scholarly journals Genetic correlations between pain phenotypes and depression and neuroticism

2019 ◽  
Vol 28 (3) ◽  
pp. 358-366 ◽  
Author(s):  
Weihua Meng ◽  
Mark J. Adams ◽  
Parminder Reel ◽  
Aravind Rajendrakumar ◽  
Yu Huang ◽  
...  

Abstract Correlations between pain phenotypes and psychiatric traits such as depression and the personality trait of neuroticism are not fully understood. In this study, we estimated the genetic correlations of eight pain phenotypes (defined by the UK Biobank, n = 151,922–226,683) with depressive symptoms, major depressive disorders and neuroticism using the the cross-trait linkage disequilibrium score regression (LDSC) method integrated in the LD Hub. We also used the LDSC software to calculate the genetic correlations among pain phenotypes. All pain phenotypes, except hip pain and knee pain, had significant and positive genetic correlations with depressive symptoms, major depressive disorders and neuroticism. All pain phenotypes were heritable, with pain all over the body showing the highest heritability (h2 = 0.31, standard error = 0.072). Many pain phenotypes had positive and significant genetic correlations with each other indicating shared genetic mechanisms. Our results suggest that pain, neuroticism and depression share partially overlapping genetic risk factors.

2018 ◽  
Author(s):  
Weihua Meng ◽  
Mark J Adams ◽  
Ian J Deary ◽  
Colin NA Palmer ◽  
Andrew M McIntosh ◽  
...  

AbstractCorrelations between pain phenotypes and psychiatric traits such as depression and the personality trait of neuroticism are not fully understood. The purpose of this study was to identify whether eight pain phenotypes, depressive symptoms, major depressive disorders, and neuroticism are correlated for genetic reasons. Eight pain phenotypes were defined by a specific pain-related question in the UK Biobank questionnaire. First we generated genome-wide association summary statistics on each pain phenotype, and estimated the common SNP-based heritability of each trait using GCTA. We then estimated the genetic correlation of each pain phenotype with depressive symptoms, major depressive disorders and neuroticism using the the cross-trait linkage disequilibrium score regression (LDSC) method integrated in the LD Hub. Third, we used the LDSC software to calculate genetic correlations among pain phenotypes. All pain phenotypes were heritable, with pain all over the body showing the highest heritability (h2=0.31, standard error=0.072). All pain phenotypes, except hip pain and knee pain, had significant and positive genetic correlations with depressive symptoms, major depressive disorders and neuroticism. The largest genetic correlations occurred between neuroticism and stomach or abdominal pain (rg=0.70, P=2.4 x 10−9). In contrast, hip pain and knee pain showed weaker evidence of shared genetic architecture with these negative emotional traits. In addition, many pain phenotypes had positive and significant genetic correlations with each other indicating shared genetic mechanisms. Pain at a variety of body sites is heritable and genetically correlated with depression and neuroticism. This suggests that pain, neuroticism and depression share partially overlapping genetic risk factors.


BMJ Open ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. e040061
Author(s):  
Getinet Ayano ◽  
Asmare Belete ◽  
Bereket Duko ◽  
Light Tsegay ◽  
Berihun Assefa Dachew

ObjectivesTo assess the global prevalence estimates of depressive symptoms, dysthymia and major depressive disorders (MDDs) among homeless people.DesignSystematic review and meta-analysis.Data sourcesDatabases including PubMed, Scopus and Web of Science were systematically searched up to February 2020 to identify relevant studies that have reported data on the prevalence of depressive symptoms, dysthymia and MDDs among homeless people.Eligibility criteriaOriginal epidemiological studies written in English that addressed the prevalence of depressive problems among homeless people.Data extraction and synthesisA random-effect meta-analysis was performed to pool the prevalence estimated from individual studies. Subgroup and sensitivity analyses were employed to compare the prevalence across the groups as well as to identify the source of heterogeneities. The Joanna Briggs Institute’s quality assessment checklist was used to measure the study quality. Cochran’s Q and the I2 test were used to assess heterogeneity between the studies.ResultsForty publications, including 17 215 participants, were included in the final analysis. This meta-analysis demonstrated considerably higher prevalence rates of depressive symptoms 46.72% (95% CI 37.77% to 55.90%), dysthymia 8.25% (95% CI 4.79% to 11.86%), as well as MDDs 26.24% (95% CI 21.02% to 32.22%) among homeless people. Our subgroup analysis showed that the prevalence of depressive symptoms was high among younger homeless people (<25 years of age), whereas the prevalence of MDD was high among older homeless people (>50 years of age) when compared with adults (25–50 years).ConclusionThis review showed that nearly half, one-fourth and one-tenth of homeless people are suffering from depressive symptoms, dysthymia and MDDs, respectively, which are notably higher than the reported prevalence rates in the general population. The findings suggest the need for appropriate mental health prevention and treatment strategies for this population group.


BJPsych Open ◽  
2021 ◽  
Vol 7 (2) ◽  
Author(s):  
Kylie P. Glanville ◽  
Jonathan R. I. Coleman ◽  
David M. Howard ◽  
Oliver Pain ◽  
Ken B. Hanscombe ◽  
...  

Background The UK Biobank contains data with varying degrees of reliability and completeness for assessing depression. A third of participants completed a Mental Health Questionnaire (MHQ) containing the gold-standard Composite International Diagnostic Interview (CIDI) criteria for assessing mental health disorders. Aims To investigate whether multiple observations of depression from sources other than the MHQ can enhance the validity of major depressive disorder (MDD). Method In participants who did not complete the MHQ, we calculated the number of other depression measures endorsed, for example from hospital episode statistics and interview data. We compared cases defined this way with CIDI-defined cases for several estimates: the variance explained by polygenic risk scores (PRS), area under the curve attributable to PRS, single nucleotide polymorphisms (SNPs)-based heritability and genetic correlations with summary statistics from the Psychiatric Genomics Consortium MDD genome-wide association study. Results The strength of the genetic contribution increased with the number of measures endorsed. For example, SNP-based heritability increased from 7% in participants who endorsed only one measure of depression, to 21% in those who endorsed four or five measures of depression. The strength of the genetic contribution to cases defined by at least two measures approximated that for CIDI-defined cases. Most genetic correlations between UK Biobank and the Psychiatric Genomics Consortium MDD study exceeded 0.7, but there was variability between pairwise comparisons. Conclusions Multiple measures of depression can serve as a reliable approximation for case status where the CIDI measure is not available, indicating sample size can be optimised using the entire suite of UK Biobank data.


1998 ◽  
Vol 55 (8) ◽  
pp. 694 ◽  
Author(s):  
Lewis L. Judd ◽  
Hagop S. Akiskal ◽  
Jack D. Maser ◽  
Pamela J. Zeller ◽  
Jean Endicott ◽  
...  

Author(s):  
Pravin Mali

Depressed mood, helplessness, worthlessness and hopelessness were the symptoms present in more than 95% of the subjects. 33 subjects displaying the symptoms of Vishada (Depression) within the inclusion criteria were included in the study. Subjects with suicidal tendencies, other psychiatric disorders, major depressive disorders, and pregnant women were excluded. A dose of 6 grams of Brahmi  Ghrita was given twice a day. The effect of the therapy was assessed using Hamilton’s Depression Rating Scale, and Self prepared. Rating Scale of Vishada, based on the scoring achieved by the subject before and after treatment. The result of the study can be summarized as follows - the overall effect of the therapy proves that after thirty days of treatment many symptoms of depression decrease in magnitude, with statistical significance. The drugs present in Brahmi  Ghrita are Srotoshodhaka  and medhya (purify the channels of the body and improves intellectual ability), Vatanulomaka ( corrects the direction of the flow of vata), Vatahara (reduce the level of Vata present in the body), and stimulant in nature. These properties inherently remove the avarana of Kapha and act on Vata. At this juncture, we can conclude that Brahmi  Ghrita has good results in managing Vishada (Depression), within thirty days of treatment.


2021 ◽  
pp. 1-10
Author(s):  
Anna E. Fürtjes ◽  
Jonathan R. I. Coleman ◽  
Jess Tyrrell ◽  
Cathryn M. Lewis ◽  
Saskia P. Hagenaars

Abstract Background People with bipolar disorder (BPD) are more likely to die prematurely, which is partly attributed to comorbid cardiometabolic traits. Previous studies report cardiometabolic abnormalities in BPD, but their shared aetiology remains poorly understood. This study examined the phenotypic associations and shared genetic aetiology between BPD and various cardiometabolic traits. Methods In a subset of the UK Biobank sample (N = 61 508) we investigated phenotypic associations between BPD (ncases = 4186) and cardiometabolic traits, represented by biomarkers, anthropometric traits and cardiometabolic diseases. To determine shared genetic aetiology in European ancestry, polygenic risk scores (PRS) and genetic correlations were calculated between BPD and cardiometabolic traits. Results Several traits were significantly associated with increased risk for BPD, namely low total cholesterol, low high-density lipoprotein cholesterol, high triglycerides, high glycated haemoglobin, low systolic blood pressure, high body mass index, high waist-to-hip ratio; and stroke, coronary artery disease and type 2 diabetes diagnosis. BPD was associated with higher polygenic risk for triglycerides, waist-to-hip ratio, coronary artery disease and type 2 diabetes. Shared genetic aetiology persisted for coronary artery disease, when correcting PRS associations for cardiometabolic base phenotypes. Associations were not replicated using genetic correlations. Conclusions This large study identified increased phenotypic cardiometabolic abnormalities in BPD participants. It is found that the comorbidity of coronary artery disease may be based on shared genetic aetiology. These results motivate hypothesis-driven research to consider individual cardiometabolic traits rather than a composite metabolic syndrome when attempting to disentangle driving mechanisms of cardiometabolic abnormalities in BPD.


2019 ◽  
Vol 3 (1) ◽  
pp. 01-13
Author(s):  
Huraira Hanif ◽  
Razia Iqbal ◽  
Sadia Sidra Aziz ◽  
Syeda Iman Fatima ◽  
Izzah Butt

The paper aims to review ECG and effects of Tricyclic Antidepressants (TCA) on ECG. ECG is the recording of the electrical conductivity of heart made by placing electrodes on the body. Antidepressants have lethal neurological and cardiovascular effects in depressive persons. TCA can cause abnormalities in the ECG pattern. It affects the conduction rate and slows the heart beat by blocking sodium channels that cause the elongation of QST complex which leads to abnormalities. QT is prolonged if > 440ms in men and > 460ms in women. Due to TCA, QT > 500ms that causes abnormalities. Brugada syndrome is also obtained by exposure to TCA. Doxepin slows down the conduction rate in patients with major depressive disorders. TCA causes symptomatic A-V blockage in patients with preexisting cardiovascular diseases. Desipramine and Immipramine cause sudden death in 6-9 years old children due to an overdose of these drugs. Antidepressants such as Agomelatine, Paroxetine, Serotonin Reuptake Inhibitors cause cardiac deformities in patients as well as pregnant women. Abnormality in ECG tells us about problems in the rhythmicity of heart. ECG can be used for the assessment of drugs that have electrophysiological effects.


Sign in / Sign up

Export Citation Format

Share Document