Countless movies and TV shows make light of women's so-called "moodiness", often jokingly attributing it to their menstrual cycle or, conversely, to menopause. In fact, mood disorders are a serious and pervasive health problem, and large-scale population studies have found women are 1.5 to 3 times more likely to suffer from major depressive disorder than are men.
In a newly published study, women's health experts from the University of Alberta argue there is an urgent need for carefully designed, gender-specific research to better understand the relationship of female sex hormones to mood states and disorders.
"The reasons for the gender disparity in rates of depression are not completely understood," says Kathy Hegadoren, the Canada Research Chair in Stress Disorders in Women at the University of Alberta.
"But there is growing evidence that estrogens have powerful effects beyond their role in reproduction that they play a critical role in mood disorders in women and this opens new avenues for research into the underlying biological mechanisms and treatment of depression."
Estrogen can be used to treat various mood disturbances in women such as perimenopausal, postmenopausal and postpartum depression but the results of these treatments can be difficult to interpret because researchers are only beginning to recognize the complex interactions among estrogens, serotonin and mood.
"Right now, clinical use of sex-hormone therapies for the treatment of mood disorders is severely hampered by the inability to predict which women would respond well to such therapies," explains study co-author and U of A nursing professor Gerri Lasiuk.
"Most animal studies looking at the causes of depression have been conducted with male animals and use chronic stress models, which are assumed to be similar to depression."
Hegadoren and Lasiuk's study recognizes that multiple factors may be at play in the development of mood disturbances, with individual, psychosocial and environmental factors interacting in complicated ways to create differential vulnerability in women and men. But they also point out that the link to sex hormones is hard to deny.
"Previous research has found that, before puberty, the rates of mood and anxiety
disorders are similar in boys and girls. It's only after females begin menstrual function that a gender differential in mood disorders manifests itself. This, coupled with the observation that women appear to be especially vulnerable to mood disturbances during times of hormonal flux, certainly lends support to the claim that a relationship exists between sex hormones and mood," says Hegadoren.
The study, co-authored by Hegadoren and Lasiuk, appears in the October 2007 issue of the journal Biological Research for Nursing.
University of Alberta
685 General Services Bldg.
Edmonton, Alberta T6E 2H1
Canada
ualberta.ca
четверг, 27 октября 2011 г.
понедельник, 24 октября 2011 г.
Low Blood Levels Of Vitamin D May Be Associated With Depression In Older Adults
Older adults with low blood levels of vitamin D and high blood levels of a hormone secreted by the parathyroid glands may have a higher risk of depression, according to a report in the May issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
About 13 percent of older individuals have symptoms of depression, and other researchers have speculated that vitamin D may be linked to depression and other psychiatric illnesses, according to background information in the article. "Underlying causes of vitamin D deficiency such as less sun exposure as a result of decreased outdoor activity, different housing or clothing habits and decreased vitamin intake may be secondary to depression, but depression may also be the consequence of poor vitamin D status," the authors write. "Moreover, poor vitamin D status causes an increase in serum parathyroid hormone levels." Overactive parathyroid glands are frequently accompanied by symptoms of depression that disappear after treatment of the condition.
Witte J. G. Hoogendijk, M.D., Ph.D., and colleagues at VU University Medical Center, Vrije Universiteit Amsterdam, the Netherlands, measured blood levels of vitamin D and parathyroid hormone and assessed symptoms of depression among 1,282 community residents age 65 to 95. Of those individuals, 26 had a diagnosis of major depressive disorder, 169 had minor depression and 1,087 were not depressed. The average blood vitamin D level was 21 nanograms per milliliter and the average parathyroid hormone level was 3.6 picograms per milliliter.
Blood vitamin D levels were 14 percent lower in individuals with major and minor depression (average, 19 nanograms per milliliter) compared with non-depressed participants (average, 22 nanograms per milliliter). In addition, parathyroid hormone thyroid levels were an average of 5 percent higher in those with minor depression (average, 3.72 picograms per milliliter) and 33 percent higher in those with major depressive disorder (average, 4.69 picograms per milliliter) than in those who were not depressed (average, 3.53 picograms per milliliter).
The findings may be important to patients because both low blood vitamin D levels and high parathyroid hormone levels can be treated with higher dietary intake of vitamin D or calcium and increased sunlight exposure. "Moreover, the clinical relevance of the present study is underscored by our finding that 38.8 percent of men and 56.9 percent of women in our community-based cohort had an insufficient vitamin D status," they conclude. Additional studies are needed to determine whether changes in levels of vitamin D and parathyroid hormone precede depression or follow it.
Arch Gen Psychiatry. 2008;65[5]:508-512.
This study was supported by a clinical fellow grant from the Netherlands Organisation for Scientific Research.
Archives of General Psychiatry
About 13 percent of older individuals have symptoms of depression, and other researchers have speculated that vitamin D may be linked to depression and other psychiatric illnesses, according to background information in the article. "Underlying causes of vitamin D deficiency such as less sun exposure as a result of decreased outdoor activity, different housing or clothing habits and decreased vitamin intake may be secondary to depression, but depression may also be the consequence of poor vitamin D status," the authors write. "Moreover, poor vitamin D status causes an increase in serum parathyroid hormone levels." Overactive parathyroid glands are frequently accompanied by symptoms of depression that disappear after treatment of the condition.
Witte J. G. Hoogendijk, M.D., Ph.D., and colleagues at VU University Medical Center, Vrije Universiteit Amsterdam, the Netherlands, measured blood levels of vitamin D and parathyroid hormone and assessed symptoms of depression among 1,282 community residents age 65 to 95. Of those individuals, 26 had a diagnosis of major depressive disorder, 169 had minor depression and 1,087 were not depressed. The average blood vitamin D level was 21 nanograms per milliliter and the average parathyroid hormone level was 3.6 picograms per milliliter.
Blood vitamin D levels were 14 percent lower in individuals with major and minor depression (average, 19 nanograms per milliliter) compared with non-depressed participants (average, 22 nanograms per milliliter). In addition, parathyroid hormone thyroid levels were an average of 5 percent higher in those with minor depression (average, 3.72 picograms per milliliter) and 33 percent higher in those with major depressive disorder (average, 4.69 picograms per milliliter) than in those who were not depressed (average, 3.53 picograms per milliliter).
The findings may be important to patients because both low blood vitamin D levels and high parathyroid hormone levels can be treated with higher dietary intake of vitamin D or calcium and increased sunlight exposure. "Moreover, the clinical relevance of the present study is underscored by our finding that 38.8 percent of men and 56.9 percent of women in our community-based cohort had an insufficient vitamin D status," they conclude. Additional studies are needed to determine whether changes in levels of vitamin D and parathyroid hormone precede depression or follow it.
Arch Gen Psychiatry. 2008;65[5]:508-512.
This study was supported by a clinical fellow grant from the Netherlands Organisation for Scientific Research.
Archives of General Psychiatry
пятница, 21 октября 2011 г.
Mindfulness-Based Therapy Helps Prevent Depression Relapse
Mindfulness-based cognitive therapy appears to be similar to maintenance antidepressant medication for preventing relapse or recurrence among patients successfully treated for depression, according to a report in the December issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
"Relapse and recurrence after recovery from major depressive disorder are common and debilitating outcomes that carry enormous personal, familial and societal costs," the authors write as background information in the article. The current standard for preventing relapse is maintenance therapy with a single antidepressant. This regimen is generally effective if patients take their medications, but as many as 40 percent of them do not. "Alternatives to long-term antidepressant monotherapy, especially those that address mood outcomes in a broader context of well-being, may appeal to patients wary of continued intervention."
Zindel V. Segal, Ph.D., of the Centre for Addiction and Mental Health, Toronto, Ontario, Canada, and colleagues studied 160 patients age 18 to 65 who met criteria for major depressive disorder and had experienced at least two episodes of depression. After eight months of treatment, 84 (52.5 percent) achieved remission. Patients in remission were then randomly assigned to one of three treatment groups: 28 continued taking their medication; 30 had their medication slowly replaced by placebo; and 26 tapered their medication and then received mindfulness-based cognitive behavioral therapy.
In this therapy, patients learn to monitor and observe their thinking patterns when they feel sad, changing automatic reactions associated with depression (such as rumination and avoidance) into opportunities for useful reflection. "This is accomplished through daily homework exercises featuring (1) guided (taped) awareness exercises directed at increasing moment-by-moment nonjudgmental awareness of bodily sensations, thoughts, and feelings; (2) accepting difficulties with a stance of self-compassion; and (3) developing an 'action plan' composed of strategies for responding to early warning signs of relapse/recurrence," the authors write.
During the 18-month follow-up period, relapse occurred among 38 percent of those in the cognitive behavioral therapy group, 46 percent of those in the maintenance medication group and 60 percent of those in the placebo group, making both medication and behavioral therapy effective at preventing relapse.
About half (51 percent) of patients were classified as unstable remitters, defined as individuals who had symptom "flurries" or intermittently higher scores on depression rating scales despite having a low enough average score to qualify for remission. The other half (49 percent) were stable remitters with consistently low scores. Among unstable remitters, those taking maintenance medication or undergoing cognitive behavioral therapy were about 73 percent less likely to relapse than those taking placebo. Among stable remitters, there were no differences between the three groups.
"Our data highlight the importance of maintaining at least one active long-term treatment in recurrently depressed patients whose remission is unstable," the authors write. "For those unwilling or unable to tolerate maintenance antidepressant treatment, mindfulness-based cognitive therapy offers equal protection from relapse during an 18-month period." It is unclear exactly how mindfulness-based therapy works, but it may change neural pathways to support patterns that lead to recovery instead of to deeper depression, they note.
Arch Gen Psychiatry. 2010;67[12]:1256-1264.
Source
Archives of General Psychiatry
"Relapse and recurrence after recovery from major depressive disorder are common and debilitating outcomes that carry enormous personal, familial and societal costs," the authors write as background information in the article. The current standard for preventing relapse is maintenance therapy with a single antidepressant. This regimen is generally effective if patients take their medications, but as many as 40 percent of them do not. "Alternatives to long-term antidepressant monotherapy, especially those that address mood outcomes in a broader context of well-being, may appeal to patients wary of continued intervention."
Zindel V. Segal, Ph.D., of the Centre for Addiction and Mental Health, Toronto, Ontario, Canada, and colleagues studied 160 patients age 18 to 65 who met criteria for major depressive disorder and had experienced at least two episodes of depression. After eight months of treatment, 84 (52.5 percent) achieved remission. Patients in remission were then randomly assigned to one of three treatment groups: 28 continued taking their medication; 30 had their medication slowly replaced by placebo; and 26 tapered their medication and then received mindfulness-based cognitive behavioral therapy.
In this therapy, patients learn to monitor and observe their thinking patterns when they feel sad, changing automatic reactions associated with depression (such as rumination and avoidance) into opportunities for useful reflection. "This is accomplished through daily homework exercises featuring (1) guided (taped) awareness exercises directed at increasing moment-by-moment nonjudgmental awareness of bodily sensations, thoughts, and feelings; (2) accepting difficulties with a stance of self-compassion; and (3) developing an 'action plan' composed of strategies for responding to early warning signs of relapse/recurrence," the authors write.
During the 18-month follow-up period, relapse occurred among 38 percent of those in the cognitive behavioral therapy group, 46 percent of those in the maintenance medication group and 60 percent of those in the placebo group, making both medication and behavioral therapy effective at preventing relapse.
About half (51 percent) of patients were classified as unstable remitters, defined as individuals who had symptom "flurries" or intermittently higher scores on depression rating scales despite having a low enough average score to qualify for remission. The other half (49 percent) were stable remitters with consistently low scores. Among unstable remitters, those taking maintenance medication or undergoing cognitive behavioral therapy were about 73 percent less likely to relapse than those taking placebo. Among stable remitters, there were no differences between the three groups.
"Our data highlight the importance of maintaining at least one active long-term treatment in recurrently depressed patients whose remission is unstable," the authors write. "For those unwilling or unable to tolerate maintenance antidepressant treatment, mindfulness-based cognitive therapy offers equal protection from relapse during an 18-month period." It is unclear exactly how mindfulness-based therapy works, but it may change neural pathways to support patterns that lead to recovery instead of to deeper depression, they note.
Arch Gen Psychiatry. 2010;67[12]:1256-1264.
Source
Archives of General Psychiatry
вторник, 18 октября 2011 г.
Voluntary Exercise Does Not Appear To Alleviate Anxiety And Depression
Voluntary physical activity does not appear to cause a reduction in anxiety and depression, but exercise and mood may be associated through a common genetic factor, according to a report in the August issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
In the general population, regular exercise is associated with reduced anxious and depressive symptoms, according to background information in the article. Experiments involving specific clinical populations have suggested that exercise causes this reduction in anxiety and depression. However, it is unclear whether this causal effect also occurs in the larger population or whether there is a third underlying factor influencing both physical activity and the risk for mood disorders.
Marleen H. M. De Moor, M.Sc., of VU University Amsterdam, the Netherlands, and colleagues studied 5,952 twins from the Netherlands Twin Register, along with 1,357 additional siblings and 1,249 parents. Participants, all aged 18 to 50, filled out surveys about leisure-time exercise and completed four scales measuring anxious and depressive symptoms.
Associations observed between exercise and anxious and depressive symptoms "were small and were best explained by common genetic factors with opposite effects on exercise behavior and symptoms of anxiety and depression," the authors note. "In genetically identical twin pairs, the twin who exercised more did not display fewer anxious and depressive symptoms than the co-twin who exercised less." Exercise behavior in one identical twin predicted anxious and depressive symptoms in the other, meaning that if one twin exercised more, the other tended to have fewer symptoms.
However, the same was not true of dizygotic (fraternal) twins or other siblings, who share only part of their genetic material. In addition, analyses over time showed that individuals who increased their level of exercise did not experience a decrease in anxious and depressive symptoms.
"It is unknown which genes might be involved in voluntary exercise behavior and in the risk for anxiety and depression," the authors write, but genes involved in the brain pathways that process dopamine, norepinephrine, opioids or serotonin are likely candidates.
The results do not mean that exercise cannot benefit those with anxiety or depression, the authors note, only that additional trials would be needed to justify this type of therapy. "Only voluntary leisure-time exercise is influenced by genetic factors, whereas the other type of exercise [directed and monitored by someone else] is environment-driven. The absence of causal effects of voluntary exercise on symptoms of anxiety and depression does not imply that manipulation of exercise cannot be used to change such symptoms," they write. "The antidepressant effects of exercise may only occur if the exercise is monitored and part of a therapeutic program."
Arch Gen Psychiatry. 2008;65[8]:897-905.
archpsyc.ama-assn
This study was supported by grants from the Netherlands Organization for Scientific Research.
Marleen H. M. De Moor, M.Sc.
JAMA and Archives Journals
In the general population, regular exercise is associated with reduced anxious and depressive symptoms, according to background information in the article. Experiments involving specific clinical populations have suggested that exercise causes this reduction in anxiety and depression. However, it is unclear whether this causal effect also occurs in the larger population or whether there is a third underlying factor influencing both physical activity and the risk for mood disorders.
Marleen H. M. De Moor, M.Sc., of VU University Amsterdam, the Netherlands, and colleagues studied 5,952 twins from the Netherlands Twin Register, along with 1,357 additional siblings and 1,249 parents. Participants, all aged 18 to 50, filled out surveys about leisure-time exercise and completed four scales measuring anxious and depressive symptoms.
Associations observed between exercise and anxious and depressive symptoms "were small and were best explained by common genetic factors with opposite effects on exercise behavior and symptoms of anxiety and depression," the authors note. "In genetically identical twin pairs, the twin who exercised more did not display fewer anxious and depressive symptoms than the co-twin who exercised less." Exercise behavior in one identical twin predicted anxious and depressive symptoms in the other, meaning that if one twin exercised more, the other tended to have fewer symptoms.
However, the same was not true of dizygotic (fraternal) twins or other siblings, who share only part of their genetic material. In addition, analyses over time showed that individuals who increased their level of exercise did not experience a decrease in anxious and depressive symptoms.
"It is unknown which genes might be involved in voluntary exercise behavior and in the risk for anxiety and depression," the authors write, but genes involved in the brain pathways that process dopamine, norepinephrine, opioids or serotonin are likely candidates.
The results do not mean that exercise cannot benefit those with anxiety or depression, the authors note, only that additional trials would be needed to justify this type of therapy. "Only voluntary leisure-time exercise is influenced by genetic factors, whereas the other type of exercise [directed and monitored by someone else] is environment-driven. The absence of causal effects of voluntary exercise on symptoms of anxiety and depression does not imply that manipulation of exercise cannot be used to change such symptoms," they write. "The antidepressant effects of exercise may only occur if the exercise is monitored and part of a therapeutic program."
Arch Gen Psychiatry. 2008;65[8]:897-905.
archpsyc.ama-assn
This study was supported by grants from the Netherlands Organization for Scientific Research.
Marleen H. M. De Moor, M.Sc.
JAMA and Archives Journals
суббота, 15 октября 2011 г.
Social Form Of Bullying Linked To Depression, Anxiety In Adults
Spreading rumors and gossiping may not cause bruises or black eyes, but the psychological consequences of this social type of bullying could linger into early adulthood, a new University of Florida study shows.
In a study of 210 college students, UF researchers discovered a link between what psychologists call relational victimization in adolescence and depression and anxiety in early adulthood, according to findings published online this month in the journal Psychology in the Schools. Rather than threatening a child with physical violence, these bullies target a child's social status and relationships by shunning them, excluding them from social activities or spreading rumors, said Allison Dempsey, a doctoral student in the UF College of Education and the study's lead author.
"Even though people are outside of high school, the memories of these experiences continue to be associated with depression and social anxiety," said Dempsey, who graduated from Columbine High School in Colorado one year before the 1999 school shooting there and now studies school prevention programs. "It was interesting to see these relationships still continue to exist even though they are in early adulthood now and in a completely different setting.
"I'm hoping this study will help shed light on the fact that this is a real problem and continues to be a real problem after students leave school."
To uncover the relationships between social bullying and loneliness, depression and anxiety, researchers surveyed college undergraduates between the ages of 18 and 25 and asked them to recall their experiences from high school. They were also looking to see if having friends mitigated some of the effects of bullying and if there was any relationship between gender and the severity of psychological symptoms, said Eric Storch, Ph.D., an assistant professor of psychiatry in the UF College of Medicine and a co-author of the study.
"About 20 years ago people thought of bullying as very physical," Storch said. "As a result people thought guys did the bullying, and that it wasn't really a big experience for girls. The problem is that isn't actually true. There are different types of aggression.
"Boys do tend to be more physical, but both sexes engage in relational victimization. We wanted to see if gender affected strength of the relationship between depressive symptoms and victimization."
But researchers found no gender difference in the link between this type of bullying and depression. They also discovered that having friends or other positive social relationships didn't lessen rates of depression and anxiety in adulthood, a finding that surprised them, Dempsey said.
For some children, having friends and positive support can help make them more resilient to the slings and arrows from bullies, Storch said. But other children take the words and abuse more to heart and begin to believe what's being said about them.
"Those types of negative thoughts are actually believed to be at the core of things like depression and anxiety," Storch said. "Behaviorally what starts happening is you avoid interactions and situations that could be quite positive for you."
Currently, there are few prevention or intervention programs that focus specifically on relational victimization, in part because it's tougher to pinpoint and stop, Dempsey said.
"If a child tries to punch someone or kick someone, there's evidence of that happening," Dempsey said. "There's a definite aggressor and a definite victim. When it comes to spreading rumors and gossiping, that's a lot more difficult to prove who's doing it. And it's harder to provide consequences."
Dempsey said she hopes this study and others will help other researchers and psychologists design programs that can help stop this form of bullying in schools.
"I think many people have the belief that victimization is a normal rite of passage in childhood," Storch said. "While it certainly does happen to most kids, it's not acceptable. And while I think it would be difficult to completely curtail it, by reducing it you're going to help someone a tremendous amount to not have to go to school and be plagued by this environment of being tortured day in and day out.
"This isn't a normative experience and we need to do something about it and recognize that not doing something could affect children who are really rising stars."
Wendy Troop-Gordon, Ph.D., an assistant professor of psychology at North Dakota State University, said understanding how past relational bullying affects people in adulthood is an important step forward for research in this field.
"Turning 18 is not a magical age when you leave all of these experiences behind," said Troop-Gordon, who is not affiliated with the study. "People do seem to carry these experiences with them."
The University of Florida Health Science Center - the most comprehensive academic health center in the Southeast - is dedicated to high-quality programs of education, research, patient care and public service. The Health Science Center encompasses the colleges of Dentistry, Public Health and Health Professions, Medicine, Nursing, Pharmacy and Veterinary Medicine, as well as the Veterinary Medical Teaching Hospital and an academic campus in Jacksonville offering graduate education programs in dentistry, medicine, nursing and pharmacy. Patient care activities, under the banner UF&Shands, are provided through teaching hospitals and a network of clinics in Gainesville and Jacksonville. The Health Science Center also has a statewide presence through satellite medical, dental and nursing clinics staffed by UF health professionals; and affiliations with community-based health-care facilities stretching from Hialeah and Miami to the Florida Panhandle.
University of Florida Health Science Center
In a study of 210 college students, UF researchers discovered a link between what psychologists call relational victimization in adolescence and depression and anxiety in early adulthood, according to findings published online this month in the journal Psychology in the Schools. Rather than threatening a child with physical violence, these bullies target a child's social status and relationships by shunning them, excluding them from social activities or spreading rumors, said Allison Dempsey, a doctoral student in the UF College of Education and the study's lead author.
"Even though people are outside of high school, the memories of these experiences continue to be associated with depression and social anxiety," said Dempsey, who graduated from Columbine High School in Colorado one year before the 1999 school shooting there and now studies school prevention programs. "It was interesting to see these relationships still continue to exist even though they are in early adulthood now and in a completely different setting.
"I'm hoping this study will help shed light on the fact that this is a real problem and continues to be a real problem after students leave school."
To uncover the relationships between social bullying and loneliness, depression and anxiety, researchers surveyed college undergraduates between the ages of 18 and 25 and asked them to recall their experiences from high school. They were also looking to see if having friends mitigated some of the effects of bullying and if there was any relationship between gender and the severity of psychological symptoms, said Eric Storch, Ph.D., an assistant professor of psychiatry in the UF College of Medicine and a co-author of the study.
"About 20 years ago people thought of bullying as very physical," Storch said. "As a result people thought guys did the bullying, and that it wasn't really a big experience for girls. The problem is that isn't actually true. There are different types of aggression.
"Boys do tend to be more physical, but both sexes engage in relational victimization. We wanted to see if gender affected strength of the relationship between depressive symptoms and victimization."
But researchers found no gender difference in the link between this type of bullying and depression. They also discovered that having friends or other positive social relationships didn't lessen rates of depression and anxiety in adulthood, a finding that surprised them, Dempsey said.
For some children, having friends and positive support can help make them more resilient to the slings and arrows from bullies, Storch said. But other children take the words and abuse more to heart and begin to believe what's being said about them.
"Those types of negative thoughts are actually believed to be at the core of things like depression and anxiety," Storch said. "Behaviorally what starts happening is you avoid interactions and situations that could be quite positive for you."
Currently, there are few prevention or intervention programs that focus specifically on relational victimization, in part because it's tougher to pinpoint and stop, Dempsey said.
"If a child tries to punch someone or kick someone, there's evidence of that happening," Dempsey said. "There's a definite aggressor and a definite victim. When it comes to spreading rumors and gossiping, that's a lot more difficult to prove who's doing it. And it's harder to provide consequences."
Dempsey said she hopes this study and others will help other researchers and psychologists design programs that can help stop this form of bullying in schools.
"I think many people have the belief that victimization is a normal rite of passage in childhood," Storch said. "While it certainly does happen to most kids, it's not acceptable. And while I think it would be difficult to completely curtail it, by reducing it you're going to help someone a tremendous amount to not have to go to school and be plagued by this environment of being tortured day in and day out.
"This isn't a normative experience and we need to do something about it and recognize that not doing something could affect children who are really rising stars."
Wendy Troop-Gordon, Ph.D., an assistant professor of psychology at North Dakota State University, said understanding how past relational bullying affects people in adulthood is an important step forward for research in this field.
"Turning 18 is not a magical age when you leave all of these experiences behind," said Troop-Gordon, who is not affiliated with the study. "People do seem to carry these experiences with them."
The University of Florida Health Science Center - the most comprehensive academic health center in the Southeast - is dedicated to high-quality programs of education, research, patient care and public service. The Health Science Center encompasses the colleges of Dentistry, Public Health and Health Professions, Medicine, Nursing, Pharmacy and Veterinary Medicine, as well as the Veterinary Medical Teaching Hospital and an academic campus in Jacksonville offering graduate education programs in dentistry, medicine, nursing and pharmacy. Patient care activities, under the banner UF&Shands, are provided through teaching hospitals and a network of clinics in Gainesville and Jacksonville. The Health Science Center also has a statewide presence through satellite medical, dental and nursing clinics staffed by UF health professionals; and affiliations with community-based health-care facilities stretching from Hialeah and Miami to the Florida Panhandle.
University of Florida Health Science Center
среда, 12 октября 2011 г.
European Medicines Agency Recommends Acomplia Must Not Be Used In Patients On Antidepressants Or With Major Depression
The European Medicines Agency (EMEA) recommended contraindicating
Acomplia (rimonabant) from sanofi-aventis, in patients with ongoing
major depression or who are being treated with antidepressants, because
of the risk of psychiatric side effects. Doctors in the EU have already
been warned about this since June 2006 but the Agency's Committee for
Medicinal Products for Human Use (CHMP) has now recommended upgrading
this warning.
Acomplia has been authorised in the EU since June 2006 as an adjunct to
diet and exercise for the treatment of obese or overweight adult
patients. Psychiatric side effects, in particular depression, were
identified as the main safety issue at the time of approval. They were
reflected in the medicine's product information as a warning that
doctors should not prescribe Acomplia in patients with uncontrolled
serious psychiatric conditions such as major depression.
As part of its continuous monitoring of the safety of medicines, the
CHMP requested sanofi-aventis in June 2007 to submit all available
information on the psychiatric side effects of Acomplia. Finalising the
assessment of the available data at its 16-19 July 2007 meeting, the
CHMP concluded that the benefits of Acomplia continue to outweigh its
risks, except in patients with ongoing major depression or taking
antidepressants.
The CHMP also recommended adding a warning that treatment with Acomplia
should be stopped if a patient develops depression, as well as the
inclusion of additional information on the psychiatric safety of
Acomplia.
Doctors will be sent a letter to inform them about the updated
prescribing information. Patients and their carers should be aware of
the risk of depression in patients taking Acomplia.
The CHMP recommendation will now be forwarded to the European Commission
for adoption of a Decision.
1. For more information, see the accompanying question-and-answer
document
, which also includes the recommended updated product
information (in Annex 1).
2. Acomplia is authorised in the European Union/European Economic
Area, and is marketed in 13 European countries. Rimonabant is also
authorised as Zimulti, but this product is not marketed in the European
Union.
3. The European Public Assessment Report for Acomplia can be found
here.
4. This press release, together with other information on the work
of the EMEA, can be found on the EMEA website: emea.europa.eu.
Acomplia (rimonabant) from sanofi-aventis, in patients with ongoing
major depression or who are being treated with antidepressants, because
of the risk of psychiatric side effects. Doctors in the EU have already
been warned about this since June 2006 but the Agency's Committee for
Medicinal Products for Human Use (CHMP) has now recommended upgrading
this warning.
Acomplia has been authorised in the EU since June 2006 as an adjunct to
diet and exercise for the treatment of obese or overweight adult
patients. Psychiatric side effects, in particular depression, were
identified as the main safety issue at the time of approval. They were
reflected in the medicine's product information as a warning that
doctors should not prescribe Acomplia in patients with uncontrolled
serious psychiatric conditions such as major depression.
As part of its continuous monitoring of the safety of medicines, the
CHMP requested sanofi-aventis in June 2007 to submit all available
information on the psychiatric side effects of Acomplia. Finalising the
assessment of the available data at its 16-19 July 2007 meeting, the
CHMP concluded that the benefits of Acomplia continue to outweigh its
risks, except in patients with ongoing major depression or taking
antidepressants.
The CHMP also recommended adding a warning that treatment with Acomplia
should be stopped if a patient develops depression, as well as the
inclusion of additional information on the psychiatric safety of
Acomplia.
Doctors will be sent a letter to inform them about the updated
prescribing information. Patients and their carers should be aware of
the risk of depression in patients taking Acomplia.
The CHMP recommendation will now be forwarded to the European Commission
for adoption of a Decision.
1. For more information, see the accompanying question-and-answer
document
, which also includes the recommended updated product
information (in Annex 1).
2. Acomplia is authorised in the European Union/European Economic
Area, and is marketed in 13 European countries. Rimonabant is also
authorised as Zimulti, but this product is not marketed in the European
Union.
3. The European Public Assessment Report for Acomplia can be found
here.
4. This press release, together with other information on the work
of the EMEA, can be found on the EMEA website: emea.europa.eu.
воскресенье, 9 октября 2011 г.
Genetic Link To Premenstrual Depression
A specific genetic variation may be tied to an increased risk for severe premenstrual depression, scientists at the University of North Carolina at Chapel Hill and the National Institute of Mental Health have found.
Known medically as premenstrual dysphoric disorder, or PMDD, this psychiatric condition affects roughly 8 percent of women in their childbearing years. It's characterized by bouts of major depression and/or anxiety and severe irritability during the second half of the menstrual cycle. Symptoms subside with the onset of each menstrual period.
While PMDD has been thought to be linked to hormonal changes over the course of the menstrual cycle, until now an explanation for the susceptibility to hormone-related mood changes has been elusive. "Our initial hope in the study was that by looking at steroid-related genes like those for receptors for steroid hormones such as estrogen, we would be able to find gene differences that might explain why some women have these mood disorders and others don't," said Dr. David R. Rubinow, the study's senior author and the Meymandi distinguished professor and chair of psychiatry at UNC School of Medicine. "This study may begin to provide important clues to the nature of that susceptibility."
The study is the first to identify a genetic variation linked to a mood disorder associated with endocrine changes during the menstrual cycle, Rubinow said. The results will appear in an upcoming print edition of the journal Biological Psychiatry and were published online June 30, 2007. The study was supported by funds from the Intramural Research Program at the National Institute of Mental Health (NIMH).
The research involved 91 women for whom the authors prospectively confirmed a diagnosis of PMDD over at least three months. Another 56 women who had no history of mood disorders related to the menstrual cycle served as a comparison group. All the women provided blood samples for genetic analysis.
The team discovered four specific genetic variants, called single nucleotide polymorphisms, in one of the two genes that encode the estrogen receptor. The variants, which are differences in strings of DNA nucleotides A, G, C, or T, were identified in the estrogen receptor alpha gene, ESR1.
Compared to the control group, women with PMDD were significantly more likely to have the ESR1 gene variants, the study found.
"While these are preliminary findings that require replication in larger studies, we would argue that this may explain part of the variance among women in the susceptibility to developing this mood disorder," Rubinow said. "Studies have shown that PMDD is characterized by abnormal sensitivity to reproductive steroids like estrogen. As a receptor for the hormone that can trigger the onset of PMDD symptoms, ESR1 has clear physiologic relevance for this disorder."
The authors acknowledge that as with other complex genetic disorders, the contribution to PMDD of polymorphisms in a single gene may not be large. In addition, they also noted that the findings may be telling us more about the control group.
These women, who have no history of psychiatric problems or menstrual cycle-related symptoms, may have gene variants that protect against PMDD. According to Rubinow, "this is equally interesting because it may help us to understand resilience and protection, which are also very important."
Dr. Susan S. Girdler, professor of psychiatry and director of the UNC Psychiatry Stress and Health Research Program, pointed out that the severity of PMDD symptoms are as great or can be as great as those of women with full-blown major depression or major anxiety disorder. "But what makes them different is that the symptoms are very time-limited and linked strongly with the women's menstrual cycle."
Girdler emphasizes that to qualify for PMDD, symptoms must be severe enough to interfere with everyday functioning - to disrupt relationships, result in social withdrawal, even prompt thoughts of suicide. "We are talking about women who meet very stringent diagnostic criteria for PMDD. This is not the garden variety PMS."
Rubinow's coauthors were from the National Institute of Mental Health's Behavioral Endocrinology Branch and Program on Genes, Cognition and Psychosis.
The UNC Center for Women's Mood Disorders is conducting follow-up studies on the genetic and environmental contributors to PMDD. Eligible women will receive free diagnostic and medical evaluations, and may be eligible to take part in reatment studies or studies providing monetary compensation.
Known medically as premenstrual dysphoric disorder, or PMDD, this psychiatric condition affects roughly 8 percent of women in their childbearing years. It's characterized by bouts of major depression and/or anxiety and severe irritability during the second half of the menstrual cycle. Symptoms subside with the onset of each menstrual period.
While PMDD has been thought to be linked to hormonal changes over the course of the menstrual cycle, until now an explanation for the susceptibility to hormone-related mood changes has been elusive. "Our initial hope in the study was that by looking at steroid-related genes like those for receptors for steroid hormones such as estrogen, we would be able to find gene differences that might explain why some women have these mood disorders and others don't," said Dr. David R. Rubinow, the study's senior author and the Meymandi distinguished professor and chair of psychiatry at UNC School of Medicine. "This study may begin to provide important clues to the nature of that susceptibility."
The study is the first to identify a genetic variation linked to a mood disorder associated with endocrine changes during the menstrual cycle, Rubinow said. The results will appear in an upcoming print edition of the journal Biological Psychiatry and were published online June 30, 2007. The study was supported by funds from the Intramural Research Program at the National Institute of Mental Health (NIMH).
The research involved 91 women for whom the authors prospectively confirmed a diagnosis of PMDD over at least three months. Another 56 women who had no history of mood disorders related to the menstrual cycle served as a comparison group. All the women provided blood samples for genetic analysis.
The team discovered four specific genetic variants, called single nucleotide polymorphisms, in one of the two genes that encode the estrogen receptor. The variants, which are differences in strings of DNA nucleotides A, G, C, or T, were identified in the estrogen receptor alpha gene, ESR1.
Compared to the control group, women with PMDD were significantly more likely to have the ESR1 gene variants, the study found.
"While these are preliminary findings that require replication in larger studies, we would argue that this may explain part of the variance among women in the susceptibility to developing this mood disorder," Rubinow said. "Studies have shown that PMDD is characterized by abnormal sensitivity to reproductive steroids like estrogen. As a receptor for the hormone that can trigger the onset of PMDD symptoms, ESR1 has clear physiologic relevance for this disorder."
The authors acknowledge that as with other complex genetic disorders, the contribution to PMDD of polymorphisms in a single gene may not be large. In addition, they also noted that the findings may be telling us more about the control group.
These women, who have no history of psychiatric problems or menstrual cycle-related symptoms, may have gene variants that protect against PMDD. According to Rubinow, "this is equally interesting because it may help us to understand resilience and protection, which are also very important."
Dr. Susan S. Girdler, professor of psychiatry and director of the UNC Psychiatry Stress and Health Research Program, pointed out that the severity of PMDD symptoms are as great or can be as great as those of women with full-blown major depression or major anxiety disorder. "But what makes them different is that the symptoms are very time-limited and linked strongly with the women's menstrual cycle."
Girdler emphasizes that to qualify for PMDD, symptoms must be severe enough to interfere with everyday functioning - to disrupt relationships, result in social withdrawal, even prompt thoughts of suicide. "We are talking about women who meet very stringent diagnostic criteria for PMDD. This is not the garden variety PMS."
Rubinow's coauthors were from the National Institute of Mental Health's Behavioral Endocrinology Branch and Program on Genes, Cognition and Psychosis.
The UNC Center for Women's Mood Disorders is conducting follow-up studies on the genetic and environmental contributors to PMDD. Eligible women will receive free diagnostic and medical evaluations, and may be eligible to take part in reatment studies or studies providing monetary compensation.
четверг, 6 октября 2011 г.
Younger White Male Veterans At Increased Risk Of Suicide
Male veterans are three times more likely than female veterans to commit suicide. Also, whites have a much higher rate of suicide compared with patients of other races.
Researchers examined associations between demographic and clinical characteristics and risk of suicide among veterans treated for depression in the Veteran's Health Administration (VA) system. Out of 807,694 veterans included in the study, 1,683 - or 0.21 percent - committed suicide during the study period. Data suggests that the rate of suicide among male veterans is three times higher than the rate among female veterans, less than the 4:1 ratio reported for the general population. In addition, the rate of suicide among whites was 95.01 per 100,000 person-years, much higher than the 27.08 per 100,000 person-years for blacks and 56.17 per 100,000 person-years for other races. Younger veterans aged 18-44 had moderately higher suicide rates than did middle-aged patients aged 45-65 and modestly higher rates than elderly patients (94.98, 77.93 and 90.06 per 100,000 person-years, respectively). Surprisingly, veterans diagnosed with posttraumatic stress disorder (PTSD) had a lower rate of suicide than those without PTSD.
"These findings can help identify depressed veterans at greatest risk of suicide, allowing providers in the VA health care system to more closely monitor these patients and can provide policy-makers with valuable information about high-risk veterans," the study's authors said. [From: "Suicide Mortality Among Individuals Receiving Treatment for Depression in the Veterans Affairs Health System: Associations with Patient and Treatment Setting Characteristics." Contact: Kara Gavin, kegavinumich.]
The American Journal of Public Health is the monthly journal of the American Public Health Association (APHA), the oldest organization of public health professionals in the world. APHA is a leading publisher of books and periodicals promoting sound scientific standards, action programs and public policy to enhance health.
American Journal of Public Health .
Researchers examined associations between demographic and clinical characteristics and risk of suicide among veterans treated for depression in the Veteran's Health Administration (VA) system. Out of 807,694 veterans included in the study, 1,683 - or 0.21 percent - committed suicide during the study period. Data suggests that the rate of suicide among male veterans is three times higher than the rate among female veterans, less than the 4:1 ratio reported for the general population. In addition, the rate of suicide among whites was 95.01 per 100,000 person-years, much higher than the 27.08 per 100,000 person-years for blacks and 56.17 per 100,000 person-years for other races. Younger veterans aged 18-44 had moderately higher suicide rates than did middle-aged patients aged 45-65 and modestly higher rates than elderly patients (94.98, 77.93 and 90.06 per 100,000 person-years, respectively). Surprisingly, veterans diagnosed with posttraumatic stress disorder (PTSD) had a lower rate of suicide than those without PTSD.
"These findings can help identify depressed veterans at greatest risk of suicide, allowing providers in the VA health care system to more closely monitor these patients and can provide policy-makers with valuable information about high-risk veterans," the study's authors said. [From: "Suicide Mortality Among Individuals Receiving Treatment for Depression in the Veterans Affairs Health System: Associations with Patient and Treatment Setting Characteristics." Contact: Kara Gavin, kegavinumich.]
The American Journal of Public Health is the monthly journal of the American Public Health Association (APHA), the oldest organization of public health professionals in the world. APHA is a leading publisher of books and periodicals promoting sound scientific standards, action programs and public policy to enhance health.
American Journal of Public Health .
понедельник, 3 октября 2011 г.
Antidepressants May Be Associated With Modestly Increased Risk Of Suicidality In Children
An analysis of data from 24 clinical trials suggests that antidepressant medications may be linked to a modest increase in the risk of suicidal thoughts and behaviors in children, according to an article in the March issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
For decades, some physicians have suspected that patients' risk of suicidality (suicidal thoughts and behavior) increased when pediatric patients first began taking antidepressants, according to background information in the article. Research indicates that there is no such association in adults. In 2003, a report submitted to the Food and Drug Administration (FDA) suggested a link between the antidepressant paroxetine and suicidality in pediatric patients. The FDA then requested pediatric data from the manufacturers of eight other antidepressant drugs, the authors report.
Tarek A. Hammad, M.D., Ph.D., and colleagues at the FDA performed a meta-analysis of data from 23 short-term clinical trials received in response to the request, as well as one trial funded by the National Institute of Mental Health (NIMH). The 24 studies included 4,582 pediatric patients taking one of nine antidepressant medications for depression, anxiety or other psychiatric disorder.
No children committed suicide in any of the trials. Although the NIMH-funded trial was the only individual trial to show a significant increase in suicidality among children taking antidepressants, the analysis of all the trials together showed a higher risk of suicidal ideation and behavior for children taking the drugs compared with those who were not. "When considering 100 treated patients, we might expect one to three patients to have an increase in suicidality beyond the risk that occurs with depression itself owing to short-term treatment with an antidepressant," the authors write.
The FDA now requires warnings regarding the risk of suicidality in children on antidepressant labeling and the distribution of a patient medication guide to patients, families and caregivers, the authors write. "Although there remain differences of opinion in the clinical community about the strength of this signal for antidepressant drug??"induced suicidality in pediatric patients and the implications for clinical practice, it is important to be clear that the FDA has not contraindicated any of the antidepressant drugs for pediatric use," they conclude. "The FDA recognizes that depression and other psychiatric disorders in pediatric patients can have significant consequences if not appropriately treated. The new warning language recognizes this need but advises close monitoring of patients as a way of managing the risk of suicidality."
(Arch Gen Psychiatry. 2006;63:332-339. Available pre-embargo to the media at jamamedia/.)
Editorial: Suicidal Behavior Different from Suicide Attempts The small number of suicide attempts across the trials make the results of the meta-analysis difficult for physicians and policymakers to use, write Ross J. Baldessarini, M.D., of McLean Hospital, Belmont, Mass., and colleagues in an accompanying editorial.
Measuring suicidality rather than suicides or suicide attempts may not paint an accurate picture of the risk associated with the drugs, they continue. "Only a small fraction of patients with suicidal thoughts attempt suicide, few attempts prove to be fatal and risk factors for suicide attempts (e.g., younger, female) and completions (e.g., older, male) differ markedly," they write. "Moreover, suicidal ideation, but usually not suicidal behavior, has been reduced with antidepressant drug treatment."
"When adverse responses do occur, they are often detectable with close clinical follow-up and psychological support, especially early in treatment, as recommended in recent FDA clinical advisories," they conclude. "Moreover, they may be reversed with appropriately modified treatment."
(Arch Gen Psychiatry. 2006;63:127-128. Available pre-embargo to the media at jamamedia/.)
Editor's Note: This commentary was supported, in part, by a grant from the Bruce J. Anderson Foundation, Boston, and the McLean Private Donors Bipolar Disorders and Psychopharmacology Research Fund, Boston (Dr. Baldessarini), by a University of Rome fellowship and by National Alliance for Research on Schizophrenia and Depression, Great Neck, N.Y. Full financial disclosures are available in the article.
To contact corresponding editorialist Ross J. Baldessarini, M.D., call Cynthia Lepore at 617-855-2110.
Contact: Susan Cruzan
JAMA and Archives Journals
For decades, some physicians have suspected that patients' risk of suicidality (suicidal thoughts and behavior) increased when pediatric patients first began taking antidepressants, according to background information in the article. Research indicates that there is no such association in adults. In 2003, a report submitted to the Food and Drug Administration (FDA) suggested a link between the antidepressant paroxetine and suicidality in pediatric patients. The FDA then requested pediatric data from the manufacturers of eight other antidepressant drugs, the authors report.
Tarek A. Hammad, M.D., Ph.D., and colleagues at the FDA performed a meta-analysis of data from 23 short-term clinical trials received in response to the request, as well as one trial funded by the National Institute of Mental Health (NIMH). The 24 studies included 4,582 pediatric patients taking one of nine antidepressant medications for depression, anxiety or other psychiatric disorder.
No children committed suicide in any of the trials. Although the NIMH-funded trial was the only individual trial to show a significant increase in suicidality among children taking antidepressants, the analysis of all the trials together showed a higher risk of suicidal ideation and behavior for children taking the drugs compared with those who were not. "When considering 100 treated patients, we might expect one to three patients to have an increase in suicidality beyond the risk that occurs with depression itself owing to short-term treatment with an antidepressant," the authors write.
The FDA now requires warnings regarding the risk of suicidality in children on antidepressant labeling and the distribution of a patient medication guide to patients, families and caregivers, the authors write. "Although there remain differences of opinion in the clinical community about the strength of this signal for antidepressant drug??"induced suicidality in pediatric patients and the implications for clinical practice, it is important to be clear that the FDA has not contraindicated any of the antidepressant drugs for pediatric use," they conclude. "The FDA recognizes that depression and other psychiatric disorders in pediatric patients can have significant consequences if not appropriately treated. The new warning language recognizes this need but advises close monitoring of patients as a way of managing the risk of suicidality."
(Arch Gen Psychiatry. 2006;63:332-339. Available pre-embargo to the media at jamamedia/.)
Editorial: Suicidal Behavior Different from Suicide Attempts The small number of suicide attempts across the trials make the results of the meta-analysis difficult for physicians and policymakers to use, write Ross J. Baldessarini, M.D., of McLean Hospital, Belmont, Mass., and colleagues in an accompanying editorial.
Measuring suicidality rather than suicides or suicide attempts may not paint an accurate picture of the risk associated with the drugs, they continue. "Only a small fraction of patients with suicidal thoughts attempt suicide, few attempts prove to be fatal and risk factors for suicide attempts (e.g., younger, female) and completions (e.g., older, male) differ markedly," they write. "Moreover, suicidal ideation, but usually not suicidal behavior, has been reduced with antidepressant drug treatment."
"When adverse responses do occur, they are often detectable with close clinical follow-up and psychological support, especially early in treatment, as recommended in recent FDA clinical advisories," they conclude. "Moreover, they may be reversed with appropriately modified treatment."
(Arch Gen Psychiatry. 2006;63:127-128. Available pre-embargo to the media at jamamedia/.)
Editor's Note: This commentary was supported, in part, by a grant from the Bruce J. Anderson Foundation, Boston, and the McLean Private Donors Bipolar Disorders and Psychopharmacology Research Fund, Boston (Dr. Baldessarini), by a University of Rome fellowship and by National Alliance for Research on Schizophrenia and Depression, Great Neck, N.Y. Full financial disclosures are available in the article.
To contact corresponding editorialist Ross J. Baldessarini, M.D., call Cynthia Lepore at 617-855-2110.
Contact: Susan Cruzan
JAMA and Archives Journals
пятница, 30 сентября 2011 г.
New FDA-Approved Device Offers Hope to Depressed Patients
The Saint Louis University Health Sciences Center medical team involved in the research and development of an innovative therapy for depression - vagal nerve stimulation (VNS) - is starting a new clinic for patients who have treatment-resistant depression.
The vagal nerve stimulator was approved Friday by the Food and Drug Administration for treatment-resistant depression following clinical trials around the United States, including Saint Louis University.
"This important service could dramatically improve the quality of life for some of the sickest patients, patients who had been on seven to 10 medications and continued to be depressed for years," says Dr. Charles Conway, who researched vagal nerve stimulation and now will lead the Saint Louis University Vagal Nerve Stimulation Clinic.
The small device is implanted in front of the armpit and has leads that run under the skin to the vagal nerve in the neck. It has been used for and is FDA-approved to treat epilepsy as well.
Charles Donovan, who had participated in the clinical research at Saint Louis University and written a book about his experience, says vagal nerve stimulation changed his life.
"I feel giddy that I've gone from the depths of despair to a normal life," he says. "For over 20 years I had tried every available treatment to give me some relief from the unbearable suffering I experienced from chronic depression.
"When I was implanted with the vagus nerve stimulator in April of 2001, I was desperate. I didn't want to continue to live a life of utter despair. I had absolutely no idea that my life was about to be completely changed."
Conway was the principal investigator at the Saint Louis University study site, one of 20 sites across the country to participate in a 200-patient clinical trial between 2000 and 2003.
"One of the most rewarding things I've done as a psychiatrist is to conduct research that shows we can help people who have lived essentially all of their lives with severe depression get better," says Conway, an assistant professor of psychiatry at Saint Louis University School of Medicine and a SLUCare psychiatrist. "Dr. George Grossberg, who directs our division of geriatric psychiatry, and I have found the treatment is successful in helping numerous patients who have failed all other existing therapies.
"Now, with a new treatment option on the horizon, I am excited we will reach more patients through the Saint Louis University Vagal Nerve Stimulation Clinic. These are patients who had given up hope of ever feeling better."
Richard Bucholz, M.D., director of the division of neurosurgery at Saint Louis University, brings his experience surgically implanting the device during the study to SLU's Vagal Nerve Stimulation Clinic. He also was involved in studies that led to the FDA's approval of vagal nerve stimulation to treat epilepsy.
Patients who are interested in the service will receive an initial consultation to see if the treatment is appropriate; a surgical consultation if they are eligible; and follow-up appointments to monitor and adjust the device settings.
The Saint Louis University Vagal Nerve Stimulation Clinic is located at the Wohl Memorial Institute, 1221 S. Grand Blvd. For information about the service, call 314-268-5385.
Saint Louis University Health Sciences Center
St. Louis, MO 63103
United States
slu/pr
The vagal nerve stimulator was approved Friday by the Food and Drug Administration for treatment-resistant depression following clinical trials around the United States, including Saint Louis University.
"This important service could dramatically improve the quality of life for some of the sickest patients, patients who had been on seven to 10 medications and continued to be depressed for years," says Dr. Charles Conway, who researched vagal nerve stimulation and now will lead the Saint Louis University Vagal Nerve Stimulation Clinic.
The small device is implanted in front of the armpit and has leads that run under the skin to the vagal nerve in the neck. It has been used for and is FDA-approved to treat epilepsy as well.
Charles Donovan, who had participated in the clinical research at Saint Louis University and written a book about his experience, says vagal nerve stimulation changed his life.
"I feel giddy that I've gone from the depths of despair to a normal life," he says. "For over 20 years I had tried every available treatment to give me some relief from the unbearable suffering I experienced from chronic depression.
"When I was implanted with the vagus nerve stimulator in April of 2001, I was desperate. I didn't want to continue to live a life of utter despair. I had absolutely no idea that my life was about to be completely changed."
Conway was the principal investigator at the Saint Louis University study site, one of 20 sites across the country to participate in a 200-patient clinical trial between 2000 and 2003.
"One of the most rewarding things I've done as a psychiatrist is to conduct research that shows we can help people who have lived essentially all of their lives with severe depression get better," says Conway, an assistant professor of psychiatry at Saint Louis University School of Medicine and a SLUCare psychiatrist. "Dr. George Grossberg, who directs our division of geriatric psychiatry, and I have found the treatment is successful in helping numerous patients who have failed all other existing therapies.
"Now, with a new treatment option on the horizon, I am excited we will reach more patients through the Saint Louis University Vagal Nerve Stimulation Clinic. These are patients who had given up hope of ever feeling better."
Richard Bucholz, M.D., director of the division of neurosurgery at Saint Louis University, brings his experience surgically implanting the device during the study to SLU's Vagal Nerve Stimulation Clinic. He also was involved in studies that led to the FDA's approval of vagal nerve stimulation to treat epilepsy.
Patients who are interested in the service will receive an initial consultation to see if the treatment is appropriate; a surgical consultation if they are eligible; and follow-up appointments to monitor and adjust the device settings.
The Saint Louis University Vagal Nerve Stimulation Clinic is located at the Wohl Memorial Institute, 1221 S. Grand Blvd. For information about the service, call 314-268-5385.
Saint Louis University Health Sciences Center
St. Louis, MO 63103
United States
slu/pr
вторник, 27 сентября 2011 г.
Children And Teens Taking Antidepressants Might Be More Likely To Attempt, Complete Suicide
Antidepressant medications may be associated with suicide attempts and death in severely depressed children and adolescents but not in adults, according to an article in the August issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
The U.S. Food and Drug Administration (FDA) recently began requiring drug manufacturers to include a warning regarding the risk of suicidal behavior among children and teens treated with antidepressants after a large analysis of clinical trials revealed a potential link. It is uncertain whether there is an association between treatment with antidepressants and suicidal behavior in adults, according to background information in the article. Because relatively few completed suicides occur, suicidal behavior is used instead in studies assessing the risks associated with antidepressant medications and few studies have examined the risk of suicide attempts or deaths in patients treated with antidepressants.
Mark Olfson, M.D., M.P.H., College of Physicians and Surgeons of Columbia University Medical Center and New York State Psychiatric Institute, New York, and colleagues analyzed the medical records of 5,469 Medicaid patients who were hospitalized for depression at least once in 1999 or 2000. The researchers first selected all cases of completed suicides (eight children and adolescents and 86 adults) and suicide attempts (263 children and adolescents, 521 adults). They then matched each case with one to five controls based on demographic information, period following hospital discharge, presence or absence of a suicide attempt prior to hospital admission, state of residence, other medication use and presence or absence of a substance abuse disorder.
Severely depressed children and adolescents ages 6 to 18 years were 1.5 times as likely to attempt suicide and also significantly more likely to complete suicide if they were treated with an antidepressant medication than if they were not treated with an antidepressant. More specifically, children and adolescents who died from suicide (eight cases) were more likely to have been treated with an SSRI antidepressant than their matched controls (39 controls, 37.5 percent vs. 7.7 percent). Among adults age 19 to 64 years, however, treatment with antidepressants was not associated with either suicide attempts or suicide deaths.
The link between completed suicides and antidepressants in young patients was based on only eight cases, and it is possible that the sickest children were more likely to be treated with such medications, skewing the results, the authors write. "With these caveats in mind, the present findings are consistent with the recommendations for careful clinical monitoring during the treatment of depressed children and adolescents with antidepressant medications," they conclude. "In practice, physicians face the difficult challenge of balancing safety concerns against evidence that depression is a key risk factor for adult and adolescent suicide and that antidepressant agents are effective for adult and adolescent depression." (Arch Gen Psychiatry. 2006;63:865-872.)
Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
For more information, contact JAMA/Archives Media Relations at 312/464-JAMA (5262) or e-mail mediarelationsjama-archives.
Contact: Craig LeMoult
JAMA and Archives Journals
The U.S. Food and Drug Administration (FDA) recently began requiring drug manufacturers to include a warning regarding the risk of suicidal behavior among children and teens treated with antidepressants after a large analysis of clinical trials revealed a potential link. It is uncertain whether there is an association between treatment with antidepressants and suicidal behavior in adults, according to background information in the article. Because relatively few completed suicides occur, suicidal behavior is used instead in studies assessing the risks associated with antidepressant medications and few studies have examined the risk of suicide attempts or deaths in patients treated with antidepressants.
Mark Olfson, M.D., M.P.H., College of Physicians and Surgeons of Columbia University Medical Center and New York State Psychiatric Institute, New York, and colleagues analyzed the medical records of 5,469 Medicaid patients who were hospitalized for depression at least once in 1999 or 2000. The researchers first selected all cases of completed suicides (eight children and adolescents and 86 adults) and suicide attempts (263 children and adolescents, 521 adults). They then matched each case with one to five controls based on demographic information, period following hospital discharge, presence or absence of a suicide attempt prior to hospital admission, state of residence, other medication use and presence or absence of a substance abuse disorder.
Severely depressed children and adolescents ages 6 to 18 years were 1.5 times as likely to attempt suicide and also significantly more likely to complete suicide if they were treated with an antidepressant medication than if they were not treated with an antidepressant. More specifically, children and adolescents who died from suicide (eight cases) were more likely to have been treated with an SSRI antidepressant than their matched controls (39 controls, 37.5 percent vs. 7.7 percent). Among adults age 19 to 64 years, however, treatment with antidepressants was not associated with either suicide attempts or suicide deaths.
The link between completed suicides and antidepressants in young patients was based on only eight cases, and it is possible that the sickest children were more likely to be treated with such medications, skewing the results, the authors write. "With these caveats in mind, the present findings are consistent with the recommendations for careful clinical monitoring during the treatment of depressed children and adolescents with antidepressant medications," they conclude. "In practice, physicians face the difficult challenge of balancing safety concerns against evidence that depression is a key risk factor for adult and adolescent suicide and that antidepressant agents are effective for adult and adolescent depression." (Arch Gen Psychiatry. 2006;63:865-872.)
Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
For more information, contact JAMA/Archives Media Relations at 312/464-JAMA (5262) or e-mail mediarelationsjama-archives.
Contact: Craig LeMoult
JAMA and Archives Journals
суббота, 24 сентября 2011 г.
Does Depression Predict Mortality In Heart Attacks?
A group of Danish investigators, headed by Per Bech (Hillerod) surveyed the literature on depression in patients with
myocardial infarction to assess the methodological quality and to test whether depression leads to an increased
postmyocardial infarction mortality.
Medline, Psycinfo, and UMI were searched, and researchers were contacted in the autumn of 2003. Thirty-one articles
were reviewed. Only seven articles scored above a predefined level of 75% for acceptable quality. The articles lack
description of non-responders, recall period for depressive symptoms, validation of applied instrument on target population,
and sample size large enough to show differences between groups.
The prevalence rates of depression ranged from 1.6 to 50%. In eight articles, a diagnostic test was applied, in the rest of
the studies, questionnaires were used. The prevalence of depression was highest in those using patient-completed
questionnaires. A significant positive association was shown between depression and postmyocardial infarction mortality in 15
studies, a non-significant association in 14, and in two articles, this was not reported. In articles with data collection
starting after 1994, a non-significant relation tended to be reported. The studies were generally not of acceptable quality.
They lacked sufficient power to show differences in stated end points between groups. Application of non-validated
instruments caused large differences in prevalence rates of depression. Future studies should include a minimum of 1,000
patients, use a validated instrument, re-examine the patients, and describe participants and non-participants in detail.
The conclusion of their analysis is that the data are not conclusive and it is premature o suggest a massive use of
antidepressant drugs with hear attacks.
Reference URL
karger
alphagalileo
myocardial infarction to assess the methodological quality and to test whether depression leads to an increased
postmyocardial infarction mortality.
Medline, Psycinfo, and UMI were searched, and researchers were contacted in the autumn of 2003. Thirty-one articles
were reviewed. Only seven articles scored above a predefined level of 75% for acceptable quality. The articles lack
description of non-responders, recall period for depressive symptoms, validation of applied instrument on target population,
and sample size large enough to show differences between groups.
The prevalence rates of depression ranged from 1.6 to 50%. In eight articles, a diagnostic test was applied, in the rest of
the studies, questionnaires were used. The prevalence of depression was highest in those using patient-completed
questionnaires. A significant positive association was shown between depression and postmyocardial infarction mortality in 15
studies, a non-significant association in 14, and in two articles, this was not reported. In articles with data collection
starting after 1994, a non-significant relation tended to be reported. The studies were generally not of acceptable quality.
They lacked sufficient power to show differences in stated end points between groups. Application of non-validated
instruments caused large differences in prevalence rates of depression. Future studies should include a minimum of 1,000
patients, use a validated instrument, re-examine the patients, and describe participants and non-participants in detail.
The conclusion of their analysis is that the data are not conclusive and it is premature o suggest a massive use of
antidepressant drugs with hear attacks.
Reference URL
karger
alphagalileo
среда, 21 сентября 2011 г.
New Preclinical Data Confirm Naurex's Novel Antidepressant GLYX-13 Appears Free Of The Behavioral Impairment And Abuse Potential Seen With Ketamine
Naurex Inc., a clinical-stage company developing innovative treatments to address unmet needs in psychiatry and neurology, reported that data being presented at the 49th Annual Meeting of the American College of Neuropsychopharmacology (ACNP) further confirm that its lead antidepressant candidate GLYX-13 appears free of the behavioral impairment and abuse potential that have limited the clinical utility of other NMDA receptor (NMDAR) modulator drugs such as ketamine.
Ketamine and similar NMDAR-modulating agents act very rapidly to alleviate the symptoms of depression and bipolar disorder, but their clinical utility has been hampered by their potential for abuse and behavioral impairment, including schizophrenia-like effects, at doses near the therapeutic dose. GLYX-13 is Naurex's lead glycine-site functional partial agonist (GFPA) selective modulator of the NMDA receptor. The novel GFPA class of compounds has been specifically designed to achieve the well-documented efficacy of classic NMDAR-modulating drugs, while avoiding their serious side effects.
In previously reported preclinical studies, GLYX-13 demonstrated the robust antidepressant-like activity of ketamine, including its rapid onset and long duration of effect, with no signs of side effects. In preclinical studies, GLYX-13 has demonstrated the widest therapeutic ratio between efficacy and side effects (>500:1) of any known NMDAR modulator.
In the new study, researchers employed a sophisticated preclinical model measuring whether subjects detect and respond to the presence of a specific drug. Rats were trained to accurately discriminate whether ketamine or saline was present in a routine injection, by choosing one of two levers that delivers a reward when correctly matched to the injected substance. The tests were run using increasing doses of ketamine and GLYX-13, including doses that are known to produce antidepressant effects in preclinical models. The rats receiving ketamine selected the "ketamine trained" lever over the "saline trained" lever as the dose was increased, until they were overcome by impairment from the drug. In contrast, the rats receiving increasing doses of GLYX-13 did not preferentially select the "ketamine" lever over the "saline" lever and continued responding until the end of the experiment.*
"This well-validated model shows dramatically different responses in rats dosed with ketamine and with GLYX-13," said Robert Balster, Ph.D., professor of Pharmacology and Toxicology and director of the Institute for Drug and Alcohol Studies at Virginia Commonwealth University, an author of the study and a recognized expert on drug dependence. "Despite its therapeutic potential, the NMDAR modulator ketamine is a well-known drug of abuse with sedative and dissociative effects. GLYX-13 also acts at the NMDA receptor, but it has a different pharmacology and appears to be devoid of these effects, making it a promising candidate for development as a medication."
Numerous studies have shown that ketamine has a markedly faster onset of action than other antidepressants (within hours, instead of weeks) and alleviates depression symptoms in a greater proportion of patients. In studies in preclinical models of depression, GLYX-13 demonstrates antidepressant-like effects consistent with those of ketamine, with antidepressant-like efficacy that was evident within minutes of administering a single dose and lasted more than two weeks post-dosing. No ketamine-like side effects were observed.
J. David Leander, Ph.D., chief scientific adviser to Naurex and an author of the study, commented, "These new data produced by experts in the pharmacology of drug dependence further confirm the clean side effect profile we have seen to date with GLYX-13. In our Phase I trial, there was no sign of any behavioral impairment or ketamine-like subjective effects at drug exposures that exceeded the 'therapeutic range' established in our animal studies. We are currently initiating a Phase II trial of GLYX-13 in patients who are not achieving an adequate response to their current antidepressant agents."
In addition to GLYX-13, Naurex is developing the NRX-1050 series of GFPAs, including numerous second-generation, orally available molecules with structures and mechanisms of action similar to GLYX-13.
The 49th Annual Meeting of the American College of Neuropsychopharmacology is being held at the Fontainebleau Resort, Miami Beach, Florida, December 5-9, 2010.
*Lack of ketamine-like discriminative effects of GLYX-13: A novel NMDA receptor glycine site functional partial agonist with antidepressant-like preclinical effects, J. David Leander, Katherine Nicholson, Robert Balster, Jeffrey Burgdorf, Joseph Moskal.
About NMDA Receptor Modulators and Depression
The glutamate receptor subtype known as NMDA plays a central role in modulating aspects of brain activity. The antidepressant effects of known NMDAR modulators, such as ketamine, have been confirmed in multiple clinical studies over the last decade. These studies have shown dramatic efficacy in patients with treatment-resistant and bipolar depression, demonstrating response rates greater than 50%, fast onset of action within hours of a single dose and a long duration of effect. The antidepressant efficacy of ketamine has been underscored in recent studies published in Science and the Archives of General Psychiatry. But ketamine and other known NMDAR blockers are also associated with significant toxicities at or near their therapeutic doses. These side effects, which include schizophrenia-like effects, behavioral impairment and abuse liability, have limited the therapeutic potential of these agents.
About Glycine-Site Functional Partial Agonists
GFPAs modulate the NMDA receptor in a novel and selective way that results in the largest therapeutic index of any known NMDAR modulator. GFPAs are being developed with the goal of achieving the antidepressant efficacy and rapid onset seen with conventional NMDAR modulators, but without their limiting side effects. The efficacy potential of GFPAs has been demonstrated in animal models in a number of CNS disorders, including major depressive disorder, neuropathic pain, schizophrenia, anxiety, Alzheimer's disease and other cognition disorders. In these studies, GFPAs did not exhibit the schizophrenia-like effects associated with conventional NMDAR-modulating drugs.
Ketamine and similar NMDAR-modulating agents act very rapidly to alleviate the symptoms of depression and bipolar disorder, but their clinical utility has been hampered by their potential for abuse and behavioral impairment, including schizophrenia-like effects, at doses near the therapeutic dose. GLYX-13 is Naurex's lead glycine-site functional partial agonist (GFPA) selective modulator of the NMDA receptor. The novel GFPA class of compounds has been specifically designed to achieve the well-documented efficacy of classic NMDAR-modulating drugs, while avoiding their serious side effects.
In previously reported preclinical studies, GLYX-13 demonstrated the robust antidepressant-like activity of ketamine, including its rapid onset and long duration of effect, with no signs of side effects. In preclinical studies, GLYX-13 has demonstrated the widest therapeutic ratio between efficacy and side effects (>500:1) of any known NMDAR modulator.
In the new study, researchers employed a sophisticated preclinical model measuring whether subjects detect and respond to the presence of a specific drug. Rats were trained to accurately discriminate whether ketamine or saline was present in a routine injection, by choosing one of two levers that delivers a reward when correctly matched to the injected substance. The tests were run using increasing doses of ketamine and GLYX-13, including doses that are known to produce antidepressant effects in preclinical models. The rats receiving ketamine selected the "ketamine trained" lever over the "saline trained" lever as the dose was increased, until they were overcome by impairment from the drug. In contrast, the rats receiving increasing doses of GLYX-13 did not preferentially select the "ketamine" lever over the "saline" lever and continued responding until the end of the experiment.*
"This well-validated model shows dramatically different responses in rats dosed with ketamine and with GLYX-13," said Robert Balster, Ph.D., professor of Pharmacology and Toxicology and director of the Institute for Drug and Alcohol Studies at Virginia Commonwealth University, an author of the study and a recognized expert on drug dependence. "Despite its therapeutic potential, the NMDAR modulator ketamine is a well-known drug of abuse with sedative and dissociative effects. GLYX-13 also acts at the NMDA receptor, but it has a different pharmacology and appears to be devoid of these effects, making it a promising candidate for development as a medication."
Numerous studies have shown that ketamine has a markedly faster onset of action than other antidepressants (within hours, instead of weeks) and alleviates depression symptoms in a greater proportion of patients. In studies in preclinical models of depression, GLYX-13 demonstrates antidepressant-like effects consistent with those of ketamine, with antidepressant-like efficacy that was evident within minutes of administering a single dose and lasted more than two weeks post-dosing. No ketamine-like side effects were observed.
J. David Leander, Ph.D., chief scientific adviser to Naurex and an author of the study, commented, "These new data produced by experts in the pharmacology of drug dependence further confirm the clean side effect profile we have seen to date with GLYX-13. In our Phase I trial, there was no sign of any behavioral impairment or ketamine-like subjective effects at drug exposures that exceeded the 'therapeutic range' established in our animal studies. We are currently initiating a Phase II trial of GLYX-13 in patients who are not achieving an adequate response to their current antidepressant agents."
In addition to GLYX-13, Naurex is developing the NRX-1050 series of GFPAs, including numerous second-generation, orally available molecules with structures and mechanisms of action similar to GLYX-13.
The 49th Annual Meeting of the American College of Neuropsychopharmacology is being held at the Fontainebleau Resort, Miami Beach, Florida, December 5-9, 2010.
*Lack of ketamine-like discriminative effects of GLYX-13: A novel NMDA receptor glycine site functional partial agonist with antidepressant-like preclinical effects, J. David Leander, Katherine Nicholson, Robert Balster, Jeffrey Burgdorf, Joseph Moskal.
About NMDA Receptor Modulators and Depression
The glutamate receptor subtype known as NMDA plays a central role in modulating aspects of brain activity. The antidepressant effects of known NMDAR modulators, such as ketamine, have been confirmed in multiple clinical studies over the last decade. These studies have shown dramatic efficacy in patients with treatment-resistant and bipolar depression, demonstrating response rates greater than 50%, fast onset of action within hours of a single dose and a long duration of effect. The antidepressant efficacy of ketamine has been underscored in recent studies published in Science and the Archives of General Psychiatry. But ketamine and other known NMDAR blockers are also associated with significant toxicities at or near their therapeutic doses. These side effects, which include schizophrenia-like effects, behavioral impairment and abuse liability, have limited the therapeutic potential of these agents.
About Glycine-Site Functional Partial Agonists
GFPAs modulate the NMDA receptor in a novel and selective way that results in the largest therapeutic index of any known NMDAR modulator. GFPAs are being developed with the goal of achieving the antidepressant efficacy and rapid onset seen with conventional NMDAR modulators, but without their limiting side effects. The efficacy potential of GFPAs has been demonstrated in animal models in a number of CNS disorders, including major depressive disorder, neuropathic pain, schizophrenia, anxiety, Alzheimer's disease and other cognition disorders. In these studies, GFPAs did not exhibit the schizophrenia-like effects associated with conventional NMDAR-modulating drugs.
воскресенье, 18 сентября 2011 г.
Minnesota Health Care Group To Launch Pilot 'Pay-for-Performance' Initiative To Reduce Treatment Costs For Depression
The Buyers Health Care Action Group, a health care purchasing coalition in Minnesota for large employers, on Wednesday announced a pay-for-performance pilot program that will reward physicians who effectively treat depressed patients, the St. Paul Pioneer Press reports. The program will start in 2009 (Forster, St. Paul Pioneer Press, 5/28). The program is modeled after similar pay-for-performance initiatives launched in recent years to improve treatment of diabetes and cardiovascular problems (Lerner, Minneapolis Star Tribune, 5/29). Some of the employers participating in the new program include the state of Minnesota, 3M, Wells Fargo, the University of Minnesota, Target, Medtronic and Carlson (St. Paul Pioneer Press, 5/28).
Under the program, patients will complete a nine-question survey to help primary care physicians determine whether a patient is depressed and gauge the severity of his or her condition. Patients will be reassessed at six months and throughout the course of treatment (Minneapolis Star Tribune, 5/29). The goal of the program is to reduce depression within the first six months and achieve full recovery in one year. Physicians who meet the goal would receive a $100 bonus per patient. Insurance companies participating in the program have committed to paying the bonuses through 2010.
Participating employers also plan to share information next year about which physicians provided the most effective treatment for patients with depression. In addition, the program will evaluate how better depression management affects health care costs (St. Paul Pioneer Press, 5/28). Francois de Brantes -- CEO of Bridges to Excellence, a national pay-for-performance group working with the Minnesota project -- said, "Ultimately, we're not about dictating to physicians how they should practice medicine but rather holding them accountable for the results of how they practice."
Opponents of the initiative say it could have an adverse effect on patient care. Sue Abderholden, executive director of the National Alliance on Mental Illness, said, "Anytime we tie pay for performance to people getting better in terms of a mental illness, I always worry that there's going to be an incentive not to treat the hard-to-treat," adding, "Some people are harder to treat than others. So what happens with those folks?" (Minneapolis Star Tribune, 5/29).
Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation.
© 2008 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
Under the program, patients will complete a nine-question survey to help primary care physicians determine whether a patient is depressed and gauge the severity of his or her condition. Patients will be reassessed at six months and throughout the course of treatment (Minneapolis Star Tribune, 5/29). The goal of the program is to reduce depression within the first six months and achieve full recovery in one year. Physicians who meet the goal would receive a $100 bonus per patient. Insurance companies participating in the program have committed to paying the bonuses through 2010.
Participating employers also plan to share information next year about which physicians provided the most effective treatment for patients with depression. In addition, the program will evaluate how better depression management affects health care costs (St. Paul Pioneer Press, 5/28). Francois de Brantes -- CEO of Bridges to Excellence, a national pay-for-performance group working with the Minnesota project -- said, "Ultimately, we're not about dictating to physicians how they should practice medicine but rather holding them accountable for the results of how they practice."
Opponents of the initiative say it could have an adverse effect on patient care. Sue Abderholden, executive director of the National Alliance on Mental Illness, said, "Anytime we tie pay for performance to people getting better in terms of a mental illness, I always worry that there's going to be an incentive not to treat the hard-to-treat," adding, "Some people are harder to treat than others. So what happens with those folks?" (Minneapolis Star Tribune, 5/29).
Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation.
© 2008 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
четверг, 15 сентября 2011 г.
Patients, Be Patient: Brain Images Suggest New Therapy For Severe Depression Can Take Months To Work
It takes time - between three and 12 months - before a new type of therapy for treatment-resistant depression starts to benefit patients, according to new preliminary brain scan research that confirms earlier observations by psychiatrists about vagal nerve stimulation.
Saint Louis University, working in collaboration with Washington University School of Medicine, conducted a pilot study of brain scans of a small group of depressed patients who received vagal nerve stimulation after failing other therapies.
Positron emission tomography (PET) scans showed significant changes in brain activity starting three months after vagal nerve stimulation treatment began. These changes continued to evolve over the course of the next 21 months.
These changes in brain scans appear to "roughly parallel" the significantly delayed effects that psychiatrists observed in improvement in mood.
"The effects come after a significant period of treatment time," said Charles Conway, M.D., an assistant professor of psychiatry at Saint Louis University School of Medicine and the lead investigator of a vagal nerve stimulation research project conducted between 2000 and 2004.
Psychiatrists are not used to such a long time lag before a treatment begins to be effective, he added.
"This is very different from the delays we see with existing treatments for depression, including pharmacotherapy and electroconvulsive therapy (ECT)," Dr. Conway said. "The biggest changes in the brain that we're noting occur between 12 and 24 months after patients began receiving vagal nerve stimulation. In psychiatry, we're used to seeing results after six to 12 weeks."
Dr. Conway cautioned the findings are preliminary and need replication.
"But they suggest that in this type of therapy, the brain takes a relatively long time to change, perhaps as long as a year or more. In this sense, vagal nerve stimulation may represent a paradigm shift in the way we view depression treatment. Patients may have to be instructed to 'be patient,' with the expectations that the antidepressant effects will be slow to come."
The good news, however, seems to be that those who benefit from the treatment stay better.
"The existing evidence suggests that about 70 percent of patients who get better from vagal nerve stimulation at one year, stay better at two years," Dr. Conway said. "That is unheard of in a depressed population this severe, and suggests that the brain changes induced by this treatment appear to be long-lasting."
Dr. Conway examined the brain scans of patients at three, six, 12 and 24 months intervals after they began receiving vagal nerve stimulation. Eight patients participated in the study for the three and six month scans, six patients at 12 months and four patients at 24 months. The size of the study group grew smaller during the two year investigation.
"This is admittedly a very tiny population and the findings of this study are very preliminary. We need to do more research with a larger group of patients," Dr. Conway said. "That said, I think the findings are real and promising and beg more research."
Vagal nerve stimulation was approved in 2005 by the U.S. Food and Drug Administration to treat severe treatment-resistant depression. A vagal nerve stimulator is similar to a cardiac pacemaker and is implanted in the chest with leads that run under the skin to the vagal nerve in the neck. The device emits electrical pulses to simulate the brain, and also is used to treat epilepsy.
Doctors don't know exactly why vagal nerve therapy works, but Dr. Conway says his new research gives some clues.
When Dr. Conway examined the neuroimages of four patients 24 months after they began receiving vagal nerve stimulation, he found brain activity that was similar to what doctors see in patients who have received ECT.
"There actually appears to be decreased activity in regions of the prefrontal cortex, which is very much parallel to the findings of treatment response in ECT, and the opposite of findings seen in medication-response to depression."
He found unexpected action in the prefrontal cortex of the brain that is similar to brain activity in depressed patients immediately after they have received ECT and before its effect wears off.
"No one knows exactly how vagal nerve stimulation works. This suggests that one way in which it works may parallel ECT," Dr. Conway said.
"ECT had been considered to be the best therapy for treatment-resistant depression, but unfortunately the effects are not long-lasting. The data so far shows that one-third of the depressed patients who are treatment resistant are responsive to vagal nerve simulations and those who respond stay well."
Dr. Conway collaborated with John Chibnall, Ph.D, a psychologist and researcher in Saint Louis University's department of psychiatry; Yvette Sheline, M.D., a psychiatrist and researcher, and Mark Mintun, M.D., a radiologist/neuroimager and researcher, both of Washington University in St. Louis.
Dr. Conway is presenting his research results at the annual meeting of the Society of Biological Psychiatrists on May 18-20, and at the annual meeting of the American Psychiatrists Association in May 20-25.
Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first M.D. degree west of the Mississippi River. Saint Louis University School of Medicine is a pioneer in geriatric medicine, organ transplantation, chronic disease prevention, cardiovascular disease, neurosciences and vaccine research, among others. The School of Medicine trains physicians and biomedical scientists, conducts medical research, and provides health services on a local, national and international level.
Nancy Solomon
solomonnslu
Saint Louis University
slu/
Saint Louis University, working in collaboration with Washington University School of Medicine, conducted a pilot study of brain scans of a small group of depressed patients who received vagal nerve stimulation after failing other therapies.
Positron emission tomography (PET) scans showed significant changes in brain activity starting three months after vagal nerve stimulation treatment began. These changes continued to evolve over the course of the next 21 months.
These changes in brain scans appear to "roughly parallel" the significantly delayed effects that psychiatrists observed in improvement in mood.
"The effects come after a significant period of treatment time," said Charles Conway, M.D., an assistant professor of psychiatry at Saint Louis University School of Medicine and the lead investigator of a vagal nerve stimulation research project conducted between 2000 and 2004.
Psychiatrists are not used to such a long time lag before a treatment begins to be effective, he added.
"This is very different from the delays we see with existing treatments for depression, including pharmacotherapy and electroconvulsive therapy (ECT)," Dr. Conway said. "The biggest changes in the brain that we're noting occur between 12 and 24 months after patients began receiving vagal nerve stimulation. In psychiatry, we're used to seeing results after six to 12 weeks."
Dr. Conway cautioned the findings are preliminary and need replication.
"But they suggest that in this type of therapy, the brain takes a relatively long time to change, perhaps as long as a year or more. In this sense, vagal nerve stimulation may represent a paradigm shift in the way we view depression treatment. Patients may have to be instructed to 'be patient,' with the expectations that the antidepressant effects will be slow to come."
The good news, however, seems to be that those who benefit from the treatment stay better.
"The existing evidence suggests that about 70 percent of patients who get better from vagal nerve stimulation at one year, stay better at two years," Dr. Conway said. "That is unheard of in a depressed population this severe, and suggests that the brain changes induced by this treatment appear to be long-lasting."
Dr. Conway examined the brain scans of patients at three, six, 12 and 24 months intervals after they began receiving vagal nerve stimulation. Eight patients participated in the study for the three and six month scans, six patients at 12 months and four patients at 24 months. The size of the study group grew smaller during the two year investigation.
"This is admittedly a very tiny population and the findings of this study are very preliminary. We need to do more research with a larger group of patients," Dr. Conway said. "That said, I think the findings are real and promising and beg more research."
Vagal nerve stimulation was approved in 2005 by the U.S. Food and Drug Administration to treat severe treatment-resistant depression. A vagal nerve stimulator is similar to a cardiac pacemaker and is implanted in the chest with leads that run under the skin to the vagal nerve in the neck. The device emits electrical pulses to simulate the brain, and also is used to treat epilepsy.
Doctors don't know exactly why vagal nerve therapy works, but Dr. Conway says his new research gives some clues.
When Dr. Conway examined the neuroimages of four patients 24 months after they began receiving vagal nerve stimulation, he found brain activity that was similar to what doctors see in patients who have received ECT.
"There actually appears to be decreased activity in regions of the prefrontal cortex, which is very much parallel to the findings of treatment response in ECT, and the opposite of findings seen in medication-response to depression."
He found unexpected action in the prefrontal cortex of the brain that is similar to brain activity in depressed patients immediately after they have received ECT and before its effect wears off.
"No one knows exactly how vagal nerve stimulation works. This suggests that one way in which it works may parallel ECT," Dr. Conway said.
"ECT had been considered to be the best therapy for treatment-resistant depression, but unfortunately the effects are not long-lasting. The data so far shows that one-third of the depressed patients who are treatment resistant are responsive to vagal nerve simulations and those who respond stay well."
Dr. Conway collaborated with John Chibnall, Ph.D, a psychologist and researcher in Saint Louis University's department of psychiatry; Yvette Sheline, M.D., a psychiatrist and researcher, and Mark Mintun, M.D., a radiologist/neuroimager and researcher, both of Washington University in St. Louis.
Dr. Conway is presenting his research results at the annual meeting of the Society of Biological Psychiatrists on May 18-20, and at the annual meeting of the American Psychiatrists Association in May 20-25.
Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first M.D. degree west of the Mississippi River. Saint Louis University School of Medicine is a pioneer in geriatric medicine, organ transplantation, chronic disease prevention, cardiovascular disease, neurosciences and vaccine research, among others. The School of Medicine trains physicians and biomedical scientists, conducts medical research, and provides health services on a local, national and international level.
Nancy Solomon
solomonnslu
Saint Louis University
slu/
понедельник, 12 сентября 2011 г.
AstraZeneca Presents New Depression And Anxiety Results For SEROQUEL XR
The first data from the SEROQUEL XR™ (quetiapine fumarate) Extended Release clinical development programme in major depressive disorder (MDD)1,2 and generalised anxiety disorder (GAD)3 were presented at the 7th International Forum on Mood and Anxiety Disorders (IFMAD) in Budapest, AstraZeneca announced today. The data showed that patients who received SEROQUEL XR once daily experienced significant reductions in symptom severity compared to those on placebo in each of three trials, which investigated SEROQUEL XR as monotherapy in MDD,1 adjunctive therapy in patients with MDD2 with inadequate response to antidepressant therapy, and as monotherapy in GAD.3 These studies are part of a clinical development programme that involved over 7000 patients - one of the largest conducted in depression and anxiety. SEROQUEL® and SEROQUEL XR™ are not approved for the treatment of MDD or GAD.
Reductions in symptom severity were measured by improved (lowered) symptom scale scores. Two randomised, double-blind Phase III studies in MDD reported significantly reduced total scores on the Montgomery-?…sberg Depression Rating Scale (MADRS) after 6 weeks of treatment with once daily SEROQUEL XR. In the MDD monotherapy study, mean MADRS score was significantly improved for patients receiving SEROQUEL XR 150 mg (-14.81; p
Martin Brecher, Executive Director Medical Science, AstraZeneca said: "The data are very encouraging and suggest SEROQUEL XR has the potential to provide a new treatment choice in this area particularly among patients who fail antidepressant therapy with existing treatment. The study program not only covers adjunct treatment but extended also to monotherapy. New therapy options are needed for treating MDD and GAD because currently available antidepressants do not achieve symptom remission in a substantial proportion of patients. Over the coming months and years we will learn more about how far an antipsychotic like SEROQUEL XR may provide a new option for these patients. AstraZeneca plans regulatory submissions in 2008."
Recently presented data may help to explain the study data in MDD and GAD alongside SEROQUEL's known efficacy in bipolar depression. A pre-clinical study used brain imaging with positron emission tomography (PET) to investigate the mechanism of action of SEROQUEL® in non-human primates.4 SEROQUEL (quetiapine fumarate), both directly and indirectly (via its major active metabolite norquetiapine), was found to target the dopamine D2 and the serotonin 5-HT2A receptors in the brain at blood concentrations similar to those during treatment with clinically recommended doses of SEROQUEL in humans. Additionally, SEROQUEL's major active metabolite norquetiapine was shown to target NET - the transporter for norepinephrine (noradrenaline). Inhibition of NET elevates norepinephrine (noradrenaline) levels in specific areas of the brain, an effect that is associated with antidepressant action.
Launched in 1997, it is estimated that SEROQUEL has been prescribed to more than 25 million* patients worldwide. It is approved in 88 countries for the treatment of schizophrenia, in 77 countries for the treatment of bipolar mania, and in 11 countries including the USA for the treatment of bipolar depression. SEROQUEL XR was launched for the treatment of schizophrenia in the US in 2007, and its clinical development program and planned regulatory filings extend through bipolar disorder to major depressive disorder (MDD) and generalised anxiety disorder (GAD).
AstraZeneca is a major international healthcare business engaged in the research, development, manufacture and marketing of prescription pharmaceuticals and the supply of healthcare services. It is one of the world's leading pharmaceutical companies with healthcare sales of $26.47 billion and leading positions in sales of gastrointestinal, cardiovascular, neuroscience, respiratory, oncology and infection products. AstraZeneca is listed in the Dow Jones Sustainability Index (Global) as well as the FTSE4Good Index.
SEROQUEL XR™ and SEROQUEL® are trademarks of the AstraZeneca group of companies.
References
1. Montgomery S, et al. A randomised, placebo-controlled study of once-daily extended release quetiapine fumarate (quetiapine XR) monotherapy in patients with major depressive disorder (MDD). Presented at the International Forum on Mood and Anxiety Disorders, Budapest, Hungary, 5-7 December, 2007
2. Bauer M, et al. Results from a phase III study of extended release quetiapine fumarate (quetiapine XR) as add-on to antidepressants in patients with major depressive disorder (MDD). Presented at the International Forum on Mood and Anxiety Disorders, Budapest, Hungary, 5-7 December, 2007
3. Bandelow B, et al. Results from a phase III study of once-daily extended release quetiapine fumarate (quetiapine XR) monotherapy in patients with generalised anxiety disorder. Presented at the International Forum on Mood and Anxiety Disorders, Budapest, Hungary, 5-7 December, 2007
4. Nyberg S et al. PET-measured D2, 5-HT2, and NET occupancy by quetiapine and N-desalkyl-quetiapine in non-human primates. Presented at the European Congress of Neuropsychopharmacology, Vienna, Austria, 13-17 October, 2007
*This estimate is based upon: (1) assumptions as to persistence (the number of prescriptions per patient) based upon 2002 market research; and (2) projections of prescriptions since launch based upon information available in the US and 13 of the 50 other countries in which SEROQUEL is marketed.
For further information, please visit astrazeneca or astrazenecapressoffice.
What is Anxiety?
For more information on what anxiety is and what to do about it, please see:
What is Anxiety? What Causes Anxiety? What To Do About It.
View drug information on Seroquel.
Reductions in symptom severity were measured by improved (lowered) symptom scale scores. Two randomised, double-blind Phase III studies in MDD reported significantly reduced total scores on the Montgomery-?…sberg Depression Rating Scale (MADRS) after 6 weeks of treatment with once daily SEROQUEL XR. In the MDD monotherapy study, mean MADRS score was significantly improved for patients receiving SEROQUEL XR 150 mg (-14.81; p
Martin Brecher, Executive Director Medical Science, AstraZeneca said: "The data are very encouraging and suggest SEROQUEL XR has the potential to provide a new treatment choice in this area particularly among patients who fail antidepressant therapy with existing treatment. The study program not only covers adjunct treatment but extended also to monotherapy. New therapy options are needed for treating MDD and GAD because currently available antidepressants do not achieve symptom remission in a substantial proportion of patients. Over the coming months and years we will learn more about how far an antipsychotic like SEROQUEL XR may provide a new option for these patients. AstraZeneca plans regulatory submissions in 2008."
Recently presented data may help to explain the study data in MDD and GAD alongside SEROQUEL's known efficacy in bipolar depression. A pre-clinical study used brain imaging with positron emission tomography (PET) to investigate the mechanism of action of SEROQUEL® in non-human primates.4 SEROQUEL (quetiapine fumarate), both directly and indirectly (via its major active metabolite norquetiapine), was found to target the dopamine D2 and the serotonin 5-HT2A receptors in the brain at blood concentrations similar to those during treatment with clinically recommended doses of SEROQUEL in humans. Additionally, SEROQUEL's major active metabolite norquetiapine was shown to target NET - the transporter for norepinephrine (noradrenaline). Inhibition of NET elevates norepinephrine (noradrenaline) levels in specific areas of the brain, an effect that is associated with antidepressant action.
Launched in 1997, it is estimated that SEROQUEL has been prescribed to more than 25 million* patients worldwide. It is approved in 88 countries for the treatment of schizophrenia, in 77 countries for the treatment of bipolar mania, and in 11 countries including the USA for the treatment of bipolar depression. SEROQUEL XR was launched for the treatment of schizophrenia in the US in 2007, and its clinical development program and planned regulatory filings extend through bipolar disorder to major depressive disorder (MDD) and generalised anxiety disorder (GAD).
AstraZeneca is a major international healthcare business engaged in the research, development, manufacture and marketing of prescription pharmaceuticals and the supply of healthcare services. It is one of the world's leading pharmaceutical companies with healthcare sales of $26.47 billion and leading positions in sales of gastrointestinal, cardiovascular, neuroscience, respiratory, oncology and infection products. AstraZeneca is listed in the Dow Jones Sustainability Index (Global) as well as the FTSE4Good Index.
SEROQUEL XR™ and SEROQUEL® are trademarks of the AstraZeneca group of companies.
References
1. Montgomery S, et al. A randomised, placebo-controlled study of once-daily extended release quetiapine fumarate (quetiapine XR) monotherapy in patients with major depressive disorder (MDD). Presented at the International Forum on Mood and Anxiety Disorders, Budapest, Hungary, 5-7 December, 2007
2. Bauer M, et al. Results from a phase III study of extended release quetiapine fumarate (quetiapine XR) as add-on to antidepressants in patients with major depressive disorder (MDD). Presented at the International Forum on Mood and Anxiety Disorders, Budapest, Hungary, 5-7 December, 2007
3. Bandelow B, et al. Results from a phase III study of once-daily extended release quetiapine fumarate (quetiapine XR) monotherapy in patients with generalised anxiety disorder. Presented at the International Forum on Mood and Anxiety Disorders, Budapest, Hungary, 5-7 December, 2007
4. Nyberg S et al. PET-measured D2, 5-HT2, and NET occupancy by quetiapine and N-desalkyl-quetiapine in non-human primates. Presented at the European Congress of Neuropsychopharmacology, Vienna, Austria, 13-17 October, 2007
*This estimate is based upon: (1) assumptions as to persistence (the number of prescriptions per patient) based upon 2002 market research; and (2) projections of prescriptions since launch based upon information available in the US and 13 of the 50 other countries in which SEROQUEL is marketed.
For further information, please visit astrazeneca or astrazenecapressoffice.
What is Anxiety?
For more information on what anxiety is and what to do about it, please see:
What is Anxiety? What Causes Anxiety? What To Do About It.
View drug information on Seroquel.
пятница, 9 сентября 2011 г.
Spirituality Protects Against Depression Better Than Church Attendance
Those who worship a higher power often do so in different ways. Whether they are active in their religious community, or prefer to simply pray or meditate, new research out of Temple University suggests that a person's religiousness - also called religiosity - can offer insight into their risk for depression.
Lead researcher Joanna Maselko, Sc.D., characterized the religiosity of 918 study participants in terms of three domains of religiosity: religious service attendance, which refers to being involved with a church; religious well-being, which refers to the quality of a person's relationship with a higher power; and existential well-being, which refers to a person's sense of meaning and their purpose in life.
In a study published on-line this month in Psychological Medicine, Maselko and fellow researchers compared each domain of religiosity to their risk of depression, and were surprised to find that the group with higher levels of religious well-being were 1.5 times more likely to have had depression than those with lower levels of religious well-being.
Maselko theorizes this is because people with depression tend to use religion as a coping mechanism. As a result, they're more closely relating to God and praying more.
Researchers also found that those who attended religious services were 30 percent less likely to have had depression in their lifetime, and those who had high levels of existential well-being were 70 percent less likely to have had depression than those who had low levels of existential well-being.
Maselko says involvement in the church provides the opportunity for community interaction, which could help forge attachments to others, an important factor in preventing depression. She added that those with higher levels of existential-well being have a strong sense of their place in the world.
"People with high levels of existential well-being tend to have a good base, which makes them very centered emotionally," said Maselko. "People who don't have those things are at greater risk for depression, and those same people might also turn to religion to cope."
Maselko admits that researchers have yet to determine which comes first: depression or being religious, but is currently investigating the time sequence of this over people's lives to figure out the answer.
"For doctors, psychiatrists and counselors, it's hard to disentangle these elements when treating mental illness," she said. "You can't just ask a patient if they go to church to gauge their spirituality or coping behaviors. There are other components to consider when treating patients, and its important information for doctors to have."
Other authors on this study are Stephen Gilman, Sc.D., and Stephen Buka, Sc.D., from the department of Public Health at Harvard University and Brown University Medical School. This research was funded by a grant from the National Institutes of Mental Health and by the Jack Shand Award from the Society for the Scientific Study of Religion.
Lead researcher Joanna Maselko, Sc.D., characterized the religiosity of 918 study participants in terms of three domains of religiosity: religious service attendance, which refers to being involved with a church; religious well-being, which refers to the quality of a person's relationship with a higher power; and existential well-being, which refers to a person's sense of meaning and their purpose in life.
In a study published on-line this month in Psychological Medicine, Maselko and fellow researchers compared each domain of religiosity to their risk of depression, and were surprised to find that the group with higher levels of religious well-being were 1.5 times more likely to have had depression than those with lower levels of religious well-being.
Maselko theorizes this is because people with depression tend to use religion as a coping mechanism. As a result, they're more closely relating to God and praying more.
Researchers also found that those who attended religious services were 30 percent less likely to have had depression in their lifetime, and those who had high levels of existential well-being were 70 percent less likely to have had depression than those who had low levels of existential well-being.
Maselko says involvement in the church provides the opportunity for community interaction, which could help forge attachments to others, an important factor in preventing depression. She added that those with higher levels of existential-well being have a strong sense of their place in the world.
"People with high levels of existential well-being tend to have a good base, which makes them very centered emotionally," said Maselko. "People who don't have those things are at greater risk for depression, and those same people might also turn to religion to cope."
Maselko admits that researchers have yet to determine which comes first: depression or being religious, but is currently investigating the time sequence of this over people's lives to figure out the answer.
"For doctors, psychiatrists and counselors, it's hard to disentangle these elements when treating mental illness," she said. "You can't just ask a patient if they go to church to gauge their spirituality or coping behaviors. There are other components to consider when treating patients, and its important information for doctors to have."
Other authors on this study are Stephen Gilman, Sc.D., and Stephen Buka, Sc.D., from the department of Public Health at Harvard University and Brown University Medical School. This research was funded by a grant from the National Institutes of Mental Health and by the Jack Shand Award from the Society for the Scientific Study of Religion.
вторник, 6 сентября 2011 г.
Corcept Therapeutics Completes Enrollment In Second Phase 3 Study For Treating Psychotic Major Depression
Corcept
Therapeutics Incorporated (Nasdaq: CORT) announced today that it completed
patient enrollment in Corcept 09, the second of three Phase 3 clinical
trials in which CORLUX(R) (mifepristone) is being evaluated for treating
the psychotic features of psychotic major depression (PMD).
"We recently announced that patient enrollment was completed in our
first Phase 3 study, Corcept 07, and that we expect to report the results
of that trial in August," said Corcept's Chief Executive Officer Joseph K.
Belanoff, M.D. "In addition, we now expect to report the results from
Corcept 09 in September 2006. We expect to report the results of our third
Phase 3 trial, Corcept 06, in the fourth quarter."
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.
A Description of Study 09
Study 09 is a randomized, double-blind, placebo-controlled study that
is being conducted in Europe. The primary endpoint is 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 28, a responder analysis. A secondary endpoint is the proportion of patients
with at least a 50 percent improvement in the BPRS PSS at both Day 7 and
Day 56. The BPRS is an 18-item rating instrument used to assess
psychopathology, and the PSS includes the four items in the BPRS that
specifically measure psychosis. Patients must have at least mild psychotic
symptoms (BPRS PSS greater than or equal to 12) to enter the study. Study
enrollees may be either inpatients or outpatients. BPRS PSS assessments are
made at Days 14, 42 and 56.
Patients may not take any antidepressant or antipsychotic medication
for at least one week before study randomization. At randomization, they
are placed in a one-to-one distribution into either a treatment group or a
placebo group. Patients in the treatment group receive 600 mg of CORLUX
once daily for a period of seven days. All patients receive antidepressant
therapy starting on Day 1 and through Day 56. Treatment with antipsychotic
medications or electroconvulsive therapy at any time during the study
results in the patient being classified as a non-responder.
Previously Completed Trials
The company has completed four studies of CORLUX for treating the
psychotic features of PMD. In January 2001, a dose-finding clinical trial
evaluated the efficacy, tolerability of and dose response to CORLUX. The
results showed that after one week of treatment, approximately two-thirds
of the patients in the two higher dosage groups (600 mg and 1200 mg)
experienced clinically meaningful reductions in psychosis, as measured by
the BPRS PSS. Based on these encouraging results, Corcept conducted two
double-blind, placebo-controlled safety and efficacy clinical trials (Study
02 and Study 03) in which a total of 429 patients were enrolled.
Study 02 indicated that CORLUX was well tolerated, and there were no
discernible problems with drug interactions between CORLUX and commonly
prescribed antipsychotic and antidepressant medications. Study 03
demonstrated with statistical significance that patients in the CORLUX
group were more likely than patients in the placebo group to achieve a 50
percent reduction in the BPRS PSS at Day 7, sustained to Day 28. At the
request of the FDA, approximately one third of the 221 patients enrolled in
this study had efficacy measures taken at Day 56. Of those patients who
exhibited at least mild psychotic symptoms on Day 0 (BPRS PSS greater than
or equal to 12) Study 03 showed with statistical significance that patients
receiving CORLUX were more likely than patients receiving placebo to
achieve a 50% reduction in the BPRS PSS at day 7 sustained to day 56.
A fourth trial involved an open-label study of the safety of
retreatment in patients with a favorable response to treatment in Studies
02 and 03. The results indicated that patients tolerated their retreatment
well. Twenty-eight patients participated in this study.
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, FDA
agreements, and the timing of the completion of pivotal Phase 3 trials.
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, completion or success of clinical
trials; the regulatory process or regulatory approvals; or commercial
success; in addition, 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) announced today that it completed
patient enrollment in Corcept 09, the second of three Phase 3 clinical
trials in which CORLUX(R) (mifepristone) is being evaluated for treating
the psychotic features of psychotic major depression (PMD).
"We recently announced that patient enrollment was completed in our
first Phase 3 study, Corcept 07, and that we expect to report the results
of that trial in August," said Corcept's Chief Executive Officer Joseph K.
Belanoff, M.D. "In addition, we now expect to report the results from
Corcept 09 in September 2006. We expect to report the results of our third
Phase 3 trial, Corcept 06, in the fourth quarter."
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.
A Description of Study 09
Study 09 is a randomized, double-blind, placebo-controlled study that
is being conducted in Europe. The primary endpoint is 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 28, a responder analysis. A secondary endpoint is the proportion of patients
with at least a 50 percent improvement in the BPRS PSS at both Day 7 and
Day 56. The BPRS is an 18-item rating instrument used to assess
psychopathology, and the PSS includes the four items in the BPRS that
specifically measure psychosis. Patients must have at least mild psychotic
symptoms (BPRS PSS greater than or equal to 12) to enter the study. Study
enrollees may be either inpatients or outpatients. BPRS PSS assessments are
made at Days 14, 42 and 56.
Patients may not take any antidepressant or antipsychotic medication
for at least one week before study randomization. At randomization, they
are placed in a one-to-one distribution into either a treatment group or a
placebo group. Patients in the treatment group receive 600 mg of CORLUX
once daily for a period of seven days. All patients receive antidepressant
therapy starting on Day 1 and through Day 56. Treatment with antipsychotic
medications or electroconvulsive therapy at any time during the study
results in the patient being classified as a non-responder.
Previously Completed Trials
The company has completed four studies of CORLUX for treating the
psychotic features of PMD. In January 2001, a dose-finding clinical trial
evaluated the efficacy, tolerability of and dose response to CORLUX. The
results showed that after one week of treatment, approximately two-thirds
of the patients in the two higher dosage groups (600 mg and 1200 mg)
experienced clinically meaningful reductions in psychosis, as measured by
the BPRS PSS. Based on these encouraging results, Corcept conducted two
double-blind, placebo-controlled safety and efficacy clinical trials (Study
02 and Study 03) in which a total of 429 patients were enrolled.
Study 02 indicated that CORLUX was well tolerated, and there were no
discernible problems with drug interactions between CORLUX and commonly
prescribed antipsychotic and antidepressant medications. Study 03
demonstrated with statistical significance that patients in the CORLUX
group were more likely than patients in the placebo group to achieve a 50
percent reduction in the BPRS PSS at Day 7, sustained to Day 28. At the
request of the FDA, approximately one third of the 221 patients enrolled in
this study had efficacy measures taken at Day 56. Of those patients who
exhibited at least mild psychotic symptoms on Day 0 (BPRS PSS greater than
or equal to 12) Study 03 showed with statistical significance that patients
receiving CORLUX were more likely than patients receiving placebo to
achieve a 50% reduction in the BPRS PSS at day 7 sustained to day 56.
A fourth trial involved an open-label study of the safety of
retreatment in patients with a favorable response to treatment in Studies
02 and 03. The results indicated that patients tolerated their retreatment
well. Twenty-eight patients participated in this study.
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, FDA
agreements, and the timing of the completion of pivotal Phase 3 trials.
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, completion or success of clinical
trials; the regulatory process or regulatory approvals; or commercial
success; in addition, 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/
суббота, 3 сентября 2011 г.
Antidepressants may lower risk of recurrent heart attack in depressed heart attack patients
In depressed patients who have experienced a heart attack, use of antidepressants, especially selective serotonin reuptake inhibitors (SSRIs), was associated with a reduced risk of death and recurrent heart attack, according to an article in the July issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
Cardiovascular disease (CVD) is the leading cause of death, major disease and disability among U.S. men and women, according to background information in the article. Major depression was found in approximately 20 percent of patients with a recent myocardial infarction (MI; heart attack); a similar prevalence was found for minor depression. Depression is a risk factor for recurrent non-fatal heart attack and cardiac death in patients who experience an acute MI (AMI), independent of cardiac disease severity. Despite their effectiveness in treating depression, the use of antidepressants in patients with CVD remains controversial.
C. Barr Taylor, M.D., from Stanford Medical Center, Stanford, Calif., and colleagues conducted a secondary analysis of data from the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial to determine the effects of antidepressants on post-MI patients. The ENRICHD trial randomized 2,481 depressed and/or socially isolated patients from October 1, 1996 to October 31, 1999. The analysis in this report is based on 1834 patients (985 men and 849 women) who had depression, with or without low social support. Of these, 446 patients took antidepressants during the study, including 301 who were prescribed SSRIs (a class of drugs that increases the levels of serotonin in the body); and 145 patients who were prescribed other types of antidepressants.
During an average follow-up of 29 months, 457 fatal and non-fatal cardiovascular events occurred. Twenty-six percent (361 of 1,388) of the patients who did not receive antidepressants died or had a recurrent MI, compared to 21.5 percent (96 of 446) of the patients who did take antidepressants. After adjusting for baseline depression and cardiac risk, SSRI use was associated with 43 percent lower risk of death or recurrent non-fatal MI, and 43 percent lower risk of death from all causes, compared with patients not receiving SSRIs. Risk of death or recurrent MI, all-cause death, or recurrent MI was 28 percent, 36 percent, and 27 percent lower, respectively, in patients taking non-SSRI antidepressants, compared with nonusers.
"The main finding of this study is that antidepressant use post-AMI by depressed patients in the ENRICHD clinical trial was associated with significantly lower rates of the study primary end points, death and reinfarction [recurrent heart attack]," the authors write.
(Arch Gen Psychiatry. 2005; 62: 792-798. Available pre-embargo to the media at jamamedia.)
Editor's Note: This study was supported by contracts from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
Editorial: Does Treating Post-Myocardial Infarction Depression Reduce Medical Mortality?
In an editorial accompanying this study, Alexander H. Glassman, M.D., of the New York State Psychiatric Institute, writes that in the ENRICHD trial "only the most depressed patients, those known to be at higher risk for cardiac events, were offered antidepressants. In addition, there was no control over when the drug was started or stopped, and even the reported start and stop times were only estimates. However, the sample was large, the number of events reasonable, and the magnitude of the effect is hard to ignore. Had the ENRICHD study observed an uncontrolled 40 percent increase in mortality with antidepressant drug treatment, public advocates would be clamoring for review by the Food and Drug Administration, label changes, or even 'black box' warnings. Yet this observation of a 40 percent decrease in life-threatening outcomes has been in the literature for almost three years with no systematic follow-up and minimal medical or psychiatric awareness."
"There are multiple mechanisms by which depression could increase vascular disease," Dr. Glassman writes. "It increases platelet activation and inflammatory markers, reduces heart variability, and leads to multiple adverse health behaviors; all are associated with increased cardiovascular risk and death. Whatever links depression and heart disease, it is more likely to involve all of the above rather than any single pathway."
"Acknowledging the implications of MDD [major depressive disorder] for cardiac morbidity and mortality would validate depression as a systemic disease with implications for the entire body, and reduce the stigma of this diagnosis for medical professionals, the public, and the patients themselves," Dr. Glassman concludes. "The ENRICHD investigators have made a significant step in that direction."
(Arch Gen Psychiatry. 2005; 62: 711-712. Available pre-embargo to the media at jamamedia.)
For more information, contact JAMA/Archives Media Relations at 312-464-JAMA (5262) or email mediarelationsjama-archives.
JAMA and Archives Journals
jamamedia
Cardiovascular disease (CVD) is the leading cause of death, major disease and disability among U.S. men and women, according to background information in the article. Major depression was found in approximately 20 percent of patients with a recent myocardial infarction (MI; heart attack); a similar prevalence was found for minor depression. Depression is a risk factor for recurrent non-fatal heart attack and cardiac death in patients who experience an acute MI (AMI), independent of cardiac disease severity. Despite their effectiveness in treating depression, the use of antidepressants in patients with CVD remains controversial.
C. Barr Taylor, M.D., from Stanford Medical Center, Stanford, Calif., and colleagues conducted a secondary analysis of data from the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial to determine the effects of antidepressants on post-MI patients. The ENRICHD trial randomized 2,481 depressed and/or socially isolated patients from October 1, 1996 to October 31, 1999. The analysis in this report is based on 1834 patients (985 men and 849 women) who had depression, with or without low social support. Of these, 446 patients took antidepressants during the study, including 301 who were prescribed SSRIs (a class of drugs that increases the levels of serotonin in the body); and 145 patients who were prescribed other types of antidepressants.
During an average follow-up of 29 months, 457 fatal and non-fatal cardiovascular events occurred. Twenty-six percent (361 of 1,388) of the patients who did not receive antidepressants died or had a recurrent MI, compared to 21.5 percent (96 of 446) of the patients who did take antidepressants. After adjusting for baseline depression and cardiac risk, SSRI use was associated with 43 percent lower risk of death or recurrent non-fatal MI, and 43 percent lower risk of death from all causes, compared with patients not receiving SSRIs. Risk of death or recurrent MI, all-cause death, or recurrent MI was 28 percent, 36 percent, and 27 percent lower, respectively, in patients taking non-SSRI antidepressants, compared with nonusers.
"The main finding of this study is that antidepressant use post-AMI by depressed patients in the ENRICHD clinical trial was associated with significantly lower rates of the study primary end points, death and reinfarction [recurrent heart attack]," the authors write.
(Arch Gen Psychiatry. 2005; 62: 792-798. Available pre-embargo to the media at jamamedia.)
Editor's Note: This study was supported by contracts from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
Editorial: Does Treating Post-Myocardial Infarction Depression Reduce Medical Mortality?
In an editorial accompanying this study, Alexander H. Glassman, M.D., of the New York State Psychiatric Institute, writes that in the ENRICHD trial "only the most depressed patients, those known to be at higher risk for cardiac events, were offered antidepressants. In addition, there was no control over when the drug was started or stopped, and even the reported start and stop times were only estimates. However, the sample was large, the number of events reasonable, and the magnitude of the effect is hard to ignore. Had the ENRICHD study observed an uncontrolled 40 percent increase in mortality with antidepressant drug treatment, public advocates would be clamoring for review by the Food and Drug Administration, label changes, or even 'black box' warnings. Yet this observation of a 40 percent decrease in life-threatening outcomes has been in the literature for almost three years with no systematic follow-up and minimal medical or psychiatric awareness."
"There are multiple mechanisms by which depression could increase vascular disease," Dr. Glassman writes. "It increases platelet activation and inflammatory markers, reduces heart variability, and leads to multiple adverse health behaviors; all are associated with increased cardiovascular risk and death. Whatever links depression and heart disease, it is more likely to involve all of the above rather than any single pathway."
"Acknowledging the implications of MDD [major depressive disorder] for cardiac morbidity and mortality would validate depression as a systemic disease with implications for the entire body, and reduce the stigma of this diagnosis for medical professionals, the public, and the patients themselves," Dr. Glassman concludes. "The ENRICHD investigators have made a significant step in that direction."
(Arch Gen Psychiatry. 2005; 62: 711-712. Available pre-embargo to the media at jamamedia.)
For more information, contact JAMA/Archives Media Relations at 312-464-JAMA (5262) or email mediarelationsjama-archives.
JAMA and Archives Journals
jamamedia
среда, 31 августа 2011 г.
Teen Pregnancy May Be Symptom, Not Cause, Of Emotional Distress
It would make sense that teenage mothers have a lot of psychological stress in their lives, but a new study shows that the distress comes before the pregnancy, not because of it.
"Psychological distress does not appear to be caused by teen childbearing, nor does it cause teen childbearing, except apparently among girls from poor households," said Stefanie Mollborn, Ph.D., an assistant professor of sociology at the Institute of Behavioral Science of the University of Colorado at Boulder.
The study, published in the September issue of the Journal of Health and Social Behavior, used data from two large long-term U.S. surveys that followed thousands of teen girls and women. Participants responded to items on symptoms associated with depression, such as how often they found things that did not usually bother them to be bothersome, how easily they could shake off feeling blue or whether they had trouble concentrating. The researchers did not use the term "depression," which is a clinical diagnosis.
Only the combination of poverty and existing distress was a good predictor of teen pregnancy.
Previous studies had shown high levels of depression among teen mothers, but nationally representative studies had not examined if distress was present before the pregnancy and stresses of young motherhood.
"Psychologically distressed girls are at risk for teen childbearing and vice versa, even if the two things usually do not cause each other," Mollborn said. "This could help educators and clinicians identify at-risk adolescents."
Looking for symptoms of depression or distress should be part of normal health screening for all teenagers, said Diane Merritt, M.D., director of Pediatric and Adolescent Gynecology at the Washington University School of Medicine in St. Louis. "Talking to teenagers about their sexuality and responsible behavior is key," she said. Responsible behavior would include the use of birth control if the teenager were sexually active.
One of the best ways to prevent teen pregnancy is for teens to have long-term goals and good self-esteem, Merritt added.
High levels of depression have long-term negative consequences for both mothers and children, Mollborn said. The higher levels of psychological distress in women who had teenage pregnancies continued well into adulthood, she added.
The Journal of Health and Social Behavior is a quarterly journal of the American Sociological Association.
Source
Health Behavior News Service
"Psychological distress does not appear to be caused by teen childbearing, nor does it cause teen childbearing, except apparently among girls from poor households," said Stefanie Mollborn, Ph.D., an assistant professor of sociology at the Institute of Behavioral Science of the University of Colorado at Boulder.
The study, published in the September issue of the Journal of Health and Social Behavior, used data from two large long-term U.S. surveys that followed thousands of teen girls and women. Participants responded to items on symptoms associated with depression, such as how often they found things that did not usually bother them to be bothersome, how easily they could shake off feeling blue or whether they had trouble concentrating. The researchers did not use the term "depression," which is a clinical diagnosis.
Only the combination of poverty and existing distress was a good predictor of teen pregnancy.
Previous studies had shown high levels of depression among teen mothers, but nationally representative studies had not examined if distress was present before the pregnancy and stresses of young motherhood.
"Psychologically distressed girls are at risk for teen childbearing and vice versa, even if the two things usually do not cause each other," Mollborn said. "This could help educators and clinicians identify at-risk adolescents."
Looking for symptoms of depression or distress should be part of normal health screening for all teenagers, said Diane Merritt, M.D., director of Pediatric and Adolescent Gynecology at the Washington University School of Medicine in St. Louis. "Talking to teenagers about their sexuality and responsible behavior is key," she said. Responsible behavior would include the use of birth control if the teenager were sexually active.
One of the best ways to prevent teen pregnancy is for teens to have long-term goals and good self-esteem, Merritt added.
High levels of depression have long-term negative consequences for both mothers and children, Mollborn said. The higher levels of psychological distress in women who had teenage pregnancies continued well into adulthood, she added.
The Journal of Health and Social Behavior is a quarterly journal of the American Sociological Association.
Source
Health Behavior News Service
воскресенье, 28 августа 2011 г.
Sudden Death Of A Parent Raises Risk Of Depression, Post-Traumatic Stress Disorder For Surviving Children, Pitt Researchers Find
The children of parents who die suddenly - whether by suicide, accident or natural causes - are three times more likely to develop depression and are at higher risk for post-traumatic stress disorder (PTSD) than children who don't face such a difficult life event, according to a University of Pittsburgh School of Medicine study published in the current issue of the Archives of Pediatric & Adolescent Medicine, one of the JAMA/Archives journals.
In the first controlled, population-based study of its kind, the team of Pitt and University of Pittsburgh Medical Center (UPMC) researchers also found that parents who died of suicide had higher rates of bipolar disorder, alcohol and substance abuse disorders and personality disorders. Higher rates of these disorders are expected in suicide victims; however, those who died accidentally or from sudden natural death also had higher rates of psychiatric disorders, specifically, alcohol and substance abuse and personality disorders, and showed a trend toward higher rates of bipolar disorder.
While the death of a parent is consistently rated as one of the most stressful events that a child can experience, little has been known about the psychiatric outcomes in bereaved children until now. "Our study shows that when premature parental death occurs, physicians should be alert to the increased risk for depression and post-traumatic stress disorder in bereaved offspring and in their surviving caregivers," said David A. Brent, M.D., academic chief of child and adolescent psychiatry at Western Psychiatric Institute and Clinic and professor of psychiatry, pediatrics and epidemiology at the University of Pittsburgh School of Medicine. "Not surprisingly, we found that bereaved offspring are at increased risk for adverse outcomes in part because of factors that may have contributed to the parent's death."
The study involved 140 families in which one parent had died of either suicide, accidental death - such as drug overdoses and car accidents - or sudden natural death, while a control group consisted of 99 families with two living biological parents who were matched to the deceased parents in the study group based on sex, age and neighborhood. Ages of the children at their parents' deaths ranged from seven to 25 years.
Other factors that affected outcomes included the nature of the last conversation with the deceased. Researchers found that a caregiver's recollection of a supportive conversation led to a higher risk of depression. "Understanding the effects of bereavement is essential to identifying those at highest risk who should be targeted for future prevention and intervention efforts," noted Nadine Melhem, Ph.D., first author and assistant professor of psychiatry at the University of Pittsburgh School of Medicine.
These findings point out the importance of improving the detection and treatment of bipolar illness, substance and alcohol abuse, and personality disorders, as well as the significance of addressing the lifestyle associations of these illnesses that lead to premature deaths, according to Dr. Brent.
"The caregivers should be monitored for depression and PTSD because restoring their normal mental functioning could lead to more positive outcomes for the children," said Dr. Brent. "However, given the increased risk of depression and PTSD, the bereaved children also should be monitored and, if necessary, referred and treated for their psychiatric disorders."
Co-authors of the study include Monica Walker, M.A., Western Psychiatric Institute and Clinic, and the Department of Psychiatry, University of Pittsburgh School of Medicine; and Grace Moritz, M.S.W., Division of Collaborative Care Medicine, UPMC.
Drs. Brent and Melhem were supported by funding provided by the National Institute of Mental Health and the American Foundation for Suicide Prevention.
The University of Pittsburgh School of Medicine is one of the nation's leading medical schools, renowned for its curriculum that emphasizes both the science and humanity of medicine and its remarkable growth in National Institutes of Health (NIH) grant support, which has more than doubled since 1998. For fiscal year 2006, the University ranked sixth out of more than 3,000 entities receiving NIH support with respect to the research grants awarded to its faculty. The majority of these grants were awarded to the faculty of the medical school. As one of the university's six Schools of the Health Sciences, the School of Medicine is the academic partner to the University of Pittsburgh Medical Center. Their combined mission is to train tomorrow's health care specialists and biomedical scientists, engage in groundbreaking research that will advance understanding of the causes and treatments of disease and participate in the delivery of outstanding patient care.
University of Pittsburgh Medical Center
In the first controlled, population-based study of its kind, the team of Pitt and University of Pittsburgh Medical Center (UPMC) researchers also found that parents who died of suicide had higher rates of bipolar disorder, alcohol and substance abuse disorders and personality disorders. Higher rates of these disorders are expected in suicide victims; however, those who died accidentally or from sudden natural death also had higher rates of psychiatric disorders, specifically, alcohol and substance abuse and personality disorders, and showed a trend toward higher rates of bipolar disorder.
While the death of a parent is consistently rated as one of the most stressful events that a child can experience, little has been known about the psychiatric outcomes in bereaved children until now. "Our study shows that when premature parental death occurs, physicians should be alert to the increased risk for depression and post-traumatic stress disorder in bereaved offspring and in their surviving caregivers," said David A. Brent, M.D., academic chief of child and adolescent psychiatry at Western Psychiatric Institute and Clinic and professor of psychiatry, pediatrics and epidemiology at the University of Pittsburgh School of Medicine. "Not surprisingly, we found that bereaved offspring are at increased risk for adverse outcomes in part because of factors that may have contributed to the parent's death."
The study involved 140 families in which one parent had died of either suicide, accidental death - such as drug overdoses and car accidents - or sudden natural death, while a control group consisted of 99 families with two living biological parents who were matched to the deceased parents in the study group based on sex, age and neighborhood. Ages of the children at their parents' deaths ranged from seven to 25 years.
Other factors that affected outcomes included the nature of the last conversation with the deceased. Researchers found that a caregiver's recollection of a supportive conversation led to a higher risk of depression. "Understanding the effects of bereavement is essential to identifying those at highest risk who should be targeted for future prevention and intervention efforts," noted Nadine Melhem, Ph.D., first author and assistant professor of psychiatry at the University of Pittsburgh School of Medicine.
These findings point out the importance of improving the detection and treatment of bipolar illness, substance and alcohol abuse, and personality disorders, as well as the significance of addressing the lifestyle associations of these illnesses that lead to premature deaths, according to Dr. Brent.
"The caregivers should be monitored for depression and PTSD because restoring their normal mental functioning could lead to more positive outcomes for the children," said Dr. Brent. "However, given the increased risk of depression and PTSD, the bereaved children also should be monitored and, if necessary, referred and treated for their psychiatric disorders."
Co-authors of the study include Monica Walker, M.A., Western Psychiatric Institute and Clinic, and the Department of Psychiatry, University of Pittsburgh School of Medicine; and Grace Moritz, M.S.W., Division of Collaborative Care Medicine, UPMC.
Drs. Brent and Melhem were supported by funding provided by the National Institute of Mental Health and the American Foundation for Suicide Prevention.
The University of Pittsburgh School of Medicine is one of the nation's leading medical schools, renowned for its curriculum that emphasizes both the science and humanity of medicine and its remarkable growth in National Institutes of Health (NIH) grant support, which has more than doubled since 1998. For fiscal year 2006, the University ranked sixth out of more than 3,000 entities receiving NIH support with respect to the research grants awarded to its faculty. The majority of these grants were awarded to the faculty of the medical school. As one of the university's six Schools of the Health Sciences, the School of Medicine is the academic partner to the University of Pittsburgh Medical Center. Their combined mission is to train tomorrow's health care specialists and biomedical scientists, engage in groundbreaking research that will advance understanding of the causes and treatments of disease and participate in the delivery of outstanding patient care.
University of Pittsburgh Medical Center
четверг, 25 августа 2011 г.
Depression Returns In About Half Of Treated Teens
Most depressed teens who receive treatment appear to recover, but the condition recurs in almost half of adolescent patients and even more often among females, according to a report posted online today that will appear in the March 2011 print issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
Major depressive disorder affects approximately 5.9 percent of teen females and 4.6 percent of teen males, according to background information in the article. "It is associated with functional impairment, risk of suicide and risk of adult depression," the authors write. "Thus, it is important to investigate not only the efficacy of adolescent major depressive disorder treatments but also whether they reduce the risk of subsequent negative outcomes, especially depression recurrence."
John Curry, Ph.D., of Duke University Medical Center, Durham, N.C., and colleagues studied 196 adolescents (86 males and 110 females) who participated in the Treatment for Adolescents With Depression Study (TADS). The teens were randomly assigned to one of four short-term treatment interventions (medication with fluoxetine hydrochloride, cognitive behavioral therapy, a combination of the two or placebo) and followed up for five years.
Almost all participants (96.4 percent) recovered from their initial episode of depression during the follow-up period, including 88.3 percent who recovered within two years. Those who responded to a 12-week treatment session (short-term responders) were more likely to have recovered by two years (96.2 percent vs. 79.1 percent). However, two-year recovery was not associated with any particular type of treatment.
Of the 189 teens who recovered from depression, 88 (46.6 percent) experienced a recurrence. "Contrary to our hypotheses, neither full response to short-term treatment nor treatment with a combination of fluoxetine and cognitive behavioral therapy reduced the risk of recurrence," the authors write. "However, short-term treatment non-responders were more likely to experience recurrence than full and partial responders. Females were significantly more likely to have a recurrence than males."
Teens who also had an anxiety disorder were more likely to experience recurrence (61.9 percent vs. 42.2 percent of those without anxiety disorders). In addition, participants whose depression returned had higher scores on scales of suicidal thoughts and behaviors.
"Our results reinforce the importance of modifying a short-term treatment that leads to partial response or non-response because these were associated with less likelihood of recovery in two years," the authors write. "The finding that recurrence rates increased significantly from two to three years after baseline suggests that recurrence prevention efforts, such as symptom or medication monitoring or cognitive behavioral therapy booster sessions may be of value beyond the [18-week] maintenance period included in TADS."
"Female sex was the most robust predictor of recurrence, indicating the importance of understanding and reducing the vulnerabilities of female adolescents to recurrent episodes."
(Arch Gen Psychiatry. Published online November 1, 2010. doi:10.1001/archgenpsychiatry.2010.150.)
Major depressive disorder affects approximately 5.9 percent of teen females and 4.6 percent of teen males, according to background information in the article. "It is associated with functional impairment, risk of suicide and risk of adult depression," the authors write. "Thus, it is important to investigate not only the efficacy of adolescent major depressive disorder treatments but also whether they reduce the risk of subsequent negative outcomes, especially depression recurrence."
John Curry, Ph.D., of Duke University Medical Center, Durham, N.C., and colleagues studied 196 adolescents (86 males and 110 females) who participated in the Treatment for Adolescents With Depression Study (TADS). The teens were randomly assigned to one of four short-term treatment interventions (medication with fluoxetine hydrochloride, cognitive behavioral therapy, a combination of the two or placebo) and followed up for five years.
Almost all participants (96.4 percent) recovered from their initial episode of depression during the follow-up period, including 88.3 percent who recovered within two years. Those who responded to a 12-week treatment session (short-term responders) were more likely to have recovered by two years (96.2 percent vs. 79.1 percent). However, two-year recovery was not associated with any particular type of treatment.
Of the 189 teens who recovered from depression, 88 (46.6 percent) experienced a recurrence. "Contrary to our hypotheses, neither full response to short-term treatment nor treatment with a combination of fluoxetine and cognitive behavioral therapy reduced the risk of recurrence," the authors write. "However, short-term treatment non-responders were more likely to experience recurrence than full and partial responders. Females were significantly more likely to have a recurrence than males."
Teens who also had an anxiety disorder were more likely to experience recurrence (61.9 percent vs. 42.2 percent of those without anxiety disorders). In addition, participants whose depression returned had higher scores on scales of suicidal thoughts and behaviors.
"Our results reinforce the importance of modifying a short-term treatment that leads to partial response or non-response because these were associated with less likelihood of recovery in two years," the authors write. "The finding that recurrence rates increased significantly from two to three years after baseline suggests that recurrence prevention efforts, such as symptom or medication monitoring or cognitive behavioral therapy booster sessions may be of value beyond the [18-week] maintenance period included in TADS."
"Female sex was the most robust predictor of recurrence, indicating the importance of understanding and reducing the vulnerabilities of female adolescents to recurrent episodes."
(Arch Gen Psychiatry. Published online November 1, 2010. doi:10.1001/archgenpsychiatry.2010.150.)
понедельник, 22 августа 2011 г.
Depressed People Have High Rates Of Physical Illness
People with recurrent depression have high rates of many common physical illnesses, such as gastric ulcer, rhinitis/hay fever, osteoarthritis, thyroid disease, hypertension and asthma, a new study has found.
Published in the May 2008 issue of the British Journal of Psychiatry, the study compared 1546 people with recurrent depression with 884 psychiatrically healthy controls in terms of past treatment for 16 different physical disorders.
Since many medical disorders are related to obesity, the researchers also examined body mass index (BMI) in both groups.
It was found that 15 physical disorders were significantly more frequent in people with recurrent depression than in controls. However, when BMI, age and gender were taken into account, depression was found to predict 6 disorders - gastric ulcer, asthma, rhinitis, hypertension, thyroid disease and osteoarthritis.
For the remaining physical health problems - diabetes, epilepsy, hypercholesterolaemia (high blood fats), kidney disease, liver disease, heart attack, osteoporosis, rheumatoid arthritis and stroke - the difference between those with and without each disorder could be accounted for by BMI, age or gender.
Both men and women with recurrent depression had significantly higher BMIs than men and women in the control group.
Although the percentages of the two groups were similar in the overweight range, a greater proportion of people with depression were in the obese range, and substantially fewer were in the normal range, compared with controls.
Thus, around a quarter of the men and women with depression were obese, which increases their susceptibility to physical health problems. In this study, obesity was associated with an increase in self-reported rates of hypercholesterolaemia, type II diabetes and heart attack.
High rates of obesity may be caused by some antidepressant medications, or arise because people who are depressed take less exercise and/or 'comfort' eat. However, it is also possible that genetic factors may be involved.
Evidence from previous research, and from this study, lends some support to the hypothesis that there are shared causal factors between recurrent depression, obesity and certain physical disorders.
One possible explanation for this is the effect that stress, and stress hormones, have on the brain and body. For instance, high levels of the stress hormone cortisol may link both obesity and gastric ulcers with depression.
The researchers comment that inflammatory processes that activate stress hormones may also link depression with asthma, hay fever, osteoarthritis and hypertension. These are speculations, however, and need confirmation from further studies.
Although long neglected, the physical health of people with schizophrenia is starting to be addressed, particularly in relation to the weight gain caused by antipsychotic drugs. This study suggests that attention needs to be paid to the physical health needs of people with depression.
"Medical disorders in people with recurrent depression."
Farmer A. et al (2008)
British Journal of Psychiatry, 192, 5, pages 351-355.
Click here to view Abstract online
The Royal College of Psychiatrists
The Royal College of Psychiatrists is the professional and educational body for psychiatrists in the United Kingdom and the Republic of Ireland. We promote mental health by:
-- Setting standards and promoting excellence in mental health care
-- Improving understanding through research and education
-- Leading, representing, training and supporting psychiatrists
-- Working with patients, carers and their organisations
As well as running its membership examination (MRCPsych), and visiting and approving hospitals for training purposes, the College organises scientific and clinical conferences and lectures and continuing professional development activities. The College publishes books, reports and educational material for professionals and the general public. It also publishes the British Journal of Psychiatry, Psychiatric Bulletin and Advances in Psychiatric Treatment, all of which are now available on-line.
The Royal College of Psychiatrists has been in existence in some form since 1841. First as the "Association of Medical Officers of Asylums and Hospitals for the Insane" (later changed to the Medico Psychological Association) then, in 1926 receiving its Royal Charter to become the "Royal Medico Psychological Association, and finally, in 1971 receiving a Supplemental Charter to become the "Royal College of Psychiatrists" we know today.
rcpsych.ac.uk
Published in the May 2008 issue of the British Journal of Psychiatry, the study compared 1546 people with recurrent depression with 884 psychiatrically healthy controls in terms of past treatment for 16 different physical disorders.
Since many medical disorders are related to obesity, the researchers also examined body mass index (BMI) in both groups.
It was found that 15 physical disorders were significantly more frequent in people with recurrent depression than in controls. However, when BMI, age and gender were taken into account, depression was found to predict 6 disorders - gastric ulcer, asthma, rhinitis, hypertension, thyroid disease and osteoarthritis.
For the remaining physical health problems - diabetes, epilepsy, hypercholesterolaemia (high blood fats), kidney disease, liver disease, heart attack, osteoporosis, rheumatoid arthritis and stroke - the difference between those with and without each disorder could be accounted for by BMI, age or gender.
Both men and women with recurrent depression had significantly higher BMIs than men and women in the control group.
Although the percentages of the two groups were similar in the overweight range, a greater proportion of people with depression were in the obese range, and substantially fewer were in the normal range, compared with controls.
Thus, around a quarter of the men and women with depression were obese, which increases their susceptibility to physical health problems. In this study, obesity was associated with an increase in self-reported rates of hypercholesterolaemia, type II diabetes and heart attack.
High rates of obesity may be caused by some antidepressant medications, or arise because people who are depressed take less exercise and/or 'comfort' eat. However, it is also possible that genetic factors may be involved.
Evidence from previous research, and from this study, lends some support to the hypothesis that there are shared causal factors between recurrent depression, obesity and certain physical disorders.
One possible explanation for this is the effect that stress, and stress hormones, have on the brain and body. For instance, high levels of the stress hormone cortisol may link both obesity and gastric ulcers with depression.
The researchers comment that inflammatory processes that activate stress hormones may also link depression with asthma, hay fever, osteoarthritis and hypertension. These are speculations, however, and need confirmation from further studies.
Although long neglected, the physical health of people with schizophrenia is starting to be addressed, particularly in relation to the weight gain caused by antipsychotic drugs. This study suggests that attention needs to be paid to the physical health needs of people with depression.
"Medical disorders in people with recurrent depression."
Farmer A. et al (2008)
British Journal of Psychiatry, 192, 5, pages 351-355.
Click here to view Abstract online
The Royal College of Psychiatrists
The Royal College of Psychiatrists is the professional and educational body for psychiatrists in the United Kingdom and the Republic of Ireland. We promote mental health by:
-- Setting standards and promoting excellence in mental health care
-- Improving understanding through research and education
-- Leading, representing, training and supporting psychiatrists
-- Working with patients, carers and their organisations
As well as running its membership examination (MRCPsych), and visiting and approving hospitals for training purposes, the College organises scientific and clinical conferences and lectures and continuing professional development activities. The College publishes books, reports and educational material for professionals and the general public. It also publishes the British Journal of Psychiatry, Psychiatric Bulletin and Advances in Psychiatric Treatment, all of which are now available on-line.
The Royal College of Psychiatrists has been in existence in some form since 1841. First as the "Association of Medical Officers of Asylums and Hospitals for the Insane" (later changed to the Medico Psychological Association) then, in 1926 receiving its Royal Charter to become the "Royal Medico Psychological Association, and finally, in 1971 receiving a Supplemental Charter to become the "Royal College of Psychiatrists" we know today.
rcpsych.ac.uk
пятница, 19 августа 2011 г.
New Study From University Of Leicester On Breast Feeding & Post Natal Depression, UK
The commonly held belief that mothers suffering from post natal depression will not be able to breastfeed has been challenged by research from the University of Leicester, which also suggests that the manner in which current breastfeeding promotion strategies are communicated may contribute to feelings of guilt and fears of inadequacy by mothers suffering from depression.
These results arise from research carried out by Ellen Homewood, Alison Tweed and Jon Crossley of the Department of Clinical Psychology at the University, and Michelle Cree of the Derbyshire Mental Health Services NHS Trust.
They found that mothers with post natal depression felt occluded in their attempts to meet their infants' demands for sustenance and nurturance. These feelings seemed to be triggered by experiences of feeding, as it represented a central aspect of the women's interaction with their infants.
In some cases, breastfeeding contributed to depression by increasing women's sense of being trapped by the dependency of their babies at the expense of their own well-being, and intensifying their feelings of responsibility for keeping their babies alive.
The authors concluded that the self-confidence of mothers with post natal depression could suffer as a result of perceived pressure to breastfeed, by prompting them to judge themselves as mothers on the basis of how successful their breast-feeding experiences were.
The research suggests that depressed mothers may well need individual, psychologically-based breastfeeding support to understand and manage their feelings of ambivalence in motherhood.
The findings on breastfeeding were not all negative, however, and for some mothers who had been diagnosed with postnatal depression, breastfeeding reassured them of their ability to satisfy, nurture and connect with their infants. Breastfeeding enabled them to feel more confident as mothers because they were fulfilling a maternal role that they valued, and consequently, this enhanced their ability to create more positive relationships with their babies.
Clinical Psychologist Ellen Homewood commented: "The findings of our study into breastfeeding experiences in women with postnatal depression highlight the effects of women's expectations about motherhood and breastfeeding on their behaviour and emotional experiences, and warn against the assumption that depressed mothers will not be able to breastfeed. The results also point to the need for further research into the potential benefits of breastfeeding for depressed mothers."
University Of Leicester
- A member of the 1994 Group of universities that share a commitment to research excellence, high quality teaching and an outstanding student experience.
-- Ranked joint top for two consecutive years for the quality of teaching and overall satisfaction amongst full-time students at English universities
-- Ranked as a Top 20 university by The Times Good University Guide and The Guardian University League Table
-- One of just 19 UK universities to feature in world's top 200- Shanghai Jiao Tong International Index, 2005 and 2006.
-- Short listed Higher Education Institution of the Year - THES awards 2005 and 2006
-- Students' Union of the Year award 2005, short listed 2006
Founded in 1921, the University of Leicester has 19,000 students from 136 countries. Teaching in 18 subject areas has been graded Excellent by the Quality Assurance Agency- including 14 successive scores - a consistent run of success matched by just one other UK University. Leicester is world renowned for the invention of DNA Fingerprinting by Professor Sir Alec Jeffreys and houses Europe's biggest academic Space Research Centre. 90% of staff are actively engaged in high quality research and 13 subject areas have been awarded the highest rating of 5* and 5 for research quality, demonstrating excellence at an international level. The University's research grant income places it among the top 20 UK research universities. The University employs over 3,000 people, has an annual turnover of ??173m, covers an estate of 94 hectares and is engaged in a ??300m investment programme- among the biggest of any UK university.
le.ac.uk
These results arise from research carried out by Ellen Homewood, Alison Tweed and Jon Crossley of the Department of Clinical Psychology at the University, and Michelle Cree of the Derbyshire Mental Health Services NHS Trust.
They found that mothers with post natal depression felt occluded in their attempts to meet their infants' demands for sustenance and nurturance. These feelings seemed to be triggered by experiences of feeding, as it represented a central aspect of the women's interaction with their infants.
In some cases, breastfeeding contributed to depression by increasing women's sense of being trapped by the dependency of their babies at the expense of their own well-being, and intensifying their feelings of responsibility for keeping their babies alive.
The authors concluded that the self-confidence of mothers with post natal depression could suffer as a result of perceived pressure to breastfeed, by prompting them to judge themselves as mothers on the basis of how successful their breast-feeding experiences were.
The research suggests that depressed mothers may well need individual, psychologically-based breastfeeding support to understand and manage their feelings of ambivalence in motherhood.
The findings on breastfeeding were not all negative, however, and for some mothers who had been diagnosed with postnatal depression, breastfeeding reassured them of their ability to satisfy, nurture and connect with their infants. Breastfeeding enabled them to feel more confident as mothers because they were fulfilling a maternal role that they valued, and consequently, this enhanced their ability to create more positive relationships with their babies.
Clinical Psychologist Ellen Homewood commented: "The findings of our study into breastfeeding experiences in women with postnatal depression highlight the effects of women's expectations about motherhood and breastfeeding on their behaviour and emotional experiences, and warn against the assumption that depressed mothers will not be able to breastfeed. The results also point to the need for further research into the potential benefits of breastfeeding for depressed mothers."
University Of Leicester
- A member of the 1994 Group of universities that share a commitment to research excellence, high quality teaching and an outstanding student experience.
-- Ranked joint top for two consecutive years for the quality of teaching and overall satisfaction amongst full-time students at English universities
-- Ranked as a Top 20 university by The Times Good University Guide and The Guardian University League Table
-- One of just 19 UK universities to feature in world's top 200- Shanghai Jiao Tong International Index, 2005 and 2006.
-- Short listed Higher Education Institution of the Year - THES awards 2005 and 2006
-- Students' Union of the Year award 2005, short listed 2006
Founded in 1921, the University of Leicester has 19,000 students from 136 countries. Teaching in 18 subject areas has been graded Excellent by the Quality Assurance Agency- including 14 successive scores - a consistent run of success matched by just one other UK University. Leicester is world renowned for the invention of DNA Fingerprinting by Professor Sir Alec Jeffreys and houses Europe's biggest academic Space Research Centre. 90% of staff are actively engaged in high quality research and 13 subject areas have been awarded the highest rating of 5* and 5 for research quality, demonstrating excellence at an international level. The University's research grant income places it among the top 20 UK research universities. The University employs over 3,000 people, has an annual turnover of ??173m, covers an estate of 94 hectares and is engaged in a ??300m investment programme- among the biggest of any UK university.
le.ac.uk
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