Depression occurs in as many as one-third of patients after a stroke, and women are at somewhat higher risk, according to a large new review of studies. Post-stroke depression is associated with greater disability, reduced quality of life and an increased risk of death.
The systematic review appears in the November-December issue of the journal Psychosomatics.
Brittany Poynter, M.D., and colleagues from the University of Toronto looked at 56 studies on stroke and depression comprising more than 75,000 people, about 12,000 of them women. The time between the stroke and onset of depression ranged from less than two weeks to 15 years.
In women, rates of post-stroke depression ranged from about 6 percent to 78 percent, while in men depression rates ranged from 4.7 percent to about 65 percent.
These findings are important, Poynter said, because women who have had a stroke generally do more poorly than men. They tend to have higher rates of disability and longer hospitalization times. The authors say this might be due in part to higher rates of depression. In addition, "women may have less access to care," Poynter said.
"People think of stroke as a 'male' disease and it is slightly more common in men but because it increases with age, more women end up having strokes because they live longer," said Linda S. Williams, M.D., chief of neurology at the Roudebush VA Medical Center in Indianapolis. She is not associated with the review.
"Post-stroke depression is often unrecognized, both by the patient and the provider," Williams said. "Patients may have symptoms, but they think that's a natural reaction to having a stroke. Providers may think it is natural that the patient feels down after having this major life event. So there is a watch-and-see approach instead of a more of an aggressive screening-and-treatment approach."
It is uncertain what the best treatments for post-stroke depression might be. "There may be multiple treatments beyond antidepressants and counseling, such as exercise, physical rehabilitation and support groups," Poynter said. "A multimodal approach may be the most effective."
Both Poynter and Williams emphasized that all stroke patients should be routinely screened for depression
Psychosomatics, the official journal of the Academy of Psychosomatic Medicine, publishes peer-reviewed research and clinical experiences in the practice of psychosomatic medicine/consultation-liaison psychiatry.
Poynter B, et al. Sex differences in the prevalence of post-stroke depression: a systematic review. Psychosomatics 50(6), 2009.
четверг, 30 июня 2011 г.
среда, 29 июня 2011 г.
Relationship Between Borderline Personality Disorder And Bipolar Disorder, Long-Term Study
Results from a long-term study indicate that borderline personality disorder (BPD) and bipolar disorder do not commonly coexist, a finding which has important implications for treatment. The findings are reported in the July 2006 issue of The American Journal of Psychiatry (AJP), the official journal of the American Psychiatric Association (APA).
BPD is a long-term, pervasive pattern of impulsive behavior, instability and changeable mood. Whether it is a variant of bipolar disorder is the focus of the AJP article, "Descriptive and Longitudinal Observations on the Relationship of Borderline Personality Disorder and Bipolar Disorder" by John G. Gunderson, M.D., medical director for the Borderline Personality Disorder Treatment Center at McLean Hospital.
The study found only modest connections to bipolar disorder among 196 patients with BPD. The rate of co-occurring bipolar disorder in these patients was 19 percent. In patients with other personality disorders, the rate was eight percent. Among the patients who did not have bipolar disorder at the beginning of the study, eight percent of the BPD patients developed bipolar disorder over the next four years, compared to three percent of the patients with other personality disorders.
Despite these differences, the rates of bipolar disorder in the BPD patients remained under 20 percent. This low frequency has important implications for treatment, as many BPD patients receive only a diagnosis of bipolar disorder and the two diagnoses generally are treated with different approaches. Psychosocial interventions are important in the treatment of BPD, whereas medication is generally the first choice for bipolar disorder.
"The diagnosis of borderline personality disorder arose from psychoanalytic psychotherapy practice, whereas bipolar disorder is the subject of intensive neurobiological research and psychopharmacological treatment," stated Robert Freedman, M.D., AJP editor-in-chief. "This study is an important step in examining the extent of overlap between the two disorders."
The co-occurrence of bipolar disorder did not worsen the course of BPD over four years. Remission occurred in two-thirds of both the BPD patients with and without bipolar disorder.
In an accompanying editorial, Michael H. Stone, M.D., of Columbia University notes the article's "more balanced position on the controversy" about the relationship of borderline personality to bipolar disorder. He suggests that the moderately higher rates of bipolar disorder in patients with BPD disorder may indicate a subgroup of BPD patients with higher genetic risk for bipolar disorder.
This study was funded by the National Institute of Mental Health.
(Am J Psychiatry. 2006; 163: 1173-1178).
About the American Journal of Psychiatry
The American Journal of Psychiatry, the official journal of the American Psychiatric Association, publishes a monthly issue with scientific articles submitted by psychiatrists and other scientists worldwide. The peer review and editing process is conducted independently of any other American Psychiatric Association components. Therefore, statements in this press release or the articles in the Journal are not official policy statements of the American Psychiatric Association. The Journal's editorial policies conform to the Uniform Requirements of the International Committee of Medical Journal Editors, of which it is a member.
For further information about the Journal visit ajp.psychiatryonline.
About the American Psychiatric Association:
The American Psychiatric Association is a national medical specialty society whose more than 36,000 physician members specialize in diagnosis, treatment, prevention and research of mental illnesses including substance use disorders.
Visit the APA at psych and healthyminds.
BPD is a long-term, pervasive pattern of impulsive behavior, instability and changeable mood. Whether it is a variant of bipolar disorder is the focus of the AJP article, "Descriptive and Longitudinal Observations on the Relationship of Borderline Personality Disorder and Bipolar Disorder" by John G. Gunderson, M.D., medical director for the Borderline Personality Disorder Treatment Center at McLean Hospital.
The study found only modest connections to bipolar disorder among 196 patients with BPD. The rate of co-occurring bipolar disorder in these patients was 19 percent. In patients with other personality disorders, the rate was eight percent. Among the patients who did not have bipolar disorder at the beginning of the study, eight percent of the BPD patients developed bipolar disorder over the next four years, compared to three percent of the patients with other personality disorders.
Despite these differences, the rates of bipolar disorder in the BPD patients remained under 20 percent. This low frequency has important implications for treatment, as many BPD patients receive only a diagnosis of bipolar disorder and the two diagnoses generally are treated with different approaches. Psychosocial interventions are important in the treatment of BPD, whereas medication is generally the first choice for bipolar disorder.
"The diagnosis of borderline personality disorder arose from psychoanalytic psychotherapy practice, whereas bipolar disorder is the subject of intensive neurobiological research and psychopharmacological treatment," stated Robert Freedman, M.D., AJP editor-in-chief. "This study is an important step in examining the extent of overlap between the two disorders."
The co-occurrence of bipolar disorder did not worsen the course of BPD over four years. Remission occurred in two-thirds of both the BPD patients with and without bipolar disorder.
In an accompanying editorial, Michael H. Stone, M.D., of Columbia University notes the article's "more balanced position on the controversy" about the relationship of borderline personality to bipolar disorder. He suggests that the moderately higher rates of bipolar disorder in patients with BPD disorder may indicate a subgroup of BPD patients with higher genetic risk for bipolar disorder.
This study was funded by the National Institute of Mental Health.
(Am J Psychiatry. 2006; 163: 1173-1178).
About the American Journal of Psychiatry
The American Journal of Psychiatry, the official journal of the American Psychiatric Association, publishes a monthly issue with scientific articles submitted by psychiatrists and other scientists worldwide. The peer review and editing process is conducted independently of any other American Psychiatric Association components. Therefore, statements in this press release or the articles in the Journal are not official policy statements of the American Psychiatric Association. The Journal's editorial policies conform to the Uniform Requirements of the International Committee of Medical Journal Editors, of which it is a member.
For further information about the Journal visit ajp.psychiatryonline.
About the American Psychiatric Association:
The American Psychiatric Association is a national medical specialty society whose more than 36,000 physician members specialize in diagnosis, treatment, prevention and research of mental illnesses including substance use disorders.
Visit the APA at psych and healthyminds.
вторник, 28 июня 2011 г.
Protein Trafficking Trouble Links Lowe Syndrome Symptoms In Brain And Kidney
Yale researchers have provided new insight into how mutations in a single gene may cause mental retardation and kidney problems in Lowe syndrome, a rare genetic condition that affects only boys.
Lowe syndrome causes cataracts, mental retardation, and a kidney dysfunction in which small proteins and ions are lost in the urine, which may lead to bone deformation and stunted growth.
The syndrome is caused by mutations in a gene that encodes an enzyme known as OCRL. Although researchers understand OCRL's biochemical properties, it has been unclear how gene mutations that affect this enzyme's function might contribute to the symptoms of Lowe syndrome.
In a new study in Developmental Cell, senior author Pietro De Camilli, professor of cell biology and neurobiology, said that the kidney defects associated with Lowe syndrome suggested that kidney cells might be improperly regulating receptor proteins on their surfaces that control the exchange of certain molecules between the urine and the blood.
DeCamilli is co-director of the medical school's interdisciplinary program in Cellular Neuroscience, Neurodegeneration and Repair, a member of the Kavli Institute for Neuroscience, and a Howard Hughes Medical Institute investigator.
Using fluorescent tags to localize OCRL in human and monkey cells, De Camilli and his colleagues observed that the protein concentrates at structures on the cell's surface called clathrin coated pits. The receptor molecules concentrate at these sites, which then pinch off from the cell membrane to form spherical vesicles. These vesicles transport the receptors and other proteins to intracellular compartments known as endosomes. Endosomes sort the transported proteins, sending some back to the cell surface and targeting others for destruction.
The researchers showed that normally OCRL attaches itself to APPL1, a protein which is associated with newly formed endocytic vesicles and endosomes and which is part of a protein scaffold that controls endocytic traffic and signaling of receptors. However, mutations that cause Lowe syndrome abolish the association of OCRL with APPL1, and this disruption may affect kidney cells' ability to reabsorb materials bound by some of their cell surface receptors. OCRL also interacts with APPL1 in brain cells, where APPL1 is involved in transporting a nerve growth factor receptor. De Camilli and his colleagues suggest that the cognitive deficits seen in Lowe syndrome may be partly caused when the mutated OCRL gene impairs intracellular traffic and signaling in the brain.
"Our next steps will be to provide further evidence for the functional relevance in the disease of the new properties of OCRL that we have identified," said De Camilli. "We hope that these studies will help design therapeutic strategies for the treatment of Lowe syndrome patients."
Co-authors included Kai Erdmann, Yuxin Mao, Heather McCrea, Roberto Zoncu, Sangyoon Lee, Summer Paradise, Jan Modregger, Daniel Biemesderfer, Derek Toomre.
Developmental Cell 13: pp 377-390 September 4, 2007
yale.edu
Lowe syndrome causes cataracts, mental retardation, and a kidney dysfunction in which small proteins and ions are lost in the urine, which may lead to bone deformation and stunted growth.
The syndrome is caused by mutations in a gene that encodes an enzyme known as OCRL. Although researchers understand OCRL's biochemical properties, it has been unclear how gene mutations that affect this enzyme's function might contribute to the symptoms of Lowe syndrome.
In a new study in Developmental Cell, senior author Pietro De Camilli, professor of cell biology and neurobiology, said that the kidney defects associated with Lowe syndrome suggested that kidney cells might be improperly regulating receptor proteins on their surfaces that control the exchange of certain molecules between the urine and the blood.
DeCamilli is co-director of the medical school's interdisciplinary program in Cellular Neuroscience, Neurodegeneration and Repair, a member of the Kavli Institute for Neuroscience, and a Howard Hughes Medical Institute investigator.
Using fluorescent tags to localize OCRL in human and monkey cells, De Camilli and his colleagues observed that the protein concentrates at structures on the cell's surface called clathrin coated pits. The receptor molecules concentrate at these sites, which then pinch off from the cell membrane to form spherical vesicles. These vesicles transport the receptors and other proteins to intracellular compartments known as endosomes. Endosomes sort the transported proteins, sending some back to the cell surface and targeting others for destruction.
The researchers showed that normally OCRL attaches itself to APPL1, a protein which is associated with newly formed endocytic vesicles and endosomes and which is part of a protein scaffold that controls endocytic traffic and signaling of receptors. However, mutations that cause Lowe syndrome abolish the association of OCRL with APPL1, and this disruption may affect kidney cells' ability to reabsorb materials bound by some of their cell surface receptors. OCRL also interacts with APPL1 in brain cells, where APPL1 is involved in transporting a nerve growth factor receptor. De Camilli and his colleagues suggest that the cognitive deficits seen in Lowe syndrome may be partly caused when the mutated OCRL gene impairs intracellular traffic and signaling in the brain.
"Our next steps will be to provide further evidence for the functional relevance in the disease of the new properties of OCRL that we have identified," said De Camilli. "We hope that these studies will help design therapeutic strategies for the treatment of Lowe syndrome patients."
Co-authors included Kai Erdmann, Yuxin Mao, Heather McCrea, Roberto Zoncu, Sangyoon Lee, Summer Paradise, Jan Modregger, Daniel Biemesderfer, Derek Toomre.
Developmental Cell 13: pp 377-390 September 4, 2007
yale.edu
Anti-Depressant Drugs Can Double Risk Of Gastrointestinal Bleeding
New research shows that selective serotonin reuptake inhibitors (SSRIs), a group of drugs commonly used to treat depression, may double the risk of gastrointestinal bleeding, according to researchers from Wake Forest University School of Medicine and colleagues. When the drugs are taken with aspirin and other similar pain medications, the risk is more than 600 percent higher.
"Clinicians who prescribe these medications should be aware of the potential risk and may need to consider alternatives," said Sonal Singh, M.D., senior researcher and an assistant professor of internal medicine. "In addition, regulatory authorities should consider revising existing package inserts to highlight the magnitude of the risk."
The research was reported online this month in Alimentary Pharmacology & Therapeutics. Emerging evidence has shown that SSRIs may be associated with bleeding of the lining of the digestive tract including the esophagus, stomach or upper part of the small intestine, which together are called the upper gastrointestinal (GI) tract. Upper gastrointestinal bleeding may be potentially serious and require hospitalization for blood transfusions and other treatments.
The drugs are widely used to treat depression, panic disorder and obsessive-compulsive disorder. The researchers undertook the study because of a lack of information on the exact magnitude of the risk. They also looked at the effects of taking SSRIs at the same time as non-steroidal anti-inflammatory drugs (NSAIDs), which are also associated with upper GI bleeding. NSAIDs include prescription medications such as Celebrex® and over-the-counter drugs such as aspirin and Aleve®.
The researchers pooled data from four studies involving 153,000 patients, which allowed them to detect effects that might not show up in the individual studies. They found patients taking SSRIs were nearly twice as likely to develop upper GI bleeding than patients not taking the drugs. When the patients also took NSAIDs, the risk of upper gastrointestinal bleeding was six times higher than in patients taking neither medication.
The authors said the combined use of NSAIDs and SSRIs may have a synergistic effect, which results in the elevated risk of bleeding beyond that seen with each agent alone.
"While the risk to an individual may increase by only a small amount, the impact to the general population is likely to be substantial because of the large numbers of people who use these drugs," said Singh.
He said that depressed, older adults may be most vulnerable because they are more likely to have conditions such as osteoarthritis that require the use of NSAIDs.
Based on their findings, the authors estimate that for every 411 patients over age 50 taking SSRIs, one is likely to develop upper GI bleeding requiring hospital admission. In patients taking both SSRIs and NSAIDs, one out of 82 would be expected to develop the problem.
"We estimate that roughly 18,000 additional cases of upper GI bleeding occurred in the United States and United Kingdom in 2003 as a result of taking SSRIs," said Singh.
In addition to the clinical studies, the researchers analyzed 101 reports on adverse effects submitted to the Canadian Adverse Events Database and the U.S. Food and Drug Administration's Adverse Event Reporting System. They found that bleeding associated with SSRI use occurred after a median of 25 weeks on the drugs. About 67 percent of those patients were also taking NSAIDs. The adverse reaction was not limited to the elderly, with 38 percent of cases occurring in patients below the age of 60.
"These findings emphasize the importance of clinicians taking a detailed gastrointestinal history from patients and targeting the use of SSRIs to patients who are at relatively low risk for upper GI bleeding," said Singh.
The research did not distinguish between specific drugs and whether one was associated with more bleeding than another. However, previous studies have shown that paroxetine (Paxil®), sertraline (Zoloft®) and fluoxetine (Prozac®) are most often associated with abnormal bleeding. Singh said future research should address the question of which specific drugs and combinations of drugs are associated with the highest risk.
Singh's co-researchers were Apurva Trivedi, M.D., with Wake Forest, and Yoon K. Loke, M.D., lead author, with the University of East Anglia, Norwich, United Kingdom.
Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university's School of Medicine. The system comprises 1,187 acute care, psychiatric, rehabilitation and long-term care beds and is consistently ranked as one of "America's Best Hospitals" by U.S. News & World Report.
Wake Forest University Baptist Medical Center
Medical Center Blvd.
Winston-Salem, NC 27157-1015
United States
www1.wfubmc
View drug information on Paxil CR; Prozac Weekly; Zoloft.
"Clinicians who prescribe these medications should be aware of the potential risk and may need to consider alternatives," said Sonal Singh, M.D., senior researcher and an assistant professor of internal medicine. "In addition, regulatory authorities should consider revising existing package inserts to highlight the magnitude of the risk."
The research was reported online this month in Alimentary Pharmacology & Therapeutics. Emerging evidence has shown that SSRIs may be associated with bleeding of the lining of the digestive tract including the esophagus, stomach or upper part of the small intestine, which together are called the upper gastrointestinal (GI) tract. Upper gastrointestinal bleeding may be potentially serious and require hospitalization for blood transfusions and other treatments.
The drugs are widely used to treat depression, panic disorder and obsessive-compulsive disorder. The researchers undertook the study because of a lack of information on the exact magnitude of the risk. They also looked at the effects of taking SSRIs at the same time as non-steroidal anti-inflammatory drugs (NSAIDs), which are also associated with upper GI bleeding. NSAIDs include prescription medications such as Celebrex® and over-the-counter drugs such as aspirin and Aleve®.
The researchers pooled data from four studies involving 153,000 patients, which allowed them to detect effects that might not show up in the individual studies. They found patients taking SSRIs were nearly twice as likely to develop upper GI bleeding than patients not taking the drugs. When the patients also took NSAIDs, the risk of upper gastrointestinal bleeding was six times higher than in patients taking neither medication.
The authors said the combined use of NSAIDs and SSRIs may have a synergistic effect, which results in the elevated risk of bleeding beyond that seen with each agent alone.
"While the risk to an individual may increase by only a small amount, the impact to the general population is likely to be substantial because of the large numbers of people who use these drugs," said Singh.
He said that depressed, older adults may be most vulnerable because they are more likely to have conditions such as osteoarthritis that require the use of NSAIDs.
Based on their findings, the authors estimate that for every 411 patients over age 50 taking SSRIs, one is likely to develop upper GI bleeding requiring hospital admission. In patients taking both SSRIs and NSAIDs, one out of 82 would be expected to develop the problem.
"We estimate that roughly 18,000 additional cases of upper GI bleeding occurred in the United States and United Kingdom in 2003 as a result of taking SSRIs," said Singh.
In addition to the clinical studies, the researchers analyzed 101 reports on adverse effects submitted to the Canadian Adverse Events Database and the U.S. Food and Drug Administration's Adverse Event Reporting System. They found that bleeding associated with SSRI use occurred after a median of 25 weeks on the drugs. About 67 percent of those patients were also taking NSAIDs. The adverse reaction was not limited to the elderly, with 38 percent of cases occurring in patients below the age of 60.
"These findings emphasize the importance of clinicians taking a detailed gastrointestinal history from patients and targeting the use of SSRIs to patients who are at relatively low risk for upper GI bleeding," said Singh.
The research did not distinguish between specific drugs and whether one was associated with more bleeding than another. However, previous studies have shown that paroxetine (Paxil®), sertraline (Zoloft®) and fluoxetine (Prozac®) are most often associated with abnormal bleeding. Singh said future research should address the question of which specific drugs and combinations of drugs are associated with the highest risk.
Singh's co-researchers were Apurva Trivedi, M.D., with Wake Forest, and Yoon K. Loke, M.D., lead author, with the University of East Anglia, Norwich, United Kingdom.
Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university's School of Medicine. The system comprises 1,187 acute care, psychiatric, rehabilitation and long-term care beds and is consistently ranked as one of "America's Best Hospitals" by U.S. News & World Report.
Wake Forest University Baptist Medical Center
Medical Center Blvd.
Winston-Salem, NC 27157-1015
United States
www1.wfubmc
View drug information on Paxil CR; Prozac Weekly; Zoloft.
понедельник, 27 июня 2011 г.
New Report Finds Little Evidence To Determine The Usefulness Of Genetic Tests In The Treatment Of Depression
There is insufficient
evidence to determine if current gene-based tests intended to personalize
the dose of medications in a class of drugs called selective serotonin
reuptake inhibitors (SSRIs) improve patient outcomes or aid in treatment
decisions in the clinical setting, according to a new evidence report
supported by a collaboration of the Agency for Healthcare Research and
Quality (AHRQ) and the Centers for Disease Control and Prevention's (CDC)
National Office of Public Health Genomics.
This evidence report is the first step in the two-step process of CDC's
Evaluation of Genomic Applications in Practice and Prevention (EGAPP) pilot
project to evaluate and make recommendations regarding the use of
gene-based tests. Funding for the report was provided by CDC.
The report found that tests evaluating differences in genes belonging
to the Cytochrome P450, or CYP450, family that affect the rate at which a
person metabolizes SSRIs are largely accurate. However, the researchers did
not find any evidence that such tests led to improved patient outcomes or
had an impact on treatment decisions for patients with depression. The
researchers noted that other genetic factors and non-genetic factors such
as diet and other medical conditions may have an impact on a patient's
response to treatment.
"This report highlights how systematically reviewing scientific
findings can help guide future research," said Beth A. Collins Sharp,
Ph.D., R.N., director of AHRQ's Evidence-based Practice Center Program.
"This information will help identify the types of studies that are
necessary to help better understand various treatment response issues."
Researchers performed a comprehensive review of the literature and
found no well-designed studies that evaluated clinical outcomes of tests to
detect differences in genes belonging to the CYP450 family. These genes
produce enzymes that break down SSRIs and many other classes of drugs. Most
studies included a small number of people, did not test for all variations
of the enzymes and were poorly designed, according to the researchers. The
majority of studies also reported the rate of metabolism after just one
dose or were done in patients without depression -- factors that do not
accurately represent the long-term use of these drugs in patients with
depression.
Because patient response to SSRIs varies, there has been strong
interest in using gene-based tests to predict whether the person will be a
poor, intermediate, extensive or ultra-rapid metabolizer. Theoretically,
ultra-rapid metabolizers could require higher doses than those who
metabolize the drug slowly. Poor metabolizers might respond to a lower
dose, which could also prevent side effects. The goal of testing is to
personalize health care by selecting therapy based on a patient's genetic
makeup.
The report found a relationship between genetic differences and the
occurrence of adverse effects from SSRIs in depressed patients in only two
of six studies. However, the researchers concluded that all six studies
were poorly designed, which limits the ability to draw conclusions about
how differences in CYP450 genes influence adverse effects of SSRIs.
"This report emphasizes that well-designed observational studies and
clinical trials are needed to clearly establish the clinical validity and
utility of the many emerging genomic tests for treatment and prevention of
common diseases of public health significance," said Muin Khoury, M.D.,
Ph.D., director of CDC's National Office of Public Health Genomics. "Early
availability of the evidence base is key to the effective use of genomics
for the benefit of population health."
Since their introduction in the late 1980s, SSRIs (such as citalopram,
fluoxetine, paroxetine and sertraline) have become the most commonly
prescribed class of drugs for treatment of depression. However, the
likelihood that a person will experience relief from all symptoms of
depression after one year of treatment is approximately 40 percent, and
side effects cause 12 percent to 15 percent of people who start treatment
to stop taking the drug. Following the recent FDA approval of a test to
predict differences in the CYP450 gene, clinicians and patients must decide
whether using such tests to choose a type or dose of an SSRI might improve
the patient's response to treatment.
In early 2007, the EGAPP working group, an independent, non-federal
panel that advises the CDC, will issue recommendations on the use of CYP450
tests in the treatment of depression based on the evidence report and other
considerations, including alternative approaches for dosing and monitoring
of drug therapy, patient access to testing and cost. The working group will
also assess current knowledge gaps and describe additional research needs
identified by the report. Future evidence reports that are part of the
AHRQ/CDC collaboration will evaluate the use of genomic tests for specific
diseases or conditions, such as a rare type of inherited colorectal cancer.
The report was prepared by a team of researchers led by David Matchar,
M.D., and Mugdha Thakur, M.D., of AHRQ's Duke University Evidence-based
Practice Center in Durham, N.C. "Testing for CYP450 Polymorphisms in Adults
With Non-Psychotic Depression Treated With SSRIs" can be found online at ahrq/clinic/tp/cyp450tp.htm.
Agency for Healthcare Research and Quality
ahrq/clinic/tp/cyp450tp.htm
evidence to determine if current gene-based tests intended to personalize
the dose of medications in a class of drugs called selective serotonin
reuptake inhibitors (SSRIs) improve patient outcomes or aid in treatment
decisions in the clinical setting, according to a new evidence report
supported by a collaboration of the Agency for Healthcare Research and
Quality (AHRQ) and the Centers for Disease Control and Prevention's (CDC)
National Office of Public Health Genomics.
This evidence report is the first step in the two-step process of CDC's
Evaluation of Genomic Applications in Practice and Prevention (EGAPP) pilot
project to evaluate and make recommendations regarding the use of
gene-based tests. Funding for the report was provided by CDC.
The report found that tests evaluating differences in genes belonging
to the Cytochrome P450, or CYP450, family that affect the rate at which a
person metabolizes SSRIs are largely accurate. However, the researchers did
not find any evidence that such tests led to improved patient outcomes or
had an impact on treatment decisions for patients with depression. The
researchers noted that other genetic factors and non-genetic factors such
as diet and other medical conditions may have an impact on a patient's
response to treatment.
"This report highlights how systematically reviewing scientific
findings can help guide future research," said Beth A. Collins Sharp,
Ph.D., R.N., director of AHRQ's Evidence-based Practice Center Program.
"This information will help identify the types of studies that are
necessary to help better understand various treatment response issues."
Researchers performed a comprehensive review of the literature and
found no well-designed studies that evaluated clinical outcomes of tests to
detect differences in genes belonging to the CYP450 family. These genes
produce enzymes that break down SSRIs and many other classes of drugs. Most
studies included a small number of people, did not test for all variations
of the enzymes and were poorly designed, according to the researchers. The
majority of studies also reported the rate of metabolism after just one
dose or were done in patients without depression -- factors that do not
accurately represent the long-term use of these drugs in patients with
depression.
Because patient response to SSRIs varies, there has been strong
interest in using gene-based tests to predict whether the person will be a
poor, intermediate, extensive or ultra-rapid metabolizer. Theoretically,
ultra-rapid metabolizers could require higher doses than those who
metabolize the drug slowly. Poor metabolizers might respond to a lower
dose, which could also prevent side effects. The goal of testing is to
personalize health care by selecting therapy based on a patient's genetic
makeup.
The report found a relationship between genetic differences and the
occurrence of adverse effects from SSRIs in depressed patients in only two
of six studies. However, the researchers concluded that all six studies
were poorly designed, which limits the ability to draw conclusions about
how differences in CYP450 genes influence adverse effects of SSRIs.
"This report emphasizes that well-designed observational studies and
clinical trials are needed to clearly establish the clinical validity and
utility of the many emerging genomic tests for treatment and prevention of
common diseases of public health significance," said Muin Khoury, M.D.,
Ph.D., director of CDC's National Office of Public Health Genomics. "Early
availability of the evidence base is key to the effective use of genomics
for the benefit of population health."
Since their introduction in the late 1980s, SSRIs (such as citalopram,
fluoxetine, paroxetine and sertraline) have become the most commonly
prescribed class of drugs for treatment of depression. However, the
likelihood that a person will experience relief from all symptoms of
depression after one year of treatment is approximately 40 percent, and
side effects cause 12 percent to 15 percent of people who start treatment
to stop taking the drug. Following the recent FDA approval of a test to
predict differences in the CYP450 gene, clinicians and patients must decide
whether using such tests to choose a type or dose of an SSRI might improve
the patient's response to treatment.
In early 2007, the EGAPP working group, an independent, non-federal
panel that advises the CDC, will issue recommendations on the use of CYP450
tests in the treatment of depression based on the evidence report and other
considerations, including alternative approaches for dosing and monitoring
of drug therapy, patient access to testing and cost. The working group will
also assess current knowledge gaps and describe additional research needs
identified by the report. Future evidence reports that are part of the
AHRQ/CDC collaboration will evaluate the use of genomic tests for specific
diseases or conditions, such as a rare type of inherited colorectal cancer.
The report was prepared by a team of researchers led by David Matchar,
M.D., and Mugdha Thakur, M.D., of AHRQ's Duke University Evidence-based
Practice Center in Durham, N.C. "Testing for CYP450 Polymorphisms in Adults
With Non-Psychotic Depression Treated With SSRIs" can be found online at ahrq/clinic/tp/cyp450tp.htm.
Agency for Healthcare Research and Quality
ahrq/clinic/tp/cyp450tp.htm
воскресенье, 26 июня 2011 г.
Sleep Durations Associated With Increased Mortality More Likely In Minorities
African-Americans and other racial minorities have sleep durations associated with increased mortality. This is consistent with the belief that unhealthy sleep patterns among minorities -- long sleep or short sleep -- may contribute to health differentials, according to a study published in the journal SLEEP.
The study, authored by Lauren Hale, PhD, assistant professor in the graduate program in public health at Stony Brook University, focused on the responses of 32,749 people 18 years of age and older to a National Health Interview Survey (NHIS).
According to the results, African-American respondents had an increased risk of being short and long sleepers (less than or equal to six hours and greater than or equal to nine hours, respectively) relative to Caucasian respondents. Hispanics, excluding Mexican-Americans, and non-Hispanic "others" were also associated with increased risk of short sleeping.
The study also found that living in an inner city was associated with increased risk of short sleeping and reduced risk of long sleeping, compared to non-urban areas. Some of the higher risk of short sleeping among African-Americans can be explained by a higher prevalence of African-Americans' habitation in the inner city.
"Inadequate or prolonged sleep durations may be due to an abundance of life stressors among racial minorities and residents of urban environments," said Dr. Hale. "For example, people from disadvantaged communities may not have the luxury of sleeping through the night if they work night shifts or multiple jobs. People in poorer neighborhoods may also experience greater levels of psychosocial stress or depression that makes it difficult to fall or stay asleep."
Social factors may also play a role in explaining these relationships, said Dr. Hale, adding that, for example, late-night socializing may be more common in the large cities because of the proximity of friends, households and increased opportunities for various social activities.
Structural conditions related to neighborhood and living environment may also contribute to the increased likelihood of high-risk sleep duration among racial minorities and city residents, noted Dr. Hale.
"Environmental factors of the inner city may prevent a solid night's rest. Noise or light pollution may keep city residents awake later or wake them up earlier than those in less urban areas. These factors might lead to either shortening sleep or increasing fragmentation of sleep leading to prolonged reported sleep durations," said Dr. Hale.
Lastly, Dr. Hale added that there may also be physiological differences in the demand for or the ability to sleep by racial category that are also associated with neighborhood characteristics.
Dr. Hale warned that these cross-sectional relationships are not sufficient to identify a causal link between race and sleep duration, and should not be over-interpreted.
"There may also be concerns about the use of self-reported data," said Dr. Hale. "For example, people with sleep apnea may be reporting longer sleep times because they are in bed for longer, but they may not be sleeping more. That said, the results of this study are consistent with the hypothesis that unhealthy sleep patterns among African-Americans and city residents may contribute to health differentials."
Dr. Hale noted that this information can assist public health and health care professionals in identifying segments of the population that are at a higher risk for sleep or sleep-related disorders. An understanding of the correlations between race, neighborhood context and sleep duration may also provide help in explaining outcomes where there are other racial disparities, such as test score gaps, educational attainment, employment and crime, said Dr. Hale. It may also lead to the incorporation of sleep and other biological variables in future public health, urban planning and social science research, added Dr. Hale.
Since 1957, the NHIS has conducted nationwide household interviews to collect information concerning the health of the U.S. civilian non-institutionalized population. The survey collects information on race/ethnicity, socioeconomic characteristics and health status.
Experts recommend that adults get 7-8 hours of sleep each night for good health and optimum performance.
Those who suspect that they might be suffering from a sleep disorder are encouraged to discuss their problem with their primary care physician or a sleep specialist.
SLEEP is the official journal of the Associated Professional Sleep Societies, LLC, a joint venture of the American Academy of Sleep Medicine (AASM) and the Sleep Research Society.
SleepEducation, a Web site maintained by the AASM, provides information about the various sleep disorders that exist, the forms of treatment available, recent news on the topic of sleep, sleep studies that have been conducted and a listing of sleep facilities.
Article, entitled, "Racial Differences in Self-Reports in a Population-Based Study"
The study, authored by Lauren Hale, PhD, assistant professor in the graduate program in public health at Stony Brook University, focused on the responses of 32,749 people 18 years of age and older to a National Health Interview Survey (NHIS).
According to the results, African-American respondents had an increased risk of being short and long sleepers (less than or equal to six hours and greater than or equal to nine hours, respectively) relative to Caucasian respondents. Hispanics, excluding Mexican-Americans, and non-Hispanic "others" were also associated with increased risk of short sleeping.
The study also found that living in an inner city was associated with increased risk of short sleeping and reduced risk of long sleeping, compared to non-urban areas. Some of the higher risk of short sleeping among African-Americans can be explained by a higher prevalence of African-Americans' habitation in the inner city.
"Inadequate or prolonged sleep durations may be due to an abundance of life stressors among racial minorities and residents of urban environments," said Dr. Hale. "For example, people from disadvantaged communities may not have the luxury of sleeping through the night if they work night shifts or multiple jobs. People in poorer neighborhoods may also experience greater levels of psychosocial stress or depression that makes it difficult to fall or stay asleep."
Social factors may also play a role in explaining these relationships, said Dr. Hale, adding that, for example, late-night socializing may be more common in the large cities because of the proximity of friends, households and increased opportunities for various social activities.
Structural conditions related to neighborhood and living environment may also contribute to the increased likelihood of high-risk sleep duration among racial minorities and city residents, noted Dr. Hale.
"Environmental factors of the inner city may prevent a solid night's rest. Noise or light pollution may keep city residents awake later or wake them up earlier than those in less urban areas. These factors might lead to either shortening sleep or increasing fragmentation of sleep leading to prolonged reported sleep durations," said Dr. Hale.
Lastly, Dr. Hale added that there may also be physiological differences in the demand for or the ability to sleep by racial category that are also associated with neighborhood characteristics.
Dr. Hale warned that these cross-sectional relationships are not sufficient to identify a causal link between race and sleep duration, and should not be over-interpreted.
"There may also be concerns about the use of self-reported data," said Dr. Hale. "For example, people with sleep apnea may be reporting longer sleep times because they are in bed for longer, but they may not be sleeping more. That said, the results of this study are consistent with the hypothesis that unhealthy sleep patterns among African-Americans and city residents may contribute to health differentials."
Dr. Hale noted that this information can assist public health and health care professionals in identifying segments of the population that are at a higher risk for sleep or sleep-related disorders. An understanding of the correlations between race, neighborhood context and sleep duration may also provide help in explaining outcomes where there are other racial disparities, such as test score gaps, educational attainment, employment and crime, said Dr. Hale. It may also lead to the incorporation of sleep and other biological variables in future public health, urban planning and social science research, added Dr. Hale.
Since 1957, the NHIS has conducted nationwide household interviews to collect information concerning the health of the U.S. civilian non-institutionalized population. The survey collects information on race/ethnicity, socioeconomic characteristics and health status.
Experts recommend that adults get 7-8 hours of sleep each night for good health and optimum performance.
Those who suspect that they might be suffering from a sleep disorder are encouraged to discuss their problem with their primary care physician or a sleep specialist.
SLEEP is the official journal of the Associated Professional Sleep Societies, LLC, a joint venture of the American Academy of Sleep Medicine (AASM) and the Sleep Research Society.
SleepEducation, a Web site maintained by the AASM, provides information about the various sleep disorders that exist, the forms of treatment available, recent news on the topic of sleep, sleep studies that have been conducted and a listing of sleep facilities.
Article, entitled, "Racial Differences in Self-Reports in a Population-Based Study"
суббота, 25 июня 2011 г.
Newly-Discovered Genetic Mutations Increase Risk Of Childhood Obesity, Says Study
Three new genetic variations that increase the risk of obesity are revealed in a new study, published today in the journal Nature Genetics. The authors suggest that if each acted independently, these variants could be responsible for up to 50% of cases of severe obesity.
Together with existing research, the new findings should ultimately provide the tools to predict which young children are at risk of becoming obese. Health professionals could then intervene to help such children before they develop weight problems, say the researchers from Imperial College London, the French National Research Institute CNRS and other international institutions.
In the UK, one in ten children under the age of six is obese, according to the Department of Health's National Child Measurement Programme 2007/08.
For today's ten-year study, scientists looked at the genetic makeup of obese children under six and morbidly obese adults, most of whom had been obese since childhood or adolescence, and compared this with age matched people of normal weight. The study reveals three previously unidentified genetic variations that increase the risk of severe obesity significantly, giving new insight into the reasons why some people become obese and others do not.
The gene variant most strongly associated with childhood obesity and adult morbid obesity in the study is located near the PTER gene, the function of which is not known. This variant is estimated to account for up to a third of all childhood obesity, and a fifth of all cases of adult obesity.
The second variant associated with child and adult obesity is found in the NPC1 gene. Previous studies in mice have suggested that this gene has a role in controlling appetite, as mice with a non-functioning NPC1 gene suffer late-onset weight loss and have poor food intake. This gene variant accounts for around 10 per cent of all childhood obesity and about 14 per cent of adult morbid obesity cases.
The final variant is found near the MAF gene, which controls the production of the hormones insulin and glucagon, as well as chains of amino acids called glucagon-like peptides. These hormones and peptides are known to play key roles in people's metabolisms by metabolising glucose and carbohydrates in the body. In addition, glucagon and glucagon-like peptides appear to have a strong effect on people's ability to feel 'full' or satiated after eating. This variant accounts for about 6 per cent of early-onset obesity in children, and 16 per cent of adult morbid obesity.
Further research is needed to determine whether the gene variants are acting independently, but if they are, then together these three new variations may account for up to half of all cases of severe adult and child obesity.
Professor Philippe Froguel, one of the authors of the study from the Department of Genomic Medicine at Imperial College London said: "When young children become obese, their lives can be affected in a very negative way. Sadly, obese children are often unfairly stigmatised and they can suffer heart and lung problems, painful joints, diabetes and cancer as they grow up.
"Understanding the genetic basis of obesity is the first step towards helping these children. Once we identify the genes responsible, we can develop ways to screen children to find out who is most at risk of becoming obese. Hopefully we can then intervene with measures such as behavioural therapy, to make sure a child forms healthy eating habits and does not develop a weight problem," added Professor Froguel.
The researchers reached their conclusions by conducting a genome-wide association study of 1,380 Europeans with early-onset childhood obesity and adult morbid obesity, and 1,416 age-matched normal weight controls. The study revealed 38 genetic markers with a strong association to a higher than normal body mass index, which the researchers evaluated in 14,186 Europeans, identifying three mutations that are significantly linked to obesity.
This work was supported by grants from the Medical Research Council, the Agence Nationale de la Recherche, the Conseil Regional Nord-Pas de Calais / Fonds europ?©en de d?©veloppement ?©conomique et r?©gional, and Genome Quebec / Genome Canada. The German cohorts and projects were supported by grants from the German Research Council.
Source: Laura Gallagher
Imperial College London
View drug information on Glucagon.
Together with existing research, the new findings should ultimately provide the tools to predict which young children are at risk of becoming obese. Health professionals could then intervene to help such children before they develop weight problems, say the researchers from Imperial College London, the French National Research Institute CNRS and other international institutions.
In the UK, one in ten children under the age of six is obese, according to the Department of Health's National Child Measurement Programme 2007/08.
For today's ten-year study, scientists looked at the genetic makeup of obese children under six and morbidly obese adults, most of whom had been obese since childhood or adolescence, and compared this with age matched people of normal weight. The study reveals three previously unidentified genetic variations that increase the risk of severe obesity significantly, giving new insight into the reasons why some people become obese and others do not.
The gene variant most strongly associated with childhood obesity and adult morbid obesity in the study is located near the PTER gene, the function of which is not known. This variant is estimated to account for up to a third of all childhood obesity, and a fifth of all cases of adult obesity.
The second variant associated with child and adult obesity is found in the NPC1 gene. Previous studies in mice have suggested that this gene has a role in controlling appetite, as mice with a non-functioning NPC1 gene suffer late-onset weight loss and have poor food intake. This gene variant accounts for around 10 per cent of all childhood obesity and about 14 per cent of adult morbid obesity cases.
The final variant is found near the MAF gene, which controls the production of the hormones insulin and glucagon, as well as chains of amino acids called glucagon-like peptides. These hormones and peptides are known to play key roles in people's metabolisms by metabolising glucose and carbohydrates in the body. In addition, glucagon and glucagon-like peptides appear to have a strong effect on people's ability to feel 'full' or satiated after eating. This variant accounts for about 6 per cent of early-onset obesity in children, and 16 per cent of adult morbid obesity.
Further research is needed to determine whether the gene variants are acting independently, but if they are, then together these three new variations may account for up to half of all cases of severe adult and child obesity.
Professor Philippe Froguel, one of the authors of the study from the Department of Genomic Medicine at Imperial College London said: "When young children become obese, their lives can be affected in a very negative way. Sadly, obese children are often unfairly stigmatised and they can suffer heart and lung problems, painful joints, diabetes and cancer as they grow up.
"Understanding the genetic basis of obesity is the first step towards helping these children. Once we identify the genes responsible, we can develop ways to screen children to find out who is most at risk of becoming obese. Hopefully we can then intervene with measures such as behavioural therapy, to make sure a child forms healthy eating habits and does not develop a weight problem," added Professor Froguel.
The researchers reached their conclusions by conducting a genome-wide association study of 1,380 Europeans with early-onset childhood obesity and adult morbid obesity, and 1,416 age-matched normal weight controls. The study revealed 38 genetic markers with a strong association to a higher than normal body mass index, which the researchers evaluated in 14,186 Europeans, identifying three mutations that are significantly linked to obesity.
This work was supported by grants from the Medical Research Council, the Agence Nationale de la Recherche, the Conseil Regional Nord-Pas de Calais / Fonds europ?©en de d?©veloppement ?©conomique et r?©gional, and Genome Quebec / Genome Canada. The German cohorts and projects were supported by grants from the German Research Council.
Source: Laura Gallagher
Imperial College London
View drug information on Glucagon.
'Informed Consent' Abortion Laws Scientifically Flawed, Washington Post Opinion Piece States
The latest abortion-rights battles are "being fought less over women's bodies than over their minds," with several states passing laws mandating that women seeking abortions are told the procedure places them at risk for mental health problems, Brenda Major, a University of California-Santa Barbara psychology professor and fellow at Stanford University's Center for Advanced Study in the Behavioral Sciences, writes in a Washington Post opinion piece. According to the Guttmacher Institute, pre-abortion counseling about mental health risks is mandatory in Mississippi, Nebraska, South Carolina, South Dakota, Texas, Utah and West Virginia.
Major argues that "informed choice requires accurate information. And these laws mandate that women be misled." The laws are part of a political strategy "aimed at dissuading women from terminating a pregnancy and at making abortions difficult, if not impossible to obtain," she continues. The strategy "distorts scientific principles, even if it uses the umbrella of scientific research to advance its aims," Major states.
According to Major, "rigorous" scientific studies "have not substantiated the claim that abortion, compared with its alternatives, causes an increased incidence of mental health problems." In 2008, a task force of American Psychological Association -- chaired by Major -- and an independent team of scholars at Johns Hopkins University reached the same conclusion. Most recently, Oregon State University researchers released a study "showing that teenagers who have an abortion are not more likely to become depressed or to have low self-esteem one year or five years later, compared with their peers who deliver," Major notes.
Errors in Logic
Major argues that there are "at least two logical flaws at play" in the arguments of the laws' supporters. "The first is the confusion of correlation with causation," she writes, noting that the "most plausible explanation for the association that some studies find between abortion and mental health is that it reflects pre-existing differences between women who continue a pregnancy and those who end one." This difference was "willfully ignored" in April when Nebraska lawmakers passed a law (LB 594) that requires doctors to screen women prior to an abortion for risk factors that the law's supporters say could indicate whether they might develop physical or mental problems after an abortion, Major writes.
The Nebraska law "ignores the fact that the very characteristics that predispose women to emotional or mental health problems following an abortion also predispose them to postpartum depression if they deliver or to mental health problems in general, even if they do not become pregnant," Major argues. She adds, "Following the logic of this purportedly protective law, women wanting to deliver a child should likewise be screened to ascertain that they are not predisposed to poor mental health afterward."
According to Major, the "second logical failing in the campaign to convince women that abortion harms their mental health involves what psychologists call the 'availability heuristic,'" which means that "vivid, first-person accounts that can be easily brought to mind ... influence our estimates of the frequency of an event more than dry, statistical data do." The "emotionally evocative stories of a minority of women can lead people to overestimate the frequency of those experiences," Major writes. Her research involving more than 400 women who had abortions early in pregnancy "shows that women who terminate an unplanned pregnancy report a range of feelings, including sadness and loss as well as relief." She adds that two years after the procedure, "most women say they would make the same decision if they had it to do over again under the same circumstances."
However, "most women feel they can't talk about their abortions -- unless they repent" because of the "stigma associated with abortion," Major argues. "Women who think they made the right decision in having an abortion must be able to say so without fear and condemnation and without feeling that something is wrong with them," she continues, concluding, "And women who feel sadness and regret should feel free to share their feelings as well. But their words should not be used to deceive women or to limit their choices" (Major, Washington Post, 11/7).
Reprinted with kind permission from nationalpartnership. You can view the entire Daily Women's Health Policy Report, search the archives, or sign up for email delivery here. The Daily Women's Health Policy Report is a free service of the National Partnership for Women & Families.
© 2010 National Partnership for Women & Families. All rights reserved.
пятница, 24 июня 2011 г.
What Model Organisms Can Teach Us About Emotion
Scientists know little about how the brain creates and controls emotions - an uncertainty that presents a major obstacle in the effort to develop treatments for emotional disorders. "The study of the brain science of emotion is in its infancy," says Howard Hughes Medical Institute (HHMI) investigator David Anderson, "yet emotional and psychiatric disorders continue to take an enormous toll on human society."
On February 20, 2010, at the American Association for the Advancement of Science's Annual Meeting in San Diego, Anderson, a neuroscientist at the California Institute of Technology, discussed how studies of model organisms such as mice and fruit flies can improve scientists' understanding of the neural basis of emotion. That understanding, he says, is essential for developing more specific therapies for emotion disorders such as depression, anxiety, or attention deficit hyperactivity disorder (ADHD).
Anderson explains that while functional magnetic imaging (fMRI) studies of the human brain have linked neural activity in specific regions of the brain to particular emotional responses, there are limits to what can be learned from these types of studies. "We cannot tell which of these hotspots represents the actual cause of an emotional response, and which of them represents a reaction to the response," he says.
To makes that distinction, scientists must alter the activity of brain circuits in a targeted way, and then determine the consequences of the changes on emotional behavior. Such experiments are not possible on human subjects, and so scientists turn to model organisms. Anderson, whose own studies at Caltech and HHMI's Janelia Farm Research Campus explore the link between neural circuitry and emotional behaviors such as fear and aggression in both mice and fruit flies, will discuss the power and limitations of these types of experiments.
"We are in the midst of a revolution in the development of new technologies for experimentally manipulating brain circuitry," he says. Molecular and genetic tools that allow scientists to control when specific neurons are turned on in model organisms is already beginning to transform scientists' understanding of many aspects of brain function, including sensation, perception, cognition, and motor control. Anderson's presentation will address how to best apply these tools to the study of emotion.
"We need to know which animals are most suitable for studying this complex subject," he says. The laboratory mouse is amenable to powerful genetics techniques and it has a brain structure that is fundamentally similar to that of humans. But, he says, mouse research is slow, costly, technically difficult, and presents ethical challenges. Invertebrate model organisms, like the fruit fly Drosophila melanogaster, have simpler brains, more powerful genetic tools, and allow for faster, less expensive studies. "But can one study emotional behavior in a fly?" Anderson asks.
"Unexpected Discoveries on Brain Function and Development from Model Organisms"
Saturday, February 20, 2010
Room 2 of the San Diego Convention Center
In addition to David Anderson, other speakers were HHMI investigator Larry Zipursky, University of California, Los Angeles, and HHMI investigator Catherine Dulac, Harvard University.
On February 20, 2010, at the American Association for the Advancement of Science's Annual Meeting in San Diego, Anderson, a neuroscientist at the California Institute of Technology, discussed how studies of model organisms such as mice and fruit flies can improve scientists' understanding of the neural basis of emotion. That understanding, he says, is essential for developing more specific therapies for emotion disorders such as depression, anxiety, or attention deficit hyperactivity disorder (ADHD).
Anderson explains that while functional magnetic imaging (fMRI) studies of the human brain have linked neural activity in specific regions of the brain to particular emotional responses, there are limits to what can be learned from these types of studies. "We cannot tell which of these hotspots represents the actual cause of an emotional response, and which of them represents a reaction to the response," he says.
To makes that distinction, scientists must alter the activity of brain circuits in a targeted way, and then determine the consequences of the changes on emotional behavior. Such experiments are not possible on human subjects, and so scientists turn to model organisms. Anderson, whose own studies at Caltech and HHMI's Janelia Farm Research Campus explore the link between neural circuitry and emotional behaviors such as fear and aggression in both mice and fruit flies, will discuss the power and limitations of these types of experiments.
"We are in the midst of a revolution in the development of new technologies for experimentally manipulating brain circuitry," he says. Molecular and genetic tools that allow scientists to control when specific neurons are turned on in model organisms is already beginning to transform scientists' understanding of many aspects of brain function, including sensation, perception, cognition, and motor control. Anderson's presentation will address how to best apply these tools to the study of emotion.
"We need to know which animals are most suitable for studying this complex subject," he says. The laboratory mouse is amenable to powerful genetics techniques and it has a brain structure that is fundamentally similar to that of humans. But, he says, mouse research is slow, costly, technically difficult, and presents ethical challenges. Invertebrate model organisms, like the fruit fly Drosophila melanogaster, have simpler brains, more powerful genetic tools, and allow for faster, less expensive studies. "But can one study emotional behavior in a fly?" Anderson asks.
"Unexpected Discoveries on Brain Function and Development from Model Organisms"
Saturday, February 20, 2010
Room 2 of the San Diego Convention Center
In addition to David Anderson, other speakers were HHMI investigator Larry Zipursky, University of California, Los Angeles, and HHMI investigator Catherine Dulac, Harvard University.
четверг, 23 июня 2011 г.
Commonly Used Anti-depressants Safe And Effective For Treating Postpartum Depression
Two antidepressants commonly used to treat depression in the general population also can effectively and safely treat postpartum depression, according to a University of Pittsburgh School of Medicine-led study published as a lead article in the August issue of the Journal of Clinical Psychopharmacology.
The study is among the first to compare the effectiveness of selective serotonin reuptake inhibitors (SSRIs) and tricyclics, two commonly used classes of antidepressants, in women who experience major depression after childbirth.
"We've been treating postpartum depression based on the assumption that drugs that work for a woman with depression under usual circumstances will work for a woman who experiences depression after giving birth, but there have not been studies that provide scientific proof that this was an effective and safe course of treatment," said Katherine L. Wisner, M.D., M.S., professor of psychiatry and obstetrics, gynecology and reproductive sciences at the University of Pittsburgh School of Medicine. "Treating these women based on that assumption was simply not good enough, and we felt compelled to provide scientific evidence to guide postpartum depression treatment decisions."
In the study, researchers compared the tricyclic nortriptyline and the SSRI sertraline because both drugs were proven effective in treating general depression in women. In addition, previous studies showed the two drugs were acceptable for use in breastfeeding women. Researchers interviewed 420 women who had major depression with postpartum onset at three sites: Pittsburgh, Cleveland and Louisville, Ky. Of those, 109 qualified and chose to participate in the study. They were randomized to receive either nortriptyline or sertraline. A placebo was not used, as researchers felt it would be unethical and dangerous to the mother and her infant to not treat the illness actively. Using common tools for assessment of depression, the investigators evaluated the women for remission of depressive symptoms at four, eight and 24 weeks. The latter evaluation point included only women who had responded after eight weeks. Of the original 109 participants, 95 provided response data at four weeks, 83 provided data at eight weeks, and 29 completed between 20 and 24 weeks of the study.
The proportion of women who responded with a reduction in depressive symptoms, and those who remitted, having few depressive symptoms consistent with wellness, did not significantly differ between the two drugs at any of the study's time points. By week four, 46 percent of the participants taking sertraline had responded and 27 percent remitted, while 56 percent of those taking nortriptyline responded and 30 percent remitted. At eight weeks, 56 percent of the participants on sertraline had a reduction of symptoms and 46 percent had no symptoms, while the participants taking nortriptyline had 69 percent respond and 48 percent remit. Of the 29 participants who remained in the study until 20-24 weeks, 93 percent taking sertraline responded and 73 percent remitted, while 100 percent taking nortriptyline responded and 79 percent remitted. None of these differences were significant by statistical analyses.
Additionally, researchers found that psychosocial functioning improved similarly with use of both drugs. Neither drug proved to be superior to the other in treating aggressive obsessional thoughts. Side-effect burdens were the same, although side effects differed between the drugs. Overall, the majority of women responded to both of the drugs within two to four weeks.
"Conventional wisdom says that it can take six to eight weeks for a person to respond to an antidepressant. Several weeks is simply too long to wait for a response in postpartum depression," said Dr. Wisner. "It's encouraging to see that these women responded quickly and well to the study medications and that now we have scientific proof on which to base our treatment decisions."
Co-authors of the study include Barbara H. Hanusa, Ph.D., James M. Perel, Ph.D., Dorothy K.Y. Sit, M.D., and Eydie Moses-Kolko, M.D., from Women's Behavioral Health CARE at the Western Psychiatric Institute and Clinic of the University of Pittsburgh Medical Center; Kathleen S. Peindl, Ph.D., department of psychiatry, Duke University Medical Center, Catherine M. Piontek, M.D., Interlink Health Care Communications, Lawrenceville, N.J.; and Robert L. Findline, M.D., department of psychiatry, Case Western Reserve University and University Hospitals Health System, Cleveland.
This study was funded through grants from the National Institute of Mental Health, one of the National Institutes of Health.
The sertraline used in this study was donated by Pfizer, but Pfizer did not provide any direct financial support for the conduct of the study. Dr. Wisner is a member of Pfizer's speaker's bureau and has a grant from Pfizer for a study of ziprasidone pharmacokinetics during pregnancy. Dr. Wisner also is a member of the speaker's bureau for GlaxoSmithKline. She has research funding from the Stanley Medical Research Institute. Full financial disclosures of all the authors can be found in the article, available on request.
Contact: Jocelyn Uhl Duffy
University of Pittsburgh Medical Center
View drug information on Ziprasidone.
The study is among the first to compare the effectiveness of selective serotonin reuptake inhibitors (SSRIs) and tricyclics, two commonly used classes of antidepressants, in women who experience major depression after childbirth.
"We've been treating postpartum depression based on the assumption that drugs that work for a woman with depression under usual circumstances will work for a woman who experiences depression after giving birth, but there have not been studies that provide scientific proof that this was an effective and safe course of treatment," said Katherine L. Wisner, M.D., M.S., professor of psychiatry and obstetrics, gynecology and reproductive sciences at the University of Pittsburgh School of Medicine. "Treating these women based on that assumption was simply not good enough, and we felt compelled to provide scientific evidence to guide postpartum depression treatment decisions."
In the study, researchers compared the tricyclic nortriptyline and the SSRI sertraline because both drugs were proven effective in treating general depression in women. In addition, previous studies showed the two drugs were acceptable for use in breastfeeding women. Researchers interviewed 420 women who had major depression with postpartum onset at three sites: Pittsburgh, Cleveland and Louisville, Ky. Of those, 109 qualified and chose to participate in the study. They were randomized to receive either nortriptyline or sertraline. A placebo was not used, as researchers felt it would be unethical and dangerous to the mother and her infant to not treat the illness actively. Using common tools for assessment of depression, the investigators evaluated the women for remission of depressive symptoms at four, eight and 24 weeks. The latter evaluation point included only women who had responded after eight weeks. Of the original 109 participants, 95 provided response data at four weeks, 83 provided data at eight weeks, and 29 completed between 20 and 24 weeks of the study.
The proportion of women who responded with a reduction in depressive symptoms, and those who remitted, having few depressive symptoms consistent with wellness, did not significantly differ between the two drugs at any of the study's time points. By week four, 46 percent of the participants taking sertraline had responded and 27 percent remitted, while 56 percent of those taking nortriptyline responded and 30 percent remitted. At eight weeks, 56 percent of the participants on sertraline had a reduction of symptoms and 46 percent had no symptoms, while the participants taking nortriptyline had 69 percent respond and 48 percent remit. Of the 29 participants who remained in the study until 20-24 weeks, 93 percent taking sertraline responded and 73 percent remitted, while 100 percent taking nortriptyline responded and 79 percent remitted. None of these differences were significant by statistical analyses.
Additionally, researchers found that psychosocial functioning improved similarly with use of both drugs. Neither drug proved to be superior to the other in treating aggressive obsessional thoughts. Side-effect burdens were the same, although side effects differed between the drugs. Overall, the majority of women responded to both of the drugs within two to four weeks.
"Conventional wisdom says that it can take six to eight weeks for a person to respond to an antidepressant. Several weeks is simply too long to wait for a response in postpartum depression," said Dr. Wisner. "It's encouraging to see that these women responded quickly and well to the study medications and that now we have scientific proof on which to base our treatment decisions."
Co-authors of the study include Barbara H. Hanusa, Ph.D., James M. Perel, Ph.D., Dorothy K.Y. Sit, M.D., and Eydie Moses-Kolko, M.D., from Women's Behavioral Health CARE at the Western Psychiatric Institute and Clinic of the University of Pittsburgh Medical Center; Kathleen S. Peindl, Ph.D., department of psychiatry, Duke University Medical Center, Catherine M. Piontek, M.D., Interlink Health Care Communications, Lawrenceville, N.J.; and Robert L. Findline, M.D., department of psychiatry, Case Western Reserve University and University Hospitals Health System, Cleveland.
This study was funded through grants from the National Institute of Mental Health, one of the National Institutes of Health.
The sertraline used in this study was donated by Pfizer, but Pfizer did not provide any direct financial support for the conduct of the study. Dr. Wisner is a member of Pfizer's speaker's bureau and has a grant from Pfizer for a study of ziprasidone pharmacokinetics during pregnancy. Dr. Wisner also is a member of the speaker's bureau for GlaxoSmithKline. She has research funding from the Stanley Medical Research Institute. Full financial disclosures of all the authors can be found in the article, available on request.
Contact: Jocelyn Uhl Duffy
University of Pittsburgh Medical Center
View drug information on Ziprasidone.
среда, 22 июня 2011 г.
United States FDA Clears The REGEN Trial To Test Bioheart's Combination Gene And Stem Cell Therapy In Heart Failure Patients
Bioheart, Inc., (OTC Bulletin Board: BHRT) a company committed to delivering intelligent devices and biologics that help monitor, diagnose and treat heart failure and cardiovascular diseases announced today that the US FDA cleared a phase I clinical trial for MyoCell SDF-1 (Stromal Derived Factor - 1) to treat congestive heart failure. The REGEN trial will enroll 15 patients in a multicenter, randomized, dose escalation study to assess the safety and cardiovascular effects of the implantation of MyoCell SDF-1 in congestive heart failure patients post myocardial infarction(s).
MyoCell SDF-1 is a composition of myogenic stem cells derived from a patient's own thigh muscle that has been modified to over express the SDF-1 protein. The product candidate is prepared with an 18-step proprietary method in a cGMP laboratory. Utilizing a needle-tipped catheter inserted into the groin of a patient who is suffering from heart failure, the cells are injected into the scar tissue that has formed in the patient's heart. The goal of MyoCell SDF-1 is to grow new contractile muscle within the scar tissue that will have the ability to release additional beneficial proteins to assist in the tissue repair process and improve the patient's heart function, exercise capacity and quality of life. In preclinical studies, MyoCell SDF-1 provided a 54 percent improvement of heart function compared to 27 percent for the original MyoCell composition while the placebo control treated animals declined by 10 percent. The preclinical studies also demonstrated that this product candidate can enhance blood vessel formation in damaged hearts.
"We are happy to be able to begin the REGEN trial to test this promising product candidate in heart failure patients after completing very successful preclinical testing," said Howard Leonhardt, Bioheart's Chairman and CEO. "To our knowledge, this will be the first clinical trial ever to test a combination gene and stem cell therapy for cardiovascular disease."
The U.S. trial is expected to begin this year. After completing the REGEN safety protocol with one-month follow-up, the company hopes to transition this second-generation product into its FDA-authorized Phase II/III MARVEL study. MyoCell SDF-1 is substantially similar to the original MyoCell composition that has been active in clinical trials since early 2001 at more than 50 centers worldwide.
The patents Bioheart has acquired covering the myogenic cells and SDF-1 compositions and methods are expected to provide intellectual property protection until 2023.
About Bioheart, Inc.
Bioheart, Inc. is committed to delivering intelligent devices and biologics that help monitor, diagnose and treat heart failure and cardiovascular diseases. Its goals are to improve a patient's quality of life and reduce health care costs and hospitalizations. Specific to biotechnology, Bioheart is focused on the discovery, development and, subject to regulatory approval, commercialization of autologous cell therapies for the treatment of chronic and acute heart damage. Its lead product candidate, MyoCell((R)), is an innovative clinical muscle-derived stem cell therapy designed to populate regions of scar tissue within a patient's heart with new living cells for the purpose of improving cardiac function in chronic heart failure patients. The Company's pipeline includes multiple product candidates for the treatment of heart damage, including Bioheart Acute Cell Therapy, an autologous, adipose tissue-derived stem cell treatment for acute heart damage, and MyoCell((R)) SDF-1, a therapy utilizing autologous cells that are genetically modified to express additional potentially therapeutic growth proteins.
MyoCell and MyoCell SDF-1 are trademarks of Bioheart, Inc.
Forward-Looking Statements:
Except for historical matters contained herein, statements made in this press release are forward-looking and are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Without limiting the generality of the foregoing, words such as "may," "will," "to," "plan," "expect," "believe," "anticipate," "intend," "could," "would", "estimate", or "continue" or the negative other variations thereof or comparable terminology are intended to identify forward-looking statements.
Investors and others are cautioned that a variety of factors, including certain risks, may affect our business and cause actual results to differ materially from those set forth in the forward-looking statements. These risk factors include, without limitation, (i) our ability to obtain additional financing; (ii) our ability to control and reduce our expenses; (iii) our ability to establish a distribution network for and commence distribution of certain products for which we have acquired distribution rights; (iv) our ability to timely and successfully complete our clinical trials; (v) the occurrence of any unacceptable side effects during or after preclinical and clinical testing of our product candidates; (vi) the timing of and our ability to obtain and maintain regulatory approvals for our product candidates; (vii) our dependence on the success of our lead product candidate; (viii) our inability to predict the extent of our future losses or if or when we will become profitable; (ix) our ability to protect our intellectual property rights; and (x) intense competition. The Company is also subject to the risks and uncertainties described in its filings with the Securities and Exchange Commission, including the section entitled "Risk Factors" in its Annual Report on Form 10-K for the year ended December 31, 2008, as amended by its Annual Report on Form 10-K/A, and its Quarterly Reports on Form 10-Q for the quarters ended March 31, 2008; June 30, 2008 and September 30, 2008.
Source: Bioheart, Inc
MyoCell SDF-1 is a composition of myogenic stem cells derived from a patient's own thigh muscle that has been modified to over express the SDF-1 protein. The product candidate is prepared with an 18-step proprietary method in a cGMP laboratory. Utilizing a needle-tipped catheter inserted into the groin of a patient who is suffering from heart failure, the cells are injected into the scar tissue that has formed in the patient's heart. The goal of MyoCell SDF-1 is to grow new contractile muscle within the scar tissue that will have the ability to release additional beneficial proteins to assist in the tissue repair process and improve the patient's heart function, exercise capacity and quality of life. In preclinical studies, MyoCell SDF-1 provided a 54 percent improvement of heart function compared to 27 percent for the original MyoCell composition while the placebo control treated animals declined by 10 percent. The preclinical studies also demonstrated that this product candidate can enhance blood vessel formation in damaged hearts.
"We are happy to be able to begin the REGEN trial to test this promising product candidate in heart failure patients after completing very successful preclinical testing," said Howard Leonhardt, Bioheart's Chairman and CEO. "To our knowledge, this will be the first clinical trial ever to test a combination gene and stem cell therapy for cardiovascular disease."
The U.S. trial is expected to begin this year. After completing the REGEN safety protocol with one-month follow-up, the company hopes to transition this second-generation product into its FDA-authorized Phase II/III MARVEL study. MyoCell SDF-1 is substantially similar to the original MyoCell composition that has been active in clinical trials since early 2001 at more than 50 centers worldwide.
The patents Bioheart has acquired covering the myogenic cells and SDF-1 compositions and methods are expected to provide intellectual property protection until 2023.
About Bioheart, Inc.
Bioheart, Inc. is committed to delivering intelligent devices and biologics that help monitor, diagnose and treat heart failure and cardiovascular diseases. Its goals are to improve a patient's quality of life and reduce health care costs and hospitalizations. Specific to biotechnology, Bioheart is focused on the discovery, development and, subject to regulatory approval, commercialization of autologous cell therapies for the treatment of chronic and acute heart damage. Its lead product candidate, MyoCell((R)), is an innovative clinical muscle-derived stem cell therapy designed to populate regions of scar tissue within a patient's heart with new living cells for the purpose of improving cardiac function in chronic heart failure patients. The Company's pipeline includes multiple product candidates for the treatment of heart damage, including Bioheart Acute Cell Therapy, an autologous, adipose tissue-derived stem cell treatment for acute heart damage, and MyoCell((R)) SDF-1, a therapy utilizing autologous cells that are genetically modified to express additional potentially therapeutic growth proteins.
MyoCell and MyoCell SDF-1 are trademarks of Bioheart, Inc.
Forward-Looking Statements:
Except for historical matters contained herein, statements made in this press release are forward-looking and are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Without limiting the generality of the foregoing, words such as "may," "will," "to," "plan," "expect," "believe," "anticipate," "intend," "could," "would", "estimate", or "continue" or the negative other variations thereof or comparable terminology are intended to identify forward-looking statements.
Investors and others are cautioned that a variety of factors, including certain risks, may affect our business and cause actual results to differ materially from those set forth in the forward-looking statements. These risk factors include, without limitation, (i) our ability to obtain additional financing; (ii) our ability to control and reduce our expenses; (iii) our ability to establish a distribution network for and commence distribution of certain products for which we have acquired distribution rights; (iv) our ability to timely and successfully complete our clinical trials; (v) the occurrence of any unacceptable side effects during or after preclinical and clinical testing of our product candidates; (vi) the timing of and our ability to obtain and maintain regulatory approvals for our product candidates; (vii) our dependence on the success of our lead product candidate; (viii) our inability to predict the extent of our future losses or if or when we will become profitable; (ix) our ability to protect our intellectual property rights; and (x) intense competition. The Company is also subject to the risks and uncertainties described in its filings with the Securities and Exchange Commission, including the section entitled "Risk Factors" in its Annual Report on Form 10-K for the year ended December 31, 2008, as amended by its Annual Report on Form 10-K/A, and its Quarterly Reports on Form 10-Q for the quarters ended March 31, 2008; June 30, 2008 and September 30, 2008.
Source: Bioheart, Inc
Understanding The Sleep-Wake Cycle
Lack of sleep is a common complaint but for many, falling asleep involuntarily during the day poses a very real and dangerous problem. A new study from the Montreal Neurological Institute (MNI) at McGill University demonstrates interestingly, that sleep-wake states are regulated by two different types of nerve cells (neurons), melanin-concentrating hormone (MCH) neurons and orexin (Orx) neurons, which occupy the same region of the brain but perform opposite functions. The MNI study is the first to discover that MCH neurons are activated during sleep and could thus be important in regulating the sleep state. The study, published in this week's issue of the journal Proceedings of the National Academy of Sciences (PNAS), provides deeper understanding of the sleep-wake cycle and vital insight into the basis of sleep disorders such as narcolepsy and possibly also other diseases such as depression and Parkinson's.
Sleep is regulated by processes in the brain in response to how long we are awake in addition to the light/dark cycle controlled by the circadian rhythm. With Drs. Oum Hassani and Maan Gee Lee, Dr. Barbara Jones at the MNI were studying a structure in the brain called the lateral hypothalamus (LH) known to be critical for maintaining wakefulness. MCH neurons, co-distributed with Orx neurons, constitute less than 10% of the LH. Previous studies have shown that Orx neurons are essential for maintenance of the awake state. These neurons are active in the waking state and turn off during sleep and in their absence, animals and humans experience narcolepsy with cataplexy or sudden loss of mucle tone. However, the role of MCH neurons was until now, unclear. Evidence from earlier knockout studies suggested that MCH neurons might play a different role than Orx neurons in regulating activity and sleep-wake states. Therefore the team at the MNI set up experiments to study the function of MCH neurons during the sleep-wake states.
"Remarkably, what we found is that MCH neurons are actually silent during waking, which is a surprising finding especially in this wake-promoting region of the brain. The neurons fire during sleep, and are most active during REM sleep," says Dr. Barbara Jones, neuroscientist at the MNI and principal investigator in the study. "Our study markedly demonstrates that MCH neurons discharge in a reciprocal manner to the Orx neurons across the sleep-wake cycle." Dr. Jones and colleagues used their expertise to apply and develop a difficult technique which allowed them to selectively record, label and thus identify a nerve cell containing a particular chemical. This allowed them to isolate the functions of the MCH and Orx cells even though they comprise less than 10% of the nerve cells in the LH.
The reciprocal profiles and roles of the Orx and MCH neurons could be significant in the manifestation of sleep disorders. It is possible that narcolepsy, which occurs with the loss of Orx neurons, is provoked in part by the MCH neurons that remain intact in the narcoleptic patients. A growing body of research shows that regular and normal sleep is necessary for overall health; regulating hormone levels, blood pressure, metabolism, alertness, mood, and consolidating memory. This study presents potential therapeutic avenues and targets for the treatment of various sleep disorders including the development of drugs that will act on receptors for Orx and MCH, to stimulate or block these receptors accordingly.
This work was supported by the Canadian Institutes of Health Research (CIHR) and the National Institutes of Health (NIH).
MNI:
October 2009 marks the 75th anniversary of the MNI. The MNI is a McGill University research and teaching institute, dedicated to the study of the nervous system and neurological diseases. Founded in 1934 by the renowned Dr. Wilder Penfield, the MNI is one of the world's largest institutes of its kind. MNI researchers are world leaders in cellular and molecular neuroscience, brain imaging, cognitive neuroscience and the study and treatment of epilepsy, multiple sclerosis and neuromuscular disorders. The MNI, with its clinical partner, the Montreal Neurological Hospital (MNH), part of the McGill University Health Centre, continues to integrate research, patient care and training, and is recognized as one of the premier neuroscience centres in the world. At the MNI, we believe in investing in the faculty, staff and students who conduct outstanding research, provide advanced, compassionate care of patients and who pave the way for the next generation of medical advances. Highly talented, motivated people are the engine that drives research - the key to progress in medical care. A new building, the North Wing Expansion, is currently under construction and will house state-of-the-art brain imaging facilities. Once the construction is completed and the new building is fully equipped, the scientific community focused on brain imaging research at the MNI will be without equivalent anywhere in the world.
Sleep is regulated by processes in the brain in response to how long we are awake in addition to the light/dark cycle controlled by the circadian rhythm. With Drs. Oum Hassani and Maan Gee Lee, Dr. Barbara Jones at the MNI were studying a structure in the brain called the lateral hypothalamus (LH) known to be critical for maintaining wakefulness. MCH neurons, co-distributed with Orx neurons, constitute less than 10% of the LH. Previous studies have shown that Orx neurons are essential for maintenance of the awake state. These neurons are active in the waking state and turn off during sleep and in their absence, animals and humans experience narcolepsy with cataplexy or sudden loss of mucle tone. However, the role of MCH neurons was until now, unclear. Evidence from earlier knockout studies suggested that MCH neurons might play a different role than Orx neurons in regulating activity and sleep-wake states. Therefore the team at the MNI set up experiments to study the function of MCH neurons during the sleep-wake states.
"Remarkably, what we found is that MCH neurons are actually silent during waking, which is a surprising finding especially in this wake-promoting region of the brain. The neurons fire during sleep, and are most active during REM sleep," says Dr. Barbara Jones, neuroscientist at the MNI and principal investigator in the study. "Our study markedly demonstrates that MCH neurons discharge in a reciprocal manner to the Orx neurons across the sleep-wake cycle." Dr. Jones and colleagues used their expertise to apply and develop a difficult technique which allowed them to selectively record, label and thus identify a nerve cell containing a particular chemical. This allowed them to isolate the functions of the MCH and Orx cells even though they comprise less than 10% of the nerve cells in the LH.
The reciprocal profiles and roles of the Orx and MCH neurons could be significant in the manifestation of sleep disorders. It is possible that narcolepsy, which occurs with the loss of Orx neurons, is provoked in part by the MCH neurons that remain intact in the narcoleptic patients. A growing body of research shows that regular and normal sleep is necessary for overall health; regulating hormone levels, blood pressure, metabolism, alertness, mood, and consolidating memory. This study presents potential therapeutic avenues and targets for the treatment of various sleep disorders including the development of drugs that will act on receptors for Orx and MCH, to stimulate or block these receptors accordingly.
This work was supported by the Canadian Institutes of Health Research (CIHR) and the National Institutes of Health (NIH).
MNI:
October 2009 marks the 75th anniversary of the MNI. The MNI is a McGill University research and teaching institute, dedicated to the study of the nervous system and neurological diseases. Founded in 1934 by the renowned Dr. Wilder Penfield, the MNI is one of the world's largest institutes of its kind. MNI researchers are world leaders in cellular and molecular neuroscience, brain imaging, cognitive neuroscience and the study and treatment of epilepsy, multiple sclerosis and neuromuscular disorders. The MNI, with its clinical partner, the Montreal Neurological Hospital (MNH), part of the McGill University Health Centre, continues to integrate research, patient care and training, and is recognized as one of the premier neuroscience centres in the world. At the MNI, we believe in investing in the faculty, staff and students who conduct outstanding research, provide advanced, compassionate care of patients and who pave the way for the next generation of medical advances. Highly talented, motivated people are the engine that drives research - the key to progress in medical care. A new building, the North Wing Expansion, is currently under construction and will house state-of-the-art brain imaging facilities. Once the construction is completed and the new building is fully equipped, the scientific community focused on brain imaging research at the MNI will be without equivalent anywhere in the world.
вторник, 21 июня 2011 г.
Incidence, Precursors And Psychiatric Sequelae Of Major Psychiatric Disorders Revealed By NIH Study
A new study by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) presents results on the first onset of substance use disorders (i.e., alcohol and drug abuse and dependence) and major mood and anxiety disorders, based on Wave 2 of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC).
This landmark survey is the first conducted in the U.S. to identify rates of first episodes (i.e., incidence) of these disorders in the U.S. population. In addition, it provides information on sociodemographic and psychopathologic risk factors for those disorders - information critical for developing evidence-based preventive interventions - and estimates risk for subsequent comorbid disorders.
Bridget Grant, Ph.D., Chief of NIAAA's Laboratory of Biometry and Epidemiology, and her colleagues found that 1-year incidence rates were highest for DSM-IV alcohol dependence (1.70%), alcohol abuse (1.02%), major depressive disorder (1.51%) and generalized anxiety disorder (1.12%), followed by panic disorder (0.62%), bipolar I disorder (0.53%) and specific phobia (0.44%). One-year incidence rates of DSM-IV social phobia (0.32%), bipolar II (0.21%) and drug abuse (0.28%) and drug dependence (0.32%) were lower but not insignificant. These rates are comparable to or exceed corresponding incidence rates for other common medical diseases such as lung cancer (0.06%), stroke (0.45%) and cardiovascular disease (1.5%).
The study found that men were at greater risk of first onset alcohol abuse, alcohol dependence and drug dependence, and 1-year incidence rates were greatest among 20- to 29-year-olds and individuals who had been separated/divorced/widowed or never married. By contrast, the risk of most incident DSM-IV anxiety disorders, including panic disorder, specific but not social phobia, and generalized anxiety disorder, was greatest among women, and all anxiety disorder incidence rates were greater in the youngest age groups (20- to 54-year-olds). Among DSM-IV mood disorders examined in this study, the risk of first onset of major depressive disorder (MDD) was greatest among women, and no sex differences in incidence were found for bipolar I and II disorders. Taken together, these results highlight age as an important general risk factor for first onset DSM-IV substance use, mood and anxiety disorders, whereas the effects of sex and marital status appear to be disorder-specific.
Consistent with earlier studies, baseline dysthymia in this study predicted incident MDD, and baseline MDD predicted incident bipolar II disorder, suggesting that MDD precedes hypomania in the development of bipolar II disorder. Consistent with other prospective studies, alcohol abuse and dependence showed strong reciprocal temporal relationships, whereas drug abuse predicted only incident drug dependence. "The reciprocal relationship between alcohol abuse and dependence suggests that strong common factors may underlie the relationship and provides support for eliminating the hierarchy between the disorders in future DSM revisions," state the authors. Other intriguing findings include reciprocal temporal relationships between MDD and GAD, and GAD and panic disorder, suggesting that common causes underlie those disorders. In addition, substance use disorders did not predict any incident mood or anxiety disorder, the authors note.
"Information on psychiatric risk factors prospectively identified in this study can begin to inform a new class of preventive interventions aimed at preventing a second disorder or set of disorders," said Grant. "As to clinical implications, this study helps to clarify the risk of future disorders posed by chronologically primary disorders, information that may be used to improve treatment planning and counsel patients at risk of developing secondary disorders."
Citation source:
Sociodemographic and Psychopathologic Predictors of First Incidence of DSM-IV Substance Use, Mood, and Anxiety Disorders: Results from the Wave 2 National Epidemiologic Survey on Alcohol and Related Conditions
Bridget F. Grant, Ph.D., Ph.D.a
Ris?« B. Goldstein, Ph.D., M.P.H. a
S. Patricia Chou, Ph.D. a
Boji Huang, M.D., Ph.D. a
Frederick S. Stinson, Ph.D. a
Deborah A. Dawson, Ph.D. a
Tulshi D. Saha, Ph.D. a
Sharon M. Smith, Ph.D. a
Attila J. Pulay, M.D. a
Roger P. Pickering, M.S. a
W. June Ruan, M.A. a
Wilson M. Compton, M.D., M.P.E.b
Affiliation:
a Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5635 Fishers Ln., M.S. 9304, Bethesda, MD, USA 20892-9304.
b Division of Epidemiology, Services, and Prevention Research, National Institute on Drug Abuse, National Institutes of Health, 6001 Executive Blvd., M.S. 9589, Bethesda, MD, USA 20892-9589.
Molecular Psychiatry
Molecular Psychiatry advance online publication
Molecular Psychiatry is a peer-reviewed independent journal that publishes groundbreaking research in psychiatry and related fields. The journal's Impact Factor is 11.804, 2nd of 95 in Psychiatry
Website: nature/mp
Editor: Julio Licinio, M.D.
University of Miami Miller School of Medicine
This landmark survey is the first conducted in the U.S. to identify rates of first episodes (i.e., incidence) of these disorders in the U.S. population. In addition, it provides information on sociodemographic and psychopathologic risk factors for those disorders - information critical for developing evidence-based preventive interventions - and estimates risk for subsequent comorbid disorders.
Bridget Grant, Ph.D., Chief of NIAAA's Laboratory of Biometry and Epidemiology, and her colleagues found that 1-year incidence rates were highest for DSM-IV alcohol dependence (1.70%), alcohol abuse (1.02%), major depressive disorder (1.51%) and generalized anxiety disorder (1.12%), followed by panic disorder (0.62%), bipolar I disorder (0.53%) and specific phobia (0.44%). One-year incidence rates of DSM-IV social phobia (0.32%), bipolar II (0.21%) and drug abuse (0.28%) and drug dependence (0.32%) were lower but not insignificant. These rates are comparable to or exceed corresponding incidence rates for other common medical diseases such as lung cancer (0.06%), stroke (0.45%) and cardiovascular disease (1.5%).
The study found that men were at greater risk of first onset alcohol abuse, alcohol dependence and drug dependence, and 1-year incidence rates were greatest among 20- to 29-year-olds and individuals who had been separated/divorced/widowed or never married. By contrast, the risk of most incident DSM-IV anxiety disorders, including panic disorder, specific but not social phobia, and generalized anxiety disorder, was greatest among women, and all anxiety disorder incidence rates were greater in the youngest age groups (20- to 54-year-olds). Among DSM-IV mood disorders examined in this study, the risk of first onset of major depressive disorder (MDD) was greatest among women, and no sex differences in incidence were found for bipolar I and II disorders. Taken together, these results highlight age as an important general risk factor for first onset DSM-IV substance use, mood and anxiety disorders, whereas the effects of sex and marital status appear to be disorder-specific.
Consistent with earlier studies, baseline dysthymia in this study predicted incident MDD, and baseline MDD predicted incident bipolar II disorder, suggesting that MDD precedes hypomania in the development of bipolar II disorder. Consistent with other prospective studies, alcohol abuse and dependence showed strong reciprocal temporal relationships, whereas drug abuse predicted only incident drug dependence. "The reciprocal relationship between alcohol abuse and dependence suggests that strong common factors may underlie the relationship and provides support for eliminating the hierarchy between the disorders in future DSM revisions," state the authors. Other intriguing findings include reciprocal temporal relationships between MDD and GAD, and GAD and panic disorder, suggesting that common causes underlie those disorders. In addition, substance use disorders did not predict any incident mood or anxiety disorder, the authors note.
"Information on psychiatric risk factors prospectively identified in this study can begin to inform a new class of preventive interventions aimed at preventing a second disorder or set of disorders," said Grant. "As to clinical implications, this study helps to clarify the risk of future disorders posed by chronologically primary disorders, information that may be used to improve treatment planning and counsel patients at risk of developing secondary disorders."
Citation source:
Sociodemographic and Psychopathologic Predictors of First Incidence of DSM-IV Substance Use, Mood, and Anxiety Disorders: Results from the Wave 2 National Epidemiologic Survey on Alcohol and Related Conditions
Bridget F. Grant, Ph.D., Ph.D.a
Ris?« B. Goldstein, Ph.D., M.P.H. a
S. Patricia Chou, Ph.D. a
Boji Huang, M.D., Ph.D. a
Frederick S. Stinson, Ph.D. a
Deborah A. Dawson, Ph.D. a
Tulshi D. Saha, Ph.D. a
Sharon M. Smith, Ph.D. a
Attila J. Pulay, M.D. a
Roger P. Pickering, M.S. a
W. June Ruan, M.A. a
Wilson M. Compton, M.D., M.P.E.b
Affiliation:
a Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5635 Fishers Ln., M.S. 9304, Bethesda, MD, USA 20892-9304.
b Division of Epidemiology, Services, and Prevention Research, National Institute on Drug Abuse, National Institutes of Health, 6001 Executive Blvd., M.S. 9589, Bethesda, MD, USA 20892-9589.
Molecular Psychiatry
Molecular Psychiatry advance online publication
Molecular Psychiatry is a peer-reviewed independent journal that publishes groundbreaking research in psychiatry and related fields. The journal's Impact Factor is 11.804, 2nd of 95 in Psychiatry
Website: nature/mp
Editor: Julio Licinio, M.D.
University of Miami Miller School of Medicine
понедельник, 20 июня 2011 г.
A New Mental Treatment Based On Attention Improves Anxiety And Depression In Secondary Education Teachers
A doctoral thesis carried out at the University of Granada has proved that a mental training based on mindfulness - an emotional self-regulating tool that consists in focusing on what we are doing, thinking about or feeling at every moment - helps to fight against psychological diseases such as anxiety, depression, concern or complaints about health, very common among secondary education teachers, and is very positive for emotional regulation.
This research work has analysed the psycho-physiological mechanisms related to the mindfulness, checking the effectiveness of a training programme that works as an emotional self-regulating tool. Mindfulness is a type of mental training increasingly popular in the U.S., based on the practice of self-awareness and in terms such as attention, awareness and the reference to a specific moment.
The work, developed by Luis Carlos Delgado Pastor and supervised by professor Jaime Vila Castellar, of the department of Personality, Assessment and Psychological Treatment, has confirmed the effectiveness of training mindfulness abilities applying it to two different groups with defined features: a 20-girls sample with high-level concern and a group of 25 secondary education teachers.
Improvement in both groups
Besides, as a consequence of the mental training, both the girls with chronic concern and the teachers improved their subjective rates of anxiety, depression, concern, complaints about health and emotional regulation, together with certain con psycho-physiological such as, for example, cardiac, muscular and respiratory variables.
Delgado Pastor says that, in the light of the results obtained, they have proved the "effectiveness of training mindfulness abilities and human values in the teaching sector as an emotional self-regulating tool, stress prevention for teachers and students, as well as to facilitate the teaching-learning process".
Accordingly, says the UGR researchers, mindfulness is also useful for persons who are suffering from desadaptative emotional processes, such as chronic concern, anxiety and depression.
Reference: Luis Carlos Delgado Pastor. Department of Personality, Assessment and Psychological Treatment of the University of Granada.
This research work has analysed the psycho-physiological mechanisms related to the mindfulness, checking the effectiveness of a training programme that works as an emotional self-regulating tool. Mindfulness is a type of mental training increasingly popular in the U.S., based on the practice of self-awareness and in terms such as attention, awareness and the reference to a specific moment.
The work, developed by Luis Carlos Delgado Pastor and supervised by professor Jaime Vila Castellar, of the department of Personality, Assessment and Psychological Treatment, has confirmed the effectiveness of training mindfulness abilities applying it to two different groups with defined features: a 20-girls sample with high-level concern and a group of 25 secondary education teachers.
Improvement in both groups
Besides, as a consequence of the mental training, both the girls with chronic concern and the teachers improved their subjective rates of anxiety, depression, concern, complaints about health and emotional regulation, together with certain con psycho-physiological such as, for example, cardiac, muscular and respiratory variables.
Delgado Pastor says that, in the light of the results obtained, they have proved the "effectiveness of training mindfulness abilities and human values in the teaching sector as an emotional self-regulating tool, stress prevention for teachers and students, as well as to facilitate the teaching-learning process".
Accordingly, says the UGR researchers, mindfulness is also useful for persons who are suffering from desadaptative emotional processes, such as chronic concern, anxiety and depression.
Reference: Luis Carlos Delgado Pastor. Department of Personality, Assessment and Psychological Treatment of the University of Granada.
воскресенье, 19 июня 2011 г.
IOF World Congress On Osteoporosis, 2008
Fourteen of the world's leading osteoporosis experts will present plenary lectures at the 2008 IOF World Congress on Osteoporosis (IOF WCO) in Bangkok, Thailand.
"We have selected these speakers for their ability to present the latest science in a format that will be useful for the thousands of health care professionals attending the IOF World Congress on Osteoporosis," noted Professor Cyrus Cooper, Chairman, IOF Committee of Scientific Advisors and Chairman, IOF World Congress on Osteoporosis 2008 Scientific Committee.
The IOF WCO, which will be held from December 3-7, 2008, is the world's largest scientific congress devoted specifically to osteoporosis.
"IOF decided to hold this important event in Asia partly because of the enormous projected growth in osteoporosis in the region," noted Professor Cooper, who pointed out that in 2050 one out of every two osteoporotic fractures will occur in Asia. "Asia also has a large number of committed health care professionals who want to meet with their colleagues from around the world to learn the latest in diagnostics and treatment."
The confirmed plenary lectures and presenters:
Worldwide Epidemiology of Fractures: Differences between East and West
Professor Jane Cauley, USA
An update on the Genetics of Osteoporosis
Dr Andre Uitterlinden, The Netherlands
Brain and Bone: CNS Control of Bone Metabolism
Professor Florent Elefteriou, USA
Cancer Induced Bone Loss
Professor Robert E. Coleman, UK
Novel Mechanisms of Bone Formation (mechanotransduction to sclerostin)
Professor John Bilezikian, USA
Absolute Fracture Risk/Determination and Clinical Usefulness
Professor Eugene McCloskey, UK
Vitamin D Insufficiency: Myth or Reality
Professor Steven Boonen, Belgium
Approaches to the Prevention of Bone Fragility throughout Life: Diet and Exercise
Professor Ego Seeman, Australia
Immune System and Bone
Professor Hiroshi Takayanagi, Japan
Estrogen and Bone in Men and Women
Professor Sundeep Khosla, USA
Economically Effective Osteoporosis Treatment Worldwide
Professor John A. Kanis, UK
Novel / Biologic Therapies in Osteoporosis
Professor Pierre D. Delmas, France
Epidemiology and Risk factors for Osteoarthritis
Professor Cyrus Cooper, UK
Structure Modification in Osteoarthritis: fact or fantasy?
Professor Jean-Yves Reginster, Belgium
Osteoporosis, in which the bones become porous and break easily, is one of the world's most common and debilitating diseases. The result: pain, loss of movement, inability to perform daily chores, and in many cases, death. One out of three women over 50 will experience osteoporotic fractures, as will one out of five men 1, 2, 3. Unfortunately, screening for people at risk is far from being a standard practice. Osteoporosis can, to a certain extent, be prevented, it can be easily diagnosed and effective treatments are available.
The International Osteoporosis Foundation (IOF) is the only worldwide organization dedicated to the fight against osteoporosis. It brings together scientists, physicians, patient societies and corporate partners. Working with its 182 member societies in 88 locations, and other healthcare-related organizations around the world, IOF encourages awareness and prevention, early detection and improved treatment of osteoporosis.
IOF World Congress on Osteoporosis, held every two years, is the only global congress dedicated specifically to all aspects of osteoporosis. Besides the opportunity to learn about the latest science and developments in diagnosis, treatment and the most recent socio-economic studies, participants have the chance to meet and exchange ideas with other physicians from around the world. All aspects of osteoporosis will be covered during the Congress which will comprise lectures by invited speakers presenting cutting edge research in the field, and a large number of oral presentations and poster sessions selected from submitted abstracts. More than 40 Meet the Expert Sessions covering many practical aspects of diagnosis and management of osteoporosis are also on the program.
1. Melton U, Chrischilles EA, Cooper C et al. How many women have osteoporosis? Journal of Bone Mineral Research, 1992; 7:1005-10 2. Kanis JA et al. Long-term risk of osteoporotic fracture in Malmo. Osteoporosis International, 2000; 11:669-674 3. Melton LJ, et al. Bone density and fracture risk in men. JBMR. 1998; 13:No 12:1915
For more information on osteoporosis and IOF please visit: iofbonehealth/
Source: Janice Blondeau
International Osteoporosis Foundation
"We have selected these speakers for their ability to present the latest science in a format that will be useful for the thousands of health care professionals attending the IOF World Congress on Osteoporosis," noted Professor Cyrus Cooper, Chairman, IOF Committee of Scientific Advisors and Chairman, IOF World Congress on Osteoporosis 2008 Scientific Committee.
The IOF WCO, which will be held from December 3-7, 2008, is the world's largest scientific congress devoted specifically to osteoporosis.
"IOF decided to hold this important event in Asia partly because of the enormous projected growth in osteoporosis in the region," noted Professor Cooper, who pointed out that in 2050 one out of every two osteoporotic fractures will occur in Asia. "Asia also has a large number of committed health care professionals who want to meet with their colleagues from around the world to learn the latest in diagnostics and treatment."
The confirmed plenary lectures and presenters:
Worldwide Epidemiology of Fractures: Differences between East and West
Professor Jane Cauley, USA
An update on the Genetics of Osteoporosis
Dr Andre Uitterlinden, The Netherlands
Brain and Bone: CNS Control of Bone Metabolism
Professor Florent Elefteriou, USA
Cancer Induced Bone Loss
Professor Robert E. Coleman, UK
Novel Mechanisms of Bone Formation (mechanotransduction to sclerostin)
Professor John Bilezikian, USA
Absolute Fracture Risk/Determination and Clinical Usefulness
Professor Eugene McCloskey, UK
Vitamin D Insufficiency: Myth or Reality
Professor Steven Boonen, Belgium
Approaches to the Prevention of Bone Fragility throughout Life: Diet and Exercise
Professor Ego Seeman, Australia
Immune System and Bone
Professor Hiroshi Takayanagi, Japan
Estrogen and Bone in Men and Women
Professor Sundeep Khosla, USA
Economically Effective Osteoporosis Treatment Worldwide
Professor John A. Kanis, UK
Novel / Biologic Therapies in Osteoporosis
Professor Pierre D. Delmas, France
Epidemiology and Risk factors for Osteoarthritis
Professor Cyrus Cooper, UK
Structure Modification in Osteoarthritis: fact or fantasy?
Professor Jean-Yves Reginster, Belgium
Osteoporosis, in which the bones become porous and break easily, is one of the world's most common and debilitating diseases. The result: pain, loss of movement, inability to perform daily chores, and in many cases, death. One out of three women over 50 will experience osteoporotic fractures, as will one out of five men 1, 2, 3. Unfortunately, screening for people at risk is far from being a standard practice. Osteoporosis can, to a certain extent, be prevented, it can be easily diagnosed and effective treatments are available.
The International Osteoporosis Foundation (IOF) is the only worldwide organization dedicated to the fight against osteoporosis. It brings together scientists, physicians, patient societies and corporate partners. Working with its 182 member societies in 88 locations, and other healthcare-related organizations around the world, IOF encourages awareness and prevention, early detection and improved treatment of osteoporosis.
IOF World Congress on Osteoporosis, held every two years, is the only global congress dedicated specifically to all aspects of osteoporosis. Besides the opportunity to learn about the latest science and developments in diagnosis, treatment and the most recent socio-economic studies, participants have the chance to meet and exchange ideas with other physicians from around the world. All aspects of osteoporosis will be covered during the Congress which will comprise lectures by invited speakers presenting cutting edge research in the field, and a large number of oral presentations and poster sessions selected from submitted abstracts. More than 40 Meet the Expert Sessions covering many practical aspects of diagnosis and management of osteoporosis are also on the program.
1. Melton U, Chrischilles EA, Cooper C et al. How many women have osteoporosis? Journal of Bone Mineral Research, 1992; 7:1005-10 2. Kanis JA et al. Long-term risk of osteoporotic fracture in Malmo. Osteoporosis International, 2000; 11:669-674 3. Melton LJ, et al. Bone density and fracture risk in men. JBMR. 1998; 13:No 12:1915
For more information on osteoporosis and IOF please visit: iofbonehealth/
Source: Janice Blondeau
International Osteoporosis Foundation
New Model For Probing Antidepressant Actions
The most widely prescribed antidepressants - medicines such as Prozac, Lexapro and Paxil - work by blocking the serotonin transporter, a brain protein that normally clears away the mood-regulating chemical serotonin. Or so the current thinking goes.
That theory about how selective serotonin reuptake inhibitors (SSRIs) work can now be put to the test with a new mouse model developed by neuroscientists at Vanderbilt University.
These mice, described in the online edition of the Proceedings of the National Academy of Sciences (PNAS), express a serotonin transporter that has been genetically altered so that it does not respond to many SSRIs or cocaine.
In addition to testing the theory about how SSRIs work, the new mouse model could lead to the development of entirely new classes of antidepressant medications, said Randy Blakely, Ph.D., Allan D. Bass Professor of Pharmacology and Psychiatry at Vanderbilt and senior author of the PNAS paper.
"Many antidepressants have been shown to target other proteins besides the serotonin transporter and ... their efficacy in treating depression takes many weeks to develop," Blakely said. "There is likely a lot that we don't know about how these drugs act."
To generate the mouse model, Blakely and colleagues at Vanderbilt and the University of Texas Health Science Center at San Antonio first determined exactly which parts of the serotonin transporter protein interact with SSRIs. They took advantage of the fact that the fruit fly expresses a serotonin transporter that is relatively insensitive to the drugs.
By changing the protein's amino acid building blocks, they converted parts of the human serotonin transporter into its fruit fly equivalent, and in so doing identified the single amino acid required for potent binding to many SSRIs as well as to cocaine.
As predicted, the genetically-modified mice displayed normal serotonin transporter levels, and their transporter exhibited normal activity in clearing serotonin from the synapses between nerve cells. But the mice did not respond to Prozac or Lexapro, indicating that the transporter is indeed the specific target of these medications for blocking serotonin inactivation.
"Interestingly, one SSRI, paroxetine (Paxil), retains its normal powerful action on the transporter, revealing that - at a molecular level - different antidepressants interact with the transporter in different ways," Blakely said.
The researchers are now evaluating chronic administration of SSRIs to determine how much the transporter contributes to the more clinically relevant, delayed effects of these drugs, as well as for the side effects experience with antidepressant medications.
Because the serotonin transporter in the mouse also lost cocaine sensitivity, the model also may help researchers determine exactly how cocaine acts in the brain. "Perhaps what started as a hunt for better ways to treat depression may also spill over into a better understanding of addiction," Blakely said.
Notes:
Brent Thompson, Ph.D., is the first author of the PNAS paper. Blakely directs the Center for Molecular Neuroscience and the Silvio O. Conte Center for Neuroscience Research at Vanderbilt.
Douglas McMahon, Ph.D., professor of Biological Sciences and Pharmacology at Vanderbilt, also collaborated on the research, which was supported by the National Institutes of Health.
That theory about how selective serotonin reuptake inhibitors (SSRIs) work can now be put to the test with a new mouse model developed by neuroscientists at Vanderbilt University.
These mice, described in the online edition of the Proceedings of the National Academy of Sciences (PNAS), express a serotonin transporter that has been genetically altered so that it does not respond to many SSRIs or cocaine.
In addition to testing the theory about how SSRIs work, the new mouse model could lead to the development of entirely new classes of antidepressant medications, said Randy Blakely, Ph.D., Allan D. Bass Professor of Pharmacology and Psychiatry at Vanderbilt and senior author of the PNAS paper.
"Many antidepressants have been shown to target other proteins besides the serotonin transporter and ... their efficacy in treating depression takes many weeks to develop," Blakely said. "There is likely a lot that we don't know about how these drugs act."
To generate the mouse model, Blakely and colleagues at Vanderbilt and the University of Texas Health Science Center at San Antonio first determined exactly which parts of the serotonin transporter protein interact with SSRIs. They took advantage of the fact that the fruit fly expresses a serotonin transporter that is relatively insensitive to the drugs.
By changing the protein's amino acid building blocks, they converted parts of the human serotonin transporter into its fruit fly equivalent, and in so doing identified the single amino acid required for potent binding to many SSRIs as well as to cocaine.
As predicted, the genetically-modified mice displayed normal serotonin transporter levels, and their transporter exhibited normal activity in clearing serotonin from the synapses between nerve cells. But the mice did not respond to Prozac or Lexapro, indicating that the transporter is indeed the specific target of these medications for blocking serotonin inactivation.
"Interestingly, one SSRI, paroxetine (Paxil), retains its normal powerful action on the transporter, revealing that - at a molecular level - different antidepressants interact with the transporter in different ways," Blakely said.
The researchers are now evaluating chronic administration of SSRIs to determine how much the transporter contributes to the more clinically relevant, delayed effects of these drugs, as well as for the side effects experience with antidepressant medications.
Because the serotonin transporter in the mouse also lost cocaine sensitivity, the model also may help researchers determine exactly how cocaine acts in the brain. "Perhaps what started as a hunt for better ways to treat depression may also spill over into a better understanding of addiction," Blakely said.
Notes:
Brent Thompson, Ph.D., is the first author of the PNAS paper. Blakely directs the Center for Molecular Neuroscience and the Silvio O. Conte Center for Neuroscience Research at Vanderbilt.
Douglas McMahon, Ph.D., professor of Biological Sciences and Pharmacology at Vanderbilt, also collaborated on the research, which was supported by the National Institutes of Health.
суббота, 18 июня 2011 г.
Low Income Associated With Mental Disorders And Suicide Attempts
Low levels of household income are associated with several lifetime mental disorders and suicide attempts, and a decrease in income is associated with a higher risk for anxiety, substance use, and mood disorders, according to a report in the April issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
"To date, findings on the relationship between income and mental illness have been mixed," the authors write as background information in the article. "Some studies have found that lower income is associated with mental illness, while other studies have not found this relationship."
Jitender Sareen, M.D., FRCPC, of the University of Manitoba, Winnipeg, Canada, and colleagues analyzed data from the U.S. National Epidemiologic Survey of Alcohol and Related Conditions - the largest longitudinal, population-based mental health survey - to examine the relationship between income, mental disorders, and suicide attempts. A total of 34,653 non-institutionalized U.S. adults, age 20 years and older, were interviewed twice, three years apart.
"Participants with household income of less than $20,000 per year were at increased risk of incident mood disorders during the three-year follow-up period in comparison with those with income of $70,000 or more per year," the authors report.
"A decrease in household income during the two time points was also associated with an increased risk of incident mood, anxiety, or substance use disorders in comparison with respondents with no change in income," they write.
An increase in income during the follow-up period was not associated with any increase or decrease in the risk of developing mental disorders.
The authors believe their study findings have important public health implications.
"Most important, the findings suggest that income below $20,000 per year is associated with substantial psychopathologic characteristics and that there is a need for targeted interventions to treat and prevent mental illness in this low-income sector of the population," they conclude. "The findings also suggest that adults with reduction in income are at increased risk of mood and substance use disorders."
Arch Gen Psychiatry. 2011;68[4]:419-427.
"To date, findings on the relationship between income and mental illness have been mixed," the authors write as background information in the article. "Some studies have found that lower income is associated with mental illness, while other studies have not found this relationship."
Jitender Sareen, M.D., FRCPC, of the University of Manitoba, Winnipeg, Canada, and colleagues analyzed data from the U.S. National Epidemiologic Survey of Alcohol and Related Conditions - the largest longitudinal, population-based mental health survey - to examine the relationship between income, mental disorders, and suicide attempts. A total of 34,653 non-institutionalized U.S. adults, age 20 years and older, were interviewed twice, three years apart.
"Participants with household income of less than $20,000 per year were at increased risk of incident mood disorders during the three-year follow-up period in comparison with those with income of $70,000 or more per year," the authors report.
"A decrease in household income during the two time points was also associated with an increased risk of incident mood, anxiety, or substance use disorders in comparison with respondents with no change in income," they write.
An increase in income during the follow-up period was not associated with any increase or decrease in the risk of developing mental disorders.
The authors believe their study findings have important public health implications.
"Most important, the findings suggest that income below $20,000 per year is associated with substantial psychopathologic characteristics and that there is a need for targeted interventions to treat and prevent mental illness in this low-income sector of the population," they conclude. "The findings also suggest that adults with reduction in income are at increased risk of mood and substance use disorders."
Arch Gen Psychiatry. 2011;68[4]:419-427.
пятница, 17 июня 2011 г.
Early Abuse Tied To More Depression In Children
Although children can be depressed for many reasons, new evidence suggests that there are physiological differences among depressed children based on their experiences of abuse before age 5. Early abuse may be especially damaging due to the very young age at which it occurs.
Those are the findings of a new study of low-income children that was conducted by researchers at the University of Minnesota and the University of Rochester, Mt. Hope Family Center. The study appears in the January/February 2010 issue of the journal Child Development.
Children who experience maltreatment, including physical, sexual, and emotional abuse or neglect, grow up with a lot of stress. Cortisol, termed the "stress hormone," helps the body regulate stress. But when stress is chronic and overloads the system, cortisol can soar to very high levels or plummet to lows, which in turn can harm development and health.
The researchers studied more than 500 low-income children ages 7 to 13, about half of whom had been abused and/or neglected, to find out whether abuse early in life and feelings of depression affected their levels of cortisol. High levels of depression were more frequent among children who were abused in the first five years of their lives than among maltreated children who weren't abused early in life or children who weren't maltreated at all.
More importantly, only children who were abused before age 5 and depressed had an atypical flattening of cortisol production during the day, whereas other children, whether they were depressed or not, showed an expected daily decline in cortisol from morning to afternoon. This finding means that the body's primary system for adapting to stress had become compromised among children who were depressed and abused early in life. The results suggest that there are different subtypes of depression, with atypical cortisol regulation occurring among children who were abused before age 5.
The authors suggest that early abuse may be more damaging to developing emotion and stress systems because it happens as the brain is rapidly developing and when children are more dependent on caregivers' protection. Moreover, because it's harder for very young children to discern the clues predicting an abusive attack, they may be chronically stressed and overly vigilant, even when they're not being abused.
"In the United States, more than 1.5 million children are abused and neglected every year, though it's estimated that the actual rates are substantially greater," according to Dante Cicchetti, McKnight Presidential Chair and professor of child development and psychiatry at the University of Minnesota, who led the study.
"The results of this study have significant implications for children in the child welfare population and underscore the importance of providing early preventive interventions to children who have been abused."
Those are the findings of a new study of low-income children that was conducted by researchers at the University of Minnesota and the University of Rochester, Mt. Hope Family Center. The study appears in the January/February 2010 issue of the journal Child Development.
Children who experience maltreatment, including physical, sexual, and emotional abuse or neglect, grow up with a lot of stress. Cortisol, termed the "stress hormone," helps the body regulate stress. But when stress is chronic and overloads the system, cortisol can soar to very high levels or plummet to lows, which in turn can harm development and health.
The researchers studied more than 500 low-income children ages 7 to 13, about half of whom had been abused and/or neglected, to find out whether abuse early in life and feelings of depression affected their levels of cortisol. High levels of depression were more frequent among children who were abused in the first five years of their lives than among maltreated children who weren't abused early in life or children who weren't maltreated at all.
More importantly, only children who were abused before age 5 and depressed had an atypical flattening of cortisol production during the day, whereas other children, whether they were depressed or not, showed an expected daily decline in cortisol from morning to afternoon. This finding means that the body's primary system for adapting to stress had become compromised among children who were depressed and abused early in life. The results suggest that there are different subtypes of depression, with atypical cortisol regulation occurring among children who were abused before age 5.
The authors suggest that early abuse may be more damaging to developing emotion and stress systems because it happens as the brain is rapidly developing and when children are more dependent on caregivers' protection. Moreover, because it's harder for very young children to discern the clues predicting an abusive attack, they may be chronically stressed and overly vigilant, even when they're not being abused.
"In the United States, more than 1.5 million children are abused and neglected every year, though it's estimated that the actual rates are substantially greater," according to Dante Cicchetti, McKnight Presidential Chair and professor of child development and psychiatry at the University of Minnesota, who led the study.
"The results of this study have significant implications for children in the child welfare population and underscore the importance of providing early preventive interventions to children who have been abused."
четверг, 16 июня 2011 г.
Persons With Serious Mental Illness Face Higher Prevalence Of Obesity
Obesity is a public health crisis within the general population; however, overweight and obesity issues are even more prevalent in persons with serious mental illness, according to a new report, scheduled to be released on October 3, 2008 by the National Association of State Mental Health Program Directors (NASMHPD).
Findings and recommendations from the report appear in the September 22 issue of Mental Health Weekly, making the journal the first major media outlet to inform the public of this new technical report.
NASMHPD calls the crisis "an epidemic within an epidemic," and say they hope the new report will go a long way toward improving the systems that provide care and treatment to the SMI population.
The specific recommendations, when implemented, should substantially reduce the weight and improve the overall health of a population with SMI, according to NASMHPD. "This report can be viewed as a rallying call for more prevention and intervention strategies for people with SMI struggling with obesity issues," said Robert W. Glover, Ph.D., NASMHPD executive director.
The report also notes that some medications can cause weight gain for people with SMI, and notes that medications that are more weight neutral should be considered by physicians. "Medical interventions are needed to address issues with medications that can cause obesity and that includes behavior and counseling treatments, medications for weight loss, and surgery," said Joseph Parks, M.D., chair of the NASMHPD Medical Directors Council and medical director for the Missouri Department of Mental Health.
The report, Obesity & Prevention Strategies for Individuals with Serious Mental Illness, represents the 15th in a series of technical reports. Two years ago, NASMHPD released its report, Morbidity and Mortality in People with Serious Mental Illness, which found that people with SMI die 25 years sooner than the general population.
In its new report, NASMHPD has issued a series of recommendations at the national, state and local levels. Recommendations include the implementation of national obesity surveillance/monitoring system for persons with SMI and the promotion of opportunities for healthcare providers, including peer specialists, to teach health lifestyles to families, individuals and older adults.
Mental Health Weekly provides information on business trends, state funding and policy issues, litigation, and more. The publication is a trustworthy source for community-based mental health program directors, hospital administrators and others in the mental healthcare profession.
About Wiley
Founded in 1807, John Wiley & Sons provides must-have content and services to customers worldwide. Its core businesses include scientific, technical, and medical journals, encyclopedias, books and online products and services; professional and consumer books and subscription services; and educational materials for undergraduate and graduate students and lifelong learners. Wiley has publishing, marketing, and distribution centers in the United States, Canada, Europe, Asia, and Australia. The company's corporate headquarters is located in Hoboken, New Jersey. The company is listed on the New York Stock Exchange under the symbols JWa and JWb. Wiley's internet site can be accessed at wiley.
John Wiley & Sons
Findings and recommendations from the report appear in the September 22 issue of Mental Health Weekly, making the journal the first major media outlet to inform the public of this new technical report.
NASMHPD calls the crisis "an epidemic within an epidemic," and say they hope the new report will go a long way toward improving the systems that provide care and treatment to the SMI population.
The specific recommendations, when implemented, should substantially reduce the weight and improve the overall health of a population with SMI, according to NASMHPD. "This report can be viewed as a rallying call for more prevention and intervention strategies for people with SMI struggling with obesity issues," said Robert W. Glover, Ph.D., NASMHPD executive director.
The report also notes that some medications can cause weight gain for people with SMI, and notes that medications that are more weight neutral should be considered by physicians. "Medical interventions are needed to address issues with medications that can cause obesity and that includes behavior and counseling treatments, medications for weight loss, and surgery," said Joseph Parks, M.D., chair of the NASMHPD Medical Directors Council and medical director for the Missouri Department of Mental Health.
The report, Obesity & Prevention Strategies for Individuals with Serious Mental Illness, represents the 15th in a series of technical reports. Two years ago, NASMHPD released its report, Morbidity and Mortality in People with Serious Mental Illness, which found that people with SMI die 25 years sooner than the general population.
In its new report, NASMHPD has issued a series of recommendations at the national, state and local levels. Recommendations include the implementation of national obesity surveillance/monitoring system for persons with SMI and the promotion of opportunities for healthcare providers, including peer specialists, to teach health lifestyles to families, individuals and older adults.
Mental Health Weekly provides information on business trends, state funding and policy issues, litigation, and more. The publication is a trustworthy source for community-based mental health program directors, hospital administrators and others in the mental healthcare profession.
About Wiley
Founded in 1807, John Wiley & Sons provides must-have content and services to customers worldwide. Its core businesses include scientific, technical, and medical journals, encyclopedias, books and online products and services; professional and consumer books and subscription services; and educational materials for undergraduate and graduate students and lifelong learners. Wiley has publishing, marketing, and distribution centers in the United States, Canada, Europe, Asia, and Australia. The company's corporate headquarters is located in Hoboken, New Jersey. The company is listed on the New York Stock Exchange under the symbols JWa and JWb. Wiley's internet site can be accessed at wiley.
John Wiley & Sons
среда, 15 июня 2011 г.
Prozac Gene Test Good For Patients, Royal College Of Psychiatrists
People who suffer depression that does not respond to medication could be treated successfully if a simple genetic blood test was made more widely available in the UK.
Four out of 10 people with depression have a genetic abnormality that prevents them responding to anti-depressant medication, according to research presented at the Royal College of Psychiatrists' Annual Meeting in London this week.
The research, which was carried out at the Mayo Clinic Mood Disorders Unit in the USA, showed that a quarter of those with a genetic abnormality produce a liver enzyme that either stops Prozac working or causes unpleasant side-effects.
Since 2003, the Mayo Clinic has offered genotyping to patients who either report significant side-effects to antidepressants or have no response.
They have identified four genes that interfere with the efficacy of antidepressant medication, including two that prevent metabolising the drug (CYP2D6 and CYP2C19) and two more that prevent the brain from absorbing or transporting serotonin.
Professor David Mrazek, chair of the Department of Psychiatry at the Mayo Clinic College of Medicine, said: "One in 10 of our patients have abnormal CYP2D6, the gene most commonly implicated in treatment-resistant depression. This means that they are poor at metabolising some common anti-depressant medication including Prozac and Seroxat. As a result, they may get adverse effects including nausea, headache, vomiting and sexual problems, from a regular or even low dose of the drug."
So far, genotyping - which costs about ??150 per gene tested - is not widely available in the UK.
"The cost of the test may be a barrier to more frequent use of genotyping," Professor Mrazek said. "But most good insurance companies now pay for the test for people who have treatment-resistant depression, either because the drugs don't work or they suffer excessive side-effects. It is now proven beyond doubt that in many cases, unpleasant side effects can be avoided with this simple blood test."
Genotyping for depression became widely known in the USA following publication of the best-seller autobiography, Mommies Cry Too, by Carolyn Brink in 2006. Brink was diagnosed with severe postpartum depression shortly after the birth of her first child. But her treatment with three different antidepressants made the depression worse and led to suicidal feelings. She claimed the Mayo Clinic saved her life when the genotyping test showed that the antidepressant medication she was taking became toxic in her bloodstream due to her low metabolism rate for this type of medication.
Reference
The Annual Meeting of the Royal College of Psychiatrists, Imperial College, London,
1 - 4 July 2008
The Royal College of Psychiatrists
rcpsych.ac.uk
View drug information on Prozac Weekly.
Four out of 10 people with depression have a genetic abnormality that prevents them responding to anti-depressant medication, according to research presented at the Royal College of Psychiatrists' Annual Meeting in London this week.
The research, which was carried out at the Mayo Clinic Mood Disorders Unit in the USA, showed that a quarter of those with a genetic abnormality produce a liver enzyme that either stops Prozac working or causes unpleasant side-effects.
Since 2003, the Mayo Clinic has offered genotyping to patients who either report significant side-effects to antidepressants or have no response.
They have identified four genes that interfere with the efficacy of antidepressant medication, including two that prevent metabolising the drug (CYP2D6 and CYP2C19) and two more that prevent the brain from absorbing or transporting serotonin.
Professor David Mrazek, chair of the Department of Psychiatry at the Mayo Clinic College of Medicine, said: "One in 10 of our patients have abnormal CYP2D6, the gene most commonly implicated in treatment-resistant depression. This means that they are poor at metabolising some common anti-depressant medication including Prozac and Seroxat. As a result, they may get adverse effects including nausea, headache, vomiting and sexual problems, from a regular or even low dose of the drug."
So far, genotyping - which costs about ??150 per gene tested - is not widely available in the UK.
"The cost of the test may be a barrier to more frequent use of genotyping," Professor Mrazek said. "But most good insurance companies now pay for the test for people who have treatment-resistant depression, either because the drugs don't work or they suffer excessive side-effects. It is now proven beyond doubt that in many cases, unpleasant side effects can be avoided with this simple blood test."
Genotyping for depression became widely known in the USA following publication of the best-seller autobiography, Mommies Cry Too, by Carolyn Brink in 2006. Brink was diagnosed with severe postpartum depression shortly after the birth of her first child. But her treatment with three different antidepressants made the depression worse and led to suicidal feelings. She claimed the Mayo Clinic saved her life when the genotyping test showed that the antidepressant medication she was taking became toxic in her bloodstream due to her low metabolism rate for this type of medication.
Reference
The Annual Meeting of the Royal College of Psychiatrists, Imperial College, London,
1 - 4 July 2008
The Royal College of Psychiatrists
rcpsych.ac.uk
View drug information on Prozac Weekly.
вторник, 14 июня 2011 г.
Comprehensive Analysis Shows Sertraline And Escitalopram Are The Best Of 12 New-Generation Antidepressants
A comprehensive meta-analysis of 12 new-generation antidepressants has shown sertraline and escitalopram have clear advantages in terms of efficacy and acceptability, while reboxetine was shown to be the significantly less efficacious than the other 11 drugs. The findings appear in an Article published Online First and in an upcoming edition of The Lancet, written by Dr Andrea Cipriani, University of Verona, Italy, and colleagues.
The study analysed results of 117 randomised controlled trials from 1991-2007, which compared the effects of these antidepressants in more than 25,000 patients with major depression. The drugs tested were bupropion, citalopram, duloxetine, escitalopram, fluoxetine, fluvoxamine, milnacipran, mirtazapine, paroxetine, reboxetine, sertraline, and venlafaxine. The main outcomes were the proportion of patients who responded to or dropped out of the allocated treatment.
Sertraline and escitalopram were found to be the best antidepressants overall in terms of efficacy and acceptability. Sertraline was more efficacious than duloxetine (by 30%), than both duloxetine and fluvoxamine (by 27% for both), 25% fluoxetine (by 25%), paroxetine (by 22%), reboxetine (by 85%). Escilatopram was more efficacious than duloxetine (by 33%), fluoxetine (by 32%), fluvoxamine (by 35%), paroxetine (by 30%), and reboxetine (by 95%). As with sertraline and escitalopram, mirtazapine and venlafaxine were also more efficacious than these other drugs. However, escilatopram and sertraline showed the best profile of acceptability, leading to significantly fewer discontinuations of treatment than did duloxetine, fluvoxamine, paroxetine, reboxetine, and venlafaxine.
The authors conclude: "The most important clinical implication of the results is that escitalopram and sertraline might be the best choice when starting a treatment for moderate to severe major depression because they have the best possible balance between efficacy and acceptability."
They add: "Sertraline seems to be better than escitalopram because of its lower cost in most countries. However, in the absence of a full economic model, this recommendation cannot be made unequivocally because several other costs are associated with the use of antidepressants."
In an accompanying Comment, Dr Sagar V Parikh, Department of Psychiatry, University of Toronto and University Health Network, Toronto, ON, Canada, says: "A key challenge now involves the issue of costs and benefits; while the generic agents are cheaper to buy, proper studies are needed to aid societal choices among the four strongest antidepressants. As Cipriani and colleagues have emphasised, such cost concerns are particularly crucial from a global perspective, because most people live in low-income and middle-income countries."
Tony Kirby
Press Officer
The Lancet
32 Jamestown Road
Camden
London
NW1 7B
thelancet
The study analysed results of 117 randomised controlled trials from 1991-2007, which compared the effects of these antidepressants in more than 25,000 patients with major depression. The drugs tested were bupropion, citalopram, duloxetine, escitalopram, fluoxetine, fluvoxamine, milnacipran, mirtazapine, paroxetine, reboxetine, sertraline, and venlafaxine. The main outcomes were the proportion of patients who responded to or dropped out of the allocated treatment.
Sertraline and escitalopram were found to be the best antidepressants overall in terms of efficacy and acceptability. Sertraline was more efficacious than duloxetine (by 30%), than both duloxetine and fluvoxamine (by 27% for both), 25% fluoxetine (by 25%), paroxetine (by 22%), reboxetine (by 85%). Escilatopram was more efficacious than duloxetine (by 33%), fluoxetine (by 32%), fluvoxamine (by 35%), paroxetine (by 30%), and reboxetine (by 95%). As with sertraline and escitalopram, mirtazapine and venlafaxine were also more efficacious than these other drugs. However, escilatopram and sertraline showed the best profile of acceptability, leading to significantly fewer discontinuations of treatment than did duloxetine, fluvoxamine, paroxetine, reboxetine, and venlafaxine.
The authors conclude: "The most important clinical implication of the results is that escitalopram and sertraline might be the best choice when starting a treatment for moderate to severe major depression because they have the best possible balance between efficacy and acceptability."
They add: "Sertraline seems to be better than escitalopram because of its lower cost in most countries. However, in the absence of a full economic model, this recommendation cannot be made unequivocally because several other costs are associated with the use of antidepressants."
In an accompanying Comment, Dr Sagar V Parikh, Department of Psychiatry, University of Toronto and University Health Network, Toronto, ON, Canada, says: "A key challenge now involves the issue of costs and benefits; while the generic agents are cheaper to buy, proper studies are needed to aid societal choices among the four strongest antidepressants. As Cipriani and colleagues have emphasised, such cost concerns are particularly crucial from a global perspective, because most people live in low-income and middle-income countries."
Tony Kirby
Press Officer
The Lancet
32 Jamestown Road
Camden
London
NW1 7B
thelancet
понедельник, 13 июня 2011 г.
Depression And Alzheimer's
"Depression may increase the risk of developing Alzheimer's", The Daily Telegraph says. It reports on a study that followed more than 900 Catholic clergy for up to 13 years. The study found that those who developed the disease had more symptoms of depression at the beginning of the study.
The main aim of the research was to look at changes in depressive symptoms in the early stages of Alzheimer's. There is a known association between dementia and depression. However, there are different theories as to whether depression causes Alzheimer's or whether they both develop because of a separate cause. By investigating changes in the severity of depression around the time that dementia develops, the researchers hoped to shed some light on the debate.
Their study found no increase in depressive symptoms before Alzheimer's became evident. This suggests that depression is not an early sign of the same processes that cause dementia. The researchers say that this therefore implies that depressive symptoms are a risk factor for Alzheimer's.
This study challenges the theory that depression and dementia are caused by another factor. It therefore adds weight to, but does not prove, the theory that depression is a risk factor for dementia. However, this study has shortcomings, and further research that is free of these should provide a clearer picture. Until more is known, depression sufferers should not be overly worried that they will develop dementia.
Where did the story come from?
Dr Robert Wilson and colleagues from the Rush University Medical Center, Chicago, and the Center for Neurobiology and Behaviour at the University of Pennsylvania carried out the research. The study was funded by the National Institute of Aging. It was published in Archives of General Psychiatry, a peer-reviewed medical journal.
What kind of scientific study was this?
This was a cohort study designed to investigate the theory that depressive symptoms increase during the early stages of Alzheimer's.
The researchers used participants from the Religious Orders Study, which has been investigating ageing and Alzheimer's in a group of Catholic nuns, priests and brothers since 1994. The researchers excluded those who already had dementia by giving the participants a clinical assessment to identify those with mild cognitive impairment or Alzheimer's.
The researchers then identified those with depression using a recognised scale and gave them a score that related to the number of symptoms reported. They also asked about certain personality characteristics and looked at past medical history.
Each year, the participants completed a depression scale to score their symptoms, and underwent a complete neurological examination to identify any mild cognitive impairment or onset of dementia.
When the researchers analysed their results, 917 people were available who had been in the study for an average of eight years. Alzheimer's was the only form of dementia that the researchers were interested in, so people who developed other types of dementia were excluded.
The researchers were particularly interested in how depressive symptoms changed once Alzheimer's had developed while taking into account other factors that could affect depression, such as age, sex, level of education, personality and vascular conditions. They also considered whether the number of symptoms at the start of the study was associated with an increased risk of Alzheimer's disease.
What were the results of the study?
The main finding from this study was that depressive symptoms did not change prior to the diagnosis of Alzheimer's disease being made, or following diagnosis.
During follow up, 190 participants went on to develop Alzheimer's after an average of four years of follow up. They tended to be older and had poorer mental state scores as well as greater problems with memory and cognition at the beginning of the study.
The researchers confirmed the findings of previous studies by noting an association (not necessarily causal) between the measure of depression at the start of the study and incidence of Alzheimer's disease. Those who developed Alzheimer's were also older, had lower levels of cognitive function, were more concerned about their memory and had different personalities.
What interpretations did the researchers draw from these results?
The authors conclude that there is no increase in depressive symptoms during the early stages of Alzheimer's disease. They say that these results do not support the 'reverse causality' theory about depression and Alzheimer's, i.e. that depression is an early sign of the processes leading to dementia. The study therefore implies that depression may be a risk factor for Alzheimer's disease.
What does the NHS Knowledge Service make of this study?
This study was set up to investigate whether symptoms of depression increased prior to dementia becoming established. It was carefully conducted and included a large number of medical assessments using recognised clinical criteria for diagnosing disease.
However, it should be noted that the participants were all older members of a religious order whose lifestyle and health behaviour may differ significantly from the general population. The participants also reported their symptoms themselves. Self reporting can introduce some error, particularly in people with cognitive impairment. Additionally, despite being a relatively large study, the number of people who went on to develop Alzheimer's was quite small. Much larger numbers would be useful to draw more meaningful results. Finally, although the researchers tried to account for factors associated with the condition, such as age and family history, it is unclear whether their analysis has accomplished this fully.
Rather than investigating whether depression causes Alzheimer's, this study was actually set up to investigate the theory that depression is an early indicator of the processes that cause dementia. It did not find evidence to support this theory.
It is often difficult to unpick the complexities of causation and association. Studies such as this add to the body of evidence behind the different theories. With the current level of knowledge, sufferers of depression should not be overly worried that they are at an increased risk of developing Alzheimer's.
Links to the headlines
Depression linked to Alzheimer's. BBC News, April 09 2008
This news comes from NHS Choices
The main aim of the research was to look at changes in depressive symptoms in the early stages of Alzheimer's. There is a known association between dementia and depression. However, there are different theories as to whether depression causes Alzheimer's or whether they both develop because of a separate cause. By investigating changes in the severity of depression around the time that dementia develops, the researchers hoped to shed some light on the debate.
Their study found no increase in depressive symptoms before Alzheimer's became evident. This suggests that depression is not an early sign of the same processes that cause dementia. The researchers say that this therefore implies that depressive symptoms are a risk factor for Alzheimer's.
This study challenges the theory that depression and dementia are caused by another factor. It therefore adds weight to, but does not prove, the theory that depression is a risk factor for dementia. However, this study has shortcomings, and further research that is free of these should provide a clearer picture. Until more is known, depression sufferers should not be overly worried that they will develop dementia.
Where did the story come from?
Dr Robert Wilson and colleagues from the Rush University Medical Center, Chicago, and the Center for Neurobiology and Behaviour at the University of Pennsylvania carried out the research. The study was funded by the National Institute of Aging. It was published in Archives of General Psychiatry, a peer-reviewed medical journal.
What kind of scientific study was this?
This was a cohort study designed to investigate the theory that depressive symptoms increase during the early stages of Alzheimer's.
The researchers used participants from the Religious Orders Study, which has been investigating ageing and Alzheimer's in a group of Catholic nuns, priests and brothers since 1994. The researchers excluded those who already had dementia by giving the participants a clinical assessment to identify those with mild cognitive impairment or Alzheimer's.
The researchers then identified those with depression using a recognised scale and gave them a score that related to the number of symptoms reported. They also asked about certain personality characteristics and looked at past medical history.
Each year, the participants completed a depression scale to score their symptoms, and underwent a complete neurological examination to identify any mild cognitive impairment or onset of dementia.
When the researchers analysed their results, 917 people were available who had been in the study for an average of eight years. Alzheimer's was the only form of dementia that the researchers were interested in, so people who developed other types of dementia were excluded.
The researchers were particularly interested in how depressive symptoms changed once Alzheimer's had developed while taking into account other factors that could affect depression, such as age, sex, level of education, personality and vascular conditions. They also considered whether the number of symptoms at the start of the study was associated with an increased risk of Alzheimer's disease.
What were the results of the study?
The main finding from this study was that depressive symptoms did not change prior to the diagnosis of Alzheimer's disease being made, or following diagnosis.
During follow up, 190 participants went on to develop Alzheimer's after an average of four years of follow up. They tended to be older and had poorer mental state scores as well as greater problems with memory and cognition at the beginning of the study.
The researchers confirmed the findings of previous studies by noting an association (not necessarily causal) between the measure of depression at the start of the study and incidence of Alzheimer's disease. Those who developed Alzheimer's were also older, had lower levels of cognitive function, were more concerned about their memory and had different personalities.
What interpretations did the researchers draw from these results?
The authors conclude that there is no increase in depressive symptoms during the early stages of Alzheimer's disease. They say that these results do not support the 'reverse causality' theory about depression and Alzheimer's, i.e. that depression is an early sign of the processes leading to dementia. The study therefore implies that depression may be a risk factor for Alzheimer's disease.
What does the NHS Knowledge Service make of this study?
This study was set up to investigate whether symptoms of depression increased prior to dementia becoming established. It was carefully conducted and included a large number of medical assessments using recognised clinical criteria for diagnosing disease.
However, it should be noted that the participants were all older members of a religious order whose lifestyle and health behaviour may differ significantly from the general population. The participants also reported their symptoms themselves. Self reporting can introduce some error, particularly in people with cognitive impairment. Additionally, despite being a relatively large study, the number of people who went on to develop Alzheimer's was quite small. Much larger numbers would be useful to draw more meaningful results. Finally, although the researchers tried to account for factors associated with the condition, such as age and family history, it is unclear whether their analysis has accomplished this fully.
Rather than investigating whether depression causes Alzheimer's, this study was actually set up to investigate the theory that depression is an early indicator of the processes that cause dementia. It did not find evidence to support this theory.
It is often difficult to unpick the complexities of causation and association. Studies such as this add to the body of evidence behind the different theories. With the current level of knowledge, sufferers of depression should not be overly worried that they are at an increased risk of developing Alzheimer's.
Links to the headlines
Depression linked to Alzheimer's. BBC News, April 09 2008
This news comes from NHS Choices
воскресенье, 12 июня 2011 г.
"Cosmetic Surgery And The Use Of Antidepressant Medication"
It has been proven that plastic surgery can improve self-esteem, but can it also act as a natural mood enhancer? A significant number of patients stopped taking antidepressant medication after undergoing plastic surgery, according to a study presented at the American Society of Plastic Surgeons (ASPS) Plastic Surgery 2006 conference in San Francisco.
"Plastic surgery patients are taking a proactive approach in making themselves happier by improving something that has truly bothered them," said Bruce Freedman, MD, ASPS Member Surgeon and study author. "While we are not saying that cosmetic plastic surgery alone is responsible for the drop in patients needing antidepressants, it surely is an important factor."
In the study, 362 patients had cosmetic plastic surgery - 17 percent or 61 patients were taking antidepressants. Six months after surgery, however, that number decreased 31 percent, down to 42 patients. In addition, 98 percent of patients said cosmetic plastic surgery had markedly improved their self-esteem.
All of the patients, who were primarily middle-aged women, had an invasive cosmetic plastic surgery procedure such as breast augmentation, tummy tuck or facelift. The authors did not identify any other major life changes that may have affected patients' use of antidepressants.
"We have just begun to uncover the various physical and psychological benefits of plastic surgery," said Dr. Freedman. "By helping our patients take control over something they were unhappy about, we helped remove a self-imposed barrier and ultimately improved their self-esteem."
For referrals to ASPS Member Surgeons certified by the American Board of Plastic Surgery visit plasticsurgery/ where you can also learn more about cosmetic and reconstructive plastic surgery.
The American Society of Plastic Surgeons is the largest organization of board-certified plastic surgeons in the world. With more than 6,000 members, the society is recognized as a leading authority and information source on cosmetic and reconstructive plastic surgery. ASPS comprises 94 percent of all board-certified plastic surgeons in the United States. Founded in 1931, the society represents physicians certified by The American Board of Plastic Surgery or The Royal College of Physicians and Surgeons of Canada.
Note: The study "Cosmetic Surgery and the Use of Antidepressant Medication" is being presented in electronic format, Sunday, Oct. 8 - Tuesday, Oct. 10, at the Moscone Convention Center, San Francisco.
Contact: LaSandra Cooper
American Society of Plastic Surgeons
"Plastic surgery patients are taking a proactive approach in making themselves happier by improving something that has truly bothered them," said Bruce Freedman, MD, ASPS Member Surgeon and study author. "While we are not saying that cosmetic plastic surgery alone is responsible for the drop in patients needing antidepressants, it surely is an important factor."
In the study, 362 patients had cosmetic plastic surgery - 17 percent or 61 patients were taking antidepressants. Six months after surgery, however, that number decreased 31 percent, down to 42 patients. In addition, 98 percent of patients said cosmetic plastic surgery had markedly improved their self-esteem.
All of the patients, who were primarily middle-aged women, had an invasive cosmetic plastic surgery procedure such as breast augmentation, tummy tuck or facelift. The authors did not identify any other major life changes that may have affected patients' use of antidepressants.
"We have just begun to uncover the various physical and psychological benefits of plastic surgery," said Dr. Freedman. "By helping our patients take control over something they were unhappy about, we helped remove a self-imposed barrier and ultimately improved their self-esteem."
For referrals to ASPS Member Surgeons certified by the American Board of Plastic Surgery visit plasticsurgery/ where you can also learn more about cosmetic and reconstructive plastic surgery.
The American Society of Plastic Surgeons is the largest organization of board-certified plastic surgeons in the world. With more than 6,000 members, the society is recognized as a leading authority and information source on cosmetic and reconstructive plastic surgery. ASPS comprises 94 percent of all board-certified plastic surgeons in the United States. Founded in 1931, the society represents physicians certified by The American Board of Plastic Surgery or The Royal College of Physicians and Surgeons of Canada.
Note: The study "Cosmetic Surgery and the Use of Antidepressant Medication" is being presented in electronic format, Sunday, Oct. 8 - Tuesday, Oct. 10, at the Moscone Convention Center, San Francisco.
Contact: LaSandra Cooper
American Society of Plastic Surgeons
суббота, 11 июня 2011 г.
Research Links Music and Listeners' Emotions
If you really want to get out of a foul mood, try listening to a little music.
A new study out of Penn State (USA) finds that music really can soothe the savage beast, up to a point, and it really doesn't matter what kind of music you listen to. As long as you like it.
'If you like music and choose to listen to it, it's probably going to make you feel better regardless of what type it is,' says associate professor of psychology Valerie N. Stratton.
Stratton and associate music professor Annette H. Zalanowski, of Penn State's Altoona campus, teamed up to take music research out of the laboratory and put it in the real world in which we live. They wanted to see when people listen to music, what types of music they prefer, and what types of moods that music induces.
It turns out that most of us listen to it a lot, but usually when we're doing something else.
'We've been looking at music and behavior for quite a few years, and it finally struck us that most of the things we were doing, and most of the things that other people were doing, were within lab settings,' says Stratton.
'There was really very little out there that looked at how people listened to music in their daily lives.'
So the researchers recruited 47 college students, including 25 music majors, and asked them to keep a diary for 14 days, noting the kinds of music they listened to. They were also asked to pick various moods from a list, showing their moods before, during and after listening to the music.
The Kids Like Rock
This is not exactly a startling finding, but the researchers found that college-age students overwhelmingly prefer to listen to rock music, whether hard, heavy or modern, and that includes music majors. If they weren't listing to hard rock, the non-music majors preferred country and soft rock. The music majors opted for classical and jazz after rock.
The researchers were a bit surprised to find that non-music majors listened to more music than the music majors. The non-music majors listened to an average of 161 minutes of music per day, compared to 117.7 minutes for the music majors.
It's not clear exactly why that turned out to be the case, but it may be that the music students spend more time listening to music in their classes, so listening during their free time is too much like the proverbial postman taking a walk on his day off.
Mood Music
If the results of the study apply to all of us, regardless of age, we don't spend a whole lot of time just sitting and listening to music. Most of the participants in the study listened to music while doing something else, and that activity apparently influenced their choice of music.
Soft background music is neat while socializing with your friends, but if it's time to hop on the exercise machine and work on those abs, a little jazz might be preferable, the researchers found.
The results of the study suggest that music is terrific when it comes to reinforcing, or elevating our positive moods, and can chase away some of our negative feelings, with one peculiar finding.
Among the non-music majors, sad, hateful and aggressive moods eased up a bit. But that didn't work for the music majors. For them, those feelings remained either unchanged, or rose slightly.
Stratton speculates that perhaps students who are hoping for a career in music may be a little more in tune to the emotional impact of music, and may even choose certain types of music to stimulate that effect. Maybe it's that old bromide at work, to be a great artist you've got to suffer along the way. So turn on a little Mahler and weep.
But oddly enough, the study found that the type of music was less important than rather the listeners really liked whatever they were listening to. Rock, the music of choice, made just about all the students 'optimistic, joyful, friendly, relaxed and calm,' according to the findings, published in a recent issue of Psychology and Education/ An Interdisciplinary Journal.
Melodies and Memories
It probably wouldn't do that for everybody, and that gives rise to an old question. Why does music have such a profound impact on our emotions?
Stratton says there are probably some physiological reasons. Different types of music may induce different 'brain rhythms,' she says. Fast music may cause the heart to speed up, for example.
But there are also cultural reasons why some music works for us, provoking very specific emotions.
Our 'past associations' with certain pieces may have a major impact on how we react to a particular song.
Hearing a very happy tune may have a sad affect on someone who associates that song with an unfortunate experience.
'If you heard that song during a very sad event in your life, that's going to bring back that kind of memory,' Stratton says. 'It's a very personal thing.'
My layman's opinion is that music works for us because it expresses the harmonics of the soul.
I haven't the foggiest idea what that means, but it sounds neat.
A new study out of Penn State (USA) finds that music really can soothe the savage beast, up to a point, and it really doesn't matter what kind of music you listen to. As long as you like it.
'If you like music and choose to listen to it, it's probably going to make you feel better regardless of what type it is,' says associate professor of psychology Valerie N. Stratton.
Stratton and associate music professor Annette H. Zalanowski, of Penn State's Altoona campus, teamed up to take music research out of the laboratory and put it in the real world in which we live. They wanted to see when people listen to music, what types of music they prefer, and what types of moods that music induces.
It turns out that most of us listen to it a lot, but usually when we're doing something else.
'We've been looking at music and behavior for quite a few years, and it finally struck us that most of the things we were doing, and most of the things that other people were doing, were within lab settings,' says Stratton.
'There was really very little out there that looked at how people listened to music in their daily lives.'
So the researchers recruited 47 college students, including 25 music majors, and asked them to keep a diary for 14 days, noting the kinds of music they listened to. They were also asked to pick various moods from a list, showing their moods before, during and after listening to the music.
The Kids Like Rock
This is not exactly a startling finding, but the researchers found that college-age students overwhelmingly prefer to listen to rock music, whether hard, heavy or modern, and that includes music majors. If they weren't listing to hard rock, the non-music majors preferred country and soft rock. The music majors opted for classical and jazz after rock.
The researchers were a bit surprised to find that non-music majors listened to more music than the music majors. The non-music majors listened to an average of 161 minutes of music per day, compared to 117.7 minutes for the music majors.
It's not clear exactly why that turned out to be the case, but it may be that the music students spend more time listening to music in their classes, so listening during their free time is too much like the proverbial postman taking a walk on his day off.
Mood Music
If the results of the study apply to all of us, regardless of age, we don't spend a whole lot of time just sitting and listening to music. Most of the participants in the study listened to music while doing something else, and that activity apparently influenced their choice of music.
Soft background music is neat while socializing with your friends, but if it's time to hop on the exercise machine and work on those abs, a little jazz might be preferable, the researchers found.
The results of the study suggest that music is terrific when it comes to reinforcing, or elevating our positive moods, and can chase away some of our negative feelings, with one peculiar finding.
Among the non-music majors, sad, hateful and aggressive moods eased up a bit. But that didn't work for the music majors. For them, those feelings remained either unchanged, or rose slightly.
Stratton speculates that perhaps students who are hoping for a career in music may be a little more in tune to the emotional impact of music, and may even choose certain types of music to stimulate that effect. Maybe it's that old bromide at work, to be a great artist you've got to suffer along the way. So turn on a little Mahler and weep.
But oddly enough, the study found that the type of music was less important than rather the listeners really liked whatever they were listening to. Rock, the music of choice, made just about all the students 'optimistic, joyful, friendly, relaxed and calm,' according to the findings, published in a recent issue of Psychology and Education/ An Interdisciplinary Journal.
Melodies and Memories
It probably wouldn't do that for everybody, and that gives rise to an old question. Why does music have such a profound impact on our emotions?
Stratton says there are probably some physiological reasons. Different types of music may induce different 'brain rhythms,' she says. Fast music may cause the heart to speed up, for example.
But there are also cultural reasons why some music works for us, provoking very specific emotions.
Our 'past associations' with certain pieces may have a major impact on how we react to a particular song.
Hearing a very happy tune may have a sad affect on someone who associates that song with an unfortunate experience.
'If you heard that song during a very sad event in your life, that's going to bring back that kind of memory,' Stratton says. 'It's a very personal thing.'
My layman's opinion is that music works for us because it expresses the harmonics of the soul.
I haven't the foggiest idea what that means, but it sounds neat.
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