scholarly journals Shared Genetic Factors in the Co-Occurrence of Depression and Fatigue

2016 ◽  
Vol 19 (6) ◽  
pp. 610-618 ◽  
Author(s):  
Elizabeth C. Corfield ◽  
Nicholas G. Martin ◽  
Dale R. Nyholt
Keyword(s):  
Genetic Relationship ◽  
Genetic Factors ◽  
Control Method ◽  
Prevalence Ratio ◽  
Additive Genetic Correlation ◽  
Relative Risks ◽  
Genetic Components ◽  
Increased Risk ◽  
The Relationship ◽  
Shared Genetic

Depression and fatigue have previously been suggested to share an underlying genetic contribution. The present study aims to investigate and characterize the familiality and genetic relationship between depression and fatigue. The familiality of depression and fatigue was assessed by calculating relative risks, measured by the prevalence ratio, within 643 monozygotic (MZ) and 577 dizygotic (DZ) twin pairs. Bivariate twin modeling was utilized to assess the magnitude of shared heritability between depression and fatigue. Finally, the relationship between depression and fatigue was investigated using the co-twin control method, to determine whether the association is explained by causal or non-causal models. We observed an increased risk of fatigue in co-twins of probands with depression and increased risk of depression in co-twins of probands with fatigue. Higher risks were observed in MZ compared to DZ twin pairs, and bivariate heritability analyses indicated significant genetic components for depression and fatigue, with heritability estimates of 48% and 41%, respectively. Importantly, a significant additive genetic correlation of 0.71 [95% CI = 0.51–0.92) and bivariate heritability of 21% [95% CI = 10–35%] was observed between depression and fatigue. Furthermore, results from the co-twin control method indicate a non-causal genetic relationship that likely explains the association between depression and fatigue. Notably, the contribution of shared genetic factors remained significant, independent of the overlapping symptoms, indicating that the relationship between co-occurring depression and fatigue is primarily due to shared genetic factors rather than overlapping symptomatology.

scholarly journals Tobacco and type 2 diabetes: is the association explained by genetic factors?

2019 ◽  
Vol 48 (3) ◽  
pp. 926-933
Author(s):  
Sofia Carlsson ◽  
Ralf Kuja-Halkola ◽  
Cecilia Magnusson ◽  
Ylva Trolle Lagerros ◽  
Tomas Andersson
Keyword(s):  
Type 2 Diabetes ◽  
Structural Equation ◽  
Genetic Factors ◽  
Structural Equation Models ◽  
Genetic Correlations ◽  
Patient Registries ◽  
Genetic Components ◽  
Increased Risk ◽  
Shared Genetic

Abstract Background Smoking and use of Swedish smokeless tobacco (snus) are associated with increased risk of type 2 diabetes (T2D). Our aim was to estimate the unique and shared genetic components of these traits and to what extent the association is explained by shared genetic factors. Methods We used twins of the Swedish Twin Registry who responded to a questionnaire between 1998 and 2006 (n = 40 247) and were followed until 2015 in the National Prescription and Patient Registries. We estimated hazard ratios (HRs) and odds ratios (ORs) for the association between smoking/snus use and T2D (n = 2130) and used structural equation models to estimate genetic and environmental variance components and genetic correlations. Results Current smokers [HR 1.69, 95% confidence interval (CI), 1.49–1.92] and snus users (HR 1.19, 95% CI 1.01–1.41) had an increased risk of T2D. In within-pair analyses of monozygotic twins, corresponding ORs were 1.36, 95% CI 0.75–2.46 (smoking) and 1.54, 95% CI 0.80–2.99 (snus). Heritability was 43% (95% CI 36–51) for ever smoking, 58% (95% CI 44– 70) for ever snus use and 66% (95% CI 59–72) for T2D. The genetic correlation with T2D was 18% (95% CI 1–35) for smoking and –6% (95% CI –24 to 4) for snus use, indicating that only a small fraction of the genetic influence is shared. Conclusions We could confirm that consumers of snus and cigarettes are at increased risk of T2D. Both snus use and smoking have strong genetic components, which appears to be attributable primarily to genes that are distinct from those promoting T2D.

scholarly journals Risk of psychiatric disorders among the surviving twins after a co-twin loss

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Huan Song ◽  
Henrik Larsson ◽  
Fang Fang ◽  
Catarina Almqvist ◽  
Nancy L Pedersen ◽  
...  
Keyword(s):  
Psychiatric Disorders ◽  
Early Life ◽  
Genetic Factors ◽  
Genetic Relatedness ◽  
Life Experiences ◽  
Stressful Event ◽  
Relative Risks ◽  
Dizygotic Twins ◽  
Increased Risk ◽  
Age And Sex

Losing a co-twin by death is a severely stressful event yet with unknown impact on the surviving twin’s risk of psychiatric disorders. We identified all Swedish-born twins who lost a co-twin by death between 1973 and 2013 (n = 4,528), their 4939 non-twin full siblings, together with 22,640 age- and sex-matched non-bereaved twins. Compared to the non-bereaved twins, exposed twins were at increased risk of receiving a first diagnosis of psychiatric disorders (hazard ratio = 1.65, 95% confidence interval1.48–1.83), particularly during the first month after loss. Similarly, compared to non-twin full siblings, the relative risks were significantly increased after loss of monozygotic co-twin (2.45-fold), and loss of a dizygotic co-twin (1.29-fold), with higher HR observed with greater age gaps between twins and non-twin siblings. As dizygotic twins share equal genetic relatedness to the deceased twin as their full siblings, this pattern suggests that beyond the contribution of genetic factors, shared early life experiences and attachment contribute to the risk of psychiatric disorders among surviving twins after co-twin loss.

scholarly journals Prediction of primary venous thromboembolism based on clinical and genetic factors within the U.K. Biobank

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
David A. Kolin ◽  
Scott Kulm ◽  
Olivier Elemento
Keyword(s):  
Risk Factors ◽  
Venous Thromboembolism ◽  
Risk Score ◽  
Genetic Risk ◽  
Genetic Factors ◽  
External Validation ◽  
Predictive Score ◽  
Polygenic Risk Score ◽  
Genetic Components ◽  
Increased Risk

AbstractBoth clinical and genetic factors drive the risk of venous thromboembolism. However, whether clinically recorded risk factors and genetic variants can be combined into a clinically applicable predictive score remains unknown. Using Cox proportional-hazard models, we analyzed the association of risk factors with the likelihood of venous thromboembolism in U.K. Biobank, a large prospective cohort. We then created a polygenic risk score of 36 single nucleotide polymorphisms and a clinical score determined by age, sex, body mass index, previous cancer diagnosis, smoking status, and fracture in the last 5 years. Participants were at significantly increased risk of venous thromboembolism if they were at high clinical risk (subhazard ratio, 4.37 [95% CI, 3.85–4.97]) or high genetic risk (subhazard ratio, 3.02 [95% CI, 2.63–3.47]) relative to participants at low clinical or genetic risk, respectively. The combined model, consisting of clinical and genetic components, was significantly better than either the clinical or the genetic model alone (P < 0.001). Participants at high risk in the combined score had nearly an eightfold increased risk of venous thromboembolism relative to participants at low risk (subhazard ratio, 7.51 [95% CI, 6.28–8.98]). This risk score can be used to guide decisions regarding venous thromboembolism prophylaxis, although external validation is needed.

scholarly journals The relationship between anxiety, health, and potential stressors among adults in the United States during the COVID-19 pandemic

2020 ◽  
Author(s):  
Angela M Parcesepe ◽  
McKaylee Robertson ◽  
Amanda Berry ◽  
Andrew Maroko ◽  
Rebecca Zimba ◽  
...  
Keyword(s):  
United States ◽  
Cohort Study ◽  
Prevalence Ratio ◽  
The United States ◽  
Anxiety Symptoms ◽  
Poisson Models ◽  
Increased Risk ◽  
The Relationship ◽  
Severe Anxiety ◽  
The U.S

ABSTRACTObjectiveTo estimate the prevalence of anxiety symptoms and the association between moderate or severe anxiety symptoms and health and potential stressors among adults in the U.S. during the COVID-19 pandemicMethodsThis analysis includes data from 5,250 adults in the Communities, Households and SARS/CoV-2 Epidemiology (CHASING) COVID Cohort Study surveyed in April 2020. Poisson models were used to estimate the association between moderate or severe anxiety symptoms and health and potential stressors among U.S. adults during the COVID-19 pandemic.ResultsGreater than one-third (35%) of participants reported moderate or severe anxiety symptoms. Having lost income due to COVID-19 (adjusted prevalence ratio [aPR] 1.27 (95% CI 1.16, 1.30), having recent COVID-like symptoms (aPR 1.17 (95% CI 1.05, 1,31), and having been previously diagnosed with depression (aPR 1.49, (95% CI 1.35, 1.64) were positively associated with anxiety symptoms.ConclusionsAnxiety symptoms were common among adults in the U.S. during the COVID-19 pandemic. Strategies to screen and treat individuals at increased risk of anxiety, such as individuals experiencing financial hardship and individuals with prior diagnoses of depression, should be developed and implemented.

scholarly journals Shared genetic factors do not account for the observed co-occurrence of depression and autoimmune diseases in the UK Biobank

2020 ◽  
Author(s):  
Kylie P Glanville ◽  
Jonathan R I Coleman ◽  
Paul F O’Reilly ◽  
James Galloway ◽  
Cathryn M Lewis
Keyword(s):  
Autoimmune Diseases ◽  
Genetic Factors ◽  
Disease Status ◽  
Epidemiological Studies ◽  
Polygenic Risk Score ◽  
Uk Biobank ◽  
Increased Risk ◽  
Case Status ◽  
The Uk ◽  
Shared Genetic

AbstractBackgroundEpidemiological studies have shown increased comorbidity between depression and autoimmune diseases. The mechanisms driving the comorbidity are poorly understood, and a highly powered investigation is needed to understand the relative importance of shared genetic influences. We investigated the evidence for pleiotropy from shared genetic risk alleles between these traits in the UK Biobank (UKB).MethodsWe defined autoimmune and depression cases using information from hospital episode statistics, self-reported conditions and medications, and mental health questionnaires. Pairwise comparisons of depression prevalence between autoimmune cases and controls, and vice-versa, were performed. Cross-trait polygenic risk score (PRS) analyses were performed to test for pleiotropy, i.e. testing whether PRS for depression could predict autoimmune disease status, and vice-versa.ResultsWe identified 28k cases of autoimmune diseases (pooling across 14 traits), and 65k cases of depression. The prevalence of depression was significantly higher in autoimmune cases compared to controls, and vice-versa. PRS for myasthenia gravis and psoriasis were significantly associated with depression case-status (p < 5.2×10−5, R2 <= 0.04%). PRS for depression were significantly associated with case-status for coeliac disease, inflammatory bowel disease, psoriasis, psoriatic arthritis, rheumatoid arthritis and type 1 diabetes (p < 5.8×10−5, R2 range 0.06% to 0.27%).ConclusionsConsistent with the literature, depression was more common in individuals with autoimmune diseases compared to controls, and vice-versa, in the UKB. PRS showed some evidence for involvement of shared genetic factors, but the modest R2 values suggest that shared genetic architecture accounts for only a small proportion of the increased risk across traits.

scholarly journals Influence of Rapid Urbanization on Thyroid Autoimmune Disease in China

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Yingchao Chen ◽  
Bing Han ◽  
Jie Yu ◽  
Yi Chen ◽  
Jing Cheng ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Genetic Factors ◽  
Autoimmune Thyroid Diseases ◽  
Rapid Urbanization ◽  
Autoimmune Thyroid ◽  
Locus Model ◽  
Thyroid Autoimmune Disease ◽  
Increased Risk ◽  
The World ◽  
The Relationship

Background. The prevalence of autoimmune thyroid diseases (AITDs), especially Hashimoto’s thyroiditis (HT), has increased dramatically in China. Moreover, China is experiencing the largest scale of urbanization in the world. We intended to explore the relationship between rapid urbanization and HT. Methods. A total of 2946 subjects in Zhejiang Shangyu (SY) (n = 1546) and Jiangsu Nanjing (NJ) (n = 1400) were enrolled in this study. Serum TPOAb, TGAb, and thyrotropin (TSH) were measured, and ultrasonography of the thyroid was performed in all subjects. DNA was extracted from all subjects, and four SNPs were selected for genotyping. Generalized multifactor dimensionality reduction (GMDR) was used to screen the best interaction between genetic factors and environment factors. Results. TPOAb and TGAb concentrations were higher in NJ than in SY (34.60 vs. 14.00 IU/ml and 21.05 vs. 7.50 IU/ml). People in NJ also had higher TPOAb and TGAb positivity rates than those in SY (7.8% vs. 12.7% and 8.7% vs. 16.3%). Logistic regression analysis indicated that rapid urbanization was an independent risk factor for TPOAb (OR = 1.473) and TGAb (OR = 1.689). Genotype TT in rs11675434 was associated with an increased risk of TPOAb positivity both in SY (OR = 2.955) and in NJ (OR = 1.819). GMDR analysis showed a two-locus model (SNP2 × urbanization) and a three-locus model (SNP2 × SNP3 × urbanization), which had testing accuracies of 56.88% and 57.25%, respectively ( P values were 0.001 and 0.001). Conclusion. Rapid urbanization influences the incidence of TPOAb and TGAb positivity. We should pay more attention to thyroid autoimmune disease in areas of China experiencing rapid urbanization.

Genetic contribution to the relationship between personality and depressive symptoms among older women

2009 ◽  
Vol 40 (8) ◽  
pp. 1357-1366 ◽  
Author(s):  
I. Pakkala ◽  
S. Read ◽  
J. Kaprio ◽  
M. Koskenvuo ◽  
M. Kauppinen ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Old Age ◽  
Genetic Relationship ◽  
Depressive Disorders ◽  
Middle Age ◽  
Depression Scale ◽  
Epidemiologic Studies ◽  
Eysenck Personality Inventory ◽  
The Relationship ◽  
Shared Genetic

BackgroundPrior studies suggest that certain types of personality are at higher risk for developing depressive disorders. This study examined the relationship between old age depressive symptoms and two middle-age personality dimensions, neuroticism and extraversion.MethodThe present study is part of the Finnish Twin Study on Aging, where altogether 409 female twins who had completed the Eysenck Personality Inventory at the age of 38–51 years were studied for depressive symptoms 28 years later using Center for the Epidemiologic Studies Depression Scale. Logistic regression analysis suitable for dependent data and univariate and Cholesky models for decomposing the genetic and environmental factor were used.ResultsMiddle age extraversion protected from later depressive symptoms while neuroticism increased the risk. Twin modeling indicated that the association between neuroticism and depressive symptoms resulted from shared genetic risk factors common to both traits. However, a substantial proportion of the genetic vulnerability was specific to old age depressive symptoms and was not shared with neuroticism. Middle age extraversion had no genetic relationship with old age depressive symptoms.ConclusionsThe relationship between middle age neuroticism and old age depressive symptoms is strong but only partly the result of genetic factors that predispose to both neuroticism and depressive symptoms. Extraversion, by contrast, has no genetic relationship with depressive symptoms experienced in old age.

Abdominal obesity and risk of CVD: a dose–response meta-analysis of thirty-one prospective studies

2021 ◽  
pp. 1-11
Author(s):  
Ran Xue ◽  
Qianwen Li ◽  
Yaping Geng ◽  
Hao Wang ◽  
Fudi Wang ◽  
...  
Keyword(s):  
Abdominal Obesity ◽  
Dose Response ◽  
Prospective Studies ◽  
Meta Analysis ◽  
Response Analysis ◽  
Random Effects Models ◽  
Relative Risks ◽  
Increased Risk ◽  
Unit Increase ◽  
The Relationship

Abstract This meta-analysis aimed to study the relationship between abdominal obesity and the risk of CVD by waist circumference (WC), waist:hip ratio (WHR) and waist:height ratio (WHtR). We systematically searched PubMed, Embase and Web of Science. Prospective studies that estimated cardiovascular events by WC, WHR and WHtR were included in this study. Pooled relative risks with 95 % CI were calculated using random effects models. A total of thirty-one studies were included in the meta-analysis, including 669 560 participants and 25 214 cases. Compared the highest with the lowest category of WC, WHR and WHtR, the summary risk ratios were 1·43 (95 % CI, 1·30, 1·56, P < 0·001), 1·43 (95 % CI, 1·33, 1·54, P < 0·001) and 1·57 (95 % CI, 1·37, 1·79, P < 0·001), respectively. The linear dose–response analysis revealed that the risk of CVD increased by 3·4 % for each 10 cm increase of WC, and by 3·5 and 6·0 % for each 0·1 unit increase of WHR and WHtR in women, respectively. In men, the risk of CVD increased by 4·0 % for each 10 cm increase of WC, and by 4·0 and 8·6 % for each 0·1 unit increase of WHR and WHtR, respectively. Collectively, abdominal obesity is associated with an increased risk of CVD. WC, WHR and WHtR are good indicators for the prediction of CVD.

Clustering of metabolic comorbidity in schizophrenia: a genetic contribution?

2005 ◽  
Vol 19 (6_suppl) ◽  
pp. 47-55 ◽  
Author(s):  
Stephen C. L. Gough ◽  
Michael C. O’Donovan
Keyword(s):  
Type 2 Diabetes ◽  
Genetic Basis ◽  
Genetic Factors ◽  
Susceptibility Loci ◽  
Environmental Determinants ◽  
Pharmacological Interventions ◽  
Increased Risk ◽  
Develop Type ◽  
Shared Genetic

People with schizophrenia are more likely to develop type 2 diabetes than the general population. Although an increased risk of diabetes has been attributed to environmental determinants such as diet, lifestyle and antipsychotic drugs, the association between these two disorders was noticed well before the advent of current lifestyles and pharmacological interventions, raising the possibility of a shared genetic basis. Schizophrenia and type 2 diabetes are common diseases with a complex mode of inheritance which includes both genetic factors and environmental determinants. As susceptibility genes for both type 2 diabetes and schizophrenia are beginning to be identified there is increasing interest in the possibility of shared susceptibility loci between the two conditions. This article reviews the genetic basis to schizophrenia and type 2 diabetes and discusses the potential for shared loci between both conditions.

scholarly journals Short night sleeping is associated with higher risk of diabetes in older adults

2018 ◽  
Vol 5 (6) ◽  
pp. 2164 ◽  
Author(s):  
Mohammed Atiah Ahmed Bakri ◽  
Mohammad Abdullah Tarish Alharbi ◽  
Abdulaziz Ahmed Mesfir Alzaher ◽  
Alzhrani Mordi A. Alzhrani ◽  
Wafaa Ahmed Alkaf ◽  
...  
Keyword(s):  
Sleep Duration ◽  
Type Ii Diabetes ◽  
Meta Analysis ◽  
Diabetes Type ◽  
Cochrane Central Register ◽  
Type Ii ◽  
Relative Risks ◽  
Increased Risk ◽  
Incident Cases ◽  
The Relationship

Background: It remains unclear how many hours of sleep are associated with the lowest risk of diabetes type II. This meta-analysis was completed to evaluate the dose-response relationship between sleep duration and risk of diabetes type II.Methods: We conducted this meta-analysis using a comprehensive search of Medline, Pubmed, EMBASE, Cochrane database of systematic reviews, and Cochrane central register of controlled trials till 01 May 2017 for prospective observational studies that assessed the relationship of sleep duration and risk of type II diabetes. Both semiparametric and parametric methods were used.Results: Ten articles with 7 reports were eligible for inclusion in the meta-analysis. A total of 16,123 incident cases of type II diabetes were ascertained among 402,397 participants with follow-up periods ranging from 3 to 17 years. The relationship was observed between sleep duration and risk of type II diabetes, with the lowest risk observed at a sleep duration category of 7–8 h per day. Compared with 7-h sleep duration per day, the pooled relative risks for type II diabetes were 1.11 (95% CI 1.06–1.17) for each 1-h shorter sleep duration among individuals who slept <7 h per day and 1.13 (1.05–1.31) for each 1-h increment of sleep duration among individuals with longer sleep duration.Conclusions: Both short and long sleep duration are linked with a considerably increased risk of type II diabetes, underscoring the significance of appropriate sleep duration in the delay or prevention of type II diabetes.

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