Sunday, March 4, 2012

Doctors on call: Cholesterol drugs linked to brain damage

Cholesterol lowering medications have become the most popular and widely distributed drugs in the world.
New health warnings have been added to the statin group such as muscle pain, memory loss and diabetes. These damaging side effects have been known long-term but pharmaceutical companies and healthcare officialshave simply turned their backs and ignored this growing concern in the past.

The United States Food and Drug Administration has now linked the use of cholesterol lowering medications with cognitive brain dysfunction.

Symptoms of statin induced brain damage include memory loss and mental confusion. The statins that have been identified as the culprits include Lipitor, Crestor, Vytornin and Zocor.

Doctor induced dementia
Cholesterol lowering medications targets and attempts to lower all fat and cholesterol in the body.

There are many areas that require a high density of fat and cholesterol to function properly including your brain. The ingestion of statin medications effect the amount of cholesterol in ones brain and will cause memory loss and mental confusion.

Statin medication specifically destroys Coenzyme Q10 (CoQ10). CoQ10 damage directly impacts the heart, skeletal muscle and the brain. Studies have confirmed CoQ10 depletion to cause further memory loss as well.The destruction of this enzyme by statins also causes weakness and muscle pain.

No cholesterol, no response
The brain and nervous system is the primary system that controls and regulates every function in the human body.

The direct side effects of statin medications inhibit and damage that master control system. One of the primary purposes of the brain is to communicate to every cell in the body and tell them how to respond to any given stimulus.

A stimulus can be positive and negative and is commonly called stress. Artificially lowering cholesterol in your brain will lower the ability of the body to identify and respond to stress.

Pharmaceutical medication can be classified as a chemical stress on the body. It is normal for the body to be able to respond to this stress, but long-term medication abuse, poor diet, lack of exercise and high levels of toxicity will diminish the bodys ability to respond to stress.

Statins cause heart disease
When your blood sugar and risk of developing diabetes increases from taking a statin medication, what is happening?

The chemical stress posed by the statin medication damages neurological tissue and reduces the bodys ability to respond to the stress. Compounding factors such as poor lifestyle indicators further inhibit the natural response to this stress.

What is the natural blood sugar response to a body that is overwhelmed with physical, mental and emotional stress? It increases and youre diagnosed with diabetes.

Diabetes is the leading contributor to the development of heart disease.

Statin medication should not be used if you desire to achieve optimal health. Optimal health means living to your potential without developing self-induced health conditions.

Many people think that heart disease, cancer and diabetes are genetic and their personal choices make no impact. This is false. Research has shown us that the majority of health conditions can be completely eliminated, reduced and reversed with the proper lifestyle indicators.

Heart disease is not a lack of statin medication. Take initiative and implement a health recovery programme.

This programme should include weight loss or maintaining a healthy weight, optimal nutrition, adequate exercise, healthy neurology and the reduction of stress. Health is a choice, what do you choose?

Alzheimer's: Ayurveda may have the cure

NEW DELHI: The late US President Ronald Reagan had it; former Union minister George Fernandes is battling it, and actor Amitabh Bachchan made it a street word with his role in the 2005 movie Black. But a cure for Alzheimer's - a degenerative disorder of the brain - may be around the corner, going by the results achieved in studies at the National Brain Research Centre (NBRC).

The disorder marked by memory and judgment loss usually occurs in people older than 65, and has defied a cure so far. But researchers working with the extract of a herb used in Ayurveda since ancient times have reported promising results. Using an extract of the Ashwagandha root on mice with Alzheimer's disease, NBRC scientists found it can reverse memory loss and may prove to be an effective cure for the disease in humans.

NBRC neuroscientist Vijayalakshmi Ravindranath tested the semi-purified sample extracted at Delhi University on genetically modified mice with Alzheimer's disease. Two sets of test mice - middle aged (9-10 months) and old (2 years) - were given oral doses of the extract for 30 days and monitored. Over the month, scientists found a reduction in amyloid plaques (a symptom of Alzheimer's) in the mice brains and improvement in the animals' cognitive abilities. Their study was published recently in the Proceedings of The National Academy of Sciences (PNAS), and the Nature India Journal.

The mice used for the experiment carry the mutation that is characteristic of Alzheimer's disease and produce the amyloid in greater quantities.

"We got the mice from Jackson Labs in US. They were tested on a radial arm maze, where they are trained to go and pick food from four of the maze's eight arms. Since the mice had Alzheimer's, they were neither able to learn nor retain the learning. But after 20 days of the Ashwagandha treatment, we noticed a difference, and after 30 days they had started behaving normally," said Ravindranath, former founder-director of NBRC, and chairperson of Centre of Neurosciences, Indian Institute of Science.

She explained that the extract didn't work directly on the brain. It enhanced a protein in the liver that is thrown out in the blood and acts like a sponge to pull out the amyloid from the brain. "I am very interested in Ayurveda. This experiment gives us hope," Ravindranath said.

The NBRC's results have also boosted morale at DU's Natural Products Laboratory. "Professor Vijayalakshmi had approached us to evaluate some plants and their effect on neurological disorders. Most medicines that are currently being used for Alzheimer's and Parkinson's are synthetic drugs that have some side effects," said professor Subhash Chand Jain of Delhi University. The team at DU selected the root of Ashwagandha and followed up with a series of extractions at the lab.

"We did the extraction using a solvent system. And then it was further fractionalized to see which fraction was most active. At this point, Vijayalakshmi was very excited because she saw that some of the fractions were active. Then we worked on pinning down the fraction that was most active," Jain said.

Drug Might Limit Stroke Brain Damage

An experimental drug could help protect against brain damage during a stroke, reducing the risk of permanent disability.
experimental drug could help protect against brain damage during a 
stroke, reducing the risk of permanent disability.
An experimental drug could protect stroke victims from brain damage. The treatment has shown very promising results in animal tests, and early results with humans are also encouraging.

There is currently only one effective treatment for stroke. Tissue plasminogen activator (tPA) can dissolve the blood clots that cause a stroke.
But it has to be given very soon after symptoms appear, and doctors first have to make sure that the stroke was not caused by a ruptured blood vessel, in which case tPA can make the situation a lot worse.

Michael Tymianski and his team, at the Toronto Western Hospital Research Institute in Canada, devised a different kind of stroke treatment, a drug known as a PSD-95 inhibitor. It works by blocking a key protein in the chain reaction of events that leads to brain-cell death.

"So by inhibiting this protein, by having a drug that binds to it so the protein can't do what it usually does, we prevent the formation of a toxic free radical called nitric oxide. And as a result of that, brain cells that are treated with this drug become more resilient to a stroke," he said.

In a new scientific paper published online in Nature, Tymianski has published the results of research on macaques - primates with complex brains much like ours.

"Animals that were treated with the placebo drug got very large strokes and were very disabled from their strokes. But animals that received the drug had much smaller strokes on their MRI scans and they were neurologically much better off."

Those encouraging results have already led to human trials, and Tymianski says "the top-line results of that particular trial have already been announced at the International Stroke Conference in New Orleans in February. So we already know that when this drug is given to humans the same way that it's given to the primates and at the same doses, it reduces stroke damage in the human brain."

Tymianski says that, unlike current treatment with tPA, the PSD-95 inhibitor can help patients with hemorrhagic strokes, which are caused by a ruptured blood vessel, and it may even be useful in treating other brain injuries as well. 

Some memory changes in aging brain are normal

Dementia and Alzheimer's have moved ahead of cancer on the list of most feared diseases. 

 Dementia and its evil twin, Alzheimer’s, may have moved ahead of cancer on the list of most feared diseases, especially among baby boomers, who have begun to believe it is their inescapable fate if they have the bad luck to live too long.
So we grasp at any news about aging, hoping that medical science has indeed found a way to preserve that most essential part of who we are — our memories.
Do we protect our minds by doing The New York Times crossword puzzle or by doing aerobics? By eating more leafy greens, absorbing more vitamin D from sunshine or memorizing poetry?
“There is such a thing as normal memory change with age,” said Dr. Susan Lehmann, who specializes in geriatric psychiatry at Johns Hopkins Hospital, “just as there are normal changes in vision.” Our brain will not always work as fast, for example, and we won’t be as good at multitasking. But these are all considered normal changes, according to Lehmann.
Some of our memory will not change. Our knowledge of the world, our autobiography, certain skills, such as playing an instrument. And we won’t forget how to read.
“But it will be harder to recall specific events, harder to make new memories and remember new things,” said Lehmann. “These can be annoying and they can be embarrassing, but they don’t herald dementia or mean that you will have more memory problems.”
It is true that we will see more dementia and more Alzheimer’s disease in the near future, but that has more to do with the fact that we are on the cusp of a huge demographic shift. Boomers are a large group, they are getting older at the same time, and they are living longer.
“The expectation is that 45 percent of those will have some form of dementia by age 85 or 90,” said Lehmann. “But that is not 100 percent.”
True, there is no cure for Alzheimer’s and no treatment to significantly modify the terrible course it takes.
“But there is a lot of emerging research that suggests that there are things we can do as early as midlife that may have a positive impact on brain function,” she said.
Research has found a correlation — but not a cause and effect — between seven risk factors and their implications for the brain. Not surprisingly, Lehmann said, they are also risk factors that have implications for the heart: Diabetes, high blood pressure, obesity and smoking.
“A healthy heart also promotes a healthy brain,” Lehmann said.
The other risk factors include cognitive inactivity and physical inactivity. This is where the crossword puzzles and the daily exercise come in.
“No study has proven that cognitive activity prevents dementia or that lack of cognitive activity causes it,” said Lehmann. “But it is possible to improve and strengthen memory at every age. It is possible to get better at it with focused approaches.”
It is also true, she said, that the more you use your brain, the more connections you lay down inside the brain, the more brainpower you have and the longer it takes to erode.
Likewise, no study has proved that exercise can prevent dementia. But there have been studies in which women who reported the highest levels of physical activity also had the slowest cognitive decline, she said.
“And there have been a number of studies that show that people who are more physically active have an increased sense of well-being in general. There may be a direct benefit to the brain as well.”
The most puzzling risk factor in dementia is depression, and it is of particular concern to women, who are twice as likely to suffer from depression across all ages.
“When someone is depressed,” Lehmann said, “it slows down their ability to think and process and remember. But sometimes, depression can be a first symptom of dementia. It is a complicated relationship.
“Treating depression improves memory, the ability to concentrate, organize, problem-solve and all of that. Untreated depression can be a risk factor for future dementia. In any case, depression needs to be taken seriously.”
And finally, sleep, which becomes more elusive as we age, may have a role in all of this.
“Sleep often gets short shrift,” said Lehmann. “Sleep is important for the consolidation of memory and fatigue degrades the ability to remember.”
The message might be that there will be changes in memory as we age that are as normal and stable over time as the changes in our eyeglass prescriptions. Those changes don’t mean that you are condemned to forget who you are or who you love.
“This should be exciting and reassuring,” Lehmann said. “The things that we want to do anyway, that are good for our health in general and for our sense of well-being, are also good for our brains.”

Experimental drug could mitigate brain damage caused by strokes

New Canadian research suggests an experimental drug can help protect the brain during the initial stages of a stroke, providing doctors with extra time to restore normal blood flow and thereby reducing the risks of permanent disability.

Although the study was conducted on macaque monkeys, the researchers think the findings should also apply to people and are eager to move forward with clinical trials.

“We believe this may have great promise for humanity,” said lead researcher Michael Tymianski of the Krembil Neuroscience Centre at Toronto Western Hospital.

There is currently only one treatment for stroke – a clot-busting drug known as tPA (tissue plasminogen activator). But it must be given within 4.5 hours of the onset of symptoms to be beneficial. As well, therapy can’t commence until after certain medical tests, including a brain scan, confirm the patient is suffering from an ischemic stroke caused by a clot that blocks blood flow to part of the brain. There is good reason to do these time-consuming precautionary tests; if tPA is given to patients with hemorrhagic strokes – or brain bleeds – it will kill them.

Less than 10 per cent of patients get tPA within 4.5 hours, at which point the brain can suffer permanent damage. As time passes, the loss of oxygen-rich blood sets in motion a chain of chemical reactions that produce toxic free radicals, which kill nerve cells.

The experimental drug – called Tat-NR2B9c – puts a halt to this destructive process.

“We’re blocking these reactions, and when you don’t get an accumulation of free radicals, the cells don’t die,” said Dr. Tymianski, who has been developing the drug for more than a decade.

His team’s study, published this week in the journal Nature, showed that the drug prevents brain cell death and preserves brain function in non-human primates.

He envisions a day when ambulance paramedics and emergency-room attendants routinely give the drug to anyone showing symptoms of a stroke. Then, with the patient’s condition stabilized, doctors could perform tests to determine whether tPA is warranted.

“If you could buy the brain a few more hours, it would lead to an exponential increase in the number of patients who would benefit from reperfusion [clot-busting therapy],” said Dr. Tymianski.

Of course, lengthy clinical trials will have to demonstrate that the drug works on people. Over the past 50 years, more than 1,000 promising stroke treatments have met with failure, and pharmaceutical companies have grown increasingly reluctant to invest in this area of research.

Due to the lack of industry involvement, Dr. Tymianski and colleagues created their own company, called NoNO Inc., to raise private capital for the drug’s initial phases of development. Dr. Tymianski, who is both president and CEO, believes the new stroke treatment could on the market in five years. “I have a huge conflict of interest,” he said half-jokingly about his role as researcher and drug company executive. “Nonetheless, if we don’t do it, who will?”

Virtual model can tell how human brain works

A European neuroscientist is planning to build a virtual human brain to understand how brains function, and why they sometimes fail.
 Henry Markram, a neuroscientist at the Swiss Federal Institute of Technology, believes the only way to truly understand how human brains work - and why they often don't - is to create one, then subject it to a barrage of experiments.
 Markram has established the Human Brain Project to do just that. The effort aims to integrate the hundreds of thousands of pieces of the brain puzzle that have been discovered by neuroscientists over the past few decades, from the structures of ion channels to the mechanisms of conscious decision-making, into a single supercomputer model: a virtual brain, Live Science reported.
 If the plan works, then the resulting model will be capable of learning and will gradually develop complex cognitive abilities, much like a living human.
 More importantly, its programmed structure, the brain code developed by the Human Brain Project, will become available for all the world's neuroscientists to do with as they please, whether that's subjecting it to virtual X-ray experiments, flooding it with the programmable equivalents of new experimental drugs, or disrupting its processes at any level and observing the effects.
 The plan is controversial; some scientists think it simply won't work, while others predict a virtual brain will be just as mysterious and difficult to work with as a real one.
 Nonetheless, the Human Brain Project has been selected as a finalist for the European Union's two new Flagship initiatives - grants worth 1 billion Euros apiece.
 "We already have prototype systems in place, ready to expand, refine and perfect," Markram told Life's Little Mysteries.
 He says the process can be broken down into seven key steps.
 First the scientists must decide on the volume of brain tissue to construct, and, second, they must distribute mathematical models of neurons throughout this volume in a manner consistent with experimental data from real human brains.
 Next, they'll connect the model neurons to each other via virtual synapses - signal-carrying pathways. As for signal speeds, even an exa-scale supercomputer, which can perform 1 billion billion calculations per second, will fall short of the simultaneous processing capabilities of actual human brains, and so the model brain will always complete tasks and generate thoughts in slow motion (relative to us).
 The fourth step in brain-building is to fire the system up. The scientists will functionalize the model neurons and synapses, as well as the glial cells (non-neuronal brain cells) and blood flow, by computer-programming these components' processes.
 To get the behaviour of these parts as close to their real-brain analogs as possible, "we mine all existing data in the literature and in databases ... organize the results and analyze it for patterns and its value in helping to specify models more and more biologically accurately," Markram said.
 Where the function of a certain brain part is not yet known to science, the team scientists either will collaborate with other neuroscientists to find what it is, or will insert placeholders into their programs and fill in the gaps when they can.
 Next, the team will run experiments on its model to validate that the cell and synapse types and densities all match experimental data.
 "The models serve to integrate biological data systematically, and therefore they can only get more and more biologically accurate with time as they take more and more biological data into account - like a sponge," Markram said.
 Unless it's capable of interacting with an outside world, a simulated brain is just the virtual equivalent of an organ floating in formaldehyde. Thus, Markram said the sixth step of the Human Brain Project is to connect the brain to a virtual environment and run training protocols so that the model brain can learn and, in so doing, develop complex cognitive capabilities.
 "When one builds a model like this, it still has to be taught to sense, act and make decisions. That is a slow process and will need extremely powerful supercomputers," he said.
 Because the scientists will build an adult brain, it won't have to undergo the neuron- and synapse-building processes that occur in childhood, but they still have to teach their brain about reality in order for it to generate meaningful thoughts. The brain will learn via interactions with "virtual agents behaving in virtual worlds," Markram said.
 And lastly, the scientists will design and perform experiments on the brain, hoping to investigate everything from the neural roots of human behaviour to the effects of new drugs on the brain to the cause of any of the 560 crippling diseases that afflict the human mind.

The Joy of Your Brain… and the Dark Side of Laughter

A “seemingly quirky finding” peers into animal minds. It may also help show how Nazis abused play and laughter to horrid ends.

Nature’s Edge Notebook #19

Observation, Analysis, Reflection, New Questions
What is it like to be a squirrel?
Or, say, a bat… or a giraffe, or a chickadee?

gty joyful chimpanzees jt 120301 wblog The Joy of Your Brain... 
and the Dark Side of LaughterSuppose you could actually feel what it’s like to be another animal … not just guess, after observing its actions and behavior from the outside, but actually break through the prison of subjectivity — both yours and the squirrel’s — and know you can feel it, as if from inside the squirrel’s brain.
Of course, no two species have exactly the same set of sensory inputs. For example, we lack the bat’s special sonic radar, its “echolocation” systems. So ultimately we humans could only guess what it’s fully “like.”
But one scientist’s “seemingly quirky finding” — that rats emit a sort of giggling laughter when they are tickled by humans — is opening a new path for scientists and philosophers in their quest to answer this ancient question.
It’s all about emotion, and especially joy, that great reward in the brain, which, once experienced, we then naturally seek to achieve again … and which can help “make life worth living.”
As a result of their discovery that tickling rats makes them laugh, brain scientist Jaak Panksepp and his colleagues are now producing what they hope will prove to be more effective anti-depressants — chemicals that not only dull negative feelings, but safely enhance positive ones.
Their work on how play and laughter can automatically produce the feeling of joy in the brain may also help clarify the difference between the artificially induced “high” produced by addictive drugs and the true “joy” that may be produced naturally and safely.
On the dark side, his work on animal laughter offers insights into how the group-bonding effects of play behavior may be susceptible to manipulation for cruel ends. It seems to illuminate such abuses as the Nazi’s manipulation of the Olympic Games to advance racist ideology, and even an infamous anti-Semitic board game marketed in Hitler’s Germany in 1936.
The Hunt For Hard Evidence
To believe that you may well be able to “feel” at least something of what it’s “like” to be another kind of animal would, of course, need some sort of evidence that your feelings and those of the other animal could be reasonably presumed to be in any way the same  and that you experience those similar feelings in similar ways — be they in a human and a squirrel, or a human and a bat …  or a salamander, or a Dover sole on the floor of the English Channel, or a goldfish in a fishbowl on a dresser peering down at a sleeping child.
After Panksepp made his delightful discovery in the 1990s that rats emit repeated chirps of laughter when tickled (as seen in this brief video in our previous Nature’s Edge Notebook), he and his team began to suspect they might just have discovered a way to get rats (and eventually perhaps other animals) to, in effect, tell us what they were feeling … and even, in a sense, something of what it is generally like to be a rat or a race horse or a three-wattled bell-bird.
(To see and hear a three-wattled bell-bird make its otherworldly “bell call”… and ponder what it might be like to be that bellbird, you can watch a brief tree-top video here.)
Some scientists are even playing with the idea that the happily chirping lab rats might eventually lead the way to new notions of how consciousness itself, or at least the general feeling of awareness, might be similar, if not exactly the same, in many species.
Towards a Solid Science of the Emotional Feelings of Animals (though other neuroscientists remain doubtful)
In an email to ABC News, Panksepp explains that his team is still exploring the chirping laughter of tickled lab rats 15 years after they discovered it, partly because “the laughter response … allows us to monitor the positive affective states (feelings) of animals objectively.”
He speaks of his “intent in really making a solid science of this seemingly quirky finding, … a science of the emotional feelings of animals … as opposed to just (of their) behaviors.”
Panksepp says that “most neuroscientists are still dead-set against talking about the feelings of animals — as if it were just a matter of opinion, as opposed to a conclusion based on the weight of abundant evidence.”
Enter his ticklish laughing rats.
In experiment after experiment, Panksepp’s labs have found them reacting to the feelings of joy in ways similar to humans and (apparently) other animals – seeking it out, “self-stimulating” for it, sometimes in ways that even demonstrate that such play-induced joy has a liability to addiction.”
If Panksepp is right, his rats could, in effect, be laughing in the faces of those scientists who, he says, still “deem the emotional feelings of animals to be outside the bounds of empirical measurement.”
His discovery that his rats’ laughter arises from inborn structures deep in the brain, combined with years of experiments to determine what sort of activity and other stimulation does and does not produce “rat vocalizations” (laughing chirps), has led Panksepp to declare (in the journal “Future Neurology”) that the happy chirps may indeed “be used as direct readouts of emotional states.”
What Pet Owners May Already ‘Know’
This may all seem rather obvious to pet owners, in a non-scientific sort of way.
They often report that they and their beloved dogs or cats share mutual languages rich in vocabularies of an endless variety of modulated meows and purrs, yips and barks, growls and groans, sweet whimpers, sly screeches, subtle hums, and half-gurgles, ruffs, gruffs and rawls.
These subtly varied sounds, say pet owners, communicate emotions common to human and cat, or human and dog — and even, they claim, can convey not only emotions but plain and practical “intellectual ideas” involving food, shelter, and the need for creative play, as well as observations about important disruptions in the status quo.
But after years of steady work in his lab, Panksepp says he and his colleagues can now present something far more testable — more scientific — than the declarations of happy pet owners.
They report that they have now tracked communicative sounds (at least in rats, but with well-established and reasonable analogues in other animals including humans) to the specific deep-brain structures that produce specific emotions.
For his fellow scientists, he labels these sounds “validated emotional vocalizations.”
If you’re not a scientist, you can get a sense of their work — have a bit of fun, engage in a little word play — by reading just the titles of three of the jargon-rich and peer-reviewed scientific articles in which he and his team have reported these findings over the years.
Don’t be afraid.
This reporter is certainly no scientist either, but I find that if you read these titles slowly and calmly, they start to make sense pretty quickly:
“‘Laughing rats’ and the evolutionary antecedents of human joy?” (Panksepp and Bergdorf in Physiology & Behavior, 4/2003.)
“Cross-Species Affective Neuroscience Decoding of the Primal Affective Experiences of Humans and Related Animals.” (Panksepp in PLoS Public Library of Science  9/2011)
(That phrase, “Primal Affective Experiences,” refers roughly to basic emotions or feelings that evolved long ago in various species… including in those animals that eventually evolved into the likes of us.)
And if you’re really feeling frisky, try this:
“Frequency-modulated 50 kHz ultrasonic vocalizations: a tool for uncovering the molecular substrates of positive affect” (Burgdorf, Panksepp, Moskal in Neuroscience & Biobehavioral Reviews35 / 2011)
(Rough translation: how “ultrasonic vocalizations” — i.e., the laughter of tickled rats — may help lead scientists to find “molecular substrates of positive affect”  – i.e., those structures in the brain that help make you feel good.)
‘The Dark Side of Laughter’… and ‘An Ancient Heritage’
The study of laughter and play has a long lineage.
Many philosophers have offered their insights. Aristotle and Plato wrote that laughter showed derision, asserted superiority.
The Bible’s Book of Proverbs says, “a merry heart doeth good like a medicine.”
Modern writer Umberto Eco built an entire detective novel around, among other things, the subversive power of laughter:
Eco’s “The Name of the Rose,” set in a remote monastery in medieval Liguria in the coastal mountains of northwest Italy, circles around the vexed (for some) theological question of whether Jesus Christ ever laughed.
(Some grouchy monks apparently just couldn’t stand the idea, thought it dangerous.)
In their 2003 article above, “‘Laughing rats’ and the evolutionary antecedents of human joy?“, Panksepp and Burgdorf assert that there has been little meaningful scientific work on the nature and purpose of laughter since French physician Laurent Joubert published his “Treatise on Laughter” in 1579, until now.
This fascinating article is not all that hard to read — at least the one-paragraph summary “Abstract” at the beginning.
It also tells how it all started — how one day, sometime “during the spring in 1997, the senior author came to the Lab, and suggested to the junior author, ‘Let’s go tickle some rats.’ ”
In considering the nature and the mystery of human laughter, they remark on the fact that laughter first appears in human babies soon after birth, and thus seems to be inborn:
They say the fact that the “vocal pattern of human laughter, that first appears in rudimentary form at 2-3 months of age, suggests an ancient heritage.”
In other words, that laughter seems to have evolved long ago in animals far more “primitive” than us, and survived through the bloody struggles of natural selection (the fittest not making it to pass on their laughter-loving DNA)… making survival more likely, and thus being “preserved” (kept) by evolution right up to the modern human, to say nothing of the modern lab rat.
All of which suggests that laughter can help confer a powerful advantage in the world’s hard struggles in which an animal must stay alive long enough to pass on its genes… otherwise why would laughter be so widespread and long-lived down through the great eons of time?
A sobering section in the article is headed, “… And the dark side of laughter.”
It cites evidence that “Usually the children that prevail in play tend to laugh the most, suggesting that, to some extent, laughter may reflect a social dominance-seeking response, which may pave the way for laughter to stigmatize and degrade others through such behavior.”
The authors also evoke painful playground memories:
“All too often, especially in children, laughter tends to become a psychological tool for teasing and taunting — the establishment of exclusionary group identities that can set the stage for finding mirth in the misfortunes of others. These tendencies may arise rather naturally from the fact that within-group laughter promotes group solidarity, which can then be used to ostracize and exhibit scorn toward those outside the group.”
They are careful to say: “We doubt if most other animals are capable of exhibiting such psychological tendencies, but such possibilities certainly need to be considered in future research…”
But they go on to cite other studies of human laughter and play that open the possibility of play behavior (and the instinctive inborn laughter and joy that attends it) being used even for horrendous ends, since laughter “can also serve as the basis for social ridicule.”
An Insight Into the Horrors of Hitler?
We asked a scholar of the Third Reich, Professor Geoffrey Cocks, author of several books on psychiatry and medicine in Hitler’s Germany, for his general thoughts about whether play and laughter might have been enlisted in that regime’s development — something that might resonate with the above description of how “within-group laughter promotes group solidarity, which can then be used to ostracize and exhibit scorn toward those outside the group.”
Cocks replied to ABC News in an email that “First, there is a sequence in Leni Riefenstahl’s Triumph of the Will (1935) in which Hitler Youth at the 1934 Nuremberg rally are shown at play: one scene shows boys being tossed high in the air off a tarpaulin and another scene shows ‘chariot races’ with two boys the ‘horses’ and another standing on their backs as the ‘charioteer.’”
Director Riefenstahl’s infamous propaganda film “Triumph of the Will” shows Hitler’s massively choreographed rallies in Nuremburg — enormous plays of pageantry — apparently reinforcing group solidarity.
She followed it with her 1938 film “Olympia,” which depicts the 1936 Olympic Games in Berlin Germany as a similarly cohesive display of imputed German “Aryan” racial superiority, displayed through the muscular German teamwork in these “games.”
The film was advertised with a poster of happily smiling young blond women.
Cocks also suggested a possible example of the abuse of play in the Hitler Youth: “It is true that the Nazi youth organizations in particular did put a special emphasis on physical activity, including play, as a means of ‘toughening’ Germany’s youth as well promoting solidarity.”
He added this grim note:
“There were board games in Nazi Germany that were designed to strengthen racial and national resolve. The most infamous was the board game Juden Raus! ["Out With the Jews!"] (1936), in which the object was to collect the most Jews and throw them out of town.”
But a quick check online, after Googling the three words “Nazi board games,” suggests some ironic news about the limits of this dark side of play and laughter.
It seems that the board game “Juden Raus!” was an “unsuccessful commercial product,” attempting to ride the wave of official anti-Semitism and racism that was being whipped up by Hitler and his propaganda minister, Joseph Goebbels.
Ironically, according to citations in recent historical research, this board game was “criticized by an SS journal that felt it trivialized anti-Semitic policies.”
Perhaps not serious enough? — And let’s have no laughter; you never know where it might be redirected?
Did even the mere possibility of fun and play, whatever might trigger it, frighten the SS as being somehow too free?
Modern play studies find abundant evidence that play has evolved to keep brains and minds open and flexible, free to consider a wide range of options — something dictators might well fear.
‘By and Large a Grim and Humorless Group’
In any case, Cocks, while noting that “It may well be that the subject of laughter and humor as a weapon of exclusion under Nazism is a subject waiting to be explored,” does reflect that the Nazis “were by and large a grim, humorless group.”
Which is, of course, in no way to say that they might not still have won World War Two. History tells of many victories by grim and humorless leaders who led brutal regimes.
But we instinctively sense a big difference between derisive vaunting laughter that excludes and truly joyful laughter that seems evidence of open-heartedness, the kind of laughter we’d find it hard to imagine in a cruel despot.
It seems that something in addition to “mere play” — perhaps from brain structures that promote empathy and sympathy — needs to moderate pure play if it is to resist abuse for cruel ends.
A Possible Explanation of the Modern ‘Roast’
As Panksepp and Burgdorf point out, the neurobiological study of laughter (and its attendant emotion, joy) as inborn impulses of the brain — both seated deeply in the brainstem right alongside other basic impulses including fear, lust and rage — is in its infancy.
But they do offer a hint about our society’s evolving use of laughter as a way to keep dominant personalities from taking themselves too seriously, which can always be a dangerous characteristic, especially in potential role models.
They point out the complex play of dominance and group-building in a recent comic invention that might have been incomprehensible to some past cultures that took dominance very seriously — the modern “roast.”
“In adults, most laughter occurs in the midst of simple friendly social interactions while greeting and ‘ribbing’ each other rather than in response to explicit verbal jokes,” they write in the “‘laughing’ rats…” article:
“The two are brought together in our institution of ‘roasting’ those we love and admire: The more dominant the targets of the roast, the more mirth there is to be had at their good-humored expense.”
It may lead you to think of the annual Correspondents’ Dinner in Washington, D.C.
In it, the president of the richest and most powerful country on earth is expected to publicly suffer probing jibes of wit and humor — possibly even offer some of his own — to the accompaniment of a great deal of merry laughter, that fertile signal of instructive play in which, say scientists, we learn a great deal about each other … knowledge that may be vital when, all together, we must face some future crisis.

The brain science behind economics

Paul Zak, a pioneer in the field of neuroeconomics, talks about the genes that can make or break a Wall Street trader, and about the chemical that helps us all get along.

TradersNeuroscience might seem to have little to do with economics, but over the last decade researchers have begun combining these disparate fields, mining the latest advances in brain imaging and genetics to get a better understanding of the biological basis for human behavior.

Paul Zak is a pioneer in this nascent field of neuroeconomics. In a recent paper published in the journal PLoS One, he examined genes that may predict success among traders on Wall Street. His forthcoming book, "The Moral Molecule," will explore how a chemical in the brain called oxytocin compels cooperation in society.

Zak, director of the Center for Neuroeconomic Studies at Claremont Graduate University, discussed this work with The Times.

What does a neuroeconomist do?

Neuroeconomics measures brain activity while people make decisions. The reason for doing that is that people can't often clearly articulate why they're doing what they're doing.

About 12 years ago, I had this idea that economists really have the wrong view of the world. The stereotypical view is that human beings are highly rational and primarily motivated by self-interest. But we see people helping strangers all the time. We see people doing things that seem "irrational." So I don't think that's the right approach.

What kinds of questions do you explore?

Why would two people ever trust each other if they're strangers? We do it all the time. We eat meals in restaurants, and we don't see the cooks prepare the food. We get on airplanes with pilots we've never met. We buy all kinds of things over the Internet. Countries with higher levels of trust are more prosperous. Countries with low levels of trust have very few economic transactions and don't create wealth.

If trust is kind of a social glue that sustains societies and economies, we need to understand why. That will help us improve life for the 2 or 3 billion people who live on less than $2 a day.

How do you study the biological basis of trust?

My first focus was on a chemical in the brain called oxytocin. In humans, it was thought to be released only during childbirth and sex. But in rodents, it was known to allow animals to tolerate their burrowmates.

I said, "Gee, toleration of burrowmates and trusting a stranger — maybe that's the same mechanism." So I started taking blood samples to see whether your brain would release oxytocin if someone sent you money via computer in a lab experiment. I also wanted to explore whether the oxytocin effect would motivate you to reciprocate.

And that's what we found. When you trust someone, their brain releases oxytocin. When you give someone a hug, their brain will release oxytocin. If I'm trustworthy, generous, kind, compassionate and empathic, that makes me a nice person to be around, and it sustains me in my social group.

We have a biology for reciprocation. I call oxytocin "the moral molecule." It's a chemical that motivates us to engage and care about others — and that's the basis for moral behavior.

You've also studied dopamine, a chemical that's released in the brain when you're doing something pleasurable.

Yes, in professional stock traders on Wall Street. We asked if there were particular genetic variants that made a trader successful on Wall Street. We collected saliva samples and other information from 60 professional traders and then compared those to MBA students at Claremont who were not trading stocks professionally.

We asked what differentiates the two groups, and whether there was some combination of genes that predicted how long the professional traders could survive on Wall Street. So we looked for genetic markers associated with dopamine, which modulates risk-taking and reward-seeking behaviors.

We found that indeed there was a difference between the traders and the MBA students, and that there was a particular combination of genes that made the traders successful. It was a Goldilocks result. Traders who were most successful had genes that gave them moderate levels of dopamine. They could take a risk when it seemed to have a good payoff and avoid a risk when it seemed likely to blow up in their face. This is what kept them successful on Wall Street.

Super-human brain technology sparks ethics debatbase

LONDON: A British ethics group has launched a debate on the ethical dilemmas posed by new technologies that tap into the brain and could bring super-human strength, highly enhanced concentration or thought-controlled weaponry.

With the prospect of future conflicts between armies controlling weapons with their minds, the Nuffield Council on Bioethics launched a consultation on Thursday to consider the risks of blurring the lines between humans and machines.

"Intervening in the brain has always raised both hopes and fears in equal measure. Hopes of curing terrible diseases, and fears about the consequences of trying to enhance human capability beyond what is normally possible," said Thomas Baldwin, a professor of philosophy at Britain's York University who is leading the study.

"These challenge us to think carefully about fundamental questions to do with the brain: What makes us human? What makes us an individual? And how and why do we think and behave in the way we do?."

The Council, an independent body which looks at ethical issues raised by new developments in biology and medicine, wants to focus on three main areas of neurotechnologies that change the brain: brain-computer interfaces (BCIs), neurostimulation techniques such as deep brain stimulation (DBS) or transcranial magnetic stimulation (TMS), and neural stem cell therapy.

These technologies are already at various stages of development for use in the treatment of medical conditions including Parkinson's disease, depression and stroke, and experts think they could bring significant benefits, especially for patients with severe brain disease or damage.


But they also have huge potential outside the health context. In military applications, BCIs are being used to develop weapons or vehicles controlled remotely by brain signals, and there is big commercial scope in the gaming industry with the development of computer games controlled by people's thoughts.

Speaking at a briefing to launch the consultation, Baldwin said the estimated total global market for all neurotechnologies - including pharmaceuticals for the treatment of brain disorders - is around $150 billion.

"Setting pharmaceuticals aside, the value of the market for the devices and technologies we are dealing with is something in the region of $8 billion, and growing fast," he said.

Kevin Warwick, a professor of Cybernetics at the University of Reading and a supporter of more neurotechnology research, said some experimental brain technologies had great potential in medicine.

"From the brain signals, a brain computer interface could translate a person's desire to move ... and then use those signals to operate a wheelchair or other piece of technology," he said. "For someone who has locked-in syndrome, for example, and cannot communicate, a BCI could be life-changing."

But he and Baldwin also stressed there are concerns about safety of some experimental techniques that involve implants in the brain, and about the ethics of using such technology in other medicine and other fields.

"If brain-computer interfaces are used to control military aircraft or weapons from far away, who takes ultimate responsibility for the actions? Could this be blurring the line between man and machine?" Baldwin said.

Study: Old flu drug speeds brain injury recovery

NEW YORK (AP) - Researchers are reporting the first treatment to speed recovery from severe brain injuries caused by falls and car crashes: a cheap flu medicine whose side benefits were discovered by accident decades ago.
Severely injured patients who were given amantadine got better faster than those who received a dummy medicine. After four weeks, more people in the flu drug group could give reliable yes-and-no answers, follow commands or use a spoon or hairbrush - things that few of them could do at the start. Far fewer patients who got amantadine remained in a vegetative state, 17 percent versus 32 percent.
"This drug moved the needle in terms of speeding patient recovery, and that's not been shown before," said neuropsychologist Joseph Giacino of Boston's Spaulding Rehabilitation Hospital, co-leader of the study. He added, "It really does provide hope for a population that is viewed in many places as hopeless."
Many doctors began using amantadine for brain injuries years ago, but until now there's never been a big study to show that it works. The results of the federally funded study appear in Thursday's New England Journal of Medicine.
A neurologist who wasn't involved in the research called it an important step. But many questions remain, including whether people less severely injured would benefit, and whether amantadine actually improves patients' long-term outcome or just speeds up their recovery.
Each year, an estimated 1.7 million Americans suffer a traumatic brain injury. Falls, car crashes, colliding with or getting hit by an object, and assaults are the leading causes. About three-quarters are concussions or other mild forms that heal over time. But about 52,000 people with brain injuries die each year and 275,000 are hospitalized, many with persistent, debilitating injuries, according to government figures.
With no proven remedies to rely on, doctors have used a variety of medicines approved for other ailments in the hopes that they would help brain injury patients. Those decisions are based on "hunches and logic rather than data," said Dr. John Whyte, of the Moss Rehabilitation Research Institute in suburban Philadelphia. He led the study along with Giacino.
Amantadine, an inexpensive generic, was approved for the flu in the mid-1960s. The first inkling that it might have other uses came a few years later when it appeared to improve Parkinson's symptoms in nursing home patients who got it. It was found to have an effect on the brain's dopamine system, whose many functions include movement and alertness, and it was later approved for Parkinson's.
It's now commonly used for brain injuries, and the researchers felt it was important to find out "whether we're treating patients with a useful drug, a harmful drug or a useless drug," Whyte said.
The study was done in the U.S., Denmark and Germany and involved 184 severely disabled patients, about 36 years old on average. About a third were in a vegetative state, meaning unconscious but with periods of wakefulness. The rest were minimally conscious, showing some signs of awareness. They were treated one to four months after getting injured, a period when a lot of patients get better on their own, Giacino noted.
They were randomly assigned to receive amantadine or a dummy drug daily for four weeks. Both groups made small but significant improvement, but the rate of recovery was faster in the group getting amantadine. When treatment stopped, recovery in the drug group slowed. Two weeks later, the level of recovery in the two groups was about the same.
There was no group difference in side effects, which included seizure, insomnia and rigid muscles.
The study was short, and the effect on long-term outcome is unknown. But Giacino said the drug still has value even if it only hastens recovery.
"What condition would we not jump for joy if we could have it over with faster?" he said.
The study didn't include those with penetrating head injuries, like the gunshot wound former Rep. Gabrielle Giffords suffered, but Giacino said the drug should have similar effects in those patients. Whether it would work in patients with brain injuries not caused by trauma, such as a stroke, isn't known.
Whyte said the researchers want to test the drug for longer periods.
Dr. Ramon Diaz-Arrastia said the results were welcome news in a field that has seen many failed efforts. He is director of clinical research at the government's Center for Neuroscience and Regenerative Medicine, which works with the military and government scientists on brain injury research.
"It's an important step toward developing better therapies," he said.
Since amantadine is so commonly used, he said U.S. troops with severe brain injuries in Iraq or Afghanistan probably get it, or should get it now. Since 2000, some 233,000 troops have suffered traumatic brain injuries, including about 6,100 serious cases, many of them from bomb blasts or shrapnel.
Laura Bacon said amantadine seems to be helping her brother recover from a car accident in Vermont last October. Nicholas Gnazzo, 47, of Rochester, N.H., was in a coma for weeks before he was taken for rehabilitation to Spaulding, where doctors put him on amantadine in January.
Since then he has been more alert, able to communicate with nods or gestures - like pointing to his eyes when he wants his glasses, his sister said. Giacino agreed her brother has gotten better, but whether it is because of the drug can't be determined. Gnazzo wasn't part of the study.
"It's been four months now, and we know we still have a long way to go," Bacon said. "Anything that could be faster - or feel faster to us - is a positive."

Finding unseen damage of traumatic brain injury

This undated handout artist rendering provided by the Schneider Lab, University of Pittsburgh shows an experimental type of scan showing damage to the brain's nerve fibers after a traumatic brain injury. The yellow shows missing fibers on one side of the brain, as compared to the uninjured side in green, in a man left with limited use of his left arm and hand. The soldier on the fringes of an explosion. The survivor of a car wreck. The football player who took yet another skull-rattling hit. Too often, only time can tell when a traumatic brain injury will leave lasting harm _ there's no good way to diagnose the damage. Now scientists are testing a tool that promises to light up breaks that these injuries leave in the brain's wiring, much like X-rays show broken bones. (AP Photo/Schneider Lab, University of Pittsburgh)

The soldier on the fringes of an explosion. The survivor of a car wreck. The football player who took yet another skull-rattling hit. Too often, only time can tell when a traumatic brain injury will leave lasting harm _ there's no good way to diagnose the damage.

Now scientists are testing a tool that lights up the breaks these injuries leave deep in the brain's wiring, much like X-rays show broken bones.

Research is just beginning in civilian and military patients to learn if this new kind of MRI-based test really could pinpoint their injuries and one day guide rehabilitation. It's an example of the hunt for better brain scans, maybe even a blood test, to finally tell when a blow to the head causes damage that today's standard testing simply can't see.

"We now have, for the first time, the ability to make visible these previously invisible wounds," says Walter Schneider of the University of Pittsburgh, who is leading development of the experimental scan. "If you cannot see or quantify the damage, it is hard to treat it."

About 1.7 million people suffer a traumatic brain injury, or TBI, in the U.S. each year. Some survivors suffer obvious disability, but most TBIs are concussions or other milder injuries that generally heal on their own. TBI also is a signature injury of the wars in Iraq and Afghanistan, affecting more than 200,000 soldiers by military estimates.

Not being able to see underlying damage leads to frustration for patients and doctors alike, says Dr. Walter Koroshetz, deputy director of the National Institute of Neurological Disorders and Stroke.

Some people experience memory loss, mood changes or other problems after what was deemed a mild concussion, only to have CT scans indicate nothing's wrong.

Repeated concussions raise the risk of developing permanent neurologic problems later in life, a concern highlighted when some retired football players sued the National Football League. But Koroshetz says there's no way to tell how much damage someone is accumulating, if the next blow "is really going to cause big trouble."

And with more serious head injuries, standard scans cannot see beyond bleeding or swelling to tell if the brain's connections are broken in a way it can't repair on its own.

"You can have a patient with severe swelling who goes on to have a normal recovery, and patients with severe swelling who go on to die," says Dr. David Okonkwo, a University of Pittsburgh Medical Center neurosurgeon who is part of the research. Current testing "doesn't tell you what the consequence of that head injury is going to be."

Hence the increasing research into new options for diagnosing TBI. In a report published Friday in the Journal of Neurosurgery, Schneider's team describes one potential candidate, called high-definition fiber tracking.

Brain cells communicate with each other through a system of axons, or nerve fibers, that acts like a telephone network. They make up what's called the white matter of the brain, and run along fiber tracts, cable-like highways containing millions of connections.

The new scan processes high-powered MRIs through a special computer program to map major fiber tracts, painting them in vivid greens, yellows and purples that designate their different functions. Researchers look for breaks in the fibers that could slow, even stop, those nerve connections from doing their assigned job.

Daniel Stunkard of New Castle, Pa., is among the first 50 TBI patients in Pitt's testing. The 32-year-old spent three weeks in a coma after his all-terrain vehicle crashed in late 2010. CT and regular MRI scans showed only some bruising and swelling, unable to predict if he'd wake up and in what shape.

When Stunkard did awaken, he couldn't move his left leg, arm or hand. Doctors started rehabilitation in hopes of stimulating healing, and Okonkwo says the high-def fiber tracking predicted what happened. The scan found partial breaks in nerve fibers that control the leg and arm, and extensive damage to those controlling the hand. In six months, Stunkard was walking. He now has some arm motion. But he still can't use his hand, his fingers curled tightly into a ball. Okonkwo says those nerve fibers were too far gone for repair.

"They pretty much knew right off the bat that I was going to have problems," Stunkard says. "I'm glad they did tell me. I just wish the number (of missing fibers) had been a little better."

The new tool promises a much closer look at nerve fibers than is now possible through a technique called diffusion tensor imaging, says Dr. Rocco Armonda, a neurosurgeon at Walter Reed National Military Medical Center.

"It's like comparing your fuzzy screen black-and-white TV with a high-definition TV," he says.

Armonda soon will begin studying the high-def scan on soldiers being treated for TBI at Walter Reed, to see if its findings correlate with their injuries and recovery. It's work that could take years to prove.

Other attempts are in the pipeline. For example, the military is studying whether a souped-up kind of CT scan could help spot TBI by measuring changes in blood flow inside the brain. The National Institutes of Health is funding a search for substances that might leak into the bloodstream after a brain injury, allowing for a blood test that might at least tell "if a kid can go back to sports next week," Koroshetz says.

He cautions that just finding an abnormality doesn't mean it's to blame for someone's symptoms.

And however the hunt for better tests pans out, Walter Reed's Armonda says the bigger message is to take steps to protect your brain.

"What makes the biggest difference is everybody _ little kids riding their bicycles, athletes playing sports, soldiers at war _ is aware of TBI," he says.