Estrogen Receptor 1 Gene rs22346939 and rs9340799 Variants are associated with Major Depressive Disorder and its Clinical Features

2021 ◽  
Vol 18 ◽  
Author(s):  
Filiz Ozsoy ◽  
Ayse Feyda Nursal ◽  
Nevin Karakus ◽  
Meral Oran Demir ◽  
Serbulent Yigit

Objective: Major depressive disorder (MDD) is a major health problem worldwide. Estrogen interacts with the central nervous system and has been shown to affect anxiety and depressive behavior. Estrogen mediates its effects by connecting its receptors, estrogen receptors 1 and 2. The purpose of this case-control study was to clarify the association between MDD risk and estrogen receptor 1 (ESR1) gene variants. Methods: This study included 245 individuals (125 MDD patients and 120 healthy controls). Polymerase Chain Reaction (PCR) and Restriction Fragment Length Polymorphism (RFLP) technics were used for genotyping ESR1 XbaI (rs9340799) and PvuII (rs22346939) variants. Results: There were statistically significant differences between the groups in terms of genotype frequencies of the ESR1 PvuII (-397 T > C) variant (p = 0.049) but not for the XbaI (-351 A > G) variant (p > 0.05). However, a correlation was observed between MDD and ESR1 XbaI variant after male participants were excluded (p = 0.028). Also, the high pain score of MDD patients was associated with the ESR1 PvuII variant, especially in female patients (p = 0.021). According to the results of combined genotype analysis, AA-TC combined genotype was correlated with a decreased risk in patients with MDD compared to controls (p = 0.016), while the combined genotype of GG-CC was associated with increased risk in the patients with MDD compared to controls (p = 0.042). Conclusion: he two ESR1 variants were associated with MDD risk and its features in both individual and combined forms.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rona J. Strawbridge ◽  
Keira J. A. Johnston ◽  
Mark E. S. Bailey ◽  
Damiano Baldassarre ◽  
Breda Cullen ◽  
...  

AbstractUnderstanding why individuals with severe mental illness (Schizophrenia, Bipolar Disorder and Major Depressive Disorder) have increased risk of cardiometabolic disease (including obesity, type 2 diabetes and cardiovascular disease), and identifying those at highest risk of cardiometabolic disease are important priority areas for researchers. For individuals with European ancestry we explored whether genetic variation could identify sub-groups with different metabolic profiles. Loci associated with schizophrenia, bipolar disorder and major depressive disorder from previous genome-wide association studies and loci that were also implicated in cardiometabolic processes and diseases were selected. In the IMPROVE study (a high cardiovascular risk sample) and UK Biobank (general population sample) multidimensional scaling was applied to genetic variants implicated in both psychiatric and cardiometabolic disorders. Visual inspection of the resulting plots used to identify distinct clusters. Differences between these clusters were assessed using chi-squared and Kruskall-Wallis tests. In IMPROVE, genetic loci associated with both schizophrenia and cardiometabolic disease (but not bipolar disorder or major depressive disorder) identified three groups of individuals with distinct metabolic profiles. This grouping was replicated within UK Biobank, with somewhat less distinction between metabolic profiles. This work focused on individuals of European ancestry and is unlikely to apply to more genetically diverse populations. Overall, this study provides proof of concept that common biology underlying mental and physical illness may help to stratify subsets of individuals with different cardiometabolic profiles.


2018 ◽  
Vol 49 (2) ◽  
pp. 243-249 ◽  
Author(s):  
Bart N. Ford ◽  
Robert H. Yolken ◽  
Faith B. Dickerson ◽  
T. Kent Teague ◽  
Michael R. Irwin ◽  
...  

AbstractBackgroundDepression can impair the immunogenicity of vaccine administration in adults. Whereas many vaccinations are administered in childhood, it is not known whether adolescent or adult onset depression is associated with impairments in the maintenance of protection of childhood vaccines. This study tested the hypothesis that individuals with adolescent or adult onset mood disorders would display compromised immunity to measles, a target of childhood vaccination.MethodsIgG antibodies to measles were quantified using a solid phase immunoassay in volunteers with bipolar disorder (BD, n = 64, mean age of onset = 16.6 ± 5.6), currently depressed individuals with major depressive disorder (cMDD, n = 85, mean age of onset = 17.9 ± 7.0), remitted individuals with a history of MDD (rMDD, n = 82, mean age of onset = 19.2 ± 8.6), and non-depressed comparison controls (HC, n = 202), all born after the introduction of the measles vaccine in the USA in 1963.ResultsRelative to HC, both the cMDD group (p = 0.021, adjusted odds ratios (OR) = 0.47, confidence interval (CI) = 0.24–0.90), and the rMDD group (p = 0.038, adjusted OR = 0.50, CI = 0.26–0.97) were less likely to test seropositive for measles. Compared with unmedicated MDD participants, currently medicated MDD participants had a longer lifetime duration of illness and were less likely to test seropositive for measles.ConclusionsIndividuals with adolescent or adult onset MDD are less likely to test seropositive for measles. Because lower IgG titers are associated with increased risk of measles infection, MDD may increase the risk and severity of infection possibly because of impaired maintenance of vaccine-related protection from measles.


1999 ◽  
Vol 174 (2) ◽  
pp. 112-120 ◽  
Author(s):  
Hartwin S. Sadowski ◽  
Blanca Ugarte ◽  
Israel Kolvin ◽  
Carole E. Kaplan ◽  
Jacqueline Barnes

BackgroundThere is evidence that exposure to social and family disadvantages in childhood are a risk factor for adult depression.AimsTo explore the effects of multiple adversity in early childhood on adult depression, and the relative effects of the different adversities.MethodThis study utilises data from the Newcastle Thousand Family Study. Information on childhood disadvantages was collected when the participants were 5 years old, and information on mental health was gathered when they were 33 years old. Mental health data were scrutinised blind to the evidence of early disadvantage, and best-estimate diagnoses of major depressive disorder were made according to DSM–III–R criteria.ResultsMultiple family disadvantages in childhood substantially increase the risk of suffering a major depressive disorder in adulthood. Such disadvantages include family or marital relationship instability, a combination of poor mothering and poor physical care, and a combination of dependence on social welfare and overcrowding. For females major depression was linked in particular to the quality of parenting in early life.ConclusionsSocial and family (especially multiple family) disadvantages during childhood predispose individuals to an increased risk of major depression in adulthood.


2020 ◽  
Author(s):  
Rona J. Strawbridge ◽  
Keira J. A. Johnston ◽  
Mark E. S. Bailey ◽  
Damiano Baldasarre ◽  
Breda Cullen ◽  
...  

AbstractUnderstanding why individuals with severe mental illness (Schizophrenia, Bipolar Disorder and Major Depressive Disorder) have increased risk of cardiometabolic disease (including obesity, type 2 diabetes and cardiovascular disease), and identifying those at highest risk of cardiometabolic disease are important priority areas for researcher. We explored whether genetic variation could identify individuals with different metabolic profiles. Loci previously associated with schizophrenia, bipolar disorder and major depressive disorder were identified from literature and those overlapping loci genotyped on the Illumina CardioMetabo and Immuno chips (representing cardiometabolic processes and diseases) were selected. In the IMPROVE study (high cardiovascular risk) and UK Biobank (general population) multidimensional scaling was applied to genetic variants implicated in both mental and cardiometabolic illness. Visual inspection of the resulting plots used to identify distinct clusters. Differences between clusters were assessed using chi-squared and Kruskall-Wallis tests. In IMPROVE, genetic loci associated with both cardiometabolic disease and schizophrenia (but not bipolar or major depressive disorders) identified three groups of individuals with distinct metabolic profiles. The grouping was replicated in UK Biobank, albeit with less distinction between metabolic profiles. This study provides proof of concept that common biology underlying mental and physical illness can identify subsets of individuals with different cardiometabolic profiles.


2019 ◽  
Vol 2 (3) ◽  
pp. 20-28 ◽  
Author(s):  
Munn Sann Lye ◽  
Aishah-Farhana Shahbudin ◽  
Yin Yee Tey ◽  
Yin Sim Tor ◽  
King Hwa Ling ◽  
...  

Major depressive disorder (MDD) compromises the individual’s capacity for self-care and productivity. Single nucleotide polymorphisms (SNP) of a number of genes have been associated with MDD. The zinc transporter-3 protein, encoded by the ZnT3 (SLC30A3) gene, maintains zinc-glutamate homeostasis at the glutamatergic synapse, a disruption of which increases risk of MDD. We hypothesise that variation in SLC30A3 (rs11126936) SNP increases risk of MDD. We recruited 300 MDD cases and 300 controls, matched in the ratio of 1:1 by age, gender and ethnicity. PCR-restriction fragment length polymorphism analysis was used in DNA genotyping, validated by sequencing 10% of samples. Deviation from the Hardy-Weinberg equilibrium was tested using the chi-square test. Conditional logistic regression was used to estimate adjusted odds ratios, controlling for age, gender, ethnicity, occupation and family monthly income. Genotypes G/G and G/T showed two times greater odds of developing MDD compared to variant genotype T/T (OR=1.983, 95% CI=1.031-3.815; p=0.040 and OR=2.232, 95% CI=1.100-4.533; p=0.026 respectively). Carriers of genotypes G/G and G/T of the SNP rs11126936 in SLC30A3 are associated with increased risk of MDD.


2017 ◽  
Author(s):  
Nicholas Kavish ◽  
Eric J. Connolly ◽  
Brian B. Boutwell

AbstractResearch suggests victims of violent crime are more likely to suffer from major depressive disorder (MDD) compared to non-victims. Less research has utilized longitudinal data to evaluate the directionality of this relationship or examined the genetic and environmental contributions to this association across the life course. The current study evaluated 473 full-sibling pairs and 209 half-sibling pairs (N = 1,364) from the National Longitudinal Survey of Youth (Mage = 20.14, SD = 3.94). Cross-lagged models were used to examine the directionality of effects between violent victimization and MDD over time. Biometric liability models were used to examine genetic and environmental influences on single and chronic violent victimization and MDD. Violent victimization was associated with increases in MDD during late adolescence, but MDD was more associated with increased risk for violent victimization across young adulthood. Biometric analysis indicated that 20% and 30% of the association between MDD and single and chronic victimization, respectively, was accounted for by common genetic influences. Results from the current study suggest individuals who exhibit symptoms of MDD are at higher risk for chronic victimization rather than developing MDD as a result of victimization. Shared genetic liability accounted for between 20 to 30% of this longitudinal relationship.


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