HOW TO SELECT THE LEADER OF YOUR BUSINESS

Should You Be the Leader of Your Small Business?

BY CAROL TICE| 

Some entrepreneurs are born to start businesses – often more than one. But not all of these idea people really want to lead a company. They simply don’t have the leadership traits that would make them the best choice to head the company, especially as it grows larger. That’s why so many founders are replaced before a company goes public – investors want to know that a vibrant, inspiring figure whose core competency is leadership will be there to drive growth.

It’s common for founders to step back from being CEO and take on some other role — common titles for founders who have stepped away from the top spot include chief technology officer, board director, chief operating officer or research and development director. Some people are full of creative spark and have a passion for coming up with new concepts or for marketing their idea. Others love to lead teams of people and inspire them to do their best.

But rarely do these two innate drives reside in one person. Many entrepreneurs cling to leadership simply because they fear the loss of control, even though their business would be better off if they brought a passionate leader to the helm and focused on the part of the business they love.

So how do you know if you should lead your business? Here are some questions you should ask yourself:

• Do you get a bigger thrill out of energizing workers and seeing your employees succeed than you do when you are successful yourself?
• Do you feel that you wouldn’t know what to do with yourself if you weren’t heading the company?

Continue reading this article at Entrepreneur.com after the break!

Coconut

Did You Know... 

. . . that coconuts are one of the wonder foods on earth that amply provides for all human needs?  They can even save your life! 

     Few people (even fewer doctors) understand how important the coconut is to stabilizing blood sugar; lowering cholesterol; healing; hydration; and evenreplacing blood plasma in an emergency.
     Referred to as kalpa vriksha (Sanskrit for "the tree that supplies all that is needed to live") in ancient India, the coconut palm has been recognized as a top immune booster,antifungal, antibiotic, antiviral andantibacterial remedy for thousands of years all over the world.  Yet, it has only been recently that modern researchers have begun to fully discover the massive health benefits this amazing fruit seed offers.

     To give just one example of coconuts' live-saving properties, they were used extensively in the Pacific during World War II.  Since blood plasma supplies were scarce, it was very common for medics to siphon pure coconut water from young coconuts to be used as emergency plasma transfusions for soldiers who were injured.  Since coconut water is nearly identical to human blood, it was suitable for people of all blood types. 

     Because of its strong antioxidant properties, the coconut can be used to:

==> Lower cholesterol ==> Improve digestion ==> Ward off wrinkles ==> Stabilize glucose levels ==> Fight off viruses ==> Build cells ==> Regulate hormones ==> Increase thyroid production ==> Lose weight ==> Increase metabolism ==> Fight infections ==> Stave off memory loss ==> Kill bacteria ==> And more!

     Considered one of the most treasured foods of all time, coconut products -- including coconut flesh, coconut water, coconut oil, and coconut cream -- each deliver superb health benefits.
    
     Coconut oil, for instance, is considered the best and safest oil to use for cooking -- even superior to extra virgin olive oil when it comes to giving the body what it needs for optimum health.  Unlike other fats and oils that we  typically use for cooking and baking, coconut oil does not form polymerized oils or dangerous trans fatty acids in our bodies, which can raise our cholesterol levels; clog our arteries and even make our skin sag and wrinkle.  Plus, this ultra-safe oil can give your body important antioxidants that can help build stronger cells and improve your overall health and well being.

     Here are a few ways that you can use coconut products to stave off disease and to recapture the look and feeling of youth:

Coconut Water - The coconut is a natural water filter.  It takes almost 9 months for a coconut to filter every quart of water stored within its shell.  This makes the resulting coconut water completely pure and sterile, which is one reason why it can be used for blood transfusions.

     Another benefit of coconut water is the fact that it has the highest concentration of electrolytes than anything else found in nature. This makes it an excellent source of hydration.
Coconut Oil - In addition to being superior for cooking and baking, coconut oil also makes a superb topical oil that can help to naturally rid the skin of dangerous toxins.  It also gives the skin the perfect mix of hydration and antioxidants that it needs to stay healthy, smooth and younger-looking longer.

     Another great benefit of coconut oil is in protecting your teeth from the bacteria that can cause cavities and disease.  Simply rubbing a little fresh coconut oil on your gums and teeth can keep them stronger and healthier than virtually any other dental treatment.

     Most people don't realize that coconut oil can actually help you lose weight!  Yes, simply changing your cooking oil from the unsaturated fat variety to coconut oil can help you lose those extra pounds.  Here's why:  Unsaturated fats found in canola, corn and other vegetables oils, as well as margarine  suppress the metabolism, which makes it harder to lose weight -- and easier to gain it.  Over time, this metabolism suppression may result in 20-30 pounds of excess weight that your body cannot get rid of.  Coconut oil, on the other hand, helps to increase thyroid function and boost your metabolism-- 2 important components to shedding unwanted pounds.

Coconut Cream - The best skin treatment product one can use to achieve flawless skin may quite possibly be coconut cream.  Unlike traditional skin creams which can actually introduce fats and oils to the skin that will break it down over time, making it look older, creams derived from the coconut can actually replenish the skin, giving it a more youthful and healthy glow than most other skin care products on the market.

     When it comes to buying coconut products, coconuts are not all created equal.  Wild coconuts are always best, but can be hard to obtain if you don't live in a tropical country.  Whether you are using this wonder food to boost your immune system; increase your metabolism or fight wrinkles, using products from young coconuts will help you reap the most benefit.
     Young coconuts contain the purest unsaturated fat, compared to the fat found in the more mature varieties.  This is why they offer the most rejuvenation properties for the body's tissues.  But how can you tell how old a coconut is?  Young coconuts are usually green in color and oddly shaped.  The brown hairy ones are mature coconuts, and while they offer a lot of healthy benefits, they aren't nearly as good for you as younger varieties.

     The best place to find young fresh coconuts is, of course, in the markets of the tropics, so be sure to seek them out if you travel to those areas.  Coconut-producing regions export coconuts all over the world, however, so it's relatively easy to find coconuts at your local health food store or Asian grocer.

Neuroscience and the pursuit of justice

Dr. Judith Edersheim of the Center for Law, Brain and Behavior delivered the 13th annual Francine and Michael Saferstein Memorial Lecture in Forensic Science on Tuesday. Photo by Dominick Reuter.

Dr. Judith Edersheim, co-founder and co-director of the Center for Law, Brain and Behavior at Massachusetts General Hospital, explores how neuroscience can enhance the pursuit of justice.

“If neuroscience could shed light on mental states, it might be able to illuminate whether someone meant the crime or intended to harm someone,” Edersheim told approximately 200 students, faculty, staff and community members who filled Northeastern’s Raytheon Amphitheater on Tuesday for the 13th annual Francine and Michael Saferstein Memorial Lecture in Forensic Science.

The lecture series — which is co-sponsored by the Barnett Institute of Chemical and Biological Analysis and the School of Criminology and Criminal Justice — was established by forensic scientist Richard Saferstein in memory of his wife and child, who were killed in 1978 when a bomb discharged inside the family’s garage.

Barry Karger — the James L. Waters Chair in Analytical Chemistry in Northeastern’s College of Science and director of the Barnett Institute of Chemical and Biological Analysis — introduced Edersheim by praising her for “performing a broad range of psychiatric evaluations in criminal and civil forensic settings.”

Edersheim, who holds both an MD and JD, said “neurolaw” is similar to  “neuropolitics” and “neuromarketing,” in that the field tries to incorporate both neuroscience and psychology into a more established practice.

One’s genetic composition as well as the electrical activity and physical structure of the working brain, she explained, can all be explored to shed light on the question of criminal responsibility.

But Edersheim added a note of caution in taking this approach: If biology single-handedly determines behavior, then the very notion of free will becomes compromised. Technological, procedural, constitutional and deterministic limitations, she said, must all be considered when applying neuroscience to the law.

“The science has to be respected in the community and it has to be peer reviewed,” Edersheim said. “It has to be reliable, reproducible and there have to be known error rates. Judges are gatekeepers and they should keep evidence out that doesn’t meet those tests.”

Edersheim also addressed the constitutionality of neurolaw. If brain scans are examples of involuntary search and seizure or if they force defendants to unwillingly incriminate themselves, then the procedure, she said, could be in violation of the Fourth and Fifth amendments, respectively.

“Thoughts may be subject to constitutional protection,” Edersheim explained, adding that the law and the brain “live in different worlds.”

The law, she said, gives us a set of rules we must abide by, but we must decide as a society whether neurobiological explanations of human behavior should matter when determining criminality.

Edersheim said the Center for Law, Brain and Behavior has an “operational philosophy for the faithful translation of law into neuroscience,” meaning that courtroom use of neurological and biological data should be limited to instances when the science is inextricably and causally linked to a behavior.

Provided by Northeastern University

"Neuroscience and the pursuit of justice." March 26th, 2012. http://medicalxpress.com/news/2012-03-neuroscience-pursuit-justice.html

Posted by
Robert Karl Stonjek

Sleeping too much or too little can be bad for your heart

Getting too little sleep – or even too much – appears to spell trouble for the heart. New data reveal that adults who get less than six hours of sleep a night are at significantly greater risk of stroke, heart attack and congestive heart failure. Even those who reportedly sleep more than eight hours a night have a higher prevalence of heart problems, namely chest pain (angina) and coronary artery disease, a narrowing of the blood vessels that supply blood and oxygen to the heart, according to research presented today at the American College of Cardiology's 61st Annual Scientific Session. The Scientific Session, the premier cardiovascular medical meeting, brings cardiovascular professionals together to further advances in the field.

While these findings echo those from previous, smaller studies, investigators say this is the first nationally representative sample to find an association between sleep duration and heart health, and the first to look at five different conditions at one time. Researchers retrospectively studied approximately 3,019 patients over the age of 45 years who participated in the National Health and Nutrition Examination Survey (NHANES), a survey of U.S. households that assessed a broad range of health issues. Analyses showed that people getting too little sleep were two times more likely to have a stroke or heart attack and 1.6 times more likely to have congestive heart failure. Those reporting more than eight hours of sleep a night were two times more likely to have angina and 1.1 times more likely to have coronary artery disease.

"We now have an indication that sleep can impact heart health, and it should be a priority," said Rohit R. Arora, MD, FACC, chairman of cardiology and professor of medicine, the Chicago Medical School, and the study's principal investigator. "Based on these findings, it seems getting six to eight hours of sleep everyday probably confers the least risk for cardiovascular disease over the long term."

Insufficient sleep has previously been linked to the hyper-activation of the sympathetic nervous system, glucose intolerance, diabetes and an increase in cortisone levels, blood pressure, resting heart rate and inflammatory markers – all of which are associated with cardiovascular disease. However, researchers are still unclear as to why longer sleep duration might be linked to heart problems.

Dr. Arora speculates that the people sleeping more than eight hours, who report chest pains to their doctor, may have been given a greater clinical workup than people getting less than six hours of sleep, who are not presenting chest pains, which may explain why there are more significant cardiovascular events in this group; however, this needs to be evaluated in future long-term studies. In addition, unknown factors not yet elucidated and other co-morbid conditions like diabetes mellitus, obesity or hypertension may cause higher risk in those sleeping under six hours.

What is clear, according to Dr. Arora, is the need for clinicians and patients to talk about sleep patterns.

"Clinicians need to start asking patients about sleep, especially with those who are already at greater risk for heart disease," he said. "It's a really simple thing to assess as part of a physical exam, it doesn't cost anything and it may help encourage patients to adopt better sleep habits."

Respondents were asked about sleep duration and subsequently stratified into one of three categories: 1) less than six hours of sleep a night, 2) between six and eight hours of sleep a night, 3) over eight hours of sleep a night. Each patient was also asked if they were ever told they had congestive heart failure, heart attack, coronary artery disease, angina or stroke. Analyses adjusted for covariates such as age, gender, total cholesterol, high-density lipoprotein, systolic blood pressure, smoking status, diabetes mellitus and body mass index. Investigators also controlled for sleep apnea and other sleep disturbances that have previously been linked to heart problems.

Dr. Arora says larger prospective studies are needed to confirm these findings and, if proven, to determine whether asking about sleep patterns presents a cost-effective way to further screen and identify patients who may be at high risk for heart disease.

Provided by American College of Cardiology

"Sleeping too much or too little can be bad for your heart." March 26th, 2012. http://medicalxpress.com/news/2012-03-linked-heart-woes.html

Posted by
Robert Karl Stonjek

The innate ability to learn language

Psychology professor Iris Berent is using behavioral and neuroimaging techniques to investigate whether our ability to learn language is innate. Credit: Mary Knox Merrill

All human languages contain two levels of structure, said Iris Berent, a psychology professor in Northeastern’s College of Science. One is syntax, or the ordering of words in a sentence. The other is phonology, or the sound structure of individual words.

Berent — whose research focuses on the phonological structure of language — examines the nature of linguistic competence, its origins and its interaction with reading. While previous studies have all centered on adult language acquisition, she is now working with infants to address two core questions.

“First,” she said, “do infants have the capacity to encode phonological rules? And, second, are some phonological rules innate?”

To address the first issue, Berent collaborated with neuroscientists Janet Werker, of the University of British Columbia, and Judit Gervain, of the Paris-based Centre National de la Recherche Scientifique.

By utilizing an optical brain imaging technique called near-infrared spectroscopy, or NIRS, the researchers found that newborns have the capacity to learn linguistic rules. This finding — published this month in the Journal of Cognitive Neuroscience — suggests that the neural foundations of language acquisition are present at birth.

Armed with this knowledge, Berent has begun conducting behavioral studies on more than two-dozen infants to explore whether linguistic rules are innate or entirely learned.

“We want to see whether infants prefer certain sound patterns to others even if neither occurs in their language,” Berent explained. “For instance, we know that human languages prefer sequences such as bnog over bdog. Would six-month-old infants show this preference even if their language (English) does not include either sequence?”

For the study, each child is placed in front of a video screen that displays an image pulsing in coordination with rotating sounds, such as “bnog” and “bdog.” Berent hypothesized that infants would look longer at the video screen when they hear sounds to which they are innately biased.

Preliminary results have upheld the hypothesis, but Berent is still accepting new subjects for the study. Her entire research program forms part of a new book called “The Phonological Mind,” which will be published by Cambridge University Press this year.

More information: A symposium on the nature, origins and use of language will take place on March 30 at 12:30 p.m. in the Curry Student Center Ballroom.

Provided by Northeastern University

"The innate ability to learn language." March 26th, 2012. http://medicalxpress.com/news/2012-03-innate-ability-language.html

Posted by
Robert Karl Stonjek

Genetic risk, stressful early infancy join to increase risk for schizophrenia

Green neurons with reduced DISC1 protein. Red neurons have less effective GABA.

Working with genetically engineered mice and the genomes of thousands of people with schizophrenia, researchers at Johns Hopkins say they now better understand how both nature and nurture can affect one’s risks for schizophrenia and abnormal brain development in general.

The researchers reported in the March 2 issue of Cell that defects in schizophrenia-risk genes and environmental stress right after birth together can lead to abnormal brain development and raise the likelihood of developing schizophrenia by nearly one and half times.

“Our study suggests that if people have a single genetic risk factor alone or a traumatic environment in very early childhood alone, they may not developmental disorders like schizophrenia,” says Guo-li Ming, M.D., Ph.D., professor of neurology and member of the Institute for Cell Engineering at the Johns Hopkins University School of Medicine. “But the findings also suggest that someone who carries the genetic risk factor and experiences certain kinds of stress early in life may be more likely to develop the disease.”

Pinpointing the cause or causes of schizophrenia has been notoriously difficult, owing to the likely interplay of multiple genes and environmental triggers, Ming says. Searching for clues at the molecular level, the Johns Hopkins team focused on the interaction of two factors long implicated in the disease: Disrupted-in-Schizophrenia 1 (DISC1) protein, which is important for brain development, and GABA, a brain chemical needed for normal brain function.

To find how these factors impact brain development and disease susceptibility, the researchers first engineered mice to have reduced levels of DISC1 protein in one type of neuron in the hippocampus, a region of the brain involved in learning, memory and mood regulation. Through a microscope, they saw that newborn mouse brain cells with reduced levels of DISC1 protein had similarly sized and shaped neurons as those from mice with normal levels of DISC1 protein. To change the function of the chemical messenger GABA, the researchers engineered the same neurons in mice to have more effective GABA. Those brain cells looked much different than normal neurons, with longer appendages or projections. Newborn mice engineered with both the more effective GABA and reduced levels of DISC1 showed the longest projections, suggesting, Ming said, that defects in both DISC1 and GABA together could change the physiology of developing neurons for the worse.

Meanwhile, other researchers at the University of Calgary and at the National Institute of Physiological Sciences in Japan had shown in newborn mice that changes in the environment and routine stress can impede GABA from working properly during development. In the next set of experiments, the investigators paired reducing DISC1 levels and stress in mice to see if it could also lead to developmental defects. To stress the mice, the team separated newborns from their mothers for three hours a day for ten days, then examined neurons from the stressed newborns and saw no differences in their size, shape and organization compared with unstressed mice. But when they similarly stressed newborn mice with reduced DISC1 levels, the neurons they saw were larger, more disorganized and had more projections than the unstressed mouse neurons. The projections, in fact, went to the wrong places in the brain.

Next, to see if their results in mice correlated to suspected human schizophrenia risk factors, the researchers compared the genetic sequences of 2,961 schizophrenia patients and healthy people from Scotland, Germany and the United States. Specifically, they determined if specific variations of DNA letters found in two genes, DISC1 and a gene for another protein, NKCC1, which controls the effect of GABA, were more likely to be found in schizophrenia patients than in healthy individuals. They paired 36 DNA “letter” changes in DISC1 and two DNA letter variations in NKCC1 — one DNA letter change per gene — in all possible combinations. Results showed that if a person’s genome contained one specific combination of single DNA letter changes, then that person is 1.4 times more likely than people without these DNA changes to develop schizophrenia. Having these single DNA letter changes in either one of these genes alone did not increase risk.

“Now that we have identified the precise genetic risks, we can rationally search for drugs that correct these defects,” says Hongjun Song, Ph.D., co-author, professor of neurology and director of the Stem Cell Program at the Institute for Cell Engineering.

Provided by Johns Hopkins University

"Genetic risk, stressful early infancy join to increase risk for schizophrenia." March 26th, 2012. http://medicalxpress.com/news/2012-03-genetic-stressful-early-infancy-schizophrenia.html

Posted by

Robert Karl Stonjek

Specialized training of complex motor skills may induce sports-specific structural changes in the human brain

A new study, using brain imaging technology, reveals structural adaptations in short-track speed skaters' brains which are likely to explain their extraordinary balance and co-ordination skills. The work by Im Joo Rhyu from the Korea University College of Medicine, and colleagues, is published online in Springer's journal Cerebellum.

The cerebellum in the brain plays an essential role in balance control, coordinated movement, and visually guided movement, which are key abilities required for short-track speed skaters as they glide on perfectly smooth ice, cornering and passing at high speeds. Previous studies have shown that damage to the cerebellum results in impaired balance and coordination. In addition, structural changes in the brain have been documented following training of complex motor skills, in both jugglers and basketball players for instance. Are these changes sports-specific?

To assess the effect of short-track speed skating training on the relative structure and size of the two brain hemispheres, the authors analyzed brain MRI scans of 16 male professional short-track speed skaters. They compared them to scans of 18 non-skaters, who did not engage in regular exercise.

They found that skaters had larger right hemispheres of the cerebellum and vermian lobules VI-VII (the lobes connecting the left and right parts of the cerebellum) than non-skaters. These results suggest that the specialized abilities of balance and coordination in skaters are associated with a certain amount of flexibility in the structure of the right hemisphere of the cerebellum and vermian VI-VII.

Why do the structural changes occur to the right side of the cerebellum? Gliding on smooth ice requires specialized abilities to control dynamic balance and coordination. During cornering at high speed, short-track speed skaters turn only to the left while maintaining balance on their right foot. Standing on the right foot activates the right lobes of the cerebellum.

In addition, learning a visually guided task is thought to occur in the right side of the brain. Therefore the larger volume of the right hemisphere of the cerebellum in these skaters is likely to be associated with the type of movements which the sport requires, for strong visual guidance while cornering and passing.

The authors conclude: "Short-track speed skaters' specialized abilities of balance and coordination stimulate specific structural changes in the cerebellum, following extensive training. These changes reflect the effects of extraordinary abilities of balance and coordination on the right region of the brain."

More information: Park IS, Rhyu IJ et al (2012). Volumetric analysis of cerebellum in short-track speed skating players. Cerebellum; DOI 10.1007/s12311-012-0366-6

Provided by Springer

"Specialized training of complex motor skills may induce sports-specific structural changes in the human brain." March 26th, 2012.http://medicalxpress.com/news/2012-03-specialized-complex-motor-skills-sports-specific.html

Posted by
Robert Karl Stonjek

Antipsychotic medication associated with modest heart attack risk in older patients with dementia

Antipsychotic medication was associated with a modest and time-limited increased risk of myocardial infarction (heart attack) among older patients treated with cholinesterase inhibitors for dementia, according to a study published Online First byArchives of Internal Medicine.

Antipsychotic medications are commonly prescribed for older patients to manage the symptoms of dementia, which can include physical aggression, agitation and hallucinations. For this indication, previous studies have suggested the use of antipsychotic agents (APs) was linked to an increased risk of stroke and safety warnings were issued in several countries. Studies focusing on the risk of death from all causes led to similar conclusions. However, the effect of AP use on the risk of acute myocardial infarction (MI) in patients with treated dementia "remains poorly examined," the authors write in their study background. .

Antoine Pariente, M.D., Ph.D., then of the Université de Montreal, Canada, now of Université Bordeaux Ségalen, France, and colleagues investigated the risk of MI associated with the use of APs in patients with dementia treated with cholinesterase inhibitors (ChIs). Using the Quebec, Canada, prescription claims database, the authors identified 37,138 patients during the study period (January 2000 through December 2009) who were 66 years or older and had ChI treatment. Of them, 10,969 (29.5 percent) started AP treatment during the study period. They were matched with 10,969 non-AP users.

"Our study results indicate that the use of APs is associated with a modest increase in the risk of MI among community-dwelling older patients with treated dementia," the authors note. "The increased risk seems to be highest at the beginning of treatment and seems to decrease thereafter, with the first month of treatment accounting for the highest period of risk."

The results indicate that within one year of starting AP treatment, 1.3 percent of the patients had an incident MI. Hazard ratios for the risk of MI after initiating AP treatment were 2.19 for the first 30 days; 1.62 for the first 60 days; 1.36 for the first 90 days and 1.15 for the first 365 days.

Researchers also performed a self-controlled case series (SCCS) study among 804 new AP users who had an incident MI. The results indicate incidence rate ratios of 1.78 for the one- to 30-day period; 1.67 for the 31- to 60-day period; 1.37 for the 61-to 90-day period; 1.18 for the remaining exposure period; and 0.80 for the withdrawal period.

"Because AP use is frequent in patients with dementia (29.5 percent in our study population), the increased risk of MI may have a major public health effect, which highlights the need for communicating such risk and for close monitoring of patients during the first weeks of treatment," the authors conclude.

In an invited commentary, Sudeep S. Gill, M.D., M.Sc., and Dallas P. Seitz, M.D., of Queen's University, Kingston, Ontario, Canada, write: "The increased risk for death associated with antipsychotic use has raised several important questions, and among them is the question of how exposure to these drugs leads to death."

"Important lessons about the pathogenesis of cardiovascular disease may underlie the observed association between antipsychotic drug use and AMI (acute myocardial infarction) that is described by Pariente et al, but we must await further research to clarify the mechanisms contributing to this association," they comment.

"Meanwhile, physicians should limit prescribing of antipsychotic drugs to patients with dementia and instead use other techniques when available, such as environmental and behavioral strategies, to keep these patients safe and engaged."

More information: Arch Intern Med. Published online March 26, 2012. doi:10.1001/archinternmend.2012.28 
Arch Intern Med. Published online March 26, 2012. doi:10.1001/archinternmed.2012.682

Provided by JAMA and Archives Journals

"Antipsychotic medication associated with modest heart attack risk in older patients with dementia." March 26th, 2012.http://medicalxpress.com/news/2012-03-antipsychotic-medication-modest-heart-older.html

Posted by
Robert Karl Stonjek

Does the brain 'remember' antidepressants?

Individuals with major depressive disorder (MDD) often undergo multiple courses of antidepressant treatment during their lives. This is because the disorder can recur despite treatment and because finding the right medication for a specific individual can take time.

While the relationship between prior treatment and the brain's response to subsequent treatment is unknown, a new study by UCLA researchers suggests that how the brain responds to antidepressant medication may be influenced by its remembering of past antidepressant exposure.

Interestingly, the researchers used a harmless placebo as the key to tracking the footprints of prior antidepressant use.

Aimee Hunter, the study's lead author and an assistant professor of psychiatry at UCLA's Semel Institute for Neuroscience and Human Behavior, and colleagues showed that a simple placebo pill, made to look like actual medication for depression, can "trick" the brain into responding in the same manner as the actual medication.

The report was published online March 23 in the journal European Neuropsychopharmacology.

The investigators examined changes in brain function in 89 depressed persons during eight weeks of treatment, using either an antidepressant medication or a similar-looking placebo pill. They set out to compare the two treatments — medication versus placebo — but they also added a twist: They separately examined the data for subjects who had never previously taken an antidepressant and those who had.

The researchers focused on the prefrontal cortex, an area of the brain thought to be involved in planning complex cognitive behavior, personality expression, decision-making and moderating social behavior, all things depressed people wrestle with.

Brain changes were assessed using electroencephalograph (EEG) measures developed at UCLA by study co-authors Dr. Ian Cook, UCLA's Miller Family Professor of Psychiatry, and Dr. Andrew Leuchter, a professor of psychiatry and director of the Laboratory of Brain, Behavior and Pharmacology at UCLA's Semel Institute. The EEG measure, recorded from scalp electrodes, is linked to blood flow in the cerebral cortex, which suggests the level of brain activity.

The antidepressant medication given during the study appeared to produce slight decreases in prefrontal brain activity, regardless of whether subjects had received prior antidepressant treatment during their lifetime or not. (A decrease in brain activity is not necessarily a bad thing, the researchers note; with depression, too much activity in the brain can be as bad as too little.)

However, the researchers observed striking differences in the power of placebo, depending on subjects' prior antidepressant use. Subjects who had never been treated with an antidepressant exhibited large increases in prefrontal brain activity during placebo treatment. But those who had used antidepressant medication in the past showed slight decreases in prefrontal activity — brain changes that were indistinguishable from those produced by the actual drug.

"The brain's response to the placebo pill seems to depend on what happened previously — on whether or not the brain has ever 'seen' antidepressant medication before," said Hunter, who is a member of the placebo research team at the Laboratory of Brain, Behavior and Pharmacology. "If it has seen it before, then the brain's signature 'antidepressant-exposure' response shows up."

According to Hunter, the effect looks conspicuously like a classical conditioning phenomenon, wherein prior exposure to the actual drug may have produced the specific prefrontal brain response and subsequent exposure to the cues surrounding drug administration — the relationship with the doctor or nurse, the medical treatment setting, the act of taking a prescribed pill and so forth — came to elicit a similar brain response through 'conditioning' or 'associative learning.'

While medication can have a powerful effect on our physiology, said Hunter, "the behaviors and cues in the environment that are associated with taking medication can come to elicit their own effects. One's personal treatment history is one of the many factors that influence the overall effects of treatment."

Still, she noted, there are other possible explanations, and further research is needed to tease out changes in brain function that are related to antidepressant exposure, compared with brain changes that are related to clinical improvement during treatment.

Provided by University of California - Los Angeles

"Does the brain 'remember' antidepressants?." March 26th, 2012. http://medicalxpress.com/news/2012-03-brain-antidepressants.html

Posted by
Robert Karl Stonjek

Essential tremor patient regains independence following surgery

For nearly 30 years, Tom Rogers' left hand would shake when he tried to use it, making even simple tasks such as drinking a glass of water, writing a check, or making a sandwich challenging. The tremor eventually became so disruptive that he lost use of his dominant hand. Rogers sought care and learned that his tremor was a symptom of Parkinson's disease, yet felt he was suffering from something different.

"I was familiar with Parkinson's because my father had it and I knew this wasn't the same," said Rogers, a 66-year-old retired truck driver who resides in Oswego, Ill. "It was exactly the opposite of my dad's tremor which would start when he was still or relaxed. My hand would shake when I had something in it or tried to use it."

Also convinced that her husband was suffering from something other than Parkinson's, Pam Rogers began searching the internet. Through her research the couple learned about another movement disorder called essential tremor and found their way to Northwestern's Parkinson's Disease and Movement Disorders Center. Northwestern Medicine® movement disorder specialists diagnosed Rogers with essential tremor, a neurological disorder that causes shaking in the hands, head, voice and occasionally the legs and trunk. An estimated 10 million Americans have essential tremor making it eight times more prevalent than Parkinson's, yet the two are often confused.

"Essential tremor is not a life-threatening disease, but it worsens over time and can be very debilitating," explained Joshua Rosenow, MD, director of functional neurosurgery at Northwestern Memorial Hospital and associate professor of neurosurgery at Northwestern University Feinberg School of Medicine. "Severe cases can profoundly impact a person's quality of life and limit the ability to function independently. As the condition progresses, it becomes more challenging for these patients to eat, feed themselves, write or drive. Some even become too frustrated or embarrassed to go out in public because of their tremor."

The disorder can be treated with medications, but many do not adequately control the tremor or cause negative side effects that outweigh the benefit. Patients are encouraged to eliminate any stimuli that increase their tremor, such as caffeine or life stress. When those treatments fail, deep brain stimulation (DBS) surgery is an option for some patients.

"Essential tremor is a vastly undertreated disorder, but DBS is tremendously effective, often much more so than medications," explained Rosenow. "DBS involves implanting small electrodes into very specific region deep in the brain to deliver continuous high frequency electrical impulses. Each electrode is connected to an extension wire that runs under the skin down to the chest where a battery pack is implanted. This pack acts as a 'pacemaker' for the brain and helps control the tremor."

This video is not supported by your browser at this time.

After medication failed to control his tremor, Rogers made the decision to have DBS surgery. "It got to the point where I couldn't even sign my own name with my left hand and it was beginning to affect my right hand as well," said Rogers. "I knew if I ignored it, eventually I wouldn't be able to function on my own."

During DBS, the surgeon first plans the surgery by mapping out the best path for the electrode using detailed 3-D images of the brain. The patient is awake for part of the surgery and becomes a key member of the team as they map out the correct location for the electrode. Local anesthetic is given so that no discomfort is felt.

"The surgeon and neurophysiologist determine the exact placement for the electrode by listening to the nerve cell signals, which have a unique pattern in each area of the brain," said Rosenow, who performed Rogers' DBS surgery. "The patient's legs and arms are moved to see what effect the electrode is having and the patient is also asked to speak, look around and relate if there is any tingling or pulling in the arms, legs or face. In Tom's case, we asked him to mimic bringing a glass to his mouth because this was something that was impacted greatly by his tremor."

Rogers immediately felt a change when his surgical team found the right spot in his brain. "It was instantaneous," he recalled. "I said 'Doc, you found ground zero.' It was shaking and then all of a sudden it stopped."

A permanent electrode is placed once the correct location is found and the surgical team tests it by turning on the charge. They look for both a decrease in tremor, as well as any unwanted side effects. Once satisfied with the location, the electrode is secured and the patient is put back under general anesthesia for the remainder of the surgery. In the months following surgery, the implanted battery pack is programmed to achieve the optimal balance between stimulation and medication.

"Following surgery, we work with the patient to tailor the level of stimulation and treatment to their needs," said Cindy Zadikoff, MD, a movement disorders specialist at Northwestern Memorial and assistant professor of neurology at the Feinberg School, who helps select patients for DBS surgery and has special expertise in programming the stimulation devices. "In rare cases, the surgery itself turns off the tremor by causing what is known as a micro-lesion effect. Tom was one of these unique situations; in more than six months since surgery his device has not been turned on and his tremor has not returned."

DBS surgery allowed Rogers to regain use of his left hand and gave him the ability to do things that most people take for granted like write checks to pay his bills or drink a glass of water. "My hand is steady as a rock, it's amazing," Rogers said. "It's like I've been given back a new life."

Along with essential tremor, DBS is approved as a treatment for other movement disorders including Parkinson's and dystonia. Brain stimulation is currently being studied as a potential treatment for a wide range of disorders including chronic pain, bipolar depression, addiction, epilepsy and a number of other conditions.

"Millions of people have essential tremor and suffer without ever knowing they can explore an option such as brain stimulation surgery," said Rosenow. "This surgery can have tremendous benefit for essential tremor and allow patients to regain the ability to do things that may have been lost because of their tremor."

Provided by Northwestern Memorial Hospital

"Essential tremor patient regains independence following surgery." March 26th, 2012. http://medicalxpress.com/news/2012-03-essential-tremor-patient-regains-independence.html

Comment:
Katharine Hepburn had this condition.

Posted by
Robert Karl Stonjek

Increased production of neurons in hypothalamus found in mice fed high fat diets

Hypothalamic proliferative zone. For more details, Nature Neuroscience (2012) doi:10.1038/nn.3079

(Medical Xpress) -- A research team made up of people from a wide variety of biological sciences has found that mice fed a diet high in fat tend to see an increase in the number of neurons created in the hypothalamus, a region of the brain associated with regulating energy use in the body. The team, as they describe in their paper published in Nature Neuroscience, write that the increase in neurons occurs in a part of the hypothalamus called the median eminence, which lies outside the blood-brain barrier.

Suspecting that something unusual goes on with the hypothalamus and the median eminence in particular, when mice eat more fat, the research team put a group of mice on a diet very high in it. In the lab, mice are usually fed a diet that is approximately thirty five percent fat, which keeps them from gaining weight. In this study, the fat content was raised to sixty percent, which of course caused the mice to get fat. But, the team found, it also caused the creation of new brain cells in the median eminence to increase, from one to five percent.

Next the researchers forced the mouse brains to stop creating new brain cells while continuing to feed the mice the high fat diet. And surprisingly, the mice weight gain slowed and the mice demonstrated more energy. Adding to the good news was the fact that the median eminence lies outside of the blood-brain area (a separation of blood and brain fluid that prevents many materials in blood from reaching brain cells) meaning that the possibility of developing a therapy based on this research to help humans lose weight might be possible.

The researchers are quick to point out, however, that there is no evidence yet that increased neuron production occurs in people who eat extra amounts of fat, or even in any other animal. They also say they don’t yet understand why new neuron growth occurs when mice are fed a high-fat diet but speculate that it may have something to do with detecting chemicals in the bloodstream and responding by sending signals to the rest of the hypothalamus.

More information: Tanycytes of the hypothalamic median eminence form a diet-responsive neurogenic niche, Nature Neuroscience (2012)doi:10.1038/nn.3079

Abstract 

Adult hypothalamic neurogenesis has recently been reported, but the cell of origin and the function of these newborn neurons are unknown. Using genetic fate mapping, we found that median eminence tanycytes generate newborn neurons. Blocking this neurogenesis altered the weight and metabolic activity of adult mice. These findings reveal a previously unreported neurogenic niche in the mammalian hypothalamus with important implications for metabolism.

© 2012 Medical Xpress

"Increased production of neurons in hypothalamus found in mice fed high-fat diets." March 26th, 2012. http://medicalxpress.com/news/2012-03-production-neurons-hypothalamus-mice-fed.html

Posted by

Robert Karl Stonjek