Open Door Review III

S0*!0*Y$%)*90*(!%0<2($)*6!$*!&01%066$)*?!8#$<02*!@$<<0**$B9! aB7<0B6?!s/647#)<)D$72

aB0Y)_!5>_!A0$D#()*_!8>_!OB**_!S>_!O)Z%$7M_!8>_!A0#($*0*_!V>_!O2!Q>_!=4B6)E@2(0)6_!i>!A>![+,-,^>!;9127(!):! 60Y0%$(4!2*&!(410!):!&01%066$)*!)*!UB2<$(4!):!<$:0!$*!72606!$&0*($:$0&!$*!(#0!7)99B*$(4>!/647#)<)D$72!&)$?!-,>-,-du6,,PP+\-d-,,,,-g]! W1/RY($-#'! Gen environment relations in the origin of depression and well being Genetically our differences are small, so it can be assumed, that the relation with the unique environment that each person suffers since conceived plays an important role in creating our uniqueness. Depression constitutes a recurrent, frequently chronic condition requiring long-term clinical management (Angst, 1997). Both genetic and environmental factors have been implicated in developmental pathways to depression (Saveanu & Nemeroff, 2012; Sullivan, Neale, & Kendler, 2000). With regard to depression, much research has focused on interactions between environmental factors and polymorphisms, since the leading study of Caspi and colleagues (Caspi et al., 2003) demonstrating that individuals with one or two copies of the short allele of the serotonin transporter gene promoter region exhibited more depressive symptoms, diagnosable depression, and suicidality in relation to stressful life events than individuals homozygous for the long allele. This has led to a renewed focus on stress (Hammen, 2005) and early and later adversity in particular in explaining vulnerability for depression, especially among genetically predisposed individuals (Heim & Nemeroff, 2001; Heim, Newport, Mletzko, Miller, & Nemeroff, 2008; Risch et al., 2009). Research in this area has mainly focused on studying the moderation of negative environment from a diathesis- stress perspective. In recent years, studies began to include positive variables such as preventive interventions, positive parenting styles, or even no trauma, it was noted that in some cases, the same alleles that were more sensitive to negative events, were also more sensitive to positive events. Hence, the model began to shift from a model of diathesis to stress or vulnerable phenotype to the model of differentiated sensitivity to the environment or social susceptibility (Bakermans- Kranenburg & van Ijzendoorn, 2011; Bakermans-Kranenburg, Van, Pijlman, Mesman, & Juffer, 2008; Belsky & Pluess, 2009; Boyce & Ellis, 2005; Cicchetti & Rogosch, 2012; Ellis & Boyce, 2008; Ellis, Boyce, Belsky, Bakermans-Kranenburg, & Van Ijzendoorn, 2011; Ellis, Essex, & Boyce, 2005; Oreland, Nilsson, Damberg, & Hallman, 2007; Pluess, Belsky, Way, & Taylor, 2010; Roisman et al., 2012; Sheese, Voelker, Rothbart, & Posner, 2007), which contends that more susceptible individuals in a positive environment will show more favourable outcomes but if they experience negative environments will show more negative results. This model argues that certain genes make us more sensitive or reactive to the environment "for better or for worse”, leading to the notion of plasticity or malleability genes. The importance of including recent and positive events in the interaction of gene and environment studies is that maybe transforming the environment in a positive one by psychotherapy or promoting social positive policies, could have a positive and effective outcome, especially in more sensitive people. Noticing the importance and power of social context to modify risky vulnerabilities. >-X%($[&/.2! Two systematic reviews are taking place in this field: (1) DIFFERENTIAL SUSCEPTIBILITY GENES; A SYSTEMATIC REVIEW OF GXE and (2) GENETIC POLYMORPHISMS, OXYTOCIN AND DEPRESSION

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