Following are the latest news and information resources for the various mental health topics that we cover. We hope you will find the news educational and the links in the resources section useful in helping you to get even more in-depth data.
The literature reviewed here is consistent in showing that GAD is a common mental disorder that typically has an early age of onset, a chronic course, and a high degree of comorbidity with other anxiety and mood disorders.
Comorbid GAD is often temporally primary, especially in relation to mood disorders, and is associated with an increased risk for the subsequent onset and severity of secondary disorders. The weight of evidence reviewed here argues against the view expressed by early commentators that GAD is better conceptualized as a prodrome, residual, or severity marker of other disorders than as an independent disorder. Focused studies of comorbidity between GAD and major depression, in which comorbidity is high, lead to the same conclusion.
The crucial evidence for this conclusion includes the following: 1. Contrary to the findings of clinical studies, GAD in the community does not have a higher comorbidity than do most other anxiety or mood disorders. 2. The symptoms of GAD form an empiric cluster distinct from the symptoms of major depression in studies of symptom profiles. 3. Family studies show distinct aggregation of GAD and major depression. 4. Twin studies show that the environmental determinants of GAD are different from the environmental determinants of major depression. 5. The sociodemographic predictors of GAD in epidemiologic studies are different from the predictors of major depression. 6. The clinical course of GAD is less consistently related to comorbidity than is the course of other anxiety and mood disorders. 7. The impairments associated with GAD are equivalent to, or greater than, those associated with other severely impairing chronic physical and mental disorders.
These findings show that the status of GAD as an independent disorder is at least as strongly supported by available evidence as is that of other anxiety or mood disorders.
This article also shows that uncertainty remains regarding even the basic epidemiologic characteristics of the GAD syndrome. Lingering concerns about the independence of GAD have conspired to exacerbate this problem by promoting repeated changes in the diagnostic criteria for GAD from the DSM-III to DSM-III-R and to DSM-IV. These successive changes have made it difficult to amass consistent long-term data on the natural history of GAD.
Available evidence on the empiric validity of current diagnostic thresholds for GAD raises questions about the requirements, such as whether a 6-month minimum duration and four or more additional psychophysiologic symptoms are optimal for identifying all of the people in the general population who suffer from a clinically significant GAD syndrome.
An additional source of potential bias in this regard is that the DSM system requires that anxiety be excessive or unrealistic for a diagnosis of GAD. Interestingly, there is no comparable DSM requirement that dysphoria must be excessive or unrealistic to qualify as major depression.
These diagnostic uncertainties make it difficult to gain a clear understanding of the true breadth and depth of the GAD syndrome in the general population. Additional research is needed, ideally from unbiased epidemiologic samples, to resolve these basic uncertainties.
The strong comorbidity between GAD and major depression, the fact that most people with this type of comorbidity report that the onset of GAD occurred before the onset of depression, and the fact that temporally primary GAD significantly predicts the subsequent onset of depression and other secondary disorders raise the question of whether early intervention and treatment of primary GAD would effectively prevent the subsequent first onset of secondary anxiety and depression.
Unfortunately, little is known about this possibility because, as mentioned earlier, few people with pure GAD seek treatment. Why this is true is unknown. Given the early onset of GAD and its strong effects in predicting the subsequent onset, severity, and persistence of other disorders, efforts are needed to collect epidemiologic data on the reasons for the low rate of help seeking among people with pure GAD and to develop outreach strategies that may correct this situation.Read article >>
People who are depressed have lower concentrations of zinc in their peripheral blood compared with nondepressed individuals, a meta-analysis suggests.
"The pathophysiological relationships between zinc status and depression, and the potential benefits of zinc supplementation in depressed patients, warrant further investigation," write Walter Swardfager, PhD, from the Sunnybrook Research Institute, University of Toronto, Canada, and colleagues.
Their findings were published in the December 15 issue of Biological Psychiatry.
Link to Zinc Deficiency
"A growing body of evidence demonstrates that experimental zinc deficiency can induce depressive-like behavior in animals, which can be effectively reversed by zinc supplementation," the authors write. Furthermore, preliminary clinical trials have suggested that zinc added to antidepressant therapy may produce more rapid or more effective improvement in depressive symptoms.
Many, although not all, studies that have measured zinc concentrations of peripheral blood in depressed and nondepressed individuals during the past several decades have suggested that depression might be associated with lower zinc concentrations in various population samples, the researchers note.
The aim of this meta-analysis was to determine whether the clinical evidence collectively supports lower zinc concentrations in depressed patients compared with nondepressed individuals.
The analysis included 17 studies that measured peripheral blood–zinc concentrations in 1643 depressed patients and 804 control participants. Ten of these studies reported on psychiatric inpatients, and 7 reported on community samples. Of the participants, 34.4% were male; the mean age was 37.7 years.
The researchers found that mean peripheral blood–zinc concentrations were lower by approximately 1.85 µmol/L in depressed individuals compared with control participants (95% confidence interval [CI], -2.51 to -1.19; P < .00001).
More severe depression was associated with greater differences in zinc levels between depressed and control participants (P = .026).
Further, the authors report that effect sizes were larger in studies of inpatients (weighted mean difference [WMD], -2.543; 95% CI, -3.522 to -1.564; P < .0001) vs community samples (WMD, -.943; 95% CI, -1.563 to -.323; P = .003) and in studies with higher methodologic quality (WMD, -2.354; 95% CI, -2.901 to -1.807; P < .0001).
"Although association studies cannot determine the direction of causation, a causal association between zinc status and depression is biologically plausible," the authors write.
"Zinc has antioxidant properties, helps to maintain endocrine homeostasis and immune function, and plays multiple roles in regulating the hippocampal and cortical glutamatergic circuits that subserve affective regulation and cognitive function. Thus, changes in zinc homeostasis might compromise neuroplasticity and contribute to long-term neuropsychological and psychiatric decline," they write.
Zinc also plays an important role in immune function. Lower serum levels of zinc have been associated with disturbances in fatty acid metabolism and in serum lipid levels, which might affect brain function and vascular health. Lower zinc levels have also been associated cardiovascular disease, a common comorbidity of major depressive disorder (MDD), the authors note.
The investigators point out limitations of their study. The quality and risk of bias "were uneven among studies included in this meta-analysis," they write.
Not all studies reported demographic data "sufficiently to be included in investigations of heterogeneity, the use of antidepressants and other concomitant medications were not consistently reported, and data on diet and alcohol use were often not reported," the authors write.
Limitations notwithstanding, the authors conclude that their results suggest that depression is associated with reduced concentrations of zinc in peripheral blood.
"The findings suggest the need to further investigate potential roles of zinc in the pathophysiology of depression, the potential utility of zinc and related biomarkers in monitoring MDD and its clinical sequelae, and potential benefits of zinc supplementation in MDD patients," they conclude.
The study was supported by the Ontario Mental Health Foundation. Dr. Swardfager was supported by fellowships from the Heart and Stroke Foundation Center for Stroke Recovery and the Toronto Rehabilitation Institute. Dr. Swardfager and the other authors report no relevant financial relationships.Read article >>
New research has drawn links between depression in women and a heightened risk of suffering a stroke. Experts from the US looked at the cases of over 80,000 women and reached the conclusion that where depression was a factor, the risk of stork increased by an alarming 29%.
Now published in Stroke: Journal of the American Heart Association, the paper urges doctors and other medical professionals to pay more attention to the ways in which depressed individuals are more prone to neglecting their health.
Stroke professionals from the UK have however countered the research with comments suggesting that stroke risk is unlikely to be affected by depression alone.
The US study examined the cases of women between the ages of 54 and 79 from the year 2000 to 2006. None of the women involved had suffered a stroke prior to the commencement of the research, though 22% were known to be suffering from depression.
When compared like for like, the women with a history of depression were considerably more likely to be less physically active, smoke tobacco and be single. In addition, the depressed group was also more widely affected by conditions like heart disease, high blood pressure and diabetes.
By the conclusion of the study, 1,033 of those observed had suffered a stroke.
Along with depression as a whole being linked with higher stroke risk, the study also highlighted how the women that had taken anti-depressant medication were a full 39% more likely to suffer a stroke.
However, lead researcher Dr Kathryn Rexrode insisted that such a sharp increase was most likely due to the serious nature of the person in question’s illness, rather than the medication itself.
“I don’t think the medications themselves are the primary cause of the risk. This study does not suggest that people should stop their medications to reduce the risk of stroke,” she said
“Depression can prevent individuals from controlling other medical problems such as diabetes and hypertension, from taking medications regularly or pursuing other healthy lifestyle measures such as exercise. All these factors could contribute to increased risk.”
Dr. An Pan of the Harvard School of Public Health insisted that regardless of the reasons for the link, doctors need to be more proactive in recognizing and addressing it.
“Regardless of the mechanism, recognizing that depressed individuals may be at a higher risk of stroke may help the physician focus on not only treating the depression, but treating stroke risk factors such as hypertension, diabetes and elevated cholesterol as well as addressing lifestyle behaviors such as smoking and exercise,” he wrote.Read article >>
Children with depression are more likely to be obese, smoke and be inactive, and can show the effects of heart disease as early as their teen years, according to a newly published study by University of South Florida Associate Professor of Psychology Jonathan Rottenberg.
The research, by Rottenberg and his colleagues at Washington University and the University of Pittsburgh, suggests that depression may increase the risk of heart problems later in life. The researchers also observed higher rates of heart disease in the parents of adolescents that had been depressed as children. The research is published online in Psychosomatic Medicine and will be included in the medical journal’s February 2014 issue.
“Given that the parents in this sample were relatively young, we were quite surprised to find that the parents of the affected adolescents were reporting a history of heart attacks and other serious events,” Rottenberg explained.
Cardiologists and mental health professionals have long known a link exists between depression and heart disease. Depressed adults are more likely to suffer a heart attack, and if they do have a heart attack, it’s more likely to be fatal.
However it was unclear when the association between clinical depression and cardiac risk develops, or how early in life the association can be detected. These findings suggest improved prevention and treatment of childhood depression could reduce adult cardiovascular disease.
Heart disease is the leading cause of death for men and women- accounting for one in every four deaths in the United States every year, according to the Centers for Disease Control and Prevention.
During the study, Rottenberg and his colleagues followed up on Hungarian children who had participated in a 2004 study of the genetics of depression. The researchers compared heart disease risk factors – such as smoking, obesity, physical activity level, and parental history – across three categories of adolescents.
The investigators surveyed more than 200 children with a history of clinical depression, as well as about 200 of their siblings who have never suffered from depression. They also gathered information from more than 150 unrelated children of the same age and gender with no history of depression.
Rottenberg plans to conduct additional research in order to understand why depression early in life may put people at increased risk for cardiovascular disease. Further studies planned with the Hungarian group will also examine whether any early warning signs of heart disease are present as these adolescents move into young adulthood.Read article >>
"I hit a breaking point the other day," a friend recently told me. "My daughter was being difficult about an upcoming curfew and I just lost it. I'm already dealing with an irate boss, an overly demanding husband and 50-hour workweeks. I couldn't take anything else, and my daughter sent me over the edge."
Welcome to 2014, where chronic stress becomes the new normal and our fast-faster society juggles a never-ending to-do list even as we're still frantically catching up from last month's agenda.
Doesn't it sometimes feel like one of those reality-show contests to see who can do the most? One problem: Nobody wins. There's always more to do.
As my friend dramatically expressed, jobs often become a major source of stress. One study found increased work demands and worrying about work during free time could disturb sleep and impair awakening. Older folks (45 and up), females and people with higher body mass indexes (BMIs) were especially susceptible to work-related stress that impaired sleep.
A vicious cycle ensues. Work and other stressors mean you sleep less, neglect exercise, and down-regulate "me" time all while grabbing a low-fat muffin with your morning java jolt to keep you going.
All that delivers a serious whammy to your quality of life, not to mention your hormones. Adrenal hormones like cortisol stay ramped up, leading to a miserable "wired and tired" feeling. One study found even one night of poor sleep can knock your hormone insulin out of balance, triggering insulin resistance and diabetes.
Chronic stress can also make you sick. One meta-analysis of 300 studies found chronic stress could seriously crash your immune system. Studies show stress can make you fat and increase your risk for serious problems like cardiovascular disease.
Shall I go on? I think you understand the very ugly repercussions of chronic stress. You can't eliminate stress, but you can learn to better cope and reduce its impact. I've found these five simple but powerfully effective strategies can help:
1. Dump the sweet stuff.
You've had the day from hell, so along with your dark roast you impulsively order an apple fritter or whatever your coffee shop weakness might be. Rather than assuage stress, sugary foods only worsen it as metabolic havoc ensues. "Consuming refined sugar... [and other] refined carbohydrates leads to a spike and then drop in blood sugar levels, which can result in anxiety, nervousness and irritability," says Trudy Scott, author of The Antianxiety Food Solution. She points out a study that shows chronic stress sometimes triggers comfort food binges. Trade the processed, high-sugar foods for lean protein, healthy fats, lots of cruciferous and leafy veggies, and slow-release high-fiber starches to steady your blood sugar and insulin levels, leading to consistent energy and mood levels.
2. Burst your stress away.
Studies show stress impairs your efforts to stay physically active. The opposite is also true: Staying active reduces stress. You've likely felt that post-workout stress-zapping endorphin rush. That's because, according to Matthew Stults-Kolehmainen, Ph.D., a kinesiologist at the Yale Stress Center, exercise can boost hormones like norepinephrine that elevate mood and even improve stress-damaged thinking. Burst training, or high-intensity interval training, is my favorite exercise for busy, stressed-out professionals to better cope with the challenges life throws their way. "When stress hits, our physiology is designed to fight or flee," says Dr. Jade Teta, co-author of The Metabolic Effect Diet. "Short, intense exercise engages recovery aspects of physiology and helps the body learn to reengage the parasympathetic nervous system."
3. Get deep sleep.
I wrote about seven hormones that become out of whack with too little sleep. On a practical level, sleep deprivation makes morning rush-hour traffic an amped-up hell, as you imagine your boss reprimanding you for being late while devouring your third dark roast. Frustrating episodes throughout your sleep-deprived day become monumental events that leave you even more stressed. A chicken-or-egg cycle ensues as stress cuts into your sleep. Among other problems, studies show chronic stress and sleep loss increase your risk for depression and other mood disorders. Make time for seven to nine hours of high-quality, uninterrupted sleep every night. You'll find you're more productive and capable of rolling with whatever stress the following day throws at you.
4. Chill out.
"I just don't know how to relax," a colleague told me recently. Leisure time gets short shift as our work-more mentality pervades. Schedule relaxation and prioritize it just like you would an important client. One study shows a massage could lower your stress hormone cortisol while boosting your feel-good neurotransmitters serotonin and dopamine. Another study among the elderly, found acupuncture could reduce stress and boost lymphocyte production. Studies also show regularly practicing Transcendental Meditation (TM) can be effective against chronic stress. What matters most is what works for you, even if that means watching a silly movie or having a coffee date with your beset friend. Find it and make it a daily habit.
5. Mind your gut.
Researchers are learning more about the mind-gut connection and how chronic stress can adversely impact your gut, leading to intestinal permeability and other issues. One study showed stress-induced prolonged combat-training increases intestinal permeability. (With its numerous demands, your life might sometimes feel similarly to combat training.) Chronic stress can also contribute to irritable bowel syndrome (IBS) and numerous other gastrointestinal conditions. Repopulating healthy microorganisms with a probiotic supplement is among my gut-healing protocol. One study found stress suppressed inflammasome, which is needed to maintain healthy gut flora. In this mice study, probiotics reversed that detrimental effect.
As you can see, chronic stress creates a domino effect that can affect numerous areas of your life. You can't eliminate stress, but you can learn to reduce its impact and attain grace under pressure (to quote Hemingway) with the right strategies.Read article >>
The people in generation Y, often called the @ generation, are considered the one’s who’ve immersed themselves in technology the most, for the way they’ve replaced traditional ways of communication with social media, and how they’ve embraced technology from very early on.
But, some have complained that the younger generation relies too much on technology and gadgetry, to the point where it’s impacted their lives in a negative way. In fact, there is a new study conducted by the University of Texas Health Science Center in Houston, that shows a lot of modern day technology is robbing young people of proper sleep, and that lack of sleep is causing depression.
Researchers gathered 4,000 teenagers over the course of one year and noticed the ones who were lacking the proper amount of sleep were four times more likely to develop major depressive disorders, compared to the teenagers who were getting enough sleep. And being online or texting to all hours of the night were the main culprits in robbing the teenagers of sufficient rest.
Robert Roberts, the lead author of the study, says the correlation between today’s technology and a lack of sleep is a strong one for young people, and it’s created a huge problem.
“That’s a pretty strong reciprocal relationship,” Roberts said. “When you throw in all the video games and iPods and all the phones, sleep starts to become less of a priority.”
In addition, Roberts said it’s important for adults to monitor how much their kids are staying online and texting at night, and if they notice their child isn’t properly rested, they should nip it in the bud immediately, because sleep deprivation is one of those conditions that parents shouldn’t take lightly.
“[Sleep deprivation] is a highly prevalent public health problem,” said Roberts. “If parents and teachers are able to pick up early on that teenagers aren’t sleeping enough, they might be able to help before things get worse.”Read article >>
Many autistic children seem to be living in their own worlds, a place they are perfectly happy to be in, withdrawn from their surroundings. Many also have trouble sleeping, are hyperactive and it seems to be impossible to shut off their brains for even a moment. The truth of the matter is that they cannot shut it all off, with the autistic mind working an average of 42% more, according to the latest findings in a University of Toronto and Case Western Reserve University joint study. What does that mean though?
Thoughts on Autism
Autism in itself is an interesting disorder. Many specialists might even prefer to use the word "condition" instead, while the opposite end of the argument might call it a mental disease. I call it disorder, personally, because the brain's structure becomes disordered, with different neurons firing about and a generally larger brain looked at. Furthermore, you have the staunch believers in vaccinations causing autism, a theory I cannot follow as twin studies show an extremely high prevalence among identical twins, compared with fraternal or siblings of different ages. As such, autism is a genetic disorder, aggravated by environmental aspects.
An autistic child's brain simply never seems to stop. This might very well account for much of their behavior, as well as the manifestation of savantism or high-functioning gifted attributes. A diagnosis on the spectrum does not mean a child is of low IQ. They may very well be the smartest children in their classrooms, simply misunderstood and mishandled.
What the Study Found
The aforementioned study followed up on a previous finding where the brains of autistic children were found to be unique, with different connections made within. According to lead investigator Dr. Roberto Fernández Galán. "Our results suggest that autistic children are not interested in social interactions because their brains generate more information at rest, which we interpret as more introspection in line with early descriptions of the disorder.”
The brain is a complex structure in itself and what was discovered is that the "Intense World Theory" is quite certainly correct, referring to the autistic mind as the result of the hyper-functioning of brain circuitry leading to over-stimulation. This means that what is absolutely impossible to comprehend for the neurotypical individual is a daily norm for the autistic, including hyper-perception, hyper-attention, hyper-memory and hyper-emotionality. As such, the theory proposes that the autistic becomes trapped in a limited, but highly secure, internal world with minimal extremes and surprises.
A 42% increase in average brain activity during rest is not a small number. It is mind-boggling and absolutely fascinating when one begins to explore the most minuscule of details, only to find something as magnanimous as this study's results. The brain needs to rest in order to recuperate, but it seems that for an autistic child, it is almost an impossible feat. Some of these tips might help in the long run, but the truth of the matter is that we should probably allow our children to enter their own worlds from time to time in order to find the rest that they require so desperately.
An autistic brain is incredible in its abilities, and I for one hope to see science unravel all the secrets it holds, including why they withdraw into themselves, ensuring better awareness and understanding in how to teach, parent and work with those diagnosed to be on the spectrum, high or low.Read article >>
By activating a brain circuit that controls compulsive behavior, MIT neuroscientists have shown that they can block a compulsive behavior in mice — a result that could help researchers develop new treatments for diseases such as obsessive-compulsive disorder (OCD) and Tourette’s syndrome.
About 1 percent of U.S. adults suffer from OCD, and patients usually receive antianxiety drugs or antidepressants, behavioral therapy, or a combination of therapy and medication. For those who do not respond to those treatments, a new alternative is deep brain stimulation, which delivers electrical impulses via a pacemaker implanted in the brain.
For this study, the MIT team used optogenetics to control neuron activity with light. This technique is not yet ready for use in human patients, but studies such as this one could help researchers identify brain activity patterns that signal the onset of compulsive behavior, allowing them to more precisely time the delivery of deep brain stimulation.
“You don’t have to stimulate all the time. You can do it in a very nuanced way,” says Ann Graybiel, an Institute Professor at MIT, a member of MIT’s McGovern Institute for Brain Research and the senior author of a Science paper describing the study.
The paper’s lead author is Eric Burguière, a former postdoc in Graybiel’s lab who is now at the Brain and Spine Institute in Paris. Other authors are Patricia Monteiro, a research affiliate at the McGovern Institute, and Guoping Feng, the James W. and Patricia T. Poitras Professor of Brain and Cognitive Sciences and a member of the McGovern Institute.
In earlier studies, Graybiel has focused on how to break normal habits; in the current work, she turned to a mouse model developed by Feng to try to block a compulsive behavior. The model mice lack a particular gene, known as Sapap3, which codes for a protein found in the synapses of neurons in the striatum — a part of the brain related to addiction and repetitive behavioral problems, as well as normal functions such as decision-making, planning and response to reward.
For this study, the researchers trained mice whose Sapap3 gene was knocked out to groom compulsively at a specific time, allowing the researchers to try to interrupt the compulsion. To do this, they used a Pavlovian conditioning strategy in which a neutral event (a tone) is paired with a stimulus that provokes the desired behavior — in this case, a drop of water on the mouse’s nose, which triggers the mouse to groom. This strategy was based on therapeutic work with OCD patients, which uses this kind of conditioning.
After several hundred trials, both normal and knockout mice became conditioned to groom upon hearing the tone, which always occurred just over a second before the water drop fell. However, after a certain point their behaviors diverged: The normal mice began waiting until just before the water drop fell to begin grooming. This type of behavior is known as optimization, because it prevents the mice from wasting unnecessary effort.
This behavior optimization never appeared in the knockout mice, which continued to groom as soon as they heard the tone, suggesting that their ability to suppress compulsive behavior was impaired.
The researchers suspected that failed communication between the striatum, which is related to habits, and the neocortex, the seat of higher functions that can override simpler behaviors, might be to blame for the mice’s compulsive behavior. To test this idea, they used optogenetics, which allows them to control cell activity with light by engineering cells to express light-sensitive proteins.
When the researchers stimulated light-sensitive cortical cells that send messages to the striatum at the same time that the tone went off, the knockout mice stopped their compulsive grooming almost totally, yet they could still groom when the water drop came. The researchers suggest that this cure resulted from signals sent from the cortical neurons to a very small group of inhibitory neurons in the striatum, which silence the activity of neighboring striatal cells and cut off the compulsive behavior.
“Through the activation of this pathway, we could elicit behavior inhibition, which appears to be dysfunctional in our animals,” Burguière says.
The researchers also tested the optogenetic intervention in mice as they groomed in their cages, with no conditioning cues. During three-minute periods of light stimulation, the knockout mice groomed much less than they did without the stimulation.
Scott Rauch, president and psychiatrist-in-chief of McLean Hospital in Belmont, Mass., says the MIT study “opens the door to a universe of new possibilities by identifying a cellular and circuitry target for future interventions.”
“This represents a major leap forward, both in terms of delineating the brain basis of pathological compulsive behavior and in offering potential avenues for new treatment approaches,” adds Rauch, who was not involved in this study.
Graybiel and Burguière are now seeking markers of brain activity that could reveal when a compulsive behavior is about to start, to help guide the further development of deep brain stimulation treatments for OCD patients.
The research was funded by the Simons Initiative on Autism and the Brain at MIT, the National Institute of Child Health and Human Development, the National Institute of Mental Health, and the Simons Foundation Autism Research Initiative.Read article >>
Building on what they hope will be an important insight into the cause of autism, French researchers are testing a high blood pressure medication on dozens of European children with autism.
The team, which has a financial stake in the drug, has tried it on 30 children with autism; now they are testing it in more, hoping to improve core characteristics of autism for the first time.
There are drugs to treat some of autism's symptoms, but none that address the underlying social and communication difficulties and repetitive behaviors, which define the condition. Previous attempts to develop an effective drug against the condition, which affects at least one in 88 U.S. schoolchildren, have either failed or are also still experimental.
In a study out today in the journal Science, the researchers offer an explanation for the promise of their drug, bumetanide, a generic diuretic long used to treat the fluid retention of high blood pressure.
The researchers found that the drug, given during pregnancy, could reverse autism symptoms in newborn mice bred with a genetic condition that often causes autism in people, and in rats exposed to the epilepsy drug valproic acid, which is known to trigger autism.
They suspect that bumetanide is flipping a chemical switch in the brain — changing the chemical GABA from stimulating electrical activity in the brain to tamping it down. This switch needs to be flipped during or near birth for the brain to develop normally, says lead researcher Yehezkel Ben-Ari of the French Institut National de la Santé et de la Recherche Médicale, in Marseilles, France.
Because this switch fails to flip in rodents with two very different triggers of autism, the researchers say they may have found an underlying cause of the condition.
That is a "pretty incredible finding and really great," says Andrew Zimmerman, a pediatric neurologist and autism expert at the University of Massachusetts Medical School in Worcester, Mass.
He and other researchers note that it's too early for people to try the drug outside of carefully watched clinical trials. There are just so many unknowns, from what the drug will do to the developing brain to how much of the drug to give and when.
"So many things cure cancer in mice and rats, and so many things cure all kinds of things and then when we give them to humans they have adverse effects and don't fix the problems we thought they could fix," says Gary Goldstein, president and CEO of the Kennedy Krieger Institute, a Baltimore-based clinic and research center. "I wouldn't give it to my child, I can tell you that."
Ben-Ari and his colleagues have patented a version of bumetanide and formed a company, Neurochlore, in Marseilles, to test the drug in children. He says bumetanide should not be given to pregnant women — despite his success with rodents — because it is impossible to determine which children will go on to develop autism and unethical to test on healthy ones.
It should be used as early in childhood as possible, Ben-Ari says, and his team is testing the drug in children as young as 2. Autism is typically diagnosed around age 4, but experts are working to push that diagnosis earlier. It is widely believed that the sooner treatment begins, the more effective it is likely to be.
Ben-Ari says he is hopeful that the drug will show benefits across a broad spectrum of children with autism, but behavioral therapy and possibly other pharmaceutical treatments will likely still be needed, too, he says.
"It's important for people to understand there is no drug to cure a medical disease as complicated as autism," he says.Read article >>
Thanks to on-stage brainwashing sessions and movies featuring disgruntled workers taking a baseball bat to the printer (Office Space, anyone?), hypnosis has a rep for being little more than pure entertainment.
Not true. Hypnosis was birthed from the brains of psychologists and researchers, and while its story was sullied by decades of disrepute, it's now making its way back into the mainstream.
The British Psychological Society has now officially declared hypnosis a proven therapeutic medium to curb stress, anxiety, pain, insomnia, irritable bowel syndrome, and migraines. "Improvements from hypnosis can be as specific as eliminating erectile dysfunction or premature ejaculation, remaining committed to a workout plan, delivering a dynamic sales presentation—or as broad as improving motivation and increasing confidence," said psychologist and certified hypnotherapist Marty Lerman, Ph.D., author of Mindshift.
And while it's strongly linked to the psycho-sciences, hypnosis is gaining popularity in broader mind-body arenas as well. In fact, one Harvard study found that patients who underwent hypnosis during surgery had fewer complications and required shorter procedures and less post-op medication.
Meanwhile, celebrities including Matt Damon, Tiger Woods, Andre Agassi, and Fergie have all been cited as using hypnotherapy for one reason or another: to stop smoking, improve focus, and lose weight.
The Science of Suggestibility
While most people equate hypnosis with swinging pocket watches and the old "you are getting very sleepy" line, it's actually very similar to guided meditation and helps coax the patient into a hyper-attentive mental state in which he or she is most open to positive suggestions from the hypnotherapist. Think of it as plugging affirmations straight into your brain, sans self-doubt.
"By accessing this subconscious part of the brain, we can bypass all the negative critical thinking and open inward to an awareness of potential and knowledge. Your imagination and creativity are free to explore all kinds of solutions and game plans to situations," Lerman said, who equates a hypnotic trance to something we've all encountered at one point or another. Ever been so absorbed in an activity that you didn't hear our name when it was called?
Only about three-fourths of people can be hypnotized, though. And not just the most gullible or submissive, said David Spiegel, M.D., a professor of psychiatry and behavioral sciences at the Stanford School of Medicine. Quite the contrary: A 2012 study from Spiegel's team found that in people who are easily hypnotized, the brain's executive-control network (responsible for making decisions) is activated in tandem with the salience network, which helps you focus.
In people that can't be hypnotized, the two brain regions don't work together the same way. That might explain why people who become engrossed in day-to-day activities—such as reading, working, or just brainstorming—tend to be most easily hypnotized.
Hypnotize Me, Baby
There's no universal licensing process for hypnotists—and since you don't want just anybody having their way with your brain—you need to do your homework before going under.Read article >>