Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort
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 s...
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| Veröffentlicht in: | Molecular psychiatry 2020-07, Vol.25 (7), p.1477-1486 |
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| creator | Khandaker, Golam M. Zuber, Verena Rees, Jessica M. B. Carvalho, Livia Mason, Amy M. Foley, Christopher N. Gkatzionis, Apostolos Jones, Peter B. Burgess, Stephen |
| description | 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] 16–24%,
p
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| doi_str_mv | 10.1038/s41380-019-0395-3 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7303009</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A627034312</galeid><sourcerecordid>A627034312</sourcerecordid><originalsourceid>FETCH-LOGICAL-c565t-92aea77f6289075d5820ec98b9ddcc97fbe8f9aeb25e15f58ba65361edd40b7f3</originalsourceid><addsrcrecordid>eNp9kk1vFSEUhidGY2v1B7gxJK6nwgADuDBpGr9iExfaNWHgMEMzAyPMrem_l5tbW5uoYQHhPOc9H3mb5iXBpwRT-aYwQiVuMVEtpoq39FFzTJjoW86FfFzflKuWEcmOmmelXGG8D_KnzRHFUvaUsuPm5ttkMji0gJ1MDGUpaIDtJ0BENuUUTb5BE5i8IRcKmALIRIccrBlKCSm-RT5EF-JYkM9pQQbNJo-ALr-gESJkM6M1rbvZbBVuhyrgqvCU8va8eeLNXODF7X3SXH54__38U3vx9ePn87OL1vKeb63qDBghfN9JhQV3XHYYrJKDcs5aJfwA0isDQ8eBcM_lYHpOewLOMTwIT0-adwfddTcs4CzErXal1xyWOpxOJuiHkRgmPaZrLSimGKsq8PpWIKcfOyibvkq7HGvPuqv7FKzHHf0_RRgXvVLsnhrNDDpEn2pJu4Ri9VnfCUwZJV2lTv9C1eNgCTZF8KH-P0gghwSbUykZ_N14BOu9VfTBKrpaRe-tovcNv_pzL3cZv71Rge4AlBqKI-T7if6t-gvZWMqA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2414576994</pqid></control><display><type>article</type><title>Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Khandaker, Golam M. ; Zuber, Verena ; Rees, Jessica M. B. ; Carvalho, Livia ; Mason, Amy M. ; Foley, Christopher N. ; Gkatzionis, Apostolos ; Jones, Peter B. ; Burgess, Stephen</creator><creatorcontrib>Khandaker, Golam M. ; Zuber, Verena ; Rees, Jessica M. B. ; Carvalho, Livia ; Mason, Amy M. ; Foley, Christopher N. ; Gkatzionis, Apostolos ; Jones, Peter B. ; Burgess, Stephen</creatorcontrib><description>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] 16–24%,
p
< 0.0001), but a genetic risk score that is strongly associated with CHD risk was not associated with depression. An increase of 1 standard deviation in the CHD genetic risk score was associated with 71% higher CHD risk, but 1% higher depression risk (95% CI 0–3%;
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 1.09–1.27;
p
= 2 × 10
−5
); per unit increase in genetically-predicted log-transformed IL-6 was 1.35 (95% CI 1.12–1.62;
p
= 0.0012); and per unit increase in genetically-predicted log-transformed CRP was 1.18 (95% CI 1.07–1.29;
p
= 0.0009). Our analyses suggest that comorbidity between depression and CHD arises largely from shared environmental factors. IL-6, CRP and triglycerides are likely to be causally linked with depression, so could be targets for treatment and prevention of depression.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/s41380-019-0395-3</identifier><identifier>PMID: 30886334</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>38/43 ; 631/154/53/2421 ; 631/208 ; 692/53/2421 ; 692/699/476/1414 ; Adult ; Aged ; Analysis ; Behavioral Sciences ; Biological Psychology ; C-reactive protein ; C-Reactive Protein - analysis ; Cardiovascular disease ; Cardiovascular diseases ; Cohort Studies ; Comorbidity ; Coronary artery disease ; Coronary Disease - blood ; Coronary Disease - epidemiology ; Coronary Disease - genetics ; Coronary heart disease ; Depression - blood ; Depression - epidemiology ; Depression - genetics ; Depression, Mental ; Environmental factors ; Female ; Health risk assessment ; Heart diseases ; Humans ; Interleukin 6 ; Interleukin-6 - blood ; Interleukins ; Male ; Medical research ; Medicine ; Medicine & Public Health ; Medicine, Experimental ; Mendelian Randomization Analysis ; Mental depression ; Middle Aged ; Neurosciences ; Odds Ratio ; Pharmacotherapy ; Polymorphism, Single Nucleotide ; Population studies ; Psychiatry ; Risk Factors ; Standard deviation ; Triglycerides ; Triglycerides - blood ; United Kingdom - epidemiology</subject><ispartof>Molecular psychiatry, 2020-07, Vol.25 (7), p.1477-1486</ispartof><rights>The Author(s) 2019</rights><rights>COPYRIGHT 2020 Nature Publishing Group</rights><rights>The Author(s) 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-92aea77f6289075d5820ec98b9ddcc97fbe8f9aeb25e15f58ba65361edd40b7f3</citedby><cites>FETCH-LOGICAL-c565t-92aea77f6289075d5820ec98b9ddcc97fbe8f9aeb25e15f58ba65361edd40b7f3</cites><orcidid>0000-0002-8019-0777 ; 0000-0001-5365-8760 ; 0000-0001-8862-0148 ; 0000-0002-0387-880X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41380-019-0395-3$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41380-019-0395-3$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30886334$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Khandaker, Golam M.</creatorcontrib><creatorcontrib>Zuber, Verena</creatorcontrib><creatorcontrib>Rees, Jessica M. B.</creatorcontrib><creatorcontrib>Carvalho, Livia</creatorcontrib><creatorcontrib>Mason, Amy M.</creatorcontrib><creatorcontrib>Foley, Christopher N.</creatorcontrib><creatorcontrib>Gkatzionis, Apostolos</creatorcontrib><creatorcontrib>Jones, Peter B.</creatorcontrib><creatorcontrib>Burgess, Stephen</creatorcontrib><title>Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort</title><title>Molecular psychiatry</title><addtitle>Mol Psychiatry</addtitle><addtitle>Mol Psychiatry</addtitle><description>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] 16–24%,
p
< 0.0001), but a genetic risk score that is strongly associated with CHD risk was not associated with depression. An increase of 1 standard deviation in the CHD genetic risk score was associated with 71% higher CHD risk, but 1% higher depression risk (95% CI 0–3%;
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 1.09–1.27;
p
= 2 × 10
−5
); per unit increase in genetically-predicted log-transformed IL-6 was 1.35 (95% CI 1.12–1.62;
p
= 0.0012); and per unit increase in genetically-predicted log-transformed CRP was 1.18 (95% CI 1.07–1.29;
p
= 0.0009). Our analyses suggest that comorbidity between depression and CHD arises largely from shared environmental factors. IL-6, CRP and triglycerides are likely to be causally linked with depression, so could be targets for treatment and prevention of depression.</description><subject>38/43</subject><subject>631/154/53/2421</subject><subject>631/208</subject><subject>692/53/2421</subject><subject>692/699/476/1414</subject><subject>Adult</subject><subject>Aged</subject><subject>Analysis</subject><subject>Behavioral Sciences</subject><subject>Biological Psychology</subject><subject>C-reactive protein</subject><subject>C-Reactive Protein - analysis</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cohort Studies</subject><subject>Comorbidity</subject><subject>Coronary artery disease</subject><subject>Coronary Disease - blood</subject><subject>Coronary Disease - epidemiology</subject><subject>Coronary Disease - genetics</subject><subject>Coronary heart disease</subject><subject>Depression - blood</subject><subject>Depression - epidemiology</subject><subject>Depression - genetics</subject><subject>Depression, Mental</subject><subject>Environmental factors</subject><subject>Female</subject><subject>Health risk assessment</subject><subject>Heart diseases</subject><subject>Humans</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - blood</subject><subject>Interleukins</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Medicine, Experimental</subject><subject>Mendelian Randomization Analysis</subject><subject>Mental depression</subject><subject>Middle Aged</subject><subject>Neurosciences</subject><subject>Odds Ratio</subject><subject>Pharmacotherapy</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Population studies</subject><subject>Psychiatry</subject><subject>Risk Factors</subject><subject>Standard deviation</subject><subject>Triglycerides</subject><subject>Triglycerides - blood</subject><subject>United Kingdom - epidemiology</subject><issn>1359-4184</issn><issn>1476-5578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kk1vFSEUhidGY2v1B7gxJK6nwgADuDBpGr9iExfaNWHgMEMzAyPMrem_l5tbW5uoYQHhPOc9H3mb5iXBpwRT-aYwQiVuMVEtpoq39FFzTJjoW86FfFzflKuWEcmOmmelXGG8D_KnzRHFUvaUsuPm5ttkMji0gJ1MDGUpaIDtJ0BENuUUTb5BE5i8IRcKmALIRIccrBlKCSm-RT5EF-JYkM9pQQbNJo-ALr-gESJkM6M1rbvZbBVuhyrgqvCU8va8eeLNXODF7X3SXH54__38U3vx9ePn87OL1vKeb63qDBghfN9JhQV3XHYYrJKDcs5aJfwA0isDQ8eBcM_lYHpOewLOMTwIT0-adwfddTcs4CzErXal1xyWOpxOJuiHkRgmPaZrLSimGKsq8PpWIKcfOyibvkq7HGvPuqv7FKzHHf0_RRgXvVLsnhrNDDpEn2pJu4Ri9VnfCUwZJV2lTv9C1eNgCTZF8KH-P0gghwSbUykZ_N14BOu9VfTBKrpaRe-tovcNv_pzL3cZv71Rge4AlBqKI-T7if6t-gvZWMqA</recordid><startdate>20200701</startdate><enddate>20200701</enddate><creator>Khandaker, Golam M.</creator><creator>Zuber, Verena</creator><creator>Rees, Jessica M. 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B.</creatorcontrib><creatorcontrib>Carvalho, Livia</creatorcontrib><creatorcontrib>Mason, Amy M.</creatorcontrib><creatorcontrib>Foley, Christopher N.</creatorcontrib><creatorcontrib>Gkatzionis, Apostolos</creatorcontrib><creatorcontrib>Jones, Peter B.</creatorcontrib><creatorcontrib>Burgess, Stephen</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khandaker, Golam M.</au><au>Zuber, Verena</au><au>Rees, Jessica M. B.</au><au>Carvalho, Livia</au><au>Mason, Amy M.</au><au>Foley, Christopher N.</au><au>Gkatzionis, Apostolos</au><au>Jones, Peter B.</au><au>Burgess, Stephen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort</atitle><jtitle>Molecular psychiatry</jtitle><stitle>Mol Psychiatry</stitle><addtitle>Mol Psychiatry</addtitle><date>2020-07-01</date><risdate>2020</risdate><volume>25</volume><issue>7</issue><spage>1477</spage><epage>1486</epage><pages>1477-1486</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><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] 16–24%,
p
< 0.0001), but a genetic risk score that is strongly associated with CHD risk was not associated with depression. An increase of 1 standard deviation in the CHD genetic risk score was associated with 71% higher CHD risk, but 1% higher depression risk (95% CI 0–3%;
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 1.09–1.27;
p
= 2 × 10
−5
); per unit increase in genetically-predicted log-transformed IL-6 was 1.35 (95% CI 1.12–1.62;
p
= 0.0012); and per unit increase in genetically-predicted log-transformed CRP was 1.18 (95% CI 1.07–1.29;
p
= 0.0009). Our analyses suggest that comorbidity between depression and CHD arises largely from shared environmental factors. IL-6, CRP and triglycerides are likely to be causally linked with depression, so could be targets for treatment and prevention of depression.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30886334</pmid><doi>10.1038/s41380-019-0395-3</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-8019-0777</orcidid><orcidid>https://orcid.org/0000-0001-5365-8760</orcidid><orcidid>https://orcid.org/0000-0001-8862-0148</orcidid><orcidid>https://orcid.org/0000-0002-0387-880X</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular psychiatry, 2020-07, Vol.25 (7), p.1477-1486 |
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| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7303009 |
| source | MEDLINE; SpringerLink Journals |
| subjects | 38/43 631/154/53/2421 631/208 692/53/2421 692/699/476/1414 Adult Aged Analysis Behavioral Sciences Biological Psychology C-reactive protein C-Reactive Protein - analysis Cardiovascular disease Cardiovascular diseases Cohort Studies Comorbidity Coronary artery disease Coronary Disease - blood Coronary Disease - epidemiology Coronary Disease - genetics Coronary heart disease Depression - blood Depression - epidemiology Depression - genetics Depression, Mental Environmental factors Female Health risk assessment Heart diseases Humans Interleukin 6 Interleukin-6 - blood Interleukins Male Medical research Medicine Medicine & Public Health Medicine, Experimental Mendelian Randomization Analysis Mental depression Middle Aged Neurosciences Odds Ratio Pharmacotherapy Polymorphism, Single Nucleotide Population studies Psychiatry Risk Factors Standard deviation Triglycerides Triglycerides - blood United Kingdom - epidemiology |
| title | Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort |
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