Abstract well as adaptation is affected by genes.

Abstract

Obesity
has always been in existence in the population of humans, although lately, it
has been comparatively rare. The availability of plentiful, processed foods
that are rich in energy in the previous decades has, on the other hand,
contributed to an increase of obesity in countries that are westernized. Even
though the main problem in healthcare is as a result of an obesogenic environment,
its action is by revealing a genetic predilection that is pre-existing in a
sub-population to additional adiposity. Considerable indication exists for the
obesity heritability, and research in obesity’s rare as well as common forms
has recognized genes with an essential part to play in its etiology.

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            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, arthritis
and so on. It is clear that fat deposition location, as well as adipokines
secretion differences, impact the way obese individuals develop difficulties.
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, the scale of
environmental interactions of the genes, the complex interplay between our
make-up of genes and our experiences of life. 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 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.

            In today’s obesogenic environment,
individuals who have these genes might be overeating. This is evident in groups
that are at high risks including Pima Indians as well as Pacific Islanders.
Recently, a study conducted 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. Support for the theory of the thrifty gene
has indicated that glucose, as well as lipid metabolism involved genes, have
been subject to positive selection in the past several decades, predominantly
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, and depression are 0.81, 0.90, 0.29, and
0.5 respectively. Moreover, a precise, measurable obesity sub-phenotypes usage
has led to 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, and
the receptor of melanocortin. Further, obesity is a hallmark of numerous
syndromes of genes caused by mutation or other abnormalities of the
chromosomes, for instance, Prader-Willi and 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; 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 have shed some light
into the common obesity genetics. According to the twin pairs, as well as
biological/adaptive members of the family, body mass index’s mean correlations
estimate are 0.74, 0.32, 0.25, 0.19,0.06, and 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 relationship
of the gene of glutamic acid decarboxylase on obesity as well as morosely obese
adults feeding activities. Subsequently, the result replicated on children that
were obese. However, 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 disapprove that variants in etiology have not been genotyped.

Visfatin

            Primarily, the cell colony of Pre-B
has been documented as a lymphocyte secreted protein for the past decade. Lately,
it has been re-named as Visfatin where it was stated in adipocytes as well as
the expression was enlarged in adipose tissue that is visceral when a contrast
is made with subcutaneous. Initial studies have inferred that mimetic
activities of insulin have been noticed in Visfatin. The early research in
genetics published confirmed that the tested variants played no role in obesity
or 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 discovered that ghrelin
hormone is secreted by the stomach as well as the small intestines and play a vital
role 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 as 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 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. This 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 polymorphisms of a single nucleotide.
Researchers using the studies of genome-wide association, 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. Until 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 likely
account for the genes that are associated with obesity susceptibility.

Interactions of Gene-Environment

            The rapid obesity eruption spreading
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 the difficulty 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; 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 and 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 of 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 needs an alteration in diet, lifestyle, or 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).

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