Although overwhelming evidence suggests that genetic and environmental risk factors both contribute to the aetiology of major depression (MD), we know little of how these two risk factor domains inter-relate. In particular, can the genetic liability to MD increase the risk of experiencing stressful life events (SLEs)?
Using discrete time survival analysis in a population-based sample of 2164 female twins, we examined whether the risks for nine personal and three aggregate network SLEs were predicted by the level of genetic liability to MD, indexed by the lifetime history of MD in monozygotic and dizygotic co-twins.
Genetic liability to MD was associated with a significantly increased risk for six personal SLEs (assault, serious marital problems, divorce/breakup, job loss, serious illness and major financial problems) and one network SLE (trouble getting along with relatives/friends). This effect was not due to SLEs occurring during depressive episodes. Similar results were found using structural equation twin modelling. In contrast to the pattern observed with MD, the genetic liability to alcoholism impacted on the risk for being robbed and having trouble with the law.
In women, genetic risk factors for MD increase the probability of experiencing SLEs in the interpersonal and occupational/financial domains. Genes can probably impact on the risk for psychiatric illness by causing individuals to select themselves into high risk environments.
"Some physiological conditions might enhance the inflammatory response to LPS and account for the diversity in symptoms and course of PD, as well as for individuals’ responses to medication after the onset of PD
. Stress is widely acknowledged to be a predisposing and precipitating factor in psychiatric illnesses
[35,36] and some neurodegenerative diseases. It was one of the earliest proposed causes of PD
[Show abstract][Hide abstract] ABSTRACT: Parkinson's disease is an irreversible neurodegenerative disease linked to progressive movement disorders and is accompanied by an inflammatory reaction that is believed to contribute to its pathogenesis. Since sensitivity to inflammation is not the same in all brain structures, the aim of this work was to test whether physiological conditions as stress could enhance susceptibility to inflammation in the substantia nigra, where death of dopaminergic neurons takes place in Parkinson's disease.
To achieve our aim, we induced an inflammatory process in nonstressed and stressed rats (subject to a chronic variate stress) by a single intranigral injection of lipopolysaccharide, a potent proinflammogen. The effect of this treatment was evaluated on inflammatory markers as well as on neuronal and glial populations.
Data showed a synergistic effect between inflammation and stress, thus resulting in higher microglial activation and expression of proinflammatory markers. More important, the higher inflammatory response seen in stressed animals was associated with a higher rate of death of dopaminergic neurons in the substantia nigra, the most characteristic feature seen in Parkinson's disease. This effect was dependent on glucocorticoids.
Our data demonstrate that stress sensitises midbrain microglia to further inflammatory stimulus. This suggests that stress may be an important risk factor in the degenerative processes and symptoms of Parkinson's disease.
Journal of Neuroinflammation 02/2014; 11(1):34. DOI:10.1186/1742-2094-11-34 · 5.41 Impact Factor
"In the present study we set out to investigate the heritability of maternal negativity, paternal negativity and negative life events in an adolescent twin sample. As has been reported previously in this sample (Button et al. 2008) and others (Kendler et al. 1993; Plomin et al. 1990; Saudino et al. 1997), all 3 measures are heritable. Multivariate genetic analyses revealed that this heritability could be accounted for by the association of these environmental stressors with common behavioural and emotional difficulties experienced during adolescence. "
[Show abstract][Hide abstract] ABSTRACT: An increasing body of evidence shows that many 'environmental' measures are heritable, indicating genetic involvement in environmental exposure (or gene-environment correlation). In the present study we attempt to clarify why three such 'environmental' measures (maternal negativity, paternal negativity and negative life events) are consistently found to be heritable. Through multivariate genetic analysis of a sample of adolescent twins from the UK we show that the heritability of these putative environmental measures can be explained via their association with five behavioural phenotypes: oppositionality, delinquency, physical aggression, depression and anxiety. This is consistent with the notion that being genetically susceptible to certain behavioural difficulties could lead to exposure to certain life events, and this may account for the reported heritability of 'environmental' measures. Results are discussed in the context of possible active, evocative and passive gene-environment correlations.
"Classic biometric modeling of independent ACE contributions to trait variance has generally not supported a significant role of the common environment for temperament and related constructs (e.g. Kendler et al., 1996; McCall, 1991; Mullineaux, Deater-Deckard, Petrill, Thompson, & DeThorne, 2009; Plomin, Defries, McClearn, & McGuffin, 2001; Saudino, 2005; Saudino & Cherny, 2001; Slutske et al., 1997), with the reduced AE model often best representing the variance. As a result, several theorists have stressed that family environments within the normal range are not important for child development (Bouchard, 2004; Harris, 1998; Rowe, 1994; Scarr, 1992). "
[Show abstract][Hide abstract] ABSTRACT: Biological parents pass on genotypes to their children, as well as provide home environments that correlate with their genotypes; thus, the association between the home environment and children's temperament can be genetically (i.e., passive gene-environment correlation) or environmentally mediated. Furthermore, family environments may suppress or facilitate the heritability of children's temperament (i.e., gene-environment interaction). The sample comprised 807 twin pairs (mean age = 7.93 years) from the longitudinal Wisconsin Twin Project. Important passive gene-environment correlations emerged, such that home environments were less chaotic for children with high effortful control, and this association was genetically mediated. Children with high extraversion/surgency experienced more chaotic home environments, and this correlation was also genetically mediated. In addition, heritability of children's temperament was moderated by home environments, such that effortful control and extraversion/surgency were more heritable in chaotic homes, and negative affectivity was more heritable under crowded or unsafe home conditions. Modeling multiple types of gene-environment interplay uncovered the complex role of genetic factors and the hidden importance of the family environment for children's temperament and development more generally.
Development and Psychopathology 02/2013; 25(1):51-63. DOI:10.1017/S0954579412000892 · 4.89 Impact Factor
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