Your Face, Your Brain, Emotions and Botox

Faces tell stories. A smile of happiness; eyes that open wide in amazement; or a tightening of the forehead that accompanies intense anger; whatever the emotions we are experiencing, they are oftentimes written into our faces.Indeed, most emotions are associated with very distinct facial expressions, involving highly selective recruitment among the muscles of the face.
One of the primary roles our facial muscles play lays in conveying our emotions to others, and we are all natural experts at using our faces to add additional meaning to the words we use in conversation.
Still, our faces do even more than simply translate our emotional state to the outside world; they also read information from the outside world to us:
From the theoretical perspective of embodied cognition, cognitive activity and bodily perception are intricately linked, and even abstract thoughts take shape in the mind by drawing upon the more concrete physical realities of bodily experience. For example, it is not merely a coincidental figure of speech that makes us refer to the future as laying ahead and to the past being behind us, but people who think of the future actually lean slightly forward, and thoughts of the past accompany the physical expression of shifting one's weight backwards.  Likewise inducing forward or backward motion can make future or past thoughts more readily available.
Similarly, embodied cognition theory might suggest that processing emotion-related information should also recruit the bodily representation of these emotions; part of which involve the sensory feedback that our facial muscles send to the brain when we smile, frown, or make any of the other facial expressions that signify our emotions. And indeed, experiments in which people are asked to read and judge the meaning of sentences describing pleasant situations, do show that people are generally quicker at understanding emotional-language when they are holding a pen between their teeth while reading, and slower when try to hold a pen between their lips.
Whhat is the connection, you ask? It's because holding a pen between your teeth forces you to use many of the same muscles you would use in a smile, and holding a pen between your lips requires using muscles that would prevent a smile. Simply using these muscles appeares to subconsciously induce the corresponding emotional state, which then makes it easier (in the case of the smile) or more difficult to comprehend the description of a pleasant situation
So here's a question for you: If the nerves leading to your facial muscles are so important to your brain's ability to process emotion-related information, what might be the effect of injecting a neurotoxin into certain areas of your face? A neurotoxin that that causes temporary muscular denervation in order to decrease activity of specific muscle fibers? A neurotoxin such as botulinum toxin-A, generally referred to as cosmetic botox?
The answer to this question is now documented in the June edition of the Journal Psychological Science, thanks to an experiment by David Havas and colleagues. For their experiment they recruited 41 first-time botox recipients to read emotion-related statements; some describing happy states; others describing angry or even sad states. The researchers measured the time it took participants to understand the meaning of these sentences (participants pressed a button to indicate they were ready), and then immediately sent them off to receive their very first botox shot.
To give you an idea of the different types of sentences, a happy sentence would read

"The water park is refreshing on the hot summer day."

An angry one might read

"The pushy telemarketer won't let you return to your dinner."

And a sad one could read

"You hold back your tears as you enter the funeral home."

In receiving their botox treatment, participants were injected the nerve toxin into the corrugator supercilii muscle; the muscle that pulls the eyebrows down and inward when experiencing negative emotions, and one of the main culprits in producing vertical wrinkles on the forehead.
Since use of the currogator supercilii is associated with the experience of negative emotions, but not with the experience of happy emotions, embodiment theory would suggest that directed denervation through the use of botox would make participants slower at processing sad and angry sentences, but leave their ability to process happy sentences unaffected.
Two weeks after the botox injection, participants were therefore asked back into the lab, where they performed - and were timed on - the same sentence comprehension task as in the first session (sentences were randomized and counterbalanced over participants in both sessions).
The table below shows the statistically significant increase in processing time for the sad and angry sentence, as well as the basically unchanged processing time for happy sentences that David Havas and his colleagues found in the experiment.

The authors interpret these finding as a demonstration that

"blocking facial expression by peripheral denervation of facial musculature selectively hinders emotional-language processing. This finding is consistent with embodied-simulation accounts of cognition, according to which neural systems used in experiencing emotions are also used to understand emotions in language. The finding also offers evidence of a functional role for peripheral activation in processing emotional language, and it suggests a bidirectional link between emotion and language that is mediated in part by moving the face. Finally, the finding provides novel evidence supporting facial- feedback theories of emotion-related processing"

The paper offers further explanations of the possible mechanisms via which botox inhibits emotional-language processing and discusses the theoretical implications.
From a practical perspective, I should point out that - although statistically significant - the effect size is relatively small (around 200 ms). Also, it is not clear to me whether the effect would remain for long-term botox users, or whether their brains would become accustomed to the denervation of particular muscles and compensate for this. Nonetheless, this is an interesting finding that should give many people something to think about. I - for one - wonder what is so bad about wrinkles in the first place...

Damage To The Frontal Cortex Of The Brain Affects Our Ability To React Quickly To A Stimulus

Researchers of the University of Granada have demonstrated that patients who have damage to the right prefrontal cortex of the brain present a deficit in intentional anticipation (for example, when we put the vehicle in gear before the traffic light turns green). The findings of this study were published in the prestigious journal Brain.
Researchers of the University of Granada have demonstrated that patients who have damage to the right prefrontal cortex of the brain –the part involved in anticipation and quick reaction to stimuli- present a deficit in intentional anticipation  (for example, when we put the vehicle in gear before the light turns green). However, these patients keep unintentional anticipation functions intact, which could help develop new therapies.
This study was published in the last issue of the prestigious journal Brain, and was led by Mónica Triviño (Department of Neuropsychology, University Hospital San Rafael, in Granada) and Ángel Correa, Marisa Arnedo and Juan Lupiáñez (Department of Experimental Psychology and Behavioural Physiology, University of Granada).

What is important about the study is that the researchers of the University of Granada have studied for the first time the neural basis in temporal preparation in patients and its connection to other two effects: the reaction-stimulus interval effect, and sequential effects. To this purpose, patients who had prefrontal damage, patients with injuries to basal ganglia circuits and healthy individuals underwent an experimental test.
Methodology
Patients were shown a sign that anticipated a stimulus to which a reaction was expected. The sign did not always anticipate correctly the stimulus, since it sometimes was shown too early or too late. Consequently, there were valid tests (the stimulus appeared just after the sign) and invalid tests (the sign and the stimulus were not synchronized, since the sign was shown too early or too late).
The results showed clear evidence that patients with right prefrontal damage presented deficient temporal preparation, while the other patients (those with damage to the left frontal cortex and to the basal ganglia) obtained the same results as healthy individuals.
As regards the response-stimulus interval, the researchers found that patients with prefrontal damage presented deficient preparation effects, while patients with damaged basal ganglia circuits showed normal effects. Finally, none of the groups –not even frontal-damage related patients– showed any altered sequential reaction.
At present, the authors of this study are analysing the relation between deficit in intentional preparation during reaction time foreperiods exhibited by prefrontal damage-related patients and their precipitation when it comes to react to a stimulus. Within their therapeutical application, researchers are analysing in what measure patients provided with rhythms (that is, basing on unintentional responses) this type of patients can improve their temporal preparation.

How crack works

Crack cocaine makes you feel like a new man; the only problem is the new guy wants more cocaine.
That maxim, part of a 1990s public service campaign in the United States, conveys a hard truth: crack delivers an intense, but brief high that can trigger powerful cravings for more stimulation.
Crack invaded inner cities in the mid-1980s, offering a cheap alternative to the powdered form of cocaine. More than two decades later, crack remains a central feature of the drug landscape in Ottawa and other North American cities.
The physiology of crack use helps to explain why it has become so firmly entrenched.
Crack speeds delivery of cocaine’s powerful chemical impact. When a rock of crack is heated — usually in a small glass pipe — it produces smoke that’s drawn into the lungs. The lungs are super efficient at transferring the vapourized cocaine from air sacs (alveoli) to tiny blood vessels (capillaries).
Once in the bloodstream, the drug is whisked to the brain’s main pleasure centre within seconds.
That centre, known as the ventral tegmantal area (VTA), is made up neurons in the middle of the brain. The centre is vital to the survival of the human species since it generates a pleasurable sensation for behaviour that sustains people — eating, drinking … sex.
An evolutionary feature, the system reinforces essential human behaviour with what amounts to brain candy: dopamine. That chemical messenger informs other parts of the brain’s reward circuit that the body’s fundamental needs are being met.
The cocaine molecule produced by smoking crack hijacks this reward system.
Cocaine overstimulates the circuit by preventing dopamine from being reabsorbed by those neurons that first issued the neurotransmitter. As a result, the brain is flooded with dopamine that continues to send its euphoric message to other neurons.
Crack’s impact on brain chemistry means users can also experience surges in confidence and energy. But the high, while quickly delivered, is fleeting: a typical hit lasts anywhere from five to 15 minutes.
While it works on the brain, cocaine also changes the body. Its short-term effects include constricted blood vessels, dilated pupils and an increase in the body’s heart rate, respiratory rate, temperature and blood pressure. Some people become agitated or nervous under influence of the drug.
In rare cases, first-time cocaine users can suffer fatal effects.
“Cocaine-related deaths are often a result of cardiac arrest or seizures followed by respiratory arrest,” according to a 2009 research report by the U.S. National Institute on Drug Abuse. “Research has also revealed a potentially dangerous interaction between cocaine and alcohol. In fact, this mixture is the most common two-drug combination that results in drug-related death.”
Not everyone who smokes crack becomes addicted. But because the drug produces such a quick, intense high, it is dangerous, particularly to those with a genetic predisposition to addiction.
Studies have shown that people with naturally low dopamine levels — those with depression often suffer the condition — experience more intense highs from stimulants such as crack.
“So if you have a genetic predisposition, you get a bigger bang for your buck whenever you use the drug: You get a greater amount of dopamine released,” explains Dr. Peter Selby, clinical director at Toronto’s Centre for Addiction and Mental Health.
Cocaine can cause people to “crash” when they stop using it, he said, because they move quicky between euphoria and irritability. That can bring powerful cravings for more of the drug, which in turn can lead to binges and addiction.
The physiological effects of long-term crack use are profound.
The brain can develop an increased tolerance to the drug that requires users to smoke more crack to obtain the same high. Computer imaging has revealed that cocaine physically alters the brain: the number of available dopamine receptors is significantly reduced in an addict.
Chronic crack smokers are more likely to suffer panic, paranoia, hallucinations, depression, nausea and seizures.

“New optimism” as brain scans point to Alzheimer’s gene targets

US researchers have shown that genetic variations associated with Alzheimer’s can affect brain imaging measurements, strengthening evidence that the genes have a role in the development of the disease and for their importance as treatment targets.

The UK’s leading dementia scientists describe the findings as marking “a new period of optimism” for research. The findings are reported in Archives of Neurology today.

Recent genome wide association studies (GWAS) identified several genetic variations associated with Alzheimer’s disease. In this study the researchers studied the influence of the variations on specific brain imaging measurements, including the size of the hippocampus – the part of the brain that makes new memories.
The well known APOE gene had the strongest association with clinical Alzheimer's and was associated with all but one of the imaging measurements. The other, potential, genes showed a significant cumulative effect on the neuroimaging measures analyzed.
Prof John Hardy, University College London, Institute of Neurology, and Prof Julie Williams, Medical Research Council Centre for Neuropsychiatric Genetics and Genomics, Cardiff University write in an accompanying editorial:
"These findings, and the genome-wide studies that presaged them, mark a new period of optimism for those of us who study ... complex diseases of the nervous system."
"While the drought of genetic findings in Alzheimer's disease has lasted a long time, the flood of new findings have been a reward worth waiting for."
Rebecca Wood, Chief Executive of the Alzheimer’s Research Trust, said:
“Our understanding of the genetics of Alzheimer’s is growing, and this important development helps us zero in on treatment targets. The Alzheimer’s Research Trust is investing heavily to capitalise on the potential of genetic studies as quickly as possible to give hope for effective treatments.
“Research like this offers the only chance of abating the coming dementia crisis. With 820,000 people in the UK living with dementia now, we must invest in research to equip our scientists with everything they need to give us hope for a treatment breakthrough.”

Excessive cell phone use enhances risk of brain tumor--study

Service providers and customers may call it a ring tone, but researchers have categorized it as a danger bell!

If findings of a new study are anything to go by, incessant use of the cell phone may result in brain tumor.
Previous studies have also established the link between excessive mobile phone use and brain tumor.

Previous studies have also established the link between excessive mobile phone use and brain tumor.
However the present 17 million pounds study establishes that the risk of contracting the disease is at least 25 percent higher than what the earlier studies showed.
The decade-long Interphone study, initiated by an UN World Health Organization agency, concluded that making calls for more than half an hour a day enhances users’ risk of developing brain cancer by as much as 40 percent.
Need to educate users
"What we have discovered indicates there is going to be one hell of a brain tumor pandemic unless people are warned and encouraged to change current cell phone use behaviours,” noted Lloyd Morgan, a member of America’s Environmental Health Trust lobby group.
Morgan highlighted that urgent steps, including education of the masses, must be initiated by the government immediately.
“Governments should not soft-peddle this critical public health issue but instead rapidly educate citizens on the risks,” he said.
“People should hear the message clearly that cell phones should be kept away from one’s head and body at all times,” opined Morgan.
Findings blown out of proportion
Cancer charities claim that the findings of the study, which was carried out in 13 countries across the world, were “overblown”.
Ed Yong, head of health information at Cancer Research UK, said, "The warnings of a ‘brain tumour pandemic’ are overblown.
“The majority of studies in people have found no link between mobile phones and cancer, national brain cancer rates have not increased in proportion to skyrocketing phone use and there are still no good consistent explanations for how mobile phones could cause cancer.”
He said that the findings of the present study, even after minor adjustments are incorporated, are still not statistically significant.
Researchers also admit that the results of the study are not irrefutable and that some element of statistical error or bias may have crept in.
Morgan feels that the main problem in the study was the “selection bias”. Many of the healthy participants chosen for assessment with tumor sufferers were apt to be mobile phone users themselves.
Other subjects, whose experience would have been helpful to the study, were either too ill to take part or did not take part in the study on their own.
“This means that any link between mobile phones and cancer that the conference presentation quotes could well be down to chance or anomalies in the data they collected,” Yong said.

Female stress: Brain chemistry link

Women may be more prone to emotional stress than men because of their brain chemistry, scientists have said.
A study has shown that females are more sensitive to low levels of a key stress hormone.
Although the research was conducted on rats, the same signalling pathway is known to play a role in human psychiatric conditions.
"This may help to explain why women are twice as vulnerable as men to stress-related disorders," said US study leader Dr Rita Valentino, from the Children's Hospital of Philadelphia.
Women have higher rates of depression, post-traumatic stress disorder and other anxiety problems than men.
However no-one has yet been able to pinpoint a biological reason for the difference.
The new research, published in the online journal Molecular Psychiatry, focuses on a hormone that organises stress responses in mammals called corticotropin-releasing factor (CRF).
A study of rats undergoing a swim stress test showed female animals had neurons that were more sensitive to CRF. The scientists also found that stressed male rats adapted by making themselves less responsive to the hormone, but females did not.
Dr Valentino pointed out that other mechanisms also played a role in human stress responses. But it was already known that CRF regulation was disrupted in people with stress-related psychiatric disorders. Since much of the previous animal research on stress used only male rodents, important sex differences may have gone undetected, she added.
"Pharmacology researchers investigating CRF antagonists (blocking agents) as drug treatments for depression may need to take into account gender differences at the molecular level," said Dr Valentino.

Guys, relax... sex is all in your brain

I have some excellent news for guys.
It's not our fault. If you do not catch my general drift, I will gladly spell it out for you -- S-E-X.
Yes, guys, if you take the time to remove all the hyphens, you will see I'm talking about sex. Specifically, I am talking about the fact that, according to statistics I once heard on TV, your average man thinks about sex roughly every seven seconds.
That means persons of my gender think about sex more often than... OK, sorry, what was I saying... Oh, yes, I was talking about the fact guys think about sex almost as much as they think about their barbecues and watching sports highlights.
Like I was saying, this is not our fault. This is not just my opinion; it's the opinion of top scientists. According to a news story I read and partially understood, these scientists have just discovered that sex addiction -- defined as when you care more about sex than you do about watching NASCAR -- is caused by a dysfunction in "a critical brain region that controls decision-making."
Yes, you read that sentence correctly, men. According to actual federally funded scientific research, YOU are not the problem. YOUR BRAIN is the problem. Is that great scientific news, or what? (Hint to male readers: Yes, if you know what's good for you, it is.) This is also the kind of news that tends to divide readers along gender lines as follows:
Typical male reaction: "I told you it wasn't my fault!"
Typical female reaction: "I want a divorce!"
This news story, which appeared on this page Monday under the headline "Brain dysfunction, sex addiction linked," states researchers have discovered male rats with a damaged prefrontal cortex become hooked on sex.
The story quotes Dr. Lique Coolen, Canada Research Chair in the Neurobiology of Motivation and Reward, as saying: "We're always very cautious to draw parallels between studies in rodents with human behaviours."
So, yes, we need to be cautious if we are trying to draw conclusions about human beings, but it's a different story if we are talking about lawyers, teenagers, telemarketers and probably every guy I have ever met in my life.
For the study, the scientists taught male rats to associate having sex with a negative consequence, such as getting sick to their stomachs. We assume the rats were also provided with tiny cigarettes and tiny stereo systems playing Barry White albums.
Anyway, when lesions were made in their prefrontal cortexes (I am talking about the rats' brains, not the researchers), the male rats were still eager to have sex, even though their brains knew something really bad was going to happen.
This is typical guy behaviour. History has shown most guys will want to go to bed with any woman who will look in their general direction, even if scientists warn them this kind of "risky behaviour" may result in the male eventually having to deal with a negative consequence in the form of creating teenagers who think he is a major dork.
However, this study does raise some troubling questions, such as: How the heck do these researchers ever get dates? Seriously, what do they talk about when they go to singles bars?
Single woman: "So, what do you do?"
Researcher: "I watch rats get busy?"
Single woman: "Did I mention I'm carrying a gun?"
I personally am not surprised by the results of this brain research, especially the fact that guys are still interested in sex, even if they know it will be followed by a terrible outcome.
This is because guys my age learned about sex in school. Back in the 1950s and early 60s, we had something called "Hygiene Class," wherein we would be shown grainy black-and-white movies featuring two innocent teenagers, usually Billy and Sally, who would do something brazenly foolish, such as openly holding hands at the school dance, which would result in a negative consequence in the form of Billy and Sally being crushed to death by a comet.
The important thing is science has given us a reasonable explanation for the behaviour of normal guys like Tiger Woods and Jesse James. They couldn't help themselves.
I tried to explain this scientific concept to my wife, but she didn't seem to buy it.
"It's all in your head," she sniffed.
"I know," I told her, "That's the problem!"

Brain Circuitry May Develop Through Adulthood

Working with mice, researchers detect changes in wiring previously thought to be fixed

TUESDAY, June 15 (HealthDay News) -- The brain's wiring isn't fixed in early life, and circuits in the adult brain are continually modified by experience, suggests a new study involving mice.
U.S. researchers found that neurons responsible for receiving input from an adult mouse's whiskers alter their relationships with one another after single whiskers are removed.
The findings show that changes in adulthood can occur in a region of the brain called the somatosensory cortex, which processes input from various parts of the body that respond to touch.
The Rockefeller University study was published June 15 in the journal PLoS Biology.
"We are just beginning to tease apart the mechanisms of adult cortical plasticity," team leader Charles D. Gilbert, head of the neurobiology laboratory at Rockefeller, said in a journal news release.

'Adult brain is continually modified by experience'

Washington: Experience shapes the brain's circuitry throughout adulthood, according to a new American study.
The research, conducted by Rockefeller University scientists, will be published next week in the online, open access journal PLoS Biology.
The researchers, led by Charles D. Gilbert, Arthur and Janet Ross Professor and head of the Laboratory of Neurobiology, observed how neurons responsible for receiving input from a mouse's whiskers shift their relationships with one another after single whiskers are removed.
The experiments explain how the circuitry of a region of the mouse brain called the somatosensory cortex, which processes input from the various systems in the body that respond to the sense of touch, can change.
In the new study, Sally Marik and other members of the Gilbert lab looked at excitatory and inhibitory neurons within the mouse cortex during periods of sensory deprivation to determine how experience shapes different components of cortical circuitry.
For this study they used the whisker-barrel system in adult mice. The barrel cortex, part of the somatosensory cortex, receives sensory input from the animal's whiskers.
Scientists have shown that after a row of whiskers is removed, barrels shift their representation to adjacent intact whiskers.
Marik, together with Homare (Matias) Yamahachi and Justin McManus, found that after a whisker was plucked excitatory connections projecting into the deprived barrels underwent exuberant and rapid axonal sprouting.
This axonal restructuring occurred rapidly - within minutes or hours after whiskers were plucked - and continued over the course of several weeks.
At the same time that excitatory connections were invading the deprived columns, there was a reciprocal outgrowth of the axons of inhibitory neurons from the deprived to the non-deprived barrels.
This suggests that the process of reshaping cortical circuits maintains the balance between excitation and inhibition that exists in the normal cortex.
Gilbert said: "Previously we showed changes only in excitatory connections.
"We've now demonstrated a parallel involvement of inhibitory connections, and we think that inhibition may play a role equal in importance to excitation in inducing changes in cortical functional maps."
The new study also showed that changes in the inhibitory circuits preceded those seen in the excitatory connections, suggesting that the inhibitory changes may mediate the excitatory ones.
This process, Gilbert said, mimics what happens in the brain during early postnatal development.
Gilbert said: "It's surprising that the primary visual or somatosensory cortices are involved in plasticity and capable of establishing new memories, which previously had been considered to be a specialized function of higher brain centers.
"We are just beginning to tease apart the mechanisms of adult cortical plasticity. We hope to determine whether the circuit changes associated with recovery of function following lesions to the central and peripheral nervous systems also occur under normal conditions of perceptual learning."