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Alcohol use disorder (AUD) is common and associated with increased risk of suicide.
To examine healthcare utilisation prior to suicide in persons with AUD in a large population-based cohort, which may reveal opportunities for prevention.
A national cohort study was conducted of 6 947 191 adults in Sweden in 2002, including 256 647 (3.7%) with AUD, with follow-up for suicide through 2015. A nested case–control design examined healthcare utilisation among people with AUD who died by suicide and 10:1 age- and gender-matched controls.
In 86.7 million person-years of follow-up, 15 662 (0.2%) persons died by suicide, including 2601 (1.0%) with AUD. Unadjusted and adjusted relative risks for suicide associated with AUD were 8.15 (95% CI 7.86–8.46) and 2.22 (95% CI 2.11–2.34). Of the people with AUD who died by suicide, 39.7% and 75.6% had a healthcare encounter <2 weeks or <3 months before the index date respectively, compared with 6.3% and 25.4% of controls (adjusted prevalence ratio (PR) and difference (PD), <2 weeks: PR = 3.86, 95% CI 3.50–4.25, PD = 26.4, 95% CI 24.2–28.6; <3 months: PR = 2.03, 95% CI 1.94–2.12, PD = 34.9, 95% CI 32.6–37.1). AUD accounted for more healthcare encounters within 2 weeks of suicide among men than women (P = 0.01). Of last encounters, 48.1% were in primary care and 28.9% were in specialty out-patient clinics, mostly for non-psychiatric diagnoses.
Suicide among persons with AUD is often shortly preceded by healthcare encounters in primary care or specialty out-patient clinics. Encounters in these settings are important opportunities to identify active suicidality and intervene accordingly in patients with AUD.
Although the rise of operationalized diagnostic criteria and the creation of DSM-III were influenced in the USA by a neo-Kraepelinian ‘revival’ of interest in psychiatric nosology, Kraepelin was only a distal influence on the specific diagnostic criteria proposed. The historical origins of the DSM-III criteria for mania and major depression (MD) are traceable back to the 1950s and contain no direct link to Kraepelin's writings. George Dreyfus, a student and assistant to Kraepelin, authored in 1907 a monograph on Involutional Melancholia which reviewed cases seen by Kraepelin in Heidelberg. In this monograph, Dreyfus presents the ‘characteristic’ symptoms for mania and depression ‘as described by Kraepelin.’ This historical finding provides the unprecedented opportunity to examine the resemblance between the criteria proposed for mania and depression in DSM-III, inspired by Kraepelin's nosologic vision, and those specifically suggested by Kraepelin 73 years earlier. Kraepelin's symptoms and signs for mania paralleled seven of the eight DSM-III criteria (except the decreased need for sleep), with two not included in DSM-III (increased mental activity and short bursts of sadness). Kraepelin's signs and symptoms paralleled six of the nine DSM-III criteria for MD, lacking suicidal ideation and changes in appetite/weight and sleep but including obsessions, reduced expressive movements, and decreased mood responsiveness. Although Kraepelin's overall approach to mania and depression emphasized their close inter-relationship in the cyclic course of manic-depressive illness, it is noteworthy Kraepelin's ‘characteristic’ symptoms for mania and depression as described by Dreyfus, bear substantial but incomplete resemblance to the criteria proposed in DSM-III.
Although alcohol use disorder (AUD) runs strongly within families, studies examining the impact of rearing environment, unconfounded by genetic effects, are rare and, to date, contradictory. We here seek to conduct such a study using an adoptive co-sib control design.
Defining high-risk as having ⩾1 biological parent with an externalizing syndrome (AUD, drug abuse or crime), we identified 1316 high-risk full-sibships and 4623 high-risk half-sibships containing at least one member who was home-reared and one who was adopted-away. Adoptive families are carefully screened in Sweden to provide high-quality rearing environment for adoptees. AUD was assessed from national medical, criminal and pharmacy registries.
Controlling for sex, parental age at birth, and, for half-siblings, affection status of the non-shared parent, hazard ratios (±95% CI) for AUD in the matched adopted v. home-reared full- and half-siblings were, respectively, 0.76 (0.65–0.89) and 0.77 (0.70–0.84). The protective effect of adoption on AUD risk was stronger in the full- and half-sibling pairs with very high familial liability (two high-risk parents) and significantly weaker when the adoptive family was broken by death or divorce or contained a high-risk adoptive parent.
In both full- and half-sibling pairs, we found evidence that the rearing environment substantially impacts on the risk for AUD. High-quality rearing environments can meaningfully reduce the risk for AUD, especially in those at high familial risk.
As Bilder makes clear, the birth of RDoC was closely inter-related with growing frustration at the slow pace of etiologic research on the DSM-defined psychiatric disorders. Part of the argument underlying the effort was that these syndromally defined diagnostic categories were at the “wrong level” to propel the needed progress. This should come as no surprise as the charge of the DSM is to develop clinically useful and reliable categories. Given the probable heterogeneity of psychiatric disorders and the massive many-to-many relationships likely between underlying mind/brain dysfunctions and clinical manifestations of psychiatric symptoms and signs, the expectation of a simple single road from DSM categories to etiology is unrealistic. RDoC was based on the assumption that the created matrix, especially the psychological constructs making up the rows, would be a more fruitful focus for etiological research than the DSM categories.
Woodward, who has for several decades been a leader in the philosophical analysis of causal processes, takes us on a detailed and somewhat demanding tour – a philosophical analysis of “levels talk.” While several other essays in this volume explore the implications of multilevel approaches to issues psychiatric, in this essay Woodward leads us into the philosophical/conceptual nitty-gritty of multilevel processes, with a focus on the problem of top-down causation.
Stephen Heckers, a psychiatrist and neuroscientist, who began pursuing a philosophy degree before changing his mind and attending medical school, provides a succinct and multifaceted introduction to the problem of levels and the attractions and problems of reduction in psychiatric research and practice. On first reading, this essay is deceptively simple. It repays a second visit.
During the development of psychiatric nosology during the nineteenth century, faculty psychological systems, often proposed by philosophers, played a substantial role in the development of psychiatric diagnostic systems. The most important of those faculties proposed were cognition and emotion. Because patients often displayed dysfunction in multiple faculties, alienists had to understand how these faculties interrelated. To address this question, nineteenth-century psychiatric diagnosticians postulated causal relationships based on folk criteria of understandability (although longitudinal observations were also utilized). This history puts efforts to apply hard reductionist models to the resulting psychiatric diagnostic categories in a conundrum. The naïve inductivist view of the origins of our psychiatric diagnostic categories – that they arose from raw observations by great skilled clinicians of the past – is untenable. Rather, the road from clinical observations to diagnostic categories passed through both theories of mental functioning (aka faculties) and hypotheses of mental causation between different disordered faculties.