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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.

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

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.

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.

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

Sunday, 4 January 2015

Early exposure to antidepressants affects adult anxiety, serotonin transmission

Monday, 15 December 2014

Move over Prozac: New drug offers hope for depression

The brain chemistry that underlies depression is incompletely understood, but research suggests that aberrant signaling by a chemical called Brain-Derived Neurotrophic Factor through its receptor TrkB, may contribute to anxiety and depression. Here, researchers describe a screen for stable small molecules that could specifically inhibit TrkB action. They identified one they dubbed ANA-12, which had potent behavioral effects when administered to mice that suggest it will have antidepressant and anti-anxiety activity in humans.

An estimated 19 million Americans suffer from depression, and though the symptoms might be recognizable, the brain chemistry that underlies them is incompletely understood. Research suggests that aberrant signaling by a chemical called Brain-Derived Neurotrophic Factor (BDNF) through its receptor TrkB, may contribute to anxiety and depression, and inhibiting this pathway in mice can reduce anxiety and depression-related behaviors. However, translating these findings to clinical studies will require the development of small molecule inhibitors of the BDNF/TrkB pathway that could be used pharmacologically.
In this paper, researchers led by Maxime Cazorla, of Columbia University in New York, and Didier Rognan, of the Université de Strasbourg in France, describe a screen for stable small molecules that could specifically inhibit TrkB action. They identified one they dubbed ANA-12, which had potent behavioral effects when administered to mice that suggest it will have antidepressant and anti-anxiety activity in humans. The researchers are hopeful that this new compound could be used to develop a new class of psychiatric drugs.

Source: http://www.sciencedaily.com/releases/2011/04/110418122314.htm

Monday, 8 December 2014

Social media 'glorifies and normalises suicidal behaviours'

A review into social media and its role in children's suicides 'glorifies and normalises suicidal behaviours' a recent study has shown.

The Commission for Children and Young People in Queensland, concerned at suicide rates amongst Australian youngsters, released some of the 140 submissions they have made on Sunday night, exploring the way social media plays a part.

One child a week commits suicide, with another 50-60 admitted to hospital for self-harming - and boys are twice as likely to end their own lives than girls, writes The Australian.

More and more Australian youngsters are exposed to suicide via the internet and socia media, sparking some copycat cases says a new submission by the Commission for Children and Young People in Queensland

The submission report, spear-headed by Megan Mitchell, the National Children's Commissioner says that several have killed themselves after looking up instructions on the internet.

But even more worrying, some of the 140 submissions that were released on Sunday show that youngsters can be drawn into the social leverage and immortalisation it gives them.

There is proof that one teenager chose to end her life after seeing the outpouring of grief another youngster had received online after killing herself, with one user's condolence message attracting 190 likes.

The submission says: 'It can be interpreted that there is clearly a social status in not only knowing a suicide occurred but even more so in contributing and participating in the shared grief. There is a social reward for this behaviour.'

Because the internet and SMS has replaced the traditional way in which children and teenagers communicate, access to suicide is instantaneous and un-policed.

'The fear of missing out and the status of participation outweigh any negative stigma in being associated with a suicide death,' says the submission

More than 2000 young people have signed up to websites set up in memory of recent youngsters who committed suicide in Queensland, even though the majority didn't even know the troubled teenagers.

That figure is five times the number of people who would usually be exposed to suicide in the community.

'The instant outpouring of grief and love means that 'young people are actively engaging in activities that expose them to youth suicide, such as seeking out suicide tribute pages online,' says the submission.

'The fear of missing out and the status of participation outweigh any negative stigma in being associated with a suicide death.'

A quick Google search flags up pro-suicide websites and the report clearly states, 'There are pro-suicide forums with content that glorifies and normalises suicidal behaviours'.

'The fear of missing out and the status of participation outweigh any negative stigma in being associated with a suicide death,' says the submission

According to the Australian Institute of Health and Welfare there were 18,277 hospitalisations for young people intentional self-harming between the ages of 3 and 17 in 2007 and 2013.

And 333 youngsters between the ages of four and 17 died from their injuries which were cause by self-harming between 2007 - 2012.

Alarmingly the report also found that of the 187 Queensland children and youngsters who have committed suicide, one third knew someone who had done it before them.

The National Children's Commissioner is demanding the government to do more on a national level to raise awareness and train those who are in a position to spot the risks and warning signs before it's too late.

If you are suicidal, self-harming, depressed or need someone to talk to contact Beyond Blue or Kids Helpline or dial them on 1 800 55 1800.

Source: http://www.dailymail.co.uk/news/article-2864313/Social-media-glorifies-normalises-suicidal-behaviours-young-people-teenagers-recent-study-shows.html#ixzz3LJ0JTQpk

Tuesday, 2 December 2014

What is Depression?

Depression is a serious condition that should not be taken lightly. Depression is an illness that can affect the body as well as your emotional state. It is not just feeling down or unhappiness when something does not go your way, but usually a more sever problem. Real depression takes over the mind and the body. Clinical Depression: Sever cases of Depression are referred to as clinical depression. It has an effect on your routine activities and the way feel physically the way you think and the way you behave. You may be unable to do everyday activities, and in sever cases you may have suicidal feelings. Depression is not just a mood you can “get over”. It is an illness that often requires medication and treatment. What are the Symptoms of Depression? Depression can occur in anyone and is not only rooted in genetic predisposition. There are many reasons why we get depressed. Sometimes its temporary, which would not be considered clinical depression which we are discussing here. But other times, in the cases of clinical depression, it can lest for years and sometimes a lifetime. It is important you realize the symptoms of depression so you can eventually treat it. Symptoms of Depression include:

Feeling unhappy and sad most of the time
Getting frustrated over small things
Lack of desire for sexual intimacy
Difficulty sleeping or too much sleep
Difficulty eating or overeating
Trouble keeping your thoughts clear
Feeling like you are in slow motion
Decreased concentration
Self blame, feeling useless and worthless
Memory failure
Crying for no reason

What Causes Depression? Because depression is a real illness, it is just that you had a bad day. That may cause temporary feelings of sadness, but it takes more to cause true depression. Often times, people suffer from depression because of major life changing events, life the death of a loved one, a divorce, or bankruptcy. Some people have gone through traumatic life changing physical events. For example those who have been abused, raped or assaulted find that their life seems to be spinning out of control. Is Depression Hereditary? There have been many studies that show that people suffering from depression actually have different wave patterns in their brains. They also may have a hormone imbalance or chemical imbalance due to life changes, physical or medical problems. Sometimes depression can be genetic and passed onto other family members through someones genetic makeup. Scientists are still researching the connection between a persons genes and clinical depression. Prevention and Treatment: While we do not usually have the ability to prevent traumatic events from happening, but we can try to build up our support systems. Having people to turn to when life changing events happen can be the best medication. However, there are times when we need to seek professional help. Seeking Professional Help: Counseling can help prevent depression from getting worse and can also give you the support you need to get through the difficult times. And other times you may need the help of a prescription medication. It is important to see your doctor if you are feeling depressed. They can evaluate your symptoms and guide you to the best treatment.
Source: http://www.consumerhealthreview.org/brain-health/depression/

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Monday, 19 January 2015

Early exposure to antidepressants affects adult anxiety, serotonin transmission

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Wednesday, 14 January 2015

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Sunday, 11 January 2015

How early trauma influences behavior

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Early exposure to antidepressants affects adult anxiety, serotonin transmission

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Monday, 15 December 2014

Move over Prozac: New drug offers hope for depression

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Monday, 8 December 2014

Social media 'glorifies and normalises suicidal behaviours'

Tuesday, 2 December 2014

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