genetics and obesity

Although it has become more uncommon recently, obesity has always existed in the human community. On the other side, the availability of cheap, processed foods with lots of calories in recent decades has led to a substantial increase in the prevalence of obesity in westernized nations. Although the obesogenic environment is the main cause of the healthcare problem, this environment's impact reveals a genetic propensity that was already present in a subpopulation to more adiposity. There is strong evidence for the heredity of obesity, and studies of both rare and common types of the disease have identified genes as key players in the etiology. Patient care application of this idea has been relaxed.
Lately, obesity risks were assumed to be understood well, with an association that is straightforward between growing obesity as well as health issue risks including the type 2 diabetes, as well as arthritis and so on. It is clear that fat deposition location, as well as adipokines secretion variation, influence the way obese individuals develop complications. Research in obesity health risk prediction is still ongoing, and researchers are working on an improved technology in diagnosis.

Key words: obesity, etiology, genes











Obesity and Genetics

Every human physiology aspect, development, as well as adaptation is affected by genes. Relatively, there is little information concerning specific obesity contributing genes as well as the scale of environmental interactions of the genes the complex interplay between our make-up of the genes as well as our experiences of life. In 2014, a study found out that fried food consumption could interact with obesity-related genes, underscoring the essence of fried food consumption reduction in people that are genetically obesity predisposed. Human obesity genes search started many decades ago. The search was intensified by rapid molecular biology advances as well as the Human Genome Project. The research pointed out numerous genetic factors responsible for single-gene obesity forms that are very rare. Developing research has started identifying common obesity genetic underpinnings which are subjective to hundreds of genes.

Moreover, a study into the specific foods as well as obesity association makes it clear regarding diet, genes, as well as obesity interaction. The early findings are even more apparent in the way they state that identified genetic factors contribute slightly to the risks of obesity. Moreover, genes are not the destiny of an individual. Numerous obesity genes carrying individuals do not necessarily become overweight, as well as the effects of genes can be counteracted by healthy lifestyles. The Organization of World Health asserts that the intensifying widespread obesity is now an ill health substantial contributor. More than 30 percent of the adults in the United States are obese. This paper outlines genes contributions as well as interactions of the gene-environment obesity development.

Neel proposed the hypothesis of the thrifty gene, in the 1960s, stating that obesity predisposing genes have a selective advantage in frequently experiencing starvation population. In today’s obesogenic environment, individuals who have these genes might be that overeating. This is evident in groups that are at high risks including Pima Indians as well as Pacific Islanders. Recently, a study done in the United States showed the existence of an obesity stage of disproportionality in the African as well as Hispanic Americans as related to the Caucasians. Pritchard has provided support for the hypothesis of the thrifty gene, recently, and has found out that glucose, as well as lipid metabolism involved genes, have been subject to positive selection in past several decades, particularly in the Asian as well as African ethnic groups.

Heritability Traits

The estimates of obesity caused by heritability issues are typically greater than 0.7, while that of schizophrenia, autism, hypertension, as well as depression are 0.81, 0.90, 0.29, and 0.5 respectively. Moreover, an accurate, measurable obesity sub-phenotypes usage has led to a substantial heritability procedures for the thickness of skinfold, the circumference of the waist, as well as the total and regional distribution of fat (Butte et al., 2016).

Monogenic Obesity

Numerous rare obesity forms come from single-gene spontaneous mutation referred to monogenic mutation. Such modifications are present in appetite control genes, intake of food, as well as energy homeostasis, in hormone leptin coding genes, the receptor of leptin, as well as the receptor of melanocortin. Besides, obesity is a hallmark of numerous syndromes of genes caused by mutation or else abnormalities of the chromosomes, for instance, Prader-Willi as well as Bardet-Biedl syndromes. Mental retardation, anomalies of the reproductive system accompany obesity, in these syndromes.

Common Obesity Causing Multiple Mutation

Now, obesity is a health issue distressing the society of the rich as well as the poor, in the 21st century. The level of the body fats varies in individuals, on the other hand, some individuals tend to have more fats in the body as compared to others. Evidence from models of animals, studies of human linkage, twin studies, as well as significant population associated studies suggests that this obesity susceptibility variation has a component of genes. It is thought that a single-gene does not control it; however, common obesity susceptibility is affected by multiple genes.

Twin studies shade some light into the common obesity genetics. According to the twin pairs as well as biological also adaptive members of the family, body mass index’s mean correlations estimate are 0.74, 0.32, 0.25, 0.19,0.06, as well as 0.12 for identical, and fraternal twins, siblings, pairs of parent-offspring, relatives that have been adopted, as well as for spouses respectively. The high body mass index correlation between twins who are identical and its lesser degree attenuation of genes that are shared put a strong BMI influence of the gene forwards. On the other hand, it is concluded that the theory that identical as well as fraternal twins pose the same shared degree of the environment. In practice, this assumption does not hold.

GAD2

There were reports on the association of the gene of glutamic acid decarboxylase on obesity as well as morbidly obese adults feeding behaviors. Subsequently, the result replicated on children that were obese. On the other hand, the findings were not replicated by independent studies. This demonstrates the difficulty in defining if there is an association between the gene and the complex disease caused by the gene. The recent findings illustrate that the research that has been done so far is not enough to prove or else disapprove that variants in etiology have not been genotyped.

Visfatin

Primarily, the cell colony of Pre-B has recognized as a lymphocyte secreted protein for the past decade. Recently, it has been re-named as Visfatin where it was expressed in adipocytes as well as the expression was amplified in adipose tissue that is visceral when a comparison is made with subcutaneous. Initial studies have informed that mimetic activities of insulin have been noticed in Visfatin. The initial research in genetics published demonstrated that the tested variants played no role in obesity or else T2DM. Neither is Visfatin articulated by adipose tissue nor representative cytokine. Moreover, it has a resolved type 11 phosphoribosyltransferase structure.

Ghrelin and Ghrelin Receptor

It has been found out that ghrelin hormone is secreted by the stomach as well as the small intestines and play an essential part in the regulation of appetite as well as gastrointestinal function. Ghrelin evidence has remained unclear, but it is believed that the identification of another hormone regulating appetite, referred to obestatin, opposes the ghrelin effects. Recently, the variants of Ghrelin have been found to associate with the common obesity as well as the rare monogenic obesity genes.

Obesity-Related Genes Identification by Use of Genome Studies.

An extensive association study of a genome scans several genetic markers across thousands of complete sets of DNA of individuals to find a variation of genes related to a specific disease. These research can find use in detecting changes of genes playing a standard part in complex diseases including obesity. Frequently, an alteration in the DNA cell that encodes for a gene can result in gene action difference. Risks of diseases are caused by variations in DNA or else polymorphisms of a single nucleotide. Researchers using the studies of genome-wide association, in 2007, identified the first gene variants that are obesity-related. In comparison, the individuals carrying these common genes have an obesity health risk of 20 to 30 percent to people lacking them.

The second variant of the gene that is obesity-related recognized by researchers lies on chromosome 18, near to the receptor gene of melanocortin-4. Up to now, studies of the genome-wide association have succeeded in identifying 30 candidate genes located on 12 chromosomes related to BMI. Most importantly, even the candidate genes that are likely account for the genes that are associated with obesity susceptibility.

Interactions of Gene-Environment

The rapid obesity spread around the world is hardly explained by changes in genes, since the pool of genes for many generations remains stable across a population. For new mutations to spread, it takes a long time. If for the last 40 years the genes of individuals have remained the same, rising levels of obesity could be because of the physical, social, as well as political surroundings influencing the amount of food we eat. Changes in the environment that make people overeat, as well as more difficult for individuals to exercise their bodies, have led to the recent increase in overweight as well as obesity.

Work on the ecological interactions of the genes that are related to obesity is still at an infancy stage. So far, the evidence states that the individuals having obesity genes do not necessarily become overweight. Relatively, it has been found that healthy diets, as well as physical exercise, counteract the risk of obesity that is related to genes. For instance, Andreasen as well as his colleagues established, in 2008, that physical activities offset a single obesity-promoting gene’s effect, which is a common variant in fat mass as well as the obesity related gene. The research found out that inactive individuals who are carrying the gene promoting obesity have higher body mass index compared to inactive individuals without a gene variant. Genetic obesity predisposition did not matter although, for inactive individuals their Body Mass Index were neither higher nor lower compared to the individuals without the gene causing obesity (Pigeyre et al., 2016).

Subsequently, the study on the connection between fat mass also obesity-related genes (FTO), physical activity, as well as obesity generated results that were contradicting. They found out that individuals who are carrying the FTO gene variant promoting obesity had a 23 percent higher risk obesity as compared to the individuals who did not. Again, physical exercise lowered the risk of obesity. Physically active adults had a 30 percent lower obesity risk compared to adults who are inactive and had the gene. Most individuals have their genetic obesity predisposition, from their history of the family as well as ethnicity backgrounds. A change in the susceptibility to obesity to obesity needs an alteration in diet, lifestyle, or else other factors of the environment.

Conclusion

Understanding the contributions of genes to obesity, particularly the common obesity gene as well as the interactions of the gene and the environment will help individuals generate a better causal pathway understanding that leads to obesity. Obesity information could provide promising approaches for obesity treatment as well as prevention. Overall, the risk of genes contributing to obesity is minimal, however toxic food, as well as activity environment profoundly, adds to the threat. Efforts on preventing obesity must focus on making health decisions by changing the setting (Allison et al., 2016).







References

Allison, K. C., Lundgren, J. D., & Wadden, T. A. (2016). Albert J. Stunkard: His Research on Obesity and Its Psychological Impact. Current obesity reports, 5(1), 140-144.

Butte, N. F., Bacino, C. A., Cole, S. A., & Comuzzie, A. G. (2016). 6 Genetics of Childhood Obesity. Handbook of Pediatric Obesity: Etiology, Pathophysiology, and Prevention, 79.

Pigeyre, M., Yazdi, F. T., Kaur, Y., & Meyre, D. (2016). Recent progress in genetics, epigenetics and metagenomics unveils the pathophysiology of human obesity. Clinical science, 130(12), 943-986.