More and more children are being diagnosed with depression. However, whether or not children should be treated with antidepressants is hotly disputed. You can read a Head to Head - where one person writes in favor, while another writes against, in this week's issue of The British Medical Journal (BMJ).
Yes - Children should be given antidepressants
We should not deny depressed children one of the few evidence-based available treatments, says Andrew Cotgrove, Clinical Director and Consultant in Adolescent Psychiatry at Pine Lodge Young People's Centre, Chester England.
The most controversial prescribing has been that of SSRIs (selective serotonin reuptake inhibitors) for children. Nevertheless, objective analysis of studies demonstrates a substantial benefit, when compared to a placebo, for some SSRIs. Guidelines recommend their use for young people with depression and OCD (obsessive-compulsive disorder).
Previous research has indicated that the use of SSRIs raises the risk of suicide related events. However, the risk is tiny and can be lessened even further with careful monitoring, Cotgrove writes.
Although cognitive behavioral therapy, interpersonal therapy and family therapy have some effect for young depressed patients, their effects are very small.
Cotgrove explains that disturbing procedural mistakes, exclusion of evidence in the conducting and reporting of some SSRI clinical trials, have justifiably alarmed doctors and members of the public. However, when one reviews the evidence carefully and objectively, the indications are that antidepressants have a role to play in treating young people with depression and OCD.
Young patients and their parents need to be told of the benefits and risks, given advice and support when choosing an evidence-based treatment. If we removed antidepressants as one of the options we would be taking away one of the few potentially effective interventions for these disabling conditions, Cotgrove concludes.
No - Children should not be given antidepressants
Prescribing SSRIs for young people is dangerous, not ethically sound, and poor value for money, writes Sami Timimi, Consultant Child and Adolescent Psychiatrist, Lincolnshire, England.
Timimi explains that as far as childhood depression is concerned, none of the SSRI studies has shown significant benefits over a placebo. Even so, national guidelines indicate the fuoxetine has more benefits than risks for young patients.
However, fluoxetine's profile is not that different from that of other SSRIs - efficacy is small and there is a potential danger. Timimi does acknowledge that a high placebo response makes it difficult for doctors to accept that SSRIs may be ineffective when faced with a distressed young person.
Timimi adds that a combination of fuzzy reporting and marketing spin have taken precedence over scientific accuracy, which have not helped the situation.
A reason for carrying out the studies in the first place was to validate well established prescribing patterns. It led to a trend which has been hard to undo, in spite of all the evidence. This does not mean we do not reverse it - for that we must, Timimi argues. SSRIs are neither value for money, nor clinically useful, moreover a small but tragic number of deaths may have happened because of their use.
In the majority of childhood cases distress is self limiting and does not need extensive intervention. However, when intervention is needed psychotherapy has shown itself to be effective, Timimi concludes.
"Should young people be given antidepressants? Yes"
Andrew Cotgrove
BMJ 2007;335:750 (13 October), doi:10.1136/bmj.39316.399931.94
Click here to read first 150 words online
"Should young people be given antidepressants? No"
Sami Timimi
BMJ 2007;335:751 (13 October), doi:10.1136/bmj.39316.406470.94
Click here to read first 150 words online
вторник, 30 августа 2011 г.
воскресенье, 28 августа 2011 г.
Targacept Initiates Phase I Clinical Trial Of TC-2216
Targacept, Inc.
(Nasdaq: TRGT), a clinical-stage biopharmaceutical company developing a new
class of drugs known as NNR Therapeutics(TM), today announced that it has
initiated a Phase I clinical trial of TC-2216, its product candidate for
the treatment of depression and anxiety disorders.
The trial is designed to evaluate the safety and tolerability of
TC-2216 and to assess its pharmacokinetic profile. The trial is a
double-blind, placebo-controlled crossover study, with sequential ascending
single oral doses administered to healthy male volunteers.
TC-2216 is a novel compound discovered using Targacept's proprietary
drug design platform known as Pentad(TM). The compound targets specific
neuronal nicotinic receptors (NNRs), a class of receptors found in the
central nervous system that play a critical role in regulating nervous
system activity. TC- 2216 selectively inhibits the alpha4beta2 NNR to
modulate the release of neurotransmitters that are involved in mood
regulation. In preclinical studies, TC-2216 showed greater potency than and
anti-depressant effects comparable to selective serotonin reuptake
inhibitors and tricyclics, which are commonly used treatments for
depression, as well as anxiety-relieving effects.
Targacept currently plans to develop TC-2216 as an oral monotherapy. In
November, the company announced positive top line results from a Phase II
clinical trial of TRIDMAC(TM), a treatment combination comprised of
mecamylamine hydrochloride as an augmentation therapy to citalopram
hydrobromide, in patients who did not respond adequately to citalopram
alone. Mecamylamine hydrochloride binds non-selectively to various NNR
subtypes, but there is a body of scientific evidence that suggests that its
anti-depressant activity is derived through its antagonism at the
alpha4beta2 NNR.
"Depression is a highly debilitating illness, and millions of people
who suffer with it are not gaining adequate relief from existing
therapies," said J. Donald deBethizy, Ph.D., Targacept's President and
Chief Executive Officer. "The results of our TRIDMAC trial not only
substantiate the promise of the NNR mechanism in the treatment of
depression and other mood disorders, but also further bolster our
enthusiasm for the potential of TC-2216."
About Targacept
Targacept is a clinical-stage biopharmaceutical company that discovers
and develops NNR Therapeutics(TM), a new class of drugs for the treatment
of central nervous system diseases and disorders. Targacept's product
candidates selectively modulate neuronal nicotinic receptors that serve as
key regulators of the nervous system activity to promote therapeutic
effects and limit adverse side effects. Targacept has product candidates in
development for Alzheimer's disease and cognitive deficits in
schizophrenia, pain and depression, and multiple preclinical programs.
Targacept is located in Winston-Salem, North Carolina. For more information
about Targacept, please visit targacept.
Forward-Looking Statements
Any statements in this press release about expectations, plans and
prospects for Targacept, Inc., including, without limitation, statements
regarding the progress, timing and scope of research and development of TC-
2216 and related regulatory filings and clinical trials, and all other
statements that are not purely historical in nature, constitute "forward-
looking statements" within the meaning of the Private Securities Litigation
Reform Act of 1995. Without limiting the foregoing, the words "may,"
"will," "could," "would," "should," "expect," "intend," "plan,"
"anticipate," "believe," "estimate," "predict," "project," "potential,"
"promise," "continue," "ongoing" and similar expressions are intended to
identify forward-looking statements. Actual results may differ materially
from those expressed or implied by forward-looking statements as a result
of various important factors, including our critical accounting policies
and risks and uncertainties relating to: the results of non-clinical
studies and assessments and clinical trials with respect to TC-2216 or our
other current and future product candidates in development; the conduct of
clinical trials, including the performance of third parties that we engage
to execute the trials and difficulties or delays in the completion of
patient enrollment or data analysis; and the timing and success of
submission, acceptance and approval of regulatory filings. These and other
risks and uncertainties are described in greater detail under the heading
"Risk Factors" in our most recent Quarterly Report on Form 10-Q and in
other filings that we make with the Securities and Exchange Commission. As
a result of the risks and uncertainties, the results or events indicated by
the forward-looking statements may not occur. We caution you not to place
undue reliance on any forward-looking statement.
In addition, any forward-looking statements in this release represent
our views only as of the date of this release and should not be relied upon
as representing our views as of any subsequent date. We anticipate that
subsequent events and developments may cause our views to change. Although
we may elect to update these forward-looking statements publicly at some
point in the future, whether as a result of new information, future events
or otherwise, we specifically disclaim any obligation to do so, except as
required by applicable law. Our forward-looking statements do not reflect
the potential impact of any future acquisitions, mergers, dispositions,
joint ventures or investments we may make.
Targacept, Inc.
targacept
(Nasdaq: TRGT), a clinical-stage biopharmaceutical company developing a new
class of drugs known as NNR Therapeutics(TM), today announced that it has
initiated a Phase I clinical trial of TC-2216, its product candidate for
the treatment of depression and anxiety disorders.
The trial is designed to evaluate the safety and tolerability of
TC-2216 and to assess its pharmacokinetic profile. The trial is a
double-blind, placebo-controlled crossover study, with sequential ascending
single oral doses administered to healthy male volunteers.
TC-2216 is a novel compound discovered using Targacept's proprietary
drug design platform known as Pentad(TM). The compound targets specific
neuronal nicotinic receptors (NNRs), a class of receptors found in the
central nervous system that play a critical role in regulating nervous
system activity. TC- 2216 selectively inhibits the alpha4beta2 NNR to
modulate the release of neurotransmitters that are involved in mood
regulation. In preclinical studies, TC-2216 showed greater potency than and
anti-depressant effects comparable to selective serotonin reuptake
inhibitors and tricyclics, which are commonly used treatments for
depression, as well as anxiety-relieving effects.
Targacept currently plans to develop TC-2216 as an oral monotherapy. In
November, the company announced positive top line results from a Phase II
clinical trial of TRIDMAC(TM), a treatment combination comprised of
mecamylamine hydrochloride as an augmentation therapy to citalopram
hydrobromide, in patients who did not respond adequately to citalopram
alone. Mecamylamine hydrochloride binds non-selectively to various NNR
subtypes, but there is a body of scientific evidence that suggests that its
anti-depressant activity is derived through its antagonism at the
alpha4beta2 NNR.
"Depression is a highly debilitating illness, and millions of people
who suffer with it are not gaining adequate relief from existing
therapies," said J. Donald deBethizy, Ph.D., Targacept's President and
Chief Executive Officer. "The results of our TRIDMAC trial not only
substantiate the promise of the NNR mechanism in the treatment of
depression and other mood disorders, but also further bolster our
enthusiasm for the potential of TC-2216."
About Targacept
Targacept is a clinical-stage biopharmaceutical company that discovers
and develops NNR Therapeutics(TM), a new class of drugs for the treatment
of central nervous system diseases and disorders. Targacept's product
candidates selectively modulate neuronal nicotinic receptors that serve as
key regulators of the nervous system activity to promote therapeutic
effects and limit adverse side effects. Targacept has product candidates in
development for Alzheimer's disease and cognitive deficits in
schizophrenia, pain and depression, and multiple preclinical programs.
Targacept is located in Winston-Salem, North Carolina. For more information
about Targacept, please visit targacept.
Forward-Looking Statements
Any statements in this press release about expectations, plans and
prospects for Targacept, Inc., including, without limitation, statements
regarding the progress, timing and scope of research and development of TC-
2216 and related regulatory filings and clinical trials, and all other
statements that are not purely historical in nature, constitute "forward-
looking statements" within the meaning of the Private Securities Litigation
Reform Act of 1995. Without limiting the foregoing, the words "may,"
"will," "could," "would," "should," "expect," "intend," "plan,"
"anticipate," "believe," "estimate," "predict," "project," "potential,"
"promise," "continue," "ongoing" and similar expressions are intended to
identify forward-looking statements. Actual results may differ materially
from those expressed or implied by forward-looking statements as a result
of various important factors, including our critical accounting policies
and risks and uncertainties relating to: the results of non-clinical
studies and assessments and clinical trials with respect to TC-2216 or our
other current and future product candidates in development; the conduct of
clinical trials, including the performance of third parties that we engage
to execute the trials and difficulties or delays in the completion of
patient enrollment or data analysis; and the timing and success of
submission, acceptance and approval of regulatory filings. These and other
risks and uncertainties are described in greater detail under the heading
"Risk Factors" in our most recent Quarterly Report on Form 10-Q and in
other filings that we make with the Securities and Exchange Commission. As
a result of the risks and uncertainties, the results or events indicated by
the forward-looking statements may not occur. We caution you not to place
undue reliance on any forward-looking statement.
In addition, any forward-looking statements in this release represent
our views only as of the date of this release and should not be relied upon
as representing our views as of any subsequent date. We anticipate that
subsequent events and developments may cause our views to change. Although
we may elect to update these forward-looking statements publicly at some
point in the future, whether as a result of new information, future events
or otherwise, we specifically disclaim any obligation to do so, except as
required by applicable law. Our forward-looking statements do not reflect
the potential impact of any future acquisitions, mergers, dispositions,
joint ventures or investments we may make.
Targacept, Inc.
targacept
пятница, 26 августа 2011 г.
Scientists Identify Elusive Neuronal Targets Of Deep Brain Stimulation
Shooting steady pulses of electricity through slender electrodes into a brain area that controls complex behaviors has proven to be effective against several therapeutically stubborn neurological and neuropsychiatric disorders. Now, a new study has found that this technique, called deep brain stimulation (DBS), targets the same class of neuronal cells that are known to respond to physical exercise and drugs such as Prozac.
The study, led by Associate Professor Grigori Enikolopov, Ph.D., of Cold Spring Harbor Laboratory (CSHL), is the cover story in the January 1st issue of The Journal of Comparative Neurology, which is currently available online.
The targeted neuronal cells, which increase in number in response to DBS, are a type of precursor cell that ultimately matures into adult neurons in the brain's hippocampus, the control center for spatial and long-term memory, emotion, behavior and other functions that go awry in diseases such as Alzheimer's, Parkinson's, epilepsy and depression. DBS has been successful in treating some cases of Parkinson's. And recently, it has also proven to work against other brain disorders such as epilepsy and severe depression.
"But the clinical application of DBS to treat neuropsychiatric disorders is still problematic because there isn't a clear rationale or a guide for which brain regions need to be stimulated to achieve maximum therapeutic benefit," says Enikolopov. "Our study now points to the brain region whose stimulation results in new cell growth in the hippocampus, an area that is implicated in many behavioral and cognitive disorders."
Enikolopov has long been interested in understanding how neuronal and neuroendocrine circuits are involved in mood regulation. "To that end, the question we've been asking is whether different types of stimuli, such as exercise or drugs or DBS, target different types of brain cells and circuits or converge on the same targets," he explains.
"There is a well-established correlation between the use of antidepressants and new neuronal growth in the hippocampus," says Enikolopov. "But what we didn't know was which steps in the cascade of events that eventually leads to the birth of new neurons are actually affected." Brain stem cells eventually differentiate into mature neurons following a cascade of steps, each of which produces a different intermediary cell type or precursor.
To identify the specific cell type affected by DBS, the CSHL team developed mouse models in which different classes of neural cells such as stem and progenitor cells produce different fluorescent colors. This enabled the scientists to visually track these cell populations and quantitatively assess how they change in response to neuronal triggers such as DBS.
To examine the effect of DBS on the hippocampus, Enikolopov teamed up with Andres Lozano, M.D., a leading Canadian neurosurgeon who pioneered its use against depression. The scientists found that stimulating the anterior thalamic nucleus - an area in the mouse brain that is equivalent to a human brain area where DBS is often therapeutically applied - resulted in an increase in cell division among the neural stem and progenitor cells, which in turn manifested as an increase in the number of new adult neurons in the hippocampus.
"By tracking new cell growth in the hippocampus and using it as a sensitive readout, we could potentially pinpoint other brain sites at which therapeutic DBS or other stimuli such as drugs might work best for various neurological and psychiatric conditions," explains Enikolopov.
Notes:
"Neurogenic hippocampal targets of deep brain stimulation" appears in the January 1 issue of the Journal of Comparative Neurology. The full citation is: Juan M. Encinas, Clement Hamani, Andres M. Lozano, and Grigori Enikolopov.
The study, led by Associate Professor Grigori Enikolopov, Ph.D., of Cold Spring Harbor Laboratory (CSHL), is the cover story in the January 1st issue of The Journal of Comparative Neurology, which is currently available online.
The targeted neuronal cells, which increase in number in response to DBS, are a type of precursor cell that ultimately matures into adult neurons in the brain's hippocampus, the control center for spatial and long-term memory, emotion, behavior and other functions that go awry in diseases such as Alzheimer's, Parkinson's, epilepsy and depression. DBS has been successful in treating some cases of Parkinson's. And recently, it has also proven to work against other brain disorders such as epilepsy and severe depression.
"But the clinical application of DBS to treat neuropsychiatric disorders is still problematic because there isn't a clear rationale or a guide for which brain regions need to be stimulated to achieve maximum therapeutic benefit," says Enikolopov. "Our study now points to the brain region whose stimulation results in new cell growth in the hippocampus, an area that is implicated in many behavioral and cognitive disorders."
Enikolopov has long been interested in understanding how neuronal and neuroendocrine circuits are involved in mood regulation. "To that end, the question we've been asking is whether different types of stimuli, such as exercise or drugs or DBS, target different types of brain cells and circuits or converge on the same targets," he explains.
"There is a well-established correlation between the use of antidepressants and new neuronal growth in the hippocampus," says Enikolopov. "But what we didn't know was which steps in the cascade of events that eventually leads to the birth of new neurons are actually affected." Brain stem cells eventually differentiate into mature neurons following a cascade of steps, each of which produces a different intermediary cell type or precursor.
To identify the specific cell type affected by DBS, the CSHL team developed mouse models in which different classes of neural cells such as stem and progenitor cells produce different fluorescent colors. This enabled the scientists to visually track these cell populations and quantitatively assess how they change in response to neuronal triggers such as DBS.
To examine the effect of DBS on the hippocampus, Enikolopov teamed up with Andres Lozano, M.D., a leading Canadian neurosurgeon who pioneered its use against depression. The scientists found that stimulating the anterior thalamic nucleus - an area in the mouse brain that is equivalent to a human brain area where DBS is often therapeutically applied - resulted in an increase in cell division among the neural stem and progenitor cells, which in turn manifested as an increase in the number of new adult neurons in the hippocampus.
"By tracking new cell growth in the hippocampus and using it as a sensitive readout, we could potentially pinpoint other brain sites at which therapeutic DBS or other stimuli such as drugs might work best for various neurological and psychiatric conditions," explains Enikolopov.
Notes:
"Neurogenic hippocampal targets of deep brain stimulation" appears in the January 1 issue of the Journal of Comparative Neurology. The full citation is: Juan M. Encinas, Clement Hamani, Andres M. Lozano, and Grigori Enikolopov.
среда, 24 августа 2011 г.
FDA Approves EMSAM(R) (selegiline Transdermal System), The First Transdermal Patch For The Treatment Of Major Depressive Disorder
Bristol-Myers Squibb Company (NYSE: BMY) and Somerset Pharmaceuticals, Inc., a joint venture between Mylan Laboratories Inc. (NYSE: MYL) and Watson Pharmaceuticals, Inc., (NYSE:WPI), announced today that the U.S. Food and Drug Administration (FDA) approved EMSAM(R) (selegiline transdermal system), the first transdermal patch for the treatment of major depressive disorder (MDD) in adults. EMSAM, a transdermal delivery system manufactured by Mylan Technologies, Inc. for Somerset, is a monoamine oxidase inhibitor (MAOI) that has been shown to relieve depressive symptoms in patients with MDD.
"We are pleased to be able to provide this important treatment to people with major depressive disorder," said Peter R. Dolan, chief executive officer, Bristol-Myers Squibb Company. "We believe EMSAM will help physicians treat their patients living with this illness through a new and unique delivery system."
"Together with Bristol-Myers Squibb, we are excited to be able to utilize transdermal technology to administer EMSAM, belonging to the MAOI class of agents that have proven antidepressant efficacy," said Mel Sharoky, M.D., president and chief executive officer, Somerset Pharmaceuticals.
About Monoamine Oxidase Inhibitors (MAOIs)
Although their mechanisms of action are not fully understood, MAOIs, including EMSAM, are presumed to work through potentiation of monoamine neurotransmitter activity in the brain by inhibiting the MAO enzyme. In an in vivo animal model, EMSAM exhibited antidepressant properties only at doses that inhibited both MAO-A and MAO-B in the brain. In the brain, MAO-A and MAO-B play important roles in the breakdown of neurotransmitter amines such as norepinephrine, dopamine and serotonin.
Oral MAOI antidepressants pass through the digestive tract, thus inhibiting intestinal
MAO-A, which is needed to break down tyramine,1 a substance found in certain foods and beverages such as aged cheese and tap beer.2 If a large amount of tyramine is absorbed systemically it can lead to a sudden and large increase in blood pressure called a hypertensive crisis, which is potentially life-threatening and requires immediate medical treatment. While most foods contain negligible amounts or no tyramine, a few food products may contain large amounts of tyramine that represent a potential risk for patients with significant inhibition of intestinal MAO-A resulting from administration of MAO inhibitors. As a result, patients taking oral MAOIs for MDD are required to avoid foods high in tyramine.3
About Transdermal Delivery of EMSAM
Through transdermal delivery, EMSAM is directly and continuously absorbed into the bloodstream over a 24-hour period. As a result, initial exposure of the drug to the digestive tract is minimized. As indicated in animal studies, the EMSAM 6 mg/24 hr patch allows for levels of medicine to inhibit MAO in the brain thought to be necessary for antidepressant effect while sufficiently preserving MAO-A in the digestive tract to break down tyramine. In its entirety, the data for EMSAM 6 mg/24 hr support the recommendation that tyramine dietary modifications are not needed. To reduce the risk of hypertensive crisis, dietary modifications are required with the EMSAM 9 mg/24 hr patch and the 12 mg/24 hr patch.
Clinical Studies
The efficacy of EMSAM in relieving depressive symptoms was established in two double-blind, placebo-controlled studies of six- (N=176) and eight- (N=265) week durations that included adult outpatients ages 18- to 70-years-old with single and recurrent episodes of MDD. The antidepressant action of EMSAM in hospitalized depressed patients has not been studied.
The six-week trial showed that a 6 mg/24 hr dose of EMSAM was significantly more effective than placebo in improving depressive symptoms as determined using the 17-item Hamilton Depression Rating Scale (HAM-D).
In the eight-week dose titration trial, patients with major depressive disorder who received EMSAM or placebo at a starting dose of 6 mg/24 hr, with possible increases to 9 mg/24 hr or 12 mg/24 hr based on clinical response, showed significant improvement compared with placebo on the primary outcome measure, the 28-item HAM-D total score.
The benefit of maintaining patients with MDD on therapy with EMSAM after achieving a responder status for an average of 25 days was demonstrated in controlled clinical trial. Three hundred twenty-two patients with major depressive disorder who had responded to EMSAM
6 mg/24 hr during an initial 10-week open-label treatment phase were randomized either to continuation of EMSAM 6 mg/24 hr (n=159), or to placebo (n=163) under double-blind conditions for observation of relapse. Approximately 52 percent of the EMSAM-treated patients as well as about 52 percent of the placebo-treated patients had discontinued treatment by week 12 of the double-blind phase. Patients continually receiving EMSAM experienced a significantly longer time to relapse.
"Using an innovative antidepressant delivery system, EMSAM provides significant relief of depressive symptoms with demonstrated safety and tolerability," said Alexander Bodkin, M.D., chief of the Clinical Psychopharmacology Research Program at Harvard University-affiliated McLean Hospital. "Major depressive disorder is a serious illness and not all treatments work equally well in all patients. The FDA approval of EMSAM is important because it adds another valuable treatment option to our armamentarium."
In clinical trials with EMSAM, application site reaction was the most commonly reported adverse event (EMSAM, 24 percent; placebo, 12 percent). Most were mild to moderate in severity with only two percent resulting in discontinuation. Overall, the rate of discontinuation due to adverse events was low (EMSAM 7.1 percent; placebo 3.6 percent). Additionally, EMSAM patients reported sexual dysfunction at a rate similar to placebo and experienced minimal weight change (mean weight change from baseline: EMSAM -1.2 lbs.; placebo +0.3 lbs.).
Dosing and Dietary ModificationsThe recommended starting and target dose of EMSAM is one 6 mg/24 hr patch administered once daily without tyramine dietary modifications. EMSAM will also be available in 9 mg/24 hr and 12 mg/24 hr once-daily doses (one patch per day). The trials were not designed to assess if higher doses are more effective than the starting and target dose of 6 mg/24 hr. To reduce the risk of hypertensive crisis, which is potentially life-threatening, foods and beverages high in tyramine must be avoided while on EMSAM 9 mg/24 hr or 12 mg/24 hr, and for two weeks following discontinuation of EMSAM at these doses or reducing the dose to EMSAM 6 mg/24 hr. Patients should be instructed to inform all of their health care professionals that they are using EMSAM, and not to stop or change treatment with EMSAM without consulting their health care professional.
Important Safety Information
Antidepressants increased the risk of suicidal thinking and behavior (suicidality) in short-term studies in children and adolescents with major depressive disorder (MDD) and other psychiatric disorders. All pediatric patients being treated with antidepressants for any indication should be observed closely for clinical worsening, suicidality, or unusual changes in behavior, especially during the initial few months of a course of drug therapy, or at time of dose changes, either increases or decreases. Families and caregivers should be advised for the need for close observation and communication with the prescriber. EMSAM is not approved for use in pediatric patients (see Boxed WARNING).
Pooled analyses of short-term (4 to 16 weeks) placebo-controlled trials of nine antidepressant drugs (SSRIs and others) in children and adolescents with major depressive disorder (MDD), obsessive compulsive disorder (OCD), or other psychiatric disorders (a total of 24 trials involving over 4,400 patients) have revealed a greater risk of adverse events representing suicidal thinking and behavior (suicidality) during the first few months of treatment in those receiving antidepressants. The average risk of such events in patients
receiving antidepressants was 4 percent, twice the placebo risk of 2 percent. No suicides occurred in these trials.
To reduce the risk of hypertensive crisis, which is potentially life-threatening, foods and beverages high in tyramine must be avoided while on EMSAM 9 mg/24 hr or 12 mg/24 hr, and for two weeks following discontinuation of EMSAM at these doses or reducing the dose to EMSAM 6 mg/24 hr.
Due to the potential for serotonin syndrome, which is potentially life-threatening, EMSAM should not be used with the following antidepressants: selective serotonin reuptake inhibitors (SSRIs), dual serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), mirtazapine, and bupropion; meperidine and analgesics such as tramadol, methadone, propoxyphene, and pentazocine; the antitussive dextromethorphan; cyclobenzaprine; oral selegiline; and St. John's wort.
After stopping treatment with SSRIs, SNRIs, TCAs, MAOIs, mirtazapine, bupropion; meperidine and analgesics such as: tramadol, methadone, and propoxyphene; dextromethophan; St. John's wort; and buspirone, approximately 1 week (5 weeks for fluoxetine) should elapse before starting therapy with EMSAM. At least 2 weeks should elapse after stopping EMSAM before starting therapy with buspirone or a drug that is contraindicated with EMSAM.
Carbamazepine and oxcarbazepine are contraindicated in patients taking MAO inhibitors, including EMSAM.
The use of EMSAM is contraindicated for use with sympathomimetic amines, including amphetamines as well as cold products and weight-reducing preparations that contain vasoconstrictors (e.g., pseudoephedrine, phenylephrine, phenylpropanolamine, and ephedrine).
Patients taking EMSAM should not undergo elective surgery requiring general anesthesia or be given local anesthesia containing sympathomimetic vasoconstrictors.
EMSAM should not be used in the presence of pheochromocytoma since such tumors secrete pressor substances.
Adults with MDD or co-morbid depression in the setting of other psychiatric illness being treated with antidepressants should be observed for clinical worsening and suicidality, especially during the initial few months of a course of drug therapy, or at times of dose changes, either increases or decreases.
Risk of bipolar disorder should be ruled out prior to initiating antidepressant therapy. EMSAM is not approved for the treatment of bipolar depression.
Due to the potential for elevated blood pressure, the use of EMSAM with buspirone is not recommended.
As with other MAOIs, postural hypotension can occur with EMSAM therapy. Dose increases in the elderly should be made with caution and patients should be observed closely for postural changes in blood pressure throughout treatment.
EMSAM should be used with caution in patients with certain concomitant systemic illnesses that can produce altered metabolism or hemodynamic responses.
As with other psychoactive drugs, EMSAM may have the potential to impair judgment, thinking, or motor skills. Patients should not drive or operate hazardous machinery until they are certain EMSAM does not impair their ability to engage in such activities.
The use of alcohol is not recommended while taking EMSAM.
EMSAM should not be used in combination with tyramine-containing nutritional supplements.
EMSAM should be used in pregnancy only if the potential benefit justifies the potential risk to the fetus. Caution should be exercised when administering EMSAM to a nursing mother. EMSAM is contraindicated in patients with known hypersensitivity to selegiline or to any component of the transdermal system.
Treatment-emergent adverse events in short-term clinical trials that occurred at a greater than or equal to 2 percent incidence with EMSAM and for which the incidence was greater than placebo include: application site reaction (24 percent vs 12 percent), headache (18 percent vs 17 percent), insomnia (12 percent vs 7 percent), diarrhea (9 percent vs 7 percent), dry mouth (8 percent vs 6 percent), dyspepsia (4 percent vs 3 percent), rash (4 percent vs 2 percent), pharyngitis (3 percent vs 2 percent), and sinusitis (3 percent vs 1 percent).
Full EMSAM (Selegiline Transdermal System) Prescribing Information, including Boxed WARNING
About Major Depression
According to the DSM-IV diagnosis, major depressive disorder is characterized by one or more major depressive episodes, (i.e., at least two weeks of depressed mood or loss of interest accompanied by at least four additional symptoms of depression)4 and impairs social and occupational or other important areas of functioning.4 Major depression affects approximately 14 million American adults in a given year5 and is the most common mental health disorder after anxiety.6 It is a leading cause of disability and disease burden worldwide.7
The illness is one and a half to three times more common among people with a family history than among the general population,4 and studies indicate that depressive episodes occur twice as frequently in women as in men.4
Today many patients with MDD do not achieve adequate symptom relief.8 If depression is not treated successfully, the chances that it will become recurrent increase.8 More than 80 percent of patients who have one episode of MDD will have at least one subsequent episode.9
Bristol-Myers Squibb and Somerset Pharmaceuticals, Inc.
EMSAM was developed by Somerset Pharmaceuticals, Inc. In December 2004, Bristol-Myers Squibb and Somerset entered into an agreement that provides Bristol-Myers Squibb with exclusive distribution rights to commercialize EMSAM after approval in the U.S. and Canada.
About Bristol-Myers Squibb
Bristol-Myers Squibb is a global pharmaceutical and related health care products company whose mission is to extend and enhance human life.
About Somerset Pharmaceuticals, Inc.
Somerset Pharmaceuticals, Inc. is a joint venture between Mylan Laboratories Inc. (NYSE: MYL) and Watson Pharmaceuticals, Inc. (NYSE: WPI). For more information about Somerset, visit somersetpharm.
References
1 - Youdim, MBH. Therapeutic Applications of Selective and Non-Selective Inhibitors of Monoamine Oxidase A and B that do not Cause Significant Tyramine Potentiation, Neuro Toxicology, 2003: 25. P. 243-250.
2 - Shulman KI, Walker SE. Psychiatric Annals. A Reevaluation of Dietary Restrictions for Irreversible Monoamine Oxidase Inhibitors. Psychiatric Annals, June 2001, 31:6;378-384.
3 - Kennedy SH, McKenna KF, Baker GB. Monamine Oxidase Inhibitors. In: Sadock BJ, Sadock BA. Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 7th Edition. New York, NY: Lippincott, Williams & Wilkins; 2000: 2398-2406.
4 - Diagnostic and Statistical Manual of Mental Disorders. Fourth ed. Washington, DC. American Psychiatric Association; 1994.
5 - Kessler RC, Berglund P, Demler O, et al. The Epidemiology of Major Depressive Disorder: Results from the National Comorbidity Survey Replication (NCS-R). Journal of the American Medical Association (JAMA), 2003; 289(23);3095-3105. P. 3099.
6 - Merck Manual of Medical Information - Second Home Edition. Whitehouse Station, NJ: Merck Research Laboratories; Copyright 1995-2005 Merck & Co.
7 - Ustun TB, et al. Global Burden of Depressive Disorders. British J Psychiatry. 2004; 184. 386-392.
8 Greden, JF. Unmet Need: What Justifies the Search for a New Antidepressant? J Clin Psychiatry, 2002;63 (suppl. 2), 3-6.
9 - Hirschfeld RMA. Clinical Importance of Long-Term Antidepressant Treatment. British J Psychiatry. 2001; 179 (suppl. 42): s4-s8.9.
bms
View drug information on Selegiline tablets.
"We are pleased to be able to provide this important treatment to people with major depressive disorder," said Peter R. Dolan, chief executive officer, Bristol-Myers Squibb Company. "We believe EMSAM will help physicians treat their patients living with this illness through a new and unique delivery system."
"Together with Bristol-Myers Squibb, we are excited to be able to utilize transdermal technology to administer EMSAM, belonging to the MAOI class of agents that have proven antidepressant efficacy," said Mel Sharoky, M.D., president and chief executive officer, Somerset Pharmaceuticals.
About Monoamine Oxidase Inhibitors (MAOIs)
Although their mechanisms of action are not fully understood, MAOIs, including EMSAM, are presumed to work through potentiation of monoamine neurotransmitter activity in the brain by inhibiting the MAO enzyme. In an in vivo animal model, EMSAM exhibited antidepressant properties only at doses that inhibited both MAO-A and MAO-B in the brain. In the brain, MAO-A and MAO-B play important roles in the breakdown of neurotransmitter amines such as norepinephrine, dopamine and serotonin.
Oral MAOI antidepressants pass through the digestive tract, thus inhibiting intestinal
MAO-A, which is needed to break down tyramine,1 a substance found in certain foods and beverages such as aged cheese and tap beer.2 If a large amount of tyramine is absorbed systemically it can lead to a sudden and large increase in blood pressure called a hypertensive crisis, which is potentially life-threatening and requires immediate medical treatment. While most foods contain negligible amounts or no tyramine, a few food products may contain large amounts of tyramine that represent a potential risk for patients with significant inhibition of intestinal MAO-A resulting from administration of MAO inhibitors. As a result, patients taking oral MAOIs for MDD are required to avoid foods high in tyramine.3
About Transdermal Delivery of EMSAM
Through transdermal delivery, EMSAM is directly and continuously absorbed into the bloodstream over a 24-hour period. As a result, initial exposure of the drug to the digestive tract is minimized. As indicated in animal studies, the EMSAM 6 mg/24 hr patch allows for levels of medicine to inhibit MAO in the brain thought to be necessary for antidepressant effect while sufficiently preserving MAO-A in the digestive tract to break down tyramine. In its entirety, the data for EMSAM 6 mg/24 hr support the recommendation that tyramine dietary modifications are not needed. To reduce the risk of hypertensive crisis, dietary modifications are required with the EMSAM 9 mg/24 hr patch and the 12 mg/24 hr patch.
Clinical Studies
The efficacy of EMSAM in relieving depressive symptoms was established in two double-blind, placebo-controlled studies of six- (N=176) and eight- (N=265) week durations that included adult outpatients ages 18- to 70-years-old with single and recurrent episodes of MDD. The antidepressant action of EMSAM in hospitalized depressed patients has not been studied.
The six-week trial showed that a 6 mg/24 hr dose of EMSAM was significantly more effective than placebo in improving depressive symptoms as determined using the 17-item Hamilton Depression Rating Scale (HAM-D).
In the eight-week dose titration trial, patients with major depressive disorder who received EMSAM or placebo at a starting dose of 6 mg/24 hr, with possible increases to 9 mg/24 hr or 12 mg/24 hr based on clinical response, showed significant improvement compared with placebo on the primary outcome measure, the 28-item HAM-D total score.
The benefit of maintaining patients with MDD on therapy with EMSAM after achieving a responder status for an average of 25 days was demonstrated in controlled clinical trial. Three hundred twenty-two patients with major depressive disorder who had responded to EMSAM
6 mg/24 hr during an initial 10-week open-label treatment phase were randomized either to continuation of EMSAM 6 mg/24 hr (n=159), or to placebo (n=163) under double-blind conditions for observation of relapse. Approximately 52 percent of the EMSAM-treated patients as well as about 52 percent of the placebo-treated patients had discontinued treatment by week 12 of the double-blind phase. Patients continually receiving EMSAM experienced a significantly longer time to relapse.
"Using an innovative antidepressant delivery system, EMSAM provides significant relief of depressive symptoms with demonstrated safety and tolerability," said Alexander Bodkin, M.D., chief of the Clinical Psychopharmacology Research Program at Harvard University-affiliated McLean Hospital. "Major depressive disorder is a serious illness and not all treatments work equally well in all patients. The FDA approval of EMSAM is important because it adds another valuable treatment option to our armamentarium."
In clinical trials with EMSAM, application site reaction was the most commonly reported adverse event (EMSAM, 24 percent; placebo, 12 percent). Most were mild to moderate in severity with only two percent resulting in discontinuation. Overall, the rate of discontinuation due to adverse events was low (EMSAM 7.1 percent; placebo 3.6 percent). Additionally, EMSAM patients reported sexual dysfunction at a rate similar to placebo and experienced minimal weight change (mean weight change from baseline: EMSAM -1.2 lbs.; placebo +0.3 lbs.).
Dosing and Dietary ModificationsThe recommended starting and target dose of EMSAM is one 6 mg/24 hr patch administered once daily without tyramine dietary modifications. EMSAM will also be available in 9 mg/24 hr and 12 mg/24 hr once-daily doses (one patch per day). The trials were not designed to assess if higher doses are more effective than the starting and target dose of 6 mg/24 hr. To reduce the risk of hypertensive crisis, which is potentially life-threatening, foods and beverages high in tyramine must be avoided while on EMSAM 9 mg/24 hr or 12 mg/24 hr, and for two weeks following discontinuation of EMSAM at these doses or reducing the dose to EMSAM 6 mg/24 hr. Patients should be instructed to inform all of their health care professionals that they are using EMSAM, and not to stop or change treatment with EMSAM without consulting their health care professional.
Important Safety Information
Antidepressants increased the risk of suicidal thinking and behavior (suicidality) in short-term studies in children and adolescents with major depressive disorder (MDD) and other psychiatric disorders. All pediatric patients being treated with antidepressants for any indication should be observed closely for clinical worsening, suicidality, or unusual changes in behavior, especially during the initial few months of a course of drug therapy, or at time of dose changes, either increases or decreases. Families and caregivers should be advised for the need for close observation and communication with the prescriber. EMSAM is not approved for use in pediatric patients (see Boxed WARNING).
Pooled analyses of short-term (4 to 16 weeks) placebo-controlled trials of nine antidepressant drugs (SSRIs and others) in children and adolescents with major depressive disorder (MDD), obsessive compulsive disorder (OCD), or other psychiatric disorders (a total of 24 trials involving over 4,400 patients) have revealed a greater risk of adverse events representing suicidal thinking and behavior (suicidality) during the first few months of treatment in those receiving antidepressants. The average risk of such events in patients
receiving antidepressants was 4 percent, twice the placebo risk of 2 percent. No suicides occurred in these trials.
To reduce the risk of hypertensive crisis, which is potentially life-threatening, foods and beverages high in tyramine must be avoided while on EMSAM 9 mg/24 hr or 12 mg/24 hr, and for two weeks following discontinuation of EMSAM at these doses or reducing the dose to EMSAM 6 mg/24 hr.
Due to the potential for serotonin syndrome, which is potentially life-threatening, EMSAM should not be used with the following antidepressants: selective serotonin reuptake inhibitors (SSRIs), dual serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), mirtazapine, and bupropion; meperidine and analgesics such as tramadol, methadone, propoxyphene, and pentazocine; the antitussive dextromethorphan; cyclobenzaprine; oral selegiline; and St. John's wort.
After stopping treatment with SSRIs, SNRIs, TCAs, MAOIs, mirtazapine, bupropion; meperidine and analgesics such as: tramadol, methadone, and propoxyphene; dextromethophan; St. John's wort; and buspirone, approximately 1 week (5 weeks for fluoxetine) should elapse before starting therapy with EMSAM. At least 2 weeks should elapse after stopping EMSAM before starting therapy with buspirone or a drug that is contraindicated with EMSAM.
Carbamazepine and oxcarbazepine are contraindicated in patients taking MAO inhibitors, including EMSAM.
The use of EMSAM is contraindicated for use with sympathomimetic amines, including amphetamines as well as cold products and weight-reducing preparations that contain vasoconstrictors (e.g., pseudoephedrine, phenylephrine, phenylpropanolamine, and ephedrine).
Patients taking EMSAM should not undergo elective surgery requiring general anesthesia or be given local anesthesia containing sympathomimetic vasoconstrictors.
EMSAM should not be used in the presence of pheochromocytoma since such tumors secrete pressor substances.
Adults with MDD or co-morbid depression in the setting of other psychiatric illness being treated with antidepressants should be observed for clinical worsening and suicidality, especially during the initial few months of a course of drug therapy, or at times of dose changes, either increases or decreases.
Risk of bipolar disorder should be ruled out prior to initiating antidepressant therapy. EMSAM is not approved for the treatment of bipolar depression.
Due to the potential for elevated blood pressure, the use of EMSAM with buspirone is not recommended.
As with other MAOIs, postural hypotension can occur with EMSAM therapy. Dose increases in the elderly should be made with caution and patients should be observed closely for postural changes in blood pressure throughout treatment.
EMSAM should be used with caution in patients with certain concomitant systemic illnesses that can produce altered metabolism or hemodynamic responses.
As with other psychoactive drugs, EMSAM may have the potential to impair judgment, thinking, or motor skills. Patients should not drive or operate hazardous machinery until they are certain EMSAM does not impair their ability to engage in such activities.
The use of alcohol is not recommended while taking EMSAM.
EMSAM should not be used in combination with tyramine-containing nutritional supplements.
EMSAM should be used in pregnancy only if the potential benefit justifies the potential risk to the fetus. Caution should be exercised when administering EMSAM to a nursing mother. EMSAM is contraindicated in patients with known hypersensitivity to selegiline or to any component of the transdermal system.
Treatment-emergent adverse events in short-term clinical trials that occurred at a greater than or equal to 2 percent incidence with EMSAM and for which the incidence was greater than placebo include: application site reaction (24 percent vs 12 percent), headache (18 percent vs 17 percent), insomnia (12 percent vs 7 percent), diarrhea (9 percent vs 7 percent), dry mouth (8 percent vs 6 percent), dyspepsia (4 percent vs 3 percent), rash (4 percent vs 2 percent), pharyngitis (3 percent vs 2 percent), and sinusitis (3 percent vs 1 percent).
Full EMSAM (Selegiline Transdermal System) Prescribing Information, including Boxed WARNING
About Major Depression
According to the DSM-IV diagnosis, major depressive disorder is characterized by one or more major depressive episodes, (i.e., at least two weeks of depressed mood or loss of interest accompanied by at least four additional symptoms of depression)4 and impairs social and occupational or other important areas of functioning.4 Major depression affects approximately 14 million American adults in a given year5 and is the most common mental health disorder after anxiety.6 It is a leading cause of disability and disease burden worldwide.7
The illness is one and a half to three times more common among people with a family history than among the general population,4 and studies indicate that depressive episodes occur twice as frequently in women as in men.4
Today many patients with MDD do not achieve adequate symptom relief.8 If depression is not treated successfully, the chances that it will become recurrent increase.8 More than 80 percent of patients who have one episode of MDD will have at least one subsequent episode.9
Bristol-Myers Squibb and Somerset Pharmaceuticals, Inc.
EMSAM was developed by Somerset Pharmaceuticals, Inc. In December 2004, Bristol-Myers Squibb and Somerset entered into an agreement that provides Bristol-Myers Squibb with exclusive distribution rights to commercialize EMSAM after approval in the U.S. and Canada.
About Bristol-Myers Squibb
Bristol-Myers Squibb is a global pharmaceutical and related health care products company whose mission is to extend and enhance human life.
About Somerset Pharmaceuticals, Inc.
Somerset Pharmaceuticals, Inc. is a joint venture between Mylan Laboratories Inc. (NYSE: MYL) and Watson Pharmaceuticals, Inc. (NYSE: WPI). For more information about Somerset, visit somersetpharm.
References
1 - Youdim, MBH. Therapeutic Applications of Selective and Non-Selective Inhibitors of Monoamine Oxidase A and B that do not Cause Significant Tyramine Potentiation, Neuro Toxicology, 2003: 25. P. 243-250.
2 - Shulman KI, Walker SE. Psychiatric Annals. A Reevaluation of Dietary Restrictions for Irreversible Monoamine Oxidase Inhibitors. Psychiatric Annals, June 2001, 31:6;378-384.
3 - Kennedy SH, McKenna KF, Baker GB. Monamine Oxidase Inhibitors. In: Sadock BJ, Sadock BA. Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 7th Edition. New York, NY: Lippincott, Williams & Wilkins; 2000: 2398-2406.
4 - Diagnostic and Statistical Manual of Mental Disorders. Fourth ed. Washington, DC. American Psychiatric Association; 1994.
5 - Kessler RC, Berglund P, Demler O, et al. The Epidemiology of Major Depressive Disorder: Results from the National Comorbidity Survey Replication (NCS-R). Journal of the American Medical Association (JAMA), 2003; 289(23);3095-3105. P. 3099.
6 - Merck Manual of Medical Information - Second Home Edition. Whitehouse Station, NJ: Merck Research Laboratories; Copyright 1995-2005 Merck & Co.
7 - Ustun TB, et al. Global Burden of Depressive Disorders. British J Psychiatry. 2004; 184. 386-392.
8 Greden, JF. Unmet Need: What Justifies the Search for a New Antidepressant? J Clin Psychiatry, 2002;63 (suppl. 2), 3-6.
9 - Hirschfeld RMA. Clinical Importance of Long-Term Antidepressant Treatment. British J Psychiatry. 2001; 179 (suppl. 42): s4-s8.9.
bms
View drug information on Selegiline tablets.
понедельник, 22 августа 2011 г.
Study Suggests Salt Might Be 'Nature's Antidepressant'
UI psychologist Kim Johnson and colleagues found in their research that when rats are deficient in sodium chloride, common table salt, they shy away from activities they normally enjoy, like drinking a sugary substance or pressing a bar that stimulates a pleasant sensation in their brains.
"Things that normally would be pleasurable for rats didn't elicit the same degree of relish, which leads us to believe that a salt deficit and the craving associated with it can induce one of the key symptoms associated with depression," Johnson said.
The UI researchers can't say it is full-blown depression because several criteria factor into such a diagnosis, but a loss of pleasure in normally pleasing activities is one of the most important features of psychological depression. And, the idea that salt is a natural mood-elevating substance could help explain why we're so tempted to over-ingest it, even though it's known to contribute to high blood pressure, heart disease and other health problems.
Past research has shown that the worldwide average for salt intake per individual is about 10 grams per day, which is greater than the U.S. Food and Drug Administration recommended intake by about 4 grams, and may exceed what the body actually needs by more than 8 grams.
Johnson, who holds appointments in psychology and integrative physiology in the College of Liberal Arts and Sciences and in pharmacology in the Carver College of Medicine, published a review of these findings in the July issue of the journal Physiology & Behavior with Michael J. Morris and Elisa S. Na, UI graduate students. In addition to reporting their own findings, the authors reviewed others' research on the reasons behind salt appetite.
High levels of salt are contained in everything from pancakes to pasta these days, but once upon a time, it was hard to come by. Salt consumption and its price skyrocketed around 2000 B.C. when it was discovered as a food preservative. Roman soldiers were paid in salt; the word salary is derived from the Latin for salt. Even when mechanical refrigeration lessened the need for salt in the 19th century, consumption continued in excess because people liked the taste and it had become fairly inexpensive. Today, 77 percent of our salt intake comes from processed and restaurant foods, like frozen dinners and fast food.
Evolution might have played an important part in the human hankering for salt. Humans evolved from creatures that lived in salty ocean water. Once on land, the body continued to need sodium and chloride because minerals play key roles in allowing fluids to pass in and out of cells, and in helping nerve cells transfer information throughout the brain and body. But as man evolved in the hot climate of Africa, perspiration robbed the body of sodium. Salt was scarce because our early ancestors ate a veggie-rich diet and lived far from the ocean.
"Most of our biological systems require sodium to function properly, but as a species that didn't have ready access to it, our kidneys evolved to become salt misers," Johnson said.
Behavior also came to play a key role in making sure we have enough salt on board. Animals like us come equipped with a taste system designed to detect salt and a brain that remembers the location of salt sources -- like salt licks in a pasture. A pleasure mechanism in the brain is activated when salt is consumed.
So the body needs salt and knows how to find it and how to conserve it. But today scientists are finding evidence that it's an abused, addictive substance -- almost like a drug.
One sign of addiction is using a substance even when it's known to be harmful. Many people are told to reduce sodium due to health concerns, but they have trouble doing so because they like the taste and find low-sodium foods bland.
Another strong aspect of addiction is the development of intense cravings when drugs are withheld. Experiments by Johnson and colleagues indicate similar changes in brain activity whether rats are exposed to drugs or salt deficiency.
"This suggests that salt need and cravings may be linked to the same brain pathways as those related to drug addiction and abuse," Johnson said.
University of Iowa Health Sciences
5141 Westlawn
Iowa City
IA 52242
United States
uihealthcare
"Things that normally would be pleasurable for rats didn't elicit the same degree of relish, which leads us to believe that a salt deficit and the craving associated with it can induce one of the key symptoms associated with depression," Johnson said.
The UI researchers can't say it is full-blown depression because several criteria factor into such a diagnosis, but a loss of pleasure in normally pleasing activities is one of the most important features of psychological depression. And, the idea that salt is a natural mood-elevating substance could help explain why we're so tempted to over-ingest it, even though it's known to contribute to high blood pressure, heart disease and other health problems.
Past research has shown that the worldwide average for salt intake per individual is about 10 grams per day, which is greater than the U.S. Food and Drug Administration recommended intake by about 4 grams, and may exceed what the body actually needs by more than 8 grams.
Johnson, who holds appointments in psychology and integrative physiology in the College of Liberal Arts and Sciences and in pharmacology in the Carver College of Medicine, published a review of these findings in the July issue of the journal Physiology & Behavior with Michael J. Morris and Elisa S. Na, UI graduate students. In addition to reporting their own findings, the authors reviewed others' research on the reasons behind salt appetite.
High levels of salt are contained in everything from pancakes to pasta these days, but once upon a time, it was hard to come by. Salt consumption and its price skyrocketed around 2000 B.C. when it was discovered as a food preservative. Roman soldiers were paid in salt; the word salary is derived from the Latin for salt. Even when mechanical refrigeration lessened the need for salt in the 19th century, consumption continued in excess because people liked the taste and it had become fairly inexpensive. Today, 77 percent of our salt intake comes from processed and restaurant foods, like frozen dinners and fast food.
Evolution might have played an important part in the human hankering for salt. Humans evolved from creatures that lived in salty ocean water. Once on land, the body continued to need sodium and chloride because minerals play key roles in allowing fluids to pass in and out of cells, and in helping nerve cells transfer information throughout the brain and body. But as man evolved in the hot climate of Africa, perspiration robbed the body of sodium. Salt was scarce because our early ancestors ate a veggie-rich diet and lived far from the ocean.
"Most of our biological systems require sodium to function properly, but as a species that didn't have ready access to it, our kidneys evolved to become salt misers," Johnson said.
Behavior also came to play a key role in making sure we have enough salt on board. Animals like us come equipped with a taste system designed to detect salt and a brain that remembers the location of salt sources -- like salt licks in a pasture. A pleasure mechanism in the brain is activated when salt is consumed.
So the body needs salt and knows how to find it and how to conserve it. But today scientists are finding evidence that it's an abused, addictive substance -- almost like a drug.
One sign of addiction is using a substance even when it's known to be harmful. Many people are told to reduce sodium due to health concerns, but they have trouble doing so because they like the taste and find low-sodium foods bland.
Another strong aspect of addiction is the development of intense cravings when drugs are withheld. Experiments by Johnson and colleagues indicate similar changes in brain activity whether rats are exposed to drugs or salt deficiency.
"This suggests that salt need and cravings may be linked to the same brain pathways as those related to drug addiction and abuse," Johnson said.
University of Iowa Health Sciences
5141 Westlawn
Iowa City
IA 52242
United States
uihealthcare
суббота, 20 августа 2011 г.
No Matter What Stage Of Cancer, Including Remission, Physical Symptoms Prevalent
Twenty-two physical symptoms associated with cancer - symptoms often unrecognized and undertreated - are prevalent in all types of cancers regardless of whether the patient is newly diagnosed, undergoing treatment or is a cancer survivor, according to researchers from the Regenstrief Institute and the Indiana University schools of medicine and nursing.
Common symptoms include fatigue, pain, weakness, appetite loss, dry mouth, constipation, insomnia and nausea. These physical symptoms are associated with substantial functional impairment, disability and diminished quality of life.
The study of 405 patients was reported in the Oct. 11, 2010, issue of the Archives of Internal Medicine. Numerous physical symptoms, rather than just a few, were prevalent in patients with cancer and this prevalence did not diminish after completion of therapy.
"We found that regardless of where they are in the course of their diseases, many individuals with cancer have a high symptom burden," said Kurt Kroenke, M.D., the study's principal investigator and first author. Dr. Kroenke is a Regenstrief Institute investigator and a Chancellor's Professor of Medicine in the IU School of Medicine.
"These symptoms impact them at home and at work throughout their lives," he said.
Study participants, all of whom had pain, depression or both, experienced substantial disability, reporting on average 17 of the past 28 days as either bed days or days in which they had to cut down on activities by at least 50%. Almost all patients reported feeling tired (97.5%) and most (78.8%) were bothered "a lot" by this symptom. Of the 22 symptoms studied, 15 were reported by more than half of the study participants.
In spite of high symptom prevalence, the researchers did not uncover greater use of the health care system. There may be several explanations for this including patients' inclinations to focus on cancer treatment while with their physicians or to accept the symptoms as an inevitable result of the disease or its treatment. Alternatively, the explanation may lie with the fact that those in the study, as cancer patients or former patients, were already frequently interacting with many parts of the health care system.
"Patients and their families should be encouraged to bring up symptoms like pain or insomnia with physicians. But because oncologists are necessarily focused on treatment of the cancer itself, they often have insufficient time to optimally evaluate and manage symptoms and other factors impacting quality of life. We have shown in an earlier study that one effective solution might be a partnership between a telephone-based symptom management team and community-based oncology practices,," said Dr. Kroenke, who is a research scientist with the Center for Implementing Evidence-Based Practice at the Richard Roudebush VA Medical Center and an Indiana University Melvin and Bren Simon Cancer Center member.
The previous study, published earlier in 2010 in the Journal of the American Medical Association, reported that an economical, centralized approach is feasible to conduct and significantly improved symptoms of pain and depression in patients in any phase of cancer. That approach gave patients, many of whom lived in underserved rural areas, one-stop assistance they probably wouldn't have had access to unless they went to a major cancer center, Kroenke said.
Recognizing and managing physical symptoms such as fatigue, pain, nausea, and insomnia may make a significant difference regardless of type or phase of cancer. The researchers plan to investigate medical and behavioral strategies and combinations of both approaches to control these symptoms.
Notes:
In addition to Dr. Kroenke, co-authors of "Somatic Symptoms in Patients with Cancer Experiencing Pain or Depression" are "Xin Zhong, R.N. and Janet Carpenter, Ph.D., R.N., of the IU School of Nursing; Dale Theobald, M.D., Ph.D. of Community Home Health Hospice and Symptom Management Group; Jingwei Wu, M.S., of the IU School of Medicine; and Wanzhu Tu, Ph.D., of the Regenstrief Institute and the IU School of Medicine. The study was supported by a grant from the National Cancer Institute.
Common symptoms include fatigue, pain, weakness, appetite loss, dry mouth, constipation, insomnia and nausea. These physical symptoms are associated with substantial functional impairment, disability and diminished quality of life.
The study of 405 patients was reported in the Oct. 11, 2010, issue of the Archives of Internal Medicine. Numerous physical symptoms, rather than just a few, were prevalent in patients with cancer and this prevalence did not diminish after completion of therapy.
"We found that regardless of where they are in the course of their diseases, many individuals with cancer have a high symptom burden," said Kurt Kroenke, M.D., the study's principal investigator and first author. Dr. Kroenke is a Regenstrief Institute investigator and a Chancellor's Professor of Medicine in the IU School of Medicine.
"These symptoms impact them at home and at work throughout their lives," he said.
Study participants, all of whom had pain, depression or both, experienced substantial disability, reporting on average 17 of the past 28 days as either bed days or days in which they had to cut down on activities by at least 50%. Almost all patients reported feeling tired (97.5%) and most (78.8%) were bothered "a lot" by this symptom. Of the 22 symptoms studied, 15 were reported by more than half of the study participants.
In spite of high symptom prevalence, the researchers did not uncover greater use of the health care system. There may be several explanations for this including patients' inclinations to focus on cancer treatment while with their physicians or to accept the symptoms as an inevitable result of the disease or its treatment. Alternatively, the explanation may lie with the fact that those in the study, as cancer patients or former patients, were already frequently interacting with many parts of the health care system.
"Patients and their families should be encouraged to bring up symptoms like pain or insomnia with physicians. But because oncologists are necessarily focused on treatment of the cancer itself, they often have insufficient time to optimally evaluate and manage symptoms and other factors impacting quality of life. We have shown in an earlier study that one effective solution might be a partnership between a telephone-based symptom management team and community-based oncology practices,," said Dr. Kroenke, who is a research scientist with the Center for Implementing Evidence-Based Practice at the Richard Roudebush VA Medical Center and an Indiana University Melvin and Bren Simon Cancer Center member.
The previous study, published earlier in 2010 in the Journal of the American Medical Association, reported that an economical, centralized approach is feasible to conduct and significantly improved symptoms of pain and depression in patients in any phase of cancer. That approach gave patients, many of whom lived in underserved rural areas, one-stop assistance they probably wouldn't have had access to unless they went to a major cancer center, Kroenke said.
Recognizing and managing physical symptoms such as fatigue, pain, nausea, and insomnia may make a significant difference regardless of type or phase of cancer. The researchers plan to investigate medical and behavioral strategies and combinations of both approaches to control these symptoms.
Notes:
In addition to Dr. Kroenke, co-authors of "Somatic Symptoms in Patients with Cancer Experiencing Pain or Depression" are "Xin Zhong, R.N. and Janet Carpenter, Ph.D., R.N., of the IU School of Nursing; Dale Theobald, M.D., Ph.D. of Community Home Health Hospice and Symptom Management Group; Jingwei Wu, M.S., of the IU School of Medicine; and Wanzhu Tu, Ph.D., of the Regenstrief Institute and the IU School of Medicine. The study was supported by a grant from the National Cancer Institute.
четверг, 18 августа 2011 г.
Workplace Burden Of Depression Magnified By Co-morbid Fatigue And Anxiety, New Study Shows
Depression, well known to reduce workplace productivity, causes significantly greater productivity declines when accompanied by common co-occurring conditions such as fatigue, sleep problems or anxiety, according to a large new study presented today at the American Psychiatric Association's 160th Annual Meeting in San Diego.[i] The study also showed that co-occurring fatigue or sleep problems significantly increased depression-related healthcare costs.1
In the study, which used an integrated database of healthcare claims and surveys of almost 14,000 employees at two large U.S. firms, researchers analyzed data on healthcare spending and presenteeism (i.e., employees' estimates of their own productivity while at work) to assess the impact of depression and other chronic conditions. 1
Overall, among the ten most prevalent physical and mental conditions measured, depression had the single largest negative effect on work productivity. That effect was magnified when fatigue, sleep problems and anxiety - conditions that often co-occur with depression - were also present. Further, while depression had significant adverse effects on productivity in the absence of other co-morbid conditions, effects of these other conditions in the absence of depression were not as pronounced. 1
"While depression itself has a significant economic impact, the negative effect on both workplace productivity and healthcare costs can be considerably increased when employees who are depressed also suffer from other conditions," said Ronald C. Kessler, Ph.D., Professor of Health Care Policy, Harvard Medical School, Boston, Mass. "These findings suggest we should aim to identify and minimize multiple factors associated with depression early to reduce this burden."
About the Study1
Methodology
Two large U.S. firms surveyed their employees about their productivity. The first sample, from a firm in the high-tech industry, consisted of 7,320 employees; the second, from a manufacturing company, included 6,490 employees. The companies then hired an independent data aggregation company to combine the survey data with medical and pharmacy claims data into a single database. The aggregation firm, in compliance with U.S. privacy laws, stripped out all information that could identify individual patients. This de-identified database was then used to compare and contrast the effects of depression and other conditions that often co-occur with depression, such as anxiety, chronic fatigue, and chronic sleep problems on absenteeism, work productivity and direct healthcare costs. Productivity was measured partly by reviewing absenteeism and partly by asking employees to rate their own "presenteeism"??????" their productivity on days when they were present but not performing at their usual standards ??????" using the WHO Health and Work Performance Questionnaire (HPQ). Each worker's rating was compared with the average productivity score for all employees at the company. Statistical regression analysis was used to assess the effect of the target health problems on absenteeism and productivity while controlling for socio-demographics and claims-based measures of utilization in the six-month pre-survey period. Results were weighted to adjust for differential survey non-response.
Employee samples were geographically diverse, however study findings are not nationally representative of the U.S. employed population. Employee sample characteristics include:
-- Average age
Employer #1 - 40.3
Employer #2 - 37.0
-- Proportion female
Employer #1 - 23%
Employer #2 - 34%
-- Proportion paid hourly (vs. salaried employees)
Employer #1 - 2%
Employer #2 - 26%
-- Proportion with covered spouse
Employer #1 - 77%
Employer #2 - 63%
-- Number of children (average)
Employer #1 - 1.3
Employer #2 - 1.1%
Additional Results
Among the most prevalent physical and mental conditions, depression had the largest negative effect on overall work performance, followed by fatigue, anxiety, chronic sleeping problems, obesity. Painful conditions also had large effects. However, when the effect of each condition was examined while controlling for comorbid depression, the independent effect of the condition was diminished. This suggests that the other conditions examined in this study have their biggest impact on work performance when they occur with depression.
At one of the companies, depression in the absence of anxiety or fatigue/sleep disturbance was associated with a 3.5 percent reduction in the presenteeism score, equivalent to seven to eight full-time workdays per year. Depression with anxiety or fatigue/sleep disturbance was associated with larger negative effects (6-8 percent reduction in average presenteeism score), and having depression with both anxiety and fatigue/sleep problems was associated with a 13.2 percent reduction.
Employees experiencing depression had average annual costs in excess of both employer sample averages ($4,132 and $3,504 compared to $3,286 and 2,653, respectively). Employees who reported experiencing fatigue or sleep problems with depression had significantly higher average annual costs than those with depression alone ($6,665 and $5,306). (All results noted above statistically significant, p
In the study, which used an integrated database of healthcare claims and surveys of almost 14,000 employees at two large U.S. firms, researchers analyzed data on healthcare spending and presenteeism (i.e., employees' estimates of their own productivity while at work) to assess the impact of depression and other chronic conditions. 1
Overall, among the ten most prevalent physical and mental conditions measured, depression had the single largest negative effect on work productivity. That effect was magnified when fatigue, sleep problems and anxiety - conditions that often co-occur with depression - were also present. Further, while depression had significant adverse effects on productivity in the absence of other co-morbid conditions, effects of these other conditions in the absence of depression were not as pronounced. 1
"While depression itself has a significant economic impact, the negative effect on both workplace productivity and healthcare costs can be considerably increased when employees who are depressed also suffer from other conditions," said Ronald C. Kessler, Ph.D., Professor of Health Care Policy, Harvard Medical School, Boston, Mass. "These findings suggest we should aim to identify and minimize multiple factors associated with depression early to reduce this burden."
About the Study1
Methodology
Two large U.S. firms surveyed their employees about their productivity. The first sample, from a firm in the high-tech industry, consisted of 7,320 employees; the second, from a manufacturing company, included 6,490 employees. The companies then hired an independent data aggregation company to combine the survey data with medical and pharmacy claims data into a single database. The aggregation firm, in compliance with U.S. privacy laws, stripped out all information that could identify individual patients. This de-identified database was then used to compare and contrast the effects of depression and other conditions that often co-occur with depression, such as anxiety, chronic fatigue, and chronic sleep problems on absenteeism, work productivity and direct healthcare costs. Productivity was measured partly by reviewing absenteeism and partly by asking employees to rate their own "presenteeism"??????" their productivity on days when they were present but not performing at their usual standards ??????" using the WHO Health and Work Performance Questionnaire (HPQ). Each worker's rating was compared with the average productivity score for all employees at the company. Statistical regression analysis was used to assess the effect of the target health problems on absenteeism and productivity while controlling for socio-demographics and claims-based measures of utilization in the six-month pre-survey period. Results were weighted to adjust for differential survey non-response.
Employee samples were geographically diverse, however study findings are not nationally representative of the U.S. employed population. Employee sample characteristics include:
-- Average age
Employer #1 - 40.3
Employer #2 - 37.0
-- Proportion female
Employer #1 - 23%
Employer #2 - 34%
-- Proportion paid hourly (vs. salaried employees)
Employer #1 - 2%
Employer #2 - 26%
-- Proportion with covered spouse
Employer #1 - 77%
Employer #2 - 63%
-- Number of children (average)
Employer #1 - 1.3
Employer #2 - 1.1%
Additional Results
Among the most prevalent physical and mental conditions, depression had the largest negative effect on overall work performance, followed by fatigue, anxiety, chronic sleeping problems, obesity. Painful conditions also had large effects. However, when the effect of each condition was examined while controlling for comorbid depression, the independent effect of the condition was diminished. This suggests that the other conditions examined in this study have their biggest impact on work performance when they occur with depression.
At one of the companies, depression in the absence of anxiety or fatigue/sleep disturbance was associated with a 3.5 percent reduction in the presenteeism score, equivalent to seven to eight full-time workdays per year. Depression with anxiety or fatigue/sleep disturbance was associated with larger negative effects (6-8 percent reduction in average presenteeism score), and having depression with both anxiety and fatigue/sleep problems was associated with a 13.2 percent reduction.
Employees experiencing depression had average annual costs in excess of both employer sample averages ($4,132 and $3,504 compared to $3,286 and 2,653, respectively). Employees who reported experiencing fatigue or sleep problems with depression had significantly higher average annual costs than those with depression alone ($6,665 and $5,306). (All results noted above statistically significant, p
вторник, 16 августа 2011 г.
DBSA Anxiety, Depression Awareness Week Survey Underscores Strong Relationship Between Common Mental Disorders
People living with depression
or bipolar disorder are also likely to have significant problems with
anxiety, both diagnosed and undiagnosed, according to an online survey
conducted by the Depression and Bipolar Support Alliance (DBSA). The
nation's largest patient- run organization focusing on two of the most
prevalent mental illnesses conducted the survey to mark National Anxiety
and Depression Awareness Week, May 6-12.
The survey of nearly 800 people with depression or bipolar disorder
reveals telling indicators that reinforce a strong relationship between
anxiety and mood disorders, a fact not unknown to mental health researchers
and clinicians, but nevertheless important for people living with these
common conditions to fully understand.
According to the National Institute of Mental Health (NIMH),
approximately 24 million Americans live with a diagnosed mood disorder
while 40 million American adults are diagnosed with an anxiety disorder.
Most people deal with anxiety on some level from time to time, but anxiety
disorders are characterized by prolonged periods (at least six months) of
exaggerated worry and fearfulness that keep people from doing things most
others take for granted.
Common anxiety disorders include generalized anxiety disorder (GAD),
obsessive compulsive disorder (OCD), panic disorder, post-traumatic stress
disorder (PTSD) and social phobias.
Eighty-seven percent of survey respondents said they either had a
diagnosed anxiety disorder or an undiagnosed problem with anxiety. Those
findings echo the Bipolar Genetics Initiative study conducted by NIMH in
2006 that found more than 90 percent of people with panic disorder also had
some form of depression or bipolar disorder.
Respondents with both depressive and anxiety diagnoses cited
generalized anxiety disorder (68%), panic disorder (57%) and PTSD (30%) as
the most common anxiety conditions. Since some people are diagnosed with
more than one anxiety disorder, the survey allowed for multiple answers.
Seventy-three percent of respondents reported that their anxiety and mood
disorders were related, with 43 percent saying their anxiety worsened their
depressive illness and 30 percent reporting the opposite.
"For people living with our illnesses it's important to manage stress
and anxiety," said DBSA president Sue Bergeson. "Whether we have a
diagnosed anxiety disorder or not, it's imperative that we develop and
adhere to wellness plans and strategies that minimize stress so that we are
living full, happy and productive lives with the goal of full and sustained
recovery."
When asked about potential triggers that worsened their anxiety, survey
respondents most commonly cited disrupted sleep patterns (57%), stressful
social situations (51%) and being in crowded areas (43%). Other anxiety
inducing situations included workplace pressures, familial problems and
special occasions, such as holidays and birthdays.
While less than half of respondents (43%) expressed confidence that
their medications and/or treatment plans were effective in helping manage
anxiety, they were quick to acknowledge that medication was the most
important thing they did to treat their conditions. Nearly three quarters
(72%) of respondents said taking medication was the best way to alleviate
their symptoms. Other helpful activities cited included sleep or rest (56%)
and talk therapy (40%).
The findings from the survey reinforce much of the research done on the
relationship between anxiety and mood disorders. Monitoring sleep patterns
and being aware of the types of social situations that induce stress and
anxiety are good ways of managing the illnesses, Bergeson suggested.
"We can't view or treat these illnesses separately; we need to take a
holistic approach so that we are addressing anything and everything that
impedes recovery," she added. "Medication and therapy may be only part of
the equation; many people are relying on peer-led support groups, mood
trackers, journaling and other types of techniques and strategies to
achieve wellness."
For more information on mood and anxiety disorders, visit
DBSAlliance
Depression and Bipolar Support Alliance
dbsalliance
or bipolar disorder are also likely to have significant problems with
anxiety, both diagnosed and undiagnosed, according to an online survey
conducted by the Depression and Bipolar Support Alliance (DBSA). The
nation's largest patient- run organization focusing on two of the most
prevalent mental illnesses conducted the survey to mark National Anxiety
and Depression Awareness Week, May 6-12.
The survey of nearly 800 people with depression or bipolar disorder
reveals telling indicators that reinforce a strong relationship between
anxiety and mood disorders, a fact not unknown to mental health researchers
and clinicians, but nevertheless important for people living with these
common conditions to fully understand.
According to the National Institute of Mental Health (NIMH),
approximately 24 million Americans live with a diagnosed mood disorder
while 40 million American adults are diagnosed with an anxiety disorder.
Most people deal with anxiety on some level from time to time, but anxiety
disorders are characterized by prolonged periods (at least six months) of
exaggerated worry and fearfulness that keep people from doing things most
others take for granted.
Common anxiety disorders include generalized anxiety disorder (GAD),
obsessive compulsive disorder (OCD), panic disorder, post-traumatic stress
disorder (PTSD) and social phobias.
Eighty-seven percent of survey respondents said they either had a
diagnosed anxiety disorder or an undiagnosed problem with anxiety. Those
findings echo the Bipolar Genetics Initiative study conducted by NIMH in
2006 that found more than 90 percent of people with panic disorder also had
some form of depression or bipolar disorder.
Respondents with both depressive and anxiety diagnoses cited
generalized anxiety disorder (68%), panic disorder (57%) and PTSD (30%) as
the most common anxiety conditions. Since some people are diagnosed with
more than one anxiety disorder, the survey allowed for multiple answers.
Seventy-three percent of respondents reported that their anxiety and mood
disorders were related, with 43 percent saying their anxiety worsened their
depressive illness and 30 percent reporting the opposite.
"For people living with our illnesses it's important to manage stress
and anxiety," said DBSA president Sue Bergeson. "Whether we have a
diagnosed anxiety disorder or not, it's imperative that we develop and
adhere to wellness plans and strategies that minimize stress so that we are
living full, happy and productive lives with the goal of full and sustained
recovery."
When asked about potential triggers that worsened their anxiety, survey
respondents most commonly cited disrupted sleep patterns (57%), stressful
social situations (51%) and being in crowded areas (43%). Other anxiety
inducing situations included workplace pressures, familial problems and
special occasions, such as holidays and birthdays.
While less than half of respondents (43%) expressed confidence that
their medications and/or treatment plans were effective in helping manage
anxiety, they were quick to acknowledge that medication was the most
important thing they did to treat their conditions. Nearly three quarters
(72%) of respondents said taking medication was the best way to alleviate
their symptoms. Other helpful activities cited included sleep or rest (56%)
and talk therapy (40%).
The findings from the survey reinforce much of the research done on the
relationship between anxiety and mood disorders. Monitoring sleep patterns
and being aware of the types of social situations that induce stress and
anxiety are good ways of managing the illnesses, Bergeson suggested.
"We can't view or treat these illnesses separately; we need to take a
holistic approach so that we are addressing anything and everything that
impedes recovery," she added. "Medication and therapy may be only part of
the equation; many people are relying on peer-led support groups, mood
trackers, journaling and other types of techniques and strategies to
achieve wellness."
For more information on mood and anxiety disorders, visit
DBSAlliance
Depression and Bipolar Support Alliance
dbsalliance
воскресенье, 14 августа 2011 г.
Wellness Expert Offers Tips On Coping With Economic Turmoil
America's financial crises is fueling chronic stress and limiting some people's ability to think clearly, control emotions and regulate bodily functions in a healthy manner. University of Alabama at Birmingham (UAB) Associate Professor Josh Klapow, Ph.D., says now is the time to take control of emotions and better regulate the mind-body stress response. Klapow is a clinical psychologist and author of "Living SMART: 5 Essential Skills to Change Your Health Habits Forever."
Klapow breaks the financial crises stress and anxiety triggers into two parts: productive worry vs. unproductive worry. "Productive worry is thinking on situations you can control, and you should use productive worry to take actions that reduce stress and relieve anxiety. Unproductive worry is thinking about things you cannot control," he said. He offers four 'action points' to get a handle on emotions and the make country's economic turmoil easier to bare. Those four points are spelled out on Klapow's new blog blogs.uab/drjoshk. They include:
1. Take action. "Make a family budget, meet with an accountant, trade in a vehicle for a more fuel-efficient model, carpool - do things to help reduce your stress," Klapow said.
2. Take a step back. "Don't saturate yourself with stressful information. Stay informed, but take a news break. Most people don't need to track the markets minute by minute."
3. Stay connected. "Don't let the rest of your life dwindle away. Make sure you are paying attention to daily activities: family, friends, social occasions and recreation."
4. Pay attention to yourself. "Remember that stress takes a physical toll. Learn meditation and do muscle relaxation. More simply, pay attention to your stress level throughout the day and occasionally breathe slowly and deeply," Klapow said.
blogs.uab/drjoshk
University of Alabama at Birmingham
Klapow breaks the financial crises stress and anxiety triggers into two parts: productive worry vs. unproductive worry. "Productive worry is thinking on situations you can control, and you should use productive worry to take actions that reduce stress and relieve anxiety. Unproductive worry is thinking about things you cannot control," he said. He offers four 'action points' to get a handle on emotions and the make country's economic turmoil easier to bare. Those four points are spelled out on Klapow's new blog blogs.uab/drjoshk. They include:
1. Take action. "Make a family budget, meet with an accountant, trade in a vehicle for a more fuel-efficient model, carpool - do things to help reduce your stress," Klapow said.
2. Take a step back. "Don't saturate yourself with stressful information. Stay informed, but take a news break. Most people don't need to track the markets minute by minute."
3. Stay connected. "Don't let the rest of your life dwindle away. Make sure you are paying attention to daily activities: family, friends, social occasions and recreation."
4. Pay attention to yourself. "Remember that stress takes a physical toll. Learn meditation and do muscle relaxation. More simply, pay attention to your stress level throughout the day and occasionally breathe slowly and deeply," Klapow said.
blogs.uab/drjoshk
University of Alabama at Birmingham
пятница, 12 августа 2011 г.
Looking On The Bright Side Improves Life Expectancy Of Cardiac Patients
A positive mental attitude appears to have a more powerful impact on the 15-year survival chances of cardiac patients even after the severity of their disease is taken into account, scientists from Duke University Medical Center revealed in the journal Archives of Internal Medicine.
Lead study author, John Barefoot, PhD, explained that theirs was a unique study because it demonstrated that an individual's attitude towards their illness has a double impact:
It influences their return to a normal lifestyle
It significantly improves their long-term health and survival chances (helps patients live longer)
Barefoot and team tracked the progress of heart patients after they had undergone coronary angiography to evaluate blood flow in the heart. Even though previous studies had gauged how a patient's expectations influenced how well they went about their work, exercise and other daily activities, this study showed how it also influenced overall physical health and longevity.
Over 2,800 cardiac patients were asked to evaluate how well they expected to recover and return to a normal lifestyle - each was given a psychological questionnaire.
1,637 of them died within fifteen years. 885 (54%) from cardiovascular disease.
Even after taking into account several impacting factors, such as coronary disease severity, sex, socioeconomic status, social support, age, and general functional ability when hospitalized, the higher risk of death remained.
Barefoot said:
"We know there is a relationship between depression and increased rates of mortality. These findings demonstrate the magnitude of the impact of patient expectations on the recovery process above and beyond depression and other psychological or social factors."
The authors explained that positive thinkers had several things that favored them, such as better treatment compliance (adherence), and a higher likelihood of trying things out that are good for their physical and mental health. Some say that pessimism, i.e. negative thinking, leads to stress and tension, which can be damaging for health.
Barefoot said:
"The take-home message is that having positive expectations can not only make you feel better but also potentially live longer."
"Recovery Expectations and Long-term Prognosis of Patients With Coronary Heart Disease"
John C. Barefoot, PhD; Beverly H. Brummett, PhD; Redford B. Williams, MD; Ilene C. Siegler, PhD, MPH; Michael J. Helms, BS; Stephen H. Boyle, PhD; Nancy E. Clapp-Channing, RN, MPH; Daniel B. Mark, MD
Arch Intern Med. Published online February 28, 2011. doi:10.1001/archinternmed.2011.41
Lead study author, John Barefoot, PhD, explained that theirs was a unique study because it demonstrated that an individual's attitude towards their illness has a double impact:
It influences their return to a normal lifestyle
It significantly improves their long-term health and survival chances (helps patients live longer)
Barefoot and team tracked the progress of heart patients after they had undergone coronary angiography to evaluate blood flow in the heart. Even though previous studies had gauged how a patient's expectations influenced how well they went about their work, exercise and other daily activities, this study showed how it also influenced overall physical health and longevity.
Over 2,800 cardiac patients were asked to evaluate how well they expected to recover and return to a normal lifestyle - each was given a psychological questionnaire.
1,637 of them died within fifteen years. 885 (54%) from cardiovascular disease.
Even after taking into account several impacting factors, such as coronary disease severity, sex, socioeconomic status, social support, age, and general functional ability when hospitalized, the higher risk of death remained.
Barefoot said:
"We know there is a relationship between depression and increased rates of mortality. These findings demonstrate the magnitude of the impact of patient expectations on the recovery process above and beyond depression and other psychological or social factors."
The authors explained that positive thinkers had several things that favored them, such as better treatment compliance (adherence), and a higher likelihood of trying things out that are good for their physical and mental health. Some say that pessimism, i.e. negative thinking, leads to stress and tension, which can be damaging for health.
Barefoot said:
"The take-home message is that having positive expectations can not only make you feel better but also potentially live longer."
"Recovery Expectations and Long-term Prognosis of Patients With Coronary Heart Disease"
John C. Barefoot, PhD; Beverly H. Brummett, PhD; Redford B. Williams, MD; Ilene C. Siegler, PhD, MPH; Michael J. Helms, BS; Stephen H. Boyle, PhD; Nancy E. Clapp-Channing, RN, MPH; Daniel B. Mark, MD
Arch Intern Med. Published online February 28, 2011. doi:10.1001/archinternmed.2011.41
среда, 10 августа 2011 г.
Prescribing Exercise For Depression, Anxiety
Exercise is a magic drug for many people with depression and anxiety disorders, and it should be more widely prescribed by mental health care providers, according to researchers who analyzed the results of numerous published studies.
"Exercise has been shown to have tremendous benefits for mental health," says Jasper Smits, director of the Anxiety Research and Treatment Program at Southern Methodist University in Dallas. "The more therapists who are trained in exercise therapy, the better off patients will be."
Smits and Michael Otto, psychology professor at Boston University, based their finding on an analysis of dozens of population-based studies, clinical studies and meta-analytic reviews related to exercise and mental health, including the authors' meta-analysis of exercise interventions for mental health and studies on reducing anxiety sensitivity with exercise. The researchers' review demonstrated the efficacy of exercise programs in reducing depression and anxiety.
The traditional treatments of cognitive behavioral therapy and pharmacotherapy don't reach everyone who needs them, says Smits, an associate professor of psychology.
"Exercise can fill the gap for people who can't receive traditional therapies because of cost or lack of access, or who don't want to because of the perceived social stigma associated with these treatments," he says. "Exercise also can supplement traditional treatments, helping patients become more focused and engaged."
The researchers presented their findings March 6 in Baltimore at the annual conference of the Anxiety Disorder Association of America. Their workshop was based on their therapist guide "Exercise for Mood and Anxiety Disorders," with accompanying patient workbook (Oxford University Press, September 2009).
"Individuals who exercise report fewer symptoms of anxiety and depression, and lower levels of stress and anger," Smits says. "Exercise appears to affect, like an antidepressant, particular neurotransmitter systems in the brain, and it helps patients with depression re-establish positive behaviors. For patients with anxiety disorders, exercise reduces their fears of fear and related bodily sensations such as a racing heart and rapid breathing."
After patients have passed a health assessment, Smits says, they should work up to the public health dose, which is 150 minutes a week of moderate-intensity activity or 75 minutes a week of vigorous-intensity activity. At a time when 40 percent of Americans are sedentary, he says, mental health care providers can serve as their patients' exercise guides and motivators.
"Rather than emphasize the long-term health benefits of an exercise program - which can be difficult to sustain - we urge providers to focus with their patients on the immediate benefits," he says. "After just 25 minutes, your mood improves, you are less stressed, you have more energy - and you'll be motivated to exercise again tomorrow. A bad mood is no longer a barrier to exercise; it is the very reason to exercise."
Smits says health care providers who prescribe exercise also must give their patients the tools they need to succeed, such as the daily schedules, problem-solving strategies and goal-setting featured in his guide for therapists.
"Therapists can help their patients take specific, achievable steps," he says. "This isn't about working out five times a week for the next year. It's about exercising for 20 or 30 minutes and feeling better today."
"Exercise has been shown to have tremendous benefits for mental health," says Jasper Smits, director of the Anxiety Research and Treatment Program at Southern Methodist University in Dallas. "The more therapists who are trained in exercise therapy, the better off patients will be."
Smits and Michael Otto, psychology professor at Boston University, based their finding on an analysis of dozens of population-based studies, clinical studies and meta-analytic reviews related to exercise and mental health, including the authors' meta-analysis of exercise interventions for mental health and studies on reducing anxiety sensitivity with exercise. The researchers' review demonstrated the efficacy of exercise programs in reducing depression and anxiety.
The traditional treatments of cognitive behavioral therapy and pharmacotherapy don't reach everyone who needs them, says Smits, an associate professor of psychology.
"Exercise can fill the gap for people who can't receive traditional therapies because of cost or lack of access, or who don't want to because of the perceived social stigma associated with these treatments," he says. "Exercise also can supplement traditional treatments, helping patients become more focused and engaged."
The researchers presented their findings March 6 in Baltimore at the annual conference of the Anxiety Disorder Association of America. Their workshop was based on their therapist guide "Exercise for Mood and Anxiety Disorders," with accompanying patient workbook (Oxford University Press, September 2009).
"Individuals who exercise report fewer symptoms of anxiety and depression, and lower levels of stress and anger," Smits says. "Exercise appears to affect, like an antidepressant, particular neurotransmitter systems in the brain, and it helps patients with depression re-establish positive behaviors. For patients with anxiety disorders, exercise reduces their fears of fear and related bodily sensations such as a racing heart and rapid breathing."
After patients have passed a health assessment, Smits says, they should work up to the public health dose, which is 150 minutes a week of moderate-intensity activity or 75 minutes a week of vigorous-intensity activity. At a time when 40 percent of Americans are sedentary, he says, mental health care providers can serve as their patients' exercise guides and motivators.
"Rather than emphasize the long-term health benefits of an exercise program - which can be difficult to sustain - we urge providers to focus with their patients on the immediate benefits," he says. "After just 25 minutes, your mood improves, you are less stressed, you have more energy - and you'll be motivated to exercise again tomorrow. A bad mood is no longer a barrier to exercise; it is the very reason to exercise."
Smits says health care providers who prescribe exercise also must give their patients the tools they need to succeed, such as the daily schedules, problem-solving strategies and goal-setting featured in his guide for therapists.
"Therapists can help their patients take specific, achievable steps," he says. "This isn't about working out five times a week for the next year. It's about exercising for 20 or 30 minutes and feeling better today."
понедельник, 8 августа 2011 г.
Psychologist Counsels Junking The Self-Help Books And Using More Realistic Yardsticks
In the not-too-distant past, young people aspired to become lawyers and doctors. Now they yearn to achieve the celebrity of a Mark Zuckerberg or Oprah Winfrey - and these goals extend to adults as well. This has wreaked havoc with our self-image, says a Tel Aviv University psychologist, and undermined our sense of self-worth.
Extensive research from Dr. Carlo Strenger of Tel Aviv University's Department of Psychology demonstrates that people over the past ten years have been suffering from an increasing fear of their own "insignificance," something he first recognized in his own clinical practice. Noticing a surge of this fear in his patients, he began an interdisciplinary research project on the phenomenon.
His findings are presented in a new book, The Fear of Insignificance: Searching for Meaning in the Twenty-first Century (Palgrave Macmillan), which illustrates his decade-long investigation into an unprecedented increase in levels of anxiety and depression. It's the first study of its kind to address the issue on a large scale.
The evolution of "homo globalis": Hot or not?
The phenomenon of global angst in the last 10 years is well established by research findings, he notes, but it has never been analyzed and explained in its entirety. "To see the whole elephant and not just its parts," he says, "you need a wide-ranging interdisciplinary framework."
The research reported in his book integrates hundreds of research projects, from economic models to sociological studies and experimental existential psychology. Strenger concludes that the fear of insignificance is due global access - comparing ourselves with the most "significant" people around the world.
"The impact of the global infotainment network on the individual is to blame," says Strenger. "A new species is born: homo globalis - global man - and we are defined by our intimate connection to the global infotainment network, which has turned ranking and rating people on scales of wealth and celebrity into an obsession."
In the past being a lawyer or doctor was a very reputable profession, he explains. Today, even high achievers constantly fear that they are insignificant when they compare themselves to success stories promulgated by the print and electronic media, constantly afraid that their rating on a variety of scales may drop. "This creates highly unstable self-esteem and an unstable society," he says.
In his book, Strenger also attacks new pop-spiritualism that promises instant change and instant relief. Instead of solving an existential unease, such resources just create ever growing disappointment. The cheap-fix guru books for instant spirituality that line airport shelves do not provide any long-term solutions, he says.
The cure? Dump the junk and look inside
Strenger counsels that people stop measuring their achievement through cultural fantasies of riches and celebrity, which reflect a media craze for ranking and rating people and cannot lead to fulfillment. The remedy is a process that he calls "active self-acceptance" through a sustained quest for self-knowledge as part of our process of maturation. The fear of insignificance can only be overcome through strong individual and cultural identity over and above measurable achievement.
He believes that people need to invest as much time in developing their worldviews as their careers. "Stable meaning cannot be found in cheap paperbacks. The media are feeding people spiritual junk food. People should invest time and thought to their worldviews and self-understanding in the same way they invest in medical studies and law school," Strenger advises.
A liberal education is a good way to start, but the process must continue through a lifetime. To live a fulfilling life, we need to engage in a life-long process of learning and evolving, he concludes.
Extensive research from Dr. Carlo Strenger of Tel Aviv University's Department of Psychology demonstrates that people over the past ten years have been suffering from an increasing fear of their own "insignificance," something he first recognized in his own clinical practice. Noticing a surge of this fear in his patients, he began an interdisciplinary research project on the phenomenon.
His findings are presented in a new book, The Fear of Insignificance: Searching for Meaning in the Twenty-first Century (Palgrave Macmillan), which illustrates his decade-long investigation into an unprecedented increase in levels of anxiety and depression. It's the first study of its kind to address the issue on a large scale.
The evolution of "homo globalis": Hot or not?
The phenomenon of global angst in the last 10 years is well established by research findings, he notes, but it has never been analyzed and explained in its entirety. "To see the whole elephant and not just its parts," he says, "you need a wide-ranging interdisciplinary framework."
The research reported in his book integrates hundreds of research projects, from economic models to sociological studies and experimental existential psychology. Strenger concludes that the fear of insignificance is due global access - comparing ourselves with the most "significant" people around the world.
"The impact of the global infotainment network on the individual is to blame," says Strenger. "A new species is born: homo globalis - global man - and we are defined by our intimate connection to the global infotainment network, which has turned ranking and rating people on scales of wealth and celebrity into an obsession."
In the past being a lawyer or doctor was a very reputable profession, he explains. Today, even high achievers constantly fear that they are insignificant when they compare themselves to success stories promulgated by the print and electronic media, constantly afraid that their rating on a variety of scales may drop. "This creates highly unstable self-esteem and an unstable society," he says.
In his book, Strenger also attacks new pop-spiritualism that promises instant change and instant relief. Instead of solving an existential unease, such resources just create ever growing disappointment. The cheap-fix guru books for instant spirituality that line airport shelves do not provide any long-term solutions, he says.
The cure? Dump the junk and look inside
Strenger counsels that people stop measuring their achievement through cultural fantasies of riches and celebrity, which reflect a media craze for ranking and rating people and cannot lead to fulfillment. The remedy is a process that he calls "active self-acceptance" through a sustained quest for self-knowledge as part of our process of maturation. The fear of insignificance can only be overcome through strong individual and cultural identity over and above measurable achievement.
He believes that people need to invest as much time in developing their worldviews as their careers. "Stable meaning cannot be found in cheap paperbacks. The media are feeding people spiritual junk food. People should invest time and thought to their worldviews and self-understanding in the same way they invest in medical studies and law school," Strenger advises.
A liberal education is a good way to start, but the process must continue through a lifetime. To live a fulfilling life, we need to engage in a life-long process of learning and evolving, he concludes.
суббота, 6 августа 2011 г.
A Risk Factor In Childhood Asthma Symptoms May Be Mother's Depression
Asthma symptoms can worsen in children with depressed mothers, according to research from Johns Hopkins Children's Center published online in the Journal of Pediatric Psychology.
Analyzing data from interviews with 262 mothers of African-American children with asthma - a population disproportionately affected by this inflammatory airway disorder - the Hopkins investigators found that children whose mothers had more depressive symptoms had more frequent asthma symptoms during the six-months of the study. Conversely, children whose mothers reported fewer depressive symptoms had less frequent asthma symptoms.
Researchers tracked ups and downs in maternal depression as related to the frequency of symptoms among children.
"Even though our research was not set up to measure just how much a mom's depression increased the frequency of her child's symptoms, a clear pattern emerged in which the latter followed the earlier," says senior investigator Kristin Riekert, Ph.D., a pediatric psychologist and co-director of the Johns Hopkins Adherence Research Center.
But while maternal depression appeared to aggravate a child's asthma, the opposite was not true: How often a child had symptoms did not seem to affect the mother's depressive symptoms, an important finding that suggests maternal depression is an independent risk factor that can portend a child's symptoms, researchers say.
Past studies have shown that children with chronic health conditions fare worse if their primary caregiver is depressed, but none have teased out the exact interplay between the two.
"Intuitively, it may seem that we're dealing with a chicken-egg situation, but our study suggests otherwise," Riekert says. "The fact that mom's depression was not affected by how often her child had symptoms really caught us off guard, but it also suggested which factor comes first."
Researchers did not study why and how a mother's depression affects a child's asthma status, but because depression often involves fatigue, memory lapses and difficulty concentrating, it can affect a parent's ability to manage the child's chronic condition, which can involve daily, and sometimes complex, drug regimens and frequent visits to the doctor.
"Mom is the one who must implement the doctor's recommendations for treatment and follow-up, and if she is depressed she can't do it well, so the child will suffer," says lead investigator Michiko Otsuki, Ph.D., a behavioral medicine fellow at Johns Hopkins at the time of the study, now at the University of South Florida St. Petersburg.
Investigators say their findings should prompt pediatricians who treat children with asthma to pay close attention to the child's primary caregiver - whether or not it is the mother - and screen and refer them for treatment if needed.
"We ask these parents if they are smokers all the time, so maybe it's time to start asking them if they are coping well emotionally," said co-investigator Arlene Butz, Sc.D., a pediatric asthma specialist at Johns Hopkins Children's Center. "Doctors are trained to pick up on subtle clues, so if they see a red flag in mom, they should follow-up with a depression screener and referral if needed."
Treating depressed mothers whose children are at high-risk for asthma complications will likely benefit both mother and child, researchers say, while providing a clear treatment target to help reduce the burden of asthma in the United States. Asthma is the country's leading pediatric chronic illness, affecting 6.5 million children under the age of 18, according to the CDC.
The Hopkins study included only mothers but investigators believe a similar pattern would emerge regardless of who the primary caregiver is.
Researchers caution that the mothers in their study were screened for depression with a standard questionnaire, which is a reliable detector of symptoms but not a firm diagnosis.
The Hopkins findings came from a high-risk, inner-city population and thus cannot be statistically extended to other ethnic and socioeconomic groups, but researchers say the effect of caregiver depression on a child's asthma likely transcends demographics.
The research was funded by the National Heart Lung Blood Institute.
Other Hopkins researchers involved in the study included Michelle Eakin, Ph.D., Lisa Arceneaux, Psy.D., Cynthia Rand, Ph.D.
Analyzing data from interviews with 262 mothers of African-American children with asthma - a population disproportionately affected by this inflammatory airway disorder - the Hopkins investigators found that children whose mothers had more depressive symptoms had more frequent asthma symptoms during the six-months of the study. Conversely, children whose mothers reported fewer depressive symptoms had less frequent asthma symptoms.
Researchers tracked ups and downs in maternal depression as related to the frequency of symptoms among children.
"Even though our research was not set up to measure just how much a mom's depression increased the frequency of her child's symptoms, a clear pattern emerged in which the latter followed the earlier," says senior investigator Kristin Riekert, Ph.D., a pediatric psychologist and co-director of the Johns Hopkins Adherence Research Center.
But while maternal depression appeared to aggravate a child's asthma, the opposite was not true: How often a child had symptoms did not seem to affect the mother's depressive symptoms, an important finding that suggests maternal depression is an independent risk factor that can portend a child's symptoms, researchers say.
Past studies have shown that children with chronic health conditions fare worse if their primary caregiver is depressed, but none have teased out the exact interplay between the two.
"Intuitively, it may seem that we're dealing with a chicken-egg situation, but our study suggests otherwise," Riekert says. "The fact that mom's depression was not affected by how often her child had symptoms really caught us off guard, but it also suggested which factor comes first."
Researchers did not study why and how a mother's depression affects a child's asthma status, but because depression often involves fatigue, memory lapses and difficulty concentrating, it can affect a parent's ability to manage the child's chronic condition, which can involve daily, and sometimes complex, drug regimens and frequent visits to the doctor.
"Mom is the one who must implement the doctor's recommendations for treatment and follow-up, and if she is depressed she can't do it well, so the child will suffer," says lead investigator Michiko Otsuki, Ph.D., a behavioral medicine fellow at Johns Hopkins at the time of the study, now at the University of South Florida St. Petersburg.
Investigators say their findings should prompt pediatricians who treat children with asthma to pay close attention to the child's primary caregiver - whether or not it is the mother - and screen and refer them for treatment if needed.
"We ask these parents if they are smokers all the time, so maybe it's time to start asking them if they are coping well emotionally," said co-investigator Arlene Butz, Sc.D., a pediatric asthma specialist at Johns Hopkins Children's Center. "Doctors are trained to pick up on subtle clues, so if they see a red flag in mom, they should follow-up with a depression screener and referral if needed."
Treating depressed mothers whose children are at high-risk for asthma complications will likely benefit both mother and child, researchers say, while providing a clear treatment target to help reduce the burden of asthma in the United States. Asthma is the country's leading pediatric chronic illness, affecting 6.5 million children under the age of 18, according to the CDC.
The Hopkins study included only mothers but investigators believe a similar pattern would emerge regardless of who the primary caregiver is.
Researchers caution that the mothers in their study were screened for depression with a standard questionnaire, which is a reliable detector of symptoms but not a firm diagnosis.
The Hopkins findings came from a high-risk, inner-city population and thus cannot be statistically extended to other ethnic and socioeconomic groups, but researchers say the effect of caregiver depression on a child's asthma likely transcends demographics.
The research was funded by the National Heart Lung Blood Institute.
Other Hopkins researchers involved in the study included Michelle Eakin, Ph.D., Lisa Arceneaux, Psy.D., Cynthia Rand, Ph.D.
четверг, 4 августа 2011 г.
50% of depression patients still suffer from depression 18 months later
Half of patients treated for depression in primary care facilities during a recent study still suffered from the condition 18 to 24 months later, according to recent research.
Patients who were unemployed, had suicidal thoughts at the beginning of the study and who stopped taking antidepressant medication on their own, before their doctor told them to quit the treatment were more likely to suffer persistent depression symptoms than those who recovered from depression over the course of the study, according to Catherine Sherbourne, Ph.D., of RAND and colleagues.
Their findings are published in the General Hospital Psychiatry.
Those with persistent depression were also the most likely to pursue aggressive therapy that combined medication and counseling sessions "suggesting that the persistent depression was not because of less intensive treatment and may represent true treatment resistance," Sherbourne says.
Researchers and physicians need to learn more about the track record of depression treatment in primary care, since primary care settings like clinics and hospitals treat more than half of all depressed patients in the United States, the authors say.
"Relative to patients who recovered, patients with poor treatment responses continued to use both general medical and mental health specialty services of all types, placing a burden on themselves, friends and family and on the health care system," Sherbourne says.
Sherbourne and colleagues followed the treatment outcomes for 1,248 people diagnosed with depression at 46 primary care clinics nationwide. Of this group, less than half received "minimally appropriate treatment" for their depression, defined as four or more special counseling sessions during six months or the use of approved antidepressant drugs for at least two months. Patients in the study could choose whether to receive therapy only, drugs only, a combination of the two or no treatment at all.
Only 442 patients received at least two six-month sessions of treatment. Of those patients, 261 people remained depressed and 181 had recovered from depression 18 to 24 months after the study started.
Patients with persistent depression were more likely than those who recovered to report side effects from their medication, to be in worse mental and physical health at the start of the study and to have sought prior treatment for depression. Patients who recovered were more likely to prefer counseling at the start of the study.
Those with persistent depression were also more likely to say they received less care from their doctors than they wanted. When asked why they did not seek further help, many said "they didn't think they could be helped" or said they were too embarrassed or afraid to bring up the issue with their health care provider, Sherbourne says.
The study was supported by Eli Lilly and Co., which manufactures the antidepressant Prozac, the Agency for Healthcare Research and Quality, the National Institute of Mental Health and the John D. and Catherine T. MacArthur Foundation (which also supports the Health Behavior News Service).
Health Behavior News Service: (202) 387-2829 or hbns.
Interviews: Contact Catherine Sherbourne at cathy_sherbournerand.
General Hospital Psychiatry: Don R. Lipsitt, M.D., at (617) 661-3544.
By Becky Ham, Science Writer
Health Behavior News Service
Center for the Advancement of Health
Contact: Ira R. Allen
Director of Public Affairs
202.387.2829
presscfah
View drug information on Prozac Weekly.
Patients who were unemployed, had suicidal thoughts at the beginning of the study and who stopped taking antidepressant medication on their own, before their doctor told them to quit the treatment were more likely to suffer persistent depression symptoms than those who recovered from depression over the course of the study, according to Catherine Sherbourne, Ph.D., of RAND and colleagues.
Their findings are published in the General Hospital Psychiatry.
Those with persistent depression were also the most likely to pursue aggressive therapy that combined medication and counseling sessions "suggesting that the persistent depression was not because of less intensive treatment and may represent true treatment resistance," Sherbourne says.
Researchers and physicians need to learn more about the track record of depression treatment in primary care, since primary care settings like clinics and hospitals treat more than half of all depressed patients in the United States, the authors say.
"Relative to patients who recovered, patients with poor treatment responses continued to use both general medical and mental health specialty services of all types, placing a burden on themselves, friends and family and on the health care system," Sherbourne says.
Sherbourne and colleagues followed the treatment outcomes for 1,248 people diagnosed with depression at 46 primary care clinics nationwide. Of this group, less than half received "minimally appropriate treatment" for their depression, defined as four or more special counseling sessions during six months or the use of approved antidepressant drugs for at least two months. Patients in the study could choose whether to receive therapy only, drugs only, a combination of the two or no treatment at all.
Only 442 patients received at least two six-month sessions of treatment. Of those patients, 261 people remained depressed and 181 had recovered from depression 18 to 24 months after the study started.
Patients with persistent depression were more likely than those who recovered to report side effects from their medication, to be in worse mental and physical health at the start of the study and to have sought prior treatment for depression. Patients who recovered were more likely to prefer counseling at the start of the study.
Those with persistent depression were also more likely to say they received less care from their doctors than they wanted. When asked why they did not seek further help, many said "they didn't think they could be helped" or said they were too embarrassed or afraid to bring up the issue with their health care provider, Sherbourne says.
The study was supported by Eli Lilly and Co., which manufactures the antidepressant Prozac, the Agency for Healthcare Research and Quality, the National Institute of Mental Health and the John D. and Catherine T. MacArthur Foundation (which also supports the Health Behavior News Service).
Health Behavior News Service: (202) 387-2829 or hbns.
Interviews: Contact Catherine Sherbourne at cathy_sherbournerand.
General Hospital Psychiatry: Don R. Lipsitt, M.D., at (617) 661-3544.
By Becky Ham, Science Writer
Health Behavior News Service
Center for the Advancement of Health
Contact: Ira R. Allen
Director of Public Affairs
202.387.2829
presscfah
View drug information on Prozac Weekly.
вторник, 2 августа 2011 г.
St. Jude Medical Announces First Patient Implants In Clinical Study Evaluating Deep Brain Stimulation For Depression
ST. PAUL, Minn. - June 26, 2008 - St. Jude Medical, Inc. (NYSE:STJ) today announced the first patient implants in a clinical study that is investigating whether deep brain stimulation (DBS) therapy will help people who suffer from major depressive disorder, a severe form of depression. The patients, a 59-year-old woman and a 42-year-old man, were implanted at Alexian Brothers Behavioral Health Hospital in Chicago, with the St. Jude Medical Libra® Deep Brain Stimulation System, an investigational device.
The study, called BROADEN™ (BROdmann Area 25 DEep brain Neuromodulation), is a controlled, multi-site, blinded study that is evaluating the safety and effectiveness of DBS in patients with depression for whom currently available treatments are not effective.
"We are excited to be part of the first double-blind study of Deep Brain Stimulation for depression and remain hopeful that this therapy may prove beneficial for this seriously ill patient population," said Anthony D'Agostino, M.D., medical director of Alexian Brothers Behavioral Health Hospital and the principal investigator at the study site. "The study is an important contribution to the advancement of treatment options for severely depressed patients."
This study is researching a specific area in the brain called Brodmann Area 25 that is thought to be involved in depression. The first research of DBS for depression was conducted in Toronto, Canada, by neurologist Helen S. Mayberg, M.D., and neurosurgeon Andres Lozano, M.D., in 2003. They published their findings in Neuron in March 2005, reporting that brain imaging studies indicate that Brodmann Area 25 appears to be overactive in profoundly sad and depressed people.
St. Jude Medical owns the intellectual property rights, and has various patents issued and pending, for the use of neurostimulation at Brodmann Area 25. The Libra Deep Brain Stimulation System provides mild pulses of current from a device implanted near the collarbone and connected to small electrical leads placed at specific targets in the brain.
"This depression study represents a continuation of our commitment to provide solutions for those who are suffering and in need of additional therapy options," said Chris Chavez, president of the St. Jude Medical ANS Division. "The Brodmann Area 25 study is an important step in bringing physicians and their patients a neuromodulation therapy that, if successful, will treat this debilitating form of depression."
The National Institute of Mental Health estimates that more than 21 million U.S. adults suffer from some kind of depressive disorder. Current therapies are effective for about 80 percent of this patient population according to the National Advisory Mental Health Council. That means approximately 4 million adult Americans live with depression that doesn't respond to medications, psychotherapy or electroconvulsive therapy.
To be eligible for this study, participants must:
-- Currently be diagnosed with major depressive disorder
-- Be between 21- and 70 years old, with onset of first episode before age 45
-- Have tried at least four treatments in their current episode, such as different medications, various combinations of medications or electroconvulsive therapy
-- Have been depressed for at least one year
For more information about this study, call toll-free at 866-787-4332, visit BROADENstudy.
Sponsored by St. Jude Medical, the BROADEN study is being conducted under a U.S. Food and Drug Administration (FDA) investigational device exemption (IDE). Initial study centers are located in Chicago, Dallas and New York City. This clinical study was preceded by a smaller pilot study of 20 patients at three sites in Canada which found that six months after the procedure, 56 percent of the patients experienced at least a 40 percent decrease in depressive symptoms. At last follow-up, 78 percent of the patients were responders, and eight of the patients have re-engaged in life activities such as work, school, travel and relationships, and three of the study patients are considered to be in remission. Patients' symptoms were measured using the Hamilton Rating Scale for Depression.
About St. Jude Medical
St. Jude Medical develops medical technology and services that focus on putting more control into the hands of those who treat cardiac, neurological and chronic pain patients worldwide. The company is dedicated to advancing the practice of medicine by reducing risk wherever possible and contributing to successful outcomes for every patient. Headquartered in St. Paul, Minn., St. Jude Medical employs more than 12,000 people worldwide and has five major focus areas that include: cardiac rhythm management, atrial fibrillation, cardiac surgery, cardiology and neuromodulation. For more information, please visit sjm.
About the ANS Division of St. Jude Medical
The ANS Division (Advanced Neuromodulation Systems) became a part of St. Jude Medical in 2005. The ANS Division is an innovative technology leader dedicated to the design, development, manufacturing and marketing of implantable neuromodulation systems to improve the quality of life for people suffering from disabling chronic pain and other nervous system disorders (ans-medical).
Forward-Looking Statements
This news release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that involve risks and uncertainties. Such forward-looking statements include the expectations, plans and prospects for the Company, including potential clinical successes, anticipated regulatory approvals and future product launches, and projected revenues, margins, earnings, and market shares. The statements made by the Company are based upon management's current expectations and are subject to certain risks and uncertainties that could cause actual results to differ materially from those described in the forward-looking statements. These risks and uncertainties include market conditions and other factors beyond the Company's control and the risk factors and other cautionary statements described in the Company's filings with the SEC, including those described in the Risk Factors and Cautionary Statements sections of the Company's Annual Report on Form 10-K filed on February 27, 2008. The Company does not intend to update these statements and undertakes no duty to any person to provide any such update under any circumstance.
The study, called BROADEN™ (BROdmann Area 25 DEep brain Neuromodulation), is a controlled, multi-site, blinded study that is evaluating the safety and effectiveness of DBS in patients with depression for whom currently available treatments are not effective.
"We are excited to be part of the first double-blind study of Deep Brain Stimulation for depression and remain hopeful that this therapy may prove beneficial for this seriously ill patient population," said Anthony D'Agostino, M.D., medical director of Alexian Brothers Behavioral Health Hospital and the principal investigator at the study site. "The study is an important contribution to the advancement of treatment options for severely depressed patients."
This study is researching a specific area in the brain called Brodmann Area 25 that is thought to be involved in depression. The first research of DBS for depression was conducted in Toronto, Canada, by neurologist Helen S. Mayberg, M.D., and neurosurgeon Andres Lozano, M.D., in 2003. They published their findings in Neuron in March 2005, reporting that brain imaging studies indicate that Brodmann Area 25 appears to be overactive in profoundly sad and depressed people.
St. Jude Medical owns the intellectual property rights, and has various patents issued and pending, for the use of neurostimulation at Brodmann Area 25. The Libra Deep Brain Stimulation System provides mild pulses of current from a device implanted near the collarbone and connected to small electrical leads placed at specific targets in the brain.
"This depression study represents a continuation of our commitment to provide solutions for those who are suffering and in need of additional therapy options," said Chris Chavez, president of the St. Jude Medical ANS Division. "The Brodmann Area 25 study is an important step in bringing physicians and their patients a neuromodulation therapy that, if successful, will treat this debilitating form of depression."
The National Institute of Mental Health estimates that more than 21 million U.S. adults suffer from some kind of depressive disorder. Current therapies are effective for about 80 percent of this patient population according to the National Advisory Mental Health Council. That means approximately 4 million adult Americans live with depression that doesn't respond to medications, psychotherapy or electroconvulsive therapy.
To be eligible for this study, participants must:
-- Currently be diagnosed with major depressive disorder
-- Be between 21- and 70 years old, with onset of first episode before age 45
-- Have tried at least four treatments in their current episode, such as different medications, various combinations of medications or electroconvulsive therapy
-- Have been depressed for at least one year
For more information about this study, call toll-free at 866-787-4332, visit BROADENstudy.
Sponsored by St. Jude Medical, the BROADEN study is being conducted under a U.S. Food and Drug Administration (FDA) investigational device exemption (IDE). Initial study centers are located in Chicago, Dallas and New York City. This clinical study was preceded by a smaller pilot study of 20 patients at three sites in Canada which found that six months after the procedure, 56 percent of the patients experienced at least a 40 percent decrease in depressive symptoms. At last follow-up, 78 percent of the patients were responders, and eight of the patients have re-engaged in life activities such as work, school, travel and relationships, and three of the study patients are considered to be in remission. Patients' symptoms were measured using the Hamilton Rating Scale for Depression.
About St. Jude Medical
St. Jude Medical develops medical technology and services that focus on putting more control into the hands of those who treat cardiac, neurological and chronic pain patients worldwide. The company is dedicated to advancing the practice of medicine by reducing risk wherever possible and contributing to successful outcomes for every patient. Headquartered in St. Paul, Minn., St. Jude Medical employs more than 12,000 people worldwide and has five major focus areas that include: cardiac rhythm management, atrial fibrillation, cardiac surgery, cardiology and neuromodulation. For more information, please visit sjm.
About the ANS Division of St. Jude Medical
The ANS Division (Advanced Neuromodulation Systems) became a part of St. Jude Medical in 2005. The ANS Division is an innovative technology leader dedicated to the design, development, manufacturing and marketing of implantable neuromodulation systems to improve the quality of life for people suffering from disabling chronic pain and other nervous system disorders (ans-medical).
Forward-Looking Statements
This news release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that involve risks and uncertainties. Such forward-looking statements include the expectations, plans and prospects for the Company, including potential clinical successes, anticipated regulatory approvals and future product launches, and projected revenues, margins, earnings, and market shares. The statements made by the Company are based upon management's current expectations and are subject to certain risks and uncertainties that could cause actual results to differ materially from those described in the forward-looking statements. These risks and uncertainties include market conditions and other factors beyond the Company's control and the risk factors and other cautionary statements described in the Company's filings with the SEC, including those described in the Risk Factors and Cautionary Statements sections of the Company's Annual Report on Form 10-K filed on February 27, 2008. The Company does not intend to update these statements and undertakes no duty to any person to provide any such update under any circumstance.
воскресенье, 31 июля 2011 г.
Link Between Insomnia And Depression In Young Adults - New Study In The Journal SLEEP
A study published in the April 1 issue of the journal SLEEP confirms the persistent nature of insomnia and the increased risk of subsequent depression among individuals with insomnia.
The study, conducted by Jules Angst, MD, of Zurich University Psychiatric Hospital in Switzerland, focused on 591 young adults, whose psychiatric, physical, and sleep symptoms were assessed with six interviews spanning 20 years. Four duration-based subtypes of insomnia were distinguished: one-month insomnia associated with significant distress, two-to-three-week insomnia, recurrent brief insomnia, and occasional brief insomnia.
According to the results, the annual prevalence of one-month insomnia increased gradually over time, with a cumulative prevalence rate of 20 percent and a greater than two-fold risk among women. In 40 percent of subjects, insomnia developed into more chronic forms over time. Insomnia either with or without comorbid depression was highly stable over time. Insomnia lasting two weeks or longer predicted major depressive episodes and major depressive disorder at subsequent interviews. Seventeen to 50 percent of subjects with insomnia lasting two weeks or longer developed a major depressive episode in a later interview. "Pure" insomnia and "pure" depression were not longitudinally related to each other, whereas insomnia comorbid with depression was longitudinally related to both.
"We used to think that insomnia was most often just a symptom of depression. However, a growing body of evidence suggests that insomnia is not just a symptom of depression, but that it may actually precede depression. In other words, people who have insomnia but no depression are at increased risk for later developing depression. This study adds to our knowledge by including a much longer follow-up period than most previous studies," said Daniel J. Buysse, MD, of the University of Pittsburgh, lead author of the paper. "We were also able to look separately at insomnia alone, depression alone, and combined insomnia-depression. The results show that insomnia seems to be followed by depression more consistently than the other way around. In addition, we found that insomnia tended to be a chronic problem that gets more persistent over time, whereas depression was a more intermittent problem."
Insomnia is a classification of sleep disorders in which a person has trouble falling asleep, staying asleep or waking up too early. It is the most commonly reported sleep disorder. About 30 percent of adults have symptoms of insomnia. It is more common among elderly people and women.
It is recommended that adults get between seven and eight hours of nightly sleep.
The American Academy of Sleep Medicine (AASM) offers the following tips on how to get a good night's sleep:
- Follow a consistent bedtime routine.
- Establish a relaxing setting at bedtime.
- Get a full night's sleep every night.
- Avoid foods or drinks that contain caffeine, as well as any medicine that has a stimulant, prior to bedtime.
- Do not bring your worries to bed with you.
- Do not go to bed hungry, but don't eat a big meal before bedtime either.
- Avoid any rigorous exercise within six hours of your bedtime.
- Make your bedroom quiet, dark and a little bit cool.
- Get up at the same time every morning.
Those who suspect that they might be suffering from insomnia, or another sleep disorder, are encouraged to consult with their primary care physician or a sleep specialist.
More information about insomnia is available from the AASM at SleepEducation/Disorder.aspx?id=6.
SLEEP is the official journal of the Associated Professional Sleep Societies, LLC, a joint venture of the AASM and the Sleep Research Society.
SleepEducation, a patient education Web site created by the AASM, provides information about various sleep disorders, the forms of treatment available, recent news on the topic of sleep, sleep studies that have been conducted and a listing of sleep facilities.
SLEEP 2008, the 22nd Annual Meeting of the Associated Professional Sleep Societies and the world's largest annual gathering of sleep scientists and sleep medicine professionals, will take place in Baltimore, Maryland, from June 9-12, 2008. SLEEP 2008 will bring together an international body of 5,000 leading researchers and clinicians, who will present and discuss over 1,100 new findings and medical developments related to sleep and sleep disorders. The deadline to register is Friday, May 30, 2008. Contact Jim Arcuri at (708) 492-0930, ext. 9317, or jarcuriaasmnet for more information or to register for a free press pass. More details, including the program schedule and a list of invited lecturers, are available at SleepMeeting.
journalsleep
The study, conducted by Jules Angst, MD, of Zurich University Psychiatric Hospital in Switzerland, focused on 591 young adults, whose psychiatric, physical, and sleep symptoms were assessed with six interviews spanning 20 years. Four duration-based subtypes of insomnia were distinguished: one-month insomnia associated with significant distress, two-to-three-week insomnia, recurrent brief insomnia, and occasional brief insomnia.
According to the results, the annual prevalence of one-month insomnia increased gradually over time, with a cumulative prevalence rate of 20 percent and a greater than two-fold risk among women. In 40 percent of subjects, insomnia developed into more chronic forms over time. Insomnia either with or without comorbid depression was highly stable over time. Insomnia lasting two weeks or longer predicted major depressive episodes and major depressive disorder at subsequent interviews. Seventeen to 50 percent of subjects with insomnia lasting two weeks or longer developed a major depressive episode in a later interview. "Pure" insomnia and "pure" depression were not longitudinally related to each other, whereas insomnia comorbid with depression was longitudinally related to both.
"We used to think that insomnia was most often just a symptom of depression. However, a growing body of evidence suggests that insomnia is not just a symptom of depression, but that it may actually precede depression. In other words, people who have insomnia but no depression are at increased risk for later developing depression. This study adds to our knowledge by including a much longer follow-up period than most previous studies," said Daniel J. Buysse, MD, of the University of Pittsburgh, lead author of the paper. "We were also able to look separately at insomnia alone, depression alone, and combined insomnia-depression. The results show that insomnia seems to be followed by depression more consistently than the other way around. In addition, we found that insomnia tended to be a chronic problem that gets more persistent over time, whereas depression was a more intermittent problem."
Insomnia is a classification of sleep disorders in which a person has trouble falling asleep, staying asleep or waking up too early. It is the most commonly reported sleep disorder. About 30 percent of adults have symptoms of insomnia. It is more common among elderly people and women.
It is recommended that adults get between seven and eight hours of nightly sleep.
The American Academy of Sleep Medicine (AASM) offers the following tips on how to get a good night's sleep:
- Follow a consistent bedtime routine.
- Establish a relaxing setting at bedtime.
- Get a full night's sleep every night.
- Avoid foods or drinks that contain caffeine, as well as any medicine that has a stimulant, prior to bedtime.
- Do not bring your worries to bed with you.
- Do not go to bed hungry, but don't eat a big meal before bedtime either.
- Avoid any rigorous exercise within six hours of your bedtime.
- Make your bedroom quiet, dark and a little bit cool.
- Get up at the same time every morning.
Those who suspect that they might be suffering from insomnia, or another sleep disorder, are encouraged to consult with their primary care physician or a sleep specialist.
More information about insomnia is available from the AASM at SleepEducation/Disorder.aspx?id=6.
SLEEP is the official journal of the Associated Professional Sleep Societies, LLC, a joint venture of the AASM and the Sleep Research Society.
SleepEducation, a patient education Web site created by the AASM, provides information about various sleep disorders, the forms of treatment available, recent news on the topic of sleep, sleep studies that have been conducted and a listing of sleep facilities.
SLEEP 2008, the 22nd Annual Meeting of the Associated Professional Sleep Societies and the world's largest annual gathering of sleep scientists and sleep medicine professionals, will take place in Baltimore, Maryland, from June 9-12, 2008. SLEEP 2008 will bring together an international body of 5,000 leading researchers and clinicians, who will present and discuss over 1,100 new findings and medical developments related to sleep and sleep disorders. The deadline to register is Friday, May 30, 2008. Contact Jim Arcuri at (708) 492-0930, ext. 9317, or jarcuriaasmnet for more information or to register for a free press pass. More details, including the program schedule and a list of invited lecturers, are available at SleepMeeting.
journalsleep
пятница, 29 июля 2011 г.
Less Than 5 Hours Sleep Linked To Higher Mental Illness Risk
Young healthy adults aged between 17 and 24 years who get less than an average of 5 hours' sleep each night have three times the risk of developing a mental illness compared to individuals of the same age who sleep eight to nine hours every night, according to a study carried out by the George Institute on Global Health, published in the medical journal Sleep.
Researchers at the George Institute for Global Health carried out a survey involving 20,822 individuals aged 17-24 years across New South Wales, Australia, identified through the state vehicle licensing authority. The study ran for 18 months and revealed a clear link between lack of sleep and mental ill health, the authors wrote.
Lead author, Professor Nick Glozier, said:
The study has revealed a number of links between mental health problems and lack of sleep among young adults." The study, published in the journal SLEEP, also showed that mental ill health is more likely to develop into a chronic problem if a person is sleeping fewer than average hours.
Professor Glozier said that sleep disturbance is an important symptom in mental health disorders, such as depression, and often an early sign or "prodrome" of the illness.
(A prodrome is an early symptom indicating the onset of an attack or disease)
The researchers added that evidence is compelling and consistent that lack of sleep can also raise the risk of cardiovascular disease, as well as weight gain in young individuals.
Professor Glozier added:
Changes in lifestyle patterns are a contributing factor to these problems but it's evident that disrupted sleep patterns are a major contributor to many types of mental health conditions.
The study was conducted as part of collaborative work undertaken by the University of Sydney's Brain and Mind Institute and the George Institute for Global Health.
The authors concluded:
Self-reported shorter sleep duration is linearly associated with prevalent and persistent psychological distress in young adults. In contrast, only the very short sleepers had a raised risk of new onset of distress. Different approaches to sleep duration measurement yield different results and should guide any interventions to improve subjective sleep duration in young adults.
"Short Sleep Duration in Prevalent and Persistent Psychological Distress in Young Adults: The DRIVE Study"
Nicholas Glozier, MBBS, MRCPsych, PhD; Alexandra Martiniuk, MSc, PhD; George Patton, MBBS, PhD; Rebecca Ivers, MIPH, PhD; Qiang Li, MSc; Ian Hickie, MBBS, MD; Teresa Senserrick, PhD; Mark Woodward, PhD; Robyn Norton, PhD; Mark Stevenson, MPH, PhD
SLEEP 2010;33(9):1139-1145.
Researchers at the George Institute for Global Health carried out a survey involving 20,822 individuals aged 17-24 years across New South Wales, Australia, identified through the state vehicle licensing authority. The study ran for 18 months and revealed a clear link between lack of sleep and mental ill health, the authors wrote.
Lead author, Professor Nick Glozier, said:
The study has revealed a number of links between mental health problems and lack of sleep among young adults." The study, published in the journal SLEEP, also showed that mental ill health is more likely to develop into a chronic problem if a person is sleeping fewer than average hours.
Professor Glozier said that sleep disturbance is an important symptom in mental health disorders, such as depression, and often an early sign or "prodrome" of the illness.
(A prodrome is an early symptom indicating the onset of an attack or disease)
The researchers added that evidence is compelling and consistent that lack of sleep can also raise the risk of cardiovascular disease, as well as weight gain in young individuals.
Professor Glozier added:
Changes in lifestyle patterns are a contributing factor to these problems but it's evident that disrupted sleep patterns are a major contributor to many types of mental health conditions.
The study was conducted as part of collaborative work undertaken by the University of Sydney's Brain and Mind Institute and the George Institute for Global Health.
The authors concluded:
Self-reported shorter sleep duration is linearly associated with prevalent and persistent psychological distress in young adults. In contrast, only the very short sleepers had a raised risk of new onset of distress. Different approaches to sleep duration measurement yield different results and should guide any interventions to improve subjective sleep duration in young adults.
"Short Sleep Duration in Prevalent and Persistent Psychological Distress in Young Adults: The DRIVE Study"
Nicholas Glozier, MBBS, MRCPsych, PhD; Alexandra Martiniuk, MSc, PhD; George Patton, MBBS, PhD; Rebecca Ivers, MIPH, PhD; Qiang Li, MSc; Ian Hickie, MBBS, MD; Teresa Senserrick, PhD; Mark Woodward, PhD; Robyn Norton, PhD; Mark Stevenson, MPH, PhD
SLEEP 2010;33(9):1139-1145.
среда, 27 июля 2011 г.
FDA Approves Lilly's Cymbalta for the Treatment of Depression
Dual-reuptake inhibitor judged safe and effective, giving doctors and patients a new option for treating the emotional and painful physical symptoms of depression
The U.S. Food and Drug Administration has approved Cymbalta® (duloxetine HCl; pronounced SIM-BALL-TA), judging it a safe and effective treatment for major depressive disorder, Eli Lilly and Company announced today.
Cymbalta, a balanced and potent reuptake inhibitor of serotonin and norepinephrine, has been studied in more than 6,000 adults with major depression worldwide. Its approval gives healthcare professionals and patients a long-awaited new option for treating the broad range of emotional and physical symptoms of depression. Today, only 25-35 percent of patients treated for depression in clinical studies experience relief from all of their disease symptoms.1
"Depression is a whole-body illness, but most modern antidepressants treat the emotional symptoms, such as crying and sadness, better than they treat the physical symptoms of depression," said Dr. Stephen Stahl, chairman of the Neuroscience Education Institute and adjunct professor of psychiatry at the University of California at San Diego School of Medicine. "Because of its dual action on serotonin and norepinephrine, Cymbalta offers physicians a new opportunity to help patients with depression, particularly those who experience the common physical symptoms of the disease, such as vague aches and pains."
Neurotransmitters are believed to help regulate a person's emotions and sensitivity to pain. Scientists believe that if these neurotransmitters are out of balance, a person may become depressed and be more likely to feel painful physical symptoms. The combination of emotional and painful physical effects of depression can have a tremendous negative impact on a person's quality of life.2
"Lilly's leadership in neuroscience and dedication to the treatment of depression is well established," said Sidney Taurel, Lilly's chairman, president and chief executive officer. "Lilly is committed to solving the world's most pressing neuroscience problems, through research programs in Alzheimer's and Parkinson's as well as through our established expertise in depression, schizophrenia, bipolar disorder and Attention-Deficit/Hyperactivity Disorder."
Lilly demonstrated Cymbalta's effectiveness in treating major depression with data from four placebo-controlled clinical studies, all in adults. The safety and efficacy of Cymbalta in children have not been studied.
Milt Meyers, a participant in a Cymbalta clinical trial, found it worked for him. "Cymbalta worked for me," Meyers said. "I felt really good for the first time in a long time. I really felt like I was on the right track."
Cymbalta comes in a capsule and can be taken once a day. In clinical trials, Cymbalta was studied in a dose range of 40-120 mg per day. The recommended daily dose is 60 mg.
Duloxetine hydrochloride also is being studied for the treatment of stress urinary incontinence and diabetic neuropathic pain, conditions believed to respond to treatment with both serotonin and norepinephrine.
About Depression
Nearly 19 million Americans suffer from depression each year, making it one of the leading causes of disability according to the World Health Organization. Current medical literature suggests that patients who are successfully treated for all their depressive symptoms, including both the emotional and painful physical ones, may be more likely to achieve remission than those whose physical symptoms are not alleviated.1, 3, 4, 5
Patient Experience
In clinical trials, Cymbalta was safe and effective. Not all patients respond the same. The experience of the patient quoted in this release might not be typical.
Important Safety Information
Depression, as a disease, can be associated with periods when the symptoms can worsen or thoughts of suicide can emerge. Patients and their families should watch for these as well as for anxiety, agitation, panic, difficulty sleeping, irritability, hostility, aggressiveness, impulsivity, restlessness, or overexcitement and hyperactivity. Call the doctor if any of these are severe or occur suddenly. Be especially observant at the initiation of antidepressant drug therapy and whenever there is a change in dose.
Prescription Cymbalta is not for everyone. People who are allergic to duloxetine hydrochloride or the other ingredients in Cymbalta should not take it. If you are taking thioridazine or if you are taking or have recently taken a type of antidepressant called a monoamine oxidase inhibitor (MAOI), you should not take Cymbalta. It also should not be administered to patients with any hepatic insufficiency, end-stage renal disease or uncontrolled, narrow-angle glaucoma. Cymbalta ordinarily should not be prescribed to patients with substantial alcohol use. Women who are pregnant should talk with their doctor before taking Cymbalta. Nursing while taking Cymbalta is not recommended.
In clinical studies, the most common side effects were nausea, dry mouth, constipation, decreased appetite, fatigue, sleepiness and increased sweating. Most people were not bothered enough by side effects to stop taking Cymbalta. Your doctor may periodically check your blood pressure. Don't stop taking Cymbalta without talking to your doctor.
For full patient information, visit Cymbalta.
About Lilly
Lilly, a leading innovation-driven corporation, is developing a growing portfolio of first-in-class and best-in-class pharmaceutical products by applying the latest research from its own worldwide laboratories and from collaborations with eminent scientific organizations. Headquartered in Indianapolis, Ind., Lilly provides answers - through medicines and information - for some of the world's most urgent medical needs. Additional information about Lilly is available at lilly.
This press release contains forward-looking statements about the potential of Cymbalta for the treatment of major depressive disorder and reflects Lilly's current beliefs. However, as with any pharmaceutical product, there are substantial risks and uncertainties in the process of development and commercialization. There is no guarantee that the product will prove to be commercially successful. For further discussion of these and other risks and uncertainties, see Lilly's filings with the United States Securities and Exchange Commission. Lilly undertakes no duty to update forward-looking statements.
1. Tran PV, Bymaster FP, McNamara RK, et al. Dual Monoamine Modulation for Improved Treatment of Major Depressive Disorder, J Clin Psychopharmacology, 2003; 23: 78-86.
2. The Regents of the University of Michigan. Beyond Sadness. Bridging the gap between emotional and physical symptoms of depression. Ann Arbor, MI, 2002.
3. Nemeroff CB et al. Duloxetine for the Treatment of Major Depressive Disorder. Psychoharmacol Bul. 2002; 36 (4):106-132.
4. Ohayon, M., et al. Using Chronic Pain to Predict Depressive Morbidity in the General Population. Arch Gen Psychiatry 2003; 60: 39-47.
5. Poster presented at American Psychiatric Association annual meeting. May 19, 2003. San Francisco, CA.
View drug information on Cymbalta.
The U.S. Food and Drug Administration has approved Cymbalta® (duloxetine HCl; pronounced SIM-BALL-TA), judging it a safe and effective treatment for major depressive disorder, Eli Lilly and Company announced today.
Cymbalta, a balanced and potent reuptake inhibitor of serotonin and norepinephrine, has been studied in more than 6,000 adults with major depression worldwide. Its approval gives healthcare professionals and patients a long-awaited new option for treating the broad range of emotional and physical symptoms of depression. Today, only 25-35 percent of patients treated for depression in clinical studies experience relief from all of their disease symptoms.1
"Depression is a whole-body illness, but most modern antidepressants treat the emotional symptoms, such as crying and sadness, better than they treat the physical symptoms of depression," said Dr. Stephen Stahl, chairman of the Neuroscience Education Institute and adjunct professor of psychiatry at the University of California at San Diego School of Medicine. "Because of its dual action on serotonin and norepinephrine, Cymbalta offers physicians a new opportunity to help patients with depression, particularly those who experience the common physical symptoms of the disease, such as vague aches and pains."
Neurotransmitters are believed to help regulate a person's emotions and sensitivity to pain. Scientists believe that if these neurotransmitters are out of balance, a person may become depressed and be more likely to feel painful physical symptoms. The combination of emotional and painful physical effects of depression can have a tremendous negative impact on a person's quality of life.2
"Lilly's leadership in neuroscience and dedication to the treatment of depression is well established," said Sidney Taurel, Lilly's chairman, president and chief executive officer. "Lilly is committed to solving the world's most pressing neuroscience problems, through research programs in Alzheimer's and Parkinson's as well as through our established expertise in depression, schizophrenia, bipolar disorder and Attention-Deficit/Hyperactivity Disorder."
Lilly demonstrated Cymbalta's effectiveness in treating major depression with data from four placebo-controlled clinical studies, all in adults. The safety and efficacy of Cymbalta in children have not been studied.
Milt Meyers, a participant in a Cymbalta clinical trial, found it worked for him. "Cymbalta worked for me," Meyers said. "I felt really good for the first time in a long time. I really felt like I was on the right track."
Cymbalta comes in a capsule and can be taken once a day. In clinical trials, Cymbalta was studied in a dose range of 40-120 mg per day. The recommended daily dose is 60 mg.
Duloxetine hydrochloride also is being studied for the treatment of stress urinary incontinence and diabetic neuropathic pain, conditions believed to respond to treatment with both serotonin and norepinephrine.
About Depression
Nearly 19 million Americans suffer from depression each year, making it one of the leading causes of disability according to the World Health Organization. Current medical literature suggests that patients who are successfully treated for all their depressive symptoms, including both the emotional and painful physical ones, may be more likely to achieve remission than those whose physical symptoms are not alleviated.1, 3, 4, 5
Patient Experience
In clinical trials, Cymbalta was safe and effective. Not all patients respond the same. The experience of the patient quoted in this release might not be typical.
Important Safety Information
Depression, as a disease, can be associated with periods when the symptoms can worsen or thoughts of suicide can emerge. Patients and their families should watch for these as well as for anxiety, agitation, panic, difficulty sleeping, irritability, hostility, aggressiveness, impulsivity, restlessness, or overexcitement and hyperactivity. Call the doctor if any of these are severe or occur suddenly. Be especially observant at the initiation of antidepressant drug therapy and whenever there is a change in dose.
Prescription Cymbalta is not for everyone. People who are allergic to duloxetine hydrochloride or the other ingredients in Cymbalta should not take it. If you are taking thioridazine or if you are taking or have recently taken a type of antidepressant called a monoamine oxidase inhibitor (MAOI), you should not take Cymbalta. It also should not be administered to patients with any hepatic insufficiency, end-stage renal disease or uncontrolled, narrow-angle glaucoma. Cymbalta ordinarily should not be prescribed to patients with substantial alcohol use. Women who are pregnant should talk with their doctor before taking Cymbalta. Nursing while taking Cymbalta is not recommended.
In clinical studies, the most common side effects were nausea, dry mouth, constipation, decreased appetite, fatigue, sleepiness and increased sweating. Most people were not bothered enough by side effects to stop taking Cymbalta. Your doctor may periodically check your blood pressure. Don't stop taking Cymbalta without talking to your doctor.
For full patient information, visit Cymbalta.
About Lilly
Lilly, a leading innovation-driven corporation, is developing a growing portfolio of first-in-class and best-in-class pharmaceutical products by applying the latest research from its own worldwide laboratories and from collaborations with eminent scientific organizations. Headquartered in Indianapolis, Ind., Lilly provides answers - through medicines and information - for some of the world's most urgent medical needs. Additional information about Lilly is available at lilly.
This press release contains forward-looking statements about the potential of Cymbalta for the treatment of major depressive disorder and reflects Lilly's current beliefs. However, as with any pharmaceutical product, there are substantial risks and uncertainties in the process of development and commercialization. There is no guarantee that the product will prove to be commercially successful. For further discussion of these and other risks and uncertainties, see Lilly's filings with the United States Securities and Exchange Commission. Lilly undertakes no duty to update forward-looking statements.
1. Tran PV, Bymaster FP, McNamara RK, et al. Dual Monoamine Modulation for Improved Treatment of Major Depressive Disorder, J Clin Psychopharmacology, 2003; 23: 78-86.
2. The Regents of the University of Michigan. Beyond Sadness. Bridging the gap between emotional and physical symptoms of depression. Ann Arbor, MI, 2002.
3. Nemeroff CB et al. Duloxetine for the Treatment of Major Depressive Disorder. Psychoharmacol Bul. 2002; 36 (4):106-132.
4. Ohayon, M., et al. Using Chronic Pain to Predict Depressive Morbidity in the General Population. Arch Gen Psychiatry 2003; 60: 39-47.
5. Poster presented at American Psychiatric Association annual meeting. May 19, 2003. San Francisco, CA.
View drug information on Cymbalta.
понедельник, 25 июля 2011 г.
New Mothers' Postpartum Lifestyle And Parenting Stress
Post-pregnancy excess weight is likely caused by the impact of new parenthood stress on physical activity, Georgia Health Sciences University researchers say.
In a study of 60 first-time mothers, researchers linked higher post-pregnancy body mass index - weight in relation to height - to a combination of a high BMI before pregnancy, excessive weight gain during pregnancy, parenting stress and a sedentary lifestyle, according to a study published in Women & Health.
The study gauged parental stress by asking participants to rate statements such as "I feel like I have less time to myself" and "I enjoy being a parent." They were also asked to recall their physical activity over the previous 24 hours, categorizing that activity from light to vigorous.
"Sedentary lifestyle, or a low amount of physical activity, was most influenced by the type of parenting stress the mothers reported," says Dr. Deborah Young-Hyman, behavioral psychologist with the Georgia Prevention Institute. "More parenting stress, especially depression, was associated with less physical activity and a higher postpartum BMI."
Interestingly, social interaction, generally considered a measure of well-being, correlated with a higher body mass index, she noted.
"We think women are socializing with their friends, not isolating themselves, but they are doing sedentary things like talking on the phone, watching television or hanging out at home, instead of taking their babies on a walk together."
New moms with a higher BMI did report more depressive symptoms, but overall felt competent as parents. Those with lower BMIs reported more physical activity (and less depressive symptoms) but more concern about their competence as parents.
"We know that physical activity improves your mood and helps you lose weight, but no one has ever asked how physical activity is related to parenting stress in first-time moms," Young-Hyman said. "The bottom line is that parenting stress does impact the postpartum lifestyles of new moms," she said.
Based on a current study tracking how first-time mothers adjust to parenthood, researchers will develop an intervention to help new moms create healthy lifestyles for both themselves and their babies ??" preventing overweight mothers and children.
In a study of 60 first-time mothers, researchers linked higher post-pregnancy body mass index - weight in relation to height - to a combination of a high BMI before pregnancy, excessive weight gain during pregnancy, parenting stress and a sedentary lifestyle, according to a study published in Women & Health.
The study gauged parental stress by asking participants to rate statements such as "I feel like I have less time to myself" and "I enjoy being a parent." They were also asked to recall their physical activity over the previous 24 hours, categorizing that activity from light to vigorous.
"Sedentary lifestyle, or a low amount of physical activity, was most influenced by the type of parenting stress the mothers reported," says Dr. Deborah Young-Hyman, behavioral psychologist with the Georgia Prevention Institute. "More parenting stress, especially depression, was associated with less physical activity and a higher postpartum BMI."
Interestingly, social interaction, generally considered a measure of well-being, correlated with a higher body mass index, she noted.
"We think women are socializing with their friends, not isolating themselves, but they are doing sedentary things like talking on the phone, watching television or hanging out at home, instead of taking their babies on a walk together."
New moms with a higher BMI did report more depressive symptoms, but overall felt competent as parents. Those with lower BMIs reported more physical activity (and less depressive symptoms) but more concern about their competence as parents.
"We know that physical activity improves your mood and helps you lose weight, but no one has ever asked how physical activity is related to parenting stress in first-time moms," Young-Hyman said. "The bottom line is that parenting stress does impact the postpartum lifestyles of new moms," she said.
Based on a current study tracking how first-time mothers adjust to parenthood, researchers will develop an intervention to help new moms create healthy lifestyles for both themselves and their babies ??" preventing overweight mothers and children.
суббота, 23 июля 2011 г.
Experimental Medication Kicks Depression In Hours Instead Of Weeks
People with treatment-resistant depression experienced symptom relief in as little as two hours with a single intravenous dose of ketamine, a medication usually used in higher doses as an anesthetic in humans and animals, in a preliminary study. Current antidepressants routinely take eight weeks or more to exert their effect in treatment-resistant patients and four to six weeks in more responsive patients - a major drawback of these medications. Some participants in this study, who previously had tried an average of six medications without relief, continued to show benefits over the next seven days after just a single dose of the experimental treatment, according to researchers conducting the study at the National Institutes of Health's National Institute of Mental Health.
This is among the first studies of humans to examine the effects of ketamine on depression, a debilitating illness that affects 14.8 million people in any given year. Used in very low doses, the medication is important for research, but is unlikely to become a widely used clinical treatment for depression because of potential side effects, including hallucinations and euphoria, at higher doses. However, scientists say this research could point the way toward development of a new class of faster- and -longer-acting medications. None of the patients in this study, all of whom received a low dose, had serious side effects. Study results were published in the August issue of the Archives of General Psychiatry.
"The public health implications of being able to treat major depression this quickly would be enormous," said NIH Director Elias A. Zerhouni, M.D. "These new findings demonstrate the importance of developing new classes of antidepressants that are not simply variations of existing medications."
For this study 18 treatment-resistant, depressed patients were randomly assigned to receive either a single intravenous dose of ketamine or a placebo (inactive compound). Depression improved within one day in 71 percent of all those who received ketamine, and 29 percent of these patients became nearly symptom-free within one day. Thirty-five percent of patients who received ketamine still showed benefits seven days later. Participants receiving a placebo infusion showed no improvement. One week later, participants were given the opposite treatment, unless the beneficial effects of the first treatment were still evident. This "crossover" study design strengthens the validity of the results.
"To my knowledge, this is the first report of any medication or other treatment that results in such a pronounced, rapid, prolonged response with a single dose. These were very treatment-resistant patients," said NIMH Director Thomas R. Insel, M.D.
Ketamine blocks a brain protein called the N-methyl-D-aspartic acid (NMDA) receptor. Previous studies have shown that agents that block the NMDA receptor reduce depression-like behaviors in animals.
NMDA receptors are critical for receiving the signals of glutamate, a brain chemical that enhances the electrical flow among brain cells that is required for normal function. Studies indicate that dysregulation in glutamate could be among the culprits in depression. Using ketamine to block glutamate's actions on the NMDA receptor appears to improve function of another brain receptor - the AMPA receptor - that also helps regulate brain cells' electrical flow.
Scientists think the reason current antidepressant medications take weeks to work is that they act on targets close to the beginning of a series of biochemical reactions that regulate mood. The medications' effects then have to trickle down through the rest of the reactions, which takes time. Scientists theorize that ketamine skips much of this route because its target, the NMDA receptor, is closer to the end of the series of reactions in question.
"This may be a key to developing medications that eliminate the weeks or months patients have to wait for antidepressant treatments to kick in," said lead researcher Carlos A. Zarate Jr., of the NIMH Mood and Anxiety Disorders Program.
The researchers who conducted the study now are zeroing in on other areas of the glutamate system. Specifying which components of the system are affected by compounds such as ketamine may help scientists understand how and why depression occurs, reveal biological markers that may one day aid in diagnosis, and point the way to more precise targets for new medications.
Dr. Zarate was joined in this research by Husseini K. Manji, chief of the NIMH Mood and Anxiety Disorders Program, and colleagues Jaskaran B. Singh, Paul J. Carlson, Nancy E. Brutsche, Rezvan Ameli, David A. Luckenbaugh, and Dennis S. Charney.
NIMH is part of the National Institutes of Health (NIH), the Federal Government's primary agency for biomedical and behavioral research. NIH is a component of the U.S. Department of Health and Human Services.
Contact: Susan Cahill
NIH/National Institute of Mental Health
This is among the first studies of humans to examine the effects of ketamine on depression, a debilitating illness that affects 14.8 million people in any given year. Used in very low doses, the medication is important for research, but is unlikely to become a widely used clinical treatment for depression because of potential side effects, including hallucinations and euphoria, at higher doses. However, scientists say this research could point the way toward development of a new class of faster- and -longer-acting medications. None of the patients in this study, all of whom received a low dose, had serious side effects. Study results were published in the August issue of the Archives of General Psychiatry.
"The public health implications of being able to treat major depression this quickly would be enormous," said NIH Director Elias A. Zerhouni, M.D. "These new findings demonstrate the importance of developing new classes of antidepressants that are not simply variations of existing medications."
For this study 18 treatment-resistant, depressed patients were randomly assigned to receive either a single intravenous dose of ketamine or a placebo (inactive compound). Depression improved within one day in 71 percent of all those who received ketamine, and 29 percent of these patients became nearly symptom-free within one day. Thirty-five percent of patients who received ketamine still showed benefits seven days later. Participants receiving a placebo infusion showed no improvement. One week later, participants were given the opposite treatment, unless the beneficial effects of the first treatment were still evident. This "crossover" study design strengthens the validity of the results.
"To my knowledge, this is the first report of any medication or other treatment that results in such a pronounced, rapid, prolonged response with a single dose. These were very treatment-resistant patients," said NIMH Director Thomas R. Insel, M.D.
Ketamine blocks a brain protein called the N-methyl-D-aspartic acid (NMDA) receptor. Previous studies have shown that agents that block the NMDA receptor reduce depression-like behaviors in animals.
NMDA receptors are critical for receiving the signals of glutamate, a brain chemical that enhances the electrical flow among brain cells that is required for normal function. Studies indicate that dysregulation in glutamate could be among the culprits in depression. Using ketamine to block glutamate's actions on the NMDA receptor appears to improve function of another brain receptor - the AMPA receptor - that also helps regulate brain cells' electrical flow.
Scientists think the reason current antidepressant medications take weeks to work is that they act on targets close to the beginning of a series of biochemical reactions that regulate mood. The medications' effects then have to trickle down through the rest of the reactions, which takes time. Scientists theorize that ketamine skips much of this route because its target, the NMDA receptor, is closer to the end of the series of reactions in question.
"This may be a key to developing medications that eliminate the weeks or months patients have to wait for antidepressant treatments to kick in," said lead researcher Carlos A. Zarate Jr., of the NIMH Mood and Anxiety Disorders Program.
The researchers who conducted the study now are zeroing in on other areas of the glutamate system. Specifying which components of the system are affected by compounds such as ketamine may help scientists understand how and why depression occurs, reveal biological markers that may one day aid in diagnosis, and point the way to more precise targets for new medications.
Dr. Zarate was joined in this research by Husseini K. Manji, chief of the NIMH Mood and Anxiety Disorders Program, and colleagues Jaskaran B. Singh, Paul J. Carlson, Nancy E. Brutsche, Rezvan Ameli, David A. Luckenbaugh, and Dennis S. Charney.
NIMH is part of the National Institutes of Health (NIH), the Federal Government's primary agency for biomedical and behavioral research. NIH is a component of the U.S. Department of Health and Human Services.
Contact: Susan Cahill
NIH/National Institute of Mental Health
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