Common genetic contributions to depressive symptoms and inflammatory markers in middle-aged men: The twins heart study

Shaoyong Su, Andrew H. Miller, Harold Snieder, J. Douglas Bremner, James Ritchie, Carisa Maisano, Linda Jones, Nancy V. Murrah, Jack Goldberg, Viola Vaccarino

Research output: Contribution to journalArticle

54 Citations (Scopus)

Abstract

OBJECTIVE:: To examine the extent to which a common genetic pathway is also involved in the relationship between depressive symptoms, in the absence of major depressive disorder (MDD), and inflammation. Recent data suggested that MDD and inflammation share common genes. METHODS:: We recruited 188 male twins from the Vietnam Era Twin Registry who were free of symptomatic coronary artery disease and MDD, with mean ± standard deviation (SD) age of 55 ± 2.75 years, including 54 monozygotic and 40 dizygotic twin pairs. These pairs were assessed for two inflammatory markers, interleukin (IL)-6 and C-reactive protein (CRP). Current depressive symptoms were measured with the Beck Depression Inventory-II. Generalized estimating equations were used to examine the phenotypic association between depression and inflammatory markers. Biometrical genetic modeling was performed to estimate the genetic and environmental contributions to this association. RESULTS:: An association was observed between severity of current depressive symptoms and increased levels of inflammatory markers (p < .001 for IL-6 and p = .005 for CRP). After adjustment for other factors, the association was slightly attenuated but remained statistically significant for IL-6 (p = .002). The heritability of IL-6, CRP, and depressive symptoms were estimated as 0.37, 0.65, and 0.48, respectively. Genetic modeling found a significant genetic correlation between IL-6 and depressive symptoms (rG = 0.22, p = .046), indicating that about 66% of the covariance between them can be explained by shared genetic influences. CONCLUSIONS:: Current depressive symptoms are significantly correlated with inflammatory markers. This covariation is due, in large part, to genes that are common to depressive symptoms and inflammation.

Original languageEnglish (US)
Pages (from-to)152-158
Number of pages7
JournalPsychosomatic Medicine
Volume71
Issue number2
DOIs
StatePublished - Jan 1 2009

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Twin Studies
Depression
Interleukin-6
Major Depressive Disorder
C-Reactive Protein
Inflammation
Dizygotic Twins
Vietnam
Genes
Registries
Coronary Artery Disease
Equipment and Supplies

Keywords

  • Common genes
  • Depression
  • Inflammation
  • Middle-aged
  • Twin study

ASJC Scopus subject areas

  • Applied Psychology
  • Psychiatry and Mental health

Cite this

Common genetic contributions to depressive symptoms and inflammatory markers in middle-aged men : The twins heart study. / Su, Shaoyong; Miller, Andrew H.; Snieder, Harold; Bremner, J. Douglas; Ritchie, James; Maisano, Carisa; Jones, Linda; Murrah, Nancy V.; Goldberg, Jack; Vaccarino, Viola.

In: Psychosomatic Medicine, Vol. 71, No. 2, 01.01.2009, p. 152-158.

Research output: Contribution to journalArticle

Su, S, Miller, AH, Snieder, H, Bremner, JD, Ritchie, J, Maisano, C, Jones, L, Murrah, NV, Goldberg, J & Vaccarino, V 2009, 'Common genetic contributions to depressive symptoms and inflammatory markers in middle-aged men: The twins heart study', Psychosomatic Medicine, vol. 71, no. 2, pp. 152-158. https://doi.org/10.1097/PSY.0b013e31819082ef
Su, Shaoyong ; Miller, Andrew H. ; Snieder, Harold ; Bremner, J. Douglas ; Ritchie, James ; Maisano, Carisa ; Jones, Linda ; Murrah, Nancy V. ; Goldberg, Jack ; Vaccarino, Viola. / Common genetic contributions to depressive symptoms and inflammatory markers in middle-aged men : The twins heart study. In: Psychosomatic Medicine. 2009 ; Vol. 71, No. 2. pp. 152-158.
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AU - Ritchie, James

AU - Maisano, Carisa

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AU - Murrah, Nancy V.

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N2 - OBJECTIVE:: To examine the extent to which a common genetic pathway is also involved in the relationship between depressive symptoms, in the absence of major depressive disorder (MDD), and inflammation. Recent data suggested that MDD and inflammation share common genes. METHODS:: We recruited 188 male twins from the Vietnam Era Twin Registry who were free of symptomatic coronary artery disease and MDD, with mean ± standard deviation (SD) age of 55 ± 2.75 years, including 54 monozygotic and 40 dizygotic twin pairs. These pairs were assessed for two inflammatory markers, interleukin (IL)-6 and C-reactive protein (CRP). Current depressive symptoms were measured with the Beck Depression Inventory-II. Generalized estimating equations were used to examine the phenotypic association between depression and inflammatory markers. Biometrical genetic modeling was performed to estimate the genetic and environmental contributions to this association. RESULTS:: An association was observed between severity of current depressive symptoms and increased levels of inflammatory markers (p < .001 for IL-6 and p = .005 for CRP). After adjustment for other factors, the association was slightly attenuated but remained statistically significant for IL-6 (p = .002). The heritability of IL-6, CRP, and depressive symptoms were estimated as 0.37, 0.65, and 0.48, respectively. Genetic modeling found a significant genetic correlation between IL-6 and depressive symptoms (rG = 0.22, p = .046), indicating that about 66% of the covariance between them can be explained by shared genetic influences. CONCLUSIONS:: Current depressive symptoms are significantly correlated with inflammatory markers. This covariation is due, in large part, to genes that are common to depressive symptoms and inflammation.

AB - OBJECTIVE:: To examine the extent to which a common genetic pathway is also involved in the relationship between depressive symptoms, in the absence of major depressive disorder (MDD), and inflammation. Recent data suggested that MDD and inflammation share common genes. METHODS:: We recruited 188 male twins from the Vietnam Era Twin Registry who were free of symptomatic coronary artery disease and MDD, with mean ± standard deviation (SD) age of 55 ± 2.75 years, including 54 monozygotic and 40 dizygotic twin pairs. These pairs were assessed for two inflammatory markers, interleukin (IL)-6 and C-reactive protein (CRP). Current depressive symptoms were measured with the Beck Depression Inventory-II. Generalized estimating equations were used to examine the phenotypic association between depression and inflammatory markers. Biometrical genetic modeling was performed to estimate the genetic and environmental contributions to this association. RESULTS:: An association was observed between severity of current depressive symptoms and increased levels of inflammatory markers (p < .001 for IL-6 and p = .005 for CRP). After adjustment for other factors, the association was slightly attenuated but remained statistically significant for IL-6 (p = .002). The heritability of IL-6, CRP, and depressive symptoms were estimated as 0.37, 0.65, and 0.48, respectively. Genetic modeling found a significant genetic correlation between IL-6 and depressive symptoms (rG = 0.22, p = .046), indicating that about 66% of the covariance between them can be explained by shared genetic influences. CONCLUSIONS:: Current depressive symptoms are significantly correlated with inflammatory markers. This covariation is due, in large part, to genes that are common to depressive symptoms and inflammation.

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