Heather Brotchie

Gender differences in depression

It is commonly suggested that a female preponderance in depression is universal and substantial. This review considers that proposition and explanatory factors. The view that depression rates are universally higher in women is challenged with exceptions to the proposition helping clarify candidate explanations. ‘Real’ and artefactual explanations for any such phenomenon are considered, and the contribution of sex role changes, social factors and biological determinants are overviewed. While artefactual factors make some contribution, it is concluded that there is a higher order biological factor (variably determined neuroticism, ‘stress responsiveness’ or ‘limbic system hyperactivity’) that principally contributes to the gender differentiation in some expressions of both depression and anxiety, and reflects the impact of gonadal steroid changes at puberty. Rather than conclude that ‘anatomy is destiny’ we favour a diathesis stress model, so accounting for differential epidemiological findings. Finally, the impact of gender on response to differing antidepressant therapies is considered briefly.

Gender differences in response to differing antidepressant drug classes: two negative studies.

BACKGROUND A recent US study presented data suggesting that depressed women are more likely to respond to selective serotonin reuptake inhibitor (SSRI) than tricyclic (TCA) antidepressant drug therapies. We have undertaken replication studies in two independent databases. METHOD We have examined for gender differences in SSRI and TCA antidepressant response in both retrospective and prospective naturalistic uncontrolled studies, and in subsets of melancholic and non-melancholic depressed subjects. As the US study had indicated that women under the age of 40 years were particularly likely to show a differential response to SSRIs, we examined for age, gender and interactional effects. In addition, we examined for differential SSRI and TCA responsiveness in a subset of patients who had received drugs from both classes. RESULTS We failed to find evidence of women having a preferential response to SSRI medication or, conversely, of men having a superior response to TCA medication. Older age, however, was associated with a superior TCA response and younger age with a superior SSRI response. CONCLUSION As few studies have examined for differential gender and age effects in response to narrow action and broad action antidepressant drugs across major depressive subtypes, gender differential effects remain to be established.

From diathesis to dimorphism: the biology of gender differences in depression.

Unipolar depression is more common in women than men. We pursue a unifying explanation for the sex difference in the incidence of depression that emerges at puberty and is unlikely to be fully explained as an artifact or as a result of socialization or contemporary sex roles. Because symptomatic anxiety disorders show a similar female preponderance in women, we consider the biology of anxiety disorders and their links to depression. Rather than viewing gender as directly determining differential unipolar depression rates, we hypothesize a primary postpubertal effect of gonadal hormones on limbic system hyperactivity, which predisposes women to potentially higher rates of certain anxiety and depressive disorders.

'D' for depression: any role for vitamin D? 'Food for Thought' II.

Parker G, Brotchie H. ‘D’ for depression: any role for vitamin D?.

Low levels of docosahexaenoic acid identified in acute coronary syndrome patients with depression

As deficiencies in n-3 PUFAs have been linked separately to depression and to cardiovascular disease, they could act as a higher order variable contributing to the established link between depression and cardiovascular disease. We therefore examine the relationship between depression and omega-3 polyunsaturated fatty acids (n-3 PUFA), including total n-3 PUFA, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), in patients with acute coronary syndrome (ACS). Plasma phospholipid levels of n-3 PUFA were measured in 100 patients hospitalized with ACS. Current major depressive episode was assessed by the Composite International Diagnostic Interview (CIDI). Depression severity was assessed by the 18-item Depression in the Medically Ill (DMI-18) measure. Patients clinically diagnosed with current depression had significantly lower mean total n-3 PUFA and DHA levels. Higher DMI-18 depression severity scores were significantly associated with lower DHA levels, with similar but non-significant trends observed for EPA and total n-3 PUFA levels. The finding that low DHA levels were associated with depression variables in ACS patients may explain links demonstrated between cardiovascular health and depression, and may have prophylactic and treatment implications.

Do the old psychostimulant drugs have a role in managing treatment-resistant depression?

Parker G, Brotchie H. Do the old psychostimulant drugs have a role in managing treatment‐resistant depression?

Mood effects of the amino acids tryptophan and tyrosine: 'Food for Thought' III.

Parker G, Brotchie H. Mood effects of the amino acids tryptophan and tyrosine.

Psychomotor change as a feature of depressive disorders: an historical overview.

Psychomotor disturbance has generally been viewed as a feature of all depressive disorders, merely varying in severity as a consequence of the mood state. As we have elsewhere argued for psychomotor change being specific to melancholia, its definition, measurement and capacity to sub-type depressive disorders may benefit from close consideration. Here we overview historical views and contemporary measures of psychomotor change, noting variable interest in behavioural manifestations of depression, as against symptoms, over time.

The impact of differing anxiety disorders on outcome following an acute coronary syndrome: time to start worrying?†

Background: Both depression and anxiety have been implicated as influencing survival following an acute coronary syndrome (ACS). Studies evaluating the contribution of anxiety have produced varying results, perhaps reflecting the use of dimensional self‐report measures of state anxiety and failure to control for co‐morbid depression. We sought to assess the impact of anxiety on outcome in ACS patients using DSM‐IV diagnoses, in addition to self‐report measures, controlling for effects of concurrent depressive diagnosis as well as medical and socio‐demographic variables. Methods: Some 489 patients hospitalized with an ACS were assessed for lifetime and current DSM‐IV anxiety disorders using both Composite International Diagnostic Interview (CIDI) decisions and such decisions complemented by clinical judgments of impairment. Patients were re‐interviewed over the next 12 months to assess cardiac outcome (ACS readmission and cardiac mortality). Results: Univariate analyses revealed a trend for those with a lifetime history of agoraphobia to experience poorer cardiac outcome and for those with a lifetime diagnosis of generalized anxiety disorder (GAD) to experience a superior cardiac outcome. After controlling for post‐ACS depression and key medical and demographic covariates, agoraphobia was a significant predictor of poorer cardiac outcome while the trend for those with a history of GAD to experience a superior cardiac outcome remained. Conclusions: Any impact of “anxiety” on post‐ACS outcome appears to be influenced by the clinical sub‐type. The seemingly paradoxical finding that GAD might improve outcome may reflect “apprehensive worrying” being constructive, by improving self‐management of the individuals cardiac problems. Depression and Anxiety, 2010.

Specificity of depression following an acute coronary syndrome to an adverse outcome extends over five years.

Many studies have demonstrated that depression is associated with a worse cardiovascular outcome and increased risk of death in those experiencing an acute coronary syndrome (ACS). Recent studies have suggested, however, that any association is strongly influenced by the timing of the depression, with post-ACS depression providing the greatest risk. Establishing any timing impact should assist etiological clarification. We initially recruited 489 subjects hospitalized for an ACS, assessed lifetime and current depression, and then - at 1 and 12 months - assessed subsequent depression. Subjects were followed for up to 5 years to assess cardiovascular outcome and the impact of depression at differing time points, with three defined poor outcome categories (i.e. cardiac admission and/or cardiac rehospitalization). While outcome was associated with a number of non-depression variables, a poor outcome was most clearly associated with depressive episodes emerging at the time of the ACS but with some risk affected by episodes that commenced prior to the ACS and being persistent. Neither lifetime depressive episodes nor transient depressive episodes occurring around the baseline ACS event appeared to provide any risk. Study findings indicate that any differential deleterious impact of post-ACS depression has both short-term and longer-term outcomes, and, by implicating the centrality of post-ACS depression, should assist studies seeking to identify causal explanations.