Antidepressants are prescription drugs used to treat depression and a variety of other psychological conditions such as anxiety, panic, posttraumatic stress disorder (PTSD) and obsessive compulsive disorder (OCD). Some depression drugs are also used to treat medical conditions (e.g. some tricyclic antidepressants are given for chronic pain).
Here is a list of helpful information about antidepressants (not in order of importance).
Antidepressants help correct chemical imbalances in your brain by affecting certain brain chemicals called neurotransmitters, which are responsible for sending messages between nerve cells. Neurotransmitters are responsible for different functions in the body. For example, some antidepressants help alleviate depression by increasing the neurotransmitter, Serotonin which plays a role in a variety of functions such as mood, appetite, sleep, memory and sexual behavior. Other antidepressants increase the neurotransmitters, Norepinephrine and Dopamine. Norepinephrine manages functions in the sympathetic nervous system (e.g. fight or flight response, blood pressure, heart rate and concentration) while Dopamine plays a part in emotion, learning, motivation, pleasure, memory, movement and other roles.
There are basically three major types of antidepressants. The different categories of antidepressants differ in terms of the neurotransmitters affected and the process involved in increasing these neurotransmitters.
Selective Serotonin Reuptake Inhibitors (SSRI) - SSRIs (e.g. Zoloft, Lexapro, Prozac, Paxil, Celexa) are the most commonly prescribed antidepressants. SSRIs increase the amount of Serotonin by hindering the process involved in eliminating Serotonin (which is called Reuptake). After Serotonin is released from a nerve cell, the Reuptake process removes any Serotonin that is not used. Since the re-absorption of Serotonin is blocked, the level of Serotonin is increased.
Tricyclic Antidepressants (TCA) - TCAs (e.g. Elavil, Nortriptyline) increase Seratonin, Norepinephrine and Dopamine by also blocking the Reuptake process (the removal of these neurotransmitters). Because of more adverse side effects, TCAs are prescribed less often than SSRIs.
Monoamine Oxidase Inhibitors (MAOI) - MAOIs (e.g. Nardil, Marplan) inhibit the action of an enzyme called monoamine oxidase, which breaks down certain neurotransmitters. As a result, the amounts of Serotonin and Norepinephrine are increased. MAOIs are less prescribed than SSRIs and TCAs because of possible severe side effects and drug interactions. They are often used to treat depression that has not responded to other depression medications.
There are other antidepressants that don't fall in any of the above categories, which affect a different combination of neurotransmitters. For example, Wellbutrin is a Dopamine and Norepinephrine Reuptake Inhibitors (DNRI), which increases both Dopamine and Norepinephrine by blocking the removal of these two neurotransmitters.
Be patient when working with your doctor. It often takes several tries to find the right antidepressant. A doctor will select the most appropriate antidepressant based on your symptoms, the antidepressant's potential side effects, your medical conditions and any medications you're taking. Because of the many antidepressants on the market today, doctors have many options to choose from. So don't worry if the first antidepressant is not working well for you.
Antidepressants are not a quick fix and take time to work. They often take several weeks (or more) before positive results are noticed. Because everyone's brain chemistry is different, antidepressants will affect individuals differently.
Each antidepressant will have its own particular side effects. Many side effects are temporary and will go away once your body adjusts to the medication. Ask your doctor about the typical side effects, how long they may last and when you should contact your doctor.
Don't stop antidepressants too early. If you do, the chances of re-experiencing depression are increased. For most people, it is not necessary to take antidepressants for the rest of your life. Many individuals take antidepressants for six months to a year or more.
The beliefs that antidepressants will change your personality or not allow you to feel are myths. If you truly need antidepressants, they should make you feel better and not worse. If you feel any of these concerns, talk to your doctor. You may be on the wrong medication or dose.
Antidepressants are not habit forming (addictive). Often people cope with depression and other problems in less healthy ways such as using alcohol or illicit drugs. Taking depression medication is a healthier alternative with less negative consequences.
Don't stop taking antidepressants without talking to your doctor first. For example, some SSRIs (e.g. Paxil) which are short-acting (stays in the body for a short period of time) may cause withdrawal like symptoms if they are stopped suddenly or dosage is reduced too quickly. If you stop or reduce certain SSRIs suddenly, you may experience SSRI Discontinuation Syndrome which is characterized by flu like symptoms such as nausea, chills, diarrhea, fatigue, headache, vomiting and dizziness. See a doctor if you start to experience these symptoms.
There has been recent concern about using antidepressants with children. Short-term studies have shown that children using antidepressants have an increased risk of suicidal thinking and behavior in the first few months of treatment. Children should be closely monitored when beginning antidepressants or changing dosage. Likewise, adults who have depression (or other psychiatric conditions) and a history of suicidal behavior should also be closely watched.
About the Author
Dr. Joanne Chao is a psychologist practicing in California and is the editor of Depression Help Resource, a website providing information about antidepressants, treatment options and depression related articles and resources.
depression-help-resource
View drug information on Celexa; Lexapro; Marplan Tablets.
понедельник, 30 мая 2011 г.
суббота, 28 мая 2011 г.
Untreated Depressed People Have Fewer Serotonin & Opioid Receptors, And Variation Is Linked To Symptoms And Treatment Response
Depressed people may have far fewer of the receptors for some of the brain's "feel good" stress-response chemicals than non-depressed people, new University of Michigan Depression Center research shows.
And even among depressed people, the numbers of these receptors can vary greatly. What's more, the number of receptors a depressed person has appears to be linked with the severity of their symptoms - and the chances that they'll feel better after taking a medication.
These preliminary findings, presented at the American Psychiatric Association's annual meeting in Washington, D.C., amplify a growing understanding of depression as a condition that affects different people in different ways, and is solidly rooted in genetic and molecular factors that are unique to each individual.
The lead U-M researcher, Jon-Kar Zubieta, M.D., Ph.D., says these new results bolster what other researchers have been finding in recent years.
"There's a substantial amount of biological difference even among people who have major depression, which is just as important as the biological differences between people with depression and people without," he says. "The more we can understand about these differences, the better we can address treatment to the individual and have the greatest effect on symptoms."
At the APA meeting, Zubieta presented data from positron emission tomography, or PET, scans of the brains of patients who met the criteria for major depression but had not yet received treatment for it. Those scans were compared with scans of the brains of non-depressed comparison volunteers.
In one group of depressed and non-depressed volunteers, the scans were made using a tracer that can reveal the location and concentration of a particular type of receptor. Called the 5HT1a receptor, it allows brain cells to receive signals from serotonin, a chemical neurotransmitter produced by the brain.
Serotonin levels in the brain are linked to depression, but the importance of 5HT1a receptor concentrations in the brains of depressed people has been cloudy. That's why Zubieta's team chose to scan only people who had not yet received antidepressant medications, since some such medications may actually encourage the brain's cells to make more serotonin receptors - and masking the actual level of receptors that the person has naturally.
In the study, 5HT1a receptor concentrations were markedly lower in depressed people compared with non-depressed people, in both the left and right hippocampus region of the brain.
But even among depressed people, the lower a person's the 5HT1 receptor levels were, the worse he or she scored on assessments of their ability to function day-to-day - and they less likely he or she was to get relief from symptoms when the researchers prescribed them a common antidepressant.
This finding of individual variation may help explain why in current depression treatment, some patients find great relief from a medication that doesn't help other equally depressed patients, says Zubieta, who is the Phil F. Jenkins Research Professor of Depression in the U-M Department of Psychiatry. He also holds positions in the U-M Nuclear Medicine division, and the Molecular & Behavioral Neuroscience Institute.
The other group of depressed volunteers - both depressed and non-depressed - received PET scans with a tracer that allowed the researchers to see the mu-opioid receptors in their brains. These receptors are the gateway for signals sent by chemicals called endogenous opioids -- the brain's natural "painkillers" - which are involved in stress response including response to pain.
Another name for the neurotransmitters that bind to mu-opioid receptors is endorphins, which have become known as a "feel good" chemical involved in reinforcing rewarding experiences. Illicit drugs such as heroin also act upon mu-opioid receptors, creating the "high" sensation and probably playing a role in the addiction process.
In this group of depressed and non-depressed volunteers, the researchers studied the distribution of the mu-opioid receptors and looked at how active the receptors were when the volunteers were asked to summon a sad memory or scenario to mind.
Depressed volunteers had lower concentrations of mu-opioid receptors to begin with. But when they underwent the "sadness challenge", those receptors were much more active than the receptors in non-depressed people. And, just as with the serotonin 5HT1a receptors, the fewer mu-opioid receptors a person had, the less well they responded to an antidepressant medication.
Zubieta and his colleagues are now working to submit these new data for publication. At the same time, they are continuing to recruit depressed volunteers who are not taking medication for more brain imaging studies. To find out more about how to participate in depression research at the U-M Depression Center, visit umengage/.
For more on research by Zubieta and other researchers at the U-M Depression Center, visit depressioncenter/.
The study was funded by the National Institutes of Health, the Pritzker Foundation, and by NARSAD, a leading mental health charity.
What are Opioids?
For more information on what opioids are, and opioid-induced constipation (OIC), please see:
All About Opioids and Opioid-Induced Constipation (OIC)
And even among depressed people, the numbers of these receptors can vary greatly. What's more, the number of receptors a depressed person has appears to be linked with the severity of their symptoms - and the chances that they'll feel better after taking a medication.
These preliminary findings, presented at the American Psychiatric Association's annual meeting in Washington, D.C., amplify a growing understanding of depression as a condition that affects different people in different ways, and is solidly rooted in genetic and molecular factors that are unique to each individual.
The lead U-M researcher, Jon-Kar Zubieta, M.D., Ph.D., says these new results bolster what other researchers have been finding in recent years.
"There's a substantial amount of biological difference even among people who have major depression, which is just as important as the biological differences between people with depression and people without," he says. "The more we can understand about these differences, the better we can address treatment to the individual and have the greatest effect on symptoms."
At the APA meeting, Zubieta presented data from positron emission tomography, or PET, scans of the brains of patients who met the criteria for major depression but had not yet received treatment for it. Those scans were compared with scans of the brains of non-depressed comparison volunteers.
In one group of depressed and non-depressed volunteers, the scans were made using a tracer that can reveal the location and concentration of a particular type of receptor. Called the 5HT1a receptor, it allows brain cells to receive signals from serotonin, a chemical neurotransmitter produced by the brain.
Serotonin levels in the brain are linked to depression, but the importance of 5HT1a receptor concentrations in the brains of depressed people has been cloudy. That's why Zubieta's team chose to scan only people who had not yet received antidepressant medications, since some such medications may actually encourage the brain's cells to make more serotonin receptors - and masking the actual level of receptors that the person has naturally.
In the study, 5HT1a receptor concentrations were markedly lower in depressed people compared with non-depressed people, in both the left and right hippocampus region of the brain.
But even among depressed people, the lower a person's the 5HT1 receptor levels were, the worse he or she scored on assessments of their ability to function day-to-day - and they less likely he or she was to get relief from symptoms when the researchers prescribed them a common antidepressant.
This finding of individual variation may help explain why in current depression treatment, some patients find great relief from a medication that doesn't help other equally depressed patients, says Zubieta, who is the Phil F. Jenkins Research Professor of Depression in the U-M Department of Psychiatry. He also holds positions in the U-M Nuclear Medicine division, and the Molecular & Behavioral Neuroscience Institute.
The other group of depressed volunteers - both depressed and non-depressed - received PET scans with a tracer that allowed the researchers to see the mu-opioid receptors in their brains. These receptors are the gateway for signals sent by chemicals called endogenous opioids -- the brain's natural "painkillers" - which are involved in stress response including response to pain.
Another name for the neurotransmitters that bind to mu-opioid receptors is endorphins, which have become known as a "feel good" chemical involved in reinforcing rewarding experiences. Illicit drugs such as heroin also act upon mu-opioid receptors, creating the "high" sensation and probably playing a role in the addiction process.
In this group of depressed and non-depressed volunteers, the researchers studied the distribution of the mu-opioid receptors and looked at how active the receptors were when the volunteers were asked to summon a sad memory or scenario to mind.
Depressed volunteers had lower concentrations of mu-opioid receptors to begin with. But when they underwent the "sadness challenge", those receptors were much more active than the receptors in non-depressed people. And, just as with the serotonin 5HT1a receptors, the fewer mu-opioid receptors a person had, the less well they responded to an antidepressant medication.
Zubieta and his colleagues are now working to submit these new data for publication. At the same time, they are continuing to recruit depressed volunteers who are not taking medication for more brain imaging studies. To find out more about how to participate in depression research at the U-M Depression Center, visit umengage/.
For more on research by Zubieta and other researchers at the U-M Depression Center, visit depressioncenter/.
The study was funded by the National Institutes of Health, the Pritzker Foundation, and by NARSAD, a leading mental health charity.
What are Opioids?
For more information on what opioids are, and opioid-induced constipation (OIC), please see:
All About Opioids and Opioid-Induced Constipation (OIC)
четверг, 26 мая 2011 г.
Mental Health 101 - American Psychiatric Association
Across the country, students are preparing to start or return to college. This is an
exciting time, though for some it's overwhelming and stressful. Depression, substance use and eating
disorders are increasingly common mental health issues on college campuses. According to a recent
survey1, the rate of students reporting ever being diagnosed with depression has increased 56 percent
in the last six years, from 10 percent in spring 2000 to 16 percent in spring 2005.
Major depression increases the likelihood of substance abuse, impairs functioning at school; and
influences an individual's subsequent development in negative ways. Depression can also co-occur
with other disorders, including physical illnesses and other mental disorders, such as anxiety and
eating disorders.
"We are seeing more students coming to college with mental health issues," said Jerald Kay, M.D.,
chair of the American Psychiatric Association's Corresponding Committee on Mental Health on
College and University Campuses. "Tragedies like at Virginia Tech only amplify the importance of
the availability of mental health services on college campuses. It is important for college-age students
to seek care so they can have a healthy mind and lead a healthy life."
The American Psychiatric Association (APA) encourages everyone to learn more about the warnings
signs of mental illnesses. For August, HealthyMinds, the APA's free consumer Web site,
features information to help parents learn more about college mental health on topics such as:
-- NEW: Suicide Prevention TV Public Service Announcement
-- "Let's Talk Facts" brochure: College Students and Alcohol Abuse
-- College Students and Alcohol Abuse Statistics
-- College Mental Health Fact Sheet: Depression
-- Disasters: Mental Health Recommendations for Students and Colleges
-- Eating Disorders: Tips for College Students
About the American Psychiatric Association
The American Psychiatric Association is the nation's leading medical specialty society whose more than 38,000
physician members specialize in diagnosis, treatment, prevention and research of mental illnesses including
substance use disorders. Visit the APA at psych and HealthyMinds.
"Healthy Minds. Healthy Lives." is APA's consumer campaign to improve understanding of mental illnesses,
psychiatry, and successful treatment options, as well as to reduce stigma. Learn more about these issues and
hear people's real-life stories by visiting the campaign's Web site at HealthyMinds .
1 American College Health Association. American College Health Association-National College Health
Assessment: Reference Group Executive Summary Fall 2006. Baltimore: American College Health
Association; 2007.
exciting time, though for some it's overwhelming and stressful. Depression, substance use and eating
disorders are increasingly common mental health issues on college campuses. According to a recent
survey1, the rate of students reporting ever being diagnosed with depression has increased 56 percent
in the last six years, from 10 percent in spring 2000 to 16 percent in spring 2005.
Major depression increases the likelihood of substance abuse, impairs functioning at school; and
influences an individual's subsequent development in negative ways. Depression can also co-occur
with other disorders, including physical illnesses and other mental disorders, such as anxiety and
eating disorders.
"We are seeing more students coming to college with mental health issues," said Jerald Kay, M.D.,
chair of the American Psychiatric Association's Corresponding Committee on Mental Health on
College and University Campuses. "Tragedies like at Virginia Tech only amplify the importance of
the availability of mental health services on college campuses. It is important for college-age students
to seek care so they can have a healthy mind and lead a healthy life."
The American Psychiatric Association (APA) encourages everyone to learn more about the warnings
signs of mental illnesses. For August, HealthyMinds, the APA's free consumer Web site,
features information to help parents learn more about college mental health on topics such as:
-- NEW: Suicide Prevention TV Public Service Announcement
-- "Let's Talk Facts" brochure: College Students and Alcohol Abuse
-- College Students and Alcohol Abuse Statistics
-- College Mental Health Fact Sheet: Depression
-- Disasters: Mental Health Recommendations for Students and Colleges
-- Eating Disorders: Tips for College Students
About the American Psychiatric Association
The American Psychiatric Association is the nation's leading medical specialty society whose more than 38,000
physician members specialize in diagnosis, treatment, prevention and research of mental illnesses including
substance use disorders. Visit the APA at psych and HealthyMinds.
"Healthy Minds. Healthy Lives." is APA's consumer campaign to improve understanding of mental illnesses,
psychiatry, and successful treatment options, as well as to reduce stigma. Learn more about these issues and
hear people's real-life stories by visiting the campaign's Web site at HealthyMinds .
1 American College Health Association. American College Health Association-National College Health
Assessment: Reference Group Executive Summary Fall 2006. Baltimore: American College Health
Association; 2007.
вторник, 24 мая 2011 г.
A New Troublesome Long-Term Effect Of Antidepressant Drugs; Tardive Dysphoria.
Treatment-resistant depression (TRD) may be related to inadequate dosing of antidepressants or antidepressant tolerance. Alternatively, there are reasons to believe that antidepressant treatment itself may contribute to a chronic depressive syndrome. This study reports a case of antidepressant discontinuation in a TRD patient, a 67-year-old white man with onset of major depressive illness at the age of 45. He was homozygous for the short form of the serotonin transporter. He was treated off and on until the age of 59 and had been on an antidepressant continuously until the age of 67. Over the previous 2 years he had been depressed without any relief by medication or 2 electroconvulsive treatments. His medications at the time of evaluation included paroxetine 10 mg daily, venlafaxine 75 mg daily and clonazepam 3 mg daily. His 17-item Hamilton depression score was 22. Over the subsequent 6 months, he was started on bupropion and then tapered off all antidepressants, including the bupropion. His Hamilton depression score dropped to 18. The patient was not satisfied with his progress and sought another opinion to restart antidepressants. One year later, on duloxetine 60 mg daily, he continued to complain of unremitting depression.
A possible prodepressant effect of antidepressants has been previously proposed. Fava was the first to suggest that an antidepressant-related neurobiochemical mechanism of increasing vulnerability to depression might play a role in worsening the long-term outcome of the illness. Understanding of potential mechanisms of this phenomenon can be gleaned from observations regarding the short form of the serotonin transporter (5HTTR). Patients with the short form of the 5HTTR and prolonged antidepressant exposure, may be particularly vulnerable to antidepressant-related worsening. In other words, prolonged exposure to antidepressants can induce neuroplastic changes that result in the genesis of antidepressant-induced dysphoric symptoms. The investigators propose the term 'tardive dysphoria' to describe such a phenomenon and describe diagnostic criteria for it. Tapering or discontinuing the antidepressant might reverse the dysphoric state. Antidepressant discontinuation may not provide immediate relief. In fact, it is likely that transient symptoms of withdrawal will occur in the initial 2-4 weeks following antidepressant discontinuation or tapering. However, after a prolonged period of antidepressant abstinence, one may see a gradual return to the patient's baseline.
A possible prodepressant effect of antidepressants has been previously proposed. Fava was the first to suggest that an antidepressant-related neurobiochemical mechanism of increasing vulnerability to depression might play a role in worsening the long-term outcome of the illness. Understanding of potential mechanisms of this phenomenon can be gleaned from observations regarding the short form of the serotonin transporter (5HTTR). Patients with the short form of the 5HTTR and prolonged antidepressant exposure, may be particularly vulnerable to antidepressant-related worsening. In other words, prolonged exposure to antidepressants can induce neuroplastic changes that result in the genesis of antidepressant-induced dysphoric symptoms. The investigators propose the term 'tardive dysphoria' to describe such a phenomenon and describe diagnostic criteria for it. Tapering or discontinuing the antidepressant might reverse the dysphoric state. Antidepressant discontinuation may not provide immediate relief. In fact, it is likely that transient symptoms of withdrawal will occur in the initial 2-4 weeks following antidepressant discontinuation or tapering. However, after a prolonged period of antidepressant abstinence, one may see a gradual return to the patient's baseline.
понедельник, 16 мая 2011 г.
Stephen Fry Named BT Mind Champion Of The Year 2007, UK
Mental health charity Mind yesterday announced Stephen Fry as BT Mind Champion of the Year at its annual awards ceremony in central London hosted by Melvyn Bragg.
Last year, in his BBC documentary The Secret Life of the Manic Depressive, Stephen talked candidly about his personal experience of bipolar disorder as well as interviewing others about how they live with the condition. The humour and sincerity with which he presented the programme moved audiences and has helped to raise awareness about an often misunderstood condition.
For the first time, Mind enabled the public to vote on its website for the person they thought had made the most significant contribution to challenging discrimination against people with mental health problems over the last year. The shortlist featured mental health activists, campaigners and fundraisers but Stephen received hundreds of votes to win the prestigious prize.
On receiving the accolade, Stephen said: "I would like to accept this award on behalf of all the people involved in making the film. I learnt a lot from making the documentary, not just about my own condition, but about what it is to be human. Mood disorders are like your own internal weather. You need to accept when it is raining but you must recognise that it will be sunny again."
"Mental health is a pressing problem for all people in Britain. A quarter of the problem with mental health is experienced by the people who are actually taking the medication or using the talking treatments and three quarters of the problem lies with the mentally healthy and their attitude to mental health."
Mind Chief Executive Paul Farmer said: "As one of Britain's best loved entertainers, Stephen has used his high profile to draw mass attention to mental health issues. In his powerful documentary, Stephen opened people's eyes to the reality of what it is like to live with manic depression. He has challenged the stigma surrounding bipolar disorder and has helped to increase public understanding."
Awards were also presented for BT Mind Book of the Year - which went to Michele Hanson for Living With Mother, her accounts of her mother's dementia; BT Mind Journalist of the Year - which went to joint winners Derek Draper and Dr Cecilia d'Felice for their detailed and innovative feature on depression in Psychologies magazine and BT Mind Student Journalist of the Year - which was awarded to Helen Thompson of the University of Cardiff newspaper, Gair Rhydd for her article on Asperger's syndrome.
This year BT sponsored the Mind Awards. BT's work on employee mental health makes them a leader in the field for promoting mental wellbeing in the workplace.
The BT Mind Awards are part of Mind Week, which this year focuses on the mental health benefits of green exercise - exercise outdoors - and the potential to use ecotherapy to treat mental health problems.
Last year, in his BBC documentary The Secret Life of the Manic Depressive, Stephen talked candidly about his personal experience of bipolar disorder as well as interviewing others about how they live with the condition. The humour and sincerity with which he presented the programme moved audiences and has helped to raise awareness about an often misunderstood condition.
For the first time, Mind enabled the public to vote on its website for the person they thought had made the most significant contribution to challenging discrimination against people with mental health problems over the last year. The shortlist featured mental health activists, campaigners and fundraisers but Stephen received hundreds of votes to win the prestigious prize.
On receiving the accolade, Stephen said: "I would like to accept this award on behalf of all the people involved in making the film. I learnt a lot from making the documentary, not just about my own condition, but about what it is to be human. Mood disorders are like your own internal weather. You need to accept when it is raining but you must recognise that it will be sunny again."
"Mental health is a pressing problem for all people in Britain. A quarter of the problem with mental health is experienced by the people who are actually taking the medication or using the talking treatments and three quarters of the problem lies with the mentally healthy and their attitude to mental health."
Mind Chief Executive Paul Farmer said: "As one of Britain's best loved entertainers, Stephen has used his high profile to draw mass attention to mental health issues. In his powerful documentary, Stephen opened people's eyes to the reality of what it is like to live with manic depression. He has challenged the stigma surrounding bipolar disorder and has helped to increase public understanding."
Awards were also presented for BT Mind Book of the Year - which went to Michele Hanson for Living With Mother, her accounts of her mother's dementia; BT Mind Journalist of the Year - which went to joint winners Derek Draper and Dr Cecilia d'Felice for their detailed and innovative feature on depression in Psychologies magazine and BT Mind Student Journalist of the Year - which was awarded to Helen Thompson of the University of Cardiff newspaper, Gair Rhydd for her article on Asperger's syndrome.
This year BT sponsored the Mind Awards. BT's work on employee mental health makes them a leader in the field for promoting mental wellbeing in the workplace.
The BT Mind Awards are part of Mind Week, which this year focuses on the mental health benefits of green exercise - exercise outdoors - and the potential to use ecotherapy to treat mental health problems.
воскресенье, 15 мая 2011 г.
Fifth Annual Conference On College Depression
Every year, more than a thousand college students die by suicide, and thousands more attempt to kill themselves. Tens of thousands of other students struggle with depression, bipolar disorder and related problems such as addiction, prescription drug and alcohol abuse, anorexia and bulimia, and self-mutilation or "cutting".
Colleges and universities across the country are working to help students understand these issues and get help. On March 19 and 20, representatives from many campuses will gather at the University of Michigan to share information about what has worked for them and to get the latest research results.
The fifth annual Depression on College Campuses Conference, organized by the University of Michigan Depression Center in collaboration with many U-M schools and colleges, takes place at a time when new national statistics suggest that suicide is on the rise among teenagers, and when parents are worried about the safety of treating depressed young people with antidepressant medications.
At the same time, colleges are struggling with an ever-increasing demand for counseling services, and with legal issues involving suicidal students.
The conference will begin with a first-person account of what it's like to develop and get help for depression while in college, from Aimee Belisle, who sought treatment for depression while a student at Bentley College, and later made depression awareness her platform during her time as the 2004 Miss Rhode Island. She is now a member of the American Psychiatric Association's Presidential Task Force on Mental Health on College Campuses. Other students will also share stories of their own experience with depression in college during a special panel on March 20.
The conference will also feature speakers from around U-M, and from institutions such as Harvard, Stanford, Cornell, Penn State and New York University. John Greden, M.D., executive director of the UMDC and chair of the Department of Psychiatry at the U-M Medical School, will give opening and closing remarks.
Several conference sessions will focus on treatment options including talk therapy, carefully monitored medication regimens, Internet-based tools, and telemedicine consultations with psychiatrists for students at rural colleges. Panel discussions will examine University policies and protocols for helping severely distressed students, and also identify key sources of data on student mental health which can be used to help determine appropriate programs and services.
Much of the conference is designed to give college personnel, mental health professionals, student group organizers and others the kind of specific information they need to bring about change on their own campuses. Special breakout sessions for academic advisors, campus administrators, mental health clinicians, faculty, student housing officials and students will foster that sharing.
The conference will also include presentations about current research. For example, Daniel Eisenberg, Ph.D., a member of the UMDC and assistant professor in the U-M School of Public Health, and other researchers, will discuss surveys that are trying to accurately assess how many college students are experiencing or getting treatment for depression, anxiety and related issues. Eisenberg leads the Healthy Minds Study, which will be fielded at nine schools around the country this spring. (For more information, visit healthymindsstudy/)
Another highlight of the conference will be the presentation of the first-ever Student Mental Health Advocate Award during a banquet lunch on March 19. Student advocates around the country have poured their energy into raising awareness of depression symptoms, suicide warning signs, and treatment options among their fellow students, and the award was created to recognize those who have made the greatest impact.
The award will be presented by Kathy Cronkite, an author and advocate who has spoken publicly of her own struggle with depression. Nominations are being accepted until Feb. 16 at med.umich/depression/docc/award.htm.
Registration for the conference is free for students, including physicians in training. The fee for all others is $99 before March 1, and $115 afterward. Group discounts are available for five or more people from the same campus who register together before March 1. Lunch on March 19 is available for $20 per person.
Continuing medical education credit is available for physicians, psychologists, nurses and social workers.
To register or for more information, visit med.umich/depression/docc
The University of Michigan Depression Center is the nation's only comprehensive center dedicated to patient care, research, education and public policy in depression and bipolar disorder. Founded in 2001, its mission is to detect depression and bipolar disorders early, treat them earlier and more effectively, prevent recurrences and progression, counteract stigma, and improve public policy. More than 160 faculty, staff and students from throughout the University are members of the Center. More information is available at med.umich/depression.
Contact: Kara Gavin
University of Michigan Health System
Colleges and universities across the country are working to help students understand these issues and get help. On March 19 and 20, representatives from many campuses will gather at the University of Michigan to share information about what has worked for them and to get the latest research results.
The fifth annual Depression on College Campuses Conference, organized by the University of Michigan Depression Center in collaboration with many U-M schools and colleges, takes place at a time when new national statistics suggest that suicide is on the rise among teenagers, and when parents are worried about the safety of treating depressed young people with antidepressant medications.
At the same time, colleges are struggling with an ever-increasing demand for counseling services, and with legal issues involving suicidal students.
The conference will begin with a first-person account of what it's like to develop and get help for depression while in college, from Aimee Belisle, who sought treatment for depression while a student at Bentley College, and later made depression awareness her platform during her time as the 2004 Miss Rhode Island. She is now a member of the American Psychiatric Association's Presidential Task Force on Mental Health on College Campuses. Other students will also share stories of their own experience with depression in college during a special panel on March 20.
The conference will also feature speakers from around U-M, and from institutions such as Harvard, Stanford, Cornell, Penn State and New York University. John Greden, M.D., executive director of the UMDC and chair of the Department of Psychiatry at the U-M Medical School, will give opening and closing remarks.
Several conference sessions will focus on treatment options including talk therapy, carefully monitored medication regimens, Internet-based tools, and telemedicine consultations with psychiatrists for students at rural colleges. Panel discussions will examine University policies and protocols for helping severely distressed students, and also identify key sources of data on student mental health which can be used to help determine appropriate programs and services.
Much of the conference is designed to give college personnel, mental health professionals, student group organizers and others the kind of specific information they need to bring about change on their own campuses. Special breakout sessions for academic advisors, campus administrators, mental health clinicians, faculty, student housing officials and students will foster that sharing.
The conference will also include presentations about current research. For example, Daniel Eisenberg, Ph.D., a member of the UMDC and assistant professor in the U-M School of Public Health, and other researchers, will discuss surveys that are trying to accurately assess how many college students are experiencing or getting treatment for depression, anxiety and related issues. Eisenberg leads the Healthy Minds Study, which will be fielded at nine schools around the country this spring. (For more information, visit healthymindsstudy/)
Another highlight of the conference will be the presentation of the first-ever Student Mental Health Advocate Award during a banquet lunch on March 19. Student advocates around the country have poured their energy into raising awareness of depression symptoms, suicide warning signs, and treatment options among their fellow students, and the award was created to recognize those who have made the greatest impact.
The award will be presented by Kathy Cronkite, an author and advocate who has spoken publicly of her own struggle with depression. Nominations are being accepted until Feb. 16 at med.umich/depression/docc/award.htm.
Registration for the conference is free for students, including physicians in training. The fee for all others is $99 before March 1, and $115 afterward. Group discounts are available for five or more people from the same campus who register together before March 1. Lunch on March 19 is available for $20 per person.
Continuing medical education credit is available for physicians, psychologists, nurses and social workers.
To register or for more information, visit med.umich/depression/docc
The University of Michigan Depression Center is the nation's only comprehensive center dedicated to patient care, research, education and public policy in depression and bipolar disorder. Founded in 2001, its mission is to detect depression and bipolar disorders early, treat them earlier and more effectively, prevent recurrences and progression, counteract stigma, and improve public policy. More than 160 faculty, staff and students from throughout the University are members of the Center. More information is available at med.umich/depression.
Contact: Kara Gavin
University of Michigan Health System
Avoiding Employee Depression In A Recession
As employees become increasingly anxious about job security and financial worries during an economic recession, satisfaction with the job they have, commitment to their company and engagement with their work are all affected detrimentally. This trend could be self-fulfilling in that disengaged employees could have a negative impact on a company's products or services and lead to its decline which would inevitably see the company failing.
Researchers in business and management have now formulated a model of how such employee engagement can change during an economic downturn. The model could help management identify and acknowledge the impact of employee anxiety and implement workplace actions that help staff stay engaged, committed and improve job satisfaction.
Kenneth Green of the Department of Management at Southern Arkansas University and Bobby Medlin of the College of Business at the University of Arkansas at Fort Smith have collected data from several hundred full-time employees in a range of jobs regarding job satisfaction and worries. The data were collected at the height of the 2009 US recession, during which gross domestic product fell dramatically and corporate bankruptcies were at a level not seen since the Great Depression of the 1930s. Workers were rightly concerned about whether or not they would keep their jobs and whether or not they would be compensated if their company did not survive the recession.
The team uses an obvious definition of employee engagement that says an engaged employee is one who is fully involved in and enthusiastic about the work. This might be qualified by adding that a fully engaged worker is prepared to offer discretionary effort or be willing to "go the extra mile", the team explains. They add that intuitively one would assume that workplace anxiety would have negative consequences on level of engagement and earlier research has supported this notion in recent years. The Arkansas team has now quantified this issue and suggests that it can be used by management to improve employee engagement, organizational commitment, and job satisfaction by helping individuals overcome their recession anxiety.
The team recommends that managers acknowledge the impact of the anxiety generated during recessionary times and take actions to reduce the negative impact of workplace anxiety by providing employees with information related to the organization's current situation and each employee's status.
"Impact of recession-based workplace anxiety" in Int. J. Management and Enterprise Development, 2010, 9, 213-232
Researchers in business and management have now formulated a model of how such employee engagement can change during an economic downturn. The model could help management identify and acknowledge the impact of employee anxiety and implement workplace actions that help staff stay engaged, committed and improve job satisfaction.
Kenneth Green of the Department of Management at Southern Arkansas University and Bobby Medlin of the College of Business at the University of Arkansas at Fort Smith have collected data from several hundred full-time employees in a range of jobs regarding job satisfaction and worries. The data were collected at the height of the 2009 US recession, during which gross domestic product fell dramatically and corporate bankruptcies were at a level not seen since the Great Depression of the 1930s. Workers were rightly concerned about whether or not they would keep their jobs and whether or not they would be compensated if their company did not survive the recession.
The team uses an obvious definition of employee engagement that says an engaged employee is one who is fully involved in and enthusiastic about the work. This might be qualified by adding that a fully engaged worker is prepared to offer discretionary effort or be willing to "go the extra mile", the team explains. They add that intuitively one would assume that workplace anxiety would have negative consequences on level of engagement and earlier research has supported this notion in recent years. The Arkansas team has now quantified this issue and suggests that it can be used by management to improve employee engagement, organizational commitment, and job satisfaction by helping individuals overcome their recession anxiety.
The team recommends that managers acknowledge the impact of the anxiety generated during recessionary times and take actions to reduce the negative impact of workplace anxiety by providing employees with information related to the organization's current situation and each employee's status.
"Impact of recession-based workplace anxiety" in Int. J. Management and Enterprise Development, 2010, 9, 213-232
The Importance Of Early Detection Of Depression In Very Young Children
It is difficult to imagine a depressed third-grader. It is even more difficult to imagine a depressed preschooler. Although childhood depression is a well-recognized and treated disorder, only recently have research studies begun looking at depression in children younger than six years old. In the new Current Directions in Psychological Science, a journal of the Association for Psychological Science, child psychiatrist/researcher Joan Luby from Washington University in St. Louis reports on recent findings examining depression in preschool-age children and the importance of early detection.
Depression in preschool-aged children does not always look the same as does depression in older children and adults - this is one reason that preschool depression has been largely neglected. For example, in depressed adults, anhedonia (the inability to enjoy pleasurable experiences) tends to show up in the form of a decreased libido. In young children however, anhedonia may appear as an inability to enjoy playtime. In addition, preschool depression may go unnoticed by parents because the symptoms may not be disruptive; these children may not seem obviously sad (as do many depressed adults) and may have periods of normal functioning during the day. A key advance for the recognition of preschool depression has been the development of age-appropriate psychiatric interviews. These interviews have shown that preschool-age children do in fact exhibit typical symptoms of depression, including appearing less joyful, being prone to guilt, and changes in sleep patterns.
Research suggests that preschool depression is not just a temporary occurrence but may instead be an early manifestation of the same chronic disorder occurring later on - studies have demonstrated that depressed preschoolers are more likely to have depression in later childhood and adolescence than are healthy preschoolers. Due to the potentially long-lasting effect of preschool depression, early identification and intervention become very important. Young children's brains are very "plastic" - that is, their brains easily adapt and change to new experiences and events. This plasticity may explain why developmental interventions are more effective if started early on and this may also prove true for psychotherapy.
More research is needed for the development of treatments for preschool depression. Luby notes that while one study has shown that SSRI antidepressants may be effective in school aged children, there are concerns about side effects of these medications. A novel treatment for preschool depression is currently undergoing testing and may be promising. This treatment is based on Parent Child Interaction Therapy (PCIT) and has been modified to emphasize the child's emotion development (ED). Early changes in emotion skills may be critical to risk for depression and PCIT-ED may help to correct those changes very early in development.
Depression in preschool-aged children does not always look the same as does depression in older children and adults - this is one reason that preschool depression has been largely neglected. For example, in depressed adults, anhedonia (the inability to enjoy pleasurable experiences) tends to show up in the form of a decreased libido. In young children however, anhedonia may appear as an inability to enjoy playtime. In addition, preschool depression may go unnoticed by parents because the symptoms may not be disruptive; these children may not seem obviously sad (as do many depressed adults) and may have periods of normal functioning during the day. A key advance for the recognition of preschool depression has been the development of age-appropriate psychiatric interviews. These interviews have shown that preschool-age children do in fact exhibit typical symptoms of depression, including appearing less joyful, being prone to guilt, and changes in sleep patterns.
Research suggests that preschool depression is not just a temporary occurrence but may instead be an early manifestation of the same chronic disorder occurring later on - studies have demonstrated that depressed preschoolers are more likely to have depression in later childhood and adolescence than are healthy preschoolers. Due to the potentially long-lasting effect of preschool depression, early identification and intervention become very important. Young children's brains are very "plastic" - that is, their brains easily adapt and change to new experiences and events. This plasticity may explain why developmental interventions are more effective if started early on and this may also prove true for psychotherapy.
More research is needed for the development of treatments for preschool depression. Luby notes that while one study has shown that SSRI antidepressants may be effective in school aged children, there are concerns about side effects of these medications. A novel treatment for preschool depression is currently undergoing testing and may be promising. This treatment is based on Parent Child Interaction Therapy (PCIT) and has been modified to emphasize the child's emotion development (ED). Early changes in emotion skills may be critical to risk for depression and PCIT-ED may help to correct those changes very early in development.
New guidelines for prescribing anti-depressants, UK
British doctors are to get new guidelines regarding the prescribing of anti-depressants for people with mild to moderate
depression. People with mild to moderate depression should seek/receive alternative treatments. The NICE guidelines cover
such famous brand names as Prozac and Seroxat.
Pharmaceutical companies say these anti-depressants, known as SSRIs (Selective Serotonin Reuptake Inhibitors) are much safer
than previous ones.
SSRI prescriptions in the UK reached a total of 13 million last year. Doctors prefer them to the old tricyclic medicines,
saying they have fewer side effects and lower risks of a patient overdosing.
Guidelines regarding SSRIs were in the spotlight last year when the Medicines and Healthcare products Regulatory Agency
(MHRA) banned their use for children under 18. There was concern the drugs may increase the risk of suicide.
The guidelines will also state that if you are taking SSRIs you should not stop taking them before seeing your doctor.
It is being said that the MHRA will advise people with mild to moderate depression to seek counselling rather than drugs. It
will advise doctors to offer counselling to people with mild to moderate depression.
What are SSRIs?
Selective Serotonin Reuptake Inhibitors (SSRIs) include fluoxetine (Prozac), sertraline (Lustral), fluvoxamine (Faverin),
citalopram (Cipramil) and escitalopram (Cipralex). Venlafaxine (Efexor) is a medicine that is related to SSRIs and shares
some of their effects. Venlafaxine and the SSRIs are used in the treatment of depressive illness and anxiety disorders.
SSRIs work by increasing the amount of serotonin in the brain. They are the newest class of antidepressants and have the
fewest side effects. Their toxic levels are high so they are a reasonable option for people who may be at risk for overdose.
View drug information on Prozac Weekly.
depression. People with mild to moderate depression should seek/receive alternative treatments. The NICE guidelines cover
such famous brand names as Prozac and Seroxat.
Pharmaceutical companies say these anti-depressants, known as SSRIs (Selective Serotonin Reuptake Inhibitors) are much safer
than previous ones.
SSRI prescriptions in the UK reached a total of 13 million last year. Doctors prefer them to the old tricyclic medicines,
saying they have fewer side effects and lower risks of a patient overdosing.
Guidelines regarding SSRIs were in the spotlight last year when the Medicines and Healthcare products Regulatory Agency
(MHRA) banned their use for children under 18. There was concern the drugs may increase the risk of suicide.
The guidelines will also state that if you are taking SSRIs you should not stop taking them before seeing your doctor.
It is being said that the MHRA will advise people with mild to moderate depression to seek counselling rather than drugs. It
will advise doctors to offer counselling to people with mild to moderate depression.
What are SSRIs?
Selective Serotonin Reuptake Inhibitors (SSRIs) include fluoxetine (Prozac), sertraline (Lustral), fluvoxamine (Faverin),
citalopram (Cipramil) and escitalopram (Cipralex). Venlafaxine (Efexor) is a medicine that is related to SSRIs and shares
some of their effects. Venlafaxine and the SSRIs are used in the treatment of depressive illness and anxiety disorders.
SSRIs work by increasing the amount of serotonin in the brain. They are the newest class of antidepressants and have the
fewest side effects. Their toxic levels are high so they are a reasonable option for people who may be at risk for overdose.
View drug information on Prozac Weekly.
Corcept Therapeutics Announces Negative Results From The First Of Three Phase 3 Studies Evaluating CORLUX(R) For Psychotic Major Depression
Corcept
Therapeutics, Incorporated (Nasdaq: CORT), today announced that the first
of its three Phase 3 trials evaluating CORLUX for treating the psychotic
features of Psychotic Major Depression (PMD) was negative.
Study 07 was a randomized, double-blind, placebo-controlled study. The
primary endpoint, a responder analysis, was the proportion of patients with
at least a 50 percent improvement in the Brief Psychiatric Rating Scale
Positive Symptom Subscale (BPRS PSS) at both Day 7 and Day 56.
Specifically, the BPRS is an 18-item rating instrument used to assess
psychopathology, and the PSS is a subset of four items in the BPRS that
specifically measure psychosis. The study revealed that 30.5 percent of the
patients receiving CORLUX and 28.6 percent of the patients receiving
placebo were responders (p value = .762). The two key secondary endpoints
of Study 07 were similarly negative.
"There was an unusually high placebo response rate in this trial,"
noted Robert L. Roe, M.D., Corcept's President and head of development. "At
Day 56, for example, approximately 80 percent of the patients in both of
the arms of the study were responders as measured by a 50 percent
improvement in BPRS PSS score."
"While we are of course disappointed by these results, we have two
other Phase 3 trials under way," said Joseph K. Belanoff, M.D., Corcept's
Chief Executive Officer. "Next month, we expect to announce the results of
Study 09, which completed its enrollment of 247 patients in late May. We
continue to enroll patients in Study 06 and expect to announce the results
of this trial by the end of this year or early next year."
Commenting on Corcept's financial guidance, Fred Kurland, Corcept's
Chief Financial Officer, stated, "Based on the timeline of our clinical
development program, we expect that our available cash and marketable
securities, which were $17.5 million at June 30, 2006, will enable us to
complete and announce the results of our two remaining Phase 3 clinical
studies."
Conference Call and Live Webcast on August 25, 2006
Management will host a conference call on August 25, 2006 at 9:00 a.m.
EDT to provide an update on its PMD clinical program. To participate,
please dial 800-867-0448 for domestic calls or 303-262-2140 for
international calls. A telephone replay will also be available by dialing
800-405-2236 for domestic calls or 303-590-3000 for international calls.
The access code is 11069588. The replay will be available until 4:00 p.m.
EDT on September 12, 2006.
A live webcast of the conference call can be accessed at
corcept. The event will be archived and available for replay until
4:00 p.m. EDT on September 12, 2006.
About Psychotic Major Depression
PMD is a serious psychiatric disorder that affects about three million
people in the United States every year. It is more prevalent than either
schizophrenia or manic depression. The disorder is characterized by severe
depression accompanied by delusions, hallucinations or both. People with
PMD are approximately 70 times more likely to commit suicide than the
general population and often require lengthy and expensive hospital stays.
There is no FDA-approved treatment for PMD.
About Corcept Therapeutics Incorporated
Corcept Therapeutics Incorporated is a pharmaceutical company focused
on developing drugs for treating severe psychiatric and neurological
diseases. Corcept's lead product, CORLUX, is in Phase 3 clinical trials for
treating the psychotic features of PMD. The drug is administered orally to
PMD patients once per day for seven days. CORLUX, a potent GR-II
antagonist, appears to reduce the effects of the elevated and abnormal
release patterns of cortisol seen in PMD. The company has also initiated a
proof-of-concept study to evaluate the ability of CORLUX to mitigate weight
gain associated with the use of olanzapine. For more information, please
visit corcept.
Forward-looking Statements
Statements made in this news release -- other than statements of
historical fact -- are forward-looking statements. These include
information relating to Corcept's PMD clinical development program, the
timing of the completion of pivotal Phase 3 trials and projections of the
availability of cash. Forward-looking statements are subject to a number of
known and unknown risks and uncertainties that might cause actual results
to differ materially from those expressed or implied here. For example,
there can be no assurances on the efficacy, safety, enrollment completion
or success of clinical trials; the regulatory process or regulatory
approvals; commercial success; in addition, financial projections and trial
timetables may not be accurate. Risk factors are explained in the company's
SEC filings, all of which are available from its Web site ( corcept )
or from the SEC's Web site ( sec ). The company does not have any
intention or duty to update forward-looking statements made in this news
release.
Corcept Therapeutics, Incorporated
corcept
Therapeutics, Incorporated (Nasdaq: CORT), today announced that the first
of its three Phase 3 trials evaluating CORLUX for treating the psychotic
features of Psychotic Major Depression (PMD) was negative.
Study 07 was a randomized, double-blind, placebo-controlled study. The
primary endpoint, a responder analysis, was the proportion of patients with
at least a 50 percent improvement in the Brief Psychiatric Rating Scale
Positive Symptom Subscale (BPRS PSS) at both Day 7 and Day 56.
Specifically, the BPRS is an 18-item rating instrument used to assess
psychopathology, and the PSS is a subset of four items in the BPRS that
specifically measure psychosis. The study revealed that 30.5 percent of the
patients receiving CORLUX and 28.6 percent of the patients receiving
placebo were responders (p value = .762). The two key secondary endpoints
of Study 07 were similarly negative.
"There was an unusually high placebo response rate in this trial,"
noted Robert L. Roe, M.D., Corcept's President and head of development. "At
Day 56, for example, approximately 80 percent of the patients in both of
the arms of the study were responders as measured by a 50 percent
improvement in BPRS PSS score."
"While we are of course disappointed by these results, we have two
other Phase 3 trials under way," said Joseph K. Belanoff, M.D., Corcept's
Chief Executive Officer. "Next month, we expect to announce the results of
Study 09, which completed its enrollment of 247 patients in late May. We
continue to enroll patients in Study 06 and expect to announce the results
of this trial by the end of this year or early next year."
Commenting on Corcept's financial guidance, Fred Kurland, Corcept's
Chief Financial Officer, stated, "Based on the timeline of our clinical
development program, we expect that our available cash and marketable
securities, which were $17.5 million at June 30, 2006, will enable us to
complete and announce the results of our two remaining Phase 3 clinical
studies."
Conference Call and Live Webcast on August 25, 2006
Management will host a conference call on August 25, 2006 at 9:00 a.m.
EDT to provide an update on its PMD clinical program. To participate,
please dial 800-867-0448 for domestic calls or 303-262-2140 for
international calls. A telephone replay will also be available by dialing
800-405-2236 for domestic calls or 303-590-3000 for international calls.
The access code is 11069588. The replay will be available until 4:00 p.m.
EDT on September 12, 2006.
A live webcast of the conference call can be accessed at
corcept. The event will be archived and available for replay until
4:00 p.m. EDT on September 12, 2006.
About Psychotic Major Depression
PMD is a serious psychiatric disorder that affects about three million
people in the United States every year. It is more prevalent than either
schizophrenia or manic depression. The disorder is characterized by severe
depression accompanied by delusions, hallucinations or both. People with
PMD are approximately 70 times more likely to commit suicide than the
general population and often require lengthy and expensive hospital stays.
There is no FDA-approved treatment for PMD.
About Corcept Therapeutics Incorporated
Corcept Therapeutics Incorporated is a pharmaceutical company focused
on developing drugs for treating severe psychiatric and neurological
diseases. Corcept's lead product, CORLUX, is in Phase 3 clinical trials for
treating the psychotic features of PMD. The drug is administered orally to
PMD patients once per day for seven days. CORLUX, a potent GR-II
antagonist, appears to reduce the effects of the elevated and abnormal
release patterns of cortisol seen in PMD. The company has also initiated a
proof-of-concept study to evaluate the ability of CORLUX to mitigate weight
gain associated with the use of olanzapine. For more information, please
visit corcept.
Forward-looking Statements
Statements made in this news release -- other than statements of
historical fact -- are forward-looking statements. These include
information relating to Corcept's PMD clinical development program, the
timing of the completion of pivotal Phase 3 trials and projections of the
availability of cash. Forward-looking statements are subject to a number of
known and unknown risks and uncertainties that might cause actual results
to differ materially from those expressed or implied here. For example,
there can be no assurances on the efficacy, safety, enrollment completion
or success of clinical trials; the regulatory process or regulatory
approvals; commercial success; in addition, financial projections and trial
timetables may not be accurate. Risk factors are explained in the company's
SEC filings, all of which are available from its Web site ( corcept )
or from the SEC's Web site ( sec ). The company does not have any
intention or duty to update forward-looking statements made in this news
release.
Corcept Therapeutics, Incorporated
corcept
Can Aspirin Treat And Prevent Depression?
A study that appears in the current issue of Psychotherapy and Psychosomatics addresses the association between use of aspirin and statins and the risk of major depression.
Chronic disease states characterised by inflammation are often accompanied by depression. Furthermore, depression is commonly reported among patients following exposure to cytokine-based immunotherapy, systemic inflammation has been implicated in the development of depressive symptoms in the elderly, and recent twin studies support a genetic contribution to inflammation and the pathogenesis of depression. As statins and aspirin both have anti-inflammatory properties, the Authors of this study hypothesised that therapy with these agents would reduce the risk for depression. From an age-stratified sample of 1,494 women, randomly selected from the community and recruited for the Geelong Osteoporosis Study 1994-1997, 837 were aged at least 50 years, meeting the inclusion criterion for the study. 386 were assessed at the 10-year follow-up and agreed to a psychiatric interview.
A lifetime history of Major Depressive Disorder (MDD) and age of onset were diagnosed using the Structured Clinical Interview for DSM-IV-TR. It was decided a priori that statins and aspirin, prescribed predominantly for cardiac prophylaxis, would be the exposure variables of interest and recognised if regular use was reported for at least 6 months. Also documented was exposure to non-steroidal antiinflammatory agents, oral glucocorticoids, paracetamol (acetaminophen), hormone therapy and antidepressants.The primary design was a nested case-control study. Cases were subjects with first-episode MDD occurring >50 years of age, controls were MDD free. Use of statins and aspirin was recognised if exposure preceded MDD onset for cases and the 10-year assessment for controls.
A retrospective cohort analysis was also performed for subjects with no prior history of MDD who were followed from baseline or time of exposure to statins or aspirin, until a first episode of MDD or the 10-year follow-up. Among 386 women, 63 were diagnosed as having MDD (cases) and 323 had no history of MDD (controls). 22 cases and 323 controls were eligible for analysis. Exposure to statins was documented for 1 of 22 cases and 93 of 323 controls (5 vs. 29%, p = 0.01). Exposure to aspirin was documented for 1 of 22 cases and 103 of 323 controls (p = 0.007) (N=104). The prevalence of exposure to statins and aspirin was lower among women with MDD (p< 0.001). At the end of the investigation, the exposure to statins and aspirin appears to be associated with a reduced risk for MDD.
These associations were not explained by use of other medications or by differences in lifestyle or body habitus. The findings are consistent with immune system dysregulation in the development of depression. Protective effects of statins have been reported previously, with psychological effects potentially attributable to modulation of the immune system, improvement in blood flow and reduction in oxidative damage. Within several constraints, the results of this study support the notion that statins and aspirin are protective against the likelihood of depression in women. These agents should be further investigated as a novel approach to both the treatment and primary prevention of depression.
Sources: Journal of Psychotherapy and Psychosomatics, AlphaGalileo Foundation.
Chronic disease states characterised by inflammation are often accompanied by depression. Furthermore, depression is commonly reported among patients following exposure to cytokine-based immunotherapy, systemic inflammation has been implicated in the development of depressive symptoms in the elderly, and recent twin studies support a genetic contribution to inflammation and the pathogenesis of depression. As statins and aspirin both have anti-inflammatory properties, the Authors of this study hypothesised that therapy with these agents would reduce the risk for depression. From an age-stratified sample of 1,494 women, randomly selected from the community and recruited for the Geelong Osteoporosis Study 1994-1997, 837 were aged at least 50 years, meeting the inclusion criterion for the study. 386 were assessed at the 10-year follow-up and agreed to a psychiatric interview.
A lifetime history of Major Depressive Disorder (MDD) and age of onset were diagnosed using the Structured Clinical Interview for DSM-IV-TR. It was decided a priori that statins and aspirin, prescribed predominantly for cardiac prophylaxis, would be the exposure variables of interest and recognised if regular use was reported for at least 6 months. Also documented was exposure to non-steroidal antiinflammatory agents, oral glucocorticoids, paracetamol (acetaminophen), hormone therapy and antidepressants.The primary design was a nested case-control study. Cases were subjects with first-episode MDD occurring >50 years of age, controls were MDD free. Use of statins and aspirin was recognised if exposure preceded MDD onset for cases and the 10-year assessment for controls.
A retrospective cohort analysis was also performed for subjects with no prior history of MDD who were followed from baseline or time of exposure to statins or aspirin, until a first episode of MDD or the 10-year follow-up. Among 386 women, 63 were diagnosed as having MDD (cases) and 323 had no history of MDD (controls). 22 cases and 323 controls were eligible for analysis. Exposure to statins was documented for 1 of 22 cases and 93 of 323 controls (5 vs. 29%, p = 0.01). Exposure to aspirin was documented for 1 of 22 cases and 103 of 323 controls (p = 0.007) (N=104). The prevalence of exposure to statins and aspirin was lower among women with MDD (p< 0.001). At the end of the investigation, the exposure to statins and aspirin appears to be associated with a reduced risk for MDD.
These associations were not explained by use of other medications or by differences in lifestyle or body habitus. The findings are consistent with immune system dysregulation in the development of depression. Protective effects of statins have been reported previously, with psychological effects potentially attributable to modulation of the immune system, improvement in blood flow and reduction in oxidative damage. Within several constraints, the results of this study support the notion that statins and aspirin are protective against the likelihood of depression in women. These agents should be further investigated as a novel approach to both the treatment and primary prevention of depression.
Sources: Journal of Psychotherapy and Psychosomatics, AlphaGalileo Foundation.
Postnatal Depression Concern As Maternity Services Report Published, UK
The lack of support for women suffering from postnatal depression - and the reduction in the health visiting service supporting those mothers - have been highlighted with the publication of a hard-hitting report into maternity services.
Unite/Community Practitioners' and Health Visitors' Association raised its continuing concerns in this area as the Healthcare Commission issued its report saying that some NHS trusts could do more to make maternity services safer.
Unite/CPHVA said that there were 690,000 'live' births in 2007 and 15% of those mothers will suffer from postnatal depression.
Dr Cheryll Adams, Unite Lead Professional Officer, Strategy & Practice Development said: 'We are very concerned that mothers don't receive the level of emotional and practical support they require in the postnatal period.'
'Difficulties with maternal child attachment and other mental health problems can only have negative consequences for children and families. Emotional health issues are often unseen and have been subject to underinvestment in the past.'
'This report makes clear the current status of such services, having found that 42% trusts had no access to a specialist perinatal mental health service for women with mental health needs.'
Earlier this year, the government announced that it wanted to employ 4,000 more midwives in England over the next three years. At the time, Unite/CPHVA said that 'the next logical step' would be a large boost to the health visitor workforce to mirror this investment - and Dr Adams repeated that call today (Thursday, 10 July).
Dr Adams said: 'The report also highlights the need for additional support for teenage mothers and those with learning difficulties in the weeks after birth and suggests that specialists midwife roles can be developed to meet these needs.'
'These roles already exist in the form of health visitors, but cutbacks in health visiting have seen a major reduction in the number and quality of postnatal visits following the handover from the midwife at between ten and 14 days.'
She said that an improved service to support parents in the postnatal period and beyond, delivered by well-trained health visitors was urgently needed. This was already a recommendation of the new child health promotion programme (CHPP) and the National Institute for Health and Clinical Excellence (NICE) guidance for ante and postnatal maternal mental health.
Unite/CPHVA welcomed this comprehensive review of maternity services which will provide a benchmark for improving the standard of maternity services.
Notes
Unite NHS Day of Protest - 18 July - Cut our pay - No way!
Unite members across the country will take part in day of protest against the NHS pay offer on the 1 July, 2008. Workers will be campaigning around the slogan:
'Cut my pay? No way!'
For more information visit: unitetheunion/nhsdayofprotest
Unite/CPHVA press releases can be seen on the CPHVA website: unitetheunion/cphva
Unite is the largest union in the UK. It has seven professional sections: the Community Practitioners' and Health Visitors' Association, the Mental Health Nurses Association, the Guild of Healthcare Pharmacists, the Society of Sexual Health Advisers, the Medical Practitioners' Union, College of Healthcare Chaplains, and the Hospital Physicists Association.
Unite was formed by an amalgamation of Amicus and the Transport and General Workers' Union in May 2007.
Unite The Union
Unite/Community Practitioners' and Health Visitors' Association raised its continuing concerns in this area as the Healthcare Commission issued its report saying that some NHS trusts could do more to make maternity services safer.
Unite/CPHVA said that there were 690,000 'live' births in 2007 and 15% of those mothers will suffer from postnatal depression.
Dr Cheryll Adams, Unite Lead Professional Officer, Strategy & Practice Development said: 'We are very concerned that mothers don't receive the level of emotional and practical support they require in the postnatal period.'
'Difficulties with maternal child attachment and other mental health problems can only have negative consequences for children and families. Emotional health issues are often unseen and have been subject to underinvestment in the past.'
'This report makes clear the current status of such services, having found that 42% trusts had no access to a specialist perinatal mental health service for women with mental health needs.'
Earlier this year, the government announced that it wanted to employ 4,000 more midwives in England over the next three years. At the time, Unite/CPHVA said that 'the next logical step' would be a large boost to the health visitor workforce to mirror this investment - and Dr Adams repeated that call today (Thursday, 10 July).
Dr Adams said: 'The report also highlights the need for additional support for teenage mothers and those with learning difficulties in the weeks after birth and suggests that specialists midwife roles can be developed to meet these needs.'
'These roles already exist in the form of health visitors, but cutbacks in health visiting have seen a major reduction in the number and quality of postnatal visits following the handover from the midwife at between ten and 14 days.'
She said that an improved service to support parents in the postnatal period and beyond, delivered by well-trained health visitors was urgently needed. This was already a recommendation of the new child health promotion programme (CHPP) and the National Institute for Health and Clinical Excellence (NICE) guidance for ante and postnatal maternal mental health.
Unite/CPHVA welcomed this comprehensive review of maternity services which will provide a benchmark for improving the standard of maternity services.
Notes
Unite NHS Day of Protest - 18 July - Cut our pay - No way!
Unite members across the country will take part in day of protest against the NHS pay offer on the 1 July, 2008. Workers will be campaigning around the slogan:
'Cut my pay? No way!'
For more information visit: unitetheunion/nhsdayofprotest
Unite/CPHVA press releases can be seen on the CPHVA website: unitetheunion/cphva
Unite is the largest union in the UK. It has seven professional sections: the Community Practitioners' and Health Visitors' Association, the Mental Health Nurses Association, the Guild of Healthcare Pharmacists, the Society of Sexual Health Advisers, the Medical Practitioners' Union, College of Healthcare Chaplains, and the Hospital Physicists Association.
Unite was formed by an amalgamation of Amicus and the Transport and General Workers' Union in May 2007.
Unite The Union
Cymbalta Reduced Anxiety Symptoms in Elderly Patients with Depression, New Analysis
Cymbalta™ (duloxetine HCL) significantly reduced anxiety symptoms in elderly patients with depression, compared with
those treated with a sugar pill, according to new research presented today at the annual meeting of the American Psychiatric
Association.
In the eight-week study of people over age 65 with depression, 60 mg of Cymbalta, taken once daily, significantly reduced
psychic anxiety symptoms in depressed patients, such as worry, ability to concentrate, tension and irritability, compared to
placebo (mean change 6.2 vs. 0.18), as measured by the psychic anxiety question on the Hamilton Depression Scale (HAMD17).
Cymbalta also significantly reduced somatic anxiety -- or physical symptoms often associated with anxiety -- compared with
placebo (mean change of 1.88 vs. 0.99), according to the anxiety/somatization subscale of the HAMD17.
"When anxiety symptoms appear in elderly patients with depression it often makes treatment more complicated than when these
symptoms emerge alone. This comorbidity is associated with an increased severity of symptoms, including a greater risk for
suicide, and often less successful treatment outcomes," explained Olga Brawman-Mintzer, MD, associate professor of
psychiatry, and the director of Anxiety Disorders Program at the Medical University of South Carolina.
While depression alone affects two million Americans aged 65 and older(i), there is considerable overlap between depression
and anxiety. Half of those with major depressive disorder actually meet the criteria for an anxiety disorder. Furthermore,
one-quarter of those with anxiety disorders meet the criteria for major depressive disorder(ii).
"Since treating this population is so challenging, the fact that patients responded to medication within one week while on
Cymbalta is promising," stated Joel Raskin, MD, FRCPC, medical advisor Eli Lilly and Company. "Further research into the
benefit of Cymbalta in anxiety is needed."
Additional Study Highlights
* When elderly patients were analyzed by age:
- Patients under 75 treated with Cymbalta experienced significant improvements in both psychic anxiety symptoms, such as
worry and tension, and physical anxiety symptoms, as measured by the anxiety/somatization subscale, compared with those
treated with a sugar pill.
- Patients 75 and older treated with Cymbalta showed significant improvements in psychic anxiety, as well. They also showed a
numerical advantage on the anxiety/somatization subscale that was not statistically significant, as compared with those
treated with a sugar pill.
* A statistically significant improvement in the somatic anxiety item of the HAMD17 was not seen in patients treated with
Cymbalta.
* In this study, Cymbalta was safe and well tolerated, with discontinuations due to adverse events occurring in less than 10
percent of those treated, with no difference between Cymbalta and placebo.
* The most common (>/= 5 percent) adverse events experienced by patients treated with Cymbalta in this study included dry
mouth (14.5 percent), nausea (12.6 percent), constipation (10.1 percent), headache (7.2 percent), dizziness (8.2 percent),
diarrhea (8.2 percent), fatigue (6.3 percent) and somnolence (5.3 percent).
Methods
Data were gathered from 311 patients with major depression aged 65 and older who participated in a multicenter, parallel,
double-blind, placebo- controlled study. After one week, patients were randomly chosen to receive either Cymbalta 60 mg once
daily (n=207) or placebo (n=104) for eight weeks. At the end of the study, patients entered a one-week, double-blind
discontinuation phase where the dose of the study medication was tapered. A secondary analysis was conducted to measure
anxiety using anxiety items 10 (psychic) and 11 (somatic,) and the anxiety/somatization subscale of the HAMD17.
About Cymbalta
Serotonin and norepinephrine are two chemicals in the brain and spinal cord called neurotransmitters. Serotonin and
norepinephrine are believed to both mediate core depression symptoms and help regulate the perception of pain. Disturbances
of serotonin and/or norepinephrine may explain the presence of both the emotional and physical symptoms of depression. Based
on pre-clinical studies, Cymbalta is a balanced and potent reuptake inhibitor of serotonin and norepinephrine. While the
mechanism of action of Cymbalta is not fully known, scientists believe its effect on both emotional symptoms and pain
perception is caused by increasing the activity of serotonin and norepinephrine in the central nervous system.
Cymbalta is approved in the United States for the treatment of major depressive disorder and the management of diabetic
peripheral neuropathic pain, both in adults. Cymbalta is not specifically indicated for geriatric depression. As Cymbalta has
not been studied in children, Lilly discourages its use in those under the age of 18.
Important Safety Information
In clinical studies, antidepressants increased the risk of suicidal thinking and behavior in children and adolescents with
depression and other psychiatric disorders. Anyone considering the use of Cymbalta or any other antidepressant in a child or
adolescent must balance the risk with the clinical need. Patients who are starting therapy should be observed closely.
Families and caregivers should discuss with the doctor any observations of worsening depression symptoms, suicidal thinking
and behavior, or unusual changes in behavior. Cymbalta is not approved for use in patients under the age of 18.
Patients on antidepressants and their families or caregivers should watch for worsening depression symptoms, unusual changes
in behavior and thoughts of suicide, as well as for anxiety, agitation, panic attacks, difficulty sleeping, irritability,
hostility, aggressiveness, impulsivity, restlessness, or extreme hyperactivity. Call the doctor if you have thoughts of
suicide, or if any of these symptoms are severe or occur suddenly. Be especially observant at the beginning of treatment or
whenever there is a change in dose.
Prescription Cymbalta is not for everyone. People who are allergic to Cymbalta or the other ingredients in Cymbalta should
not take it. If you have recently taken a type of antidepressant called a monoamine oxidase inhibitor (MAOI), are taking
thioridazine or have uncontrolled narrow-angle glaucoma, you should not take Cymbalta. Talk with your doctor before taking
Cymbalta if you have liver or kidney problems, glaucoma or consume large quantities of alcohol. Women who are pregnant should
talk with their doctor before taking Cymbalta. Nursing while taking Cymbalta is not recommended.
In clinical studies of Cymbalta for depression, the most common side effects were nausea, dry mouth, constipation, decreased
appetite, fatigue, sleepiness, and increased sweating. Cymbalta is also approved for the management of neuropathic pain
associated with diabetic peripheral neuropathy. In clinical studies of Cymbalta in these patients, the most common side
effects were nausea, sleepiness, dizziness, constipation, dry mouth, increased sweating, decreased appetite, and loss of
strength or energy. In all clinical trials, most people were not bothered enough by side effects to stop taking Cymbalta.
Your doctor may periodically check your blood pressure. Don't stop taking Cymbalta without talking to your doctor.
For full Patient Information, visit Cymbalta.
For full Prescribing Information, including Boxed Warning, visit Cymbalta.
About Lilly
Lilly, a leading innovation-driven corporation, is developing a growing portfolio of first-in-class and best-in-class
pharmaceutical products by applying the latest research from its own worldwide laboratories and from collaborations with
eminent scientific organizations. Headquartered in Indianapolis, Ind., Lilly provides answers -- through medicines and
information -- for some of the world's most urgent medical needs. Additional information about Lilly is available at lilly.
P-LLY
This press release contains forward-looking statements about the potential of Cymbalta hydrochloride for the treatment of
anxiety, in addition to major depressive disorder, and reflects Lilly's current beliefs. However, as with any pharmaceutical
product, there are substantial risks and uncertainties in the process of development and commercialization. There is no
guarantee that the product will prove to be commercially successful. For further discussion of these and other risks and
uncertainties, see Lilly's filings with the United States Securities and Exchange Commission. Lilly undertakes no duty to
update forward-looking statements.
(i) Kim, Crystal. "Major Depression in the Elderly," Johns Hopkins University, Spring 2003. Available at
jhu/hurj/issue2/07C%20MajorDepress.pdf . Accessed 1/5/05.
(ii) Anxiety Disorders Association of America. Brief Overview of Anxiety Disorders. Available at:
adaa/AnxietyDisorderInfor/AnxietyElderly.cfm . Accessed March 21, 2005.
lillymedia
View drug information on Cymbalta.
those treated with a sugar pill, according to new research presented today at the annual meeting of the American Psychiatric
Association.
In the eight-week study of people over age 65 with depression, 60 mg of Cymbalta, taken once daily, significantly reduced
psychic anxiety symptoms in depressed patients, such as worry, ability to concentrate, tension and irritability, compared to
placebo (mean change 6.2 vs. 0.18), as measured by the psychic anxiety question on the Hamilton Depression Scale (HAMD17).
Cymbalta also significantly reduced somatic anxiety -- or physical symptoms often associated with anxiety -- compared with
placebo (mean change of 1.88 vs. 0.99), according to the anxiety/somatization subscale of the HAMD17.
"When anxiety symptoms appear in elderly patients with depression it often makes treatment more complicated than when these
symptoms emerge alone. This comorbidity is associated with an increased severity of symptoms, including a greater risk for
suicide, and often less successful treatment outcomes," explained Olga Brawman-Mintzer, MD, associate professor of
psychiatry, and the director of Anxiety Disorders Program at the Medical University of South Carolina.
While depression alone affects two million Americans aged 65 and older(i), there is considerable overlap between depression
and anxiety. Half of those with major depressive disorder actually meet the criteria for an anxiety disorder. Furthermore,
one-quarter of those with anxiety disorders meet the criteria for major depressive disorder(ii).
"Since treating this population is so challenging, the fact that patients responded to medication within one week while on
Cymbalta is promising," stated Joel Raskin, MD, FRCPC, medical advisor Eli Lilly and Company. "Further research into the
benefit of Cymbalta in anxiety is needed."
Additional Study Highlights
* When elderly patients were analyzed by age:
- Patients under 75 treated with Cymbalta experienced significant improvements in both psychic anxiety symptoms, such as
worry and tension, and physical anxiety symptoms, as measured by the anxiety/somatization subscale, compared with those
treated with a sugar pill.
- Patients 75 and older treated with Cymbalta showed significant improvements in psychic anxiety, as well. They also showed a
numerical advantage on the anxiety/somatization subscale that was not statistically significant, as compared with those
treated with a sugar pill.
* A statistically significant improvement in the somatic anxiety item of the HAMD17 was not seen in patients treated with
Cymbalta.
* In this study, Cymbalta was safe and well tolerated, with discontinuations due to adverse events occurring in less than 10
percent of those treated, with no difference between Cymbalta and placebo.
* The most common (>/= 5 percent) adverse events experienced by patients treated with Cymbalta in this study included dry
mouth (14.5 percent), nausea (12.6 percent), constipation (10.1 percent), headache (7.2 percent), dizziness (8.2 percent),
diarrhea (8.2 percent), fatigue (6.3 percent) and somnolence (5.3 percent).
Methods
Data were gathered from 311 patients with major depression aged 65 and older who participated in a multicenter, parallel,
double-blind, placebo- controlled study. After one week, patients were randomly chosen to receive either Cymbalta 60 mg once
daily (n=207) or placebo (n=104) for eight weeks. At the end of the study, patients entered a one-week, double-blind
discontinuation phase where the dose of the study medication was tapered. A secondary analysis was conducted to measure
anxiety using anxiety items 10 (psychic) and 11 (somatic,) and the anxiety/somatization subscale of the HAMD17.
About Cymbalta
Serotonin and norepinephrine are two chemicals in the brain and spinal cord called neurotransmitters. Serotonin and
norepinephrine are believed to both mediate core depression symptoms and help regulate the perception of pain. Disturbances
of serotonin and/or norepinephrine may explain the presence of both the emotional and physical symptoms of depression. Based
on pre-clinical studies, Cymbalta is a balanced and potent reuptake inhibitor of serotonin and norepinephrine. While the
mechanism of action of Cymbalta is not fully known, scientists believe its effect on both emotional symptoms and pain
perception is caused by increasing the activity of serotonin and norepinephrine in the central nervous system.
Cymbalta is approved in the United States for the treatment of major depressive disorder and the management of diabetic
peripheral neuropathic pain, both in adults. Cymbalta is not specifically indicated for geriatric depression. As Cymbalta has
not been studied in children, Lilly discourages its use in those under the age of 18.
Important Safety Information
In clinical studies, antidepressants increased the risk of suicidal thinking and behavior in children and adolescents with
depression and other psychiatric disorders. Anyone considering the use of Cymbalta or any other antidepressant in a child or
adolescent must balance the risk with the clinical need. Patients who are starting therapy should be observed closely.
Families and caregivers should discuss with the doctor any observations of worsening depression symptoms, suicidal thinking
and behavior, or unusual changes in behavior. Cymbalta is not approved for use in patients under the age of 18.
Patients on antidepressants and their families or caregivers should watch for worsening depression symptoms, unusual changes
in behavior and thoughts of suicide, as well as for anxiety, agitation, panic attacks, difficulty sleeping, irritability,
hostility, aggressiveness, impulsivity, restlessness, or extreme hyperactivity. Call the doctor if you have thoughts of
suicide, or if any of these symptoms are severe or occur suddenly. Be especially observant at the beginning of treatment or
whenever there is a change in dose.
Prescription Cymbalta is not for everyone. People who are allergic to Cymbalta or the other ingredients in Cymbalta should
not take it. If you have recently taken a type of antidepressant called a monoamine oxidase inhibitor (MAOI), are taking
thioridazine or have uncontrolled narrow-angle glaucoma, you should not take Cymbalta. Talk with your doctor before taking
Cymbalta if you have liver or kidney problems, glaucoma or consume large quantities of alcohol. Women who are pregnant should
talk with their doctor before taking Cymbalta. Nursing while taking Cymbalta is not recommended.
In clinical studies of Cymbalta for depression, the most common side effects were nausea, dry mouth, constipation, decreased
appetite, fatigue, sleepiness, and increased sweating. Cymbalta is also approved for the management of neuropathic pain
associated with diabetic peripheral neuropathy. In clinical studies of Cymbalta in these patients, the most common side
effects were nausea, sleepiness, dizziness, constipation, dry mouth, increased sweating, decreased appetite, and loss of
strength or energy. In all clinical trials, most people were not bothered enough by side effects to stop taking Cymbalta.
Your doctor may periodically check your blood pressure. Don't stop taking Cymbalta without talking to your doctor.
For full Patient Information, visit Cymbalta.
For full Prescribing Information, including Boxed Warning, visit Cymbalta.
About Lilly
Lilly, a leading innovation-driven corporation, is developing a growing portfolio of first-in-class and best-in-class
pharmaceutical products by applying the latest research from its own worldwide laboratories and from collaborations with
eminent scientific organizations. Headquartered in Indianapolis, Ind., Lilly provides answers -- through medicines and
information -- for some of the world's most urgent medical needs. Additional information about Lilly is available at lilly.
P-LLY
This press release contains forward-looking statements about the potential of Cymbalta hydrochloride for the treatment of
anxiety, in addition to major depressive disorder, and reflects Lilly's current beliefs. However, as with any pharmaceutical
product, there are substantial risks and uncertainties in the process of development and commercialization. There is no
guarantee that the product will prove to be commercially successful. For further discussion of these and other risks and
uncertainties, see Lilly's filings with the United States Securities and Exchange Commission. Lilly undertakes no duty to
update forward-looking statements.
(i) Kim, Crystal. "Major Depression in the Elderly," Johns Hopkins University, Spring 2003. Available at
jhu/hurj/issue2/07C%20MajorDepress.pdf . Accessed 1/5/05.
(ii) Anxiety Disorders Association of America. Brief Overview of Anxiety Disorders. Available at:
adaa/AnxietyDisorderInfor/AnxietyElderly.cfm . Accessed March 21, 2005.
lillymedia
View drug information on Cymbalta.
A New Generation Of Rapid-Acting Antidepressants?
Conventional antidepressant treatments generally require three to four weeks to become effective, thus the discovery of treatments with a more rapid onset is a major goal of biological psychiatry. The first drug found to produce rapid improvement in mood was the NMDA glutamate receptor antagonist, ketamine.
In a new issue of Biological Psychiatry, published by Elsevier, researchers from the National Institutes of Health report that another medication, scopolamine, also appears to produce replicable rapid improvement in mood. Scopolamine temporarily blocks the muscarinic cholinergic receptor, thought to be overactive in people suffering from depression.
Drs. Wayne Drevets and Maura Furey recruited outpatients with major depressive disorder who were randomly assigned to receive placebo and then scopolamine treatment, or vice versa, in a double-blinded design so that neither the researchers nor the patients knew which treatment they were receiving.
"Scopolamine was found to reduce symptoms of depression within three days of the first administration. In fact, participants reported that they experienced relief from their symptoms by the morning after the first administration of drug," explained Dr. Furey. "Moreover, one-half of participants experienced full symptom remission by the end of the treatment period. Finally, participants remained well during a subsequent placebo period, indicating that the antidepressant effects persist for at least two weeks in the absence of further treatment."
The efficacy of scopolamine is very interesting because the potent blockade of muscarinic receptors was a property of tricyclic antidepressant medications, the oldest type of antidepressants. With these medications, the muscarinic receptor blockade was mostly viewed as the cause of unwanted side effects, such as constipation, sedation, and memory impairments. Newer antidepressants, such as serotonin reuptake inhibitors or serotonin-norepinephrine reuptake inhibitors, were explicitly designed to avoid blocking muscarinic receptors. Yet, the current data raise the possibility that this strategy may have increased safety and tolerability of these medications at the expense of providing effective and timely relief for depression symptoms.
Dr. John Krystal, Editor of Biological Psychiatry, commented that these findings "have the potential to raise expectations for new antidepressant treatments. Three-to-six weeks is a long time to wait for depression symptoms to be alleviated. Depressed people describe their emotional state using terms like 'agony' and others compare their condition to 'living in hell'. Further, depression is a life-threatening condition for some, preventing them from performing basic self-care functions or causing them to exhibit self-destructive behavior."
Although these findings open the door to a conceptually different approach to the treatment of depression, it remains to be seen whether rapid acting antidepressant effects will be viable clinically. One could imagine that they might mitigate hospitalization in some patients and enhance the overall effectiveness of the treatment of depression. However, this possibility remains to be demonstrated empirically in studies that show that a rapid-acting antidepressant treatment can be smoothly transitioned to definitive long-term treatment for depression.
Notes:
The article is "Replication of Scopolamine's Antidepressant Efficacy in Major Depressive Disorder: A Randomized, Placebo-Controlled Clinical Trial" by Wayne C. Drevets and Maura L. Furey. The authors are affiliated with the Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland. The article appears in Biological Psychiatry, Volume 67, Issue 5 (March 1, 2010), published by Elsevier.
The authors' disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D. is Chairman of the Department of Psychiatry at the Yale University School of Medicine and a research psychiatrist at the VA Connecticut Healthcare System. He is a co-sponsor of a patent for one of the rapid-acting antidepressant medications, ketamine. His full disclosures of financial and conflicts of interests are available here.
In a new issue of Biological Psychiatry, published by Elsevier, researchers from the National Institutes of Health report that another medication, scopolamine, also appears to produce replicable rapid improvement in mood. Scopolamine temporarily blocks the muscarinic cholinergic receptor, thought to be overactive in people suffering from depression.
Drs. Wayne Drevets and Maura Furey recruited outpatients with major depressive disorder who were randomly assigned to receive placebo and then scopolamine treatment, or vice versa, in a double-blinded design so that neither the researchers nor the patients knew which treatment they were receiving.
"Scopolamine was found to reduce symptoms of depression within three days of the first administration. In fact, participants reported that they experienced relief from their symptoms by the morning after the first administration of drug," explained Dr. Furey. "Moreover, one-half of participants experienced full symptom remission by the end of the treatment period. Finally, participants remained well during a subsequent placebo period, indicating that the antidepressant effects persist for at least two weeks in the absence of further treatment."
The efficacy of scopolamine is very interesting because the potent blockade of muscarinic receptors was a property of tricyclic antidepressant medications, the oldest type of antidepressants. With these medications, the muscarinic receptor blockade was mostly viewed as the cause of unwanted side effects, such as constipation, sedation, and memory impairments. Newer antidepressants, such as serotonin reuptake inhibitors or serotonin-norepinephrine reuptake inhibitors, were explicitly designed to avoid blocking muscarinic receptors. Yet, the current data raise the possibility that this strategy may have increased safety and tolerability of these medications at the expense of providing effective and timely relief for depression symptoms.
Dr. John Krystal, Editor of Biological Psychiatry, commented that these findings "have the potential to raise expectations for new antidepressant treatments. Three-to-six weeks is a long time to wait for depression symptoms to be alleviated. Depressed people describe their emotional state using terms like 'agony' and others compare their condition to 'living in hell'. Further, depression is a life-threatening condition for some, preventing them from performing basic self-care functions or causing them to exhibit self-destructive behavior."
Although these findings open the door to a conceptually different approach to the treatment of depression, it remains to be seen whether rapid acting antidepressant effects will be viable clinically. One could imagine that they might mitigate hospitalization in some patients and enhance the overall effectiveness of the treatment of depression. However, this possibility remains to be demonstrated empirically in studies that show that a rapid-acting antidepressant treatment can be smoothly transitioned to definitive long-term treatment for depression.
Notes:
The article is "Replication of Scopolamine's Antidepressant Efficacy in Major Depressive Disorder: A Randomized, Placebo-Controlled Clinical Trial" by Wayne C. Drevets and Maura L. Furey. The authors are affiliated with the Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland. The article appears in Biological Psychiatry, Volume 67, Issue 5 (March 1, 2010), published by Elsevier.
The authors' disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D. is Chairman of the Department of Psychiatry at the Yale University School of Medicine and a research psychiatrist at the VA Connecticut Healthcare System. He is a co-sponsor of a patent for one of the rapid-acting antidepressant medications, ketamine. His full disclosures of financial and conflicts of interests are available here.
Guidelines To Improve Care Of Three Symptoms At End Of Life Issued By Internal Medicine Organization
The American College of Physicians (ACP) has issued new guidelines to improve palliative care at the end of life (EOL).
The guidelines say that clinicians should regularly assess people with serious illness at the end of life for symptoms of pain, shortness of breath, and depression; that they should use proven therapies to treat these conditions; and should ensure that advance care planning occurs for all patients with serious illness.
"Many Americans will face a serious illness at the end of life and their families will be involved in their care," said Amir Qaseem, MD, PhD, MHA, Senior Medical Associate in the Clinical Programs and Quality of Care Department of the Medical Education and Publishing Division at ACP. "We wanted to pull together best available evidence on improving care that relieves or soothes symptoms at the end of life. Evidence review showed that the three most common symptoms were pain, difficult breathing and depression, so our guidelines address these."
Elaborating on the recommendations to use therapies of proven effectiveness to manage pain, shortness of breath, and depression, the guidelines say that clinicians should regularly assess patients with serious illness at the end of life.
For patients with cancer, pain has been proven to be controlled with anti-inflammatory drugs, narcotic drugs and bisphosphonates.
In patients at the end of life with difficult breathing, unrelieved dyspnea can be relieved by narcotic drugs and oxygen for short-term relief of hypoxemia.
Patients with depression can be treated with antidepressants and psychosocial intervention.
ACP, through its Clinical Efficacy Assessment Subcommittee, has been developing guidelines since 1981. ACP guidelines have relied on evidence or clinical documentation rather than consensus or expert opinion.
In the case of the EOL guidelines, the reviewing committee found that high-quality evidence on end-of-life care is limited, and most of the evidence comes from literature on patients with cancer. Therefore the new evidence-based guidelines could not address many other important aspects of EOL care, such as symptoms specific to heart disease, lung disease, or dementia, or therapies such as nutritional support, complementary and alternative therapies, and spiritual care.
The EOL guidelines were passed by the ACP Board of Regents on July 14, 2007.
"End of life care has been identified by the Institute of Medicine as one of the priority areas to improve quality of health care. We hope that these guidelines would benefit physicians taking care of patients with seriously disabling or symptomatic chronic conditions."
The guidelines grade the evidence recommendations using the American College of Physicians' clinical practice guidelines grading system. All of the ACP recommendations on EOL care are considered strong recommendations, meaning that benefits clearly outweigh the risks. All of the EOL recommendations are considered to have moderate quality of evidence because most of the published literature is on patients with cancer.
Annals of Internal Medicine (annals/) is one of the most widely cited peer-reviewed medical journals in the world. The journal has been published for 80 years and accepts only seven percent of the original research studies submitted for publication.
Annals of Internal Medicine is published by the American College of Physicians (acponline/), the largest medical specialty organization and the second-largest physician group in the United States.
ACP members include 124,000 internal medicine physicians (internists), related subspecialists, and medical students. Internists specialize in the prevention, detection, and treatment of illness in adults.
Summary of guideline follows.
Summary of Clinical Practice Guideline from the American College of Physicians on Evidence-Based Interventions to Improve the Palliative Care of Pain, Dyspnea, and Depression at the End of Life:
Amir Qaseem, MD, PhD, MHA; Vincenza Snow, MD; Paul Shekelle, MD, PhD; Donald E. Casey Jr., MD, MPH, MBA; J. Thomas Cross Jr., MD, MPH; and Douglas K. Owens, MD, MS, for the Clinical Efficacy Assessment Subcommittee of the American College of Physicians*
Recommendation 1: In patients with serious illness at the end of life, clinicians should regularly assess patients for pain, dyspnea, and depression. (Grade: strong recommendation, moderate quality of evidence.)
Recommendation 2: In patients with serious illness at the end of life, clinicians should use therapies of proven effectiveness to manage pain. For patients with cancer, this includes nonsteroidal antiinflammatory drugs, opioids, and bisphosphonates. (Grade: strong recommendation, moderate quality of evidence.)
Recommendation 3: In patients with serious illness at the end of life, clinicians should use therapies of proven effectiveness to manage dyspnea, which include opioids in patients with unrelieved dyspnea and oxygen for short-term relief of hypoxemia. (Grade: strong recommendation, moderate quality of evidence.)
Recommendation 4: In patients with serious illness at the end of life, clinicians should use therapies of proven effectiveness to manage depression. For patients with cancer, this includes tricyclic antidepressants, selective serotonin reuptake inhibitors, or psychosocial intervention. (Grade: strong recommendation, moderate quality of evidence.)
Recommendation 5: Clinicians should ensure that advance care planning, including completion of advance directives, occurs for all patients with serious illness. (Grade: strong recommendation, low quality of evidence.)
Annals of Internal Medicine 2008;148:141-146.
The guidelines say that clinicians should regularly assess people with serious illness at the end of life for symptoms of pain, shortness of breath, and depression; that they should use proven therapies to treat these conditions; and should ensure that advance care planning occurs for all patients with serious illness.
"Many Americans will face a serious illness at the end of life and their families will be involved in their care," said Amir Qaseem, MD, PhD, MHA, Senior Medical Associate in the Clinical Programs and Quality of Care Department of the Medical Education and Publishing Division at ACP. "We wanted to pull together best available evidence on improving care that relieves or soothes symptoms at the end of life. Evidence review showed that the three most common symptoms were pain, difficult breathing and depression, so our guidelines address these."
Elaborating on the recommendations to use therapies of proven effectiveness to manage pain, shortness of breath, and depression, the guidelines say that clinicians should regularly assess patients with serious illness at the end of life.
For patients with cancer, pain has been proven to be controlled with anti-inflammatory drugs, narcotic drugs and bisphosphonates.
In patients at the end of life with difficult breathing, unrelieved dyspnea can be relieved by narcotic drugs and oxygen for short-term relief of hypoxemia.
Patients with depression can be treated with antidepressants and psychosocial intervention.
ACP, through its Clinical Efficacy Assessment Subcommittee, has been developing guidelines since 1981. ACP guidelines have relied on evidence or clinical documentation rather than consensus or expert opinion.
In the case of the EOL guidelines, the reviewing committee found that high-quality evidence on end-of-life care is limited, and most of the evidence comes from literature on patients with cancer. Therefore the new evidence-based guidelines could not address many other important aspects of EOL care, such as symptoms specific to heart disease, lung disease, or dementia, or therapies such as nutritional support, complementary and alternative therapies, and spiritual care.
The EOL guidelines were passed by the ACP Board of Regents on July 14, 2007.
"End of life care has been identified by the Institute of Medicine as one of the priority areas to improve quality of health care. We hope that these guidelines would benefit physicians taking care of patients with seriously disabling or symptomatic chronic conditions."
The guidelines grade the evidence recommendations using the American College of Physicians' clinical practice guidelines grading system. All of the ACP recommendations on EOL care are considered strong recommendations, meaning that benefits clearly outweigh the risks. All of the EOL recommendations are considered to have moderate quality of evidence because most of the published literature is on patients with cancer.
Annals of Internal Medicine (annals/) is one of the most widely cited peer-reviewed medical journals in the world. The journal has been published for 80 years and accepts only seven percent of the original research studies submitted for publication.
Annals of Internal Medicine is published by the American College of Physicians (acponline/), the largest medical specialty organization and the second-largest physician group in the United States.
ACP members include 124,000 internal medicine physicians (internists), related subspecialists, and medical students. Internists specialize in the prevention, detection, and treatment of illness in adults.
Summary of guideline follows.
Summary of Clinical Practice Guideline from the American College of Physicians on Evidence-Based Interventions to Improve the Palliative Care of Pain, Dyspnea, and Depression at the End of Life:
Amir Qaseem, MD, PhD, MHA; Vincenza Snow, MD; Paul Shekelle, MD, PhD; Donald E. Casey Jr., MD, MPH, MBA; J. Thomas Cross Jr., MD, MPH; and Douglas K. Owens, MD, MS, for the Clinical Efficacy Assessment Subcommittee of the American College of Physicians*
Recommendation 1: In patients with serious illness at the end of life, clinicians should regularly assess patients for pain, dyspnea, and depression. (Grade: strong recommendation, moderate quality of evidence.)
Recommendation 2: In patients with serious illness at the end of life, clinicians should use therapies of proven effectiveness to manage pain. For patients with cancer, this includes nonsteroidal antiinflammatory drugs, opioids, and bisphosphonates. (Grade: strong recommendation, moderate quality of evidence.)
Recommendation 3: In patients with serious illness at the end of life, clinicians should use therapies of proven effectiveness to manage dyspnea, which include opioids in patients with unrelieved dyspnea and oxygen for short-term relief of hypoxemia. (Grade: strong recommendation, moderate quality of evidence.)
Recommendation 4: In patients with serious illness at the end of life, clinicians should use therapies of proven effectiveness to manage depression. For patients with cancer, this includes tricyclic antidepressants, selective serotonin reuptake inhibitors, or psychosocial intervention. (Grade: strong recommendation, moderate quality of evidence.)
Recommendation 5: Clinicians should ensure that advance care planning, including completion of advance directives, occurs for all patients with serious illness. (Grade: strong recommendation, low quality of evidence.)
Annals of Internal Medicine 2008;148:141-146.
Psoriasis Drug May Also Relieve Depression And Fatigue Linked To The Disease
A drug used to treat the clinical symptoms of psoriasis may also relieve fatigue and depression associated with the disease, concludes a randomised trial published online, Thursday December 15, 2005 by The Lancet.
Psoriasis has substantial psychological and emotional effects. Ranga Krishnan (Duke University Medical Center, Durham, North Carolina, USA) and colleagues looked at the effect of etanercept, an effective treatment for the clinical symptoms of psoriasis, on fatigue and symptoms of depression.
The team recruited over 600 patients with moderate to severe psoriasis from centers in the US and Canada; half received twice weekly doses of the drug for 12 weeks and half received placebo for 12 weeks.
They found that etanercept reduced the severity of psoriasis to a much greater extent than placebo. 47% of patients on the drug achieved a 75% or greater improvement from baseline in a psoriasis area and severity index score, compared with only 5% on placebo. Furthermore, patients who were assigned etanercept had a 50% improvement in a commonly used rating scale for depression when compared to those on placebo.
Patients taking the drug also had significant improvements on a scale that assesses fatigue than those on placebo.
Professor Krishnan states: "Etanercept treatment might relieve fatigue and symptoms of depression associated with this chronic disease."
Joe Santangelo
j.santangeloelsevier
Lancet
thelancet
Psoriasis has substantial psychological and emotional effects. Ranga Krishnan (Duke University Medical Center, Durham, North Carolina, USA) and colleagues looked at the effect of etanercept, an effective treatment for the clinical symptoms of psoriasis, on fatigue and symptoms of depression.
The team recruited over 600 patients with moderate to severe psoriasis from centers in the US and Canada; half received twice weekly doses of the drug for 12 weeks and half received placebo for 12 weeks.
They found that etanercept reduced the severity of psoriasis to a much greater extent than placebo. 47% of patients on the drug achieved a 75% or greater improvement from baseline in a psoriasis area and severity index score, compared with only 5% on placebo. Furthermore, patients who were assigned etanercept had a 50% improvement in a commonly used rating scale for depression when compared to those on placebo.
Patients taking the drug also had significant improvements on a scale that assesses fatigue than those on placebo.
Professor Krishnan states: "Etanercept treatment might relieve fatigue and symptoms of depression associated with this chronic disease."
Joe Santangelo
j.santangeloelsevier
Lancet
thelancet
STAR*D, A Landmark Depression Study Releases Results
The results of the "Sequenced Treatment Alternatives to Relieve Depression" (STAR*D) study are being released in the January 2006 edition of the American Journal Of Psychiatry (AJP), a monthly psychiatric journal of the American Psychiatric Association (APA).
The AJP article, Evaluation of Outcomes With Citalopram for Depression Using Measurement-Based Care in STAR*D: Implications for Clinical Practice, finds that only 30 percent of chronically depressed patients achieve remission during initial treatment with the selective serotonin reuptake inhibitor (SSRI) citalopram.
This real-world outcome study, led by Madhukar H. Trivedi, M.D., investigated 2,876 outpatients with nonpsychotic depression at 23 psychiatric and 18 primary care sites. Nearly 80 percent had chronic or recurrent major depression and comorbid medical and psychiatric conditions. Patients in both settings did not differ in remission or response rates and a substantial number of patients achieved remission or response at or around eight weeks of treatment.
"This study raises the bar for studies of real life outcomes of treatment for depression by focusing on recovery rather than mere improvement of symptoms. The good and bad news is that 30 percent of patients achieve recovery during initial treatment. While we are pleased about the recovery of so many people, the question of how the majority who do not achieve recovery should be treated is of obvious concern," said Robert Freedman, M.D., AJP editor-in-chief. "For now, the data offer new treatment guidelines for clinicians and realistic estimates of the likelihood of successful outcomes for their patients."
Findings also show that patients who were Caucasian, female, employed, or had higher levels of education or income had higher remission rates. While patients with comorbid disorders (especially anxiety or drug abuse) and general medical disorders were associated with lower remission rates.
"This study should prompt both primary care physicians and psychiatrists to monitor their patient's response to treatment with brief assessment instruments. Currently available instruments such as the QIDS or PHQ-9 may be used to correctly identify and modify treatment for the two-thirds of patients who don't achieve remission with initial treatment," said Darrel A. Regier, M.D., M.P.H., director of the APA's Division of Research. "The scope and design of this large National Institute of Mental Health study makes it a welcome addition to evidence-based treatment with significant practical utility for guiding clinical practice."
QIDS is Quick Inventory of Depressive Symptomatology and PHQ-9 is Patient Health Questionnaire (nine questions).
The STAR*D study was designed to assess effectiveness of treatments and ensure the delivery of adequate treatments.
(Am J Psychiatry. 2006; 163: 28-40).
About the American Psychiatric Association
The American Psychiatric Association is a national medical specialty society whose more than 36,000 physician members specialize in diagnosis, treatment, prevention and research of mental illnesses including substance use disorders. Visit the APA at psych and healthyminds.
The AJP article, Evaluation of Outcomes With Citalopram for Depression Using Measurement-Based Care in STAR*D: Implications for Clinical Practice, finds that only 30 percent of chronically depressed patients achieve remission during initial treatment with the selective serotonin reuptake inhibitor (SSRI) citalopram.
This real-world outcome study, led by Madhukar H. Trivedi, M.D., investigated 2,876 outpatients with nonpsychotic depression at 23 psychiatric and 18 primary care sites. Nearly 80 percent had chronic or recurrent major depression and comorbid medical and psychiatric conditions. Patients in both settings did not differ in remission or response rates and a substantial number of patients achieved remission or response at or around eight weeks of treatment.
"This study raises the bar for studies of real life outcomes of treatment for depression by focusing on recovery rather than mere improvement of symptoms. The good and bad news is that 30 percent of patients achieve recovery during initial treatment. While we are pleased about the recovery of so many people, the question of how the majority who do not achieve recovery should be treated is of obvious concern," said Robert Freedman, M.D., AJP editor-in-chief. "For now, the data offer new treatment guidelines for clinicians and realistic estimates of the likelihood of successful outcomes for their patients."
Findings also show that patients who were Caucasian, female, employed, or had higher levels of education or income had higher remission rates. While patients with comorbid disorders (especially anxiety or drug abuse) and general medical disorders were associated with lower remission rates.
"This study should prompt both primary care physicians and psychiatrists to monitor their patient's response to treatment with brief assessment instruments. Currently available instruments such as the QIDS or PHQ-9 may be used to correctly identify and modify treatment for the two-thirds of patients who don't achieve remission with initial treatment," said Darrel A. Regier, M.D., M.P.H., director of the APA's Division of Research. "The scope and design of this large National Institute of Mental Health study makes it a welcome addition to evidence-based treatment with significant practical utility for guiding clinical practice."
QIDS is Quick Inventory of Depressive Symptomatology and PHQ-9 is Patient Health Questionnaire (nine questions).
The STAR*D study was designed to assess effectiveness of treatments and ensure the delivery of adequate treatments.
(Am J Psychiatry. 2006; 163: 28-40).
About the American Psychiatric Association
The American Psychiatric Association is a national medical specialty society whose more than 36,000 physician members specialize in diagnosis, treatment, prevention and research of mental illnesses including substance use disorders. Visit the APA at psych and healthyminds.
Legendary Singer Connie Francis Partners With Mental Health America On National Campaign On Trauma-Informed Care
Legendary singer Connie Francis and Mental Health America joined in launching a new national campaign on the importance of stress and trauma in the development of mental health problems and the need to appropriately treat them in order for people to get better.
Called S.T.A.R. of Mine (for Stress, Treatment, Awareness, Recovery), the campaign will raise awareness of the impact of trauma, help remove the stigma attached to it, and inform the public and health professionals on the importance of a new generation of treatments that puts control back in the hands of the traumatized person so that they can feel safe again and achieve recovery.
Mental Health America has established a website for the campaign at: mentalhealthamerica/STAR.
"This campaign will address itself to the millions of people in America who are currently suffering from the deleterious effects of depression and trauma of all kinds whether it be the trauma experienced by victims of violent crime, rape, domestic abuse, loss of a loved one, divorce, loss of finances or a job, and significantly in the largely-unattended area of the Post-Traumatic Stress Disorder (PTSD) experienced by our returning veterans of our two wars," Francis said. "You don't have to be in a war, however, to be victimized by PTSD; many people wage war everyday with their struggle to come to grips with emotional problems that often seem insurmountable.
"Having been involuntarily committed seventeen times in nine years to mental institutions it is now my intention to be a voice for those suffering from mental disorders and to make them aware that there is hope and light at the end of an often bleak and interminable tunnel."
"Toxic stress and trauma can ruin health and mental health," said David L. Shern, Ph.D., president and CEO of Mental Health America. "While we know what to do to help, people often don't get appropriate services. The science is clear. The time to act is now."
Trauma is an emotional response to a terrible event like an accident, rape or natural disaster. Shock and denial are typical responses immediately following the event. Longer term reactions include unpredictable emotions, flashbacks, strained relationships and even physical symptoms such as headaches or nausea.
If untreated, trauma can damage a person's physical and emotional health. It can lead to addiction, severe mental illness, and many other very harmful consequences. The earlier in life the traumatic event happens, the more harmful it is.
It is also important that appropriate care is provided or re-traumatization can occur. For example, although unintended, a situation could occur where a large male counselor is assigned to a woman who was attacked by a large male, or a woman who was locked in a closet as a child is assigned to a small room.
A new generation of care called Trauma-Informed Care encourages people to talk about their trauma in their own time and in their own way. In a trauma-informed program, people respect survivors for what they have gone through and how they have coped, rather than assuming there is something wrong with them or blaming them for their problems.
Although Trauma-Informed Care has been recognized as critical to providing appropriate care to individuals, it has not been widely adopted. The campaign will work to achieve greater acceptance and implementation across the United States through a multi-pronged campaign.
Source
Mental Health America
Called S.T.A.R. of Mine (for Stress, Treatment, Awareness, Recovery), the campaign will raise awareness of the impact of trauma, help remove the stigma attached to it, and inform the public and health professionals on the importance of a new generation of treatments that puts control back in the hands of the traumatized person so that they can feel safe again and achieve recovery.
Mental Health America has established a website for the campaign at: mentalhealthamerica/STAR.
"This campaign will address itself to the millions of people in America who are currently suffering from the deleterious effects of depression and trauma of all kinds whether it be the trauma experienced by victims of violent crime, rape, domestic abuse, loss of a loved one, divorce, loss of finances or a job, and significantly in the largely-unattended area of the Post-Traumatic Stress Disorder (PTSD) experienced by our returning veterans of our two wars," Francis said. "You don't have to be in a war, however, to be victimized by PTSD; many people wage war everyday with their struggle to come to grips with emotional problems that often seem insurmountable.
"Having been involuntarily committed seventeen times in nine years to mental institutions it is now my intention to be a voice for those suffering from mental disorders and to make them aware that there is hope and light at the end of an often bleak and interminable tunnel."
"Toxic stress and trauma can ruin health and mental health," said David L. Shern, Ph.D., president and CEO of Mental Health America. "While we know what to do to help, people often don't get appropriate services. The science is clear. The time to act is now."
Trauma is an emotional response to a terrible event like an accident, rape or natural disaster. Shock and denial are typical responses immediately following the event. Longer term reactions include unpredictable emotions, flashbacks, strained relationships and even physical symptoms such as headaches or nausea.
If untreated, trauma can damage a person's physical and emotional health. It can lead to addiction, severe mental illness, and many other very harmful consequences. The earlier in life the traumatic event happens, the more harmful it is.
It is also important that appropriate care is provided or re-traumatization can occur. For example, although unintended, a situation could occur where a large male counselor is assigned to a woman who was attacked by a large male, or a woman who was locked in a closet as a child is assigned to a small room.
A new generation of care called Trauma-Informed Care encourages people to talk about their trauma in their own time and in their own way. In a trauma-informed program, people respect survivors for what they have gone through and how they have coped, rather than assuming there is something wrong with them or blaming them for their problems.
Although Trauma-Informed Care has been recognized as critical to providing appropriate care to individuals, it has not been widely adopted. The campaign will work to achieve greater acceptance and implementation across the United States through a multi-pronged campaign.
Source
Mental Health America
Kidney Disease Linked To Depression, Even In Early Stages
Depression has long been associated with end stage kidney disease, but
a new study published today in the American Journal of Kidney Diseases,
the official journal of the National Kidney Foundation, found that 20%
of patients with early stage chronic kidney disease (CKD) also suffered
from depression.
Researchers led by Susan Hedayati, MD, at the University of Texas
Southwestern Medical Center, found that the prevalence of major
depressive episodes in chronic kidney disease patients is greater than
those reported for patients with other chronic diseases including
diabetes (11%), congestive heart failure (14%) and coronary artery
disease (16%).
Researchers studied 272 patients with CKD in stages two through five
who they categorized as depressed or nondepressed based on the presence
or absence of the Mini International Neuropsychiatric Interview (MINI)
diagnosis of a current major depressive episode. One in five patients
met Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria
for a major depressive episode.
"Unemployment, psychiatric illness and diabetes were factors that
seemed to contribute to depression in the chronic kidney disease
patients we studied," says Hedayati. "Patients with chronic kidney
disease should understand that they are at increased risk for depression
and ask physicians to monitor them regularly for signs of depression.
"Early screening is especially important since depression is
associated with poor outcomes in patients with end stage kidney disease.
In fact, long term dialysis patients with clinical depression are twice
as likely to die or require hospitalization," continues Hedayati.
To help patients manage depression, the National Kidney Foundation
offers the following tips:
- Try to be with other people and to confide in someone
- Expect your mood to improve gradually not immediately
- Aim for 8 hours of sleep per day
- Exercise regularly; even if it's taking the stairs instead of the
elevator or parking the car further away from the store
Source
The National Kidney Foundation, Inc.
a new study published today in the American Journal of Kidney Diseases,
the official journal of the National Kidney Foundation, found that 20%
of patients with early stage chronic kidney disease (CKD) also suffered
from depression.
Researchers led by Susan Hedayati, MD, at the University of Texas
Southwestern Medical Center, found that the prevalence of major
depressive episodes in chronic kidney disease patients is greater than
those reported for patients with other chronic diseases including
diabetes (11%), congestive heart failure (14%) and coronary artery
disease (16%).
Researchers studied 272 patients with CKD in stages two through five
who they categorized as depressed or nondepressed based on the presence
or absence of the Mini International Neuropsychiatric Interview (MINI)
diagnosis of a current major depressive episode. One in five patients
met Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria
for a major depressive episode.
"Unemployment, psychiatric illness and diabetes were factors that
seemed to contribute to depression in the chronic kidney disease
patients we studied," says Hedayati. "Patients with chronic kidney
disease should understand that they are at increased risk for depression
and ask physicians to monitor them regularly for signs of depression.
"Early screening is especially important since depression is
associated with poor outcomes in patients with end stage kidney disease.
In fact, long term dialysis patients with clinical depression are twice
as likely to die or require hospitalization," continues Hedayati.
To help patients manage depression, the National Kidney Foundation
offers the following tips:
- Try to be with other people and to confide in someone
- Expect your mood to improve gradually not immediately
- Aim for 8 hours of sleep per day
- Exercise regularly; even if it's taking the stairs instead of the
elevator or parking the car further away from the store
Source
The National Kidney Foundation, Inc.
'Mind' Comments On Government 'Fit Note' Plans, UK
On the 25th Novembe the UK Government announced that it will implement Dame Carol Black's 'Fit for Work' proposals and replace sickness absence 'sick notes' with 'fit notes', designed to describe what an employee can do and help them remain in work.
Commenting on the plans, Mind's Chief Executive Paul Farmer said:
"Many people with mental health problems want to work, but lack of support both in work and during sickness absence present considerable barriers in allowing people to remain in employment. Currently, people can be signed off work and lose contact with their workplace altogether, making it increasingly difficult to return. Mind welcomes the Government's plans to turn 'sick notes' into 'fit notes', which if properly implemented, should allow people to remain in work while managing their recovery and prevent them from becoming alienated from working life.
"However, GPs aren't occupational health experts, and a person who is able to do work-related tasks necessarily able to cope with the working environment. GPs will need to be extremely sensitive to ensure that people's needs are properly assessed. For the system to work, doctors and employers need to cooperate closely so that healthcare and employment support work together to retain a mentally healthy workforce."
1. Today's government report, 'Improving health and work: changing lives' is a response to the Dame Carol Black's 'Fit for Work' proposals contained in her report 'Working for a healthier tomorrow' (March 2008).
Mind is the leading mental health charity in England and Wales. We work to create a better life for everyone with experience of mental distress.
Mind
Commenting on the plans, Mind's Chief Executive Paul Farmer said:
"Many people with mental health problems want to work, but lack of support both in work and during sickness absence present considerable barriers in allowing people to remain in employment. Currently, people can be signed off work and lose contact with their workplace altogether, making it increasingly difficult to return. Mind welcomes the Government's plans to turn 'sick notes' into 'fit notes', which if properly implemented, should allow people to remain in work while managing their recovery and prevent them from becoming alienated from working life.
"However, GPs aren't occupational health experts, and a person who is able to do work-related tasks necessarily able to cope with the working environment. GPs will need to be extremely sensitive to ensure that people's needs are properly assessed. For the system to work, doctors and employers need to cooperate closely so that healthcare and employment support work together to retain a mentally healthy workforce."
1. Today's government report, 'Improving health and work: changing lives' is a response to the Dame Carol Black's 'Fit for Work' proposals contained in her report 'Working for a healthier tomorrow' (March 2008).
Mind is the leading mental health charity in England and Wales. We work to create a better life for everyone with experience of mental distress.
Mind
Gene Therapy May Be Powerful New Treatment For Major Depression
In a report published in Science Translational Medicine, researchers at NewYork-Presbyterian Hospital/Weill Cornell Medical Center say animal and human data suggest gene therapy to the brain may be able to treat patients with major depression who do not respond to traditional drug treatment.
The researchers hope to rapidly translate their findings into a human clinical trial using the same kind of gene therapy modality the investigators have pioneered to treat Parkinson's disease. A 45-patient randomized blinded phase II multicenter clinical trial using the gene therapy to treat Parkinson's has recently ended and results are being readied for publication.
"Given our findings, we potentially have a novel therapy to target what we now believe is one root cause of human depression," says the study's senior investigator, Dr. Michael Kaplitt, associate professor and vice chairman for research of neurological surgery at Weill Cornell Medical College and a neurosurgeon at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
"Current therapies for depression treat symptoms but not underlying causes, and while that works for many patients, those with advanced depression, or depression that does not respond to medication, could hopefully benefit from our new approach," adds Dr. Kaplitt.
The Science Translational Medicine study demonstrates that a brain protein known as p11 in a single, small brain area, the nucleus accumbens, is critical to the feelings of reward and pleasure that are often missing in depression. This brain region had primarily been studied in addiction research, but the inability to find satisfaction with positive life experiences is one of the major sources of disability in depression.
While investigators believe that depression is a complex disorder that likely involves a number of brain areas and neural circuits, they say their findings suggest that restoring p11 may significantly alter the course of depression in humans.
"Applying molecular neurobiology and gene therapy to depression could dramatically alter the approach to psychiatric diseases," Dr. Kaplitt says. "Our results provide further evidence that the underlying causes of psychiatric disorders are due to molecular changes in key brain circuits, so that they are much more similar to common neurological disorders -- such as Parkinson's disease -- that might be helped by restoring molecular function."
The study pulls together human and animal data contributed by a team of researchers at NewYork-Presbyterian/Weill Cornell, as well as by investigators at Rockefeller University, Karolinska Institute in Sweden, the University of Texas Southwestern Medical Center and Neurologix in Fort Lee, N.J.
The idea for the new research began in conversations between Dr. Kaplitt, a pioneer of brain gene therapy, and Dr. Paul Greengard, of Rockefeller University, a neuroscientist who won a Nobel Prize in 2000 for his work in neurotransmission between brain neurons. In 2006, Dr. Greengard and his Rockefeller colleagues discovered that the p11 gene appears to play a key role in depression. They found p11 protein is needed to bring receptors that bind to the neurotransmitter serotonin to the surface of nerve cells. In the brain, serotonin regulates mood, appetite and sleep, among other functions, and most antidepressants seek to regulate serotonin.
"In the absence of p11, a neuron can produce all the serotonin receptors it needs, but they will not be transported to the cell surface and therefore won't stick out and latch on to the neurotransmitter," says Dr. Kaplitt.
So the researchers decided to disable function of the p11 gene in mice using a virus which would produce an siRNA -- small pieces of double-stranded RNA -- that blocked the gene's expression. Once they showed this could be done, they chose to selectively target p11 expression in the nucleus accumbens brain area because human functional MRI studies at Weill Cornell had shown this area to be particularly affected in depressed patients.
"Focusing exclusively on this area is fairly novel because it had been thought to be mostly involved in behaviors that are tied to addiction," Dr. Kaplitt says.
The mice without p11 all exhibited depression-like behaviors. That prompted Dr. Kaplitt and his team to adapt the gene therapy vehicle they had successfully tested in Parkinson's disease patients in a phase I clinical trial reported in the Lancet in 2007. The therapy uses an inert "smart" virus as a Trojan horse to enter brain cells and deposit a genetic payload into the genome of neurons. These new genes then produce their protein.
To treat Parkinson's disease Dr. Kaplitt used the virus to deliver glutamic acid decarboxylase (GAD), the enzyme that synthesizes the neurotransmitter GABA. In the current study, he inserted the p11 gene into the virus and delivered them to the nucleus accumbens of the p11-free mice. The treatment effectively reversed depression-like behaviors in the mice.
This study also reports that autopsy studies of patients with severe depression revealed significantly reduced levels of the p11 protein in their nucleus accumbens, compared with individuals without depression.
"Together, these studies provide strong evidence that maintaining adequate levels of this particular protein, p11, in this pleasure-reward area of the brain may be central to preventing or treating depression," Dr. Kaplitt says.
The researchers say that not only could the gene therapy used here restore p11, but future research may identify a small molecule to restore p11.
Notes:
The study was funded by grants from the Department of Defense, the National Institutes of Health, the Skirball Foundation, National Alliance for Research on Schizophrenia and Depression, and the Swedish Royal Academy of Science.
Study co-authors also included Brian Alexander, Margarita Arango-Lievano, Mary Vernov, Mihaela Stavarache, from NewYork-Presbyterian Hospital/Weill Cornell Medical Center; Jennifer Warner Schmidt and Marc Flajolet, from Rockefeller University; Therese Eriksson and Per Svenningsson, from Karolinska Institute; Carol Tamminga and Subroto Ghose, from the University of Texas Southwestern Medical Center; and Sergei Musatov, from Neurologix Inc.
Dr. Kaplitt is a founder of and paid consultant for Neurologix Inc., which has licensed intellectual property rights to p11 gene therapy for behavioral disorders. Dr. Greengard is a founder of and equity holder in Intracellular Therapies Inc., which has licensed intellectual property rights to p11. Dr. Kaplitt and Dr. Alexander are inventors on a patent application assigned to Cornell University related to p11 gene therapy for behavioral disorders. Dr. Greengard and Dr. Svenningsson are inventors on a patent application assigned to the Rockefeller University related to the p11 gene and behavioral disorders.
The researchers hope to rapidly translate their findings into a human clinical trial using the same kind of gene therapy modality the investigators have pioneered to treat Parkinson's disease. A 45-patient randomized blinded phase II multicenter clinical trial using the gene therapy to treat Parkinson's has recently ended and results are being readied for publication.
"Given our findings, we potentially have a novel therapy to target what we now believe is one root cause of human depression," says the study's senior investigator, Dr. Michael Kaplitt, associate professor and vice chairman for research of neurological surgery at Weill Cornell Medical College and a neurosurgeon at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
"Current therapies for depression treat symptoms but not underlying causes, and while that works for many patients, those with advanced depression, or depression that does not respond to medication, could hopefully benefit from our new approach," adds Dr. Kaplitt.
The Science Translational Medicine study demonstrates that a brain protein known as p11 in a single, small brain area, the nucleus accumbens, is critical to the feelings of reward and pleasure that are often missing in depression. This brain region had primarily been studied in addiction research, but the inability to find satisfaction with positive life experiences is one of the major sources of disability in depression.
While investigators believe that depression is a complex disorder that likely involves a number of brain areas and neural circuits, they say their findings suggest that restoring p11 may significantly alter the course of depression in humans.
"Applying molecular neurobiology and gene therapy to depression could dramatically alter the approach to psychiatric diseases," Dr. Kaplitt says. "Our results provide further evidence that the underlying causes of psychiatric disorders are due to molecular changes in key brain circuits, so that they are much more similar to common neurological disorders -- such as Parkinson's disease -- that might be helped by restoring molecular function."
The study pulls together human and animal data contributed by a team of researchers at NewYork-Presbyterian/Weill Cornell, as well as by investigators at Rockefeller University, Karolinska Institute in Sweden, the University of Texas Southwestern Medical Center and Neurologix in Fort Lee, N.J.
The idea for the new research began in conversations between Dr. Kaplitt, a pioneer of brain gene therapy, and Dr. Paul Greengard, of Rockefeller University, a neuroscientist who won a Nobel Prize in 2000 for his work in neurotransmission between brain neurons. In 2006, Dr. Greengard and his Rockefeller colleagues discovered that the p11 gene appears to play a key role in depression. They found p11 protein is needed to bring receptors that bind to the neurotransmitter serotonin to the surface of nerve cells. In the brain, serotonin regulates mood, appetite and sleep, among other functions, and most antidepressants seek to regulate serotonin.
"In the absence of p11, a neuron can produce all the serotonin receptors it needs, but they will not be transported to the cell surface and therefore won't stick out and latch on to the neurotransmitter," says Dr. Kaplitt.
So the researchers decided to disable function of the p11 gene in mice using a virus which would produce an siRNA -- small pieces of double-stranded RNA -- that blocked the gene's expression. Once they showed this could be done, they chose to selectively target p11 expression in the nucleus accumbens brain area because human functional MRI studies at Weill Cornell had shown this area to be particularly affected in depressed patients.
"Focusing exclusively on this area is fairly novel because it had been thought to be mostly involved in behaviors that are tied to addiction," Dr. Kaplitt says.
The mice without p11 all exhibited depression-like behaviors. That prompted Dr. Kaplitt and his team to adapt the gene therapy vehicle they had successfully tested in Parkinson's disease patients in a phase I clinical trial reported in the Lancet in 2007. The therapy uses an inert "smart" virus as a Trojan horse to enter brain cells and deposit a genetic payload into the genome of neurons. These new genes then produce their protein.
To treat Parkinson's disease Dr. Kaplitt used the virus to deliver glutamic acid decarboxylase (GAD), the enzyme that synthesizes the neurotransmitter GABA. In the current study, he inserted the p11 gene into the virus and delivered them to the nucleus accumbens of the p11-free mice. The treatment effectively reversed depression-like behaviors in the mice.
This study also reports that autopsy studies of patients with severe depression revealed significantly reduced levels of the p11 protein in their nucleus accumbens, compared with individuals without depression.
"Together, these studies provide strong evidence that maintaining adequate levels of this particular protein, p11, in this pleasure-reward area of the brain may be central to preventing or treating depression," Dr. Kaplitt says.
The researchers say that not only could the gene therapy used here restore p11, but future research may identify a small molecule to restore p11.
Notes:
The study was funded by grants from the Department of Defense, the National Institutes of Health, the Skirball Foundation, National Alliance for Research on Schizophrenia and Depression, and the Swedish Royal Academy of Science.
Study co-authors also included Brian Alexander, Margarita Arango-Lievano, Mary Vernov, Mihaela Stavarache, from NewYork-Presbyterian Hospital/Weill Cornell Medical Center; Jennifer Warner Schmidt and Marc Flajolet, from Rockefeller University; Therese Eriksson and Per Svenningsson, from Karolinska Institute; Carol Tamminga and Subroto Ghose, from the University of Texas Southwestern Medical Center; and Sergei Musatov, from Neurologix Inc.
Dr. Kaplitt is a founder of and paid consultant for Neurologix Inc., which has licensed intellectual property rights to p11 gene therapy for behavioral disorders. Dr. Greengard is a founder of and equity holder in Intracellular Therapies Inc., which has licensed intellectual property rights to p11. Dr. Kaplitt and Dr. Alexander are inventors on a patent application assigned to Cornell University related to p11 gene therapy for behavioral disorders. Dr. Greengard and Dr. Svenningsson are inventors on a patent application assigned to the Rockefeller University related to the p11 gene and behavioral disorders.
Study Finds Male Desire To Be Strong And Protect Family, Key To Preventing Suicides
Masculine ideals of strength coupled with strong family ties can help men combat depression and overcome thoughts of suicide, according to University of British Columbia research.
In a study to appear in a forthcoming issue of Social Science and Medicine, UBC researchers John Oliffe and John Ogrodniczuk looked at how men's ideas of masculinity served or hindered them during bouts of severe depression. Their findings shed light on risk factors and prevention strategies for suicide.
The authors analyzed qualitative data from interviews with 38 men between 24 and 50 years of age living in Vancouver and Prince George. The participants were self-identified or were formally diagnosed with depression.
The study suggests that men can best counter suicidal thoughts by connecting with others - namely intimate partners and family - to regain some stability and to secure emotional support from others.
"Support from friends and connecting to other things including spirituality is often the conduit to men seeking professional help to overcome the suicidal thoughts that can accompany severe depression" says lead author Oliffe, an associate professor in the School of Nursing.
Men die by suicide at least three times more than women although it is women who are diagnosed at twice the rate of men for depression. Men aged 20-29 have the highest rate of suicide. Statistics Canada reports that in 2003, the last year for which data is available, more than 2,900 men committed suicide.
The investigators found that most study participants expressed a strong commitment to their families and turned away from suicide for the hurt and trauma it would cause loved ones.
"Here, men's strong sense of masculine roles and responsibility as a provider and protector enables men to hold on while seeking support to regain some self-control," says Oliffe.
But Ogrodniczuk says the "stoic warrior" ideal also presents a downside that can lead men to shut down and look for escape. In these situations, study participants chose to mute their feelings or disconnect from others. They often overused alcohol and other drugs.
"Instead of finding respite from their emotional, mental and physical pain, self-harm emerged as the most common outcome of these actions," says Ogrodniczuk, an associate professor in the Dept. of Psychiatry
The study received support from the Canadian Institutes of Health Research (CIHR
In a study to appear in a forthcoming issue of Social Science and Medicine, UBC researchers John Oliffe and John Ogrodniczuk looked at how men's ideas of masculinity served or hindered them during bouts of severe depression. Their findings shed light on risk factors and prevention strategies for suicide.
The authors analyzed qualitative data from interviews with 38 men between 24 and 50 years of age living in Vancouver and Prince George. The participants were self-identified or were formally diagnosed with depression.
The study suggests that men can best counter suicidal thoughts by connecting with others - namely intimate partners and family - to regain some stability and to secure emotional support from others.
"Support from friends and connecting to other things including spirituality is often the conduit to men seeking professional help to overcome the suicidal thoughts that can accompany severe depression" says lead author Oliffe, an associate professor in the School of Nursing.
Men die by suicide at least three times more than women although it is women who are diagnosed at twice the rate of men for depression. Men aged 20-29 have the highest rate of suicide. Statistics Canada reports that in 2003, the last year for which data is available, more than 2,900 men committed suicide.
The investigators found that most study participants expressed a strong commitment to their families and turned away from suicide for the hurt and trauma it would cause loved ones.
"Here, men's strong sense of masculine roles and responsibility as a provider and protector enables men to hold on while seeking support to regain some self-control," says Oliffe.
But Ogrodniczuk says the "stoic warrior" ideal also presents a downside that can lead men to shut down and look for escape. In these situations, study participants chose to mute their feelings or disconnect from others. They often overused alcohol and other drugs.
"Instead of finding respite from their emotional, mental and physical pain, self-harm emerged as the most common outcome of these actions," says Ogrodniczuk, an associate professor in the Dept. of Psychiatry
The study received support from the Canadian Institutes of Health Research (CIHR
Altered Activity Of Circadian Rhythm Gene Implicated In Depression
Depression appears to be associated with a molecular-level disturbance in the body's 24-hour clock, new research suggests.
Scientists examined genes that regulate circadian rhythm in people with and without a history of depression. As a group, those with a history of depression had a higher level of activity of the so-called Clock gene, which has a role in regulating circadian rhythm, than did people with no mood disorders.
Higher expression levels of this gene suggest something is amiss in the body's 24-hour biological and behavioral cycle, which could affect sleep patterns and other physiological functions governed by circadian rhythm. Sleep disturbance is a common symptom of depression.
But the researchers noted that the association between the gene activity and depression is just that - a link, with no demonstrated causal effect in either direction. At this point in what is known about the relationship, this genetic profile could lead to depression or depression could alter this particular gene function, or some other biological or environmental influences could combine to disrupt the circadian clock.
Though this study offers just a snapshot in time of circadian activity in people with and without depression, the finding could have important clinical implications if it is supported by additional research. People with depression who share this genetic profile might benefit most from sleep-related treatments, such as light therapy or a class of antidepressants that act on melatonin, a hormone that regulates sleep.
"We know that there are a lot of insomnia symptoms in depression, especially early morning awakening," said Jean-Philippe Gouin, a graduate student in psychology at Ohio State University and lead author of the study. "We can't say with this study that there is a direct relationship between this altered gene function and behavior, but the research suggests that over-expression of circadian genes might serve as a biomarker of vulnerability to depression."
The research is published in a recent issue of the Journal of Affective Disorders.
Gouin is currently serving a predoctoral clinical psychology internship at Rush University Medical Center. As a graduate student at Ohio State, he has worked for years on studies led by the Institute for Behavioral Medicine Research that examine the health effects of chronic stress in people who take care of loved ones with dementia. Some of the people who participated in this study were from that population.
"There was some evidence that chronic stress led to changes in circadian gene expression in animals," Gouin said. "We wanted to see if that would be the case in humans, and one of the models of chronic stress in humans is dementia caregiving stress. We found that caregiving was not related to circadian genes, but instead it was really the history of depression that distinguishes between regulation of these genes."
The researchers collected blood samples from, and conducted interviews with, 60 people: 25 who were providing at least five hours of care per week for a family member with dementia and 35 non-caregiving controls with similar demographic characteristics. Thirty participants had a lifetime history of depression, while the other 30 had never been clinically depressed.
All blood samples were drawn between 9 a.m. and 11 a.m. to control for variations in circadian clock gene activity that occur throughout the day.
The researchers analyzed the blood to determine the messenger RNA levels for four circadian genes, including Clock. Messenger RNA (mRNA) contains the set of instructions for building proteins, so its level in genes dictates how much protein each gene is making.
As a group, the participants with a history of depression had a significantly higher level of Clock mRNA expression than did participants who had never been depressed. The researchers didn't find statistically significant results for the other three genes.
The association between depression and elevated Clock mRNA levels held up even when figures were adjusted for differences in age, sex, body mass index, alcohol and tobacco use, exercise, other medical conditions and caregiving status, Gouin noted.
He said that to further define the relationship between this genetic profile and depression, researchers ideally would monitor research participants over time to measure the changes in mRNA expression in circadian genes through a 24-hour cycle.
"If we look at people who have depression, they can have very different groups of symptoms. So if some of them have a biological profile that shows circadian dysfunction, there is a chance that a circadian type of treatment might be more helpful for them than for others," Gouin said.
He conducted the study with co-authors James Connors, Janice Kiecolt-Glaser, Ronald Glaser, William Malarkey, Cathie Atkinson and Ning Quan of Ohio State's Institute for Behavioral Medicine Research, and David Beversdorf of the University of Missouri.
The research was funded by the National Institutes of Health, a General Clinical Research Center grant, a Comprehensive Cancer Center grant and a Fonds de la Recherche en Sant?© du Qu?©bec Doctoral Training Award.
Scientists examined genes that regulate circadian rhythm in people with and without a history of depression. As a group, those with a history of depression had a higher level of activity of the so-called Clock gene, which has a role in regulating circadian rhythm, than did people with no mood disorders.
Higher expression levels of this gene suggest something is amiss in the body's 24-hour biological and behavioral cycle, which could affect sleep patterns and other physiological functions governed by circadian rhythm. Sleep disturbance is a common symptom of depression.
But the researchers noted that the association between the gene activity and depression is just that - a link, with no demonstrated causal effect in either direction. At this point in what is known about the relationship, this genetic profile could lead to depression or depression could alter this particular gene function, or some other biological or environmental influences could combine to disrupt the circadian clock.
Though this study offers just a snapshot in time of circadian activity in people with and without depression, the finding could have important clinical implications if it is supported by additional research. People with depression who share this genetic profile might benefit most from sleep-related treatments, such as light therapy or a class of antidepressants that act on melatonin, a hormone that regulates sleep.
"We know that there are a lot of insomnia symptoms in depression, especially early morning awakening," said Jean-Philippe Gouin, a graduate student in psychology at Ohio State University and lead author of the study. "We can't say with this study that there is a direct relationship between this altered gene function and behavior, but the research suggests that over-expression of circadian genes might serve as a biomarker of vulnerability to depression."
The research is published in a recent issue of the Journal of Affective Disorders.
Gouin is currently serving a predoctoral clinical psychology internship at Rush University Medical Center. As a graduate student at Ohio State, he has worked for years on studies led by the Institute for Behavioral Medicine Research that examine the health effects of chronic stress in people who take care of loved ones with dementia. Some of the people who participated in this study were from that population.
"There was some evidence that chronic stress led to changes in circadian gene expression in animals," Gouin said. "We wanted to see if that would be the case in humans, and one of the models of chronic stress in humans is dementia caregiving stress. We found that caregiving was not related to circadian genes, but instead it was really the history of depression that distinguishes between regulation of these genes."
The researchers collected blood samples from, and conducted interviews with, 60 people: 25 who were providing at least five hours of care per week for a family member with dementia and 35 non-caregiving controls with similar demographic characteristics. Thirty participants had a lifetime history of depression, while the other 30 had never been clinically depressed.
All blood samples were drawn between 9 a.m. and 11 a.m. to control for variations in circadian clock gene activity that occur throughout the day.
The researchers analyzed the blood to determine the messenger RNA levels for four circadian genes, including Clock. Messenger RNA (mRNA) contains the set of instructions for building proteins, so its level in genes dictates how much protein each gene is making.
As a group, the participants with a history of depression had a significantly higher level of Clock mRNA expression than did participants who had never been depressed. The researchers didn't find statistically significant results for the other three genes.
The association between depression and elevated Clock mRNA levels held up even when figures were adjusted for differences in age, sex, body mass index, alcohol and tobacco use, exercise, other medical conditions and caregiving status, Gouin noted.
He said that to further define the relationship between this genetic profile and depression, researchers ideally would monitor research participants over time to measure the changes in mRNA expression in circadian genes through a 24-hour cycle.
"If we look at people who have depression, they can have very different groups of symptoms. So if some of them have a biological profile that shows circadian dysfunction, there is a chance that a circadian type of treatment might be more helpful for them than for others," Gouin said.
He conducted the study with co-authors James Connors, Janice Kiecolt-Glaser, Ronald Glaser, William Malarkey, Cathie Atkinson and Ning Quan of Ohio State's Institute for Behavioral Medicine Research, and David Beversdorf of the University of Missouri.
The research was funded by the National Institutes of Health, a General Clinical Research Center grant, a Comprehensive Cancer Center grant and a Fonds de la Recherche en Sant?© du Qu?©bec Doctoral Training Award.
New Links Between Cholesterol And Depression In The Elderly
Most people know that high cholesterol levels place them at increased risk for heart disease and stroke. Prior research has shown that particular types of strokes contribute to one's risk for depression, and that abnormal blood lipid levels can increase the risk of depression in the elderly.
However, new findings by French researchers, published in Biological Psychiatry, suggest the link between increased cholesterol and depression may be complicated. They evaluated a large population of elderly men and women (aged 65 and over) over a seven year follow-up period, assessing them for symptoms of depression and measuring their lipid levels.
They found that, in women, depression was associated with low levels of the "good" form of cholesterol, high density lipoprotein (HDL). This disturbance in their cholesterol levels put them at higher risk for vascular disease, including stroke, by increasing their risk for developing lesions in their blood vessels called atherosclerotic plaques.
In contrast, the men who were at greater risk of depression had low levels of the "bad" form of cholesterol, low density lipoprotein (LDL). This was especially true for those men with a genetic vulnerability to depression related to a serotonin transporter gene.
This finding in men raises important considerations. Although this pattern of low LDL levels seemingly protects them from developing cardiovascular diseases or strokes, this study suggests that it increases their mental health risk at the same time.
Dr. Marie-Laure Ancelin, corresponding author for this study, commented: "Our results suggest that clinical management of abnormal lipid levels may reduce depression in the elderly, but different treatment will be required according to sex. LDL-C serum level seems to be an important biological marker in men, with a narrow range for normal functioning. Above this range, cardio- or cerebro-vascular risk increases and below it, there is increased risk of depression."
Therefore, the authors suggest that properly regulating the levels of HDL and LDL may help to prevent depression in the elderly. However, particularly careful management of LDL levels in men seems to be warranted. Dr. John Krystal, Editor of Biological Psychiatry, agreed, noting that "these new data provide yet another important reason that doctors and patients should monitor and regulate cholesterol levels carefully, through a combination of diet and medication."
However, new findings by French researchers, published in Biological Psychiatry, suggest the link between increased cholesterol and depression may be complicated. They evaluated a large population of elderly men and women (aged 65 and over) over a seven year follow-up period, assessing them for symptoms of depression and measuring their lipid levels.
They found that, in women, depression was associated with low levels of the "good" form of cholesterol, high density lipoprotein (HDL). This disturbance in their cholesterol levels put them at higher risk for vascular disease, including stroke, by increasing their risk for developing lesions in their blood vessels called atherosclerotic plaques.
In contrast, the men who were at greater risk of depression had low levels of the "bad" form of cholesterol, low density lipoprotein (LDL). This was especially true for those men with a genetic vulnerability to depression related to a serotonin transporter gene.
This finding in men raises important considerations. Although this pattern of low LDL levels seemingly protects them from developing cardiovascular diseases or strokes, this study suggests that it increases their mental health risk at the same time.
Dr. Marie-Laure Ancelin, corresponding author for this study, commented: "Our results suggest that clinical management of abnormal lipid levels may reduce depression in the elderly, but different treatment will be required according to sex. LDL-C serum level seems to be an important biological marker in men, with a narrow range for normal functioning. Above this range, cardio- or cerebro-vascular risk increases and below it, there is increased risk of depression."
Therefore, the authors suggest that properly regulating the levels of HDL and LDL may help to prevent depression in the elderly. However, particularly careful management of LDL levels in men seems to be warranted. Dr. John Krystal, Editor of Biological Psychiatry, agreed, noting that "these new data provide yet another important reason that doctors and patients should monitor and regulate cholesterol levels carefully, through a combination of diet and medication."
Sleep Chemical Central To Effectiveness Of Deep Brain Stimulation
A brain chemical that makes us sleepy also appears to play a central role in the success of deep brain stimulation to ease symptoms in patients with Parkinson's disease and other brain disorders. The surprising finding is outlined in a paper published online Dec. 23 in Nature Medicine.
The work shows that adenosine, a brain chemical most widely known as the cause of drowsiness, is central to the effect of deep brain stimulation, or DBS. The technique is used to treat people affected by Parkinson's disease and who have severe tremor, and it's also being tested in people who have severe depression or obsessive-compulsive disorder.
Patients typically are equipped with a "brain pacemaker," a small implanted device that delivers carefully choreographed electrical signals to a very precise point in the patient's brain. The procedure disrupts abnormal nerve signals and alleviates symptoms, but doctors have long debated exactly how the procedure works.
The new research, by a team of neuroscientists and neurosurgeons at the University of Rochester Medical Center, gives an unexpected nod to a role for adenosine and to cells called astrocytes that were long overlooked by neuroscientists.
"Certainly the electrical effect of the stimulation on neurons is central to the effect of deep brain stimulation," said Maiken Nedergaard, M.D., Ph.D., the neuroscientist and professor in the Department of Neurosurgery who led the research team. "But we also found a very important role for adenosine, which is surprising."
Adenosine in the brain is largely a byproduct of the chemical ATP, the source of energy for all our cells. Adenosine levels in the brain normally build as the day wears on, and ultimately it plays a huge role in making us sleepy - it's the brain's way of telling us that it's been a long day, we've expended a lot of energy, and it's time to go to bed.
The scientists say the role of adenosine in deep brain stimulation has not been realized before. Even though scientists have recognized its ability to inhibit brain cell signaling, they did not suspect any role as part of DBS's effect of squelching abnormal brain signaling.
"There are at least a dozen theories of what is happening in the brain when deep brain stimulation is applied, but the fact is that no one has really understood the process completely," said Robert Bakos, M.D., a neurosurgeon at the University of Rochester and a co-author of the paper, who has performed more than 100 DBS surgeries in the last decade. "We've all been focused on what is happening to the nerve cells in the brain, but it may be that we've been looking at the wrong cell type."
Nedergaard's team showed that the electrical pulses that are at the heart of DBS evoke those other cells - astrocytes - in the area immediately around the surgery to release ATP, which is then broken into adenosine. The extra adenosine reduces abnormal signaling among the brain's neurons.
The team also showed that in mice, an infusion of adenosine itself, without any deep brain stimulation, reduced abnormal brain signaling. They also demonstrated that in mice whose adenosine receptors had been blocked, DBS did not work; and they showed that a drug like caffeine that blocks adenosine receptors (the reason why caffeine helps keep us awake) also diminishes the effectiveness of DBS.
"It may be possible to enhance the effectiveness of deep brain stimulation by taking advantage of the role of agents that modulate the pathways initiated by adenosine," said Nedergaard. "Or, it's possible that one could develop another type of procedure, perhaps using local targeting of adenosine pathways in a way that does not involve a surgical procedure."
The latest work continues Nedergaard's line of research showing that brain cells other than neurons play a role in a host of human diseases. ATP in the brain is produced mainly by astrocytes, which are much more plentiful in the brain than neurons. Astrocytes were long thought of as simple support cells, but in recent years, Nedergaard and colleagues have shown that they play an important role in a host of diseases, including epilepsy, spinal cord disease, migraine headaches, and Alzheimer's disease.
The research on DBS came about as a result of a presentation Nedergaard made to colleagues about her research on astrocytes. Bakos linked her detailed description of astrocyte activity to what he sees happening in the brain when deep brain stimulation is applied. Based on Bakos' experience in the operating room and with funding from the National Institute of Neurological Disorders and Stroke, Nedergaard went back to the laboratory and analyzed the effects of deep brain stimulation in a way that no one had ever before considered.
"The correlation between what we see in the clinic and Dr. Nedergaard has found in the laboratory is really quite startling," said Bakos. "All the credit goes to her and her team. This has been a nice interchange of information between the clinic and the laboratory, to speed a discovery that really could have an impact on patients."
The lead authors on the paper are post-doctoral research associate Lane Bekar, Ph.D., and neurosurgeon Witold Libionka, M.D. The Rochester team is based both in the Department of Neurosurgery and the Center for Translational Medicine. In addition to Nedergaard and Bakos, other authors from Rochester include research assistant professors Guo F. Tian and Takahiro Takano; graduate students Arnulfo Torres and Ditte Lovatt; technical associate Qiwu Xu; former post-doctoral research associate Xiaohai Wang; and Erika Williams, a Fairport native and an undergraduate student at Williams College. Jurgen Schnermann of the National Institutes of Health also contributed.
The work shows that adenosine, a brain chemical most widely known as the cause of drowsiness, is central to the effect of deep brain stimulation, or DBS. The technique is used to treat people affected by Parkinson's disease and who have severe tremor, and it's also being tested in people who have severe depression or obsessive-compulsive disorder.
Patients typically are equipped with a "brain pacemaker," a small implanted device that delivers carefully choreographed electrical signals to a very precise point in the patient's brain. The procedure disrupts abnormal nerve signals and alleviates symptoms, but doctors have long debated exactly how the procedure works.
The new research, by a team of neuroscientists and neurosurgeons at the University of Rochester Medical Center, gives an unexpected nod to a role for adenosine and to cells called astrocytes that were long overlooked by neuroscientists.
"Certainly the electrical effect of the stimulation on neurons is central to the effect of deep brain stimulation," said Maiken Nedergaard, M.D., Ph.D., the neuroscientist and professor in the Department of Neurosurgery who led the research team. "But we also found a very important role for adenosine, which is surprising."
Adenosine in the brain is largely a byproduct of the chemical ATP, the source of energy for all our cells. Adenosine levels in the brain normally build as the day wears on, and ultimately it plays a huge role in making us sleepy - it's the brain's way of telling us that it's been a long day, we've expended a lot of energy, and it's time to go to bed.
The scientists say the role of adenosine in deep brain stimulation has not been realized before. Even though scientists have recognized its ability to inhibit brain cell signaling, they did not suspect any role as part of DBS's effect of squelching abnormal brain signaling.
"There are at least a dozen theories of what is happening in the brain when deep brain stimulation is applied, but the fact is that no one has really understood the process completely," said Robert Bakos, M.D., a neurosurgeon at the University of Rochester and a co-author of the paper, who has performed more than 100 DBS surgeries in the last decade. "We've all been focused on what is happening to the nerve cells in the brain, but it may be that we've been looking at the wrong cell type."
Nedergaard's team showed that the electrical pulses that are at the heart of DBS evoke those other cells - astrocytes - in the area immediately around the surgery to release ATP, which is then broken into adenosine. The extra adenosine reduces abnormal signaling among the brain's neurons.
The team also showed that in mice, an infusion of adenosine itself, without any deep brain stimulation, reduced abnormal brain signaling. They also demonstrated that in mice whose adenosine receptors had been blocked, DBS did not work; and they showed that a drug like caffeine that blocks adenosine receptors (the reason why caffeine helps keep us awake) also diminishes the effectiveness of DBS.
"It may be possible to enhance the effectiveness of deep brain stimulation by taking advantage of the role of agents that modulate the pathways initiated by adenosine," said Nedergaard. "Or, it's possible that one could develop another type of procedure, perhaps using local targeting of adenosine pathways in a way that does not involve a surgical procedure."
The latest work continues Nedergaard's line of research showing that brain cells other than neurons play a role in a host of human diseases. ATP in the brain is produced mainly by astrocytes, which are much more plentiful in the brain than neurons. Astrocytes were long thought of as simple support cells, but in recent years, Nedergaard and colleagues have shown that they play an important role in a host of diseases, including epilepsy, spinal cord disease, migraine headaches, and Alzheimer's disease.
The research on DBS came about as a result of a presentation Nedergaard made to colleagues about her research on astrocytes. Bakos linked her detailed description of astrocyte activity to what he sees happening in the brain when deep brain stimulation is applied. Based on Bakos' experience in the operating room and with funding from the National Institute of Neurological Disorders and Stroke, Nedergaard went back to the laboratory and analyzed the effects of deep brain stimulation in a way that no one had ever before considered.
"The correlation between what we see in the clinic and Dr. Nedergaard has found in the laboratory is really quite startling," said Bakos. "All the credit goes to her and her team. This has been a nice interchange of information between the clinic and the laboratory, to speed a discovery that really could have an impact on patients."
The lead authors on the paper are post-doctoral research associate Lane Bekar, Ph.D., and neurosurgeon Witold Libionka, M.D. The Rochester team is based both in the Department of Neurosurgery and the Center for Translational Medicine. In addition to Nedergaard and Bakos, other authors from Rochester include research assistant professors Guo F. Tian and Takahiro Takano; graduate students Arnulfo Torres and Ditte Lovatt; technical associate Qiwu Xu; former post-doctoral research associate Xiaohai Wang; and Erika Williams, a Fairport native and an undergraduate student at Williams College. Jurgen Schnermann of the National Institutes of Health also contributed.
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