SATURDAY, Dec. 13, 2014 (HealthDay News) -- Looking for a way to help
reduce your stress? Try checking your emails less often, researchers
suggest.
The new study featured 124 adults -- including students,
financial analysts, medical professionals and others -- who were
divided into two groups. During the first week, one group checked their
emails only three times a day, while the other group checked their
emails as often as they liked. The groups then switched for the second
week of the study.
"Our
findings showed that people felt less stressed when they checked their
email less often," study author Kostadin Kushlev, a Ph.D. candidate in
psychology at the University of British Columbia in Canada, said in a
university news release.
However, changing email habits proved difficult for many of the study participants, the investigators found.
"Most participants in our study found it quite difficult to check their email only a few times a day," Kushlev said.
The study was published online recently in the journal Computers in Human Behavior.
Source: http://health.usnews.com/health-news/articles/2014/12/13/constant-email-checks-can-leave-you-stressed
Google Sniper
Sunday 25 January 2015
Wednesday 21 January 2015
What is Anxiety Disorder?
Anxiety is a normal
reaction to stress and can actually be beneficial in some situations.
For some people, however, anxiety can become excessive. While the person
suffering may realize their anxiety is too much, they may also have
difficulty controlling it and it may negatively affect their day-to-day
living. There are a wide variety of anxiety disorders, including
post-traumatic stress disorder, obsessive-compulsive disorder, and panic
disorder to name a few. Collectively, they are among the most common
mental disorders experienced by Americans.
The following anxiety disorders are discussed on this website:
Scientists currently think that, like heart disease and type 1 diabetes, mental illnesses are complex and probably result from a combination of genetic, environmental, psychological, and developmental factors. For instance, although NIMH-sponsored studies of twins and families suggest that genetics play a role in the development of some anxiety disorders, problems such as PTSD are triggered by trauma. Genetic studies may help explain why some people exposed to trauma develop PTSD and others do not.
Several parts of the brain are key actors in the production of fear and anxiety. Using brain imaging technology and neurochemical techniques, scientists have discovered that the amygdala and the hippocampus play significant roles in most anxiety disorders.
The amygdala is an almond-shaped structure deep in the brain that is believed to be a communications hub between the parts of the brain that process incoming sensory signals and the parts that interpret these signals. It can alert the rest of the brain that a threat is present and trigger a fear or anxiety response. The emotional memories stored in the central part of the amygdala may play a role in anxiety disorders involving very distinct fears, such as fears of dogs, spiders, or flying.
The hippocampus is the part of the brain that encodes threatening events into memories. Studies have shown that the hippocampus appears to be smaller in some people who were victims of child abuse or who served in military combat. Research will determine what causes this reduction in size and what role it plays in the flashbacks, deficits in explicit memory, and fragmented memories of the traumatic event that are common in PTSD.
By learning more about how the brain creates fear and anxiety, scientists may be able to devise better treatments for anxiety disorders. For example, if specific neurotransmitters are found to play an important role in fear, drugs may be developed that will block them and decrease fear responses; if enough is learned about how the brain generates new cells throughout the lifecycle, it may be possible to stimulate the growth of new neurons in the hippocampus in people with PTSD.
Current research at NIMH on anxiety disorders includes studies that address how well medication and behavioral therapies work in the treatment of OCD, and the safety and effectiveness of medications for children and adolescents who have a combination of anxiety disorders and attention deficit hyperactivity disorder.
Anxiety disorders commonly occur along with other mental or physical illnesses, including alcohol or substance abuse, which may mask anxiety symptoms or make them worse. In some cases, these other illnesses need to be treated before a person will respond to treatment for the anxiety disorder.
Effective therapies for anxiety disorders are available, and research is uncovering new treatments that can help most people with anxiety disorders lead productive, fulfilling lives. If you think you have an anxiety disorder, you should seek information and treatment right away.
Women are 60% more likely than men to experience an anxiety disorder over their lifetime. Non-Hispanic blacks are 20% less likely, and Hispanics are 30% less likely, than non-Hispanic whites to experience an anxiety disorder during their lifetime.
A large, national survey of adolescent mental health reported that about 8 percent of teens ages 13–18 have an anxiety disorder, with symptoms commonly emerging around age 6. However, of these teens, only 18 percent received mental health care.
People with anxiety disorders who have already received treatment should tell their current doctor about that treatment in detail. If they received medication, they should tell their doctor what medication was used, what the dosage was at the beginning of treatment, whether the dosage was increased or decreased while they were under treatment, what side effects occurred, and whether the treatment helped them become less anxious. If they received psychotherapy, they should describe the type of therapy, how often they attended sessions, and whether the therapy was useful.
Often people believe that they have “failed” at treatment or that the treatment didn’t work for them when, in fact, it was not given for an adequate length of time or was administered incorrectly. Sometimes people must try several different treatments or combinations of treatment before they find the one that works for them.
Medication
Medication will not cure anxiety disorders, but it can keep them under control while the person receives psychotherapy. Medication must be prescribed by physicians, usually psychiatrists, who can either offer psychotherapy themselves or work as a team with psychologists, social workers, or counselors who provide psychotherapy. The principal medications used for anxiety disorders are antidepressants, anti-anxiety drugs, and beta-blockers to control some of the physical symptoms. With proper treatment, many people with anxiety disorders can lead normal, fulfilling lives.
Antidepressants
Antidepressants were developed to treat depression but are also effective for anxiety disorders. Although these medications begin to alter brain chemistry after the very first dose, their full effect requires a series of changes to occur; it is usually about 4 to 6 weeks before symptoms start to fade. It is important to continue taking these medications long enough to let them work.
SSRIs
Some of the newest antidepressants are called selective serotonin reuptake inhibitors, or SSRIs. SSRIs alter the levels of the neurotransmitter serotonin in the brain, which, like other neurotransmitters, helps brain cells communicate with one another.
Fluoxetine (Prozac®), sertraline (Zoloft®), escitalopram (Lexapro®), paroxetine (Paxil®), and citalopram (Celexa®) are some of the SSRIs commonly prescribed for panic disorder, OCD, PTSD, and social phobia. SSRIs are also used to treat panic disorder when it occurs in combination with OCD, social phobia, or depression. Venlafaxine (Effexor®), a drug closely related to the SSRIs, is used to treat GAD. These medications are started at low doses and gradually increased until they have a beneficial effect.
SSRIs have fewer side effects than older antidepressants, but they sometimes produce slight nausea or jitters when people first start to take them. These symptoms fade with time. Some people also experience sexual dysfunction with SSRIs, which may be helped by adjusting the dosage or switching to another SSRI.
Tricyclics
Tricyclics are older than SSRIs and work as well as SSRIs for anxiety disorders other than OCD. They are also started at low doses that are gradually increased. They sometimes cause dizziness, drowsiness, dry mouth, and weight gain, which can usually be corrected by changing the dosage or switching to another tricyclic medication.
Tricyclics include imipramine (Tofranil®), which is prescribed for panic disorder and GAD, and clomipramine (Anafranil®), which is the only tricyclic antidepressant useful for treating OCD.
MAOIs
Monoamine oxidase inhibitors (MAOIs) are the oldest class of antidepressant medications. The MAOIs most commonly prescribed for anxiety disorders are phenelzine (Nardil®), followed by tranylcypromine (Parnate®), and isocarboxazid (Marplan®), which are useful in treating panic disorder and social phobia. People who take MAOIs cannot eat a variety of foods and beverages (including cheese and red wine) that contain tyramine or take certain medications, including some types of birth control pills, pain relievers (such as Advil®, Motrin®, or Tylenol®), cold and allergy medications, and herbal supplements; these substances can interact with MAOIs to cause dangerous increases in blood pressure. The development of a new MAOI skin patch may help lessen these risks. MAOIs can also react with SSRIs to produce a serious condition called “serotonin syndrome,” which can cause confusion, hallucinations, increased sweating, muscle stiffness, seizures, changes in blood pressure or heart rhythm, and other potentially life-threatening conditions.
Anti-Anxiety Drugs
High-potency benzodiazepines combat anxiety and have few side effects other than drowsiness. Because people can get used to them and may need higher and higher doses to get the same effect, benzodiazepines are generally prescribed for short periods of time, especially for people who have abused drugs or alcohol and who become dependent on medication easily. One exception to this rule is people with panic disorder, who can take benzodiazepines for up to a year without harm.
Clonazepam (Klonopin®) is used for social phobia and GAD, lorazepam (Ativan®) is helpful for panic disorder, and alprazolam (Xanax®) is useful for both panic disorder and GAD.
Some people experience withdrawal symptoms if they stop taking benzodiazepines abruptly instead of tapering off, and anxiety can return once the medication is stopped. These potential problems have led some physicians to shy away from using these drugs or to use them in inadequate doses.
Buspirone (Buspar®), an azapirone, is a newer anti-anxiety medication used to treat GAD. Possible side effects include dizziness, headaches, and nausea. Unlike benzodiazepines, buspirone must be taken consistently for at least 2 weeks to achieve an anti-anxiety effect.
Beta-Blockers
Beta-blockers, such as propranolol (Inderal®), which is used to treat heart conditions, can prevent the physical symptoms that accompany certain anxiety disorders, particularly social phobia. When a feared situation can be predicted (such as giving a speech), a doctor may prescribe a beta-blocker to keep physical symptoms of anxiety under control.
Taking Medications
Before taking medication for an anxiety disorder:
Psychotherapy involves talking with a trained mental health professional, such as a psychiatrist, psychologist, social worker, or counselor, to discover what caused an anxiety disorder and how to deal with its symptoms.
Cognitive-Behavioral Therapy
Cognitive-behavioral therapy (CBT) is very useful in treating anxiety disorders. The cognitive part helps people change the thinking patterns that support their fears, and the behavioral part helps people change the way they react to anxiety-provoking situations.
For example, CBT can help people with panic disorder learn that their panic attacks are not really heart attacks and help people with social phobia learn how to overcome the belief that others are always watching and judging them. When people are ready to confront their fears, they are shown how to use exposure techniques to desensitize themselves to situations that trigger their anxieties.
People with OCD who fear dirt and germs are encouraged to get their hands dirty and wait increasing amounts of time before washing them. The therapist helps the person cope with the anxiety that waiting produces; after the exercise has been repeated a number of times, the anxiety diminishes. People with social phobia may be encouraged to spend time in feared social situations without giving in to the temptation to flee and to make small social blunders and observe how people respond to them. Since the response is usually far less harsh than the person fears, these anxieties are lessened. People with PTSD may be supported through recalling their traumatic event in a safe situation, which helps reduce the fear it produces. CBT therapists also teach deep breathing and other types of exercises to relieve anxiety and encourage relaxation.
Exposure-based behavioral therapy has been used for many years to treat specific phobias. The person gradually encounters the object or situation that is feared, perhaps at first only through pictures or tapes, then later face-to-face. Often the therapist will accompany the person to a feared situation to provide support and guidance.
CBT is undertaken when people decide they are ready for it and with their permission and cooperation. To be effective, the therapy must be directed at the person’s specific anxieties and must be tailored to his or her needs. There are no side effects other than the discomfort of temporarily increased anxiety.
CBT or behavioral therapy often lasts about 12 weeks. It may be conducted individually or with a group of people who have similar problems. Group therapy is particularly effective for social phobia. Often “homework” is assigned for participants to complete between sessions. There is some evidence that the benefits of CBT last longer than those of medication for people with panic disorder, and the same may be true for OCD, PTSD, and social phobia. If a disorder recurs at a later date, the same therapy can be used to treat it successfully a second time.
Medication can be combined with psychotherapy for specific anxiety disorders, and this is the best treatment approach for many people.
If an anxiety disorder is diagnosed, the next step is usually seeing a mental health professional. The practitioners who are most helpful with anxiety disorders are those who have training in cognitive-behavioral therapy and/or behavioral therapy, and who are open to using medication if it is needed.
You should feel comfortable talking with the mental health professional you choose. If you do not, you should seek help elsewhere. Once you find a mental health professional with whom you are comfortable, the two of you should work as a team and make a plan to treat your anxiety disorder together.
Remember that once you start on medication, it is important not to stop taking it abruptly. Certain drugs must be tapered off under the supervision of a doctor or bad reactions can occur. Make sure you talk to the doctor who prescribed your medication before you stop taking it. If you are having trouble with side effects, it’s possible that they can be eliminated by adjusting how much medication you take and when you take it.
Most insurance plans, including health maintenance organizations (HMOs), will cover treatment for anxiety disorders. Check with your insurance company and find out. If you don’t have insurance, the Health and Human Services division of your county government may offer mental health care at a public mental health center that charges people according to how much they are able to pay. If you are on public assistance, you may be able to get care through your state Medicaid plan.
Ways to Make Treatment More Effective
Many people with anxiety disorders benefit from joining a self-help or support group and sharing their problems and achievements with others. Internet chat rooms can also be useful in this regard, but any advice received over the Internet should be used with caution, as Internet acquaintances have usually never seen each other and false identities are common. Talking with a trusted friend or member of the clergy can also provide support, but it is not a substitute for care from a mental health professional.
Stress management techniques and meditation can help people with anxiety disorders calm themselves and may enhance the effects of therapy. There is preliminary evidence that aerobic exercise may have a calming effect. Since caffeine, certain illicit drugs, and even some over-the-counter cold medications can aggravate the symptoms of anxiety disorders, they should be avoided. Check with your physician or pharmacist before taking any additional medications.
The family is very important in the recovery of a person with an anxiety disorder. Ideally, the family should be supportive but not help perpetuate their loved one’s symptoms. Family members should not trivialize the disorder or demand improvement without treatment.
Source: http://www.nimh.nih.gov/health/topics/anxiety-disorders/index.shtml
The following anxiety disorders are discussed on this website:
- generalized anxiety disorder (GAD)
- obsessive-compulsive disorder (OCD),
- panic disorder,
- post-traumatic stress disorder (PTSD), and
- social phobia (or social anxiety disorder).
Causes
NIMH supports research into the causes, diagnosis, prevention, and treatment of anxiety disorders and other mental illnesses. Scientists are looking at what role genes play in the development of these disorders and are also investigating the effects of environmental factors such as pollution, physical and psychological stress, and diet. In addition, studies are being conducted on the “natural history” (what course the illness takes without treatment) of a variety of individual anxiety disorders, combinations of anxiety disorders, and anxiety disorders that are accompanied by other mental illnesses such as depression.Scientists currently think that, like heart disease and type 1 diabetes, mental illnesses are complex and probably result from a combination of genetic, environmental, psychological, and developmental factors. For instance, although NIMH-sponsored studies of twins and families suggest that genetics play a role in the development of some anxiety disorders, problems such as PTSD are triggered by trauma. Genetic studies may help explain why some people exposed to trauma develop PTSD and others do not.
Several parts of the brain are key actors in the production of fear and anxiety. Using brain imaging technology and neurochemical techniques, scientists have discovered that the amygdala and the hippocampus play significant roles in most anxiety disorders.
The amygdala is an almond-shaped structure deep in the brain that is believed to be a communications hub between the parts of the brain that process incoming sensory signals and the parts that interpret these signals. It can alert the rest of the brain that a threat is present and trigger a fear or anxiety response. The emotional memories stored in the central part of the amygdala may play a role in anxiety disorders involving very distinct fears, such as fears of dogs, spiders, or flying.
The hippocampus is the part of the brain that encodes threatening events into memories. Studies have shown that the hippocampus appears to be smaller in some people who were victims of child abuse or who served in military combat. Research will determine what causes this reduction in size and what role it plays in the flashbacks, deficits in explicit memory, and fragmented memories of the traumatic event that are common in PTSD.
By learning more about how the brain creates fear and anxiety, scientists may be able to devise better treatments for anxiety disorders. For example, if specific neurotransmitters are found to play an important role in fear, drugs may be developed that will block them and decrease fear responses; if enough is learned about how the brain generates new cells throughout the lifecycle, it may be possible to stimulate the growth of new neurons in the hippocampus in people with PTSD.
Current research at NIMH on anxiety disorders includes studies that address how well medication and behavioral therapies work in the treatment of OCD, and the safety and effectiveness of medications for children and adolescents who have a combination of anxiety disorders and attention deficit hyperactivity disorder.
Signs & Symptoms
Unlike the relatively mild, brief anxiety caused by a stressful event (such as speaking in public or a first date), anxiety disorders last at least 6 months and can get worse if they are not treated. Each anxiety disorder has different symptoms, but all the symptoms cluster around excessive, irrational fear and dread.Anxiety disorders commonly occur along with other mental or physical illnesses, including alcohol or substance abuse, which may mask anxiety symptoms or make them worse. In some cases, these other illnesses need to be treated before a person will respond to treatment for the anxiety disorder.
Effective therapies for anxiety disorders are available, and research is uncovering new treatments that can help most people with anxiety disorders lead productive, fulfilling lives. If you think you have an anxiety disorder, you should seek information and treatment right away.
Who Is At Risk?
Anxiety disorders affect about 40 million American adults age 18 years and older (about 18%) in a given year, causing them to be filled with fearfulness and uncertainty.Women are 60% more likely than men to experience an anxiety disorder over their lifetime. Non-Hispanic blacks are 20% less likely, and Hispanics are 30% less likely, than non-Hispanic whites to experience an anxiety disorder during their lifetime.
A large, national survey of adolescent mental health reported that about 8 percent of teens ages 13–18 have an anxiety disorder, with symptoms commonly emerging around age 6. However, of these teens, only 18 percent received mental health care.
Diagnosis
A doctor must conduct a careful diagnostic evaluation to determine whether a person’s symptoms are caused by an anxiety disorder or a physical problem. If an anxiety disorder is diagnosed, the type of disorder or the combination of disorders that are present must be identified, as well as any coexisting conditions, such as depression or substance abuse. Sometimes alcoholism, depression, or other coexisting conditions have such a strong effect on the individual that treating the anxiety disorder must wait until the coexisting conditions are brought under control.Treatments
In general, anxiety disorders are treated with medication, specific types of psychotherapy, or both. Treatment choices depend on the problem and the person’s preference.People with anxiety disorders who have already received treatment should tell their current doctor about that treatment in detail. If they received medication, they should tell their doctor what medication was used, what the dosage was at the beginning of treatment, whether the dosage was increased or decreased while they were under treatment, what side effects occurred, and whether the treatment helped them become less anxious. If they received psychotherapy, they should describe the type of therapy, how often they attended sessions, and whether the therapy was useful.
Often people believe that they have “failed” at treatment or that the treatment didn’t work for them when, in fact, it was not given for an adequate length of time or was administered incorrectly. Sometimes people must try several different treatments or combinations of treatment before they find the one that works for them.
Medication
Medication will not cure anxiety disorders, but it can keep them under control while the person receives psychotherapy. Medication must be prescribed by physicians, usually psychiatrists, who can either offer psychotherapy themselves or work as a team with psychologists, social workers, or counselors who provide psychotherapy. The principal medications used for anxiety disorders are antidepressants, anti-anxiety drugs, and beta-blockers to control some of the physical symptoms. With proper treatment, many people with anxiety disorders can lead normal, fulfilling lives.
Antidepressants
Antidepressants were developed to treat depression but are also effective for anxiety disorders. Although these medications begin to alter brain chemistry after the very first dose, their full effect requires a series of changes to occur; it is usually about 4 to 6 weeks before symptoms start to fade. It is important to continue taking these medications long enough to let them work.
SSRIs
Some of the newest antidepressants are called selective serotonin reuptake inhibitors, or SSRIs. SSRIs alter the levels of the neurotransmitter serotonin in the brain, which, like other neurotransmitters, helps brain cells communicate with one another.
Fluoxetine (Prozac®), sertraline (Zoloft®), escitalopram (Lexapro®), paroxetine (Paxil®), and citalopram (Celexa®) are some of the SSRIs commonly prescribed for panic disorder, OCD, PTSD, and social phobia. SSRIs are also used to treat panic disorder when it occurs in combination with OCD, social phobia, or depression. Venlafaxine (Effexor®), a drug closely related to the SSRIs, is used to treat GAD. These medications are started at low doses and gradually increased until they have a beneficial effect.
SSRIs have fewer side effects than older antidepressants, but they sometimes produce slight nausea or jitters when people first start to take them. These symptoms fade with time. Some people also experience sexual dysfunction with SSRIs, which may be helped by adjusting the dosage or switching to another SSRI.
Tricyclics
Tricyclics are older than SSRIs and work as well as SSRIs for anxiety disorders other than OCD. They are also started at low doses that are gradually increased. They sometimes cause dizziness, drowsiness, dry mouth, and weight gain, which can usually be corrected by changing the dosage or switching to another tricyclic medication.
Tricyclics include imipramine (Tofranil®), which is prescribed for panic disorder and GAD, and clomipramine (Anafranil®), which is the only tricyclic antidepressant useful for treating OCD.
MAOIs
Monoamine oxidase inhibitors (MAOIs) are the oldest class of antidepressant medications. The MAOIs most commonly prescribed for anxiety disorders are phenelzine (Nardil®), followed by tranylcypromine (Parnate®), and isocarboxazid (Marplan®), which are useful in treating panic disorder and social phobia. People who take MAOIs cannot eat a variety of foods and beverages (including cheese and red wine) that contain tyramine or take certain medications, including some types of birth control pills, pain relievers (such as Advil®, Motrin®, or Tylenol®), cold and allergy medications, and herbal supplements; these substances can interact with MAOIs to cause dangerous increases in blood pressure. The development of a new MAOI skin patch may help lessen these risks. MAOIs can also react with SSRIs to produce a serious condition called “serotonin syndrome,” which can cause confusion, hallucinations, increased sweating, muscle stiffness, seizures, changes in blood pressure or heart rhythm, and other potentially life-threatening conditions.
Anti-Anxiety Drugs
High-potency benzodiazepines combat anxiety and have few side effects other than drowsiness. Because people can get used to them and may need higher and higher doses to get the same effect, benzodiazepines are generally prescribed for short periods of time, especially for people who have abused drugs or alcohol and who become dependent on medication easily. One exception to this rule is people with panic disorder, who can take benzodiazepines for up to a year without harm.
Clonazepam (Klonopin®) is used for social phobia and GAD, lorazepam (Ativan®) is helpful for panic disorder, and alprazolam (Xanax®) is useful for both panic disorder and GAD.
Some people experience withdrawal symptoms if they stop taking benzodiazepines abruptly instead of tapering off, and anxiety can return once the medication is stopped. These potential problems have led some physicians to shy away from using these drugs or to use them in inadequate doses.
Buspirone (Buspar®), an azapirone, is a newer anti-anxiety medication used to treat GAD. Possible side effects include dizziness, headaches, and nausea. Unlike benzodiazepines, buspirone must be taken consistently for at least 2 weeks to achieve an anti-anxiety effect.
Beta-Blockers
Beta-blockers, such as propranolol (Inderal®), which is used to treat heart conditions, can prevent the physical symptoms that accompany certain anxiety disorders, particularly social phobia. When a feared situation can be predicted (such as giving a speech), a doctor may prescribe a beta-blocker to keep physical symptoms of anxiety under control.
Taking Medications
Before taking medication for an anxiety disorder:
- Ask your doctor to tell you about the effects and side effects of the drug.
- Tell your doctor about any alternative therapies or over-the-counter medications you are using.
- Ask your doctor when and how the medication should be stopped. Some drugs can’t be stopped abruptly but must be tapered off slowly under a doctor’s supervision.
- Work with your doctor to determine which medication is right for you and what dosage is best.
- Be aware that some medications are effective only if they are taken regularly and that symptoms may recur if the medication is stopped.
Psychotherapy involves talking with a trained mental health professional, such as a psychiatrist, psychologist, social worker, or counselor, to discover what caused an anxiety disorder and how to deal with its symptoms.
Cognitive-Behavioral Therapy
Cognitive-behavioral therapy (CBT) is very useful in treating anxiety disorders. The cognitive part helps people change the thinking patterns that support their fears, and the behavioral part helps people change the way they react to anxiety-provoking situations.
For example, CBT can help people with panic disorder learn that their panic attacks are not really heart attacks and help people with social phobia learn how to overcome the belief that others are always watching and judging them. When people are ready to confront their fears, they are shown how to use exposure techniques to desensitize themselves to situations that trigger their anxieties.
People with OCD who fear dirt and germs are encouraged to get their hands dirty and wait increasing amounts of time before washing them. The therapist helps the person cope with the anxiety that waiting produces; after the exercise has been repeated a number of times, the anxiety diminishes. People with social phobia may be encouraged to spend time in feared social situations without giving in to the temptation to flee and to make small social blunders and observe how people respond to them. Since the response is usually far less harsh than the person fears, these anxieties are lessened. People with PTSD may be supported through recalling their traumatic event in a safe situation, which helps reduce the fear it produces. CBT therapists also teach deep breathing and other types of exercises to relieve anxiety and encourage relaxation.
Exposure-based behavioral therapy has been used for many years to treat specific phobias. The person gradually encounters the object or situation that is feared, perhaps at first only through pictures or tapes, then later face-to-face. Often the therapist will accompany the person to a feared situation to provide support and guidance.
CBT is undertaken when people decide they are ready for it and with their permission and cooperation. To be effective, the therapy must be directed at the person’s specific anxieties and must be tailored to his or her needs. There are no side effects other than the discomfort of temporarily increased anxiety.
CBT or behavioral therapy often lasts about 12 weeks. It may be conducted individually or with a group of people who have similar problems. Group therapy is particularly effective for social phobia. Often “homework” is assigned for participants to complete between sessions. There is some evidence that the benefits of CBT last longer than those of medication for people with panic disorder, and the same may be true for OCD, PTSD, and social phobia. If a disorder recurs at a later date, the same therapy can be used to treat it successfully a second time.
Medication can be combined with psychotherapy for specific anxiety disorders, and this is the best treatment approach for many people.
Living With
If you think you have an anxiety disorder, the first person you should see is your family doctor. A physician can determine whether the symptoms that alarm you are due to an anxiety disorder, another medical condition, or both.If an anxiety disorder is diagnosed, the next step is usually seeing a mental health professional. The practitioners who are most helpful with anxiety disorders are those who have training in cognitive-behavioral therapy and/or behavioral therapy, and who are open to using medication if it is needed.
You should feel comfortable talking with the mental health professional you choose. If you do not, you should seek help elsewhere. Once you find a mental health professional with whom you are comfortable, the two of you should work as a team and make a plan to treat your anxiety disorder together.
Remember that once you start on medication, it is important not to stop taking it abruptly. Certain drugs must be tapered off under the supervision of a doctor or bad reactions can occur. Make sure you talk to the doctor who prescribed your medication before you stop taking it. If you are having trouble with side effects, it’s possible that they can be eliminated by adjusting how much medication you take and when you take it.
Most insurance plans, including health maintenance organizations (HMOs), will cover treatment for anxiety disorders. Check with your insurance company and find out. If you don’t have insurance, the Health and Human Services division of your county government may offer mental health care at a public mental health center that charges people according to how much they are able to pay. If you are on public assistance, you may be able to get care through your state Medicaid plan.
Ways to Make Treatment More Effective
Many people with anxiety disorders benefit from joining a self-help or support group and sharing their problems and achievements with others. Internet chat rooms can also be useful in this regard, but any advice received over the Internet should be used with caution, as Internet acquaintances have usually never seen each other and false identities are common. Talking with a trusted friend or member of the clergy can also provide support, but it is not a substitute for care from a mental health professional.
Stress management techniques and meditation can help people with anxiety disorders calm themselves and may enhance the effects of therapy. There is preliminary evidence that aerobic exercise may have a calming effect. Since caffeine, certain illicit drugs, and even some over-the-counter cold medications can aggravate the symptoms of anxiety disorders, they should be avoided. Check with your physician or pharmacist before taking any additional medications.
The family is very important in the recovery of a person with an anxiety disorder. Ideally, the family should be supportive but not help perpetuate their loved one’s symptoms. Family members should not trivialize the disorder or demand improvement without treatment.
Source: http://www.nimh.nih.gov/health/topics/anxiety-disorders/index.shtml
Monday 19 January 2015
Early exposure to antidepressants affects adult anxiety, serotonin transmission
About 15
percent of women in the United States suffer from anxiety disorders and
depression during their pregnancies, and many are prescribed
antidepressants. However little is known about how early exposure to
these medications might affect their offspring as they mature into
adults.
Related Articles
The answer to that question is vital, as 5 percent of all babies born
in the U.S. -- more than 200,000 a year -- are exposed to
antidepressants during gestation via transmission from their mothers.
Now, a UCLA team has studied early developmental exposure to two different antidepressants, Prozac and Lexapro, in a mouse model that mimics human third trimester medication exposure. They found that, although these serotonin-selective reuptake inhibiting antidepressants (SSRIs) were thought to work the same way, they did not produce the same long-term changes in anxiety behavior in the adult mice.
The mice exposed to Lexapro had permanent changes in serotonin neurotransmission and were less anxious as adults than the mice exposed to Prozac, said study senior author Anne M. Andrews, professor of psychiatry and chemistry and biochemistry and the Richard Metzner Endowed Chair in Clinical Neuropharmacology at the Semel Institute for Neuroscience & Human Behavior and California NanoSystems Institute.
"This was quite surprising, since these medications belong to the same drug class and are believed to work by the same mechanism. The implications of these findings are that with additional investigation, it may be possible to identify specific antidepressants that are safer for pregnant women," Andrews said. "It's important to recognize that major depressive disorders and anxiety disorders are serious medical conditions that often require therapeutic intervention. Prescribing the safest medication for mother and child is paramount."
The results of the six-year study appear early online Dec. 19, 2014 in the peer-reviewed journal Neuropsychopharmacology.
SSRIs like Prozac and Lexapro act by blocking the actions of a protein called the serotonin transporter, which removes the neurotransmitter serotonin from the signaling space between neurons. Andrews and her team also studied mice that had been genetically engineered to have a reduction or absence of serotonin transporters in the brain. They were able to compare early antidepressant exposure to permanent reductions in serotonin transporter function.
Genetic reductions in serotonin transporters are thought to be a risk factor, particularly when combined with stressful life experiences, for developing anxiety and mood disorders. And in fact, the genetically engineered mice Andrews studied showed more anxiety as adults.
"It might be possible that when mothers are treated for depression or anxiety during pregnancy that certain SSRIs may promote resilience to developing these disorders in children later in life," Andrews said. "However, it will take much more research for us to understand whether this is true and whether certain SSRIs may be better at promoting these effects."
Going forward, Andrews and her team plan to investigate the effects of early exposure to antidepressants on the architectures of serotonin neurons. Based on the current findings, they suspect that early exposure to Lexapro may alter the way serotonin neurons innervate brain regions involved in mood and anxiety behavior. They also plan to investigate other SSRIs such as Paxil and Zoloft.
"Current antidepressant therapies are ineffective in treating anxiety and depression in large numbers of patients, and advances in predicting individual responses are hindered by difficulties associated with characterizing complex influences of genetic and environmental factors on serotonergic transmission in humans," the study states. "Highly controlled animal models, such as those studied here, represent avenues by which to identify factors potentially influencing behavioral domains associated with emotion-related disorders."
Source: http://www.sciencedaily.com/releases/2014/12/141219160606.htm
Now, a UCLA team has studied early developmental exposure to two different antidepressants, Prozac and Lexapro, in a mouse model that mimics human third trimester medication exposure. They found that, although these serotonin-selective reuptake inhibiting antidepressants (SSRIs) were thought to work the same way, they did not produce the same long-term changes in anxiety behavior in the adult mice.
The mice exposed to Lexapro had permanent changes in serotonin neurotransmission and were less anxious as adults than the mice exposed to Prozac, said study senior author Anne M. Andrews, professor of psychiatry and chemistry and biochemistry and the Richard Metzner Endowed Chair in Clinical Neuropharmacology at the Semel Institute for Neuroscience & Human Behavior and California NanoSystems Institute.
"This was quite surprising, since these medications belong to the same drug class and are believed to work by the same mechanism. The implications of these findings are that with additional investigation, it may be possible to identify specific antidepressants that are safer for pregnant women," Andrews said. "It's important to recognize that major depressive disorders and anxiety disorders are serious medical conditions that often require therapeutic intervention. Prescribing the safest medication for mother and child is paramount."
The results of the six-year study appear early online Dec. 19, 2014 in the peer-reviewed journal Neuropsychopharmacology.
SSRIs like Prozac and Lexapro act by blocking the actions of a protein called the serotonin transporter, which removes the neurotransmitter serotonin from the signaling space between neurons. Andrews and her team also studied mice that had been genetically engineered to have a reduction or absence of serotonin transporters in the brain. They were able to compare early antidepressant exposure to permanent reductions in serotonin transporter function.
Genetic reductions in serotonin transporters are thought to be a risk factor, particularly when combined with stressful life experiences, for developing anxiety and mood disorders. And in fact, the genetically engineered mice Andrews studied showed more anxiety as adults.
"It might be possible that when mothers are treated for depression or anxiety during pregnancy that certain SSRIs may promote resilience to developing these disorders in children later in life," Andrews said. "However, it will take much more research for us to understand whether this is true and whether certain SSRIs may be better at promoting these effects."
Going forward, Andrews and her team plan to investigate the effects of early exposure to antidepressants on the architectures of serotonin neurons. Based on the current findings, they suspect that early exposure to Lexapro may alter the way serotonin neurons innervate brain regions involved in mood and anxiety behavior. They also plan to investigate other SSRIs such as Paxil and Zoloft.
"Current antidepressant therapies are ineffective in treating anxiety and depression in large numbers of patients, and advances in predicting individual responses are hindered by difficulties associated with characterizing complex influences of genetic and environmental factors on serotonergic transmission in humans," the study states. "Highly controlled animal models, such as those studied here, represent avenues by which to identify factors potentially influencing behavioral domains associated with emotion-related disorders."
Source: http://www.sciencedaily.com/releases/2014/12/141219160606.htm
Wednesday 14 January 2015
Depression: New Medications On The Horizon
With the advent of monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants (TCAs) in the 1950s, depression
treatment was revolutionized. These medicines target the monoamine
system, including the neurotransmitters serotonin, norepinephrine and
dopamine.
For decades, the dominant hypothesis of depression has been that low levels of monoamines in the brain cause this debilitating disorder.
In the ‘80s, the selective serotonin reuptake inhibitor (SSRI) fluoxetine (brand name: Prozac) heralded a new era of safer drugs which also target the monoamine system. Since then, various SSRIs and serotonin-norepinephrine reuptake inhibitors (or SNRIs) have been developed as new antidepressants. While these drugs aren’t more effective than older antidepressants, they are less toxic.
But SSRIs and SNRIs don’t work for everyone, so MAOIs and TCAs still are prescribed.
Two out of three patients with depression do not fully recover on an antidepressant medication according to findings from STAR*D, the largest clinical trial study of treatments for major depressive disorder, funded by the National Institute of Mental Health. (One-third of patients do have a remission of their depression symptoms.)
These results “are important because previously it was unclear just how effective (or ineffective) antidepressant medications are in patients seeking treatment in real-world settings,” said James Murrough, M.D., board-certified psychiatrist and a research fellow at the Mount Sinai School of Medicine Mood and Anxiety Disorders Program.
As Murrough explained, depression treatment can be thought of in thirds: “for one third of patients, symptoms remit; another third don’t have as good of an outcome, experiencing residual symptoms and waxing and waning course or chronic course and are at risk for relapse whether they’re on or off medication; and then a third don’t get much benefit at all.”
He added that around “10 to 20 percent have persistent clinically significant symptoms that aren’t decreased by current treatment — these are the patients that we are the most worried about.”
So there’s a real need to find treatments that work for these patients. Since the 1950s and 1980s breakthroughs, researchers haven’t discovered drugs that target chemical systems in the brain other than the monoamine system.
“We haven’t been able to find any new systems, because we don’t understand the underlying biology of depression,” Murrough said.
But researchers are studying other mechanisms of depression and various drugs have recently been approved to treat depression. Below, you’ll learn about these drugs along with several chemical systems research is exploring.
Prime examples of me-too drugs are desvenlafaxine (Pristiq), an SNRI, and escitalopram (Lexapro), an SSRI, he said. Pristiq is simply Effexor’s main metabolite. Lexapro is essentially a close relative derivative of citalopram (Celexa). Interestingly, sales still skyrocketed when Lexapro came out.
As Murrough said, there is value in some me-too drugs. Generally, all drugs within the classes SSRIs and SNRIs are me-too drugs. But the side effect profiles for each drug have slight differences, which can help patients.
For instance, Prozac tends to be more activating, so a doctor may prescribe it for patients with low energy, Murrough said. In contrast, paroxetine (Paxil) makes people more tired, so it’s prescribed to patients who have trouble sleeping, he said.
The drug Oleptro was approved this year for depression. It doesn’t target new mechanisms, and it isn’t even a me-too drug, Murrough said. It’s a reformulation of trazodone, an atypical antidepressant that’s been used as a sleeping aid by psychiatrists and other doctors. Because it’s so sedating, its earlier form would just put patients to sleep. “It is unclear if the new formulation will offer any benefit for patients over the original,” Murrough said.
These recently approved medicines “characterize the state of drugs in psychiatry,” Murrough said, and speak to “what’s wrong with antidepressant drug development today.” Novel treatments just aren’t on the market.
Specifically, some research has found that adding atypical antipsychotic drugs, like aripiprazole (Abilify) and quetiapine (Seroquel), to an antidepressant can boost its effectiveness.
Atypical antipsychotics are used to treat schizophrenia and bipolar disorder. “Abilify has three strong studies that show how well it works in patients that have partially responded to antidepressants,” Marks said. According to Murrough, augmentation has become a common strategy in depression treatment.
Some research has implicated the dysfunction of the glutamate system in medical conditions, such as Huntington’s chorea and epilepsy, and psychological disorders, such as schizophrenia and anxiety disorders.
Recent research suggests that drugs targeting a specific type of glutamate receptor in the brain — called the NMDA receptor — may have antidepressant effects.
Studies have explored ketamine, an NMDA antagonist, in treating treatment-resistant depression and acute suicidal ideation. Ketamine has a long history in analgesia and anesthesiology.
Currently, when a person is at imminent risk for attempting suicide or has attempted suicide, they’re admitted to a psychiatric hospital and closely monitored. But, as Murrough explained, medically, there’s nothing doctors can do to help with suicidal ideation or intense depressed mood. Antidepressants typically four to six weeks to work.
Ketamine appears to have fast antidepressant effects — within hours or a day. Thus, it may help protect patients from suicidal thinking or acute dysphoria when they’re in the hospital. Unfortunately, its effects only last seven to 10 days.
This research is “highly experimental, and probably less than 100 patients in the country have participated in controlled depression studies of ketamine,” Murrough said. The patients in these studies typically have treatment-resistant depression: They haven’t responded to several antidepressants and have moderate to severe symptoms of depression.
They’re admitted to the hospital and receive ketamine intravenously from an anesthesiologist, while their vital signs are closely monitored.
Ketamine is a drug of abuse, known by such street names as “Special K.” It induces trance-like or hallucination states. It also produces mild to moderate cognitive side effects, like other anesthetics. People report feeling “out of it,” intoxicated and disconnected in general.
These side effects actually “introduce a potential bias to the study design” because participants know they’re getting the treatment (when saline is given in the placebo condition), Murrough said.
To eliminate this bias, Murrough and his team are conducting the first-ever study to compare ketamine to a different anesthetic — the benzodiazepine midazolam (Versed) — which has similar transient effects as ketamine, he said. The study is currently recruiting participants.
Murrough cautioned that ketamine isn’t meant to be a treatment administrated at your doctor’s office. In a recent article in the journal Nature Medicine, he said ketamine treatment may be “akin to electroconvulsive shock treatment.”
Studying ketamine may reveal mechanisms underlying depression and help to find drugs that can be prescribed as antidepressants to a wider patient population.
Pharmaceutical companies have started exploring other NMDA receptor antagonists for treatment-resistant depression. For instance, in July 2010, the pharmaceutical company Evotec Neurosciences began testing a compound in a Phase II study, which evaluates the safety and efficacy of a drug.
Source: http://psychcentral.com/lib/depression-new-medications-on-the-horizon/0005794
For decades, the dominant hypothesis of depression has been that low levels of monoamines in the brain cause this debilitating disorder.
In the ‘80s, the selective serotonin reuptake inhibitor (SSRI) fluoxetine (brand name: Prozac) heralded a new era of safer drugs which also target the monoamine system. Since then, various SSRIs and serotonin-norepinephrine reuptake inhibitors (or SNRIs) have been developed as new antidepressants. While these drugs aren’t more effective than older antidepressants, they are less toxic.
But SSRIs and SNRIs don’t work for everyone, so MAOIs and TCAs still are prescribed.
Two out of three patients with depression do not fully recover on an antidepressant medication according to findings from STAR*D, the largest clinical trial study of treatments for major depressive disorder, funded by the National Institute of Mental Health. (One-third of patients do have a remission of their depression symptoms.)
These results “are important because previously it was unclear just how effective (or ineffective) antidepressant medications are in patients seeking treatment in real-world settings,” said James Murrough, M.D., board-certified psychiatrist and a research fellow at the Mount Sinai School of Medicine Mood and Anxiety Disorders Program.
As Murrough explained, depression treatment can be thought of in thirds: “for one third of patients, symptoms remit; another third don’t have as good of an outcome, experiencing residual symptoms and waxing and waning course or chronic course and are at risk for relapse whether they’re on or off medication; and then a third don’t get much benefit at all.”
He added that around “10 to 20 percent have persistent clinically significant symptoms that aren’t decreased by current treatment — these are the patients that we are the most worried about.”
So there’s a real need to find treatments that work for these patients. Since the 1950s and 1980s breakthroughs, researchers haven’t discovered drugs that target chemical systems in the brain other than the monoamine system.
“We haven’t been able to find any new systems, because we don’t understand the underlying biology of depression,” Murrough said.
But researchers are studying other mechanisms of depression and various drugs have recently been approved to treat depression. Below, you’ll learn about these drugs along with several chemical systems research is exploring.
Recently Approved Drugs for Depression
Recently approved drugs for depression are generally “me-too” drugs. A “me-too drug is a drug whose mechanism of action (what it does at the molecular level in the brain) is not meaningfully different than its predecessor,” Dr. Murrough said.Prime examples of me-too drugs are desvenlafaxine (Pristiq), an SNRI, and escitalopram (Lexapro), an SSRI, he said. Pristiq is simply Effexor’s main metabolite. Lexapro is essentially a close relative derivative of citalopram (Celexa). Interestingly, sales still skyrocketed when Lexapro came out.
As Murrough said, there is value in some me-too drugs. Generally, all drugs within the classes SSRIs and SNRIs are me-too drugs. But the side effect profiles for each drug have slight differences, which can help patients.
For instance, Prozac tends to be more activating, so a doctor may prescribe it for patients with low energy, Murrough said. In contrast, paroxetine (Paxil) makes people more tired, so it’s prescribed to patients who have trouble sleeping, he said.
The drug Oleptro was approved this year for depression. It doesn’t target new mechanisms, and it isn’t even a me-too drug, Murrough said. It’s a reformulation of trazodone, an atypical antidepressant that’s been used as a sleeping aid by psychiatrists and other doctors. Because it’s so sedating, its earlier form would just put patients to sleep. “It is unclear if the new formulation will offer any benefit for patients over the original,” Murrough said.
These recently approved medicines “characterize the state of drugs in psychiatry,” Murrough said, and speak to “what’s wrong with antidepressant drug development today.” Novel treatments just aren’t on the market.
Augmentation of Depression Drugs
Recently, the biggest development in depression treatment has been the use of augmenting agents, said David Marks, M.D., assistant professor at the Department of Psychiatry & Behavioral Sciences at the Duke University Medical Center.Specifically, some research has found that adding atypical antipsychotic drugs, like aripiprazole (Abilify) and quetiapine (Seroquel), to an antidepressant can boost its effectiveness.
Atypical antipsychotics are used to treat schizophrenia and bipolar disorder. “Abilify has three strong studies that show how well it works in patients that have partially responded to antidepressants,” Marks said. According to Murrough, augmentation has become a common strategy in depression treatment.
The Glutamate System and Depression
Researchers have looked at the role of the glutamate system in depression. Glutamate is abundant in the brain and is one of the most common neurotransmitters. It’s involved in memory, learning and cognition.Some research has implicated the dysfunction of the glutamate system in medical conditions, such as Huntington’s chorea and epilepsy, and psychological disorders, such as schizophrenia and anxiety disorders.
Recent research suggests that drugs targeting a specific type of glutamate receptor in the brain — called the NMDA receptor — may have antidepressant effects.
Studies have explored ketamine, an NMDA antagonist, in treating treatment-resistant depression and acute suicidal ideation. Ketamine has a long history in analgesia and anesthesiology.
Currently, when a person is at imminent risk for attempting suicide or has attempted suicide, they’re admitted to a psychiatric hospital and closely monitored. But, as Murrough explained, medically, there’s nothing doctors can do to help with suicidal ideation or intense depressed mood. Antidepressants typically four to six weeks to work.
Ketamine appears to have fast antidepressant effects — within hours or a day. Thus, it may help protect patients from suicidal thinking or acute dysphoria when they’re in the hospital. Unfortunately, its effects only last seven to 10 days.
This research is “highly experimental, and probably less than 100 patients in the country have participated in controlled depression studies of ketamine,” Murrough said. The patients in these studies typically have treatment-resistant depression: They haven’t responded to several antidepressants and have moderate to severe symptoms of depression.
They’re admitted to the hospital and receive ketamine intravenously from an anesthesiologist, while their vital signs are closely monitored.
Ketamine is a drug of abuse, known by such street names as “Special K.” It induces trance-like or hallucination states. It also produces mild to moderate cognitive side effects, like other anesthetics. People report feeling “out of it,” intoxicated and disconnected in general.
These side effects actually “introduce a potential bias to the study design” because participants know they’re getting the treatment (when saline is given in the placebo condition), Murrough said.
To eliminate this bias, Murrough and his team are conducting the first-ever study to compare ketamine to a different anesthetic — the benzodiazepine midazolam (Versed) — which has similar transient effects as ketamine, he said. The study is currently recruiting participants.
Murrough cautioned that ketamine isn’t meant to be a treatment administrated at your doctor’s office. In a recent article in the journal Nature Medicine, he said ketamine treatment may be “akin to electroconvulsive shock treatment.”
Studying ketamine may reveal mechanisms underlying depression and help to find drugs that can be prescribed as antidepressants to a wider patient population.
Pharmaceutical companies have started exploring other NMDA receptor antagonists for treatment-resistant depression. For instance, in July 2010, the pharmaceutical company Evotec Neurosciences began testing a compound in a Phase II study, which evaluates the safety and efficacy of a drug.
Source: http://psychcentral.com/lib/depression-new-medications-on-the-horizon/0005794
Sunday 11 January 2015
How early trauma influences behavior
Traumatic
events leave their mark. People exposed to a traumatic experience early
in life are more likely to be affected by illnesses such as borderline
personality disorder or depression. However such experience can also
have positive effects in certain circumstances. Thus, moderate stress in
childhood may help a person develop strategies to better cope with
stress in adulthood.
Related Articles
Further, it has long been recognised by psychologists and
psychiatrists that the negative effects of trauma experienced by parents
can be seen in their children, but the molecular mechanisms underlying
such transmission are only beginning to be identified. A research team
led by Isabelle Mansuy, Professor of Neuroepigenetics at the University
of Zurich and ETH Zurich, has for the first time tested in mice the
degree to which the beneficial effects of stress can be passed to
following generations.
Flexible and goal-oriented in critical situations
The researchers subjected newborn male mice to traumatic stress by removing them from their mother at irregular and frequent intervals and by severely stressing the mothers in addition. They then used tests to analyse the behaviour of these pups when adult and their offspring in comparison to control mice not subjected to stress. They observed that the offspring of the stressed mice handled complex tasks more efficiently than the control group.
For example, one test revealed that the offspring of stressed fathers adapted better to changing rules on a task to earn a drink reward when they were thirsty. They reacted more flexibly. In another test, the mice had to poke their nose into a hole when prompted by a light signal but only after a pre-determined delay of 6, 12 or 18 seconds to get water. The stressed mice and their offspring performed the task better than the control mice at the long time interval of 18 seconds, which was especially challenging. This result was interpreted by the researchers as evidence for improved goal-oriented behaviour in difficult situations. Since the fathers were kept apart from their offspring and the mothers, the young animals cannot have learned this behaviour. Rather, they must have inherited it via molecular pathways in germ cells.
To determine how this behaviour is expressed and transmitted to the next generation, the researchers examined the activity of a gene, a mineralocorticoid receptor gene previously implicated in flexible behaviour. Mansuy's team discovered that 'epigenetic' marks, which determine how much a gene is expressed, were altered on this gene, both in the brain and sperm of the stressed mice when adult. The altered marks were passed on to the next generation probably through the sperm, and may partly be responsible for the altered behaviour. The mineralocorticoid receptor in question binds signal messengers such as the stress hormone cortisone which initiates a signalling cascade in neurons.
Help in overcoming problems
"Our results show that environmental factors change behaviour and that these changes can be passed on to the next generation," explains Mansuy. This finding -- that not only a parent's susceptibility to psychological disorders can be passed on to its offspring, but also its improved goal-oriented behaviour in difficult situations -- might prove to be of value to the clinic. Doctors could help post-trauma patients suffering from depression to build on these sorts of strength. The implication of the mineralocorticoid receptor gene could also be a good starting point for potential future medical therapies.
"We are not in any way suggesting that early-childhood trauma is somehow positive," says Mansuy. But she adds that her study on mice demonstrates how extreme stress can affect the brain and behaviour across generations -- negatively, but also in some ways positively.
Source: http://www.sciencedaily.com/releases/2014/12/141201125158.htm
Flexible and goal-oriented in critical situations
The researchers subjected newborn male mice to traumatic stress by removing them from their mother at irregular and frequent intervals and by severely stressing the mothers in addition. They then used tests to analyse the behaviour of these pups when adult and their offspring in comparison to control mice not subjected to stress. They observed that the offspring of the stressed mice handled complex tasks more efficiently than the control group.
For example, one test revealed that the offspring of stressed fathers adapted better to changing rules on a task to earn a drink reward when they were thirsty. They reacted more flexibly. In another test, the mice had to poke their nose into a hole when prompted by a light signal but only after a pre-determined delay of 6, 12 or 18 seconds to get water. The stressed mice and their offspring performed the task better than the control mice at the long time interval of 18 seconds, which was especially challenging. This result was interpreted by the researchers as evidence for improved goal-oriented behaviour in difficult situations. Since the fathers were kept apart from their offspring and the mothers, the young animals cannot have learned this behaviour. Rather, they must have inherited it via molecular pathways in germ cells.
To determine how this behaviour is expressed and transmitted to the next generation, the researchers examined the activity of a gene, a mineralocorticoid receptor gene previously implicated in flexible behaviour. Mansuy's team discovered that 'epigenetic' marks, which determine how much a gene is expressed, were altered on this gene, both in the brain and sperm of the stressed mice when adult. The altered marks were passed on to the next generation probably through the sperm, and may partly be responsible for the altered behaviour. The mineralocorticoid receptor in question binds signal messengers such as the stress hormone cortisone which initiates a signalling cascade in neurons.
Help in overcoming problems
"Our results show that environmental factors change behaviour and that these changes can be passed on to the next generation," explains Mansuy. This finding -- that not only a parent's susceptibility to psychological disorders can be passed on to its offspring, but also its improved goal-oriented behaviour in difficult situations -- might prove to be of value to the clinic. Doctors could help post-trauma patients suffering from depression to build on these sorts of strength. The implication of the mineralocorticoid receptor gene could also be a good starting point for potential future medical therapies.
"We are not in any way suggesting that early-childhood trauma is somehow positive," says Mansuy. But she adds that her study on mice demonstrates how extreme stress can affect the brain and behaviour across generations -- negatively, but also in some ways positively.
Source: http://www.sciencedaily.com/releases/2014/12/141201125158.htm
Sunday 4 January 2015
Early exposure to antidepressants affects adult anxiety, serotonin transmission
About 15
percent of women in the United States suffer from anxiety disorders and
depression during their pregnancies, and many are prescribed
antidepressants. However little is known about how early exposure to
these medications might affect their offspring as they mature into
adults.
Related Articles
The answer to that question is vital, as 5 percent of all babies born
in the U.S. -- more than 200,000 a year -- are exposed to
antidepressants during gestation via transmission from their mothers.
Now, a UCLA team has studied early developmental exposure to two different antidepressants, Prozac and Lexapro, in a mouse model that mimics human third trimester medication exposure. They found that, although these serotonin-selective reuptake inhibiting antidepressants (SSRIs) were thought to work the same way, they did not produce the same long-term changes in anxiety behavior in the adult mice.
The mice exposed to Lexapro had permanent changes in serotonin neurotransmission and were less anxious as adults than the mice exposed to Prozac, said study senior author Anne M. Andrews, professor of psychiatry and chemistry and biochemistry and the Richard Metzner Endowed Chair in Clinical Neuropharmacology at the Semel Institute for Neuroscience & Human Behavior and California NanoSystems Institute.
"This was quite surprising, since these medications belong to the same drug class and are believed to work by the same mechanism. The implications of these findings are that with additional investigation, it may be possible to identify specific antidepressants that are safer for pregnant women," Andrews said. "It's important to recognize that major depressive disorders and anxiety disorders are serious medical conditions that often require therapeutic intervention. Prescribing the safest medication for mother and child is paramount."
The results of the six-year study appear early online Dec. 19, 2014 in the peer-reviewed journal Neuropsychopharmacology.
SSRIs like Prozac and Lexapro act by blocking the actions of a protein called the serotonin transporter, which removes the neurotransmitter serotonin from the signaling space between neurons. Andrews and her team also studied mice that had been genetically engineered to have a reduction or absence of serotonin transporters in the brain. They were able to compare early antidepressant exposure to permanent reductions in serotonin transporter function.
Genetic reductions in serotonin transporters are thought to be a risk factor, particularly when combined with stressful life experiences, for developing anxiety and mood disorders. And in fact, the genetically engineered mice Andrews studied showed more anxiety as adults.
"It might be possible that when mothers are treated for depression or anxiety during pregnancy that certain SSRIs may promote resilience to developing these disorders in children later in life," Andrews said. "However, it will take much more research for us to understand whether this is true and whether certain SSRIs may be better at promoting these effects."
Going forward, Andrews and her team plan to investigate the effects of early exposure to antidepressants on the architectures of serotonin neurons. Based on the current findings, they suspect that early exposure to Lexapro may alter the way serotonin neurons innervate brain regions involved in mood and anxiety behavior. They also plan to investigate other SSRIs such as Paxil and Zoloft.
"Current antidepressant therapies are ineffective in treating anxiety and depression in large numbers of patients, and advances in predicting individual responses are hindered by difficulties associated with characterizing complex influences of genetic and environmental factors on serotonergic transmission in humans," the study states. "Highly controlled animal models, such as those studied here, represent avenues by which to identify factors potentially influencing behavioral domains associated with emotion-related disorders."
Source: http://www.sciencedaily.com/releases/2014/12/141219160606.htm
Now, a UCLA team has studied early developmental exposure to two different antidepressants, Prozac and Lexapro, in a mouse model that mimics human third trimester medication exposure. They found that, although these serotonin-selective reuptake inhibiting antidepressants (SSRIs) were thought to work the same way, they did not produce the same long-term changes in anxiety behavior in the adult mice.
The mice exposed to Lexapro had permanent changes in serotonin neurotransmission and were less anxious as adults than the mice exposed to Prozac, said study senior author Anne M. Andrews, professor of psychiatry and chemistry and biochemistry and the Richard Metzner Endowed Chair in Clinical Neuropharmacology at the Semel Institute for Neuroscience & Human Behavior and California NanoSystems Institute.
"This was quite surprising, since these medications belong to the same drug class and are believed to work by the same mechanism. The implications of these findings are that with additional investigation, it may be possible to identify specific antidepressants that are safer for pregnant women," Andrews said. "It's important to recognize that major depressive disorders and anxiety disorders are serious medical conditions that often require therapeutic intervention. Prescribing the safest medication for mother and child is paramount."
The results of the six-year study appear early online Dec. 19, 2014 in the peer-reviewed journal Neuropsychopharmacology.
SSRIs like Prozac and Lexapro act by blocking the actions of a protein called the serotonin transporter, which removes the neurotransmitter serotonin from the signaling space between neurons. Andrews and her team also studied mice that had been genetically engineered to have a reduction or absence of serotonin transporters in the brain. They were able to compare early antidepressant exposure to permanent reductions in serotonin transporter function.
Genetic reductions in serotonin transporters are thought to be a risk factor, particularly when combined with stressful life experiences, for developing anxiety and mood disorders. And in fact, the genetically engineered mice Andrews studied showed more anxiety as adults.
"It might be possible that when mothers are treated for depression or anxiety during pregnancy that certain SSRIs may promote resilience to developing these disorders in children later in life," Andrews said. "However, it will take much more research for us to understand whether this is true and whether certain SSRIs may be better at promoting these effects."
Going forward, Andrews and her team plan to investigate the effects of early exposure to antidepressants on the architectures of serotonin neurons. Based on the current findings, they suspect that early exposure to Lexapro may alter the way serotonin neurons innervate brain regions involved in mood and anxiety behavior. They also plan to investigate other SSRIs such as Paxil and Zoloft.
"Current antidepressant therapies are ineffective in treating anxiety and depression in large numbers of patients, and advances in predicting individual responses are hindered by difficulties associated with characterizing complex influences of genetic and environmental factors on serotonergic transmission in humans," the study states. "Highly controlled animal models, such as those studied here, represent avenues by which to identify factors potentially influencing behavioral domains associated with emotion-related disorders."
Source: http://www.sciencedaily.com/releases/2014/12/141219160606.htm
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