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Because almost all (93%)", default", subjects with ADHD had been exposed to stimulants, we cannot be certain that our results are not drug related.

By Fred A. Baughman Jr., MD

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.

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].

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.

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.”

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.

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

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. 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).

Castellanos et al [8] (1996), took magnetic resonance images (scans), of the brains of 57 boys 5-18

” “Total brain volume was 5% smaller in the ADHD boys…”

The majority of these patients were treated either with methylphenidate (Ritalin) or d-amphetamine (Dexedrine).

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

 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.

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-nave boys with ADHD is under way”

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)?

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…”

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.

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].

Semrud-Clikeman M, et al [12] (2000). Under “METHOD, subjects,” writes: “The volumetric MRI measures from these subjects, who were participants in a larger study, have been reported previously by Filipek et al (1997). Ten children with ADD/H from the previous study and 11 normal controls were selected.” “Volumetric” means structural, anatomic, morphological. By repeat reading of this manuscript I get the impression that the ADD/H subjects were scanned for the 1997 study and not since. Dates of the MRI and of psychometric tests are not given. This means that all 10 of the ADD/H subjects (just the Ritalin responders), herein were subjects in the previous Filipek (1997) study. This study’s purpose is to correlate previous MRI scan findings to current (or whenever) psychometric “neuropsychological” tests (not merely to do MRI scans on ADHD subjects). And yet I do not see specific dates of either MRIs or the psychometric tests. This study assumes these psychometric test abnormalities are part of ADD/H, at least in treatment- responding ADD/H subjects, and has as it’s main intent to perform psychometric tests and correlate them with the brain changes i.e., smaller volume of the left caudate head; smaller volume of white matter of the right frontal lobe. These are pipe-dreams. In neurology, my specialty, we regularly see large, entirely asymptomatic frontal and temporal lobe tumors with no behavior changes and no IQ or other psychometric changes. We regularly see patients with dementia as in Huntington’s disease, or Alzheimer’s disease, with clear, disabling behavioral abnormality but normal psychometric batteries. I have seen children with clear mental retardation with false normal psychometric test results. To hope for and test for such correlations is pure pseudo-science.

Semrud-Clikeman et al [12], continue: “Since structural differences varied depending on response/nonresponse to stimulant medication within the ADHD group in our previous study (Filipek,1997), participants were selected to be as homogeneous as possible on this variable (responders only), to control for a possible confounding variable.” This was their excuse for eliminating ADD/H non-responders and therefore, non-exposed and not brain-damaged by the Ritalin. I suspect they know that Ritalin non-responders and therefore, Ritalin non-exposed [FB: at least not for long, as would probably be required to cause permanent change], would look like ADHD (untreated) which looks like, NORMAL! It appears they know the ADHD responders (and therefore long on the drugs), would be the only ones to have brain atrophy/changes. But do they speak of the drug being the cause of the changes? Of course not. Of children with ADHD being normal, having normal brains? Of course not. “Using DSM-III criteria (1980), we selected 10 children with ADHD (called ADD in 1980), because they were favorable responders…” And because they were long exposed to the brain-toxic effects of Ritalin and would have brain atrophy on their MRI.


In their joint presentation to the National Institutes of Health, Consensus Conference on ADHD, November 16-18, 1998. James Swanson, Ph.D., of the University of California at Irvine (also, remarkably of the National Professional Medical Board of CHADD) , and F. Xavier Castellanos [13] of the National Institute of Mental Health (NIMH), among the most prominent of ADHD researchers, reviewed the Biological Bases of Attention Deficit Hyperactivity Disorder: Neuroanatomy, Genetic, and Pathophysiology. Who would guess, having heard their title, that there is no biological basis for ADHD? Swanson and Castellanos wrote: “One of the most important current developments has been the convergence of findings from magnetic resonance imaging studies of brain anatomy (aMRI).” What, I wonder, does ‘convergence of findings’ mean relative to proof? Those in “biological” psychiatry seem fond of the expression, “convergence of findings,” perhaps having to do with the fact that there are no proofs in “biological” psychiatry, just as there are no actual diseases. They continue: “We will present a meta-analysis of studies from several independent laboratories that have reported ADHD/HKD (hyperkinetic disorder, a term used in the UK), abnormalities in two specific but still coarsely defined brain regions of the frontal lobes and basal ganglia. For example, Filipek and colleagues [9], reported that a group of children with ADHD/HKD had brain volumes about 10 percent smaller than normal in anterior superior regions (posterior prefrontal, motor association, and mid-anterior cingulate, anterior inferior regions, and anterior basal ganglia), and Castellanos and colleagues [8] reported that right anterior frontal, caudate, and globus pallidus regions were about 10% smaller in an ADHD/HKD group than in a control group.

“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.

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.”

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.

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?”

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].

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-nave 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.].

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.”

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..."

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.”

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

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.”

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:

“ ...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.”

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.

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.”

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

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.

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.

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.

2001-2010 National Alliance against Mandated Mental Health Screening & Psychiatric Drugging of Children. All rights reserved.

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