Psychological disorders are often manifested through abnormal behaviours. To be considered abnormal, a behaviour must meet three conditions: (1) it must cause distress to the individual; (2) it must be dysfunctional either for the society or the individual and finally, (3) it must not conform to society’s norms – behavioural written and unwritten rules that specify how an individual is expected to think, feel and behave -, in other words, it must be considered a deviant behaviour. In a recent study by Wittchen et al. (2011), it was estimated that approximately 38.2% – 164.8 million people – of the European population suffers from a psychological disorder; and, in the UK alone, 17% of the population experiences suicidal thoughts (HSCIC, 2009). Scientific research on psychological disorders, while broadening our understanding of the disorders, has also shown the gaps in our knowledge. One of the most considerable gaps regards the causal factors of psychological disorders. In fact, although there seems to be agreement on the fact that both genetic and environmental factors contribute to the development of psychological disorders, it is still unclear to what extent. Here, we will focus on a particular group of psychological disorders – mood affective disorders – and on their genetic and environmental causal factors. More specifically, we will discuss the role of frontal asymmetry (FA) as a potential index of vulnerability to developing psychological disorders.Mood affective disorders are psychological disorders which present as main underlying feature the disturbance in one individual’s mood. They fall into the sub-groups of elevated mood, depressed mood and moods that cycle between mania and depression. Elevated mood disorders are characterized by two states, namely mania – a state of abnormally elevated affect, and energy level – and hypomania – characterized by persistent disinhibition and elevation (euphoria). Depressed mood disorders, of which the best-known is major depressive disorder (MDD), are at the opposite end of the spectrum of disorders; whereas moods which cycle between mania and depression, the most known being bipolar disorder, exhibit an alternation between elevated and depressed mood disorders. Research has shown that mood disorders cluster in families (Smoller & Finn, 2003); parents affected by mood disorders are more likely to have children with psychological disorder than are unaffected parents (Weissman et al., 1997). Genetic factors surface in twin and family studies (McGuffin, Owen, & Gottesmann, 2005) and have been linked to depression (Comer, 2009) and to bipolar disorder. The concordance rate of identical twins for experiencing clinical depression is about 67%, whereas fraternal twins present a rate of 15% (Gershon, Berrettini & Golden, 1989). Moreover, 50% of the population affected by bipolar disorder has a close parent or child with the disorder (Barondes, 1999). The concordance rate for bipolar disorder is five times higher in identical twins than in fraternal twins – which suggests a genetic link. However, these statistics also suggest that depression and bipolar disorder are not caused solely by genetic factors – otherwise, we would expect the concordance rate for monozygotic twins to be 100%. Therefore, individuals are likely to inherit a predisposition – or vulnerability – to develop the disorder, if environmental factors such as significant losses and low social support are present (Barondes, 1999). Accordingly, the vulnerability-stress model posits that the development of psychological disorders takes place due to two factors: vulnerability and stressors – or the stress experienced in a given moment (such as economic adversity, environmental trauma or interpersonal losses). Vulnerability is the degree to which an individual is likely to develop a disorder and it includes genetic factors, psychological traits and low social support. Hence, the genetic predisposition appears to create a disorder only when triggered by stressing factors (Keenan, Dillenburger, Doherty, Byrne, & Gallagher, 2010). A study by Bowlby (2000) showed that experiencing the death of a parent during childhood is associated with a higher risk of developing depression (Barnes & Prosen, 1985; Brown & Harris, 1978). However, the role of stressors in the development of disorders is not completely clear. Freud (1957) believed that stressors such as early traumatic losses or rejections are the cause of vulnerability for later depression, for they trigger emotional processes of grief and rage that become part of the individual’s personality. This theory does not take into account genetic factors, since it present vulnerability as an outcome of traumatic life event, rather than a genetic predisposition. From a neurochemical perspective, depression may be caused by underactivity of certain neurotransmitters such as norepinephrine, dopamine and serotonin (Anisman, 2010). These neurotransmitters are particularly active in brain regions involved in experiencing reward and pleasure. The decrease of neural transmission in these brain areas may result in the lack of pleasure and loss of motivation characteristic of depression (Donaldson, 1998). As previously mentioned, abnormal behaviours are diagnostic phenotypes – the set of observable characteristics of a person, resulting from the interaction between its genotype and the environment – for psychological disorders. Since diagnostic phenotypes vary largely and are very complex, they hinder the identification of those genes that confer vulnerability to disorders. Thus, an alternative approach focuses on ”endophenotypes” – hereditary characteristics associated with a disorder, which are not a direct symptom of that condition (Gottesman and Gould, 2003). In bipolar disorder, for example, an endophenotype is considered to be a deficit in face emotion labelling or face perception – that is the understanding and perception of an individual’s face. To be considered an endophenotype, a characteristic must meet certain criteria, which we will analyse in relationship to frontal brain asymmetry (FA).The term frontal brain asymmetry refers to neuroanatomical differences between the two hemispheres of the brain – left and right. It is generally used to indicate the tendency of some cognitive processes and neural function to be more dominant in one hemisphere than in the other. Anokhin, Heath and Myers (2006) suggested that frontal asymmetry may be associated with individual differences in vulnerability to mood disorders. As observed by Anokhin, Heath and Myers (2006), FA meets the criteria to be considered a endophenotype: (1) it is a stable trait measure; (2) abnormal patterns in frontal asymmetry correlate to a history of psychiatric diagnosis and are present during remission; (3) frontal asymmetry is associated with indicators of diathesis – hereditary predisposition to a disorder – such as traits indicating a de?cit of approach behaviors; (4) it develops early in life and is associated with emotionality in infants and children; and (5) frontal asymmetry is linked to neurobiological mechanisms of emotion and mood disorders – evidence for this has been provided by neuroimaging and brain lesion data. However, to be considered an endophenotype for genetic research frontal asymmetry must be heritable. Based on the findings of previous research, it is reasonable to hypothesize that FA may re?ect genetically transmitted individual differences in neurophysiological substrates of emotion. Emotionally evocative ?lm clips and other similar experimental factors aimed at eliciting emotions produced asymmetric patterns of EEG activation. In these experiments, higher right frontal activation was associated with negative affect, whereas greater left frontal activation was associated with positive emotional states (Davidson, 2003). If the tendency of the right hemisphere – associated with negative affect – to be the dominant one is passed by parents to the offspring, frontal asymmetry might constitute a genetic vulnerability to psychological disorders. Furthermore, developmental studies have shown that individual differences in FA emerge early in life and are associated with individual differences in infants’ behaviour (Davidson, 1992; Fox & Davidson, 1986). Jones, Field, Fox, Lundy and Davalos (1997) observed that children of mothers suffering from depression exhibit reduced left frontal activation at 1 month of age (Dawson et al., 1999). Moreover, FA had a greater sensitivity than behavioural measures in discriminating between infants of depressed and non- depressed mothers (Dawson et al., 1997). A study by Anokhin and Rohrbaugh (1998) found a signi?cant familial transmission of FA and Anokhin et al. (1997) found an association between brain asymmetry patterns and familial risk for depression. These ?ndings suggest that FA can be a biological marker of familial and genetic risk for mood disorders. To conclude, the studies here presented suggest that genetic factors contribute to the development of psychological disorders, in that they confer vulnerability to the disorders. However they are not to be considered the only causal factors. If biological factors were the only variable, we would expect to find a 100% correspondence rate in monozygotic twins with psychological disorders. This is not the case. Environmental factors also must be taken into account for two important reasons: (1) the difference in the concordance rate for monozygotic twins cannot be explained by genetic factors and it is likely to be explained by environmental causes; and (2) the finding that psychological disorders cluster in families has to be carefully evaluated, for families, apart from sharing part of genetic information, also share, most of the times, the environment (they usually live together and share similar habits). Regardless, genetic factors appear to be a more reliable indicator, although more difficult to measure, of future development of psychological disorders.