British Journal of Psychiatry, 192(4), April 2008, pp.275-278.
Publisher:
Cambridge University Press
Few studies have examined whether attributional style (an individual's explanation of why events happen) is a genetically influenced vulnerability factor for depression. The aim was to investigate whether attributional style is an enduring vulnerability trait for recurrent depression. As part of the Cardiff Depression Study, we interviewed 108 people with depression and their siblings, and a control group of 105 healthy individuals and their siblings, using the Schedules for Clinical Assessment in Neuropsychiatry and the Life Events and Difficulties Schedule. Participants also completed the Attributional Style Questionnaire. Regression analyses showed that attributional style results from mood state and is not a familial risk factor for depression. However, the tendency to internalise negative events was related to having had a prior episode of depression, suggesting a `scarring' effect. Also, non-severe events were associated with one subset of optimistic attributions. Attributional style mainly measures current mood and does not reflect a familial risk factor for depression.
Few studies have examined whether attributional style (an individual's explanation of why events happen) is a genetically influenced vulnerability factor for depression. The aim was to investigate whether attributional style is an enduring vulnerability trait for recurrent depression. As part of the Cardiff Depression Study, we interviewed 108 people with depression and their siblings, and a control group of 105 healthy individuals and their siblings, using the Schedules for Clinical Assessment in Neuropsychiatry and the Life Events and Difficulties Schedule. Participants also completed the Attributional Style Questionnaire. Regression analyses showed that attributional style results from mood state and is not a familial risk factor for depression. However, the tendency to internalise negative events was related to having had a prior episode of depression, suggesting a `scarring' effect. Also, non-severe events were associated with one subset of optimistic attributions. Attributional style mainly measures current mood and does not reflect a familial risk factor for depression.
British Journal of Psychiatry, 192(2), February 2008, pp.83-85.
Publisher:
Cambridge University Press
Recent developments in the classification of major depressive disorder are reviewed in light of the predictions made by Kendell in the 1970s. Particularly, the institution of operational diagnoses along with the contentious issues of subdividing major depressive disorder and its characterisation on a dimensional as opposed to a categorical scale.
Recent developments in the classification of major depressive disorder are reviewed in light of the predictions made by Kendell in the 1970s. Particularly, the institution of operational diagnoses along with the contentious issues of subdividing major depressive disorder and its characterisation on a dimensional as opposed to a categorical scale.
Subject terms:
literature reviews, psychiatry, depression, diagnosis;
British Journal of Psychiatry, 186(3), March 2005, pp.179-181.
Publisher:
Cambridge University Press
... of variance explained by additive genetic factors) of around 80%, followed by major depression (40-70%) and anxiety disorders (40-50%). For affective disorders in adult life the role as precipitants of certain proximal factors such as severe and threatening life events has been well replicated. There is also much evidence of distal factors such as childhood adversity contributing to vulnerability. Important developmental aspects include continuities between childhood depressive symptoms and adult depression and changing contributions of genes and environment throughout the life span. For example, recent findings support and extend earlier work that has shown increasing genetic influence on depressive symptoms as children grow into adolescence. With the completion of the sequencing of all the base pairs such as depression. Although genetic variation in humans can now be determined relatively easily from a single DNA sample derived from blood or even scrapings from the inside of the cheek, experimental manipulation of the environment of human subjects is clearly not possible. Consequently, alternative methods are required to measure the ‘environment’. One is to examine the genotypes of individuals who have all been
It is probable that the genetic components of affective disorders (bipolar affective disorder, major depressive disorder and anxiety states) result from multiple genes conferring susceptibility or liability to develop the disorder when other (environmental) risk factors are also present. In general, bipolar affective disorder has been found to have the highest heritability (the proportion of variance explained by additive genetic factors) of around 80%, followed by major depression (40-70%) and anxiety disorders (40-50%). For affective disorders in adult life the role as precipitants of certain proximal factors such as severe and threatening life events has been well replicated. There is also much evidence of distal factors such as childhood adversity contributing to vulnerability. Important developmental aspects include continuities between childhood depressive symptoms and adult depression and changing contributions of genes and environment throughout the life span. For example, recent findings support and extend earlier work that has shown increasing genetic influence on depressive symptoms as children grow into adolescence. With the completion of the sequencing of all the base pairs in the human genome we are entering a ‘post-genomic’ era, although identifying the genes involved in the aetiology of affective disorders remains a major research pre-occupation. However, many geneticists as well as researchers from other disciplines are turning their attention to environmental risk factors and how these interact and co-act with genes to lead to the expression of pathological phenotypes such as depression. Although genetic variation in humans can now be determined relatively easily from a single DNA sample derived from blood or even scrapings from the inside of the cheek, experimental manipulation of the environment of human subjects is clearly not possible. Consequently, alternative methods are required to measure the ‘environment’. One is to examine the genotypes of individuals who have all been exposed to a specific risk factor, such as childhood adversity or severe threatening life events, comparing those who have expressed the phenotype, for example by becoming depressed, and those who have not (resilient individuals). Some longitudinal and twin studies, as well as others currently being conducted, will lend themselves to this type of analysis.
British Journal of Psychiatry, 185(10), October 2004, pp.280-282.
Publisher:
Cambridge University Press
The Centre’s focus is on common psychiatric disorders, covering three domains: mood disorders (especially anxiety and depression), ‘externalising’ disorders (especially disruptive behaviour including hyperactivity) and cognitive disorders (especially language disorders and mild learning disability, including autistic symptoms). The Centre concentrates on the aetiological aspects – developmental
The Centre’s focus is on common psychiatric disorders, covering three domains: mood disorders (especially anxiety and depression), ‘externalising’ disorders (especially disruptive behaviour including hyperactivity) and cognitive disorders (especially language disorders and mild learning disability, including autistic symptoms). The Centre concentrates on the aetiological aspects – developmental as well as genetic and environmental origins – of behavioural disorders. However, there is a strong emphasis on methods of measurement and classification and an attempt to foresee the practical, clinical and public health implications of the Centre’s findings
Subject terms:
learning disabilities, psychiatry, research dissemination, research methods, conduct disorders, depression;