Girls born weighing less than 2,500 grams (about 5.5 pounds) may be more likely to develop depression between ages 13 to 16 than those born at a normal weight, while the same does not appear to be true for boys, according to a report in the March issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
Several previous studies have linked low birth weight with depression in adolescence and adulthood, according to background information in the article. Some suggest that, like adult-onset diabetes or cardiovascular disease, the potential for depression may lie dormant in individuals born with low birth weight, emerging under stressful conditions. However, previous research has not considered differences in rates of depression by age and sex, the authors note.
Elizabeth Jane Costello, Ph.D., Duke University Medical School, Durham, N.C., and colleagues examined the association between low birth weight and depression in 1,420 participants between the ages of 9 and 16 years, 49 percent of whom were female. Children from 11 North Carolina counties were enrolled in the Great Smoky Mountains Study in 1993 and assessed yearly for depression and other psychiatric disorders during childhood (age 9 to 12) and adolescence (age 13 to 16 years). The children's mothers gave information about birth weight and other indicators of adversity, such as having a mother younger than age 18 at birth or having a parent who left school before the 11th grade.
A total of 5.7 percent of the girls in the study were born weighing less than 2,500 grams. Of those, 38.1 percent experienced at least one episode of depression between ages 13 and 16, compared with 8.4 percent of those born at a normal weight. The risk of depression attributable to low birth weight was 18 percent - in other words, if all female babies were born at a normal weight, 18 percent fewer teen girls would have episodes of depression. On average, 23.5 percent of teen girls with low birth weight were depressed each year, compared with 3.4 percent of those with normal birth weight.
The same effect was not observed in boys - throughout childhood and adolescence, no more than 4.9 percent of boys experienced depression, regardless of birth weight. Low birth weight was not associated with an increased risk of any other psychiatric condition, including anxiety disorders, in either boys or girls.
"The findings need replication in larger samples that include prospective data from birth to adulthood. Important next steps will include separate examination of the many different hormonal, morphological, psychological and social aspects of puberty that might best explain the increase in risk seen in adolescence, herein indexed by age," the authors conclude. "For the present, the findings suggest that pediatricians and parents of girls who were of low birth weight should pay close attention to their mental health as they enter puberty."
(Arch Gen Psychiatry. 2007;64:338-344. Available pre-embargo to the media at jamamedia.)
This study was supported by grants from the National Institute of Mental Health, the National Institute on Drug Abuse and the William T. Grant Foundation. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
Contact: Tracey Koepke
JAMA and Archives Journals
вторник, 30 августа 2011 г.
воскресенье, 28 августа 2011 г.
Postpartum Mood Disturbances In Healthy New Mothers May Be Predicted By Their Perception Of Poor Sleep
A study of healthy new mothers in the April 1 issue of the journal Sleep found that the perception of poor sleep and the conscious awareness of its impact on daytime functioning might be stronger predictors of immediate postpartum mood disturbances than actual sleep quality and quantity.
Results indicate that both objective and subjective nighttime sleep significantly worsened with decreased total sleep time and sleep efficiency after giving birth. However, variables related to the subjective perception of sleep and sleep-related daytime dysfunction were stronger predictors of postpartum mood. After giving birth, subjective total sleep time at night fell from 437 minutes to 348 minutes, and mean subjective sleep efficiency decreased from 79 percent to 66 percent. Seventeen participants (46 percent) experienced some deterioration of mood after delivery.
Lead author Bei Bei, DPsych, clinical psychologist at the University of Melbourne in Victoria, Australia, said that while pregnancy is a joyous and exciting time, it also exposes women to many stressors, including disturbed sleep.
"We were surprised that while objective sleep was not irrelevant, subjective perception of sleep shared a much stronger relationship with mood," said Bei. "Women who are concerned about their sleep and/or mood should speak to health care professionals about cognitive-behavioral therapy, which is effective for improving both sleep and mood."
The two-stage longitudinal study measured sleep and mood during the third trimester and one week postpartum in 44 healthy women at low risk for postpartum depression. The average age of participants was 30 years, with a range from 18 to 41 years. The sample included 20 first-time mothers (45.5 percent) and 24 mothers with multiple children (54.5 percent). The majority of participants (91 percent) were married or in a stable relationship.
Objective sleep was measured by actigraphy, and subjective sleep by the Pittsburgh Sleep Quality Index. Mood was assessed by the Depression Anxiety Stress Scale, the Hospital Anxiety Depression Scale, and the Positive and Negative Affect Schedule. Subjective sleep and mood scales were administered during both phases of the study, and objective sleep measures were recorded continuously for seven days during the third trimester and seven days after delivery.
Poorer subjective nighttime sleep both during the third trimester and after delivery was associated with worse postpartum mood. As women's nighttime sleep worsened following delivery, their perceived sleep-related daytime dysfunction and napping behavior became relevant to their mood changes: higher sleep-related daytime dysfunction and more frequent naps were associated with higher reported distress. Sleep obtained in a daytime nap did not appear to provide the same restorative value as sleep obtained at night.
Objective sleep deteriorated after delivery as the mean total sleep time at night fell from 428 minutes during the third trimester to 373 minutes postpartum, and average sleep efficiency dropped from 77 percent to 63 percent. The average amount of time spent awake in bed after initially falling asleep at night increased from 77 minutes to 150 minutes, and mean daily nap time increased from 32 minutes to 101 minutes.
However, evidence supporting a relationship between objective nighttime sleep and mood was weak. Lower positive affect after delivery was related to poorer overall objective sleep during the third trimester but was unrelated to objective postpartum sleep. A series of analyses also found no significant difference in postpartum mood between women who had daytime labor and those who had nighttime labor.
The authors noted that the study was unable to determine if it was poor sleep that led to emotional distress, or if poor mood caused sleep complaints. However, they proposed that women with higher levels of psychological distress might perceive their sleep to be poorer; this perception of disturbed sleep at night might exacerbate subjective stress and frustration, thus creating a potentially vicious cycle.
The study: "Subjective Perception of Sleep, but not its Objective Quality, is Associated with Immediate Postpartum Mood Disturbances in Healthy Women"
Results indicate that both objective and subjective nighttime sleep significantly worsened with decreased total sleep time and sleep efficiency after giving birth. However, variables related to the subjective perception of sleep and sleep-related daytime dysfunction were stronger predictors of postpartum mood. After giving birth, subjective total sleep time at night fell from 437 minutes to 348 minutes, and mean subjective sleep efficiency decreased from 79 percent to 66 percent. Seventeen participants (46 percent) experienced some deterioration of mood after delivery.
Lead author Bei Bei, DPsych, clinical psychologist at the University of Melbourne in Victoria, Australia, said that while pregnancy is a joyous and exciting time, it also exposes women to many stressors, including disturbed sleep.
"We were surprised that while objective sleep was not irrelevant, subjective perception of sleep shared a much stronger relationship with mood," said Bei. "Women who are concerned about their sleep and/or mood should speak to health care professionals about cognitive-behavioral therapy, which is effective for improving both sleep and mood."
The two-stage longitudinal study measured sleep and mood during the third trimester and one week postpartum in 44 healthy women at low risk for postpartum depression. The average age of participants was 30 years, with a range from 18 to 41 years. The sample included 20 first-time mothers (45.5 percent) and 24 mothers with multiple children (54.5 percent). The majority of participants (91 percent) were married or in a stable relationship.
Objective sleep was measured by actigraphy, and subjective sleep by the Pittsburgh Sleep Quality Index. Mood was assessed by the Depression Anxiety Stress Scale, the Hospital Anxiety Depression Scale, and the Positive and Negative Affect Schedule. Subjective sleep and mood scales were administered during both phases of the study, and objective sleep measures were recorded continuously for seven days during the third trimester and seven days after delivery.
Poorer subjective nighttime sleep both during the third trimester and after delivery was associated with worse postpartum mood. As women's nighttime sleep worsened following delivery, their perceived sleep-related daytime dysfunction and napping behavior became relevant to their mood changes: higher sleep-related daytime dysfunction and more frequent naps were associated with higher reported distress. Sleep obtained in a daytime nap did not appear to provide the same restorative value as sleep obtained at night.
Objective sleep deteriorated after delivery as the mean total sleep time at night fell from 428 minutes during the third trimester to 373 minutes postpartum, and average sleep efficiency dropped from 77 percent to 63 percent. The average amount of time spent awake in bed after initially falling asleep at night increased from 77 minutes to 150 minutes, and mean daily nap time increased from 32 minutes to 101 minutes.
However, evidence supporting a relationship between objective nighttime sleep and mood was weak. Lower positive affect after delivery was related to poorer overall objective sleep during the third trimester but was unrelated to objective postpartum sleep. A series of analyses also found no significant difference in postpartum mood between women who had daytime labor and those who had nighttime labor.
The authors noted that the study was unable to determine if it was poor sleep that led to emotional distress, or if poor mood caused sleep complaints. However, they proposed that women with higher levels of psychological distress might perceive their sleep to be poorer; this perception of disturbed sleep at night might exacerbate subjective stress and frustration, thus creating a potentially vicious cycle.
The study: "Subjective Perception of Sleep, but not its Objective Quality, is Associated with Immediate Postpartum Mood Disturbances in Healthy Women"
пятница, 26 августа 2011 г.
Low Cholesterol, Depression Linked To Early Death
New Geisinger research shows that men with a combination of low total cholesterol and depression were seven times more likely to die prematurely from unnatural causes, such as suicide and accidents.
The study, which was published recently in Journal of Psychiatric Research, found that men with low total cholesterol (165 milligrams of cholesterol per deciliter or less) and depression were at very high risk for premature death from "external causes" including suicide, drug overdose, accidental poisoning and unintended injuries.
"While it's generally understood that having low cholesterol is a good health sign, combined with other factors, it could actually put a person at risk," said Geisinger senior investigator Joseph Boscarino, PhD, MPH.
Low cholesterol levels in a person's blood may lead to decreased serotonin, which is a neurotransmitter that helps relay signals to various parts of the brain. Decreased serotonin is linked to depression, anger, sleep loss and other problems, Dr. Boscarino said.
Those with anti-social personality disorder, which is associated with high risk-taking and thrill-seeking, were twice as likely to die prematurely, according to the study. Men with morbid depression had a similar risk.
Cholesterol is important because it serves as a key component or "constituent" of nerve cells in the body, said Geisinger neurologist and study co-author Stuart Hoffman, DO.
"A certain amount of cholesterol needs to be present for neurons to function normally," Dr. Hoffman said. "Our study shows that if a person's cholesterol is too low, nervous system problems could develop."
For the study, Dr. Boscarino reviewed medical histories and medical exams performed on nearly 4,500 Vietnam veterans in 1985/86. These reports included comprehensive mental health assessments, physical exams and assessment of lipid levels, including total cholesterol. Dr. Boscarino also reviewed death certificate data for the veterans that were available in 2000.
The research was funded, in part, with a National Institute of Mental Health Training Grant to Dr. Boscarino.
About Geisinger Health System
Founded in 1915, Geisinger Health System is one of the nations largest integrated health services organizations. Serving more than 2.6 million residents throughout central and northeastern Pennsylvania, the physician-led organization is a nationally recognized leader in the use of electronic health records, patient access and engagement in their healthcare, and in medical education for the next generation. Geisinger is comprised of three medical center campuses, a 740-member group practice, a not-for-profit health insurance company and research that extends across our large system- all dedicated to creating new models for scientific discovery, quality patient care, and successful clinical outcomes. Geisinger's Weis Center, Center for Health Research and Center for Clinical Studies include basic science, population-based and clinical trials research, complemented by collaborative relationships with top academic centers. Geisinger Ventures, the system's for profit entrepreneurial arm, seeks and promotes opportunities to speed the delivery of medical innovation to benefit patients. For more information, visit geisinger.
Geisinger Health System
100 N Academy Ave.
Danville
PA
United States
geisinger
The study, which was published recently in Journal of Psychiatric Research, found that men with low total cholesterol (165 milligrams of cholesterol per deciliter or less) and depression were at very high risk for premature death from "external causes" including suicide, drug overdose, accidental poisoning and unintended injuries.
"While it's generally understood that having low cholesterol is a good health sign, combined with other factors, it could actually put a person at risk," said Geisinger senior investigator Joseph Boscarino, PhD, MPH.
Low cholesterol levels in a person's blood may lead to decreased serotonin, which is a neurotransmitter that helps relay signals to various parts of the brain. Decreased serotonin is linked to depression, anger, sleep loss and other problems, Dr. Boscarino said.
Those with anti-social personality disorder, which is associated with high risk-taking and thrill-seeking, were twice as likely to die prematurely, according to the study. Men with morbid depression had a similar risk.
Cholesterol is important because it serves as a key component or "constituent" of nerve cells in the body, said Geisinger neurologist and study co-author Stuart Hoffman, DO.
"A certain amount of cholesterol needs to be present for neurons to function normally," Dr. Hoffman said. "Our study shows that if a person's cholesterol is too low, nervous system problems could develop."
For the study, Dr. Boscarino reviewed medical histories and medical exams performed on nearly 4,500 Vietnam veterans in 1985/86. These reports included comprehensive mental health assessments, physical exams and assessment of lipid levels, including total cholesterol. Dr. Boscarino also reviewed death certificate data for the veterans that were available in 2000.
The research was funded, in part, with a National Institute of Mental Health Training Grant to Dr. Boscarino.
About Geisinger Health System
Founded in 1915, Geisinger Health System is one of the nations largest integrated health services organizations. Serving more than 2.6 million residents throughout central and northeastern Pennsylvania, the physician-led organization is a nationally recognized leader in the use of electronic health records, patient access and engagement in their healthcare, and in medical education for the next generation. Geisinger is comprised of three medical center campuses, a 740-member group practice, a not-for-profit health insurance company and research that extends across our large system- all dedicated to creating new models for scientific discovery, quality patient care, and successful clinical outcomes. Geisinger's Weis Center, Center for Health Research and Center for Clinical Studies include basic science, population-based and clinical trials research, complemented by collaborative relationships with top academic centers. Geisinger Ventures, the system's for profit entrepreneurial arm, seeks and promotes opportunities to speed the delivery of medical innovation to benefit patients. For more information, visit geisinger.
Geisinger Health System
100 N Academy Ave.
Danville
PA
United States
geisinger
среда, 24 августа 2011 г.
New 'Smart' Materials For The Brain
Research done by scientists in Italy and Switzerland has shown that carbon nanotubes may be the ideal "smart" brain material. Their results, published in the advance online edition of the journal Nature Nanotechnology, are a promising step forward in the search to find ways to "bypass" faulty brain wiring.
The research shows that carbon nanotubes, which, like neurons, are highly electrically conductive, form extremely tight contacts with neuronal cell membranes. Unlike the metal electrodes that are currently used in research and clinical applications, the nanotubes can create shortcuts between the distal and proximal compartments of the neuron, resulting in enhanced neuronal excitability.
The study was conducted in the Laboratory of Neural Microcircuitry at EPFL in Switzerland and led by Michel Giugliano (now an assistant professor at the University of Antwerp) and University of Trieste professor Laura Ballerini. "This result is extremely relevant for the emerging field of neuro-engineering and neuroprosthetics," explains Giugliano, who hypothesizes that the nanotubes could be used as a new building block of novel "electrical bypass" systems for treating traumatic injury of the central nervous system. Carbon nano-electrodes could also be used to replace metal parts in clinical applications such as deep brain stimulation for the treatment of Parkinson's disease or severe depression. And they show promise as a whole new class of "smart" materials for use in a wide range of potential neuroprosthetic applications.
Henry Markram, head of the Laboratory of Neural Microcircuitry and an author on the paper, adds: "There are three fundamental obstacles to developing reliable neuroprosthetics:
stable interfacing of electromechanical devices with neural tissue,
understanding how to stimulate the neural tissue, and
understanding what signals to record from the neurons in order for the device to make an automatic and appropriate decision to stimulate.
The new carbon nanotube-based interface technology discovered together with state of the art simulations of brain-machine interfaces is the key to developing all types of neuroprosthetics -- sight, sound, smell, motion, vetoing epileptic attacks, spinal bypasses, as well as repairing and even enhancing cognitive functions."
Contact information:
Michele Giugliano, Department of Biomedical Sciences, University of Antwerp
Laura Ballerini, MD, Life Sciences Department, Center for Neuroscience B.R.A.I.N. University of Trieste
Henry Markram, professor, EPFL Laboratory of Neural Microcircuitry
The research shows that carbon nanotubes, which, like neurons, are highly electrically conductive, form extremely tight contacts with neuronal cell membranes. Unlike the metal electrodes that are currently used in research and clinical applications, the nanotubes can create shortcuts between the distal and proximal compartments of the neuron, resulting in enhanced neuronal excitability.
The study was conducted in the Laboratory of Neural Microcircuitry at EPFL in Switzerland and led by Michel Giugliano (now an assistant professor at the University of Antwerp) and University of Trieste professor Laura Ballerini. "This result is extremely relevant for the emerging field of neuro-engineering and neuroprosthetics," explains Giugliano, who hypothesizes that the nanotubes could be used as a new building block of novel "electrical bypass" systems for treating traumatic injury of the central nervous system. Carbon nano-electrodes could also be used to replace metal parts in clinical applications such as deep brain stimulation for the treatment of Parkinson's disease or severe depression. And they show promise as a whole new class of "smart" materials for use in a wide range of potential neuroprosthetic applications.
Henry Markram, head of the Laboratory of Neural Microcircuitry and an author on the paper, adds: "There are three fundamental obstacles to developing reliable neuroprosthetics:
stable interfacing of electromechanical devices with neural tissue,
understanding how to stimulate the neural tissue, and
understanding what signals to record from the neurons in order for the device to make an automatic and appropriate decision to stimulate.
The new carbon nanotube-based interface technology discovered together with state of the art simulations of brain-machine interfaces is the key to developing all types of neuroprosthetics -- sight, sound, smell, motion, vetoing epileptic attacks, spinal bypasses, as well as repairing and even enhancing cognitive functions."
Contact information:
Michele Giugliano, Department of Biomedical Sciences, University of Antwerp
Laura Ballerini, MD, Life Sciences Department, Center for Neuroscience B.R.A.I.N. University of Trieste
Henry Markram, professor, EPFL Laboratory of Neural Microcircuitry
понедельник, 22 августа 2011 г.
Two Years Later: DIAMOND Program Continues To Get Nearly 50% Of Patients With Depression Into Remission Within Six Months
The DIAMOND program (Depression Improvement Across Minnesota, Offering a New Direction) continues to get at least five times as many patients into remission by six months than patients receiving typical primary care treatment, according to two-year findings reported by the Institute for Clinical Systems Improvement.
Of the 1,752 patients contacted six months after entering into the DIAMOND program to date, 45% were in remission and another 16% had at least a 50% reduction in the severity of their depression. An additional 1,285 DIAMOND patients unable to be reached at six months to determine their progress are presumed to be still depressed, although they could have gotten better. Using this measurement, 26% of DIAMOND clinic patients were in remission at six months, compared to only 5.8% of patients treated in 184 primary care and behavioral health clinics reporting in 2009 to MN Community Measurement, a nonprofit organization that publicly reports on medical group's quality results in Minnesota.
"Among the clinics reporting on patient outcomes stemming from their treatment plans, seven offering the DIAMOND program were in the top 10," said Jim Chase, president of MN Community Measurement. "Mayo Clinic had two of the state's top performing clinics, and clinics run by Family HealthServices Minnesota, HealthPartners Medical Group and Allina Medical Clinic that also offered the DIAMOND program all posted top 10 results."
"What's exciting about our latest data is that we continue to see significant positive patient response to DIAMOND treatment after two years of implementation and across metro and rural clinics," says Nancy Jaeckels, ICSI vice president of member relations and strategic initiatives. "DIAMOND was modeled on a concept proven in almost 40 research studies; now our consistent results across thousands of patients demonstrate that this program is replicable in virtually any 'real world' setting."
The DIAMOND Program
Medical groups, health plans, employers, patients and the Minnesota Department of Human Services, under the auspices of ICSI, collaborated to develop the DIAMOND program. Launched in March 2008 through 10 clinics and now offered through a total of 83 primary care clinics, it is the first depression treatment program in the nation to integrate a collaborative care model with a reimbursement structure that enables medical groups to provide enhanced care support to patients with depression.
Key elements of the program, based on the IMPACT model created by Dr. Jurgen Unutzer, University of Washington, include: use of a standard assessment tool to improve the diagnosis and management of depression, the addition of a care manager and consulting psychiatrist to the patient's primary care treatment team, an evidence-based stepped-care approach to treatment, a tracking system to monitor follow-up care and treatment effectiveness, and tools to prevent the patient from relapsing back into depression. This extra bundle of care means the patient with depression is more frequently contacted, educated, encouraged and supported.
"Our two-year data also show that the DIAMOND program's approach to treatment including involving patients in their own recovery and giving them tools to avoid falling back into depressio works. Among 735 patients contacted a year after entering DIAMOND, 50% are in remission and another 17% have had at least a 50% reduction in the severity of their depression," says Jaeckels.
Payment Model
A key to the program's success has been a new payment model whereby medical groups receive a monthly fee from health plans to cover the costs of these additional care services. Without changes to the payment structure, medical groups would not be able to provide the care manager and consulting psychiatrist services to patients.
Health plans currently reimbursing clinics for delivering DIAMOND services include Blue Cross Blue Shield of Minnesota, HealthPartners, Mayo Clinic MMSI, Medica, Metropolitan Health Plan, PreferredOne, PrimeWest Health and UCare.
HealthPartners Research Foundation is nearing the halfway point of a five-year study on the DIAMOND program that is funded by a $3 million grant from the National Institute of Mental Health. That study is evaluating all aspects of the initiative, including changes in care delivery, patient outcomes (including productivity effects), and health care cost-effectiveness. The findings of that study will help determine the full value of the DIAMOND program.
"Our mission at ICSI is to improve the quality and lower the cost of care," said Kent Bottles, MD, president of ICSI. "DIAMOND is an excellent example of how collaboration among medical groups, health plans, employers and patients enables us to deliver on that mission."
The Institute for Clinical Systems Improvement (icsi) is a non-profit health care improvement organization that brings diverse stakeholders together to find solutions to complex health care problems. Sponsored by six health plans in Minnesota and Wisconsin, ICSI helps its 56 medical group and hospital members deliver higher quality and lower cost health care.
Of the 1,752 patients contacted six months after entering into the DIAMOND program to date, 45% were in remission and another 16% had at least a 50% reduction in the severity of their depression. An additional 1,285 DIAMOND patients unable to be reached at six months to determine their progress are presumed to be still depressed, although they could have gotten better. Using this measurement, 26% of DIAMOND clinic patients were in remission at six months, compared to only 5.8% of patients treated in 184 primary care and behavioral health clinics reporting in 2009 to MN Community Measurement, a nonprofit organization that publicly reports on medical group's quality results in Minnesota.
"Among the clinics reporting on patient outcomes stemming from their treatment plans, seven offering the DIAMOND program were in the top 10," said Jim Chase, president of MN Community Measurement. "Mayo Clinic had two of the state's top performing clinics, and clinics run by Family HealthServices Minnesota, HealthPartners Medical Group and Allina Medical Clinic that also offered the DIAMOND program all posted top 10 results."
"What's exciting about our latest data is that we continue to see significant positive patient response to DIAMOND treatment after two years of implementation and across metro and rural clinics," says Nancy Jaeckels, ICSI vice president of member relations and strategic initiatives. "DIAMOND was modeled on a concept proven in almost 40 research studies; now our consistent results across thousands of patients demonstrate that this program is replicable in virtually any 'real world' setting."
The DIAMOND Program
Medical groups, health plans, employers, patients and the Minnesota Department of Human Services, under the auspices of ICSI, collaborated to develop the DIAMOND program. Launched in March 2008 through 10 clinics and now offered through a total of 83 primary care clinics, it is the first depression treatment program in the nation to integrate a collaborative care model with a reimbursement structure that enables medical groups to provide enhanced care support to patients with depression.
Key elements of the program, based on the IMPACT model created by Dr. Jurgen Unutzer, University of Washington, include: use of a standard assessment tool to improve the diagnosis and management of depression, the addition of a care manager and consulting psychiatrist to the patient's primary care treatment team, an evidence-based stepped-care approach to treatment, a tracking system to monitor follow-up care and treatment effectiveness, and tools to prevent the patient from relapsing back into depression. This extra bundle of care means the patient with depression is more frequently contacted, educated, encouraged and supported.
"Our two-year data also show that the DIAMOND program's approach to treatment including involving patients in their own recovery and giving them tools to avoid falling back into depressio works. Among 735 patients contacted a year after entering DIAMOND, 50% are in remission and another 17% have had at least a 50% reduction in the severity of their depression," says Jaeckels.
Payment Model
A key to the program's success has been a new payment model whereby medical groups receive a monthly fee from health plans to cover the costs of these additional care services. Without changes to the payment structure, medical groups would not be able to provide the care manager and consulting psychiatrist services to patients.
Health plans currently reimbursing clinics for delivering DIAMOND services include Blue Cross Blue Shield of Minnesota, HealthPartners, Mayo Clinic MMSI, Medica, Metropolitan Health Plan, PreferredOne, PrimeWest Health and UCare.
HealthPartners Research Foundation is nearing the halfway point of a five-year study on the DIAMOND program that is funded by a $3 million grant from the National Institute of Mental Health. That study is evaluating all aspects of the initiative, including changes in care delivery, patient outcomes (including productivity effects), and health care cost-effectiveness. The findings of that study will help determine the full value of the DIAMOND program.
"Our mission at ICSI is to improve the quality and lower the cost of care," said Kent Bottles, MD, president of ICSI. "DIAMOND is an excellent example of how collaboration among medical groups, health plans, employers and patients enables us to deliver on that mission."
The Institute for Clinical Systems Improvement (icsi) is a non-profit health care improvement organization that brings diverse stakeholders together to find solutions to complex health care problems. Sponsored by six health plans in Minnesota and Wisconsin, ICSI helps its 56 medical group and hospital members deliver higher quality and lower cost health care.
суббота, 20 августа 2011 г.
A new culprit in depression?
The brains of people with severe depression have lower levels of several related molecules that are key to the
development, organization, growth and repair of the brain than the brains of people without the disease, or those with the
bipolar form of depression, a new study finds.
The discovery, which surprised researchers in the multi-university consortium that made it, suggests a whole new direction
for understanding depression and developing new depression treatments. It may even help scientists understand how some
antidepressant medications work in the brain to ease symptoms, and why there is wide variation in how depressed people
respond to different antidepressants.
The finding was made in two specific areas of the brain known to be important to depression. The study relied on microarray
analysis of 32 post-mortem brain samples -- the microarray method can simultaneously measure the level of activity of tens of
thousands of genes that are functional in a given tissue.
The researchers found that levels of molecules called fibroblast growth factors (FGFs), and two of the receptors that bind to
them, were significantly lower among people who had been diagnosed with severe clinical depression and had died in a
depressed state. There was also some indication that those depressed people who had been taking antidepressants before their
deaths had levels of FGF and FGF receptors that were closer to normal.
The results are published online this week in the early edition of the Proceedings of the National Academy of Sciences by
researchers from the Pritzker Neuropsychiatric Disorders Research Consortium, which is supported by the Pritzker Family
Philanthropic Fund and by the National Institute of Mental Health. The research team consisted of scientists from the
University of Michigan's Mental Health Research Institute and Department of Psychiatry, working in close collaboration with
researchers from the University of California's Davis and Irvine campuses and from Stanford University.
"This finding comes from a completely unbiased search that began with no hypothesis, to find what genes best differentiate
major depression brains from normal and bipolar brains," says senior author Huda Akil, Ph.D., the Gardner C. Quarton
Distinguished Professor of Neurosciences in Psychiatry at U-M. "A wide set of individual genes came up as different between
the depressed and control individuals, but the family of genes that was most different and showed the highest significance as
a coherent group was the FGF family. This suggests a more profound change in an entire system of communication and control
within the brain."
No previous studies have directly examined the role of FGFs or their receptors in psychiatric illnesses. Another growth
factor, called Brain Derived Neurotrophic Factor, has been hypothesized to play a role in the effects of stress on the brain
and in the mode of action of antidepressants.
FGFs are a family of molecules that stimulate cell growth in many areas of the body, and are involved in the growth of
multiple tissues and in growth that takes place at various stages of life. They have potent effects during embryonic, fetal
and child development, and can modify the size and structure of particular brain regions. They are also involved in the
repair of adult tissues after injury and may mediate the cross-talk between different cell types in the brain.
As a result, they can be seen as mediators of the property that neuroscientists call "neural plasticity" -- the ability of
the brain to adapt to stress, experience, disease and the effects of drugs.
The research group started their study by measuring levels of approximately 20,000 different kinds of messenger RNA in
dissected brain samples from people who died from suicide, accidents and sudden medical causes. Messenger RNA levels are a
measure of how active different genes are, and the researchers took care only to study brains that had no complicating
factors that would have changed their mRNA levels at death.
The analysis was conducted on samples from two areas of the brain involved in the coordination of thinking and emotion: the
dorsolateral prefrontal cortex and the anterior cingulate cortex. Both are located toward the front of the brain behind the
forehead. Previously, brain scan studies have found differences in brain activity levels and size in these areas in people
with psychiatric illnesses.
In the current paper, the researchers report what they found when they zeroed in on a group of six kinds of related mRNA that
had the most coordinated differences between the samples from depressed brains, the non-depressed brains and the bipolar
brains.
These turned out to be mRNAs for four different FGF molecules and two receptors that bind to FGF and are key to their
function. Levels of all of the mRNAs encoding these proteins were lower in the brains of people with major depression. Lower
mRNA levels mean the brain may not produce enough protein to carry out normal function.
The team confirmed its finding using another genetic technique called PCR analysis, which revealed that the most significant
differences were in levels of mRNA for one of the FGFs, called FGF1, and for the two receptors, FGFR2 and FGFR3.
The researchers emphasize that they do not yet know whether the depressed people were born with lower levels of these
molecules, or whether the lower levels were brought on by the effects of depression on the brain or by external factors such
as stressful events. Other studies have shown that genes involved in brain chemistry and stress response are expressed
differently in the brains of depressed people and non-depressed people.
"We can't say whether these FGF gene expression changes are a predisposing factor for depression, or a consequence of the
disease process itself," says lead author and U-M research investigator Simon Evans, Ph.D. "There may be totally normal
people out there with compromised FGF systems, but if they don't experience stressful life events they may never develop
major depression. We need to study this system further to unravel this question."
Even as they made their discovery, the researchers grasped the potential significance of the FGF finding. "It's a new
direction for depression research to go," says Evans. "Given the known roles of this FGF family in neural development and
maintenance, it's not a huge leap to see how compromising the system could lead to changes in neural circuitry and contribute
to mood disorders."
"The bottom line is, the FGF system is less active in depressed individuals and presumably, correcting that would be part of
how you can make them better," says Akil, who is co-director of the U-M Mental Health Research Institute. "This finding gives
us a new target and a new set of ideas for pursuing better treatment."
Akil notes that the brains of bipolar people in the study did not show the decreased FGF gene activity. "This was all the
more remarkable since both groups of individuals were severely depressed at the time of death," she says. "This is yet
another indication that bipolar illness, though classified with depression as a mood disorder, is biologically a very
different disease.
The Pritzker Neuropsychiatric Disorders Research Fund L.L.C. has filed a patent application related to this research, but the
research team has made all of its data on mRNA levels for all types of growth factors available on the Internet. These can be
found with the paper on the PNAS web site, pnas.
With these results in hand, the research team hopes now to look at FGF levels in other areas of the brain including the
hippocampus, and to look for differences in levels of other families of growth factors. They also hope to look at the
different layers of the brain's cortex to see if there are any differences by layer. And, they hope to look at the genes that
encode FGFs and their receptors, to see if slight differences in gene sequence could modify the activity level of these genes
in the brain and contribute to the observed differences.
Akil also says it might be possible someday to study FGF differences in living people, if scientists can develop tools to
measure levels of the FGF receptors using brain imaging such as positron emission tomography, or PET.
In addition to Evans and Akil, the study's authors are: from the University of Michigan, Stanley J. Watson, Juan F. Lopez,
Robert C. Thompson, J. D. Stead, C.R. Neal and F. Meng; from UC Davis, P.V. Choudary and E.G. Jones, who communicated the
article to PNAS; from Stanford's Human Genome Center, J.Z. Li and R.M. Myers; and from UC Irvine, M.P. Vawter, H. Tomita,
D.M. Walsh, and W.E. Bunney. Several authors are members of the U-M Depression Center, the nation's first comprehensive
center devoted to research, treatment, education and public policy on depressive disorders.
Reference: Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0406788101 (open access paper)
Contact: Sally Pobojewski
poboumich
734-764-2220
University of Michigan Health System
development, organization, growth and repair of the brain than the brains of people without the disease, or those with the
bipolar form of depression, a new study finds.
The discovery, which surprised researchers in the multi-university consortium that made it, suggests a whole new direction
for understanding depression and developing new depression treatments. It may even help scientists understand how some
antidepressant medications work in the brain to ease symptoms, and why there is wide variation in how depressed people
respond to different antidepressants.
The finding was made in two specific areas of the brain known to be important to depression. The study relied on microarray
analysis of 32 post-mortem brain samples -- the microarray method can simultaneously measure the level of activity of tens of
thousands of genes that are functional in a given tissue.
The researchers found that levels of molecules called fibroblast growth factors (FGFs), and two of the receptors that bind to
them, were significantly lower among people who had been diagnosed with severe clinical depression and had died in a
depressed state. There was also some indication that those depressed people who had been taking antidepressants before their
deaths had levels of FGF and FGF receptors that were closer to normal.
The results are published online this week in the early edition of the Proceedings of the National Academy of Sciences by
researchers from the Pritzker Neuropsychiatric Disorders Research Consortium, which is supported by the Pritzker Family
Philanthropic Fund and by the National Institute of Mental Health. The research team consisted of scientists from the
University of Michigan's Mental Health Research Institute and Department of Psychiatry, working in close collaboration with
researchers from the University of California's Davis and Irvine campuses and from Stanford University.
"This finding comes from a completely unbiased search that began with no hypothesis, to find what genes best differentiate
major depression brains from normal and bipolar brains," says senior author Huda Akil, Ph.D., the Gardner C. Quarton
Distinguished Professor of Neurosciences in Psychiatry at U-M. "A wide set of individual genes came up as different between
the depressed and control individuals, but the family of genes that was most different and showed the highest significance as
a coherent group was the FGF family. This suggests a more profound change in an entire system of communication and control
within the brain."
No previous studies have directly examined the role of FGFs or their receptors in psychiatric illnesses. Another growth
factor, called Brain Derived Neurotrophic Factor, has been hypothesized to play a role in the effects of stress on the brain
and in the mode of action of antidepressants.
FGFs are a family of molecules that stimulate cell growth in many areas of the body, and are involved in the growth of
multiple tissues and in growth that takes place at various stages of life. They have potent effects during embryonic, fetal
and child development, and can modify the size and structure of particular brain regions. They are also involved in the
repair of adult tissues after injury and may mediate the cross-talk between different cell types in the brain.
As a result, they can be seen as mediators of the property that neuroscientists call "neural plasticity" -- the ability of
the brain to adapt to stress, experience, disease and the effects of drugs.
The research group started their study by measuring levels of approximately 20,000 different kinds of messenger RNA in
dissected brain samples from people who died from suicide, accidents and sudden medical causes. Messenger RNA levels are a
measure of how active different genes are, and the researchers took care only to study brains that had no complicating
factors that would have changed their mRNA levels at death.
The analysis was conducted on samples from two areas of the brain involved in the coordination of thinking and emotion: the
dorsolateral prefrontal cortex and the anterior cingulate cortex. Both are located toward the front of the brain behind the
forehead. Previously, brain scan studies have found differences in brain activity levels and size in these areas in people
with psychiatric illnesses.
In the current paper, the researchers report what they found when they zeroed in on a group of six kinds of related mRNA that
had the most coordinated differences between the samples from depressed brains, the non-depressed brains and the bipolar
brains.
These turned out to be mRNAs for four different FGF molecules and two receptors that bind to FGF and are key to their
function. Levels of all of the mRNAs encoding these proteins were lower in the brains of people with major depression. Lower
mRNA levels mean the brain may not produce enough protein to carry out normal function.
The team confirmed its finding using another genetic technique called PCR analysis, which revealed that the most significant
differences were in levels of mRNA for one of the FGFs, called FGF1, and for the two receptors, FGFR2 and FGFR3.
The researchers emphasize that they do not yet know whether the depressed people were born with lower levels of these
molecules, or whether the lower levels were brought on by the effects of depression on the brain or by external factors such
as stressful events. Other studies have shown that genes involved in brain chemistry and stress response are expressed
differently in the brains of depressed people and non-depressed people.
"We can't say whether these FGF gene expression changes are a predisposing factor for depression, or a consequence of the
disease process itself," says lead author and U-M research investigator Simon Evans, Ph.D. "There may be totally normal
people out there with compromised FGF systems, but if they don't experience stressful life events they may never develop
major depression. We need to study this system further to unravel this question."
Even as they made their discovery, the researchers grasped the potential significance of the FGF finding. "It's a new
direction for depression research to go," says Evans. "Given the known roles of this FGF family in neural development and
maintenance, it's not a huge leap to see how compromising the system could lead to changes in neural circuitry and contribute
to mood disorders."
"The bottom line is, the FGF system is less active in depressed individuals and presumably, correcting that would be part of
how you can make them better," says Akil, who is co-director of the U-M Mental Health Research Institute. "This finding gives
us a new target and a new set of ideas for pursuing better treatment."
Akil notes that the brains of bipolar people in the study did not show the decreased FGF gene activity. "This was all the
more remarkable since both groups of individuals were severely depressed at the time of death," she says. "This is yet
another indication that bipolar illness, though classified with depression as a mood disorder, is biologically a very
different disease.
The Pritzker Neuropsychiatric Disorders Research Fund L.L.C. has filed a patent application related to this research, but the
research team has made all of its data on mRNA levels for all types of growth factors available on the Internet. These can be
found with the paper on the PNAS web site, pnas.
With these results in hand, the research team hopes now to look at FGF levels in other areas of the brain including the
hippocampus, and to look for differences in levels of other families of growth factors. They also hope to look at the
different layers of the brain's cortex to see if there are any differences by layer. And, they hope to look at the genes that
encode FGFs and their receptors, to see if slight differences in gene sequence could modify the activity level of these genes
in the brain and contribute to the observed differences.
Akil also says it might be possible someday to study FGF differences in living people, if scientists can develop tools to
measure levels of the FGF receptors using brain imaging such as positron emission tomography, or PET.
In addition to Evans and Akil, the study's authors are: from the University of Michigan, Stanley J. Watson, Juan F. Lopez,
Robert C. Thompson, J. D. Stead, C.R. Neal and F. Meng; from UC Davis, P.V. Choudary and E.G. Jones, who communicated the
article to PNAS; from Stanford's Human Genome Center, J.Z. Li and R.M. Myers; and from UC Irvine, M.P. Vawter, H. Tomita,
D.M. Walsh, and W.E. Bunney. Several authors are members of the U-M Depression Center, the nation's first comprehensive
center devoted to research, treatment, education and public policy on depressive disorders.
Reference: Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0406788101 (open access paper)
Contact: Sally Pobojewski
poboumich
734-764-2220
University of Michigan Health System
четверг, 18 августа 2011 г.
Brain Changes Linked To Depression Caused By Light At Night
Exposure to even dim light at night is enough to cause physical changes in the brains of hamsters that may be associated with depression, a new study shows.
Researchers found that female Siberian hamsters exposed to dim light every night for eight weeks showed significant changes in a part of the brain called the hippocampus.
This is the first time researchers have found that light at night, by itself, may be linked to changes in the hippocampus.
These alterations may be a key reason why the researchers also found that the hamsters exposed to dim light at night showed more depressive symptoms when compared to hamsters in a standard light-dark cycle.
"Even dim light at night is sufficient to provoke depressive-like behaviors in hamsters, which may be explained by the changes we saw in their brains after eight weeks of exposure," said Tracy Bedrosian, co-author of the study and doctoral student in neuroscience at Ohio State University.
Bedrosian and her colleagues presented the result in San Diego at the annual meeting of the Society for Neuroscience.
The results are significant because the night-time light used in the study was not bright: 5 lux, or the equivalent of having a television on in a darkened room, said Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State.
"You would expect to see an impact if we were blasting these hamsters with bright lights, but this was a very low level, something that most people could easily encounter every night," said Nelson, who is also a member of Ohio State's Institute for Behavioral Medicine Research.
The study involved female Siberian hamsters, which had their ovaries removed to ensure that hormones produced in the ovary would not interfere with the results.
Half were housed in a standard light-dark cycle of 16 hours of light (at 150 lux) and eight hours of total darkness. The other half were housed in 16 hours of daylight (150 lux) and eight hours of dim light (5 lux).
After eight weeks in their lighting condition, they were tested for depressive-like behaviors. These tests are the same ones used by pharmaceutical companies to test anti-depressive and anti-anxiety drugs in animals before they are used in humans.
One depression test, for example, measured how much sugar water the mice drank. Mice generally like the drink, but those with depressive-like symptoms will not drink as much, presumably because they don't get as much pleasure from activities they usually enjoy.
Results showed that hamsters that lived in the dim light at night showed more symptoms of depression compared to the hamsters in the standard light-dark cycle.
At the end of the experiment, the researchers examined the hippocampus area of the hamsters' brains.
Results showed that mice that lived in the dim light had a significantly reduced density of dendritic spines - hairlike growths on brain cells, which are used to send chemical messages from one cell to another.
"The hippocampus plays a key role in depressive disorders, so finding changes there is significant," Bedrosian said.
The researchers found no difference between the two groups of hamsters in terms of concentrations of the stress hormone cortisol. That's important because hormones like cortisol have been linked to changes in the hippocampus.
"To the best of our knowledge, this is the first study to document that light at night is a sufficient stimulus to induce changes in the hippocampus, without changes in cortisol levels," Nelson said.
How is light at night causing the changes in the hippocampus? The researchers believe it is related to production of the hormone melatonin. Light at night suppresses secretion of melatonin, which is involved in how the body knows it is nighttime.
The lower levels of melatonin at night may be the cause of the lower density of dendritic spines in the hippocampus, Bedrosian said.
The researchers are continuing this work by investigating the exact role of melatonin in the findings of this study.
These results are consistent with an earlier study by Nelson and his colleagues which found that constant bright light at night is linked to depressive symptoms in male mice. In another recent study, they found that light at night is also linked to weight gain in mice.
Other co-authors of the current study were Laura Fonken and James Walton, both graduate students at Ohio State.
Researchers found that female Siberian hamsters exposed to dim light every night for eight weeks showed significant changes in a part of the brain called the hippocampus.
This is the first time researchers have found that light at night, by itself, may be linked to changes in the hippocampus.
These alterations may be a key reason why the researchers also found that the hamsters exposed to dim light at night showed more depressive symptoms when compared to hamsters in a standard light-dark cycle.
"Even dim light at night is sufficient to provoke depressive-like behaviors in hamsters, which may be explained by the changes we saw in their brains after eight weeks of exposure," said Tracy Bedrosian, co-author of the study and doctoral student in neuroscience at Ohio State University.
Bedrosian and her colleagues presented the result in San Diego at the annual meeting of the Society for Neuroscience.
The results are significant because the night-time light used in the study was not bright: 5 lux, or the equivalent of having a television on in a darkened room, said Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State.
"You would expect to see an impact if we were blasting these hamsters with bright lights, but this was a very low level, something that most people could easily encounter every night," said Nelson, who is also a member of Ohio State's Institute for Behavioral Medicine Research.
The study involved female Siberian hamsters, which had their ovaries removed to ensure that hormones produced in the ovary would not interfere with the results.
Half were housed in a standard light-dark cycle of 16 hours of light (at 150 lux) and eight hours of total darkness. The other half were housed in 16 hours of daylight (150 lux) and eight hours of dim light (5 lux).
After eight weeks in their lighting condition, they were tested for depressive-like behaviors. These tests are the same ones used by pharmaceutical companies to test anti-depressive and anti-anxiety drugs in animals before they are used in humans.
One depression test, for example, measured how much sugar water the mice drank. Mice generally like the drink, but those with depressive-like symptoms will not drink as much, presumably because they don't get as much pleasure from activities they usually enjoy.
Results showed that hamsters that lived in the dim light at night showed more symptoms of depression compared to the hamsters in the standard light-dark cycle.
At the end of the experiment, the researchers examined the hippocampus area of the hamsters' brains.
Results showed that mice that lived in the dim light had a significantly reduced density of dendritic spines - hairlike growths on brain cells, which are used to send chemical messages from one cell to another.
"The hippocampus plays a key role in depressive disorders, so finding changes there is significant," Bedrosian said.
The researchers found no difference between the two groups of hamsters in terms of concentrations of the stress hormone cortisol. That's important because hormones like cortisol have been linked to changes in the hippocampus.
"To the best of our knowledge, this is the first study to document that light at night is a sufficient stimulus to induce changes in the hippocampus, without changes in cortisol levels," Nelson said.
How is light at night causing the changes in the hippocampus? The researchers believe it is related to production of the hormone melatonin. Light at night suppresses secretion of melatonin, which is involved in how the body knows it is nighttime.
The lower levels of melatonin at night may be the cause of the lower density of dendritic spines in the hippocampus, Bedrosian said.
The researchers are continuing this work by investigating the exact role of melatonin in the findings of this study.
These results are consistent with an earlier study by Nelson and his colleagues which found that constant bright light at night is linked to depressive symptoms in male mice. In another recent study, they found that light at night is also linked to weight gain in mice.
Other co-authors of the current study were Laura Fonken and James Walton, both graduate students at Ohio State.
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