The exact etiology of ADHD is unknown. No one is claiming to know that, at least not right now. However, in regards to statements about there being "no scientific basis"(/B) for these disorders,

Here's the "proof" : These are ALL from unrestricted research grants published in (the cream of the crop) peer reviewed journals.

1) The neurobiological nature of ADHD.....THE PROOF YOU SAY DOESNT EXIST: was conclusively proven in the 1990 landmark glucose brainscan research study published in the New England Journal of Medicine....


Zametkin,A.J.,Nordahl,T.E.,Gross,M.,King,A.K.,Semp le,W.E.,Rumsey,J.,Hamburger,S.,& Cohen,R.M.(1990) Cerebral glucose metabolism in adults with hyperactivity of childhood onset. The New England Journal of Medicine,323,(30).1361-1366.

The "proof" is in the PET scans that showed that the harder a person with ADHD concentrated the "slower" their brain went vs the exact opposite for the non ADHD group. However, that was remedied when the ADHD subjects took stimulant medication.

THE definitive study proving the existence of ADHD as a "real" disorder;signed off on by over 80 of the world's leading scientists (with over 19 pages of references) is :

Consortium of international scientists:International Consensus Statement on ADHD, January 2002. (http://www.chadd.org). It can also be viewed at Russell Barkley's website.


You can turn to pages 22-24 of Sandra Rief's 2003 book.............The ADHD Book of Lists ....................to find the section (1-7) WHAT THE RESEARCH IS REVEALING ABOUT ADHD

Within that section is the reference for the Landmark MTA Study:

"There has been significant research with regards to treatments for ADHD and their relative effectiveness. The longest and most thorough study of the effects of ADHD interventions was the 1999 Multimodal Treatment Study of Children with ADHD (MTA) by the National Institute of Mental Health (NIMH).

MTA Cooperative Group" A 14-month Randomized Clinincal Trial of Treatment Strategies for AD/HD,"Archives of General Psychiatry,[I] 56:1073-1086;1999.

ADHD is primarily thought to be largely (80%) genetic/inherited.THE GENETIC LANDMARK FOR ADHD WAS FOUND IN 995. That study is as follows:


Cook,et.al.,(1995) Association of attention-deficit disorder and the dopamine transporter gene.American Journal of Human Genetics,56.993-998.

The US Surgeon General's Report on Mental Health: Chapter 3: Disorders of Infancy, Childhood & Adolescence has excellent background info supporting in great detail (with another 19 pages of scientific references).Here's a small segment on what I'm talking about:
" The exact etiology of ADHD is unknown,although neurotransmitter deficits,genetics and perinatal complications have been implicated." It goes on to say:

"Research to pinpoint abnormal genes is honing in on 2 genes;a dopamine receptor gene (DRD) gene on chromosome 11 and the dopamine -transporter gene (DAT1) on chromosome 5 (Cook,et.al.,1995:Smalley,et.al.;1998).

The latter reference is : Smalley,et.at.(1998) Evidence that the dopamine D4 receptor is a succeptibility gene in attention-deficit hyperactivity disorder,Molecular Psychiatry,3,427-430.

Recently (3/25/05), I participated in a teleconference on ADHD in children put on by United Behavioral Health (UBH: a managed care company). The presenter was Russell Barkley, PhD. He is largely viewed as the world's leading researcher on ADHD. During that presentation, he listed the following (evidenced based/research derived) data regarding the neurology of ADHD.

Decreased Cerebral Metabolism
(from Thomas Spencer, M.D.)

global and regional glucose metabolism by PET scan reduced in adults who have been hyper since childhood (thats Zametkin's research again).
Largest reductions in:
1) pre motor cortex
2) superior prefrontal cortex

Anterior Cingulate Dysfunction in ADHD, fMRI and the Counting Stroop.
Bush,et.al.,(1998).


Etiologies-Neurological

Smaller, less active,less developed brain
Regions found on MRI,fMRI and PET scans incluse the following areas of the brain:
1) Orbital-Prefrontal Cortex( primarily on the right side)

2) Basal Ganglia (mainly striatum and globus pallidus)

3) Cerebellum (central vermis area, right side) - there were some other posts about this particualr area of the brain being a key component of ADHD in a different thread I believe

Suspected Neurochemical Deficiency:

1) Dopamine dysregulation likely but not definitive....... the mere fact that stimulant
medication works at all to relieve symptoms of ADHD forms a solid basis
for helping to substantiate this (and the first medication study was done in 1937 in
Rhode Island)

2) Norepinephrine dysregulation probable

Etiologies- Genetic ( these data were all derived from research studies) The usual maker for statistical significance is 1.5 SD (standard deviation) 's from the mean, which equates to a %tile ranking of 93. In other words, the absolute lowest chance of these data being accurate is 93%.

1) Family aggregation of the disorder: 25-35% of siblings; 78-92% of idnetical twins;15-20% of mothers, and 25-30% of fathers; If the parent is ADHD, then theres a 20-54% chance of the offspring being ADHD (increases the odds 8fold)

2) Twin studies of Heritability 57-97%)

3) Shared environment 0-6% (not significant)

4) Unique environment (15-20% )


Molecular Genetics : Candidate genes on DRD4,DAT1,DBH-Taq1 (on chromosomes 3,5,and 11)

Candidate region: chromosome 26p13 region


Lastly, the answer to your questions about the difference between ADHD and ADD can be found in Barkley's ADHD and the Nature of Self-Control (1997).
It's also addressed in his 2002 book Taking Charge of ADHD (pages 137-138) and in You Mean Im Not Lazy,Stupid Or Crazy? by Kate Kelly & Peg Ramundo (Chapter 2).

As for depression, it is considered to be a Medical disorder on the basis of the chemical imbalance of the neurotransmitter serotonin. I don't know anyone who considers it to be a "disease".

There's no cure for the common cold but people know it exists. The Biogenic Amine Hypothesis was derived (via research) over 20 years ago. Here's what that says: "The concept that abnormalities in the physiology and metabolism of certain biogenic amines, particularly catecholamines[I](norepinephrine and dopamine ) and an indoleamine(serotonin) , are involved in the causes and courses of certain psychiatric illnesses."
That qoute was from an older issue of A Psychiatric Glossary of the AMerican Psychiatric Association, page 28. The new one is at the office.

The Biogenic Amine Hypothesis is what eventually led to the development of the class of antidepressants we now know as SSRI's (Select Serotonin Reuptake Inhibitor's:Zoloft, Prozaz,etc.).


This MORE than refutes your remarks. As of the summer of 2003 there were over 6k research articles,professional papers, chapters in book and books on ADHD.

If you go to the International Consensus 2002 journal article, you will also find on page 89:

"ADHD is recognized as a disorder/medical condition by the American Medical Association, the American Psychiatric Association, the American Psychological Association and the American Academy of Pediatrics."


THIS ISN'T AN EXACT SCIENCE .NO ONE EVER SAID IT WAS. But I can tell you that a T score of 70+% on the Conners Parent Rating Scale is one of the most accurate predictors of ADHD currently available (when used in concert with a thorough developemental and medical screening, behavioral observations and other screenings for executive functions; to name a few).


I could go on but I've made my point. I spent hours on this post and still had to cut it short. There's your scientific basis.

mctavish23,

Thank you so much for taking the time to put this on the forum. I have a hard time reading it all at once, so I do it in peices. I also reread it.

It is very comforting having you here, with your extended knowledge base, education, and passion for helping the rest of us understand more about ADD.

Again, thank you so much for taking the time to research and post this.

Have a wonderous day!!!!

mctavish I appreciate you taking the time to provide all this great information.
Thank You very much.:)

Thank you so very much, mctavish!

That's so extremely helpful, thank you! I'm reading it over a few times. I want to be ready for the next moron that tries to say ADHD doesn't exist.

I may take to carrying this around to present as a hand out. Sick and fed up with the bs and Mctavish here has put that to rest with a firm hand.
Long my you live mctavish23. :D

Don't forget it's also acknowledged by the American's with Disabilities Act (ADA).

"the harder a person with ADHD concentrated the "slower" their brain went vs the exact opposite for the non ADHD group. "


Hmm, I keep coming back to this board, in part wondering if my diagnosis could be for real and thinking I was fine, I just need to get shed of all the crazy people around me. Then I find information like this, which describes me to a T. My wife, people around me say I' so slow at doing things, but I have to move very slowly to focus and do them right.

I hate the medication, but I do notice I seem to think much faster. Especially in meetings, I am able to listen, think, and articulate a reply. In the past I couldn't process both what was being said and what I wanted to say simultaneously (a real disadvantage for an IT person).

Maybe I'll go see the doc and work back up to the full dose, I've been taking 1/2. I hate the side effects, I feel like my heart's going to jump out of my chest and get extremely irritable.

Thanks for the post.

I stuggled for a long time trying to get away from the Dex, but finally gave up a month or so ago. I really don't like the idea of taking meds but they help. I used to go off them periodically for a week or so to check the differences.

I got tired of going off the meds and rail roading conversations by not being able to wait my turn, and burning bridges of first impressions with new people, overwhelming the situation with too much of ME.

With dex, I become blended into the mix and that allows more freedom for me. I can enjoy not being medicated, but I like to be among friends that know me well, and can enjoy my rapid fire enthusiasm. :D
Cheers! Ian.

Nice to see McT's post up there. I have the greatest respect for the man.

You and me both. I fear he's had his fill of disrespect from less rational quarters here. I'm glad his record remains public here. He sets the bar very high.

Some drink at the fountain of knowledge...others just gargle.

Im glad that this thread is still open. There has to be a way of confronting misinformation that goes beyond a simple matter of personal opinion.

With the science of ADHD things are spelled out in the research. The thing is, it continues to progress, so you have to stay on top of it.

I was thinking about this earlier, regardless of a person's motivation, each time there is an "attack" or "challenge" or whatever you want to call it, it actually provides an excellent opportunity to help teach the "basics," of ADHD to everyone.

I remember about 5 or 6 years ago, a woman came into ADD Support chat in Yahoo. She was angry and bitter over being challenged by a school psychologist about her copy of CHADD FACTS #1 and it's mention of the 1990 "landmark" glucose brain scan research study that conclusively established the neurobiological nature of ADHD, having not been replicated.Unfortunately, she left before I could tell her the rest of the story.

Zametkin ( 1993 ) did establish the proof of diminished metabloic activity ,even tho (Zametkin et.al.,1997) could not replicate the original 1990 study.

The point is, Zametkin 1990 can STILL be referred to as being a "landmark" study because of the 1993 findings. It was the first study to show diminshed metabolic activity.

What I especially like is that in confronting the misinformation,irrespective of the intent,parents have an opportunity to read up on how to handle those same potential challenges they may encounter later on.

In the process, they can "arm" themselves if you will, with what the research really has to say in terms of "the big picture" about the legitimate science behind ADHD.

I recognize that there is a huge difference between "content and intent." If a person has ulterior motives, I believe that they will surface at some point, so that doesn't bother me. Either way, situations like these provide the opportunity to help educate , which is a very good thing.

take care

mctavish23 (Robert)

McTavish, Did Zametkin suggest any possible reasons the 1997 study did not find the same differences as the previous two?

Scattered

Better would have been to keep the thread locked and start a part 2 using the original post. McT and others posted a lot of good information on the original thread which has now been lost on this truncated thread.

Barkley explained the reason on p.166 (Chapter 5- Etiologies) of his 1998 Second Edition of: Attention Deficit Disorder: A Handbook for Diagnosis and Treatment.


"More recently, studies using PET to assess cerebral glucose metabolism found diminished metabolism in adults (Zametkin,et.al.,1990) and adolescent females with ADHD (Ernst,et.al.,1994) but proved negative in adolescent males with ADHD (Zametkin,et.al.,1993). An attempt to replicate the findings with adolescent females who have ADHD in younger female ADHD children failed to find such diminished metabolism (Ernst,Cohen,Liebenauer,Jons & Zametkin,1997).

Here's where he explains it : "Such studies are often plagued by their exceptionally small sample sizes,which results in low power to detect group differences and considerable unreliability in replicating previous findings."

Now,here's the most important part because it gives you the whole story and not just part of it,which in turn,would have been misleading.

He states in that same paragraph: "However, significant correlations have been noted between diminished metabolic activity in the left anterior frontal region and severity of ADHD symptoms in adolescent girls with ADHD (Zametkin,1993). This demonstration of an association between the metabolic activity of certain brain regions and symptoms of ADHD is critical to proving a connection between the findings pertaining to brain activation and the behavior comprising ADHD."

Unless you'd read those journal articles or a book like this one in which they're summarized, you would come away thinking that the "proof" had been debunked. However, the reality is that it's actually the other way around.

Because (Zametkin,1993) DID find significant correlations to support diminished metabolic activity that in turn helped prove a connection between brain activation and ADHD behavior, Zametkin's original 1990 study (that was published in the New England Journal of Medicine) can still be called "landmark" because it was the first study to show any evidence of diminished metabolic activity.

Thanks, McTavish, for once again improving my understand of all this!:)

Scattered

YW:)

I'm home for lunch right now.I'm doing 1/2 days today and tomorrow. Now I'll be able to spend the afternoon working on letters to schools requesting different accomodations, as well as an eval., without interruption.

There's also some references and definitions that I still need to post. Hopefulyl, I can get to that but Im still struggling cognitively.

In addition,there's also some more info that I'd like to post on how Cook,et.al.,(1995) is just like Zametkin, 1990, in terms of still being called a 'landmark " molecular genetics study, even tho one of the candidate genes (DAT1) wasn't replicated,while the other one (DRD4) was.

The point Id like to make here is that things do change in terms of how you arrive at determining "the proof." That's why you have to stay on top of the research. Having said that, I try and do that as much as possible, but it's very difficult.

(Since I've been a member of the Forum, I've been shown so many great links that I would have never known about. I'm very grateful for that, as I'm always striving to learn more).

At the same time, "landmark(s)" will still remain as the first studies in their respective areas to determine something of importance regarding ADHD.

take care

mctavish23 (Robert)

Not to confuse the issue, Robert, but do you have any response to our observation that it hasn’t been established that diminished metabolic activity actually indicates a defect of some sort?

Our work clearly establishes two different types of logical structure in use in the brain, and our characterization of the web-like form of the newer type of structure has been verified by some recent research, particularly in females.

By our estimation, the web-like structures are significantly more efficient. This would mean we should expect less metabolic activity for equivalent operations. In fact, one might wonder why there isn’t more of a difference. What is the more efficient structure doing, that the older, less efficient structure doesn’t get around to?

Any comment? It seems to us that the idea that less == defective is ingrained in the articles you cite. If so, the assumption deserves challenge.

--Tom and Kay

It's always good to ask questions and your questions sound reasonable. Wish I could answer.

Stabile,

My understanding is that the task involved had to do with reading. The idea was to measure glucose metabilism and brain activation on a specific task. Its been years since I read the study but that's the premise.

For example, the harder the non med ADHD group concentrated the slower their brains went, as opposed to the non ADHD group who's brains "kicked in" right away.

Stabile,

My understanding is that the task involved had to do with reading. The idea was to measure glucose metabilism and brain activation on a specific task. Its been years since I read the study but that's the premise.

For example, the harder the non med ADHD group concentrated the slower their brains went, as opposed to the non ADHD group who's brains "kicked in" right away.
Thanks. That’s pretty much what I expected; we haven’t seen much that actually attempts to establish a correlation between diminished metabolic activity and diminished capacity of some sort.

I know it seems like a no-brainer, but life (and medical science in particular) is full of that exact kind of mistaken assumption, one that is so obvious that the assumption itself is difficult to see, let alone discuss.

So on the one hand, we have the idea that the brain functions and uses energy in doing so, and if less energy is used, less actual work must have been done. And in any specific brain that is exactly correct, as long as we’re looking at the same neurons.

But there is no theory that says any two brains should use similar amounts of energy to perform equivalent functions. Again, this seems like a no-brainer, because neurons only work one way, and that is true as far as we can determine.

But no such principle of equivalence can be assumed to operate on the level of neural structures themselves. Here is where we believe the logic begins to fall through the cracks; it seems dimly reasonable that we all might have the same logical structures in our heads, but everyone’s really working in a vacuum when we get to this point.

Those issues are in a different context, too, one that embraces questions of how neural structures are defined, ultimately the whole nature vs. nurture debate as it’s unfolded over recent years.

There isn’t even much speculative work about the actual form of these structures. When Kay and I started to look at the problem, we realized we were traversing virgin territory on an almost daily basis.

The upshot is this: it seems premature to assume that any two individuals will have the same neural structures operating in their heads, simply because there is no research suggesting that similar logical structures are necessarily in use.

There’s a persuasive argument that any two human brains might implement the same functions with at least two different types of logical structures. Since logical structures are expressed in neural structures, it seems likely that different physical arrangements of neurons might be expected to support the same high level functions in different individuals.

And different arrangements of neurons should be expected to expend different amounts of energy to perform their allotted task. I know it probably still seems reasonable to you to assume that there must be some value to the scans measuring tagged glucose uptake and similar techniques, but however counterintuitive it might be, the deep analysis suggests otherwise.

The best analogous example that leaps to mind is the way that the medical community spent years blaming surgeons for being sloppy and missing (or even accidentally releasing) ‘seed’ cells that caused cancer to metastasize after an apparently successful operation to remove a solitary primary tumor.

Surgeons tried desperately to refine their technique, usually with little success, and there was a considerable amount of problematical distress that occurred, as might be expected.

Then cancer researchers discovered that primary tumors excreted a ‘tumor growth inhibition factor’, a substance that apparently is intended to suppress the flowering of pre-existing ‘micro tumors’ located throughout the body that would have sapped the resources available to the primary tumor had they been allowed to grow freely.

Removing the primary tumor also removed the inhibiting agent, of course, and the ‘micro tumors’ were then free to grow. The surgeons had been causing the problem, but not because of any lack of skill or lapse of attention. It wasn’t really their fault, but the surgery’s fault. The approach was wrong because they didn’t understand the situation.

This is similar to the case with brain scans and assumptions about what differences in metabolic uptake indicate. The surgeons didn’t know the ‘micro tumors’ existed; if they had known, they might have tried to look for them, somehow, before operating.

In a similar way, nobody knows what the neural structures in two different brains look like, whether they’re similar or perhaps radically different; we know the logical structures they support can be radically different. Different physical structures (with different numbers and arrangements of neurons) would be expected to function at different metabolic rates.

The problem may go far deeper than this, though. We also have good reasons to believe that similar functions might not necessarily arise as neural operation in the traditionally expected regions of the brain. That is, ADDers may perform entirely different physical and logical operations to evidence the same high-level behavioral functions, as in some aspects of the reading tasks you mention.

If that’s true, everything has to be thrown out and done over from the beginning. Personally, I believe it may not be quite that dramatic. But I have no doubt that the assumptions currently at work need some drastic revamping before we can accurately tell if there’s any real data in these scans.

And I definitely would recommend against incorporating these apparently premature conclusions into any theory about AD/HD and the brain.

They are very likely the product of impeccable science, done by world class scientists. But just because it’s good science doesn’t mean it’s right. In this case, it certainly seems likely not everything has been accounted for, and caution would be highly recommended.

We’ve got enough problems with wingnut theories and people with actual bad intentions and agendas to match. We certainly don’t need to leave holes in our own structures they can take pot shots through.

Thanks again. --Tom

It would be interesting to see a link to that study. That the non-medicated ADHD'ers brain's use of energy actually decreased when they tried to concentrate, is not explained by your model Stabile.

Stabile, you guys are definately way over my head, but on the surface one flaw that I see is that generally what brings folks with AD/HD in for treatment is not that their brain are working more efficiently utilizing less energy -- generally quite the opposite, they are less functional and alert mentally unless they are very stimulated by the activity (I would actually love to hear about a brain scan done while an ADDer was in hyperfocus mode). On a personal level, I've experienced a major decrease in function when asked to concentrate under pressure (especially time pressure), to the point where I can't read a map, fill out a basic form, or comprehend a test questions (I have two master's degrees and these activities are not beyond my normal functioning ability).

I do see advantages in the many connections the ADD mind is likely to make in the creative process and in long term memory, but I don't see that with the PET studies being discussed when the area being studied is concentration and glucose metabolism.

Scattered

I believe what they did was then give the ADHD group (stimulant) meds for the first time and that created more glucose, which in turn, increased the activity .The idea being that it would help the ADHD person read and comprehend better.

Thats far from scientific but I think thats the idea.

It would be interesting to see a link to that study. That the non-medicated ADHD'ers brain's use of energy actually decreased when they tried to concentrate, is not explained by your model Stabile.
Not explained well enough by me, perhaps. But I think our models are OK here.

Our models don’t really predict anything about what happens when an ADDer tries to concentrate. But they do allow us to know something about what general structures and operations may be involved, because they limit the range of possibilities on the level that these brain scans probe.

We can also predict quite a bit about what is going to happen in the brain during the test on an entirely different level, the one on which the behavior itself is a recognizable abstraction, and we can speak of things like ‘concentration’ with meaning.

So we know (for example) that what we call ‘attention’ is related to the way we regulate our internal ‘view’ of the cacophony of all of the firing patterns being presented to our conscious centers at any particular moment, from both external and internal sources. (Here, ‘external’ means external to the conscious centers, not external to the brain itself.)

The actual mechanism of ‘attention’ is not continuous. We each have a certain quantity, in a sense, but ‘attention’ itself is quantified; it’s a discrete mechanism. The ‘amount’ of attention we have at any moment to devote to a particular task will always be expressed as an integer. It’s more proper to refer to ‘attention mechanisms’ that ‘attention’ per se.

Any task requires at least one devoted attention mechanism, and if we pop down a level or two we’ll find that a ‘one task, one attention mechanism’ rule is universal. Any task that appears to use multiple attention mechanisms has been partitioned logically on a lower level into multiple parallel tasks.

(This description is entirely misleading in some important points, in order to make the mechanisms understandable. Much of the actual causality is reversed. For example, attention mechanisms define what a task is; there are no ‘tasks’ on the neural level, only the activity we recognize as attention. The appearance that a task exists independently is an illusion.)

This follows from the way that actual neural structures function; they’re naturally indiscriminate, every network firing at will, and we couldn’t do much with them unless there was a way to control and organize their output from moment to moment.

One way this is accomplished is by creating many-layered hierarchical structures; stuff happening on lower layers is naturally muffled a bit. But ultimately, we have to discriminate amongst the patterns presented, and this is the function of attention mechanisms.

Normally our strategy would be to suppress all but the most active firing pattern, but there is a mechanism by which that ‘loudest first’ principle may be temporarily overcome, and attention paid to a less active, quieter pattern. The conscious experience of this mechanism is ‘shock’, and it evolved as a tool for survival during chaotic moments.

Why talk about this special kind of mechanism, which allows us to temporarily focus on stuff (like not tripping on the steps) that seems less important than, say, the flames licking our legs? Because one of the hallmarks of having/being AD/HD is a dawning conscious awareness of these internal processes, and that awareness can in turn affect how we respond even in ordinary circumstances.

Adders not only appear to have a few more attention processes (perhaps only one more) than normals, but we are slowly gaining control of the process of assigning them to a specific task. We’re new at this, and sometimes we don’t quite get it right. (And remember, tasks don’t really exist, anyway. Some fun.)

We don’t know what exactly to expect when ADDer’s try to concentrate during a brain scan. But we do know that it involves these high level neural mechanisms, and it would be unusual if the result was exactly the same as a normal’s response.

But we would expect some aspects of the neural activity to remain the same: if we watch the cupboard carefully, we’ll see the same soup can disappear regardless of whether I reach in a pick it up in the usual way, or my new dinner fixin’ robot snatches it up on its way to the strove.

Totally different mechanisms at work, but with the same goal and result on a higher level (having soup for dinner) and same observable effect on a lower level (the can sits in the cupboard now, and now it’s gone).

And if you were measuring my energy expenditure, you would see it decrease once the robot is introduced. That’s the point, isn’t it?

* * * * *

The question of how we’re accomplishing these tasks internally must be better addressed before we can interpret the scan results. We only stated that we know a more efficient structure is in use, and that it would be expected to require less energy for equivalent function.

We don’t know if that’s why the scans show less energy uptake under some conditions, and they don’t either. I think we ought to find out, don’t you?

Stabile, you guys are definately way over my head, but on the surface one flaw that I see is that generally what brings folks with AD/HD in for treatment is not that their brain are working more efficiently utilizing less energy -- generally quite the opposite, they are less functional and alert mentally unless they are very stimulated by the activity (I would actually love to hear about a brain scan done while an ADDer was in hyperfocus mode). On a personal level, I've experienced a major decrease in function when asked to concentrate under pressure (especially time pressure), to the point where I can't read a map, fill out a basic form, or comprehend a test questions (I have two master's degrees and these activities are not beyond my normal functioning ability).

I do see advantages in the many connections the ADD mind is likely to make in the creative process and in long term memory, but I don't see that with the PET studies being discussed when the area being studied is concentration and glucose metabolism.

Scattered

Good points, but I doubt our stuff is as far over your head as you think.

The idea that some aspects of our normal brain function are handled by these more efficient structures is not directly coupled with the stuff you mention, like an inability to focus under some circumstances. In a way, the efficiency is just a side effect, although it does have some important implications down the line.

The impact of the use of these structures filters out to stuff like concentration through two effects. First, the operation of the structure itself is not identical, although it is wrong to think of this as a defect, because the overall function of a system built of these structures is guaranteed to be correct. The alternatives aren’t recognizable as such; everything would simply fail, and there would be no result, and no person, either.

Secondly, there are deeper implications to the use of the structure that occasionally cause us to make a decision that is unexpected (and thus wrong) to a person using the older normal structures.

It’s like this: you live near some caves, and know that when it rains you can run around a bit and find shelter without too much trouble, a place to wait out the storm before getting back to the business of finding dinner.

Then one day, for reasons you don’t understand, your vision begins to improve, until finally you can see there’s an umbrella vendor’s stand set up on the opposite side of the valley.

The next time it rains, you cross the valley, running away from the caves, and purchase an umbrella. And you stroll back to the vicinity of the caves, and continue your search for berries, protected from the storm.

This is not going to look like the expected normal behavior to your friends huddled in the caves, and by most measures might not be judged entirely sane. And as obvious as it seems to us now, it might take a while to catch on.

Our problems with having/being AD/HD are all double-edged in this way. Even where there’s an inherent advantage to a particular mode in which our brains seem to function, there are multiple disadvantages that accrue when it’s put to use.

Some of the measures of our ability to function (like your casual assessment of your own ability to concentrate under pressure) may be incorrectly applied in subtle ways.

Think of a test that times how quickly you find a cave when it starts to rain. The instant you snap open an umbrella, you fail. If you believe you’ve failed strongly enough, you might throw away the umbrella.

Other tests fail to judge our abilities in a similar way on many different levels. We have no difficulty recognizing that an experienced carpenter is a skilled craftsman, even though he is at present doing a butcher job on laying brick for his new fireplace.

He’s not a mason, he’s a carpenter, and part of our problem isn’t that we’re broke, but that the labels for what we’re good at haven’t been invented.

There’s a problem with that argument; for it to hold up, we must posit a special circumstance in which it is difficult or impossible for some reason for us to invent the right description of our particular craft, so that we may be recognized as skilled even though we might not be able to read a map under pressure.

And Occam’s Razor tells us that’s unlikely, because it’s a more complex explanation requiring an even more complex circumstance to occur. The simplest explanation is the most likely, and that’s the one that says we’re just not very good at doing normal stuff.

But Occam’s Razor is suspended under certain conditions, and we happen to have just those conditions in our own case. We didn’t set out to explain AD/HD; we set out to understand human communications, and in particular a problem in which it seems impossible to form words for a thing regardless of how long and hard we try.

The answer to our problem is also the answer to the problem of describing ADDers in a benevolent and respectful way, one that celebrates and engenders our unique abilities rather than (potentially) vilifying us.

This is intimately tied to the difference in the two types of logical structures in use in our brains, and in particular to the difference in how they hold and organize information, and how we access it. In a way, you can think of words as being restricted to the range of experience and understanding possible when using the older structures.

Carpentry and masonry are both accessible in terms of those older structures, so we have no difficulty describing both, and perceiving the bumbling carpenter as a skilled craftsman despite his poor attempt at laying brick.

But our ADDer abilities are (in part) due to the use of logical structures that by definition lie outside the range of any possible words. We literally can’t describe normal function and ADDer function on equal terms, like the carpenter and mason, and some of us wind up being a bit wounded by the experience.

It’s not a simple problem, and if we hadn’t backed into it with the unobvious and seemingly unlikely communications bits already in place, I wouldn’t buy it either.

We’re also suffering from the same exact problem of not having words to correctly express the concepts, and to tell the truth, we’re using a trick to sneak by. But it doesn’t work in the general case; sometimes it feels like we’re shouting through a hole in the wall.

So we have a tough job explaining these ideas sometimes, and that, more than anything else, might be why you think they seem a bit over your head.

I assure it’s not. It’s just a bit far out, and as such a bit complicated at first glance. And it requires the use of the web-like structures to talk about at all.

Think about that the next time you’re lookin’ in the mirror. (grins…)

--Tom

The upshot is this: it seems premature to assume that any two individuals will have the same neural structures operating in their heads, simply because there is no research suggesting that similar logical structures are necessarily in use.
There is indirect evidence for this hypothesis of similarity. The work on recurrant syntatical structures across cultures and languages pioneered by Chompsky, for example.

If all humans share similar verbal structures that contain nouns, verbs, etc., in differnet cultures around the world, this would indicate similar underlying neurological structures. Similar forms arise from similar structures, in this case.

Nuanced human language, however, may integrate other parts of the brain and different neuro-networks beyond the fundamental language structures. Such nuances and integration may differ between individuals, but all humans use the fundamental verbal neurological structures to do language.

Many regions of the cortex have been mapped crudely. You can use glucose metabolism and positron emissions to show activity in a speech center.

While the brain is somewhat plastic, fundamental structures within the brain are not so variable. The sense of touch will map to the language centers when a blind person learns braille. You can show this on a brain scan.

But, I agree with Stabile to some extent, I don't think you can show the workings of the ADHD mind in brain scans, yet. But I do think real, identifyable differences exist between the brains of people with different flavors of ADHD and normal people (although each flavor may have its own source).

An analogy for scans:

Surgeons have heard patient complaints of back pain and followed up with xrays or spinal scans. They find something amiss; a compressed or leaky disk, a suspected entrapped nerve. They operated to correct the deficiency only to discover afterwards that the patient feels no relief.

Then, someone did a large blinded series of spinal scans on healthy and pained individuals. They found the statistical distribution of spinal abnormalities was similar between the pained and the healthy who did not complain of pain.

This result doesn't mean there is no difference or no organic source for complaints of back pain, but that the methods in use to identify the cause were useless, especially when no one considered what 'normal' spines might look like.

Brain scans have a similar problem. Not enough comparison data, not enough resolution and an unsophisticated tool.

But I do believe ADHD will someday resolve into identifiable structural (or neuro-transmitter) abnormailities (or differences) in the brain.

But I do believe ADHD will someday resolve into identifiable structural (or neuro-transmitter) abnormailities (or differences) in the brain.Stan, I agree with this and I'm also sure your right that our sample of both normal and ADD brains are too limited to date.

Stabile, Thanks for your response. I'm understanding a bit more where you are coming from and am interested in understanding more. Your analogies are quite helpful in grasping the general concepts.

Scattered

We said necessarily in use, in the sense that similar function must imply similar structure.

There is no such requirement in nature, nor does any research we know of suggest it. But it seems so self-evident that it’s difficult to get a decent discussion going about it.


While the brain is somewhat plastic, fundamental structures within the brain are not so variable. The sense of touch will map to the language centers when a blind person learns braille. You can show this on a brain scan…
This is the commonly accepted view, all right. But again, it hasn’t actually been established.

It sure seems like it makes sense, though, and that’s the problem we’re facing on every level.

The truth about the fundamental structures in the brain is that they don’t do anything like what we might expect; in fact, we’re certain the there is an additional layer of logic between the neural structures and the logical structures we’ve been trying to discuss.

A scan is assumed to show the neural activity underlying the logical activity associated with the high level behavior being studied, and that’s quite a stretch already.

But if the neural activity is actually supporting an emulation in which the logical activity in turn supports different logical activity which is ultimately responsible for the behavior of interest, there isn’t much hope of understanding the (supposed) chain of causal relationships that connect the image to the behavior.

But note that this circumstance would create the impression that the structures in our brains are pretty much similar in all individuals, exactly as you noted. In a sense you can think of the differences being hidden by the intermediate layer of logic; a ‘ghost’ brain within the physical brain does a lot of the work, and scans don’t show that at all.

If you’re curious as to why we posit this extra layer, it’s related to several observations, including the fact that real physical neurons can’t adapt quickly enough to serve as (for example) short term memory.

Chemistry is relatively slow. Logical models of chemistry operate at the speed of thought.


…Brain scans have a similar problem. Not enough comparison data, not enough resolution and an unsophisticated tool.
Good point. But we would add that the tool probably can’t be refined much beyond its current state. It’s firmly rooted in logical models that don’t support metalevels, and the walls are closing in.

An entirely new way of thinking about scans is necessary, one that models the problem with an awareness of the inherent metalevels.

The limitations (which appear as irresolvable ambiguity) of logical models that don’t incorporate metalevels can’t be overemphasized. Metalevels allow us to identify an infinite number of layers in our models; when we need finer resolution we can always add dimensions to accommodate it.

In contrast, models without metalevels are effectively limited to the projection of the metalevel enabled model onto a surface, like the shadow of a complex structure. Any element that lies in another’s shadow is indistinguishable in the projection.

We think this is a pretty cool analogy; it’s actually what’s going on in our heads when we experience ambiguity of this particular sort.

* * * * *

Note that your examples all address high level function that is directly due to activity in logical structures in the brain, not physical structures. Scans show the activity of the physical structures that support the logical structures, but again, there isn’t any particular reason to assume they necessarily imply similar function.

This has been a particular problem in linguistics, not made any easier by the fact that you can show a correlation between verbalization under controlled circumstances and particular neural activity, in particular regions that are roughly similar in most of us.

Chomsky considers the attempt to explain linguistics in terms of neural activity a waste of resources or worse. He did abandon his original approach of generative grammars in the late ‘90s, favoring a much more elegant black-box model with ‘switches’. Set the switches this way, and you have Japanese. Set them another way and you get Tagalog, and so on. The rest he considers hard-wired.

But he doesn’t consider the question of why the mechanism of ‘switches’ should exist, and I don’t believe he feels it’s appropriate to do so. It is an interesting problem: if the main bulk of the logical apparatus can converge on a single solution across a wide-spread population, why wouldn’t the switches settle into a single appropriate setting as well?

We might all speak something like modern French, and it’s hard to find a reasonable argument that would suggest such an arrangement wouldn’t work. So why switches, and different languages, if the rest of the system has managed to lock onto a single common solution without any trouble?

There is an answer, found in our work (of course), but it’s complicated by the fact that the linguistic faculty doesn’t exactly work the way it seems. By far the largest part of the business of acquiring language involves the structure of reality, in the form of the internal reality model in which we experience being.

We may be the only people so far to notice the fact that the bandwidth of the oral-aural channel is insufficient for the task at hand, by at least several orders of magnitude. If we were to actually transfer the information in any ordinary conversation, it would require years of careful listening.

How do we communicate, then? By having the conversation entirely within an internal reality, complete with models of all the participants, where there are no bandwidth restrictions to slow us down.

Of course we still need a way to extend the conversation to other real external participants, and so we have evolved a system of complex mechanisms that allow us to very precisely synchronize all of the individual versions of the conversation in each of the participants’ heads.

That’s probably not what you expected us to describe, but it does fit the requirements in quite a few important ways. And note how the experiment has changed: where we originally expected a scan to show brain activity related to forming sentences and so on, now most of the activity must be assumed to serve the purpose of establishing and maintaining this synchronization among the participants.

In absolute terms, researchers are probably setting their imagination way too low, in the sense that a particular amount of activity on a scan probably represents at least an order of magnitude more logical activity than they expect.

As far as the switches are concerned, they match nicely a property of neural structures that we first recognized fifteen years ago. Hierarchical neural structures represent a functional transform of the inputs on the outputs of arbitrary form; that is the definition of an arbitrary logical model, theoretically capable of representing anything.

These models are initially in a ‘blank’ state, really more of an average than a null (which relates directly to things like conventional standards of beauty, believe it or not). As the model is exercised, the state is modified until it converges on the final form, a representation that can be astonishingly accurate.

But there are restrictions on how that convergence occurs; the process must be limited to operations that can only improve the state, or there is a risk the model won’t converge at all, or worse, appear to converge on an incorrect state.

Neural networks in the brain are pretty good at converging and not messing up, but there is one flaw – a certain kind of ambiguity in the data while certain models are being developed can cause what we call bimodal convergence.

This simply means that there are two stable states that the network may take, and the process of convergence is data sensitive. If we start over here, we’ll converge in this state; but if we start over there, we’ll converge in a different (but still stable and useful) state.

Not long ago Kay realized that Chomsky’s switches are almost certainly the most common example of bimodal convergence. We exchanged emails with Chomsky about this, but he wasn’t very enthusiastic. In his opinion, it just didn’t seem relevant.

We have a different opinion, of course; we believe understanding the mechanism itself is superior to merely being able to predict the response of a black box, regardless of how accurate the prediction may be. The example of scans used for linguistic research is appropriate exactly because the interpretation of what the neural activity represents has so far been made without accounting for much of the work that must be done to complete even a simple sentence.

Again, we’re not criticizing the work of linguists, or saying that their models of language are wrong. What we’re trying to communicate is a sense of how vastly different the problem really is once you get into the realm of actual neurons. It’s not at all what our simplistic deterministic view of things like language and behavior (and even neurons) leads us to believe.

In many cases we’re probably looking for the wrong things, in the wrong places. The clues necessary to find the appropriate places are right there, stuff like applying information theory to the process of communicating with words. That in particular is not rocket science, yet nobody we’ve mentioned it to has seen fit to check it out.

That’s just another example for the foolish human tricks spotlight reel, in our opinion, and it’s hard to get too upset about it. But it would be nice to get over it and try to get some real work done.

In that respect, Chomsky was right. A lot of this is wasted effort, and will be until we get on the right track understanding how neural and logical structures really function.

Then we can start to figure out what scans are really showing us, and if some of it’s the differences that represent AD/HD, well, that’s OK with us. There isn’t really anything inherently wrong with being different, is there?

Oh well. Enough for now. Enough for later too. I think I’ll shut up for a while.

Good comments here lately, by the way. This has been fun.

--Tom & Kay

Those were all excellent posts. Right now, I think we're still in the Stone Age when it comes to understanding ADHD .The cool thing is that it keeps moving forward.

Theres nothing to understand

This is the way we were born
This is the way we are supposed to be
Its the rest of society that has ther head up there *********
as they are the ones
That cant accept us for what we are

That was very well said Gary.

It's like when someone comes in here or perhaps the ADD Support chat in Yahoo, and starts DEMANDING that we "prove ADHD exists" OR attacks existing research that is looked upon as "landmark."

You have to ask yourself a (rhetorical) question about their intent.If the tone remains critical and/or abrasvie, it's doubtful (but not impossible) that they're here to help further knowledge or offer support.

The reality is that this is THEIR PROBLEM and not ours.

The really manipulative thing about it is that in taking that approach (attacking us),it also helps keep us off balance so that they don't have to offer any evidence to the contrary (because there's not any).

I'm guilty of getting caught up in that. In fact, that's where :Here's the Proof " came from in the first place.

The thing to remember tho, is that if you score a slam dunk (by posting a response that answers the question in no uncertain terms and proves the point) on these people and they don't respond or simply re-post what you just posted,then you're not dealing with a rational person.

I've said this before, but by not responding to anything you posted (and re-posting what you just said is NOT a response because it doesn't address any of the the points you made), these people don't have to read the references and admit they're wrong;which they are.

Unfortunately, we've been bombarded by *******s for so long that we naturally take a defensive posture.

The satisfaction, however, is in making these people either leave or stfu.

In the process, the rest of the Forum can become better educated on the etiologies and (real) science behind ADHD. That way, they'll be better prepared if they have to defend themselves or their kids in any meetings, etc.

The people that do these types of things don't realize they're actually providing an "in vivo (real world experience)" demonstration of How To Handle Criticism's of ADHD.

That not only proves to be educational, it's also heuristic (serves to encourage discovery of problem solving), because it leads to looking up the "real" research and learning something as you proceed


take care
mcatvish23 (Robert).

Well said, everybody. Hear, hear.

You guys all rock !
In all the ways you say it, elequont, scientific, or in just plain 'there it is'..
You just rock !!!

This info is so helpful to me. I grow tired of my family treating me like a lazy parent who has just decided whimsically to have my kids pop pills. Thanks for sharing all of the info. I read lots and lots of books, but this boils it all down into something more valuable.

Theres nothing to understand

This is the way we were born
This is the way we are supposed to be
Its the rest of society that has ther head up there *********
as they are the ones
That cant accept us for what we are
Garry I am glad to see I am not the only one who sees it this way.
We are stigmatized to believe and waste our times trying to figure something out that is using the wrong perspective to study it with.

Hello All,

On Good Friday my partner of ten years broke up with me saying, "Baby - I am so sorry this had to happen this way -- please take this as a chance to do the right thing -- Love --Me"

Over the course of that night I decided that I wanted her back. I also decided that in order to do that I would need to change. I had known I had ADHD for years but had never sought out any type of help or treatment. I also never really educated myself as to what ADHD really was other than a few basics and that I had been diagnosed with it. Well, the last month has been one of some major ups and downs, discovery, education, medication and quite a few changes. I still hope that she will be able to heal. I still hope that we will be able to spend the rest of our lives together. No matter what though, I will never ever be the same person again. And, with her or without her I will be a better person because of it. Heh, when you can think of the worse possible crazy depressed drugged angry money spending ADHD poster child out there, you'd be thinking of me. Or at least the person I was....

I am now on Strattera and must be one of the very few lucky ones because, so far, I would fight tooth and nail to stay on this medicine. I actually have finger nails for the first time in 37 years!!! And so far none of the side effects. Well not sure about the sex ones since I'm not having any heh but anyways... The ammount of impulse controle I have, though not perfect, is way way WAY more than I have ever had before...

The darn thing is I am from the Washington D.C. area and for the last two weeks and for the next one to two months I am in Denver, CO for work. My Father took pity on me and hired me and brought me ought here to help him. Even though he is helping and he is err somewhat supportive I really have no friends or real support out here at all. So I took to the net and consider myself very lucky to have found this board.

So that's my introduction. I'm sure we'll talk more about me and my issues with ADHD as time goes by. I started reading this thread and felt that some info I had recently come accross on another site would fit right in. So, here is the Consensus Statement:

Oh and thanks for taking the time to listen :)

Eric

International Consensus Statement on ADHD
Mainstream media coverage about attention deficit hyperactivity disorder has historically been biased, full of misinformation and heavily influenced by anti-psychiatry groups.


In response to this unfortunate trend, Dr. Russell Barkley and 74 other prominent medical doctors and researchers in AD/HD issued the following statement.

January 2002

We, the undersigned consortium of 75 international scientists, are deeply concerned about the periodic inaccurate portrayal of attention deficit hyperactivity disorder (ADHD) in media reports. This is a disorder with which we are all very familiar and toward which many of us have dedicated scientific studies if not entire careers. We fear that inaccurate stories rendering ADHD as myth, fraud, or benign condition may cause thousands of sufferers not to seek treatment for their disorder. It also leaves the public with a general sense that this disorder is not valid or real or consists of a rather trivial affliction.

We have created this consensus statement on ADHD as a reference on the status of the scientific findings concerning this disorder, its validity, and its adverse impact on the lives of those diagnosed with the disorder as of this writing (January 2002).

Occasional coverage of the disorder casts the story in the form of a sporting event with evenly matched competitors. The views of a handful of non-expert doctors that ADHD does not exist are contrasted against mainstream scientific views that it does, as if both views had equal merit. Such attempts at balance give the public the impression that there is substantial scientific disagreement over whether ADHD is a real medical condition. In fact, there is no such disagreement --at least no more so than there is over whether smoking causes cancer, for example, or whether a virus causes HIV/AIDS.

The U.S. Surgeon General, the American Medical Association (AMA), the American Psychiatric Association, the American Academy of Child and Adolescent Psychiatry (AACAP), the American Psychological Association, and the American Academy of Pediatrics (AAP), among others, all recognize ADHD as a valid disorder. While some of these organizations have issued guidelines for evaluation and management of the disorder for their membership, this is the first consensus statement issued by an independent consortium of leading scientists concerning the status of the disorder. Among scientists who have devoted years, if not entire careers, to the study of this disorder there is no controversy regarding its existence.

ADHD and Science

We cannot over emphasize the point that, as a matter of science, the notion that ADHD does not exist is simply wrong. All of the major medical associations and government health agencies recognize ADHD as a genuine disorder because the scientific evidence indicating it is so is overwhelming.

Various approaches have been used to establish whether a condition rises to the level of a valid medical or psychiatric disorder. A very useful one stipulates that there must be scientifically established evidence that those suffering the condition have a serious deficiency in or failure of a physical or psychological mechanism that is universal to humans. That is, all humans normally would be expected, regardless of culture, to have developed that mental ability.

And there must be equally incontrovertible scientific evidence that this serious deficiency leads to harm to the individual. Harm is established through evidence of increased mortality, morbidity, or impairment in the major life activities required of one's developmental stage in life. Major life activities are those domains of functioning such as education, social relationships, family functioning, independence and self-sufficiency, and occupational functioning that all humans of that developmental level are expected to perform.

As attested to by the numerous scientists signing this document, there is no question among the world's leading clinical researchers that ADHD involves a serious deficiency in a set of psychological abilities and that these deficiencies pose serious harm to most individuals possessing the disorder. Current evidence indicates that deficits in behavioral inhibition and sustained attention are central to this disorder -- facts demonstrated through hundreds of scientific studies. And there is no doubt that ADHD leads to impairments in major life activities, including social relations, education, family functioning, occupational functioning, self-sufficiency, and adherence to social rules, norms, and laws. Evidence also indicates that those with ADHD are more prone to physical injury and accidental poisonings. This is why no professional medical, psychological, or scientific organization doubts the existence of ADHD as a legitimate disorder.

The central psychological deficits in those with ADHD have now been linked through numerous studies using various scientific methods to several specific brain regions (the frontal lobe, its connections to the basal ganglia, and their relationship to the central aspects of the cerebellum). Most neurological studies find that as a group those with ADHD have less brain electrical activity and show less reactivity to stimulation in one or more of these regions. And neuro-imaging studies of groups of those with ADHD also demonstrate relatively smaller areas of brain matter and less metabolic activity of this brain matter than is the case in control groups used in these studies.

These same psychological deficits in inhibition and attention have been found in numerous studies of identical and fraternal twins conducted across various countries (US, Great Britain, Norway, Australia, etc.) to be primarily inherited. The genetic contribution to these traits is routinely found to be among the highest for any psychiatric disorder (70-95% of trait variation in the population), nearly approaching the genetic contribution to human height. One gene has recently been reliably demonstrated to be associated with this disorder and the search for more is underway by more than 12 different scientific teams worldwide at this time.

Numerous studies of twins demonstrate that family environment makes no significant separate contribution to these traits. This is not to say that the home environment, parental management abilities, stressful life events, or deviant peer relationships are unimportant or have no influence on individuals having this disorder, as they certainly do. Genetic tendencies are expressed in interaction with the environment. Also, those having ADHD often have other associated disorders and problems, some of which are clearly related to their social environments. But it is to say that the underlying psychological deficits that comprise ADHD itself are not solely or primarily the result of these environmental factors.

This is why leading international scientists, such as the signers below, recognize the mounting evidence of neurological and genetic contributions to this disorder. This evidence, coupled with countless studies on the harm posed by the disorder and hundreds of studies on the effectiveness of medication, buttresses the need in many, though by no means all, cases for management of the disorder with multiple therapies. These include medication combined with educational, family, and other social accommodations. This is in striking contrast to the wholly unscientific views of some social critics in periodic media accounts that ADHD constitutes a fraud, that medicating those afflicted is questionable if not reprehensible, and that any behavior problems associated with ADHD are merely the result of problems in the home, excessive viewing of TV or playing of video games, diet, lack of love and attention, or teacher/school intolerance.

ADHD is not a benign disorder. For those it afflicts, ADHD can cause devastating problems. Follow-up studies of clinical samples suggest that sufferers are far more likely than normal people to drop out of school (32-40%), to rarely complete college (5-10%), to have few or no friends (50-70%), to under perform at work (70-80%), to engage in antisocial activities (40-50%), and to use tobacco or illicit drugs more than normal. Moreover, children growing up with ADHD are more likely to experience teen pregnancy (40%) and sexually transmitted diseases (16%), to speed excessively and have multiple car accidents, to experience depression (20-30%) and personality disorders (18-25%) as adults, and in hundreds of other ways mismanage and endanger their lives.

Yet despite these serious consequences, studies indicate that less than half of those with the disorder are receiving treatment. The media can help substantially to improve these circumstances. It can do so by portraying ADHD and the science about it as accurately and responsibly as possible while not purveying the propaganda of some social critics and fringe doctors whose political agenda would have you and the public believe there is no real disorder here. To publish stories that ADHD is a fictitious disorder or merely a conflict between today's Huckleberry Finns and their caregivers is tantamount to declaring the earth flat, the laws of gravity debatable, and the periodic table in chemistry a fraud. ADHD should be depicted in the media as realistically and accurately as it is depicted in science -- as a valid disorder having varied and substantial adverse impact on those who may suffer from it through no fault of their own or their parents and teachers.

Sincerely, Russell A. Barkley, Ph.D.
Professor
Depts. Of Psychiatry and Neurology
University of Massachusetts Medical School
55 Lake Avenue North
Worcester, MA 01655

Edwin H. Cook, Jr., M.D.
Professor
Departments of Psychiatry and Pediatrics
University of Chicago
5841 S. Maryland Ave.
Chicago, IL

Mina Dulcan, M.D.
Professor
Department of Child and Adolescent
Psychiatry
2300 Children’s Plaza #10
Children’s Memorial Hospital
Chicago, IL 60614

Susan Campbell, Ph.D.
Professor
Department of Psychology
4015 O’Hara Street
University of Pittsburgh
Pittsburgh, PA 15260

Margot Prior, Ph.D.
Professor
Department of Psychology
Royal Children’s Hospital
Parkville, 3052 VIC
Australia


Marc Atkins, Ph.D.
Associate Professor
University of Illinois at Chicago
Institute for Juvenile Research
Department of Psychiatry
840 South Wood Street, Suite 130
Chicago, IL 60612-7347

Christopher Gillberg, M.D.
Professor
Department of Child and Adolescent
Psychiatry
University of Gothenberg
Gothenberg, Sweden

Mary Solanto-Gardner, Ph.D.
Associate Professor
Division of Child and Adolescent Psychiatry
The Mt. Sinai Medical Center
One Gustave L. Levy Place
New York, NY 10029-6574

Jeffrey Halperin, Ph.D.
Professor,
Department of Psychology
Queens College, CUNY
65-30 Kissena Ave.
Flushing, NY 11367

Jose J. Bauermeister, Ph.D.
Professor,
Department of Psychology
University of Puerto Rico
San Juan, PR 00927

Steven R. Pliszka, M.D.
Associate Professor and Chief
Division of Child and Adolescent Psychiatry
University of Texas Health Sciences Center
7703 Floyd Curl Drive
San Antonio, TX 78229-3900

Mark A. Stein, Ph.D.
Chair of Psychology
Children’s National Medical Center and
Professor of Psychiatry & Pediatrics
George Washington Univ. Med. School
111 Michigan Ave. NW
Washington, DC 20010


John S. Werry, M.D.
Professor Emeritus
Department of Psychiatry
University of Auckland
Auckland, New Zealand

Joseph Sergeant, Ph.D.
Chair of Clinical Neuropsychology
Free University
Van der Boecharst Straat 1
De Boelenlaan 1109
1018 BT Amsterdam
The Netherlands

Ronald T. Brown, Ph.D.
Associate Dean, College of Health Professions
Professor of Pediatrics
Medical University of South Carolina
19 Hagood Avenue
P. O. Box 250822
Charleston, SC 29425

Alan Zametkin, M.D.
Child Psychiatrist
Kensington, MD

Arthur D. Anastopoulos, Ph.D.
Professor, Co-Director of Clinical Training
Department of Psychology
University of North Carolina at Greensboro
P. O. Box 26164
Greensboro, NC 27402-6164

James J. McGough, M.D.
Associate Professor of Clinical Psychiatry
UCLA School of Medicine
760 Westwood Plaza
Los Angeles, CA 90024

George J. DuPaul, Ph.D.
Professor of School Psychology
Lehigh University
111 Research Drive, Hilltop Campus
Bethlehem, PA 18015

Stephen V. Faraone, Ph.D.
Associate Professor of Psychology
Harvard University
750 Washington St., Suite 255
South Easton, MA 02375

Florence Levy, M.D.
Associate Professor
School of Psychiatry
University of New South Wales
Avoca Clinic
Joynton Avenue
Zetland, NSW, 2017, Australia

Mariellen Fischer, Ph.D.
Professor,
Department of Neurology
Medical College of Wisconsin
9200 W. Wisconsin Avenue
Milwaukee, WI 53226

Joseph Biederman, M.D.
Professor and Chief
Joint Program in Pediatric
Psychopharmacology
Massachusetts General Hospital and
Harvard Medical School
15 Parkman St., WACC725
Boston, MA 02114

Cynthia Hartung, Ph.D.
Postdoctoral Fellow
Department of Psychology
Department of Psychology
University of Denver
2155 S. Race St.
Denver, CO 80208

Stephen Houghton, Ph.D.
Professor of Psychology
Director, Centre for Attention & Related Disorders
The University of Western Australia
Perth, Australia

Gabrielle Carlson, M.D.
Professor and Director,
Division of Child and Adolescent Psychiatry
State University of New York at Stony Brook, Putnam Hall
Stony Brook, NY 11794

Charlotte Johnston, Ph.D.
Professor
Department of Psychology
University of British Columbia
2136 West Mall
Vancouver, BC, Canada V6T 1Z4

Thomas Spencer, M.D.
Associate Professor and Assistant
Director, Pediatric Psychopharmacology
Harvard Medical School and
Massachusetts General Hospital
15 Parkman St., WACC725
Boston, MA 02114

Thomas Joiner, Ph.D.
The Bright-Burton Professor of Psychology
Florida State University
Tallahassee, FL 32306-1270

Rosemary Tannock, Ph.D.
Professor of Psychiatry,
Brain and Behavior Research
Hospital for Sick Children
55 University Avenue
Toronto, Ontario, Canada M5G 1X8

Adele Diamond, Ph.D.
Professor of Psychiatry
Director, Center for Developmental
Cognitive Neuroscience
University of Massachusetts Medical School
Shriver Center
Trapelo Rd.
Waltham, MA

Carol Whalen, Ph.D.
Professor
Department of Psychology and Social Behavior
University of California at Irvine
3340 Social Ecology II
Irvine, CA 02215

Stephen P. Hinshaw, Ph.D.
Professor,
Department of Psychology #1650
University of California at Berkeley
3210 Tolman Hall
Berkeley, CA 94720-1650

Herbert Quay, Ph.D.
Professor Emeritus
University of Miami
2525 Gulf of Mexico Drive, #5C
Long Boat Key, FL 34228

John Piacentini, Ph.D.
Associate Professor
Department of Psychiatry
UCLA Neuropsychiatric Institute
760 Westwood Plaza
Los Angeles, CA 90024-1759

Philip Firestone, Ph.D.
Professor
Departments of Psychology & Psychiatry
University of Ottawa
120 University Priv.
Ottawa, Canada K1N 6N5

Salvatore Mannuzza, M.D.
Research Professor of Psychiatry
New York University School of Medicine
550 First Avenue
New York, NY 10016

Howard Abikoff, Ph.D.
Pevaroff Cohn Professor of Child and Adolescent Psychiatry
NYU School of Medicine
Director of Research
NYU Child Study Center
550 First Avenue
New York, NY 10016

Keith McBurnett, Ph.D.
Associate Professor
Department of Psychiatry
University of California at San Francisco
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I was just moving my car and my husband keeps it on AM radio - Rush Limbaugh (sp?) was on. and right as i turned the car on he's saying "ADD DOESN'T EXIST!" something to the effect of it was invented by drug companies and parents who don't want to deal with normal little boys, and adults who want something to blame their "road rage" on. ???? Also said there's scientific evidence because there's money in doing research studies. maybe im just ridiculously biased because I pretty much take anything he says as a load of you-know-what ... but ughhhhhh

Well, Rush Limbaugh certainly knows a thing or two about prescription drugs. He's also a hypocrite, as he believes that all drug addicts should be thrown in jail...except for him, he deserves treatment.

I think the fact that the two most prominent anti-ADD people out there are Tom Cruise and Rush Limbaugh pretty much says all you need to know about people with that viewpoint.

That Rush Limbaugh idea just made me think, once again, that every time I see Carlos Mencia I think "This dude is LOADED with ADD" and his humor cracks me up...yet I am terrified to contact him in any way about that lest he find a way to work ADD into his routine in a negative way. Then I would have to get annoyed and stop watching his show ;).

And now back to your regularly scheduled thread.

I think the fact that the two most prominent anti-ADD people out there are Tom Cruise and Rush Limbaugh pretty much says all you need to know about people with that viewpoint.



:D :rolleyes: :p

Most execellent point!

The International Consensus 2002 is THE definitive research article on the existence of ADHD as a real disorder.

Thanks for posting it.

Nice 2 cya'll. Just passing thru.Am still alive & well.

tc
mctavish23
(Robert)

It's awesome to know you're doing well, McT, and see you on here, even if it's briefly.

I'm always wishing you well.

I have a warm fuzzy feeling and I haven't even been drinking!

Heres one thing we can all agree about, McT is the best.

Heres one thing we can all agree about, McT is the best.Ditto to that! Always nice to see you posting McT!:)

Scattered

Just been back from seeing my doctor again, having had to take him by the nose through the recommended doses for Strattera and get him to up my dose from 40 to 80 (day 30 on 40mg, not much yet, should I keep going up?). He has already told me this is the first time he's come across an adult with an ADHD diagnosis (this is one I fought for against all the prejudice here 10 years ago, when I was 28 and in a break up like Lostnomore, but later 'shelved' because the ritalin didn't work and i didn't like defining myself as someone with a disorder). The psychiatrist with whom he has 'shared care' over me (the UK system - which applies in this part of Ireland - requires 'Shared care' between a psychiatrist and General Practitioner (GP)), is not much better - he has been reluctant to see me (this is the public health system, so they prioritise 'real' illnesses) and, in spite of a diagnosis made by one of his colleagues in Dublin, has indicated his skepticism over this, citing an opinion by another from 11 years ago that I may have a 'personality disorder' (which one is unspecified). It seems therefore that I am taking Strattera only because this guy is humouring me. Both the GP and the Psychiatrist in my case have little Rush Lymbaughs in their heads it seems! If I am right about being 'humoured' it means that if the Strattera doesn't work for me It's going to mean re-evaluating for ADHD before I can try another treatment. A pain in the ****!

Anyway your posts are very helpful for me in being able to produce hard evidence for these flat-earthers. Any pointers anyone to tests for ADHD in neuroscience? (any breakthroughs in neurology, neuropsychiatry, neuropsychology etc which could demonstrate that ADHD is what I have?). Sorry for the disorganised thoughts, but, em, you know...

Anyway your posts are very helpful for me in being able to produce hard evidence for these flat-earthers. Any pointers anyone to tests for ADHD in neuroscience? (any breakthroughs in neurology, neuropsychiatry, neuropsychology etc which could demonstrate that ADHD is what I have?). Sorry for the disorganised thoughts, but, em, you know...Sorry for the hassles with your doctor. I understand they're coming close to a diagnositic type SPECT and PET scan thingy but I don't think it's on the market yet.


...and now the real possibly of brain scans not only to learn but objectively diagnosis ADHD.http://www.news-medical.net/?id=19410

Quote:
<TABLE cellSpacing=0 cellPadding=6 width="100%" border=0><TBODY><TR><TD class=alt2 style="BORDER-RIGHT: 1px inset; BORDER-TOP: 1px inset; BORDER-LEFT: 1px inset; BORDER-BOTTOM: 1px inset">Boston Life Sciences announces issuance of U.S. patent for methods to diagnose ADHD


Boston Life Sciences has announced that the U.S. Patent and Trademark Office has issued a patent to the President and Fellows of Harvard College, the General Hospital Corporation and Organix that covers methods of diagnosing and monitoring attention deficit hyperactivity disorder (ADHD) by assessing the level of dopamine transporter (DAT) in at least one region of a patient's central nervous system.

The patent is exclusively licensed to BLSI under a worldwide licensing arrangement between BLSI and Harvard University. The patent is based on the work of the inventors, Dr. Bertha Madras of Harvard, Dr. Peter Meltzer of Organix, Inc., and Dr. Alan Fischman of Massachusetts General Hospital. Both Dr. Fischman and Dr. Meltzer serve as advisors to BLSI. The patent claims a variety of diagnostic and monitoring methods for assessing ADHD utilizing labeled compounds that bind to the dopamine transporter and are measured using any imaging technique including single photon emission computed tomography (SPECT) and positron emission tomography (PET). An example of a compound covered by the patent is the Company's ALTROPANE(R) molecular imaging agent currently in Phase II clinical trials as an aid to ADHD diagnosis. The Company is currently analyzing imaging results and clinical data, both of which were obtained from patients enrolled to-date, to verify findings in prior studies and ensure that the trial design and quantification algorithms are appropriate.

In addition to methods used to objectively diagnose ADHD in adults or children, the patent covers methods that could enable physicians to determine the most effective ADHD drug treatment and/or dosage level for an individual patient, monitor the long-term progress of treatment for ADHD, and aid in identifying individuals at risk for ADHD.

Mark Hurtt, BLSI's Chief Medical Officer, comments, "The use of imaging techniques and dopamine transporter specific imaging agents has the potential to provide an objective, biologically-based diagnosis for ADHD. We are very pleased with the potential scope of this patent. We believe that the new patent enhances our position in this significant area of medical need. According to the Centers for Disease Control, between 3% and 7% of school-aged children and 2 to 4% of adults have been diagnosed with ADHD. We believe that imaging agents may assist physicians in confirming a diagnosis, resolving conflicting diagnoses, calling into question a diagnosis or non-diagnosis of ADHD, or selecting medication."
</TD></TR></TBODY></TABLE>
For the moment, as far as I know, the individual's history is still the best tool in the hands of someone who understand Adult ADD (I know that's where the trouble lies, eh -- finding that practioner). Hope Strattera works well for you.

Even with a valid diagnosis of ADHD a 30 + percent of folks are considered non responders (not a significant enough improvement in their symptoms or they can't tolerate the medication). I recently got a book that comes very highly recommended by Russell Barkley one of the leaders in the field of ADHD called Mastering Your Adult ADHD: A Cognitive-Behavioral Treatment Program --Client Workbook. It can be used to maximize your results with medication or "for the 50 percent of individuals who derive relativelylittle benefit fom medication, this program may be sufficient. -- David Barlow, Editor-in-Chief, Treatments That Work.

Russell Barkley says of it, "This is groundbreaking work...In this manual, patients will find highly useful information about the disorder, and just as important, scientifically proven tactics for dealing with their ADHD symptoms and assoicated impairments. Thank you, Drs. Safred, Sprich, Perlman, and Otto."

Nice to have another tool available in addition to psychotherapy and medication.

Take care,

Scattered

Heres one thing we can all agree about, McT is the best.

Okay this this three times in one day I have agreed with you this could be a frightening trend. . . . should we head for the bomb shelters yet. :p

McT it is good to see you!

Ok, this is why I could not be a scientist or a debater.....I do not have a clue what any of this says.........
I know what the bottom line is, but how can anyone follow any of this, it makes my head spin.
This is the kind of stuff that makes me feel inferior:( ...........

The exact etiology of ADHD is unknown. No one is claiming to know that, at least not right now. However, in regards to statements about there being "no scientific basis"(/B) for these disorders,

Here's the "proof" : These are ALL from unrestricted research grants published in (the cream of the crop) peer reviewed journals.

1) The neurobiological nature of ADHD.....THE PROOF YOU SAY DOESNT EXIST: was conclusively proven in the 1990 landmark glucose brainscan research study published in the New England Journal of Medicine....


Zametkin,A.J.,Nordahl,T.E.,Gross,M.,King,A.K.,Semp le,W.E.,Rumsey,J.,Hamburger,S.,& Cohen,R.M.(1990) Cerebral glucose metabolism in adults with hyperactivity of childhood onset. The New England Journal of Medicine,323,(30).1361-1366.

The "proof" is in the PET scans that showed that the harder a person with ADHD concentrated the "slower" their brain went vs the exact opposite for the non ADHD group. However, that was remedied when the ADHD subjects took stimulant medication.

THE definitive study proving the existence of ADHD as a "real" disorder;signed off on by over 80 of the world's leading scientists (with over 19 pages of references) is :

Consortium of international scientists:International Consensus Statement on ADHD, January 2002. (http://www.chadd.org (http://www.chadd.org/)). It can also be viewed at Russell Barkley's website.


You can turn to pages 22-24 of Sandra Rief's 2003 book.............The ADHD Book of Lists ....................to find the section (1-7) WHAT THE RESEARCH IS REVEALING ABOUT ADHD

Within that section is the reference for the Landmark MTA Study:

"There has been significant research with regards to treatments for ADHD and their relative effectiveness. The longest and most thorough study of the effects of ADHD interventions was the 1999 Multimodal Treatment Study of Children with ADHD (MTA) by the National Institute of Mental Health (NIMH).

MTA Cooperative Group" A 14-month Randomized Clinincal Trial of Treatment Strategies for AD/HD,"Archives of General Psychiatry,[I] 56:1073-1086;1999.

ADHD is primarily thought to be largely (80%) genetic/inherited.THE GENETIC LANDMARK FOR ADHD WAS FOUND IN 995. That study is as follows:


Cook,et.al.,(1995) Association of attention-deficit disorder and the dopamine transporter gene.American Journal of Human Genetics,56.993-998.

The US Surgeon General's Report on Mental Health: Chapter 3: Disorders of Infancy, Childhood & Adolescence has excellent background info supporting in great detail (with another 19 pages of scientific references).Here's a small segment on what I'm talking about:
" The exact etiology of ADHD is unknown,although neurotransmitter deficits,genetics and perinatal complications have been implicated." It goes on to say:

"Research to pinpoint abnormal genes is honing in on 2 genes;a dopamine receptor gene (DRD) gene on chromosome 11 and the dopamine -transporter gene (DAT1) on chromosome 5 (Cook,et.al.,1995:Smalley,et.al.;1998).

The latter reference is : Smalley,et.at.(1998) Evidence that the dopamine D4 receptor is a succeptibility gene in attention-deficit hyperactivity disorder,Molecular Psychiatry,3,427-430.

Recently (3/25/05), I participated in a teleconference on ADHD in children put on by United Behavioral Health (UBH: a managed care company). The presenter was Russell Barkley, PhD. He is largely viewed as the world's leading researcher on ADHD. During that presentation, he listed the following (evidenced based/research derived) data regarding the neurology of ADHD.

Decreased Cerebral Metabolism
(from Thomas Spencer, M.D.)

global and regional glucose metabolism by PET scan reduced in adults who have been hyper since childhood (thats Zametkin's research again).
Largest reductions in:
1) pre motor cortex
2) superior prefrontal cortex

Anterior Cingulate Dysfunction in ADHD, fMRI and the Counting Stroop.
Bush,et.al.,(1998).


Etiologies-Neurological

Smaller, less active,less developed brain
Regions found on MRI,fMRI and PET scans incluse the following areas of the brain:
1) Orbital-Prefrontal Cortex( primarily on the right side)

2) Basal Ganglia (mainly striatum and globus pallidus)

3) Cerebellum (central vermis area, right side) - there were some other posts about this particualr area of the brain being a key component of ADHD in a different thread I believe

Suspected Neurochemical Deficiency:

1) Dopamine dysregulation likely but not definitive....... the mere fact that stimulant
medication works at all to relieve symptoms of ADHD forms a solid basis
for helping to substantiate this (and the first medication study was done in 1937 in
Rhode Island)

2) Norepinephrine dysregulation probable

Etiologies- Genetic ( these data were all derived from research studies) The usual maker for statistical significance is 1.5 SD (standard deviation) 's from the mean, which equates to a %tile ranking of 93. In other words, the absolute lowest chance of these data being accurate is 93%.

1) Family aggregation of the disorder: 25-35% of siblings; 78-92% of idnetical twins;15-20% of mothers, and 25-30% of fathers; If the parent is ADHD, then theres a 20-54% chance of the offspring being ADHD (increases the odds 8fold)

2) Twin studies of Heritability 57-97%)

3) Shared environment 0-6% (not significant)

4) Unique environment (15-20% )


Molecular Genetics : Candidate genes on DRD4,DAT1,DBH-Taq1 (on chromosomes 3,5,and 11)

Candidate region: chromosome 26p13 region


Lastly, the answer to your questions about the difference between ADHD and ADD can be found in Barkley's ADHD and the Nature of Self-Control (1997).
It's also addressed in his 2002 book Taking Charge of ADHD (pages 137-138) and in You Mean Im Not Lazy,Stupid Or Crazy? by Kate Kelly & Peg Ramundo (Chapter 2).

As for depression, it is considered to be a Medical disorder on the basis of the chemical imbalance of the neurotransmitter serotonin. I don't know anyone who considers it to be a "disease".

There's no cure for the common cold but people know it exists. The Biogenic Amine Hypothesis was derived (via research) over 20 years ago. Here's what that says: "The concept that abnormalities in the physiology and metabolism of certain biogenic amines, particularly catecholamines[I](norepinephrine and dopamine ) and an indoleamine(serotonin) , are involved in the causes and courses of certain psychiatric illnesses."
That qoute was from an older issue of A Psychiatric Glossary of the AMerican Psychiatric Association, page 28. The new one is at the office.

The Biogenic Amine Hypothesis is what eventually led to the development of the class of antidepressants we now know as SSRI's (Select Serotonin Reuptake Inhibitor's:Zoloft, Prozaz,etc.).


This MORE than refutes your remarks. As of the summer of 2003 there were over 6k research articles,professional papers, chapters in book and books on ADHD.

If you go to the International Consensus 2002 journal article, you will also find on page 89:

"ADHD is recognized as a disorder/medical condition by the American Medical Association, the American Psychiatric Association, the American Psychological Association and the American Academy of Pediatrics."


THIS ISN'T AN EXACT SCIENCE .NO ONE EVER SAID IT WAS. But I can tell you that a T score of 70+% on the Conners Parent Rating Scale is one of the most accurate predictors of ADHD currently available (when used in concert with a thorough developemental and medical screening, behavioral observations and other screenings for executive functions; to name a few).


I could go on but I've made my point. I spent hours on this post and still had to cut it short. There's your scientific basis.

ADD is just about the most real thing there is.

... one in a long line of remarkable perspective changes which current society will need to take on - as we vanish off into the future.

The peculiar humour of ADD - is that instead of a neutral other current perspective - much of what we see on ADD - at least currently - {out there} - is diametrically opposed to how it will come to be seen.

Whether each of us will look back on our gross mischaracterization of ADD in the future - as peculiar, funny or humourous - ~though~ - depends on our individual context.

Really so ...

... winds of change

... did you ever really believe that ADD was a straight-up disease?

andreapurple, I hear you. I guess I'm not sure what to believe anymore.

Scattered, since you mention Barkley, this is what I've read.

1. "The overwhelming majority of individuals with ADD have no history of significant brain injuries" (Barkley, 1998)

2. "Neuropsychological testing of ADD individuals has detected some differences in frontal lobe functions, but those findings are inconsistent". (Barkley, 1997)

3. "Researchers have been unable to document with any certainty neurochemical or neurotransmitter deficiencies as causal factors for ADD" (Barkley, 1998)

4. "Nervous system psychophysiological measures have been inconsistent in demonstrating significant group differences between ADD individuals and controls" (Baumeister & Hawkins, 2001)

5. "ADD neuro-imaging studies have not found evidence for any type of brain structural damage" (Leo & Cohen, 2002; Overmeyer & Tayler, 2001; Frank & Pavakis, 2001)

6. "There is no compelling evidence that pregnancy or birth complications cause ADD" (Barkley, 1998)

7. "Due to serious methodological limitations, the evidence that ADD is caused by environmental toxins, for example, prenatal exposure to alcohol and tobacco smoke or elevated body lead levels, must be viewed with caution" (Barkley, 1995)

8. "No evidence exists to show that ADD is the result of abnormal, damaged, or extra chromosomes. There is convincing evidence of family heredity basis or genetic link for ADD" (Biederman et al., 1995; Faraone, 2000)

9. "Although the present technology of neuro-imaging studies may help determine the volumn and shape of brain structures involved in specific cognitive task, they cannot provide information about the timing and rapid order of neuronal firing, nor can they show the oscillations between cortical and subcortical brain networks that are hypothesized to bind and integrate neural systems" (Durston et al., 2001; Stern & Silbersweig, 2001)

I would love to know why there are so many contradictions within the research of ADD.

Thanks for all of your work MCT, I am only questioning the contradications here. What do you think is going on here? How can they say one thing and something else too?

When it comes to "How do you get ADHD?" There are main 2 "types" of ADHD:

1) 80+% genetic inherited;

2) approx 20% "acquired"

That refers to pre, peri and post natal brain damage.

pre natal refers to inuetero exposure to nicotine and to alcohol : each of which increases the risk factor by 2.5X's


peri natal covers birth complications, with pre-mature birth having the greatest impact 3+x's the risk;

post natal refers to head trauma, lead paint (much less of a big deal as once thought), the impact of chemotherapy and a rare brain infection involving a strep like infection (If I remember correctly, I think it involves the basal ganglia).


Those data came directly from Russ's power points from a United Behavioral Health (UBH) teleconference on ADHD in Adults on 3/24/05.

The very same info can be found in : ADHD and the Nature of Self-control (1997) and The ADHD Handbook (both second & third editions (2002 & 2005).


Lastly, in his presentation in San Francisco (2000), he remarks on the genetic propensity of ADHD being greater than human height & IQ.


These are old data. Be careful how you try and interpret things, as they may be inadvertently taken out of context.

Those data were and are accurately reported.

tc

hope ya'll are all well.

mctavish23

Robert

Thanks for the clarification, McT! Always good to hear from you! Hope things are going well.

Oddjobace, they are still on a pretty high learning curve when it comes to the brain. Hopefully between the brain imaging that is being done and the human genome project, we'll soon have some more definative scientific information. In the mean time finding what combination (medication, and/or exercise, meditation, diet/supplements, behavioral therapy, family counseling, education, environmental adaptations, etc) helps you function best, is the most practical approach I know to dealing with ADHD. I think when first diagnosed, it's very easy to want absolutes and proof that this is why you are the way you are. I know I did. At some point coming to understand yourself and realize that most of us (including yourself) are doing the best we can most of the time can help with self acceptance and finding a path that fits for you.


Take care!
Scattered

re post #53, Mct.


The beginning of that post gives the impression that ADHD is due to brain damage. I hope that is not what you meant. With the exception of children who have suffered obvious brain damage in utero or after birth, the vast majority of ADHD people have no gross neurological deficits and no demonstrable CNS deficits on electrophysiologic studies or scans.

The examples of prenatal, postnatal causes should not be interpreted as known direct causes, but only as predisposing factors, i.e. those things result in a higher percentage of offspring with ADHD than children who don't have those factors in their histories. Obviously for example, if a child was a premi with respiratory problems, had a CT scan during neonatal period which showed hemorrhages, there will be a stronger likelihood of later problems, but again this is not 100% by a longshot.

The point should be that a high percentage of children with ADHD have one or more parent with ADHD but not all. Both parents having ADHD will increase the probability, but it will never be 100%.

BEtter way of looking at things: Most ADHD is caused by genetic factors influencing a child's temperament, mood, neurological make up. Given the fertile set up with a family which can't handle it effectively, some of these children will develop clinical problems, but some will be manageable if the parent/s happen to be wise/strong/capable/able to afford help.

Some of what looks like ADHD is a result of inadequate parenting techniques.

How does one tell the difference? Sometimes its not possible. But in my mind, the familial inheritable type is likely to be obvious within the first year, and sometimes before birth, but certainly prior to school age if there is a hyperactivity component; age of diagnosis is more variab in females without hyperactivity., often well after KG.

I hope this is clear.

hey richard,

I think McT was describing the probable causes of "acquired" ADHD ... the type of ADHD which is represented by the 20% figure he referenced.

welcome to the forums. :)

wheezie

Better way of looking at things: Most ADHD is caused by genetic factors influencing a child's temperament, mood, neurological make up. Given the fertile set up with a family which can't handle it effectively, some of these children will develop clinical problems, but some will be manageable if the parent/s happen to be wise/strong/capable/able to afford help.

Some of what looks like ADHD is a result of inadequate parenting techniques.
I'm not sure if I understand what you're saying in this paragraph or not. I hope you're not saying that poor parenting is responsible for ADHD (although I would agree that poor parents may produce pseudo-ADD like behavior). I was adopted at birth by very non ADHD folks who were wise, strong, capable,and able to afford help. I was still diagnosed with hyperactivity by age 4 and I'm told they knew something was up by age one. Having met my birth family as an adult, I know I came by it honestly and it was inspite of good parenting, not because of it (although I have no doubt that excellent parenting and scaffolding helped minimize the damaging aspects of having ADHD).

Scattered

I have heard of tribes in other parts of the world that are all ADD like with few people that are Non-ADD like. Just the opposite as in our society.

I really doubt that scientific studies will ever be able to find an absolute reason or even close to a reason why ADDers think the way they do in comparison to the non-ADDers.

How would they prossibly be able to compare how two differant subjects process information. I'm using two because that would be the least amount of differenciations.

Lets look at an example of a study room and two subjects. They are both ten years old. That's about as much as they are alike. Even that could be inaccurate depending on the conditions when they were born, when exactly they were born, how they were born, where they born, was it a cold room? Did one fall when he was two and skin his knee? Did the other see an elephant at the circus? Let's look at the room they are in for the study. If they are looking around, has one of them experienced a birthday in a room similar to this years ago and maybe the other had a real bad experience in a room like this? What did they eat for dinner today, yesterday, two weeks ago, five years ago? Does one have 20/20 vision and the other 20/30? What have they seen, touched, smelled, heard, tasted, or sensed? Are they of German heritage or from the North Pole? One Millionth of a second could change what has happened with the neurotransmitters in either of thier brains at any point in the study. There are just too many variables that would have to be stable and known for it to be a controlled environment and subject.

There can never be an absolute controlled study of two subjects to make a comparison.

What does this mean? ADD still exists and you could call it anything you want and it would still mean we process things differantly.

We have to just be able to love our uniqueness and use all the gifts it can give us and the world. There will never be another like you or me.

Now to carry the message to the ill informed . . . . .going main stream!

The lack of proof is due to different reasons for developing ADHD

glad to see some of you can see through the garbage. haven't you noticed scientists have proof for everything then we find out the next day they were wrong. at least they didn't go wrong when they figured the earth was flat or the center of the universe.

glad to see some of you can see through the garbage. haven't you noticed scientists have proof for everything then we find out the next day they were wrong. at least they didn't go wrong when they figured the earth was flat or the center of the universe.
…which scientists did that figuring, exactly? Are you sure you’re talking about science?

It’s clear we’re not talking apple and oranges here. Some forum members are concerned about people who reject the idea that there is any scientific proof that AD/HD exists, but in general the culprits tend to be Normals, not ADDers.

The presentation of proof here got a little mixed up with the contentious debate that led directly to the creation of this parti