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Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort

Golam M Khandaker, Verena Zuber, Jessica MB Rees, Livia Carvalho, Amy M Mason, Christopher N Foley, Apostolos Gkatzionis, Peter B Jones, Stephen Burgess
doi: https://doi.org/10.1101/533828
Golam M Khandaker
1Department of Psychiatry, University of Cambridge, Cambridge, UK
2Cambridgeshire and Peterborough NHS Foundation Trust, Cambridge, UK
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Verena Zuber
3MRC Biostatistics Unit, University of Cambridge, Cambridge, UK
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Jessica MB Rees
4Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK
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Livia Carvalho
5Department of Clinical Pharmacology, Queen Mary University of London, London, UK
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Amy M Mason
4Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK
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Christopher N Foley
3MRC Biostatistics Unit, University of Cambridge, Cambridge, UK
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Apostolos Gkatzionis
3MRC Biostatistics Unit, University of Cambridge, Cambridge, UK
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Peter B Jones
1Department of Psychiatry, University of Cambridge, Cambridge, UK
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Stephen Burgess
3MRC Biostatistics Unit, University of Cambridge, Cambridge, UK
4Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK
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ABSTRACT

While comorbidity between coronary heart disease (CHD) and depression is evident, it is unclear whether the two diseases have shared underlying mechanisms. We performed a range of analyses in 367,703 unrelated middle-aged participants of European ancestry from UK Biobank, a population based cohort study, to assess whether comorbidity is primarily due to genetic or environmental factors, and to test whether cardiovascular risk factors and CHD are likely to be causally related to depression using Mendelian randomization. We showed family history of heart disease was associated with a 20% increase in depression risk (95% confidence interval [CI] 16% to 24%, p<0.0001), but a genetic risk score that is strongly associated with CHD risk was not associated with depression. An increase of one standard deviation in the CH D genetic risk score was associated with 71% higher CHD risk, but 1% higher depression risk (95% CI 0% to 3%; p=0.11). Mendelian randomization analyses suggested that triglycerides, interleukin-6 (IL-6), and C-reactive protein (CRP) are likely causal risk factors for depression. The odds ratio for depression per standard deviation increase in genetically-predicted triglycerides was 1.18 (95% CI 1.09 to 1.27; p=2×10-5); per unit increase in genetically-predicted log-transformed I L-6 was 0.74 (95% CI 0.62 to 0.89; p=0.0012); and per unit increase in genetically-predicted log-transformed CRP was 1.18 (95% CI 1.07 to 1.29; p=0.0009). Our analyses suggest that comorbidity between depression and CHD arises largely from shared environmental factors. I L-6, CRP and triglycerides, are likely to be causally linked with depression, so could be targets for treatment and prevention of depression.

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Posted January 29, 2019.
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Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort
Golam M Khandaker, Verena Zuber, Jessica MB Rees, Livia Carvalho, Amy M Mason, Christopher N Foley, Apostolos Gkatzionis, Peter B Jones, Stephen Burgess
bioRxiv 533828; doi: https://doi.org/10.1101/533828
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Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort
Golam M Khandaker, Verena Zuber, Jessica MB Rees, Livia Carvalho, Amy M Mason, Christopher N Foley, Apostolos Gkatzionis, Peter B Jones, Stephen Burgess
bioRxiv 533828; doi: https://doi.org/10.1101/533828

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