Decreased Bone Mineral Density in Subjects Carrying Familial Defective Apolipoprotein B-100
Context:Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this association remain to be clarified. One hypothesis is that hyperlipidemia may be a common predisposing factor to both atherosclerotic heart dis...
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| Published in | The journal of clinical endocrinology and metabolism Vol. 98; no. 12; pp. E1999 - E2005 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Oxford University Press
01.12.2013
Copyright by The Endocrine Society Endocrine Society |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Context:Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this association remain to be clarified. One hypothesis is that hyperlipidemia may be a common predisposing factor to both atherosclerotic heart disease and bone fragility.Objective:To evaluate this, we compared bone mineral density (BMD) between subjects with and without the R3500Q APOB mutation, the cause of familial defective apolipoprotein B-100, which has been previously shown to markedly increase low-density lipoprotein cholesterol (LDL-C). We hypothesized that R3500Q carriers would have lower BMD due to lifetime, elevated LDL-C.Design:This was a a cross-sectional study in the Old Order Amish (OOA) population.Participants:The R3500Q APOB mutation is present at a high frequency (∼6% vs <0.5%) in the OOA population due to a founder effect. Therefore, we conducted analysis on 1097 Amish individuals of whom 125 were R3500Q carriers.Main Outcome Measure:BMD was measured by dual-energy x-ray absorptiometry.Results:After adjusting for age, age2, sex, body mass index, and family structure, carriers for the Q risk allele had significantly lower BMD than noncarriers at the femoral neck (P = .037), lumbar spine (P = .035) and whole body (P = .016). Adjusting for LDL-C attenuated the association between R3500Q genotype and BMD but did not completely explain the relationship. Subgroup analyses showed no significant interactions with sex, age, or presence of metabolic syndrome.Conclusion:These results use the unique genetic architecture of the OOA population to provide a novel line of evidence supporting a causal role for elevated LDL-C in lowering BMD. |
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| AbstractList | Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this association remain to be clarified. One hypothesis is that hyperlipidemia may be a common predisposing factor to both atherosclerotic heart disease and bone fragility.
To evaluate this, we compared bone mineral density (BMD) between subjects with and without the R3500Q APOB mutation, the cause of familial defective apolipoprotein B-100, which has been previously shown to markedly increase low-density lipoprotein cholesterol (LDL-C). We hypothesized that R3500Q carriers would have lower BMD due to lifetime, elevated LDL-C.
This was a a cross-sectional study in the Old Order Amish (OOA) population.
The R3500Q APOB mutation is present at a high frequency (∼6% vs <0.5%) in the OOA population due to a founder effect. Therefore, we conducted analysis on 1097 Amish individuals of whom 125 were R3500Q carriers.
BMD was measured by dual-energy x-ray absorptiometry.
After adjusting for age, age(2), sex, body mass index, and family structure, carriers for the Q risk allele had significantly lower BMD than noncarriers at the femoral neck (P = .037), lumbar spine (P = .035) and whole body (P = .016). Adjusting for LDL-C attenuated the association between R3500Q genotype and BMD but did not completely explain the relationship. Subgroup analyses showed no significant interactions with sex, age, or presence of metabolic syndrome.
These results use the unique genetic architecture of the OOA population to provide a novel line of evidence supporting a causal role for elevated LDL-C in lowering BMD. Context:Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this association remain to be clarified. One hypothesis is that hyperlipidemia may be a common predisposing factor to both atherosclerotic heart disease and bone fragility.Objective:To evaluate this, we compared bone mineral density (BMD) between subjects with and without the R3500Q APOB mutation, the cause of familial defective apolipoprotein B-100, which has been previously shown to markedly increase low-density lipoprotein cholesterol (LDL-C). We hypothesized that R3500Q carriers would have lower BMD due to lifetime, elevated LDL-C.Design:This was a a cross-sectional study in the Old Order Amish (OOA) population.Participants:The R3500Q APOB mutation is present at a high frequency (∼6% vs <0.5%) in the OOA population due to a founder effect. Therefore, we conducted analysis on 1097 Amish individuals of whom 125 were R3500Q carriers.Main Outcome Measure:BMD was measured by dual-energy x-ray absorptiometry.Results:After adjusting for age, age2, sex, body mass index, and family structure, carriers for the Q risk allele had significantly lower BMD than noncarriers at the femoral neck (P = .037), lumbar spine (P = .035) and whole body (P = .016). Adjusting for LDL-C attenuated the association between R3500Q genotype and BMD but did not completely explain the relationship. Subgroup analyses showed no significant interactions with sex, age, or presence of metabolic syndrome.Conclusion:These results use the unique genetic architecture of the OOA population to provide a novel line of evidence supporting a causal role for elevated LDL-C in lowering BMD. Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this association remain to be clarified. One hypothesis is that hyperlipidemia may be a common predisposing factor to both atherosclerotic heart disease and bone fragility.CONTEXTAlthough numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this association remain to be clarified. One hypothesis is that hyperlipidemia may be a common predisposing factor to both atherosclerotic heart disease and bone fragility.To evaluate this, we compared bone mineral density (BMD) between subjects with and without the R3500Q APOB mutation, the cause of familial defective apolipoprotein B-100, which has been previously shown to markedly increase low-density lipoprotein cholesterol (LDL-C). We hypothesized that R3500Q carriers would have lower BMD due to lifetime, elevated LDL-C.OBJECTIVETo evaluate this, we compared bone mineral density (BMD) between subjects with and without the R3500Q APOB mutation, the cause of familial defective apolipoprotein B-100, which has been previously shown to markedly increase low-density lipoprotein cholesterol (LDL-C). We hypothesized that R3500Q carriers would have lower BMD due to lifetime, elevated LDL-C.This was a a cross-sectional study in the Old Order Amish (OOA) population.DESIGNThis was a a cross-sectional study in the Old Order Amish (OOA) population.The R3500Q APOB mutation is present at a high frequency (∼6% vs <0.5%) in the OOA population due to a founder effect. Therefore, we conducted analysis on 1097 Amish individuals of whom 125 were R3500Q carriers.PARTICIPANTSThe R3500Q APOB mutation is present at a high frequency (∼6% vs <0.5%) in the OOA population due to a founder effect. Therefore, we conducted analysis on 1097 Amish individuals of whom 125 were R3500Q carriers.BMD was measured by dual-energy x-ray absorptiometry.MAIN OUTCOME MEASUREBMD was measured by dual-energy x-ray absorptiometry.After adjusting for age, age(2), sex, body mass index, and family structure, carriers for the Q risk allele had significantly lower BMD than noncarriers at the femoral neck (P = .037), lumbar spine (P = .035) and whole body (P = .016). Adjusting for LDL-C attenuated the association between R3500Q genotype and BMD but did not completely explain the relationship. Subgroup analyses showed no significant interactions with sex, age, or presence of metabolic syndrome.RESULTSAfter adjusting for age, age(2), sex, body mass index, and family structure, carriers for the Q risk allele had significantly lower BMD than noncarriers at the femoral neck (P = .037), lumbar spine (P = .035) and whole body (P = .016). Adjusting for LDL-C attenuated the association between R3500Q genotype and BMD but did not completely explain the relationship. Subgroup analyses showed no significant interactions with sex, age, or presence of metabolic syndrome.These results use the unique genetic architecture of the OOA population to provide a novel line of evidence supporting a causal role for elevated LDL-C in lowering BMD.CONCLUSIONThese results use the unique genetic architecture of the OOA population to provide a novel line of evidence supporting a causal role for elevated LDL-C in lowering BMD. CONTEXT:Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this association remain to be clarified. One hypothesis is that hyperlipidemia may be a common predisposing factor to both atherosclerotic heart disease and bone fragility. OBJECTIVE:To evaluate this, we compared bone mineral density (BMD) between subjects with and without the R3500Q APOB mutation, the cause of familial defective apolipoprotein B-100, which has been previously shown to markedly increase low-density lipoprotein cholesterol (LDL-C). We hypothesized that R3500Q carriers would have lower BMD due to lifetime, elevated LDL-C. DESIGN:This was a a cross-sectional study in the Old Order Amish (OOA) population. PARTICIPANTS:The R3500Q APOB mutation is present at a high frequency (∼6% vs <0.5%) in the OOA population due to a founder effect. Therefore, we conducted analysis on 1097 Amish individuals of whom 125 were R3500Q carriers. MAIN OUTCOME MEASURE:BMD was measured by dual-energy x-ray absorptiometry. RESULTS:After adjusting for age, age, sex, body mass index, and family structure, carriers for the Q risk allele had significantly lower BMD than noncarriers at the femoral neck (P = .037), lumbar spine (P = .035) and whole body (P = .016). Adjusting for LDL-C attenuated the association between R3500Q genotype and BMD but did not completely explain the relationship. Subgroup analyses showed no significant interactions with sex, age, or presence of metabolic syndrome. CONCLUSION:These results use the unique genetic architecture of the OOA population to provide a novel line of evidence supporting a causal role for elevated LDL-C in lowering BMD. Context:Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this association remain to be clarified. One hypothesis is that hyperlipidemia may be a common predisposing factor to both atherosclerotic heart disease and bone fragility.Objective:To evaluate this, we compared bone mineral density (BMD) between subjects with and without the R3500Q APOB mutation, the cause of familial defective apolipoprotein B-100, which has been previously shown to markedly increase low-density lipoprotein cholesterol (LDL-C). We hypothesized that R3500Q carriers would have lower BMD due to lifetime, elevated LDL-C.Design:This was a a cross-sectional study in the Old Order Amish (OOA) population.Participants:The R3500Q APOB mutation is present at a high frequency ( similar to 6% vs <0.5%) in the OOA population due to a founder effect. Therefore, we conducted analysis on 1097 Amish individuals of whom 125 were R3500Q carriers.Main Outcome Measure:BMD was measured by dual-energy x-ray absorptiometry.Results:After adjusting for age, age2, sex, body mass index, and family structure, carriers for the Q risk allele had significantly lower BMD than noncarriers at the femoral neck (P = .037), lumbar spine (P = .035) and whole body (P = .016). Adjusting for LDL-C attenuated the association between R3500Q genotype and BMD but did not completely explain the relationship. Subgroup analyses showed no significant interactions with sex, age, or presence of metabolic syndrome.Conclusion:These results use the unique genetic architecture of the OOA population to provide a novel line of evidence supporting a causal role for elevated LDL-C in lowering BMD. |
| Author | Ryan, Kathleen A. Mitchell, Braxton D. Shen, Haiqing Streeten, Elizabeth A. Yerges-Armstrong, Laura M. Shuldiner, Alan R. |
| AuthorAffiliation | Program in Personalized and Genomic Medicine (L.M.Y.-A., H.S., K.A.R., E.A.S., A.R.S., B.D.M.) and Department of Medicine, Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine; and Geriatric Research and Education Clinical Center (E.A.S., A.R.S., B.D.M.), Veterans Administration Medical Center, Baltimore, Maryland 21201 |
| AuthorAffiliation_xml | – name: Program in Personalized and Genomic Medicine (L.M.Y.-A., H.S., K.A.R., E.A.S., A.R.S., B.D.M.) and Department of Medicine, Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine; and Geriatric Research and Education Clinical Center (E.A.S., A.R.S., B.D.M.), Veterans Administration Medical Center, Baltimore, Maryland 21201 |
| Author_xml | – sequence: 1 givenname: Laura M. surname: Yerges-Armstrong fullname: Yerges-Armstrong, Laura M. email: lyerges@medicine.umaryland.edu organization: 1Program in Personalized and Genomic Medicine (L.M.Y.-A., H.S., K.A.R., E.A.S., A.R.S., B.D.M.) and Department of Medicine, Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine – sequence: 2 givenname: Haiqing surname: Shen fullname: Shen, Haiqing organization: 1Program in Personalized and Genomic Medicine (L.M.Y.-A., H.S., K.A.R., E.A.S., A.R.S., B.D.M.) and Department of Medicine, Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine – sequence: 3 givenname: Kathleen A. surname: Ryan fullname: Ryan, Kathleen A. organization: 1Program in Personalized and Genomic Medicine (L.M.Y.-A., H.S., K.A.R., E.A.S., A.R.S., B.D.M.) and Department of Medicine, Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine – sequence: 4 givenname: Elizabeth A. surname: Streeten fullname: Streeten, Elizabeth A. organization: 1Program in Personalized and Genomic Medicine (L.M.Y.-A., H.S., K.A.R., E.A.S., A.R.S., B.D.M.) and Department of Medicine, Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine – sequence: 5 givenname: Alan R. surname: Shuldiner fullname: Shuldiner, Alan R. organization: 1Program in Personalized and Genomic Medicine (L.M.Y.-A., H.S., K.A.R., E.A.S., A.R.S., B.D.M.) and Department of Medicine, Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine – sequence: 6 givenname: Braxton D. surname: Mitchell fullname: Mitchell, Braxton D. organization: 1Program in Personalized and Genomic Medicine (L.M.Y.-A., H.S., K.A.R., E.A.S., A.R.S., B.D.M.) and Department of Medicine, Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine |
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| Snippet | Context:Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this... CONTEXT:Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this... Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this... |
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| SubjectTerms | Adult Aged Aged, 80 and over Alleles Amino Acid Substitution Amish Apolipoprotein B Apolipoprotein B-100 - genetics Apolipoprotein B-100 - metabolism Apolipoproteins Arteriosclerosis Body mass index Bone Density Bone mineral density Bone Resorption - etiology Cardiovascular diseases Cholesterol Cholesterol, LDL - blood Cross-Sectional Studies Dual energy X-ray absorptiometry Epidemiology Female Founder Effect Genotypes Heart diseases Heterozygote Humans Hyperlipidemia Hyperlipoproteinemia Type II - blood Hyperlipoproteinemia Type II - genetics Hyperlipoproteinemia Type II - metabolism Hyperlipoproteinemia Type II - physiopathology JCEM Online: Advances in Genetics Low density lipoprotein Male Metabolic syndrome Middle Aged Mutation Mutation Rate Osteoporosis Pennsylvania Point Mutation Population genetics Population studies Spine (lumbar) Young Adult |
| Title | Decreased Bone Mineral Density in Subjects Carrying Familial Defective Apolipoprotein B-100 |
| URI | https://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00004678-201312000-00078 https://www.ncbi.nlm.nih.gov/pubmed/24106285 https://www.proquest.com/docview/3164461892 https://www.proquest.com/docview/1465866051 https://www.proquest.com/docview/1611621436 https://pubmed.ncbi.nlm.nih.gov/PMC3849668 |
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