Posts tagged science
Articles and news from the latest research reports.
N.C. Coal Plant Emissions Might Play Role in State Suicide Numbers
New research from Wake Forest Baptist Medical Center finds that suicide, while strongly associated with psychiatric conditions, also correlates with environmental pollution.
Lead researcher John G. Spangler, M.D., M.P.H., a professor of family medicine at Wake Forest Baptist, looked specifically at the relationship between air pollution and emissions from coal-fired electricity plants.
"This study raises interesting questions about suicide rates in counties where coal-fired electrical plants operate and suggests that the quality of air can affect people suffering from different mood disorders," Spangler said.
For this ecological study, Spangler evaluated air level contaminates in 20 North Carolina counties where coal-fired electricity plants existed, using data from the 2000 U.S. Census, 2001-2005 mortality rates from the N.C. State Center for Health Statistics and the U.S. Environmental Protection Agency.
County-level suicide rates were higher overall in North Carolina (12.4 per 100,000 population) compared to the U.S. population (10.8 per 100,000). The study found that for each additional coal-fired electricity plant per N.C. county, there were about two additional suicides per 100,000 population annually per county. As there were 20 coal-fired electricity plants in North Carolina when this study was carried out, that means there were about 40 suicides a year per 100,000 population related to the plants. When applied to the state’s year 2,000 population of 8,049,313, this equals about 3,220 suicides a year associated with coal-fired electricity plants.
The study is published in the most recent online edition of the Journal of Mood Disorders.
"The presence of a coal-fired electricity plant correlated with airborne levels of nickel, mercury, lead, chromium, cadmium, beryllium and arsenic," Spangler said.
While prior research has evaluated the association between environmental contamination and mood disorders and suicide, coal emissions have not been looked at in this fashion, Spangler said. “This is the first study to show that the existence of coal-fired electricity plants is related to population-level suicide rates. Because suicide might be associated with environmental pollution, this study may help inform regulations not only of air pollutants, but also of coal-fired electrical power plant emissions.”
Spangler has conducted previous ecological research into environmental heavy metals, looking at their correlation to diabetes mortality, chronic liver disease death, cancer mortality and infant mortality. Spangler said the study was subject to a number of limitations because it only looked at county-level characteristics and could not control for factors in individual residents.
"Still, it raises the interesting question of whether suicide in a given population is related to the presence or absence of coal-fired electricity plants and the air quality," he said. "Further research is needed to understand what factors related to coal burning actually are at play and suggest that tighter regulation of coal-fired power plant emissions might cut down on county suicide rates in North Carolina."
(Image: David Freund)
Grammar errors? The brain detects them even when you are unaware
Your brain often works on autopilot when it comes to grammar. That theory has been around for years, but University of Oregon neuroscientists have captured elusive hard evidence that people indeed detect and process grammatical errors with no awareness of doing so.
Participants in the study — native-English speaking people, ages 18-30 — had their brain activity recorded using electroencephalography, from which researchers focused on a signal known as the Event-Related Potential (ERP). This non-invasive technique allows for the capture of changes in brain electrical activity during an event. In this case, events were short sentences presented visually one word at a time.
Subjects were given 280 experimental sentences, including some that were syntactically (grammatically) correct and others containing grammatical errors, such as “We drank Lisa’s brandy by the fire in the lobby,” or “We drank Lisa’s by brandy the fire in the lobby.” A 50 millisecond audio tone was also played at some point in each sentence. A tone appeared before or after a grammatical faux pas was presented. The auditory distraction also appeared in grammatically correct sentences.
This approach, said lead author Laura Batterink, a postdoctoral researcher, provided a signature of whether awareness was at work during processing of the errors. “Participants had to respond to the tone as quickly as they could, indicating if its pitch was low, medium or high,” she said. “The grammatical violations were fully visible to participants, but because they had to complete this extra task, they were often not consciously aware of the violations. They would read the sentence and have to indicate if it was correct or incorrect. If the tone was played immediately before the grammatical violation, they were more likely to say the sentence was correct even it wasn’t.”
When tones appeared after grammatical errors, subjects detected 89 percent of the errors. In cases where subjects correctly declared errors in sentences, the researchers found a P600 effect, an ERP response in which the error is recognized and corrected on the fly to make sense of the sentence.
When the tones appear before the grammatical errors, subjects detected only 51 percent of them. The tone before the event, said co-author Helen J. Neville, who holds the UO’s Robert and Beverly Lewis Endowed Chair in psychology, created a blink in their attention. The key to conscious awareness, she said, is based on whether or not a person can declare an error, and the tones disrupted participants’ ability to declare the errors. But, even when the participants did not notice these errors, their brains responded to them, generating an early negative ERP response. These undetected errors also delayed participants’ reaction times to the tones.
"Even when you don’t pick up on a syntactic error your brain is still picking up on it," Batterink said. "There is a brain mechanism recognizing it and reacting to it, processing it unconsciously so you understand it properly."
The study was published in the May 8 issue of the Journal of Neuroscience.
The brain processes syntactic information implicitly, in the absence of awareness, the authors concluded. “While other aspects of language, such as semantics and phonology, can also be processed implicitly, the present data represent the first direct evidence that implicit mechanisms also play a role in the processing of syntax, the core computational component of language.”
It may be time to reconsider some teaching strategies, especially how adults are taught a second language, said Neville, a member of the UO’s Institute of Neuroscience and director of the UO’s Brain Development Lab.
Children, she noted, often pick up grammar rules implicitly through routine daily interactions with parents or peers, simply hearing and processing new words and their usage before any formal instruction. She likened such learning to “Jabberwocky,” the nonsense poem introduced by writer Lewis Carroll in 1871 in “Through the Looking Glass,” where Alice discovers a book in an unrecognizable language that turns out to be written inversely and readable in a mirror.
For a second language, she said, “Teach grammatical rules implicitly, without any semantics at all, like with jabberwocky. Get them to listen to jabberwocky, like a child does.”
How Multitasking Can Improve Judgments
Research has revealed that multitasking impedes performance across a variety of tasks. Emergency room nurses that are interrupted multiple times while treating a patient can be more likely to make medication errors. Driving while speaking on a mobile phone significantly increases the probability of an automobile accident. At the same time, however, experienced golfers putt better when distracted than experienced golfers who are focusing on performance. Distractions resulting from the presence of other people can increase an individual’s performance, too. Why?
Addressing the Contradictions
In a forthcoming issue of Psychological Science, one of the world’s top-ranked empirical journals in psychology, a team of researchers from the University of Basel helps to clarify these apparent contradictions. Lead author Janina Hoffmann, a Ph.D. student in Economic Psychology, and her co-authors Dr. Bettina von Helversen and Prof. Dr. Jörg Rieskamp, find that the type of judgment strategy that an individual employs strongly conditions how the “cognitive load” induced by multitasking affects performance. Higher cognitive load can actually improve performance when the task can be best completed using a less demanding, similarity-based strategy that informs judgments by retrieving past instances from memory.
The study is supported by the findings of two experiments conducted at the University of Basel. The first study exposed 90 participants to variable cognitive loads as they were asked to solve a judgment task whose solution was best achieved through the use of a similarity-based strategy (predicting how many cartoon characters another cartoon character could catch). Most participants switched to using a similarity-based strategy and produced more accurate judgments. The second study then exposed 60 participants to a linear task whose solution was not conducive to similarity-based strategies but rather rule- based strategies. Those participants who employed a similarity-based strategy made poorer judgments. The experiments were conducted with financial support from the Swiss National Science Foundation.
Moving Forward
Cognitive load does not per se lead to worse performance, but rather it can, dependent on strategy choice, lead to better performance. The researchers believe that it is important to decipher cognitive strategies that people choose under given levels of cognitive load. Hoffmann claims, “A better understanding of these cognitive strategies may permit future studies to predict the precise circumstances under which people can solve a problem particularly well.”
Brain frontal lobes not sole centre of human intelligence
Human intelligence cannot be explained by the size of the brain’s frontal lobes, say researchers.
Research into the comparative size of the frontal lobes in humans and other species has determined that they are not - as previously thought - disproportionately enlarged relative to other areas of the brain, according to the most accurate and conclusive study of this area of the brain.
It concludes that the size of our frontal lobes cannot solely account for humans’ superior cognitive abilities.
The study by Durham and Reading universities suggests that supposedly more ‘primitive’ areas, such as the cerebellum, were equally important in the expansion of the human brain. These areas may therefore play unexpectedly important roles in human cognition and its disorders, such as autism and dyslexia, say the researchers.
The study is published in the Proceedings of the National Academy of Sciences (PNAS) today.
The frontal lobes are an area in the brain of mammals located at the front of each cerebral hemisphere, and are thought to be critical for advanced intelligence.
Lead author Professor Robert Barton from the Department of Anthropology at Durham University, said: “Probably the most widespread assumption about how the human brain evolved is that size increase was concentrated in the frontal lobes.
"It has been thought that frontal lobe expansion was particularly crucial to the development of modern human behaviour, thought and language, and that it is our bulging frontal lobes that truly make us human. We show that this is untrue: human frontal lobes are exactly the size expected for a non-human brain scaled up to human size.
"This means that areas traditionally considered to be more primitive were just as important during our evolution. These other areas should now get more attention. In fact there is already some evidence that damage to the cerebellum, for example, is a factor in disorders such as autism and dyslexia."
The scientists argue that many of our high-level abilities are carried out by more extensive brain networks linking many different areas of the brain. They suggest it may be the structure of these extended networks more than the size of any isolated brain region that is critical for cognitive functioning.
Previously, various studies have been conducted to try and establish whether humans’ frontal lobes are disproportionately enlarged compared to their size in other primates such as apes and monkeys. They have resulted in a confused picture with use of different methods and measurements leading to inconsistent findings.
The Durham and Reading researchers, funded by The Leverhulme Trust, analysed data sets from previous animal and human studies using phylogenetic, or ‘evolutionary family tree’, methods, and found consistent results across all their data. They used a new method to look at the speed with which evolutionary change occurred, concluding that the frontal lobes did not evolve especially fast along the human lineage after it split from the chimpanzee lineage.
(Source: eurekalert.org)
Serotonin Mediates Exercise-Induced Generation of New Neurons
Mice that exercise in running wheels exhibit increased neurogenesis in the brain. Crucial to this process is serotonin signaling. These are the findings of a study by Dr. Friederike Klempin, Daniel Beis and Dr. Natalia Alenina from the research group led by Professor Michael Bader at the Max Delbrück Center (MDC) Berlin-Buch. Surprisingly, mice lacking brain serotonin due to a genetic mutation exhibited normal baseline neurogenesis. However, in these serotonin-deficient mice, activity-induced proliferation was impaired, and wheel running did not induce increased generation of new neurons. (Journal of Neuroscience)
Scientists have known for some time that exercise induces neurogenesis in a specific brain region, the hippocampus. However, until this study, the underlying mechanism was not fully understood. The hippocampus plays an important role in learning and in memory and is one of the brain regions where new neurons are generated throughout life.
Serotonin facilitates precursor cell maturation
The researchers demonstrated that mice with the ability to produce serotonin are likely to release more of this hormone during exercise, which in turn increases cell proliferation of precursor cells in the hippocampus. Furthermore, serotonin seems to facilitate the transition of stem to progenitor cells that become neurons in the adult mouse brain.
For Dr. Klempin and Dr. Alenina it was surprising that normal baseline neurogenesis occurs in mice that, due to a genetic mutation, cannot produce serotonin in the brain. However, they noted that some of the stem cells in serotonin-deficient mice either die or fail to become neurons.
Yet, these animals seem to have a mechanism that allows compensation for the deficit, in that progenitor cells, an intermediate stage in the development from a stem cell to a neuron, divide more frequently. According to the researchers, this is to maintain the pool of these cells.
However, the group of wheel-running mice that do not produce serotonin did not exhibit an exercise-induced increase in neurogenesis. The compensatory mechanism failed following running. The researchers concluded: “Serotonin is not necessarily required for baseline generation of new neurons in the adult brain, but is essential for exercise-induced hippocampal neurogenesis.”
Hope for new approaches to treat depression and memory loss in the elderly
Deficiency in serotonin, popularly known as the “molecule of happiness”, has been considered in the context of theories linking major depression to declining neurogenesis in the adult brain. “Our findings could potentially help to develop new approaches to prevent and treat depression as well as age-related decline in learning and memory,” said Dr. Klempin and Dr. Alenina.
Out of sync with the world: Brain study shows body clocks of depressed people are altered at cell level
Finding of disrupted brain gene orchestration gives first direct evidence of circadian rhythm changes in depressed brains, opens door to better treatment
Every cell in our bodies runs on a 24-hour clock, tuned to the night-day, light-dark cycles that have ruled us since the dawn of humanity. The brain acts as timekeeper, keeping the cellular clock in sync with the outside world so that it can govern our appetites, sleep, moods and much more.
But 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.
It’s the first direct evidence of altered circadian rhythms in the brain of people with depression, and shows that they operate out of sync with the usual ingrained daily cycle. The findings, in the Proceedings of the National Academy of Sciences, come from scientists from the University of Michigan Medical School and other institutions.
The discovery was made by sifting through massive amounts of data gleaned from donated brains of depressed and non-depressed people. With further research, the findings could lead to more precise diagnosis and treatment for a condition that affects more than 350 million people worldwide.
What’s more, the research also reveals a previously unknown daily rhythm to the activity of many genes across many areas of the brain – expanding the sense of how crucial our master 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, suggesting that studying this “stopped clock” could conceivably be useful in forensics. By contrast, 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.
The work was funded in large part by the Pritzker Neuropsychiatric Disorders Research Fund, and involved researchers from the University of Michigan, University of California’s Irvine and Davis campuses, Weill Cornell Medical College, the Hudson Alpha Institute for Biotechnology, and Stanford University.
The team uses material from donated brains obtained shortly after death, along with extensive clinical information about the individual. Numerous regions of each brain are dissected by hand or even with lasers that can capture more specialized cell types, then analyzed to measure gene activity. The resulting flood of information is picked apart with advanced data-mining tools.
Lead author Jun Li, Ph.D., an assistant professor in the U-M Department of Human Genetics, describes how this approach allowed the team 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. But when the team tried to do the same in the brains of 34 depressed individuals, the gene activity was off by hours. The cells looked as if it were an entirely different time of day.
“There really was a moment of discovery,” says Li, who led the analysis of the massive amount of data generated by the rest of the team and is a research assistant professor in U-M’s Department of Computational Medicine at Bioinformatics. “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.”
Huda Akil, Ph.D., the co-director of the U-M Molecular & Behavioral Neuroscience Institute and co-director of the U-M site of the Pritzker Neuropsychiatric Disorders Research Consortium, notes that the findings go beyond previous research on circadian rhythms, using animals or human skin cells, which were more easily accessible than human brain tissues.
“Hundreds of new genes that are very sensitive to circadian rhythms emerged from this research — not just the primary clock genes that have been studied in animals or cell cultures, but other genes whose activity rises and falls throughout the day,” she says. “We were truly able to watch the daily rhythm play out in a symphony of biological activity, by studying where the clock had stopped at the time of death. And then, in depressed people, we could see how this was disrupted.”
Now, she adds, scientists must use this information to help find new ways to predict depression, fine-tune treatment for each depressed patient, and even find new medications or other types of treatment to develop and test. One possibility, she notes, could be to identify biomarkers for depression – telltale molecules that can be detected in blood, skin or hair.
And, the challenge of determining why the circadian clock is altered in depression still remains. “We can only glimpse the possibility that the disruption seen in depression may have more than one cause. We need to learn more about whether something in the nature of the clock itself is affected, because if you could fix the clock you might be able to help people get better,” Akil notes.
The team continues to mine their data for new findings, and to probe additional brains as they are donated and dissected. The high quality of the brains, and the data gathered about how their donors lived and died, is essential to the project, Akil says. Even the pH level of the tissue, which can be affected by the dying process and the time between death and freezing tissue for research, can affect the results. The team also will have access to blood and hair samples from new donors.
(Source: uofmhealth.org)
Reversing Paralysis with a Restorative Gel
Some parts of the body, like the liver, can regenerate themselves after damage. But others, such as our nervous system, are considered either irreparable or slow to recover, leaving thousands with a lifetime of pain, limited mobility, or even paralysis.
Now a team of Tel Aviv University researchers, including Dr. Shimon Rochkind of TAU’s Sackler Faculty of Medicine and Tel Aviv Sourasky Medical Center and Prof. Zvi Nevo of TAU’s Department of Human Molecular Genetics and Biochemistry, has invented a method for repairing damaged peripheral nerves. Through a biodegradable implant in combination with a newly-developed Guiding Regeneration Gel (GRG) that increases nerve growth and healing, the functionality of a torn or damaged nerve could ultimately be restored.
This innovative project is now gaining international recognition. Its initial successes were reported recently at several renowned scientific congresses, including the World Federation of Neurological Societies and the European Neurological Society. And the therapy, already tested in animal models, is only a few years away from clinical use, says Dr. Rochkind.
Like healing in the womb
A nerve is like an electrical cable. When severed or otherwise damaged, power can no longer be transferred and the cable loses its functionality. Similarly, a damaged nerve loses the ability to transfer signals for movement and feeling through the nervous system.
But Dr. Rochkind and Prof. Nevo found a way to breach the gap. In their method, two severed ends of a damaged nerve are reconnected by implanting a soft, biodegradable tube, which serves as a bridge to help the nerve ends connect. The innovative gel which lines the inside of the tube nurtures nerve fibers’ growth, encouraging the nerve to reconnect the severed ends through the tube, even in cases with massive nerve damage, Dr. Rochkind says.
The key lies in the composition of the gel, the researchers say, which has three main components: anti-oxidants, which exhibit high anti-inflammatory activities; synthetic laminin peptides, which act as a railway or track for the nerve fibers to grow along; and hyaluronic acid, commonly found in the human fetus, which serves as a buffer against drying, a major danger for most implants. These components allow the nerve to heal the way a fetus does in the womb — quickly and smoothly.
Keeping cells safe for transplant
The implant has already been tested in animal models, and the gel by itself can be used as a stand-alone product, acting as an aid to cell therapy. GRG is not only able to preserve cells, it can support their survival while being used for therapy and transplantation, says Dr. Rochkind. When grown in the gel, cells show excellent development, as well as intensive fiber growth. This could have implications for the treatment of diseases such as Parkinson’s, for which researchers are actively exploring cell therapy as a potential solution.
Scientists develop drug that slows Alzheimer’s in mice
A drug developed by scientists at the Salk Institute for Biological Studies, known as J147, reverses memory deficits and slows Alzheimer’s disease in aged mice following short-term treatment. The findings, published May 14 in the journal Alzheimer’s Research and Therapy, may pave the way to a new treatment for Alzheimer’s disease in humans.
"J147 is an exciting new compound because it really has strong potential to be an Alzheimer’s disease therapeutic by slowing disease progression and reversing memory deficits following short-term treatment," says lead study author Marguerite Prior, a research associate in Salk’s Cellular Neurobiology Laboratory.
Despite years of research, there are no disease-modifying drugs for Alzheimer’s. Current FDA-approved medications, including Aricept, Razadyne and Exelon, offer only fleeting short-term benefits for Alzheimer’s patients, but they do nothing to slow the steady, irreversible decline of brain function that erases a person’s memory and ability to think clearly.
According to the Alzheimer’s Association, more than 5 million Americans are living with Alzheimer’s disease, the sixth leading cause of death in the country and the only one among the top 10 that cannot be prevented, cured or even slowed.
J147 was developed at Salk in the laboratory of David Schubert, a professor in the Cellular Neurobiology Laboratory. He and his colleagues bucked the trend within the pharmaceutical industry, which has focused on the biological pathways involved in the formation of amyloid plaques, the dense deposits of protein that characterize the disease. Instead, the Salk team used living neurons grown in laboratory dishes to test whether their new synthetic compounds, which are based upon natural products derived from plants, were effective at protecting brain cells against several pathologies associated with brain aging. From the test results of each chemical iteration of the lead compound, they were able to alter their chemical structures to make them much more potent. Although J147 appears to be safe in mice, the next step will require clinical trials to determine whether the compound will prove safe and effective in humans.
"Alzheimer’s disease research has traditionally focused on a single target, the amyloid pathway," says Schubert, "but unfortunately drugs that have been developed through this pathway have not been successful in clinical trials. Our approach is based on the pathologies associated with old age-the greatest risk factor for Alzheimer’s and other neurodegenerative diseases-rather than only the specificities of the disease."
To test the efficacy of J147 in a much more rigorous preclinical Alzheimer’s model, the Salk team treated mice using a therapeutic strategy that they say more accurately reflects the human symptomatic stage of Alzheimer’s. Administered in the food of 20-month-old genetically engineered mice, at a stage when Alzheimer’s pathology is advanced, J147 rescued severe memory loss, reduced soluble levels of amyloid, and increased neurotrophic factors essential for memory, after only three months of treatment.
In a different experiment, the scientists tested J147 directly against Aricept, the most widely prescribed Alzheimer’s drug, and found that it performed as well or better in several memory tests.
"In addition to yielding an exceptionally promising therapeutic, both the strategy of using mice with existing disease and the drug discovery process based upon aging are what make the study interesting and exciting," says Schubert, "because it more closely resembles what happens in humans, who have advanced pathology when diagnosis occurs and treatment begins." Most studies test drugs before pathology is present, which is preventive rather than therapeutic and may be the reason drugs don’t transfer from animal studies to humans.
Prior and her colleagues say that several cellular processes known to be associated with Alzheimer’s pathology are affected by J147, including an increase in a protein called brain-derived neurotrophic factor (BDNF), which protects neurons from toxic insults, helps new neurons grow and connect with other brain cells, and is involved in memory formation. Postmortem studies show lower than normal levels of BDNF in the brains of people with Alzheimer’s.
Because of its broad ability to protect nerve cells, the researchers believe that J147 may also be effective for treating other neurological disorders, such as Parkinson’s disease, Huntington’s disease and amyotrophic lateral sclerosis (ALS), as well as stroke, although their study did not directly explore the drug’s efficacy as a therapy for those diseases.
The Salk researchers say that J147, with its memory enhancing and neuroprotective properties, along with its safety and availability as an oral medication, would make an “ideal candidate” for Alzheimer’s disease clinical trials. They are currently seeking funding for such a trial.
Stroke turned ex-con into rhyming painter
Name: Tommy McHugh
Disorder: Sudden artistic output following brain damage
"I was sitting on the toilet. I suddenly felt an explosion in the left side of my head and ended up on the floor. I think the only thing that kept me conscious was that I didn’t want to be found with my pants down. Then the other side of my head went bang! I woke up in hospital and looked out of the window to see the tree was sprouting numbers. 3, 6, 9. Then I started talking in rhyme…"
Ten days after having a subarachnoid haemorrhage – a stroke caused by bleeding in and around the brain – Tommy McHugh, an ex-con who’d been in his fair share of scraps, became a new man, with a personality that nobody recognised.
When he was a young man, Tommy did time in prison. But after his stroke at age 51, everything changed. “I could taste the femininity inside of myself,” he said. “My head was full of rhymes and images and pictures.”
Not only did he feel a sudden urge to write poetry, but he also began to paint and draw obsessively for up to 19 hours a day. He was never artistic before – in fact, he joked that he’d never even been in an art gallery “except to maybe steal something”.
Desperate to find out what was going on, Tommy wrote to several neuroscientists and end up working closely with Alice Flaherty at Harvard Medical School and Mark Lythgoe at University College London.
Going Zen
Flaherty says the haemorrhage sent blood squirting around the brain surface, affecting a lot of areas. It left Tommy unusually emotional and unable to hurt anyone, “like Zen monks sweeping steps before they walk,” says Flaherty. “Everything strikes him as beautiful and cosmically meaningful.”
Scanning Tommy’s brain was impossible after an operation to treat the stroke damage left him with a piece of metal in his head. Instead, Lythgoe performed a neuropsychological evaluation. Tommy’s IQ was in the normal range. However, he showed verbal disinhibition – he tended to talk a lot – and had difficulty with tests that required him to switch between different cognitive tasks. All of which suggested problems with the frontal lobes.
The frontal lobes play a vital role in abstract thought and creativity. They are constantly bombarded with raw sensory data from the world around us, most of which is deemed irrelevant by the brain and screened from conscious awareness. Blocking this inhibition using magnetic pulses can make people more creative, even unleashing savant-like skills.
"That’s what Tommy’s mind does all the time," says Lythgoe. Everything he heard and saw triggered a stream of associations that he found difficult to stop. Tommy saw it as having a brain that shows him "endless, endless corridors". He said his paintings represented a snapshot of a millisecond in his brain.
"I’ll paint three or six or nine pictures at a time. I see those numbers in my head all the time. Canvases became too costly, so I started painting the ceilings and the wallpaper and the floor. I can’t stop painting and sculpting. Give me a mountain and I’ll turn it into a profile. If you give me a bare tree I’ll change it, so when spring come all the leaves will create the face, the mouth, the lips. Without hurting the tree."
Offering advice for others with brain damage, he said that people who have had strokes need to learn not to think of themselves as ill, with the dangers of depression that can bring. “Some repairs to the brain are constructive, some are negative. One has to learn to develop one’s damaged brain, adapt and start to live again. You can either sit on your bum or look in the mirror and say ‘I’m alive’.”
He wouldn’t even have wanted his old mind back: “The most wonderful thing that happened to Tommy McHugh,” he laughed, “is having a stroke while doing a poo.”
He wouldn’t have changed a thing. “My two strokes have given me 11 years of a magnificent adventure that nobody could have expected.”
Tommy McHugh passed away on 19 September 2012, having spoken to New Scientist several times that year. Samples of his artwork can be viewed on his website.
To suppress or to explore? Emotional strategy may influence anxiety
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.
The study appears in the journal Emotion.
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."