these genes are leptin and its receptor, proopiomelanocortin (POMC) melanocortin receptor 4 (MC4R) and

The previously mentioned peak and the positions where obesity has greatly amassed revealed a genetic trait that tends towards obesity. In the 1960’s, people developed the “thrifty gene” hypothesis, saying that genes leading to obesity could be inherited. The hypothesis was supported by the knowledge that digestive metabolisms have been naturally selected to favor obese traits.

Genes control almost every aspect of human life, and when it comes to weight there is no exception. Little is known, however, how much of an individual’s genes actually control the weight of certain individuals. Body fat can vary from person to person, yet some people have always carried more weight than others. Often times, when one person is overweight in the family, most of the other individuals in the same family are overweight as well. However, more than just genetics can go into being overweight, and a person’s genes are not the end all be all of obesity. Many times the environment surrounding people who are obese contributes to the overall weight of the individual, and when obesity promoting genes are mixed

Obesity is a condition where an individual’s weight is disproportionate to their height. There are many factors

Environment factors, including sedentary lifestyles, high energy intake and social aspects enhance the risk for obesity. A recently published evaluation of the Framingham Study provides an interesting alternative explanation for the worldwide increase in the prevalence of obesity, by demonstrating that the chance of a person to become obese is significantly higher when a friend, sibling or spouse are obese (Christakis and Fowler, 2007). Thus the social net work could be a relevant factor in the obesity epidemic.

Although the mechanism of obesity development is not fully understood, it is confirmed that obesity occurs when energy intake exceeds energy expenditure. There are multiple etiologies for this imbalance, hence, and the rising prevalence of obesity cannot be addressed by a single etiology (Dehghan et al., 2005, p.

Obesity is a highly prevalent condition in America, affecting approximately one third of the adult American population. Obesity can be caused by a myriad of factors: genetics,

genetic variations effect obesity will make it much easier to prevent and treat the condition of

Although many individuals are uncertain about the increasing statistics associated with obesity, more than seventy percent of men and virtually sixty-two percent of women within the United States adult population are overweight or obese (Wilmore, Costill, & Kenney). Obesity refers to the condition of having an excessive amount of body fat. If an individual’s amount of body fat becomes too excessive, he/she is at a much greater risk of developing life-altering diseases such as heart failure, hypertension, type II diabetes, cancer, gallbladder disease, osteoarthritis, etc. (Wilmore, et al., 2008).

In recent discussion of obesity, a controversial issue has been whether there should be involvement of society and the government. On one hand, some argue that obese people harm everyone, therefore, everyone should be involved. One the other hand, people argue that obese people should decide whether or not they want to be healthy.In sum, then, the issue is whether society and the government should do something about obesity. My own view is that while I do think that the government and society should encourage healthy living, however, there should be less pressure from society.

Over the past twenty five years, obesity ratio has been rising dramatically. And it is continued to become a problem in the United States. Obesity is a serious problem which should be concerned and solved by our society. The negative effects it has on individual are much larger than we think. Gaining extra weight, heart disease, and serious problems can change our human life forever. Furthermore, obesity also affects the society by costing tax payers and the government money to treat these issues. There are currently many ways of how to fight and stop the problem while it is increasing. One of the ways to help us combat with the obesity is to look at the causes such as: lack of energy balance, physical activity, and heredity.

Obesity is a disorder of the Endocrine System. Obesity means having too much body fat, it occurs over time when more calories are eaten than being use. The balance between calories-in and calories-out differs for each person. Factors that might affect weight consist of your genetic makeup, overeating, eating high-fat foods, and not being physically active. Furthermore, several endocrine abnormalities are reported in obesity. Some of these abnormalities are considered as contributory factors for the development of obesity, whereas others are considered to be secondary effects of obesity and usually are restored after weight loss. Thyroid hormones usually are normal in obesity, with the exception of T3 which is elevated. Prolactin is normal but prolactin response to different stimuli is dulled. GH is low and GH response to stimuli is dulled. IGF-I levels are normal or elevated. Cortisol, ACTH, and urine free cortisol levels are usually normal; however, a hyperresponsiveness of the HPA axis with increased cortisol and ACTH response to stimulatory tests is observed in extremely obese individuals.

The topic that I have chosen to look at is obesity. The aim of this topic is to find out whether “the ignorance of genetics as a contra factor of obesity”. I have chosen to look at this topic because obesity is concerns me. Obesity has always been a bid debate for a long time now and I was intrigued to find out more about the topic and the cause of obesity. The fact that obesity has made deadlines news in recent years. There are a lot of misconceptions about obesity such as overweight is caused by a sow metabolism. There have been a lot of beliefs and myths about obesity in society today and he above myths is on of them. According to Donnellan (1998) ‘ ‘people who are overweight have told their doctors that they eat no more and

Everybody knows the child that can eat any type of food all day and never seem to gain weight. This occurrence has led researchers to investigate the role that genetics plays in childhood obesity. Not all children who are inactive or who eat poorly are obese, much in the same way that some obese children eat fairly healthy, and exercise moderately. Heredity has recently been shown to influence body fat percentage, regional fat storage, and the body?s response to overeating (Rush, 1). Children who have obese parents are 80% more likely to be obese than their lean parented counterparts (Buffington, 16). This familial correlation is contributed to genetics as well as the parents eating habits. Children with obese parents typically aren?t taught the correct way to choose when and what food to eat, leading to poor eating habits and eventually obesity. Many genetic defects can have a significant effect on obesity such as variable thyroid activity and pituitary defects. Abnormalities in any one of these regulators could be responsible for appetite abnormalities and weight gain. Furthermore, obesity leads to defects in appetite regulation, hormone production, and metabolic events (Oklahoma Cooperative, 4) that are responsible for further weight gain,

Obesity is one of the most genetically predisposed traits (Walley, A et al 2006). Genetic studies have shown that heritability estimates for obesity are high (typically >70%), which parallels with other polygenic diseases like