Vitamin D deficiency at birth linked to schizophrenia

Vitamin D deficiency at birth is associated with a significantly increased risk of schizophrenia, according to a new study, confirming a potential way to prevent the disease in the future.

Researcher Professor McGrath, from UQ’s Queensland Brain Institute, told doctorportal: “it’s very unusual that we find risk factors that are so readily treated by safe, cheap and publically accessible interventions.”

“Obviously it’s not a done deal yet. It’s a correlational study and randomised controlled trials need to be done. But we feel we need to keep chasing down this hypothesis.”

The case-controlled study, published in Scientific Reports, included 2602 participants. They were randomly selected from all infants born in Denmark between 1981 and 2000, who received a diagnosis of schizophrenia.

Controls, drawn from the same birth cohort, were individually matched on sex, date of birth and were alive and free of schizophrenia at the time of onset of the matched case. The concentration of 25 hydroxyvitamin D (25OHD) was assessed from neonatal dried blood samples, which have been collected and systematically stored since 1981.

The researchers found that those with 25OHD below 20.4 nmol/L (consistent with standard definitions of vitamin D deficiency) had a 44% increased risk of schizophrenia compared to those in the reference category.

Unlocking an enduring mystery around schizophrenia

Professor McGrath said that researchers have known for a long time – since around 1920 – that people born in winter have a slightly increased risk of developing schizophrenia than those born in other seasons.

“This has always been a bit of mystery. People thought it might have been due to infection and other factors, but we proposed it could be vitamin D, which is mostly known to be linked to bone health.”

Professor McGrath said that most of the work done at the Queensland Brain Institute has demonstrated that if vitamin D is removed from animal models, brain development will be altered.

“That was the hypothesis, so we needed to find a sample. Fortunately, our colleagues in Denmark have access to a biobank, and in 2010 we did a study with this and showed that vitamin D deficiency at birth was linked to an increased risk of schizophrenia.”

“In this new paper, we’ve looked at the research question in a much bigger sample of 2602 and we’ve found exactly the same thing – that babies who have vitamin D deficiency at birth have a 44% increased risk of schizophrenia.

Biological mechanism behind the association is complex and still being probed

“Vitamin D is related to steroid hormones, and we know that if you have steroid hormones you reduce the rate of cell division and you drive cell differentiation.”

New emerging theories relate to the common genetic variants in calcium pathways, which have been shown to increase schizophrenia risk.

“It turns out that vitamin D in many areas of the body, including the brain, alters these exact same channels and we’re exploring that question currently”, Professor McGrath said.

“The problem with vitamin D is that it is one of those hormones which does lots of things to lots of different tissues, so we’ve got a very big sandpit to play in and it will be a challenge to sort out what the mechanisms are.”

Research to tease out a link between vitamin D and other brain disorders

Professor McGrath studies an active area of research: “We have funding from a Danish research agency to measure vitamin D in a very large sample of 80,000 babies and we’ve started that now in Copenhagen, and it will be about two years before those results are ready.”

“We’re looking at whether low vitamin D impacts on other brain disorders. We’ve done some work in the Netherlands a couple of years ago where we measured vitamin D in maternal sera that was taken at 20 weeks of gestation.”

This large study showed that for mothers who had low vitamin D during mid-gestation, their offspring had an increased risk of autism and related symptoms at age 6.

“So we’re wondering whether vitamin D deficiency is just bad for brain development,” Professor McGrath said.

“Most kids that are exposed to vitamin D deficiency are fine – they might have weak bones but most don’t get mental illness. However, we have not been able to reject the hypothesis yet based on epidemiology.”

Better off not knowing? The self-fulfilling risks of genetic testing

Simply knowing you’re at increased genetic risk for an illness can precipitate symptoms of the disease, new research shows.

Researchers from Stanford University’s Department of Psychology ran DNA tests on around 100 adults for two genes associated with obesity – one related to exercise capacity (CREB1), and the other to appetite (FTO rs9939609).

Instead of giving the individuals their actual DNA test results, the researchers randomly told participants they had either “high-risk” or “protective” genotypes.*

In the first experiment, 116 participants were asked to run a treadmill test before and after receiving personalised genetic information on their aerobic exercise capacity.

After being told they had a “high risk” genotype, people exhibited worse cardiorespiratory fitness –poorer metabolic gas exchange (CO2:02) and lower maximum ventilator flow rate compared to baseline, the study found. They also ran a shorter distance before giving up, and also reported feeling more exerted and hotter.

By contrast, individuals who were told they had the protective genotype did not exhibit any significant changes in their treadmill performance compared with baseline.

In the second experiment, 107 participants were given a meal before and after receiving personalised results on the gene linked with appetite.

Those told they had a protective genotype experienced greater satiety at the second meal – measured by self-reported feelings of “fullness” as well as by post-consumption gut peptide physiology (GLP-1 response).

By contrast, participants assigned the “high-risk” genotype experienced no significant changes in post-consumption feelings of fullness or GLP-1 response compared with baseline.

Across both experiments, the size of the effects due to “perceived genetic risk” were sometimes greater than effect sizes associated with actual genetic risk.

A potent mindset

Writing in the journal Nature Human Behaviour this month, the authors warned: “If simply conveying genetic risk information can alter actual risk, clinicians and ethicists should wrestle with appropriate thresholds for when revealing genetic risks is warranted.”

“Receiving genetic risk information has the potential to instil a potent mindset,” they wrote. “Many studies show that providing people with a genetic causal explanation reduces perceived control compared with providing people with an environmental or lifestyle causal account for a range of conditions and situations, including mental illness, maths performance, and obesity.”

The study comes amid an explosion in genetic testing, with genetic risk estimates now available for over 10,000 conditions, according to the authors.

Although the aim of genetic testing may be to motivate patients toward risk-reducing behaviours, its efficacy is dubious. A recent meta-analysis of 18 studies found communicating the genetic risk of disease had no effect on recipients’ motivation to change behavior, or actual engagement in risk-reducing behavior.

Lifestyle and personality

Dr Sarah Edelman (PhD), a Sydney-based clinical psychologist and author of the book Change Your Thinking, said patients who underwent genetic testing needed to be informed that health outcomes were influenced by both genes and lifestyle.

“Whilst we can’t control our genes, we do have control over lifestyle choices,” she said. “When providing test results, genetic counsellors need to focus on the individual’s potential to influence health outcomes and to frame it in terms of how they can make a difference. For example, saying things like: ‘when people do regular exercise and follow [the prescribed] eating guidelines, they reduce their risk by 30%.’”

Personality also plays a role in how people responded to knowing their personal genetic risk, she said.

“For some people, knowing their genetic risk will be a motivator; for others, it will have the opposite effect. For people who don’t believe they can make a difference to the things that happen to them (low self-efficacy), discovering that they have a high genetic risk for a particular condition may reinforce feelings of hopelessness, and may be unhelpful.”

*The researchers noted ethical challenges in their study design – notably, that some participants were falsely informed of their genotype. It was for this reason that the researchers chose to focus on the effects of genetic risk information for obesity, rather than a more emotionally charged disease such as Alzheimer’s or cancer. They also limited the time under which participants would hold a potentially false belief about their genetic risk to around 1 hour, while under clinical supervision.

New hope for COPD patients with anxiety: study

The link between anxiety and chronic obstructive pulmonary disease (COPD) has long been a treatment challenge.

Now a well-designed trial has found cognitive behavioural therapy (CBT) reduces anxiety and keeps COPD patients out of hospital.

UK researchers randomised 279 patients with COPD of varying levels of severity and concomitant anxiety to either CBT plus self-help leaflets or self-help leaflets alone.

The intervention was delivered one-to-one by respiratory nurses who had completed at least three days of training in CBT, and included components such as breathing control, relaxation, distraction to avoid triggers for panic and positive self-talk. Patients received up to six 30-minute CBT sessions, depending on their need.

In both the treatment and control groups, patients experienced improvements in anxiety at three months (as assessed by the Hospital Anxiety and Depression Anxiety Subscale). However, the change in the CBT group was superior by a clinically important difference (mean difference 1.52, 95% CI 0.49-2.54, p=0.003).

CBT was associated with fewer emergency department attendances and hospital admissions and more Quality Adjusted Life Years. It was also found to be more cost-effective than self-help leaflets alone, with the advantages sustained at 12 months.

Writing in the European Respiratory Society’s journal ERJ Open Research, the authors concluded CBT should be incorporated into routine clinical care pathways for patients with COPD.

“Training respiratory staff can lead to better recognition and treatment of breathlessness and anxiety symptoms, in patients who otherwise may not have engaged with mental health services,” they wrote.

“Begging for an intervention”

Professor Christine Jenkins, head of the Respiratory Group at the George Institute for Global Health, welcomed the study, saying it was “a well-designed trial showing good outcomes in an area begging for an intervention”.

“We are generally not good at managing anxiety in COPD, even though we know there is a strong feedback loop between anxiety and respiratory symptoms,” she said. “When a patient becomes anxious their breathing rate goes up and they can experience dynamic hyperinflation. Beta-agonists also ramp up anxiety.”

Professor Jenkins said she had seen many COPD patients for whom anxiety had played a major role in their presentation.

“I can recall patients who have been extremely breathless, but who within an hour of getting into the ED and being in the reassuring presence of health professionals, have completely calmed down such that they are very stable,” she said.

Previous studies of pharmacotherapy or cognitive behavioural therapy to treat anxiety in COPD patients had been small or inconclusive, Professor Jenkins said.

“It’s really nice to see this adequately powered randomised controlled trial showing you can train nurses to deliver CBT and it leads to patients gaining better control over their breathing so they have fewer hospital visits,” she said.

“Using CBT in this way is entirely feasible in Australia, whether it were to be delivered by respiratory nurses or clinical psychologists involved in pulmonary rehab programs.”

Removing barriers to CBT

The researchers screened 1518 COPD outpatients and found 59% had a HADS-Anxiety Subscale of eight or more, making them eligible for the study.

However, around one quarter of eligible patients (26%) declined to take part. The authors said while this was not unusual in a clinical trial setting, it was unknown whether a similar refusal rate would occur outside of trial conditions.

“Screening for comorbid anxiety symptoms in the clinic and having a nurse skilled in both respiratory and CBT management may remove stigma or other barriers to CBT, improve engagement and allow more holistic care,” they wrote.

The study found no correlation between baseline anxiety score and severity of lung function. Patients with major psychiatric problems or receiving current psychological treatment were excluded from the trial.

Bipolar Australians needed for study

Bipolar Australians are being urged to volunteer for the world’s largest study on the chronic disorder.

Researchers have called on 5000 Australians who have undergone treatment for the mental illness to help crack its genetic code in a bid to revolutionise treatments and find a cure.

The national call-out, announced on Tuesday, has been backed by federal Health Minister Greg Hunt – whose mother lived with bipolar disorder – and mental health advocates like former Wallaby Enrique “Topo” Rodriguez.

The Australian Genetics of Bipolar Disorder Study hopes to identify the genes that predispose people to bipolar disorder and how this influences their response to medications.

Participants will be asked to submit a saliva sample for DNA analysis and answer an online questionnaire.

Co-investigator Professor Nick Martin says researchers hope the results will mean more effective, personalised drugs and treatments.

“That’s going to save a lot of patients suffering and save a lot of government funding for medications that are subsidised,” he told AAP.

Unlike depression, which can sometimes be treated without drugs, medication underpins the treatment for nearly everyone with bipolar disorder, alongside other lifestyle interventions, he said.

It is unknown exactly what causes the condition, which affects about one-in-50 Australians but genetics account for 70 per cent of the risk, researchers say.

Those living with the illness are 15 times more likely to commit suicide than the general population and account for 25 per cent of all suicides.

Sydneysider Alex Pettigrew says he struggled with the disorder throughout high school until a diagnosis and correct medication helped him manage his life.

The 22-year-old music composer spent years battling depressive and manic periods and inflicted harm on himself, especially when bullied at school.

Mr Pettigrew, who says he has never taken drugs and doesn’t drink alcohol, felt “high” during his manic highs and would “pump out the music” on his piano.

“I can’t remember much, the medication I was taking made me forget a lot of things … I do remember there were some really bad times,” he told AAP.

Now, the combination of a diagnosis and correct medication has meant he can live a normal life, pursuing his music career ambitions while working at a child care centre in Sydney.

“I do take time off when I’m not well, there are very few times of the year where I will have some psychotic symptoms,” he said.

“I have an action plan and I know what I need to do to get myself well again.”

He hoped speaking out would encourage others to join the study but more importantly give other young people with bipolar disorder some hope.

“Men hold things in for such a long time, it can do a lot of damage,” he said.

“It took me so long to finally open up and tell someone what was going on.”

People can volunteer to take part in the study at www.geneticsofbipolar.org.au.

LifeLine 13 11 14

Beyond Blue 1300 22 4636

Let’s be clear eyed while moving forward on private health insurance

BY ASSOCIATE PROFESSOR JULIAN RAIT, CHAIR, COUNCIL OF PRIVATE SPECIALIST PRACTICE

On October 11, Health Minister Greg Hunt announced the final rules that support the new private health insurance clinical categories and the Gold, Silver, Bronze and Basic classification system.

CPSP and the AMA have called on these reforms to deliver simplified, better value private health insurance products for consumers. A system that offers more comprehensive coverage, with clear definitions, and less caveats and carve outs. Will the new system deliver total clarity and transparency? Not quite, but it is going to be a lot simpler for consumers than trying to navigate through the current 70,000 policy offerings.

The AMA has always supported, two key aspects of these reforms:

Clarity about what medical conditions are covered in each tier of benefits; and
The use of standard clinical categories across all private health policies.

The new classification system categorises existing policies into easier to understand tiers. These tiers, in combination with new Private Health Information Statement (which includes mandatory information about what each policy covers), should make it easier for people to compare policies, to shop around and actually see what they are covered for.

This should enable consumers to know that when they book in for a procedure they are covered now and not have to wait an additional 12 months or try the public system.

The tiers outline minimum requirements, but they still allow insurers to add additional cover. The legislation clarifies that insurers can move people onto new products, closing old products, but introduces new protections about warning and information for consumers. Additionally, the Minister is on the record stating that “importantly consumers will not be forced to change their policy cover if they are happy with it”.

There are also some more hidden benefits that will come in with the new system.

That the system provides full mandatory cover for the medical conditions in each tier; partial cover is not permitted (except in Basic cover and for Psychiatry, Rehabilitation, and Palliative Care – except in Gold cover where there are no exclusions allowed at all);
The inclusion of gynaecology, breast surgery, cancer treatment, and breast reconstruction in bronze tier products;
That a clinical category covers the entire episode of hospital care for the investigation or treatment;
That an episode of hospital treatment covers the miscellaneous services allied to the primary service; and
Patients with limited cover for psychiatric care can upgrade their cover (once) to access higher benefits for in-hospital treatment without serving a waiting period.

While these look obvious, they haven’t always been included in policies. From next year they will be.

The Minister has called for an April 1, 2019 commencement to coincide with the annual announcement of new premiums. However, as with most major changes, not all groups can adapt as quickly as others. So, while the reforms start next year, insurers have a further 12 months to ensure that each of their products is compliant and to move people onto new products if required. This is not ideal, but the transition for the smaller insurers is likely to be very resource intensive. The Minister has stated that his expectation is that the great majority of policies will be ready to go by April 1 next year. He has also stated that these reforms will have an overall neutral to -0.3 per cent impact on premiums compared with current policy settings.

But we also need to be clear eyed here. This will not solve the wider issue of how to bridge the ongoing premium increases in the 4-5 per cent range, and wages growth at 2 per cent range. That fundamental paradox to a long-term, sustainable private health insurance system remains. These reforms will not address the concerns around private health insurer behavior, nor will they address the variation in rebates. These reforms are about making life a little easier for our patients, and our practices. But the AMA will need the support of all our members going forward – for clearly, the bigger problem is yet to be addressed.

One in four Australians are lonely: research

The most comprehensive report on loneliness in Australia has revealed that a quarter of adults are lonely for three or more days of the week, and this has significant implications for their mental and physical health.

The Australian Loneliness Report, released by the Australian Psychological Society and Swinburne University, also found that one in two (50.5 per cent) Australians feels lonely for at least one day in a week, while more than one-fifth of people rarely or never feel they have someone to talk to or turn to for help.

These results come from an online survey completed by 1,678 people from across Australia between 29 May and 1 October 2018. The survey continues to be run by Swinburne University to track loneliness levels over time.

As part of the research. loneliness was measured using the UCLA Loneliness Scale, a comprehensive gold standard measure of loneliness, with a range from 20-80 with higher scores indicating a higher level of loneliness.

Dr Michelle Lim, senior lecturer and clinical psychologist from Swinburne University of Technology told doctorportal that “loneliness matters as it affects our health and the social fabric of our community – there may be evidence that it affects workplace productivity.”

Lonely Australians have significantly worse mental and physical health.

The report found that lonely Australians are 15.2% more likely to be depressed and 13.1% more likely to be anxious about social interactions than those who are not lonely.

Higher levels of loneliness are also associated with less social interaction, poorer psychological well-being and poorer quality of life.

Previous research has established that loneliness increases the likelihood of an earlier death by 26%. High levels of loneliness are associated with poorer overall physical health, increased number of headaches, poor sleep and worse experience of physical pain.

Loneliness did not discriminate significantly by age. The oldest Australians (over 65 years) were the least lonely, while there were no differences in loneliness levels between other age groups. Younger adults reported significantly more social interaction anxiety than older adults.

What causes loneliness and how can we address it?

Dr Lim said that while the specific causes of loneliness are unknown at present, there are correlates of loneliness that can be measured, such as marital status or living alone, which indicates these may influence loneliness.

The report found that Australians who are married are the least lonely compared to those who are single, separated or divorced. Australians in a de facto relationship are also less lonely than those who are not.

Dr Lim said that at present, service providers encountering loneliness do not have any guidance or training to assist with it, and there continues to be a lack of awareness of the consequences of loneliness.

“Educating and normalising loneliness as a normal human condition is the first step.”

Dr Lim said that in particular, “we need guidelines, for example for first responders on how to deal with lonely people who present at health services”. These guidelines must outline where a lonely person can go for support and highlight the kind of resources that will be made available to that person.

She said that strategies also needed to be developed and implemented to encourage people experiencing loneliness to make more meaningful connections.

[Perspectives] Voice-hearing in 19th-century psychiatry

The roots of many current psychiatric concepts can be found in the 19th century, including the view that auditory verbal hallucinations (AVHs) are phenomenologically different from other kinds of “false” beliefs and experiences. This way of understanding voice-hearing only gradually emerged in the late 19th century. During the early decades of psychiatry, doctors did not always differentiate between a patient hearing an external voice or feeling as if they were being communicated to or commanded by an imagined entity.

Youngest kids in class more likely to be diagnosed with ADHD

New research has shown that the youngest child in a classroom is more likely to be diagnosed with ADHD, throwing into question the value of the ADHD label.

Dr Martin Whitely, research fellow at the John Curtin Institute of Public Policy based at Curtin University, told doctorportal that “I personally think the label of ADHD is not at all useful.”

“It masks a whole host of factors. Late birthdate isn’t the only thing that characterises ADHD – it’s kids that are sleep deprived, kids who have suffered trauma, kids whose parents are going through a messy divorce, kids who are being bullied, kids who have been sexually abused.”

“There’s research showing that all of these other factors are associated with ADHD diagnosis.”

“What we can do is stop labelling kids and start looking at their individual circumstances. And even if you don’t accept that, we have to give kids the time they need to mature.”

Late birthdate effect just as strong in low and high prescribing countries

Dr Whitely co-authored the systematic review, published in the Journal of Child Psychology and Psychiatry, which looked at a total of 19 studies in 13 countries, covering over 15.4 million children.

A total of 17 of the 19 studies found that the youngest children in a school year were considerably more likely to be diagnosed and/or medicated for ADHD than their older classmates. Two Danish studies found either a weak or no late birth date effect.

Dr Whitely said that what was especially interesting was that “this effect was just as strong in a high prescribing country like the US, Canada or Iceland, or a relatively low prescribing country like Denmark, Sweden or Taiwan, or to a lesser extent Australia which is on the lower to middle end.”

A lack of a strong effect in Denmark may be accounted for by the common practice of academic ‘redshirting’, where children judged by parents as immature have a delayed school start. Redshirting may prevent and/or disguise late birthdate effects and further research is warranted

Dr Whitely said that the findings of the study are significant because previously, it had been argued that the birthdate effect was evidence of high prescribing countries like the US.

“This actually brings into question: is there a safe level of prescribing that eliminates misdiagnosis? Based on this evidence, there isn’t.”

“We can’t have confidence that even when prescribing rates are low, there isn’t misdiagnosis”, he said.

Teachers can mistake immaturity for ADHD in the classroom

Dr Whitely explained that a potential reason for the late birthdate effect stems from the fact that parent perception of these children differs considerably from how teachers see them.

“Parents don’t rank them against other kids in the class, whereas teachers do, so the teachers are ranking the youngest kids in the class as having behavioural problems, when this is actually just a perfectly normal function of their age-related immaturity.”

He said there is evidence to indicate that while teachers do not diagnose ADHD, they are often the first person to suggest a diagnosis.

“Teachers start off the diagnostic process by talking to parents and even when they don’t do that, they provide information via a behavioural checklist and report on the kid’s behaviour.”

“If they’re ranking a child in the class who is aged 5 against other kids in the class who are 6 years old, and they’ve seen him acting very immaturely, then they’re ranking him based on 20% less life experience and that’s leading to kids being labelled as psychiatrically disordered”, Dr Whitely said.

Hair reading for mental health

Children’s hair could help identify their mental health.

At least that is what a groundbreaking Townsville-based research project is investigating.

A James Cook University medical researcher hopes to pave the way for earlier and more accurate identification of mental health disorders in children by reading their hair.

Dr Hani Mikhail’s is examining the potential for the measurement of cortisol, a stress-related hormone stored in hair, to help screen children for a range of mental conditions, as well as flag those at risk of developing one.

“The current model of mental health relies on analysing symptoms and their impact on a patient’s life, then trying to figure out what is going on at a psychological level,” he said.

“There is no way of looking beneath the surface, and treatment can involve a long process of trial and error.

“Cortisol is the primary chronic stress hormone of the endocrine system, and assists in the fight, flight or freeze response. As a bio marker, it may assist in reducing treatment delays, by helping to flag mental illnesses before symptoms even arise.

“This is particularly important in the context of child psychiatry, as symptoms are a lot more non-specific and early interventions often have life-long ramifications.”

The Rockhampton Base Hospital intern began his research as an honours student last year.

Dr Mikhail’s study is the first Australian research project to trial the collection and analysis of hair cortisol from children visiting a mental health facility.

His primary goal is to see hair cortisol employed as a diagnostic tool to screen and identify children at risk, before they tip over the edge.

“Ultimately, my colleagues and I want to see hair cortisol enable clinicians to detect if a child is brewing a mental health disorder, before they show any symptoms – so they can intervene to prevent something bad happening later on,” he said.

Since December last year, Dr Mikhail has collected hair samples and background questionnaire data from more than 150 children, aged five to 18, who have attended the Child and Youth Mental Health Service in Townsville.

Each child has contributed strands of hair at least three centimetres in length for analysis.

“Just like a tree, when you cut it down and can see the rings which record each year of growth, each centimeter of hair collected is roughly equivalent to one month of growth,” Dr Mikhail said.

“So we can analyse the cortisol level in a particular segment of hair and say, three months ago, this is what your average stress level was like. What was happening then?”

Previous studies have indicated that cortisol levels can change significantly in response to stress imposed by an existing mental health disorder, or due to external stress factors that could herald the onset of a mental health problem.

Conditions such as depression and psychosis raise cortisol levels, while anxiety disorders actually do the opposite.

“Bizarrely enough, Post Traumatic Stress Disorder, anxiety and eating disorders all tend to decrease the hair cortisol,” Dr Mikhail said.

“The theory is that these people have been chronically stressed for so long that the endocrine system begins to tire and starts to suppress itself.”

About half of the study participants initially assessed by the Townsville clinic were accepted for treatment.

The current phase of the study will examine hair cortisol samples to see if they predict which children were deemed in need of clinical assistance.

Dr Mikhail’s work is being supervised by JCU neuroscientist, Professor Zoltan Sarnyai, and JCU’s Head of Psychiatry, Professor Brett McDermott.

Why predicting suicide is a difficult and complex challenge

Who is going to die by suicide? This terrible mystery of human behavior takes on particular poignancy in the wake of suicides by high-profile and much-beloved celebrities Kate Spade and Anthony Bourdain. It is only natural that people want to know why such tragedies occur. Those closest to those who take their lives are often tormented, wondering if there is something they could have – or should have – known to prevent their loved one’s suicide.

As a scientist who has focused on this question for the past decade, I should have a pretty good idea of who is and isn’t going to die by suicide. But the sad truth is, I don’t. The sadder truth is, neither do any other suicide experts, psychiatrists or physicians. The sum of the research on suicide shows that it does not matter how long we’ve known someone or how much we know about them. In my research, my colleagues and I have shown that we can only predict who is going to die by suicide slightly more accurately than random guessing.

The need for answers

The fact that suicide is so hard to predict unfortunately took about 50 years for most scientists to appreciate. About the same time that this recognition became widespread a few years ago, a new hope emerged: a form of artificial intelligence called machine learning. As several research groups have demonstrated in recent years, machine learning may be able to predict who is going to attempt or die by suicide with up to 90 percent accuracy.

To understand why this is, and why we humans won’t ever be able to accurately predict suicide on our own, one needs to take a step back and understand a little more about the nature of human cognition, suicide and machine learning.

As humans, we love explanations that have two qualities. First, explanations should be simple, meaning that they involve one or a small number of things. For example, depression is a simple explanation for suicide.

Second, explanations should be determinate, meaning that there is one set explanation that accounts for all or most of something. For example, the idea that depression causes most suicides is a determinate explanation. This simple and determinate explanatory style is highly intuitive and very efficient. It’s great for helping us to survive, procreate, and get through our days.

But this style of thinking is terrible for helping us understand nature. This is because nature is not simple and determinate. In recent decades, scientists have come to recognize that nearly everything – from physics to biology to human behavior – is complex and indeterminate. In other words, a very large number of things combined in a complex way are needed to explain most things, and there’s no set recipe for most physical, biological or behavioral phenomena.

I know that this latter idea of indeterminacy is especially counterintuitive, so let me provide a straightforward example of it. The math equation X plus Y equals 1 is indeterminate. As humans, we instinctively try to find one solution to this equation (e.g., X equals 1, Y equals 0). But there is no set recipe for solving this equation; there are nearly infinite solutions to this equation. Importantly, however, this does not mean that “anything goes.” There are also near infinite values for X and Y that do not solve this equation. This indeterminate middle ground between “one solution” and “anything goes” is difficult for most humans to grasp, but it’s how much of nature works.

The sum of our scientific evidence indicates that, just like most other things in nature, the causes and predictors of suicide are complex and indeterminate. Hundreds, and maybe thousands, of things are relevant to suicide, but nothing predicts suicide much more accurately than random guessing. For example, depression is often considered to be an extremely important predictor of suicide. But about 2 percent of severely depressed people eventually die by suicide, which is only slightly higher than the 1.6 percent of people from the general United States population who eventually die by suicide. Such a pattern is consistent with complexity because it suggests that we must put a lot of factors together to account for suicide.

Empathy will always matter

So how should we put all of these factors together? One intuitive solution is to add many of these factors together. But even when summing hundreds of factors, this doesn’t work – prediction is still only slightly more accurate than random guessing.

A much better solution would be to somehow find an optimized combination of tens or even hundreds of factors. How can we do this? One promising answer is machine learning. In short, machine learning programs can process a large amount of data and learn an optimal combination of factors for a given task. For example, most existing machine learning studies have used data from electronic health records, spanning hundreds of factors related to mental health diagnoses, physical health problems, medications, demographics and hospital visit patterns. Results from several groups in recent years have shown that this approach can consistently predict future suicide attempts and death with 80-90 percent accuracy. Multiple groups are currently working on applying these algorithms to actual clinical practice.

One important thing to keep in mind is that there isn’t, and never will be, a single algorithm or recipe for suicide prediction. This is because suicide is indeterminate, much like the X plus Y equals 1 equation. There are likely near-infinite algorithms that could predict suicide with 80-90 percent accuracy, as a number of studies have shown. Research has already demonstrated that no particular factors are necessary for a good algorithm, and many different types of algorithms can produce accurate prediction. But again, this indeterminacy also means that there are near-infinite bad algorithms, too.

About 2 percent of severely depressed people die by suicide.
Fure/Shutterstock.com

All of this research shows that suicide is unfortunately too complex and indeterminate for humans to predict. Neither I nor anyone else can accurately predict who is going to die by suicide or truly explain why a particular person died by suicide (this includes the suicide decedents themselves). Machine learning can do a much better job of approximating the complexity of suicide, but even it falls far short. Although it can accurately predict who will eventually die by suicide, it cannot yet tell us when someone will die by suicide. This “when” dimension of prediction is critical, and we are likely still many years away from accounting for it.

In the meantime, what can we humans do? While we don’t have the ability to know whether someone is going to die by suicide or not, we do have the ability to be supportive and caring. If you believe that someone may be struggling, talk with them and let them know about resources such as the US National Suicide Prevention Lifeline (1-800-273-8255).

If this article has raised issues for you or if you’re concerned about someone you know, call Lifeline on 13 11 14.

Joseph Franklin, Assistant professor of Psychology, Florida State University

This article was originally published on The Conversation. Read the original article.