Mood disorders frequently co-occur with medical diseases that involve inflammatory pathophysiologic mechanisms. Immune responses can affect the brain and might increase the risk of mood disorders, but longitudinal studies of comorbidity are lacking.
To estimate the effect of autoimmune diseases and infections on the risk of developing mood disorders.
Nationwide, population-based, prospective cohort study with 78 million person-years of follow-up. Data were analyzed with survival analysis techniques and adjusted for calendar year, age, and sex.
Individual data drawn from Danish longitudinal registers.
A total of 3.56 million people born between 1945 and 1996 were followed up from January 1, 1977, through December 31, 2010, with 91,?637 people having hospital contacts for mood disorders.
The risk of a first lifetime diagnosis of mood disorder assigned by a psychiatrist in a hospital, outpatient clinic, or emergency department setting. Incidence rate ratios (IRRs) and accompanying 95% CIs are used as measures of relative risk.
A prior hospital contact because of autoimmune disease increased the risk of a subsequent mood disorder diagnosis by 45% (IRR, 1.45; 95% CI, 1.39-1.52). Any history of hospitalization for infection increased the risk of later mood disorders by 62% (IRR, 1.62; 95% CI, 1.60-1.64). The 2 risk factors interacted in synergy and increased the risk of subsequent mood disorders even further (IRR, 2.35; 95% CI, 2.25-2.46). The number of infections and autoimmune diseases increased the risk of mood disorders in a dose-response relationship. Approximately one-third (32%) of the participants diagnosed as having a mood disorder had a previous hospital contact because of an infection, whereas 5% had a previous hospital contact because of an autoimmune disease.
Autoimmune diseases and infections are risk factors for subsequent mood disorder diagnosis. These associations seem compatible with an immunologic hypothesis for the development of mood disorders in subgroups of patients.
Comment In: Evid Based Ment Health. 2014 Feb;17(1):2024327367
From the aDepartment of Political Science, University of Copenhagen, Copenhagen, Denmark; bDepartment of Political Science, Stanford University, Stanford, CA; cDepartment of Political Science, Aarhus University, Aarhus, Denmark; dPsychiatric Center Copenhagen, Copenhagen University Hospital, Copenhagen, Denmark; eDepartment of Clinical Medicine, Aarhus University, Aarhus, Denmark; and fPsychosis Research Unit, Aarhus University Hospital, Risskov, Denmark.
Daylight savings time transitions affect approximately 1.6 billion people worldwide. Prior studies have documented associations between daylight savings time transitions and adverse health outcomes, but it remains unknown whether they also cause an increase in the incidence rate of depressive episodes. This seems likely because daylight savings time transitions affect circadian rhythms, which are implicated in the etiology of depressive disorder. Therefore, we investigated the effects of daylight savings time transitions on the incidence rate of unipolar depressive episodes.
Using time series intervention analysis of nationwide data from the Danish Psychiatric Central Research Register from 1995 to 2012, we compared the observed trend in the incidence rate of hospital contacts for unipolar depressive episodes after the transitions to and from summer time to the predicted trend in the incidence rate.
The analyses were based on 185,419 hospital contacts for unipolar depression and showed that the transition from summer time to standard time were associated with an 11% increase (95% CI = 7%, 15%) in the incidence rate of unipolar depressive episodes that dissipated over approximately 10 weeks. The transition from standard time to summer time was not associated with a parallel change in the incidence rate of unipolar depressive episodes.
This study shows that the transition from summer time to standard time was associated with an increase in the incidence rate of unipolar depressive episodes. Distress associated with the sudden advancement of sunset, marking the coming of a long period of short days, may explain this finding. See video abstract at, http://links.lww.com/EDE/B179.
CommentIn: BMJ. 2016 Oct 31;355:i5857 PMID 27803014
Both preclinical studies and clinical trials have indicated that the combination of a selective serotonin reuptake inhibitor (SSRI) and a statin may have superior antidepressant effects compared with SSRI treatment alone. The authors sought to assess whether this beneficial effect can be generalized to a more heterogeneous population of SSRI users.
In a nationwide cohort study that included all incident SSRI users in Denmark between 1997 and 2012, the authors compared people who had periods of concomitant use of SSRIs and statins with people who had periods of SSRI treatment alone. Outcomes included the rates of psychiatric hospital contacts (any cause), psychiatric hospital contacts due to depression, suicidal behavior, and all-cause mortality. Using Cox regression and competing risk analysis, the authors calculated crude and adjusted hazard ratios for these outcomes.
The authors identified 872,216 incident SSRI users, of whom 113,108 (13.0%) used a statin concomitantly. Compared with SSRI treatment alone, the combined use of an SSRI and a statin was associated with a significantly lower risk for both psychiatric hospital contacts (adjusted hazard ratio=0.75 (95% CI=0.69, 0.82) and psychiatric hospital contacts due to depression (adjusted hazard ratio=0.64, 95% CI=0.55, 0.75). Compared with SSRI treatment alone, the concomitant use of SSRIs and statins was not associated with significant increases in all-cause mortality (adjusted hazard ratio=1.04, 95% CI=0.96, 1.12) or suicidal behavior (adjusted hazard ratio=0.85, 95% CI=0.61, 1.18).
In a large naturalistic cohort, concomitant treatment with SSRIs and statins resulted in robust advantages compared with SSRIs alone.
From the aDepartment of Political Science, University of Copenhagen, Copenhagen, Denmark; bDepartment of Political Science, Stanford University, Stanford, CA; cDepartment of Clinical Medicine, Aarhus University, Aarhus, Denmark; and dPsychosis Research Unit, Aarhus University Hospital, Risskov, Denmark.
On 22 July 2011, Anders Breivik killed 77 adults and children in Norway. Having recently documented increases in the incidence of trauma- and stressor-related disorders in Denmark after the 9/11 attacks, we hypothesized that the Breivik attacks-due to their geographic proximity-would be followed by even larger increases in Denmark.
Using population-based data from the Danish Psychiatric Central Research Register (1995-2012), we conducted an intervention analysis of the change in the incidence of trauma- and stressor-related disorders after the Breivik attacks.
The incidence rate increased by 16% over the following 1½ years after the Breivik attacks, corresponding to 2736 additional cases. In comparison, 9/11 was followed by a 4% increase. We also present evidence of a subsequent surge in incidence stimulated by media attention.
This study bolsters previous findings on extra-national consequences of terrorism and indicates that geographic proximity and media coverage may exacerbate effects.
Unit for Psychiatric Research, Aalborg Psychiatric Hospital, Aalborg University Hospital, Aalborg, Denmark; Psychiatric research Unit, Psychiatric Center North Zealand, University of Copenhagen, Hillerød, Denmark. Electronic address: email@example.com.
Severe unipolar depression is associated with increased risk of suicide, but it remains unknown whether the same risk factors are present in the non-psychotic (non-PD) and psychotic (PD) subtypes respectively. Therefore, this study aimed to identify risk factors for suicide in non-PD and PD separately, and to investigate if the presence of psychotic symptoms is an independent risk factor for suicide in severe depression.
This register-based, nationwide, historical prospective cohort study used logistic regression analyses to ascertain risk factors for suicide among all adults diagnosed with severe depression at Danish psychiatric hospitals between January 1, 1994 and December 31, 2010. The risk for suicide was expressed as adjusted odds ratios (AOR).
A total of 34,671 individuals with severe depression (non-PD: n=26,106 and PD: n=12,101) were included in the study. Of these, 755 completed suicide during follow up. PD was not found to be an independent risk factor for suicide in severe depression (AOR=0.97 [0.83-1.15]). Older age (non-PD AOR=1.05 [per year], PD AOR=1.04 [per year]), male sex (non-PD AOR=1.89, PD AOR=1.98), and a previous incident of self-harm (non-PD AOR=5.02, PD AOR=5.17) were significant risk factors for both groups.
As the study population was comprised only of patients with contact to psychiatric hospitals, the results cannot be extrapolated to the primary care setting.
The following risk factors for non-PD and PD were identified: older age, male gender and previous incidents of self-harm. In suicide prevention efforts, equal attention should be paid to non-PD and PD patients.