Mortality following treatment for cannabis use disorders: predictors and causes.

The aim of the study was to determine excess mortality associated with cannabis use disorders. Individuals entering treatment for cannabis use disorders were followed by use of Danish registers and standardized mortality ratios (SMRs) estimated. Predictors of different causes of death were determined. A total of 6445 individuals were included and 142 deaths recorded during 26,584 person-years of follow-up. Mortality was predicted by age, comorbid use of opioids, and lifetime injection drug use. For different causes of death the SMRs were: accidents: 8.2 (95% CI 6.3-10.5), suicide: 5.3 (95% CI 3.3-7.9), homicide/violence: 3.8 (95% CI 1.5-7.9), and natural causes: 2.8 (95% CI 2.0-3.7). Following exclusion of those with secondary use of opioids, cocaine, amphetamine, or injection drug use, SMRs for all causes of death remained significantly elevated except for homicide/violence. The study underlines the need to address mortality risk associated with cannabis use disorders.

Mortality among individuals with cannabis, cocaine, amphetamine, MDMA, and opioid use disorders: a nationwide follow-up study of Danish substance users in treatment.

This is a register-based cohort study of 20,581 individuals in treatment for illicit substance use disorders in Denmark between 1996 and 2006. All in all, 1441 deaths were recorded during 111,445 person-years of follow-up. Standardized mortality ratios (SMRs) associated with different primary substance types were calculated and Cox-regression analyses were performed in order to establish hazard ratios (HR) associated with injection drug use and psychiatric comorbidity. SMRs for primary users of specific substances were: cannabis: 4.9 (95% confidence interval (CI): 4.2-5.8), cocaine: 6.4 (CI: 3.9-10.0), amphetamine: 6.0 (CI: 4.2-8.3), heroin: 9.1 (CI: 8.5-9.8), and other opioids 7.7 (CI: 6.6-8.9). For MDMA ('ecstasy') the crude mortality rate was 1.7/1000 person-years (CI: 0.4-7.0) and the SMR was not significantly elevated. Injection drug use was associated with significantly increased hazard ratios in users of opioids and cocaine/amphetamine. Overall, psychiatric comorbidity was not associated with increased mortality (HR: 1.1 [CI: 0.9-1.2], p=.28), but an association was found specifically among cocaine/amphetamine users (HR: 3.6 [CI: 2.1-6.4], p<.001).

Brain stimulation in posttraumatic stress disorder.

Posttraumatic stress disorder (PTSD) is a complex, heterogeneous disorder that develops following trauma and often includes perceptual, cognitive, affective, physiological, and psychological features. PTSD is characterized by hyperarousal, intrusive thoughts, exaggerated startle response, flashbacks, nightmares, sleep disturbances, emotional numbness, and persistent avoidance of trauma-associated stimuli. The efficacy of available treatments for PTSD may result in part from relief of associated depressive and anxiety-related symptoms in addition to treatment of core symptoms that derive from reexperiencing, numbing, and hyperarousal. Diverse, heterogeneous mechanisms of action and the ability to act broadly or very locally may enable brain stimulation devices to address PTSD core symptoms in more targeted ways. To achieve this goal, specific theoretical bases derived from novel, well-designed research protocols will be necessary. Brain stimulation devices include both long-used and new electrical and magnetic devices. Electroconvulsive therapy (ECT) and Cranial electrotherapy stimulation (CES) have both been in use for decades; transcranial magnetic stimulation (TMS), magnetic seizure therapy (MST), deep brain stimulation (DBS), transcranial Direct Current Stimulation (tDCS), and vagus nerve stimulation (VNS) have been developed recently, over approximately the past twenty years. The efficacy of brain stimulation has been demonstrated as a treatment for psychiatric and neurological disorders such as anxiety (CES), depression (ECT, CES, rTMS, VNS, DBS), obsessive-compulsive disorder (OCD) (DBS), essential tremor, dystonia (DBS), epilepsy (DBS, VNS), Parkinson Disease (DBS), pain (CES), and insomnia (CES). To date, limited data on brain stimulation for PTSD offer only modest guidance. ECT has shown some efficacy in reducing comorbid depression in PTSD patients but has not been demonstrated to improve most core PTSD symptoms. CES and VNS have shown some efficacy in reducing anxiety, findings that may suggest possible utility in relieving PTSD-associated anxiety. Treatment of animal models of PTSD with DBS suggests potential human benefit. Additional research and novel treatment options for PTSD are urgently needed. The potential usefulness of brain stimulation in treating PTSD deserves further exploration.

Short exposure to light treatment improves depression scores in patients with seasonal affective disorder: A brief report.

Light therapy is an effective treatment of seasonal affective disorder (SAD), when administered daily for at least several weeks. We have previously reported a small improvement in mood in SAD patients following exposure to the first hour of treatment. We now reevaluate retrospectively mood changes during shorter exposures comparing depression ratings at baseline, 20, 40, and 60 minutes of light. Participants were 15 depressed patients with SAD, untreated, who were tested during the winter season. The treatment consisted of 10,000 lux of white cool fluorescent light. Depression was measured using the 24-item NIMH scale (24-NIMH). The data were analyzed using ANOVA on ranks and Wilcoxon signed rank tests. Light resulted in significant improvement in mood at every interval when compared with baseline (p< .001). The 40 minute exposure resulted in a greater improvement than the 20 minute exposure (p < .001) but was not different from the 60 minute exposure (p < = .068). We conclude that immediate improvement in mood can be detected after the first session of light with exposures as short as 20 minutes, and that 40 minutes of exposure is not less effective than 60 minutes.

Role of selenium depletion in the etiopathogenesis of depression in patients with alcoholism [corrected].

Chronic heavy alcohol consumption adversely affects both macronutrients and micronutrients. Alcohol use affects selenium status. Considerable evidence suggests that selenium status may modify mental function. The author suggests that the effects of alcohol intake on mood, behavior, and cognition may be partly mediated by biological changes related to selenium deficiency. It has been observed that there is a trend towards the normalization of selenium levels in patients with alcoholism after a relatively short period of abstinence from alcohol. It has also been observed that when depression develops in persons with alcoholism, they are likely to improve fairly rapidly after a relatively short period of abstinence from alcohol without therapy aimed at the depressive symptoms. The author suggests that improvement in depressed patients after a period of abstinence from alcohol might be in part related to the normalization of selenium status. Treatment and prevention of comorbid alcoholism and mood disorders require more attention by research workers, practicing physicians, and the general public. Future studies of the etiology and pathogenesis of mood disorders in patients with alcoholism are merited.

Role of selenium depletion in the effects of dialysis on mood and behavior.

Depression and behavioral problems are common in patients undergoing dialysis. Researchers have reported that serum selenium concentrations are generally lower in dialysis patients than in healthy controls. Considerable evidence suggests that selenium deprivation leads to depressed mood, and high dietary or supplementary selenium seems to improve mood. Low plasma selenium concentrations in the elderly are significantly associated with senility and cognitive decline. The author suggests that dialysis-related selenium loss may play a role in biological mechanisms of psychiatric disorders in dialysis patients.