Depression in Grandmothers who care for Grandchildren

Grandmothers who care for their grandkids fulltime need help for depression and family strains, report researchers from the Case Western Reserve University's Frances Payne Bolton School of Nursing.

Carol Musil, PhD, RN, FAAN, professor of nursing, recently conducted one the longest-running studies on grandmothers in various family situations, from serving as their grandkids' fulltime caregivers to those not caring for their grandchildren as a comparison.

"Although we expected the primary caregiver grandmothers raising grandchildren would have more strain and depressive symptoms, " Musil said, "we were surprised at how persistent these were over the years examined in the study."

Results of the study, funded by a grant from the National Institute of Nursing Research, were reported in Nursing Outlook, the journal of the American Academy of Nursing and the Council for the Advancement of Nursing Science.

Some 6.2 million, or 5.3 percent of all U.S. households, have a grandparent living in the house, according to U.S. Census data.

Musil said over 1 million grandmothers are responsible for raising grandchildren whose parents do not live in the home.

Musil tracked and focused on the health and wellbeing of 240 grandmothers they studied for 6 1/2 years to see how the responsibilities of caring for their grandchildren 16 years and younger affected their health over time.

The subjects were surveyed about their physical and mental health annually for the first three years, and two more times, 2- 2 ½ years apart at the end of study.

The grandmothers, who averaged 57.5 years old at study onset, were in three caregiving situations: those who are fulltime caregivers for their grandchildren, living in multigenerational homes or non-caregivers.

They were randomly selected throughout Ohio, representing rural, suburban and urban backgrounds.

Despite the signs of depression and family stress, researchers also found that the grandmothers, especially those raising grandchildren, were generally open to receiving various forms of help.

That implies, Musil said, that grandmothers might be open to resourcefulness training, which has helped to reduce depressive symptoms in grandmothers in pilot studies conducted with Jaclene Zauszniewski.

"They need support from others," she said, "but the most important thing is to maintain and perhaps develop new cognitive and behavioral skills and approaches for handling some very challenging family issues."

Grandparents: Strong bond with Grandchildren reduces Depression in both parties

A new study shows that grandparents and grandchildren have real, measurable effects on each other's psychological well-being long into grandchildren's adulthood.

Sara M. Moorman

"We found that an emotionally close grandparent-adult grandchild relationship was associated with fewer symptoms of depression for both generations," said Sara M. Moorman, an assistant professor in the Department of Sociology and the Institute on Aging at Boston College, who will present the study at the 108th Annual Meeting of the American Sociological Association.

"The greater emotional support grandparents and adult grandchildren received from one another, the better their psychological health."

The study also revealed that giving tangible support to or receiving it from their grandchildren affected the psychological well-being of grandparents but not grandchildren.

Tangible support, also called functional solidarity or instrumental support, includes anything from rides to the store and money to assistance with household chores and advice.

"Grandparents who experienced the sharpest increases in depressive symptoms over time received tangible support, but did not give it," said Moorman, who co-authored the study with Jeffrey E. Stokes, a PhD candidate in sociology at Boston College.

"There's a saying, 'It's better to give than to receive.' Our results support that folk wisdom—if a grandparent gets help, but can't give it, he or she feels badly.

Grandparents expect to be able to help their grandchildren, even when their grandchildren are grown, and it's frustrating and depressing for them to instead be dependent on their grandchildren."

Comparatively, the researchers found that grandparents who both gave and received tangible support experienced the fewest symptoms of depression over time.

"Therefore, encouraging more grandparents and adult grandchildren to engage in this type of exchange may be a fruitful way to reduce depression in older adults," said Moorman.

In their study, the researchers used data from the Longitudinal Study of Generations, a survey of 3- and 4-generation U.S. families that included seven waves of data collection between 1985 and 2004.

The sample was comprised of 376 grandparents and 340 grandchildren. The average grandparent was born in 1917 and the average grandchild in 1963, making them 77 years old and 31 years old, respectively, at the midpoint of the study in 1994.

In terms of the study's implications, Moorman said her research suggests that efforts to strengthen families shouldn't stop with the nuclear family or focus only on families with younger children.

"Extended family members, such as grandparents and grandchildren, serve important functions in one another's daily lives throughout adulthood," she said.

The study also indicates that helping older people remain functionally independent may aid their psychological well-being, according to Moorman.

"Most of us have been raised to believe that the way to show respect to older family members is to be solicitous and to take care of their every need," Moorman said.

"But all people benefit from feeling needed, worthwhile, and independent. In other words, let granddad write you a check on your birthday, even if he's on Social Security and you've held a real job for years now."

More information: The paper, "Does Solidarity in the Grandparent/Grandchild Relationship Protect Against Depressive Symptoms?," will be presented on Monday, Aug. 12, at 4:30 p.m. EDT in New York City at the American Sociological Association's 108th Annual Meeting.

UK Childline asks; Do you know your children well enough?

A growing “worry gap” between the problems children actually face and the issues that most concern their parents could be putting young people at risk, experts warned last night.

Most parents of primary school children choose “traditional” concerns such as stranger-danger or bullying when asked what most worries them about youngsters’ well-being, polling seen by The IoS shows.

Yet records from the UK charity ChildLine show their most common calls from children relate to depression, self-harm or thoughts of suicide.

More than half of all parents polled by YouGov for the helpline picked stranger-danger as an issue that worried them, while two-thirds chose bullying.

Yet fewer than one in five parents identified mental health as something they would worry about with a child – despite it being the most common thing for which children seek help.

Of ChildLine’s 1.5 million phone calls and online counselling sessions last year, more than 42,000 related to mental health problems, suicidal thoughts or self-harm.

Esther Rantzen, the charity’s founder, said: “It’s really important for us to hear the message that’s coming from young people who ring ChildLine. The fact is that unhappiness of this seriousness has not been on our agenda as parents and we need to take time to see what our children’s attitude to life is.”

Mental health-related issues are also among the fastest growing concerns for UK youngsters. In 2012 more than 16,000 children called ChildLine about self-harm, up 68 per cent on the previous year.

There were 12,000 calls about suicide, an annual increase of 39 per cent, and 14,000 calls about depression and mental health, up 19 per cent.

Siobhan Freegard, the founder of the parenting website Netmums, said: “We see it here at Netmums, that when parents start noticing mental health problems it actually seems quite late.

Because we’re not so aware of it and it’s not on our list of key worries it seems to me we don’t pick it up early enough, and by the time we’re aware it’s often fully entrenched.

“It’s still a bit of a taboo that your child could have a mental health problem. People need to realise that this absolutely could be my child.”

Parents did not identify the impact of troublesome family relationships as a major worry, but this was the second most common source of concern for children and young people seeking help from ChildLine.

Almost 40,000 phone and online counselling sessions by the charity last year were about family relationship issues, such as parents getting divorced.

Peter Liver, director of ChildLine, said: “There have been notable changes in the problems children contact us about since ChildLine launched in 1986. Originally, sexual abuse was the major issue but now the pendulum is swinging towards family problems, self-harm and suicide.

We know from polls of parents that they are still having more traditional conversations with their children about issues such as stranger-danger, which is great, but are unlikely to speak to them about emerging issues like self-harm.”

He added: “It can be hard for parents to keep up and I think it’s easier to understand more traditional issues as we’ve been through them ourselves or were warned about them by our own parents.”

Mothers and fathers are not entirely out of touch, however. One in 10 ChildLine counselling sessions – more than 30,000 – related to bullying and around 16,000, or 5 per cent, of their counselling sessions were about sexual abuse.

Two-fifths of parents were worried about their children accessing pornography – though this did not feature in the top 10 worries of children contacting the charity.

US DSM-5 for diagnosing mental disorders published - Asperger's is Out!

In the manual, grief is newly medicalised as major depressive disorder (MDD). 

Credit: Adam G. Gregor /Alamy

The field of mental health will face its greatest upset in years on Saturday with the publication of the long-awaited and deeply-controversial US manual for diagnosing mental disorders.

Early drafts of the book, the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, or DSM-5, have divided medical opinion so firmly that authors of previous editions are among the most prominent critics.

Known informally as the psychiatrists' bible, the $199 tome from the American Psychiatric Association is the guidebook that US doctors will use to diagnose mental disorders. The latest edition is the first major update in 20 years.

Though not used in the UK, where doctors turn to the World Health Organisation's International Statistical Classification of Diseases (ICD), the US manual has global influence. It defines groups of patients, and introduces new names for disorders.

Those names can spread, and become the norm elsewhere, but more importantly, the categories redefine the populations that are targeted by drugs companies.

Criticisms have come from almost every corner. There are claims of expansionism, with common experiences and behaviours becoming newly medicalised.

Allen Frances

Temper tantrums become Disruptive Mood Dysregulation Disorder (DMDD); grief becomes major Depressive Disorder (MDD), according to Allen Frances, an American psychiatrist who chaired the task force behind the fourth edition of the manual.

Other behaviours get their own labels: overeating becomes binge eating disorder; keeping too much junk, a hoarding disorder; a bit forgetful could be mild neurocognitive disorder.

David Clark

David Clark, professor of experimental psychology at Oxford University, said "Mental health disorders are often hard to divide into clear categories, because too little is known about them, and there can be major overlaps. But the definitions are often valuable. For example, greater distinctions between various types of anxiety have led to more specific and effective treatments."

Nick Craddock, professor of psychiatry at Cardiff University, and director of the National Centre for Mental Health in Wales, said "Some of the stranger aspects of the US manual will have no impact in Britain. DSM-5 was flawed because definitions of disorders were sometimes changed on the basis of too little fresh scientific evidence."

"I don't believe the science has advanced sufficiently in 20 years since DSM-4 to warrant making a new system," he said. "That essentially is just a group of people agreeing on tweaking things and making them appear a little bit different. That to me is not a very helpful stage in the develop of psychiatric diagnosis. This is the wrong time in history to change the diagnostic system."

Changing the definitions of disorders alters who has them. That affects who gets drugs and other support, and who interventions are trialled on. If the criteria for attention Deficit Hyperactivity Disorder (ADHD) are broadened, then more people are likely to be diagnosed with the condition.

The arrival of DSM-5 will mean the end of Asperger's syndrome in the professional eyes of the US psychiatric arena.

Along with some other autism-related conditions, Asperger's will now be consumed by the new category of "autism spectrum disorder".

Carol Povey

Some people diagnosed with Asperger's are unhappy about the coming change. Carol Povey, director of the National Autistic Society's Centre for Autism, said: "The term Asperger Syndrome is a core part of their identity for many people and they understandably feel anxious about moves to remove the term. The changes won't prevent people from continuing to use it to define themselves and nor should it," she said.

Debbie Tucker, chair of the Asperger's Syndrome Foundation, said the label can be useful in treating people, but that some did not want to be labelled. "Labels only become unhelpful and sometimes dangerous if used to discriminate. People with Aspergers are vulnerable to this," she said.

Thomas Inse

Last month, Thomas Insel, director of the National Institute of Mental Health, declared that the organisation would not use DSM-5 definitions to set its research priorities. Writing about DSM-5 on his blog, he said: "The weakness is its lack of validity. Unlike our definitions of ischaemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure."

Instead, he said the NIHM would lay the foundations for a new classification system, based on brain imaging, genetics, cognitive science and other research.

"We need to begin collecting the genetic, imaging, physiologic, and cognitive data to see how all the data – not just the symptoms – cluster and how these clusters relate to treatment response," he said.

Depression in Adolescent Girls linked to Father Absence

New research from the Children of the 90s study at the UK University of Bristol shows that girls whose fathers were absent during the first five years of life were more likely to develop depressive symptoms in adolescence than girls whose fathers left when they were aged five to ten years or than boys in both age groups (0-5 and 5-10). 

This finding has been found to be true, even after a range of factors was taken into account.

While previous studies have looked at the effect of childhood separation and divorce on the risk of depression in adolescence, this new research, published 15 May in Psychological Medicine, is one of only a few studies to look specifically at the effect of a father's absence and the timing of his departure on adolescents' mental health.

The study is one of the largest of its kind (5,631 children) and because Children of the 90s has charted the health and well-being of its participants since birth, it is one of only a few able to demonstrate a strong link between early childhood father absence and teenage girls' risk of depressive symptoms.

The finding has been found to be true, even after a wide range of other factors that can contribute to depression – including home ownership, social status, financial problems, family size, parental conflict, the mother's educational background and history of depression – are taken into account.

The authors say their findings are in line with previous studies suggesting that young children are more likely to suffer depression because they have developed fewer 'coping mechanisms' than older children, who also have more opportunities and resources to cope, as well as more social support networks, e.g. friends, outside the family.

Previous studies suggest that the stronger negative effect of father absence on the mental health of teenage girls over boys could be because girls are more vulnerable to negative interpersonal and family life events.

Iryna Culpin, the paper's lead author, said: "These findings indicate a need to include fathers in research related to child and adolescent mental health issues."

She also suggests that support for depression could be aimed at teenage girls whose father left before the age of five.

The authors highlight that it does not necessarily follow that a teenage girl who experiences depression as a teenager will continue to be affected later in life.

They also point out that the study did not examine the level of contact nor the quality of the relationship between a child and an absent father, all of which could influence the risk of depression.

More information: Culpin, I. et al. Father absence and depressive symptoms in adolescence: findings from a UK cohort, Psychological Medicine.

Depression: Patients Body Clocks are Altered at Cell Level

The researchers used gene expression patterns to try to predict the time of death for each person in the study (inner circles), and then compared it with the actual time of death (outer circles). 

The two matched closely in healthy people, as shown by the short lines between the two points in the left diagram. 

But in depressed people, the two were out of sync, as seen with the longer lines at right. 

Credit: Image courtesy of University of Michigan Health System

Every cell in our bodies runs on a 24-hour clock, tuned to the night-day, light-dark cycles that have ruled us since the dawn of humanity.

The brain acts as timekeeper, keeping the cellular clock in sync with the outside world so that it can govern our appetites, sleep, moods and much more.

But new research shows that the clock may be broken in the brains of people with depression -- even at the level of the gene activity inside their brain cells.

It's the first direct evidence of altered circadian rhythms in the brain of people with depression, and shows that they operate out of sync with the usual ingrained daily cycle.

The findings, in the Proceedings of the National Academy of Sciences, come from scientists from the University of Michigan Medical School and other institutions.

The discovery was made by sifting through massive amounts of data gleaned from donated brains of depressed and non-depressed people.

With further research, the findings could lead to more precise diagnosis and treatment for a condition that affects more than 350 million people worldwide.

What's more, the research also reveals a previously unknown daily rhythm to the activity of many genes across many areas of the brain -- expanding the sense of how crucial our master clock is.

In a normal brain, the pattern of gene activity at a given time of the day is so distinctive that the authors could use it to accurately estimate the hour of death of the brain donor, suggesting that studying this "stopped clock" could conceivably be useful in forensics.

By contrast, in severely depressed patients, the circadian clock was so disrupted that a patient's "day" pattern of gene activity could look like a "night" pattern -- and vice versa.

Read more of this article here

Journal Reference:

1. Jun Z. Li, Blynn G. Bunney, Fan Meng, Megan H. Hagenauer, David M. Walsh, Marquis P. Vawter, Simon J. Evans, Prabhakara V. Choudary, Preston Cartagena, Jack D. Barchas, Alan F. Schatzberg, Edward G. Jones, Richard M. Myers, Stanley J. Watson, Jr., Huda Akil, and William E. Bunney. Circadian patterns of gene expression in the human brain and disruption in major depressive disorder. PNAS, 2013 DOI: 10.1073/pnas.1305814110

Depression Stems from Miscommunication Between Brain Cells; Study Challenges Role of Serotonin in Depression

A new study from the University of Maryland School of Medicine suggests that depression results from a disturbance in the ability of brain cells to communicate with each other. 

Credit: © Artur Golbert / Fotolia

A new study from the University of Maryland School of Medicine suggests that depression results from a disturbance in the ability of brain cells to communicate with each other.

The study indicates a major shift in our understanding of how depression is caused and how it should be treated. Instead of focusing on the levels of hormone-like chemicals in the brain, such as serotonin, the scientists found that the transmission of excitatory signals between cells becomes abnormal in depression.

Scott M. Thompson

The research, by senior author Scott M. Thompson, Ph.D., Professor and Interim Chair of the Department of Physiology at the University of Maryland School of Medicine, was published online in the March 17 issue of Nature Neuroscience.

According to the Centers for Disease Control and Prevention, between 2005 and 2008, approximately one in 10 Americans were treated for depression, with women more than twice as likely as men to become depressed.

The most common antidepressant medications, such as Prozac (Fluoxetine), Zoloft (Setraline) and Celexa (Citalopram), work by preventing brain cells from absorbing serotonin, resulting in an increase in its concentration in the brain.

Unfortunately, these medications are effective in only about half of patients. Because elevation of serotonin makes some depressed patients feel better, it has been thought for over 50 years that the cause of depression must therefore be an insufficient level of serotonin.

The new University of Maryland study challenges that long-standing explanation.

"Dr. Thompson's groundbreaking research could alter the field of psychiatric medicine, changing how we understand the crippling public health problem of depression and other mental illness," says E. Albert Reece, M.D., Ph.D., M.B.A., Vice President for Medical Affairs at the University of Maryland and John Z. and Akiko K. Bowers Distinguished Professor and Dean at the University of Maryland School of Medicine.

"This is the type of cutting-edge science that we strive toward at the University of Maryland, where discoveries made in the laboratory can impact the clinical practice of medicine."

Depression affects more than a quarter of all U.S. adults at some point in their lives, and the World Health Organization (WHO) predicts that by 2020 it will be the second leading cause of disability worldwide.

Depression is also the leading risk factor for suicide, which causes twice as many deaths as murder, and is the third leading cause of death for 15-24 year olds.

The first major finding of the study was the discovery that serotonin has a previously unknown ability to strengthen the communication between brain cells.

"Like speaking louder to your companion at a noisy cocktail party, serotonin amplifies excitatory interactions in brain regions important for emotional and cognitive function and apparently helps to make sure that crucial conversations between neurons get heard," says Dr. Thompson.

"Then we asked, does this action of serotonin play any role in the therapeutic action of drugs like Prozac?"

To understand what might be wrong in the brains of patients with depression and how elevating serotonin might relieve their symptoms, the study team examined the brains of rats and mice that had been repeatedly exposed to various mildly stressful conditions, comparable to the types of psychological stressors that can trigger depression in people.

The researchers could tell that their animals became depressed because they lost their preference for things that are normally pleasurable.

For example, normal animals given a choice of drinking plain water or sugar water strongly prefer the sugary solution. Study animals exposed to repeated stress, however, lost their preference for the sugar water, indicating that they no longer found it rewarding.

This depression-like behaviour strongly mimics one hallmark of human depression, called anhedonia, in which patients no longer feel rewarded by the pleasures of a nice meal or a good movie, the love of their friends and family, and countless other daily interactions.

A comparison of the activity of the animals' brain cells in normal and stressed rats revealed that stress had no effect on the levels of serotonin in the 'depressed' brains.

Instead, it was the excitatory connections that responded to serotonin in strikingly different manner. These changes could be reversed by treating the stressed animals with antidepressants until their normal behaviour was restored.

"In the depressed brain, serotonin appears to be trying hard to amplify that cocktail party conversation, but the message still doesn't get through," says Dr. Thompson.

Using specially engineered mice created by collaborators at Johns Hopkins University School of Medicine, the study also revealed that the ability of serotonin to strengthen excitatory connections was required for drugs like antidepressants to work.

Sustained enhancement of communication between brain cells is considered one of the major processes underlying memory and learning.

The team's observations that excitatory brain cell function is altered in models of depression could explain why people with depression often have difficulty concentrating, remembering details, or making decisions.

Additionally, the findings suggest that the search for new and better antidepressant compounds should be shifted from drugs that elevate serotonin to drugs that strengthen excitatory connections.

"Although more work is needed, we believe that a malfunction of excitatory connections is fundamental to the origins of depression and that restoring normal communication in the brain, something that serotonin apparently does in successfully treated patients, is critical to relieving the symptoms of this devastating disease," Dr. Thompson explains.

The above story is reprinted from materials provided by University of Maryland Medical Center.

Depression: Is This Peptide a Key to Happiness?

What makes us happy? Family? Money? Love? How about a peptide? The neurochemical changes underlying human emotions and social behaviour are largely unknown. 

Now though, for the first time in humans, UCLA scientists have measured the release of a specific peptide, a neurotransmitter called hypocretin (Orexin), that greatly increased when subjects were happy but decreased when they were sad. 

Credit: © lassedesignen / Fotolia

The finding suggests that boosting hypocretin could elevate both mood and alertness in humans, thus laying the foundation for possible future treatments of psychiatric disorders like depression by targeting measureable abnormalities in brain chemistry.

In addition, the study measured for the first time the release of another peptide, this one called melanin concentrating hormone, or MCH.

Researchers found that its release was minimal in waking but greatly increased during sleep, suggesting a key role for this peptide in making humans sleepy.

The study is published in the March 5 online edition of the journal Nature Communications.

"The current findings explain the sleepiness of narcolepsy, as well as the depression that frequently accompanies this disorder," said senior author Jerome Siegel, a professor of psychiatry and director of the Center for Sleep Research at UCLA's Semel Institute for Neuroscience and Human Behavior.

"The findings also suggest that hypocretin deficiency may underlie depression from other causes."

In 2000, Siegel's team published findings showing that people suffering from narcolepsy, a neurological disorder characterized by uncontrollable periods of deep sleep, had 95 percent fewer hypocretin nerve cells in their brains than those without the illness.

The study was the first to show a possible biological cause of the disorder.

Since depression is strongly associated with narcolepsy, Siegel's lab began to explore hypocretin and its possible link to depression.

Depression is the leading cause of psychiatric disability in the U.S, Siegel noted. More than 6 percent of the population is affected each year, with lifetime prevalence exceeding 15 percent.

Yet the use of antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), has not been based on evidence of a deficiency, or excess, of any neurotransmitter. Several recent studies have questioned whether SSRIs, as well as other depression-fighting drugs, are any more effective than placebos.

In the current study, the researchers obtained their data on both hypocretin and MCH directly from the brains of eight patients who were being treated for intractable epilepsy.

The patients had been implanted with intra-cranial depth electrodes by Dr. Itzhak Fried, a UCLA professor of neurosurgery and psychiatry and a co-author of the study, to identify seizure foci for potential surgical treatment. The location of electrodes was based solely on clinical criteria.

The researchers, with the patients' consent, used these same electrodes to "piggyback" their research. A membrane similar to that used for kidney dialysis and a very sensitive radio-immunoassay procedure were used to measure the release of hypocretin and MCH.

The patients were recorded while they watched television; engaged in social interactions such as talking to physicians, nursing staff or family; ate; underwent various clinical manipulations; and experienced sleep-wake transitions.

Notes of activities were made throughout the study every 15 minutes in synchrony with a 15-minute microdialysis sample collection by a researcher in the patients' rooms.

The subjects rated their moods and attitudes on a questionnaire, which was administered every hour during waking.

The researchers found that hypocretin levels were not linked to arousal in general but were maximized during positive emotions, anger, social interactions and awakening.

In contrast, MCH levels were maximal during sleep onset and minimal during social interactions.

"These results suggest a previously unappreciated emotional specificity in the activation of arousal and sleep in humans," Siegel said.

"The findings suggest that abnormalities in the pattern of activation of these systems may contribute to a number of psychiatric disorders."

Siegel noted that hypocretin antagonists are now being developed by several drug companies for use as sleeping pills. The current work suggests that these drugs will alter mood as well sleep tendency.

The Siegel lab has also previously reported that hypocretin is required for the "pursuit of pleasure" in rodents but plays no role in avoidance behavior.

"These results, in conjunction with the current findings, suggest that hypocretin administration will elevate both mood and alertness in humans," Siegel said.

Childhood Bullying Has Long term Effects: Mood Disorders

Bullying by peers changes the structure surrounding a gene involved in regulating mood, making victims more vulnerable to mental health problems as they age.

This is the reported finding of a recent study by a researcher at the Centre for Studies on Human Stress (CSHS) at the Hôpital Louis-H. Lafontaine and professor at the Université de Montréal suggests that .

The study published in the journal Psychological Medicine seeks to better understand the mechanisms that explain how difficult experiences disrupt our response to stressful situations.

"Many people think that our genes are immutable; however this study suggests that environment, even the social environment, can affect their functioning. This is particularly the case for victimization experiences in childhood, which change not only our stress response but also the functioning of genes involved in mood regulation," says Isabelle Ouellet-Morin, lead author of the study.

A previous study by Ouellet-Morin, conducted at the Institute of Psychiatry in London (UK), showed that bullied children secrete less cortisol -- the stress hormone -- but had more problems with social interaction and aggressive behaviour.

The present study indicates that the reduction of cortisol, which occurs around the age of 12, is preceded two years earlier by a change in the structure surrounding a gene (SERT) that regulates or transports serotonin, and is a neurotransmitter involved in mood regulation and depression.

To achieve these results, 28 pairs of identical twins with a mean age of 10 years were analyzed separately according to their experiences of bullying by peers: one twin had been bullied at school while the other had not.

"Since they were identical twins living in the same conditions, changes in the chemical structure surrounding the gene cannot be explained by genetics or family environment. Our results suggest that victimization experiences are the source of these changes," says Ouellet-Morin.

According to the author, it would now be worthwhile to evaluate the possibility of reversing these psychological effects, in particular, through interventions at school and support for victims.

Stages of Grief - Is It Time For a New Model?

The face of Grief and mourning in our society is changing.

One wonders why the myth, that mourning or grieving happens in stages or phases, is still so prevalent in our enlightened society.

After all, there are other, more descriptive models that better describe the process. So what’s wrong with stage-based models of mourning?Well, several things.


Stage Theories
If there is a multitude of stage theories, which one is correct? There are theories involving three, four, five, six, seven, ten, and twelve different stages.

DABDA
The most famous model is a misapplication of Elizabeth Kubler-Ross’s five stages of coping with dying. The stages, popularly known by the acronym DABDA, include:

1. Denial — "I feel fine."; "This can't be happening, not to me."
   Denial is usually only a temporary defense for the individual. This feeling is generally replaced with heightened awareness of possessions and individuals that will be left behind after death. Denial can be conscious or unconscious refusal to accept facts, information, or the reality of the situation. Denial is a defense mechanism and some people can become locked in this stage.
2. Anger — "Why me? It's not fair!"; "How can this happen to me?"; '"Who is to blame?"
   Once in the second stage, the individual recognizes that denial cannot continue. Because of anger, the person is very difficult to care for due to misplaced feelings of rage and envy. Anger can manifest itself in different ways. People can be angry with themselves, or with others, and especially those who are close to them. It is important to remain detached and nonjudgmental when dealing with a person experiencing anger from grief.
3. Bargaining — "I'll do anything for a few more years."; "I will give my life savings if..."
   The third stage involves the hope that the individual can somehow postpone or delay death. Usually, the negotiation for an extended life is made with a higher power in exchange for a reformed lifestyle. Psychologically, the individual is saying, "I understand I will die, but if I could just do something to buy more time..." People facing less serious trauma can bargain or seek to negotiate a compromise. For example "Can we still be friends?.." when facing a break-up. Bargaining rarely provides a sustainable solution, especially if it's a matter of life or death.
4. Depression — "I'm so sad, why bother with anything?"; "I'm going to die soon so what's the point?"; "I miss my loved one, why go on?"
   During the fourth stage, the dying person begins to understand the certainty of death. Because of this, the individual may become silent, refuse visitors and spend much of the time crying and grieving. This process allows the dying person to disconnect from things of love and affection. It is not recommended to attempt to cheer up an individual who is in this stage. It is an important time for grieving that must be processed. Depression could be referred to as the dress rehearsal for the 'aftermath'. It is a kind of acceptance with emotional attachment. It's natural to feel sadness, regret, fear, and uncertainty when going through this stage. Feeling those emotions shows that the person has begun to accept the situation.
5. Acceptance — "It's going to be okay."; "I can't fight it, I may as well prepare for it."
   In this last stage, individuals begin to come to terms with their mortality, or that of a loved one, or other tragic event. This stage varies according to the person's situation. People dying can enter this stage a long time before the people they leave behind, who must pass through their own individual stages of dealing with the grief.

This model for mourning is the most egregious one since it is a totally erroneous application of her work.

Complex Process
Regardless of which one you chose, each stage theory attempts to portray a complex process involving the emotional, behavioral, cognitive, spiritual, and social facets of a person with a few simplistic terms.

While simplicity can help describe something, it can also be very misleading. There is no empirical proof that any stage-based model describes everyone’s bereavement experience.

The models have been based on observations of select populations and not, until recently, subjected to empirical study.

A Car Wash Approach

Stages imply that mourning is passive. A good analogy is a car wash. First is the “vacuuming the floor” stage, followed by the “clean the bugs off the windshield” stage, followed by the “wash, and rinse” stage, followed by the last stage - the “drying off” stage.

The car doesn’t do anything but be there, and everything happens to it so it comes out of the process bright and shiny clean. Mourning is not a passive process like a car wash; it is a highly active one.

Simple Expectations
Stage models create expectations of what mourning is supposed to be like. To me, this is a major shortcoming because of the potentially detrimental effect on the bereaved.

A widely published list of stages sets people up to expect certain reactions after the death of a loved one.

When those expectations don’t happen or don’t happen in the “correct” order, the bereaved individuals can think there is something wrong with them.

I have had several clients come to me stating they haven’t experienced one stage or another, and they're scared they're not grieving the way they should.

Once I explained to them that stages are an artificial construct, they were definitely relieved. There are typically enough complex and emotional possibilities for a bereaved person to work through, without adding whether he/she has adequately encountered all the 'defined' stages of grieving or whether the stages have occurred in the 'proper' sequence.


Conclusion
It is NOT a checklist that defines an established path. It is time we stopped trying to distill the inter-personal and intra-personal complexities of mourning into a simplistic template and a set of dogmatic steps.

Mourning is a highly individualistic process based on many complex factors in the bereaved person’s life.

It is a process for finding meaning in a distressing time of loss, transforming and /or creating a new relationship with the deceased, reintegrating the deceased into the bereaved person’s being, and learning how to live in the world under a new set of conditions and assumptions.

If you or anyone you know is experiencing difficulties dealing with their loss and bereavement then they should seek advice and support from a professional who can provide guidance and insight.

PTSD: Anti-anxiety Drug Calms Fears by Altering Brain Chemistry

An advance in understanding the brain’s fear circuitry has been revealed by a research team. They say it may hold particular promise for people at risk for anxiety disorders, including those suffering post-traumatic stress disorder (PTSD). Findings are reported in the journal Molecular Psychiatry.

“What is most compelling is our ability to translate first from mice to human neurobiology and then all the way out to human behaviour,” says Ahmad Hariri, a neurobiologist at Duke University. “That kind of translation is going to define the future of psychiatry and neuroscience.”

Read the original study DOI: 10.1038/mp.2012.72

 

The common thread in their studies is a gene encoding an enzyme called fatty acid amide hydrolase, or FAAH.

The enzyme breaks down a natural endo-cannabinoid chemical in the brain that acts in essentially the same way that Cannabis, aka marijuana, does (hence the name endo-cannabinoid).

Earlier studies had suggested that blocking the FAAH enzyme could decrease fear and anxiety by increasing endo-cannabinoids, which is consistent with the decreased anxiety some experience after smoking marijuana.

In 2009, Hariri’s lab found that a common variant in the human FAAH gene leads to decreased enzyme function with affects on the brain’s circuitry for processing fear and anxiety.

In the new study, Andrew Holmes’ group at the National Institute on Alcoholism and Alcohol Abuse tested the effects of a drug that blocks FAAH activity in fear-prone mice that had also been trained to be fearful through experiences in which they were delivered foot shocks.

Tests for the ability of those mice to get over their bad experiences found that the drug allowed a faster recovery from fear thanks to higher brain endo-cannabinoid levels.

More specifically, the researchers showed that those drug effects traced to the amygdala, a small area of the brain that serves as a critical hub for fear processing and learning.

To test for the human relevance of the findings, Hariri’s group went back to the genetic variant they had studied earlier in a group of middle-aged adults.

They showed study participants a series of pictures depicting threatening faces while they monitored the activity of their amygdalas using functional magnetic resonance imaging (fMRI) scans. They then looked for how the genetic variant affected this activity.

While the activity of the amygdala in all participants decreased over repeated exposures to the pictures. But people who carried the version of the FAAH gene associated with lower enzyme function and higher endo-cannabinoid levels showed a greater decrease in activity.

Hariri says that suggests that those individuals may be better able to control and regulate their fear response.

Further confirmation came from an analysis led by Duke’s Avshalom Caspi and Terrie Moffitt of 1,000 individuals in the Dunedin Study, who have been under careful observation since their birth in the 1970s in New Zealand.

Consistent with the mouse and brain imaging studies, those New Zealanders carrying the lower-expressing version of the FAAH gene were found to be more likely to keep their cool under stress.

“This study in mice reveals how a drug that boosts one of the brain’s naturally occurring endo-cannaboids enables fear extinction, a process that forms the basis of exposure therapy for PTSD,” Holmes says.

“It also shows how human gene variation in the same chemical pathways modulates the amygdala’s processing of threats and predicts how well people cope with stress.”

Studies are now needed to further explore both the connections between FAAH variation and PTSD risk as well as the potential of FAAH inhibition as a novel therapy for fear-related disorders, the researchers say.

More news from Duke University: http://today.duke.edu/

Antidepressants in water trigger Autism genes in fish

Low levels of antidepressants and other psychoactive drugs in water supplies can trigger the expression of genes associated with autism, in fish at least.

The use of antidepressants has increased dramatically over the past 25 years, says Michael Thomas of Idaho State University in Pocatello. 

Around 80 per cent of each drug passes straight through the human body without being broken down, and so they are present in waste water. In most communities, water purification systems cannot filter out these pharmaceuticals. 

"They just fly right through," says Thomas, which means they ultimately find their way into the water supply.

The concentration of these drugs in drinking water is very low – at most, they are present at levels several orders of magnitude lower than the prescription doses. 

But since the drugs are specifically designed to act on the nervous system, Thomas hypothesised that even a small dose could affect a developing fetus.

Thomas's group created a cocktail of the anti-epileptic drug carbamazepine and two selective serotonin uptake inhibitor (SSRI) antidepressants, fluoxetine and venlafaxine, at this low concentration. 

They exposed fathead minnows (Pimephales promelas) to the drugs for 18 days, then analysed the genes that were being expressed in the fishes' brains.

Although the researchers had expected the drugs might activate genes involved in all kinds of neurological disorders, only 324 genes associated with autism in humans appeared to be significantly altered. Most of these genes are involved in early brain development and wiring.

The finding fits with previous research which had found that pregnant women who take SSRIs are slightly more likely to have autistic children. (Archives of General Psychiatry, DOI: 10.1001/archgenpsychiatry.2011.73).

To test whether these changes actually altered the fish's behaviour, the researchers did an experiment in which they startled the fish. Fish exposed to the drugs tended to panic and behave differently from a control group of fish.

Thomas emphasises that the research is very preliminary – there's no need for pregnant women to worry about their drinking water yet, he says. The researchers next plan to study whether the drugs have a similar effect in mammals. 

They are testing this by lacing the drinking water of pregnant mice with the low-concentration cocktail. 

They are also studying water supplies in areas around the country where there are particularly high concentrations of drugs to determine whether the fish – and people – in these areas have autism-like gene expression patterns.

Journal reference: PLoS One, DOI: 10.1371/journal.pone.0032917

Three Messages You Should Never Give to Kids about Anxiety

Kids don’t generally develop anxiety disorders all on their own. Oh sure, genes and biology have some influence, but these factors largely just predispose kids in the direction of acquiring problems with anxiety.

The wrong messages can push both anxiously disposed kids as well as otherwise normal kids in the direction of struggling with anxiety for the rest of their lives.

If you’re a parent or someone who cares about kids, you just might want to know what type of messages instill insecurity.

Let's start by laying out three common mistakes that parents make; in other words, the kinds of messages you “don’t” want to give them:

1. Invalidating or Denying Your Children’s Feelings. If your kids seem worried, fearful, upset, or distraught, sometimes it’s tempting to tell them “there’s no reason that they should feel that way” or even that they “shouldn’t” be feeling what they are obviously feeling. Parents give these messages because they don’t want their kids to feel distress. So, they reason that their kids will understand, if their bad feelings have no real basis, they won’t feel the way they do. Big mistake. Children need to hear that it’s normal and OK to have a little fear or distress sometimes.
2. Providing Incessant Reassurance. Messages that “everything will turn out OK” sound so very much like what you should tell kids, and if you don’t say them too often, there’ll probably be no problem. However, when you frequently reassure your kids, you end up giving them the message that they need to turn to you (as an adult or parent) to help them see that things will turn out alright. They fail to learn that they can get through fear on their own. 
3. Protecting Your Kids from All Harm. No one ever wants to see a child in harm’s way. However, growing, developing and learning require kids to face challenges and even take a few small risks along the way. Parents that try to constantly clear all dangers and risks that their kids confront teach them that the world is a scary place and that they need their parents to guide them through it. That message hardly fosters the independence and maturity they’ll need as adolescents and young adults.

So what’s a parent to do instead? One of the best ways to help prevent kids from developing anxiety disorders is to model how to cope.

I recommend that parents express when they’re feeling anxious and tell their kids how they plan to cope with it. For example, you might say, “Sometimes I feel nervous when I have to climb a ladder, but I just need to take a deep breath, be careful, and do it.

If I get too nervous, I can always climb back down, but it feels good to get through difficult tasks.”

Another good strategy is for parents to praise their kids when they make efforts to do things that are a little anxiety arousing for them.

The bottom line: Gently encourage your kids to confront their fears, let them know that a little anxiety is normal, and don’t try to keep them away from all challenges and risks.

Teenage Depression: SPARX Game as effective as Traditional Treatment

An innovative computer-based intervention for depressed young people, developed by researchers from The University of Auckland, has been shown to be at least as effective as standard treatments mainly comprising face-to-face therapy.

A research team led by Associate Professor Sally Merry developed and trialled the intervention called SPARX with the aim of giving young people easier, lower cost access to treatment.

In a study published in the British Medical Journal (BMJ) they assessed the effectiveness of SPARX in 24 sites around New Zealand, including youth clinics, schools and general practices.

Half of the young people participating used the new game and half received standard treatment through their doctor, school counsellor or other provider. SPARX was shown to be at least as good as the standard treatments.

SPARX uses CD-Rom based computer gaming to teach self-help for depression. It includes an interactive 3D fantasy game to teach young people the skills they need to cope with challenges and manage their mood.

In contrast to many other e-therapies, SPARX has been designed to help young people learn through action in a virtual world. It is based on cognitive behavioural therapy, a proven therapeutic approach.

“Using computer technology that young people are comfortable with is one way of making therapy more accessible, practical, and hopefully more fun,” says Dr Merry.

It has been designed to be easily accessed by young people directly or to be delivered easily in primary care settings. In 2011, SPARX won a UN World Summit Award recognising creativity and innovation in e-health interventions.

 

Depression is common among young people internationally and accessing help can be difficult. One in five New Zealanders will have experienced clinical depression by their eighteenth birthday.

Three quarters of young people with depression never receive treatment. “We want to intervene earlier and more effectively,” says Dr Merry.

SPARX was initiated by researchers, clinicians, and learning technologists at the University’s Werry Centre for Child and Adolescent Mental Health in the Department of Psychological Medicine.

It was developed with input from Māori, Pacific people, and other cultural groups in New Zealand. The programme was created with the assistance of a local game development company, Metia Interactive.

A number of actors, musicians and artists have generously donated their time and skills to the project.

The work was funded by the NZ Ministry of Health as part of the Primary Health Care Strategy to build and strengthen the capacity of the primary care sector to respond to mental health needs, and in this case adolescent depression.

More information on SPARX is available on www.sparx.org.nz.

Drugs: Speed and Ecstasy Use Linked to Teen Depression

The use of speed and ecstasy by secondary school pupils appears to increase the risk of depression by up to 70 percent, a study claims.

Scientists at the University of Montreal carried out research on almost 4,000 secondary school pupils to explore concerns that the two drugs, which have spread from the clubbing scene into schools, could cause long-term damage.

The study, published in the Journal of Epidemiology and Community Health, found that those students who used either drug were between 60 and 70 percent more likely to exhibit heightened symptoms of depression.

The authors tracked the mental health of a sample of 3,880 teenagers from deprived areas in Quebec between 2003 and 2008, quizzing them on their drug use and later testing their mental health on a validated scale.

The use of speed (meth/amphetamine) was found to be more common, with 11.6 percent (451) admitting taking it, while 8 percent (310) admitted taking ecstasy (MDMA).

The use of both drugs was admitted by 6.7 percent of the sample. Teenagers in this group were found to be twice as likely to have depressive symptoms as those who used neither drug.

The authors claimed this pointed toward "additive or synergistic adverse effects of concurrent use".

"Our results provide, to the best of our knowledge, the first compelling evidence that recreational [ecstasy] and [speed] use places developing secondary school students at greater risk of experiencing depressive symptoms," the researchers concluded.

While they admit that the causative contribution of drug use itself to depression is "relatively modest", they caution that even a modest contribution can have "significant clinical implications from a population health perspective".

They propose that further research should be undertaken to look into whether depressive symptoms are an effect of neurological damage, which adolescent brains could be more susceptible to, and are keen to examine the differences between adults and adolescents in this area.

Speed, or amphetamine, is a widely used drug in the clubbing and rave scene. The drug make people more awake, overactive and chatty. it is generally followed by a long comedown and can put a strain on the user's heart. It can also lead to anxiety, aggression and paranoia.

Ecstasy is popular because it makes users feel energetic and happy, allowing them to stay up partying into the early hours. Its use has been linked to liver, kidney and heart problems, while its comedown often leads users to feel lethargic or depressed.

Blood Test Diagnoses Depression In Teens

Diagnosing depression may soon include a simple blood test, according to research published Tuesday. new study. Researchers developed a blood test to identify markers for depression in teenagers that maylead to better treatments and lessen the stigma surrounding the condition.

Doctors currently rely on patients coming forward with symptoms to diagnose depression. However, differentiating between types of depression can be difficult without an objective diagnosis, researchers said. Instead, using a diagnostic blood test could allow for more personalized treatment.

"Right now depression is treated with a blunt instrument," Dr. Eva Redei, study author and professor of psychiatry at Northwestern University, said in a statement. "It's like treating type 1 diabetes and type 2 diabetes exactly the same way. We need to do better."

Previous studies identified 26 potential genetic markers for depression in rats. Redei and her team found 11 similar markers in depressed teens that they did not find in the control group.

"These 11 genes are probably the tip of the iceberg because depression is a complex illness," Redei said in a statement. "But it's an entree into a much bigger phenomenon that has to be explored. It clearly indicates we can diagnose from blood and create a blood diagnosis test for depression."

Some doctors remain skeptical of the findings since the study examined only 28 volunteers. Skeptics said research needs to show whether the markers can test a wider population and whether the markers are present in adults as well before the test can be considered viable.

"I think people are looking for a magic bullet, a single answer," Dr. Carol Bernstein, an associate professor of psychiatry at New York University, told ABC News. "But these disorders are much too complicated."

One in 20 Americans over the age of 12 reported feeling symptoms of depression between 2005 and 2006, according to the Centers for Disease Control and Prevention. Symptoms include hopelessness, feeling like a failure, poor appetite and lack of interest in activities.

Depression affects approximately 1 percent of children under the age of 12, researchers said. But as children enter their teenage years, depression affects almost 25 percent. Depression that sets in during the teenage years has a poorer prognosis than depression that sets in in adulthood, increasing the risk of substance abuse, suicide and physical illness, researchers said.

Being able to diagnose depression with a blood test could mean more people getting treatment. None of the teens who were diagnosed with depression over the course of the study opted for treatment, most likely due to the stigma that comes with it, Redei said.

Depression is treated through a combination of medication and therapy, but many people see the disease as a defect and think it will make people view them as "broken", Dr. Jonathan Rottenberg, an associate professor of psychology at the University of South Florida, said in a Psychology Today blog post.

 The journal Translational Psychiatry published the study on Tuesday.

Antidepressants During Pregnancy: What Are the Risks?

What is a woman struggling with depression supposed to do when she becomes pregnant?

A study published on Monday in the Archives of General Psychiatry tackles the tough decision of deciding to keep taking the medication, or risk harming the fetus.

Roughly six percent of pregnant women are taking antidepressants. The struggle to live with depression or risk your baby's health has plagued women for quite some time.

The latest study included 7,696 pregnant women. Five hundred and seventy of the women suffering from depression were not on medication, and 99 women with depression "were being treated with selective serotonin reuptake inhibitors (SSRIs), a common class of antidepressants."

What this study found is that women going untreated for depression gave birth to babies that had a reduction in total body growth.

This affected the fetal head growth as well. Those women taking prenatal SSRI also had babies that suffered from a reduced growth of the fetal head, but the overall growth of the body during pregnancy was not affected.

What are the risks for the fetus during pregnancy with antidepressants? Mothers taking antidepressants could have preterm babies, who face higher health risks like respiratory and gastrointestinal disorders.

Not only could these children be born preterm, but according to the authors of the study, reduced fetal head-growth can lead to behavioural problems and psychiatric disorders later on.

However, the risks for the mother may outweigh the risks of the pregnancy, if she discontinues antidepressant medication.

Dr. Sudeepta Varma, clinical assistant professor of psychiatry at NYU Langone School of Medicine reported "If we are talking about a woman who can't take care of her health as a result of battling with moderate to severe depression, she faces risks to herself as well as the baby that are associated with untreated depression during pregnancy."

According to Varma, "if you don't take care of the mom, there may be no baby to speak of."

These findings however are inconclusive according to the authors of the study. "More long-term drug safety studies are needed before evidence-based recommendations can be derived," concluded the authors.