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.

Highlights

  • Pain is a global public health priority

  • A Supplementary Table 1 presenting the age, sex, and body mass index (BMI) of participants contributing to the eight genomewide association study (GWAS) and of the non-responders is included

  • The narrow-sense single nucleotide polymorphisms (SNPs) heritabilities of each pain phenotype are presented in the Table 2

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Summary

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Pain is a global public health priority. In the Global Burden of Diseases Study 2017, low back and headache disorders were the leading cause of years lived with disability (YLDs) worldwide, with neck pain ranked among the top ten causes [1]. Both depression and neuroticism (a personality trait) are common comorbidities of pain [6, 7]. Many pain phenotypes have been shown to be associated with depression and neuroticism in epidemiological studies [9,10,11,12,13,14,15,16,17,18] This epidemiological coexistence could arise in part because of shared genetic factors [19, 20]. We used the same ‘no pain’ control population for all pain phenotypes in different body sites

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