scholarly journals Roma socioeconomic status has higher impact on smoking behaviour than genetic susceptibility

2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
M A Merzah ◽  
P Pikó ◽  
R Ádány ◽  
S Fiatal

Abstract Background Prevalence of smoking in Hungarian Roma (HR) population is two to five times higher than in Hungarian general (HG) population. Our study aims to examine genetic susceptibility and other possible determinants associated to smoking behaviours in these populations. Methods A questionnaire based cross-sectional study was designed in HG (N = 412) and HR (N = 402) populations. Ten Single Nucleotide Polymorphisms (SNPs) were genotyped known to be robustly linked to smoking behaviours. Risk allele frequencies were compared. Additive genetic risk scores (unweighted GRS and weighted GRS) were constructed to compare genetic load from SNPs in genes NRXN1, CHRNA5/4, AGPHD1, MAOA, TRPC7, KCNJ6, GABRA4, and CYP2A6. Smoking behaviour were associated with GRSs and confounders (age, gender, BMI, socioeconomic status-SES) in several regression models. SES was calculated based on Modified Kuppuswamy scale 2019. Results Risk allele frequencies of four SNPs were found to be different between populations (p < 0.01). Median of GRS was equivalent among in populations; whilst wGRS median was slightly higher among Roma (5.2 compared to Hungarian 4.9; P = 0.02). In Roma both genders were more likely to be heavy smoker (OR = 2.05, 95%CI: 1.47-2.86; OR = 1.89, 95%CI: 1.58-2.25, for males and females, respectively) compared to counterparts from general population. GRS were higher among heavy smokers of both populations compared to other smoking behaviours (ORRoma= 1.06, 95%CI:0.98-1.15; ORHungarian=1.05, 95%CI=0.91-1.2). Strong reversible relationship was found between SES and smoking behaviours among study populations (p < 0.0001). Heavy, moderate, and former smokers were having lower SES compared to never smokers of both populations (SES β=-0.037, P = 0.04 for Hungarian; β=-0.039, P = 0.02 for Roma). Conclusions Socioeconomic status was shown as a priority indicator based on multifactorial regression analysis. The highest efforts should be focused on improving the SES of Roma population. Key messages Result of this study indicate the priority impact of SES instead of genetic susceptibility on Roma smoking behaviours variations. Interventions on improving socioeconomic status of the Roma might result in decreasing their cigarette consumption.

Author(s):  
Mohammed Merzah ◽  
Zsigmond Kósa ◽  
János Sándor ◽  
Shewaye Natae ◽  
Péter Pikó ◽  
...  

It is a matter of speculation whether the high prevalence of smoking among Hungarian Roma (HR) is related to genetic, gene-environmental interactions or cultural factors. Our aim is to compare the genetic susceptibility and possible effects of determinants associated with smoking behaviours in the Hungarian general (HG) and Roma populations. A complex health survey including three pillars (questionnaire, physical and laboratory examinations) was carried out (NHG = 412 and NHR = 402). Risk allele frequencies of ten single-nucleotide polymorphisms (SNPs) were compared, and their combined effect was estimated by computing unweighted and weighted genetic risk scores (GRS, wGRS). The effects of genetic and environmental factors were investigated in regression analyses after confounders were introduced. Socio-economic status (SES) was calculated based on the Kuppuswamy scale 2019. Risk allele frequencies of only four SNPs were found to be different between populations (p < 0.01). Median values of GRS did not differ, while the wGRS median was slightly higher among Roma individuals (5.2 vs. 4.9; p = 0.02). Roma individuals were more likely to be heavy smokers (ORmales = 2.05, 95% CI [1.47–2.86]; ORfemales = 1.89, 95% CI [1.58–2.25]. Smokers have lower SES compared to never smokers (SES βHR = −0.039, p = 0.023; βHG = −0.010, p = 0.049). An inverse relationship was found between SES and smoking behaviours (p < 0.0001) and was found to be a better predictor of smoking behaviours than genetic susceptibility. Our study findings suggest that the high prevalence of smoking behaviours and nicotine-dependence were not revealed to have a genetic susceptibility among HR individuals; therefore, the highest efforts should be focused on targeting SES-related factors in the Roma population. Strengths of the study: This is the first study carried out to investigate and detect the most relevant factors and the possible genetic background of the extremely high prevalence of smoking based in the Roma population. Limitations of the study: No standard instrument has been used to assess the intensity of addiction to nicotine. Because of some participants’ unwillingness to define themselves as Roma, the overall HR population was not represented by the sample of this study.


2014 ◽  
Vol 46 (6) ◽  
pp. 207-215 ◽  
Author(s):  
Kumpei Tanisawa ◽  
Tomoko Ito ◽  
Xiaomin Sun ◽  
Zhen-Bo Cao ◽  
Shizuo Sakamoto ◽  
...  

High cardiorespiratory fitness (CRF) is associated with a reduced risk for dyslipidemia; however, blood lipid levels are also affected by individual genetic variations. We performed a cross-sectional study to determine whether CRF modifies polygenic risk for dyslipidemia. Serum levels of triglycerides (TG), LDL cholesterol (LDL-C), and HDL cholesterol (HDL-C) were measured in 170 Japanese men (age 20–79 yr). CRF was assessed by measuring maximal oxygen uptake (V̇o2max), and subjects were divided into low-fitness and high-fitness groups according to the reference V̇o2max value for health promotion in Japan. We analyzed 19 single nucleotide polymorphisms (SNPs) associated with TG, LDL-C, or HDL-C levels. Based on these SNPs, we calculated three genetic risk scores (GRSs: TG-GRS, LDL-GRS, and HDL-GRS), and subjects were divided into low, middle, and high groups according to the tertile for each GRS. Serum TG levels of low-fitness individuals were higher in the high and middle TG-GRS groups than in the low TG-GRS group ( P < 0.01 and P < 0.05, respectively), whereas no differences were detected in the TG levels of high-fitness individuals among the TG-GRS groups. In contrast, the high LDL-GRS group had higher LDL-C levels than did the low LDL-GRS group, and HDL-C levels were lower in the high HDL-GRS group than in the low HDL-GRS group regardless of the fitness level ( P < 0.05). These results suggest that high CRF attenuates polygenic risk for hypertriglyceridemia; however, high CRF may not modify the polygenic risk associated with high LDL-C and low HDL-C levels in Japanese men.


2021 ◽  
Vol 12 ◽  
Author(s):  
P. Prakrithi ◽  
Priya Lakra ◽  
Durai Sundar ◽  
Manav Kapoor ◽  
Mitali Mukerji ◽  
...  

Host genetic variants can determine their susceptibility to COVID-19 infection and severity as noted in a recent Genome-wide Association Study (GWAS). Given the prominent genetic differences in Indian sub-populations as well as differential prevalence of COVID-19, here, we compute genetic risk scores in diverse Indian sub-populations that may predict differences in the severity of COVID-19 outcomes. We utilized the top 100 most significantly associated single-nucleotide polymorphisms (SNPs) from a GWAS by Pairo-Castineira et al. determining the genetic susceptibility to severe COVID-19 infection, to compute population-wise polygenic risk scores (PRS) for populations represented in the Indian Genome Variation Consortium (IGVC) database. Using a generalized linear model accounting for confounding variables, we found that median PRS was significantly associated (p &lt; 2 x 10−16) with COVID-19 mortality in each district corresponding to the population studied and had the largest effect on mortality (regression coefficient = 10.25). As a control we repeated our analysis on randomly selected 100 non-associated SNPs several times and did not find significant association. Therefore, we conclude that genetic susceptibility may play a major role in determining the differences in COVID-19 outcomes and mortality across the Indian sub-continent. We suggest that combining PRS with other observed risk-factors in a Bayesian framework may provide a better prediction model for ascertaining high COVID-19 risk groups and to design more effective public health resource allocation and vaccine distribution schemes.


2017 ◽  
Author(s):  
Michelle S Kim ◽  
Kane P Patel ◽  
Andrew K Teng ◽  
Ali J Berens ◽  
Joseph Lachance

AbstractBackgroundAccurate assessment of health disparities requires unbiased knowledge of genetic risks in different populations. Unfortunately, most genome-wide association studies use genotyping arrays and European samples. Here, we integrate whole genome sequence data from global populations, results from thousands of GWAS, and extensive computer simulations to identify how genetic disease risks can be misestimated.ResultsIn contrast to null expectations, we find that risk allele frequencies at known disease loci are significantly different for African populations compared to other continents. Strikingly, ancestral risk alleles are found at 9.51% higher frequency in Africa and derived risk alleles are found at 5.40% lower frequency in Africa. By simulating GWAS with different study populations, we find that non-African cohorts yield disease associations that have biased allele frequencies and that African cohorts yield disease associations that are relatively free of bias. We also find empirical evidence that genotyping arrays and SNP ascertainment bias contribute to continental differences in risk allele frequencies. Because of these causes, polygenic risk scores can be grossly misestimated for individuals of African descent. Importantly, continental differences in risk allele frequencies are only moderately reduced if GWAS use whole genome sequences and hundreds of thousands of cases and controls. Finally, comparisons between uncorrected and corrected genetic risk scores reveal the benefits of considering whether risk alleles are ancestral or derived.ConclusionsOur results imply that caution must be taken when extrapolating GWAS results from one population to predict disease risks in another population.


Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3064
Author(s):  
Sooad Alsulami ◽  
Dhanasekaran Bodhini ◽  
Vasudevan Sudha ◽  
Coimbatore Subramanian Shanthi Rani ◽  
Rajendra Pradeepa ◽  
...  

The increasing prevalence of type 2 diabetes among South Asians is caused by a complex interplay between environmental and genetic factors. We aimed to examine the impact of dietary and genetic factors on metabolic traits in 1062 Asian Indians. Dietary assessment was performed using a validated semi-quantitative food frequency questionnaire. Seven single nucleotide polymorphisms (SNPs) from the Transcription factor 7-like 2 and fat mass and obesity-associated genes were used to construct two metabolic genetic risk scores (GRS): 7-SNP and 3-SNP GRSs. Both 7-SNP GRS and 3-SNP GRS were associated with a higher risk of T2D (p = 0.0000134 and 0.008, respectively). The 3-SNP GRS was associated with higher waist circumference (p = 0.010), fasting plasma glucose (FPG) (p = 0.002) and glycated haemoglobin (HbA1c) (p = 0.000066). There were significant interactions between 3-SNP GRS and protein intake (% of total energy intake) on FPG (Pinteraction = 0.011) and HbA1c (Pinteraction = 0.007), where among individuals with lower plant protein intake (<39 g/day) and those with >1 risk allele had higher FPG (p = 0.001) and HbA1c (p = 0.00006) than individuals with ≤1 risk allele. Our findings suggest that lower plant protein intake may be a contributor to the increased ethnic susceptibility to diabetes described in Asian Indians. Randomised clinical trials with increased plant protein in the diets of this population are needed to see whether the reduction of diabetes risk occurs in individuals with prediabetes.


2012 ◽  
Vol 97 (12) ◽  
pp. 1027-1033 ◽  
Author(s):  
Geeta A Thakur ◽  
Sarojini M Sengupta ◽  
Natalie Grizenko ◽  
Zia Choudhry ◽  
Ridha Joober

ObjectiveTo investigate five top single nucleotide polymorphisms (SNPs) located in different genes and loci (CHRNA3, BDNF, DBH and LOC100188947) that were highly associated with different dimensions of smoking behaviour, in relation to attention-deficit hyperactivity disorder (ADHD).DesignCohort study consisting of a clinical sample of children with ADHD.SettingDouglas Institute ADHD Clinic, Montreal, Canada.PatientsFamilies of 454 children with ADHD aged 6–12 years old.InterventionsFamily-based association tests used to study the transmission of risk alleles within these five genetic markers.Main outcome measuresClinical diagnosis of ADHD, and a number of behavioural and neurocognitive phenotypes relevant to the disorder.ResultsOne SNP (rs1329650) from a non-coding RNA (LOC100188947) was significantly associated with overall ADHD diagnosis with the C* risk allele being over-transmitted from parents to children with ADHD (p=0.02). It was also over-transmitted to children with higher scores on Conners’ Parents (p=0.01) and Conners’ Teacher (p=0.002) index scores, and Child Behaviour Checklist withdrawn (p=0.001) and aggressive (p=0.007) behaviours. Children with poorer performances on executive and attention tasks were more likely to inherit the risk allele.ConclusionsThe C* allele of rs1329650 may be increasing the risk for ADHD and smoking behaviour through a common mechanism, possibly externalising behaviours and specific cognitive deficits that manifest as ADHD in childhood and are the gateway to smoking behaviour later in life. This exploratory study illustrates the use of comorbid disorders to investigate ADHD genetics. In spite of its relatively large sample size, replication in future studies is warranted.Trial Registration NumberNCT00483106.


2017 ◽  
Vol 41 (1) ◽  
pp. 7
Author(s):  
Nicole Hale ◽  
Andrea M. Murphy ◽  
Jon R. Adams ◽  
Cylie M. Williams

Objective In 2010, Peninsula Health (Vic., Australia), became smoke free as part of the locally developed smoking prevention and cessation strategy. The aim of the present study was to determine the effect of a smoke-free policy on smoking status and employee attitudes over a 3-year period. Methods Data were collected by three surveys 6 months before and 6 months and 3 years after policy introduction. Demographic data, smoking status and attitudes to the introduction of the smoke-free policy were collected for analysis. Results There were 3224 individual responses collected over three time points with similar demographics at each time. There were fewer employees smoking at 6 months (P = 0.010) and 3 years (P < 0.001) after implementation of the policy. There were more employees who felt positive towards the policy 3 years after its introduction (P = 0.028). There were greater odds of an employee not identifying as a smoker after the policy was in place than before the policy was implemented. Conclusions The introduction of a smoke-free policy within a health service was an upstream health intervention that was well accepted by staff and appeared to have a positive effect on smoking behaviours. What is known about the topic? There are an increasing number of environmental changes that seek to decrease smoking behaviours. Bans within workplaces have a direct effect on employee smoking behaviour. What does this paper add? Some employee groups demonstrated the greater odds of smoking when a smoke-free policy was in place. Employees felt positive towards this policy. What are the implications for practitioners? This policy change supports environmental changes affecting individual health-related behaviours.


2020 ◽  
Author(s):  
Doreen Mhandire ◽  
Kudakwashe Mhandire ◽  
Mulalo Magadze ◽  
Ambroise Wonkam ◽  
Andre P Kengne ◽  
...  

Abstract Background: Maternal cytomegalovirus (CMV) infection and/or reactivation in pregnancy is associated with a myriad of adverse infant outcomes. However, the role of host genetic polymorphisms in modulating maternal CMV status is inconclusive. This study investigated the possible association of single nucleotide polymorphisms in toll like receptor (TLR) and cytokine genes with maternal plasma CMV DNA status in black Zimbabweans. Methods: In a cross-sectional study, 110 women in late gestation who included 36 CMV infected cases and 74 CMV uninfected, age and HIV status matched controls were enrolled. Twenty single nucleotide polymorphisms in 10 genes which code for proteins involved in immunity against CMV were genotyped using Iplex GOLD SNP genotyping protocol on the Agena MassARRAY® system. Statistical analyses were performed using Stata SE and the ‘Genetics’ and ‘SNPassoc’ packages of the statistical package R. Results: The TLR7 rs179008A>T (p<0.001) polymorphism was associated while the TLR9 rs352139T>C (p=0.049) polymorphism was on the borderline for association with CMV positive (CMV+) status. In contrast, the interleukin ( IL)-6 rs10499563T>C (p<0.001) and TLR2 rs1816702C>T (p=0.001) polymorphisms were associated with CMV negative (CMV-) status. Furthermore, allele frequencies of SNPs in TLR2, TLR4, TLR9, TLR7 , IL - 6 , IL-10 , IL-28B , IL-1A and interferon AR1 ( IFNAR1 ) genes are being reported here for the first time in a Zimbabwean population. The allele frequencies in the Zimbabwean population re generally comparable to other African populations but different when compared to European and Asian populations. Conclusions: Toll like receptor and interleukin genetic polymorphisms influence CMV status in late gestation among black Zimbabweans. This is attributable to possible modulation of immune responses to CMV reactivation in a population previously exposed to CMV infection.


2020 ◽  
Author(s):  
Doreen Mhandire ◽  
Kudakwashe Mhandire ◽  
Mulalo Magadze ◽  
Ambroise Wonkam ◽  
Andre P Kengne ◽  
...  

Abstract Background: Maternal cytomegalovirus (CMV) infection and/or reactivation in pregnancy is associated with a myriad of adverse infant outcomes. However, the role of host genetic polymorphisms in modulating maternal CMV status is inconclusive. This study investigated the possible association of single nucleotide polymorphisms in toll like receptor (TLR) and cytokine genes with maternal plasma CMV DNA status in black Zimbabweans. Methods: In a cross-sectional study, 110 women in late gestation who included 36 CMV infected cases and 74 CMV uninfected, age and HIV status matched controls were enrolled. Twenty single nucleotide polymorphisms in 10 genes which code for proteins involved in immunity against CMV were genotyped using Iplex GOLD SNP genotyping protocol on the Agena MassARRAY® system. Statistical analyses were performed using Stata SE and the ‘Genetics’ and ‘SNPassoc’ packages of the statistical package R. Results: The TLR7 rs179008A>T (p<0.001) polymorphism was associated while the TLR9 rs352139T>C (p=0.049) polymorphism was on the borderline for association with CMV positive (CMV+) status. In contrast, the interleukin ( IL)-6 rs10499563T>C (p<0.001) and TLR2 rs1816702C>T (p=0.001) polymorphisms were associated with CMV negative (CMV-) status. Furthermore, allele frequencies of SNPs in TLR2, TLR4, TLR9, TLR7 , IL - 6 , IL-10 , IL-28B , IL-1A and interferon AR1 ( IFNAR1 ) genes are being reported here for the first time in a Zimbabwean population. The allele frequencies in the Zimbabwean population re generally comparable to other African populations but different when compared to European and Asian populations. Conclusions: Toll like receptor and interleukin genetic polymorphisms influence CMV status in late gestation among black Zimbabweans. This is attributable to possible modulation of immune responses to CMV reactivation in a population previously exposed to CMV infection.


2020 ◽  
Author(s):  
Doreen Mhandire ◽  
Kudakwashe Mhandire ◽  
Mulalo Magadze ◽  
Ambroise Wonkam ◽  
Andre P Kengne ◽  
...  

Abstract Background: Maternal cytomegalovirus (CMV) infection and/or reactivation in pregnancy is associated with a myriad of adverse infant outcomes. However, the role of host genetic polymorphisms in modulating maternal CMV status is inconclusive. This study investigated the possible association of single nucleotide polymorphisms in toll like receptor (TLR) and cytokine genes with maternal plasma CMV DNA status in black Zimbabweans.Methods: In a cross-sectional study, 110 women in late gestation who included 36 CMV infected cases and 74 CMV uninfected, age and HIV status matched controls were enrolled. Twenty single nucleotide polymorphisms (SNPs) in 10 genes which code for proteins involved in immunity against CMV were genotyped using Iplex GOLD SNP genotyping protocol on the Agena MassARRAY® system. Statistical analyses were performed using Stata SE and the ‘Genetics’ and ‘SNPassoc’ packages of the statistical package R.Results: The TLR7 rs179008A>T (p<0.001) polymorphism was associated while the TLR9 rs352139T>C (p=0.049) polymorphism was on the borderline for association with CMV positive (CMV+) status. In contrast, the interleukin (IL)-6 rs10499563T>C and (p<0.001) TLR2 rs1816702C>T (p=0.001) polymorphisms were associated with CMV negative (CMV-) status. Furthermore, allele frequencies of SNPs in TLR2, TLR4, TLR9, TLR7, IL-6, IL-10, IL-28B, IL-1A and interferon AR1 (IFNAR1) genes are being reported here for the first time in a Zimbabwean population. The allele frequencies in the Zimbabwean population re generally comparable to other African populations but different when compared to European and Asian populations.Conclusions: Toll like receptor and interleukin genetic polymorphisms influence CMV status in late gestation among black Zimbabweans. This is attributable to possible modulation of immune responses to CMV reactivation in a population previously exposed to CMV infection.


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