Posts tagged neuroscience
Articles and news from the latest research reports.
Stimulating brain cells stops binge drinking, animal study finds
Researchers at the University at Buffalo have found a way to change alcohol drinking behavior in rodents, using the emerging technique of optogenetics, which uses light to stimulate neurons.
Their work could lead to powerful new ways to treat alcoholism, other addictions, and neurological and mental illnesses; it also helps explain the underlying neurochemical basis of drug addiction.
The findings, published in November in Frontiers in Neuroscience, are the first to demonstrate a causal relationship between the release of dopamine in the brain and drinking behaviors of animals. Research like this, which makes it possible to map the neuronal circuits responsible for specific behaviors, is a major focus of President Obama’s Brain Research for Advancing Innovative Neurotechnologies initiative, known as BRAIN.
In the experiments, rats were trained to drink alcohol in a way that mimics human binge-drinking behavior.
First author Caroline E. Bass, PhD, assistant professor of pharmacology and toxicology in the UB School of Medicine and Biomedical Sciences explains: “By stimulating certain dopamine neurons in a precise pattern, resulting in low but prolonged levels of dopamine release, we could prevent the rats from binging. The rats just flat out stopped drinking,” she says.
Bass’s co-authors are at Wake Forest University, where she worked previously.
Interestingly, the rodents continued to avoid alcohol even after the stimulation of neurons ended, she adds.
“For decades, we have observed that particular brain regions light up or become more active in an alcoholic when he or she drinks or looks at pictures of people drinking, for example, but we didn’t know if those changes in brain activity actually governed the alcoholic’s behavior,” says Bass.
The researchers activated the dopamine neurons through a type of deep brain stimulation, but unlike techniques now used to treat certain neurological disorders, such as severe tremors in Parkinson’s disease patients, this new technique, called optogenetics, uses light instead of electricity to stimulate neurons.
“Electrical stimulation doesn’t discriminate,” Bass explains. “It hits all the neurons, but the brain has many different kinds of neurons, with different neurotransmitters and different functions. Optogenetics allows you to stimulate only one type of neuron at a time.”
Bass specializes in using viral vectors to study the brain in substance abuse. In this study, she used a virus to introduce a gene encoding a light-responsive protein into the animals’ brains. That protein then activated a specific subpopulation of dopamine neurons in the brain’s reward system.
“I created a virus that will make this protein only in dopaminergic neurons,” Bass says.
The neuronal pathways affected in this research are involved in many neurological disorders, she says. For that reason, the results have application not only in understanding and treating alcohol-drinking behaviors in humans, but also in many devastating mental illnesses and neurological diseases that have a dopamine component.
Bass notes that this ability to target genes to dopamine neurons could potentially lead to the use of gene therapy in the brain to mitigate many of these disorders.
“We can target dopamine neurons in a part of the brain called the nigrostriatal pathway, which is what degenerates in Parkinson’s disease,” she says. “If we could infuse a viral vector into that part of the brain, we could target potentially therapeutic genes to the dopamine neurons involved in Parkinson’s. And by infusing the virus into other areas of the brain, we could potentially deliver therapeutic genes to treat other neurological diseases and mental illnesses, including schizophrenia and depression.”
Researchers report technique that enables patient with ‘word blindness’ to read again
In the journal Neurology, researchers report a novel technique that enables a patient with “word blindness” to read again.
Word blindness is a rare neurological condition. (The medical term is “alexia without agraphia.”) Although a patient can write and understand the spoken word, the patient is unable to read.
The article is written by Jason Cuomo, Murray Flaster, MD, PhD and Jose Biller, MD, of Loyola University Medical Center.
Here’s how the technique works: When shown a word, the patient looks at the first letter. Although she clearly sees it, she cannot recognize it. So beginning with the letter A, she traces each letter of the alphabet over the unknown letter until she gets a match. For example, when shown the word Mother, she will trace the letters of the alphabet, one at a time, until she comes to M and finds a match. Three letters later, she guesses correctly that the word is Mother.
"To see this curious adaption in practice is to witness the very unique and focal nature" of the deficit, the authors write.
The authors describe how word blindness came on suddenly to a 40-year-old kindergarten teacher and reading specialist. She couldn’t make sense of her lesson plan, and her attendance sheet was as incomprehensible as hieroglyphs. She also couldn’t tell time.
The condition was due to a stroke that probably was caused by an unusual type of blood vessel inflammation within the brain called primary central nervous system angiitis.
Once a passionate reader, she was determined to learn how to read again. But none of the techniques that she had taught her students – phonics, sight words, flash cards, writing exercises, etc. – worked. So she taught herself a remarkable new technique that employed tactile skills that she still possessed.
The woman can have an emotional reaction to a word, even if she can’t read it. Shown the word “dessert,” she says “Oooh, I like that.” But when shown “asparagus,” she says, “Something’s upsetting me about this word.”
Shown two personal letters that came in the mail, she correctly determined which was sent by a friend of her mother’s and which was sent by one of her own friends. “When asked who these friends were, she could not say, but their names nevertheless provoked an emotional response that served as a powerful contextual clue,” the authors write.
What she most misses is reading books to children. She teared up as she told the authors: “One day my mom was with the kids in the family, and they were all curled up next to each other, and they were reading. And I started to cry, because that was something I couldn’t do.”
(Source: eurekalert.org)
Brain training works, but just for the practiced task
Search for “brain training” on the Web. You’ll find online exercises, games, software, even apps, all designed to prepare your brain to do better on any number of tasks. Do they work? University of Oregon psychologists say, yes, but “there’s a catch.”
The catch, according to Elliot T. Berkman, a professor in the Department of Psychology and lead author on a study published in the Jan. 1 issue of the Journal of Neuroscience, is that training for a particular task does heighten performance, but that advantage doesn’t necessarily carry over to a new challenge.
The training provided in the study caused a proactive shift in inhibitory control. However, it is not clear if the improvement attained extends to other kinds of executive function such as working memory, because the team’s sole focus was on inhibitory control, said Berkman, who directs the psychology department’s Social and Affective Neuroscience Lab.
"With training, the brain activity became linked to specific cues that predicted when inhibitory control might be needed," he said. "This result is important because it explains how brain training improves performance on a given task — and also why the performance boost doesn’t generalize beyond that task."
Sixty participants (27 male, 33 females and ranging from 18 to 30 years old) took part in a three-phase study. Change in their brain activity was monitored with functional magnetic resonance imaging (fMRI).
Half of the subjects were in the experimental group that was trained with a task that models inhibitory control — one kind of self-control — as a race between a “go” process and a “stop” process. A faster stop process indicates more efficient inhibitory control.
In each of a series of trials, participants were given a “go” signal — an arrow pointing left or right. Subjects pressed a key corresponding to the direction of the arrow as quickly as possible, launching the go process. However, on 25 percent of the trials, a beep sounded after the arrow appeared, signaling participants to withhold their button press, launching the stop process.
Participants practiced either the stop-signal task or a control task that didn’t affect inhibitory control every other day for three weeks. Performance improved more in the training group than in the control group.
Neural activity was monitored using functional magnetic resonance imaging (fMRI), which captures changes in blood oxygen levels, during a stop-signal task. MRI work was done in the UO’s Robert and Beverly Lewis Center for Neuroimaging. Activity in the inferior frontal gyrus and anterior cingulate cortex — brain regions that regulate inhibitory control — decreased during inhibitory control but increased immediately before it in the training group more than in the control group.
The fMRI results identified three regions of the brain of the trained subjects that showed changes during the task, prompting the researchers to theorize that emotional regulation may have been improved by reducing distress and frustration during the trials. Overall, the size of the training effect is small. A challenge for future research, they concluded, will be to identify protocols that might generate greater positive and lasting effects.”Researchers at the University of Oregon are using tools and technologies to shed new light on important mechanisms of cognitive functioning such as executive control,” said Kimberly Andrews Espy, vice president for research and innovation and dean of the UO Graduate School. “This revealing study on brain training by Dr. Berkman and his team furthers our understanding of inhibitory control and may lead to the design of better prevention tools to promote mental health.”
Molecule discovered that protects the brain from cannabis intoxication
Two INSERM research teams led by Pier Vincenzo Piazza and Giovanni Marsicano (INSERM Unit 862 “Neurocentre Magendie” in Bordeaux) recently discovered that pregnenolone, a molecule produced by the brain, acts as a natural defence mechanism against the harmful effects of cannabis in animals. Pregnenolone prevents THC, the main active principle in cannabis, from fully activating its brain receptor, the CB1 receptor, that when overstimulated by THC causes the intoxicating effects of cannabis. By identifying this mechanism, the INSERM teams are already developing new approaches for the treatment of cannabis addiction.
These results are to be published in Science on 3 January.
Over 20 million people around the world are addicted to cannabis, including a little more than a half million people in France. In the last few years, cannabis addiction has become one of the main reasons for seeking treatment in addiction clinics. Cannabis consumption is particularly high (30%) in individuals between 16 to 24 years old, a population that is especially susceptible to the harmful effects of the drug.
While cannabis consumers are seeking a state of relaxation, well-being and altered perception, there are many dangers associated to a regular consumption of cannabis. Two major behavioural problems are associated with regular cannabis use in humans: cognitive deficits and a general loss of motivation. Thus, in addition to being extremely dependent on the drug, regular users of cannabis show signs of memory loss and a lack of motivation that make quite hard their social insertion.
The main active ingredient in cannabis, THC, acts on the brain through CB1 cannabinoid receptors located in the neurons. THC binds to these receptors diverting them from their physiological roles, such as regulating food intake, metabolism, cognitive processes and pleasure. When THC overstimulates CB1 receptors, it triggers a reduction in memory abilities, motivation and gradually leads to dependence.
Increase of dopamine release
Developing an efficient treatment for cannabis addiction is becoming a priority of research in the fiend of drug addiction.
In this context, the INSERM teams led by Pier Vincenzo Piazza and Giovanni Marsicano have investigated the potential role of pregnenolone a brain produced steroid hormone. Up to now, pregnenolone was considered the inactive precursor used to synthesize all the other steroid hormones (progesterone, estrogens, testosterone, etc.). The INSERM researchers have now discovered that pregnenolone has quite an important functional role: it provide a natural defence mechanism that can protect the brain from the harmful effects of cannabis.
Essentially, when high doses of THC (well above those inhaled by regular users) activate the CB1 cannabinoid receptor they also trigger the synthesis of pregnenolone. Pregnenole then binds to a specific site on the same CB1 receptors (see figure) and reducing the effects of THC.
The administration of pregnenolone at doses that increase the brain’s level of this hormone even more, antagonize the behavioral effects of cannabis.
At the neurobiological level, pregnenolone greatly reduces the release of dopamine triggered by THC. This is an important effect, since the addictive effects of drugs involve an excessive release of dopamine.
This negative feedback mediated by pregnenolone (THC is what triggers the production of pregnenolone, which then inhibits the effects of THC) reveal a previously unknown endogenous mechanism that protects the brain from an over-activation of CB1 receptor.
A protective mechanism that opens the doors to a new therapeutic approach.
The role of pregnenolone was discovered when, rats were given equivalent doses of cocaine, morphine, nicotine, alcohol and cannabis and the levels of several brain steroids (pregnenolone, testosterone, allopregnenolone, DHEA etc..) were measured. It was then found that only one drug, THC, increased brain steroids and more specifically selectively one steroid, pregnenolone, that went up3000% for a period of two hours.
The effect of administering THC on the pregnenolone synthesis (PREG) and other brain steroids
This increase in pregnenolone is a built-in mechanism that moderates the effects of THC. Thus, the effects of THC increase when pregnenolone synthesis is blocked. Conversely, when pregnenolone is administered to rats or mice at doses (2-6 mg/kg) that induce even greater concentrations of the hormone in the brain, the negative behavioural effects of THC are blocked. For example, the animals that were given pregnenolone recover their normal memory abilities, are less sedated and less incline to self-administer cannabinoids.
Experiments conducted in cell cultures that express the human CB1 receptor confirm that pregnenolone can also counteract the molecular action of THC in humans.
Pier Vincenzo Piazza explains that pregnenolone itself cannot be used as a treatment “Pregnenolone cannot be used as a treatment because it is badly absorbed when administerd orally and once in the blood stream it is rapidly transformed in other steroids”.
However, the researcher says that there is strong hope of seeing a new addiction therapy emerge from this discovery. “We have now developed derivatives of pregnenolone that are well absorbed and stable. They then present the characteristics of compounds that can be used as new class of therapeutic drugs. We should be able to begin clinical trials soon and verify whether we have indeed discovered the first pharmacological treatment for cannabis dependence.”
Odor receptors discovered in lungs
Your nose is not the only organ in your body that can sense cigarette smoke wafting through the air. Scientists at Washington University in St. Louis and the University of Iowa have shown that your lungs have odor receptors as well.
Unlike the receptors in your nose, which are located in the membranes of nerve cells, the ones in your lungs are in the membranes of neuroendocrine cells. Instead of sending nerve impulses to your brain that allow it to “perceive” the acrid smell of a burning cigarette somewhere in the vicinity, they trigger the flask-shaped neuroendocrine cells to dump hormones that make your airways constrict.
The newly discovered class of cells expressing olfactory receptors in human airways, called pulmonary neuroendocrine cells, or PNECs, were found by a team led by Yehuda Ben-Shahar, PhD, assistant professor of biology, in Arts & Sciences, and of medicine at Washington University in St. Louis, and including colleagues Steven L. Brody, MD, and Michael J. Holtzman, MD, of the Washington University School of Medicine, and Michel J. Welsh, MD, of the University of Iowa Carver College of Medicine.
“We forget,” said Ben-Shahar, “that our body plan is a tube within a tube, so our lungs and our gut are open to the external environment. Although they’re inside us, they’re actually part of our external layer. So they constantly suffer environmental insults,” he said, “and it makes sense that we evolved mechanisms to protect ourselves.”
In other words, the PNECs, described in the March issue of the American Journal of Respiratory Cell and Molecular Biology, are sentinels, guards whose job it is to exclude irritating or toxic chemicals.
The cells might be responsible for the chemical hypersensitivity that characterizes respiratory diseases, such as chronic obstructive pulmonary disease (COPD) and asthma. Patients with these diseases are told to avoid traffic fumes, pungent odors, perfumes and similar irritants, which can trigger airway constriction and breathing difficulties.
The odor receptors on the cells might be a therapeutic target, Ben-Shahar suggests. By blocking them, it might be possible to prevent some attacks, allowing people to cut down on the use of steroids or bronchodilators.
Every breath you take
When a mammal inhales, volatile chemicals flow over two patches of specialized epithelial tissue high up in the nasal passages. These patches are rich in nerve cells with specialized odorant-binding molecules embedded in their membranes.
If a chemical docks on one of these receptors, the neuron fires, sending impulses along the olfactory nerve to the olfactory bulb in the brain, where the signal is integrated with those from hundreds of other similar cells to conjure the scent of old leather or dried lavender.
Aware that airway diseases are characterized by hypersensitivity to volatile stimuli, Ben-Shahar and his colleagues realized that the lungs, like the nose, must have some means of detecting inhaled chemicals.
Earlier, a team at the University of Iowa, where Ben-Shahar was a postdoctoral research associate, had searched for genes expressed by patches of tissue from lung transplant donors. They found a group of ciliated cells that express bitter taste receptors. When offending substances were detected, the cilia beat more strongly to sweep them out of the airway. This result was featured on the cover of the Aug. 28, 2009, issue of Science.
But since people are sensitive to many inhaled substances, not just bitter ones, Ben-Shahar decided to look again. This time he found that these tissues also express odor receptors, not on ciliated cells but instead on neuroendocrine cells, flask-shaped cells that dump serotonin and various neuropeptides when they are stimulated.
This made sense. “When people with airway disease have pathological responses to odors, they’re usually pretty fast and violent,” said Ben-Shahar. “Patients suddenly shut down and can’t breathe, and these cells may explain why.”
Ben-Shahar stresses the differences between chemosensation in the nose and in the lung. The cells in the nose are neurons, he points out, each with a narrowly tuned receptor, and their signals must be woven together in the brain to interpret our odor environment.
The cells in the airways are secretory, not neuronal, cells, and they may carry more than one receptor, so they are broadly tuned. Instead of sending nerve impulses to the brain, they flood local nerves and muscles with serotonin and neuropeptides. “They are possibly designed,” he said, “to elicit a rapid, physiological response if you inhale something that is bad for you.”
The different mechanisms explain why cognition plays a much stronger role in taste and smell than in coughing in response to an irritant. It is possible, for example, to develop a taste for beer. But nobody learns not to cough; the response is rapid and largely automatic.
The scientists suspect these pulmonary neuroscretory cells contribute to the hypersensitivity of patients with COPD to airborne irritants. COPD is a group of diseases, including emphysema, that is characterized by coughing, wheezing, shortness of breath and chest tightness.
When the scientists looked at the airway tissues from patients with COPD, they discovered that they had more of these neurosecretory cells than airway tissues from healthy donors.
Of mice and men
As a geneticist, Ben-Shahar would like to go farther, knocking out genes to make sure that the derangement of neurosecretory cells isn’t just correlated with airway diseases but instead suffices to produce it.
But there is a problem. “For example, a liver from a mouse and a liver from a human are pretty similar, they express the same types of cells. But the lungs from different mammalian species are often very different; you can see it at a glance,” Ben-Shahar said.
“Clearly, primates have evolved distinct cell lineages and signaling systems for respiratory-specific functions.”
This makes it challenging to unravel the biomolecular mechanisms of respiratory diseases.
Still, he is hopeful that the PNEC pathways will provide targets for drugs that would better control asthma, COPD and other respiratory diseases. They would be welcome. There has been a steep rise in these diseases in the past few decades, treatment options have been limited, and there are no cures.
Want a good night’s sleep in the new year? Quit smoking
As if cancer, heart disease and other diseases were not enough motivation to make quitting smoking your New Year’s resolution, here’s another wake-up call: New research published in the January 2014 issue of The FASEB Journal suggests that smoking disrupts the circadian clock function in both the lungs and the brain. Translation: Smoking ruins productive sleep, leading to cognitive dysfunction, mood disorders, depression and anxiety.
"This study has found a common pathway whereby cigarette smoke impacts both pulmonary and neurophysiological function. Further, the results suggest the possible therapeutic value of targeting this pathway with compounds that could improve both lung and brain functions in smokers," said Irfan Rahman, Ph.D., a researcher involved in the work from the Department of Environmental Medicine at the University of Rochester Medical Center in Rochester, N.Y. "We envisage that our findings will be the basis for future developments in the treatment of those patients who are suffering with tobacco smoke-mediated injuries and diseases.
Rahman and colleagues found that tobacco smoke affects clock gene expression rhythms in the lung by producing parallel inflammation and depressed levels of brain locomotor activity. Short- and long- term smoking decreased a molecule known as SIRTUIN1 (SIRT1, an anti-aging molecule) and this reduction altered the level of the clock protein (BMAL1) in both lung and brain tissues in mice. A similar reduction was seen in lung tissue from human smokers and patients with chronic obstructive pulmonary disease (COPD). They made this discovery using two groups of mice which were placed in smoking chambers for short-term and long-term tobacco inhalation. One of the groups was exposed to clean air only and the other was exposed to different numbers of cigarettes during the day. Researchers monitored their daily activity patterns and found that these mice were considerably less active following smoke exposure.
Scientists then used mice deficient in SIRT1 and found that tobacco smoke caused a dramatic decline in activity but this effect was attenuated in mice that over expressed this protein or were treated with a small pharmacological activator of the anti-aging protein. Further results suggest that the clock protein, BMAL1, was regulated by SIRT1, and the decrease in SIRT1 damaged BMAL1, resulting in a disturbance in the sleep cycle/molecular clock in mice and human smokers. However, this defect was restored by a small molecule activator of SIRT1.
"If you only stick to one New Year’s resolution this year, make it quitting smoking," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “Only Santa Claus has a list longer than that of the ailments caused or worsened by smoking. If you like having a good night’s sleep, then that’s just another reason to never smoke.”
Going from Good to Great with Complex Tasks
It is a common belief that consciously thinking about what we are doing interferes with our performance. The origins of this idea go far back. Consider, for instance, the centipede’s dilemma:
A centipede was happy – quite!
Until a toad in fun
Said, “Pray, which leg moves after which?”
This raised her doubts to such a pitch,
She fell exhausted in the ditch
Not knowing how to run.
The centipede performs a very complex task with ease, unless she thinks about the task. The story was thought to illustrate something fundamental about human nature. English psychologist George Humphrey wrote “[the poem] contains a profound truth which is illustrated daily in the lives of all of us.” Humphrey and others thought that not having to think about everything that we do provides a great advantage. According to the famed philosopher Alfred North Whitehead, “Civilization advances by extending the number of important operations which we can perform without thinking about them.” Whitehead believed that thinking must be reserved only for decisive moments.
Though common, this idea is misleading. It is never optimal to run on autopilot. Even the motor tasks that we have learned to do fluently without much cognitive control are better performed while engaged. The key is to realize that we can apply cognitive control at a higher level. Moreover, gaining fluency at a motor task often comes at a cost. The cost is rigidity and deliberately breaking the flow in response to changing contexts often pays off. Musicians, athletes, public speakers, architects, designers, and others whose jobs require complex sequential actions can increase their performance if they understand that they are not trapped in the centipede’s dilemma.
In a fascinating paper, Brain researchers Eitan Globerson and Israel Nelken started with the observation that piano playing involves a very complex sequential motor task. The task is often executed in speeds that do not allow cognitive control of individual muscle movements. Through practice, pianists learn to execute fast and complex motor tasks with little cognitive control. Once this is achieved, it is possible to play in a disengaged way with little cognitive involvement. However, Globerson and Nelken suggest another way. Instead of focusing on individual finger movements or not focusing on anything, pianists may focus on higher-level mental events, such as the character of a longer musical phrase. This allows constant engagement with the music making and deliberate control without disrupting the mechanics of playing. Globerson and Nelken argue that this may dramatically improve performance.
If we follow their argument, it is easy to come up with our own examples about how to use higher-level cognitive control. While playing, a pianist may actively focus on the relationships between different musical ideas. A public speaker may develop a “mental script” that includes bigger-picture ideas, the connections between those ideas, where the climax of the speech should be, and what general effects should the speech make on the audience. During the speech, the public speaker may be constantly engaged with this mental script instead of trying to select words individually or mechanically replicating a previous performance. While shooting, a basketball player may focus on the arc that the ball should follow instead of focusing on arm movements or focusing on nothing. You can create your own examples of higher-level cognitive control for dancing, driving a car, designing a house, or doing the work of a carpenter.
Experts have long been aware of the power of focusing on higher-level mental processes. In 1924, Russian pianist and piano teacher Josef Lhevinne wrote the book Basic Principles in Pianoforte Playing, which later became a classic. In his discussion of memory, he wrote, “the thing to remember is the thought, not the symbols. When you remember a poem you do not remember the alphabetical symbols, but the poet’s beautiful vision, his thought pictures. … Get the thought, the composer’s idea; that is the thing that sticks.”
Higher-level cognitive control is capable of changing the motor action in a beneficial way. When a pianist decides to play a passage in an expressive fashion, for instance, this high-level command changes the character of playing through initiating a sequence of associated motor movements. There is experimental evidence that suggests that performance in highly automatized tasks can be improved by increasing the level of engagement. Musicians in symphony orchestras are typically asked to play the same pieces many times over the course of their careers. The playing of these pieces becomes mostly automatic; and the job satisfaction of orchestra players is typically dismal. Psychologists Ellen Langer, Timothy Russell, and Noah Eisenkraft recently asked a symphony orchestra to record, under different experimental conditions, the finale from Brahms’s Symphony No. 1. A local community chorus listened to and rated the recordings. The musicians were either asked to replicate a previous fine performance or to offer “subtle new nuances” to their performance. Musicians enjoyed the latter performance more; and the majority of the listeners preferred the recording of the latter performance.
There is always an unconscious component of the link between our intentions and the motor actions those intentions create. Even if I deliberately stretch my arm to grab a coffee mug, I do not have conscious control over the way the individual muscles in my arm operate to give rise to the specific stretching movement. Deliberate cognitive control is always less complex than the actual motor action. However, we often learn to apply cognitive control in an even more summary-like way. That is, we can learn to apply cognitive control in a single step over longer and more complex sequences of motor actions. Through practice, sequences of motor actions merge into a single unit that can be initiated by a single deliberate command. This is often called chunking. When children first learn how to brush their teeth or lace their shoes, they deliberately control individual movements that make up the task. After some practice, the individual movements are chunked and the whole sequence can be initiated by a single mental command. Many other daily activities such as riding a bike or writing one’s signature involve chunking. It is possible to merge chunked sequences into even longer sequences and reduce cognitive involvement even more.
Once initiated, a chunked motor sequence is executed automatically. As a consequence, we lose control over individual movements. This type of rigidity is often undesirable because we live in a constantly changing environment. In her book The Power of Mindful Learning Harvard psychologist Ellen Langer talks about how automaticity may get in the way of adapting to new circumstances. Overlearned driving skills may put one in danger while driving in a different country or in different weather conditions. Holding a baseball bat in the same overlearned way after getting older or stronger will hinder performance.
We can disrupt automaticity and appropriately respond to the situation at hand by orienting ourselves in the present and being sensitive to different contexts. We can think at a level higher than the mechanics of the motor action. We can be engaged with the task by making use of these two approaches simultaneously. In any case, thinking should never be reserved.
Disease and sleep: Recent studies find new links
One in five U.S. adults shows signs of chronic sleep deprivation, and a shortage of sleep has been linked to health problems as different as diabetes and Alzheimer’s disease. Recent studies have found some interesting connections between illness and what is happening in our brains as we snooze.
A new study from Uppsala University, Sweden, shows that one night of sleep deprivation increases morning blood concentrations of NSE and S-100B in healthy young men. These molecules are typically found in the brain. Thus, their rise in blood after sleep loss may indicate that a lack of snoozing might be conducive to a loss of brain tissue. The findings are published in the journal SLEEP.
Fifteen normal-weight men participated in the study. In one condition they were sleep-deprived for one night, while in the other condition they slept for approximately 8 hours.
“We observed that a night of total sleep loss was followed by increased blood concentrations of NSE and S-100B. These brain molecules typically rise in blood under conditions of brain damage. Thus, our results indicate that a lack of sleep may promote neurodegenerative processes”, says sleep researcher Christian Benedict at the Department of Neuroscience, Uppsala University, who lead the study.
“In conclusion, the findings of our trial indicate that a good night’s sleep may be critical for maintaining brain health”, says Christian Benedict.
Alcohol, tobacco, drug use far higher in severely mentally ill
In the largest ever assessment of substance use among people with severe psychiatric illness, researchers at Washington University School of Medicine in St. Louis and the University of Southern California have found that rates of smoking, drinking and drug use are significantly higher among those who have psychotic disorders than among those in the general population.
The study is published online in the journal JAMA Psychiatry.
The finding is of particular concern because individuals with severe mental illness are more likely to die younger than people without severe psychiatric disorders.
“These patients tend to pass away much younger, with estimates ranging from 12 to 25 years earlier than individuals in the general population,” said first author Sarah M. Hartz, MD, PhD, assistant professor of psychiatry at Washington University. “They don’t die from drug overdoses or commit suicide — the kinds of things you might suspect in severe psychiatric illness. They die from heart disease and cancer, problems caused by chronic alcohol and tobacco use.”
The study analyzed smoking, drinking and drug use in nearly 20,000 people. That included 9,142 psychiatric patients diagnosed with schizophrenia, bipolar disorder or schizoaffective disorder — an illness characterized by psychotic symptoms such as hallucinations and delusions, and mood disorders such as depression.
The investigators also assessed nicotine use, heavy drinking, heavy marijuana use and recreational drug use in more than 10,000 healthy people without mental illness.
The researchers found that 30 percent of those with severe psychiatric illness engaged in binge drinking, defined as drinking four servings of alcohol at one time. In comparison, the rate of binge drinking in the general population is 8 percent.
Among those with mental illness, more than 75 percent were regular smokers. This compares with 33 percent of those in the control group who smoked regularly. There were similar findings with heavy marijuana use: 50 percent of people with psychotic disorders used marijuana regularly, versus 18 percent in the general population. Half of those with mental illness also used other illicit drugs, while the rate of recreational drug use in the general population is 12 percent.
“I take care of a lot of patients with severe mental illness, many of whom are sick enough that they are on disability,” said Hartz. “And it’s always surprising when I encounter a patient who doesn’t smoke or hasn’t used drugs or had alcohol problems.”
Hartz said another striking finding from the study is that once a person develops a psychotic illness, protective factors such as race and gender don’t have their typical influence.
Previous research indicates that Hispanics and Asians tend to have lower rates of substance abuse than European Americans. The same is true for women, who tend to smoke, drink and use illicit drugs less often than men.
“We see protective effects in these subpopulations,” Hartz explained. “But once a person has a severe mental illness, that seems to trump everything.”
That’s particularly true, she said, with smoking. During the last few decades, smoking rates have declined in the general population. People over age 50 are much more likely than younger people to have been regular smokers at some point in their lives. For example, about 40 percent of those over 50 used to smoke regularly. Among those under 30, fewer than 20 percent have been regular smokers. But among the mentally ill, the smoking rate is more than 75 percent, regardless of the patient’s age.
“With public health efforts, we’ve effectively cut smoking rates in half in healthy people, but in the severely mentally ill, we haven’t made a dent at all,” she said.
Until recently, smoking was permitted in most psychiatric hospitals and mental wards. Hartz believes that many psychiatrists decided that their sickest patients had enough problems without having to worry about quitting smoking, too. There also were concerns about potential dangers from using nicotine-replacement therapy, while continuing to smoke since smoking is so prevalent among the mentally ill. Recent studies, however, have found those concerns were overblown.
The question, she said, is whether being more aggressive in trying to curb nicotine, alcohol and substance use in patients with severe psychiatric illness can lengthen their lives. Hartz believes health professionals who treat the mentally ill need to do a better job of trying to get them to stop smoking, drinking and using drugs.
“Some studies have shown that although we psychiatrists know that smoking, drinking and substance use are major problems among the mentally ill, we often don’t ask our patients about those things,” she said. “We can do better, but we also need to develop new strategies because many interventions to reduce smoking, drinking and drug use that have worked in other patient populations don’t seem to be very effective in these psychiatric patients.”
(Source: news.wustl.edu)