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  #61  
Old 09-01-05, 12:51 PM
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Quote:
Originally Posted by Scattered
If you're truly interested in learning more about current AD/HD research and not just proving your point, these books are a good place to start in addition to Wender's very scholarly book (I also really like Barkley's book Taking Charge of ADHD: The Complete, Authoritative Guide for Parents, but you seem to have already written him off in your mind):

Driven to Distraction, Answers to Distraction, and Delivered from Distraction by Hallowell and Ratey give lots of the current research in layman's terms. There are many others, but these were the ones I found easiest to understand.

Scattered
Barkley is on the the DSM-IV workgroup. That can be updated long before 2010 to reflect the current state of science by himself. He suggested calling it something other than ADHD. I will just leave it at this so it doesn't sound like I am bickering.

27 adults with no control subjects says nothing. All of the studies have been small, contradictory and the largest ever was flawed. It is the most researched disorder in the world and all we have are theories in 2005 and a statement by Barkley because the science isn't there.

The only method for average people to determine if medication is going to work is to be diagnosed, take it, and it improves the symptoms.

There is no known genetic cause. There is no known cause period. There is no gene identified. There may be someday, but we've been looking and looking and have virtually nothing. Nothing has changed.
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  #62  
Old 09-01-05, 01:46 PM
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Dave, if you're here to say that ADHD is a condition that impairs peoples lives which there is no medical test for. I can live with that.

You know, we have had people come in here from Scientology periodically. We can't discuss Science with them because they believe Scientistís data is corrupted by drug company money. They never tell us what ADHD is or avoid telling us that is a FRAUD because that is the end of their game. They relentlessly attack and rarely answer questions directly.

Please show us that you are different and tell us specifically what ADHD is, if it impairs life functioning, if the identification process is adequate, and what is mental illness. It would also be nice if you could scroll back and answer the other questions that were asked of you.

Looking forward to your response. It would be much appreciated.
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Old 09-01-05, 02:40 PM
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Dear Members,

I appreciate your concern and the reporting of certain posts instead of the use of flames and personal attacks. But, since there has been no break in forum guidelines there is nothing we can as moderators do.

I urge you all to re-read the guidelines, especially those pertaining to disagreeing with respect.

I also urge you to make use of your ignore button should you feel that you can no longer tolerate another member or their theories. This applies to both sides of the discussion.

The forums does not demand agreement on all subjects but we do demand that you show your fellow members respect and curtisy to their thoughts as well as yours when posting. If we feel there has been a break in guidelines or useless flaming of another member we will act immediatly with no further or gentle warnings.

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  #64  
Old 09-01-05, 02:50 PM
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Quote:
Originally Posted by scuro
Dave, if you're here to say that ADHD is a condition that impairs peoples lives which there is no medical test for. I can live with that.

You know, we have had people come in here from Scientology periodically. We can't discuss Science with them because they believe Scientistís data is corrupted by drug company money. They never tell us what ADHD is or avoid telling us that is a FRAUD because that is the end of their game. They relentlessly attack and rarely answer questions directly.

Please show us that you are different and tell us specifically what ADHD is, if it impairs life functioning, if the identification process is adequate, and what is mental illness. It would also be nice if you could scroll back and answer the other questions that were asked of you.

Looking forward to your response. It would be much appreciated.
Here is what ADHD is, and nothing more from a diagnostic perspective. This is the science in my opinion. This is the diagnostic criteria from the APA's DSM-IV, I grabbed it at the CDC.
(http://www.cdc.gov/ncbddd/adhd/symptom.htm):

  • Six or more of the following symptoms of inattention have been present for at least 6 months to a point that is disruptive and inappropriate for developmental level:

Inattention

  • Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities.
  • Often has trouble keeping attention on tasks or play activities.
  • Often does not seem to listen when spoken to directly.
  • Often does not follow instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions).
  • Often has trouble organizing activities.
  • Often avoids, dislikes, or doesn't want to do things that take a lot of mental effort for a long period of time (such as schoolwork or homework).
  • Often loses things needed for tasks and activities (e.g. toys, school assignments, pencils, books, or tools).
  • Is often easily distracted.
  • Is often forgetful in daily activities.

  • Six or more of the following symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level:

Hyperactivity

  • Often fidgets with hands or feet or squirms in seat.
  • Often gets up from seat when remaining in seat is expected.
  • Often runs about or climbs when and where it is not appropriate (adolescents or adults may feel very restless).
  • Often has trouble playing or enjoying leisure activities quietly.
  • Is often "on the go" or often acts as if "driven by a motor".
  • Often talks excessively.

Impulsivity

  • Often blurts out answers before questions have been finished.
  • Often has trouble waiting one's turn.
  • Often interrupts or intrudes on others (e.g., butts into conversations or games).

  • Some symptoms that cause impairment were present before age 7 years.
  • Some impairment from the symptoms is present in two or more settings (e.g. at school/work and at home).
  • There must be clear evidence of significant impairment in social, school, or work functioning.
  • The symptoms do not happen only during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder. The symptoms are not better accounted for by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder).

Based on these criteria, three types of ADHD are identified:

  • ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
  • ADHD, Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months
  • ADHD, Predominantly Hyperactive-Impulsive Type: if Criterion 1B is met but Criterion 1A is not met for the past six months.

A mental illness is any other disorder as defined in the DSM - a cluster of symptoms. The identification process if far from adequete for ADHD. Eli Lilly (www.adultadd.com) is scoring this and has you at WEBMD for a doctor in seconds. and forgeting a few steps above. They just so happens to be selling something.

It is vague, could be updated to include a more thorough assessment of twice the symptoms, but it isn't. Would 9 symptoms for hyperactivity be a bad thing? Does the APA take money from drug companies? Yes. Could that be a factor? I'm assuming there is science as to why there are 6 symptoms. I'm sure someone will tell me. I'm sure there is some science as to why it isn't going to be updated until 2010.

I do not think it is a fraud (look at the forums). However Math Disorder is real, there is criteria for it:
http://www.athealth.com/Consumer/disorders/Math.html

There are people seriously impaired by mental illness. Then there are (specifically with ADHD) borderline cases where a complete assessment would be beneficial. A few adults are under the impression it is something that develops (adult onset).

People can be corrupted by drug money, money period. Is this possible?

Here is Dr. Biederman, who is a former member of CHADD, NIMH, and the Adderall clinical trial author.

http://www.psychiatrist.com/pcc/visuals/disc.htm (Spencer [Strattera, others] is mentioned over there)
Dr. Biedermanhas received research support from Shire Richwood, Eli Lilly, Wyeth, Pfizer, Cephalon, Novartis, Janssen, Noven Pharmaceutical, Stanley Foundation, the National Institute of Mental Health (NIMH), the National Institute of Child Health & Human Development, and the National Institute on Drug Abuse (NIDA); is a member of the speakers bureaus for GlaxoSmithKline, Eli Lilly, Pfizer, Novartis, Wyeth, Shire Richwood, ALZA, and Cephalon; and is a member of the advisory boards for Eli Lilly, Celltech, Shire Richwood, Novartis, Noven Pharmaceutical, ALZA, McNeil, and Cephalon.


He prefers Adderall 3 to 1 in false advertising and is FDA regulated:
http://www.fda.gov/cder/warn/nov2000/dd9153.pdf


And now an Adderall SUD advisory:
http://www.fda.gov/cder/drug/InfoShe...adderalHCP.htm


Is there a possible relationship of drug company money influencing him, causing that SUD advisory? Sure there is.


No, I am not a scientoligist, a Lutheran who misses quite a few days of church. That label is irrelevant. Tom Cruise must have ADHD because he missed the Concerta ads in WEBMD's magazine re: Brooke Shields, see:

http://pn.psychiatryonline.org/cgi/c.../full/36/21/20


I think I answered everything - I tried.
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  #65  
Old 09-01-05, 03:11 PM
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I am much clearer on your position. Thank you. I don't share your total distrust for scientists and their funding (though I will maintain an awareness of that influence). However, it's not just Biederman who prefers Adderall. If memory serves, 75% of teachers also prefer Adderall for their students -- having been a teacher I can assure you they aren't getting any kickbacks!

Scattered

PS: As far as Tom Cruise goes -- I recently saw him on the David Letterman show twitching in the seat and wiggling his fingers almost not stop -- he's like a walking add for AD/HD. Pretty funny!

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  #66  
Old 09-01-05, 03:53 PM
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Talking

Quote:
Originally Posted by Scattered
PS: As far as Tom Cruise goes -- I recently saw him on the David Letterman show twitching in the seat and wiggling his fingers almost not stop -- he's like a walking add for AD/HD. Pretty funny!
Heehee.. I saw him on the Today Show with Matt Lauer and he could have used an IV drip of Valium or Xanax after lurching out of his chair. I thought he was having a panic attack.
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  #67  
Old 09-01-05, 04:14 PM
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I'm not interested in ADHD from a diagnostic perspective. That was just a cut and paste job. You are so opinionated else where. Shed some more light here with your opinion.

1)Can you give us a specific answer to the question is ADHD a "real" disorder?
2)If it is, does ADHD impair life functioning?
3)Again, I'm not interested about mental illness from a diagnostic perspective, I want to know if you believe that the other disorders like Schizophrenia and BP are "real" disorders, do they impair life functioning, and is the identification process adequate?

Your "digs" after the cut and paste do little to instill confidence that you are no more then a basher. It is the shotgun approach. Take aim and fire and you have a scattered attack that can't be refuted easily with a single line of logic. There are just too many divergent ideas that you bring up. Stick to one specific topic and support your main idea with secondary ideas and examples. That is communication and I can then respond likewise. At that point we are sharing knowledge. For instance you may want explain further why math disorder is real and ADHD is not.

Finally, you should look at this link. Much of what you ask about is answered here.
http://www.continuingedcourses.net/a.../course003.php
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  #68  
Old 09-01-05, 04:18 PM
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Thanks for posting the link Scuro. It looks interesting -- I think you may have just found my next CEU's for me!

You have a great way of putting things clearly and cutting to the chase.

Scattered
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Old 09-01-05, 04:39 PM
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Before I finish posting the rest of Sandra Rief's references on the Etiologies of ADHD, let me first post Russ Barkley's power points on that same subject.

These are taken from his March 24 & 25/05 teleconferences on ADHD in Children and ADHD in Adults;sponosored by United Behavioral Health (UBH).UBH is a managed care company.

The principal references for this are: 1) his 1997 book ADHD and the Nature of Self-Control (Guilford Press) and 2) Attention Deficit- Hyperactivity Disorder : A Handbook For Diagnosis and Treatment, Second Edition (1998). (Also Guilford Press).
The 3rd edition was set to come out in August, however, I haven't had a chance to check it out yet.

I believe that these data more than sufficiently support my original post. The "proof" required was "scientific." This certainly fits that description.

ETIOLOGIES : NEUROLOGICAL

1)smaller,less active,less developed brain regions (found on MRI,fMRI and PET).

As an aside, here's what Dr.Barkley has to say about the inconsistentcies in Zametkin's 1990 research not being able to be replicated by this study(Ernst,Cohen,Liebennauer,Jons and Zametkin( 1997):

"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."

He goes on to say: "However,significant correlations have been noted between diminished metabolic activity in the left anterior frontal region and the severity of ADHD symptoms in adolescents with ADHD ( Zametkin,1993). This demonstration of an association between the metabolicactivity 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." ADHD Handbook (p.166).

THIS IS WHY ZAMETKIN'S 1990 STUDY CAN STILL BE CALLED "LANDMARK," BECAUSE THERE IS DATA TO SUPPORT DIMINSHED METABOLIC ACTIVITY.

I bet you didn't know that.

This isn't some stupid *** conspiracy theory surrounding CHADD. You've read some of the research for sure, however, just enough to make your self dangerous.

2)orbital-prefrontal cortex (primarily right side);

3) basal ganglia (mainly striatum and globus pallidus);

4)cerebellum (central vermis area, right side).

ETIOLOGIES : NEUROLOGICAL- Suspected Neurochemical Deficiency:

1) dopamine dysregulation likely but not definite;

2) norepinephrine dysregulation probable.

(This is where the biogenic amine hypothesis comes into play).

POST NATAL BRAIN DAMAGE : accounts for 3-5%

1) head trauma,brain hypoxia tumors or infections;

2)lead poisoning in preschool years;

3) survival from acute lymphoblastic leukemia (ALL )- treatments for ALL caused brain damage ( resulting in part in ADHD) -these are all considered to be "acquired types."

4) post natal Streptoccocal Bacteria infection (triggers auto immune antibody attack of basal ganglia).



ETIOLOGIES : GENETIC (Some of this is a repeat of what Sandera Rief has in her book, however, keep in mind that hers is a compilation of research over the last 10-15 years)

FAMILY AGGREGATION:ADHD Runs In Families
1) 25 -25% of siblings;
2)78-92% of identical twins
3) 15-20% of mothers;
4) 25-30% of fathers
(If a parent is ADHD, then 20-54% of siblings will be) (odds are 8+ )-this is what I mean when I qoute him as saying "ADHD is 80% genetic."

TWIN STUDIES OF HERITABILITY:

Heritability - 57-97% (with a mean of 80+ % ) see above

Shared Environment = 0-6% (not significant)...... please make note of that for all of the genetics/environment discussions.The research overwhelmingly supports genetics.(This encompasses social class and family educational/occupational status, the general home environment,family nutrition.,environmental toxins, parental and childrearing characteristics that are common or shared across children in the family)



Unique Environment = 15- 20% (these are studies that indicate the extent to which individual differences in ADHD symptoms are the result of nonshared environmental factors (factors that uniquely affect one of the twins, like neurological injury).


MOLECULAR GENETICS:

1) candidate genes: DRD4 DAT1, DBH-Taq1;

2)candidate region chromosome 16p 13 region.


There are currently 12 working definitions of ADHD. One of them is that it is a Neurobiological disorder.

Deal with it.

mctavish23 (Robert)
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Old 09-01-05, 05:16 PM
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Quote:
Originally Posted by mctavish23
THIS IS WHY ZAMETKIN'S 1990 STUDY CAN STILL BE CALLED "LANDMARK," BECAUSE THERE IS DATA TO SUPPORT DIMINSHED METABOLIC ACTIVITY.
Yeah, but don't lose the big picture. Our research predicts significantly more efficient use of neural mass, so if those were our small number of scans we would be crowing about finding indications that the AD/HD brain is in fact more efficient, as predicted.

And you canít skip over the woeful lack of any reasonable connection between the appearance of diminished metabolic activity and/or size (be it due to efficiency or defect or something else entirely) and the external overt (perhaps measurable) symptoms of AD/HD.

No research or theory we know of says that diminished neural mass or apparent activity actually causes a problem of any kind. The connection is pure speculation, and everybody is guilty of bad science and lack of common sense when it comes to this, Barkley included.

Ask Barkley why a smaller neural structure is bad, how it causes problems associated with AD/HD, and he wonít have any answers. Everybody assumes smaller or less active is bad, but nobody has evidence to back that claim.

And sooner or later everybody will be forced to deal with that little fact.

As far as we know, we are the only people on the planet that have proposed an actual theory that makes a connection between activity of neural structures and behavior. Itís too big a leap for almost anyone mired in a conventional field of study.

I suppose that implies weíre mired in an unconventional field of study, and we are. We have to deal with that.

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Old 09-01-05, 05:23 PM
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Quote:
Originally Posted by scuro
I'm not interested in ADHD from a diagnostic perspective. That was just a cut and paste job. You are so opinionated else where. Shed some more light here with your opinion.

1)Can you give us a specific answer to the question is ADHD a "real" disorder?
2)If it is, does ADHD impair life functioning?
3)Again, I'm not interested about mental illness from a diagnostic perspective, I want to know if you believe that the other disorders like Schizophrenia and BP are "real" disorders, do they impair life functioning, and is the identification process adequate?

Your "digs" after the cut and paste do little to instill confidence that you are no more then a basher. It is the shotgun approach. Take aim and fire and you have a scattered attack that can't be refuted easily with a single line of logic. There are just too many divergent ideas that you bring up. Stick to one specific topic and support your main idea with secondary ideas and examples. That is communication and I can then respond likewise. At that point we are sharing knowledge. For instance you may want explain further why math disorder is real and ADHD is not.
Once ADHD (or anything) is inserted the DSM-IV, it is a real disorder. That is my opinion. Why do you seem so defensive that it is not real? I have never said it isn't.

The identification process for the disorders you mention are included in above, the DSM. Those are real.

ADHD is not life impairing in all cases in many cases opinion. None of the above mentioed are in all cases. All can, which is different than all do. It also depends if you mean impairing one's life for a time, or forever.

The DSM is the only identification process for mental disorders or conditions listed. There are no genetic causes known to any, unless you know them.

I went through the identification process once, insert any disorder you want there, although ADHD is the most vague.

Two question since I answered 3 (or tried): What (validated with science) causes ADHD? What confirms a diagnosis of ADHD?
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Old 09-01-05, 05:33 PM
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Quote:
Originally Posted by mctavish23

There are currently 12 working definitions of ADHD. One of them is that it is a Neurobiological disorder.

Deal with it.

mctavish23 (Robert)
12 theories. "Here's the Proof" is the name of the thread - I haven't seen it.
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Old 09-01-05, 05:42 PM
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I agree with some of what you said. You're dead wrong about the genetics though.

In terms of what constitutes a "disorder," the previously mentioned journal article International Consensus 2002 has the best operational definition I've ever seen.

It is from Rutger's ethics researcher James Wakefield. He defines a disorder by saying 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."

It goes on to say in a new paragraph, " 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." (p.89).

The breakdown is that "disorder" is usually defined as "harmful dysfunction in major life activites."

Since one of the other working definitions of ADHD is that it is a "normal dimensional disorder that all human beings display" at certain points in their lives, the clinical threshold is "impairment."

" No impairment, no disorder."- Russ Barkley

For kids, "major life activities are : school and peer relationships. As they get older, then throw in driving a car.

Adults are : relationships, occupational/employment ,academic and driving.

I just thought of one other aspect of ADHD that can cloud the issue and that is recognizing Executive Function deficits.

ADHD impairing the Executive FUnctions is another of the working definitions.
The biggest problems occur with the "covert" Exec.Functions,i.e., the ones you cant necessarily see. Examples would be Working Memory, Initiation (the ability to "get started" on an activity,)" Planning/Organization, especially as relates to preparing to accomplish a future goal (you have an assignment dues in so many weeks, etc).
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Old 09-01-05, 05:53 PM
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To have ADHD, it must be impairing. That is the criteria for diagnosis. Barkley has commented on this, if you have all the symptoms and no impairment, then you don't have ADHD.

What causes ADHD? In a word....mostly genetics.


From Barkley http://www.continuingedcourses.net/a.../course003.php

".....Far more consistent have been the results of quantitative electroencephalograph (QEEG) and evoked response potential (ERP) measures, sometimes taken in conjunction with vigilance tests (Frank, Lazar, & Seiden, 1992; Klorman, 1992; Klorman, Salzman, & Borgstedt, 1988; Rothenberger, 1995). Although results have varied substantially across these studies (see Tannock, 1998, for a review), the most consistent pattern for EEG research is increased slow wave, or theta, activity, particularly in the frontal lobe, and excess beta activity, all indicative of a pattern of under-arousal and under-reactivity in ADHD (Baving, Laucht, and Schmidt, 1999; Chabot & Serfontein, 1996; Kuperman, Johnson, Arndt, Lindgren, & Wolraich, 1996; Monastra, Lubar, & Linden, 2001). ADHD children have been found to have smaller amplitudes in the late positive and negative components of their evoked response patterns (ERPs). These late components are believed to be a function of the prefrontal regions of the brain, are related to poorer performances on inhibition and vigilance tests, and are corrected by stimulant medication (Johnstone, Barry, & Anderson, 2001; Pliszka, Liotti, & Woldorff, 2000; Kuperman et al., 1996). Thus, psychophysiological abnormalities related to sustained attention and inhibition indicate an under-responsiveness of ADHD children to stimulation that is corrected by stimulant medication.

Several studies have also examined cerebral blood flow using single photon emission computed tomography (SPECT) in ADHD and normal children (see Tannock, 1998; Hendren, DeBacker, & Pandina, 2000, for reviews). They have consistently shown decreased blood flow to the prefrontal regions (most recently in the right frontal area) and pathways connecting these regions to the limbic system via the striatum and specifically its anterior region known as the caudate, and with the cerebellum (Gustafson, Thernlund, Ryding, Rosen, & Cederblad, 2000; Lou, Henriksen, & Bruhn, 1984; Lou, Henriksen, Bruhn et al., 1984; Sieg, Gaffney, Preston, & Hellings, 1995). Degree of blood flow in the right frontal region has been correlated with behavioral severity of the disorder, while that in more posterior regions and the cerebellum seems related to degree of motor impairment (Gustafson et al., 2000).

Within the last few years, a radioactive chemical ligand, known as [I123] Altropane, has been developed that binds specifically to the dopamine transporter protein in the striatum of the brain and thus can be used to indicate level of dopamine transporter activity within this region. Following intravenous injection of the ligand, SPECT scanning is used to detect the binding activity of Altropane in the striatum. The dopamine transporter is responsible for the re-uptake of extracellular dopamine from the synaptic cleft after neuronal release. Several initial pilot studies found that adults with ADHD had significantly increased binding potential of Altropane and thus greater dopamine transporter activity (Dougherty et al., 1999; Krause, Dresel, Krause, Kung, & Tatsch, 2000). A third pilot study likewise replicated this difference in binding potential and found that degree of transporter activity was significantly associated with severity of ADHD symptoms but not with comorbid anxiety or depression (Barkley et al., 2002). These findings are interesting because research suggests that the drug, methylphenidate, often used to treat ADHD has a substantial effect on activity in this brain region and may produce its therapeutic effect by slowing down this dopamine transporter activity (Krause et al., 2000; Volkow et al., 2001).

Studies using positron emission tomography (PET) to assess cerebral glucose metabolism have found diminished metabolism in adults, particularly in the frontal region (Schweitzer, Faber, Grafton, tune, Hoffman, & Kilts, 2000; Zametkin et al., 1990) and adolescent females with ADHD (Ernst et al., 1994) but have proven negative in adolescent males with ADHD (Zametkin et al., 1993). An attempt to replicate the finding with adolescent females having ADHD in younger female ADHD children failed to find such diminished metabolism (Ernst, Cohen, Liebenauer, Jons, & Zametkin, 1997). Such studies are plagued by their exceptionally small sample sizes that result in very low power to detect group differences and considerable unreliability in replicating previous findings. However, significant correlations have been noted between diminished metabolic activity in the anterior frontal region and severity of ADHD symptoms in adolescents with ADHD (Zametkin et al., 1993). Also, using a radioactive tracer that indicates dopamine activity, Ernst and colleagues were able to show abnormal dopamine activity in the right midbrain region of ADHD children and that severity of symptoms was correlated with the degree of this abnormality (Ernst, Zametkin, Matochik, Pascualvaca, Jons, & Cohen, 1999). These demonstrations of an association between the metabolic activity of certain brain regions and symptoms of ADHD and associated executive deficits is critical to proving a connection between the findings pertaining to brain activation and the behavior comprising ADHD.

More recent neuro-imaging technologies offer a more fine-grained analysis of brain structures using the higher resolution magnetic resonance imaging (MRI) devices. Studies employing this technology find differences in selected brain regions in those with ADHD relative to control groups. Much of the initial work was done by Hynd and his colleagues (see Tannock, 1998, for a review). Initial studies from this group examined the region of the left and right temporal lobes associated with auditory detection and analysis (planum temporale) in ADHD, LD (reading), and normal children. Both the ADHD and LD children were found to have smaller right hemisphere plana temporale than the control group while only the LD subjects had a smaller left plana temporale (Hynd, Semrud-Clikeman, et al., 1990). In the next study, the corpus callosum was examined in those with ADHD. This structure assists with the interhemispheric transfer of information. Those with ADHD were found to have a smaller callosum, particularly in the area of the genu and splenium and that region just anterior to the splenium (Hynd, Semrud-Clikeman et al., 1991). An attempt to replicate this finding, however, failed to show any differences between ADHD and control children in the size or shape of the entire corpus callosum with the exception of the region of the splenium (posterior portion), which again was significantly smaller in subjects with ADHD (Semrud-Clikeman et al., 1994).

In a later study by Hynd and colleagues, children with ADHD had a significantly smaller left caudate nucleus creating a reversal of the normal pattern of left>right asymmetry of the caudate (Hynd, Hern et al., 1993). This finding is consistent with the earlier blood flow studies of decreased activity in this brain region. Several more recent studies have used larger samples of ADHD and control subjects using quantitative MRI technology. These studies have indicated significantly smaller anterior right frontal regions, smaller size of the caudate nucleus, reversed asymmetry of the head of the caudate, and smaller globus pallidus regions in children with ADHD compared to control subjects (Aylward et al., 1996; Castellanos et al., 1994; Castellanos et al., 1996; Filipek, et al., 1997; Singer et al., 1993). Important as well have been the findings that the size of some of these regions, particularly the structures in the basal ganglia and right frontal lobe, has been shown to correlate with the degree of impairment in inhibition and attention in ADHD children (Casey et al., 1997; Semrud-Clikeman et al., 2000). The putamen, however, has not been found to be smaller in children with ADHD (Aylward et al., 1996; Castellanos et al., 1996; Singer et al., 1993) or to be associated with behavioral inhibition deficits in these children (Casey et al., 1997).

Interestingly, the study by Castellanos et al. (1996) also found smaller cerebellar volume in those with ADHD. This would be consistent with recent views that the cerebellum plays a major role in executive functioning and the motor presetting aspects of sensory perception that derive from planning and other executive actions (Diamond, 2000).

No differences between groups on MRI were found in the regions of the corpus callosum either of the studies by Castellanos and colleagues (1994, 1996) as had been suggested in the small studies discussed above or as had been found in a prior study by this same research team (Giedd et al., 1994). However, the study by Filipek and colleagues (1997) did find smaller posterior volumes of white matter in both hemisphere in the regions of the parietal and occipital lobes that might be consistent with the earlier studies showing smaller volumes of the corpus callosum in this same area. Castellanos et al. (1996) suggest that such differences in corpus callosal volume, particularly in the posterior regions, may be more related to learning disabilities that are often found in a large minority of ADHD children than to ADHD itself.

The results for the smaller size of the caudate nucleus are quite consistent across studies but are inconsistent in indicating which side of the caudate may be smaller. The work by Hynd and colleagues (Hynd, Hern et al., 1993) discussed earlier found the left caudate to be smaller than normal in their ADHD subjects. The more recent studies by Filipek and colleagues (1997) and Semrud-Clikeman et al. (2000) found the same result. However, Castellanos et al. (1996) also reported a smaller caudate but found this to be on the right side of the caudate. The normal human brain demonstrates a relatively consistent asymmetry in volume in favor of the right frontal cortical region being larger than the left (Giedd et al., 1996). This led Castellanos et al. (1996) to conclude that a lack of frontal asymmetry (a smaller than normal right frontal region) probably mediates the expression of ADHD. However, whether this asymmetry of the caudate of right side>left side is true in normal subjects is debatable as other studies found the opposite pattern in their normal subjects (Filipek et al., 1997; Hynd, Hern et al., 1993). More consistent across these studies are the findings of smaller right prefrontal cortical regions, smaller caudate volume, and smaller regions of the cerebellar vermis (again, likely more on the right than left side).

With the advent of even more advanced MRI technology, researchers can now evaluate functional activity in various brain regions while administering psychological tests to subjects being scanned. These studies find ADHD children to have abnormal patterns of activation during attention and inhibition tasks than do normal children, particularly in the right prefrontal region, basal ganglia (striatum and putamen), and the cerebellum (Rubia et al., 1999; Teicher et al., 2000; Vaidya et al., 1998). Again, the demonstrated linkage of brain structure and function with psychological measures of ADHD symptoms and executive deficits is exceptionally important in such research to permit causal inferences to be made about the role of these brain abnormalities in the cognitive and behavioral abnormalities comprising ADHD.
Neurotransmitter Deficiencies.

Possible neurotransmitter dysfunction or imbalances have been proposed in ADHD for quite some time (see Pliszka, McCracken, & Maas, 1996 for a review). Initially, these rested chiefly on the responses of ADHD children to differing drugs. ADHD children respond remarkably well to stimulants, most of which act by increasing the availability of dopamine via various mechanisms, and producing some effects on the noradrenergic pathways as well (DuPaul, Barkley, & Connor, 1998). These children also respond well to tricyclic antidepressants giving further support to a possible noradrenergic basis to ADHD (Connor, 1998). Consequently, it seemed sensible to hypothesize that these two neurotransmitters might be involved in the disorder. Given the findings that normal children show a positive, albeit lesser, response to stimulants (Rapoport et al., 1978), however, partially undermines this logic. Other, more direct evidence comes from studies of cerebral spinal fluid in ADHD and normal children that indicated decreased brain dopamine in ADHD children (Raskin, et al., 1984). Similarly, other studies used blood and urinary metabolites of brain neurotransmitters to infer deficiencies in ADHD, largely related to dopamine regulation. Early studies of this sort proved conflicting in their results (Shaywitz, Shaywitz, Cohen, & Young, 1983; Shaywitz, Shaywitz, Jatlow, et al., 1986; Zametkin & Rapoport, 1986). A subsequent study continued to find support for reduced noradrenergic activity in ADHD as inferred from significantly lower levels of a metabolite of this neurotransmitter (Halperin et al., 1997). What limited evidence there is from this literature seems to point to a selective deficiency in the availability of both dopamine and norepinephrine, but this evidence cannot be considered conclusive at this time.
Pregnancy and Birth Complications

Some studies have not found a greater incidence of pregnancy or birth complications in ADHD compared to normal children (Barkley, DuPaul, & McMurray, 1990) while others have found a slightly higher prevalence of unusually short or long labor, fetal distress, low forceps delivery, and toxemia or eclampsia (Hartsough & Lambert, 1985; Minde, Webb, & Sykes, 1968). Nevertheless, while ADHD children may not experience greater pregnancy complications, prematurity or lower birth weight as a group, children born prematurely or who have markedly lower birth weights are at high risk for later hyperactivity or ADHD (Breslau et al., 1996; Nichols & Chen, 1981; Schothorst & Engeland, 1996; Sykes et al., 1997; Szatmari, Saigal, Rosenbaum, & Campbell, 1993). It is not merely low birth weight that seems to pose the risk for symptoms of ADHD or the disorder itself, among other psychiatric disorders, but the extent of white matter abnormalities due to birth injuries, such as parenchymal lesions and/or ventricular enlargement (Whittaker et al., 1997). These findings suggest that while certain pregnancy complications may not be the cause of most cases of ADHD, some cases may arise from such complications, especially prematurity associated with minor bleeding in the brain.

Several studies suggest that mothers of ADHD children are younger when they conceive these children than are mothers of control children and that such pregnancies may have a greater risk of adversity (Denson, Nanson, & McWatters, 1975; Hartsough & Lambert, 1985; Minde et al., 1968). Since pregnancy complications are more likely to occur among young mothers, mothers of ADHD children may have a higher risk for such complications that which may act neurologically to predispose their children toward ADHD. However, the complications that have been noted to date are rather mild and hardly compelling evidence of pre﷓ or peri﷓natal brain damage as a cause of ADHD. Furthermore, large scale epidemiological studies have generally not found a strong association between pre﷓ or peri﷓natal adversity (apart from prematurity as noted above) and symptoms of ADHD once other factors are taken into account, such as maternal smoking and alcohol use (see below) as well as socio﷓economic disadvantage, all of which may predispose to perinatal adversity and hyperactivity (Goodman & Stevenson, 1989; Nichols & Chen, 1981; Werner, Bierman, & French, 1971).

One study found that the season of a childís birth was significantly associated with risk for ADHD, at least among those subgroups who also either had learning disability or who did not have any psychiatric comorbidity (Mick, Biederman, & Faraone, 1996). Birth in September was over-represented in this subgroup of ADHD children. The authors conjecture that the season of birth may serve as a proxy for the timing of seasonally mediated viral infections to which these mothers and their fetuses may have been exposed and that this may account for approximately 10 percent of cases of ADHD.


Genetic Factors


Evidence for a genetic basis to this disorders comes from three sources: family studies, twin studies, and, most recently, molecular genetic studies identifying individual candidate genes. Again, nearly all of this research applies to the Combined Type of ADHD.
Family Aggregation Studies.

For years, researchers have noted the higher prevalence of psychopathology in the parents and other relatives of children with ADHD. Between 10 to 35 percent of the immediate family members of children with ADHD are also likely to have the disorder with the risk to siblings of the ADHD children being approximately 32 percent (Biederman et al., 1992; Biederman, Faraone, Keenan, et al., 1990; Pauls, 1991; Welner et al., 1977). Even more striking, research shows that if a parent has ADHD, the risk to the offspring is 57 percent (Biederman, Faraone, Mick, et al., 1995). Thus, ADHD clusters significantly among the biological relatives of children or adults with the disorder, strongly implying a hereditary basis to this condition. Subsequently, these elevated rates of disorders also have been noted in African-American ADHD samples (Samuel et al., 1999) as well as in ADHD girls compared to boys (Faraone et al., 2000).

These studies of families further suggest that ADHD with CD may be a distinct familial subtype of ADHD. By separating the group of ADHD children into those with and without conduct disorder (CD), it has been shown that the conduct problems, substance abuse, and depression in the parents and other relatives are related more to the presence of CD in the ADHD children than to ADHD itself (August & Stewart, 1983; Biederman, Faraone, Keenan, et al., 1992; Faraone, Biederman, et al., 1995; Faraone, Biederman, Mennin, Russell, & Tsuang, 1998; Lahey et al., 1988). Rates of hyperactivity or ADHD remain high even in relatives of the group of ADHD children without CD (Biederman, Faraone, Keenan, et al., 1992) but depression and antisocial spectrum disorders are most likely to appear in the comorbid group. Using sib-pairs in which both siblings had ADHD, Smalley and colleagues have also recently supported this view through findings that CD significantly clusters among the families of only those sib-pairs having CD (Smalley et al., 2000).

Some research has also suggested that girls who manifest ADHD may need to have a greater genetic loading (higher family member prevalence) than do males with ADHD (Smalley et al., 2000). Faraone and colleagues also found some evidence in support of this view in that male siblings from families with one affected child were more likely to have ADHD than were female siblings from these families (Faraone et al., 1995). They also reported that the gender difference noted above for ADHD (3:1 males-to-females) may apply primarily to children from families in which either the child or a parent has antisocial behavior.

Interestingly, research by Faraone and Biederman (1997) suggests that depression among family members of children with ADHD may be a nonspecific expression of the same genetic contribution that is related to ADHD. This is based on their findings that family members of children with ADHD are at increased risk for major depression while individuals having major depression have first-degree relatives at increased risk for ADHD. Even so, as noted above, the risk for depression among family members is largely among those children having ADHD with CD.

Adoption Research.

Another line of evidence for genetic involvement in ADHD has emerged from studies of adopted children. Cantwell (1975) and Morrison and Stewart (1973) both reported higher rates of hyperactivity in the biological parents of hyperactive children than in adoptive parents having such children. Both studies suggest that hyperactive children are more likely to resemble their biological parents than their adoptive parents in their levels of hyperactivity. Yet, both studies were retrospective and both failed to study the biological parents of the adopted hyperactive children as a comparison group (Pauls, 1991). Cadoret and Stewart (1991) studied 283 male adoptees and found that if one of the biological parents had been judged delinquent or to have an adult criminal conviction, the adopted away sons had a higher likelihood of having ADHD. A later study (van den Oord, Boomsma, & Verhulst, 1994) using biologically related and unrelated pairs of international adoptees identified a strong genetic component (47 percent of the variance) for the Attention Problems dimension of the Child Behavior Checklist, a rating scale commonly used in research on ADHD. More recently, a comparison of the families of adopted ADHD children to those living with their biological parents and to a control group also showed the same pattern of an elevated prevalence of ADHD among just the biological parents of the ADHD children (6% vs. 18% vs. 3% respectively) (Sprich, Biederman, Crawford, Mundy, & Faraone, 2000). Thus, like the family association studies discussed earlier, results of adoption studies point to a strong possibility of a significant hereditary contribution to hyperactivity.
Twin Studies.

Since the last edition of this text, the number of twin studies of ADHD and its underlying behavioral dimensions has increased markedly. More exciting has been the striking consistency across all of these studies. This research strategy provides a third avenue of evidence for a genetic contribution to ADHD. But it also provides a means of testing any competing environmental theories of the disorder (e.g., that ADHD is due to poor parenting, adverse family life, excessive TV viewing, etc.). That is because twin studies can not only compute the proportion of variance in a trait that is genetically influenced (heritability), but also the proportion that results from common or shared environment (things twins and siblings have in common growing up in the same family) and that which results from unique environment (all non-genetic factors or events that are unique or specific to one child and not to others in the family) (Plomin, Defries, McClearn, & Rutter, 1997).

Early research on ADHD using twins looked only at twin concordance (likelihood of twins sharing the same disorder) and did not compute these estimates of heritability, shared, and unique environment. These early studies demonstrated a greater agreement (concordance) for symptoms of hyperactivity and inattention between monozygotic (MZ) compared to dizygotic twins (DZ) (O'Connor, Foch, Sherry, & Plomin, 1980; Willerman, 1973). Studies of very small samples of twins (Heffron, Martin, & Welsh, 1984; Lopez, 1965) found complete (100%) concordance for MZ twins for hyperactivity and far less agreement for DZ twins. For instance, Gilger, Pennington, and DeFries (1992) found that if one twin was diagnosed as ADHD, the concordance for the disorder was 81 percent in MZ twins and 29 percent in DZ twins. Sherman, McGue, and Iacono (1997) found that the concordance for MZ twins having ADHD (mother identified) was 67 percent versus 0 percent for DZ twins.

Later research has computed heritability and environmental contributions to ADHD. One such study of a large sample of twins (570) found that approximately 50 percent of the variance in hyperactivity and inattention in this sample was due to heredity while 0-30 percent may have been environmental (Goodman & Stevenson, 1989). The relatively limited number of items assessing these two behavioral dimensions, however, may have reduced the sensitivity of the study to genetic effects. Later and even larger twin studies have found an even higher degree of heritability for ADHD, ranging from .75 to .97 (see Levy & Hay, 2001; Thapar, 1999 for reviews) (Burt, Krueger, McGue, Iacono, 2001; Coolidge et al., 2001; Gjone, Stevenson, & Sundet, 1996; Gjone, Stevenson, Sundet, & Eilertsen, 1996; Hudziak, 1997; Levy, Hay, McStephen, Wood, & Waldman, 1997; Rhee, Waldman, Hay, & Levy, 1995; Sherman, Iacono, & McGue, 1997; Sherman, McGue, & Iacono, 1997; Silberg et al., 1996; Thapar, Harrington, & McGuffin, 2001; Thapar, Hervas, & McGuffin, 1995; van den Oord, Verhulst, & Boomsma, 1996). Thus, twin studies indicate that the average heritability of ADHD is at least 0.80, being nearly that for human height (.80-.91) and higher than that found for intelligence (.55-.70). These studies consistently find little, if any, effect of shared (rearing) environment on the traits of ADHD while sometimes finding a small significant contribution for unique environmental events. In their totality, shared environmental factors seem to account for 0-6 percent of individual differences in the behavioral trait(s) related to ADHD. It is for this reason that I stated at the opening of this section that little attention would be given here to discussing purely environmental or social factors as involved in the causation of ADHD.

The twin studies cited above have also been able to indicate the extent to which individual differences in ADHD symptoms are the result of nonshared environmental factors. Such factors not only include those typically thought of as involving the social environment, but also all biological factors that are nongenetic in origin. Factors in the nonshared environment are those events or conditions that will have uniquely affected only one twin and not the other. Besides biological hazards or neurologically injurious events that may have befallen only one member of a twin pair, the nonshared environment also includes those differences in the manner in which parents may have treated each child. Parents do not interact with all of their children in an identical fashion and such unique parent-child interactions are believed to make more of a contribution to individual differences among siblings than do those factors about the home and child-rearing that are common to all children in the family. Twin studies to date have suggested that approximately 9-20 percent of the variance in hyperactive-impulsive-inattentive behavior or ADHD symptoms can be attributed to such nonshared environmental (nongenetic) factors (Levy et al., 1997; Sherman, Iacono et al., 1997; Silberg et al., 1996). A portion of this variance, however, must be attributed to the error of the measure used to assess the symptoms. Research suggests that the nonshared environmental factors also contribute disproportionately more to individual differences in other forms of child psychopathology than do factors in the shared environment (Pike & Plomin, 1996). Thus, if researchers were interested in identifying environmental contributors to ADHD, these studies suggest that such research should focus on those biological and social experiences that are specific and unique to the individual and are not part of the common environment to which other siblings have been exposed.
Molecular Genetic Research.

Although a quantitative genetic analysis of the large sample of families studied in Boston by Biederman and his colleagues suggested that a single gene may account for the expression of the disorder (Faraone, Biederman, et al., 1992), most investigators suspect multiple genes given the complexity of the traits underlying ADHD and their dimensional nature. The focus of research initially had been on the dopamine type 2 gene given findings of its increased association with alcoholism, Tourette's Disorder, and ADHD (Bloom, Cull, Braverman, & Comings, 1996; Comings et al., 1991) but others have failed to replicate this finding (Gelernter et al., 1991; Kelsoe et al., 1989). More recently, the dopamine transporter gene (DAT1) has been implicated in two studies of children ADHD (Cook et al., 1995; Cook, Stein, & Leventhal, 1997; Gill, Daly, Heron, Hawi, & Fitzgerald, 1997). However, here again other laboratories have not been able to replicate this association (Swanson et al., 1997).

Another gene related to dopamine, the DRD4 (repeater gene), has been the most reliably found in samples of ADHD children (Faraone et al., 1999). It is the 7-repeat form of this gene that has been found to be over represented in children with ADHD (Lahoste et al., 1996). Such a finding is quite interesting because this gene has previously been associated with the personality trait of high novelty seeking behavior, this variant of the gene affects pharmacological responsiveness, and the geneís impact on post-synaptic sensitivity is primarily found in frontal and prefrontal cortical regions believed to be associated with executive functions and attention (Swanson et al., 1997). The finding of an over-representation of the 7-repeat DRD4 gene has now been replicated in a number of other studies using not only children with ADHD, but also adolescents and adults with the disorder (Faraone et al., 1999).
Thyroid Disorder

Resistance to thyroid hormone (RTH) represents a variable tissue hyposensitivity to thyroid hormone. It is inherited as an autosomal dominant characteristic in most cases. It has been associated with mutations in the thyroid hormone beta receptor gene, thus a single gene for the disorder has been identified. One study (Hauser, Zametkin, Martinez, et al., 1991) found that 70 percent of individuals with RTH had ADHD. Other research has suggested that 64 percent of patients with RTH display hyperactivity or learning disabilities (Refetoff, Weiss, & Usala, 1993). A later study was not able to corroborate a link between RTH and ADHD (Weiss, Stein, Trommer et al., 1993). In a subsequent study, Stein, Weiss, and Refetoff (1995) did find that half of their children with RTH met clinical diagnostic criteria for ADHD. Even so, the degree of ADHD in RTH patients is believed to be milder than that seen in clinic-referred and diagnosed cases of ADHD. The RTH patients often have more learning difficulties and cognitive impairments than do the ADHD children without RTH. Given that RTH is exceptionally rare in children with ADHD (prevalence of 1:2500) (Elia et al., 1994), then thyroid dysfunction is unlikely to be a major cause of ADHD in the population. An interesting recent finding is that RTH children having ADHD may show a positive behavioral response to liothyronine, with decreased impulsiveness, than do ADHD children who do not have RTH (Weiss, Stein, & Refetoff, 1997).
Environmental Toxins

As the twin and quantitative genetic studies have suggested, unique environmental events may play some role in individual differences in symptoms of ADHD. This should not be taken to mean only those influences within the realm of psychosocial or family influences. As noted above, variance in the expression of ADHD that may be due to environmental sources means all nongenetic sources more generally. These include pre-, peri-, and post-natal complications, and malnutrition, diseases, trauma, toxin exposure, and other neurologically compromising events that may occur during the development of the nervous system before and after birth. Among these various biologically compromising events, several have been repeatedly linked to risks for inattention and hyperactive behavior.

One such factor is exposure to environmental toxins, specifically lead. Elevated body lead burden has been shown to have a small but consistent and statistically significant relationship to the symptoms comprising ADHD (Baloh, Sturm, Green, & Gleser, 1975; David, 1974; de la Burde & Choate, 1972, 1974; Needleman et al, 1979; Needleman et al., 1990). However, even at relatively high levels of lead, less than 38 percent of children are rated as having the behavior of hyperactivity on a teacher rating scale (Needleman et al., 1979) implying that most lead poisoned children do not develop symptoms of ADHD. And most ADHD children, likewise, do not have significantly elevated lead burdens, although one study indicates their lead levels may be higher than in control subjects (Eskinazi & Gittelman, 1983). Studies which have controlled for the presence of potentially confounding factors in this relationship have found the association between body lead (in blood or dentition) and symptoms of ADHD to be .10-.19 with the more factors controlled, the more likely the relationship falls below .10 (Ferguson, Ferguson, Horwood, & Kinzett, 1988; Silva, Hughes, Williams, & Faed, 1988; Thompson et al., 1989). Only 4 percent or less of the variance in the expression of these symptoms in children with elevated lead is explained by lead levels. Moreover, two serious methodological issues plague even the better conducted studies in this area: (1) None of the studies have used clinical criteria for a diagnosis of ADHD to determine precisely what percentage of lead-burdened children actually have the disorder -- all have simply used behavior ratings comprising only a small number of items of inattention or hyperactivity; and (2) none of the studies assessed for the presence of ADHD in the parents and controlled its contribution to the relationship. Given the high heritability of ADHD, this factor alone could attenuate the already small correlation between lead and symptoms of ADHD by as much as a third to a half of its present levels.

Other types of environmental toxins found to have some relationship to inattention and hyperactivity are prenatal exposure to alcohol and tobacco smoke (Bennett, Wolin, & Reiss, 1988; Denson et al., 1975; Milberger, Biederman, Faraone, Chene, & Jones, 1996a; Nichols & Chen, 1981; Shaywitz, Cohen, & Shaywitz, 1980; Streissguth et al., 1984; Streissguth, Bookstein, Sampson, & Barr, 1995). It has also been shown that parents of children with ADHD do consume more alcohol and smoke more tobacco than control groups even when not pregnant (Cunningham et al., 1988; Denson et al., 1975). Thus, it is reasonable for research to continue to pursue the possibility that these environmental toxins may be causally related to ADHD. However, as in the lead studies discussed above, most research in this area suffers from the same two serious methodological limitations -- the failure to utilize clinical diagnostic criteria to determine rates of ADHD in exposed children and the failure to evaluate and control for the presence of ADHD in the parents. Until these steps are taken in future research, the relationships demonstrated so far between these toxins and ADHD must be viewed with some caution. In the area of maternal smoking during pregnancy, at least, such improvements in methodology were used in a recent study that found the relationship between maternal smoking during pregnancy and ADHD to remain significant after controlling for symptoms of ADHD in the parent (Milberger et al., 1996a).
Psychosocial Factors

A few environmental theories of ADHD were proposed over 20 years ago (Block, 1977; Willis & Lovaas, 1977) but have not received much support in the available literature since then. Willis and Lovaas (1977) claimed that hyperactive behavior was the result of poor stimulus control by maternal commands and that this poor regulation of behavior arose from poor parental management of the children. Others have also conjectured that ADHD results from difficulties in the parentsí over-stimulating approach to caring for and managing the child as well as parental psychological problems (Carlson, Jacobvitz, & Sroufe, 1995; Jacobvitz & Sroufe, 1987; Silverman & Ragusa, 1992). But these conjectures have not articulated just how deficits in behavioral inhibition, executive functioning, and other cognitive deficits commonly associated with clinically diagnosed ADHD as described above could arise purely from such social factors. Moreover, many of these studies proclaiming to have evidence of parental characteristics as potentially causative of ADHD have not used clinical diagnostic criteria to identify their children as ADHD, instead relying merely on elevated parental ratings of hyperactivity or laboratory demonstrations of distractibility to classify the children as ADHD (Carlson et al., 1995; Silverman & Ragusa, 1992). Nor have these purely social theories received much support in the available literature that has studied clinically diagnosed children with ADHD (see Danforth et al., 1991; Johnston & Mash, 2001).

In view of the twin studies discussed above that show minimal, nonsignificant contributions of the common or shared environment to the expression of symptoms of ADHD, theories based entirely on social explanations of the origins of ADHD are difficult to take seriously any longer. This is not to say that the family and larger social environment do not matter, for they surely do. Despite the large role heredity seems to play in ADHD symptoms, they remain malleable to unique environmental influences and nonshared social learning. The actual severity of the symptoms within a particular context, the continuity of those symptoms over development, the types of comorbid disorders that will develop, the peer relationship problems that may arise, and various outcome domains of the disorder are likely to be related in varying degrees to parent, family, and larger environmental factors (Johnson, Cohen, Kasen, Smailes, & Brook, 2001; Johnston & Mash, 2001; Milberger, 1997; Pfiffner, McBurnett, &Rathouz, 2001; van den Oord & Rowe, 1997). Yet even here care must be taken in interpreting these findings as evidence of a purely social contribution to ADHD. This is because many measures of family functioning and adversity also show a strong heritable contribution to them, largely owing to the presence of similar symptoms and disorders (and genes!) in the parents as may be evident in the child (Pike & Plomin, 1996; Plomin, 1995). Thus, there is a genetic contribution to the family environment; a fact that often goes overlooked in studies of family and social factors involved in ADHD.
Summary

It should be evident from the research reviewed here that ADHD arises from multiple etiologies, neurological and genetic factors being substantial ones. Like Taylor (1999), I envision ADHD as having a heterogeneous etiology with various developmental pathways leading to this behavioral syndrome. These various etiologies and pathways, however, may give rise to the disorder through disturbances in a final common pathway in the nervous system. That pathway appears to be the integrity of the prefrontal cortical-striatal network. It now appears that hereditary factors play the largest role in the occurrence of ADHD symptoms in children. It may be that what is transmitted genetically is a tendency toward a smaller and less active prefrontal﷓striatal-cerebellar network. The condition can also be caused or exacerbated by pregnancy complications, exposure to toxins, or neurological disease. Social factors alone cannot be supported as causal of this disorder but such factors may exacerbate the condition, contribute to its persistence, and, more likely, contribute to the forms of comorbid disorders associated with ADHD. Cases of ADHD can also arise without a genetic predisposition to the disorder provided the child is exposed to significant disruption or neurological injury to this final common neurologic pathway, but this would seem to account for only a small minority of ADHD children. In general, then, research conducted since the last edition of this text has further strengthened the evidence for genetic and developmental neurological factors as likely causal of this disorder while greatly reducing the support for purely social or environmental factors as having a role. Even so, environmental factors involving family and social adversity may still serve as both exacerbating factors, determinants of comorbidity, and contributors to persistence of disorder over development...."


I'll leave what confirms a diagnosis for another post. Perhaps after we hash this one out.
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Old 09-01-05, 05:57 PM
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I didn't say that I put all 12 definitions in the "Here's the proof". I'll be glad to post them AND give you the references to back it up.

In the post on "here's the proof", I didnt have to include all of those to make my point.

The real concern with all the working definitions is that it is difficult for people to differentiate between ADHD, and things that are comorbid or things that can "mimic" ADHD.

Absent of a head injury of some type of toxicity, if ADHD is present, then it came first (because 80% of it is genetic).

I hope that helps some.
Take care.
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