Small Number of Autism Cases Linked to Depression Medications

Autism Spectrum Disorders News | 19 May 2013

In utero exposure to depression medications may increase the risk of autism spectrum disorders in less than 1 percent of cases, researchers in Sweden say.

First author Dheeraj Rai, a clinical lecturer at the Department of Public Health Sciences at Karolinska Institutet in Stockholm, and colleagues at the University of Bristol; Avon and Wiltshire Partnership Mental Health NHS Trust in Bristol, England; and Drexel University School of Public Health on Philadelphia said the study involved 4,429 cases of autism spectrum disorder -- 1,828 with and 2,601 without intellectual disability and 43,277 age and sex matched controls.

The study involved 1,679 cases of autism spectrum disorder and 16,845 controls with data on maternal anti-depressant use.

The study, published in the British Medical Journal, said parental depression and other characteristics were recorded in administrative registers before the birth of the child. Maternal anti-depressant use, recorded at the first antenatal interview, was available for children born from 1995 onwards.

A history of maternal -- but not paternal -- depression was associated with an increased risk of autism spectrum disorders in offspring, the study said. In the subsample with available data on drugs, this association was confined to women reporting anti-depressant use during pregnancy irrespective of whether selective serotonin reuptake inhibitors or non-selective monoamine reuptake inhibitors were reported, the study said.

"Whether this association is causal or reflects the risk of autism with severe depression during pregnancy requires further research," the study authors wrote in the study. "However, assuming causality, anti-depressant use during pregnancy is unlikely to have contributed significantly towards the dramatic increase in observed prevalence of autism spectrum disorders as it explained less than 1 percent of cases."

Low Intelligence and Schizophrenia

Schizophrenia News | 18 May 2013

The relationship between the heritable risk for schizophrenia and low intelligence (IQ) has not been clear.

Schizophrenia is commonly associated with cognitive impairments that may cause functional disability. There are clues that reduced IQ may be linked to the risk for developing schizophrenia. For example, reduced cognitive ability may precede the onset of schizophrenia symptoms. Also, these deficits may be present in healthy relatives of people diagnosed with schizophrenia.

In a remarkable new study published in Biological Psychiatry, Dr. Andrew McIntosh and his colleagues at the University of Edinburgh provide new evidence that the genetic risk for schizophrenia is associated with lower IQ among people who do not develop this disorder.

The authors analyzed data from 937 individuals in Scotland who first completed IQ testing in 1947, at age 11. Around age 70, they were retested and their DNA was analyzed to estimate their genetic risk for schizophrenia.

The researchers found that individuals with a higher genetic risk for schizophrenia had a lower IQ at age 70 but not at age 11. Having more schizophrenia risk-related gene variants was also associated with a greater decline in lifelong cognitive ability.

“If nature has loaded a person’s genes towards schizophrenia, then there is a slight but detectable worsening in cognitive function between childhood and old age. With further research into how these genes affect the brain, it could become possible to understand how genes linked to schizophrenia affect people’s cognitive function,” said McIntosh.

These findings suggest that common genetic variants may underlie both cognitive aging and risk of schizophrenia.

“While this study does not show that these common gene variants produce schizophrenia per se, it elegantly suggests that these variants may contribute to declines in intelligence, a clinical feature associated with schizophrenia,” commented Dr. John Krystal, Editor ofBiological Psychiatry. “However, we have yet to understand the development of cognitive impairments that produce disability in young adulthood, the period when schizophrenia develops for many affected people.”

Clearly, more research is necessary, but this new study adds to the growing and substantial effort to understand how the gene variants that contribute to the development of schizophrenia give rise to the cognitive disability commonly associated with it.

Easier to be Happy When Listening to Upbeat Music

Depression News | 17 May 2013

The song, “Get Happy,” famously performed by Judy Garland, has encouraged people to improve their mood for decades. Recent research at the University of Missouri discovered that an individual can indeed successfully try to be happier, especially when cheery music aids the process. This research points to ways that people can actively improve their moods and corroborates earlier MU research.

“Our work provides support for what many people already do – listen to music to improve their moods,” said lead author Yuna Ferguson, who performed the study while she was an MU doctoral student in psychological science. “Although pursuing personal happiness may be thought of as a self-centered venture, research suggests that happiness relates to a higher probability of socially beneficial behavior, better physical health, higher income and greater relationship satisfaction.”

In two studies by Ferguson, participants successfully improved their moods in the short term and boosted their overall happiness over a two week period. During the first study, participants improved their mood after being instructed to attempt to do so, but only if they listened to the upbeat music of Copland, as opposed to the more somber Stravinsky. Other participants, who simply listened to the music without attempting to change their mood, also didn’t report a change in happiness. In the second study, participants reported higher levels of happiness after two weeks of lab sessions in which they listened to positive music while trying to feel happier, compared to control participants who only listened to music.

However, Ferguson noted that for people to put her research into practice, they must be wary of too much introspection into their mood or constantly asking, “Am I happy yet?”

“Rather than focusing on how much happiness they’ve gained and engaging in that kind of mental calculation, people could focus more on enjoying their experience of the journey towards happiness and not get hung up on the destination,” said Ferguson.

Ferguson’s work corroborated earlier findings by Ferguson’s doctoral advisor and co-author of the current study, Kennon Sheldon, professor of psychological science in MU’s College of Arts and Science.

“The Hedonic Adaptation Prevention model, developed in my earlier research, says that we can stay in the upper half of our ‘set range’ of potential happiness as long as we keep having positive experiences, and avoid wanting too much more than we have,” said Sheldon. “Yuna’s research suggests that we can intentionally seek to make mental changes leading to new positive experiences of life. The fact that we’re aware we’re doing this, has no detrimental effect.”

Ferguson is now assistant professor of psychology at Pennsylvania State University Shenango. The study, “Trying to Be Happier Really Can Work: Two Experimental Studies,” was published in The Journal of Positive Psychology.

The Biology Behind Binge Eating

Eating Disorders News | 17 May 2013

Female rats are much more likely to binge eat than male rats, according to new research that provides some of the strongest evidence yet that biology plays a role in eating disorders.

The study, by Michigan State University scientists, is the first to establish sex differences in rates of binge eating in animals and has implications for humans. Binge eating is one of the core symptoms of most eating disorders, including bulimia nervosa and the binge/purge subtype of anorexia nervosa, and females are four to 10 times more likely than males to have an eating disorder.

“Most theories of why eating disorders are so much more prevalent in females than males focus on the increased cultural and psychological pressure that girls and women face,” said Kelly Klump, lead author and professor of psychology. “But this study suggests that biological factors likely contribute as well, since female rats do not experience the psychosocial pressures that humans do, such as pressures to be thin.”

Klump and colleagues ran a feeding experiment with 30 female and 30 male rats over a two-week period, replacing the rodents’ food pellets periodically with vanilla frosting. They found that the rate of binge eating “proneness” (i.e., the tendency to consume the highest amount of frosting across all feeding tests) was up to six times higher in female as compared to male rats.

The tendency to binge eat may be related to the brain’s natural reward system, or the extent to which someone likes and seeks reward, Klump said. The MSU researchers currently are testing the rats to see if female brains are more sensitive and/or responsive to rewarding stimuli (e.g., high-fat, high-sugar food) and the chemicals that trigger reward behavior.

The answers could ultimately help improve therapy – both counseling and medications – for those with eating disorders.

“This research suggests there is probably a biological difference between males and females that we need to explore to understand risk factors and mechanisms,” Klump said.

The study is published online in the International Journal of Eating Disorders. Klump’s co-authors are Cheryl Sisk, psychology professor, and graduate students Sarah Racine and Britny Hildebrandt.

Sensitivity to Stress Among the Offspring of Parents With Bipolar Disorder

Bipolar Disorder News | 16 May 2013

It is well known that the hypothalamic–pituitary–adrenal (HPA) axis is compromised in major depression and bipolar disorder. There is increasing evidence that subtle HPA abnormalities, such as elevated cortisol levels, precede the development of an affective disorder. Interpersonal stress is also associated with the development of affective disorders. This study sought to determine whether interpersonal chronic and episodic stress moderated the relationship between cortisol levels in the natural environment and risk status, defined as having a parent with bipolar disorder.

"Previous research has shown that children of parents with bipolar disorder are four times as likely to develop mood disorders as those from parents without the condition," said the senior author Dr. Mark Ellenbogen. "The goal of our study was to determine how this is happening."

They already knew that high levels of the stress hormone cortisol often occur in people who later develop bipolar disorder - and that high stress levels can contribute to developing bipolar disorder. What they found out in this study is that people with a bipolar parent react to both low-level and high-level stress by producing more cortisol than those with the same stress level but no bipolar parent.

These results, said Dr. Ellenbogen, might lead to finding ways to prevent the increased sensitivity from developing.

Effects of Individual Experiences on the Brain

Other News | 16 May 2013

The adult brain continues to grow with the challenges that it faces; its changes are linked to the development of personality and behavior. But what is the link between individual experience and brain structure? Why do identical twins not resemble each other perfectly even when they grew up together? To shed light on these questions, the scientists observed forty genetically identical mice that were kept in an enclosure offering a large variety of activity and exploration options.

“The animals were not only genetically identical, they were also living in the same environment,” explains principal investigator Gerd Kempermann, Professor for Genomics of Regeneration, CRTD, and Site Speaker of the DZNE in Dresden. “However, this environment was so rich that each mouse gathered its own individual experiences in it. Over time, the animals therefore increasingly differed in their realm of experience and behavior.”

New neurons for individualized brains

Each of the mice was equipped with a special micro-chip emitting electromagnetic signals. This allowed the scientists to construct the mice’s movement profiles and to quantify their exploratory behavior. The result: Despite a common environment and identical genes the mice showed highly individualized behavioral patterns. They reacted to their environment differently. In the course of the three-month experiment these differences increased in size.

“Though the animals shared the same life space, they increasingly differed in their activity levels. These differences were associated with differences in the generation of new neurons in the hippocampus, a region of the brain that supports learning and memory,” says Kempermann. “Animals that explored the environment to a greater degree also grew more new neurons than animals that were more passive.”

Adult neurogenesis, that is, the generation of new neurons in the hippocampus, allows the brain to react to new information flexibly. With this study, the authors show for the first time that personal experiences and ensuing behavior contribute to the “individualization of the brain.” The individualization they observed cannot be reduced to differences in environment or genetic makeup.

“Adult neurogenesis also occurs in the hippocampus of humans,” says Kempermann. “Hence we assume that we have tracked down a neurobiological foundation for individuality that also applies to humans.”

Impulses for discussion across disciplines

“The finding that behavior and experience contribute to differences between individuals has implications for debates in psychology, education science, biology, and medicine,” states Prof. Ulman Lindenberger, Director of the Center for Lifespan Psychology at the Max Planck Institute for Human Development (MPIB) in Berlin. “Our findings show that development itself contributes to differences in adult behavior. This is what many have assumed, but now there is direct neurobiological evidence in support of this claim. Our results suggest that experience influences the aging of the human mind.”

In the study, a control group of animals housed in a relatively unattractive enclosure was also examined; on average, neurogenesis in these animals was lower than in the experimental mice. “When viewed from educational and psychological perspectives, the results of our experiment suggest that an enriched environment fosters the development of individuality,” comments Lindenberger.

Emotional Strategy May Influence Anxiety

Anxiety News | 15 May 2013

When trouble approaches, what do you do? Run for the hills? Hide? Pretend it isn’t there? Or do you focus on the promise of rain in those looming dark clouds?

New research suggests that the way you regulate your emotions, in bad times and in good, can influence whether – or how much – you suffer from anxiety.

In a series of questionnaires, researchers asked 179 healthy men and women how they managed their emotions and how anxious they felt in various situations. The team analyzed the results to see if different emotional strategies were associated with more or less anxiety.

The study revealed that those who engage in an emotional regulation strategy called reappraisal tended to also have less social anxiety and less anxiety in general than those who avoid expressing their feelings. Reappraisal involves looking at a problem in a new way, said University of Illinois graduate student Nicole Llewellyn, who led the research with psychology professor Florin Dolcos, an affiliate of the Beckman Institute at Illinois.

“When something happens, you think about it in a more positive light, a glass half full instead of half empty,” Llewellyn said. “You sort of reframe and reappraise what’s happened and think what are the positives about this? What are the ways I can look at this and think of it as a stimulating challenge rather than a problem?”

Study participants who regularly used this approach reported less severe anxiety than those who tended to suppress their emotions.

Anxiety disorders are a major public health problem in the U.S. According to the National Institute of Mental Health, roughly 18 percent of the U.S. adult population is afflicted with general or social anxiety that is so intense that it warrants a diagnosis.

“The World Health Organization predicts that by 2020, anxiety and depression – which tend to co-occur – will be among the most prevalent causes of disability worldwide, secondary only to cardiovascular disease,” Dolcos said. “So it’s associated with big costs.”

Not all anxiety is bad, however, he said. Low-level anxiety may help you maintain the kind of focus that gets things done. Suppressing or putting a lid on your emotions also can be a good strategy in a short-term situation, such as when your boss yells at you, Dolcos said. Similarly, an always-positive attitude can be dangerous, causing a person to ignore health problems, for example, or to engage in risky behavior.

Previous studies had found that people who were temperamentally inclined to focus on making good things happen were less likely to suffer from anxiety than those who focused on preventing bad things from happening, Llewellyn said. But she could find no earlier research that explained how this difference in focus translated to behaviors that people could change. The new study appears to explain the strategies that contribute to a person having more or less anxiety, she said.

“This is something you can change,” she said. “You can’t do much to affect the genetic or environmental factors that contribute to anxiety. But you can change your emotion regulation strategies.”

The research team also included postdoctoral researcher Sanda Dolcos, graduate student Alexandru Iordan and psychology professor Karen Rudolph.

Depressed People Have Different Body Clocks

Depression News | 15 May 2013

Depressed people are out of sync with the rest of the world because their body clocks are broken, according to a new study.

The discovery of disrupted body clocks in the brains of people with depression is the first link to be found between the condition and changes in the circadian rhythm. It is hoped that the finding will allow for the development of better treatments.

Every cell in the human body runs on a 24-hour clock, tuned to the night-day, light-dark cycles in nature. The brain acts as a timekeeper, keeping this cellular clock in sync with the outside world so that it can govern our appetite, sleep and moods.

However, new research shows that the clock may be broken in the brains of people with depression - even at the level of the gene activity inside their brain cells.

The discovery, published in the journal, Proceedings of the National Academy of Sciences was made by studying differences in the donated brains of people who had been depressed and those who had not. 

The research also revealed a previously unknown daily rhythm to the activity of many genes across many areas of the brain - expanding the sense of how crucial the body’s clock is.

In a normal brain, the pattern of gene activity at a given time of the day is so distinctive that the authors could use it to accurately estimate the hour of death of the brain donor.

However, in severely depressed patients, the circadian clock was so disrupted that a patient’s ‘day’ pattern of gene activity could look like a ‘night’ pattern, and vice versa.

Lead author Dr Jun Li, an assistant professor in the Department of Human Genetics at University of Michigan Medical School, in the U.S., described how the approach allowed the researchers to accurately back-predict the hour of the day when each non-depressed individual died - literally plotting them out on a 24-hour clock by noting which genes were active at the time they died. 

They looked at 12,000 gene transcripts isolated from six regions of 55 brains from people who did not have depression. This provided a detailed understanding of how gene activity varied throughout the day in the brain regions studied. 

In severely depressed patients, the circadian clock is so disrupted that a patient's 'day' pattern of gene activity could look like a 'night' pattern

However, when the team tried to do the same in the brains of 34 depressed people, the gene activity was off by hours. The cells looked as if it were an entirely different time of day.

Dr Li said: ‘There really was a moment of discovery. ‘It was when we realized that many of the genes that show 24-hour cycles in the normal individuals were well-known circadian rhythm genes - and when we saw that the people with depression were not synchronized to the usual solar day in terms of this gene activity.

‘It’s as if they were living in a different time zone than the one they died in.’

Depression affects one in ten adults in the UK at any one time but it is slightly more common in women. At any one time one in 20 people in the UK will be experiencing severe depression.

The main symptoms are lasting feelings of sadness and hopelessness, losing interest in things you used to enjoy and feeling tearful. There can also be physical symptoms such as fatigue, sleeping badly, having no appetite and aches and pains.

Children with Autism See Movement Quicker- A Clue to Underlying Cause of the Disorder

Autism Spectrum Disorders News | 14 May 2013

Children with autism see simple movement twice as quickly as other children their age, and this hypersensitivity to motion may provide clues to a fundamental cause of the developmental disorder, according to a new study.

Such heightened sensory perception in autism may help explain why some people with the disorder are painfully sensitive to noise and bright lights. It also may be linked to some of the complex social and behavioral deficits associated with autism, says Duje Tadin, one of the lead authors on the study and an assistant professor of brain and cognitive sciences at the University of Rochester.

"We think of autism as a social disorder because children with this condition often struggle with social interactions, but what we sometimes neglect is that almost everything we know about the world comes from our senses. Abnormalities in how a person sees or hears can have a profound effect on social communication."

Although previous studies have found that people with autism possess enhanced visual abilities with static images, this is the first research to discover a heightened perception of motion, the authors write. The findings were reported in the Journal of Neuroscience on May 8 by Tadin, co-lead author Jennifer Foss-Feig, a postdoctoral fellow at the Child Study Center at Yale University, and colleagues at Vanderbilt University.

In the study, 20 children with autism and 26 typically developing children, ages 8 to 17, looked at brief video clips of moving black and white bars and simply indicated which direction the bars were heading, right or left. Each time a participant made the correct direction choice, the next video clip became slightly shorter and thus a little more difficult. When they made a mistake, the next video became a bit longer and thus easier to see. In this way, the researchers were able to measure how quickly children with autism can perceive motion.

"This dramatically enhanced ability to perceive motion is a hint that the brains of individuals with autism keep responding more and more as intensity increases. Although this could be considered advantageous, in most circumstances if the neural response doesn't stop at the right level it could lead to sensory overload," explains Foss-Feig.

Such hypersensitive perception is the neural signature for a brain that is unable to dampen its response to sensory information, note the authors. This same increase in neural "excitability" is also found in epilepsy, which is strongly linked to autism. In fact, as many as one third of individuals with autism also have epilepsy. Normally, the brain puts the brakes on its responses to sound, taste, touch, and other stimuli when they become too intense.

What's important about this dampening ability is that it's a ubiquitous mechanism controlling how humans perceive the world. "If the processing of our vision, hearing, and other sensory systems is abnormal in some way, it will have a cascading effect on other brain functions," says Carissa Cascio, assistant professor of psychiatry at Vanderbilt University, in whose lab the study was conducted. "You may be able to see better, but at some point the brain really is over responding. A strong response to high intensity stimuli in autism could be one reason for withdrawal."

The research builds on earlier findings that people with autism process visual stimuli differently. For example, previous studies have shown that individuals with autism are better able to perceive basic patterns, are able to see simple line images more quickly, and are more focused on details than individuals without the condition. By contrast, in more complex tasks, like facial recognition, these enhancements become impairments. Likewise, autism is associated with deficits in perceiving motion patterns more complex than the simple moving bars used in this study, such as detecting walking and other biological movements.

Kimberly Schauder, a research assistant at Vanderbilt University, is also an author on the paper. The research was supported by grants from the National Institutes of Health.

World First Clinical Trial Supports Use of Kava to Treat Anxiety

Anxiety News | 14 May 2013

A world-first completed clinical study by an Australian team has found Kava, a medicinal South Pacific plant, significantly reduced the symptoms of people suffering anxiety.

The study, led by the University of Melbourne and published in the Journal of Clinical Psychopharmacology, revealed Kava could be an alternative treatment to pharmaceutical products for the hundreds of thousands of Australians who suffer from Generalised Anxiety Disorders (GAD)

Lead researcher, Dr Jerome Sarris from Department of Psychiatry at the University of Melbourne, said GAD is a complex condition that significantly affected people’s day-today lives. Existing medications have a modest clinical effect and new effective options were needed for patients with anxiety.

“Based on previous work we have recognised that plant based medicines may be a viable treatment for patients with chronic anxiety.  In this study we've been able to show that Kava offers a potential natural alternative for the treatment of chronic clinical anxiety. Unlike some other options it has less risk of dependency and less potential for side effects,” he said.

The study also found that people’s genetic differences (polymorphisms) of certain neurobiological mechanisms called GABA transporters, may modify their response to Kava.

“If this finding is replicated, it may pave the way for simple genetic tests to determine which people may be likely to have a beneficial anxiety-reducing effect from taking Kava,” Dr Sarris said.

During the eight-week study, 75 patients with clinically diagnosed Generalised Anxiety Disorder were given Kava or placebo, and anxiety levels were regularly assessed.

Results showed a significant reduction in anxiety for the Kava group compared to the placebo group at the end of the study.

In participants diagnosed with moderate to severe GAD, Kava had an even greater effect in reducing anxiety. Following the completion of the controlled phase, 26 per cent of the Kava group were classified as in remission from their symptoms compared to six per cent of the placebo group.

Participants in the Kava group were given tablets twice per day consisting of water-soluble extracted Kava (peeled rootstock) for a total dose of 120mg of kavalactones for the first three-week controlled phase.  In cases of non-response this was increased to a double-dose twice per day for the second three-week controlled phase. Participants in the placebo group took matching dummy tablets in the same manner.

Kava was also well tolerated. Results showed no significant differences across the two groups for liver function which had previously been a concern for Kava’s medicinal use.  In addition there were no considerable adverse reactions that could be attributed to Kava and no difference in withdrawal or addiction between the groups.

An additional novel finding of the study, recently published in Phytotherapy Research was that Kava increased women’s sex drive compared to those in the placebo group, believed to be due to the reduction of anxiety, rather than any aphrodisiac effect.

Future studies confirming the genetic relationship to therapeutic response, and any libido-improving effects from Kava is now required. Dr Sarris said these significant findings are of importance to sufferers of anxiety and to the South Pacific region which relies on Kava as a major export.

The study was funded by the NHMRC and Integria Healthcare who manufacture MediHerb and Thompson’s Kava products.