Childhood Obesity and Genetics, Research Proposal Example

Introduction

Obesity is becoming one of the most common problems in children from industrialized and developed countries and has been growing at an increasing rate. In fact, the prevalence for obesity is at 14-20% with over 22 million children under the age of five being overweight (Sidik and Ahmad, 2004). In the United States, 25% of children are overweight with 11% of those considered obese. In addition, about 70% of obese children stay as obese adults. Furthermore, obesity in childhood has been associated with an increased mortality rate in adults. (Zhao and Grant, 2011) Childhood obesity, per the Center for Disease Control (CDC), is referred to as a child being “overweight” or “at risk for becoming overweight”. The method that is used to evaluate if a child is obese is though using the body mass index or BMI. The BMI is measured through the body weight divided by the height. If a child has a BMI greater that the 95^th percentile, they are considered overweight and if they have a BMI greater than the 85^th percentile, they are at risk of becoming overweight. (Burrage and McCandless, 2007) The problem with obesity is that is can lead to significant health problems such as, diabetes, cardiovascular, respiratory, gastrointestinal, endocrine, mortality, and psychosocial problems. (Sidik and Ahmad, 2004) There are several factors that can influence childhood obesity. One of the factors is genetics. In this research project, the genetic factors that influence childhood obesity were examined.

One of the factors that are influencing obesity in children is genetics. For instance, there are several genetic disorders such as, Prader-Willi syndrome, Bardet-Beidi syndrome, chromosomal defects, and genetic mutations that have been linked to childhood obesity. In addition, studies have shown the genetic influence through racial groups and twins. For instance, only 5% or less of Caucasian children are obese; whereas in Asian populations, there is prevalence up to 50% or more. Also, identical twin studies have shown fat mass and BMI ranges to be similar in identical twins. (Zhao and Grant, 2011) The early detection of a genetic syndrome in children can be identified through genetic evaluation due to phenotypic abnormalities, birth defects or neurological deficits; however, for children that do not exhibit these types of characteristics it is harder to detect and prevent onset of obesity. There has been recent research studies performed that has linked a single gene mutation to the early onset of obesity in children that are not associated with any type of physical or mental abnormality. The gene, leptin, the leptin-receptor and melanocortin-4 receptor have shown to be linked to obesity.

Leptin is an adipocyte-specific hormone that maintains adipose-tissue mass through effects on the hypothalamus in the brain. It acts on the hypothalamus through the leptin receptor. It has been tested in rodents and has the homozygous mutations in genes that produce both leptin and the leptin receptor has shown the early onset of obesity. The rodents also exhibited signs of hypercortisolaemia, which affects glucose levels or sugar levels, as well as increased infertility. (Clement et al., 1998)

Other research has further supported leptin as a key player in the control of human body weight through the study of leptin alleles, which are different forms of a gene. A study conducted by Stratigopoulos et al. (2008), illustrated both mice and humans having an effect in fat increases with the addition of the LEP or leptin gene. It has also shown the there are several proteins, such as insulin, ghrelin and peptide YY that are associated with the signaling pathway of leptin and are connected to weight increase. Through the different research studies conducted on Leptin, it is indicated that it places a central role in weight control; however, the extent or the degree which the gene has control over body weight is still being examined. In addition, the effect of this gene on childhood obesity is still unknown as well.

Due to the restrictions in testing these genetic factors on childhood obesity, the link between environmental factors, genetics and childhood obesity was further examined. It has been indicated that the environmental factors, such as diet and exercise influence, in combination with these genetic anomalies, can influence obesity in children. (Sidik and Ahmad, 2004) In order to determine the correlation between factors, studies have looked into the genetic component through epidemiology studies. In addition, parental obesity has been referred to as the predictor for childhood obesity. Studies have reviewed the family risk ration for adolescent obesity when the parents are obese. In addition, birth weight in children has been linked to genetic heritability in addition to the parental environmental effects. It has been found that 5% of the childhood obesity has an impaired genetic function; however, it has also been indicated that different forms of childhood obesity comes in the form of behaviors that are learned from their environment. (i.e. Parental lifestyle and eating habits). In a study by Bouchard (2009), it showed that genes coding for obesity and at risk alleles for obesity were very common in populations. The study also indicated that people at risk for these genes can deter the obesity from occurring through behavior. Therefore, the study is basically stating that if an individual is pre-disposed to these obesity genes or at risk alleles, they can eliminate their chances of becoming obese through their behavior. This study further suggests that it is the parental involvement and behavior that is taught to the children in order to decrease their risk of becoming obese; obese parents are more likely to have obese offspring than normal weight parents.

It is important to understand both the genetic factors and environmental factors associated with obesity in children. For children who do not exhibit any genetic syndrome characteristic, it might be hard to diagnosis or find a problem associated with their obesity or “at risk” obesity problems. It is therefore important to find a method in which children who are at risk for being obese have the proper treatment in order to prevent obesity. There are numerous children worldwide who are at risk for obesity or area already obese. This also leads to the risk for these children developing more serious health issues, such as diabetes, heart disease, asthma, psychological problems and emotional problems. For instance, obese children may have a harder time in school due to being teased and exclude from physical activities. This can further lead to self-esteem issues, which can affect school work and home life. The focus, therefore, should be on investigating the influence of genetic underlying issues, as well as the environmental factors, that result in an increased risk for obesity in children. Determining any genetic abnormalities can result in a treatment plan for children and prevent them from becoming obese during childhood, adolescence and adulthood.

Previous research studies have shown the link between genetics and environmental influences on childhood obesity. Previous research has found that serum-leptin levels are positively correlated with obesity in humans. (Considine et al., 1996) The link between this gene and its relation to childhood obesity or early onset of obesity has also shown direct correlation. Leptin has been found to exert both behavioral and neuroendocrine effects at the site of the hypothalamic leptin receptors. It was found that leptin levels were proportionate to the amount of fat cells or mass in humans; obese humans having higher levels than thin humans. (Hafeezullah, 2006) A study following the leptin levels in humans found that most of the severely obese individuals had a mutation in the leptin receptor. (Burrage and McCandless, 2007) The testing of the leptin receptors and hormones that are associated with the receptor, therefore, has been underway. What has been recently found is that the hormone, Proopiomelanocortin (POMC) that is produced in the hypothalamus plays an important role in feeding and that it expresses for the leptin receptor and is regulated by leptin. It has also been found that patients with early-onset of obesity have a genetic mutation in genes that process POMC. (Zhao and Grant, 2011) For instance, there have been studies correlating a mutation in the melanocortin-4 receptor (MC4R) with obesity. 6% of the obese patients had this mutation. (Burrage and McCandless).

Geneticst at the Children’s Hospital in Philadelphia has conducted the largest childhood genome study and has identified genes common in childhood obesity. Researchers found at least two genes that increase the risk. The Center for Applied Genomics at the Children’s Hospital of Philadelphia was able to collect DNA from children who were obese and study the DNA characteristics. They looked at 5,540 cases of children who were obese with 8,300 control participants. All of the children were from European heritage. The researchers were able to pinpoint two loci on the OLMF4 gene on the chromosome 13 and another on the HOXB5 gene on chromosome 17. These genes were different than the leptin genes that were previously being research and have opened doors for scientist to study the onset and risk for obesity in children and adolescents. (Azsenci, 2012)

Conclusion

Childhood obesity is becoming a major concern worldwide. Not only does this affect the health of the child, it leads to obesity as adolescent and adult and further leads to more complications in regard to health as adult. These individuals become at risk for heart disease, diabetes, and other health issues. It is important to find out both the environmental and genetic factors that are involved in detecting the onset or risks for children with obesity. Research has identified leptin gene, allele and receptor levels to be a factor in the control of human body weight. Both rodent and human DNA analysis has confirmed this as a factor; however, the extent that these genes, alleles and receptors play in the actual cause of weight gain is still unknown. In addition, research has further supported this notion through statistically linking serum-leptin levels with obesity in humans. However, in regard to childhood obesity and serum-levels, this has not been conducted. Furthermore, other factors, such as the hormone propiomelanocortin (POMC) have been linked to obesity in children. The expression of the POMC has been correlated with the leptin and the leptin receptor. In fact, obese patients have been found to have a mutation in the gene that codes for POMC.

There have been several studies that have focused on the leptin genes, alleles and receptors; however, these studies have not focused on the real issue at hand: Childhood obesity. What can our society do to decrease childhood obesity? What research is being conducted in order decrease the risk for children who are already at risk for obesity? The Children’s Hospital of Philadelphia has made great distances with their genetic profiling of obesity in children. The researchers at this hospital have identified two genes that have not ever been correlated with obesity and have obtained this information from obese children. Finding this information has opened doors for genetic researchers to find a cause and suggest preventative measurements in order to help children who are either obese or at risk. In addition, it is up to the parents to take action and transform the behaviors that they children are learning. It has been found that many people in the population carry these genes and are at risk for becoming obese; however, it inherently comes down to the type of environment and the behavioral lifestyle that is being employed on children.

Overall, the factors that are affecting obesity in children are both environmental and genetics. The first step in helping obese children or at risk obese children is changing their eating and activity lifestyle habits. Children can significantly decrease their risk levels by properly being taught how to eat properly and how to exercise. Finding out if an individual is genetically at risk, just increases the urgency for parents to change their children’s lifestyles.

References

Azcensi, J. (2012). Genes Identified for Common Childhood Obesity. Children’s Hospital of Philadelphia. http://www.eurekalert.org/pub_releases/2012-04/chop-gif040312.php

Bourchard C. (2009). Childhood obesity: are genetics differences involved? Am J Clin Nutr.89(5): 149S-1501S.

Burrage, L.C. and McCandless, S.E. (2006). Genetics of Childhood Obesity. U.S. Pediatrics Review: 60-63.

Clement, K., et al. A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Nature. 392(6674):398-401.

Hafeezullah, M.A. (2006). Review Article: Leptin: Fights Against Obesity. Pak J Physiology. 2(1): 7V. Considine, M. K. Sinha, M. L. Heiman et al. (1996).

Serum immunoreactive-leptin concentrations in normal-weight and obese humans, The New England Journal of Medicine, 334( 5):292–295.

Stratigopoulos, G., et al. 2008. Functional Consequences of the Human Leptin Receptor (LEPR) Q223R Transversion. Obesity. 17(1):126-135.

Sidik, S. M. and Ahmad, R. (2004). Childhood Obesity: Contributing Factors, Consequences and Intervention. Mal J Nutr. 10(1):13-22.

Zhao, J. and Grant, S.F.A. (2011). Genetics of Childhood Obesity. Journal of Obesity. 2011:pgs.