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Articles by D. E Stewart
Total Records ( 2 ) for D. E Stewart
  J Sacher , A. A Wilson , S Houle , P Rusjan , S Hassan , P. M Bloomfield , D. E Stewart and J. H. Meyer
 

Context  The early postpartum period is a time of high risk for a major depressive episode (or postpartum depression), with a prevalence of 13%. During this time, there is a heightened vulnerability for low mood because postpartum blues is common. Severe postpartum blues can herald the onset of postpartum depression. The neurobiological mechanisms to explain postpartum blues and the high risk for the onset of postpartum depression in the first few weeks after delivery are unclear. Estrogen levels drop 100- to 1000-fold during the first 3 to 4 days postpartum, and changes in estrogen levels have an inverse relationship with monoamine oxidase A (MAO-A) density. However, MAO-A levels have never been measured in the early postpartum period.

Objective  To determine whether brain MAO-A binding is elevated in the early postpartum period.

Design  Case-control study.

Setting  Tertiary care academic psychiatric hospital in Toronto, Ontario, Canada.

Participants  Fifteen healthy women who were 4 to 6 days postpartum and 15 healthy women who had not recently been postpartum underwent carbon 11–labeled harmine positron emission tomography scanning. All women were nonsmoking and medication free.

Main Outcome Measure  MAO-A total distribution volume, an index of MAO-A density, was measured in prefrontal cortex, anterior cingulate cortex, anterior temporal cortex, thalamus, dorsal putamen, hippocampus, and midbrain.

Results  MAO-A total distribution volume was significantly elevated (mean, 43%) throughout all analyzed brain regions during the early postpartum period.

Conclusions  Elevated MAO-A levels in the early postpartum period can be interpreted as a marker of a monoamine-lowering process that contributes to the mood change of postpartum blues. Rather than a purely psychosocial model, we propose a neurobiological model of estrogen decline, followed by elevated MAO-A binding, low mood, and subsequently a period of high risk for major depressive episodes. Our model has important implications for preventing postpartum depression and for developing therapeutic strategies that target or compensate for elevated MAO-A levels during postpartum blues.

  B. D Thombs , R. C Ziegelstein , L Pilote , D. J. A Dozois , A. T Beck , K. S Dobson , S Fuss , P de Jonge , S. L Grace , D. E Stewart , J Ormel and S. E. Abbey
 

Background

Depression measures that include somatic symptoms may inflate severity estimates among medically ill patients, including those with cardiovascular disease.

Aims

To evaluate whether people receiving in-patient treatment following acute myocardial infarction (AMI) had higher somatic symptom scores on the Beck Depression Inventory–II (BDI–II) than a non-medically ill control group matched on cognitive/affective scores.

Method

Somatic scores on the BDI–II were compared between 209 patients admitted to hospital following an AMI and 209 psychiatry out-patients matched on gender, age and cognitive/affective scores, and between 366 post-AMI patients and 366 undergraduate students matched on gender and cognitive/affective scores.

Results

Somatic symptoms accounted for 44.1% of total BDI–II score for the 209 post-AMI and psychiatry out-patient groups, 52.7% for the 366 post-AMI patients and 46.4% for the students. Post-AMI patients had somatic scores on average 1.1 points higher than the students (P<0.001). Across groups, somatic scores accounted for approximately 70% of low total scores (BDI–II <4) v. approximately 35% in patients with total BDI–II scores of 12 or more.

Conclusions

Our findings contradict assertions that self-report depressive symptom measures inflate severity scores in post-AMI patients. However, the preponderance of somatic symptoms at low score levels across groups suggests that BDI–II scores may include a small amount of somatic symptom variance not necessarily related to depression in post-AMI and non-medically ill respondents.

 
 
 
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