Social Support and Smoking Abstinence among Incarcerated Adults in the United States: A Longitudinal Study

Background: In the United States, tobacco use among prisoners is nearly three times that of the general population. While many American prisons and jails are now tobacco-free, nearly all inmates return to smoking as soon as they are released back into the community. Methods: To better understand the role that personal relationships may play in enabling return to smoking, we enrolled former-smokers who were inmates in a tobacco-free prison. Baseline assessments were conducted six weeks prior to inmates’ scheduled release and included measures of smoking prior to incarceration, motivation, confidence and plans for remaining quit after release. We also assessed global social support (ISEL) and a measure of social support specific to quitting smoking (SSQ). Smoking status was assessed three weeks after prison release and included 7-day point-prevalence abstinence validated by urine cotinine, days to first cigarette and smoking rate. Results: A diverse sample comprised of 35% women, 20% Hispanic, and 29% racial minorities (average age 35.5 years) provided baseline data (n = 247). Over 90% of participants provided follow up data at 3-weeks post-release. Prior to incarceration participants had smoked an average of 21.5 (SD = 11.7) cigarettes per day. Only 29.2% had definite plans to remain smoking-abstinent after release. Approximately half of all participants reported that “most” or “all” of their family (42.2%) and friends (68%) smoked, and 58.8% reported their spouse or romantic partner smoked. SSQ scores were not significantly predictive of smoking outcomes at three weeks, however, social support from family and friends were each significantly and positively correlated with motivation, confidence, and plans for remaining abstinent (all p values Conclusions: Inmates of smoke-free prisons have a head-start on being smoke-free for life. They have been abstinent well past the duration of nicotine withdrawal and have great financial incentive not to begin smoking again. However, this advantage may be offset by a lack of non-smoking role models among their family and friends, and perceived lack of support for remaining smoke-free. Trial Registration: ClinicalTrials.gov Identifier: NCT0168499

Forced Smoking Abstinence: Not Enough for Smoking Cessation

Importance: Millions of Americans are forced to quit smoking as they enter tobacco-free prisons and jails, but most return to smoking within days of release. Interventions are needed to sustain tobacco abstinence after release from incarceration. Objective: To evaluate the extent to which the WISE intervention (Working Inside for Smoking Elimination), based on motivational interviewing (MI) and cognitive behavioral therapy (CBT), decreases relapse to smoking after release from a smoke-free prison. Design: Participants were recruited approximately 8 weeks prior to their release from a smoke-free prison and randomized to 6 weekly sessions of either education videos (control) or the WISE intervention. Setting: A tobacco-free prison in the United States. Participants: A total of 262 inmates (35% female). Main Outcome Measure: Continued smoking abstinence was defined as 7-days point-prevelance abstinence validated by urine cotinine measurement. Results: At the 3-week follow-up, 25% of the participants in the WISE intervention (31 of 122) and 7% of the control participants (9 of 125) continued to be tobacco-abstinent (odds ration [OR], 4.4; 95% CI, 2.0-9.7). In addition to the intervention, Hispanic ethnicity, a plan to remain abstinent, and being incarcerated for more than 6 months were all associated with increased likelihood of remaining abstinent. In the logistical regression analysis, participants randomized to the WISE intervention were 6.6 times more likely to remain tobacco abstinent at the 3-week follow up than those randomized to the control condition (95% CI, 2.5-17.0). Nonsmokers at the 3-week follow-up had an additional follow-up 3 months after release, and overall 12% of the participants in the WISER intervention (14 of 122) and 2% of the control participants (3 of 125) were tobacco free at 3 months, as confirmed by urine cotinine measurement (OR, 5.3; 95% CI, 1.4-23.8). Conclusions and Relevance: Forced tobacco abstinence alone during incarceration has little impact on postrelease smoking status. A behavioral intervention provided prior to release greatly improves cotinine-confirmed smoking cessation in the community. Trial Registration: clinicaltrials.gov Identifier: NCT0112258

The association between impulsivity and alcohol/drug use among prison inmates

Background: Few studies have examined the relation between impulsivity and drug involvement with prison inmates, in spite of their heavy drug use. Among this small body of work, most studies look at clinically relevant drug dependence, rather than drug use specifically. Method: N = 242 adult inmates (34.8% female, 52% White) with an average age of 35.58 (SD = 9.19) completed a modified version of the 15-item Barratt Impulsiveness Scale (BIS) and measures assessing lifetime alcohol, opiate, benzodiazepine, cocaine, cannabis, hallucinogen, and polysubstance use. Lifetime users also reported the frequency of use for the 30 days prior to incarceration. Results: Impulsivity was higher among lifetime users (versus never users) of all substances other than cannabis. Thirty day drug use frequency was only related to impulsivity for opiates and alcohol. Discussion: This study extends prior work, by showing that a lifetime history of non-clinical substance use is positively associated with impulsivity among prison inmates. Implications for drug interventions are considered for this population, which is characterized by high rates of substance use and elevated impulsivity

Changes in Depression and Stress after Release from a Tobacco-Free Prison in the United States

Prior research has found high levels of depression and stress among persons who are incarcerated in the United States (U.S.). However, little is known about changes in depression and stress levels among inmates post-incarceration. The aim of this study was to examine changes in levels of depression and stress during and after incarceration in a tobacco-free facility. Questionnaires that included valid and reliable measures of depression and stress were completed by 208 male and female inmates approximately eight weeks before and three weeks after release from a northeastern U.S. prison. Although most inmates improved after prison, 30.8% had a worsening in levels of depression between baseline and the three-week follow-up. In addition, 29.8% had a worsening in levels of stress after release than during incarceration. While it is not surprising that the majority of inmates reported lower levels of depression and stress post-incarceration, a sizable minority had an increase in symptoms, suggesting that environmental stressors may be worse in the community than in prison for some inmates. Further research is needed to address depression and stress levels during and after incarceration in order for inmates to have a healthier transition back into the community and to prevent repeat incarcerations

A Space for Co-constructing Counter Stories Under Surveillance

Using our experiences as members of a participatory action research committee (from the City University of New York Graduate Center and the Bedford Hills Correctional Facility) documenting the impact of college in a maximum security prison, this essay illustrates the power of Participatory Action Research in the construction of counter stories. We raise for discussion a set of theoretical, methodological and ethical challenges that emerged from the co-production of counter stories under surveillance: the creation of a critical space for producing \u27counter knowledge\u27; the co-mingling of counter and dominant discourses, the negotiation of power over and within research in prison, and the opening of a dialogue between counter stories and public policy makers

Indicated school-based intervention to improve depressive symptoms among at risk Chilean adolescents: a randomized controlled trial

Background: Depression is a disabling condition affecting people of all ages, but generally starting during adolescence. Schools seem to be an excellent setting where preventive interventions may be delivered. This study aimed to test the effectiveness of an indicated school-based intervention to reduce depressive symptoms among at-risk adolescents from low-income families. Methods: A two-arm, parallel, randomized controlled trial was conducted in 11 secondary schools in vulnerable socioeconomic areas in Santiago, Chile. High-risk students in year 10 (2° Medio) were invited to a baseline assessment (n = 1048). Those who scored ≥10 (boys) and ≥15 (girls) in the BDI-II were invited to the trial (n = 376). A total of 342 students consented and were randomly allocated into an intervention or a control arm in a ratio of 2:1. The intervention consisted of 8 group sessions of 45 min each, based on cognitive-behavioural models and delivered by two trained psychologists in the schools. Primary (BDI-II) and secondary outcomes (measures of anxiety, automatic thoughts and problem-solving skills) were administered before and at 3 months post intervention. The primary outcome was the recovery rate, defined as the proportion of participants who scored in the BDI-II <10 (among boys) and <15 (among girls) at 3 months after completing the intervention. Results: There were 229 participants in the intervention group and 113 in the control group. At 3-month follow-up 81.4 % in the intervention and 81.7 % in the control group provided outcome data. The recovery rate was 10 % higher in the intervention (50.3 %) than in the control (40.2 %) group; with an adjusted OR = 1.62 (95 % CI: 0.95 to 2.77) (p = 0.08). No difference between groups was found in any of the secondary outcomes. Secondary analyses revealed an interaction between group and baseline BDI-II score. Conclusions: We found no clear evidence of the effectiveness of a brief, indicated school-based intervention based on cognitive-behavioural models on reducing depressive symptoms among Chilean adolescents from low-income families. More research is needed in order to find better solutions to prevent depression among adolescents

Prevalence and architecture of de novo mutations in developmental disorders.

The genomes of individuals with severe, undiagnosed developmental disorders are enriched in damaging de novo mutations (DNMs) in developmentally important genes. Here we have sequenced the exomes of 4,293 families containing individuals with developmental disorders, and meta-analysed these data with data from another 3,287 individuals with similar disorders. We show that the most important factors influencing the diagnostic yield of DNMs are the sex of the affected individual, the relatedness of their parents, whether close relatives are affected and the parental ages. We identified 94 genes enriched in damaging DNMs, including 14 that previously lacked compelling evidence of involvement in developmental disorders. We have also characterized the phenotypic diversity among these disorders. We estimate that 42% of our cohort carry pathogenic DNMs in coding sequences; approximately half of these DNMs disrupt gene function and the remainder result in altered protein function. We estimate that developmental disorders caused by DNMs have an average prevalence of 1 in 213 to 1 in 448 births, depending on parental age. Given current global demographics, this equates to almost 400,000 children born per year

Heterozygous Variants in KMT2E Cause a Spectrum of Neurodevelopmental Disorders and Epilepsy.

We delineate a KMT2E-related neurodevelopmental disorder on the basis of 38 individuals in 36 families. This study includes 31 distinct heterozygous variants in KMT2E (28 ascertained from Matchmaker Exchange and three previously reported), and four individuals with chromosome 7q22.2-22.23 microdeletions encompassing KMT2E (one previously reported). Almost all variants occurred de novo, and most were truncating. Most affected individuals with protein-truncating variants presented with mild intellectual disability. One-quarter of individuals met criteria for autism. Additional common features include macrocephaly, hypotonia, functional gastrointestinal abnormalities, and a subtle facial gestalt. Epilepsy was present in about one-fifth of individuals with truncating variants and was responsive to treatment with anti-epileptic medications in almost all. More than 70% of the individuals were male, and expressivity was variable by sex; epilepsy was more common in females and autism more common in males. The four individuals with microdeletions encompassing KMT2E generally presented similarly to those with truncating variants, but the degree of developmental delay was greater. The group of four individuals with missense variants in KMT2E presented with the most severe developmental delays. Epilepsy was present in all individuals with missense variants, often manifesting as treatment-resistant infantile epileptic encephalopathy. Microcephaly was also common in this group. Haploinsufficiency versus gain-of-function or dominant-negative effects specific to these missense variants in KMT2E might explain this divergence in phenotype, but requires independent validation. Disruptive variants in KMT2E are an under-recognized cause of neurodevelopmental abnormalities

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)