suicidal behavior

Depression may be our brain’s way of telling us to stop and solve a problem.

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At any given time, about 5% of Americans report symptoms of moderate or severe depression. Major depressive disorder is so common that at some point in life, one in six Americans (15%) will suffer from it.

The prevalence of depression presents economic problems as well – it’s one of the most common causes of disability, it has effects in the workplace, and it’s responsible for a host of suicide-related costs. In 2010, the economic burden of depression in the US was estimated to be $210.5 billion.

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So why does such a debilitating condition strike so many people?

The traditional understanding is that depression is just a breakdown in the way things are normally supposed to work in the brain – chemical imbalances that can be righted through a combination of medication and behavioral shifts.

But there’s also a theory that instead of being purely a disorder, depression might be a specific behavioral strategy that we’ve evolved, a biological adaptation that serves a purpose. As Matthew Hutson explains in a Nautilus feature on the potential evolutionary roots of depression and suicidal behavior , that purpose might be to make us stop, understand, and deal with an important problem.

Hutson explains that evolutionary psychologist Paul Andrews and psychiatrist J. Anderson Thomson first elaborated on this idea, called the “analytical rumination hypothesis,” in an article published in Psychological Review in 2009.

The basic concept is that what we think of as a disorder is actually a way our brains analyze and dwell on a problem in the hopes of coming up with a way to deal with it. The researchers suggest it’s possible that a difficult or complex problem triggers a “depressive” reaction in some people that sends them into a sort of analytical mode.

With depression, Hutson writes, “[t]here’s an increase in rumination, the obsessing over the source of one’s pain,” along with increased analytical activity in the brain and REM sleep, which helps with memory processing. A major symptom of depression is anhedonia, the inability to take pleasure from normal activities. According to this approach, those activities could be seen as disrupting this “processing” phase.

This hypothesis would account for the fact that the majority of depressive episodes occur after a significant life event like a death or the end of a relationship.

In their 2009 paper, Andrews and Thomson even suggest this idea could explain why depression and anxiety so frequently occur together.

“We hypothesize that depression and anxiety often co-occur because some problems require both analysis (promoted by depressed affect) and vigilance (promoted by anxiety),” they write. Analysis allows someone to understand the inciting factor, vigilance is a way of trying to prevent it from happening again.

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Implications for treatment

As fascinating as evolutionary explanations are, it’s hard to prove they are correct, especially if they haven’t yet been reinforced by other research.

The idea that depression might be a biological adaptation rather than a mental disorder is not the main consensus of the mental health community. And even if the hypothesis is correct, it’s likely incomplete and doesn’t explain all of depression.

Complex problems usually have a number of causes. About 20% of depression cases aren’t preceded by a major life event – there may be some cause in the past, but we don’t know for sure. We also know thatgenetics can play some role in a person’s susceptibility to depression. As Andrews and Thomson point out, there are different types of depression, some of which may have different causes. They also write that there are alternative evolutionary explanations that could co-exist with their hypothesis.

But if the analytical rumination hypothesis can be further validated, it could have major implications for how we treat this kind of mental illness in the future.

In that case, the approach to treating depression could shift to deal more with the underlying cause, rather than just treating symptoms. One anthropologist told Hutson that if the theory is right, treating depression with antidepressants might be like treating a broken bone with painkillers (instead of providing both painkillers and a cast to help the break heal). By that logic, therapy could be seen as an important part of treatment, since it can help people better understand and cope with whatever caused their depressive episodes.

Traditional antidepressants have been very effective , even life-changing, for some. But those approaches don’t work in the long term for everyone, which is why researchers are investigating all kinds of different therapies.

Even if depression is found to be some sort of evolutionary “tool” or adaptation, it clearly doesn’t necessarily help people solve the problem that causes it. But new understandings may help us think about new or better forms of treatment – something that’s always welcome.

Source:http://www.businessinsider.in

Family History Of Suicide: Parent’s Suicidal Behavior Could Influence Child’s.

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Parent’s suicidal behavior may influence their child’s suicidal behavior. 

It is well known that a family history of suicide increases a young person’s risk for suicidal behavior. However, very little is known about what mechanisms and pathways lead to familial transmission of suicidal behavior. A recent study published in JAMA Psychiatry has found that having a parent who attempted suicide means a child with a mood disorder could be five times more likely to exhibit suicidal behavior.

According to the National Institute of Mental Health, approximately 38,000 people die by suicide each year in the United States. Some of the most common risk factors for suicide include a family history of suicide, a family history of mental disorder or substance abuse, and family violence, including physical or sexual abuse. While tragic, suicide is often preventable, and the best method of prevention is knowing the signs and getting help.

“Impulsive aggression played an important role in increasing the likelihood of an offspring suicide attempt, but it did so by increasing the risk of the subsequent development of a mood disorder, which in turn increased the risk of an attempt,” the research team explained. “The transition from impulsive aggression to mood disorder may be particularly salient to understanding recurrent suicidal behavior because this pathway from offspring suicide attempt at baseline to an attempt at follow-up was mediated by offspring impulsive aggression and mood disorder.”

The research team, led by Dr. David A. Brent from the University of Pittsburgh Medical Center, recruited 701 children between the ages of 10 and 50, as well as 334 parents suffering from mood disorder, 191 of which had attempted suicide. Both children and parents were followed for a period of 5.6 years. At the beginning of the study, which took place between July 1997 and June 2012, participants underwent a complete psychiatric assessment as well as self-reported questionnaires.

Out of 701 children, 44 admitted to attempting suicide prior to the study and 29 made a suicide attempt during the study’s follow-up, 19 of which were first-time suicide attempts. Incidence of depression among children in the study increased from 29.6 percent in the first 1-2 years to 48.2 percent by the end of the study. After accounting for previous suicide attempts and familial transmission of a mood disorder, results indicated that children with a parent who attempted suicide were nearly five times more likely to attempt suicide.

“Parental history of a suicide attempt conveys a nearly five-fold increased odds of suicide attempt in offspring at risk for mood disorder, even after adjusting for the familial transmission of mood disorder,” the research team concluded. “Interventions that target mood disorder and impulsive aggression in high-risk offspring may attenuate the familial transmission of suicidal behavior.”

Source: Oquendo M, Melhem N, Brent D, et al. Familial Pathways to Early-Onset Suicide AttemptA 5.6-Year Prospective Study. JAMA Psychiatry. 2014.

Only Certain Newer Antiepileptic Drugs Associated with Increased Risk for Suicidal Behavior

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Current use of newer antiepileptic drugs (AEDs) that pose high risk for depression is associated with increased risk for suicidal behavior, according to an industry-funded study in Neurology. (In 2008, the FDA warned that all AEDs raise suicidality risk.)

Using a U.K. general practice database, researchers matched some 450 patients with epilepsy who had displayed self-harm or suicidal behavior with some 9000 epileptic patients without such behavior. All had used at least one AED during 5.5 years’ follow-up.

Current use of newer AEDs associated with high risk for depression (e.g., levetiracetam, topiramate) raised the odds for self-harm or suicidality threefold, compared with nonuse in the past year. Barbiturates, conventional AEDs (e.g., carbamazepine, phenytoin, valproate), and newer AEDs with low risk for depression (e.g., gabapentin, lamotrigine) did not increase risk.

Editorialists call the study a “good initial attempt” but point out various limitations that might invalidate the findings; for instance, few cases were taking high-risk drugs.