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.
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