While it is well known that there is an interaction between sleep disorders and substance abuse, it is certainly more complex than was previously thought. The effects on sleep depend on the substance used, but it has been shown that both during use and in withdrawal periods consumers have various sleep problems, and basically more fragmented sleep. We know that sleep problems must be taken into account to prevent addiction relapses.

To explain the different sleep disorders caused by substances such as alcohol and cannabis

As an example of this, two cases are introduced: the first one, a 17-year-old boy, who is diagnosed with ADHD with daily cannabis use since the age of 14. As a result of reducing consumption, he presents an episode of sleep paralysis that he had not previously had. The second one is a 50-year-old man diagnosed with a personality disorder and with dependence on cannabis and alcohol for years. He currently has abstinence from alcohol for months and maintains daily cannabis use. However, he has long-standing sleep pattern disturbances and frequent depersonalization phenomena at night.

Alcohol at low doses has no clear effects on sleep architecture. At higher doses it decreases sleep latency, as well as awakenings. In chronic alcoholic patients, a decrease in deep slow sleep, and more fragmented sleep have been found. Cannabis withdrawal reduces sleep quality, increases latency, and produces strange dreams.

There is a positive relationship both between having a substance use disorder and suffering from a sleep disorder.

No significant relationships.

Depression is strongly associated with chronic disease; yet, the direction of this relationship is poorly understood. Allostatic load (AL) provides a framework for elucidating depression-disease pathways. We aimed to investigate bidirectional, longitudinal associations of baseline depressive symptoms or AL with 5-year AL or depressive symptoms, respectively.

Data were from baseline, 2-year, and 5-year visits of 620 adults (45–75 years) enrolled in the Boston Puerto Rican Health Study. The Center for Epidemiology Studies Depression (CES-D) scale (0–60) captured depressive symptoms, which were categorized at baseline as low (<8), subthreshold (8–15), or depression-likely (⩾16) symptoms. AL was calculated from 11 parameters of biological functioning, representing five physiological systems. Baseline AL scores were categorized by the number of dysregulated parameters: low (0–2), moderate (3–5), or high (⩾6) AL. Multivariable, multilevel random intercept and slope linear regression models were used to examine associations between 3-category baseline CES-D score and 5-year continuous AL score, and between baseline 3-category AL and 5-year continuous CES-D score.

Baseline subthreshold depressive symptoms [(mean (95% CI)): 4.8 (4.5–5.2)], but not depression-likely symptoms [4.5 (4.2–4.9)], was significantly associated with higher 5-year AL scores, compared to low depressive symptoms [4.3 (3.9–4.7)]. Baseline high AL [19.4 (17.6–21.2)], but not low AL [18.5 (16.5–20.6)], was significantly associated with higher 5-year CES-D score, compared to baseline moderate AL [16.9 (15.3–18.5)].

Depressive symptoms and AL had a bi-directional relationship over time, indicating a nuanced pathway linking depression with chronic diseases among a minority population.

To test the prognostic value of suicidal status in depressed patients for responses to antidepressant treatment.

We evaluated treatment response and covariates in depressed patients diagnosed with DSM-IV major depressive (n=50) or bipolar disorders (n=32) treated initially in a day-hospital for 2 weeks, followed by 4 weeks of outpatient treatment with antidepressants, with or without a mood-stabilizer. Being suicidal was based on an item-3 of the 17-item Hamilton Depression Rating Scale (HDRS17) scored at ≥3 and verified by baseline clinical assessment; morbidity and improvement were based on the total of the remaining 16 nonsuicidal items (HDRS16).

Suicidal (n=31) and nonsuicidal subjects (n=51) were similar in baseline ratings of depressive symptom-severity (HDRS16), but were depressed longer and less likely to be married. Suicidality ratings improved by 36% during 6 weeks of treatment among initially suicidal patients, but other depressive symptoms (HDRS16) improved (13%) only half as much as in nonsuicidal subjects (25%), independent of diagnosis and treatment. Fewer than half as many suicidal subjects showed ≥20% improvement in HDRS16 scores.

Findings, based on diagnostically complex and relatively treatment-resistant subjects, may not generalize.

Being suicidal may limit response to treatment in depressed major affective disorder patients, independent of diagnosis or overall symptomatic severity.

Aberrant activity of the subcallosal cingulate (SCC) is a common theme across pharmacologic treatment efficacy prediction studies. The functioning of the SCC in psychotherapeutic interventions is relatively understudied, as are functional differences among SCC subdivisions. We conducted functional connectivity analyses (rsFC) on resting-state functional magnetic resonance imaging (fMRI) data, collected before and after a course of cognitive behavioral therapy (CBT) in patients with major depressive disorder (MDD), using seeds from three SCC subdivisions.

Resting-state data were collected from unmedicated patients with current MDD (Hamilton Depression Rating Scale-17 > 16) before and after 14-sessions of CBT monotherapy. Treatment outcome was assessed using the Beck Depression Inventory (BDI). Rostral anterior cingulate (rACC), anterior subcallosal cingulate (aSCC), and Brodmann’s area 25 (BA25) masks were used as seeds in connectivity analyses that assessed baseline rsFC and symptom severity, changes in connectivity related to symptom improvement after CBT, and prediction of treatment outcomes using whole-brain baseline connectivity.

Pretreatment BDI negatively correlated with pretreatment rACC ~ dorsolateral prefrontal cortex and aSCC ~ lateral prefrontal cortex rsFC. In a region-of-interest longitudinal analysis, rsFC between these regions increased post-treatment (p < 0.05FDR). In whole-brain analyses, BA25 ~ paracentral lobule and rACC ~ paracentral lobule connectivities decreased post-treatment. Whole-brain baseline rsFC with SCC did not predict clinical improvement.

rsFC features of rACC and aSCC, but not BA25, correlated inversely with baseline depression severity, and increased following CBT. Subdivisions of SCC involved in top-down emotion regulation may be more involved in cognitive interventions, while BA25 may be more informative for interventions targeting bottom-up processing. Results emphasize the importance of subdividing the SCC in connectivity analyses.

Several studies show that attention-deficit/hyperactivity disorder (ADHD) may persist into adulthood, increasing the risk of antisocial behaviour, drug abuse, psychiatric comorbidities, aggressive behaviour, social impairment and suicide risk.

Analyze correlations among ADHD, substances abuse, alcoholism and suicide risk.

The aim of our study is to better understand the clinical features of ADHD during adulthood.

We analyzed the presence of ADHD symptoms, suicide risk and levels of hopelessness, alcoholism and substance abuse in a sample of 50 (40% males) in/outpatients of S. Andrea Hospital in Rome, between February and May 2016. We administered the following scales: Adult-Self Report Scale (ASRS), Columbia Suicide Severity Rating Scale (C-SSRS), Beck Hopelessness Scale (BHS), Michigan Alcoholism Screening Test (MAST), Drug Abuse Screening Test (DAST).

In our sample of 50 adult patients, 20% had ADHD symptoms (10 subjects). We found that those with ADHD showed more frequently death desires (85.7%; χ2 = 1.31; P = 0.25) and higher levels of hopelessness (66.7%; χ2 = 0.83; P = =0.36) if compared to subjects without ADHD symptoms (respectively 63% and 45.8%). In the overall group of ADHD patients, 10% showed severe alcoholism, 20% (χ2 = 1.39; P = 0.49) had a borderline behavior, whereas 40% presented a substance abuse (χ2 = 1.75; P = 0.18).

ADHD may represent a psychiatric disorder with an increased suicide risk. It would be important to screen for suicidality and comorbid symptoms routinely in ADHD in order to improve the treatment of the patients.

The authors have not supplied their declaration of competing interest.

Suicidal behaviour and drug and alcohol dependence represent two different aspects of self-destructive behavior.

We evaluated the relationship between suicidal behavior and substance and alcohol addiction. It was investigated the role of childhood trauma in these self-destructive behaviors and in the development of the two mental constructions of hopelessness and mentalization.

We also assessed how a high level of hopelessness could affect suicidal ideation and how low or absent capacity of mentalization could influence the development of substance and/or alcohol addiction.

This naturalistic, observational study included 50 patients (mean age = 46.54; S.D = 14.57) recruited from the department of psychiatry (n = 18) and the centre for suicide prevention (n = 32) of Sant’Andrea Hospital (Rome). Different questionnaires were administered to each patient from February to May 2016.

There was not a statistically significant relationship between suicidal behavior and addict behavior. Childhood trauma resulted a risk factor for alcohol abuse with a relationship that tended to significance (P = 0.07). Physical and sexual abuses were significantly associated with addiction (respectively P = 0.014; P = 0.033). It was showed a statistically significant interaction between high level of hopelessness and suicidal ideation (P = 0.037). The absence of mentalization was related to the absence of alcohol abuse (P = 0.061). Finally, trauma experienced during childhood was associated with high level of hopelessness (P = 0.005).

Suicidal behavior is influenced indirectly by a childhood traumatic experience that conditioning the level of hopelessness. Childhood trauma affected directly the development of drug abuse and alcoholism. The capacity of mentalization was not related with childhood trauma.

The authors have not supplied their declaration of competing interest.

The 2009 American Recovery and Reinvestment Act (ARRA) increased monthly Supplemental Nutrition Assistance Program (SNAP) benefits and expanded SNAP eligibility, yet limited evidence exists on the potential impact of ARRA on dietary intake among at-risk individuals. We aimed to examine pre-/post-ARRA differences in food insecurity (FI) and dietary intake by SNAP participation status.

Pre/post analysis.

Boston, MA, USA.

Data were from the longitudinal Boston Puerto Rican Health Study (2007–2015). The US Department of Agriculture ten-item adult module assessed FI. A validated FFQ assessed dietary intake. Diet quality was assessed using the Alternate Healthy Eating Index-2010 (AHEI-2010). Self-reported pre-/post-ARRA household SNAP participation responses were categorized as: sustained (n 249), new (n 95) or discontinued (n 58). We estimated differences in odds of FI and in mean nutrient intakes and AHEI-2010 scores post-ARRA.

Compared with pre-ARRA, OR (95 % CI) of FI post-ARRA were lower for all participants (0·69 (0·51, 0·94)), and within sustained (0·63 (0·43, 0·92)) but not within new (0·94 (0·49, 1·80)) or discontinued (0·63 (0·25, 1·56)) participants. Post-ARRA, total carbohydrate intake was higher, and alcohol intake was lower, for sustained and new participants, and dietary fibre was higher for sustained participants, compared with discontinued participants. Scores for AHEI-2010 and its components did not differ post-ARRA, except for lower alcohol intake for sustained v. discontinued participants.

Post-ARRA, FI decreased for sustained participants and some nutrient intakes were healthier for sustained and new participants. Continuing and expanding SNAP benefits and eligibility likely protects against FI and may improve dietary intake.