What Causes Obesity Is The Relationship Of Energy Intake And Expenditure And Its Effect On Energy Balance Essay

Candidate genes allow researchers to come up with rational hypothesis of role of these genes and their contribution to different conditions, in this case obesity. Therefore, they are potential predisposition factors. Candidate genes are chosen on a basis of knowledge of their function, biochemistry and their expression pattern (what protein they encode for and where is this protein mainly expressed) in obesity. At present, there are about 300 genes that have been hypothesized to contribute (to some extent) to obesity development.

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

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

• Genetic factors; Obesity tend to be lowered, so that the genetic cause of the alleged to have. But family members not only share genes, but also food and lifestyle habits, which could push the onset of obesity. It is often difficult to separate the lifestyle factors with genetic factors. The latest research shows that the average genetic factors giving influence of 33% against a person’s body weight.

Many people struggling with morbid obesity have been fighting their weight since they were kids. Many people assume that obesity in children is the result of parents not knowing taking control of their child’s eating habits, but this is seldom the sole cause. Many research studies have shown that children typically will grow up to have a similar BMI to their parents, and siblings will have similar BMI’s to one another. Researchers use this data to show that there is a heavy genetic influence on a person’s weight and simply eating too much or not exercising enough is not the sole determinant of someone’s BMI.

There were several family members with the diagnosis of obesity. However, it seems that initially it may have been environmental factors which influenced susceptibility for obesity and later generations. This revelation was discovered by tracing the genes of JT Sr’s parents and MM’s parents. There was no genetic link to obesity until JT Sr. and MM. Research was extended to the grandparents of JT Sr. and MM with no trace of obesity.

Obesity has become an epidemic health problem. It is not only about genetics but also the environmental factors involved in obesity. According to Kaushik Prashant and James T. Anderson Epigenetic it is the study of heritable but the dynamic changes to genomic function that regulate gene expression independently of DNA sequence. The study have shown that the maternal nutrition is controlled during pregnancy that can alter the metabolic phenotype of the offspring by means of epigenetic regulation of specific genes, and this can be passed to the next generation. Obesity is associated with extensive gene expression changes throughout the body. It is a simple disease with multiple risk factors.

Factors associated to obesity include an interplay between genetic, behavioral, and envi-ronmental factors (Rogers, 2010). In fact, the combination of genetic and environmental factors increases the

Obesity is disease that involving environmental, genetic, physiologic, metabolic, and psychological components. Obesity is cause of many diseases and psychological problems. There are many causes of obesity overeating, lack of physical activity, the environment. Obesity tends to run in families, implying genetic factors. The search for an obesity gene is complicated because families also tend to share eating habits and lifestyle habits. Eating fast food such as, French fries, pizza, cheeseburgers and drinking Coca-Cola are the top metabolism in American society. By consuming such foods and drinks regularly, people are slowing their metabolism but I have a brother who always drinks soft drink everyday and still he is skinny, while other people

Many studies have been carried out to determine the genetic base of obesity. As result, mono and polygenic obesity have been revealed by scientists with the polygenic form stated as the most common. More than 100 and 200 genes respectively in human and mice have been identified to be related with obesity. As example, a defect in the gene coding for leptin, a hormone involved in regulation of appetite, abnormalities enzyme prohormone convertase that convert the hormone proopiomelanocortin (POMC) into neuropeptides, can deregulate energy metabolism. Genome wide scans in different ethnic populations have identified major obesity loci on chromosomes 2, 5, 10, 11 and 20 [9]. Recent genetic studies have identified several different causative mutations

Obesity is a serious medical condition that requires treatment to lower the risk of metabolic and cardiovascular disorders. However, one in three people in the United States is clinically obese (Overweight and Obesity Statistics) and 10-25% of obese individuals are labeled metabolically healthy (Bluher). Obesity is clinically diagnosed with a body mass index (BMI) of a score of 30 or greater in reference to the total weight in people’s body compared to their height (Overweight and Obesity Statistics). Although obesity is shown to increase mortality rate with associated metabolic and cardiovascular disorders, a recently classified observable trait of an individual, or phenotype, developed to separate the metabolically healthy from the unhealthy: Metabolically Healthy Obesity or MHO (Bluher). Whereas metabolism is the biological functions that maintain the living state of cells, metabolic health in reference to MHO is classified as being clinically obese while maintaining a waist size of a maximum 40 or 35 inches for a man and woman respectively, normal blood pressure, cholesterol and blood sugar compared to healthy individuals of their age groups, normal sensitivity to insulin and moderate physical fitness (Skerrett).

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

According to Skelton, Irby, Grzywacz, and Miller (2012), mutation in the gene that controls leptin production causes leptin deficiency, which in turn inhibits the ability of the brain to regulate body weight. This abnormality in leptin pathways is linked with around 3-4% of severe cases of childhood obesity (Skelton, Irby, Grzywacz, & Miller, 2012). Mutations in proopiomelanocortin (POMC) gene are also associated with early-onset of obesity. POMC neurons produce melanocortins and β-endorphin, hormones that are also known to regulate feeding behavior. Therefore, deficiency of these hormones due to mutations in POMC also contributes to early onset of obesity (Skelton, Irby, Grzywacz, & Miller, 2012). Other genes that are known to play a part in regulating feeding behavior in humans are MC3R and MC4R. Just like in the cases described earlier, abnormalities in MC3R and MC4R contributes to obesity in children (Skelton, Irby, Grzywacz, & Miller, 2012). Despite this, mutations in genes only account for a small proportion of cases of childhood obesity. In particular, abnormalities in genes associated with body weight regulation accounts for only 5% of childhood obesity (Flemming, 2011).