Suicide prevention: Let’s start at the very beginning

WHO’s 2014 report on suicide makes interesting reading. In the decade to 2012 Australia’s suicide rate dropped 10.6% to 10.6/100,000. Over the same period the UK rate fell by 21% to 6.2, Russia’s fell by 44% to 19.5, and the US rate increased by 24% to 12.1. What are we to make of those patterns? The question is important if we are to pursue a suggested further 25% reduction for Australia over the next 5 years, 50% in 10. Are these goals achievable, and which strategies offer the best chance of success?

That social factors on a national scale play a significant role in suicide rates is beyond dispute. So is the role of psychiatric illness: population attributable risk of 40% for ever having been admitted with a psychiatric disorder. Ten years ago, Goldney proposed a model to reconcile those factors, positing there exists a baseline human suicide ‘rate’ of 5–10, genetically determined, with higher rates attributable to social factors on a national basis (Goldney, 2003). In this era of epigenetics and g × e interactions, such an artificial separation can seem contrived, but is forced on us by the need to allocate resources: should we be focusing on illness, or on populations and the social determinants of health generally? What about personality, context, or predicament?

At a population level the principles of suicide prevention are now well established: public education, gate keeping, means prevention and improved treatment are the cornerstones. Australia is one of several countries that can claim a reduction in suicide paralleling its strategy, although causality is hard to prove.

Some of the most tangible gains in suicide prevention have come from addressing the means of suicide: changes to natural gas in the UK, the fencing of bridges and other significant jumping points, alterations to car exhaust systems, restriction of firearms and access to pesticides. In Australia most of these are already in place so there is little further to be gained.

A programme developed in Nuremberg (Hegerl 2010, cited in WHO) produced a statistically significant reduction in suicide attempts in the intervention region, and 12 fewer people died: that’s good. Whether its take-up in other European centres will produce the same results is less clear: Nuremburg started with an attempt rate almost double the comparison region, and after intervention dropped closer to where the other region remained.

In general, the most impressive results have come from sub-populations whose base rate is unusually high. Work with the Montreal police produced a 79% reduction in completed suicide (30.5 to 6.4/100,000) (Mishara 2011, cited in WHO). The US Air Force achieved a 33% reduction (~16 to ~10) (Knox 2003, cited in WHO). Australia’s ‘Mates in Construction’ intervention shows similar promise: the latest (2012) construction industry suicide rate in Queensland dropping close to that state’s base rate. These targeted programmes are developed within specified populations and involvement can to some extent be mandated. The programmes have status and visibility, and recruit ‘connectors’ (contact personnel) within their own populations: relationship is important.

The better treatment of recognised illness remains a valid focus and a recurring theme in coroner’s findings. In the UK, improvements in service delivery achieved up to a 20% reduction in completed suicide by service users, with a measurable dose–response effect reflecting the scale of implementation. Interventions covered multiple domains: removal of hanging points; improved access by way of 24/7 services and assertive outreach; mandated procedures for post-discharge follow-up, dual diagnosis and non-compliance; information sharing with families and with criminal justice; training and multidisciplinary reviews. Unfortunately the residual rate remains high in that population. Improvements in treatment in private practice are more difficult to track.

All of this is encouraging but stands in contrast to the unchanged prevalence of psychiatric disorder in our population. If, as many argue, major depression is the prime cause of suicide, can we reduce the prevalence of major depression? Our failure to do so to date may be because our attention has been on early intervention at the expense of actual prevention (Jorm, 2014).

Depression, of course, is not a single entity, and those who arrive there come by various pathways. John Mackie coined the acronym ‘inus’ to describe how various combinations of factors can interact: each is an Insufficient but Necessary component of an Unnecessary but Sufficient combination. There are other combinations. Kendler’s (2006) modelling for major depression graphically demonstrates some of those various pathways. He has framed them in developmental terms. In childhood he identifies genetics, parental warmth, sexual abuse and parental loss. In early adolescence, neuroticism, self-esteem, early anxiety, and conduct disorder. In late adolescence he tracks low education, lifetime trauma, low social support, and substance misuse. All of this potentially identifiable before our young people have become depressive ‘cases’.

The WHO report alludes to many of these as ‘Theoretically valid upstream prevention approaches’:

Childhood adversity (e.g. child maltreatment, exposure to domestic violence, parent mental disorder) and other risk factors appearing early in life (e.g. bullying, delinquency) have been linked to later morbidity and mortality, including suicide. Similarly, protective factors (e.g. connectedness) acquired in childhood may reduce later suicide risk. While effective upstream strategies exist, they remain largely unevaluated with regard to their impact on suicide and attempted suicide; however, they are theoretically valid and provide promising directions for future suicide prevention and evaluation.

A decade ago the WHO’s Global Burden of Disease project brought mental illness to public health awareness. Despite that, even in developed countries like our own, funding for mental health services and research still lags woefully behind its proportional importance. Child and adolescent mental health only arrived on the GBD map recently, and then in the most basic forms: autism, ADHD and conduct disorder. But that is the paradox: behaviour problems and unhappiness in toddlers we can actually do something about, but compared to a suicidal teenager or a psychotic adult they don’t seem that important. By the time the problems are visible, it may be too late. Thus Jacka’s recommendations in this Journal about perinatal care, parenting and early school interventions (Jacka et al., 2013). Good perinatal care and home support can improve later attachment. Parenting programmes reduce conduct problems. A growing evidence base for school intervention programmes demonstrates significant reductions in the risk factors that will later cause the illnesses behind suicide, and schools provide a captive audience. Those are the places the money needs to go.

I imagine the 17-year-old I saw recently would, if she died, appear as ‘depression’ on a psychological autopsy, yet she falls short of Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria. There is a family history of bipolar disorder. Parenting was punitive, as was her mother’s before her. She had been abused and neglected at home, then exploited and raped in her peer group. She copes by being good. Her dissociative strategies are so well established she doesn’t recognise her own unhappiness until it bursts through as an impulsive suicide attempt. She eats and sleeps, smiles and studies, and orders a rope on the internet. There is no home where she feels wanted. Her personality development has been profoundly distorted and I have grave doubts as to whether we can help her before she slips away behind that mask. We have already failed to follow up twice because she walked away, as such highly defended self-copers do, and we took her at her smiling face value. To help someone like this we need to be starting much sooner. We need to start at the very beginning.