Reprinted from Sify News, July 29, 2010

A specific part of our brain processes information about human and animal faces and is responsible for how we recognize them and interpret facial expressions. Now, Israeli researchers are exploring what makes this highly specialized area of the brain unique.

In her “Face Lab” at Tel Aviv University, Dr. Galit Yovel of TAU’s Department of Psychology is trying to understand the mechanisms at work in the face area of the brain called the “fusiform gyrus” of the brain. She is combining cognitive psychology with techniques like brain imaging and electrophysiology to study how the brain processes information about faces. Her most recent research on the brain’s face-processing mechanisms appears in the Journal of Neuroscience and Human Brain Mapping.

The study of face recognition does more than provide an explanation for embarrassing memory lapses. For instance, it may help business executives better match names with faces, and more important can lead to better facial recognition software to identify terrorists or criminals. Similar to faces, bodies are also processed by distinct brain areas. How we perceive faces is not totally intuitive, she says, and therefore raises the question of how this information is combined in our brain to understand how separate face and body areas generate a whole body-image impression. 

In her research, Dr. Yovel has found that we are better able to recognize faces when we regularly see and interact with them in meaningful settings. It’s as though the face-processing sections of the brain – the fusiform face area being the most distinct – recognizes faces holistically. Additions to your face, such as a beard or glasses, are assimilated into or incorporated into the face recognition gestalt of the brain, unlike other elements that are irrelevant to facial recognition, such as the chair you’re sitting on. This may be why fashions in hairstyle and eyewear have become so important to personal appearance, she theorizes.

The inability to recognize faces is more common than most people think. Dr. Yovel says that two percent of all people are born with “face blindness,” scientifically known as prosopagnosia. She hopes her research will enable these people to train themselves, via software and other methods, to better differentiate one face from another – especially when the face is that of a loved one.

“Faces are important. We meet so many people every day, on the street or at work, and should know whether or not each face is important to us. In principle, faces are very similar to one another. That’s probably why we’ve evolved these complex and specialized face areas in the brain – so that we can more accurately discriminate among the countless faces we encounter throughout our lives,” says Dr. Yovel, who first began to study the neurological basis of face recognition as a post-doctoral student at the Massachusetts Institute of Technology.

Dr. Yovel hopes her studies will lead to new algorithms that can help computers do a better job of recognizing faces, as well as help people who somehow lack this critical social skill. She is currently collaborating with computer scientists at Tel Aviv University to explore new computational algorithms for facial recognition. (ANI)

Integrative Management of ADHD: What the Evidence Suggests

Provided as a public service of the American Health Assistance Foundation

On this page, you will find the following:

• Risk Factors
  • Heredity
• Prevention
  • Diet
  • Exercise
  • Building Brain Reserves & Social Engagement
  • NSAIDS
  • Estrogen

Risk Factors

Scientists have identified factors that appear to play a role in the development of Alzheimer’s disease, but no definitive causes have been found for this complex disorder.

Known Risk Factors

• Age: The single greatest risk of developing Alzheimer’s disease is age. Approximately 5 percent of Americans between the ages of 65 and 74, and almost half of those 85 years and older are estimated to have Alzheimer’s.
• Genetics: The majority of Alzheimer’s cases are late-onset, usually developing after age 65, and this form of the disease shows no obvious inheritance pattern. However, in some families, clusters of cases are seen. A gene called Apolipoprotein E (ApoE) appears to be a risk factor for the late-onset form of Alzheimer’s. There are three forms of this gene: ApoE2, ApoE3 and ApoE4. Roughly one in four Americans has ApoE4 and one in twenty has ApoE2. While inheritance of ApoE4 increases the risk of developing the disease, ApoE2 substantially protects against it. Some current research is focused on the association between these two forms of ApoE and Alzheimer’s disease. Several other genes also appear to influence the development of Alzheimer’s disease, and more detailed information is available in the Heredity section.
  Familial Alzheimer’s disease (FAD) or early-onset Alzheimer’s is an inherited, rare form of the disease, affecting less than 10 percent of patients. Familial Alzheimer’s Disease develops before age 65, in people as young as 35. It is caused by one of three gene mutations on chromosomes 1, 14 and 21.

Potential Contributing Factors   

• Cardiovascular disease: Risk factors associated with heart disease and stroke, such as high blood pressure and high cholesterol, may also increase one’s risk of developing Alzheimer’s disease. High blood pressure may damage blood vessels in the brain, disrupting regions that are important in decision-making, memory and verbal skills. This could contribute to the progression of the disease. High cholesterol may inhibit the ability of the blood to clear protein from the brain.

• Type 2 Diabetes: There is growing evidence of a link between Alzheimer’s disease and type 2 diabetes. In Type 2 diabetes insulin does not work effectively to convert blood sugar into energy. This inefficiency results in production of higher levels of insulin and blood sugar which may harm the brain and contribute to the progression of Alzheimer’s.

• Oxidative Damage: Free radicals are unstable molecules that sometimes result from chemical reactions within cells. These molecules seek stability by attacking other molecules, which can harm cells and tissue and may contribute to the neuronal brain cell damage caused by Alzheimer’s.

• Inflammation: Inflammation is a natural, but sometimes harmful, healing bodily function in which immune cells rid themselves of dead cells and other waste products. As protein plaques develop, inflammation results, but it is not known whether this process is damaging and a cause of Alzheimer’s, or part of an immune response attempting to contain the disease.

• Other Possible Risk Factors: Some studies have implicated prior traumatic head injury, lower education level and female gender as possible risk factors. Alzheimer’s disease may also be associated with an immune system reaction or a virus.

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Heredity

Familial Alzheimer’s disease (FAD) or early-onset Alzheimer’s is an inherited and rare. It affects less than 10 percent of Alzheimer’s disease patients. Familial Alzheimer’s disease develops before age 65, in people as young as 35. It is caused by gene mutations on chromosomes 1, 14 and 21. If even one of these mutated genes is inherited from a parent, the person will almost always develop Familial Alzheimer’s disease. All offspring in the same generation have a 50/50 chance of developing this type of Alzheimer’s if one parent has it.

The majority of Alzheimer’s disease cases are late-onset, usually developing after age 65. Late-onset Alzheimer’s disease has no known cause and shows no obvious inheritance pattern. However, in some families, clusters of cases are seen. Although a specific gene has not been identified as the cause of late-onset Alzheimer’s disease, genetic factors do appear to play a role in the development of this form of the disease. A gene called Apolipoprotein E (ApoE) appears to be a risk factor for the late-onset form of Alzheimer’s disease. There are three forms of this gene: ApoE2, ApoE3 and ApoE4. Roughly one in four Americans has ApoE4 and one in twenty has ApoE2. While inheritance of ApoE4 increases the risk of developing Alzheimer’s disease, ApoE2 substantially protects against it.
Scientists believe that several other genes may influence the development of Alzheimer’s disease. Two of these genes, UBQLN1 and SORL1, are located on chromosomes 9 and 11. Researchers have also identified three genes on chromosome 10, one of which produces an insulin degrading enzyme that may contribute to the disease. A gene, called TOMM40, appears to significantly increase one’s susceptibility to developing Alzheimer’s when other risk factors are present, such as having the ApoE-4 gene. Several recently discovered genes that influence Alzheimer’s disease risk are CLU (also called APOJ) on chromosome 8, which produces a protein called clusterin, PICALM on chromosome 11 and CR1 on chromosome 1.

Genetic risk factors alone are not enough to cause the late-onset form of Alzheimer’s disease, so researchers are actively exploring education, diet and environment to learn what role they might play in the development of this disease.

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Prevention

Alzheimer’s disease is a complex disorder, for which there is currently no known prevention or cure. Some research has generated hope that one day it might be possible to slow the progression of Alzheimer’s disease, delay its symptoms or even prevent it from occurring at all. Although there is preliminary data to support the benefit of some interventions, such as physical activity and cardiovascular risk reduction, nothing at this time has definitively been shown to prevent Alzheimer’s disease or other dementias.  The scientific advisors of the American Health Assistance Foundation (AHAF) do not currently recommend or endorse any commercial nutritional supplement, exercise program, or cognitive training exercises for the purposes of preventing Alzheimer’s disease. In spite of this, AHAF encourages people to evaluate the role of these interventions on the overall health and spirits of both the patient and caregivers

Diet

A number of preliminary studies suggest that how we eat may raise or lower our risk of developing Alzheimer’s disease. Eating a diet that is high in whole grains, fruits, vegetables and that is low in sugar and fat can reduce the incidence of many chronic diseases, and researchers are continuing to study whether these dietary modifications are also applicable to Alzheimer’s disease.  However, the strongest research supporting these modifications has been performed in animal studies, and remains to be rigorously established in randomized and controlled clinical trials.

There are, however, some exciting reports, that though currently preliminary, may one day be shown to protect against Alzheimer’s disease. Many of these modifications have also been shown to be part of overall healthy lifestyles that are likely to protect against other diseases as well. For example,  researchers found that clinical trial participants who adhered to a Mediterranean diet have a slower decline on the mini-mental state examination (MMSE) cognitive decline.  The Mediterranean diet may be protective against other diseases as well, including age-related macular degeneration.  Also, vitamin D3 has been shown to have neuroprotective effects that may preserve cognitive function. This vitamin is produced naturally by the body from exposure to the sun, and is also being studied by AHAF supported scientists for its potential protective effects against glaucoma.

Some studies conducted in animals have shown that including blueberries, strawberries, and cranberries in the diet can lead to improved cognitive function, both in animals that age normally and in those that have been bred to develop “Alzheimer’s disease.”  Scientists are beginning to study what chemicals within these berries might be responsible for their beneficial effects.

Curcumin is a spice typically found in turmeric which is used to enhance the flavor of curries and meats in Indian cuisine. Currently researchers are studying the effects of curcumin on the human brain. Recent research implies that curcumin might actually reduce the amount of beta-amyloid plaques associated with Alzheimer’s disease.  The problem with curcumin is that, in its natural state it is very difficult for a human body to absorb curcumin consumed as food.  Once in the blood stream, it is also quite difficult for curcumin pass from the blood to the brain.   AHAF funded scientists are studying whether special preparations of curcumin might overcome these limitations.   Similarly, a study conducted on green tea and Alzheimer’s disease indicates that an antioxidant found in green tea, called epigallocatechin gallate (EGCG), has powerful anti-plaque ability and may actually prevent or delay Alzheimer’s disease.

Switching from animal based oils and vegetable oil to extra virgin olive oil may also be a good habit to adopt. According to recent research, not only is extra virgin olive oil a generally healthy food, but it may prevent Alzheimer’s disease as well. Studies suggest that oleocanthal, a naturally-occurring compound found in extra-virgin olive oil, changes the structure of Amyloid beta-Derived Diffusible Ligands (ADDLs). ADDLs are proteins that are toxic to nerve cells and may contribute to the symptoms of Alzheimer’s disease. By structurally changing ADDLs, oleocanthal may be stopping the proteins’ ability to damage nerve cells within the brain.

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Exercise

Exercise is an important activity to add to a healthy lifestyle. AHAF encourages people to discuss exercise plans with their health care provider, so that an appropriate exercise program can be tailored for your specific needs.  Studies conducted on those with mild cognitive impairment (MCI) indicate that aerobic exercise may improve cognitive agility. In one study, investigators looked at the relationship between physical activity and ones’ risk of developing Alzheimer’s disease. 1,700 adults aged 65 years and older were observed over a 6-year period in this study. Results showed that the risk of Alzheimer’s disease was 35 to 40 percent lower in those who exercised for at least 15 minutes 3 or more times a week than in those who exercised fewer than 3 times a week.

While it is not proven that exercise could prevent Alzheimer’s disease or slow its’ progression, animal studies and preliminary human studies have produced significant interest amongst scientists.  Larger, and more rigorous, randomized controlled trials will be necessary before a definitive statement on the role of exercise in the prevention of Alzheimer’s disease can be made. In spite of this, developing an exercise program as part of an Alzheimer’s disease patient’s routine may also be helpful with maintaining muscle strength, decreasing frailty, and elevating mood.

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Building Brain Reserves & Social Engagement

Many people born between 1945 and 1964 or “baby boomers” are beginning to worry about Alzheimer’s disease. Millions are already caring for their parents and watching them fade away, and they realize they may be next in line. Although there is currently no cure, scientists believe there are ways to lower the risk of developing Alzheimer’s disease by continually “exercising” our brains. Some research suggests that shoring up mental reserves as we age may protect against the onslaught of Alzheimer’s. This approach may also delay onset of the disease or possibly help retain cognitive function longer if it does strike.

Building cognitive reserves is a lifelong process that begins in childhood as we expand reading skills. According to classic neurological theory, during the early developmental stages of life, the human brain forms an enormous number of neurons, or nerve cells, but many of these cells also die. The neurons that survive do so by connecting with other neurons during the rapid-growth stage of the nervous system that occurs in childhood and adolescence. Reading progressively more challenging books, learning a musical instrument, creating art, playing chess and engaging in any mental activity all help form these vital neural connections that can last a lifetime, and appear to buffer people from cognitive decline later on.

Fortunately, according to the theory of "neuroplasticity," brain reserves can be expanded throughout life, even into advanced old age. A team of researchers led by Dr. David Bennett, M.D., director of the Rush Alzheimer’s Research Center, has studied neuroplasticity in adults. These scientists found that those who continue to learn, to embrace new activities, learn new skills – in essence, to exercise their brains — continue to build up connections that in turn lower their risk of Alzheimer’s disease. Perhaps they have begun to develop the disease, but they show no symptoms because they have brain cells to spare.

Another study led by Dr. Robert Friedland, of Case Western Reserve University School of Medicine, compared mental, physical and social activity levels in adults with rates of developing Alzheimer’s disease. The researchers discovered that the more active adults, those who played a musical instrument, gardened, and played mentally engaging board games, for example, were significantly less likely to develop Alzheimer’s disease. The benefit extended to those who were active between the ages of 40 and 60, so it’s never too late to start building intellectual muscle, and stimulating hobbies have a pay-off regardless of the age they are started.

Each of these studies, though hopeful and promising, require replication before their impact on risk of Alzheimer’s disease can be confirmed.  But what does it hurt?  While AHAF does not recommend any commercial products that advertise Alzheimer’s disease prevention, learning new skills or enriching your life in study of a favorite topic is an act of empowerment that AHAF recommends for all people at any age.

It is never too late to start new and creative activities. Continue to enjoy favorite pastimes, but challenge yourself by learning something new. Try a foreign language, read books and newspapers, solve puzzles and brain teasers, sing, dance, play board and video games, correspond by mail and email and engage in conversation. The combination of social, mental and physical stimulation is really the best medicine we have for a healthy life.

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NSAIDS

Over the past couple of years, reports have been surfacing that NSAIDs like Ibuprofen, Naproxen and COX-2 inhibitors might actually prevent Alzheimer’s disease. Researchers have been rigorously studying the relationship between NSAID use and Alzheimer’s disease and no benefit has been demonstrated. Despite these results, scientists continue to look for ways to test how other anti-inflammatory drugs might affect the development or progression of Alzheimer’s disease.

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Estrogen

Over the past several years, estrogen has been recognized as having a protective role in the brain. However, its’ potential role in the development of Alzheimer’s disease has yet to be determined. In fact, clinical trials have shown that estrogen does not slow the progression of already-diagnosed Alzheimer’s disease and is not effective in treating or preventing AD if treatment is begun in later life.

One large trial found that women older than 65 who began taking estrogen in the form of Premarin® or PremPro® were actually at an increased risk of developing Alzheimer’s disease and dementia. Although results from such studies were disappointing, many questions remain. For instance, would starting estrogen therapy closer to menopause be more effective in preventing Alzheimer’s disease? These questions and other concerns related to estrogen’s relationship with Alzheimer’s disease are currently being studied in clinical trials.

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Disclaimer: The information provided in this section is a public service of the American Health Assistance Foundation, and should not in any way substitute for the advice of a qualified healthcare professional and is not intended to constitute medical advice. Although we take efforts to keep the medical information on our website updated, we cannot guarantee that the information on our website reflects the most up-to-date research. Please consult your physician for personalized medical advice; all medications and supplements should only be taken under medical supervision. The American Health Assistance Foundation does not endorse any medical product or therapy.

Last Reviewed On: 04/22/10

By Geoff Adams-Spink , April 23, 2010
Age & disability correspondent, BBC News website

The father of a child with severe autism has developed technology to help him communicate.

Stephen Lodge said the idea for his Speaks4Me system came to him years ago but has been waiting for technology to catch up in order to make it a reality.

His eleven-year-old son, Callum, is non-verbal and uses his father’s invention to speak.

Speaks4Me was on show at Naidex 2010 – the annual disability exhibition at the NEC in Birmingham.

Mr Lodge’s system runs on any device that can run the Windows XP, Vista and Windows 7 operating system.

It uses the concept of dragging and dropping images from one area of the screen to another to form sentences.

The user then presses a speech button to "verbalise" the sentence.

"Callum has been using Speaks4Me for some time now and he has already been able to create some very expressive sentences," Mr Lodge told the BBC.

Examples include, "I want a drink of juice", "I want to go outside", and "I feel tired".

Mr Lodge – who lives in South Yorkshire – has 20 years’ experience in technology and developed Speaks4Me after deciding that other products on the market were unsatisfactory for Callum.

He cashed in his savings and raised money on his property in order to finance the venture.

Speaks4Me is currently sold on a portable, touch screen media player imported from the Far East.

But the company is finalising a "software only" price which will mean that it can run on any Windows laptop, desktop or even an interactive plasma white board in schools.

Mr Lodge says that several people have already tried the system.

"It’s fabulous to see how such an exciting but simple concept is well understood by the children that have been introduced to it," he said.

Mr Lodge estimates it takes half an hour or less to be able to understand and use the system.

He is also hoping that it will prove useful to stroke survivors – about a third of whom lose the ability to speak, either temporarily or permanently.

"Imagine waking up in hospital, not being able to speak: how would you ask for the toilet?" he said.

Speaks4Me currently retails for about £2,000.

Mr Lodge says his future plans include being able to put his software on other portable devices such as mobile phones and gaming handsets.

On call

Also having its UK launch at Naidex was a French product called the Minifone.

It is being sold in the UK by Essex-based PivoTell which describes the product as the world’s smallest digital cordless phone.

Designed with older and disabled people in mind, the Minifone is worn like a wrist watch.

It can be used to summon help from three pre-programmed numbers and has the additional option of being connected to a call centre.

Provided that the landline has caller line identification (CLI) enabled, the Minifone will also display the date and time and the name or number of an incoming caller.

The Minifone uses a built-in speaker and microphone.

"The experience in France has been that – unlike alarm pendants which have a certain stigma attached – people find these quite attractive and so are more likely to be wearing them," said Adrian Milne of PivoTell.

The device costs £150 and a subscription to the call centre is £10 per month.

Naidex 2010 was at the National Exhibition Centre in Birmingham from 20 – 22 April.

Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/technology/8634607.stm
Published: 2010/04/23 10:05:02 GMT

Since the Jan. 14 death of Phoebe Prince, the 15-year-old in South Hadley, Mass., who committed suicide after being bullied by fellow students, many onlookers have meditated on whether the circumstances that led to her after-school hanging might have been avoided.

Could teachers have stepped in and stopped the bullying? Could parents have done more to curtail bad behavior? Or could preventive measures have been started years ago, in early childhood, long before bullies emerged and started heaping abuse on their peers? (Read what can be done about bullying in school.)

Increasingly, neuroscientists, psychologists and educators believe that bullying and other kinds of violence can indeed be reduced by encouraging empathy at an early age. Over the past decade, research in empathy — the ability to put ourselves in another person’s shoes — has suggested that it is key, if not the key, to all human social interaction and morality.

Without empathy, we would have no cohesive society, no trust and no reason not to murder, cheat, steal or lie. At best, we would act only out of self-interest; at worst, we would be a collection of sociopaths.

Although human nature has historically been seen as essentially selfish, recent science suggests that it is not. The capacity for empathy is believed to be innate in most humans, as well as some other species — chimps, for instance, will protest unfair treatment of others, refusing to accept a treat they have rightfully earned if another chimp doing the same work fails to get the same reward.       

The first stirrings of human empathy typically appear in babyhood: newborns cry when hearing another infant’s cry, and studies have shown that children as young as 14 months offer unsolicited help to adults who appear to be struggling to reach something. Babies have also shown a distinct preference for adults who help rather than hinder others. (Read about the link between bullying and suicides.)

But, like language, the development of this inherent tendency may be affected by early experience. As evidence, look no further than ancient Greece — at the millennia-old child-rearing practices of Sparta and Athens. Spartans, who were celebrated almost exclusively as warriors, raised their ruling-class boys in an environment of uncompromising brutality — enlisting them in boot camp at age 7, and starving them to encourage enough deviousness and cunning to steal food — which skillfully bred yet more generations of ruthless killers.

In Athens, future leaders were brought up in a more nurturing and peaceful way, at home with their mothers and nurses, starting education in music and poetry at 6. They became pioneers of democracy, art, theater and culture. “Just like we can train people to kill, the same is true with empathy. You can be taught to be a Spartan or an Athenian — and you can taught to be both,” says Teny Gross, executive director of the outreach group Institute for the Study and Practice of Nonviolence in Providence, R.I., and a former sergeant in the Israeli army.

What the ancient Greeks intuited is supported by research today. Childhood — as early as infancy — is now known to be a critical time for the development of empathy. And although children can be astonishingly resilient, surviving and sometimes thriving despite abuse and neglect, studies show that those who experience such early trauma are at much greater risk of becoming aggressive or even psychopathic later on, bullying other children or being victimized by bullies themselves.

Simple neglect can be surprisingly damaging. In 2007, researchers published the first randomized, controlled study of the effect of being raised in an orphanage; that study, and subsequent research on the same sample of Romanian orphans, found that compared with babies placed with a foster family, those who were sent to institutions had lower IQs, slower physical growth, problems with human attachment and differences in functioning in brain areas related to emotional development.

Institutionalized infants do not experience being the center of a loving family’s attention; instead, they are cared for a rotating staff of shift workers, which is inherently neglectful. Such children miss out on intensive, one-on-one affection and attachment with a parental figure, which babies need at that vulnerable age. Without that experience, they learn early on that the world is a cold, insecure and untrustworthy place. Their emotional needs having gone unmet, they frequently have trouble understanding or appreciating the feelings of others.

Nearly 90% of brain growth takes place in the first five years of life, and the minds of young children who have been neglected or traumatized often fail to make the connection between people and pleasure. That deficit can make it difficult for them to feel or demonstrate love later on. “You can enhance empathy by the way you treat children,” says Martin Hoffman, an emeritus professor of psychology at New York University and a pioneer of empathy research, “or you can kill it by providing a harsh punitive environment.”

See pictures of a diverse group of American teens.

See The Wellness Blog.

Discipline, but Don’t Punish?

The cold environment of an orphanage can be considered on a spectrum of punishment, at the other end of which is simple child discipline — an issue that sometimes confounds even the most mindful parents. How do you teach a child right from wrong without being too tough, or slipping into abuse? Who among us has not raised our voice — O.K., screamed — while disciplining our children? (Read about what makes us moral.)

But shouting at or, worse, hitting a child results in fear, rather than an understanding on the child’s part of why he or she is being punished, say researchers. Over the long term, the routine use of corporal punishment, such as spanking, not only fails to change behavior for the better, but has also been shown to increase aggression in children.

“Instead of starting from the assumption that you have to beat the badness out of a child, turn on that empathy and compassion switch,” says Dacher Keltner, professor of psychology at the University of California, Berkeley, and author of Born to Be Good: The Science of a Meaningful Life.

In other words, start by teaching children to understand their own behavior and feelings — it provides the basic tools for understanding the behavior and feelings of others. For instance, when dealing with a child who has hurt another person, help him or her “anchor how they felt in the moment,” says Mary Gordon, founder of Roots of Empathy, a school-based program designed to foster compassion. “We always think we should start with, ‘How do you think so-and-so felt?’ But you will be more successful if you start with, ‘You must have felt very upset.’ The trick is to help children describe how they felt, so that the next time this happens, they’ve got language. Now, they can say ‘I’m feeling like I did when I bit Johnny.’”

When children are able to understand their own feelings, they are closer to being able to understand that Johnny was also hurt and upset by being bitten — that “switch” is the spark for a change in behavior.

But understanding suffering alone does not teach empathy, says Gordon, which helps explain why children who suffer more — enduring abuse at home, for instance — are more likely to become bullies. It’s not that they don’t know what it feels like to be hurt; it’s that they have learned that violence is the way to express anger or assert power.

In Gordon’s Roots of Empathy program, which is currently being used in about 3,000 kindergartens, elementary schools and middle schools in Canada, and 40 schools in Seattle, children get to see a visiting parent and infant interact in the classroom about once a month, and watch the foundations of empathy being built. When the baby cries, the Roots of Empathy instructor helps the mother and students think about what might be bothering the baby and how to make things better.

Students are taught that a crying baby isn’t a bad baby, but a baby with a problem. By trying to figure out what’s going on, the children learn to see the world through the infant’s eyes, and to understand what it might be like to have needs but not be able to express them clearly.

“We love when we get a colicky baby,” says Gordon, because then the mother usually tells the class how frustrating and annoying it is when the baby won’t stop crying. That gives children insight into the parent’s perspective — and how children’s behavior can affect adults — something they have often never thought about. “If you look at the development of empathy, one of the key features is perspective-taking,” says Gordon. “In coaching that skill, we help them [take the perspective of] their classmates.”

To date, nine separate studies have shown that Roots of Empathy has helped reduce bullying at school, and increased supportive behavior among students. Many school districts in the U.S., including New York City’s, have recently expressed interest in using Gordon’s approach. (See “The Year in Health 2009.”)

Setting an Empathetic Example

A child’s individual capacity for empathy can further be encouraged when parents model empathetic behavior themselves. When parents treat other people with compassion, selflessness and a lack of judgment, children copy those behaviors. “Empathy can’t be taught, but it can be caught,” says Gordon.

Her own family was a shining example. As a young girl in Newfoundland, Gordon says she grew up in a large, multigenerational family — including four siblings, two grandparents and a mentally disabled uncle — that also often included “strays.” Her parents liked to take in people in need: unmarried pregnant women who had no place to go, recently released prisoners who would stop by for a free meal. Gordon also tagged along with her mother, an artist (Gordon’s father was the Canadian minister of labor), as she visited poor families in the community, bringing them food, clothing and coal for heat.

When young Mary sneered and asked why a woman stored coal in her bathtub instead of bathing in it, her mother admonished her — but in private. “My mom would never embarrass anyone, so she wouldn’t embarrass me as a child either. She saw the dignity in everybody,” Gordon says. “In the car, she said, ‘You judged that woman when you made that face.’ She would say, ‘She’s made the best decisions she could with the challenges she has, and you don’t know her challenges.’”

Not every child is raised by a Mother Gordon. But even children who have survived rough environments — like the gang members Teny Gross of the Institute for the Study and Practice of Nonviolence works with in Providence — can be helped to “catch” empathy.

Gross has found that his outreach workers are most successful when they build relationships based on caring and fairness. “People have a sense of justice,” Gross says, explaining why even troubled teens respond well when counselors, with whom they have an ongoing relationship, take a firm stance with them regarding their behavior. “[Our kids are] used to injustice; they’re used to abuse at school and from the police. But when constraints come from a place of love and caring, people don’t think it violates their sense of justice.” (Read “Are Humans Selfish?”)

Gross’s program focuses on introducing young men and boys in gangs to a new network of people who not only care about them, but do so dependably — providing the kind of secure environment that many of them missed in childhood. By employing former gang members to mentor the troubled boys, Gross makes it easier for them to foster relationships of mutual understanding and connection with one another. Mentors show up consistently at the boys’ important events — court dates, funerals — demonstrating care and concern. They also organize social outings for the boys, like a trip to a local beach last summer for a day of surfing. That excursion purposefully included boys from rival gangs, in the hopes that the introductions could help reduce violence later on.

Indeed, research shows that simple exposure to other kinds of people in a friendly setting can increase your empathy toward them. Although some gangsters and sociopaths may never be reachable, Gross holds out hope. He points to statistics such as the near halving of the U.S. murder rate over the last 20 years that suggest a “different life is possible. It’s not easy, but a lot of it is common sense,” he says.

Szalavitz is the co-author of Born for Love: Why Empathy Is Essential — and Endangered (Morrow, April 2010).

Today, the “epidemic” of ADHD has grown to about seven million young people in the U.S. Most of these children are on medication. And if you add in the numbers that are on antidepressants and other psychotropic medications, the number is over 10 million. That is larger than the entire population of New York City!

By Jon Herring, Total Health Breakthroughs, March 10, 2010 

“Hey, Phillip… do you mind if I sit here and eat with you?” I asked.

“Sure, whatever…”

“How’s school going? Are you doing well?”

“Not really. I just want it to be summer.”

“Yeah, I remember how that used to feel,” I told him.

Phillip is eleven years old. He’s the son of some family friends and I was at a small party when I saw him sitting by himself. I hadn’t seen him for a few years, so I wanted to remind him who I was and get to know him a little better.

As he became comfortable, he opened up a bit more. He told me his plans for the summer. He told me about his friends and the girl he likes at school. And he also told me that he didn’t care for school all that much.

“It’s hard,” he said. “Plus, I have ADHD, so I don’t pay attention very well.”

“Really? How do you know you have ADHD?” I asked.

“That’s what my doctor said. He said I’ve had it since I was born. That’s why I have to take medicine.”

“Well, I think you’re just fine. How does that medicine make you feel?”

“It used to make me kinda nervous,” he said. “And I couldn’t go to sleep when I took it. Now, it just makes me not want to eat.”

After complimenting Phillip on his manners and intelligence, I changed the subject back to his plans for the summer. But what he said bothered me. Here was a bright young boy who was bored and frustrated in school… who probably had a few behavioral problems… and who had now been labeled as having a “disease” and put on medication.

And, unfortunately, Phillip is just one of millions…

I was bothered by his story because I could only imagine what that would do to the psyche and development of a child to be handed a lifelong sentence like that from a doctor. You are broken. You are defective. Your brain doesn’t work right. You are not acceptable in your natural state, but taking these drugs every day can help you.

It might be one thing if ADHD was actually a “disease”… but it’s not.

In 1987, attention-deficit/hyperactivity disorder (ADHD) was voted into existence by the American Psychiatric Association and inserted in the Diagnostic and Statistical Manual of Mental Disorders (DSM). Yes, that’s right… the “disease” was “voted” into existence.

Can you imagine if we had to take a “vote” to determine whether cancer is a disease… or diabetes… or heart disease? That would be patently ludicrous. But every year, more and more disorders are voted into the DSM.

In the case of ADHD, psychiatrists made a list of the most common behaviors among children that parents and teachers object to — and then termed them a disease. Within one year, more than half a million children were “diagnosed.”

Since then, the number of behaviors that constitute the disorder has continued to grow. There are now 18 of them. That opens the door for even more children to be labeled and then put on drugs.

Today, most ADHD “testing” consists of parents, teachers, school administrators, or social workers checking off these behaviors as observed at home and in the classroom. A doctor reviews the checklist, and if six or more of these behaviors are exhibited, then the child is “diagnosed” with ADHD. In almost every case, the treatment is pharmaceutical.

Today, the “epidemic” of ADHD has grown to about seven million young people in the U.S. Most of these children are on medication. And if you add in the numbers that are on antidepressants and other psychotropic medications, the number is over 10 million. That is larger than the entire population of New York City!

You might ask, where were these kids when I was growing up?

Dr. Russell Barkley, Professor of Psychiatry at the University of Massachusetts, has the answer for that. They were there, he says. “They were the class clowns. […] Back then, we didn’t have a professional label for them.

“They were the lazy kids, the no-good kids, the dropouts, the delinquents, the lay-about ne’er-do-wells who were doing nothing with their lives. Now we know better. Now we know that it is a real disability, that it is a valid condition…”

They were the dropouts, huh? The kids who didn’t fit in? The kids who found traditional schooling to be hostile, boring, and unacceptable? I wonder if Barkley was referring to “dropouts” like:

• Bill Gates & Paul Allen (college dropouts, cofounders of Microsoft)
• Sir Richard Branson (high school dropout, founder of the Virgin Group)
• Michael Dell, Larry Ellison, and Steve Jobs (college dropouts, computer company founders)
• Kirk Kerkorian (eighth-grade dropout, billionaire)
• William Faulkner (high school and college dropout, Nobel Prize-winning novelist)
• Ray Kroc (high school dropout, founder of McDonald’s)
• Dave Thomas (high school dropout, founder of Wendy’s)

Almost certainly, if many of these men were in school today, they would be “labeled” with a mental disorder.

The pharmaceutical companies and modern psychiatry represent ADHD to be a biological abnormality of the brain. Along with many other “mental illnesses,” it is often said to be caused by that catch-all phrase — “a chemical imbalance.”

The problem is that psychiatry has never validated ADHD as a biological entity. They have never shown even the slightest bit of proof of a “chemical imbalance” or that this is an actual brain disease. And yet, millions of children and parents are told fraudulently that this is the case.

Dr. Fred Baughman is a respected pediatric neurologist who has been in practice for 35 years. He knows what a real disease is. So, from 1993 to 1997, he doggedly pursued correspondence with the Food and Drug Administration (FDA), the Drug Enforcement Agency (DEA), Ciba-Geigy (the original manufacturers of Ritalin), and top ADHD researchers at the National Institute of Mental Health. He asked them to show him ANY peer-reviewed scientific literature proving a physical or chemical aberration that would qualify ADHD as a disease or a medical syndrome.

After years of persistence, Dr. Baughman finally got these groups to admit that there is NO objective validation for ADHD. Today, the National Institutes of Health state that, “We do not have an independent, valid test for ADHD, and there is no data to indicate that ADHD is due to a brain malfunction.”

And yet, hundreds of thousands of doctors still “label” children as diseased and prescribe powerful and dangerous drugs for something that they have admitted they can’t prove. That is not medicine. It is fraud.

And many doctors and social workers push these drugs forcefully and manipulatively. I heard of one doctor who asked a parent, “If your child had diabetes, you would give him insulin, wouldn’t you?”

Unfortunately, that parent probably didn’t know enough to tell the doctor that diabetes can be measured — either by blood sugar abnormalities or pancreatic malfunction — while ADHD cannot.

When you go to a doctor, they take blood, they do X-rays. They don’t ask how you behave. And yet, that is how the “disease” of ADHD (along with depression and many other “mental illnesses”) is diagnosed.

Thomas Szasz, Professor Emeritus of Psychiatry at the State University of New York, says, “No behavior or misbehavior can be a disease. That is not what diseases are.”

Diseases are malfunctions of the human body. For example, typhoid fever is a disease. Spring fever? Not so much. Spring fever is a metaphor. It is a figure of speech… just like most mental illnesses. And yet, the treatment for this figure of speech is now worth billions of dollars a year.

Though there are now many drugs used to treat ADHD, Ritalin (methylphenidate) is one of the most common. In 1970, there were an estimated 150,000 U.S. children taking Ritalin. Today, the number is estimated to be higher than five million. According to the Drug Enforcement Agency, the production of methylphenidate increased 700% between 1990 and 1997!

And the trend is to “diagnose” children at younger and younger ages. According a study published in the Journal of the American Medical Association, prescriptions for two- to four-year-olds increased by almost 300% between 1991 and 1995. I didn’t search for more recent statistics, but you can be sure the trend has continued.

And despite what those who promote them might say… these are NOT safe and harmless medications.

Ritalin, for example, is classified by the FDA and the DEA as a Schedule II Controlled Substance. It is listed in the same category as methamphetamines, cocaine, morphine, and Dilaudid (among other powerful illegal and prescription drugs). These drugs are powerful. They can cause harm. And they carry a significant risk of abuse.

Most ADHD drugs are a class of amphetamine. On the street, these stimulants are commonly known as “speed.” And while “speed” can increase alertness and productivity, the trajectory is crash and burn.

But what are the risks of long-term use of these drugs, especially by developing children?

These drugs have been known to cause depression and psychotic states. And they can be the cause of real neurological disorders like epilepsy and seizures. They can also lead to physical dependence and have been shown to precipitate illegal drug abuse.

Studies have also shown that ADHD drugs stunt the physical growth of children and cause the brain to atrophy and shrink.

But of course, the biggest risk is death. In fact, research funded by the National Institute of Mental Health showed that children and teens on drugs such as Ritalin have a 500% higher risk of sudden death than would be typical for children of a similar age and health status.

Not surprisingly, long-term use can increase the risk of heart attack.

And cancer is a known risk, too. In one study, researchers identified twelve children who met the criteria for ADHD in the DSM-IV and were to begin taking methylphenidate in daily doses between 20 and 54 mg. Because the test group was small, each child was used as his or her own control.

Chromosomal abnormalities in blood cells were measured before starting the treatment. Then these same tests were performed after three months of taking the medication. Three separate chromosomal abnormalities were evaluated. In every single child, significant increases in chromosomal aberrations were measured. On average, the aberrations increased by 323% following treatment. Researchers believe that greater frequencies of these aberrations equate to an increased risk of cancer.

And to balance out these significant risks… there are absolutely NO long-term studies that show positive effects from these drugs on learning, academic standards, or social behavior.

Certainly there are children who are misbehaving at school and at home. There are kids who are unable to achieve self-control. There are those who are unusually hyperactive.

But in the vast majority of cases, these kids do not need medication. They certainly do not need to be exposed to the dangers of these drugs. But do their doctors ever ask what kind of foods, preservatives, and additives these children are exposed to? Do they inquire about nutrition or give advice about the many ways that the foods children eat, the toxins they are exposed to, and the nutrients they are missing can affect mood and behavior? Of course, most doctors do not. That would require too much effort and follow-up. It is much easier (and more profitable) to write a quick prescription and usher in a new patient.

Today, we are constantly told to protect our children from drug abuse. And yet, there are some disturbing exceptions to that rule. Thomas Szasz put it well when he said, “Labeling a child as mentally ill is stigmatization, not diagnosis. Giving a child a psychiatric drug is poisoning, not treatment.”

To Your Health,

Jon Herring
Total Health Breakthroughs

Mind Matters -  March 2, 2010

Antidepressants: Do They “Work” or Don’t They?

A new study finds little difference between pill and placebo

By John Kelley, Scientific American

Answer: Yes!
In my view, both these statements are true: Antidepressants do work. And antidepressants don’t work.  Not to put too fine a Clintonian point on it, but determining whether antidepressants work depends on the definition of the word “work.”

A controversial article just published in the prestigious Journal of the American Medical Association concluded that antidepressants are no more effective than placebos for most depressed patients. Jay Fournier and his colleagues at the University of Pennsylvania aggregated individual patient data from six high-quality clinical trials and found that the superiority of antidepressants over placebo is clinically significant only for patients who are very severely depressed.  For patients with mild, moderate, and even severe depression, placebos work nearly as well as antidepressants.

There have been at least four other review articles published in the last eight years that have come to similar conclusions about the limited clinical efficacy of antidepressants, and one of the study authors, psychologist Irving Kirsch, has recently published a book on the topic, provocatively entitled The Emperor’s New Drugs: Exploding the Antidepressant Myth.
The recent review articles questioning the clinical efficacy of antidepressants run counter to the received wisdom in the psychiatric community that antidepressants are highly effective.  Indeed, it wasn’t so long ago that psychiatrist Peter Kramer wrote in his best-selling book Listening to Prozac that this miracle drug made patients “better than well.”  Prozac was a Rock Star. Its extraordinary success  even led to a photograph of the green and white capsule on the cover of Newsweek Magazine in 1990.

The essential facts about antidepressant efficacy are not in dispute. In double-blind, randomized controlled trials – meaning that patients are randomly assigned to receive either drug or placebo, and neither patient nor clinician knows who gets what – antidepressants show a small but statistically significant advantage over placebos.  The debate is over the interpretation of these findings, and it revolves around the distinction between clinical significance and statistical significance.

Statistical significance means that an effect is probably not due to chance and is therefore likely to be reliable.  But statistical significance says nothing about the magnitude of the effect or its practical implications.  Clinical significance indicates the degree to which an effect translates to a meaningful improvement in symptoms for patients.  Although the superiority of antidepressants over placebos has been shown to be statistically significant, the observed differences are not clinically significant.  In fact, the average difference between drug and placebo is approximately two points on a depression scale that ranges from 0 to 52.  This difference does not exceed the commonly accepted standard for a minimally significant clinical improvement of a 3 point improvement on the depression scale.

But what of the testimonials from patients and their doctors reporting dramatic relief of symptoms in response to antidepressants?  Such reports really aren’t in conflict with the data from randomized controlled trials.  In clinical trials, patients treated with antidepressants do show substantial improvement from baseline.  However, the clinical trial data also show that patients treated with placebos improve about 75% as much as patients treated with antidepressants, suggesting that only a quarter of the improvement shown by patients treated with antidepressants is actually attributable to the specific effect of the drugs.  The rest of the improvement is a placebo response.  In clinical practice, of course, there is no placebo group, and therefore patients and their doctors are likely to attribute all symptom improvement to the medication.

What seems clear from double-blind, randomized controlled trials is that antidepressants are, on average, only marginally superior to placebos.  One might reasonably ask, however, whether there might be a sub-set of patients for whom antidepressants are highly effective.  This is certainly possible, but to date no one has been able to reliably predict which subset of patients will respond best.

Moreover, because average antidepressant efficacy is small and not clinically significant, if there is a sub-set of patients for whom antidepressants are highly effective, there must also be a sub-set of patients for whom antidepressants have no effect, or are even harmful.  In addition, since pharmaceutical companies are now the major sponsors of drug trials, and they have an interest in maximizing the number of people for whom their medications can be prescribed, they have little interest in performing any trials whose aim would be to identify such sub-sets of patients.  To do so would risk reducing their profits.

Some have suggested that critics of antidepressant efficacy should keep quiet and not publicize their work.  The reasoning is that if the effectiveness of antidepressants depends in large part on the faith of patients and their doctors, then publicizing the fact that antidepressants appear to have only minimal efficacy as compared to placebos will have the practical effect of harming patients.  But this is putting our heads in the sand.  The history of medicine is littered with treatments initially thought effective that we now know to be ineffective at best and actually harmful at worst (For example, bloodletting contributed to the death of George Washington).  To ignore the evidence, is to return to a pre-scientific form of medicine.  In the long run, this will not be beneficial to patients.

So what’s the bottom line?  In clinical practice, many people suffering from depression improve after taking antidepressants.  But the evidence indicates that much of that improvement is a placebo response.  Antidepressants do work in the sense that many patients in clinical practice show substantial improvement.  However, if the standard is efficacy in comparison to placebo, the best available scientific evidence suggests that antidepressants do not work very well.  Given their cost and side effects, the psychiatric community and the general public should not be satisfied with antidepressant medications that provide only a marginal benefit over placebo.

Indeed, as early as 1994, Brown University School of Medicine psychiatrist Walter Brown suggested treating mild to moderately depressed patients with placebos for an initial 4-6 week period, and then switching to active medications if patients did not improve.  To surmount ethical concerns, Brown proposed prescribing placebos openly by informing patients that clinical trials showed that many depressed patients improved after being treated with placebos, and asking whether they would like to try a placebo initially.  It’s been sixteen years since Brown offered up his radical prescription for harnessing the placebo effect in the treatment of depression.  Is it time to fill the prescription?

This is a single stem cell-derived neuron that has migrated away from the transplantation site in the cortex and grown into a mature neuron. The blue stain shows the nuclei of the endogenous neural cells in this part of the brain. (Credit: Courtesy, with permission: Weimann et al. The Journal of Neuroscience 2010.)

ScienceDaily (Jan. 24, 2010) — Transplanted neurons grown from embryonic stem cells can fully integrate into the brains of young animals, according to new research in the Jan. 20 issue of The Journal of Neuroscience.

Healthy brains have stable and precise connections between cells that are necessary for normal behavior. This new finding is the first to show that stem cells can be directed not only to become specific brain cells, but to link correctly.

In this study, a team of neuroscientists led by James Weimann, PhD, of Stanford Medical School focused on cells that transmit information from the brain’s cortex, some of which are responsible for muscle control. It is these neurons that are lost or damaged in spinal cord injuries and amyotrophic lateral sclerosis (ALS). "These stem cell-derived neurons can grow nerve fibers between the brain’s cerebral cortex and the spinal cord, so this study confirms the use of stem cells for therapeutic goals," Weimann said.

To integrate new cells into a brain successfully, the researchers first had to condition unspecialized cells to become specific cells in the brain’s cortex. Cells that were precursors to cortical neurons were grown in a Petri dish until they displayed many of the same characteristics as mature neurons. The young neurons were then transplanted into the brains of newborn mice — specifically, into regions of the cortex responsible for vision, touch, and movement.

Until now, making these proper cellular connections has been a fundamental problem in nervous system transplant therapy. In this case, the maturing neurons extended to the appropriate brain structures, and, just as importantly, avoided inappropriate areas. For example, cells transplanted into the visual cortex reached two deep brain structures called the superior colliculus and the pons, but not to the spinal cord; cells placed into the motor area of the cortex stretched into the spinal cord but avoided the colliculus.

"The authors show that appropriate connectivity for one important class of projection neurons can be obtained in newborn animals," said Mahendra Rao, MD, PhD, an expert in stem cell biology at Life Technology, who was unaffiliated with the study.

The researchers also compared two methods used to grow transplantable cells, only one of which produced the desired results. "The authors provide a protocol for how to get the right kind of neurons to show appropriate connectivity," Rao said. "It’s a huge advance in the practical use of these cells."

Researchers will now explore whether the same results can be achieved in adult animals and, ultimately, humans. Weimann and his colleagues also hope to understand how the transplanted cells "knew" to connect in precisely the right way, and whether they can generate the right behaviors, such as vision and movement.

The research was supported by the National Institute of Neurological Disorders and Stroke, the Roman Reed Spinal Cord Injury Research Fund, and The California Institute for Regenerative Medicine.

Story Source:

Adapted from materials provided by Society for Neuroscience, via EurekAlert!, a service of AAAS.

Society for Neuroscience (2010, January 24). Neurons developed from stem cells successfully wired with other brain regions in animals. ScienceDaily. Retrieved January 24, 2010, from

http://www.sciencedaily.com­ /releases/2010/01/100119172751.htm