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Computerised cognitive–behavioural therapy (cCBT) for depression has the potential to be efficient therapy but engagement is poor in primary care trials.
We tested the benefits of adding telephone support to cCBT.
We compared telephone-facilitated cCBT (MoodGYM) (n = 187) to minimally supported cCBT (MoodGYM) (n = 182) in a pragmatic randomised trial (trial registration: ISRCTN55310481). Outcomes were depression severity (Patient Health Questionnaire (PHQ)-9), anxiety (Generalized Anxiety Disorder Questionnaire (GAD)-7) and somatoform complaints (PHQ-15) at 4 and 12 months.
Use of cCBT increased by a factor of between 1.5 and 2 with telephone facilitation. At 4 months PHQ-9 scores were 1.9 points lower (95% CI 0.5–3.3) for telephone-supported cCBT. At 12 months, the results were no longer statistically significant (0.9 PHQ-9 points, 95% CI −0.5 to 2.3). There was improvement in anxiety scores and for somatic complaints.
Telephone facilitation of cCBT improves engagement and expedites depression improvement. The effect was small to moderate and comparable with other low-intensity psychological interventions.
Antidepressant prescribing is widespread. Nonetheless, response to antidepressants is variable. If it was possible to predict response to medication and thus tailor treatment accordingly, this would not only improve patient outcomes but may also have economic benefits.
To test the hypothesis that individuals with more severe depression would benefit more from noradrenaline reuptake inhibitors (NARIs) than selective serotonin reuptake inhibitors (SSRIs) compared with individuals with less severe depression.
Individuals recruited from UK primary care who met ICD-10 criteria for a depressive episode and scored 15 or more on the Beck Depression Inventory (BDI) were randomised to either an SSRI (citalopram 20mg daily) or a NARI (reboxetine 4mg twice daily). Randomisation was by means of a remote automated telephone system. The main outcome was depressive symptoms measured by the BDI total score 6 weeks after randomisation. (Trial registration: ISRCTN31345163.)
In total, 601 participants were randomised (citalopram: n = 298, reboxetine: n = 303). Ninety-one per cent were followed up at 6 weeks (citalopram: n = 274, reboxetine: n = 272). There was little evidence to support an interaction between treatment and severity of depression (interaction term: 0.02, 95% CI −0.59 to 0.62, P = 0.96). Adjustment for potential confounders (age, gender, employment status, history of depression, number of life events and social support) did not affect the findings (interaction term: 0.06, 95% CI −0.54 to 0.66, P = 0.85).
Treatment with NARIs does not confer any advantage over SSRI treatment for outcome in those with more severe depressive illness presenting in primary care.
Antidepressants exhibit a variety of pharmacological actions including
inhibition of the serotonin and noradrenaline transporters. We wished to
investigate whether genetic variation could be used to target or
personalise treatment, in a comparison of selective serotonin reuptake
inhibitors (SSRIs) with noradrenaline reuptake inhibitors (NARIs).
To test the hypothesis that patients homozygous for the long (insertion)
polymorphism of the serotonin transporter (5-HTTLPR) have an increased
response to SSRI antidepressants but not to NARI antidepressants.
In an individually randomised, parallel-group controlled trial, people
meeting criteria for a depressive episode who were referred by their
general practitioner were randomised to receive either citalopram (an
SSRI) or reboxetine (an NARI). Randomisation was by means of a remote
automated system accessed by telephone. The main outcome was depressive
symptoms, measured by Beck Depression Inventory (BDI) total score 6 weeks
after randomisation. The trial was registered with the International
Standard Randomised Controlled Trials Number registry
Altogether 298 participants were randomised to receive citalopram and 303
were randomised to reboxetine. At 6 weeks follow-up, complete data were
available for 258 participants taking citalopram and 262 taking
reboxetine. We found no evidence to support an influence of 5-HTTLPR on
outcome following antidepressant treatment. The interaction term for BDI
score at 6 weeks was 0.50 (95% CI −2.04 to 3.03, P =
0.70), which indicated that responses to the SSRI and NARI were similar
irrespective of 5-HTTLPR genotype.
It is unlikely that the 5-HTTLPR polymorphism alone will be clinically
useful in predicting response to antidepressants in people with
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