War exposure, 5-HTTLPR genotype and lifetime risk of
                        depression

BackgroundIn 1962 approximately 1.5 million French people living in Algeria were repatriated to France in very poor and often life-threatening conditions. These people constitute a cohort for the study of the long-term impact of gene–environment interaction on depression.AimsTo examine the interaction between a highly stressful life event and subsequent depression, and its modulation by a length polymorphism of the serotonin transporter gene (5–HTTLPR).MethodA community sample of people aged 65 years and over residing in the Montpellier region of the south of France was randomly recruited from electoral rolls. Genotyping was performed on 248 repatriated persons and 632 controls. Current and lifetime major and minor depressive disorders were assessed according to DSM-IV criteria.ResultsA significant relationship was observed between exposure to repatriation and subsequent depression (P<0.002), but there was no significant effect of gene alone (P = 0.62). After controlling for age, gender, education, disability, recent life events and cognitive function, the gene–environment interaction (repatriation×5-HTTLPR) was globally significant (P<0.002; OR = 3.21, 95% CI 2.48–5.12). Individuals carrying the two short (s) alleles of 5-HTTLPR were observed to be at higher risk (P<0.005; OR = 2.34, 95% CI 1.24–4.32), particularly when repatriation occurred before age 35 years (P<0.002; OR = 2.91, 95% CI 1.44–5.88), but this did not reach significance in those who were older at the time of the event (P = 0.067).ConclusionsThe association between depression and war repatriation was significantly modulated by 5-HTTLPR genotype but this appeared to occur only in people who were younger at the time of exposure.

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Current Challenges in the Genetics of Psoriatic Arthritis: A Report from the GRAPPA 2009 Annual Meeting

The Journal of Rheumatology ◽

10.3899/jrheum.101123 ◽

2011 ◽

Vol 38 (3) ◽

pp. 564-566 ◽

Cited By ~ 2

Author(s):

PROTON RAHMAN

Keyword(s):

Psoriatic Arthritis ◽

Annual Meeting ◽

Association Studies ◽

Environment Interaction ◽

Genome Wide Association Studies ◽

Novel Genes ◽

Gene Environment Interaction ◽

Gene Environment ◽

Genome Wide

Psoriasis and psoriatic arthritis (PsA) are heterogeneous diseases. While both have a strong genetic basis, it is strongest for PsA, where fewer investigators are studying its genetics. Over the last year the number of independent genetic loci associated with psoriasis has substantially increased, mostly due to completion of multiple genome-wide association studies (GWAS) in psoriasis. At least 2 GWAS efforts are now under way in PsA to identify novel genes in this disease; a metaanalysis of genome-wide scans and further studies must follow to examine the genetics of disease expression, epistatic interaction, and gene-environment interaction. In the long term, it is anticipated that genome-wide sequencing is likely to generate another wave of novel genes in PsA. At the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) in Stockholm, Sweden, in 2009, members discussed issues and challenges regarding the advancement of the genetics of PsA; results of those discussions are summarized here.

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P.2.a.028 Gene × environment interaction in depressive disorders: which environment is of risk?

European Neuropsychopharmacology ◽

10.1016/s0924-977x(12)70357-7 ◽

2012 ◽

Vol 22 ◽

pp. S240

Author(s):

L. Mandelli ◽

C. Petrelli ◽

A. Serretti

Keyword(s):

Depressive Disorders ◽

Environment Interaction ◽

Gene Environment Interaction ◽

Gene Environment

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Psychotic Experiences Are Associated With Paternal Age But Not With Delayed Fatherhood in a Large, Multinational, Community Sample

Schizophrenia Bulletin ◽

10.1093/schbul/sbz142 ◽

2020 ◽

Vol 46 (5) ◽

pp. 1327-1334

Author(s):

Franck Schürhoff ◽

Baptiste Pignon ◽

Mohamed Lajnef ◽

Romain Denis ◽

Bart Rutten ◽

...

Keyword(s):

Community Sample ◽

Self Report ◽

Paternal Age ◽

Environment Interaction ◽

The European Union ◽

Gene Environment Interaction ◽

Gene Environment ◽

Increased Risk ◽

Psychosis Risk ◽

Subclinical Psychosis

Abstract Advanced paternal age has been consistently associated with an increased risk of schizophrenia. It is less known if such an association also exists with subclinical/attenuated forms of psychosis. Additionally, it has been suggested that it is not paternal age per se, but rather delayed fatherhood, as a marker of a genetic liability of psychosis, that is the cause of the association. The aim of the current study was to examine whether paternal age and/or delayed fatherhood (paternity age) predict self-reported positive, negative, and/or depressive dimensions of psychosis in a large sample from the general population. The sample (N = 1465) was composed of control subjects from the 6 countries participating in the European Union Gene-Environment Interaction study. The CAPE, a self-report questionnaire, was used to measure dimensions of subclinical psychosis. Paternal age at the time of respondents’ birth and age of paternity were assessed by self-report. We assessed the influence of the variables of interest (paternal age or paternity age) on CAPE scores after adjusting for potential confounders (age, gender, and ethnicity). Paternal age was positively associated with the positive dimension of the CAPE. By contrast, paternity age was not associated with any of the psychosis dimensions assessed by the CAPE. Thus, our results do not support the idea that delayed fatherhood explains the association between age of paternity and psychosis risk. Furthermore, our results provide arguments for the hypothesis of an etiologic continuum of psychosis.

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Getting to the bottom of feeding behaviour: who’s on top?

Applied Physiology Nutrition and Metabolism ◽

10.1139/h06-072 ◽

2007 ◽

Vol 32 (2) ◽

pp. 177-189 ◽

Cited By ~ 27

Author(s):

Jameason Cameron ◽

Éric Doucet

Keyword(s):

Feeding Behaviour ◽

Peptide Yy ◽

Homo Sapiens ◽

Human Model ◽

Environment Interaction ◽

Gene Environment Interaction ◽

State Dependent ◽

Gene Environment ◽

Glucagon Like Peptide 1

Traditionally there has been a tendency to focus on peripheral “bottom-up” feeding-related signals and their resulting downstream actions on hypothalamic centers when studying the feeding behaviour of animals. A problem with this hierarchal approach emerges especially with respect to acquiring a human model attempting to explain what is ultimately a distributed control of feeding and energy balance. This review focuses on illuminating the means by which we have come to understand the complexities of feeding, and takes the next step in an attempt to propose a distinctive “top-down” view of this composite behaviour. It is argued that in evolutionary terms humans demonstrate behaviours unique to all species as represented by an expanded forebrain and the resultant psychological “non-homeostatic” mediators of feeding. Emphasis is placed on a distributionist “two-tier” model, arguing that traditional short-term (cholescystokinin, ghrelin, peptide YY, glucagon-like peptide 1, etc.) and long-term (insulin and leptin) feeding signals may be actively suppressed by the nested nuclei and projections of cortical–limbic brain areas. It is the motivational state (dependent on depletion–repletion signals of hunger and satiety) that in turn has the capability to modulate how rewarding or how palatable a food item may be perceived; thus, both sides of the two-tiered model of feeding behaviour are complimentary and interdependent all at once. In the end, this paper is both commentary and critical review. This synthesis purports that as evolutionary processes spawned consciousness, the psychology of hunger and the present-day discordance of gene–environment interaction forever changed the feeding behaviour of Homo sapiens .

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Effects of Childhood Adversity and Its Interaction with the MAOA, BDNF, and COMT Polymorphisms on Subclinical Attention Deficit/Hyperactivity Symptoms in Generally Healthy Youth

Children ◽

10.3390/children7090122 ◽

2020 ◽

Vol 7 (9) ◽

pp. 122

Author(s):

Meng-Che Tsai ◽

Kai-Jyun Jhang ◽

Chih-Ting Lee ◽

Yu-Fang Lin ◽

Carol Strong ◽

...

Keyword(s):

Community Sample ◽

Univariate Analysis ◽

Childhood Adversity ◽

Monoamine Oxidase A ◽

Environment Interaction ◽

Adhd Symptoms ◽

Gene Score ◽

Gene Environment Interaction ◽

Gene Environment ◽

Interaction Term

We aimed to investigate the effects of childhood adversity and its interaction with the polymorphisms in the monoamine oxidase A (MAOA), brain-derived neurotrophic factor (BDNF), and catechol-O-methyltransferase (COMT) genes on attention and hyperactivity disorder (ADHD) symptoms in a community sample of generally healthy youth. Participants (N = 432) completed questionnaires assessing ADHD symptoms (i.e., inattention, hyperactivity, and impulsiveness) and adverse childhood experiences, such as adverse environments (AEs) and childhood maltreatment (CM). Salivary genomic DNA was used to test polymorphisms in MAOA, BDNF, and COMT genes. A gene score (GS) was created based on the number of risk allele in the studied genes. Multiple linear regressions were used to examine the genetic and environmental effects on ADHD symptoms. The univariate analysis indicated that CM was significantly associated with inattention (β = 0.48 [95% confidence interval 0.16–0.79]), hyperactivity (0.25 [0.06–0.45]), and impulsiveness (1.16 [0.26–2.05]), while the GS was associated with hyperactivity (0.22 [0.11–0.33]) and impulsiveness (0.56 [0.06–1.05]). Only the GS remained significantly associated with hyperactivity (0.25 [0.12–0.37]) and impulsiveness (0.79 [0.20–1.38]) when the gene-environment interaction term was added in the model. No effects were found for AE and the gene-environment interaction term. In conclusion, CM was associated with ADHD symptoms in emerging adulthood. Genetic factors may also play a significant role in the association with these outcomes.

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