There is news from England about some research that indicates that many children who were thought to have low intelligence actually have a problem with working memory, the ability to hold information in your head and manipulate it mentally. It is largely genetic and if it fails to function normally it can affect long-term academic success into adulthood and prevent children from achieving their potential.

The researchers from Durham University surveyed over three thousand children in 35 schools across the UK using the first tool to enabled them to assess memory capacity in the classroom. They found that ten per cent of school children across all age ranges suffer from poor working memory seriously affecting their learning. Poor working memory is rarely identified by teachers, who often describe children with this problem as inattentive or as having lower levels of intelligence.

The new tool is a combination of a checklist and computer program created after many years of research into poor working memory in children, and it should
enable psychologists and teachers to identify and assess children’s
memory capacity as early as four years old.

The hope is that early assessment of children will enable teachers to adopt new approaches to teaching.

The checklist, called the Working Memory Rating Scale (WMRS), will enable teachers to identify children who they think may have a problem with working memory without immediately subjecting them to a test. A high score on this checklist shows that a child is likely to have working memory problems that will affect his or her academic progress.

Children can be evaluated using the computerized Automated Working Memory Assessment (AWMA). The tools also suggest ways for teachers to manage the children’s working memory loads that will minimize the chances of children failing to complete tasks. Recommendations include repetition of instructions, talking in simple short sentences and breaking down tasks into smaller chunks of information.

Pearson Assessment publishes the tools.

This is interesting work, but we still need more research to answer another question: disturbances in working memory have been identified in attention deficit/hyperactivity disorder (ADHD). So the question is whether many of the children found to have defects in working memory may actually have had ADHD.

An extremely important article by researchers from the National Institute of Mental Health has just been published in the Proceedings of the National Academies of Sciences. It suggests that children with Attention Deficit Hyperactivity Disorder (ADHD) have brains that develop more slowly than those of children without ADHD. However in most cases they still follow a normal pattern of development.

In a study of 450 children, 225 of whom had ADHD, the researchers found that the cerebral cortex of children with ADHD developed about three years more slowly.

The primary measure that they used was the peak thickness of the brain, which is normally taken to be a sign of maturity. Half of the children with ADHD reached peak thickness when they were an average of 10.5 years old, compared with 7.5 years among children without ADHD.

Even if the brain is developing more slowly, the fact that it appears to grow normally is reassuring, and may explain why a substantial proportion of children with ADHD do grow out of it as they get older. Though it still leaves us with several questions:

• Why does the delay occur at all?
• Why do so many people NOT grow out of it, and have persistent symptoms in adulthood?
• Is the brain really “catching up?” The brains of people without ADHD also continue to develop and grow

The National Institute of Mental Health has also published a nice press release that includes a video of brain maturation. You can find it here.

We recently talked about the increasing evidence that insulin has many extremely important roles in the brain.

New research by investigators at the Center for Molecular Neuroscience and the Institute of Imaging Science at Vanderbilt University Medical Center researchers, working with colleagues in Texas, has found that insulin levels affect the brain’s dopamine systems. These systems are involved in motivation, reward, salience, movement and emotional processing. Disturbances in dopamine pathways have been implicated in substance abuse, as well as schizophrenia, bipolar disorder and attention deficit hyperactivity disorder (ADHD). Drugs that interfere with the dopamine pathways may produce Parkinsonism as well as elevations of the hormone prolactin.

The psychostimulant drugs amphetamine and cocaine, as well as related medications for ADHD, block the reuptake of the neurotransmitter dopamine by dopamine transporters (DATs) thereby increasing the level of dopamine signaling. Some of these compounds also cause a massive surge of dopamine through DATs, resulting in high levels of synaptic dopamine that alter attention, increases motor activity and plays an important role in the addictive properties of psychostimulants.

The reason for examining a possible relationship between dopamine and insulin goes back to the 1970s, when it was reported that amphetamine had no effect on diabetic animals and in the 1980s it was shown that diabetic rats did not show the usual stereotyped behaviors when given amphetamine. There were also odd reports about disturbances in the enzyme dopamine-beta-hydroxylase in experimental diabetes and changes in dopamine D1 receptors in the brains of rats with induced diabetes.

These observations lead to this new research into a possible link between insulin signaling and amphetamine action.

They used a standard a rat model of type 1 diabetes in which insulin levels are massively depleted, and then assessed the function of the dopaminergic pathway in the striatum, an area of the brain rich in dopamine.

In the absence of insulin, amphetamine-induced dopamine signaling was disrupted: dopamine release in the striatum was severely impaired and expression of DAT on the surface of the nerve terminal was significantly reduced.

The lack of the DAT protein on the plasma membrane prevents the amphetamine-induced increase in extracellular dopamine, and in turn, amphetamine fails to activate the dopamine pathways that stimulate reward, attention and movement.

The researchers then gave insulin into the brains of the diabetic animals and found that the system returns to normal, indicating that the lack of insulin in the striatum directly affected amphetamine action.

They also developed a probe for brain DAT activity using functional magnetic resonance imaging (fMRI). In normal, healthy rats with plenty of insulin, amphetamine increased neural activity in the striatum. But in diabetic animals, activity in the striatum was suppressed.

So there is a powerful interplay between dopamine neurotransmitter systems and insulin signaling mechanisms. The results are some of the first to link insulin levels and dopamine function in the brain and hold several implications for human health and disease.

We need to have another look at the effect of diabetes on the brain. We have known that people with diabetes are at increased risk of cognitive impairment and depression, and we had assumed that it was because of hypoglycemia and vascular disease. Those assumptions may have been wrong.

The findings may also be important for diseases with altered dopamine signaling, such as schizophrenia and ADHD. Insulin may have something to do with the underlying brain disturbances in ADHD. Then control of insulin levels and neuronal responses to the hormone may help determine the efficacy of psychostimulants in people with ADHD.

Every now and then you see people on psychostimulant medications who need huge doses. Perhaps their problem lies with insulin rather than dopamine.

The debate about the possible association between watching television and children’s behavior has been going on ever since this window on the world entered our lives fifty years ago.

A new study, indicates that consistent, heavy television viewing (more than two hours a day) throughout early childhood can cause behavior, sleep and attention problems.

Yes, you did read that correctly: heavy viewing is just two hours a day!

Researchers from the Department of Population, Family, and Reproductive Health at Johns Hopkins assessed data from the Healthy Steps for Young Children national evaluation effort that looked at the effects of early, concurrent and sustained television exposure at age two and a half and again at five and a half. They also measured the effects of having a television in the child’s bedroom at age five and a half.

Sixteen percent of parents said that their child watched television for more than two hours a day at age two and a half years only, which they called “early exposure;” 15 percent reported that their children watched more than two hours of television daily at five and a half years only, which they called “concurrent exposure;” and 20 percent reported more than two hours of television viewing daily at both times (sustained exposure).

Forty-one percent of children had a television in their bedroom by the age of five and a half. Sustained television viewing was associated with sleep, attention and aggressive behavior problems, and what is known as “externalizing” of problem behaviors: throwing or breaking things.

Excessive television exposure was associated with fewer social skills. Having a television in the bedroom was associated with sleep problems and less emotional reactivity in the five year olds. Early exposure to television for more than two hours a day, which decreased over time, did not cause behavior or social problems.

The American Academy of Pediatrics recommends no television viewing for children under age 2, and no more than two hours of daily media exposure for ages 2 and older.

This is scary research. How many children are parked in front of a television for hours at a time, just to get them out of the way. And what kinds of problems are we creating for our future?

One of the smartest people I know has several children who have never watched television. They are instead all multilingual and each is an expert in at least one musical instrument.

Makes you think, doesn’t it?

Regular readers will remember my recent article concerning food additives and hyperactivity in children.

I have just read that he British Food Standards Agency (FSA) has been accused by campaigners of “chickening out” of banning additives linked to hyperactivity in children even though they funded the research that was published in the Lancet.

After the research was published, the FSA issued updated advice that eliminating the artificial colorings from the diet might have some beneficial effects in hyperactive children.

But critics said it did not go far enough and several environmental and children’s campaign groups, including the National Union of Teachers, called on the watchdog to extend that advice to all children since the additives posed a threat to psychological health.

The FSA responded by saying that the evidence was not strong enough to justify a ban and it would wait for the European Food Safety Authority (EFSA) to make a decision on use of additives in food.

EFSA says that it is considering the research as a matter of urgency and will be making an initial response within the next month.

We shall see what they have to say.

These were the main additives incriminated in the Lancet study:
Sunset yellow (E110) - Coloring found in some drinks
Carmoisine (E122) - Red coloring in jelly
Tartrazine (E102) - New coloring in some frozen and carbonated drinks
Ponceau 4R (E124) - Red coloring
Sodium benzoate (E211) - Preservative
Quinoline yellow (E104) - Food coloring
Allura red AC (E129) - Orange / red food dye