Genetic variants affecting cross-sectional lung function in adults show little or no effect on longitudinal lung function decline
BackgroundGenome-wide association studies have identified numerous genetic regions that influence cross-sectional lung function. Longitudinal decline in lung function also includes a heritable component but the genetic determinants have yet to be defined.ObjectivesWe aimed to determine whether regio...
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Veröffentlicht in: | Thorax 2017-05, Vol.72 (5), p.400-408 |
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creator | John, Catherine Soler Artigas, María Hui, Jennie Nielsen, Sune Fallgaard Rafaels, Nicholas Paré, Peter D Hansel, Nadia N Shrine, Nick Kilty, Iain Malarstig, Anders Jelinsky, Scott A Vedel-Krogh, Signe Barnes, Kathleen Hall, Ian P Beilby, John Musk, Arthur W Nordestgaard, Børge G James, Alan Wain, Louise V Tobin, Martin D |
description | BackgroundGenome-wide association studies have identified numerous genetic regions that influence cross-sectional lung function. Longitudinal decline in lung function also includes a heritable component but the genetic determinants have yet to be defined.ObjectivesWe aimed to determine whether regions associated with cross-sectional lung function were also associated with longitudinal decline and to seek novel variants which influence decline.MethodsWe analysed genome-wide data from 4167 individuals from the Busselton Health Study cohort, who had undergone spirometry (12 695 observations across eight time points). A mixed model was fitted and weighted risk scores were calculated for the joint effect of 26 known regions on baseline and longitudinal changes in FEV1 and FEV1/FVC. Potential additional regions of interest were identified and followed up in two independent cohorts.ResultsThe 26 regions previously associated with cross-sectional lung function jointly showed a strong effect on baseline lung function (p=4.44×10−16 for FEV1/FVC) but no effect on longitudinal decline (p=0.160 for FEV1/FVC). This was replicated in an independent cohort. 39 additional regions of interest (48 variants) were identified; these associations were not replicated in two further cohorts.ConclusionsPreviously identified genetic variants jointly have a strong effect on cross-sectional lung function in adults but little or no effect on the rate of decline of lung function. It is possible that they influence COPD risk through lung development. Although no genetic variants have yet been associated with lung function decline at stringent genome-wide significance, longitudinal change in lung function is heritable suggesting that there is scope for future discoveries. |
doi_str_mv | 10.1136/thoraxjnl-2016-208448 |
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fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5520280</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1866297339</sourcerecordid><originalsourceid>FETCH-LOGICAL-b513t-ac971a59cf1177278e2ea90d83a7d7d9b8caebafc6c8f6b87644d52c4d9f6c983</originalsourceid><addsrcrecordid>eNqNkkuPFCEUhYnROO3oT9CQuHFTyqt4bEzMREeTSdzomlBAddOhYQRqRpf-c-nuseNjMxvIhe8cuHAAeI7Ra4wpf9M2uZjv2xQHgjDvg2RMPgArzLgcKFH8IVghxNDAqeBn4EmtW4SQxFg8BmdEYsEoQyvw89In34KFN6YEk1qFZp69bSGtoS251qHuq5xMhHHpi_OSDjUMCRq3xK6om3wLY2gtepgLTBn6gwfsVMxpHdriwv8GztsYkn8KHs0mVv_sbj4HXz-8_3Lxcbj6fPnp4t3VMI2YtsFYJbAZlZ17C4II6Yk3CjlJjXDCqUla4yczW27lzCcpOGNuJJY5NXOrJD0Hb4--18u088761IqJ-rqEnSk_dDZB_72Twkav840eR4KIRN3g1Z1Byd8WX5vehWp9jCb5vFSNpcJyRAKze6CcEyUoVR19-Q-6zUvpr1V1P3YUlPGRd2o8Uoc_KX4-3Rsjvc-DPuVB7_Ogj3nouhd_Nn1S_Q5AB9ARmHbbe3r-As0Ox34</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2025734656</pqid></control><display><type>article</type><title>Genetic variants affecting cross-sectional lung function in adults show little or no effect on longitudinal lung function decline</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>John, Catherine ; Soler Artigas, María ; Hui, Jennie ; Nielsen, Sune Fallgaard ; Rafaels, Nicholas ; Paré, Peter D ; Hansel, Nadia N ; Shrine, Nick ; Kilty, Iain ; Malarstig, Anders ; Jelinsky, Scott A ; Vedel-Krogh, Signe ; Barnes, Kathleen ; Hall, Ian P ; Beilby, John ; Musk, Arthur W ; Nordestgaard, Børge G ; James, Alan ; Wain, Louise V ; Tobin, Martin D</creator><creatorcontrib>John, Catherine ; Soler Artigas, María ; Hui, Jennie ; Nielsen, Sune Fallgaard ; Rafaels, Nicholas ; Paré, Peter D ; Hansel, Nadia N ; Shrine, Nick ; Kilty, Iain ; Malarstig, Anders ; Jelinsky, Scott A ; Vedel-Krogh, Signe ; Barnes, Kathleen ; Hall, Ian P ; Beilby, John ; Musk, Arthur W ; Nordestgaard, Børge G ; James, Alan ; Wain, Louise V ; Tobin, Martin D</creatorcontrib><description>BackgroundGenome-wide association studies have identified numerous genetic regions that influence cross-sectional lung function. Longitudinal decline in lung function also includes a heritable component but the genetic determinants have yet to be defined.ObjectivesWe aimed to determine whether regions associated with cross-sectional lung function were also associated with longitudinal decline and to seek novel variants which influence decline.MethodsWe analysed genome-wide data from 4167 individuals from the Busselton Health Study cohort, who had undergone spirometry (12 695 observations across eight time points). A mixed model was fitted and weighted risk scores were calculated for the joint effect of 26 known regions on baseline and longitudinal changes in FEV1 and FEV1/FVC. Potential additional regions of interest were identified and followed up in two independent cohorts.ResultsThe 26 regions previously associated with cross-sectional lung function jointly showed a strong effect on baseline lung function (p=4.44×10−16 for FEV1/FVC) but no effect on longitudinal decline (p=0.160 for FEV1/FVC). This was replicated in an independent cohort. 39 additional regions of interest (48 variants) were identified; these associations were not replicated in two further cohorts.ConclusionsPreviously identified genetic variants jointly have a strong effect on cross-sectional lung function in adults but little or no effect on the rate of decline of lung function. It is possible that they influence COPD risk through lung development. Although no genetic variants have yet been associated with lung function decline at stringent genome-wide significance, longitudinal change in lung function is heritable suggesting that there is scope for future discoveries.</description><identifier>ISSN: 0040-6376</identifier><identifier>EISSN: 1468-3296</identifier><identifier>DOI: 10.1136/thoraxjnl-2016-208448</identifier><identifier>PMID: 28174340</identifier><language>eng</language><publisher>England: BMJ Publishing Group LTD</publisher><subject>Adult ; Adults ; Age ; Chronic Obstructive Pulmonary Disease ; Cross-Sectional Studies ; Disease Progression ; Female ; Genetic Predisposition to Disease ; Genetic Variation ; Genome-Wide Association Study ; Genomes ; Genotype ; Health risk assessment ; Heart ; Humans ; Longitudinal Studies ; Male ; Middle Aged ; Principal components analysis ; Pulmonary Disease, Chronic Obstructive - genetics ; Pulmonary Disease, Chronic Obstructive - physiopathology ; Quality control ; Respiration - genetics ; Respiratory Function Tests ; Risk Assessment ; Risk Factors ; Smoking ; Spirometry ; Studies ; Time Factors ; Western Australia</subject><ispartof>Thorax, 2017-05, Vol.72 (5), p.400-408</ispartof><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.</rights><rights>Copyright: 2017 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/ 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b513t-ac971a59cf1177278e2ea90d83a7d7d9b8caebafc6c8f6b87644d52c4d9f6c983</citedby><cites>FETCH-LOGICAL-b513t-ac971a59cf1177278e2ea90d83a7d7d9b8caebafc6c8f6b87644d52c4d9f6c983</cites><orcidid>0000-0002-6057-2073</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28174340$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>John, Catherine</creatorcontrib><creatorcontrib>Soler Artigas, María</creatorcontrib><creatorcontrib>Hui, Jennie</creatorcontrib><creatorcontrib>Nielsen, Sune Fallgaard</creatorcontrib><creatorcontrib>Rafaels, Nicholas</creatorcontrib><creatorcontrib>Paré, Peter D</creatorcontrib><creatorcontrib>Hansel, Nadia N</creatorcontrib><creatorcontrib>Shrine, Nick</creatorcontrib><creatorcontrib>Kilty, Iain</creatorcontrib><creatorcontrib>Malarstig, Anders</creatorcontrib><creatorcontrib>Jelinsky, Scott A</creatorcontrib><creatorcontrib>Vedel-Krogh, Signe</creatorcontrib><creatorcontrib>Barnes, Kathleen</creatorcontrib><creatorcontrib>Hall, Ian P</creatorcontrib><creatorcontrib>Beilby, John</creatorcontrib><creatorcontrib>Musk, Arthur W</creatorcontrib><creatorcontrib>Nordestgaard, Børge G</creatorcontrib><creatorcontrib>James, Alan</creatorcontrib><creatorcontrib>Wain, Louise V</creatorcontrib><creatorcontrib>Tobin, Martin D</creatorcontrib><title>Genetic variants affecting cross-sectional lung function in adults show little or no effect on longitudinal lung function decline</title><title>Thorax</title><addtitle>Thorax</addtitle><description>BackgroundGenome-wide association studies have identified numerous genetic regions that influence cross-sectional lung function. Longitudinal decline in lung function also includes a heritable component but the genetic determinants have yet to be defined.ObjectivesWe aimed to determine whether regions associated with cross-sectional lung function were also associated with longitudinal decline and to seek novel variants which influence decline.MethodsWe analysed genome-wide data from 4167 individuals from the Busselton Health Study cohort, who had undergone spirometry (12 695 observations across eight time points). A mixed model was fitted and weighted risk scores were calculated for the joint effect of 26 known regions on baseline and longitudinal changes in FEV1 and FEV1/FVC. Potential additional regions of interest were identified and followed up in two independent cohorts.ResultsThe 26 regions previously associated with cross-sectional lung function jointly showed a strong effect on baseline lung function (p=4.44×10−16 for FEV1/FVC) but no effect on longitudinal decline (p=0.160 for FEV1/FVC). This was replicated in an independent cohort. 39 additional regions of interest (48 variants) were identified; these associations were not replicated in two further cohorts.ConclusionsPreviously identified genetic variants jointly have a strong effect on cross-sectional lung function in adults but little or no effect on the rate of decline of lung function. It is possible that they influence COPD risk through lung development. Although no genetic variants have yet been associated with lung function decline at stringent genome-wide significance, longitudinal change in lung function is heritable suggesting that there is scope for future discoveries.</description><subject>Adult</subject><subject>Adults</subject><subject>Age</subject><subject>Chronic Obstructive Pulmonary Disease</subject><subject>Cross-Sectional Studies</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic Variation</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>Genotype</subject><subject>Health risk assessment</subject><subject>Heart</subject><subject>Humans</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Principal components analysis</subject><subject>Pulmonary Disease, Chronic Obstructive - genetics</subject><subject>Pulmonary Disease, Chronic Obstructive - physiopathology</subject><subject>Quality control</subject><subject>Respiration - genetics</subject><subject>Respiratory Function Tests</subject><subject>Risk Assessment</subject><subject>Risk Factors</subject><subject>Smoking</subject><subject>Spirometry</subject><subject>Studies</subject><subject>Time Factors</subject><subject>Western Australia</subject><issn>0040-6376</issn><issn>1468-3296</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>9YT</sourceid><sourceid>ACMMV</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkkuPFCEUhYnROO3oT9CQuHFTyqt4bEzMREeTSdzomlBAddOhYQRqRpf-c-nuseNjMxvIhe8cuHAAeI7Ra4wpf9M2uZjv2xQHgjDvg2RMPgArzLgcKFH8IVghxNDAqeBn4EmtW4SQxFg8BmdEYsEoQyvw89In34KFN6YEk1qFZp69bSGtoS251qHuq5xMhHHpi_OSDjUMCRq3xK6om3wLY2gtepgLTBn6gwfsVMxpHdriwv8GztsYkn8KHs0mVv_sbj4HXz-8_3Lxcbj6fPnp4t3VMI2YtsFYJbAZlZ17C4II6Yk3CjlJjXDCqUla4yczW27lzCcpOGNuJJY5NXOrJD0Hb4--18u088761IqJ-rqEnSk_dDZB_72Twkav840eR4KIRN3g1Z1Byd8WX5vehWp9jCb5vFSNpcJyRAKze6CcEyUoVR19-Q-6zUvpr1V1P3YUlPGRd2o8Uoc_KX4-3Rsjvc-DPuVB7_Ogj3nouhd_Nn1S_Q5AB9ARmHbbe3r-As0Ox34</recordid><startdate>20170501</startdate><enddate>20170501</enddate><creator>John, Catherine</creator><creator>Soler Artigas, María</creator><creator>Hui, Jennie</creator><creator>Nielsen, Sune Fallgaard</creator><creator>Rafaels, Nicholas</creator><creator>Paré, Peter D</creator><creator>Hansel, Nadia N</creator><creator>Shrine, Nick</creator><creator>Kilty, Iain</creator><creator>Malarstig, Anders</creator><creator>Jelinsky, Scott A</creator><creator>Vedel-Krogh, Signe</creator><creator>Barnes, Kathleen</creator><creator>Hall, Ian P</creator><creator>Beilby, John</creator><creator>Musk, Arthur W</creator><creator>Nordestgaard, Børge G</creator><creator>James, Alan</creator><creator>Wain, Louise V</creator><creator>Tobin, Martin D</creator><general>BMJ Publishing Group LTD</general><general>BMJ Publishing Group</general><scope>9YT</scope><scope>ACMMV</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6057-2073</orcidid></search><sort><creationdate>20170501</creationdate><title>Genetic variants affecting cross-sectional lung function in adults show little or no effect on longitudinal lung function decline</title><author>John, Catherine ; Soler Artigas, María ; Hui, Jennie ; Nielsen, Sune Fallgaard ; Rafaels, Nicholas ; Paré, Peter D ; Hansel, Nadia N ; Shrine, Nick ; Kilty, Iain ; Malarstig, Anders ; Jelinsky, Scott A ; Vedel-Krogh, Signe ; Barnes, Kathleen ; Hall, Ian P ; Beilby, John ; Musk, Arthur W ; Nordestgaard, Børge G ; James, Alan ; Wain, Louise V ; Tobin, Martin D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b513t-ac971a59cf1177278e2ea90d83a7d7d9b8caebafc6c8f6b87644d52c4d9f6c983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Adults</topic><topic>Age</topic><topic>Chronic Obstructive Pulmonary Disease</topic><topic>Cross-Sectional Studies</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic Variation</topic><topic>Genome-Wide Association Study</topic><topic>Genomes</topic><topic>Genotype</topic><topic>Health risk assessment</topic><topic>Heart</topic><topic>Humans</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Principal components analysis</topic><topic>Pulmonary Disease, Chronic Obstructive - genetics</topic><topic>Pulmonary Disease, Chronic Obstructive - physiopathology</topic><topic>Quality control</topic><topic>Respiration - genetics</topic><topic>Respiratory Function Tests</topic><topic>Risk Assessment</topic><topic>Risk Factors</topic><topic>Smoking</topic><topic>Spirometry</topic><topic>Studies</topic><topic>Time Factors</topic><topic>Western Australia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>John, Catherine</creatorcontrib><creatorcontrib>Soler Artigas, María</creatorcontrib><creatorcontrib>Hui, Jennie</creatorcontrib><creatorcontrib>Nielsen, Sune Fallgaard</creatorcontrib><creatorcontrib>Rafaels, Nicholas</creatorcontrib><creatorcontrib>Paré, Peter D</creatorcontrib><creatorcontrib>Hansel, Nadia N</creatorcontrib><creatorcontrib>Shrine, Nick</creatorcontrib><creatorcontrib>Kilty, Iain</creatorcontrib><creatorcontrib>Malarstig, Anders</creatorcontrib><creatorcontrib>Jelinsky, Scott A</creatorcontrib><creatorcontrib>Vedel-Krogh, Signe</creatorcontrib><creatorcontrib>Barnes, Kathleen</creatorcontrib><creatorcontrib>Hall, Ian P</creatorcontrib><creatorcontrib>Beilby, John</creatorcontrib><creatorcontrib>Musk, Arthur W</creatorcontrib><creatorcontrib>Nordestgaard, Børge G</creatorcontrib><creatorcontrib>James, Alan</creatorcontrib><creatorcontrib>Wain, Louise V</creatorcontrib><creatorcontrib>Tobin, Martin D</creatorcontrib><collection>BMJ Open Access Journals</collection><collection>BMJ Journals:Open Access</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Thorax</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>John, Catherine</au><au>Soler Artigas, María</au><au>Hui, Jennie</au><au>Nielsen, Sune Fallgaard</au><au>Rafaels, Nicholas</au><au>Paré, Peter D</au><au>Hansel, Nadia N</au><au>Shrine, Nick</au><au>Kilty, Iain</au><au>Malarstig, Anders</au><au>Jelinsky, Scott A</au><au>Vedel-Krogh, Signe</au><au>Barnes, Kathleen</au><au>Hall, Ian P</au><au>Beilby, John</au><au>Musk, Arthur W</au><au>Nordestgaard, Børge G</au><au>James, Alan</au><au>Wain, Louise V</au><au>Tobin, Martin D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic variants affecting cross-sectional lung function in adults show little or no effect on longitudinal lung function decline</atitle><jtitle>Thorax</jtitle><addtitle>Thorax</addtitle><date>2017-05-01</date><risdate>2017</risdate><volume>72</volume><issue>5</issue><spage>400</spage><epage>408</epage><pages>400-408</pages><issn>0040-6376</issn><eissn>1468-3296</eissn><abstract>BackgroundGenome-wide association studies have identified numerous genetic regions that influence cross-sectional lung function. Longitudinal decline in lung function also includes a heritable component but the genetic determinants have yet to be defined.ObjectivesWe aimed to determine whether regions associated with cross-sectional lung function were also associated with longitudinal decline and to seek novel variants which influence decline.MethodsWe analysed genome-wide data from 4167 individuals from the Busselton Health Study cohort, who had undergone spirometry (12 695 observations across eight time points). A mixed model was fitted and weighted risk scores were calculated for the joint effect of 26 known regions on baseline and longitudinal changes in FEV1 and FEV1/FVC. Potential additional regions of interest were identified and followed up in two independent cohorts.ResultsThe 26 regions previously associated with cross-sectional lung function jointly showed a strong effect on baseline lung function (p=4.44×10−16 for FEV1/FVC) but no effect on longitudinal decline (p=0.160 for FEV1/FVC). This was replicated in an independent cohort. 39 additional regions of interest (48 variants) were identified; these associations were not replicated in two further cohorts.ConclusionsPreviously identified genetic variants jointly have a strong effect on cross-sectional lung function in adults but little or no effect on the rate of decline of lung function. It is possible that they influence COPD risk through lung development. Although no genetic variants have yet been associated with lung function decline at stringent genome-wide significance, longitudinal change in lung function is heritable suggesting that there is scope for future discoveries.</abstract><cop>England</cop><pub>BMJ Publishing Group LTD</pub><pmid>28174340</pmid><doi>10.1136/thoraxjnl-2016-208448</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-6057-2073</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adult Adults Age Chronic Obstructive Pulmonary Disease Cross-Sectional Studies Disease Progression Female Genetic Predisposition to Disease Genetic Variation Genome-Wide Association Study Genomes Genotype Health risk assessment Heart Humans Longitudinal Studies Male Middle Aged Principal components analysis Pulmonary Disease, Chronic Obstructive - genetics Pulmonary Disease, Chronic Obstructive - physiopathology Quality control Respiration - genetics Respiratory Function Tests Risk Assessment Risk Factors Smoking Spirometry Studies Time Factors Western Australia |
title | Genetic variants affecting cross-sectional lung function in adults show little or no effect on longitudinal lung function decline |
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