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Obesity is a topic that has elicited much interest within the wider topic of genetics. There are some studies that have been done to find out the relationship between obesity and genetics. A number of theories have also been established to explain how genetics affect obesity. This paper seeks to find out from the researches done and the existing hypotheses on the relationship between the two. Knowledge on this topic would be essential in finding a way of dealing with obesity, which is a threat to the modern world.
First and foremost, it is prudent to understand what obesity is. It is a condition that occurs when excess body fats accumulate to levels which affects the normal functioning of the body. This condition, if not dealt with can lead to an increased health problems and low life expectancy. World Health Organization predicts that “obesity and overweight will soon replace the common public health concerns, like under nutrition and infectious diseases to be the main cause of poor health” (WHO, 2000). This is due to the fact that obesity increases the chances of contracting other diseases like cancer, type 2 diabetes, heart diseases, and obstructive sleep apnea.
Body Mass Index (BMI) is the measure used to find out those that with the right weight or obese. It is found out by comparison between weight and height measurements. Bodies with BMI of between 25 and 30 Kg/m2 are termed as overweight or pre-obese. BMI of 30 Kg/m2 and above lies in the obese category. Research shows that the most affected regions are the North America, Europe, and Australia. The increase of this condition in these regions has been attributed to the low costs of food due to the production techniques and the Agricultural policy. In United States, the processed and fast food is cheaper due to the high subsidy by the U.S farm bill (Pollan, 2007). Figure 1 below is pictures of normal, overweight and obese persons respectively:
Figure 1- normal, overweight, and obese persons
Genetics has been found by different studies to play a big role in most of the obese persons. Hypotheses in place and studies have brought out conclusions that there is some passage of the obese genes to the offsprings. Observation of a family where both parents are obese most leads to the children which are obese. Other hypotheses have also shown that there exists obesity genes that can be past to subsequent generations through inheritance. Therefore, when a person is obese, there is likelihood there existed some parents or ancestors along the lineage who had the genes.
Thrifty gene hypothesis by genetist James V. Neel proposes that there exist thrifty genes which enable individuals to efficiently collect and process food during times of plenty. These deposit fat to be stored as a reserve for the times of food scarcity. The hypothesis also indicates that those with the thrifty genotype long ago in communities which experienced seasons of food abundance and scarcity would fatten. The excess fat could later be used by the body during droughts (Neel J.V, 2009).
This worked well for the adaptation in the older days. In the present, things have however changed. There is no food scarcity in most of diabetic affected areas. This means that the fat stored in the body by the genotype with an expectation of a famine, a phenomena that is rear of late. As a result, the increased fattening leads to obesity, a condition that makes the body prone to dangerous diseases like diabetes. Environmental conditions have been changing time by time. This includes the types of food eaten and other types of activities. Therefore, the only way of reducing these health conditions is by regaining the ancestral environment, something close to impossible.
Primary research studies that have been done in the past have confirmed the link between genes and obesity. Some of these studies have been conducted on twins, family members, and adoptees. A research done by Prof.Stephen O'Rahilly, MD and I. Sadaf Farooqi, MD (2005) on the genesis of obesity on humans finds out the evidence of the inherited factors that determine fat mass. In their research, they estimated the phenotypic variance attributed to genetic variation under a polygenic model. The twin studies conducted did prove the heritability of about 40% to 70% showing a concordance of 0.7-0.9 for the monozygotic twins in comparison to 0.35-0.45 for the dizygotic twins (O'Rahilly S. and Farooqi S., 2005).
On the adoption, the study was done on over 5,000 people on the Danish adoption register with all details of the subjects and the biological parents. The result shows a close relationship of the BMI between those adopted and the biological parents. There are no relationships with the adopting parents. This is a strong indication of the involvement of genes in the propagation of pleiotropic obesity syndromes.
Another primary research study on the Quantitative Trait Loci Contributing to Obesity Related Phenotypes done in 2004 shows that obesity has a strong evidence of genetic component, environmental factors, and some mode of inheritance that seems uncertain (J Clin Endocrinal Metab, 2004). The report however fails to find out the susceptibility genes of obesity. It attributes this to the interaction of many factors that lead to the disease etiologies. This is the complex situation that has made it difficult to identify the responsible gene despite the many studies over the past decades. This study also mentions the inconsistent and unproved outcomes that arise from these studies. The study, however confirms the linkage findings for the obesity phenotypes.
A research done by the University of Michigan on the Epidemiologic and Genetic Studies of Nonalcoholic Fatty Liver Disease (2011) found out the relationship between obesity and liver problems. Obesity causes the fattening of the liver, something that is dangerous. They have identified the genes that are responsible for passing the defects to the offspring. These are: PNPLA3, NCAN, GCKR, LYPLAL1, and PPP1R3B. They are shown in figure 1 below. The findings also indicate that they contain 20% of the heritability of the traits. They also contain other metabolic traits that are for the glucose and lipid abnormalities.
According the information available in their website, the same university has been able to identify 32 SNP chromosome variants that are associated with the Body Mass Index (BMI). They has also established a 3% heritability of the traits. The website says, “We have also identified two copy number variants that associate with BMI near the genes NEGR1 and GPRC5B. Some of the genes near associating variants are known to affect hypothalamic control of appetite regulation (MC4R, SH2B1, BDNF, POMC) while others are suspected to play a role in peripheral effects of nutrient sensing and insulin secretion (GIPR). At most associating sites however, the genes near the variants have never before been connected to obesity giving us new insights into the biology of body weight regulation. We are also involved in studies of body fat distribution and fat mass” (http://spelioteslab.com/page 85).
There are other hypotheses that have been made in respect to this. Thrifty phenotype hypothesis came into place as a result of Neel’s hypothesis. It is based on the theory that thrifty factors arise as a result of the immediate environment in the womb. Conditions of the womb environment within the mother play a bigger role than the genes. This is unlike Neel’s hypothesis which theorized that genetic factors were responsible for the thrifty factors. This theory continues predicting that the body is capable of predicting the life of starvation for the fetus. This in turn leads to the production of insulin (Watve and Yajnik, 2007).
Thrifty phenotype hypothesis has been linked to the type 2 diabetes, a condition caused by poor fetal and infant growth. Some metabolic syndrome and other development aspects have also been linked to this hypothesis. Epidemiological evidence of this hypothesis has been proved by the various studies conducted in most parts of the world. Research done on various age groups has also proved the insulin resistance is clear. It however does not give a clear relationship of the insulin secretion. It should be noted that these two hypotheses remain a matter of discussion in terms of contribution of environment and genes (Wells, J. C. K., 2009).
There also exists another hypothesis known as ‘thrifty epigenomic hypotheses. In The thrifty epigenotype: An acquired and heritable predisposition for obesity and diabetes? Stoger R. elaborates this hypothesis. It combines the phenotype and the thrifty genotype hypotheses. It gives the theory that an individual’s susceptibility to contracting a disease depends on the epigenetic inheritance of such risks. It therefore proposes that there are epigenetic factors that influence the disease risks in any individual (Watve and Yajnik, 2007). This is a strong support of the hypothesis at hand.
In conclusion, it is very clear that the topic of genetics of obesity is an interesting one. Many studies have been done and others are still underway to find out more on it. What comes out is the fact that there are genes that are responsible for obesity. These genes are inherited from one generation to the next. It is also evident that the specific susceptibility genes that causes obesity is what remains to unveiled but there is no doubt that genes are involved. Understanding this would an important factor in the prevention of this condition that is becoming a problem in developed nations. The effects of obesity are far reaching.