Comments by blakeacake

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  • Hey Steve,

    Why do you call ADHD a disease?

    For the odd child who can’t make it in an open classroom, you come up with another plan that works for him.

    Nothing works. Nice kid. Wonderful boy. Helps others. Leader. Polite. Respects teachers. He is unable to focus his attention on anything consistently such that his school work suffers or is not done. Scouting, choir and other activities are not engaged in. His IQ indicates he is performing below his potential. No other known factors explain this quandary.

    “Due to either early trauma or something epigenetic, or genetic, they develop psychotic characters. Real treatment, like for the rest of us, is psychotherapy of character, with the useful addition of antipsychotics to help with schizophrenic terror, reflecting the dissolution of the intactness of their sense of self, and a horrific ‘play’ of consciousness. This is spelled out in more detail, in my book, “Psychotherapy of Character, the Play of Consciousness in the Theater of the Brain”, by Robert A Berezin, MD., specifically chapter 17.

    “We may not be as far apart as it seems. I certainly judiciously use, anti-psychotics for schizophrenia and manic depression, both in the context of real psychotherapy. Where I absolutely disagree is that I find no place, and no use for antidepressants at all – either in manic-depression or any other depression. These patients can be reached in a real way in therapy, always. I continue to suggest my book to have a fuller context for my position. Then I’d be happy to discuss.”

    In your opinion, Steve, how are antipsychotics applicable in these situations Dr. Berezin alludes to? Why do suppose he uses them?

  • As for hard evidence that “Antipsychotics return intactness to a deeply terrified schizophrenic”. A cure? My golly…not even the pharmaceutical companies would dare to make such an outlandish and unrealistic claim!

    Antipsychotics return intactness to a deeply terrified schizophrenic, according to Dr. Berezin

    I quoted Dr. Berezin

  • If I focused on the information Ralph Nader published in books about the poor design and construction of cars, I would never own, rent, borrow or ride in one, ever. I love Ralph Nader. He provided an important service. We were awakened as a nation by his single-handed efforts to alert us to the grave dangers we didn’t see. At the same time, percentage wise, most drivers avoided most of the perils he described.

  • “So interesting to see how all of this plays out between Big Pharma and physicians. It’s the clients I’d be concerned about, as of course, these drugs have absolutely nothing whatsoever to do with healing. The resources used for all of this is sheer waste. Thanks for an interesting read.”

    I disagree. I am grateful for some of the meds they produce. Some of their drugs save lives.

  • If you decided to start a drug manufacturing company, what would you do? Where would you get the capital, how would you pay it back, how would you promote your products and what would you try to produce first?

    Anyone can research any drugs’ efficacy. That the drug companies publish most of the literature about their drugs, means what? Who else would we expect to invest huge sums of money to do so? Take the profit motive out of making drugs and what do you think will happen? If corporations are psychopathic monsters who don’t mind killing people, like someone posted the other day, better not get in an airplane or a car or a bus, a ship, a train, don’t eat most food sold in supermarkets, drink coffee, or enter buildings or houses or use elevators, buy t.v.s, radios, R.V.s, and away we go.

    Some drug companies have produced some drugs that have saved lives and enhanced our health. As I constantly rethink my view on the drug industry, I can’t deny some of their achievements.

  • When I read what you wrote Duane, I felt sadness. I see where you often have kind, encouraging things say to others. Even apologizing for possible, perceived slights. How awesome is that! I think almost every person posting here appreciates you and your thoughtfulness. You try to go out of your way to be open-minded and polite with everyone, even with those you don’t see eye to eye. You are the nicest person here. Know you make an important difference

    “Change does not take place by changing the brain. Personality change takes place through therapy and the brain follows suit.” This quote from Dr. Berezin is interesting. I wonder how much influence Dr. Freud has had in establishing positions like that? His work was astonishingly important, sweeping over the world of therapy and not all that that long ago.

    Dr. B describes places of great therapeutic impact that were born from small rural European communities where the wounded in spirit and life could go and be embraced by the townspeople in loving acceptance. How cool is that?

    Again, thanks for your sincere courtesy

  • Dr. Berezin, I appreciate all you have offered. Please ignore me and the questions I ask. I don’t mean to bug you. (You may have seen my uncle play football for the Crimson and dad play basketball for them.)

    I would like to know if any doctors would care to answer this question: What do you believe are the best ways to help an adult control/manage/improve his ability to concentrate consistently when he has a long history of not being able to do so. All known anatomical causes have been ruled out. The person has been unable to follow and participate intelligently throughout the course of casual or formal conversations, one-on-one or in groups, and is unable to follow lectures, regardless of the topic or presenter.


  • I found where the NYTs quotes him as having said that the week before, I just can’t find to whom he said it and where, in what context. If you look at his website, he continues to stand firm that aspirin is more dangerous.

    Regarding antipsychotics restoring intactness, I was quoting Dr. Berezin.

  • Hey Steve,

    A friendly reminder.

    “By the way, I don’t know if you are aware of this, but there was a great study back in the 80s showing that “ADHD” kids were indistinguishable from “normal” …” Was it peer-reviewed and published in the literature?

    That “odd one” who doesn’t fit in is the one I’d like to discuss further.

  • Thanks doctor. Appreciate your explanation.

    “ADHD is a ficticious disease. It does not exist.” It doesn’t have to be a disease to wreak havoc in one’s life. In my opinion, it is not as critical what it is called as it is to help those overwhelmed by its most disruptive characteristics: distractibility, impulsivity and disorganization.

    What do you believe are the best ways to help an adult who is unable to concentrate consistently, having ruled out all other health issues?

  • Ritalin, like all medications, can be useful when used properly and dangerous when used improperly. Why is it so difficult for so many people to hold to that middle ground?

    And yet difficult it is. Ritalin continues to be a political football, a hot-button issue almost on a par with abortion or capital punishment. One is pushed to be for it or against it, while the right and good position is to be for whatever will help a child lead a better life, as long as it is safe and it is legal.

    Used properly, Ritalin is safe, safer than aspirin. And it is legal, albeit highly regulated. As to its long-term use, apply common sense. Use it as long as it is helpful and causes no side effects. That may be for a day, or it may be for many years.
    Of course we need to address the complex issues that contribute to behavioral, emotional, and learning problems in children. I’ve written extensively about what I call “pseudo-ADHD,” children who look as if they had ADHD but in fact have an environmentally-induced syndrome caused by too much time spent on electronic connections and not enough time spent on human connections, i.e., family dinner, bedtime stories, walks in the park, playing outdoors with friends or relatives, time with pets, buddies, extended family, and other forms of non-electronic connection. Pseudo-ADHD is a real problem; the last thing a child with pseudo-ADHD needs is Ritalin.
    But that is not to say that no child needs Ritalin, nor that those who prescribe it are dimwits hoodwinked by drug companies to medicate children who do not need it. Sure, some doctors over-medicate, while other doctors never medicate because they “don’t believe in ADHD” and “don’t believe in Ritalin.”

    Above all, children need a loving, safe, and richly connected childhood. The long-term study that Dr. Sroufe cited in his opinion piece does indeed show that over time, medication becomes a less important force in a child’s improvement and that human connections become ever more powerful. It is good and heartening to know that human connection–i.e., love–works wonders over time. Love is our most powerful and under-prescribed “medication.” It’s free and infinite in supply, and doctors most definitely ought to prescribe it more!

    But that is not to say, as Dr. Sroufe does, that Ritalin has “gone wrong.” We may go wrong in how we use it, when we over-prescribe it, or when we use it as a substitute for love, guidance, and the human connection.

    But as long as we use it properly, it remains one of our most valuable–and tested–medications. Going all the way back to the first use of stimulants to treat what we now call ADHD in 1937, stimulants have served us well as one tool–not the tool–for helping children and adults learn how to strengthen the brakes of their race car brains and become the champions they can be.


  • You said you are offering a counterbalance to the, “monolith of mainstream perspectives on psychiatry. That ground is more than sufficiently covered elsewhere…”

    What I want to convey is that some kids have benefited profoundly through the use of medication, but we don’t hear much about them or those kinds of success stories, anywhere. I think it needs to be said, unequivocally, some kids respond favorably to treatment for ADHD. Kids with ADHD make considerable advances on drugs. Don’t forget about them. Don’t let anything obscure your sight of the boy in the straw hat whose life turned around. Some have been given a real shot a living; something they stopped dreaming of, an honest-to-goodness life unimpeded by the inability to control distractions. (Can you try to imagine what that is like? Would you try?)

  • “The fact is, ADHD is not objectively distinguishable from a number of other conditions…” But, you already made distinctions.

    “nor is it particularly distinguishable from normal childlike behavior.” But, you have already distinguished it.

    “Until there is a way to know who specifically “has ADHD” and who has something else and who has nothing but a boring classroom or incompetent or abusive parents…” Steve, you already identified kids who have it. Remember the hunters and gatherers, too.

    “it really is nothing more than a description of kids who the teacher/parent finds annoying.” You have more, no, you have way, way too much intelligence to make that statement with conviction.

    Have you seen a top notch medical doctor who is a specialist in ADHD diagnosis and treatment like Ned Hallowell, out of Harvard? Have you read, Driven To Distraction?

  • “Putting the child in a position where s/he has to think about consequences and about others’ feelings in order to get what s/he wants is also a very powerful approach.” If that doesn’t help?

    “The key is to teach them the skill and value of planning and forethought without crushing their exuberant spirits.” What if no one can teach them those skills and values?

    When you wrote, “the goal is to help people with ADHD with their difficulties in organization and focus” you gave away, you revealed, your true nature as a human being and your real agenda, didn’t you?

  • “We fulfill our natures in relation to the quality of our nurture.” And our nature cannot be flawed? Antipsychotics return intactness to a deeply terrified schizophrenic. Thank goodness. How awesome it that? A person overwhelmed by fears is enabled to benefit from psychotherapy through the use of a drug. I take for granted, all too often, the advances we’ve made in modern medicine.

  • “their difficulties in organization and focus” Steve

    I think that is a good partial definition of the traits that some people experience/have to such an extent that it interferes with their ability to progress through school and life.

    Some kids are motivated by and excel at football and cannot focus on what the coach says consistently. They are so big, strong, quick and aggressive, they can and do compensate. If the coach stops his lecture/teaching and asks him what he just said, he cannot answer. He wanted to pay attention. He tried to pay attention. His entire life revolved around his love for football. He had no idea what the coach was teaching, consistently.

    Graduating from college is a measure I think you raised. “For some of these kids, they are motivated and can use their intelligence and drive to come up with ways to overcome their difficulties in organization and focus. In other case, they don’t care about going to college and do other things instead. Why is that wrong? ” Nothing. I don’t think I said there was. In addition, if school is the only major life activity where the child is failing or struggling, he doesn’t have ADHD.

    If you can let me know how to find that study, that would be great.

    “And while there may be an odd kid who can’t function…” Can we discuss that odd kid that doesn’t do well even in an open classroom? What is it about that kid, in particular, that interferes with his ability to focus his attention?

  • The following is an article which includes the issue of tracking/measuring neurotransmissions.

    “The JAMA study said that, compared with a group of healthy subjects, brain scans of 53 adults with ADHD revealed a flaw in the way they process dopamine, which among other things, alerts people to new information and helps them anticipate pleasure and rewards. Swanson speculated that people with ADHD may even have a net deficit of dopamine.”

    “Sept. 9 report in the Journal of the American Medical Association, based on a new study that indicates a striking difference in the brain’s motivational machinery in people with ADHD symptoms.”

    “This is another big piece in the puzzle saying that there is something there, that this is not simply a matter of anxious parents,” said James Swanson, a co-author of the report and a developmental psychologist based at the University of California at Irvine.

    The JAMA study said that, compared with a group of healthy subjects, brain scans of 53 adults with ADHD revealed a flaw in the way they process dopamine, which among other things, alerts people to new information and helps them anticipate pleasure and rewards. Swanson speculated that people with ADHD may even have a net deficit of dopamine.

    “The findings offer support for a long-held theory about why people with ADHD tend to be so easily distracted and bored — so hard to teach in school, so prone to end up in high-stimulus jobs such as in sales or the media, and so susceptible to gambling and drug abuse.”

    “Volkow’s team collected detailed images of participants’ brains with positron emission tomography, or PET, scans after injecting them with a radioactive chemical that binds to dopamine receptors and transporters, which take up and recycle dopamine as it moves between neurons. The imaging showed that, in people with ADHD, the receptors and transporters are significantly less abundant in mid-brain structures…”

    *Nora Volkow, is a research psychiatrist who is director of the National Institute on Drug Abuse

    “Stephen Hinshaw, chair of the psychology department at the University of California at Berkeley, praised the study as being “above and beyond the normal rank and file” of incremental progress in the quest to solidify the dynamics of ADHD.”

    Katherine Ellison
    Special to The Washington Post
    Tuesday, September 22, 2009

  • “There are times in the treatment of schizophrenia when a patient is horrendously terrified. I don’t impose med’s on anbody. Sometimes it helps to get back intactness. I give the control to my patient. The real work has nothing to do with med’s. It is the psychotherapy.” Dr. B.

    Thanks, doctor, for your response. Meds help bring a very sick patient back to intactness where the real work can begin. (I think the meds do some important work, too. To assist the patient to the point where more work can be done, is critical.)

    How does the med do that? How is it possible? Do any medical principles, evidence, testing or theories indicate what it is specifically that that med does to recover intactness?

    I’d ask the same kinds of questions for your work with Manic-Depression when meds are applicable.

    Thanks Dr.

  • “It” exists, because “it” is a list of behaviors that make it inconvenient for these kids to function in a standard classroom environment.” Steve

    Thanks for this, Steve. I appreciate the opportunity to examine ADHD with you and Duane. I know I have much to learn.

    Responding to your opening statement, let me ask this. You say it exists because it is “inconvenient” for these kids to function in a standard school environment. What if it makes it impossible for some kids to function in a standard class or an open class (have you found that study you mentioned. I would like to see it)? What then? Is it possible some have it in a more severe form than others? Or that some people don’t have the intelligence/skills to compensate for it as well others do? Can you graduate from college with untreated ADHD and if so, is that proof everyone with it can do as well if they have the same strengths and interests, or may the traits be overpowering to some regardless how intelligent they may be?

    This is the one-step-at-a-time approach I prefer. Just trying to break things down to look carefully at the logic at each point of a discussion. So, I start with your first sentence, in this case, to try to parse it into precisely what we can deduce from it, if that is okay with you.

  • Duane, have you seen information like this.. Newer research is even more impressive.

    Nihon Yakurigaku Zasshi. 1997 Jun;109(6):259-70.

    [Neurotransmission in human brains measured by positron emission tomography (PET)].

    [Article in Japanese]

    Yanai K1.

    Author information


    Various techniques have been developed to image human brain function in the past decade. X-ray computerized tomography and magnetic resonance imaging (MR) are used to evaluate brain structure. Recently, positron emission tomography (PET) and MR are often utilized to perform human brain mapping such as attention, cognition, language comprehension, and so on. PET also makes it possible to evaluate the states of various types of neurotransmission. These techniques cannot only be used to map “brain neurochemistry” in normal human brains, but they will also increase our knowledge by demonstrating neurochemical abnormalities in a wide range of neurological and psychiatric disorders or those that occur during normal aging. The PET techniques are applicable to the development of new drugs in the pharmaceutical industry. Using PET techniques of imaging neurotransmission, it is feasible to measure the release of neurotransmitter after activation of the CNS by various methods (ligand activation study). We have developed the methodology of using 11C-labeled antagonists for mapping functional histamine H1-receptors in human brain directly and noninvasively by PET. The present review article provides an outline of the conceptual and methodological progress over the past several years that has made it possible to visualize neurotransmission in human brains by PET.

  • Indeed. Let’s identify what it is and proceed. Thanks for the references. Steve M. has just acknowledged it is real. That is a good place to start an in-depth analysis and to define it with as much specificity as is possible. It isn’t that difficult to use logic, the process of elimination and other investigative techniques, to figure out what can be known about it. One step at a time. So far, no doctor has offered an answer or her opinion.

  • “1. Prescribers will assure you that ADHD medicines are powerful yet harmless…” Dr., would you name a doctor who prescribed these drugs while making that promise?

    “2. Medicinal treatment can also take away the urgency of a problem…”
    Can you offer examples where this has been a problem with these meds and ADHD patients?

    “These drugs purportedly address the structural and biochemical deficiencies present in the brains of people diagnosed with ADHD.”

    What do you think doctor? Purportedly doesn’t mean positively.

  • “Everyone involved (including the child) adopts the belief that there is permanent incompetence and the necessity for others to provide constant surveillance and force. Therapy that promotes self-management does not occur.” Dr. Wiener

    Unless that is provable, I don’t think that statement can be made with integrity.

    “6. While medicinal therapy is certainly a reasonable treatment option when the benefits clearly outweigh the harms…”

    Dr., you are making a powerful point. You recognize ADHD exists, number 1 and that #2, medication to treat it makes sense.

  • “I do think ADHD is a characteristic or trait that is at least partly inherited”

    Great. You gave a clear answer. It exists. IT EXISTS!

    Now what?

    Can we approach further discussion about it a step at a time?
    What if an open classroom has no positive influence on some kids who have it? IOW, do some experience its symptoms more extensively or more severely than others? If so, what do we do with those kids?

  • And to anyone who cares, how do you view and what is ADHD, exactly? Same questions as above. Is it fictitious? Real, but no big deal. Typical of boys, nothing serious. Nothing that requires or justifies the use of any stimulant, period. A phase. A set of traits? Not serious. Can be disabling. A function of willpower?

    I would appreciate your thoughts.


  • “Nor is there any long-term social or emotional benefit to stimulant use over time…” That is not true.

    “If we are being scientific, your first question makes no sense. The real question is whether psychiatry has any proof that any “mental disorder IS a molecular medical disease.”” Yet, there is no proof that it isn’t.

    DR. Berezin, if you read this and are so inclined, could you explain why you would you prescribe antipsychotics for S and MD?

    “By the way, I don’t know if you are aware of this, but there was a great study back in the 80s showing that “ADHD” kids were indistinguishable from “normal” kids in an open classroom environment where they had more control of their time and activities” Would you give the name of the study or other details? I’d like to see it. What is an open classroom? Their grades were just as good? Do you know how long it lasted? Thanks

    “While both of these impositions can yield some short-term benefits…” Dr. Wiener.

    Dr., based upon what information do you make this statement? Any ideas you could share with us why drugs and organization can yield short-term benefits?

    “In this treatment protocol, diagnosed individuals are remanded into treatment that mimics institutional care (i.e., others control their access to resources and their behavior is restrained with drugs).”
    How is their behavior restrained? by drugs? They are unable to move or speak? Again, why do you suppose there can short-term benefits in this type of setting?

    Dr., do you believe ADHD exists? Is there such a trait, characteristic, disorder, illness or whatever it should be called? Or is it just nonsense? Is there nothing to it? Are some people unable to concentrate consistently when they need to, no matter how hard they try to? Can that type of problem exist? Or, is it your opinion that attention is always under the control of the individual?

    I would appreciate your thoughts and those of any and all the MIA writers.


  • The two most popular interventions for ADHD are drugs and stringent control. Those who believe in the traditional biological determinist view assert that others must provide the control that people diagnosed with ADHD lack. In this treatment protocol, diagnosed individuals are remanded into treatment that mimics institutional care (i.e., others control their access to resources and their behavior is restrained with drugs). While both of these impositions can yield some short-term benefits, they can also produce unwanted side effects much like what happens when there is incarceration

    What do you recommend when nothing works?

  • “The reason why researchers have no proof that psychiatry is a molecular medical disease, is because it isn’t so.” Dr. Berezin

    Dr. Berezin are you able to confirm your statement above through science?

    “I certainly judiciously use, anti-psychotics for schizophrenia and manic depression, both in the context of real psychotherapy.” Dr. Berezin

    Robert Berezin, MD (MIA Author)
    on February 14, 2015 at 5:17 pm said:
    I appreciate your comment. However, I am against psychiatric medictions, and psych diagnoses. I don’t use them. I certainly don’t sing their praises. I address my approach toward psychiatry to the best of my ability. I hope you will consider my offerings. you may contact me at [email protected]

    Dr., in light of your stance, I’m not clear why you would prescribe anti-psychotics for schizophrenia and manic depression?

    “We may not be as far apart as it seems. I certainly judiciously use, anti-psychotics for schizophrenia and manic depression, both in the context of real psychotherapy. Where I absolutely disagree is that I find no place, and no use for antidepressants at all – either in manic-depression or any other depression. These patients can be reached in a real way in therapy, always. I continue to suggest my book to have a fuller context for my position. Then I’d be happy to discuss.”

  • “They have persuaded parents that their children’s brains are impaired…” The power of words.

    Some doctors of medicine love to practice their craft-to bring healing to the sick. Granddad did. Still saw 18 to 25 patients in the mornings at age 75. Didn’t perform surgery any longer, though. He was as gruff as you can get but they loved him, thousands of town folks did. Absolutely no bedside manor. Actually, he was scary. A retired Admiral, his voice exploded like a 16 inch cannon when he told patients they were fine. “God Dammit, I said, there’s nothing wrong with you!” He wasn’t there to make money off of anybody’s misfortune. But if you were really sick or broken from a car wreck, he’d fix you or die trying.

    I wish he’d known about A.D.D. when I was a kid. I can’t imagine what it would have been like. To be a student, a real student, to contribute, to be seen and understood for the good, thoughtful kid I was. He could have prescribed a life-giving medicine for me and everyone would have known that I wasn’t the worst kid ever. I would have cried my eyes out, if only they could have only known I wasn’t the worst kid ever, that I wasn’t trying not to study. To have been able to participate in classroom life, to hear my teachers, to read and do my lessons, quietly, thoroughly.

    “They have persuaded parents that their children’s brains are impaired…” is a cruel thing to say. My brain was/is impaired. Many are doing the best they can to help others. Many do care.

    “Give sorrow words; the grief that does not speak knits up the o-er wrought heart and bids it break.”
    ― William Shakespeare, Macbeth

  • Very interesting. Glasses are fine. They are not dangerous. Without glasses the person is practically blind and cannot function, realistically. No question he needs and will benefit from a fine new pair, prescribed and fitted just for him. We don’t give it a second thought. Glasses are safe. He can’t see. Voila!

    Did you hear the breaking news? Pepper treats ADHD. It works great to focus one’s attention, like 20/20 focus. Stimulants are so yesterday. Pepper is here. Cheap, safe, plentiful and IT WORKS!

    One year later and no one discusses ADHD any longer. At least, no one bothers to challenge whether or not it “is”. (Bill Clinton now knows that is is is.) Take your pepper. Doesn’t bother me. It doesn’t matter if it’s real or not. It is those dangerous drugs we don’t like. Good riddance drugs.

    Hello Ms. Beachy, thank you for your response. Please share more! (I hope Dr. Berezin will join in.) I want to know your educated, sincere thoughts. Really.

    Would you give aspirin to someone with a headache even if aspirin really is more dangerous than amphetamine? I am a teetotaler. Don’t smoke or drink or do drugs, ever, at all. I would prefer pepper. Pepper doesn’t help. Should I stop my meds? Most of my life I could not function. Awakenings. Did you see it? True story. The L-Dopa drug restored life to a group of catatonic patients. Robin Williams and De Niro. I can relate.

    I don’t want to kill myself, especially now that I can read. I LOVE to read. I can watch documentaries and do Algebra II and cross word puzzles. People don’t laugh at me any more. (I’ve heard people whisper, saying how smart I am!) I want to live. I like being healthy. Should I stop?

    Here is Dr. Hallowell’s response to the December 9, 2012 New York Times article:

    “To the Editor:

    Bravo Dr. Sutherland! As a man who has both A.D.H.D. and dyslexia myself, and as a psychiatrist who’s been writing about and treating children and adults with this condition for over 30 years, I know of the rampant yet preventable damage wrong information about A.D.H.D. does to children and adults every day.

    The proper treatment of A.D.H.D. should always include education, a lifestyle review, coaching to develop organizational skills, and assessment of talents and strengths, not just a focus on what’s going wrong. The treatment also may, but need not, include medication. First used to treat what we now call A.D.H.D. in 1937, stimulant medications have stood the tests of time and scientific review. Medication should now be a welcomed option, but it usually is not, due to wild and toxic misconceptions.

    People often ask me, “Do you believe in Ritalin?” My reply is that it is not a religious principle. Yet, it is often discussed as if it were. Stimulant medications, like Ritalin and Adderall, are simply medications. When used properly, they can be a godsend, as effective in helping people who have A.D.H.D. as eyeglasses are in helping people who are near-sighted. If they do not help, or of they cause side effects, either the dosage should be changed or the medication should be discontinued. It should be as simple as that. Sadly, this sensible approach gets blown up routinely by the hyperbolic nonsense that appears too often even in responsible media. The SCIENCE IS CLEAR, used properly stimulant medication is safe, in many ways safer than aspirin, and provides the most effective short term aid we have to help people of all ages deal with the negative symptoms associated with A.D.H.D. Yet, rather than regard this medication as a helpful tool, most parents fear it, seeing it as a last resort. Stigma enshrouds stimulant medication like an impenetrable rind, preventing legions of children, as well as adults, from ever reaping the extraordinary benefits these safe and time-tested medications can provide.

    Happily, we have many other powerful tools in our toolbox we can use to help people develop the many talents that are wonderfully embedded in the mind of a person who has A.D.H.D. But it is foolish to disregard the science and subscribe to the superstitions that lead people to remove stimulant medication from that toolbox.”

    Thank you again for your response.

  • Dr. Berezin,
    If a person is terribly nearsighted and he cannot really function because his vision is so poor, but a pair of corrective lenses will bring the world into focus for him, is there any reason not to supply him with a nice pair of glasses?

  • “that kids who may be off the walls can have “symptoms” for many reasons including physical problems, that show that real medical illnesses may cause certain symptoms…”

    Just be damn sure the medical problem cannot be ADHD?

    To which medical illnesses do you refer that produce the bouncing off the walls behaviors you mention?

    I don’t think calling ADHD a bogus diagnosis is helpful, especially when there is no good reason to. As you say, labeling kids with a term like bogus can only be harmful to them.

    You know what is cool? Some of us don’t mind the term ADHD at all. Just the opposite, in fact. We are quite proud of our abilities when harnessed. Do you have any idea how fast the brains of some with ADHD compute? Do you have any idea how perceptive many are, extremely affable, generous and creative? Did you realize that we often see through complex problems and arrive at a solution in an instant, an answer no one else even considered? Do you know how big our hearts are? How sensitive we are to the pain of others? How we can walk into a room of strangers and sense who is hurting just like that? It is uncanny. Often, we are the life of the party. And when something grabs our attention, say goodbye. It is called hyper-focusing. We lose sense of time. You cannot break us away from whatever it may be, like wrestling or computer games, preparing to present a product or concept to sell.

    It is often a relief to know that there is a name for this mysterious set of symptoms.

    “psychiatry just uses its lethal drugs”
    Check that. Lethal?
    “They hide or suppress surface symptoms with no regard to the real cause..” Unfair generalization. Probably some do.
    “Whether physical or environmental, so they are totally useless.”
    “If the person really has a dangerous illness that needs immediate treatment as has been the case at times, such stigmatizing and drugging of the victim can be very deadly indeed not to mention all the drug induced deaths of normal”
    We can’t win!

    That’s about it. Said pretty much what I have to say.

  • I believe withdrawal is a serious problem for some people on some meds.

    “The next day, I came down with horrible depression when there was no reason for me to be depressed.”

    Certain types of depression attack regardless what our outward circumstances may be.

    “Not correct blakeacake. Many people stay on the meds because when they try to get off, the withdrawal symptoms are horrendous.”

    How can you assert that the reason these drugs sell so well is due to the horrible withdrawal process when you don’t know how many are taking them for that reason?

    “many people never learn that withdrawal symptoms are keeping them on the psych meds and that is why they stay on them.”

    If many never learn it is the withdrawal symptoms keeping them on the meds, how would you know that?

    “Dr. Joseph Glenmullen”

    Are you referring to the tongue guy?

    best of luck

  • “Has it ever occurred to you that if someone has difficulties with reading due to dyslexia, comprehension, visual perceptual problems, auditory processing, that they are going to have trouble attending to what they are reading…”

    Now you are talking. You bring up an excellent point. Proper diagnosis is critical. IEPs need to be based on the best information available. The subtest scores on the Woodcock-Johnson Battery pinpoints each component of the child’s cognitive functioning.

    (Test 2: Visual-Auditory Learning
    Long-Term Retrieval (Glr )
    Associative memory
    Paired-associative encoding via directed spotlight attention; storage and retrieval
    Test 3: Spatial Relations
    Visual-Spatial Thinking (Gv )
    Spatial relations
    Visual feature detection; manipulation of visual images in space; matching
    private speech
    Test 4: Sound Blending
    Auditory Processing (Ga )
    Phonetic coding
    Short-Term Memory (Gsm )
    Working memory
    Auditory Processing (Ga )
    Speech-sound discrimination Resistance to auditory-stimulus distortion

    Hope this helps

  • Ever? Has treatment for the disorder attracted one positive word or any acclamations from our media? Autism receives some serious attention. Dyslexia, too. They should. Freed from what feels like an unending, unknown, hellish nightmare of ADHD, this confounding, damnable disorder, through medication, its victims hear nothing, except, it doesn’t exist and we take speed.

    Emmeline, (Love that name) said, “rather than attempting to sing the praises of psych diagnosis and drugging to people who have been harmed by diagnosis and drugging”

    I sing the praises of a life set free from hell. I don’t care if taking pepper did the trick, and I don’t mind if an elevator operator convinced me to use it; it is being liberated from hell that makes me sing. Should I be silent? Should I refrain from telling my story? Is there room for truth? Formidable, entrenched powers crush a lot of folks. Many are overlooked. “It don’t count ‘less it sells” our modern day Bard wrote.

  • “Obviously things are very different today, and I think the fundamental questions here are: how did these changes come about? and, who’s to blame?”

    Obviously, the answer is: because drugs work. Very simple. If people did not respond favorably to the meds they were prescribed, they would have stopped taking them. Obviously, a great many people were helped. How ridiculous it would have to be to expect to sell billions and billions of dollars worth of these products if they were ineffective.

  • ” she had accessed my former records saying I had a serious mental illness. Within meeting me for 5 seconds she dismissed my physical problem by telling me to see my psychiatrist…” aria

    HIPAA Violations and Enforcement
    Failure to comply with HIPAA can result in civil and criminal penalties (42 USC § 1320d-5).
    Civil Penalties
    The “American Recovery and Reinvestment Act of 2009”(ARRA) that was signed into law on February 17, 2009, established a tiered civil penalty structure for HIPAA violations (see below). The Secretary of the Department of Health and Human Services (HHS) still has discretion in determining the amount of the penalty based on the nature and extent of the violation and the nature and extent of the harm resulting from the violation. The Secretary is still prohibited from imposing civil penalties (except in cases of willful neglect) if the violation is corrected within 30 days (this time period may be extended).
    HIPAA Violation
    Minimum Penalty
    Maximum Penalty
    Individual did not know (and by exercising reasonable diligence would not have known) that he/she violated HIPAA $100 per violation, with an annual maximum of $25,000 for repeat violations (Note: maximum that can be imposed by State Attorneys General regardless of the type of violation) $50,000 per violation, with an annual maximum of $1.5 million
    HIPAA violation due to reasonable cause and not due to willful neglect $1,000 per violation, with an annual maximum of $100,000 for repeat violations $50,000 per violation, with an annual maximum of $1.5 million

    aria, Had you signed a medical release authorization form? If not, that’s A LAWSUIT WAITING TO HAPPEN.
    Do you have his or her name and address?

  • Donna, I recommend that you locate Baughman’s most recent, published, peer-reviewed research and present it here.

    Yannis Paloyelis,corresponding author1 Fruhling Rijsdijk,1 Alexis C. Wood,1,2 Philip Asherson,1 and Jonna Kuntsi1
    Previous studies have documented the primarily genetic aetiology for the stronger phenotypic covariance between reading disability and ADHD inattention symptoms, compared to hyperactivity-impulsivity symptoms. In this study, we examined to what extent this covariation could be attributed to “generalist genes” shared with general cognitive ability or to “specialist” genes which may specifically underlie processes linking inattention symptoms and reading difficulties. We used multivariate structural equation modeling on IQ, parent and teacher ADHD ratings and parent ratings on reading difficulties from a general population sample of 1312 twins aged 7.9–10.9 years. The covariance between reading difficulties and ADHD inattention symptoms was largely driven by genetic (45%) and child-specific environment (21%) factors not shared with IQ and hyperactivity-impulsivity; only 11% of the covariance was due to genetic effects common with IQ. Aetiological influences shared among all phenotypes explained 47% of the variance in reading difficulties. The current study, using a general population sample, extends previous findings by showing, first, that the shared genetic variability between reading difficulties and ADHD inattention symptoms is largely independent from genes contributing to general cognitive ability and, second, that child-specific environment factors, independent from IQ, also contribute to the covariation between reading difficulties and inattention symptoms.

    Keywords: ADHD, Reading disability, Inattention, Comorbidity, Twins, IQ


    The co-occurrence between attention deficit-hyperactivity disorder (ADHD), which is characterized by developmentally inappropriate levels of inattentive and/or hyperactive-impulsive behaviours (American Psychiatric Association (APA) 2000), and reading disability, whether defined as diagnostic categories or quantitative traits, is well documented (August and Garfinkel 1990; Dykman and Ackerman 1991; Trzesniewski et al. 2006; Willcutt and Pennington 2000a,b). It reflects a strong phenotypic association between reading disability and ADHD inattention symptoms, which has been largely attributed to shared genes (Martin et al. 2006; Willcutt and Pennington 2000a; Willcutt et al. 2000, 2007b). The present study, using a genetically informative design, extends this research by investigating to what extent the common genetic variability between reading difficulties and ADHD inattention symptoms is also shared with general cognitive ability, as measured by IQ.

    Previous twin studies have shown that both reading ability/disability (Alarcon and DeFries 1997; Byrne et al. 2008; Gayan and Olson 2003; Harlaar et al. 2005a; Tiu et al. 2003; Wadsworth et al. 2000) and ADHD symptoms (Kuntsi et al. 2004; Wood et al. 2009) share genetic variability with IQ. Therefore, it is possible that any shared genetic variability between inattention symptoms and reading disability could reflect a common genetic association shared with general intelligence. This idea was supported by evidence that genetic and environmental influences shared with IQ accounted for the covariance between reading performance and a cognitive attention measure (Zumberge et al. 2007). However, it is not possible to generalize directly from cognitive attention processes to behavioural inattention problems (Marzocchi et al. 2009; Warner-Rogers et al. 2000). Similar manifestations of inattention problems may reflect diverse cognitive deficits, and the relationship between overt behavioural inattention and deficits in cognitive attention is neither simple nor direct (Marzocchi et al. 2009; Warner-Rogers et al. 2000).

    Indeed, behavioural and genetic evidence at the overt symptom level suggests that shared aetiological influences between inattention symptoms and reading disability are likely to be independent of IQ. A recent study reported similar estimates of common genetic influences between a brief measure of hyperactive/inattentive behaviours and a composite measure of academic achievement (including reading) before and after adjusting the latter for IQ (Saudino and Plomin 2007). Other studies have shown that early inattention symptoms predicted later reading achievement even after controlling for prior reading ability and IQ (Rabiner and Coie 2000; Rabiner and Malone 2004).

    There is a need to understand better the aetiology of the covariance between ADHD inattention symptoms and reading disability because, to be effective at improving reading performance in the context of inattention problems, intervention programs need to address the specific deficits giving rise to the covariance between these disorders (Rabiner and Malone 2004). If the covariance could be attributed to shared aetiological influences that are independent of IQ, this would indicate the presence of specific neurocognitive deficits contributing to these disorders that were independent of possible “generalist” mechanisms spanning cognitive processes and learning abilities/disabilities across domains (Haworth et al. 2009).

    Bivariate studies allow the parsing of the covariance between two phenotypes into distinct genetic and environmental components. The genetic and environmental correlations provide estimates of the degree to which the covariance between two phenotypes reflects shared genes or environmental factors, respectively. The inclusion of additional variables of interest in the multivariate case makes possible the estimation of the extent to which the genetic (or environmental) overlap is further shared with the additional variables (such as IQ). Multivariate designs offer improved power by decreasing the rate of false positive type I error rate (by decreasing the number of tests) and by taking into account the covariance among traits for each individual (Hottenga and Boomsma 2008).

    Existing studies have employed bivariate designs, examining the aetiology between reading deficits and a single ADHD subtype, or ADHD symptom dimension, at a time, excluding IQ (Martin et al. 2006; Willcutt et al. 2000, 2007b). In the present study we replicate and extend previous research by using a general population sample and employing a multivariate design, including measures of IQ and both ADHD inattention and hyperactivity-impulsivity symptoms. The use of an unselected, general population sample avoids possible selection biases associated with clinic-referred or selected community samples and allows the generalization of findings to the general population. Inattention, hyperactivity-impulsivity and reading disability are all considered to be the tails of normally distributed traits, reflecting the normal distribution of genetic risk in the population (Chen et al. 2008; Harlaar et al. 2005b; Levy et al. 1997; Shaywitz et al. 1992). Studying general population samples is useful in understanding the extremes, as quantitative genetic and epidemiological evidence supports the validity of making inferences from population data to clinical cases in ADHD (Chen et al. 2008).

    Specifically, our study aimed to: (1) Confirm the substantially larger phenotypic and genetic correlations between reading difficulties and ADHD inattention symptoms, compared to hyperactivity-impulsivity symptoms. (2) Investigate, for the first time, to what extent the common genetic variability between ADHD inattention symptoms and reading difficulties is also shared with IQ and hyperactivity-impulsivity symptoms. (3) Assess how much of the variance in reading difficulties could be attributed to aetiological influences shared with the ADHD symptom domains and IQ, thus providing an estimate of their relative importance in understanding the aetiology of reading difficulties. (4) Finally, examine the possibility of gender differences in the aetiology for the covariation between reading difficulties and inattention symptoms.


    Sample and Procedure

    Participants are members of the Study of Activity and Impulsivity Levels in children (SAIL), a general population sample of twins aged 7.9–10.9 years. They were recruited from the Twins’ Early Development Study (TEDS; Trouton et al. 2002), a birth cohort study which had invited parents of all twins born in England and Wales during 1994–1996 to enrol. Despite attrition, the TEDS families continue to be reasonably representative of the UK population with respect to parental occupation, education and ethnicity (Oliver and Plomin 2006). Zygosity has been determined using a standard zygosity questionnaire which has shown 95% accuracy (Price et al. 2000).

    TEDS families were invited to take part if they fulfilled the following SAIL project inclusion criteria: twins’ birthdates between September 1, 1995 and December 31, 1996; lived within a feasible travelling distance from the research centre; White European ethnic origin (to reduce population heterogeneity for molecular genetic studies); recent participation in TEDS, as indicated by return of questionnaires at either 4- or 7-year data collection point; no extreme pregnancy, perinatal difficulties, specific medical syndromes, chromosomal anomalies or epilepsy; not participating in other current TEDS substudies; and not on stimulant or other neuropsychiatric medications.

    Of the 1,230 suitable families contacted, 672 families (55%) agreed to participate. Overall, the sample is as representative of the general population as is feasible for a study of this kind, and previous analyses on TEDS indicated that attrition was not due to ADHD symptoms. For example, Saudino et al. (2005) found that twins who participated at age 7 assessments were not significantly different in parent ratings of hyperactivity from lost twins at age 2 (t=1.77; p=0.08). However slight bias towards higher parental occupational classification, compared to the original TEDS sample, should be noted (39% of mothers and 52% of fathers in managerial or professional jobs, compared to 28% and 40%, respectively). Thirty-two children were subsequently excluded due to: IQ<70, epilepsy, autism, obsessive-compulsive or other neurodevelopmental disorder, illness during testing or placement on stimulant medication for ADHD. The final sample consisted of 1312 individuals: 255 monozygotic (MZ) twin pairs, 183 same-sex dizygotic (DZ) and 206 opposite-sex DZ twin pairs, as well as 24 singletons coming from pairs with one of the twins excluded. Data for the 24 singleton twins were also used in the structural equation modelling (see Neale et al. 2003). Participants were invited to our research centre for cognitive assessment (see Kuntsi et al. 2006), where ratings on the Conners’ scale and the reading difficulties questionnaire were collected from parents. Teachers’ ratings on the Conners’ scale were obtained through post.

    The mean age of the sample was 8.83 (SD=0.67), and half of the sample were girls (N=663, 50.5%). Children’s IQs ranged from 70 to 158 (M=109.34, SD=14.72). Parents of all participants gave informed consent following procedures approved by the Institute of Psychiatry Ethical Committee.


    Wechsler Intelligence Scales for Children, Third Edition (WISC-III; Wechsler 1991) The vocabulary, similarities, picture completion and block design subtests from the WISC-III were used to obtain an estimate of the child’s IQ (prorated following procedures described by Sattler (1992)).

    Ratings of Inattention and Hyperactivity-Impulsivity Parents and teachers were asked to complete the Long Versions of the Conners’ Parent and Teacher Rating Scales (Conners et al. 1998a,b). Teacher ratings were collected from the main class teacher for each child. Previous analyses on the TEDS sample indicated that the majority of twins had been rated by the same teacher (Saudino et al. 2005). In a study looking at scholastic achievement and hyperactivity/inattention in the TEDS parent sample, the aetiology of the covariance was similar for ratings provided by the same or different teachers or parents (Saudino and Plomin 2007). From both scales, we used the 9-item inattention and 9-item hyperactivity-impulsivity DSM-IV symptoms sub-scales. Inter-rater agreement for parent and teacher ratings was .46 (p<.001) for inattention and .40 (p<.001) for hyperactivity-impulsivity, which are comparable to those obtained in previous studies (Saudino et al. 2005; Thapar et al. 2000). We created DSM-IV composite inattention and hyperactivity-impulsivity scores by summing up standardized parent and teacher ratings on the corresponding subscales. Teacher ratings were missing for 151 individuals and parent ratings for two individuals. Those with missing teacher ratings on the Conners’ scale did not significantly differ from the rest of the sample on the reading difficulties questionnaire (F(1, 667)=0.61, p=.43), in IQ (F(1, 667)=3.55, p=.06) or parent hyperactivity-impulsivity ratings (F(1, 666)=3.49, p=.06), but were slightly older (M=9.12, SD=0.71; F(1, 667)=17.88, p65 as indicated in the manual) (Conners 1997). These estimates match or exceed the estimated ADHD prevalence rate in the population (Ford et al. 2003; Polanczyk et al. 2007).

    Reading Difficulties Questionnaire (RDQ; Martin et al. 2006; Rommelse et al. 2009; Willcutt et al. 2010b) This 6-item parent rating scale is part of an instrument screening for learning disorders. On a scale which ranges from 1 (“Never/not at all”) to 5 (“Always/a great deal”), parents are asked to report to what extent their child has difficulties with spelling, learning letter names or phonics (sounding words out), and to what extent their child reads slowly, below expectancy level or has required extra help at school. In the validation study, using four independent referred and general population samples (N=4158), all items loaded on a single factor and the scale showed excellent internal consistency (mean Cronbach’s α=.90) and high inter-rater (r=.83) and 1-year test-retest (r=.81) reliabilities (Willcutt et al. 2010b). In that study RDQ showed high correlations with a range of objective reading and spelling measures (overall r=.64; CI:.60 to .68) but low correlations with measures of other learning difficulties (r=.07–.024), attesting to its good criterion and discriminant validity (Willcutt et al. 2010b). In our sample (using data collected as part of the TEDS project, Trouton et al. 2002), the RDQ showed similarly high correlations with a measure of word reading efficiency (r=−.63, p<.001, N=301, unpublished observations; Test of word reading efficiency, Torgesen et al. 1999) and teacher ratings for reading attainment (r=−.58, p<.001, N=975; unpublished observations). Moreover, RDQ scores have shown high heritability (h2=53% to 83%) and high genetic correlations (−.71 to−.89) with a composite measure of reading performance (Astrom et al. 2009; Martin et al. 2006). Parent and teacher ratings of inattention and hyperactivity-impulsivity showed remarkably similar correlations with RDQ scores (inattention: parents:.41 (CI95:.37 to .46), teachers:.47 (CI95:.45 to .51); hyperactivity-impulsivity: parents:.22 (CI95:.17 to .23), teachers:.17 (CI95:.11 to .18)).


    Overview of the Twin Method In univariate analyses, correlations between members of a twin pair for each trait are used to apportion phenotypic variance to additive genetic (A), dominant genetic (D) or shared environment (C), and child-specific environment (E) components (which also subsumes measurement error) (Neale and Cardon 1992; Plomin et al. 2001). Based on the assumptions that (a) MZ twins are genetically identical and therefore share 100% of genetic variation, whereas DZ twins share, on average, 50% of their segregating alleles contributing to A and 25% contributing to D, and (b) both MZ and DZ pairs share 100% of their C but are discordant for E, the phenotypic variance for a trait is partitioned into constituent A, D or C and E influences. Greater phenotypic similarity between MZ twins compared to DZ twins suggests genetic influences on trait variance. If the phenotypic similarity of MZ twins is more than twice that of DZ twins, this suggests the presence of D, otherwise only A is suggested. DZ twin correlations greater than half the MZ twin correlations suggest the presence of C. The extent to which MZ twins are not 100% concordant for a trait reflects E (Rijsdijk and Sham 2002).Structural equation modelling provides a tool for the formal estimation of variance components (A, C/D and E parameters) and for testing alternative models describing possible component contributions to trait variance or covariance. When only twin pairs reared together are used, the available information allows the estimation of only a C or D component at a time. In multivariate genetic analyses, as well as partitioning the phenotypic variance of single traits, it is also the covariance between traits that is decomposed into A, C/D and E influences following exactly the same logic as above and using the ratio of MZ:DZ differences in cross-twin cross-trait correlations, (e.g. inattention symptoms in twin 1 with reading difficulties in twin 2) (Rijsdijk and Sham 2002).As multivariate models have increased power over univariate models (Schmitz et al. 1998), we do not present parameter estimates from univariate models. Univariate modelling was used to inform the choice of parameters for the multivariate models (e.g. the choice of C or D parameters) and to test for sex effects.

    Structural Equation Modelling Structural equation modelling was performed using Mx (Neale et al. 2003). Models were fitted to age- and sex-regressed standardized residual scores, which were logarithmically transformed to minimize skewness. All estimates are provided with 95% confidence intervals (the inclusion of zero indicates non-significance). The relative goodness of fit of the competing hierarchical (or nested) models was assessed using a likelihood ratio test. This was computed as the difference in the −2LL statistics of two models, which is distributed as a χ2 with degrees of freedom (df) equal to the difference in the parameters estimated with each model. A significant χ² suggests a significant deterioration in fit for the more constrained model; if the χ² is not significant, the model with the fewer parameters is preferred for being more parsimonious. In the case of multivariate genetic analyses with large samples, the χ2 difference from the saturated model is likely to be significant. In such cases, as well as when comparing models that are not nested, Akaike’s information criteria (AIC) can be used to assess the relative fit of models. The lowest AIC value indicates the best fitting model, given the data and the set of candidate models (Wagenmakers and Farrell 2004).

    Saturated Phenotypic Model This model fully describes the data using the maximum number of free parameters and provides a baseline comparison for subsequent genetic models. We constrained this model in accordance with the assumptions of the genetic method (that is, means and variances within traits and phenotypic correlations across traits were equated across twins in a pair and zygosity groups) to obtain phenotypic correlations representative of the whole sample while taking into account the non-independence of the data (i.e. data of related subjects).

    Sex Effects Qualitative sex differences are found where the nature of the A, C/D and E influences differs, i.e. different genes or different environmental influences underlie the variance in the trait for males and females. The data indicate quantitative sex differences if the magnitude of A, C/D and E influences underlying a trait are significantly different for males and females. Scalar sex differences are found where only unstandardized A, D/C and E estimates differ (but standardized estimates are the same), due to variance differences in the trait distribution between males and females. There were neither qualitative nor quantitative sex differences underlying the variance in traits, although scalar differences were observed for reading difficulties, and inattention and hyperactivity-impulsivity symptoms. Therefore, in the multivariate modelling male phenotypic variances for these traits were pre- and post-multiplied by a scaling factor. As there are no significant qualitative or quantitative differences in variance components between the sexes, MZ and DZ correlations are not presented for each sex. However, given the scalar differences between the sexes, means and standard deviations are broken down into sex- and zygosity-specific groups (Table 1).

    Table 1

    Table 1

    Cross-Twin Correlations (with 95% Confidence Intervals in Brackets) and Means (and Standard Deviations) for and Across IQ, Inattention, Hyperactivity-Impulsivity and Reading Difficulties Ratings

    Parameter Selection for the Multivariate Models In the univariate analyses, an ACE model provided the best fit for IQ, while ADE models (with scalar sex differences) fitted best for the remaining three phenotypes (as we would predict from the MZ:DZ ratios of cross-twin correlations for these traits, Table 1). In this study we were interested to assess the contribution of broad-sense shared genetic influences to the covariation between reading difficulties and inattention (that is, not distinguishing between A and D effects), and the extent to which they are independent from genetic effects also shared with IQ. Therefore, in the multivariate models we parsed the variance contributing to the covariation among the four phenotypes into A and E components, with A reflecting broad-sense genetic effects. Due to the lack of qualitative or quantitative sex differences in the univariate analyses beyond scalar differences, the computational intensity of modelling sex effects and additional power issues (Neale et al. 2006), only scalar differences between males and females were allowed in the multivariate models.

    Multivariate Genetic analyses A Cholesky triangular decomposition, which postulates a series of hierarchical genetic (A1–A4) and child-specific environment (E1–E4) factors, was used (Fig. 1). The order of the traits in the Cholesky model was decided a priori, with a view to estimating the aetiological influences that contribute to the covariance between reading difficulties and inattention symptoms independent of the other traits. A different ordering of the traits would produce the same fit of the model, but address different questions. The Cholesky model can be converted to the mathematically equivalent correlated factors solution (Fig. 2; Loehlin 1996), in which the order of traits is of no importance. This mathematical solution allows the estimation of the extent to which the same genes or environments contribute to the covariation between traits (i.e. the genetic and environmental correlations), irrespective of the extent to which they are shared with other traits in the model. For instance, in the Cholesky model, the proportion of the covariance between reading difficulties and inattention symptoms due to common genes (or environmental factors) which are not shared with hyperactivity-impulsivity symptoms and/or IQ can be estimated as the product of the paths linking these phenotypes with latent factor A3 and dividing by their covariance. In the same model, the proportion of the variance in reading difficulties which is not due to genetic (or environmental) effects shared with any of the other traits measured in this study is estimated by dividing the square of the path linking RDQ with latent genetic factor A4 by the variance in RDQ scores.Two additional multivariate models were employed to address the question of whether the covariance between the four traits in our study could be attributed to genetic and child-specific environment effects that are common to all, either directly (common factor, independent-pathway model, Fig. 3a), or through a common latent factor (common-factor, common-pathway model, Fig. 3b).

    Fig. 1

    Fig. 1

    Multivariate Cholesky triangular decomposition with unstandardized parameter estimates. The best-fitting ACE(IQ)-AE model is presented (for twin one only)

    Fig. 2

    Fig. 2

    Correlated factors solution of the best fitting ACE(IQ)-AE multivariate Cholesky decomposition model presented in Fig. 1 (for twin one only). Path estimates presented as square roots are the unstandardized parameter estimates (the basis of the …

    Fig. 3

    Fig. 3

    Illustration of the multivariate independent pathways (a) and common pathway (b) ACE(IQ)-AE models which were compared to the multivariate Cholesky model presented in Fig. 1


    •Aim 1: Are the phenotypic and genetic correlations between reading difficulties and ADHD inattention symptoms larger compared to hyperactivity-impulsivity symptoms?

    A medium phenotypic correlation between reading difficulties and inattention symptoms was observed, which was substantially and significantly higher than the correlation with hyperactivity-impulsivity symptoms (p1 SD) below those of their peers had normal reading scores at the post-kindergarten assessment. However, existing evidence suggests that reading difficulties in the context of inattention symptoms may not be caused by inadequate tutoring, given the failure of a behavioural intervention program to improve reading performance only in the comorbid cases (Rabiner and Malone 2004).

    The findings from the current study can only apply to reading difficulties and ADHD inattention symptoms as reflected in parent and teacher ratings; they cannot be extrapolated to any specific process in either domain. ADHD inattention ratings represent pervasive inattentiveness across different domains in real life over an extended period of time. Therefore our conclusions cannot be extended to any specific cognitive attention process, as overt behavioural problems cannot be linked in a simple and direct manner to possible underlying deficits in cognitive attention processes, while similar manifestations of inattention problems may reflect diverse cognitive deficits (Marzocchi et al. 2009; Warner-Rogers et al. 2000). Studies using specific cognitive attention measures may lead to different conclusions regarding the extent of shared aetiological influences with IQ, depending on what particular measure in used (Zumberge et al. 2007).

    It is important to understand the causal links between inattention problems or deficits in cognitive attention processes and the development of normal reading skills or the act of reading. Reading disability is a multifactorial disorder (Bosse et al. 2007; Vellutino et al. 2004), and for behavioural interventions to be effective they need to address the specific aetiological factors involved in each case (e.g. focusing on self-regulation versus targeting a specific neurocognitive process) (Rabiner and Malone 2004; Stage et al. 2003). Inattention is unlikely to be associated with reading difficulties only at the behavioural level and, in line with existing research, our findings are consistent with the idea that specific neurocognitive processes underlie the covariance between these two traits, which reflects shared genetic and child-specific environment influences that are largely independent from IQ. Indeed, cognitive attentional processes are being recognized as being involved in many stages of the reading process (Bosse et al. 2007; Reynolds and Besner 2006; Shaywitz and Shaywitz 2008; Vidyasagar and Pammer 2010). In the future we need evidence from longitudinal twin studies, measuring objectively a range of specific reading skills as well as of processes likely to contribute to behavioural inattention problems. Such studies will identify with greater specificity the neurocognitive processes that link behavioural inattention with deficits in specific reading skills, and examine causal relationships between these traits though development, as well as examine whether the contribution of IQ differs throughout development.


    The Study of Activity and Impulsivity Levels in children (SAIL) is funded by a project grant from the Wellcome Trust (GR070345MF). Yannis Paloyelis is supported by a studentship from the Medical Research Council. Thank you to all who make this research possible: the TEDS-SAIL families, who give their time and support so unstintingly; Rebecca Gibbs, Hannah Rogers, Eda Salih, Greer Swinard, Kate Lievesley, Kayley O’Flynn, Suzi Marquis and Rebecca Whittemore; and everyone on the TEDS team.

    Declaration of Interest None

    Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.


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  • Neural Plasticity and Proliferation in the Generation of Antidepressant Effects: Hippocampal Implication

    Fuencisla Pilar-Cuéllar,1,2 Rebeca Vidal,1,2 Alvaro Díaz,1,2 Elena Castro,1,2 Severiano dos Anjos,1,3 Jesús Pascual-Brazo,1,2,4 Raquel Linge,1,2 Veronica Vargas,1,2 Helena Blanco,1 Beatriz Martínez-Villayandre,1 Ángel Pazos,1,2 and Elsa M. Valdizán1,2,5

    1Departamento de Fisiología y Farmacología, Instituto de Biomedicina y Biotecnología de Cantabria (IBBTEC), Universidad de Cantabria-CSIC-IDICAN, Santander, Cantabria, Spain
    2Centro de Investigación Biomédica en Red de SaludMental (CIBERSAM), Instituto de Salud Carlos III, Santander, Cantabria, Spain
    3Stem Center, Clínica Palmaplanas, Camí dels Reis 308, Palma de Mallorca, Spain
    4The Research Group for Neurobiology and Gene Therapy, KU Leuven, Leuven, Belgium
    5Department of Physiology and Pharmacology, School of Medicine, Cardenal Herrera Oria s/n, University of Cantabria 39011 Santander, Spain
    Received 4 March 2013; Revised 1 May 2013; Accepted 8 May 2013
    Academic Editor: Chitra D. Mandyam

    Copyright © 2013 Fuencisla Pilar-Cuéllar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


    It is widely accepted that changes underlying depression and antidepressant-like effects involve not only alterations in the levels of neurotransmitters as monoamines and their receptors in the brain, but also structural and functional changes far beyond. During the last two decades, emerging theories are providing new explanations about the neurobiology of depression and the mechanism of action of antidepressant strategies based on cellular changes at the CNS level. The neurotrophic/plasticity hypothesis of depression, proposed more than a decade ago, is now supported by multiple basic and clinical studies focused on the role of intracellular-signalling cascades that govern neural proliferation and plasticity. Herein, we review the state-of-the-art of the changes in these signalling pathways which appear to underlie both depressive disorders and antidepressant actions. We will especially focus on the hippocampal cellularity and plasticity modulation by serotonin, trophic factors as brain-derived neurotrophic factor (BDNF), and vascular endothelial growth factor (VEGF) through intracellular signalling pathways—cAMP, Wnt/β-catenin, and mTOR. Connecting the classic monoaminergic hypothesis with proliferation/neuroplasticity-related evidence is an appealing and comprehensive attempt for improving our knowledge about the neurobiological events leading to depression and associated to antidepressant therapies.

    As indicated in this review, the importance of either proliferation or plasticity, or both, is still a matter of debate. As the involvement of proliferation and plasticity has been mainly studied in hippocampus, we might be underestimating its role in the antidepressant effect. In this sense, as the hippocampus is responsible for the learning and cognition part of the depressive disorder, the fact that the impairment of hippocampal proliferation would not block the antidepressant effect of some drugs does not necessarily conclude that the proliferation is only dependent on hippocampus. In the last years, prefrontal cortex, a structure with a great importance in mood control and working memory, is gaining increasing relevance in the plastic changes linked to antidepressant effects promoted by drugs as ketamine. In this sense, hippocampal proliferation would be only a small part of the plastic changes that are taking place within the hippocampus, and other brain areas. Thus, we must not underestimate the implication of synaptic plasticity in those antidepressant treatments that are not accompanied with increased proliferation.

    You are encouraged to share the research you find which refutes these arguments. Thank you

  • Beyond fascinating. These processes and activities and cellular formation that make us who we are and which I rarely think about are magnificent.

    The behavioral effects of antidepressants in animal models of depression and the therapeutic effects in humans typically take several weeks to develop. Upregulation of BDNF expression and enhanced TrkB receptor signaling in the dentate gyrus, hippocampus, and cortex is implicated in the mechanism of action of antidepressant drugs such as the selective serotonin reuptake inhibitors (SSRIs). While BDNF has diverse functions, it is commonly thought that TrkB signaling during antidepressant treatment promotes or restores plasticity in affected circuits through regulation of gene expression (Castren et al. 2006; Dagestad et al. 2006). As discussed, Arc has been identified as a critical effector gene for BDNF in the context of BDNF-induced LTP in the dentate gyrus. Several studies have reported upregulation of Arc in forebrain structures in which TrkB signaling is enhanced by antidepressants (Pei et al. 2003; Alme et al. 2007; Larsen et al. 2007; Molteni et al. 2008). A recent microarray study further identified a panel of nine genes that are strongly upregulated with Arc during BDNF-LTP and HFS-LTP in the dentate gyrus and five genes selected for validation by RT-PCR and in situ hybridization were confirmed upregulated in dentate granule cells (Wibrand et al. 2006). The gene set includes several genes with known synaptic roles, such as neuronal activity-regulated pentraxin (Narp) and neuritin. Interestingly, the BDNF-regulated genes exhibited a region-specific pattern of upregulation in the prefrontal cortex, hippocampus, and dentate gyrus, after chronic (but not acute) treatment with the SSRI fluoxetine (Alme et al. 2007).

    Exp Brain Res. 2010 Jan; 200(2): 125–140.

    Published online 2009 Aug 19. doi: 10.1007/s00221-009-1959-2

  • Pirta Hotulainen, PhD
    Project leader
    P.O. Box 56, FI-00014 University of Helsinki
    Phone: 57606 (internal), +358 50 415 6606
    Email: pirta.hotulainen at

    I wouldn’t mind doing some research with Ms. HOTullainen

    The human brain consists of hundred billion neurons interconnected into functional neuronal circuits that underlie all our behaviors, thoughts, emotions, dreams and memories. The capacity of neurons to function within neuronal circuits is mediated via specialized cell junctions called synapses. Chemical synapses regulate the electric communication within neural networks and pass information directly from presynaptic axon terminals to postsynaptic dendritic regions. Precise control of the development and connectivity of synapses is critical for accurate neural network activity and normal brain function. Most excitatory synapses in the mammalian brain are formed at tiny dendritic protrusions, named dendritic spines (Bourne and Harris, 2008). Experimental evidence has shown that changes in spine morphology account for functional differences at the synaptic level (Kasai et al., 2003; Yuste and Bonhoeffer, 2001). It is now widely believed that information in the brain can be stored by strengthening or weakening existing synapses, as well as appearance or disappearance of dendritic spines, which subsequently leads to the formation or elimination of synapses. These functional and structural changes at spines and synapses are believed to be the basis of learning and memory in the brain (Kasai et al., 2010). During the last decade, numerous studies on signaling pathways demonstrated that the actin cytoskeleton plays a pivotal role in the formation and elimination, motility and stability, and size and shape of dendritic spines (reviewed in Hotulainen and Hoogenraad, 2010). In addition, modulation of actin dynamics drives the morphological changes in dendritic spines that are associated with alteration in synaptic strength (Cingolani and Goda, 2008). It has also been shown that various memory disorders involve defects in the regulation of the actin cytoskeleton (Newey et al., 2005).

    The main goal of our group is to elucidate the mechanisms of actin cytoskeleton regulation in dendritic spines and to reveal how regulation of cytoskeletal dynamics affects dendritic spine development, morphology and plasticity. Currently, we are studying the regulation of dendritic spine structural and functional plasticity from three different aspects. First, we are studying the roles of different actin-binding proteins. Second, we are studying the effects of a novel mechanism of actin regulation -actin phosphorylation. Third, we are studying the effects of intracellular pH. We have already shown that these regulatory mechanisms affect the actin treadmilling rate. Next, we will examine how that affects dendritic spine morphology, motility and synapse function. As model systems, we use cultured rat primary hippocampal neurons and living mice or rats. Spine morphology and motility, as well as actin dynamics in spines, are analyzed by using various microscopy techniques. In addition, we use electrophysiological approaches to study the role of actin regulation in neuron function. These studies will result in a comprehensive understanding on regulation of dendritic spine structural plasticity. This knowledge is fundamental in understanding cognitive processes such as learning as well as neurological diseases.

  • start here

    PMID: 15738959 [PubMed – indexed for MEDLINE]

    The chemical hypothesis of depression suggests that mood disorders are caused by a chemical imbalance in the brain, which can be corrected by antidepressant drugs. However, recent evidence indicates that problems in information processing within neural networks, rather than changes in chemical balance, might underlie depression, and that antidepressant drugs induce plastic changes in neuronal connectivity, which gradually lead to improvements in neuronal information processing and recovery of mood.

    Have you read much of the research of E Castrén and his group? Pretty interesting dude.

    Antidepressants protect against hippocampal volume loss in humans and reverse stress-induced atrophic changes in animals thus supporting the hypothesis that the pathophysiology of stress-related disorders such as depression involves reductions in neuronal connectivity and this effect is reversible by antidepressant treatment. However, it is unclear which brain areas demonstrate such alterations in plasticity in response to antidepressant treatment. The aim of the present study was to examine the effect of antidepressant treatment on the expression of three plasticity-associated marker proteins, the polysialylated form of nerve cell adhesion molecule (PSA-NCAM), phosphorylated cyclic-AMP response element binding protein (pCREB) and growth-associated protein 43 (GAP-43), in the rat brain. To this end, rats were treated either acutely (60 min) or chronically (21 days) with imipramine (30 and 15 mg/kg, respectively) and the expression of PSA-NCAM, pCREB, and GAP-43 was assessed using immunohistochemistry. Initial mapping revealed that chronic imipramine treatment increased expression of these plasticity-associated proteins in the hippocampus, medial prefrontal cortex and piriform cortex but not in the other brain regions examined. Since PSA-NCAM and pCREB are expressed in recently-generated neurons in the dentate gyrus, it is likely that chronic imipramine treatment increased their expression in the hippocampus at least partially by increasing neurogenesis. In contrast, since chronic imipramine treatment is not associated with neurogenesis in the medial prefrontal cortex, increased expression of PSA-NCAM and pCREB in the prelimbic cortex implicates changes in synaptic connectivity in this brain region. Acute treatment with imipramine increased the number of pCREB positive nuclei in the hippocampus and the prefrontal cortex but did not alter expression of GAP-43 or PSA-NCAM in any of the brain regions examined. Taken together, the results of the present study suggest that antidepressant treatment increases synaptic plasticity and connectivity in brain regions associated with mood disorders. E Castrén

    Eero Castrén group
    Induction of neuronal plasticity the adult brain: mechanisms and applications
    Eero Castrén
    Professor, Director
    P.O. Box 56, FI-00014 University of Helsinki
    Phone: 57626 (internal), +358 50 5207974
    E-mail: eero.castren at

    Our lab is investigating the role of neurotrophic factors and their receptors on neuronal plasticity and drug responses in adult brain. We have found that antidepressant drugs reactivate a developmental-like plasticity in the adult brain in rodents and we have coned this phenomenon iPlasticity. We first found that fluoxetine, a widely prescribed antidepressant drug, induces critical period-like plasticity in the adult rat visual cortex and brings about a recovery of vision in an amblyopic eye, when drug treatment is combined with patching of the healthy eye. We subsequently showed that fluoxetine treatment induces juvenile-like plasticity also in the amygdala, which may explain the enhanced effect of combined antidepressant drug treatment and psychotherapy in the treatment of traumatic memories. In iPlasticity, drugs have no functional effects of their own, but by inducing plasticity they promote the effects of rehabilitation and psychotherapy. We have shown that signaling of the neurotrophin BDNF (brain-derived neurotrophic factor) and its receptor TrkB is required and sufficient for iPlasticity and that several other drug classes also activate TrkB signaling. We are now focusing on the neuronal and molecular mechanisms underlying iPlasticity and investigating how adult plasticity could promote recovery in a variety of neuronal disorders. The lab is supported by the European Research Council Advanced investigator award and grants from Sigrid Jusélius Foundation and Academy of Finland.

  • If the product doesn’t work, it won’t be viable, economically. It will be replaced. If the product isn’t safe, the company and the doctors may be exposed to law suits and ruined reputations. If doctors receive enough negative feedback from their patients about their meds, they better stop prescribing them or they will be sued out of business or lose their customer base.

    Free markets. We have the greatest heath care industry in the world, by far. No other nation compares. Competition weeds out companies that don’t produce a better product at a better price. Notice Toyota is the worlds largest car maker, again.

    Hyundai-Kia is bigger than Chrysler and Ford. So is Volkswagen.

    If a doctor screws over her patients, they can and do move on. What, we have around 700,000 M.D.s in the U.S.?

    If drug companies don’t manufacture drugs that offer relief, or otherwise do what they publish they will do, they will go bye-bye, or lose market share. Plenty of hungry businesses out there vying for more customers.

    Lawyers love big pharmaceuticals, too. Love. They have a way of pressuring them to behave. The government dose, too, and they work with private sector lawyers to protect consumers. Look at TAP, for example.

    Have the abused by psychiatrists/psychiatric meds ever filed a class action?

  • “I also noticed that since I started taking photos, my ability to write has seriously declined. I find it very hard to write anything and writing this has taken a long time.”

    Ms. Goldstein, may I make a suggestion, if you don’t mind? If you are correct, if there is an inverse relationship between your taking photos and your diminished capacity to write, please, please take photos all day and night, 365, with one exception. Take breaks from photography when you are absolutely positive your writing skills are at an all time low or completely gone. Then, take some time to write.

    If what you’ve written here is an example how photography is destroying your talent for writing, you’ve got to do more work with your camera.

    With your second posted picture you captured the path I imagine after I die and am on my way, strolling along, to heaven.

    The last picture catches what occurs while on my trek to heaven, it suddenly bursts into view. Silent. Stunning. Lush. Indescribable. Overwhelming, piercingly beautiful, heaven.

    Thanks for touching my heart today

  • “True, the drugs seem to be helpful short-term…” Gilbert

    “you are aware that stimulants cause a manic reaction…” AA

    My ability to sustain my attention is good (a miracle) and has been ever since I started taking my meds years ago without increasing the dosage.

  • psychiatry created the eugenics theories that led to the Nazi Holocaust after psychiatrists practiced by gassing to death those they stigmatized as “mentally ill.”

    Well Donna, I don’t think we should be too concerned that we are going to be gassed by Dr. Hallowell or Dr. Ratey. Besides, I think our government officials would be at much greater risk if a new wave of persecutions targeted the mentally ill.

  • Robert Berezin, MD

    Psychiatrist and author of Psychotherapy of Character:
    The Play of Consciousness in the Theater of the Brain

    Robert Berezin says:

    December 19, 2014 at 5:18 pm

    “We may not be as far apart as it seems. I certainly judiciously use, anti-psychotics for schizophrenia and manic depression, both in the context of real psychotherapy. Where I absolutely disagree is that I find no place, and no use for antidepressants at all – either in manic-depression or any other depression. These patients can be reached in a real way in therapy, always. I continue to suggest my book to have a fuller context for my position. Then I’d be happy to discuss.”

    Dr., did I misunderstand your comments here?

  • “I suppose the comment from “a Dad” was supposed to be scientific evidence of that poor kid being destroyed…”

    I don’t think the dad was promoting a scientific fact. I think he was expressing his opinion about the healthcare his son was receiving and his pleasure that the child was doing much better. He seemed to be grateful that his son was getting a real shot to live a full life.

    I think his question was a good one and I haven’t seen a scientifically established answer to it either way. The diagnostic criteria has recently expanded to include children as young as 4 for ADHD. I don’t know why children cannot be afflicted with various kinds of illnesses. Apparently, 4 years of age is the cutoff for Bipolar.

    “I certainly judiciously use, anti-psychotics for schizophrenia and manic depression, both in the context of real psychotherapy” Dr. Berezin

    Dr. Berezin, do you or would you include 4 year olds among the patients you treat for Bipolar or Manic Depression?

  • Pretty first name, Emmeline. Any relation to Margaret? She was an incredible person.
    You said, “The arguments here are somewhat one-sided in the sense that what we’re trying to offer on this site is a counterbalance to the monolith of mainstream perspectives on psychiatry. That ground is more than sufficiently covered elsewhere — in fact it’s pretty much all you can find elsewhere — what we’re presenting is an alternate, more critical view.”

    Ms. Mead, Have you read an article in a newspaper or seen on television a segment of a show or an entire program featuring the wonders of a drug that has helped turn around a failing student into a thriving, happy student?

  • I can understand how disorienting and off-putting these conversations might feel for you. After all, you’re encountering a new and unfamiliar perspective that calls into question everything you know.

    I am familiar with their perspective.

    Meanwhile you’re trying to share your own perspective, but it isn’t a new one for the people you’re conversing with — they’re already familiar with it, and have strenuously rejected it.

    Are you sure all the other participants reject my perspective? Is it a requirement for posting that you must agree with me? If so, I wasn’t aware of it and I apologize. Maybe it would make sense to reconsider what I am saying. Science is always about learning more.

    I am calm and objective. If my experience has been different than most, are you suggesting it is better not to express it? I haven’t been presented with a reason to reject as unscientific even one of my opinions, yet, though I ask for proof that others are right or that I am. The oft repeated refrain that junk science is my foundation, I have not concluded the same about anyone else.

    Would you prefer that I stop sharing my opinions?

  • This barrage of accusations, the contempt for this breakthrough diagnosis and treatment, the cutting insults, feels like a tsunami without warning breaking over my self-esteem and new life of possibilities in churning waves of hatred. And medical experts lead the way.

    Somehow, I have become the enemy. My doctors are compared to Nazi war criminals who use me and everyone else they can for their selfish gain. If that isn’t bad enough, it turns out that as a duped believer in the myth of junk science, I too am just as guilty. I’m a Nazi. We abuse others. We sell drugs. My team, it turns out, is a cartel, a real cartel.

    We are from that school of medicine that cut off brains for bucks. When drugs came along, we saw the money making potential, so we dropped the lobotomy business and started pushing drugs. Now, I and my partners drug little kids. We make them docile puppets; we make them behave and all the bad parents and nasty teachers love us. We want to stifle creativity. We sell the idea that drugs are all you need.

    Meanwhile, unaware how diabolical I’ve become, for the first time in my life, I follow what the newsman reports. I hear every word he said. For three minutes.

  • “The chemical hypothesis of depression suggests that mood disorders are caused by a chemical imbalance in the brain, which can be corrected by antidepressant drugs. However, recent evidence indicates that problems in information processing within neural networks, rather than changes in chemical balance, might underlie depression, and that antidepressant drugs induce plastic changes in neuronal connectivity, which gradually lead to improvements in neuronal information processing and recovery of mood”

    But the antidepressants are credited with generating plasticity in the neuronal pathways which leads to mood improvement. It is a chemically induced modification of the brain! BTW, the results suggest a different application may be involved.

  • New York Times

    “A recent groundbreaking brain-imaging study found that children with attention-deficit hyperactivity disorder experience a development delay with a distinct biological basis. Investigators at the National Institute of Mental Health discovered that areas of the brain’s cortex undergo a thinning maturation process about three years later in children with A.D.H.D. than in those without the condition. Areas that integrate sensory information with executive functions like focused attention, remembering things from moment to moment and controlling movement — functions that are often compromised in people with A.D.H.D. — showed the longest lag time.

    The results of the study support the belief that A.D.H.D. is a delay in a normal pattern of development, rather than a deficit that completely derails development — a longstanding debate in A.D.H.D. research. Yet despite M.R.I. images showing biological brain differences in children with A.D.H.D., news of the findings immediately tapped into a wellspring of skepticism about the legitimacy of the condition. Web sites were inundated with postings that A.D.H.D. is “just a delay,” that kids diagnosed with the condition are actually “normal” after all, that it’s perverse to medicate children for something that “most” will outgrow.

    Estimated to affect millions of Americans — 3 percent to 7 percent of children and more than 4 percent of adults — A.D.H.D. has traveled an extraordinary arc of clinical and public opinion over the last four decades. What began as a relatively unknown disorder became broadly recognized as one of the most common psychiatric problems in children and an increasingly major consideration in adult psychiatric diagnoses as well.

    Yet even as a mountain of research confirms the disorder’s biological and genetic basis, the impulse to deny A.D.H.D.’s legitimacy persists. “It’s always generated by this underlying skepticism, this feeling that, ‘Come on, all these kids need is a kick in the pants; this is just an excuse for being lazy,’ ” said Dr. Edward M. Hallowell, author of the popular “Driven to Distraction” series of books on A.D.H.D. “Twenty-five years since I first learned about this condition, the subtext is still always there, and it’s always on the part of the people who know none of the science.”

    “Dr. Philip Shaw, the National Institute of Mental Health psychiatrist who led the imaging study, was surprised and dismayed to see the results taken up to bolster that brand of doubt. “The findings, if anything, are very good evidence of yet another major biological difference between kids with A.D.H.D. and typically developing children,” he said. “The study was very much a question about the biology of A.D.H.D., and I think the findings certainly would feed into the idea of A.D.H.D. as being a very real problem with a very clear biological basis.

    The notion of a delay also seems to have sown confusion about how often children actually outgrow A.D.H.D. In fact, the disorder persists into adulthood in a majority of cases, with hyperactivity and impulsivity generally waning while inattentiveness persists. The actual figures are widely debated, depending upon how restrictively A.D.H.D. symptoms in adults are defined.

    About a fifth of young adults still meet the strictest diagnostic criteria for A.D.H.D., Dr. Shaw said. But if you take a slightly broader definition, “about two-thirds to half of people still have a lot of problems stemming from their childhood A.D.H.D.,” he said, adding: “We were only looking at one of the first milestones of brain development. There are others to come, further down the line. And we know from a lot of other studies that teens with A.D.H.D. have very real differences in both brain function and structure.”

    Russell A. Barkley, author of “A.D.H.D. in Adults: What the Science Says,” believes that persistence may be even more common. “Between 14 and 35 percent of children will technically outgrow the disorder, falling within the normal range of behavior and impairments as adults,” Dr. Barkley said. “We have many studies showing the functional deficits in A.D.H.D. well into adulthood.”

    Dr. Shaw plans to continue imaging studies on both younger and older children. For now, he stresses that his findings mean children with A.D.H.D. face real challenges. “Just by underpinning that there is a very real biological difference, I hope it would add to the argument that kids with A.D.H.D. do often need adaptations to their learning environment to give them as good a chance as possible,” he said. “The priority still remains making sure your kid gets the best possible treatment and can realize their potential.” Publish date: 3/12/08

    After struggling for decades to try to survive in the real world of modern, technically advanced U.S. of A., the pieces of the puzzle finally come together with a diagnosis of and treatment for a disabling condition unbeknownst to you. “My gosh, you mean all this time this A.D.D. thing for kids, I’ve got? Impossible! But, I have all the characteristics. How can this be?” But sort of like the theory of quantum mechanics, it passes every test, it explains every thing that’s been inexplicable, up ’til now.”

    Wouldn’t you know, even as the reality of this damnable disorder really begins to sinks in, out there on the distant horizon a very vocal, but small minority, clamors unceasingly shouting at you at the top of their lungs that there is no such thing. You’ve got something that doesn’t exist.

    Lo and behold, you’ve been duped again. You are using a fictitious label to feel better. It gives you an excuse. It offers a cheap explanation why you have been such a doofus all your life. You like that, don’t you? Just blame everything on some poorly conceived ploy to make psychiatrists and the drug companies rich. Every study, every double blind, controlled test, every observed experiment, every SPECT scan, every PET scan, each MRI, is bull. Every doctor prescribing the cocaine to you is a drug dealer, a thug and crook. (All meds used to treat it are just some form of speed) Not one piece of real scientific data supports this crazy, concocted crap. You are a fan of those charlatans. You are just like them.

    But, I can read a book.

  • If it is sleep apnea, it is not ADHD. If it can be explained by anything other than ADHD, it is not ADHD. Onset begins by 7 years of age.

    Stimulants help people without attentional deficits to concentrate. The ability to pay attention runs along a continuum. Even those with severe ADHD pay attention on occasion and even Einstein couldn’t pay attention perfectly. Most can attend well enough to function without much difficulty. Those with ADHD do not and cannot fully tap the other mental skills we have, whether they are unexceptional or extraordinary.

    I like the eyeglasses analogy. You can be a genius but if you are legally blind or completely blind, without being aware of it and compensating for it with corrective lenses, or by becoming proficient in braille, reading is going to be tough! If you operate at about 100 FSIQ, same thing.

    Putting on a pair of corrective lenses that yields 20/20 vision, will rock your world. At the same time, glasses don’t teach you to read suddenly. Glasses don’t teach you how to identify mathematical terms, to be able to name the colors of the spectrum, to know what beauty is and what kind of impact it will have on your life. Yet, for the first time in your life, you can begin to learn all about everything you missed.

    And that is a reason to celebrate. That is a reason to feel grateful-for glasses/drugs. (If you stop wearing them after 14 months, don’t expect to keep reading. The silly study that recorded no additional gains in teens after they ceased taking their meds at 14 months, proves my point.)

    Then, you will meet people who will insist you can not see, or that you always could see, you just never knew. They will sneer and tell you your glasses are made by the Mafioso. They only want to rip you off. They charge too much and bribe optometrists and ophthalmologists to push their brand of eyewear. Glasses break, too, don’t forget. Kids have been blinded from sharp pieces of glass from busted glasses. But, the mob doesn’t care. All they want is your money. They don’t care if you stare at the sun with your glasses on! They don’t warn you you’ll burn your retinas right out of your head. They don’t tell you how hideous you’re going to appear to your friends and how your girlfriend will start heaving with one glimpse of your 4-eyed, ugly mug! O no! They just want your bread, man. No, you don’t want to go down that road of wearing glasses. Besides, only nerds wear glasses.

    In your heart you can only shout, I was blind but now I see!

  • “And the real experts” You mean other experts are not real? ” have exposed that any supposed differences” The experts don’t suppose.
    “in the brains” Pretty important organ. Unlike anything else on the face of the earth! Unreal, isn’t it? “of so called ADHD” It isn’t “so called” ADHD. If it were merely “so called”, your real experts wouldn’t identify it as that which exists only in the brains deformed by toxic drugs.
    “and normal kids are due to the toxic drugs” No data supports that belief. “given to those stuck with a junk science ADHD stigma” is circular reasoning. “due to abusive families, bullies and other social stressors and certainly not any faulty brains.” They, the ADHD labeled kids, are labeled that way because of abuse, but their brains show no signs of abnormality, except for what was caused by others who abused them for having ADHD which doesn’t exist.

    Thanks for your input. I don’t agree with you, but you are to be commended for your passionate defense of your views. Take care

  • “The real source of human suffering is not the brain. Suffering is the experience of a person, a human being, in the context of damage to his or her play of consciousness. This damage is the consequence of deprivation and abuse in our emotional environments during the formation of our personalities. This takes place in relation to the unique constellation of our temperaments.” Dr. Berezin

    Dr., I think I understand what you mean. However, if the brain itself is sick, the person will likely be sick, too.

    If I want to reflect on my childhood, I can cut my hand off and still think all I want to about my youth. Thinking doersn’t depend on my hand. If I remove my brain, well, thinking might not go too well. If my brain is not working properly, my mental state will suffer.

    You don’t entirely disagree with that position, either, do you? “I certainly judiciously use, anti-psychotics for schizophrenia and manic depression, both in the context of real psychotherapy” you said.

    How can it be that you would use drugs for those conditions but deny their usefulness in treating depression or ADHD?

    Thanks Dr.

  • “Human nature operates through our consciousness. The more we understand the workings of the mind, the more we come to understand that consciousness is organized in the brain as a play; as stories, with characters, feeling relationships between them, scenarios, plots, landscapes and set designs. We evolve our characters over the course of twenty or so years of child raising. The biology of the brain creates and informs our character as a whole. Parts of the brain — such as neurotransmitters and the various brain modules — do not operate independently. They operate as a whole to simply create the play of consciousness itself.” Dr. Berezin

    Neurotransmitters do not operate independently, in your opinion. But, do they operate perfectly? Is it your position, Dr., that neurotransmitters are not a part of human anatomy in some sense? Are there any other “modules” within the human body that behave like neurotransmitters, that is, as part of the whole without imperfection?

    These questions are intended for any MDs or PhDs not just the good doctor.

  • Dr. Brogan,

    Do you believe that ADHD not only doesn’t exist but that it cannot exist, it cannot ever be a real condition? ADHD, as defined, is impossible? The brain cannot “tune out”? That the brain cannot be distracted pathologically under any circumstances? That there is no such thing as deficits in “tuning in and tuning out” and there can be no such thing for any reason? And nothing like that could be corrected through any medicine, even if it did exist?

    Do you hold that every one can direct his attention exactly as he would like, all the time? Every one can adequately screen out extraneous signals? Every one can redirect his attention as needed–to zoom in and zoom out without any debilitating interference at all, ever?

    These questions go out to all of you doctors, not just Dr. Brogan. My questions are intended for all doctors, psychiatrists, psychologists, all the PhDs for that matter.

    I will assume that no answers would be a yes, that is your belief.
    Thank you

  • PD is caused by the progressive loss of dopamine brain cells (neurons) in a part of the brain called the substantia nigra, which produces the chemical dopamine.

    Despite intense research efforts around the world, the molecular causes of Parkinson’s disease are still unclear. What doctors and scientists do know is that PD is caused by the progressive loss of dopamine brain cells (neurons) in a part of the brain called the substantia nigra, which produces the chemical dopamine. As the cells die, less dopamine is produced and transported to the striatum, the area of the brain that co-ordinates movement

    The latest research suggests that dopamine, a neurotransmitter known to be important in the brain’s attending functions, is not responsible for ADHD. The cause appears to lie in the structure of the grey matter. ADHD sufferers have less of it than those without it.

  • What is so interesting about ADHD is the way those who are afflicted with deficits attending can hyper- focus on those things that stimulate their interest. Confounding is another appropriate term. Just the novelty of a first interview with a health care professional for an assessment often masks the ADHD. Novelty often triggers the attending “apparatus” in our brains.

    Considering the complexity of the human brain, it makes sense that it will not function perfectly at all times. Composed of roughly 1oo billion neurons, it is a marvel without competition. It is amazing that it works at all. It is susceptible to the full range of weaknesses, injuries, deformities, diseases, etc. common to the human condition. Even the blood brain barrier cannot protect the brain from all forms of assault. If it was capable of perfection, if everyone could pay attention perfectly, all the time, for example, we would be advanced beyond comprehension. Being flesh and blood, perfection isn’t possible. It would be nice! Don’t get me wrong.

  • “Unfortunately, the real, scientific studies do not support your claim. True, the drugs seem to be helpful short-term, in smaller doses than most psychiatrists prescribe; but over the long term the neuroleptics take away most peoples’ chances of living a rich and fulfilling life.” Mr. Gilbert

    Can you point to the sources for the opinions you have shared here?

    Hello Mr. Gilbert. I am still interested in your response. Thanks

  • “Unfortunately, the real, scientific studies do not support your claim. True, the drugs seem to be helpful short-term, in smaller doses than most psychiatrists prescribe; but over the long term the neuroleptics take away most peoples’ chances of living a rich and fulfilling life.” Mr. Gilbert

    Can you point to the sources for the opinions you have shared here? Thank you

  • These types of modern testing methods reveal brain function and differences on a scale unimaginable when Sir Alexander Crichton wrote about people lacking attending capacity in 1798.

    First, to differentiate between inattention and impulsivity based on type of errors made in the AX version of the Continuous Performance Task (CPT), and second, to investigate whether differences in performance between children with attention-deficit hyperactivity disorder (ADHD) and normal controls also occur in specific forms of brain activity, namely event-related potentials (ERPs), presumably related to inattention and impulsivity or inhibition.


    Sixteen ADHD and 16 normal control children performed the CPT-AX. ERPs were recorded at occipital (Oz), parietal (Pz), central (Cz), and frontal (Fz) leads.


    The ADHD children had a higher CPT-Inattention score and showed smaller parietal positive waves at a latency of approximately 300 msec in reaction to target stimuli, target P3s, likewise indicating less attention. In contrast, they showed neither higher CPT-Impulsivity nor a smaller frontocentral negative wave at about 200 msec (N2); the N2 is generally seen as reflecting inhibition. A subgroup of children with ADHD and oppositional defiant disorder (n = 6) had smaller N2 waves than controls, however.


    The ADHD group studied showed deficits in attention but not in impulsivity (or inhibition
    First, to differentiate between inattention and impulsivity based on type of errors made in the AX version of the Continuous Performance Task (CPT), and second, to investigate whether differences in performance between children with attention-deficit hyperactivity disorder (ADHD) and normal controls also occur in specific forms of brain activity, namely event-related potentials (ERPs), presumably related to inattention and impulsivity or inhibition.


    Sixteen ADHD and 16 normal control children performed the CPT-AX. ERPs were recorded at occipital (Oz), parietal (Pz), central (Cz), and frontal (Fz) leads.


    The ADHD children had a higher CPT-Inattention score and showed smaller parietal positive waves at a latency of approximately 300 msec in reaction to target stimuli, target P3s, likewise indicating less attention. In contrast, they showed neither higher CPT-Impulsivity nor a smaller frontocentral negative wave at about 200 msec (N2); the N2 is generally seen as reflecting inhibition. A subgroup of children with ADHD and oppositional defiant disorder (n = 6) had smaller N2 waves than controls, however.


    The ADHD group studied showed deficits in attention but not in impulsivity

    These tests confirm that the ADHD brain reacts to stimulus with less attending speed and energy than controls.

  • Event rate and event-related potentials in
    Roeljan Wiersema,
    Jaap van der Meere,
    Herbert Roeyers,
    Rudy Van Coster,
    and Dieter Baeyens
    Department of Experimental-Clinical and Health Psychology, Ghent University, Belgium;
    Department of Clinical
    and Developmental Psychology, Groningen University, The Netherlands;
    Department of Pediatrics and Medical
    Genetics, Ghent University, Belgium
    Background: It has been repeatedly found that performance of children with attention deficit hyper-
    activity disorder (ADHD) is more impaired when a long inter-stimulus interval (ISI) is used than when a
    short ISI is used. According to the cognitive-energetic model, this may reflect difficulty in remaining in
    an optimal motor activation state because of insufficient effort allocation. Method: Event-related
    potentials (ERPs) were evaluated during a Go/No-Go task that incorporates a condition with a fast and a slow presentation rate. Results: ADHD, whether or not comorbid with oppositional defiant/conduct disorder (ODD/CD), was associated with a steeper increase in reaction time (RT) from the fast to the slow condition accompanied by a missing increment of the parietal P3. Speed of responding was found to be correlated with P3 amplitude. In the fast condition, children with ADHD made more errors of commission, accompanied by a smaller No-Go N2, a component thought to be related to inhibition; however, after controlling for ODD/CD these differences disappeared. Conclusions: The association between the steeper increase in RT and reduced parietal P3s may indicate that the children with ADHD did not allocate enough extra effort to adjust to a potentially under-activated state. However, the event rate effects could not account for all of the differences between groups and also early automatic information processing stages seem disturbed in this disorder as indexed by larger P2 amplitudes.
    Alternative explanations are discussed. Keywords: ADHD, ODD/CD, ERP, event rate, effort, state
    In general, children with attention deficit hyper-
    activity disorder (ADHD; DSM-IV-TR, American
    Psychiatric Association, 2000) have been found to
    perform more poorly in conditions of relatively slow
    event rates as compared with fast and moderate
    event rates. This statement holds with respect to
    paired associate learning tests (Conte, Kinsbourne,
    Swanson, Zirk, & Samuels, 1986; Dalby, Kins-
    bourne, Swanson, & Sobol, 1977), memory re-
    cognition tests (Chee, Logan, Schachar, Lindsay, &
    Wachsmuth, 1989), the Computerized Matching
    Familiar Figure Test (Sonuga-Barke, 2002), Go/No-
    Go tests (Borger & van der Meere, 2000; Potgieter,
    Borger, van der Meere, & de Cock, 2000; van der
    Meere, Gunning, & Stemerdink, 1995), the Con-
    ners CPT (Purvis & Tannock, 2000), the CPT-A
    (Leung, Leung, & Tang, 2000), the stop task
    (Scheres, Oosterlaan, & Sergeant, 2001), and tap-
    ping tasks (Rubia, Taylor, Taylor, & Sergeant,
    1999). The typical slow and variable response style
    in ADHD, when stimuli are presented slowly, is a
    consistent finding in these studies, whereas with
    respect to errors of commission, the findings are
    mixed. Relative to controls, children with ADHD
    have been found to make more errors of commis-
    sion in the fast condition (Potgieter et al., 2000), in
    the slow condition (van der Meere et al., 1995), in
    both a fast and a slow condition compared to a
    medium condition (van der Meere, Vreeling, &
    Sergeant, 1992), or in neither one of the conditions
    (Borger & van der Meere, 2000; Scheres et al.,
    The finding that RT performance in children with
    ADHD is highly sensitive to presentation rate of
    stimuli has been explained by Sergeant, Oosterlaan,
    and van der Meere (1999) and by van der Meere
    (2005) in terms of the cognitive-energetic model of
    Sanders (1998). According to this model, event rate
    influences the motor activation level (tonic readiness
    to respond). Motor activation increases with an in-
    crease in presentation rate of stimuli, whereas a long
    inter-stimulus interval (ISI) may induce under-acti-
    vation. To compensate for a sub-optimal motor
    activation state, extra effort allocation is necessary.
    Consequently, the earlier mentioned RT findings
    may suggest that children with ADHD have difficulty
    in adjusting their under-activated state because of
    insufficient effort allocation.
    Borger and van der Meere (2000) underscored the
    idea that ADHD is associated with insufficient effort
    allocation and an under-activated motor state. They
    reported that children with ADHD showed decreased
    heart rate deceleration before onset of the Go
    stimulus in the slow condition but not in the fast
    condition, suggesting decreased motor activation in
    the slow condition. In addition, children with ADHD
    showed higher heart rate variability (HRV) in the
    slow condition only, suggesting less effort allocation.
    The major aim of the current study is to test
    whether children with ADHD do not allocate the
    Journal of Child Psychology and Psychiatry 47:6 (2006), pp 560–567 doi:10.1111/j.1469-7610.2005.01592.x
    Ó 2006 The Authors
    Journal compilation Ó 2006 Association for Child and Adolescent Mental Health.
    Published by Blackwell Publishing, 9600 Garsington Road, Oxford OX4 2DQ, UK and 350 Main Street, Malden, MA 02148, US

  • “this invented disorder created to drug children does not exist” Dr. Corrigan

    Pediatr Neonatol. 2012 Apr;53(2):118-24. doi: 10.1016/j.pedneo.2012.01.009. Epub 2012 Mar 2.

    Auditory event-related potentials in children with attention deficit hyperactivity disorder.

    Tsai ML1, Hung KL, Lu HH.

    Recording of event-related potentials (ERPs) from the scalp is a noninvasive technique reflecting the sensory and cognitive processes associated with attention tasks. Attention deficit hyperactivity disorder (ADHD) is a disorder involving deficits in attention and behavioral control. The aim of this study was to investigate the difference in ERPs between normal children and those with ADHD.


    We examined 50 children with ADHD and 51 age-matched controls. All children with ADHD met the full criteria for ADHD according to Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV). The auditory oddball paradigm was applied, and event-related long-latency components (N1, P2, N2 and P3) from Fz, Cz and Pz were measured in each test subject.


    Children with ADHD showed a significantly longer latency and a lower amplitude of P3 compared to normal control children (p < 0.01). Delayed N2 latency at the Pz electrode was shown in children with ADHD compared to normal controls (p 10 years of age (p < 0.05).


    We found that the endogenous ERPs (P3 and N2) were significantly affected in children with ADHD, compared to exogenous ERPs (N1 and P2). Increased latency of P3 suggests a slower processing speed, and decreased P3 amplitude is interpreted as disruption of inhibitory control in children with ADHD. These results indicate a neurocognitive abnormality in ADHD, as presented by a reduction in ERP response.

    Copyright © 2012. Published by Elsevier B.V.

  • “Beyond just describing how all kids behave while they are learning to be good students and responsible, polite adults…” Dr. Corrigan

    Dr., forgive me. I quote this older comment you made in this thread because I am unsure whether you would see my response on the original thread.

    I think and hope what I have to say to you is worthwhile. You are a sincere man. Your arguments are heartfelt. You draw out of me, and others undoubtedly, a deep desire to clarify issues surrounding ADHD. I will begin by being brief. Your statement above is representative, a fine example of the paradox we face with ADHD in so many ways.

    The symptoms described in the literature that define ADHD are like just like what everyone experiences… True. Undeniable. Plain and simple. So simple it is a wonder advocates for the diagnosis can be so blind! Well, sort of.

    Ahh! But, let’s take a closer look. This is the point where much confusion starts. You say in essence, kids are kids, “…all kids behave while they are learning…” In other words, it is normal for children to lose stuff, to get sidetracked, to be restless, etc. as they progress through school. So, why are those kinds of normal behaviors so sick, so disruptive, so difficult to manage that medication becomes necessary for a bunch of kids? Again, closer. Look closer, “just describing how all kids behave while they are learning to be good students and responsible, polite adults…”

    Do you see it? The key: to meet the conditions of the ADHD diagnosis requires that those very “symptoms” behaviors occur so frequently and are so severe that the progression through school–learning to be a good student, learning to be responsible, learning to be a polite adult, etc. does not happen! Not as it does for most kids. The normal progression is interrupted. That is the difference. ADHD prevents it. It interferes with it, to the point where the person is handicapped. He cannot will himself to do better, and his best, depending on the severity of his ADHD, holds him back significantly. It harms him- educationally, socially, with self-esteem. He is injured even as he faces common daily challenges. He tries to function like the other kids but with an unseen disadvantage as real as if he were blind. That is the difference between the child who screws up like all normal kids do and the child with ADHD.

  • “The American public has come to view ADHD drug treatment as a rather benign option for common behavioral and academic issues.” Dr. Watson
    That is hard to imagine given the uproar by some who believe it is a dangerous drug pushed on our youth by big business.

    “By most any reasonable measure, the number of children who are medicated under the guise of ADHD is out of bounds. Current levels of ADHD drug treatment are unsafe for individuals and society.” Dr. Watson
    Let’s say that is true. Do we therefore deny ADHD exists? Even if it is terribly over diagnosed, should we therefore conclude that it must not be real and debilitating for some?

    “The more a drug is prescribed, the more it will be diverted for illicit purposes.” Dr. Watson
    Which is not a reason to deny the RX for those who need it, is it?

    “Too few of the professionals who have issued lax ADHD diagnoses or overprescribed drugs for the condition realize that better and safer options exist”
    Dr., would you list those options, please, or tell me where to find them? Thank you

    “The truth is that the MTA study actually provided evidence to consider behavioral interventions — not drug therapy — as the first line of defense. As reviewed by Dr. William Pelham, a clinical psychologist who was one of the MTA researchers”

    “The Effectiveness of Short- and Long-Acting Stimulant Medications for Adolescents With ADHD in a Naturalistic Secondary School Setting”

    Dr. Pelham has been recognized by Divisions 53 and 37 of the APA and by CHADD as a model program

    Dr. Pelham disclosed that Abbott Labs contributed financially to this study

    Existing studies demonstrate that medication delivered in analogue settings clearly produces an acute effect on teen academics (Evans et al., 2001) and disruptive behavior (Smith et al., 1998). Parents also report that stimulant medication produces improvements in their adolescents’ ADHD symptoms (Fin­dling et al., 2011). These studies establish the efficacy of stimulant medication for teens

    Primary findings of this study are as follows: (a) short-acting MPH, but not long-acting pemoline, led to statisti­cally significant improvements in ADHD symptoms
    Other treatments, including individual counseling, play therapy, dietary interventions, treatment for inner ear problems, neurofeedback/biofeedback, perceptual-motor training, sensory integration training, chiropractic manipulation, pet therapy and others have no proven efficacy for ADHD.

  • A dad wrote,
    “I hope that the legitimate questions about reporting potential conflicts of interest does not obscure the fact that young children can exhibit Bipolar disorder symptoms and that medications can help. Our youngest son was diagnosed with ADHD and then bipolar after he was hospitalized just prior to his 4th birthday. Medications have helped tremendously (though not completely) to give him a chance at a normal life. If other diseases can develop at a young age, why not psychiatric disorders? Just because it has not been in standard lexicon in the past doesn’t mean that it is not legitimate. Running clinical trials on children is notoriously complicated, so I would take criticism of small studies (referring to Biederman) with a grain of salt. Large studies on every group of children would be welcome, but quite difficult. In the meantime, children like my son are able to lead more stable lives that are less harmful to themselves and others.”

    Westinghouse wanted to exploit the potential benefits of modern electricity production. Tesla invented and tested alternating current which he believed to be far superior to Edison’s DC. Westinghouse backed Tesla financially. His revolutionary concept with the support of Westinghouse changed the world.

    Although “drug” companies finance the production and testing of their experimental chemical compounds through well known medical professionals, it does not follow that they therefor produce an inferior therapeutic. Remember something important here: they want the same thing. If the product doesn’t work, it won’t be viable, economically. If the product isn’t safe, the company and the doctors may be exposed to law suits and ruined reputations. If doctors receive enough negative feedback from their patients, they will stop prescribing those drugs.

    Gary Null, personally, is being sued by consumers of his products even as he is suing his supplier.

  • “even the fictitious ADHD – are ‘illnesses’ that should be treated with pharmaceuticals such as antidepressants, benzodiazepines, anti-psychotics, and amphetamines.” Dr. Berezin

    Dr., then what is ADHD? If it is a fictitious illness, then how should it be classified? Or, are you saying that what is described as symptomatic of ADHD is really nothing at all? Nothing more than typical behavior from normal young boys with lots of energy? Do you believe that everyone has sufficient capacity “to attend to” and that any depiction of attentional deficits is bogus?

  • Can you explain what a power-based clinical relationship is? Thank you. When you say profit-driven, does that include the selling of books written by mental health professionals?

    I was asking Alex, so I’m hoping to hear from him. Thanks for your opinion. Would you confirm your claims with specific, documented examples if you get a chance? Thanks.

    “As long as ‘mental health practices’ are profit-driven” Which practices are profit driven? Considering the average indebtedness in 2012 for a medical school graduate ranged between $170,000 and $190,000, practicing medicine better generate some serious income.

  • “shine a light on the atrocities”

    Which atrocities, precisely- and committed by whom, other than Biederman, exactly?

    Biederman withheld financial information. What atrocity did he perpetrate on hundreds of people?

    “criminal offenses which led to harm of hundreds” Do we know who these hundreds are? Do we have their names and verified proof of the causes and nature of the harmful atrocities they suffered? If not, how do we know they were the victims of criminal offenses? Without specific answers to these kinds of questions, I am afraid it is all just bluster, nothing more.

    “Now, the real heroes expose the lies of the psycopharmaceutical industrial complex and shine a light on the atrocities that psychiatry continues to perpetrate under the guise of “treatment” and “medicine.”

  • Being laughed at, being called names like “big dummy”, repeated failures, not knowing what someone just told you (over and over again while you look them in the eye and nod your head at the appropriate inflection or pause-faking attention all your life, hoping to fool people into believing you are hearing what they are saying, hoping you can hear them, not knowing why you can’t except you do know you are a god damned son of a bitch lazy kid), not knowing where to go, what to do next, even when instructed several times in plain English, and on and on every hour, every day, week, month, year, at home, school, on the ball field, on and on and on

    That is hell, too

  • Frieda Fromm-Reichmann is gone, but her legend lives on and on. Joanne Greenberg was a fortunate patient and Dr. Frieda was fortunate, also. Fortunate that in Joanne she found a bright, witty, well read young lady with a passion for life. Many of her patients were older and lacked Joanne’s zest for life.

    If Dr. Frieda had not been Joanne’s therapist, she may have remained sick. Today, with the help of modern science’s most advanced medicine, someone like her, without the intervention of a Dr. F., still might enjoy a measure of mental health undreamed of just a century ago.

    I don’t think talk therapy, human relationships, unconditional love, skilled and devoted health care professional/loved ones on the one hand and drug therapy on the other are necessarily mutually exclusive.

  • To me, it is somewhat surprising that protecting air quality, and cleaning and purifying the dangerous, toxic, filthy dirty air we inhale and send into our bodies all day, doesn’t seem to attract as much attention as a key factor in overall healthy living as food products do. Billions of tons of industrial byproducts spew into our precious layer of air every year, year after year, decade after decade. Have you ever seen billions and billions of tons of noxious fumes?

    The EPA requires woodstove manufactures to meet certain output standards primarily through the use of catalytic combustors. They function using the same principle as car catalytic converters, I think. They ignite and more thoroughly burn the emissions from a wood fire.

    Sorry, but I love the smell of a nice wood fire.

  • Joe Kennedy decided to have the procedure done on his oldest daughter, Rosemary. It was an utter disaster. He’d made the decision to do so based on what he thought was expert, sound and informed medical advice.

    She had been responding well to regular injections of “Endocrines” recommended by Dr. Charles Lawrence, chief endocrinologist at the New England Medical Center.

  • Starry, starry night
    Paint your palette blue and gray
    Look out on a summer’s day
    With eyes that know the darkness in my soul

    Shadows on the hills
    Sketch the trees and the daffodils
    Catch the breeze and the winter chills
    In colors on the snowy linen land

    Now I understand
    What you tried to say to me
    And how you suffered for your sanity
    And how you tried to set them free

    They would not listen, they did not know how
    Perhaps they’ll listen now

    Starry, starry night
    Flaming flowers that brightly blaze
    Swirling clouds in violet haze
    Reflect in Vincent’s eyes of china blue

    Colors changing hue
    Morning fields of amber grain
    Weathered faces lined in pain
    Are soothed beneath the artist’s loving hand

    Now I understand
    What you tried to say to me
    And how you suffered for your sanity
    And how you tried to set them free

    They would not listen, they did not know how
    Perhaps they’ll listen now

    For they could not love you
    But still your love was true
    And when no hope was left in sight
    On that starry, starry night

    You took your life, as lovers often do
    But I could’ve told you Vincent
    This world was never meant for
    One as beautiful as you

    Starry, starry night
    Portraits hung in empty halls
    Frame-less heads on nameless walls
    With eyes that watch the world and can’t forget

    Like the strangers that you’ve met
    The ragged men in ragged clothes
    The silver thorn of bloody rose
    Lie crushed and broken on the virgin snow

    Now I think I know
    What you tried to say to me
    And how you suffered for your sanity
    And how you tried to set them free

    They would not listen, they’re not listening still
    Perhaps they never will