The DOI matches its Crossref record; 172 of the 174 references it cites were found in a registry or an index; 1 of the 97 sources its claims cite were checked for support.
Gene–environment interactions: early life stress and risk for depressive and anxiety disorders
Open accessAbstract
Rationale Prior reviews have examined how stress, broadly defined, interacts with genetic diathesis in the pathogenesis of internalizing (i.e., depressive and anxiety) disorders. Recent findings have suggested a unique role for early life stress (ELS) in the development of internalizing disorders, contributing to the rapid proliferation of research in this area.Objective This paper critically reviews studies in humans examining gene-environment interaction (GxE) effects of ELS on the risk for depression and anxiety, primarily from a candidate gene perspective. Major methodological challenges that are unique to such studies are considered.Results The majority of published studies have focused on candidates that regulate the serotonin system, especially the serotonin transporter. More recent work has addressed interactions of ELS with candidates from the hypothalamic-pituitary-adrenal axis and neurotrophin system. Available studies vary greatly with respect to definitions of ELS, examination of gene-gene interactions, consideration of gender effects, and attention to analytic limitations.Conclusions Overall, there is support for GxE effects of ELS on the risk for depressive and anxiety outcomes. Future studies of ELS in this context will require careful attention to methodologic considerations. Such studies would benefit from more systematic assessment of positive environmental factors (e.g., social support) and greater utilization of developmentally sensitive paradigms.
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70 Not checked yet · 10 No basis given · 9 Own interpretation · 3 Own method · 2 Own result · 1 Partly supported · accuracy not yet measured
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In the paper
“Findings from 15 of the 22 samples tested support increased risk for internalizing symptoms in participants with the low-expression short alleles and ELS in all participants”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
plaincorrelationaln = 15- Asserted: passes — The authors put it forward as true.
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In the paper
“many studies do not report whether they have tested for rGE between ELS and genotype”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
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In the paper
“the majority of G×ELS studies to date have involved gene variants that regulate brain serotonin systems (Tables 1 and 2); in particular, numerous studies have focused on 5-HTTLPR”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Another major source of inconsistency involves the type of early stress under study. Whereas some studies have focused on direct childhood maltreatment, such as abuse and neglect, others have included more broadly experienced events, such as parental arguing/divorce, or qualitatively distinct circumstances, such as poverty or parent education levels.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“However, relatively few studies separately test for GxE effects within gender or type of ELS.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Although no published meta-analyses have focused on gene by ELS interactions”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“published studies are characterized by considerable differences in methodology, especially in terms of ELS measurement.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
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In the paper
“Studies yielding inconsistent findings have often relied on suboptimal timing of ELS assessment (ranging from a single measurement at 3 months of age to retrospective accounts of childhood provided by advanced-age participants).”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
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In the paper
“A substantially elevated risk of internalizing (i.e., depressive and anxiety) disorders following ELS is particularly well documented”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Early life stress and risk for depressive and anxiety disorders
What the sources say
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In the paper
“Early life stress (ELS) is an established predictor of adverse outcomes across the lifespan encompassing neurocognitive, behavioral, health, and psychiatric domains”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Early life stress and risk for depressive and anxiety disorders
What the sources say
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Polanczyk et al. concluded that the GxE effect was supported, but with the effect specific to depression-relevant emotional memories assessed with the CTQ.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > HPA axis
What the sources say
- Partly supportedcites Polanczyk et al. (2009) sourceExperimental — accuracy not yet measured
The Comment reports a significant gene–environment interaction in the E-Risk Study, where maltreatment was assessed with the CTQ, but no replication in the Dunedin Study. It describes the CTQ as tapping depression-relevant emotional memories; however, the authors present the role of those memories as a hypothesis they could not test, not an established specificity of the effect. Our copy provides no page numbers for these passages. (LLM, conf=0.89)
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- Partly supported
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In the paper
“most of the studies reviewed here have either comprised racially homogeneous groups or have adjusted their models for population stratification; however, some studies have not reported on this important issue”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
plain- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“to our knowledge there is only 1 report examining interactions with ELS.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Other candidate genes
hedged- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“However, it is important to note that these reviews included studies of life events occurring throughout the lifespan and did not formally address the potentially differential effects of ELS relative to adult stressors.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Evidence from studies reviewed here supports the existence of differences in the impact of type of ELS, and these effects may be gender-specific (Cicchetti et al. 2007; Heim et al. 2009; Sjoberg et al. 2006).”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
What the sources say
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Several studies have notably failed to detect these effects.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Conclusions and future directions
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“Studies that did observe rGE should be interpreted with caution, as it is possible that rGE can account for apparent GxE effects.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“In the first of two samples tested by Chipman et al. (2007), genotype frequencies were not in HWE, and no GxE interaction was detected.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
What the sources say
- Not checked yetcites Chipman et al. (2007) source
plainn = 2- Asserted: passes — The authors put it forward as true.
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In the paper
“Achieving sufficient statistical power presents a special challenge because interaction effects require larger numbers of subjects for adequate power (Brookes et al. 2001; Luan et al. 2001; Uher 2008), and power depends on allele frequencies in addition to exposure to ELS (Munafo et al. 2009).”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Gene–environment interactions > Methodological considerations
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Similarly, Aguilera et al. (2009) showed a GxE effect of the 5-HTTLPR s allele and a history of childhood sexual abuse on depressive symptoms, but also observed rGE, in which the l/l genotype was more strongly associated with childhood sexual abuse than the l/s genotype.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
What the sources say
- Not checked yetcites Aguilera et al. (2009) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Although no main or interaction effects for the 5-HT2C VNTR were found, a significant main effect for increased depression in T allele carriers of the 5-HT2A T102C was observed.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
What the sources say
- Not checked yetcites Eley et al. (2004) source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“In the case of ELS, the nature and timing of the stress exposure may be a critical determinant of the sequelae, while the method of assessment (i.e., prospective, retrospective; interview, records, questionnaire) may be similarly critical in permitting detection of any moderation by candidate risk genes”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Gene–environment interactions > Methodological considerations
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“In addition, there was a GxE interaction such that men reporting ELS with an A allele had decreased cortisol responses compared with women reporting ELS, but responses of men and women without ELS did not differ.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > HPA axis
What the sources say
- Not checked yetcites Heim et al. (2009) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“The short (s) allele of this polymorphism confers lower transcriptional efficiency than the long (l) allele, and is associated with decreased transporter expression and serotonin reuptake”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
What the sources say
- Not checked yetcites Lesch et al. 1996 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Wichers et al. (2008), identified a three-way interaction between ELS, 5-HTTLPR, and BDNF, which the authors acknowledged must be qualified by the fact that they also found rGE between BDNF genotype and reported childhood adversity (with increased adversity reported by youth with Val/Met relative to Val/Val).”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
What the sources say
- Not checked yetcites Wichers et al. (2008) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Seven of ten single nucleotide polymorphisms (SNPs) spanning the gene showed significant interactions, with the rs110402 and rs7209436 SNPs significant even after correction for multiple tests.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > HPA axis
What the sources say
- Not checked yetcites Bradley et al. 2008 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“However, continuous measures of depression or anxiety disorders are also problematic in that they generally provide accurate assessments only of current symptoms, and therefore may miscategorize those individuals who have a history of such symptoms but are currently in remission.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Gene–environment interactions > Methodological considerations
hedgedconditional- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“The effects of genetic and environmental factors on symptoms of depression and anxiety have also been shown to differ as a function of age (Tambs and Mourn 1993) and gender (Eaves et al. 1997), so these factors should be considered in GxE analyses.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Gene–environment interactions > Methodological considerations
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Men, but not women, who were carriers of the A allele had decreased cortisol responses compared with men with the G/G genotype.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > HPA axis
What the sources say
- Not checked yetcites Heim et al. (2009) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“suggesting that prior findings of elevated depressive symptoms in individuals with this genotype and childhood maltreatment could reflect alterations in neuroendocrine stress responding.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > HPA axis
What the sources say
- Not checked yetcites Tyrka et al. (2009) source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
In the paper
“Although the replication sample did not show a departure from HWE, as the authors noted, findings from the replication sample were limited by the fact that very few adolescents categorized as having persistent adversity had high levels of depressive symptoms.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Serotonin system
What the sources say
- Not checked yetcites Chipman et al. (2007) source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Differences in both genetic and environmental determinants of childhood- vs. adult-onset disorders could be expected, limiting the validity of studies that combine these conditions.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Munafo et al. (2009) conducted a meta-analysis which led them to conclude that most of the available studies were underpowered, and that findings using logistic regression models were “compatible with chance.””
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
What the sources say
- Not checked yetcites Munafo et al. (2009) source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Reciprocal interactions between BDNF and serotonin have also been well documented (Duman 2002; MacQueen et al. 2003).”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Neurotrophins
What the sources say
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“This effect was specific to depression and did not predict anxiety symptoms.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Other candidate genes
What the sources say
- Not checked yetcites Haeffel et al. 2008 source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Psychiatric disorders tend to co-occur, and are also heterogeneous, so that efforts to examine dichotomous diagnoses, a common approach in genetic research, are problematic (Eaves 2006).”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
What the sources say
- Not checked yetcites Eaves 2006 source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Caspi et al. (2010), recently reviewing the role of 5-HTTLPR in stress sensitivity from a broader perspective, asserted a prominent role for this gene in the neurobiological and behavioral responses to stress.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
What the sources say
- Not checked yetcites Caspi et al. (2010) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Since altered sensitivity of GRs is thought to mediate HPA axis dysregulation in depression and PTSD (Raison and Miller 2003), genes regulating components of this system are likely candidates for GxE investigations of the etiopathology of depression and anxiety (Charney 2004; Wust et al. 2004a; Wust et al. 2004b).”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > HPA axis
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Dopamine, which plays a central role in motivation and pleasure, has also been implicated in the pathophysiology of depression (Dunlop and Nemeroff 2007).”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Other candidate genes
What the sources say
- Not checked yetcites Dunlop and Nemeroff 2007 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“and has been implicated in impaired extinction of conditioned fear response and atypical frontoamygdala activity in humans (Soliman et al. 2010)”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Neurotrophins
What the sources say
- Not checked yetcites Soliman et al. 2010 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“FKBP5 interacted with reported childhood maltreatment to predict PTSD symptoms.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > HPA axis
What the sources say
- Not checked yetcites Binder et al. 2008 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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The quote only partly states this claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Examination of continuous measures affords greater statistical power and may decrease statistical error due to miscategorization of “subthreshold” individuals (Caspi et al. 2010; Plomin and Davis 2009).”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Significant interactions between BDNF Val66Met and ELS were observed, with BDNF Met carriers exposed to high ELS showing poorer working memory, elevated heart rate in resting and arousal conditions, and smaller hippocampus and amygdala volumes.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > Neurotrophins
What the sources say
- Not checked yetcites Gatt et al. (2009) source
plaincorrelationaln = 374- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“a recent meta-analysis by Risch et al. (2009) examined GxE between stressful life events and 5-HTTLPR on depression using 14 studies (N=14,250). Just under half of the included studies focused on the effects of ELS. The authors concluded that there was no support for an interaction effect”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Inconsistencies in the literature: methodological issues
What the sources say
- Not checked yetcites Risch et al. (2009) source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“there was an interaction between childhood experiences of crime and abuse and FKBP5 genotype in predicting PTSD in African Americans, but not European Americans.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Candidate genes and effects of early life stress > HPA axis
What the sources say
- Not checked yetcites Xie et al. (2009) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“studies reviewed here suggest that differences in findings may be attributable to: (1) type of ELS, (2) gender-related effects, (3) additional interactive or additive environmental influences, such as social support, and (4) additional moderating genes.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Conclusions and future directions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Timing of ELS is likely also critically important, and may further explain inconsistencies in the literature.”
§ Gene–environment interactions: early life stress and risk for depressive and anxiety disorders > Conclusions and future directions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The authors state this as an assumption.
Common diseases are influenced by common genetic variants.
“Candidate gene research is predicated on the assumption that common diseases are influenced by common genetic variants”
The paper relies on this without support.
Early life stress does not invariably lead to dysfunction and is not a specific risk factor for any particular disorder.
“ELS does not invariably lead to dysfunction, nor is it a specific risk factor for any particular disorder.”
The authors state this as an assumption.
An increasingly accepted gene–environment model assumes that genes may interact with environmental influences on both ends of the spectrum, with risk and resilience resulting from exposure to negative and positive environments, respectively.
“Finally, an increasingly accepted GxE model assumes genes may interact with environmental influences on both ends of the spectrum, with risk and resilience resulting from exposure to negative and positive environments, respectively.”
The paper relies on this without support.
Some types of adversity commonly co-occur, while others, such as sexual abuse, may occur in isolation.
“A further complication is that some types of adversity commonly co-occur, while others, such as sexual abuse, may occur in isolation.”
The paper relies on this without support.
Identified stressors may occur in the context of additional adversity that is not consistently identified or examined.
“Moreover, identified stressors may occur in the context of additional adversity that is not consistently identified or examined.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Candidate genetic risk factors play functional roles in serotonin transport, activation of the HPA-axis via corticotropin releasing hormone (CRH), glucocorticoid sensitivity, and production of brain derived neurotrophic factors (BDNF).”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Nugent et al., 2011
In the citing paper
“there is evidence to support that specific genetic risk factors can predispose an individual to psychopathology in the presence of increasing life stress”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Nugent et al., 2011
In the citing paper
“It is notable that each of these identified risk factors has distinct links to functioning of the HPA-axis and inflammatory activity.”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Nugent et al., 2011
Citations
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Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene
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“Of the 13 studies including physical abuse as an ELS, ten found support for GxE with risk associated with the s/s′ allele (Aguilera et al. 2009; Åslund et al. 2009; Caspi et al. 2003; Cicchetti et al. 2007; Kaufman et al. 2006; Kaufman et al. 2004; Stein et al. 2008; Taylor et al. 2006; Wichers et al. 2008; Xie et al.…”
BackgroundMethodInfluentialLesch, K.-P., Bengel, D., Heils, A., Sabol, S. Z., Greenberg, B. D., Petri, S., Benjamin, J., Müller, C. R., Hamer, D. H., & Murphy, D. L. (1996) · Science · doi:10.1126/science.274.5292.1527 · Cited by 5,162 · cited 1×
“The short (s) allele of this polymorphism confers lower transcriptional efficiency than the long (l) allele, and is associated with decreased transporter expression and serotonin reuptake (Lesch et al. 1996).”
BackgroundStress and the brain: from adaptation to disease
de Kloet, E. R., Joëls, M., & Holsboer, F. (2005) · Nature Reviews Neuroscience · doi:10.1038/nrn1683 · Cited by 4,621 · cited 1×
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BackgroundMethodology for Genetic Studies of Twins and Families
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“The Met allele of the functional BDNF Val66Met polymorphism confers abnormal intracellular packaging and secretion of BDNF (Egan et al. 2003), and has been implicated in impaired extinction of conditioned fear response and atypical frontoamygdala activity in humans (Soliman et al. 2010), as well as…”
BackgroundA Neurotrophic Model for Stress-Related Mood Disorders
Duman, R. S., & Monteggia, L. M. (2006) · Biological Psychiatry · doi:10.1016/j.biopsych.2006.02.013 · Cited by 3,375 · cited 20×
“A study of depressed inpatients found that those with two copies of the Met allele of BDNF Val66Met had elevated adrenocorticotropic hormone and cortisol responses to the Dex/CRH text (Schule et al. 2006).”
BackgroundInfluentialBeyond diathesis stress: differential susceptibility to environmental influences
Belsky, J., & Pluess, M. (2009) · Psychological Bulletin · doi:10.1037/a0017376 · Cited by 3,039 · cited 2×
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BackgroundNature-nurture reconceptualized in developmental perspective: A bioecological model.
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BackgroundValidity of adult retrospective reports of adverse childhood experiences: review of the evidence
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“…may be a critical determinant of the sequelae, while the method of assessment (i.e., prospective, retrospective; interview, records, questionnaire) may be similarly critical in permitting detection of any moderation by candidate risk genes (Hardt and Rutter 2004; Moffitt et al. 2005; Paivio 2001).”
BackgroundMethodChristakis, D., Richards, J. A., Zimmerman, F. J., Garrison, M. M., Xu, D., & Yapanel, U. H. (2009) · Cited by 2,290
Cited by
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Child Development in the Context of Disaster, War, and Terrorism: Pathways of Risk and Resilience
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“…in stress response, also have been implicated as potential moderators of trauma response in geneby-environment (G x E) studies, including research on the corticotropin-releasing hormone type 1 receptor and glucocorticoid receptor genes (Cicchetti 2010, Nugent et al. 2011, Pratchett & Yehuda 2011).”
de Figueiredo, C. S., Sandre, P. C., Portugal, L. C. L., Mázala-de-Oliveira, T., Chagas, L. D. S., Raony, Í., Ferreira, E. S., Giestal‐de‐Araujo, E., dos Santos, A. A., & Oliveira-Silva, P. (2020) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2020.110171 · Cited by 720
Modulation of the Hypothalamic-Pituitary-Adrenal Axis by Early Life Stress Exposure
van Bodegom, M., Homberg, J. R., & Henckens, M. J. A. G. (2017) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2017.00087 · Cited by 606
Cultural evolutionary theory: How culture evolves and why it matters
Creanza, N., Kolodny, O., & Feldman, M. W. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1620732114 · Cited by 482
Future Directions in Emotion Dysregulation and Youth Psychopathology
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Neurobiology and consequences of social isolation stress in animal model—A comprehensive review
Mumtaz, F., Khan, M. I., Zubair, M., & Dehpour, A. R. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.05.086 · Cited by 369
Sex differences in anxiety and emotional behavior
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“particular relevance because acute, repeated, or chronic stress exposures are common triggers for these psychiatric disorders [273, 286], because women may have an inherently increased stress vulnerability, and because key symptoms of these disorders have been successfully modeled in animals.”
BackgroundTelomeres and early-life stress: an overview
Price, L. H., Kao, H.-T., Burgers, D. E., Carpenter, L. L., & Tyrka, A. R. (2013) · Biological Psychiatry · doi:10.1016/j.biopsych.2012.06.025 · Cited by 339
Self-citationHigh anxiety trait: A vulnerable phenotype for stress-induced depression
Weger, M., & Sandi, C. (2018) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2018.01.012 · Cited by 289
“There are excellent examples of the moderate impact of specific genes, particularly from the monoaminergic system and the HPA axis, in defining subsequent behavioral adaptations (Nugent et al., 2011; Scheuer et al., 2016; Zannas and Binder, 2014).”
Sex differences in the elevated plus-maze test and large open field test in adult Wistar rats.
Knight, P., Chellian, R., Wilson, R., Behnood-Rod, A., Panunzio, S., & Bruijnzeel, A. W. (2021) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2021.173168 · Cited by 252
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“Recently, genome-wide association studies have implicated several SNPs associated with major depression (Hek et al., 2013; Lewis et al., 2010; Nugent et al., 2011; Sullivan et al., 2009).”
Hsu, D. T., Kirouac, G. J., Zubieta, J.-K., & Bhatnagar, S. (2014) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2014.00073 · Cited by 238
“Stressful life events can facilitate and exacerbate anxiety disorders (ADs), substance use disorder (SUD), and major depressive disorder (MDD; Hammen, 2005; Andersen and Teicher, 2009; Nugent et al., 2011).”
BackgroundPrenatal stress and epigenetics
Cao-Lei, L., de Rooij, S. R., King, S., Matthews, S. G., Metz, G. A. S., Roseboom, T. J., & Szyf, M. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.05.016 · Cited by 253
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“This literature has been thoroughly and carefully reviewed and goes beyond the scope of this review (See for example Nugent et al., 2011; Tyrka et al., 2013).”
Nolte, T., Guiney, J., Fonagy, P., Mayes, L. C., & Luyten, P. (2011) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2011.00055 · Cited by 210
“Stress in a child’s early caregiving environment has been linked to lasting adverse effects on both physiological and psychological domains of development (National Scientific Council on the Developing Child, 2005; Gunnar and Quevedo, 2007; Nugent et al., 2011).”
The serotonin-BDNF duo: developmental implications for the vulnerability to psychopathology
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The gut microbiome and mental health: implications for anxiety- and trauma-related disorders
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“Investigations of gene–gene and gene– environment interactions (Nugent et al., 2011), copy number variations (Bersani et al., 2016; Fung et al., 2010; Kawamura et al., 2011), and epigenetic factors (Cappi et al., 2016; Kim et al., 2017) have yielded some additional insights into the molecular…”
Genetic Determinants of Depression: Recent Findings and Future Directions
Dunn, E. C., Brown, R. C., Dai, Y., Rosand, J., Nugent, N. R., Amstadter, A. B., & Smoller, J. W. (2015) · Harvard Review of Psychiatry · doi:10.1097/hrp.0000000000000054 · Cited by 158
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The neurobiological correlates of childhood adversity and implications for treatment
Tyrka, A. R., Burgers, D. E., Philip, N. S., Price, L. H., & Carpenter, L. L. (2013) · Acta Psychiatrica Scandinavica · doi:10.1111/acps.12143 · Cited by 142
Self-citationHow age, sex and genotype shape the stress response
Novais, A., Monteiro, S., Roque, S., Correia‐Neves, M., & Sousa, N. (2016) · Neurobiology of Stress · doi:10.1016/j.ynstr.2016.11.004 · Cited by 152
“…from mothers with depression or neglected/abused infants, is associated with increased susceptibility to the effects of stress later in life and vulnerability to develop stress-related psychiatric disorders (Graham et al., 1999; Nugent et al., 2011) and cardiovascular diseases (Loria et al., 2014).”
BackgroundYorgason, J. T., España, R. A., Konstantopoulos, J. K., Weiner, J. L., & Jones, S. R. (2013) · European Journal of Neuroscience · doi:10.1111/ejn.12113 · Cited by 136
Kendler, K. S. (2011) · Molecular Psychiatry · doi:10.1038/mp.2011.70 · Cited by 128
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Schirmbeck, F. N., & Zink, M. (2013) · Frontiers in Pharmacology · doi:10.3389/fphar.2013.00099 · Cited by 125
“GxEIs are core elements within current theories of schizophrenia (van Os and Kapur, 2009; van Os et al., 2008, 2010), depression (Keers and Uher, 2012), anxiety disorders (Gregory et al., 2008; Nugent et al., 2011) and OCD (Nicolini et al., 2009; Pauls, 2010).”
BackgroundCórdova-Palomera, A., Fatjó-Vilas, M., Gastó, C., Navarro, V, Krebs, M.-O., & Fañanás, L. (2015) · Translational Psychiatry · doi:10.1038/tp.2015.49 · Cited by 117
Childhood maltreatment and methylation of FK506 binding protein 5 gene (FKBP5)
Tyrka, A. R., Ridout, K. K., Parade, S. H., Paquette, A., Marsit, C. J., & Seifer, R. (2015) · Development and Psychopathology · doi:10.1017/s0954579415000991 · Cited by 118
Self-citationSocial isolation rearing increases dopamine uptake and psychostimulant potency in the striatum
Yorgason, J. T., Calipari, E. S., Ferris, M. J., Karkhanis, A. N., Fordahl, S. C., Weiner, J. L., & Jones, S. R. (2015) · Neuropharmacology · doi:10.1016/j.neuropharm.2015.10.025 · Cited by 114
“…in humans is associated with increased risk for developing severe psychological disorders including schizophrenia, depression, and anxiety disorders, as well as risk for abusing and becoming addicted to drugs such as psychostimulants (Scheller-Gilkey et al., 2004; Nugent et al., 2011; Enoch, 2012).”
Wang, X., Labermaier, C., Holsboer, F., Wurst, W., Deussing, J. M., Müller, M. B., & Schmidt, M. V. (2012) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2012.08148.x · Cited by 108
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“…susceptibility to depression has lead to recent theories proposing a role of gene-by-environment interactions in the etiology of depression, in which genetic predisposition modulates vulnerability in the depressogenic response to environmental stressors (Kas et al., in press; Nugent et al., 2011).”
BackgroundChronic unpredictable stress impairs endogenous antioxidant defense in rat brain
Che, Y., Zhu, Z., Shu, Y., Zhai, C., Zhu, Y., Gong, S., Cui, Y., & Wang, J. (2014) · Neuroscience Letters · doi:10.1016/j.neulet.2014.10.031 · Cited by 99
The Clinical Implications of Mouse Models of Enhanced Anxiety
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“Second, the mouse models described so far mostly reflect either genetic or environmental manipulations rather than mimicking the interaction of these two risk factors, though such interaction seems to be critical in the clinical manifestation of anxiety disorders [7,159].”
Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders
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Gene–Environment Interactions and Intermediate Phenotypes: Early Trauma and Depression
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Chronic unpredictable stress induces anxiety-like behaviors in young zebrafish
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Early Life Stress, Physiology, and Genetics: A Review
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Cohen, Z. P., Cosgrove, K. T., DeVille, D. C., Akeman, E., Singh, M. K., White, E. J., Stewart, J. L., Aupperle, R. L., Paulus, M. P., & Kirlić, N. (2021) · Frontiers in Pediatrics · doi:10.3389/fped.2021.622608 · Cited by 85
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“Anxiety and depression are stress-related common mental disorders and are caused by a combination of multiple genetic and environmental factors affecting certain brain circuits [3].”
Background“Bedside-to-Bench” Behavioral Outcomes in Animal Models of Pain: Beyond the Evaluation of Reflexes
Cobos, E. J., & Portillo-Salido, E. F. (2013) · Current Neuropharmacology · doi:10.2174/1570159x113119990041 · Cited by 78
Fesharaki‐Zadeh, A., & Datta, D. (2024) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1371213 · Cited by 83
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“In humans, however, so far only very few studies have been dedicated to G E in anxiety (see Nugent et al. 2011), mostly focussing on variation in the serotonin transporter gene (Stein et al. 2008; Laucht et al. 2009; e.g., Grabe et al. 2009; Klauke et al., 2011).”
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Interaction between the MTHFR C677T polymorphism and traumatic childhood events predicts depression
Lok, A., Bockting, C., Koeter, M. W. J., Snieder, H., Assies, J., Mocking, R. J. T., Vinkers, C. H., Kahn, R. S., Boks, M. P., & Schene, A. H. (2013) · Translational Psychiatry · doi:10.1038/tp.2013.60 · Cited by 64
“This vulnerability becomes exposed when triggered by enhanced environmental stress such as childhood trauma.(37) This could be the result of long-lasting trauma-”
BackgroundGenetic insights into the neurobiology of anxiety
Koskinen, M.-K., & Hovatta, I. (2023) · Trends in Neurosciences · doi:10.1016/j.tins.2023.01.007 · Cited by 73
The Role of Serotonin in Fear Learning and Memory: A Systematic Review of Human Studies
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Serotonin system gene polymorphisms are associated with impulsivity in a context dependent manner
Stoltenberg, S. F., Christ, C. C., & Highland, K. B. (2012) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2012.06.012 · Cited by 62
“For G × E interaction studies focused on adverse early life events, more precise measures of childhood trauma should be investigated to better understand the type, timing, perpe‐ trator, and amount of trauma that increases impulsivity later in life (Nugent et al., 2011).”
Hart, H. C., Lim, L. L., Mehta, M. A., Chatzieffraimidou, A., Curtis, C. J. C., Xu, X., Breen, G. D., Simmons, A., Mirza, K., & Rubia, K. (2017) · PLoS ONE · doi:10.1371/journal.pone.0188744 · Cited by 62
Perspectives on stress resilience and adolescent neurobehavioral function
Romeo, R. D. (2014) · Neurobiology of Stress · doi:10.1016/j.ynstr.2014.11.001 · Cited by 65
“GeneeEnvironment interactions Gene and environment (G E) interactions are another set of variables that need to be taken into consideration when discussing resilience and vulnerability to stressors (Nugent et al., 2011; Caspi and Moffitt, 2006).”
BackgroundPozzi, D., Rasile, M., Corradini, I., & Matteoli, M. (2020) · Translational Psychiatry · doi:10.1038/s41398-020-01027-6 · Cited by 57
Zhou, R., Chen, F., Feng, X., Zhou, L., Li, Y., & Chen, L. (2015) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2015.02.018 · Cited by 58
A biological perspective on differences and similarities between burnout and depression
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Loria, A. S., Ho, D. H., & Pollock, J. S. (2014) · Acta Physiologica · doi:10.1111/apha.12189 · Cited by 53
“In humans, ELS has long been linked to anxiety disorders and depression in adulthood (Nugent et al. 2011, Shapero et al. 2013).”
BackgroundGlotzbach-Schoon, E., Andreatta, M., Reif, A., Ewald, H., Tröger, C., Baumann, C., Deckert, J., Mühlberger, A., & Pauli, P. (2013) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2013.00031 · Cited by 60
“Although, threatening experiences and life stress have been reported to increase the risk for anxiety disorders (Watanabe et al., 2005; Melchior et al., 2007), the effect of environmental stress is also moderated by a genetic diathesis (Nugent et al., 2011).”
BackgroundAmiri, S., Amini-Khoei, H., Haj‐Mirzaian, A., Rahimi-Balaei, M., Naserzadeh, P., Dehpour, A. R., Mehr, S. E., & Hosseini, M. (2015) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2015.09.009 · Cited by 53
A dimensional approach to modeling symptoms of neuropsychiatric disorders in the marmoset monkey
Oikonomidis, L., Santangelo, A. M., Shiba, Y., Clarke, F. H., Robbins, T. W., & Roberts, A. C. (2017) · Developmental Neurobiology · doi:10.1002/dneu.22446 · Cited by 54
“Such behavioral traits are the product of interactions between genes and early life experiences (Nugent et al., 2011).”
BackgroundZink, M. (2014) · Advances in Medicine · doi:10.1155/2014/317980 · Cited by 55
Brietzke, E. M., Mansur, R. B., Soczynska, J. K., Powell, A. M., & McIntyre, R. S. (2012) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2012.05.004 · Cited by 56
Akkermann, K., Kaasik, K., Kiive, E., Nordquist, N., Oreland, L., & Harro, J. (2011) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2011.09.013 · Cited by 56
Epigenetic Modulation of Mood Disorders
Archer, T. (2013) · Journal of Genetic Syndromes & Gene Therapy · doi:10.4172/2157-7412.1000120 · Cited by 52
“ISSN:2157-7412 JGSGT, an open access journal traumatic stress [130,135,136], and frequently are accompanied by relative elevations of glucocorticoid stress hormones.”
BackgroundKarkhanis, A. N., Leach, A. C., Yorgason, J. T., Uneri, A., Barth, S. H., Niere, F., Alexander, N. J., Weiner, J. L., McCool, B. A., Raab‐Graham, K. F., et al. (2018) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.8b00360 · Cited by 48
Huang, C. L.-C., Wu, M., Ho, C., & Wang, J. (2017) · Journal of Psychosomatic Research · doi:10.1016/j.jpsychores.2017.07.008 · Cited by 51
“Depression and anxiety are stress-related common mental disorders and are caused by a combination of multiple environmental and genetic factors affecting certain brain circuits [3].”
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Gibb, B. E., Beevers, C. G., & McGeary, J. E. (2012) · Cognition & Emotion · doi:10.1080/02699931.2012.712950 · Cited by 53
“Although there have been some mixed findings, there is growing evidence that genes influencing serotonergic and hypothalamic–pituitary–adrenal (HPA) axis functioning moderate the impact of environmental stress on depression risk (see Karg, Burmeister, Shedden, & Sen, 2011; Nugent, Tyrka, Carpenter, & Price, 2011 , for…”
ResultLebe, M., Hasenbring, M. I., Schmieder, K., Jetschke, K., HARDERS, A. G., Epplen, J. T., Hoffjan, S., & Kötting, J. (2012) · Pain · doi:10.1016/j.pain.2012.11.017 · Cited by 52
Waters, R. C., & Gould, E. (2022) · Frontiers in Systems Neuroscience · doi:10.3389/fnsys.2022.860847 · Cited by 54
Telomeres, Early-Life Stress and Mental Illness
Ridout, S. J., Ridout, K. K., Kao, H., Carpenter, L. L., Philip, N. S., Tyrka, A. R., & Price, L. H. (2015) · Advances in psychosomatic medicine · doi:10.1159/000369088 · Cited by 51
Self-citationDoherty, T. S., Blaze, J., Keller, S. M., & Roth, T. L. (2017) · Developmental Psychobiology · doi:10.1002/dev.21547 · Cited by 50
Lowe, S. R., Quinn, J. W., Richards, C. A., Pothen, J., Rundle, A., Galea, S., Ressler, K. J., Koenen, K. C., & Bradley, B. (2015) · Child Abuse & Neglect · doi:10.1016/j.chiabu.2015.10.007 · Cited by 54
DISC1 mouse models as a tool to decipher gene-environment interactions in psychiatric disorders
Cash-Padgett, T. V., & Jaaro-Peled, H. (2013) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2013.00113 · Cited by 47
Developmental Risk I: Depression and the Developing Brain
Weir, J. M., Zakama, A. K., & Rao, U. (2012) · Child and Adolescent Psychiatric Clinics of North America · doi:10.1016/j.chc.2012.01.004 · Cited by 54
Hegde, A., Suresh, S., & Mitra, R. (2020) · Scientific Reports · doi:10.1038/s41598-020-70875-5 · Cited by 45
Soga, T., Teo, C. H., & Parhar, I. S. (2021) · Frontiers in Genetics · doi:10.3389/fgene.2020.601868 · Cited by 47
Werme, J., van der Sluis, S., Posthuma, D., & de Leeuw, C. (2021) · Translational Psychiatry · doi:10.1038/s41398-021-01288-9 · Cited by 45
Rozenblat, V., Ong, D., Fuller‐Tyszkiewicz, M., Akkermann, K., Collier, D. A., Engels, R. C. M. E., Fernández‐Aranda, F., Harro, J., Homberg, J. R., Karwautz, A. F. K., et al. (2016) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2016.09.023 · Cited by 46
“…field, where greater traumatic life events, including childhood abuse, have been found to interact with 5-HTTLPR to predict depression (Karg et al., 2011; Nugent et al., 2011), although the interaction between life events and 5-HTTLPR is not undisputed (Munaf o et al., 2009; Risch et al., 2009).”
BackgroundResultTaha, F., & Goodwin, R. D. (2014) · Journal of Affective Disorders · doi:10.1016/j.jad.2014.07.014 · Cited by 42
“Previous studies suggest that stress is strongly linked to smoking, (Kassel et al., 2003; Tsourtos et al., 2008) as well as to depressive and anxiety symptoms (Hicks et al., 2009; Kessing et al., 2003; Nugent et al., 2011).”
BackgroundMandelli, L., Antypa, N., Nearchou, F., Vaiopoulos, C., Stefanis, C. N., Serretti, A., & Stefanis, N. C. (2012) · Journal of Affective Disorders · doi:10.1016/j.jad.2012.03.047 · Cited by 44
“Gene–environment interaction (GxE) research provides a potential pathway of understanding how genetic differences influence the likelihood that exposure to environmental stress will result in psychopathology (Nugent et al., 2011).”
BackgroundCarlisi, C. O., & Robinson, O. J. (2018) · Brain and Neuroscience Advances · doi:10.1177/2398212818774223 · Cited by 48
“‘Anxious temperament’ is considered to be a stable trait across time, and those with extreme levels of such traits are at a higher risk for developing clinical or pathological anxiety (Arnaudova et al., 2013; Jones, 2013; Nugent et al., 2011).”
BackgroundCurcumin as a putative antidepressant
Seo, H., Wang, S., Han, C., Lee, S.-J., Patkar, A. A., Masand, P. S., & Pae, C. (2015) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2015.1008457 · Cited by 42
“Depression is a heterogeneous disorder with multiple complex etiologies originating from interactions between environmental and genetic factors [1].”
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Lindström, M., Fridh, M., & Rosvall, M. (2013) · Psychiatry Research · doi:10.1016/j.psychres.2013.11.018 · Cited by 39
“Recent studies suggest a substantially increased risk of internalizing depressive and anxiety disorders into adulthood following early life stress in childhood (Kendler et al., 2003; Nugent et al., 2011).”
BackgroundmiR-132/212 is induced by stress and its dysregulation triggers anxiety-related behavior
Aten, S., Page, C. E., Kalidindi, A., Wheaton, K. L., Niraula, A., Godbout, J. P., Hoyt, K. R., & Obrietan, K. H. (2018) · Neuropharmacology · doi:10.1016/j.neuropharm.2018.10.020 · Cited by 40
Early life stress impairs contextual threat expression in female, but not male, mice.
Manzano-Nieves, G., Gaillard, M., Gallo, M. E., & Bath, K. G. (2018) · Behavioral Neuroscience · doi:10.1037/bne0000248 · Cited by 35
Stress sensitivity of childhood epilepsy is related to experienced negative life events
van Campen, J. S., Jansen, F. E., Steinbusch, L. C., Joëls, M., & Braun, K. P. J. (2012) · Epilepsia · doi:10.1111/j.1528-1167.2012.03566.x · Cited by 40
“This was demonstrated for psychiatric conditions such as depression and anxiety disorders (Heim & Nemeroff 2001; Tennant, 2002; Nemeroff, 2004; Hulbert-Williams & Hastings, 2008; Nugent et al., 2011), but also cardiovascular disease, asthma, and exacerbations of multiple sclerosis have been shown to be more common in…”
BackgroundGenetic Factors in Anxiety Disorders
Domschke, K., & Maron, E. (2013) · Modern trends in psychiatry · doi:10.1159/000351932 · Cited by 42
Adult Anxiety Disorders in Relation to Trait Anxiety and Perceived Stress in Childhood
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“Notably, several methodological considerations about GxE analyses have been raised in recent literature (Koenen et al. 2008; Dick 2011; Duncan and Keller 2011; Nugent et al. 2011).”
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“Anxiety and depression are stress-related common mental disorders and are caused by a combination of multiple genetic and environmental factors affecting certain brain circuits (Nugent et al., 2011).”
BackgroundThe First Pilot Genome-Wide Gene-Environment Study of Depression in the Japanese Population
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Background
Metadata
- Authors
- Nugent, N. R., Tyrka, A. R., Carpenter, L. L., & Price, L. H.
- Affiliations
- Brown University (US)
- Corresponding author
- Nugent, Nicole R.
- Venue
- Psychopharmacology
- Published
- 2011-01-12
- Volume
- 214
- Issue
- 1
- Pages
- 175-196
- ISSN
- 0033-3158 (ISSN-L)
- 1432-2072
- PMC
- PMC3615637
- OpenAlex
- W2094951488
- Cited by
- 269
- References
- 174
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 8 · 2023: 16 · 2022: 40 · 2021: 14 · 2020: 13 · 2019: 11 · 2018: 17 · 2017: 25 · 2016: 10 · 2015: 30 · 2014: 20 · 2013: 25 · 2012: 17
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Psychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Defense
- National Institute of Mental Health (K01MH087240, R01MH083704, R01MH068767)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Clinical Psychology › Child and Adolescent Psychosocial and Emotional Development
- Keywords
- gene-environment interaction, early life stress, depression, anxiety disorders, internalizing disorders, candidate genes, serotonin transporter, serotonergic system, hypothalamic-pituitary-adrenal axis, neurotrophins, gene-gene interaction, sex differences, social support
- MeSH terms
- Animals, Anxiety Disorders, Depressive Disorder, Female, Humans, Life Change Events, Male, Risk Factors, Sex Factors, Stress, Psychological
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