University Cardiovascular Risk: Gene-Environment Interaction Report

This report examines the gene-environment interaction for cardiovascular risk, focusing on obesity and diabetes in relation to smoking, non-smoking, and other tobacco users. The study utilizes data from CINAHL, PubMed, and Medline, analyzing various study designs including systematic literature reviews, randomized control trials, and cross-sectional studies. Environmental factors such as physical activity, diet, and tobacco use are considered alongside genetic factors like SNPs and alleles. Statistical analyses, including T-tests, Chi-square tests, and ANNOVA, are employed to determine the significance of findings. The report highlights how smoking, unhealthy diets, and sedentary lifestyles interact with genetic predispositions to increase cardiovascular risk, particularly in the development of obesity and diabetes. The research also explores how tobacco use can lead to genetic mutations and impact insulin production. References from various studies are included to support the analysis.

Running head: GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
Name of the Student
Name of the University
Author Note

1
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
Table 1: GENE-environment interaction for cardiovascular risk: Obesity
Search
terms
Databa
se
Hits
“how
many
articles,
just the
numbe
r”
Type of
study
design
Sample
size and
type
Data
collection
Environmen
tal factors
Genetic
factors:
SNPs,
alleles,
biomarker
s,
genes
What
type of
Statistica
l analysis
Findings
Gene
interaction
with
environme
nt for
obesity
among
smokers
CINAH
L,
PubMed
,
Medline
196 Maximum
studies
have
conducted
considerin
g
systematic
literature
Random
sampling
focusing
on the age
and
smoking
habits of
the
Quantitativ
e survey or
meta-
analysis.
Low or no
amount of
physical
activity and
gene
interaction
with
smoking.
Monogenet
ic mutation
by
smoking
can cause
the obesity
drastically.
T-test and
Chi-
square
test for
the
significan
ce of data
collected.
Most of the
articles stated
that the
smoking and
unhealthy
diet along
with lack of
physical

2
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
review,
the
randomize
d control
trial and
cross-
sectional
study.
participant
s.
activity can
cause obesity
as the single
gene
mutation can
be developed
(Courtemanc
he, Tchernis
and Ukert
2018).
Gene
interaction
with
environme
nt for
obesity
among
CINAH
L,
PubMed
,
Medline
167 Randomiz
ed control
trial and
cross-
sectional
study.
Random
sampling
sometimes
convenien
ce
sampling.
Quantitativ
e survey
through
close ended
questionnai
re.
Big appetite
and junk food
consumption
along with
hereditary
issues.
Heredity
that is
comprised
of alleles in
the genetic
content
that are
ANNOV
A and T-
test.
Obesity is
developed
among the
non-smokers
by junk food
consumption
and sedentary

3
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
non-
smokers
responsible
for obesity
developme
nt.
lifestyle.
Moreover,
the effects of
the heredity
can also be
the cause of
this condition
(Fuller-
Thomson et
al. 2018).
Gene
interaction
with
environme
nt for
obesity
among
CINAH
L,
PubMed
,
Medline
139 Systemati
c literature
review,
the
randomize
d control
trial and
Sampling
based on
the
tobacco
consumpti
on amount
and type
Quantitativ
e survey
and meta-
analysis.
Unhealthy
diet and lack
of literacy
and also
leading
sedentary
Tobacco
products
affects the
genes by
mutating
them and
subsequent
Mean
calculatio
n and also
the Chi-
square
test to test
the
Tobacco
users other
than the
smokers can
also develop
the negative
genetic

4
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
other
tobacco
users.
cross-
sectional
study.
and age as
well.
lifestyle. ly breaking
the DNA
content in
smaller
parts. This
condition
leads to
different
deformities
in alleles
and thus
the
developme
nt of
cancerous
cells.
significan
ce of the
data.
interactions
and
subsequently
affect the
genetic
material
along with
the unhealthy
diet leads to
the
development
of obesity
among these
people (Hurt
et al. 2017).

5
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
Table 2: GENE-environment interaction for cardiovascular risk: Diabetes
Search
terms
Databas
e
Hits
“how
many
articles,
just the
number
”
Type of
study
design
Sample
size and
type
Data
collection
Environment
al factors
Genetic
factors:
SNPs,
alleles,
biomarker
s,
genes
What
type of
Statistic
al
analysis
Findings
Gene
interaction
with
environme
nt for
diabetes
among
smokers
CINAH
L,
PubMed,
Medline
267 Systemati
c
literature
review,
the
randomize
d control
trial and
Random
sampling
focusing
on the age
and
smoking
habits of
the
Quantitativ
e survey or
meta-
analysis
and follow
up through
observation
.
Sedentary
lifestyle,
unhealthy
diet, smoking
and stress.
Smoking
causes
genetic
methylation
and
subsequentl
y develop
type 2
ANNOV
A test.
Most of the
articles
stated that
the
smoking
can cause
methylatio
n of

6
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
cross-
sectional
study.
participant
and the
participants
are diabetic
patients.
diabetes. different
genetic
alleles
which lead
to the
negative
condition
developme
nt of
insulin
production
hence,
diabetes
develops
and stress
has a large
role in this

7
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
condition
developme
nt
(Asfuroğlu,
Araslı-
Yılmaz and
Aycan
2019).
Gene
interaction
with
environme
nt for
diabetes
among
non-
smokers
CINAH
L,
PubMed,
Medline
179 Systemati
c
literature
review,
randomize
d control
trial and
cross-
sectional
Random
sampling
sometimes
convenienc
e sampling
based on
the
diabetes
and the
Quantitativ
e survey
through
close ended
questionnai
re and
follow up
through
observation
Stress
regarding the
economic
status or job-
related
dissatisfaction
or age-based
diabetes
Heredity
that is
comprised
of alleles in
the genetic
content that
are
responsible
for obesity
ANNOV
A and T-
test.
Stress and
unhealthy
lifestyle
effectively
mutate the
genes and
subsequentl
y insulin
production

8
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
study. lifestyle of
the
participants
.
. development. developmen
t.
Moreover,
the stress
and
unhealthy
living can
also lead to
mutate the
genes
responsible
for insulin
production.
reduced or
stopped
which
leads to
diabetes
developme
nt
(Akinkugb
e et al.
2017).
Gene
interaction
with
environme
CINAH
L,
PubMed,
189 Systemati
c
literature
review,
Sampling
based on
the tobacco
consumptio
Quantitativ
e survey
and meta-
Unhealthy
diet and lack
of literacy
stress and
Tobacco
products
affects the
genes by
ANNOV
A and T-
test.
Tobacco
users other
than the
smokers

9
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
nt for
diabetes
among
other
tobacco
users.
Medline the
randomize
d control
trial and
cross-
sectional
study.
n amount
and type
and age as
well as the
diabetic
patients.
analysis. depression. mutating
them and
subsequentl
y breaking
the DNA
content and
thus the
negative
interaction
can lead to
termination
of insulin
production.
can also
develop the
negative
genetic
interactions
and
subsequentl
y affect the
genetic
material
which can
develop the
situation of
blood sugar
content
unchecked.
Thus, the

10
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
diabetes
develops
(Clement
et al.
2018).

11
GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK
References
Akinkugbe, A.A., Sanders, A.E., Preisser, J.S., Cai, J., Salazar, C.R. and Beck, J.D., 2017. Environmental tobacco smoke exposure
and periodontitis prevalence among nonsmokers in the hispanic community Health Study/Study of Latinos. Community dentistry and
oral epidemiology, 45(2), pp.168-177.
Asfuroğlu, P., Araslı-Yılmaz, A. and Aycan, Z., 2019. Cigarette smoking in adolescents with type 1 diabetes mellitus and congenital
adrenal hyperplasia. The Turkish Journal of Pediatrics, 61(2).
Clement, L., Clair, C., Muller, O., Gencer, B., Klingenberg, R., Raber, L., Matter, C.M., Luscher, T.F., Windecker, S., Mach, F. and
Rodondi, N., 2018. P2510 Insufficient smoking cessation in patients with diabetes after acute coronary syndrome, need for improved
secondary prevention. European Heart Journal, 39(suppl_1), pp.ehy565-P2510.
Courtemanche, C., Tchernis, R. and Ukert, B., 2018. The effect of smoking on obesity: Evidence from a randomized trial. Journal of
health economics, 57, pp.31-44.
Fuller-Thomson, E., Howden, K.E., Fuller-Thomson, L.R. and Agbeyaka, S., 2018. A strong graded relationship between level of
obesity and COPD: Findings from a National Population-Based Study of Lifelong Nonsmokers. Journal of obesity, 2018.
Hurt, R.T., Croghan, I.T., Schroeder, D.R., Hays, J.T., Choi, D.S. and Ebbert, J.O., 2017. Combination varenicline and lorcaserin for
tobacco dependence treatment and weight gain prevention in overweight and obese smokers: a pilot study. Nicotine & Tobacco
Research, 19(8), pp.994-998.

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GENE-ENVIRONMENT INTERACTION FOR CARDIOVASCULAR RISK