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Depression is almost twice as common, and poor quality of life almost five times as common, in people with bipolar disorder who have elevated or low levels of the stress hormone cortisol in the blood. Researchers at Umeå University, Sweden, report this in a study published in the journal PLOS ONE.

“In bipolar depression the stress system is often activated, which means that the affected individuals have elevated cortisol levels in the blood. We have now been able to show that both over- and underactivity in the stress system, with corresponding elevated or reduced cortisol levels, can impair mental health in terms of depression and poor quality of life in these patients,” says Martin Maripuu, a PhD student at the Department of Clinical Sciences, Psychiatry Unit Umeå University and physician at the psychiatric clinic, Ostersund Hospital.

Bipolar disorder is a lifelong disease that causes recurrent episodes of both mania and depression. Stress is a known trigger for these episodes, and depression and mania also adds to the accumulated stress load.

One of the body’s main stress systems is the HPA axis. This system regulates the production and level of the vital stress hormone cortisol. Cortisol is a hormone that everyone needs in everyday life in order to cope with various stressful situations, such as pain, illness and stress at work.

Stress causes overactivity in the stress system, resulting in elevated levels of cortisol. If the stress continues in the long-term, it is believed to cause an underactivity in the stress system, which results in low cortisol levels.

Previous studies have shown that the stress system is often overactive in patients with bipolar depression. To investigate the relationship between cortisol levels and depression among these patients, the researchers at Umeå University conducted a study with 145 patients who had bipolar disorder, as well as 145 people in a control group. The researchers measured cortisol levels in the participants, both under normal conditions and after the participants had completed a so-called dexamethasone suppression test, which is sensitive to early abnormalities in the stress system.

The results of the study show that more than half of the patients with bipolar disorder who had elevated or low levels of cortisol in the blood, also had depression. Depression was additionally almost twice as common in those who had high cortisol levels and in those who had low cortisol levels, compared with those who had normal levels of the hormone in the blood. Prevalence of low quality of life was six times more common in the group with low cortisol levels and nearly five times more common among those with high cortisol levels, compared with those who exhibited normal activity in the stress system.

The study also shows that people who had low cortisol levels, on average, have had their disease longer than those with high cortisol levels, which could suggest that chronic stress in bipolar disorder can lead to an “exhaustion” of the stress system with reduced cortisol levels as a result. The researchers also believe that the low cortisol levels, once developed, can contribute to a more chronic, manifested state of the disorder.

“These are important results that in the future could contribute to a more personally tailored medical treatment of bipolar disorder. The results may also ultimately lead to the development of new drugs that work by normalizing the stress system and cortisol levels,” says Martin Maripuu.

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In an experiment that had people with bipolar disorder playing roulette, brain scans revealed that the ‘reward centers’ of their brains were activated more than those of people without the psychiatric disorder formerly known as manic depression.

The research, published in the journal Brain, used functional MRI scans to monitor the response of a part of the brain known to be involved in reward and pleasure, the nucleus accumbens.

This center drives us to make decisions that bring satisfying short-term results, but was shown to be more active in response to risk-taking in the people with bipolar disorder, report the neuroscientists from the UK’s universities of Manchester and Liverpool.

Prof. Wael El-Deredy, a cognitive neuroscientist from the University of Manchester, says there are upsides and downsides to this response for people living with bipolar. He says:

“The greater buzz that people with bipolar disorder get from reward is a double-edged sword.

On the one hand, it helps people strive towards their goals and ambitions, which may contribute to the success enjoyed by many people with this diagnosis.

However, it comes at a cost: these same people may be swayed more by immediate rewards when making decisions and less by the long-term consequences of these actions.”

The brains with bipolar disorder showed that another, less primitive area of the brain also gave a different response. The prefrontal cortex, highly developed in humans and associated with our ability to give conscious thought, was more effective at guiding the impulses of the study participants who did not have bipolar disorder, “towards safe gambles and away from risky ones.”

This part of the brain for the control subjects was better able to temper desire for immediately rewarding decisions, in favor of maximizing overall results.

Prof. Richard Bentalla, an expert in psychology at the University of Liverpool, says: “This study shows how we can use the new tools of neuroscience to better understand the psychological mechanisms that lead to a psychiatric disorder which, until now, has been very difficult to understand.”

Dr. Liam Mason, a psychologist from the Manchester team who now works at King’s College London’s Institute of Psychiatry, says the research revelations will inform the scientific pursuit of treatments.

“Understanding how the brain works to regulate the pursuit of goals will help us to design, evaluate and monitor better therapies for bipolar disorder,” he says.

Risky pursuit of goals

Bipolar disorder results in disturbance of mood, and people with the diagnosis experience unpredictable episodes of depression and mania. The mania produces periods of intense excitement and irritability, often leading to very risky behavior.

The authors note:

“Bipolar disorder is characterized by marked difficulty in regulating the pursuit of goals, with the onset of manic and depressive episodes linked to the attainment and failure to obtain goals, respectively.

Although particularly elevated during mania, impulsivity represents a trait feature of the disorder and there is evidence of altered frontostriatal processing of reward prospects and outcomes across mood episodes.”

The patients recruited to the study were in a euthymic phase, neither in an episode of depression or mania, and were not receiving antipsychotics, so that the medications would not affect the results.

The 20 people with bipolar disorder in remission were matched with 20 healthy control subjects of the same age, gender and level of education.

All participants were between 18 and 45 years of age, and had no current alcohol problem or recent substance use.

High and low stakes

The task being performed while functional MRI was used to evaluate brain activity involved three time phases to a roulette gamble:

patient entering an mri scanner
The researchers used functional MRI scans to monitor the response of a part of the brain known to be involved in reward and pleasure, the nucleus accumbens.
◾Selection
◾Anticipation
◾Outcome.

This decision-making, and its resulting reward anticipation and receipt, was in response to two conditions of probability, and two levels of stake:
◾Safe, high probability of reward (75%)
◾Risky, low chance of reward (25%)
◾Low stake of £3
◾High stake of £9.

The safe or risky conditions were presented to participants at the beginning of each trial, and the magnitude of the stake was announced during the selection phase. The participants knew that they would be paid the actual winnings at the end.

There were 8 runs at the roulette game, of about 6 minutes each, giving a total of 272 trials for the participants. The probabilities and stakes were distributed equally in each run.

Results showed, for example, that during the anticipatory phase, the prefrontal cortex was more active across all the participants for “prospects that afforded a high probability of reward, and for prospects of larger magnitude.” The authors say this is consistent with activity in that part of the brain for “aligning with the higher-order goal of maximizing rewards.”

In the bipolar disorder group, however, the effect of probability was reduced, such that these patients “showed a smaller increase in prefrontal cortex activation” for high-probability prospects.

“Patients with bipolar disorder,” the authors continue, “responded more strongly to gains but not losses, consistent with a stronger lower-order preference for rewards.”

Written by Markus MacGill

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A neuroscientist at Rutgers University-Newark says the human brain operates much the same whether active or at rest – a finding that could provide a better understanding of schizophrenia, bipolar disorder and other serious mental health conditions that afflict an estimated 13.6 million Americans.

In newly published research in the journal Neuron, Michael Cole, an assistant professor at the Center for Molecular and Behavioral Neuroscience, determined that the underlying brain architecture of a person at rest is basically the same as that of a person performing a variety of tasks.

This is important to the study of mental illness because it is easier to analyze a brain at rest, says Cole, who made the discovery using functional magnetic resonance imaging (fMRI).

“We can now observe people relaxing in the scanner and be confident that what we see is there all the time,” says Cole, who initially feared his team might find that the brain reorganizes itself for every task. “If that had been the case, we would have had less hope that we could understand mental illness in our lifetime.”

Poor connectivity between areas of the brain
Poor connectivity between areas of the brain may be at the root of severe mental illness.
Credit: Neuron

Instead, Cole says, scientists can now make their search for causes of mental illness more focused – and he suggests at least one target of opportunity. The prefrontal cortex is a portion of the brain involved in high level thinking, as well as remembering what a person’s goal is and the task being performed.

Cole says it would be useful to explore whether connectivity between the prefrontal cortex and other areas of the brain is altered – while the brain is at rest – in people with severe mental illness. “And then we can finally say something fundamental,” he predicts, “about what’s different about the brain’s functional network in schizophrenia and other conditions.”

Those differences, in turn, could explain certain symptoms. For instance, what if a patient has visual hallucinations because poor connectivity between the prefrontal cortex and the portion of the brain that governs sight causes the hallucinations to override what the eyes actually see? Cole suggests that’s just one of the questions that analysis of the brain at rest might help to answer. Others include a person’s debilitating beliefs, such as overly negative self-assessment when depressed.

Opportunities to find better ways to improve patients’ lives might then follow. Cole notes that current medications for severe mental illness, when they help at all, typically do not relieve cognitive symptoms. It is possible the drugs will reduce hallucinations or depressing thoughts, but patients continue to have difficulty concentrating on the task at hand, and often find it hard to find or hold a job. Cole says that even solving that one issue would be a major step forward – and he hopes his new work has helped advance science toward achieving this goal.

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A new study carried out by scientists from University College London in the UK has reported on the discovery of a rare gene variant found in about 1 in every 200 people that could increase the risk of developing alcohol dependence, bipolar disorder and schizophrenia.

Their research found that people with the variant of the GRM3 gene, believed to be important in brain signaling, were approximately 2-3 times more likely to develop alcohol dependence or schizophrenia. Previous research by the same team has found that the same gene variant could triple the risk of developing bipolar disorder.

All three of these conditions are chronic and severe, often having dramatic impacts on peoples’ livelihoods and social relationships.

Treatment for schizophrenia and bipolar disorder focuses on eliminating the symptoms of the conditions, as the specific causes are unknown. The new research could, however, lead to new treatments as a further clue to the genesis of such conditions is unveiled. Co-author of the research Prof. David Curtis says:



”We could be looking at the next big drug target for treating mental illness. The work opens up new ways to prevent and treat mental illnesses by revealing the mechanisms involved in their development.”

Two studies, same findings

The researchers, who published their results in Psychiatric Genetics, arrived at their findings through a genetic analysis of 6,280 participants. Of these people, 4,971 had been diagnosed with one of the three disorders, and their results were compared with the results of the 1,309 healthy control participants.

DNA
Chronic mental illnesses such as schizophrenia and bipolar disorder tend to run in the family, suggesting a genetic cause for the conditions.

The team found that the participants who had a variant of the GRM3 gene were also more likely to develop schizophrenia, bipolar disorder or alcohol dependency.

The association between the GRM3 variant and an increased risk of schizophrenia was confirmed by a global study that also involved research from University College London (UCL), as part of a consortium of over 200 institutions.



The study, also co-authored by Prof. Curtis and published in Nature, examined the genomes of 36,989 people who had developed schizophrenia and 113,075 otherwise healthy subjects taken from different sites across the world.

The consortium identified a total of 108 different genetic locations that were associated with schizophrenia. Of these, only the GRM3 gene has had a specific mutation identified as being responsible.

Prof. Curtis says that the consortium’s findings were “particularly compelling,” as “the odds of this occurring by chance are only one in a billion.”

New treatments to be developed?

Presently, the activity of the chemical dopamine is key to methods of treating schizophrenia. Dopamine is a neurotransmitter that helps to transmit signals between brain cells, and it is believed that overactive dopamine signaling could lead to areas of the brain communicating with each other that are supposed to remain separate.

Some scientists believe that overactive dopamine signaling could be responsible for one of the prominent symptoms of schizophrenia. Being able to “hear voices” may be due to speech and hearing areas of the brain communicating between each other.

However, there are other chemicals that brain cells use in order to communicate with each other. Glutamate is another neurotransmitter that is involved, and calcium “channels” are used to control brain cell activation. The consortium’s research found that genes related to these, including GRM3 were implicated in the development of schizophrenia.

Dr. Andrew McQuillen is head of the UCL Molecular Psychiatry team that first discovered GRM3, and he says that the findings could affect future research into treating the chronic conditions that the GRM3 variant has been linked to:

“Drug treatments for schizophrenia have barely changed over the past few decades, as they still target dopamine receptors. Schizophrenia treatments targeting glutamate receptors have been tested in the past without success. However, they might be more effective at treating patient groups with mutations in glutamate receptors such as GRM3.”

Dr. McQuillen also acknowledges that drugs targeting calcium channels have previously been tested with some success against bipolar disorder and that the consortium’s findings suggest that they are viable drug targets. He says he expects “we will see increased interest in drugs against both glutamate receptors and calcium channels as a result of the research.”

At present, it is reported that 2.4 million American adults have schizophrenia, 5.7 million experience bipolar disorder and more than 18 million have alcohol dependence. Any developments related to treatment for these chronic illnesses stand to improve the lives of a considerable portion of the American population.

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Brain stimulation treatments, like electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS), are often effective for the treatment of depression. Like antidepressant medications, however, they typically have a delayed onset. For example, a patient may receive several weeks of regular ECT treatments before a full response is achieved.

Thus, there is an impetus to develop antidepressant treatments that act to rapidly improve mood.

Low field magnetic stimulation (LFMS) is one such potential new treatment with rapid mood-elevating effects, as reported by researchers at Harvard Medical School and Weill Cornell Medical College.

“LFMS is unlike any current treatment. It uses magnetic fields that are a fraction of the strength but at higher frequency than the electromagnetic fields used in TMS and ECT,” explained first author Dr. Michael Rohan.

Indeed, the potential antidepressant properties of LFMS were discovered accidentally, while researchers were conducting an imaging study in healthy volunteers. This led Rohan and his colleagues to conduct a preliminary study in which they identified the imaging parameters that seemed to be causing the antidepressant effect.

They then designed and constructed a portable LFMS device, which delivers a low strength, high frequency, electromagnetic field waveform to the brain. The next step was to test the device in depressed patients, the results of which are published in the current issue of Biological Psychiatry.

A total of 63 currently depressed patients, diagnosed with either major depressive disorder or bipolar disorder, participated in the study and were randomized to receive a single 20-minute treatment of real LFMS or sham LFMS, where the device was on but the electromagnetic fields were inactive. Since neither the patients nor the researchers knew which treatment each person actually received, the true effect of the LFMS could be measured.

An immediate and substantial improvement in mood was observed in the patients who received real LFMS, compared to those who received the sham treatment. There were no reported side effects.

This finding suggests that LFMS may have the potential to provide immediate relief of depressed mood, perhaps even in emergency situations. It also confirms the success of the device’s design.

“The idea that weak electrical stimulation of the brain could produce beneficial effects on depression symptoms is somewhat surprising,” said Dr. John Krystal, Editor of Biological Psychiatry. “Yet the data make a compelling case that this safe approach deserves further study.”

Rohan confirmed that additional research is underway to find the best parameters for LFMS use in the clinical treatment of depression. Further research will also be necessary to evaluate the effects of multiple compared to single treatments, and how long the antidepressant effects last following treatment.

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The first effective web-based treatment for Bipolar Disorder based on the latest research evidence has been developed by psychologists.

People with Bipolar Disorder have problems getting access to psychological therapy and this online intervention, published in the Journal of Affective Disorders, may offer a round the clock solution at a reduced cost to the NHS.

It was developed as part of the ‘Living with Bipolar’ project led by Dr Nicholas Todd under the supervision of Professor Fiona Lobban and Professor Steven Jones at the Spectrum Centre for Mental Health Research, Lancaster University.

92% of the participants in the trial of the online intervention found the content positive – and one said it had changed her life.

“I have encountered insights in the modules that have significantly helped me to survive the blackest moments. I cannot measure the value of this, as it has contributed to their difference between life and death. My husband and I are sincerely grateful for the immeasurable impact this has had on our family.”

Therapeutic gains for the participants included improved stability, accessing additional help from friends and family, less reliance on services and more likely to turn to self-management.

One described the online help as “…a practical intervention…very positive, empowering, recovery orientated, fostering personal responsibility. It is not patronising at all…”

Focussed on recovery, supporting people to live a fulfilling and meaningful life alongside their symptoms, the programme includes elements of Cognitive Behavioural Therapy and Psycho-education delivered via ten audio-visual modules with a mood checking tool, interactive worksheets and worked examples. The intervention is supported by a peer support forum moderated by a member of the research team and motivational emails.

Dr Todd said the online intervention may be a way of overcoming the difficulties of enabling people with a severe mental illness to manage their condition.

“The intervention was most useful for improving non-symptomatic outcomes such as quality of life, recovery and wellbeing. These packages may therefore provide a useful alternative to the symptom focussed approaches.”

Further research trials are required before this intervention can be made available within the NHS.

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Depression can hit young fathers hard — with symptoms increasing dramatically during some of the most important years of their children’s lives, a new Northwestern MedicineR study has found.

Depressive symptoms increased on average by 68 percent over the first five years of fatherhood for these young men, who were around 25 years old when they became fathers and whom lived in the same home as their children. The results of the study were published in the journal Pediatrics.

This study is the first to identify when young fathers are at increased risk of developing depressive symptoms. Craig Garfield, M.D., lead author of the paper, said the results of this longitudinal study are significant and could lead to more effective interventions and treatment for young men early in the fatherhood years.

“It’s not just new moms who need to be screened for depression, dads are at risk, too,” Garfield said. “Parental depression has a detrimental effect on kids, especially during those first key years of parent-infant attachment. We need to do a better job of helping young dads transition through that time period.”

Garfield is an associate professor in pediatrics and medical social sciences at Northwestern University Feinberg School of Medicine and a pediatrician at Ann & Robert H. Lurie Children’s Hospital and Northwestern Memorial Hospital.

Previous research has shown depressed dads will use more corporal punishment, read less and interact less with their children, and are more likely to be stressed and neglect their children. Compared to the children of non-depressed dads, these children are at risk for having poor language and reading development and more behavior problems and conduct disorders.

“We knew paternal depression existed and the detrimental effects it has on children, but we did not know where to focus our energy and our attention until this study,” Garfield said. “This is a wakeup call for anyone who knows a young man who has recently become a new father. Be aware of how he is doing during his transition into fatherhood. If he is feeling extreme anxiety or blues, or not able to enjoy things in life as he previously did, encourage him to get help.”

This paper used data collected from 10,623 young men enrolled in the National Longitudinal Study of Adolescent Health (Add Health). It includes a nationally representative sample of adolescents in the U.S. and follows them in several waves over nearly 20 years into young adulthood. All participants’ symptoms of depression were scored at each wave through a survey using a subset of the Center for Epidemiologic Studies Depression Scale.

During the most recent wave of the Add Health study, the young men were age 24 to 32, and 33 percent had become fathers.

The majority of these fathers lived in the same home as their children. Young fathers who did not live with their children did not experience such a dramatic increase in depressive symptom scores in early fatherhood, the study found. Instead, these non-residential fathers’ depression symptom scores were elevated before fatherhood and start to decrease during early fatherhood, though this sample is smaller in number. Residential fathers’ depression symptom scores were lower before fatherhood and then dramatically increased after the birth of a child and into early fatherhood.

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According to the Centers for Disease Control and Prevention, around 1 in 10 American adults report having some form of depression. Now, researchers have revealed an unlikely strategy for treating the condition; activating neurons in the brain associated with stress-induced depression may actually trigger natural resilience to it.

The research team, led by Allyson K. Friedman, PhD, of the Icahn School of Medicine at Mount Sinai in New York, NY, says their research could lead to new targets for “naturally acting antidepressants.”

To reach their findings, recently published in the journal Science, the researchers conducted a study on mice that were susceptible to depression.

The team says mice that are resilient to social defeat stress – a form of stress triggered by losing a dispute or from a hostile interaction – currents in the cation channels, or ion channels, of the brain are significantly increased, compared with depressed or control mice. The cation channels are responsible for transporting positive ions in dopamine neurons.

For their latest study, the researchers wanted to see whether increasing currents in the cation channels of mice susceptible to depression would enhance their resilience and coping mechanisms.

Brain performs a ‘complex balancing act’ to become resilient to depression

The investigators exposed the mice to optogenetics. This involves using laser optics and gene virus transfer to control the signaling of dopamine neurons.

Mouse in cage
Increased activity of dopamine neurons in mice allowed them to cope with stress without developing symptoms of depression.

The team says that when the neurons of the mice were exposed to stress from light or lamotrigine – an anticonvulsant drug used to treat epilepsy and bipolar disorder – their signaling increased.

They found that increasing such activity allowed the mice to cope with stress without developing symptoms related to depression. Furthermore, they were amazed to find that the hyperactivity of the dopamine neurons normalized.

“To our surprise, we found that resilient mice, instead of avoiding deleterious changes in the brain, experience further deleterious changes in response to stress, and use them beneficially,” says senior study author Ming-Hu Han, PhD, also of the Icahn School of Medicine at Mount Sinai.

Friedeman explains that in order to achieve this resilience when under social stress, the brain must perform a “complex balancing act,” which involves negative stress-related changes in the brain activating positive changes.

The team says their findings may lead to the development of new antidepressant medication. They add that if a drug could boost the resilience and coping mechanisms of individuals susceptible to depression, it may have fewer side effects and could tackle depression in a more natural way.

Commenting on the team’s findings, Dr. Eric Nestler, of the Icahn School of Medicine – who was not involved in the study – says:

“In this elegant study, Drs. Friedman and Han and their colleagues reveal a highly novel mechanism that controls an individual’s susceptibility or resilience to chronic social stress.

The discoveries have important implications for the development of new treatments for depression and other stress-related disorders.”

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Depression may be better predicted and understood now that University of Illinois at Chicago researchers have discovered that young adults who previously experienced the mental illness have hyper-connected emotional and cognitive networks in the brain.

Rachel Jacobs and Scott Langenecker, University of Illinois at Chicago
Rachel Jacobs, UIC research assistant professor in psychiatry, and Scott Langenecker, UIC associate professor of psychiatry and psychology, use functional magnetic resonance imaging to examine the brain connectivity of young adults.
Credit: Photo: Joshua Clark/UIC Photo Services

UIC researchers used functional magnetic resonance imaging to examine the brain connectivity of young adults ages 18 to 23 while they were in a resting state. Thirty unmedicated young adults who had previously experienced depression and 23 healthy controls were used in the study, which has been published online in the journal PLOS ONE.

“We wanted to see if the individuals who have had depression during their adolescence were different from their healthy peers,” said Rachel Jacobs, research assistant professor in psychiatry at UIC’s Institute for Juvenile Research, the lead author of the study.

The researchers found many regions that are “hyper-connected – or talking to each other a little too much – among those who have a history of depression,” Jacobs said. These hyper-connected brain networks were related to rumination, with individuals thinking about a problem over and over without actively trying to come up with a solution.

“Rumination is not a very healthy way of processing emotion,” said Scott Langenecker, associate professor of psychiatry and psychology at UIC and corresponding author of the study. “Rumination is a risk factor for depression and for reoccurrence of depression if you’ve had it in the past.”

The researchers also looked at cognitive control (the ability to engage and disengage in thought processes or behaviors), which is a predictor of response to treatment and also relapse of illness.

“Cognitive control and rumination, as you might expect, are related to each other. As rumination goes up, cognitive control goes down,” said Langenecker.

The researchers will follow these young adults over time to see whether or not these hyper-connectivities predict who will or won’t have a recurrence of illness.

Psychosocial and medication treatments for depression can be helpful, said Jacobs, but within two years of recovery half of those teenagers will relapse.

The transition to adulthood, a time when brain networks are nearly mature, may be a critical window for interventions.

“If we can help youth learn how to shift out of maladaptive strategies such as rumination, this may protect them from developing chronic depression and help them stay well as adults,” Jacobs said.

“We think that depression is a developmental outcome, and it’s not a foregone conclusion that people need to become depressed. If we can provide prevention and treatment to those people that are most at risk, we might be able to prevent depression, reduce the number of depressive episodes, or reduce their severity,” said Langenecker.

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Reported poor sleep quality, independent of a depressed mood, appears to be associated with an increased risk for suicide in older adults.

Suicide is a preventable public health problem and accounts for almost 1 million deaths annually worldwide. Late life is characterized by an increased prevalence of sleep complaints and disproportionately elevated rates of suicide. The study sample included 420 individuals (400 control patients and 20 patients who died from suicide) who were selected from 14,456 participants.

The authors examined the risk for suicide associated with poor reported sleep in a group of older adults (with an average age of nearly 75 years) during a 10-year observation period.

Those individuals who reported poorer sleep quality at baseline had a 1.4 times increased risk for suicide. When authors controlled for the effects of a depressed mood, people with poorer sleep at baseline still demonstrated a 1.2 times greater risk for suicide during the 10-year observation period. Two sleep factors in particular – difficulty falling asleep and nonrestorative sleep – were associated with increased suicide risk.

“We suggest that poor subjective sleep quality may therefore represent a useful screening tool and a novel therapeutic target for suicide prevention in late life.”

The study is published in JAMA Psychiatry.

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