Drug may increase cognition for people with Down syndrome

ScienceDaily (Aug. 1, 2011) — A University of Colorado School of Medicine scientist is completing a major clinical trial on a drug that could boost cognitive function in those with Down syndrome, significantly improving their quality of life and representing a potential milestone in research on this genetic condition.

"We are hoping to enhance memory and learning in those with Down syndrome," said Alberto Costa, MD, PhD, an associate professor of medicine and the neuroscientist leading the effort. "We have been studying this drug for three years and are now ready to analyze the data on our trial. Our team at the University of Colorado and Children's Hospital Colorado expects to have the results in the next two or three months."

Costa, whose work was recently chronicled in New York Times Magazine, is testing the drug memantine, currently used to relieve symptoms of Alzheimer's disease, in 39 people with Down syndrome. About half received the drug and the others a placebo. In 2007, Costa demonstrated that memantine could improve memory function in mice with Down syndrome.

And now, for the first time, he is taking a drug effective in the treatment of learning and memory deficits in mice with Down syndrome and applying it to humans, a move described by the New York Times as "a milestone in the history of Down syndrome research."

Costa is no disinterested researcher. His 16-year-old daughter Tyche -- named for the Greek goddess of Fortune -- has Down syndrome. Like others with the condition, she faces the specter of a steady decline in mental functioning as she gets older and a roughly 20 percent chance of getting Alzheimer's in her 50's. After that diagnosis, death is often just five years away.

"I feel I am racing the clock to find something that will at least keep her functioning at the level she is at now," Costa said. "As they age, parts of their brain will shrink and their functions will diminish."

Costa is actively pursuing links between Down and Alzheimer's disease. He says babies born with Down often carry the biological markers for Alzheimer's.

"They have the disease from the get go," he said.

Costa says the world is awash in false assumptions about Down syndrome ranging from distortions on life expectancy to educational limitations. In fact, depending on the severity of their condition, those with Down can live into their 70s, attend college, live independently and hold down jobs.

"If we are successful, it will increase hope and expectations for those with Down syndrome," Costa said. "Right now there are drugs for the signs and symptoms of medical conditions more frequent in those with Down syndrome, but nothing to improve brain function. In fact, the prevailing wisdom has been that there is essentially nothing you can do to boost memory and learning in this group. Hopefully, we can prove them wrong."

But he and other Down researchers face an overall lack of federal funding, especially when compared to other diseases and disorders.

Costa has been supported by Forest Pharmaceuticals which is funding the clinical trial, the Linda Crnic Institute for Down Syndrome, the Coleman Institute for Cognitive Disabilities and the National Institute of Child Health and Development, part of the National Institutes of Health.

"Clearly these funding sources are the unsung heroes," Costa said. "They may not get the attention or publicity but I can assure you that our efforts and the future of those with Down syndrome would be seriously compromised without their continued generosity."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Colorado Denver, via EurekAlert!, a service of AAAS.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here sciencedaily.com

New antidepressants can increase risks for elderly, study suggests

ScienceDaily (Aug. 3, 2011) — Older people taking new generation antidepressants are at more risk of dying or suffering from a range of serious health conditions including stroke, falls, fractures and epilepsy, suggests a new study involving researchers at The University of Nottingham.

The research, published on the British Medical Journal website, discovered that selective serotonin reuptake inhibitors (SSRIs) are more strongly associated with an increased risk of several adverse outcomes in people over the age of 65 with depression compared with older tricyclic antidepressants (TCAs).

The authors say the risks and benefits of different antidepressants should be carefully considered when prescribing these drugs to elderly patients and have called for further research to investigate the findings.

Dr Carol Coupland, Associate Professor in Medical Statistics in The University of Nottingham's Division of Primary Care said: "We've found some evidence from our study that the older tricyclic antidepressants may be associated with lower risks of several adverse outcomes compared with newer antidepressants in older people diagnosed as having depression.

"This was an unexpected finding, and so further research using other data sources is needed to confirm these findings as well as provide more evidence on the benefits of different antidepressants in this group of people."

Depression is a common condition in older people and antidepressants -- particularly SSRIs -- are widely used. However, very little is known about the safety of these drugs in older people.

The team of researchers from the Universities of Nottingham and East Anglia set out to investigate the potential link between antidepressant treatment and the risk of a number of potentially life-threatening outcomes in older people.

They identified 60,746 UK patients aged 65 and over with a newly diagnosed episode of depression between 1996 and 2007 using the QResearch primary care database. Many patients had other conditions, such as heart disease and diabetes, and were taking several medications.

Patients were tracked until the end of 2008. During this time, 89 per cent (54,038) received at least one prescription for an antidepressant, and a total of 1,398,359 prescriptions for antidepressants were received. Of these 57 per cent were for SSRIs, 31 per cent for TCAs, 0.2 per cent for monoamine oxidase inhibitors (MAOIs) and 13.5 per cent for other antidepressants.

Antidepressant use was then analysed against several adverse outcomes including all-cause mortality, attempted suicide or self harm, heart attack, stroke, falls, fractures, epilepsy or seizures and high salt levels in the blood (hyponatraemia).

After adjusting for factors that could affect the results, including age, sex, severity of depression, other illnesses and use of other medications, the team found that SSRIs and drugs in the group of other antidepressants were associated with an increased risk of several adverse outcomes compared with TCAs.

Those taking SSRIs were more likely to die, suffer a stroke, fall or fracture, have epilepsy or a seizure and have hyponatraemia compared with TCAs. The group of other antidepressants were associated with an increased risk of mortality, attempted suicide or self-harm, stroke, fracture and epilepsy or seizures.

Patients in the study had a seven per cent risk of dying over one year while they were not taking antidepressants, while the comparable risks were 8.1 per cent when taking TCAs, 10.6 per cent for SSRIs and 11.4 per cent for the group of other antidepressants. For stroke, one-year risks were 2.3 per cent, 2.6 per cent and three per cent (compared with 2.2 per cent when not on antidepressants) and for fracture they were 2.2 per cent, 2.7 per cent and 2.8 per cent compared with 1.8 per cent.

Among individual drugs trazodone, mirtazapine and venlafaxine carried the highest risk for some adverse outcomes.

Rates of most adverse outcomes were highest in the 28 days after starting the antidepressant and also in the 28 days after stopping.

The authors also point out that TCAs were prescribed at lower doses than SSRIs and other antidepressant drugs, which they say "could in part explain our findings." They also caution that differences between patients prescribed different antidepressant drugs may account for some of the associations seen in the study, underlining the need for further research to confirm the findings.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Nottingham, via AlphaGalileo.

Journal Reference:

C. Coupland, P. Dhiman, R. Morriss, A. Arthur, G. Barton, J. Hippisley-Cox. Antidepressant use and risk of adverse outcomes in older people: population based cohort study. BMJ, 2011; 343 (aug02 1): d4551 DOI: 10.1136/bmj.d4551

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here sciencedaily.com

Mouse with 'off switch' in key brain cell population developed; Research may increase understanding of SIDS, depressive disorders

ScienceDaily (July 30, 2011) — NIH-funded scientists have developed a strain of mice with a built-in off switch that can selectively shut down the animals' serotonin-producing cells, which make up a brain network controlling breathing, temperature regulation, and mood. The switch controls only the serotonin-producing cells, and does not affect any other cells in the animal's brains or bodies.

When the researchers powered down the animals' serotonin cells, the animals failed to sufficiently step up their breathing to compensate for an increase of carbon dioxide in the air, and their body temperatures dropped to match the surrounding temperature.

The finding has implications for understanding sudden infant death syndrome, or SIDS, which has been linked to low serotonin levels, and is thought to involve breathing abnormalities and problems with temperature control. The finding may also provide insight into depressive disorders, which also involve serotonin metabolism.

The study results appear in the current issue of the journal Science.

SIDS is the death of an infant before his or her first birthday that cannot be explained after a complete autopsy, an investigation of the scene and circumstances of the death, and a review of the medical history of the infant and of his or her family. According to the National Center for Health Statistics, SIDS is the third leading cause of infant death.

"The single most effective way to reduce the risk of SIDS is to always place infants on their backs for sleep," said Marian Willinger, Ph.D., special assistant for SIDS at the NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development, which provided major funding for the study. "This new animal model of the serotonin-producing system holds the promise of helping us to understand the biological processes contributing to SIDS, which is critical for the development of tests and interventions to prevent these deaths.'' Additional NIH support was provided by the National Institute of Mental Health, National Institute on Drug Abuse, and National Center for Research Resources.

To conduct the study, the researchers developed mice with a unique molecule, or receptor, on the surface of their serotonin-producing brain cells, or neurons. Typically, cells communicate via chemicals that bind to receptors on their surfaces, with the molecules binding to their receptors in much the same way a key fits into a lock.

The researchers added this special receptor to the animal's serotonin-producing neurons using a genetic manipulation technique they developed called intersectional genetics. The special receptor was developed by NIH-funded researcher Bryan Roth. The approach consists of manipulating the animals' genetic material so that it manufacturers an additional receptor on the surface of its neurons. In this case, the animals' serotonin-producing cells began making a receptor that is not found in nature. Rather than binding to a naturally occurring brain chemical, the receptor binds to a chemical compound manufactured in a laboratory, clozapine-N-oxide (CNO).

"CNO was identified for its ability to bind specifically to this foreign receptor that we placed into the serotonin cells, and because it does not react with other cells or tissues in the animal's body," Dr. Dymecki explained.

When CNO binds with the receptor, it deactivates only the serotonin cells, effectively switching off all communications in the serotonin network. CNO does not affect any other cells in the animals' brains or bodies.

"By selectively switching off the serotonin-producing cells, we can get a definite idea of what bodily functions the serotonin cells specifically control" she said.

The researchers exposed genetically normal mice and mice with the receptor for CNO to elevated levels of carbon dioxide. Carbon dioxide is the waste product given off when a breath is exhaled. If carbon dioxide builds up in the body, due to insufficient breathing, it can be toxic, leading to loss of consciousness and death. The response to high carbon dioxide accumulation is increased breathing and a faster breathing rate, which releases carbon dioxide through the lungs.

When the normal mice were exposed to carbon dioxide, they almost immediately began to breathe faster and more deeply. In contrast, after their serotonin-producing neurons were switched off, mice with the receptor to CNO had a smaller response to carbon dioxide and did not increase their breathing as much.

"This finding shows that the breathing response to carbon dioxide is regulated by serotonin neurons," Dr. Dymecki said.

The researchers next tested the ability of the CNO-responsive mice to regulate their body temperatures. When the room temperature was set at 74 degrees Fahrenheit, the body temperature of normal mice remained at about 98.6 degrees -- the normal temperature for mice. Normal mice can maintain a normal body temperature even when the room temperature is cool and below that of body temperature, Dr. Dymecki added. However, after their serotonin neurons were switched off with CNO, the body temperatures of the CNO mice soon plunged. Like reptiles faced with a sudden temperature drop, the body temperatures of the mice soon dropped to the 74 degree room temperature.

"Their body temperatures were equilibrating with the room temperature," Dr. Dymecki said. "Our finding affirms that temperature is regulated by the serotonergic system."

Dr. Dymecki explained that the researchers added the CNO receptor to all the animals' serotonergic neurons. In future studies, she and her colleagues plan to selectively add the receptor to subsets of serotonergic receptors, to better understand their functioning in health, and in disorders such as SIDS and depression.

The finding provides support for previous autopsy studies by NIH grantees implicating abnormalities in serotonin metabolism in the brainstem as playing a role in SIDS.

Researchers theorize that infants who die of SIDS may have been unable to respond to breathing challenges, such as low levels of oxygen or high levels of carbon dioxide. High levels of carbon dioxide may accumulate around the face of an infant sleeping face down, when the infant's exhaled breath accumulates in a pocket formed by bedding materials.

The ability to regulate body temperature is also thought to play a role in SIDS deaths. The NICHD's Back to Sleep campaign advises parents and caregivers to avoid letting infants overheat during sleep, to dress them in light sleep clothes, avoid blankets or coverings, and to keep the room at a temperature that is comfortable for an adult.

Other authors of the paper were Russell Ray and Rachael Brust, also of the Department of Genetics at Harvard Medical School; Andrea Corcoran and Eugene Nattie, Department of Physiology at Dartmouth Medical School, in Lebanon, N.H.; Jun Chul Kim, Department of Psychology, University of Toronto, Toronto, Ontario, Canada; and George B. Richerson, Department of Neurology, University of Iowa in Iowa City.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by NIH/National Institute of Child Health and Human Development.

Journal Reference:

R. S. Ray, A. E. Corcoran, R. D. Brust, J. C. Kim, G. B. Richerson, E. Nattie, S. M. Dymecki. Impaired Respiratory and Body Temperature Control Upon Acute Serotonergic Neuron Inhibition. Science, 2011; 333 (6042): 637 DOI: 10.1126/science.1205295

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Traumatic brain injury linked with tenfold increase in stroke risk

ScienceDaily (July 29, 2011) — If you suffer traumatic brain injury, your risk of having a stroke within three months may increase tenfold, according to a new study reported in Stroke: Journal of the American Heart Association.

"It's reasonable to assume that cerebrovascular damage in the head caused by a traumatic brain injury can trigger either a hemorrhagic stroke [when a blood vessel bursts inside the brain] or an ischemic stroke [when an artery in the brain is blocked]," said Herng-Ching Lin, Ph.D., senior study author and professor at the School of Health Care Administration, College of Medicine, Taipei Medical University in Taiwan. "However, until now, no research had been done showing a correlation between traumatic brain injury and stroke."

It is the first study that pinpoints traumatic brain injury as a potential risk factor for subsequent stroke.

Traumatic brain injury occurs when an external force such as a bump, blow or jolt to the head disrupts the normal function of the brain. Causes include falls, vehicle accidents, and violence.

In the United States alone, approximately 1 in 53 individuals sustain a traumatic brain injury each year, according to 2004 statistics from the Centers for Disease Control and Prevention.

Worldwide, traumatic brain injuries are a major cause of physical impairment, social disruption and death.

Using records from a nationwide Taiwanese database, researchers investigated the risk of stroke in traumatic brain injury patients during a five-year period. The records included 23,199 adult traumatic brain injury patients who received ambulatory or hospital care between 2001 and 2003. The comparison group comprised 69,597 non-traumatic brain injury patients. The average age of all patients was 42 and 54 percent were male.

During the three months after injury, 2.91 percent of traumatic brain injury patients suffered a stroke compared with only 0.30 percent of those with non-traumatic brain injury -- a tenfold difference.

Stroke risk in patients with traumatic brain injury decreased gradually over time, researchers said:

After one year, the risk was about 4.6 times greater for patients who suffered a traumatic brain injury than for those who had not.After five years, the risk was 2.3 times greater for traumatic brain injury patients.

Stroke risk among traumatic brain injury patients with skull bone fractures was more pronounced than in traumatic brain injury patients without fractures, researchers said.

During the first three months, those with skull bone fractures were 20 times more likely to have a stroke than patients without skull bone fractures. The risk decreased over time.

Furthermore, the risk of subarachnoid hemorrhage (bleeding in the area between the brain and the thin tissues that cover the brain) and intracerebral hemorrhage (bleeding in the brain caused by the rupture of a blood vessel) increased significantly in patients with traumatic brain injury versus non-traumatic brain injury patients.

After considering age and gender, patients with traumatic brain injury were more likely to have hypertension, diabetes, coronary heart disease, atrial fibrillation and heart failure than non-traumatic brain injury patients.

Early neuroimaging examinations -- such as MRI -- and intensive medical monitoring, support and intervention should be required following a traumatic brain injury, especially during the first few months and years, Lin said. Moreover, better health education initiatives could increase public awareness about the factors that cause strokes and the signs and symptoms of stroke in patients with traumatic brain injuries.

"Stroke is the most serious and disabling neurological disorder worldwide," said Lin. "Our study leads the way in identifying stroke as an additional neurological problem that may arise following traumatic brain injury."

Co-authors are: Yi-Hua-Chen, Ph.D, lead author and Jiunn-Horng Kang, M.D.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Heart Association, via EurekAlert!, a service of AAAS.

Journal Reference:

Y.-H. Chen, J.-H. Kang, H.-C. Lin. Patients With Traumatic Brain Injury: Population-Based Study Suggests Increased Risk of Stroke. Stroke, 2011; DOI: 10.1161/STROKEAHA.111.620112

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Prenatal exposure to certain antidepressants may modestly increase risk of autism spectrum disorders, study suggests

ScienceDaily (July 5, 2011) — Prenatal exposure to selective serotonin reuptake inhibitors, especially during the first trimester, is associated with a modest increase the risk of developing an autism spectrum disorder, according to a report published Online First in the Archives of General Psychiatry, one of the JAMA/Archives journals.

"The prevalence of autism spectrum disorders (ASDs) has increased over recent years," the authors write as background information in the article. "Use of antidepressant medications during pregnancy also shows a secular increase in recent decades, prompting concerns that prenatal exposure may contribute to increased risk of ASD."

To evaluate if prenatal exposure to antidepressants, including selective serotonin reuptake inhibitors (SSRIs), is associated with an increase in ASD, Lisa A. Croen, Ph.D., of Kaiser Permanente Northern California, Oakland, and colleagues examined medical records for children drawn from the Childhood Autism Perinatal Study conducted by Kaiser Permanente Medical Care Program in Northern California. The authors included 298 children with ASD (case group) and their mothers, and 1,507 control children and their mothers in the study.

Twenty mothers of children in the case group (6.7 percent) and 50 mothers of children in the control group (3.3 percent) had at least one prescription for an antidepressant in the year prior to the birth of the study child. Of the 20 case mothers who were prescribed antidepressants, 13 (65 percent) were prescribed SSRIs only, two (10 percent) were prescribed an SSRI in combination with another antidepressant and five (25 percent) were prescribed one or more non-SSRI antidepressants only. Of the 50 control mothers who were prescribed an antidepressant, 25 (50 percent) were prescribed SSRIs only, nine (18 percent) were prescribed an SSRI in combination with another antidepressant and 16 (32 percent) were prescribed one or more non-SSRI antidepressants only.

After adjusting for maternal and birth factors, mothers of children with ASD were twice as likely to have at least one antidepressant prescription in the year prior to delivery. When compared with women with no antidepressant prescription during the study period, those with a prescription for a SSRI were more than twice as likely to have a child later diagnosed with ASD. This association was not seen for the small group of women who were prescribed a non-SSRI antidepressant only.

Additionally, after adjustment for a history of depression during the year prior to delivery, SSRI exposure during the first trimester remained significantly associated with risk of ASD, as was a history of SSRI exposure at any point during the year prior to delivery. Conversely, no association was seen between risk of ASD and the indication for treatment (mother having a history of depression or any mental health disorder) for the year prior to delivery.

"Although the number of children exposed prenatally to selective serotonin reuptake inhibitors in this population was low, results suggest that exposure, especially during the first trimester, may modestly increase the risk of ASD," the authors conclude. "We recommend that our findings be considered as preliminary and treated with caution, pending results from further studies designed to address the very complex question of whether prenatal exposure to SSRIs may be etiologically linked to later diagnoses of ASDs in offspring."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by JAMA and Archives Journals.

Journal Reference:

Lisa A. Croen; Judith K. Grether; Cathleen K. Yoshida; Roxana Odouli; Victoria Hendrick. Antidepressant Use During Pregnancy and Childhood Autism Spectrum Disorders. Archives of General Psychiatry, 2011; DOI: 10.1001/archgenpsychiatry.2011.73

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Drinking, cannabis use and psychological distress increase in Ontario, Canada, survey finds

ScienceDaily (June 13, 2011) — The latest survey of Ontario adults from the Centre for Addiction and Mental Health (CAMH) shows increasing rates of daily drinking and cannabis use and high levels of psychological distress. The results of the 2009 CAMH Monitor survey, the longest running survey tracking mental health and addiction indicators among adults in Ontario, were published June 13, 2011.

Alcohol

The proportion of adults reporting daily drinking increased from 5.3% in 2002 to over 9% in 2009. The average number of drinks consumed weekly among drinkers has also increased from 3 drinks to 4.6 drinks, and the proportion of adults exceeding low-risk drinking guidelines remains at elevated levels (22%). However, there were also some encouraging findings: there was a significant decline in binge drinking from 12.6% in 2006 to 7.1% in 2009, and the decline was evident especially among young adults, from 24% to 11.5%.

Although driving within an hour of consuming two or more drinks has shown a steady decline in the past years, from 13.1% in 1996 to 6.9% in 2009, there is evidence that this trend has reversed among young adults. Driving after drinking posted a significant increase among 18 to 29 year olds, from 7.7% in 2005 to 12.8% in 2009.

"The data tell us that while the number of people who drink alcohol has not changed, the way they are drinking has -- people are drinking more often and may be consuming more alcohol when they do drink, although there may be fewer binge occasions," said Dr. Robert Mann, CAMH Senior Scientist and lead investigator on the study. "We know that the more access people have to alcohol, the more people will drink, leading to more instances of drinking and driving. Measures such as Random Breath Testing and lowering legal limits to .05% can reduce drunk driving deaths. The implementation of .05% legislation in British Columbia appears to have resulted in a 50% decrease in drinking and driving deaths in that province."

Cannabis

The prevalence of cannabis use has been steadily increasing from 8.7% in 1996 to 13.3% in 2009, for both men and women and among all age groups. Along with this, there was almost a 2-fold increase in cannabis use among those aged 18-29, from 18.3% to 35.8%.

"These increases are of concern to us," stated Dr. Mann. "We know that cannabis use may increase the risk of psychosis for people who are predisposed to schizophrenia, and may worsen the symptoms of other mental illnesses." Another noticeable change was the large increase in use of cannabis among older adults. Use by those aged 50 years and older increased more than 3-fold from 1.4% to 4.7% between 1996 and 2009 and, among past year cannabis users, the proportion of users aged 50 years and older increased from 1.9% to 13.9% during the same time period.

Tobacco

Some positive findings are that the percentage of adult Ontarians reporting smoking cigarettes declined from 19.7% in 2008 to 18.6% in 2009. Though 14% of Ontarians still report daily smoking, it is a positive sign that cigarette smoking has steadily declined since 1996, from 26.8% to 18.6% in 2009. Dr. Mann notes that the provincial government's commitment to anti- smoking legislation through smoke-free Ontario probably played an important role in the decrease in smoking rates.

Mental Health

One in seven Ontario adults (14.7%), representing 1,400,000 people, reported symptoms of elevated psychological distress, and almost 6% reported that their overall mental health was poor. Those aged 30-39 were the most likely to report poor mental health, and those over age 65 reported the lowest rates of poor mental health. Mental health was strongly correlated with education. Those who had not graduated high school reported higher levels of poor mental health, and those who had graduated from university reported lower rates. "These results suggest that the social determinants of health, such as income, play as important a role in mental health as they do in physical health," said Mann.

The use of anti-anxiety medication has remained stable over the past few years, but trend data shows that over the past 10 years, use of these medications has risen from 4.5% to nearly 7% of Ontario adults. The same pattern can also be seen in the use of antidepressant medication, which has trended upward from 3.6% in 1999 to the current rate of 6.6%. Added Dr. Mann, "Though these are marked increases, they may also be showing that more people experiencing mental health problems are seeking and receiving help, which is a positive step."

Despite several differences, there was no strong dominant pattern in regional differences. Those from Northern Ontario were the most likely to be current smokers and to smoke daily; those from Toronto were the least likely to drink alcohol; those from the South West region of the province reported the highest average number of drinks consumed per week; and driving after drinking was most likely in the South West and in the Central South regions.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Centre for Addiction and Mental Health.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Panic symptoms increase steadily, not acutely, after stressful event

ScienceDaily (June 20, 2011) — Just like everyone else, people with panic disorder have real stress in their lives. They get laid off and they fight with their spouses. How such stresses affect their panic symptoms hasn't been well understood, but a new study by researchers at Brown University presents the counterintuitive finding that certain kinds of stressful life events cause panic symptoms to increase gradually over succeeding months, rather than to spike immediately.

"We definitely expected the symptoms to get worse over time, but we also thought the symptoms would get worse right away," said Ethan Moitra, a postdoctoral researcher in the Department of Psychiatry and Human Behavior at the Warren Alpert Medical School of Brown University.

But even if the events don't seem to trigger an immediate panic attack, said Dr. Martin Keller, professor of psychiatry and human behavior and principal investigator of the research, patients, family members, or their psychiatrists need to keep their guard up.

"If they have the event and they are not feeling much different then maybe the vigilance on the individual's part decreases somewhat," Keller said. "With the knowledge we have, you may need to stay vigilant for three months or maybe longer. This is something you have to watch for."

In their study, published in advance June 11 in the Journal of Affective Disorders, lead author Moitra, Keller, and their co-authors also found that panic symptoms did not seem to increase in advance of stressful life events, even if they were predictable, such as a divorce becoming official.

The study is based annual assessments of 418 adults with panic disorder or panic disorder with agoraphobia, who were enrolled in the Harvard/Brown Anxiety Research Project (HARP) between 1998 and 2004. Research staff asked the volunteers detailed, standardized questions about important events in their lives and their levels of anxiety.

A statistical analysis of the results found that for stressful life events in the categories of "work," such as a demotion or layoff, or "friends/family/household," such as a family argument, panic symptoms that had meandering severity before the event, increased steadily but gradually for at least 12 weeks afterward.

Stressful events in seven other categories, such as "crime/legal" or "deaths" did not seem to affect panic symptoms at all.

While the findings about the effect of some stressful life events on symptoms of people already diagnosed with panic disorder are new, other researchers have connected stress to panic attacks before. Stressful events are associated with the onset of panic disorder in the vast majority of cases, Moitra said.

Moitra said a possible biological explanation for the association is that stressful life events might exacerbate an underlying proclivity in people with panic disorder to perceive oncoming bouts of hyperventilation, which in turn lead to panic responses.

But while some stressful events have proven to be associated with changes in panic symptom levels, more research is needed to determine what kind of causal role stressful events may have.

"This may be one of those reasons why panic disorders can get worse," Moitra said.

In addition to Moitra and Keller, other authors include Brown psychiatry and human behavior researchers Ingryd Dyck, Courtney Beard, Andri Bjornsson, and Nicholas Sibrava. Author Risa Weisberg is also affiliated with the Alpert Medical School's Department of Family Medicine. The National Institutes of Health funded the research.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Brown University.

Journal Reference:

Ethan Moitra, Ingrid Dyck, Courtney Beard, Andri S. Bjornsson, Nicholas J. Sibrava, Risa B. Weisberg, Martin B. Keller. Impact of stressful life events on the course of panic disorder in adults. Journal of Affective Disorders, 2011; DOI: 10.1016/j.jad.2011.05.029

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here