THE ADHD-AS-A-“DISEASE” FRAUD ROLLS ON - by Fred A. Baughman Jr., MD (10/17/02)

THE
ADHD-AS-A-“DISEASE” FRAUD ROLLS ON 

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By
Fred A. Baughman Jr., MD

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On May, 13, 1998, Castellanos
[1] of the NIMH confessed to me: “… we have not yet met the burden of
demonstrating the specific pathophysiology that we believe underlies this
condition.”

This was one of but a few
truthful statements I have extracted from the leadership of “biological”/
“drugging” psychiatry, in a decade of putting questions to them.

On October 10, 2002, this same
Castellanos [2] a pre-eminent ADHD researcher, 
(formerly of the NIMH, now of NYU, still, remarkably, on the National
Professional Advisory Board of CHADD) claimed, once again—as many times  in the past– that ADHD, not Ritalin, causes
atrophy—shrinkage, of the brain. 

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Under “Context,” they write:
“various anatomic brain abnormalities [FB: mainly whole-brain atrophy], have
been reported for attention-deficit/hyperactivity disorder (ADHD), with varying
methods, small samples, cross-sectional designs, and without accounting for
stimulant drug exposure [FB: Ritalin and amphetamines].

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The phrase, “Without accounting
for stimulant drug exposure,” refers to the fact that in all previous studies
from that of Nasrallah [3],  1986 to the
present, the ADHD subjects had been “treated”, i.e., exposed to Ritalin or
amphetamines, meaning the drugs were probably causing the brain
atrophy/shrinkage.  I say probably,
because such drugs are known to be brain- and body-toxic, and because until the
present Castellanos study, there has been no confirmation of ADHD as a
disease/physical abnormality.

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For more “context” regarding ADHD
brain scan research, let us return to 1986 and Nasrallah, et al [3], who
reported: “24 young males treated [FB: Ritalin/stimulant therapy], and followed
up for hyperactivity since childhood, as adults (mean age 23.2 years), had a
significantly greater frequency of cerebral (brain) atrophy.”  They concluded: “The possible associations
of hyperactivity [FB: now called ADHD] or perhaps stimulant drug treatment to
atrophic brain changes are discussed.”  

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Hynd, et al [4] (1991), using MRI,
compared ADHD children “judged to be favorable responders to Ritalin (treated),
and controls.  The corpus callosum (the
large bundle of nerve fibers connecting the two cerebral hemispheres), was
found to be smaller in the ADHD group and was said to be due to ADHD.  No mention was made of the possibility  that the atrophy of the corpus callosum
might be due to Ritalin. 

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Giedd, et al. [5] (1994), using
MRI, found smaller corpus callosum in hyperactive boys than in normal controls
and attributed it to their ADHD.

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Castellanos [6] (1994), wrote:
“Thirty-nine of the 50 patients had been previously treated with
psychostimulants, and all patients participated in a 12 week double-blind trial
of methylphenidate, d-amphetamine, and placebo, which is described
elsewhere.”  “The normal pattern of
slight but significantly greater right caudate volume across all ages was not
seen in ADHD.”  “Total brain volume was
5% smaller in the ADHD boys…”

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The majority of these patients
were treated either with methylphenidate (Ritalin) or

d-amphetamine (Dexedrine).  

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Lyoo, et al, [7] (1996), studied
45 males and 6 females (51 total) with ADHD, and 28 controls (normals).  Those with ADHD had significantly larger
posterior lateral ventricles [FB: when brain tissue atrophies/shrinks, the
ventricles, filled with spinal fluid, enlarge, taking up the space vacated by
brain tissue].  A number of those in the
ADHD group had co-existent conduct disorder [FB: like ADHD, never yet proved to
be a disease/physical abnormality].  
The majority on stimulants (treated). 

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Castellanos et al  [8] (1996), took magnetic resonance images
(scans), of the brains of 57 boys 5-18 years of age said to have attention
deficit hyperactivity disorder (ADHD), and of 55 “healthy” age-matched
controls.  Those in the ADHD group were
found to have significantly smaller, atrophic brains [FB: referring to the
whole of the brain; cerebrum and cerebellum], relative to the
“healthy”controls, and the loss at many sites, of right more than left
asymmetry (where right-sided structures are normally larger than that on the
left).  Under “Results,” in the abstract
of the article, we read: “Subjects with ADHD had a 4.7 % total cerebral
volume.”  Under “Conclusion:” the part
most often read, they state, unambiguously: “This first comprehensive
morphometric analysis is consistent with hypothesized dysfunction of
right-sided prefrontal-striatal system in ADHD.  [FB: don’t let the big words get in the way, they are saying the
whole brain atrophy/shrinkage is due to ADHD, and would have you believe is
THE  proof that ADHD is a disease.

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However, if you failed to read
this article thoroughly/carefully, you would have missed on the next to last
page under “Comments”:  “Because almost
all (93%), subjects with ADHD had been exposed to stimulants, we cannot be
certain that our results are not drug related.”   This comes as a shocker for the reason that the
Ritalin/amphetamine group of stimulants have long been known to be brain- and
body-poisons.  Importantly, for future
reference, they go on to say:  “A
replication study with stimulant-naïve boys with ADHD is under way” 

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If the this was the first “proof”
that ADHD is an actual disease with confirmatory, characteristic abnormalities
of the brain, what proof were Castellanos and his NIMH colleagues referring to
when, in NIH Publication 94-3572 
“Attention Deficit Hyperactivity Disorder - Decade of the Brain” (1994),
with “Scientific information and review (was) provided  by NIMH staff members (Castellanos, included)…”
in which they refer to ADHD as “the disease” (page 7)?   

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In 1997 Filipek, et al [9],  undertook volumetric MRI analysis “To test
by MRI…the a priori hypotheses that developmental anomalies exist in
attention-deficit hyperactivity disorder in left caudate and right prefrontal
frontal/ and or/ posterior parietal hemispheric regions in accord with
neurochemical, neuronal circuitry and attentional framework hypotheses, and
prior imaging studies.”  “All subjects
with ADHD had been placed on medication for at least 6 months prior to the
study and were felt to be responding favorably at the time of the MRI.”   Five of the subjects had not previously
responded to methylphenidate or dextroamphetamine, but responded to
non-stimulant medication.  Nonetheless,
Filipek et al, concludes: “This study is the first to report localized
hemispheric structural anomalies in ADHD…”

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Berquin , et al. [10]
(1998) undertook an MRI study of the cerebellum in attention-deficit
hyperactivity disorder.  In 46 boys with
ADHD, vermal  (vermis or the
cerebellum), volume was significantly less than in the 47 matched
controls.  From ‘methods’ we read, ‘The
46… boys with ADHD were recruited for a drug-treatment study and were included
in a prior report”.   The DSM-III-R 1987
was used for diagnosis herein.  They
commented on the association of cerebellar atrophy with alcohol and
acknowledged they could not fully rule out fetal alcohol exposure.  Making mention of alcohol exposure as a
possible contributor to cerebellar atrophy, and acknowledging that all of their
patients (number = 46), were recruited from among the 57 subjects in the study
of Castellanos, et al (1996), 93% of whom had been on stimulant therapy,
Berquin, et al, made no mention, as did Castellanos, of the fact that “Because
almost all (93%) subjects with ADHD had been exposed to stimulants, we cannot
be certain that our results are not drug related.”  Clearly the cerebellar atrophy described in this study could have
been, and probably was, stimulant-induced.  

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Mostofsky [11] (1999):  Brain abnormality linked to ADHD, April 20,
99 (Reuters Health) — Compared with other children of the same age, children
with attention deficit hyperactivity disorder (ADHD), have  smaller brain volumes, particularly smaller
amounts of gray matter in the right frontal area of their brains, “There
is a lot of evidence that the brain’s right hemisphere is dominant in
attentional processes,” said study author and neurologist Stewart
Mostofsky, MD, of the Kennedy Krieger Institute and Johns Hopkins School of
Medicine in Baltimore. 
“Abnormalities in the brain’s right frontal structure and function
may be contributing to the behavioral impairments associated with ADHD.”  Along with less right frontal gray matter,
there searchers also found that ADHD patients had smaller volumes of left
frontal gray matter as well as right and left frontal white matter when
compared to children without ADHD.  The
study included 12 boys diagnosed with ADHD and 14 boys without ADHD. All boys
were between the ages of seven and 13.  
Nothing was said of drug status in the press release.  I have had no answer to my letter of inquiry
to Mostofsky.  I have since learned–in
fact, Castellanos assures us in his January, 2000, Reader’s Digest
interview–that this research, too, dealt with “treated” subjects [FB: and it
has since, been published]. 

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“The convergence of findings
within and across investigators has not emerged for functional imaging studies
using positron emission tomography (PET) [FB: this is a confession, at long
last, that the much publicized 1990, PET scan “breakthrough” of Zametkin et al
[14], the “neurobiological” basis for ADHD for 5-10 years, was never once
replicated/confirmed],  as it has for
aMRI studies.”  What the authors mean
here, is that only anatomic MRI (aMRI) studies have shown
abnormalities—atrophy–in ADHD subjects, relative to normal controls. 

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Swanson, presenting at the
Consensus Conference for himself, and Castellanos   summarized: “ Recent investigations provide converging evidence
that a refined phenotype of ADHD/HKD is characterized by reduced size in
specific neuroanatomical regions of the frontal lobes and basal ganglia.”  

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Nor did Swanson leave any doubt
that he was claiming that the brain atrophy he had described was part and
parcel of ADHD/HKD (by whatever name)—it’s long-sought biological basis (ADD
having been conceptualized-invented, for the DSM-III in 1980).    Saying these brain abnormalities were a
component of the ADHD ‘phenotype,’ Swanson posited that it had genetic basis—an
abnormal ‘genotype.’  Speaking of  ‘phenotype’ one speaks of the somatic or
physical manifestation of all the genes—the genotype.  Saying one has one has an abnormal ‘phenotype,’ one implies an
abnormal gene or genes—an abnormal ‘genotype’ as it’s cause.

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Baughman, an invited presenter,
took the microphone and asked:   “Dr.
Swanson, why did you not mention that virtually all of the ADHD subjects in the
neuroimaging studies have been on chronic stimulant therapy and that this is
the likely cause of their brain atrophy?” 

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Audience:  “ooh, wow!” 
[And this is all captured in real-time on my video: “ADHD—Total, 100%
Fraud,” which I narrate and appear in, made from the official federal videotape
of the Consensus Conference].

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Swanson:  “Well, that’s a hypothesis. 
I don’t know the exact numbers of how many were or were not on
medication, and as I indicated, I understand that this is a critical issue and
in fact I am planning a study to investigate that.  I haven’t yet done it.” 
[FB: recall, Castellanos et al [8] having written, in 1996: “A
replication study with stimulant-naïve boys with ADHD is under way.”  Surely if Castellanos, his co-author was
doing such a study, Swanson would know about it.  Where is it? As we shall see via his Readers Digest, January,
2000 [16] interview, to come, it is nowhere to be found.].

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Opening the November 16-18, 1998,
NIH, Consensus Conference on ADHD, Hyman   
Director of the NIMH, posited: “ADHD affects from 0-3% in some school
districts up to 40% in others…   this
cannot be right.”

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Carey, reporting on “Is ADHD a
Valid Disorder?” concluded: “What is…described as ADHD in the United States
appears to be a set of normal behavioral variations…”

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Degrandpre, commenting on the Report
of the Panel, observed: “… it appears that you define disease as a maladaptive
cluster of characteristics. In the history of science and medicine, this would
not be a valid definition of disease.”

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Failing to prove that ADHD is a
disease, they seek to re-define the word ‘disease’.

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Baughman testified: “Without an
iota of proof … the NIMH  proclaims the
… children “brain-diseased,” “abnormal.” CHADD, funded by Ciba-Geigy, … has
spread the “neuro-biological” lie.  The
US Department of Education,   absolving
itself of controlling the children and rendering them literate, coerces the
labeling and drugging… ADHD is a total, 100% fraud.”

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Given Carey’s testimony, that ADHD
appears to be “a set of normal behavioral variations…”, and my exposing
the fact that virtually all of the ADHD brain scan literature dealt with
subjects, on chronic Ritalin/amphetamine “treatment,” the final statement of
Consensus Conference Panel  November 18,
1998, was:

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“ …we do not have an
independent, valid test for ADHD, and there are no data to indicate that ADHD
is due to a brain malfunction.”

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I specify “final statement of
Consensus Conference Panel of November 18, 1998,” because, believe it or not,
there was another one to come; another “final statement.”  This wording (above),
which appeared for an indeterminate time on the NIH web site, was subsequently
removed and replaced with wording claiming ‘validity’ for ADHD.  Myself, and a number of colleagues who had
been at the press conference when the “final statement” was passed out, wrote
to conference organizers, and got no satisfactory explanation.  Just who made this alteration remains
unknown. 

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In a Readers Digest interview in January, 2000 [15], it was
first claimed, “Castellanos and his group found three areas of the brain to be
“significantly smaller in ADHD kids than in normal children.  A series of studies also found that the
greater the shrinkage, the worse the ADHD symptoms appear to be.  According to Dr. Jay Giedd, an associate of
Castellanos, this suggests that ASDHD may arise from abnormalities in these
parts of the brain.  Some critics claim
that such brain differences in ADHD children might actually be caused by
Ritalin – meaning these smaller areas of the brain could be the result of the
stimulant treatment.  To address this,
Castellanos has now embarked on another study, imaging the brains of ADHD
youngsters who have not been treated with drugs.”

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Which study is that? 
The one of drug-naïve boys he said he was doing in 1996 or does this
refer to the study just published in JAMA, October 10, 2002? 

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Here again Castellanos cites the need to do a study of
subjects never exposed to psychiatric drugs, all of which are brain-,
body-toxins; why then in his current study has he co-mingled the ADHD subjects
who have been treated/exposed (68%), with the few never-treated, never exposed
(32%), thus necessitating so such statistical “massaging” to arrive at the
desired conclusion: always, in biological psychiatry, that the disorder is as
disease needing, requiring treatment, and that the drug(s) are never addictive,
dangerous or deadly, and that, most of all, it never causes the brain to
shrivel. 

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In order to know if the brains of
children with an ADHD diagnosis are equal to those of normals or atrophic, all
that needs to be done is to compare the brain scans of normals with those of
ADHD-diagnosed children, never, ever exposed to psychiatric drugs.  It is as if they were afraid to do such a
study, afraid the children with this non-disease, might just have normal
healthy brains, and then of course Big Pharma, Novartis in particular, would be
mad at them because that would mean the atrophic, shrunken, shriveled brains
had been due to Ritalin all along. It is almost as if they knew the drugs were
doing it (atrophying, shrinking, shriveling the brains), and planned to
represent/report it to medicine and to the public and parents and children as
proof of this terrible
disorder/disease/syndrome/epidemic/plague/concoction. 

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Actually, the answer to the
AD/HD “disease”/ “no disease” question was delivered by Swanson himself, March
7, 1998, in an address to he American Society of Adolescent Psychiatry, in San
Diego  (I was there).  He confessed:“I would like to have an
objective diagnosis for the disorder (ADHD). 
Right now psychiatric diagnosis is completely subjective…We would like
to have biological tests—a dream of psychiatry for many years.” 

Swanson’s saying this means
there is no such thing as an actual disease/physical abnormality in all of
psychiatry; means the brain atrophy in all of the studies, from that of
Nasrallah, et al, in 1986, up to and including that of Castellanos, et al, in
JAMA, October, 10, 2002 could only be due to their Ritalin/amphetamine therapy;
and means that every physical consequence/side effect, of every psychiatric
“disease” can only be due to drugs/treatments themselves—there being no such
thing as an actual, real, genuine, bona fide, psychiatric disease. 

Swanson’s saying this also means
that the 6 million children in the US with ADHD, were entirely normal until the
moment their Ritalin/amphetamine “treatment” was begun. 

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BIBLIOGRAPHY

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1. Castellanos,
   FX.   Personal correspondence to
   F.Baughman of May, 13, 1998.

2.     
Castellanos, et
al. Developmental Trajectories of Brain Volume Abnormalities in Children and
Adolescents with attention-deficit/hyperactivity disorder.  JAMA, 2002;288: 1740-1748.

3. Giedd,
   J.N., et.al., American Journal of Psychiatry 1994;151:665)
4. Nasrallah
   H, et al [1986] Cortical atrophy in young adults with a history of
   hyperactivity in childhood. 
   Psychiatric Research, 
   1986;17:241-246.
5. Hynd
   GW, Semrud-Clikeman M, Lorys AR , Novey ES, Eliopulos D & Lyytenen, H.
   Corpus callosum morphoilogy in attention deficit-hyperactivity disorder:
   Morphometric analysis of MRI.  J of
   Learning Disabilities, 24 (3), 141-146)  
   
6. Castellanos
   FX, et al. Quantitive Morphology of the Caudate Nucleus in Attention
   Deficit Hyperactivity Disorder.  Am
   J Psychiatry 1994; 151:1791-1796.
7. Lyoo,
   et al. The corpus callosum an lateral ventricles in children with
   attention-deficit hyperactivity disorder: a brain MRI study.  Biological Psychiatry.
   1996;40:1060-1063.)   
8. Castellanos
   et al.  Quantitative brain magnetic
   resonance imaging in attention-deficit/hyperactivity disorder. Archives of
   General Psychiatry. 1996;53:607-616.
9. Filipek
   et al. 1997  Volumetric MRI
   analysis comparing subjects having attention-deficit hyperactivity
   disorder with normal controls. Neurology 1997;48:589-601.
10. Berquin
    PC, et al. Cerebellum in attention-deficit hyperactivity disorder: A
    morphometric MRI study.  Neurology
    1998;50:1087-1093. 
11. Mostofsky
    S. Brain abnormality linked to ADHD, April 20, 1999 (Reuters Health) 

Semrud-Clikeman M, et al.  Notes on Using MRI to Examine
Brain-Behavior Relationships in Males with Attention Deficit Disorder With
Hyperactivity. Semrud-Clikeman M, et al. 
J. Am Acad Child Adolesc. Psychiatry, 2000, 39 (4):477-484.

13. Swanson
    J, Castellanos FX. Biological Basises of Attention Deficit Hyperactivity
    Disorder. Invited presentation at the NIH, Consensus Development
    Conference on ADHD, November 16-18, 1998.
14. Zametkin
    AJ, et al. Cerebral Glucose Metabolism in Adults with Hyperactivity of
    Childhood Onset.  N Engl. J. Med.
    1990;323:1361-6.
15. John
    Pekkanen.  Making Sense of Ritalin
    (interview with FX Castellanos). Readers Digest, January, 2000:159-168.

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