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Scientific Discussion This forum is limited to published/presented scientific research, in a quasi-academic format, with references where appropriate; clear and structured discourse is encouraged

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  #1  
Old 04-14-05, 12:49 AM
mctavish23 mctavish23 is offline
 

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Thumbs up "No scientific basis" - Here's the Proof

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" 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, 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,[/i]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.

Last edited by namazu; 09-20-16 at 02:46 PM.. Reason: fixed formatting tag
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  #2  
Old 04-20-05, 01:26 PM
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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!!!!
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Old 04-20-05, 04:50 PM
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mctavish I appreciate you taking the time to provide all this great information.
Thank You very much.
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Old 04-21-05, 10:02 PM
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Thank you so very much, mctavish!
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Old 05-04-05, 03:33 AM
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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.
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Old 05-04-05, 10:38 AM
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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.
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Old 05-04-05, 11:35 AM
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Don't forget it's also acknowledged by the American's with Disabilities Act (ADA).
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Old 05-05-05, 11:14 PM
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"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.
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Old 05-06-05, 02:27 PM
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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.
Cheers! Ian.
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Old 05-06-05, 05:43 PM
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Nice to see McT's post up there. I have the greatest respect for the man.
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Old 05-07-05, 01:07 AM
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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.
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Old 09-05-05, 05:54 PM
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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)
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Old 09-05-05, 06:05 PM
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McTavish, Did Zametkin suggest any possible reasons the 1997 study did not find the same differences as the previous two?

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Old 09-05-05, 07:00 PM
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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.
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Old 09-05-05, 07:55 PM
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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.
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