For kids with ADHD, regular ‘green time’ is linked to milder symptoms

A new study adds to the evidence that time spent in green outdoor settings benefits children with ADHD.

A study of more than 400 children diagnosed with Attention Deficit Hyperactivity Disorder has found a link between the children’s routine play settings and the severity of their symptoms, researchers report.

Full article:
http://medicalxpress.com/news/2011-09-kids-adhd-regular-green-linked.html

tl;dr:
Those who regularly play in outdoor settings with lots of green (grass and trees, for example) have milder ADHD symptoms than those who play indoors or in built outdoor environments. The association holds even when the researchers controlled for income and other variables.

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Use Herbal Remedies for ADHD

ADHD is typically treated with the medications methylphenidate or amphetamine, which are stimulant drugs. While they have been proven to be effective they also have a high risk for abuse and have many side effects such as weight changes, appetite changes, insomnia, and nervous tics.

Full article:
http://www.naturalnews.com/026081.html

tl;dr:
Due to the troubling side effects of medications more and more parents are looking into alternative options for dealing with ADHD. Use of herbal remedies for ADHD shows beneficial results without the risk of abuse found in pharmacological medications and usually with significantly less side effects. 

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Alterations in Brain Dopamine Pathway Appears to be Associated with Certain Symptoms of ADHD

Among the findings of the authors: “This study provides evidence in favor of the predicted disruption in the mesoaccumbens dopamine pathway in ADHD. With PET imaging, lower D2/D3 receptor and DAT [dopamine transporters] availability in those with ADHD than in the control group was documented in 2 key brain regions for reward and motivation (accumbens and midbrain),” they write.

“The lower than normal D2/D3 receptor and DAT availability in the accumbens and midbrain regions supports the hypothesis of an impairment of the dopamine reward pathway in ADHD.”

This pathway plays a key role in reinforcement-motivation and in learning stimuli-reward associations, and its involvement in ADHD supports the use of interventions to enhance the saliency of school and work tasks to improve performance.

Full article:
http://www.medicalnewstoday.com/releases/163864.php

tl;dr:
Researchers find a dopamine pathway with fewer receptors and transporters in ADHD adults. They interpret this as an “impairment” which supports the use of “interventions”.

My comments:
An alternative possibility : Could it also mean the ADHD adults aren’t naturally hard-wired for a certain self-reinforcing dopamine feedback loop? Is it more desirable for everyone to be the “happy” or “content” person that would be an “addict” in other contexts and bored to happiness with the status quo in this one? Where has that gotten us?  🙄

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Addiction: Pay Attention

Heroin and chocolate cake have a nasty way of crowding out the rest of the universe. The country’s chief addiction expert argues that the propensity to drink, overeat and take drugs is a matter of attention gone awry.

By Kathleen McGowan, published on November 01, 2004 – last reviewed on December 08, 2010

Meeting her now, it is hard to believe that the Mexican-Russian great-granddaughter of the revolutionary Leon Trotsky ever felt the need to impress her friends. But the universal teenage urge to look more glamorous drove a young Nora Volkow, then in high school, to smoke her first cigarette. It could have been the first step toward a nasty habit, but something in her neurochemistry rebelled. She hated it.Volkow, now one of the country’s most prominent drug addiction researchers and the director of the National Institute on Drug Abuse (NIDA), doesn’t think that her disgust for cigarettes had anything to do with morals or self-control. She says she’s just naturally intense; the additional stimulation provided by the nicotine was simply too much for her. “I like coffee, but I cannot even drink it because I get so wired,” she says. “I was probably born like that. I’m very protected against drugs. It’s my neurobiology, and I’m lucky.”

Listening to her explain her theories about addiction and the brain, her self-diagnosis sounds right on target. Even though she’s petite, with a jogger’s lean physique, she dominates the room. She speaks very fast, with a Spanish accent that rounds her vowels, and ideas tumble out one after the other so quickly that it’s almost impossible to keep up.

She’s a fast-moving example of one of her most interesting theories: that addiction may be a malfunction of the normal human craving for stimulation. Volkow thinks that drugs and other addictive habits tap into some of the deepest forces within us—our lust for newness, our yearning for vitality and the deep-down thrill of being alive. “We all seek that intensity,” she says. “There’s something very powerful about that.”

This idea is based on a new understanding of dopamine, the brain chemical involved in motivation, pleasure and learning. Because addictive drugs like cocaine and nicotine cause a flood of dopamine in the brain, researchers once thought that the neurochemical was a simple pleasure switch, the body’s own “reward” button. Yet something didn’t add up. If dopamine delivers the pleasure message, addicts should be in a continual state of bliss—but most of them get very little pleasure from the drug, despite the surge of neurochemicals. “I’ve seen hundreds of addicted people, and never have I come across one who wanted to be addicted,” says Volkow. As she began doing brain-imaging studies with drug addicts, that contradiction haunted her.

In response, Volkow and other researchers are developing a new understanding of addiction. Rather than just telling us to feel good, dopamine tells us what’s salient—the unexpected bits of new information we need to pay attention to in order to survive, like alerts about sex, food and pleasure, as well as danger and pain. If you are hungry and you get a whiff of a bacon cheeseburger, Volkow’s research team has shown, your dopamine skyrockets. But the chemical will also surge if a lion leaps into your cubicle. Dopamine’s role is to shout: “Hey! Pay attention to this!” Only as an afterthought might it whisper “Wow, this feels great.” So maybe addicts aren’t just chasing a good time. Perhaps their brains have somehow mistakenly learned that drugs are the most important thing to pay attention to, as crucial to survival as food or sex.

The salience theory of dopamine also provides new explanations for other self-destructive human tendencies, from binge eating to gambling. It may explain why we crave the stimulation of new information. The experiments that Volkow and her team are conducting may also reveal some of the most powerful behavioral machinery in our brains, the equipment that motivates and inspires us. If they are right, dopamine is more than a joyride. It’s more like the drug of life. Its mission is more profound and philosophical: to connect us to the world and supply us with the will to stay alive.

Nora Volkow has science in her blood. Her father is a chemist, her grandfather and her great-grandfather were physicists. But her family, which emigrated from Russia to Mexico in the 1930s, has another intellectual legacy. One of her great-grandfathers was the brilliant Bolshevik leader Leon Trotsky, and Volkow grew up in the Mexico City home where he spent the last days of his life—and where he was killed on Stalin’s orders in 1940. Parts of the house became a museum of Trotsky’s life, and when Volkow was a child, people like the Nobel Prize-winning novelist Gabriel Garcia Marquez would stop by.

Volkow, though, was more interested in psychiatry than in politics. She graduated at the top of her medical school class at the National University of Mexico, then came to the United States to pursue the new science of brain imaging. During the 1980s, at New York University and then at University of Texas, Austin, she used brain imaging techniques to study schizophrenia and cocaine addiction—and established herself as a leader in the field. She then moved to Brookhaven National Laboratory in Upton, New York, where she won a reputation as an intellectual powerhouse, respected for her creativity as well as for her productivity. “Nora has that enthusiasm, that spark,” says NYU Medical Center psychiatry chair Robert Cancro, who worked with her early in her career. “She’d get excited about things, talk 160 words a minute—and that was in English!”

Her colleagues say she is a bold and unconventional thinker. Early on, she demonstrated that cocaine physically damaged the brain. It took years before this controversial finding was accepted, but other research eventually proved her right. She was also an early champion of the idea that drug addiction is a medical problem, rather than a lack of willpower or moral fiber. That formerly radical view is now considered mainstream.

Since she was chosen to direct NIDA, Volkow has brought new visibility to the controversial theory about dopamine that has percolated in the scientific community for approximately the past decade. According to the salience theory of dopamine, the neurochemical is released when something surprisingly important happens, whether that’s an unexpected reward or accidentally stepping on a nail. Since dopamine is also involved in learning, memory and motivation, the chemical helps us pay attention to the information we need to survive, act upon it, and remember it for the future. But drugs hijack that machinery, sending 5 to ten times as much dopamine surging through the nucleus accumbens and forcing the brain’s motivational and attentional mechanisms to focus purely on the drug. It becomes the most interesting and important thing in the world. “In any addicted person, what’s salient is the drug,” says Volkow. “There’s no competition.”

Over time, the addict’s brain adapts to the torrent of dopamine by dampening the system down. Imaging experiments show that cocaine addicts’ brains don’t react to the things that turn on the rest of us, whether that’s romantic passion, food or cold, hard cash. Volkow’s research has also shown that addicts have fewer dopamine D2 receptors, which are found in parts of the brain involved in motivation and reward behavior. With fewer receptors, the dopamine system is desensitized, and the now-understimulated addict needs more and more of the drug to feel anything at all. Meanwhile, pathways associated with other interesting stimuli are left idle and lose strength. The prefrontal cortex—the part of the brain associated with judgment and inhibitory control—also stops functioning normally. It’s a neurological recipe for disaster. “You have enhanced motivation for the drug, and you have impaired prefrontal cortical systems. So you want the drugs pathologically, and you have reduced control of behavior, and what you’ve got is an addict,” says University of Michigan, Ann Arbor psychology professor Terry Robinson, who pioneered this new way of thinking about dopamine with his University of Michigan colleague Kent Berridge.

Some people are apparently born with fewer dopamine receptors, and they are more likely to enjoy the rush of addictive drugs. In one imaging experiment, Volkow gave Ritalin, which gently lifts dopamine levels, to a group of ordinary volunteers. Some loved the feeling of the drug, but others hated it so much that they threatened to drop out of the study. Volkow was puzzled until she imaged their brains. She found that those who liked the rush from the drug had fewer dopamine D2 receptors than those who hated it. Volkow thinks that some people have a sensitive dopamine circuitry; they can’t take the additional stimulation of drugs.

Obesity may involve similar malfunctions in the dopamine system. Volkow’s longtime Brookhaven collaborator Gene-Jack Wang has discovered that the brains of seriously obese people seem to be tuned toward food. Even when they are lying quietly in the scanning machine, the sensory cortex of their mouth, tongue and lips is more active than it is in normal-weight people, he says: “They are putting out their antennae.” Yet he also found that the dopamine circuitry of heavy people is less responsive, with fewer dopamine D2 receptors. Even among the obese, there are dopamine differences. The heaviest people in his study had fewer dopamine receptors than the lightest. Like addicts, overeaters may be compensating for a sluggish dopamine system by turning to the one thing that gets their neurons pumping.

It’s a mark of changing times—and more sophisticated science—that the head of the National Institute on Drug Abuse is thinking about doughnuts as well as heroin. Just as blaming drug addiction on moral weakness was a shortsighted and unscientific way of framing a social problem, Volkow believes that focusing solely on metabolism, or blaming fat people for overindulgence and gluttony, are intellectual dead ends. “What motivates us to eat is clearly much more than hunger,” she says. “We need to expand the way we think about eating.” Wang and Volkow suggest that dopamine may provide a new window into weight loss: Animal studies have shown, for example, that exercise elevates dopamine release and increases dopamine D2 receptors.

Volkow and the other champions of the new view of dopamine don’t deny that the chemical helps us register pleasure. But they think that pleasure is just part of a set of interconnected dopamine-related behaviors. Volkow recently found that adults with attention deficit disorder who took dopamine-boosting Ritalin before taking a math test found it easier to concentrate, in part, because the task seemed more interesting, so they felt more motivated to do the problem.

From this angle, it makes sense that the cognitive process of absorbing new information is closely tied to the brain’s pleasure mechanisms. You might say that what the brain really “wants” is new information, suggests Gregory Berns, associate professor of psychiatry and behavioral sciences at Emory University in Atlanta. “Neurons really exist to process information. That’s what neurons do. If you want to anthropomorphize neurons, you can say that they are happiest when they are processing information.”

This urge to connect to the world and learn from it is more important than mere pleasure, says Volkow. It’s part of the most basic force in behavior: the will to live. It’s not automatic, she points out. Seriously ill or very depressed people can lose the will to survive. “What is the motivation we all have to be alive, to do things?” she asks. “It’s not pleasure. Our lives would be so much simpler if we were motivated just for the sake of pleasure.”

But dopamine sensitivity and addiction aren’t genetically determined or inevitable. One experiment with monkeys showed that the dopamine system may be influenced by social interactions: Animals that lost social status also lost D2 receptors. Context is also crucial. Obviously, it’s easier to get hooked if drugs are easy to get in your neighborhood, but it’s not just a question of supply and demand. People who grow up in stimulating, engaging surroundings are protected against addiction, Volkow believes, even if they don’t have a naturally responsive dopamine system. If you connect to the world in a meaningful way, and have more chances to get excited about natural stimuli, you’re less likely to need an artificial boost.

“If you don’t get excited by everyday things in life, if things look gray, and the drug makes things look extraordinary, that puts you at risk,” she says. “But if you get great excitement out of a great multiplicity of things, and intensely enjoy these things—seeing a movie, or climbing a mountain—and then you try a drug, you’ll think: What’s the big deal?” For those lucky enough to grow up as Volkow did, surrounded by sharp minds and fascinating history, drugs are just nowhere near as interesting as everyday life.
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Stop or Go?

Stop or go…inhibit or excite? There seems to be some confusion regarding the claim that dopamine is a neuro-inhibitor in the dopamine addiction model, leading some people to have difficulty with the excitatory / inhibitory thing. Let me see if I can offer some clarification.

Excitatory means turning on, or firing, or increasing the rate of firing of the neuron. In this context, the “dopaminergic” neuron or, dopamine sensitive neuron. Inhibitory means the opposite: to turn off, or decrease the rate of firing of the neuron.

So whether dopamine excites the neuron, or turns it off depends on the receptor. When speaking about whether the neuron’s effect is to excite, or inhibit, in the sense of alertness, or dullness, it would probably be more appropriate, nevermind less confusing, to view it as character, or quality of effect, rather than excitory, or inhibitory (for instance, whether this dopaminergic character, and quality is trance-like, as opposed to alertness), perhaps as a function of pathway, or whatever else.

In this light, I think anyway, the question raised is whether ADHD is a result of increased XOR decreased dopamine type neuron activity — that is, does turning off dopamine neurons give ADHD like symptoms, or does more of them being turned on give ADHD type symptoms. The popular contention is there’s too many in the turned off category — thus the administration of cocaine-like dopaminergic stimulate.

I have come across an article or two showing increased learning, and concentration associated with increased dopaminergic activity. Still, there is a fine line between concentration, and trance — that’s how I’d view this particular instance of description of the dopaminergic stimulation character, and quality.

Most importantly though, if this dopaminergic quality is “inhibitory”, the obvious question is, with respect to what? What’s the dopaminergic neuron, having been turned on, inhibiting? Other neurons? Gets one or more of the dopamine circuits firing so as to limit other brain activity?

Again, concentration and trance, a fine line. Does it dampen other aspects of the central, and peripheral nervous system? This is, I think, the necessary direction of inquiry. So far, it does seem to go back to concentration, and trance. Dopamine seems to have the quality of pulling the organism together so to speak, neurally, and physically, and a part of this includes dampening excitability, and alertness.

This seems to naturally lead to a fine article in ‘psychology today’ by Kathleen McGowan:
Summary: Heroin and chocolate cake have a nasty way of crowding out the rest of the universe. The country’s chief addiction expert argues that the propensity to drink, overeat and take drugs is a matter of attention gone awry.

Read the full article here or here.

tl;dr:

Some confusion with the meanings of the words: “excite” and “inhibit”, with respect to the action of dopamine, may be leading researchers to confuse “concentration” with slipping into a trance.

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Imbicilica

Imbicilica: stuff that is imbicilic.

Imbicilic: like or as an imbecile; so senseless as to be laughable; absurd, foolish, harebrained, idiotic
en.wiktionary.org/wiki/imbecilic

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According to the fourth edition of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), a child has ADHD if, for a period of six months, he or she exhibits at least six symptoms from a list of 14.

Among them: “often has difficulty organizing tasks and activities,” “is often easily distracted by extraneous stimuli,” “often fidgets with hands or feet or squirms in seat,” and “often blurts out answers before questions have been completed.”

(In the full listing, please note the precise language used in the DSM-IV definition, such as “often,” “excessively” and “extraneous”).

Parents are frequently surprised to learn that the clinical observation of these symptoms, over the span of a 10-minute doctor’s consultation, is the sole basis of an ADHD diagnosis.

After all, aren’t all kids “easily distracted” some of the time? Isn’t a certain amount of hyperactivity a natural part of childhood?
_http://reason.com/archives/2000/05/01/dangerous-distraction

Check out this Consensus Development Conference on ADD/ADHD 1998:

Even a panel of Doctors can’t seem to describe ADD/ADHD.

Note the part of the video where this panel of ‘experts’ are unable to define the symptoms or diagnosis of ADD or ADHD. Sorry, but I couldn’t watch the whole thing.
http://www.youtube.com/watch?v=KcgYQfvjMD8

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You can be sincere and still be stupid.  ~Charles F. Kettering

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Executive Functions Model Part 3 – Ruination

On his web page, Russell A. Barkley, Ph.D., is described as an internationally recognized authority on attention deficit hyperactivity disorder (ADHD) in children and adults. Dr. Barkley has specialized in ADHD for more than 30 years and is currently a Clinical Professor of Psychiatry at the Medical University of South Carolina.

In 1997 when Barkley first presented a variation on Strang and Rourke’s 1983 Executive Functions model to explain ADHD, Barkely chose to incorporate into his model the existing body of literature of brain function, and to emphasize the similarity between symptoms of pseudopsychopathy (right frontal lobe damage – remember our story about Phineas Gage in Part 1?) and ADHD.

The right-frontal-lobe brain damaged individual has been shown to experience increases in motor activity, talkativeness, and a lack of tact and restraint; symptoms commonly associated with ADHD. Animals with frontal lobe damage cannot adapt to new situations or environments, while humans with such lesions similarly experience extreme difficulties in situations requiring problem solving and unique solutions.

Because he only focuses on similarity of symptoms and because he assumes ADHD to be synonymous with this type of brain damage, Barkley concluded, rather amateurishly and incorrectly, that persons with ADHD are also less capable of creative thought, and stated this hypothesis concerning ADHD and creativity explicitly in several of his writings.

Boy, is that such an obvious gaffe, and yet he still promotes the idea!

As an aside, the Executive Functions model Barkley chose to modify (Strang and Rourke’s 1983 Executive Functions model) was being applied to problems in the relatively new field of NLVD (non-verbal learning disorder) which attempts to identify the neurocognitive, psychosocial and adaptive characteristics of children with learning disabilities, whatever the cause. Strang and Rourke never mentioned anything related to “AD/HD” from what I have read.

So, back to Barkley: About a year after presenting his model for the expressly stated purpose of “explaining ADHD”, Barkley announces the discovery of the polymorphic DRD4 receptor gene and describes his version of the executive functions – presenting both in the September, 1998 edition of Scientific American magazine:

Russell Barkley states that the Executive Functions can be grouped as a set of 4 mental activities:

1) Working memory: Holding information in mind while working on a task, even after the original stimulus is gone. Said to be crucial to timeliness and goal-directed behavior. Also provides the means for hindsight, forethought, preparation and the ability to imitate the novel behavior of others.

2) Internalizing self-directed speech. Said to allow one to reflect to oneself, to follow rules and instructions, to use self-questioning as a form of problem solving and to construct “meta-rules”, the basis for understanding rules about rules – all quickly without tipping one’s hand to others. The idea is to make this self-talk private, preventing others from knowing one’s thoughts.

3) Controlling emotions, motivation and state of arousal. Said to help individuals achieve goals by delaying or altering potentially distracting emotional reactions to a particular event and to generate private emotions and motivations. Those who rein in their immediate passions can behave in more socially accepted ways.

4) Reconstitution. Said to encompass two separate processes: breaking down observed behaviors and combining the parts into new actions not previously learned from experience. Said to give humans a great degree of fluency, flexibility and creativity and allows them to propel themselves toward a goal without having to learn all the steps by rote. Also said to permit children, as they mature, to direct their behavior across increasingly longer intervals by combining behaviors into ever longer chains to attain a goal.

Barkley states the essence of his ADHD model thusly:

“In the early years [In all children], the executive functions are performed externally: children might talk out loud to themselves while remembering a task or puzzling out a problem. As children mature, they internalize, or make private, such executive functions, which prevents others from knowing their thoughts. Children with ADHD, in contrast, seem to lack the restraint to inhibit the public performance of these executive functions.”

…and he states it again:

All 4 Executive functions become internalized during typical neural development in childhood. As normal children grow and develop, they develop the capacity to behave covertly, to mask some of their behaviors or feelings from others. Either through faulty genetics or embryonic development, ADHD children have not attained these covert abilities and therefore display too much public behavior and speech.

The first three things I noticed is 1) the obvious value judgment: “too much public behavior and speech”. How much is too much and who gets to decide and why? 2) the high value that is placed on covert thought and emotion as if the mere expressing of one’s living thoughts and feelings were a criminal offense; and 3) how the focus of this model is obviously on reinforcing the concept of social conformity – the mistaken view that the most important thing is to be approved of by one’s peers and to avoid their punishments.

The same overt justifications can be found in his description of Ritalin’s “benefits”. Here it is in his own words:

“…they tend to be liked better by other children and to experience less punishment for their actions, which improves their self-image.”

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Conclusion?

In my opinion, it’s a very unhappy camper who can abuse a position of trust as a psychiatrist by first, attempting to demolish an individual’s self-esteem –  teaching them that they were born ‘defective’ and that what they must do is to take pills to be ‘acceptable’. Then, to improve the self-esteem he devastates, he reassures them that all they must do is whatever it takes to get people to like them and to not want to punish them.

Perhaps he just feels a bit guilty concerning the rumors of being paid by Novartis (maker of Ritalin), never mind the devastating effects of psycho-stimulants on so many innocent, bright, creative and loving kids.

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Thom Hartmann commentary:
Thom Hartmann states the he and his son is diagnosed ADHD. He’s a prolific author on ADHD and the inventor of the  Hunter vs. farmer theory of the condition.Hartmann (with co-author Vaudree Lavallee) has this to say about Barkley’s doings:
If brain damage research had been used to build the Hunter/Farmer hypothesis, “ADD: A Different Perception” may have explored the difficulties associated with being a right-frontal-lobe-damaged individual in a world taken over by people with left-frontal-lobe-damage.
Described in non-disorder (difference) terms, left-frontal-lobe-damaged “Farmers” could be seen as objective (rather than indifferent), exerting emotional self-control (rather than showing little overt emotion), able to show enough self-regulation to remain silent (rather than showing little or no verbal output), and speaking only when spoken to (rather than failure to initiate conversations).
However, this silly analogy was never used in “ADD: A Different Perception,” or any subsequent Thom Hartmann book or article for that matter, because Hunters are not right-frontal-lobe brain damaged persons, and Farmers are not left-frontal-lobe brain damaged persons: each are, instead, two end-points on a continuum of human variability.
To understand the role of brain pathology research in validating the Executive Functions model, we need to first determine what the Executive Functions model would look like without reference to brain damage.
The Executive Functions model would still compare the more liberal and flamboyant ADHDers unfavorably to the more conservative and restrained “statistical norm.” Americas “brick” factory-like schoolhouses would still be seen as the epitome of human civilization and accomplishment. And, like Phillip Rushton, the Executive Functions model would still see a negative correlation between IQ and promiscuity.
In summary, we would still have an ethnocentric (almost Aryan) commentary of genetic endowment differences.
Without these highly questionable (and, in the opinion of these authors, outright flawed) ideological underpinnings, however, what remains of the Executive Functions model is simply a theory of individual variation.
The Executive Functions model tends to focus on post base-line variation in human response to environmental stimulation while ignoring important differences in how such stimulation may initially be experienced by the individual.
We agree that after controlling for base-line differences between Hunters and Farmers, there may be important executive function differences among Hunters and among Farmers. Additionally, these “executive function” differences may turn out to be one among the many variables which help determine whether ADHD will produce an entrepreneurial success or a chronic criminal.
As the Hunter/Farmer hypothesis predicts, there are base-line differences in the ways individual Hunters and Farmers each experience and cope with depression, boredom, frustration and joy. However, these base-line differences do not fully explain why one Hunter (or Farmer for that matter) may or may not experience depression at a dysfunctional level.
Instead, the Hunter/Farmer hypothesis suggests that it’s the driving need or hunger for aliveness which animates most ADHD/ADD behaviors, and executive function is only a small (but significant) variable that determines how this need or hunger is satisfied (through socially adaptive means, such as a high-stimulation job in an emergency room, or socially maladaptive means like becoming a barroom brawler).
Seen in this light, Barkley’s so called executive system may be nothing more than a fight or flight response mechanism, acting like a rubber band that exerts its influence at both ends of the ADHD continuum. Evidence which indicates that having a “happy temperament” as an infant is associated with improved prognosis for Hunters while some environmental factors, such as having experienced abuse, are associated with negative life chances lends support to the prospect that the Executive Functions model is a theory of within-Hunter variation rather than of Hunter/Farmer differences.
To recapitulate, if one were to divide the population into groups based on individual differences in tolerance of (or desire for) novelty, the individuals in each group would still vary in both their tolerance of and their exposure to adversity or stress.
Theoretically, those in each group whose threshold for stress has been exceeded may exhibit many of the cognitive difficulties associated with the so-called executive functions.
From: ADHD – disorder or difference?, Thom Hartmann & Vaudree Lavallee
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Notes on NLVD:
Principles of neuropsychology, By Eric Zillmer, Mary Spiers, William C. Culbertson, 2008-2001, Thompson-Wadsworth, p. 305-309NLVD non-verbal learning disorder attempts to identify the neurocognitive, psychosocial and adaptive characteristics of children with learning disabilities. His investigations have led him to make two subtypes: R-S for reading and spelling disability and NLVD.
Rourke (1993) considers that NLVD reflects right-hemisphere (particularly posterior) damage, or dysfunction, whereas R-S deficits more closely reflect problems in the left, language-dominant hemisphere system.Also:
Nonverbal learning disabilities represent a discrete and separate diagnostic entity. However, some of the symptoms identified are similar to those described for other disorders.
Individuals with right hemisphere dysfunction (Semrud-Clikeman & Hynd, 1990; Weintraub & Mesulam, 1983), Asperger’s syndrome (Klin, Sparrow, Volkmar, Cicchetti, & Rourke, 1995; Semrud-Clikeman & Hynd, 1990; Wing, 1981), and “central processing disorders” (Rourke, 1982) each possess a number of symptoms that overlap with those seen in NVLD. Nevertheless, these disorders can be differentiated through proper assessment.
The Syndrome of Nonverbal Learning Disabilities:
Clinical Description and Applied Aspects Michael A. Roman
The University of Texas
http://www.nldline.com/michaelr.htm
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