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dc.contributor.authorSigurdsson, Gunnar
dc.contributor.authorHalldorsson, Bjarni V
dc.contributor.authorStyrkarsdottir, Unnur
dc.contributor.authorKristjansson, Kristleifur
dc.contributor.authorStefansson, Kari
dc.date.accessioned2008-12-02T11:29:09Z
dc.date.available2008-12-02T11:29:09Z
dc.date.issued2008-10-01
dc.date.submitted2008-12-02
dc.identifier.citationJ. Bone Miner. Res. 2008, 23(10):1584-90en
dc.identifier.issn1523-4681
dc.identifier.pmid18505373
dc.identifier.doi10.1359/jbmr.080507
dc.identifier.urihttp://hdl.handle.net/2336/41714
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractLow bone mass in adults is a major risk factor for low-impact fractures and is considered of complex origin because of interaction of environmental and genetic factors, each with modest effect. The objective was to assess the relative impact of genetics and environment and quantify the risk in relatives of osteopenic individuals. We studied 440 Icelandic nuclear families with 869 first-degree relatives of both sexes. Index cases (male or female) had BMD in the lumbar spine or hip >1.5 SD less than sex-matched controls. Heritability of BMD was estimated by maximum likelihood method, and variance component analysis was used to partition the genetic and environmental effects. Relative risk of low BMD (< -1 SD) in first-degree relatives was estimated, and heritable decrement in BMD was calculated compared with controls. Heritability was estimated as 0.61-0.66. Relative risk among first-degree relatives was 2.28, and the yield of screening was as high as 36%. The genetic influence was consistent with one or a few genes with considerable effect in addition to multiple genes each with a small effect. The genetic deficit in BMD was already present before 35 yr of age and equaled bone loss during 8-30 yr after menopause. We confirmed that genetics are more important than environment to low bone mass in adults. Our results are consistent with a few underlying genes with considerable effect. The prevalence among first-degree relatives of both sexes is common, suggesting that screening them should be cost effective and informative to elucidate the underlying genetics.
dc.language.isoenen
dc.publisherAmerican Society for Bone and Mineral Researchen
dc.relation.urlhttp://dx.doi.org/10.1359/jbmr.080507en
dc.subject.meshGenetic Predisposition to Diseaseen
dc.subject.meshBone Densityen
dc.subject.meshAdulten
dc.titleImpact of genetics on low bone mass in adultsen
dc.typeArticleen
dc.contributor.departmentDepartment of Endocrinology and Metabolism, Landspitali-University Hospital, University of Iceland, Reykjavik, Iceland. gunnars@landspitali.isen
dc.identifier.journalJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Researchen
html.description.abstractLow bone mass in adults is a major risk factor for low-impact fractures and is considered of complex origin because of interaction of environmental and genetic factors, each with modest effect. The objective was to assess the relative impact of genetics and environment and quantify the risk in relatives of osteopenic individuals. We studied 440 Icelandic nuclear families with 869 first-degree relatives of both sexes. Index cases (male or female) had BMD in the lumbar spine or hip >1.5 SD less than sex-matched controls. Heritability of BMD was estimated by maximum likelihood method, and variance component analysis was used to partition the genetic and environmental effects. Relative risk of low BMD (< -1 SD) in first-degree relatives was estimated, and heritable decrement in BMD was calculated compared with controls. Heritability was estimated as 0.61-0.66. Relative risk among first-degree relatives was 2.28, and the yield of screening was as high as 36%. The genetic influence was consistent with one or a few genes with considerable effect in addition to multiple genes each with a small effect. The genetic deficit in BMD was already present before 35 yr of age and equaled bone loss during 8-30 yr after menopause. We confirmed that genetics are more important than environment to low bone mass in adults. Our results are consistent with a few underlying genes with considerable effect. The prevalence among first-degree relatives of both sexes is common, suggesting that screening them should be cost effective and informative to elucidate the underlying genetics.


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