Institutional smoking bans reduce secondhand smoke exposure and harms, but more research is needed

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It’s been almost 9 years since the introduction of SmokeFree legislation in the UK (although we elves still return from a night out smelling of campfire smoke). However, secondhand smoke is still accountable for 600,000 deaths annually.

Smoke free policies can be implemented at the micro-level (i.e. the individual level or in homes), the meso-level (i.e. in organisations, such as public healthcare facilities, higher education centres and prisons) or the macro-level (i.e. in an entire country). In many countries, smokefree legislation is at the macro-level, although exemptions exist at the meso-level. For example, in the UK, specific rooms in prisons and care homes are exempt from this legislation.

In their Cochrane review, Frazer and colleagues review the evidence for meso-level smoking bans (in venues not typically included in smokefree legislation) on 1) passive smoke exposure, 2) other health-related outcomes and 3) active smoking, including tobacco consumption and smoking prevalence.

Worldwide, secondhand smoke is still accountable for 600,000 deaths annually.

Worldwide, secondhand smoke is still accountable for 600,000 deaths annually.

Methods

Identification of included studies

The authors searched online databases of clinical trials, reference lists of identified studies and contacted authors to identify ongoing studies. Studies were included if they:

The introduction of smoking bans in psychiatric hospitals and prisons is extremely controversial.

The introduction of smoking bans in psychiatric hospitals and prisons is extremely controversial.

Results

Characteristics of included studies

No randomised controlled trials (RCTs) were found. 17 observational studies were identified (three using a controlled before-and-after design with another site for comparison and 14 using an uncontrolled before-and-after design). Of these 17 studies:

  • 12 were based in hospitals;
  • 3 in prisons;
  • 2 in universities.

Five studies investigated the impact of smoking bans on two participant groups (i.e. staff and either patients or prisoners).

The 17 studies were conducted in 8 countries: the USA (6 studies), Spain (3 studies), Switzerland (3 studies), Australia, Canada, Croatia, Ireland and Japan (all 1 study). Eight of these were conducted in US states or countries with macro-level (i.e. national) smoke-free legislation, eight with no legislative bans and one which compared all 50 US states (some with national bans and others without).

Main findings

There was considerable heterogeneity between the 17 studies and so a meta-analysis of all studies was not conducted. Instead studies were analysed using aqualitative narrative synthesis according to each of the outcome measures:

Reducing secondhand smoke exposure

Four studies assessed secondhand smoke exposure, finding that a reduction in exposure was observed in all three settings after smoking bans. However, none of the studies in the review used a biochemically validated measure of smoke exposure such as cotinine or carbon monoxide levels.

Other health outcomes

Four studies examined the impact of partial or complete smoking bans on health outcomes including smoking-related mortality. Two were conducted in prisons, one in a hospital and one in a secure mental hospital (Etter et al, 2007). All of these studies observed improvements in smoking-related morbidity and mortality after smoking bans. One of these assessed the impact of smoking bans in prisons in all 50 US states and found that smoking-related mortality was reduced in those prisons that had a smoking ban for more than 9 years.

Tobacco consumption and smoking prevalence

Thirteen studies reported data on the effect of smoking bans on smoking prevalence and five of these reported data on two populations within settings (i.e. prisoners and prison staff).

Eleven of these studies were included in a meta-analysis (using the Mantel-Haenszel fixed-effect method) and the data from the 12,485 participants in these studies was pooled. Although there was considerable heterogeneity between these studies (I2 = 72%; where a higher I2 value is evidence of higher levels of heterogeneity), this heterogeneity was lower within subgroups (e.g. in prisoners or hospital staff).

Ten studies conducted in hospital settings found mixed evidence for the impact of smoking bans on smoking prevalence. Eight of these studies were included in the meta-analysis and there was evidence that smoking bans reduced active smoking rates among hospital staff (risk ratio (RR) 0.71, 95% confidence interval (CI) 0.64 to 0.78, n = 4,544, I2 = 76%) and patients (RR 0.84, CI 0.76 to 0.98, n = 1442, I2 = 20%).

The one study in a prison setting found no evidence of a change in smoking prevalence among staff or prisoners after a smoking ban (RR 0.99, CI 0.84 to 1.16, n = 130).

Two studies in university settings observed reductions in smoking prevalence after smoking bans (RR 0.72, CI 0.64 to 0.80, n = 6,369, I2 = 59%), although one study only observed this among male ‘frequent’ smokers.

Quality of the evidence

The evidence was judged to be of low quality as all of the studies wereobservational (none used a RCT design) and the risk of bias was rated as high.

Banning smoking in hospitals and universities increased the number of smoking quit attempts and reduced the number of people smoking.

Banning smoking in hospitals and universities increased the number of smoking quit attempts and reduced the number of people smoking.

Conclusion

Overall, this review finds evidence of smoking bans on:

  • reducing smoking prevalence in hospitals and universities, with the greatest reductions among hospital staff;
  • reduced mortality and exposure to secondhand smoke in hospitals, universities and prisons.

Limitations

The quality of the evidence was low and the authors conclude that ‘we therefore need more robust studies assessing evidence for smoking bans and policies in these important specialist settings’. Limitations with the studies included in the review include: small sample sizes in some studies, a lack of a control location for comparison in all but three studies and a high level of heterogeneity between and within the different settings (e.g. the hospital settings included a cancer hospital, psychiatric hospitals and general hospitals).

We need more robust studies assessing the evidence for smoking bans and policies in specialist settings.

We need more robust studies assessing the evidence for smoking bans and policies in specialist settings.

Discussion

The authors report that given this evidence, smoking bans at the meso-level should be considered as part of multifactorial tobacco control activities to reduce secondhand smoke exposure and smoking prevalence.

Given that the introduction of these bans particularly in psychiatric hospitals and prisons is controversial, the introduction of these bans should be sensitive to the needs of populations. For example, bans in psychiatric hospitals should be implemented in consultation with psychiatrists to ensure that the improved health outcomes of patients is considered first and foremost. As the evidence is currently weak, with a high risk of bias, any interventions should be closely monitored.

More robust studies are needed, using a control group for comparison, assessing smoke exposure using biochemically validated measures, using long-term follow-ups of at least 6 months and reporting smoking prevalence both before and after the introduction of the ban.

It is not possible to draw firm conclusions about institutional smoking bans from the current evidence.

It is not possible to draw firm conclusions about institutional smoking bans from the current evidence.

Links

Primary paper

Frazer K, McHugh J, Callinan JE, Kelleher C. (2016) Impact of institutional smoking bans on reducing harms and secondhand smoke exposure. Cochrane Database of Systematic Reviews 2016, Issue 5. Art. No.: CD011856. DOI: 10.1002/14651858.CD011856.pub2.

Other references

Etter M, Etter JF. (2007) Acceptability and impact of a partial smoking ban in a psychiatric hospital.. Preventive Medicine 2007;44(1):649. [PubMed abstract]

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Treatment for depression in traumatic brain injury: Cochrane find no evidence for non-pharmacological interventions

by Eleanor Kennedy @Nelllor_

This blog originally appeared on the Mental Elf site on 31st May 2016.

Traumatic Brain Injury has been associated with increased occurrence of depression (Gertler et al, 2015). Traumatic Brain Injury results from damage to the brain by external forces, such as direct impact or rapid acceleration; consequences of a traumatic brain injury may be temporary or permanent and can lead to problems with cognition, emotion and behaviour (Maas, Stocchetti, & Bullock, 2008).

The main feature of depression is either a depressed mood or loss of interest and pleasure in usual activities, or both, consistently for a two week period. Depression can present as a major risk factor for suicide after Traumatic Brain Injury.

A recent Cochrane systematic review aimed to measure “the effectiveness of non-pharmacological interventions for depression in adults and children with Traumatic Brain Injury at reducing the diagnosis and severity of symptoms of depression.”

People who experience traumatic brain injury are at an increased risk of depression.

People who experience traumatic brain injury are at an increased risk of depression.

Methods

The Cochrane Injuries Group searched eight electronic databases for randomised controlled trials (RCTs) of non-pharmacological interventions for depression in adults and children who had a Traumatic Brain Injury. For inclusion in the review, study participants had to fulfil the following criteria:

  • A history of Traumatic Brain Injury due to external forces; samples that included participants with non-traumatically acquired brain injury, such as stroke, were also included if the data allowed for separate analysis of those with Traumatic Brain Injury
  • Fulfilment of diagnostic criteria for an applicable mood disorder, such as major depressive disorder or adjustment disorder with depressive mood, based on DSM or ICD criteria
  • Presenting with clinically significant depressive symptoms based on standardised measures

The primary outcome was “the presence or remission of depressive disorders, as determined by the use of accepted diagnostic criteria (e.g. DSM-IV or ICD-10), by the use of a standardised structured interview based on such criteria (e.g. Structured Clinical Interview for the DSM Disorders), or the results of validated self- or observer-rated questionnaires of depressive symptoms.”

The secondary outcomes were:

  • Neuropsychological functioning, psychosocial adjustment, everyday functioning, quality of life, and participation
  • Medication and healthcare service usage
  • Treatment compliance, based on the proportion of withdrawals from intervention
  • The occurrence of suicide or self-harm
  • Any adverse effects of the intervention.

Results

Six studies were included in the review. Three of the studies were carried out in the USA (Ashman, Cantor, Tsaousides, Spielman, & Gordon, 2014; Ashman & Tsaousides, 2012; Fann et al., 2015; Hoffman et al., 2010), one in China (He, Yu, Yang, & Yang, 2004), one in Canada (Bedard et al., 2014) and one in Australia (Simpson, Tate, Whiting, & Cotter, 2011). Participants in all studies were over 18 years of age.

Summary of interventions in included studies

Study NParticipants Intervention Duration of Treatment Outcome measure
Ashman 2014 (Ashman et al., 2014; Ashman & Tsaousides, 2012) 77(43 completed) Cognitive Behaviour Therapy (CBT) or Supportive Psychotherapy (SPT) 16 sessions over 3 months Structured Clinical Interview for DSM-IVBeck Depression Inventory – second edition (BDI-II)
Bedard 2013 (Bedard et al., 2014) 105(76 completed) Mindfulness-based cognitive therapy (MBCT) modified to suit those with TBI 10 weekly session plus recommended daily meditation BDI-II
Fann 2015 (Fann et al., 2015) 100(86 with follow up data) CBT in person or by telephone 8 to 12 weekly sessions Hamilton Depression Rating Scale (HAMD-17)
He 2004 (He et al., 2004) 64(63 completed) Repetitive transcranial magnetic stimulation (rTMS) 4 treatment sessions each lasting 5 days, with an interval of 2 days between sessions HAMD
Hoffman 2010 (Hoffman et al., 2010) 80(76 completed) Supervised exercise training 10 weekly sessions, plus a home program BDI
Simpson 2011 (Simpson et al., 2011) 17(16 completed) Group-based CBT 10 weekly sessions Hospital Anxiety and Depression Scale (HADS)

Primary outcomes

The review reported on four comparative analyses:

  1. CBT, or a variant of CBT, vs waiting list; included a meta-analysis of three studies (Bedard, Fann, Simpson). There was no indication of a difference in depression symptoms attributable to the intervention (standardised mean difference (SMD) -0.14, 95% CI -0.47 to 0.19; Z = 0.83, p = .41).
  2. CBT to SPT; based on one study (Ashman), the difference in depression remission was not statistically supported (RR 0.76; 95% CI 0.58 to 1.00; Z = 1.96; P = 0.05) nor was the difference between groups in depression symptoms (SMD -0.09; 95% CI -0.65 to 0.48; Z = 0.30; P = 0.77).
  3. rTMS plus tricyclic antidepressants (TCA) to TCA; based on one study (He). There was a reduction in depression symptoms seen in the rTMS plus TCA group, (0.84; 95% CI -1.36 to -0.32; Z = 3.19; P = 0.001), however the difference was not considered to be clinically relevant. This was the only study to report adverse effects as two participants reported transient tinnitus with spontaneous remission.
  4. Supervised exercise and exercise as usual; based on a single study (Hoffman). There was no difference in depression symptoms between groups following the intervention (SMD -0.43; 95% CI -0.88 to 0.03; Z = 1.84; P = 0.07).

Secondary outcomes

Secondary outcomes were reported for each individual study. There was no difference in treatment compliance between intervention and comparison group in each study. One study (He et al., 2004) reported adverse effects as two participants reported transient tinnitus with spontaneous remission.

Most other secondary outcomes showed no difference between intervention and treatment groups.

There is insufficient evidence to recommend any particular non-pharmacological treatment for depression in traumatic brain injury.

There is insufficient evidence to recommend any particular non-pharmacological treatment for depression in traumatic brain injury.

Strengths and limitations

Some studies were not included because of the narrow focus of the review. The primary outcome of these studies was quality of life or psychological well-being and as such did not require included participants to have a diagnosis of depression or a particular cut-off score on a depression scale. While these may have been of interest, this is not necessarily a limitation as it allowed the authors to concentrate on a clinically relevant treatment effect for depression.

The authors found the quality of evidence to be low or very low in all comparisons, mainly due to the lack of blinding participants and personnel to the treatment. This lack of blinding could have affected the self-report depression symptom scales in particular. The authors suggested some suitable placebo treatments such as sham rTMS to imitate real TMS or a social contact intervention to compare to CBT.

Conclusion

The paucity of studies included makes it difficult to draw any firm conclusions. There was no strong evidence to support any of the interventions explored here. All of the studies are very recent which suggests there may be an increase in this kind of research.

The authors point to some implications for future research in this area, such as the careful consideration of what will be meaningful to the individual participants and the question of the suitability of RCT design for CBT interventions.

The review calls for future RCTs that compare active interventions with controls that replicate the effect of the attention given to participants during an active treatment.

The review calls for future RCTs that compare active interventions with controls that replicate the effect of the attention given to participants during an active treatment.

Links

Primary paper

Gertler P, Tate RL, Cameron ID. (2015) Non-pharmacological interventions for depression in adults and children with traumatic brain injury. Cochrane Database of Systematic Reviews 2015, Issue 12. Art. No.: CD009871. DOI: 10.1002/14651858.CD009871.pub2.

Other references

Ashman, T., Cantor, J. B., Tsaousides, T., Spielman, L., & Gordon, W. (2014). Comparison of cognitive behavioral therapy and supportive psychotherapy for the treatment of depression following traumatic brain injury: A randomized controlled trial. Journal of Head Trauma Rehabilitation, 29(6), 467–478. [PubMed abstract]

Ashman, T., & Tsaousides, T. (2012). Cognitive behavioral therapy for depression following traumatic brain injury: FINDINGS of a randomized controlled trial. Brain Impairment. Cambridge University Press.

Bedard, M., Felteau, M., Marshall, S., Cullen, N., Gibbons, C., Dubois, S., … Moustgaard, A. (2014). Mindfulness-based cognitive therapy reduces symptoms of depression in people with a traumatic brain injury: results from a randomized controlled trial. J Head Trauma Rehabil, 29(4), E13–22. [PubMed abstract]

Fann, J. R., Bombardier, C. H., Vannoy, S., Dyer, J., Ludman, E., Dikmen, S., … Temkin, N. (2015). Telephone and in-person cognitive behavioral therapy for major depression after traumatic brain injury: a randomized controlled trial. Journal of Neurotrauma, 32(1), 45–57. [PubMed abstract]

He, C. S., Yu, Q., Yang, D. J., & Yang, M. (2004). Interventional effects of low-frequency repetitive transcranial magnetic stimulation on patients with depression after traumatic brain injury. Chinese Journal of Clinical Rehabilitation, 8, 6044–6045.

Hoffman, J. M., Bell, K. R., Powell, J. M., Behr, J., Dunn, E. C., Dikmen, S., & Bombardier, C. H. (2010). A randomized controlled trial of exercise to improve mood after traumatic brain injury. Physical Medicine and Rehabilitation, 2(10), 911–919. [PubMed abstract]

Maas, A. I. R., Stocchetti, N., & Bullock, R. (2008). Moderate and severe traumatic brain injury in adults. Lancet Neurology, 7 (August), 728 – 741. [PubMed abstract]

Simpson, G. K., Tate, R. L., Whiting, D. L., & Cotter, R. E. (2011). Suicide prevention after traumatic brain injury: a randomized controlled trial of a program for the psychological treatment of hopelessness. The Journal of Head Trauma Rehabilitation, 26(4), 290–300. [PubMed abstract]

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– See more at: http://www.nationalelfservice.net/mental-health/depression/treatment-for-depression-in-traumatic-brain-injury-cochrane-find-no-evidence-for-non-pharmacological-interventions/#sthash.oqwXaf7W.dpuf

Medication for cognitive impairment in traumatic brain injury: little evidence to support its use

by Eleanor Kennedy @Nelllor_

This blog originally appeared on the Mental Elf site on 18th January 2016.

Traumatic Brain Injury (TBI) is classified by The World Health Organization as the leading cause of death and disability among children and young adults worldwide (WHO, 2006, p. 164). An estimated 235 per 100,000 Europeans acquire brain injuries each year, with more than  6 million TBI survivors already living in Europe (Tagliaferri et al, 2006).

There are many long-lasting consequences of TBI including cognitive, behavioural and emotional problems (Barnes & Ward, 2005). Pharmacotherapy interventions have been suggested to alleviate cognitive impairment in TBI sufferers. The current review aimed to assess the evidence for such interventions (Dougall et al, 2015).

skateboardTraumatic brain injury is the leading cause of death and disability among children and young adults worldwide.

Methods

The Cochrane Dementia and Cognitive Improvement Group’s Specialised Register was searched for studies that examined the effectiveness of pharmacological treatment for cognitive impairment in people with traumatic brain injury. The search included both healthcare databases and trial registers. Studies were included if:

  • The study design was either a randomised controlled trial (RCT) or cross-over design study
  • The study investigated one centrally acting pharmacological agent that modulate one or more of the main neurotransmitter systems
  • Participants had to have experienced the TBI resulting in chronic cognitive impairment at least 12 months prior to assessment

The primary outcomes of interest were performance on psychometric and neuropsychological tests or scores on screening measures that measured memory and cognitive function; global severity of cognitive impairment and global impression of change. Acceptability of treatment (as measured by withdrawal from trial), safety, mortality and subjective benefit were all secondary outcomes.

Analyses were carried out on results from phase one of each included study.

Results

Four studies in total were included in the review (3 from the United States, one from Sweden). Seven RCTs that matched inclusion criteria were found, however, two cross-over design studies could not be included as data for phase one was not available from the authors; another study was not included due to the lack of a placebo control. Table 1 summarises the treatments and participants.

Study N Participants Treatment Duration of treatment
Jhaet al. 2008 51 (age 16 to 65) Modafinil; effects histaminergic, serotonergic, and glutaminergic activity 4 weeks
Johansson et al. 2012 12 (age 30 to 65) (−)-OSU6162; monoamine stabiliser agent with dopaminergic and serotonergic effects 4 weeks
Ripley et al. 2014 60 (age 18 to 65) Atomoxetine; noradrenaline reuptake inhibitor 2 weeks
Silver et al., 2006 157 (age 18 to 50) Rivastigmine; an acetylcholinesterase and butyrylcholinesterase inhibitor 12 weeks

Primary outcome

Neither modafinil nor atomoxetine demonstrated superiority over placebo on any measure of cognition. The effects of rivastigmine were superior on one measure in the current review (CANTAB RVIP −44.54 milliseconds, 95% CI −88.62 to −0.46), but not in the original trial. Rivastigmine was also effective on the same measure in a subgroup of participants with greater cognitive impairment.

Superiority over placebo for (−)-OSU6162 was demonstrated in Trail Making Test A (−9.20 seconds, 95% CI −12.19 to −6.21), Trail Making Test B (−6.20 seconds, 95%CI,−7.81 to−4.59) and WAIS-III digit symbol coding (8.60, 95% CI 6.47 to 10.73), however the score in Trail Making Test D was higher for placebo (53.80 seconds, 95% CI 36.76 to 70.24) (Johansson 2012).

Secondary outcomes

Safety and acceptability were two secondary outcomes that were reported on. Participants reported more adverse effects for modafinil and atomoxetine, however this was not statistically supported. One participant required a dose reduction in the (-)-OSU6162 trial due to adverse effects. More participants taking rivastigmine reported nausea compared to those taking placebo (19/80, 23.8%versus 6/77, 7.8%, risk ratio 3.05, 95% CI 1.29 to 7.22). Two people dropped out of the modafinil treatment arm, none in the placebo group. There were no deaths reported in any of the included studies.

Strengths and limitations

The review included only randomised controlled trials to assess the effects of centrally acting pharmacological agents for treatment of chronic cognitive impairment subsequent to traumatic brain injury in adults. There were very strict inclusion criteria and the authors chose to only include data from phase one of the treatment. This is a strength for cross-over design studies particularly as this controls for the possibility of long term treatment effects once a group’s treatment is switched to placebo following pharmacological treatment. However, two studies were excluded because data from phase one were unavailable.

The limited number of included studies, rather than a limitation, is likely to be indicative of a lack of well controlled research into pharmacological treatments for cognitive impairment following TBI.

Conclusions

There was no evidence to support modafinil or atomoxetine as a treatment for cognitive impairment as a result of TBI. There was weak evidence to suggest that rivastigmine may be helpful in the treatment of cognitive impairment in one measure of cognitive functioning in this review, however the same effect was not significant in the original study possibly due to the use of a different statistical test, and the findings that (−)-OSU6162 may be superior to placebo must be interpreted with caution as the sample size in this group was so small (n=6).

Overall the authors concluded that:

there is insufficient evidence to determine whether pharmacological treatment is effective in chronic cognitive impairment in TBI.

Two of the four included studies had fatigue as their primary outcome, which further suggests that more research  in the specific area of cognition may be necessary.

In closing, the review highlights a gap in the research in such treatments for TBI, the authors suggest that future research should also focus on outcomes such as neurobehavioral symptoms as well as cognitive impairment and memory performance.

This review highlights a lack of RCTs that explore the value of medication for cognitive impairment following traumatic brain injury.This review highlights a lack of RCTs that explore the potential value of medication for cognitive impairment following traumatic brain injury.

Links

Primary paper

Dougall D, Poole N, Agrawal N. Pharmacotherapy for chronic cognitive impairment in traumatic brain injury. Cochrane Database of Systematic Reviews 2015, Issue 12. Art. No.: CD009221. DOI: 10.1002/14651858.CD009221.pub2.

Other references

Barnes M, Ward A. (2005) Oxford Handbook of Rehabilitation Medicine. Oxford University Press.

Jha A, Weintraub A, Allshouse A, Morey C, Cusick C, Kittelson J, Gerber D. (2008) A randomized trial of modafinil for the treatment of fatigue and excessive daytime sleepiness in individuals with chronic traumatic brain injury. Journal of Head Trauma Rehabilitation, 23(1), 52–63. doi:10.1097/01.HTR.0000308721.77911.ea (PubMed abstract)

Johansson B, Carlsson A, Carlsson ML, Karlsson M, Nilsson MKL, Nordquist-Brandt E, Rönnbäck L. (2012) Placebo-controlled cross-over study of the monoaminergic stabiliser (-)-OSU6162 in mental fatigue following stroke or traumatic brain injury. Acta Neuropsychiatrica, 24, 266–274. doi:10.1111/j.1601-5215.2012.00678.x [PubMed record]

Ripley DL, Morey CE, Gerber D, Harrison-Felix C, Brenner LA, Pretz CR, Wesnes K. (2014) Atomoxetine for attention deficits following traumatic brain injury: Results from a randomized controlled trial. Brain Injury, 28(January 2016), 1514–1522. doi:10.3109/02699052.2014.919530 [PubMed abstract]

Silver JM, Koumaras B, Chen M, Mirski D, Potkin SG, Reyes P, Gunay I. (2006) Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology, 67, 748–755. [PubMed abstract]

Tagliaferri F, Compagnone C, Korsic M, Servadei F, Kraus J. (2006) A systematic review of brain injury epidemiology in Europe. Acta Neurochirurgica, 148(3), 255–68; discussion 268. doi:10.1007/s00701-005-0651-y [PubMed abstract]

WHO. (2006) Neurological Disorders: Public Health Challenges. World Health Organisation (p. 232).http://www.who.int/mental_health/neurology/neurological_disorders_report_web.pdf

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Drug-using offenders with co-occuring mental illness

by Meg Fluharty @MegEliz_

This blog originally appeared on the Mental Elf site on 15th October 2015.

shutterstock_314454056

Many individuals in the criminal justice system have both mental health and substance use problems. There is little evidence targeting the treatment programmes for offenders, alongside the additional challenges faced by those with co-occurring mental illnesses.

The Cochrane Drugs and Alcohol Group have published a set of four reviews centred on interventions for drug-using offenders. This is an updated review, targeting offenders with co-occurring mental illnesses, which was originally published in 2006. We blogged about the review when it was last updated in March 2014, but this new version has more evidence (3 new RCTs) included.

About 30% of acquisitive crime (burglaries, theft and robberies) are committed by individuals supporting drug use.

Methods

The review authors searched the usual comprehensive list of databases to identify randomised controlled trials (RCTs) to identify whether treatments for drug using offenders with co-occurring mental illnesses:

  • Reduced drug use
  • Reduced criminal activity
  • Whether the treatment setting affected the intervention
  • Whether the type of treatment affected the outcome

All participants, regardless of gender, age or ethnicity, were included in this analysis.

The updated search (from March 2013 – April 2014) added 3 new trials to the review, totalling 14 publications representing 8 trials published between 1999 and 2014.

Study characteristics

  • 6 studies were conducted in secure settings and 2 studies were conducted in a court setting
  • No studies assessed pharmacological treatments or were conducted in the community
  • All studies were conducted in the United States
  • Study duration varied from 3 months to 5 year follow-up
  • 7 studies investigated adult offenders, while one study investigated adolescent offenders (aged 14 -19)
  • 3 studies included female offenders, while adult male offenders filled the majority of the population in the remaining studies.

Results

Therapeutic community and aftercare versus treatment as usual

Impact on drug use (self-report)

  • Two studies reported a reduction in drug use:
    • (Sacks, 2004) (RR 0.58 95% CI 0.36 to 0.93, 139 participants)
    • (Sacks, 2008) (RR 0.73, 95% CI 0.53 to 1.01, 370 participants)
  • One study reported no reduction:
    • (Wexler, 1999) (RR 1.11 95% CI 0.82 to 1.49, 576 participants)

Impact on criminal activity

  • Two studies reported no reduction in re-arrests following treatment:
    • (Sacks, 2008) (RR 1.65, 95% CI 0.83 to 3.28, 370 participants)
    • (Wexler, 1999) (RR 0.96, 95% CI 0.82 to 1.13, 428 participants)
  • Three studies evaluated the impact of therapeutic community treatment using re-incarceration measures
    • Two studies reported reductions:
      • (Sacks, 2004) (RR 0.28, 95% CI 0.13 to 0.63, 193 participants)
      • (Sacks 2011) (RR 0.49, 95% CI 0.27 to 0.89, 127 participants)
    • One study found no effects:
      • (Sacks, 2008) (RR 0.73, 95% CI 0.45 to 1.19, 370 participants)

Mental health court and case management versus treatment as usual (standard court proceedings)

Impact on drug use (self-report)

  • No data available

Impact on criminal activity

  • One study reported no reduction in criminal activity:
    • (Cosden, 2003) (RR 1.05, 95% CI 0.90 to 1.22, 235 participants)

Motivational interviewing and cognitive skills versus relaxation therapy

Impact on drug use (self-report)

  • Two studies reported no reduction in drug use:
    • (Stein 2011) (MD -7.42, 95% CI -20.12 to 5.28, 162 participants)
    • (Lanza 2013) (RR 0.92, 95% CI 0.36 to 2.33, 41 participants)

Impact on criminal activity

  • No data available

Interpersonal psychotherapy versus a psychotherapy versus a psycho-educational intervention

Impact on drug use (self-report)

  • One study reported no reduction in drug use:
    • (Johnson 2012) (RR 0.67, 95% CI 0.30 to 1.50, 38 participants)

Impact on criminal activity

  • No data available

This review suggests that mental health programmes and drug interventions can help reduce criminal activity and re-incarceration rates, but are less effective at reducing drug use.

Discussion

This updated review included eight studies conducted within secure settings and in the judicial system. There were no studies for drug abusing offenders with mental illnesses under parole identified for inclusion within this review. Therefore, it’s difficult to compare if interventions are more beneficial within the community or under probation services.

Additionally, as all studies were conducted in the United States, it’s possible the treatments may not be generalisable outside the American judicial system, and as drug-use was self-report rather than biological measures, some caution needs to be taken when interpreting the results.

Generally, there was large variation across the studies, making comparisons difficult. However, two of the five trials displayed some evidence for therapeutic aftercare in relation to reducing subsequent re-incarceration.

All of the studies in this review were conducted in the US, so there may be issues of generalisability to other countries and judicial/health systems.

Links

Primary paper

Perry AE, Neilson M, Martyn-St James M, Glanville JM, Woodhouse R, Godfrey C, Hewitt C. Interventions for drug-using offenders with co-occurring mental illness. Cochrane Database of Systematic Reviews 2015, Issue 6. Art. No.: CD010901. DOI: 10.1002/14651858.CD010901.pub2.

Other references

Sacks S, Sacks JY, McKendrick K, Banks S, Stommel J. Modified TC for MICA inmates in correctional settings: crime outcomes. Behavioural Sciences and the Law 2004;22(4):477-501. [PubMed abstract]

Sullivan CJ, McKendrick K, Sacks S, Banks S. Modified therapeutic community treatment for offenders with MICA disorders: substance use outcomes. American Journal of Drug and Alcohol Abuse 2007; Vol. 33, issue 6:823-32. [0095-2990: (Print)] [PubMed abstract]

Sacks JY, McKendrick K, & Hamilton ZK. A randomized clinical trial of a therapeutic community treatment for female inmates: outcomes at 6 and 12 months after prison release. Journal of Addictive Diseases 2012;31(3):258-69. [PubMed abstract]

Sacks JY, Sacks S, McKendrick K, Banks S, Schoeneberger M, Hamilton Z, et al. Prison therapeutic community treatment for female offenders: Profiles and preliminary findings for mental health and other variables (crime, substance use and HIV risk). Journal of Offender Rehabilitation 2008;46(3-4):233-61. [: 1050-9674] [Abstract]

Prendergast ML, Hall EA, Wexler HK. Multiple measures of outcome in assessing a prison-based drug treatment program. Journal of Offender Rehabilitation 2003;37:65-94. [Abstract]

Prendergast ML, Hall EA, Wexler HK, Melnick G, Cao Y. Amity prison-based therapeutic community: 5-year outcomes. Prison Journal 2004;84(1):36-50. [Abstract]

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Cosden M, Ellens JK, Schnell JL, Yamini-Diouf Y, Wolfe MM. Evaluation of a mental health treatment court with assertive community treatment. Behavioral Sciences and the Law2003;21(4):415-27. [Abstract]

Stein LA, Lebeau R, Colby SM, Barnett NP, Golembeske C, Monti PM. Motivational interviewing for incarcerated adolescents: effects of depressive symptoms on reducing alcohol and marijuana use after release. Journal of Studies on Alcohol and Drugs2011;72(3):497-506. [PubMed abstract]

Lanza PV, Garcia PF, Lamelas FR, Gonzalez-Menendez A. Acceptance and commitment therapy versus cognitive behavioral therapy in the treatment of substance use disorder with incarcerated women. Journal of Clinical Psychology 2014;70(7):644-57. [DOI:10.1002/jcip.22060]

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– See more at: http://www.nationalelfservice.net/mental-health/substance-misuse/drug-using-offenders-with-co-occurring-mental-illness/#sthash.CnpCuCWr.dpuf

Reducing alcohol consumption in illicit drug users: new Cochrane review on psychotherapies

By Olivia Maynard @OliviaMaynard17

This blog originally appeared on the Mental Elf site on 28th January 2015

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Whilst we all know that excessive alcohol consumption is bad for our health, illicit drug users are one group for whom problem alcohol use can be especially harmful, causing serious health consequences.

The prevalence of the hepatitis C virus is high among illicit drug users and problem alcohol use contributes to a poorer prognosis of this disease by increasing its progression to other diseases. In addition, rates of anxiety, mood and personality disorders are higher among illicit drug users, each of which is exacerbated by problem alcohol use.

Despite these health consequences, the prevalence of problem alcohol use is high among illicit drug users, with around 38% of opiate- and 45% of stimulant-using treatment-seeking individuals having co-occurring alcohol use disorders (Hartzler 2010; Hartzler 2011).

Previous Cochrane reviews have investigated the effectiveness of psychosocial interventions (or ‘talking therapies’) for either problem alcohol use, or illicit drug use alone. However, none have investigated the effectiveness of these therapies for individuals with concurrent problem alcohol and illicit drug use. Given the significant health risk and the high prevalence of concurrent problem alcohol and illicit drug use, a Cochrane review of this kind is long over-due.

Luckily, Kilmas and colleagues have done the hard work for us and their comprehensive Cochrane review of the literature evaluates the evidence for talking therapies for alcohol reduction among illicit drug users (Klimas et al, 2014).

This updated Cochrane review looks at psychotherapy for concurrent problem alcohol and illicit drug use.

The talking therapies we’re concerned with here are psychologically based interventions, which aim to reduce alcohol consumption without using any pharmacological (i.e. drug-based) treatments. Although there’s a wide range of different talking therapies currently used in practice, the ones which are discussed in this Cochrane review are:

  • Motivational interviewing (MI): this uses a client-centered approach, where the client’s readiness to change and their motivation, is a key component of the therapy.
  • Cognitive-behavioural therapy (CBT): this focuses on changing the way a client thinks and behaves. To address problem alcohol use, CBT approaches identify the triggers associated with drug use and use behavioural techniques to prevent relapse.
  • Brief interventions (BI): often BIs are based on the principles of MI and include giving advice and information. However, as implied by the name, BIs tend to be shorter and so are more suitable for non-specialist facilities.
  • The 12-step model: this is the approach used by Alcoholics Anonymous and operates by emphasising the powerlessness of the individual over their addiction. It then uses well-established therapeutic approaches, such as group cohesiveness and peer pressure to overcome this addiction.

Methods

  • The Cochrane review included all randomised controlled trials which compared psychosocial interventions with another therapy (whether that be other psychosocial therapies (to allow for comparison between therapies), pharmacological therapies, or placebo). Participants were adult illicit drug users with concurrent problem alcohol use
  • Four studies were included, involving 594 participants in total
  • The effectiveness of these interventions were assessed and the authors were most interested in the impact of these therapies on alcohol use, but were also interested in their impact on illicit drug use, participants’ engagement in further treatment and differences in alcohol related harms
  • The quality of the studies was also assessed

The quality of trials included in this review could certainly have been a lot better.

Results

The four studies were very different, each comparing different therapies:

  • Study 1: cognitive-behavioural therapy versus the 12-step model (Carroll et al, 1998)
  • Study 2: brief intervention versus treatment as usual (Feldman et al 2013)
  • Study 3: group or individual motivational interviewing versus hepatitis health promotion (Nyamathi et al, 2010)
  • Study 4: brief motivational intervention versus assessment only (Stein et al, 2002)

Due to this heterogeneity, the results could not be combined and so each study was considered separately. Of the four studies, only Study 4 found any meaningful differences between the therapies compared. Here, participants in the brief motivational intervention condition had reduced alcohol use (by seven or more days in the past month at 6-month follow up) as compared with the control group (Risk Ratio 1.67; 95% Confidence Interval 1.08 to 2.60; P value = 0.02). However, no other differences were observed for other outcome measures.

Overall, the review found little evidence that there are differences in the effectiveness of talking therapies in reducing alcohol consumption among concurrent alcohol and illicit drug users.

The authors of this review also bemoan the quality of the evidence provided by the four studies and judged them to be of either low or moderate quality, failing to account for all potential sources of bias.

The review found no evidence that any of the four therapies was a winner when it came to reducing alcohol consumption in illicit drug users.

Conclusions

So, what does this all mean for practice?

In a rather non-committal statement, which reflects the paucity of evidence available, the authors report that:

based on the low-quality evidence identified in this review, we cannot recommend using or ceasing psychosocial interventions for problem alcohol use in illicit drug users.

However, the authors suggest that similar to other conditions, early intervention for alcohol problems in primary care should be a priority. They also argue that given the high rates of co-occurrence of alcohol and drug problems, the integration of therapy for these two should be common practice, although as shown here, the evidence base to support this is currently lacking.

And what about the comparison between the different talking therapies?

Again, rather disappointingly, the authors report that:

no reliable conclusions can be drawn from these data regarding the effectiveness of different types of psychosocial interventions for the target condition.

How about the implications for research? What do we still need to find out?

This review really highlights the scarcity of well-reported, methodologically sound research investigating the effectiveness of psychosocial interventions for alcohol and illicit drug use and the authors call for trials using robust methodologies to further investigate this.

Choosing a therapy for this group of patients is difficult with insufficient evidence to support our decision.

Links

Klimas J, Tobin H, Field CA, O’Gorman CSM, Glynn LG, Keenan E, Saunders J, Bury G, Dunne C, Cullen W. Psychosocial interventions to reduce alcohol consumption in concurrent problem alcohol and illicit drug users. Cochrane Database of Systematic Reviews 2014, Issue 12. Art. No.: CD009269. DOI: 10.1002/14651858.CD009269.pub3.

Hartzler B, Donovan DM, Huang Z. Comparison of opiate-primary treatment seekers with and without alcohol use disorderJournal of Substance Abuse Treatment 2010;39 (2):114–23.

Hartzler B, DonovanDM,Huang Z. Rates and influences of alcohol use disorder comorbidity among primary stimulant misusing treatment-seekers: meta-analytic findings across eight NIDA CTN trialsThe American Journal of Drug and Alcohol Abuse 2011;37(5):460–71.

Carroll, K.M., Nich, C. Ball, S.A, McCance, E., Rounsavile, B.J. Treatment of cocaine and alcohol dependence with psychotherapy and dislfram. Addiction 1998; 93(5):713-27. [PubMed abstract]

Feldman N, Chatton A, Khan R, Khazaal Y, Zullino D. Alcohol-related brief intervention in patients treated for opiate or cocaine dependence: a randomized controlled studySubstance Abuse Treatment, Prevention, and Policy 2011;6(22):1–8.

Nyamathi A, Shoptaw S,Cohen A,Greengold B,Nyamathi K, Marfisee M, et al. Effect of motivational interviewing on reduction of alcohol useDrug Alcohol Dependence 2010;107(1):23–30. [1879–0046: (Electronic)]

Stein MD, Charuvastra A, Makstad J, Anderson BJ. A randomized trial of a brief alcohol intervention for needle exchanges (BRAINE). Addiction 2002;97(6):691. [:09652140] [PubMed abstract]

Mikhail Pogosov / Shutterstock.com

– See more at: http://www.thementalelf.net/mental-health-conditions/substance-misuse/reducing-alcohol-consumption-in-illicit-drug-users-new-cochrane-review-on-psychotherapies/#sthash.DgftSUSM.dpuf

Cochrane review says there’s insufficient evidence to tell whether fluoxetine is better or worse than other treatments for depression

Depression is common in primary care and associated with a substantial personal, social and societal burden. There is considerable ongoing controversy regarding whether antidepressant pharmacotherapy works and, in particular, for whom. One widely-prescribed antidepressant is fluoxetine (Prozac), an antidepressant of the selective serotonin reuptake inhibitors (SSRI) class. Although a number of more recent antidepressants are available, fluoxetine (which went off patent in 2001) remains highly popular and is commonly prescribed.

This systematic review and meta-analysis, published through the Cochrane Collaboration, compares the effects of fluoxetine for depression, compared with other SSRIs, tricyclic antidepressants (TCAs), selective noradrenaline reuptake inhibitors (SNRIs), monoamine oxidase inhibitors (MAOIs) and newer agents, as well as other conventional and unconventional agents. This is an important clinical question – different antidepressants have different efficacy and side effect profiles, but direct comparisons are relatively rare.

Methods

Thank goodness for systematic reviewers who read hundreds of papers and combine the results, so you don't have to

Thank goodness for systematic reviewers who read hundreds of papers and combine the results, so you don’t have to

The review focused on studies of adults with unipolar major depressive disorder (regardless of the specific diagnostic criteria used), searching major databases for studies published up to 11 May 2012.

All randomised controlled trials comparing fluoxetine with any other antidepressant (including non-conventional agents such as hypericum, also known as St John’s wort) were included. Both dichotomous (reduction of at least 50% on the Hamilton Depression Scale) and continuous (mean scores at the end of the trial or change score on depression measures) outcomes were considered.

Results

A total of 171 studies were included in the analysis, conducted between 1984 and 2012 and comprising data on 24,868 participants.

A number of differences in efficacy and tolerability between fluoxetine and certain antidepressants were observed. However, these differences were typically small, so that the clinical meaning of these differences is not clear.

Moreover, the majority of studies failed to report detail on methodological procedures, and most were sponsored by pharmaceutical companies.

Both factors increase the risk of bias and overestimation of treatment effects.

Conclusions

The review

The review found sertraline and venlafaxine (and possibly other antidepressants) had a better efficacy profile than fluoxetine

The authors conclude that: “No definitive implications can be drawn from the studies’ results”.

There was some evidence for greater efficacy of sertraline and venlafaxine over fluoxetine, which may be clinically meaningful, but other considerations such as side-effect profile, patient acceptability and cost will also have a bearing on treatment decisions.

In other words, despite considerable effort and pooling all of the available evidence, we still can’t be certain whether one antidepressant is superior to another.

What this review really highlights is the ongoing difficulty in establishing whether some drugs are genuinely effective (and safe), because of publication bias against null results (Turner, 2008).

This situation is made worse when there are financial vested interests involved. Recently, there has been active discussion about how this problem can be resolved, for example by requiring pharmaceutical companies to release all data from clinical trials they conduct, irrespective of the nature of the findings.

Despite the mountains of trials published in this field, we still cannot say for sure which treatments work best for depression

Despite the mountains of trials published in this field, we still cannot say for sure which treatments work best for depression

Clinical decision making regarding the most appropriate medication to prescribe are complex, and made harder by the lack of direct comparisons. Moreover, the apparent efficacy of individual treatments may be inflated by publication bias. Direct comparisons between different treatments are therefore important, but remain relatively rare. This Cochrane Review provides very important information, even if only by highlighting how much we still don’t know about which treatments work best.

Links

Magni LR, Purgato M, Gastaldon C, Papola D, Furukawa TA, Cipriani A, Barbui C. Fluoxetine versus other types of pharmacotherapy for depression. Cochrane Database of Systematic Reviews 2013, Issue 7. Art. No.: CD004185. DOI: 10.1002/14651858.CD004185.pub3.

Etchells, P. We don’t know if antidepressants work, so stop bashing them. The Guardian website, 15 Aug 2013.

Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R. Selective publication of antidepressant trials and its influence on apparent efficacy. N Engl J Med. 2008 Jan 17;358(3):252-60. doi: 10.1056/NEJMsa065779. [PubMed abstract]

This article first appeared on the Mental Elf website on 1st October 2013 and is posted by Marcus Munafo