Smoking influences the association between apolipoprotein E and lipids: The National Heart, Lung, and Blood Institute Family Heart Study

Luc Djoussé; Richard H. Myers; Hilary Coon; Donna K. Arnett; Michael A. Province; R. Curtis Ellison

doi:10.1007/S11745-000-0591-1

Smoking influences the association between apolipoprotein E and lipids: The National Heart, Lung, and Blood Institute Family Heart Study

Luc Djoussé, Richard H. Myers, Hilary Coon, Donna K. Arnett, Michael A. Province, R. Curtis Ellison

Research output: Contribution to journal › Article › peer-review

13 Citations (SciVal)

Abstract

Apolipoprotein E allele 4 (apo ε₄) and smoking each have been associated with an unfavorable lipid profile. We used data collected on 1,472 subjects in the National Heart, Lung, and Blood Institute Family Heart Study to assess whether smoking interacts with apo ε₄ to influence the levels of plasma lipids. We dichotomized smoking and apo ε₄ and used analysis of covariance to estimate the means of lipids. Smokers had lower body mass index, were younger, and consumed less fruits and vegetables. Among individuals without apo ε₄, comparing nonsmokers with smokers, mean low density lipoprotein cholesterol (LDL) was 129.3 and 134.4 mg/dL, respectively, for women and 126.1 and 127.6 mg/dL, respectively, for men. Among subjects with an apo ε₄ allele, corresponding means were 132.0, and 152.9 mg/dL, respectively, for women and 131.3 and 137.3 mg/dL, respectively, for men (P for interaction <0.001 for women and 0.11 for men). A similar interaction was observed for total cholesterol among women (P = 0.02). This study shows a statistically significant effect modification of the relation of apo ε₄ to LDL and total cholesterol by smoking among women. Smoking may enhance genetic susceptibility to an unfavorable lipid profile among subjects with apo ε₄.

Original language	English
Pages (from-to)	827-831
Number of pages	5
Journal	Lipids
Volume	35
Issue number	8
DOIs	https://doi.org/10.1007/S11745-000-0591-1
State	Published - 2000

Bibliographical note

Funding Information:
Support was partially provided by the National Heart, Lung, and Blood Institute cooperative agreement grants U01 HL56563, U01 HL56564, U01 HL56565, U01 HL56566, U01 HL56567, U01 HL56568, U01 HL56569. This paper is presented on behalf of the investigators of the NHLBI Family Heart Study. Participating institutions and principal staff of the study are as follows: Forsyth County/University of North Carolina/Wake Forest University: Ger-ardo Heiss, Stephen Rich, Greg Evans; James Pankow; H.A. Tyroler, Jeannette T. Bensen, Catherine Paton, Delilah Posey, and Amy Haire; University of Minnesota Field Center: Donna K. Arnett, Aaron R. Folsom, Larry Atwood, James Peacock, and Greg Feitl; Boston University/Framingham Field Center: R. Curtis Ellison, Richard H. Myers, Yuqing Zhang, Andrew G. Bostom, Luc Djoussé, Jemma B. Wilk, and Greta Lee Splansky; University of Utah Field Center: Steven C. Hunt, Roger R. Williams (deceased), Paul N. Hopkins, Hilary Coon, and Jan Skuppin; Coordinating Center, Washington University, St. Louis: Michael A. Province, D.C. Rao, Ingrid B. Borecki, Yuling Hong, Mary Feitosa, Jeanne Cashman, and Avril Adelman; Central Biochemistry Laboratory, University of Minnesota: John H. Eckfeldt, Catherine Leiendecker-Foster, Michael Y. Tsai, and Greg Rynders; Central Molecular Laboratory, University of Utah: Mark F. Leppert, Jean-Marc Lalouel, Tena Varvil, Lisa Baird; National Heart, Lung, & Blood Institute—Project Office: Phyliss Sholinsky, Millicent Higgins (retired), Jacob Keller (retired), Sarah Knox, and Lorraine Silsbee.

ASJC Scopus subject areas

Biochemistry
Organic Chemistry
Cell Biology

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10.1007/S11745-000-0591-1

Cite this

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title = "Smoking influences the association between apolipoprotein E and lipids: The National Heart, Lung, and Blood Institute Family Heart Study",

abstract = "Apolipoprotein E allele 4 (apo ε4) and smoking each have been associated with an unfavorable lipid profile. We used data collected on 1,472 subjects in the National Heart, Lung, and Blood Institute Family Heart Study to assess whether smoking interacts with apo ε4 to influence the levels of plasma lipids. We dichotomized smoking and apo ε4 and used analysis of covariance to estimate the means of lipids. Smokers had lower body mass index, were younger, and consumed less fruits and vegetables. Among individuals without apo ε4, comparing nonsmokers with smokers, mean low density lipoprotein cholesterol (LDL) was 129.3 and 134.4 mg/dL, respectively, for women and 126.1 and 127.6 mg/dL, respectively, for men. Among subjects with an apo ε4 allele, corresponding means were 132.0, and 152.9 mg/dL, respectively, for women and 131.3 and 137.3 mg/dL, respectively, for men (P for interaction <0.001 for women and 0.11 for men). A similar interaction was observed for total cholesterol among women (P = 0.02). This study shows a statistically significant effect modification of the relation of apo ε4 to LDL and total cholesterol by smoking among women. Smoking may enhance genetic susceptibility to an unfavorable lipid profile among subjects with apo ε4.",

author = "Luc Djouss{\'e} and Myers, {Richard H.} and Hilary Coon and Arnett, {Donna K.} and Province, {Michael A.} and Ellison, {R. Curtis}",

note = "Funding Information: Support was partially provided by the National Heart, Lung, and Blood Institute cooperative agreement grants U01 HL56563, U01 HL56564, U01 HL56565, U01 HL56566, U01 HL56567, U01 HL56568, U01 HL56569. This paper is presented on behalf of the investigators of the NHLBI Family Heart Study. Participating institutions and principal staff of the study are as follows: Forsyth County/University of North Carolina/Wake Forest University: Ger-ardo Heiss, Stephen Rich, Greg Evans; James Pankow; H.A. Tyroler, Jeannette T. Bensen, Catherine Paton, Delilah Posey, and Amy Haire; University of Minnesota Field Center: Donna K. Arnett, Aaron R. Folsom, Larry Atwood, James Peacock, and Greg Feitl; Boston University/Framingham Field Center: R. Curtis Ellison, Richard H. Myers, Yuqing Zhang, Andrew G. Bostom, Luc Djouss{\'e}, Jemma B. Wilk, and Greta Lee Splansky; University of Utah Field Center: Steven C. Hunt, Roger R. Williams (deceased), Paul N. Hopkins, Hilary Coon, and Jan Skuppin; Coordinating Center, Washington University, St. Louis: Michael A. Province, D.C. Rao, Ingrid B. Borecki, Yuling Hong, Mary Feitosa, Jeanne Cashman, and Avril Adelman; Central Biochemistry Laboratory, University of Minnesota: John H. Eckfeldt, Catherine Leiendecker-Foster, Michael Y. Tsai, and Greg Rynders; Central Molecular Laboratory, University of Utah: Mark F. Leppert, Jean-Marc Lalouel, Tena Varvil, Lisa Baird; National Heart, Lung, & Blood Institute—Project Office: Phyliss Sholinsky, Millicent Higgins (retired), Jacob Keller (retired), Sarah Knox, and Lorraine Silsbee.",

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doi = "10.1007/S11745-000-0591-1",

language = "English",

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AU - Arnett, Donna K.

AU - Province, Michael A.

AU - Ellison, R. Curtis

N1 - Funding Information: Support was partially provided by the National Heart, Lung, and Blood Institute cooperative agreement grants U01 HL56563, U01 HL56564, U01 HL56565, U01 HL56566, U01 HL56567, U01 HL56568, U01 HL56569. This paper is presented on behalf of the investigators of the NHLBI Family Heart Study. Participating institutions and principal staff of the study are as follows: Forsyth County/University of North Carolina/Wake Forest University: Ger-ardo Heiss, Stephen Rich, Greg Evans; James Pankow; H.A. Tyroler, Jeannette T. Bensen, Catherine Paton, Delilah Posey, and Amy Haire; University of Minnesota Field Center: Donna K. Arnett, Aaron R. Folsom, Larry Atwood, James Peacock, and Greg Feitl; Boston University/Framingham Field Center: R. Curtis Ellison, Richard H. Myers, Yuqing Zhang, Andrew G. Bostom, Luc Djoussé, Jemma B. Wilk, and Greta Lee Splansky; University of Utah Field Center: Steven C. Hunt, Roger R. Williams (deceased), Paul N. Hopkins, Hilary Coon, and Jan Skuppin; Coordinating Center, Washington University, St. Louis: Michael A. Province, D.C. Rao, Ingrid B. Borecki, Yuling Hong, Mary Feitosa, Jeanne Cashman, and Avril Adelman; Central Biochemistry Laboratory, University of Minnesota: John H. Eckfeldt, Catherine Leiendecker-Foster, Michael Y. Tsai, and Greg Rynders; Central Molecular Laboratory, University of Utah: Mark F. Leppert, Jean-Marc Lalouel, Tena Varvil, Lisa Baird; National Heart, Lung, & Blood Institute—Project Office: Phyliss Sholinsky, Millicent Higgins (retired), Jacob Keller (retired), Sarah Knox, and Lorraine Silsbee.

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N2 - Apolipoprotein E allele 4 (apo ε4) and smoking each have been associated with an unfavorable lipid profile. We used data collected on 1,472 subjects in the National Heart, Lung, and Blood Institute Family Heart Study to assess whether smoking interacts with apo ε4 to influence the levels of plasma lipids. We dichotomized smoking and apo ε4 and used analysis of covariance to estimate the means of lipids. Smokers had lower body mass index, were younger, and consumed less fruits and vegetables. Among individuals without apo ε4, comparing nonsmokers with smokers, mean low density lipoprotein cholesterol (LDL) was 129.3 and 134.4 mg/dL, respectively, for women and 126.1 and 127.6 mg/dL, respectively, for men. Among subjects with an apo ε4 allele, corresponding means were 132.0, and 152.9 mg/dL, respectively, for women and 131.3 and 137.3 mg/dL, respectively, for men (P for interaction <0.001 for women and 0.11 for men). A similar interaction was observed for total cholesterol among women (P = 0.02). This study shows a statistically significant effect modification of the relation of apo ε4 to LDL and total cholesterol by smoking among women. Smoking may enhance genetic susceptibility to an unfavorable lipid profile among subjects with apo ε4.

AB - Apolipoprotein E allele 4 (apo ε4) and smoking each have been associated with an unfavorable lipid profile. We used data collected on 1,472 subjects in the National Heart, Lung, and Blood Institute Family Heart Study to assess whether smoking interacts with apo ε4 to influence the levels of plasma lipids. We dichotomized smoking and apo ε4 and used analysis of covariance to estimate the means of lipids. Smokers had lower body mass index, were younger, and consumed less fruits and vegetables. Among individuals without apo ε4, comparing nonsmokers with smokers, mean low density lipoprotein cholesterol (LDL) was 129.3 and 134.4 mg/dL, respectively, for women and 126.1 and 127.6 mg/dL, respectively, for men. Among subjects with an apo ε4 allele, corresponding means were 132.0, and 152.9 mg/dL, respectively, for women and 131.3 and 137.3 mg/dL, respectively, for men (P for interaction <0.001 for women and 0.11 for men). A similar interaction was observed for total cholesterol among women (P = 0.02). This study shows a statistically significant effect modification of the relation of apo ε4 to LDL and total cholesterol by smoking among women. Smoking may enhance genetic susceptibility to an unfavorable lipid profile among subjects with apo ε4.

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Smoking influences the association between apolipoprotein E and lipids: The National Heart, Lung, and Blood Institute Family Heart Study

Abstract

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