Heritability of individual depressive symptoms

Jang, Kerry L.; Livesley, W. John; Taylor, Steven; Stein, Murray B.; Moon, Erin C.

doi:10.1016/s0165-0327(03)00108-3

Cited by 74 publications

(72 citation statements)

References 15 publications

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“…Finally, different genetic regions have been associated with specific mood and anxiety traits in both mice (Henderson et al, 2004), and humans (Foley et al, 2003;Jang et al, 2004), which can affect genetic association study results (Lotrich, 2011). Consistent with this, we have found that polymorphisms affecting TNF-a and IL-28b are associated with specific mood-related symptom clusters in individuals receiving IFN-a (Lotrich et al, 2010;Lotrich et al, 2011).…”

Section: Introductionsupporting

confidence: 82%

“…In fact, different specific depression symptoms may be influenced by different genes (Jang et al, 2004), a phenomenon long noted in mice where different chromosomal regions are implicated in anxiety-depending on what behavioral test is used (Henderson et al, 2004). The possibility that the Met allele is only associated with risk for a subset of symptoms may be one plausible reason that some studies do not replicate an association between depression risk and the BDNF Val/Met polymorphism Figueira et al, 2010;Middeldorp et al, 2010;Ribeiro et al, 2007;Suchanek et al, 2011;Wray et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

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Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Lotrich

Albusaysi

Ferrell

2012

Neuropsychopharmacol

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Depression has been associated with inflammation, and inflammation may both influence and interact with growth factors such as brainderived neurotrophic factor (BDNF). Both the functional Val66Met BDNF polymorphism (rs6265) and BDNF levels have been associated with depression. It is thus plausible that decreased BDNF could mediate and/or moderate cytokine-induced depression. We therefore prospectively employed the Beck Depression Inventory-II (BDI-II), the Hospital Anxiety and Depression Scale (HADS), and the Montgomery-Asberg Depression Rating Scale (MADRS) in 124 initially euthymic patients during treatment with interferon-alpha (IFN-a), assessing serum BDNF and rs6265. Using mixed-effect repeated measures, lower pretreatment BDNF was associated with higher depression symptoms during IFN-a treatment (F 144,17.2 ¼ 6.8; Po0.0001). However, although the Met allele was associated with lower BDNF levels (F 1,83.0 ¼ 5.0; P ¼ 0.03), it was only associated with increased MADRS scores (F 4,8.9 ¼ 20.3; Po0.001), and not the BDI-II or HADS. An exploratory comparison of individual BDI-II items indicated that the Met allele was associated with suicidal ideation, sadness, and worthlessness, but not neurovegetative symptoms. Conversely, the serotonin transporter promoter polymorphism (5-HTTLPR) short allele was associated with neurovegetative symptoms such as insomnia, poor appetite and fatigue, but not sadness, worthlessness, or suicidal ideation. IFN-a therapy further lowered BDNF serum levels (F 4,37.7 ¼ 5.0; P ¼ 0.003), but this decrease occurred regardless of depression development. The findings thus do not support the hypothesis that decreasing BDNF is the primary pathway by which IFN-a worsens depression. Nonetheless, the results support the hypothesis that BDNF levels influence resiliency against developing inflammatory cytokine-associated depression, and specifically to a subset of symptoms distinct from those influenced by 5-HTTLPR. Neuropsychopharmacology (2013) 38, 985-995;

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Section: Introductionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Lotrich

Albusaysi

Ferrell

2012

Neuropsychopharmacol

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“…For NA, our present findings are comparable with those reported in multiple previous studies (15-23) on related personality traits such as neuroticism, and emphasize the difference between negative affect (referring to mood state), which was found not to be heritable (37) and NA, a stable predisposition to experience negative emotions that shows a substantial genetic contribution. This study is the first to report heritability estimates for type-D personality and SI.…”

Section: Discussionsupporting

confidence: 91%

Heritability of Type-D Personality

Kupper

Denollet

Geus

et al. 2007

Psychosomatic Medicine

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Objective: To quantify the influence of genes and environment on individual differences in type-D status, and the type-D subcomponents negative affectivity and social inhibition. Type-D personality independently predicts poor prognosis in patients with cardiovascular disease. However, no previous study has determined the heritability of type-D personality. Methods: This study determined type-D personality by applying the "combination of scales" method to survey data collected by the Netherlands Twin Register in 3331 healthy, young adult twins. Using structural equation modeling (SEM), the relative contributions of additive genetic, nonadditive genetic, and nonshared environmental factors to the variance in type-D and its subcomponents were determined. Results: SEM indicated that type-D personality was substantially heritable (52%). The subcomponents negative affectivity and social inhibition were equally heritable, with broad heritability estimates of 46% and 50%. Although negative affectivity was determined by additive genetic effects and nonshared environment, individual differences in social inhibition were predominantly determined by nonadditive genetic effects and nonshared environment. Conclusions: This study provides strong evidence that genes are important in determining individual differences in type-D personality and the type-D subcomponents negative affectivity and social inhibition.

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“…For the subscales, environmental effects explained most of the variation except for psychomotor retardation, which had a slight genetic effect, the genetic effect being more evident among older twins. Jang et al (2004) recently reported the heritability in the subscales of CES-D and other depression scales among young adults. The results indicated genetic effect (between 18% and 35%) on the subscales that reflect physiologic functions, such as loss of appetite, loss of pleasure, and cognitions such as feelings of guilt, hopelessness and positive affect.…”

mentioning

confidence: 99%