Adult Attention Deficit Disorder
RESOURCES FOR UNDERSTANDING ADULT ATTENTION DEFICIT DISORDER
-- Updated January 4, 2012 --

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    The mission of this page is to provide you with latest and best information about Adult Attention Deficit Disorder (Adult ADD).

    If you have been dealing with the challenges of ADD, this information, presented this way, will turn a light on for you. This website and Dr. Sterling's book have already been called "game changers." They are written as much for non-ADDers as they are for ADDers.

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The Short Story About Adult Attention Deficit Hyperactivity Disorder  (updated 1/06/2011)  [Back to Index]

    Attention Deficit Disorder (ADD) is technically called Attention Deficit Hyperactivity Disoder (ADHD). I use the term ADD because the more technical term tends to mislead people into thinking that hyperactivity must be present to make the diagnosis. Not true.

    Adult ADD only started receiving proper attention in the last ten years. This means that the diagnosis and treatment of ADD in adults has lagged behind. It is not a "fad" diagnosis. It has historically been underdiagnosed and undertreated, so all of us are catching up on our awareness and proper treatment of ADD. Historically, ADD in children has received the most attention because of the challenges that hyperactive, impulsive children caused for school systems. ADD has at least two types of expression -- a hyperactive type and what I call a "day-dreamer" type.

    It used to be thought that children with ADD grew out of it, but it became evident that what they were often growing out of was just the hyperactive component. Many children with ADD became adults with untreated ADD. Many were never diagnosed during their school years because they weren't causing problems (the day-dreamer type) and because awareness of the many characteristics and subtleties of the disorder have not been and still are not widely known.

    People with ADD often experience failures in higher education and have lifestyles of rapidly changing jobs, poor work skills, and difficult relationships. Due to frequent failures, adults with ADD often get depressed and experience chronic low self-esteem. In addition, adults with ADD often experience significant negative daydreaming (worrying), which sets them up for chronic mild depression and substantial moodiness. They also can get easily overwhelmed, which often translates into a feeling of chronic anxiety.

    In their book Driven to Distraction, Edward M. Hallowell, M.D. and John J. Ratey, M.D. use the term "attention inconsistency disorder" to more accurately describe the attentional problems related to ADD. ADD is not a "deficit" in attention as much as it is distractibility which leads to inconsistent attention, or "flitting" attention. I would just call it "Distractibility Disorder." I call what happens in the ADD brain "serial single-tasking," which I write about further below. The true "deficit" in Attention Deficit Disorder consists of less-than-normal levels of certain neurotransmitters in a certain part of the brain.

    Here are a few signs of ADD in adults: (1) Inattention and memory problems -- losing or forgetting things, being absent-minded, not finishing things, misjudging time, trouble getting started ("procrastination"); (2) Hyperactivity and restlessness; and, (3) Impulsivity and emotional instability -- saying things without thinking first, interrupting others, easily frustrated and angered, unpredictable moods, risky driving behavior. ADD seems to be distributed equally between women and men.

    We do not yet have the ability to directly study the living human brain at the microscopic level, so we do not yet know the precise causes of ADD symptoms. Research points toward a deficit of the neurotransmitters norepinephrine and dopamine in the prefrontal cortex of the brain. A well-functioning prefrontal cortex is crucial to judgment, organization, attention span, planning, impulse control, problem solving, critical thinking, forward thinking, and empathy. However, there are several specialized areas of the prefrontal cortex that we do not yet fully understand.

    Not all ADD is the same. In addition to the neurotransmitter deficiencies, there are neuroanatomical differences and, thus, there are subtypes of ADD. In other words, the actual brain site where the neurotransmitter deficiency exists can vary from person to person. This is likely the reason that some medications work with some people, but not with others.

    Failure of a test dose of one type of ADD medication is NOT diagnostic. About 70% of the time, methylphenidate (Concerta, Ritalin LA) is a slam-dunk solution. About 30% of the time it is not, and you should move on to trials of other ADD medications. If you are in the 30% group, it can take a little longer to find the right medication or possibly the right combination of two different medications. If you are an adult who fits the criteria for the diagnosis, 98% of the time you will find a medication or combination of two medications that will make a significant difference in your life.

    To help people understand the deficit in ADD, I use the "bridges-out" concept. This is a somewhat simplified explanation -- the brain is a very complicated organ with very complex feedback and modulation loops. The brain is made up of billions of little pieces of road (nerve cells). The pieces of road are connected by bridges (chemicals called neurotransmitters). In the human brain, there are no long roads without bridges. So, if a lot of bridges are out (low neurotransmitter levels), there are fewer roads available for transporting data. When there are only a few roads for information to travel on, much information doesn't get processed properly.

    All medications that help with ADD symptoms do similar things -- they increase certain neurotransmitters in the prefrontal cortex. Thus, they put more bridges back into operation creating more usable roads for information processing. If people with normal levels of neurotransmitters take these medications, they may get mostly side-effects. There are no advantages to increasing neurotransmitter levels to above normal. Unfortunately, there is no clear evidence yet that these medications can "fix" neurons, so their function is to temporarily add a deficient component (bridges/neurotransmitters).

    Not all people with ADD have difficulties and problems. There are people who, because of their particular circumstances, intelligence level, or support systems, do very well. They may be very creative and energetic, and accomplish a lot. However, in those people who are experiencing mostly the downside of ADD, I recommend a thorough evaluation and a treatment plan.

How to Diagnose ADD  (updated 1/06/2011)   [Back to Index]

    Although there are self-report questionnaires, symptom checklists, and even some computer-generated attentional tests, they are only useful for general screening to see if you fit many of the criteria for the diagnosis. Most of those diagnostic tools just don't go deep enough and are not fine-tuned enough to pick up on whether a person is able to adequately self-define to answer some of the questions correctly. That is, a back-and-forth conversation with a live specialist allows for further clarification and exploration which are processes that are extremely important to making a correct diagnosis.

    No questionnaire or computer program is going to pick up the subtleties of a statement or self-report that may be off the mark. Let's see "you used the word 'selfish' to describe your behavior, could it be that you just don't follow-through well?" "Empathy requires follow-through to know that it exists, it is generally not going to be recognized by others if it is only a quick thought that you had that disappears when your next thought shows up. How are you at follow-through?"

    The longer and more comprehensive Adult ADD screening questionnaires that are available have been created by Dr. Daniel Amen and can be found here and here. Another well-known shorter screening questionnaire can be found here.

    To ask enough questions, discuss answers, use clarification and explore properly, it takes me about 100 to 150 minutes to obtain enough information to come to professionally adequate conclusions about a diagnosis and to rule in or rule out the diagnosis of ADD. If you fit the criteria for ADD, then it is a matter of deciding on what treatment strategies you wish to pursue. Once that is decided, it is a matter of deciding what that particular treatment strategy might involve in terms of work and follow-up.

What do We Know for Sure about Neurotransmitters and ADD Symptoms?  (added 1/06/2011 and updated 2/28/2011)  [Back to Index]

    We know for sure from recent studies using radioisotopes to tag dopamine and dopamine transporters in the human brain that dopamine deficiency in the prefrontal cortex is clearly related to the symptoms of ADD. Those studies can be found here (2009), here (2007), here (2007), and here (2007).

    Other important neurotransmitters (bridges) found in the human brain that are generally very specialized and usually found concentrated in certain parts of the brain include norepinephrine (clearly implicated in producing the symptom mix found in ADD), serotonin (not clearly implicated in ADD yet), GABA, and glutamate.

    Neurotransmission Basics at CNS Forum is a good place to start understanding more about the brain's neurotransmitters.

    Although radioligands have been developed for tagging norepinephrine transporters, serotonin transporters, and estimating GABA and glutamate, they were developed much more recently than the dopamine-related radioligands and have not yet (to my knowledge, to date - 02/28/2011) yielded the kind of data that is currently available for the dopamine system. Thus, we don't have the same conclusive data for norepinephrine deficiency in ADD as we do for dopamine. For instance, norepinephrine levels in the normal and the ADD brain have not been definitively imaged or mapped due to the continuing analysis of whether the current radioligands used for such imaging are specific enough.

    However, there is more than enough reliable research that shows trouble in norepinephrine systems related to ADD. It is my opinion that the main obstacle to fully understanding the effects of norepinephrine deficiencies is that norepinephrine processes in the brain and body are much more complex than the dopamine processes. In addition, norepinephrine is synthesized from dopamine by dopamine beta-hydroxylase.

    Since norepinephrine is synthesized from dopamine, increasing dopamine levels alone, with the use of medications that are known to do that, could also increase norepinephrine levels. This article at Wikipedia is particularly good at describing almost all you need to know about norepinephrine.

    Serotonin, GABA, and glutamate have not been clearly implicated in producing the symptoms of ADD. However, there is nothing that says you can't have troubles with more than one neurotransmitter system and, often, with people who have not been properly treated for their ADD, it is possible to end up clinically depressed (hippocampus damage that can be fixed with serotonin antidepressants) due to the years of more-than-normal stress created by the challenges of coping with ADD.

Are Medications the Only Solution for Fixing ADD Symptoms?  (updated 1/06/2011)  [Back to Index]

    Given the clear neurobiological basis of the symptoms of ADD -- neurotransmitter deficiencies -- there is no consistently reliable non-medication method for raising those levels to normal, well, unless you want to say that being an "adrenaline junkie" can do it.

    Yes, behaviorally, you can raise dopamine and norepinephrine levels by participating in risky behavior or constant high stress situations (video games, extreme sports, risky driving, criminal activities, police, fire, security, war, emergency services, etc.), but the side effects of such behaviors is generally burn-out, injuries or legal problems. You can modify neurotransmitters with exercise, but it also is not a very potent or reliable way for raising neurotransmitter levels.

    So, in adults, I highly recommend pursuing a medication treatment strategy. Before you start accusing me of some kind of conflict of interest with respect to pharmaceutical companies and their possible "profiteering" from an increased frequency of medication treatment for ADD, you should read my disclosure statement, here.

    If you think about it a bit, the best way I could make money related to the diagnosis of ADD would be to recommend therapy for treatment, which could go on and on and on with little or no results. The most cost-effective and most effective treatment for the symptoms of ADD is the correct medication. The folks who hugely profit from the existence and under-treatment of ADD in our society are the entertainment industry, retailers, and prisons.

    With respect to children under the ages of 12 or so, I do not particularly support the use of medication strategies for treatment, or, if utilized, utilized only in the most difficult behavioral circumstances or at minimum doses.

    Although I am not an expert on the use of ADD medications in children, it is my professional opinion that there are too many variables being treated in the young child situation to be sure that treatment is proper or completely relevant. The variables include (1) children, until they get enough language skills and experience in life, are very poor self-reporters, (2) too many "authority" figures in a child's life have too many agendas of their own that may not be appropriate or entirely relevant to making correct medication decisions, and (3) children's brains are still going through neurobiological maturing processes and probably should not be "messed with" too much.

    Unfortunately, the kind of structural changes that can help kids both in and out of school who fit the criteria for ADD is not very available in the United States. Between our distraction-obsessed society, economic instability, family dysfunction and overwork, and insufficient school resources, the choices for medication strategies over structural changes can become attractive only because there are very few other available support or treatment options.

    Nevertheless, when a child reaches an age where neural development is more or less stabilized (mid-teens to late teens) and self-reporting skills are more developed, medication strategies should be offered to young people with ADD so that they can have a chance to bloom without the obstacles that ADD can present to their successes.

Medication Issues  (updated 1/06/2011)  [Back to Index]

    Generally, if you fit the criteria and do not want to explore or work on other psychological, social, or environmental issues, it is possible to find the right medication, the right dosage and the right timing of the dosage(s) within about three to six 25-minute follow-up sessions.

    If Ritalin (methylphenidate) is a slam dunk, fewer follow-up appointments are generally required for fine-tuning medication. If it is not, it may take a little longer follow-up to arrive at the right medication result. In a very few instances, there are enough complicating factors that all the available medications, even in combination with a mood stabilizer, do not bring about a good result. In my experience, that is around 2% of the adult population that fits the criteria for ADD.

    Finding and fine-tuning the correct medication for any particular person should be done fairly aggressively. Any medications that have significant side-effects such as muscle tension, increased heart rate, overstimulation, stomach upset, increased anxiety, or irritability, or adverse affects on sleep should be seen as incorrect and the trial of the next available medication should begin.

    The point of taking medication is to not have side effects or any significant downside. Those are signals that it is the wrong medication. Please note, again: Just because one ADD medication does not work for you, does not mean there is none that will work for you.

    The point of medication is to raise norepinephrine and dopamine levels to as close to normal as possible without going over normal. Since we cannot accurately measure those neurotransmitter levels to determine how much medication would be the correct medication, we have to proceed by trial and error and self-report assessments of the upside and downside of a particular medication and dosages. There is no advantage to above-normal levels of neurotransmitters. They are as problematic as below normal levels of neurotransmitters.

    Once you have established the correct medication, dosage and timing of dosages, that will be the exact regimen that will work for most of your life. Generally, ADD medications are take it or leave it medications. That is, except for Strattera (atomoxetine), they do not need to "build up" in your system nor do they need to be weaned off of. When you are utilizing your medications you will have a more normal brain than off the medications. Off the medications means returning to your ADD brain. That can be shocking for some people after they have discovered what life is like with a more normal brain (close to normal norepinephrine and dopamine functioning).

    There are many myths about ADD medications, which I will begin to address further below.

    I recommend finding the right medication and dosages before trying to come to conclusions about your possible "personality disorder," "anxiety," "anger problems," "irritability," "moodiness." "selfishness," "passive-aggressiveness" or other so-called character or psychological flaws until you see what you are when the "dust settles." The ADD brain so significantly affects thoughts, feelings and behavior, that it would be premature and difficult to make an accurate personality or other behavioral diagnosis before the ADD portion of the problems is properly treated.

    I will write more about anger, depression and anxiety related to deficiencies in norepinephrine and dopamine further below.

Why Different Medications Work for Different People  (updated 1/06/2011)  [Back to Index]

    If you hear anyone, professional or otherwise, claim that Ritalin (methylphenidate) can be used to test whether you fit the diagnosis of ADD or not, tell them they are wrong, wrong, wrong. This myth exists even among my colleagues. The truth is different medications work for different people.

    In my experience, if you fit the criteria for ADD, Ritalin (methylphenidate) is a "slam-dunk" solution about 70% of the time. About 30% of the time it is not. If you are in the 30% group, it can take more time to find the right medication. I have not been able to find any surveys which show the percentages of different medications being used by people for their diagnosis of ADD.

    Medications which can make significant differences in an ADD person's life include Ritalin (methylphenidate), Focalin (dexmethylphenidate), Adderall (mixed salts of dextroamphetamine and amphetamine -- two categories and four chemicals in one tablet), Dexedrine (dextroamphetamine), Desoxyn (methamphetamine), Vyvanse (lisdexamfetamine), Strattera (atomoxetine), Provigil (modafinil), Wellbutrin (bupropion) and, sometimes, a mood stabilizer such as Lamictal (lamotrigine). The non-mood stabilizers all have similar final effects of raising extra-cellular brain levels of dopamine and norepinephrine but their mechanisms for obtaining that result are different.

    There is no completely reliable method for predicting which medication will be helpful for a particular person unless that person has a close biological family member who has already been diagnosed with ADD and has found the correct medication. There is some evidence that SPECT scans can help predict correct medication strategies, but the expense of such a scan is far greater than aggressively pursuing appropriate trials of the useful medications and deciding which medication is the most helpful.

    Unfortunately, there is no conclusive answer to the question "Why do different drugs work differently for different people with ADD?" The current most logical answer is based on our knowledge that although all ADD clearly involves lower than normal levels of dopamine and likely lower than normal levels of norepinephine in regions of the prefrontal cortex, that there is also the additional variable of where the particular deficiency is located.

    It appears that there are several possible areas within the prefrontal cortex where a neurotransmitter deficiency can be located and that the several different medications that are helpful in the treatment of ADD are likely targeting only specific areas of the prefrontal cortex and not the whole prefrontal cortex or the whole brain. Such locational differences in ADD-implicated neurotransmitter deficiency sites have been somewhat confirmed by SPECT scans and other neuroimaging studies, but a conclusive answer has not been established. You can read more about the subparts of the prefrontal cortex here and here.

ADD Medication Myths and Facts  (updated 1/06/2011)   [Back to Index]

  • The Number One Myth: ADD Medications are "Stimulants"  (updated 1/06/2011)  [Back to Index]

    The number one myth about ADD medications is that they are "stimulants" or that they are "addictive." They are only stimulants or addictive if they are used improperly for reasons other than increasing dopamine and norepinephrine levels up to normal. People with normal levels of dopamine and norepinephrine can get a buzz or a stimulation experience from many ADD medications because that is what happens when you increase such neurotransmitters to above normal.

    There is no advantage to increasing such neurotransmitters to above normal. It confuses nerve cells in the prefrontal cortex, which produces the "buzz" but, that's about it. The myth that above normal levels of such neurotransmitters assists in learning is hogwash. It may help someone stay up late and cram for a test or meet a deadline, but if that is the only way they can make it through school or at work, then they should get an evaluation about their procrastination (a common ADD symptom).

    There is no evidence that above-normal levels of such neurotransmitters positively affect learning, memory or other positive cognitive processes. The evidence is that it only allows for a longer study period, which, if done improperly without much sleep, works against long-term memory, since sleep is important for learning and long-term memory. Of course, if you don't care about how much of your "learning" gets into your long-term memory, then go for it. Again, that sounds so ADD -- short-term versus long-term thinking.

    The truly scientific mind would not logically conclude that this particular class of ADD medications should be called "stimulants" anymore than Prozac (fluoxetine) should be called a stimulant since it is a stimulant for many people, and sometimes cannot be tolerated due to its stimulating effects. And, so are many other "non-stimulants" also "stimulating." Wellbutrin (bupropion) is also consistently a very stimulating medication, but it is not restricted, nor is it classified as a "stimulant."

    In addition, it is well known that it is very difficult to "withdraw" from many of the psychotropic medications which are not restricted, but widely "misprescribed," such as Zoloft, Effexor, Paxil, Lexapro, Seroquel, Neurontin, and the list could go on. Some people find it impossible to withdraw from these medications, even when it is clearly misprescribed and not state-of-the-art standard of care.

    It is unfortunate that the scientific community continues to tolerate the kind of negative branding of certain medications with the "stimulant" tag, because the effect of such branding scares a significant number of people and discourages the appropriate use of such medications, not to mention how the "stimulant" tag and, thus, the "restricted medication" classification create significant obstacles to access and continuity of medication treatment for ADD. The stigma attached to these profoundly useful "stimulant" medications is still very high and patients often experience it when presenting their prescriptions to pharmacists and when talking about such medications with others.

    Additionally, any experienced psychiatrist can tell you hundreds of "horror" stories about the inappropriate use of many "unrestricted" psychotropic medications from antidepressants to mood stabilizers to anti-psychotics that have unarguably caused more death, health hazards, and discontinuation tragedies, and have been inappropriately prescribed and utilized far beyond what has taken place with the "restricted" ADD medications.

  • The Number Two Myth: ADD Medications Cause Sleep Problems  (updated 1/06/2011)  [Back to Index]

    This myth is so embedded in the mainstream community that it is almost laughable, if it weren't so serious. Yes, the wrong ADD medication can create sleep problems for those with ADD. The right ADD medication will not create sleep problems. In fact, the right medication will likely create better sleep. In fact, if an ADD medication prescribed to a person with ADD is affecting sleep adversely, it is the wrong medication. There are research articles about sleep and ADD here and here.

    There is a study I read recently and lost and haven't found again. It showed how low dose Dexedrine (dextroamphetamine) in the middle of the night, taken by people who were being treated for their ADD with Dexedrine (dextroamphetamine), who had woken up but could not get back to sleep was beneficial in helping them get back to sleep. You might wonder how this could be, given the hype about the alleged stimulating effects of most ADD medications. Well, here is the true story.

    When you have taken the correct ADD medication for you, that medication changes your brain to a more normal brain. For the number of hours that the medication is effective, you don't have your ADD brain. When the medication wears off, and they all wear off pretty fast except for Strattera (atomoxetine), you are back to your ADD brain.

    Somewhere in the vicinity of 80% of adults with ADD have sleep onset insomnia -- difficulty getting to sleep -- often at both bedtime and later in the night when they wake up.

    A large number of people with untreated ADD develop certain "sleep habits." They may use a strategy of going to bed really late when they are clearly tired because they know that they have difficulty getting to sleep if they lay down earlier. Or, they may use "white noise" (television or music on in background) to distract them from thinking and to create "boredom" and sleep.

    Other strategies for sleep often involve the "misuse" of over-the-counter and prescription sleep medications to treat this common symptom of ADD when treating the ADD itself is what is required. The reason for this sleep difficulty is that when your ADD brain is operating it does not have the ability to focus so it cannot focus on sleep and the processes of getting to sleep like a normal brain. Thoughts flood in and take control and the ADD brain cannot shut them off very well and focus on sleep.

    In the past, the "stimulant" tag noted above misled even professionals to think that you cannot take these medications later in the day without messing up sleep. The opposite is actually true. However, the key is being on the right medication. If you are not on the right medication for you, it can have an adverse effect on sleep. If you are on the right medication, you should be able to take it just about anytime of day (even in the middle of the night at low doses) and it will improve sleep. There are several studies reported in 2008 and 2009 revealing the sleep problems in people with un-medicated ADD. A 2008 study and a 1995 study showed how methylphenidate improved sleep, even if taken late in the day. Those studies can be found here and here.

  • The Number Three Myth: A Trial of Ritalin (methylphenidate) Will Be Diagnostic for ADD  (updated 1/06/2011)  [Back to Index]

    The only way to properly evaluate and discover whether you fit the criteria for ADD is a properly done clinical evaluation. If you fit the criteria for ADD, it is a 98% chance that you will find a medication or a combination of two medications that will change your life. What that medication will be is somewhat unpredictable, as noted above.

    A trial of even six out of the possible seven or so medications that will change an ADD brain into something that is a more normal brain would still not be "diagnostic" and would not rule out the diagnosis. Until you have explored all the appropriate medications for ADD, you will not be able to use the medication failures as evidence that you do not actually have ADD.

    Generally, the 2% of people who cannot be helped who fit the criteria for ADD are people who have confounding factors that prevent them from utilizing ADD medications, such as epilepsy, morbid high blood pressure or serious heart conditions. In addition, people with Posttraumatic Stress Disorder or Bipolar Disorder may not be able to utilize ADD medications because it could make their co-existing disorder worse. No guarantee on that, but those are the people who are often in the 2% can't-be-medicated-without-serious-problems group.

    In the section above entitled "Why Different Medications Work for Different People," I note that about 70% of people who fit the criteria for ADD are significantly helped by Ritalin (methylphenidate) without any side effects. The remaining 30% or so of those who fit the criteria for the diagnosis of ADD are significantly helped by some other medication or combination of medications. There is relatively no way to predict what medication will work for what person.

    Just think about it for a second or two. If you wanted to test the effectiveness of a particular ADD medication and do "head-to-head" comparisons of different ADD medications, how would you do that? Since there are subtypes of ADD likely based on neuroanatomical differences among ADDers that respond differently to different medications, researchers can't really do head-to-head comparisons until they discover a way to identify the ADD subtypes in advance of trying to make head-to-head medication comparisons.

    So, if you were to test the effectiveness of Ritalin (methylphenidate) treatment you could expect a 30% failure rate. If you were to test the effectiveness of Adderall (mixed amphetamines) treatment or any other non-Ritalin medication, you could expect a very large failure rate somewhere in the 60-80% range. And, that is about what has happened when the effectiveness of these medications has been tested in the general population of ADDers. In addition, many of the studies of the effectiveness of a particular medication for ADD have, in my opinion, "forgiven" too many side effects in the assessment of the alleged effectiveness.

  • Myth Number Four: ADD Medications are Addicting  (updated 1/06/2011)  [Back to Index]

    Before discussing drug tolerance and withdrawal, I should add a little explanation about bridges (neurotransmitters) and roads (neurons). Those bridges (neurotransmitters) can only create their temporary connections by being accepted somewhere on the surface of the road (neuron) they are traveling to.

    If the bridge receptors are blocked or locked down for some reason, the bridge (neurotransmitter) has no way to connect and it ends up generally stranded and then being quickly biologically "trashed" and thrown away -- broken down quickly into a non-active metabolic by-product. (You can read more about bridges (neurotransmitters) and roads (neurons) below under Serial Single-Tasking and the ADD Brain.

    As noted above, the goal of ADD medications is to increase norepinephrine and dopamine levels in the area of the brain called the prefrontal cortex up to normal but not to above normal.

    Using prescription medications or recreational drugs (cocaine, methamphetamine) to raise such levels to above normal has no information processing advantages, but, generally, such levels produce so-called "stimulating" side effects. This is why people who don't fit the criteria for the diagnosis of ADD can get "high" or "buzzed" or "energized" by taking ADD medications -- they start with baseline normal neurotransmitters and increase them way above normal, thus, the "buzz." But, guess what? Nerve cells are very protective.

    So, to get such a "buzz" from any of the ADD medications or cocaine or methamphetamine on an ongoing basis it requires more medication or recreational drug to produce the same earlier "buzz" as drug use continues. It is called "tolerance" which can be viewed as "nerve cells trying to protect themselves" (homeostasis) by shutting down receptors (gates) and using other mechanisms to protect themselves from the damaging effects of too much neurotransmitter.

    Thus, to get the same "buzz" from nerve cells that have closed most of their gates to protect themselves, it takes more and more drug to crash through the gates. When such drug use ceases or is reduced, the gates don't open easily and they open much slower than they closed (call it appropriate nerve-cell caution), so withdrawal occurs (a period when nerve cells are gradually reopening gates and getting back to normal). Thus, all those neurological bad things take place while the affected nerve cells get back to normal -- headaches, hallucinations, cognitive slowing, fuzziness, seizures, nausea and vomiting, etc.

    There is also clear evidence that too much "gate-crashing" can do permanent brain damage. Some methamphetamine abusers never get normal cognitive function back. This review article tells most of the story -- Cocaine, metamfetamine, and MDMA abuse: the role and clinical importance of neuroadaptation.

    Three key concepts are very important: (1) Correct ADD medication targets the correct area of the prefrontal cortex and it varies from ADDer to ADDer; (2) Side effects are not to be tolerated -- if you fit the criteria for the diagnosis of ADD there is a correct medication for you 98% of the time and it is the one that has minimal to no side-effects; (3) Dosage of the right medication should not be increased to a level where it produces side effects and, if it does, it should be reduced.

    The correct use of such medications is a "take it or leave it proposition." On medications, you will have a more "normal" brain. Off medications, you will have a more ADD brain. No tolerance develops. I often say to my clients who fit the criteria for ADD and utilize medications to

    "Side effects" are generally manifestations of too much neurotransmitter. There is no advantage to too much neurotransmitter. It produces "buzz." Staying on a medication that produces significant side effects is likely to produce a tolerance to that medication and require increased dosing. Please don't do that. First, you must be sure you have the correct diagnosis. Second, you must find the right medication for you. Third, you must use the correct dosage that does not produce side-effects. Otherwise, yes, it is possible to become "addicted" to a medication.

  • Myth Number Five: Taking ADD Medications Leads to Addiction Vulnerabilities  (updated 1/06/11)  [Back to Index]

    There is no evidence that the correct use of ADD medications, as noted above, leads to any types of future addiction vulnerabilities. Several studies have been conducted to answer the question "Do 'stimulant' medications for attention-deficit hyperactivity disorder contribute significantly to later substance abuse?" They can be found here (2010), here (2008), here (2008), here (2008), here (2003), and, here (2003).

    There is much more evidence that not treating ADD with appropriate medications sets up such undertreated or untreated ADDers for later addictions of many kinds. See here (2010), here (2010), here (2010), here (2008), here (2008), and here (2007).

    It is more than abundantly clear that it takes a a dramatic increase of dopamine and norepinephrine levels to above normal (either short-term high dosages, or longer-term moderately high dosages) to "reset" nerve cells to be so self-protective. which leads to needing larger and larger doses to get the same earlier, more "undefended," neuron buzz.

  • Myth Number Six: Typical ADD Medications Cause Blood Pressure Problems  (updated 1/06/2011)  [Back to Index]

    There have been a number of studies which have been inconclusive or mixed in their results for the question "Do ADD medications adversely affect blood pressure?" Some of them can be found here , here , and here. There is not much good data about the blood pressure effects of ADD medications. The clearest result shows that those who are already being treated for hypertension are not adversely affected by ADD medications. Because of the mixed results of these studies, it is recommended that a certain amount of caution should always be used, and monitoring of blood pressure is often recommended.

    However, in my experience, treating ADD with the correct medication generally lowers blood pressure. You might wonder why this has not been studied more extensively. I have tried to find that answer, but with no success, so far.

    There are large amounts of data and research about the relationship between anger, anxiety, depression and increased blood pressure and other adverse cardiovascular events. That research has also resulted in mixed conclusions, but generally the weight of the evidence is that certain kinds of anger and chronic fear, including panic attacks, contribute significantly to increased blood pressure. It makes sense that this would be true, because we know that adrenaline (reaction to fright, and flight-or-fight hormone) increases blood pressure, among other things.

    When you are constantly in a somewhat over-whelmed, somewhat chaotic or worried state of mind, you can expect that the "fright" factor of that mindset will have chronically stimulating effects on the adrenal glands with chronic responsive adrenaline secretion, among other things. See these links for some of the research: here (2010), here (2009), here (2009), here (2008), here (2008), here (2003), and here (2005).

    The untreated ADDer's life is often characterized by significant daily anxiety, moodiness, low-frustration tolerance (resulting irritability and anger), and other stressors related to disorganization, poor follow-through, and forgetfulness, among other things. Often, people with untreated ADD experience panic attacks. When you treat the ADD-brain problem responsible for those symptoms that produce higher levels of stress, the stress goes down (the fear factor, obsessive worrying, irritability, anger, etc.) and, thus, so does blood pressure, and, you would expect, other adverse cardiovascular effects.

Myths about ADD  (updated 1/06/2011)  [Back to Index]

  • Myth Number One: ADD is a Myth Diagnosis  (updated 1/06/2011)  [Back to Index]

    There are so many myths about ADD and its treatment, that it is difficult to decide which ones to address first and which ones to address later. This particular myth is also associated with the myth, "ADD is a Fad Diagnosis." I will write a separate article about that myth.

    One of the most prolific and well-known purveyors of the concept that "ADD is a Myth" is Thomas Armstrong, Ph.D. His argument can be summed up as "ADD is in the eyes of the beholder." That is, according to him, making the diagnosis of ADD is so full of inconsistencies and poor explanations that it is too subjective of an assessment to be valid. Well, in the hands of an inexperienced evaluator, that criticism might be correct.

    In addition, Dr. Armstrong more-or-less cherry picks his arguments and focuses mostly, if not entirely, on children and the diagnosis of ADD. That, of course, is the easiest place to pick apart the diagnosis, since children, as I noted above, are very poor at self-reporting and don't have the knowledge base, the language, the experience and the maturity to do even moderately good self-reporting.

    So, the diagnosis and treatment of ADD in children is full of challenges that should be addressed but generally aren't, because parents, teachers, and schools don't have the time or resources and there is a huge lack of access to child specialists who could do a better and more thorough job of diagnosis.

    Because of the poor access to quality diagnostic and follow-up care, we should be careful about pushing medication treatments -- why? -- they could be, and may often be, wrong. Also, as noted above, too many "authority" figures in a child's life have too many agendas of their own that may not be appropriate or entirely relevant to making correct treatment decisions.

    However, making the ADD diagnosis in adults is a whole different ballgame. Yes, you need to still do it right (see above about making the diagnosis). But, in addition to doing it right, adults, by far, are better at noting what their difficulties are and describing the subtleties of such difficulties.

    In my opinion, the vast majority of children over the age of 12 can usually do a fairly good self-reporting and identify details of their experience that helps tremendously in making a correct diagnosis. With respect to children under the ages of 12 or so, I do not particularly support the use of medication strategies for treatment, or, if utilized, utilized only in the most difficult behavioral circumstances or at minimum doses.

    As noted above, we now know conclusively that ADD is related directly to a deficiency in dopamine and likely also to a deficiency in norepinephrine in the prefrontal cortex. However, we cannot yet get to the diagnosis by utilizing those research techniques that have established that fact -- it is very expensive and also somewhat daunting for the research subject, to have to be injected with a radioisotope that tags dopamine receptors to be able to measure them and see if there is a deficiency. So, current diagnosis with adults and older children consists of an experienced evaluator doing his or her job thoroughly and then, if desired, pursuing medication discovery and follow-through.

    Even if SPECT scans can make the diagnosis (and that is still arguable), SPECT scans run in the range of $4,000 and are not covered by insurance for the purpose of diagnosing ADD.

    There are genetic tests that are also very complicated and expensive, which have identified some of the genetic components giving rise to ADD symptoms, but the genetics are complicated enough to make genetic testing for ADD unreliable as a diagnostic tool.

    There are no ways to do other blood tests or measurements using spinal fluid that reliably and correctly measure dopamine and norepinephrine or their breakdown products.

    So, since we have to use what we know about the symptoms of ADD and how they correlate in research studies to lower than normal neurotransmitter levels to diagnose ADD, the younger and more inexperienced the person is, the more subjective the conclusions will be. Otherwise, an experienced evaluator doing their job correctly can come to correct diagnostic conclusions in the population of people who can adequately self-report and are not under pressure to conform answers, guess, or otherwise not be able to self-report very well.

  • Myth Number Two: ADD is a Fad Diagnosis  (updated 1/06/2011)  [Back to Index]

    Probably the best recent mainstream article addressing this notion can be found at the New York Times, by Perri Klass, M.D., dated December 13, 2010, Untangling the Myths About Attention Deficit Disorder.

    The fact is, we do not have the tools to accurately measure the prevalence of ADD in populations, since such a measurement relies on making the diagnosis. Making the diagnosis relies on people defining a problem and seeking a diagnosis. So, people's awareness of their own potential for the diagnosis drives the data. Fewer people seeking help means fewer diagnoses. More people seeking help means more diagnoses. You can only count what has been measured. Guessing at what has not been measured leads to unreliable estimates.

    There have been rough assessments made in populations using brief self-report questionnaires, but, as noted above, such questionnaires are not very accurate indicators of the percentage of actual, valid diagnoses. More people are seeking diagnostic help and more people are being diagnosed because they are seeking diagnostic help.

    So, the short answer to the question "Is it a Fad Diagnosis" is "No." It is a diagnosis that is being made more often every year as people begin to understand what ADD is and that it can be effectively treated.

    Clearly, the diagnosis in adults is being made at a much higher rate every year. Is that because the incidence of ADD is increasing, like, "are people catching it somehow?" No. In my professional and scientific opinion, what is happening is that the challenges of our "new fast and very distracting society" is too much for the average ADDer.

    What is clear is that what I call "the dopamine deficiency syndrome" (of which ADD is a significant player) is so widely genetically embedded in our population that the new complexities of life in the United States have made it seem to blossom, when, in fact, it was always lurking. Previously, simpler, less challenging, less chaotic, less multi-tasking lifestyles and demands did not overwhelm the average ADDer to the extent of bringing about the inability to keep up, or to the extent that the distractions and complex demands in combination with their impatience and impulse control problems got them into trouble.

    Why is our new fast, distraction-based, entertainment-driven, multi-tasking, financially-insecure society so challenging for people with ADD? More on that below, under "How Does Serial Single Tasking Produce Typical ADD Symptoms?"

Serial Single-Tasking and the ADD Brain  (updated 2/17/2011)  [Back to Index]

    This discussion might cause your brain to hurt a little bit -- this is a complex subject, which I will attempt to simplify in a way that does not result in any misrepresentations of what is currently known about the human brain's prefrontal cortex information processing and working memory.

    I have to say that the worst piece of writing that I have ever read related to ADHD and brain processing issues, is found at Psychology Today, entitled ADHD Brains: The Quintessential Supercomputer. The writer makes the most unscientific and undocumented claims about the ADD brain that I have seen in a long, long time.

    And, he makes those claims for all the wrong reasons -- to prop up the argument that the ADD brain is a different brain, not necessarily a worse brain. Honestly, Dr. Goodman, exaggerated misinformation is not helpful. I have no problem believing the ADD brain is special and not "worse" than any other brain and that the ADD brain, in many situations, can be exactly what the doctor ordered, so to speak. The variation in brains, whether ADD or otherwise, should be respected and you don't have to make exaggerated claims to make it so. That's my rant.

    So, for those people who don't see or experience a significant downside to the way their ADD brain works, great. And, for those who do experience a significant downside, give them a chance to choose how they want to deal with that without someone trying to make them feel guilty about their assessment of their problems or difficulties. As if, all they have to do is realize how special their brains are, and that will make it all better? Honestly, if your rant, Dr. Goodman is about how ADD folks are discriminated against and treated with disrespect, then talk about that, and kick some discriminatory butt.

    So, exactly what is the comparison between the ADD brain and computer operations that helps us better understand what is going on in the ADD brain that creates challenges to certain kinds of information processing? Well, here it is, as best as I can describe the current understanding. Unlike what Dr. Goodman claims, the ADD brain has some real problems with working memory and with functions similar to what we call RAM (random access memory) in computers. That does not make the ADD brain a supercomputer, anymore than any other brain. You can read more about IQ and ADD here and here.

    The average person already has a supercomputer brain. Yep. Huge. But each of our supercomputer's operations can be challenged by certain limitations. Intelligence Quotient (IQ) is one of those challenges. The other challenge for the ADD brain, is how much RAM is not available without getting those dopamine and norepinephrine levels up to normal. Dr. Goodman confuses IQ with ADD processing and comes up with exaggerated claims for the ADD brain. There is no evidence that the ADD population, on average, have higher IQs than the non-ADD population.

    As I noted earlier on this page, I use the "bridges-out" concept to describe at least one significant dimension of what we know is taking place in the ADD brain -- low dopamine and norepinephrine neurotransmitters in various parts of the prefrontal cortex.

    If you visualize brain cells as microscopic pieces of road all crammed in together in the form of the nervous system, and you visualize how those pieces of road cannot really transport information any farther than the extent of that one little piece of road (nerve cell) without utilizing a bridge (a chemical called a neurotransmitter) to get the information to the next piece of road (nerve cell) to send it onward along a particular brain circuit, then you can understand that without the normal (or optimal) number of bridges available to your roads, the roads are limited in their capacity to transport information.
    In other words, when the bridges are out, the roads are rendered relatively useless for transporting information very far or very fast.

    In a very real sense, the ADD brain is working with lesser amounts of Random Access Memory (RAM) than the normal brain with normal levels of dopamine and norepinephrine in the prefrontal cortex. Less RAM, as you probably know, means less "mutli-tasking," and certainly less ability to hold a thought for further processing at some near-future point.

    The RAM-like activity of neurons has been discussed here. People with more working memory are not easily distracted according to research done at University of Oregon where investigator Edward Vogel compares working memory to RAM.

    In addition, a team of investigators in Sweden has identified what parts of the brain are its "spam" filters. Their work not only showed that a good working memory depended on how well irrelevant data was screened out, but it also showed what parts of the human brain are involved in such screening activities ("spam filters"). Turns out screening out relatively "irrelevant" data (less distractibility) depends on prompt and coordinated efforts between the prefrontal cortex and the basal ganglia.

    The jump in brain activity in these areas was greatest for so-called "high working memory capacity performers" and much smaller for "low working memory capacity performers." So, if these studies are replicated, it will be more than clear that one of the functions of higher RAM (higher dopamine and norepinephrine availability) is the ability to deal with increases in data without being overwhelmed by the data. You could say that more RAM allows for more screening, and, thus, more efficiency in processing "important" data. Just what the ADD brain lacks, and wants.

    Thus, the ADD brain is essentially limited to serial single-tasking much like the older computers that had limited amounts of RAM. To open more than one program at a time was very difficult. If it could be done, it was very slow. Serial-single tasking means that one thought, one image, or one sound (one piece of data) is open at a time. To open (notice) a new data point and pay attention to it, the current data point has to be closed. Since the old data point was closed, and cannot be held in a cache (holding station) somewhere, it may just disappear and never get a second chance. So, for information processing in the ADD brain, it is pretty much one data point at a time. When the next data point shows up the old data point is closed, and on and on.

    Serial single-tasking can happen faster in higher IQ brains and is generally slower in lower IQ brains. Often, people who fit the criteria for the ADD diagnosis who have higher IQs can find work-arounds for processing information faster, but compared to someone else with the same IQ, the ADD brain cannot outperform the non-ADD brain.

    So, how does this relative lack of parallel processing and the bottleneck of limited information processing pathways in the ADD brain account for the symptoms of ADD? At this point in time, the theory is it appears to significantly adversely affect working memory and processing speeds in the prefrontal cortex. A few of the working memory deficit reports can be found here, here and here.

    The prefrontal cortex is clearly implicated in both working memory operations (the holding of information online for processing) and executive functions (deciding how to manipulate working memory). For a really good and accurate discussion of working memory, check working memory at Wikipedia. In 2008, Time Magazine published a catchy article called "Kids with ADHD May Learn Better by Fidgeting" in which Mark Rapport, a long-time ADD researcher is quoted "Don't overly tax their [ADHD students] working memory."

    Rapport said "The average teacher doesn't understand how ADHD kids process information. You might hear something like this in the typical classroom, 'Take out the book, turn to page 23, do items 1 through 8, but don't do five.' They have given four directions at once and the child with ADHD and working memory problems has lost several of them, so it's like 'I am at page 23, what am I supposed to do now?'"

    The fact is kids and adults with ADHD learn better while "fidgeting." Fidgeting is not perfect, but it does have arousal and priming effects on neural transmission in the prefrontal cortex, probably by increasing available dopamine and norepineprhine.

    As I noted earlier, the goal of medications in the ADD brain is to increase dopamine and norepinephrine up to normal but not above normal. Above normal levels of these neurotransmitters do not produce any advantages to learning other than staying up longer, which, in and of itself, can negatively impact long-term memory (I suppose if you have to cram you have to cram, but it does not really constitute learning).

    Check here for a study confirming the relative non-usefulness of ADD medications for those who do not fit the criteria for ADD. Check here for a report about the "non-medical" use of "stimulants" by college students and how it is associated with ADHD symptoms (in other words, undiagnosed ADHD).

    There have been a number of studies and discussions about cognitive "enhancing" medications generally used for ADD treatment but often used by students and others to "enhance learning" or "increase capacity for doing homework," etc. Most of the studies have confirmed that there are actually reductions in cognitive performance for those who are baseline high performers. This conclusion clearly indicates that in the population with the most "optimized" brains, putting more than normal neurotransmitter into the mix reduces performance. Why?

    If you can visualize too many bridges in a system of roads, you might also see how that over-abundance of bridges would likely confuse drivers (information flow) and reduce the efficiency of getting from one place to another (processing). The fact that previously "low performers" experienced increased performance using ADD medications is more likely than not further proof of a spectrum of "processing disorders" of the prefrontal cortex from the more subtle (low performance without clear-cut ADD) to low performance with clear-cut ADD.

    With respect to the human brain, it appears that there is an optimum level of norepinephrine and dopamine bridges (RAM) below which and above which the brain does not operate at a data processing optimum. Unlike computers, which can be outfitted with increasingly complex hardware that can allow huge amounts of RAM to be utilized, the human brain has a limited number of neurons (pieces of road). To optimize those processors (pieces of road) you need just the right amount of RAM. Too few or too many bridges (RAM) produces non-optimal performance.

    This is likely true of all the neurotransmitters in the brain. There are many of them, including some ions which can be neurotransmitters. Different neurotransmitters are specialized in different systems, regions, and pathways. Neurotransmission Basics at CNS Forum is a good place to start understanding more about the brain's neurotransmitters. Not all neurotransmitters act like RAM to optimize working memory in the general region of the prefrontal cortex. Other neurotransmitters have other functions.

How Does the Serial Single-Tasking of the ADD Brain Produce Typical ADD Symptoms?  (updated 1/06/2011)  [Back to Index]

    As I have noted above, I use the "bridges-out" concept for explaining one of the most significant deficits in the ADD brain, the low levels of dopamine (completely proven) and the low levels of norepinephrine (mostly proven).

    Many studies have clearly proven that one of the major contributors to the downside of the ADD brain are deficits in working memory in at least the prefrontal cortex, but also, possibly located in slow-processing links between the prefrontal cortex and other brain areas.

    I have compared the ADD brain to a computer with less than normal RAM to the extent that, as described in several studies, the low dopamine and norepinephrine levels cause clear deficits in working memory.

    Working memory is the term used for the brain's RAM. More RAM (up to optimum levels of neurotransmitters) allows for more ability to hold data temporarily while, among other things, making decisions about what to process first or later, without losing the data during the time interval that is required for the decisions related to priorities of processing, importance of data, and such.

    Brain processing operations are more concurrent than parallel. More concurrent processing can take place when there are more circuits available for processing data. Less bridges than normal means less available circuits and, thus, less concurrent processing. This deficiency in available circuits produces slower overall processing speed. In addition, the relative lack of concurrent processing resources in the ADD prefrontal cortex and basal ganglia lead to difficulty screening out "noise."

    Although we are all pretty much forced to pay attention to the next piece of data, when you have less RAM, you may not be able to put anything on hold for later processing and then data just becomes overwhelming with the next piece replacing the first piece and so on.

    What looks like distractibility is, in fact, data streaming relentlessly without much processing. Endless serial attention without a holding area results in constantly changing thoughts, images, and sensations resulting in overwhelming levels of unprocessed, streaming data. And you wonder why one of the major downsides of the ADD brain is distractibility?

    Major indicators of the diagnosis of ADD are (1) easy distractibility, (2) relatively uncontrollable moodiness throughout the day, (3) low frustration tolerance - easily angered, irritable, (4) moderate to severe daily anxiety, (5) impatience, (6) impulsivity, (7) hyperactivity - fidgeting, compulsion to move, (9) non-empathic, (10) "hyperfocus", (10) risk-taking or "sensation-seeking" behaviors, (12) self-harm. I will explain how the serial single-tasking of the ADD brain creates these various symptoms.

  • Easy Distractibility  (updated 1/06/2011)  [Back to Index]

    "Easy distractibility" manifests itself in several different behavioral and information processing ways. The signs that such easy ADD distractibility produce include (1) difficulty staying on task, (2) hypersensitivity to sound and touch, (3) difficulty reading, with a typical ADD scenario of read a couple of paragraphs, get distracted by some other thought (or noise), forget what was read, have to re-read a lot; (4) forgetfulness, poor follow-through, disorganization, (5) indecision, procrastination, (6) sleep-onset insomnia and difficulty returning to sleep when awakened, and (7) social "phobia" or anxiety, among other things.

    My theory is that the distractibility of ADD is primarily related to the lower processing power of the ADD brain in terms of low RAM (as above, not enough bridges with which to create enough circuits to adequately process "normal" loads of information). This sets up the ADD serial single-tasking that only allows for brief, cursory, and sometimes no processing or prioritizing of information received -- producing a stream of uncontrollable thoughts and images.

    The essence of distractibility is difficulty screening out or holding data for later processing, and, thus, having no real control of the stream of data as it presents itself to the ADD brain. It has been clearly proven that those who fit the criteria for ADD have working memory deficits (see citations above).

    Working memory deficits have been clearly implicated in distractibility which is a clear inability to screen out "irrelevant" data and to have the capability to choose data to focus in on. The phrase I use to describe this process in the ADD brain is "the data chooses you, you do not choose the data -- in that regard, you are not in control of the data, it is in control of you."

    Although it should be fairly clear how distractibility relates to the ADD brain's deficiency in working memory (low RAM), let me run through each distractibility sign again:

      (1) Difficulty staying on task -- focus and choice are relatively absent due to the limitations of serial single-tasking (one task at a time and literally hundreds of data points presenting themselves for processing);

      (2) Hypersensitivity to sound and touch -- environmental data that can't be screened out while choosing some other data to focus on -- all data "claiming" equal attention;

      (3) Difficulty reading, with a typical ADD scenario of read a couple of paragraphs, get distracted by some other thought, sensation, or noise, forget what was read, have to re-read a lot, difficulty focusing on words and sentences within all the other words on a page;

      (4) Forgetfulness, poor follow-through, disorganization, poor sense of time -- if you can't choose thoughts due to resource limitations, then you can't choose actions either, or prioritize very well, or note the passing of time;

      (5) Indecision, procrastination -- can't make a choice, can't narrow down data points or set priorities (all data gets equal attention), can't get past the inertia of the weight of too many thoughts and choices, thus, what appears to be procrastination is really more about confusion until a deadline forces action, or, as a deadline gets closer, the fear factor goes up, increasing adrenaline, and allowing for greater focus as the deadline nears;

      (6) Sleep-onset insomnia and difficulty returning to sleep when awakened -- can't shut off thoughts and images and focus on sleep; and

      (7) Social "phobia" or anxiety -- too much input in "party" situations with so many data points converging from different sources at the same time that the ADDer just wants to escape (get drunk, do drugs, or just leave or withdraw).

    People (including professionals) observing these behaviors will often conclude that the person is lacking discipline or will power, is lazy, stupid, unreliable, poor reader, unmotivated, shy, rebellious, uncooperative, passive-aggressive, dishonest (embellishing or lying), having racing thoughts or grandiose (bipolar), a loner, or autistic, alcoholic, or addiction-prone, among other things.

    • Reading Impairments  (added 2/23/2011)  [Back to Index]

      I created "Reading Impairments" as a separate category to make sure that it gets your full attention. As noted above, significant reading impairment is almost always part of the ADDer's life. It is generally not an IQ, language or knowledge problem.

      The two most common distractibility-related reading impairment scenarios are (1) read a couple of paragraphs, get distracted by some other thought (or noise), forget what was read, and have to frequently re-read, and (2) since words and sentences on a page are surrounded closely by other words and sentences above, below, and along side of what a person is attempting to read, the distractibility quotient of any typical page of text is very high and ADDers often find it difficult to focus in on the word or the sentence they are attempting to read without being distracted by the surrounding words.

      The work-arounds that are often used by ADDers are to highlight every sentence, take copious notes, or use a ruler, a pointer, or a finger to stay focused on one word or one line of words at a time.

      Check the following studies for more information:

      2011 -- "The encoding of information from one event into working memory can delay high-level, central decision-making processes for subsequent events. It is, therefore, possible that, in addition to delaying central processes, the engagement of working memory encoding (WME) also postpones perceptual processing as well. We conclude that encoding of a stimulus into working memory delays the deployment of attention to subsequent target representations in visual cortex."

      2010 -- "We found that attentional mechanisms controlled by the dorsal visual stream help in serial scanning of letters and any deficits in this process will cause a cascade of effects, including impairments in visual processing of graphemes, their translation into phonemes and the development of phonemic awareness."

      2010 -- "Cumulative incidence of reading disability (RD) by the age of 19 years was significantly higher in children with ADHD (51% in boys, 46.7% in girls) compared with those without ADHD (14.5% in boys, 7.7% in girls)."

      2010 -- "Individual differences in processing speed are influenced by genes that also increase risk for reading disability (RD), ADHD, and their comorbidity. These results suggest that processing speed measures may be useful for future molecular genetic studies of the etiology of comorbidity between RD and ADHD."

      2008 -- "Recognition of the role of attentional mechanisms in reading offers potentially new strategies for interventions in dyslexia. In particular, the use of pharmacotherapeutic agents affecting attentional mechanisms may not only provide a window into the neurochemical mechanisms underlying dyslexia but also may offer a potential adjunct treatment for facilitating dyslexic readers to read fluently and automatically. Preliminary studies suggest that agents traditionally used to treat disorders of attention, particularly attention-deficit/hyperactivity disorder, may prove to be effective in improving reading in dyslexic students (emphasis mine)."

    • Sleep Difficulties  (added 2/24/2011)  [Back to Index]

      As noted above in "The Number Two Myth: ADD Medications Cause Sleep Problems," around 80% of people with ADD have sleep onset insomnia -- difficulty getting to sleep -- often at both bedtime and later in the night when they wake up.

      A large number of people with untreated ADD develop habits of going to bed really late when they are clearly tired because they know that they have difficulty getting to sleep if they lay down earlier. The may also utilize "white noise" such as a radio, television, or fan making low volume background noise. Such consistent background sounds can be a "magnet" for the ADD brain and allow it to more-or-less "lock-out" other intrusive or streaming data and set-up the ADD brain for sleep.

      Of course, in addition to the "non-medication" strategies noted above for "treating" sleep difficulties, ADDers often resort to over-the-counter and prescribed sleep medications, illicit drugs, and alcohol for sleep. The major reason for this sleep onset difficulty is that data (thoughts, images, sounds, sensations) flood in and take control and the ADD brain, as noted above, has a very difficult time choosing a thought and focusing on it, or ignoring or otherwise screening out irrelevant data (poor "spam filter" as noted above).

      Two excellent studies of ADD sleep problems can be found here (2009) and here (2009).

      The first study entitled "Association between attention-deficit/hyperactivity disorder and sleep impairment in adulthood: evidence from a large controlled study" out of Massachusetts General Hospital, Cambridge, MA 02138, USA, showed that "adults with ADHD went to bed later than control subjects and had a wider range of bedtimes, were more likely to take over an hour to fall asleep, and were more likely to experience difficulty going to bed, going to sleep, sleeping restfully, or waking in the morning. Adults with ADHD experienced daytime sleepiness more often and reported more sleep problems than controls."

      The second study entitled "Sleep problems and disorders among adolescents with persistent and subthreshold attention-deficit/hyperactivity disorders" out of the National Taiwan University Hospital & College of Medicine, Taipei, showed that "adolescents with a childhood diagnosis of ADHD according to DSM-IV criteria, regardless of whether they had persistent ADHD, were more likely to have current and lifetime sleep problems and sleep disorders according to DSM-IV (insomnia, sleep terrors, nightmares, bruxism, and snoring)."

      With respect to research done to discover whether typical medications for the treatment of ADD symptoms also improve sleep, the results are mostly positive. One would expect that if you go to bed with an "ADD brain," you are going to be highly distractible and have a difficult time focusing on sleep. One would expect that if you went to bed with more normal levels of dopamine and norepinephrine that you would be better at choosing what to focus on and better at screening out irrelevant data. And, that is precisely what happens.

      Studies showing the positive effects of methylphenidate for sleep normalization in ADDers can be found here:

        2010 -- "According to our results we can say that the MPH not only does not make sleep worse, but that it improves the quality of the sleep in those patients with sleep disorders."

        2008 -- "Compared to controls untreated patients showed increased nocturnal activity, reduced sleep efficiency, more nocturnal awakenings and reduced percentage of REM sleep. Treatment with methylphenidate resulted in increased sleep efficiency as well as a subjective feeling of improved restorative value of sleep."

        2007 -- "Our data suggest that sleep problems are inherent in adults with ADHD and that methylphenidate reduced total sleep time but improved sleep quality by consolidating sleep."

      Again, as noted above, in my experience, 80% of adults who fit the criteria for ADD have significant sleep difficulties. When the correct medication is used to treat such a person's ADD it has significant positive effects on normalizing both the ability to get to sleep and the sleep quality. This 2004 article at ADDitudeMag.com, gets most of it right about ADD sleep problems. As Dr. Dodson says "About two-thirds of my adult patients take a full dose of their ADHD medication every night to fall asleep."

  • Relatively Uncontrollable Moodiness Throughout the Day  (updated 1/06/2011)  [Back to Index]

    As noted above under "Easy Distractibility," due to the RAM limitations found in the ADD brain, increased incoming data overwhelms the system resources and each data point more-or-less simultaneously claims attention because of the working memory limitation.

    So, as I mentioned earlier, in the ADD brain, "the data is in control of you, you are not in control of the data." You are on what I call a "data roller coaster" -- more or less at the mercy of streaming thoughts and images, unable to screen out what you don't want to think about (as if you thought that could happen). So, mixtures of "good" and "bad" thoughts take you up and down throughout the day without you being able to screen out one or the other and choose a set of data to focus on (stability). Since almost all images, memories and thoughts have emotional meaning attached to them, when you are on a thought roller coaster you are on a mood roller coaster.

    People (including professionals) observing this often classify the behavior as tempermental, moody, unpredictable, dysthymic, clinically depressed, bipolar, manic-depressive, borderline personality disorder, flighty, or overly-sensitive, among other things.

  • Low Frustration Tolerance - Often Irritable and Easily Angered  (updated 1/06/2011)  [Back to Index]

    When data processing resources are overwhelmed by data due to limited ADD brain RAM, guess what? People feel overwhelmed. The condition of feeling easily overwhelmed leads to a sense of frustration and irritability ("leave me alone"), and often to easily triggered anger ("didn't I say, leave me alone?"). If not spoken out-loud, the untreated ADDer feels it at some level, and is often puzzled, and often angry, about the unexplained limitations they keep encountering. Often, the ADDer who knows this about themselves, will try to simplify rather than react and will just withdraw or hunker down, or escape in some way.

    People (including professionals) observing this in those with ADD often classify such behavior as mean, rude, selfish, quick-tempered, passive-aggressive, borderline personality disorder, or detached, among other things.

  • Moderate to Severe Daily Anxiety  (updated 1/06/2011)  [Back to Index]

    If you sensed that you are being "attacked" by overwhelming amounts of data, wouldn't you be a little fearful? Organisms, including humans, have the "uncanny" ability to sense things.

    The main sense that most ADDers will report to you if you ask them is "I can't handle it all." That would be strike number one. What they are noticing is that life is too much for them, and the more complex or distracting elements that are introduced into their lives means even more "dreadful" data. Well, any data can be dreadful when it overwhelms system resources and produces a sense of panic. And, you wonder why so many ADDers get diagnosed with anxiety disorders or have panic attacks? Or, why driving a vehicle might be somewhat distressing?

    Then there is the whole thing about "forgetfulness." ADDers almost always know they are forgetting something. They know it, but they cannot completely control it. Higher IQ ADDers often figure out work-arounds, like certain kinds of "routines" (sometimes interpreted as "rituals") such as always putting their keys, cell phones, wallets, or purses in a specific place, no matter what. Or, double checking doors to make sure they are locked, etc., etc., etc. And you wonder why some ADDers get classified as having an obsessive compulsive disorder?

    Well, constant fear of forgetting and worry about it (and it is constant) makes for a very anxious feeling. That would be strike number two.

    Strike number three for most adult ADDers when it comes to the experience of anxiety is "more worry" -- as if worrying about forgetting is not enough. As if worrying about forgetting is not enough, adult ADDers often do "negative day-dreaming." In other words, they aren't doing positive day-dreaming.

    What appears very clear to me is that the "pool" of possible distracting negative events in a person's history gets bigger every year (I know, so does the pool of possible distracting positive events in person's history). That pool of negative experiences becomes fodder for distractions and often "plagues" the ADD brain, much more than the pool of positive experiences. Adult ADDers have this sense that they are always on the verge of failure and their "day-dreaming" is more often than not, negative, harking back to bad things that happened before.

    One recent study published in 2008, found that 33% of 97 consecutive adult patients seen in an anxiety disorder specialty clinic fit the criteria for the diagnosis of ADD and were not referred to the clinic for ADD symptoms or evaluation. Only nine of those who had been referred to the clinic for treatment for anxiety had been previously identified as fitting the criteria for ADD.

    Some untreated ADDers figure out their limitations and don't push themselves too hard or do not give in to being pushed by others for "more success." They may stubbornly simplify their lives by sticking to one job most of their life, not marrying, not having kids, and keeping their life as structured and simple as possible.

    People (including professionals) observing this often conclude that ADDers are depressed, pessimistic, worry-warts, compulsive, obsessive, inflexible, afraid of change, agoraphobic, have anxiety disorders, have clinical depression, have panic disorder, or have obsessive-compulsive disorder.

  • Impatience  (updated 1/06/2011)  [Back to Index]

    I created impatience as a separate category to make sure that it gets your full attention. Significant and problematic impatience is almost always part of the ADDer's life.

    Impatience is really associated with the low-frustration tolerance (easily overwhelmed) of the ADD brain. So, the earlier discussion about low-frustration tolerance applies here. Waiting for just about anything requires fairly good working memory, in the sense that thoughts and actions must be put on hold during the waiting process. Thus, waiting, in and of itself, produces increased distractibility and unanticipated data.

    ADDers will often interrupt others in conversations because they are not in control of their thoughts and images, and "can't put them on hold." If they attempt to put them on hold, they may lose the thought or image completely.

    ADDers usually talk much like they process information -- scattered, tangential, often losing track of the previous thought or train of thought or the thread of the conversation. They may blurt out opinions, judgments, criticisms and compliments at totally or relatively inappropriate moments in a conversation and have real trouble modulating language (that is, modifying it to match the tone of the conversation) to stay within the conversation's tonal range.

    There has been some theorizing about the ADD brain's difficulty with inhibition and some research done in the last few years has indicated that possibly inhibitory pathways in the ADD brain are malfunctioning. Research based on tests utilizing "stop-signal tasks" and go-no-go tasks have had mixed results.

    A 2010 study entitled Do working memory deficiencies underlie behavioral inhibition deficits? concluded that working memory deficits underlie the difficulties with the inhibition of behavior often seen in ADD. With lower than normal working memory it is very difficult to have a thought and decide what to do with the thought at the same time. Generally, it does not happen well in the ADD brain.

    People (including professionals) often interpret such behaviors as rude, self-centered, narcissistic, unsympathetic, dishonest, narcissistic personality disorder, or borderline personality disorder, among other things.

  • Impulsivity  (updated 1/06/2011)  [Back to Index]

    Again, ADDers behave pretty much just like how they process information -- stream of data, and, thus stream of behavior. In other words, not much thought processing, holding a thought and examining it, or thinking about long-term consequences takes place in the ADD brain.

    Without a good working memory, it is impossible to actually modify an action or reaction while moving toward an action or reaction because both processes cannot go on at the same time without more RAM. It can be thought of as a lack of inhibition, but the actual process is not about neurons having a deficit in inhibitory feedback. A better explanation is thoughts and images are pretty much in control of the ADD brain. Processing is limited, so evaluation and holding back, delay and thinking through, do not happen before action takes place.

    People (including professionals) often interpret such impulsivity as poor self-control (well, yah...), poor discipline, short-sighted, selfish, flighty, risk-taking, lack of planning, attention seeking, dramatic, excitable, entertaining, energetic, addicted to gambling or pornography, or bipolar, or borderline personality disorder, among other things.

  • Hyperactivity - Fidgeting, Restlessness, "Driven by a Motor"  (updated 1/06/2011)  [Back to Index]

    The "compulsion to move" found among many ADDers has had many explanations, from inability to inhibit actions, to reward deficiency syndrome, to being an "adrenaline junkie." There have been theories that explain such ADD hyperactivity as a way of "arousing" the prefrontal cortex to improve working memory.

    A study done by Rapport and associates became the focus of a May 2009 Time magazine article entitled "Kids with ADHD Learn Better by Fidgeting." What Rapport discovered is that during working memory tasks kids who fit the criteria for ADHD had higher activity levels ("fidgeting") than a normal population of kids and that the fidgeting could be eliminated by presenting those same fidgeting kids with non-working memory tasks.

    The current theory is that fidgeting somehow increases the "arousal" state (possibly dopamine levels) needed in the prefrontal cortex for working memory to operate properly. Although this theory makes very good sense, it has not been proven by actual brain imaging of prefrontal cortex function in children or adults with ADHD during "fidgeting" and non-fidgeting periods while doing working memory tasks.

    However, the feeling of restlessness and the "driven by a motor sensation" is a different experience and can easily be viewed as the behavioral manifestation of a stream of ideas and thoughts that are in control of the ADD brain. The behavioral equivalent of that stream of data is a "restless body and restless feelings due to a restless brain."

    People (including professionals) often interpret such hyperactivity and restlessness as trouble-making, "easily bored," sensation-seeking, risk-taking, rebelliousness, poor discipline, rudeness, or disobedience.

  • Non-Empathic  (updated 1/06/2011)  [Back to Index]

    The adult ADDer is often accused of being non-empathic, forgetful of birthdays and important events, relatively unloving (immature, superficial, with problems with intimacy, etc.) and, often, a less than attentive sexual partner. This may not seem so obvious, but empathy is more than a feeling. To be seen as empathic, one has to display the feeling for longer than a flitting second and, generally, empathy requires follow-through behavior.

    Although ADDers have feelings (tons of them) and thoughts (tons of them), those feelings and thoughts often do not stick around long enough for someone to actually get to notice them or benefit from them.

    The distractibility of the ADD brain leads to problems with follow-through and, thus, forgetfulness (or what appears to be forgetfulness), and distractibility during intimate moments and sexual encounters, which can be more than a little irritating. Such distractibility often leads to chronic or frequent "impotence" or difficulty reaching an orgasm.

    People (including professionals) often interpret ADDers and these behaviors as narcissistic, unloving, uncaring, unsympathetic, superficial, immature, and sexually compromised, among other things.

  • "Hyperfocus"  (updated 1/06/2011)  [Back to Index]

    To many people, "hyperfocus" is a very puzzling aspect of the behavior of the ADDer. How can it be that a supremely distractible person can all of a sudden be so focused on one thing that you can't get them to stop, slow-down, think of others, think of consequences, or change focus. Why do they make such good video game players who can sit and compete for hours at a time? The answer is in the serial single-tasking that takes place in the ADD brain.

    If a thought or a pursuit shows up in the ADD brain that particularly captures its attention, it can become "locked on," not unlike a resource-demanding software program that eats up all the available RAM and makes it impossible to open up any other program at all. This is the most significant variable in creating the hyperfocus of the ADD brain -- the single-tasking locked on focus that allows almost nothing else to be noticed.

    The other significant variable that leads to "hyperfocus" behavior is the need for structure and stability. So-called "simpler tasks" that may be more activity-oriented than a challenge to working memory may become a comfort zone of activity and a preferred activity due to our human need for less chaos (less distraction). In other words, it is a method of "zoning out." For the person who is being relatively "tortured" by streaming thoughts and images and those feelings of relative chaos and disorganization, an entertaining and engaging activity that helps screen out all that other stuff is a welcome relief.

    People (including professionals) interpret this as selfish, narcissistic, loner, disobedient, dedicated, autistic, or withdrawn, among other things.

  • Risk-Taking, Adventurousness, "Sensation-Seeking," and "Adrenaline Junky" Behaviors  (updated 1/06/2011)  [Back to Index]

    I have created this category for the purpose of making sure these frequent behaviors exhibited by those who fit the criteria for ADD get your attention. Although, none of the research to date has shown exactly why dangerous risk-taking behaviors are more likely to take place in the ADD population, they have shown that such behaviors are related to impulse control problems and hyperactivity. We know that impulse control problems and hyperactivity (including fidgeting) are related to deficits in working memory which, in turn, is very likely related to baseline low dopamine and norepinephrine levels.

    The term "risk-taking," of course, is a difficult term. On one hand, risk-taking is important and, without it, there would be no follow-through on curiosity, creativity, or other "adventurous" behaviors that are essential to learning, growing, inventing, and evolving. So, there is a risk-taking scale from zero to ten. Zero is as potentially unhealthy and has probably as many downsides to it as a ten.

    Risk-taking in the social sciences encompasses a huge number of possible behaviors from risky driving, risky sex, risky alcohol use, risky illicit drug use, risky tobacco use, propensity to injuries (burns, etc.) to risky gambling. You can read a number of such studies related to ADD here, here, here, here, here, here, here, here, here, here, here, here, and here.

    In addition to the contribution of low working memory resources to impulsivity and hyperactivity, there is likely another major contributor to such risk-taking or "sensation-seeking," and "adrenaline junky" behaviors (sometimes called "courageous"). It is the ability to "tolerate" dramatic increases in norepinephrine and dopamine in the brain during and around times of high epinephrine (adrenal gland hormone also called adrenaline) output secondary to fear-inducing situations, such as jumping out of planes, cliff diving, speeding, being threatened, fighting, fleeing, and so on.

    Epinephrine stimulates the release of the arousal-related neuromodulator norepinephrine in the brain by activating beta-adrenoceptors located on vagal afferents terminating on brain-stem noradrenergic cell groups in the nucleus of the solitary tract and locus coeruleus. (I knew you would want to know that!) Noradrenergic projections originating in these nuclei connect to forebrain and prefrontal cortex structures involved in learning, modulation of aggressive behavior, hyperactivity and working memory.

    Anecdotally, there is much evidence that adults who fit the criteria for ADD are often able to handle high-adrenaline situations (emergencies, threats, risky tasks, risky activities, etc.) with better focus, less confusion and ambivalence or nervousness than adults who do not fit the criteria for ADD. It is unfortunate that there are absolutely no studies on the prevalence of the diagnosis of ADD among police, firefighters, emergency medical technicians, and military enlistees. Honestly, none that I can find. So, if you know of any, let me know.

    Such data would be very important because it would clarify so many things about what I consider to be one of the greatest upsides of baseline low dopamine and norepinephrine levels in the prefrontal cortex -- the ability to do better in risk-taking and emergency situations than "normal" folks with normal baseline levels of brain norepinephrine and dopamine.

    You may be able to visualize how, if your baseline norepinephrine and dopamine levels are low, that you could tolerate an increase in those levels much better than someone who started with normal or optimal levels of those neurotransmitters.

    Remember, from above, the study that showed how higher than normal levels of such neurotransmitters, in already high performers, degraded performance rather than enhancing performance. Thus, it is highly probable that the low-baseliners may have three potential contributors to "dangerous, risky" behavior: (1) decreased working memory (Ignorance is bliss? Consequences, what's that?), (2) they can do it, and (3) they feel more normal doing it (that is, less noise in their head, more focused, "alive," and engaged).

    The other benefit of such ADD prevalence studies in certain occupational populations would be to help understand why there are such high rates of domestic and relationship problems in the above-noted occupations (see here and here).

    The scientific community is either hesitant or prohibited from researching such prevalence based on their own assumptions or biases, or the members of those occupations do not want to know the truth. The truth could set them free, literally.

    That is, maybe if a high percentage of such professionals fit the criteria for ADD, they could utilize medications when they are off work (they are all fast acting) and be able to have better personal time (less moodiness, low frustration tolerance, oversensitivity, distractibility, etc.) due to treating their low neurotransmitter levels that return after the challenges of their typical work day are over. This is a longer discussion, but I thought you might like a couple of thought provoking tidbits.

    People (including professionals) observing such dangerous risk-taking behaviors may interpret them as careless, irresponsible, illogical, undisciplined, overly aggressive, grandiose, stupid, or courageous, among other things.

  • Self-Harm  (updated 1/06/2011)  [Back to Index]

    There are many misleading beliefs about self-harm, self-injury, and suicidal inclinations. I have included self-harm as a separate category under the symptoms of ADD because I want to make sure it gets your attention.

    Self-harm, deliberate self-harm and self-injury are defined as the intentional, direct injuring of body tissue without suicidal intent. These terms are used in more recent literature in an attempt to reach a less pejorative terminology. Older and relatively inaccurate terminology was "self-mutilation."

    The most common form of self-harm is skin-cutting but self-harm also covers a wide range of behaviors including burning, severe scratching, banging or hitting body parts, interfering with wound healing, hair-pulling, and the ingestion of toxic substances or objects. Substance abuse and eating disorders are not considered "self-harm, but the spectrum of "self-harm" is wide and not perfectly categorical.

    It is unfortunate that there is a glaring lack of research about the association betweem ADD and self-harming behaviors, since it is clear that the combination of the low frustration tolerance, impatience, and the impulsivity of ADD contributes fiercely and directly to self-harm behaviors. One of the only resources I found about self-harm and ADD can be found at a UK site, Why Do Some Teenagers With ADHD Self Harm?. Otherwise, pubmed.com had no significant search results for terms such as "ADHD and self-harm."

    The fact is that such self-harm behaviors are not limited to teenagers and they take place in many adults with ADD (and other diagnoses). In my opinion, the term "self-harm" does not extend to eating disorders, illicit drug use, alcoholism, and tobacco addiction. Although those behaviors can be clearly harmful, they are often more unintentionally harmful due to their side-effects, but the behaviors, themselves, may be misdirected attempts to fix something.

    The thing that complicates the self-harm discussion is the term "harm." "Self-harm" is often a misdirected attempt at brain "stimulation" or "arousal" such as with self-pinching and self-hitting. Cutting and other self-harm behaviors are more indicators of low-frustration tolerance, in combination with self-doubts, awareness of limitations, the confusion of the ADD brain, impatience and impulsivity. Even though such behaviors are painful, they can often lead to a feeling of catharsis, relief or "normality." And, while it is true that suicide attempts and successes take place more frequently in impulsive people, self-harm is not a reliable indicator of suicidal intentions.

    Proper treatment of ADD usually eliminates such self-harm behaviors in those with ADD. Non-ADD self-harm symptoms belonging to other disorders cannot be treated the same way as ADD is treated and may be more difficult to modify.

    People (including professionals) may interpret such behavior as clinical depression, suicidal behavior, borderline personality disorder, or psychosis, among other things. However, it is a relatively common behavior among those with ADD.

Underdiagnosis and Misdiagnosis Related to Adult ADD  (updated 1/24/2011)  [Back to Index]

    If you are one of those people who have been undiagnosed or misdiagnosed for many years and have struggled with one of the significant downsides of ADD, you know what it is like to finally find relief in a correct diagnosis and treatment.

    Whether you were being mistreated for ADD-related insomnia, anxiety, moodiness, depression, anger, impulsiveness, hypersensitivity, eating disorder, narcissism, procrastination, passive-aggressiveness, disorganization, dissociation, compulsions, social phobia, self-harm, agitation, substance abuse or sociopathic behavior, you know that once the correct ADD diagnosis was made, your life changed.

    You also know how angry, temporarily confused, resentful, and sad you can get when you think about all the years you struggled. In too many such cases, you had been on the verge of suicide or almost killed yourself, you had become exhausted, chronically fatigued, clinically depressed, or you ended up with fibromyalgia.

    Getting the correct diagnosis can be a shock and can lead to a period of considerable bereavement. Such newly-diagnosed and properly treated adult ADDers often go through a mourning process related to past educational and training struggles, lost opportunities and relationships, substance abuse, financial troubles and criminality, and other significant troubles that took place while they were undiagnosed or misdiagnosed and not properly treated.

    It is very apparent to anyone who specializes in the diagnosis and treatment of adult ADD that there are hundreds of thousands of people who clearly fit the criteria for the diagnosis of ADD who have been and continue to be misdiagnosed.

    ADD mindsets and behaviors too frequently get interpreted by others, including professionals, as evidence of narcissistic or borderline personality disorders, anxiety disorder, panic disorder, major depressive disorder, eating disorder, addiction disorder, dysthymic disorder and obsessive compulsive disorder, among many others.

    The authors of an early 2009 brief report entitled Attention deficit hyperactivity disorder erroneously diagnosed and treated as bipolar disorder noted "There is a dearth of literature on patients erroneously diagnosed and treated for bipolar disorder." That would seem to be an understatement.

    I highly recommend reading the following two articles which do a good job of summarizing up to December 2009 what we know about the underdiagnosis of ADD: Unrecognized attention-deficit/hyperactivity disorder in adults presenting with other psychiatric disorders (2008 - small pdf document) and Why Now? Factors That Delay ADHD Diagnosis in Adults (2009).

    I highly recommend reading the following article -- The Prevalence and Correlates of Adult ADHD in the United States: Results From the National Comorbidity Survey Replication. Here's one important note from that article:

      "One striking implication of the high overall comorbidity is that many people with adult ADHD are in treatment for other mental or substance use disorders but not for ADHD. The 10% of respondents diagnosed with ADHD who had received treatment for adult ADHD is much lower than the rates for anxiety, mood, or substance use disorders. Direct-to-consumer outreach and physician education are needed to address this problem."

    Overall, in this circa-2004 study published in 2006, ADD was estimated to affect 4.4% of adults in the United States, but it was largely undiagnosed, and less than 11% of affected individuals were receiving treatment for ADD. No studies similar to this have been done since 2006, but many other sources of information and data clearly indicate that the non-diagnosis and misdiagnosis related to adult ADD continues to be significantly problematic.

    The authors of the book Driven to Distraction and Delivered from Distraction, Drs. Hallowelll and Ratey, discuss how easy it is to get side-tracked by one or two of the many symptoms and signs of ADD and end up coming to conclusions about a diagnosis that are incorrect. Although they do not use the term "misdiagnosis," this is the term I will use.

    Chapter 6 in Driven to Distraction is entitled "Parts of the Elephant." At the beginning of that chapter, the authors list 13 subtypes of ADD. The list includes ADD with (1) hyperactivity, (2) anxiety, (3) depression, (4) learning disorders, (5) agitation or mania, (6) substance abuse, (7) creativity, (8) high-risk behavior, (9) dissociative states, (10) borderline personality features, (11) conduct, oppositional, or sociopathic personality features, (12) obsessive compulsive disorder, and (13) pseudo-ADD.

    Unfortunately, it is rather disappointing to see that neither of the above-noted books contain a single entry in their indexes for the terms "misdiagnosis," "stigma," "discrimination," "bereavement," "mourning," or "recovery." I bring this up for a few reasons which I will write about immediately below.

    On the upside, Drs. Hallowell and Ratey do talk about some of the many factors that contribute to the dilemma of misdiagnosis and underdiagnosis, but, in my opinion, they do not say it loud enough. Also, on the upside, Drs. Hallowell and Ratey do reject the term "co-morbid" in favor of the term "co-existing" to describe disorders that may "co-exist" with adult ADD.

    So, why do I bring up those words? Because there are hundreds of thousands more adults with ADD who are either undiagnosed or misdiagnosed than there are people who have been diagnosed properly and offered correct treatment. If, for instance, 33% of the population that would typically be referred to an anxiety disorder clinic fit the criteria for the diagnosis of ADD and have not been diagnosed properly (the "Canadian Ameringen 2007 Study"), you can bet that that is just the tip of the iceberg, so to speak. You would think that the Canadian Ameringen 2007 Study would have inspired dozens of follow-up studies, but it apparently has not.

    My professional opinion is that the term "co-existing" (co-morbid) can only be correctly used if the condition with which ADD is allegedly co-existing continues to be a valid diagnosis after the ADD is properly treated. Most of the studies have looked for ADD in the midst of major depressive disorder, bipolar disorder, substance use disorders, anxiety disorders, conduct and oppositional defiance disorders, and panic disorder. There is only one study I know of that has looked at the co-morbidity of ADD in those diagnosed with borderline personality disorder. I could not find anything that looked at the actual misdiagnosis of ADD as borderline personality disorder.

    Certainly, after properly diagnosing and treating adult ADD, a professional should stay tuned for what might still need to be fixed, because it is very possible to have complicating co-existing disorders such as posttraumatic stress disorder, major depressive disorder, or some other significant set of problematic symptoms.

    It is not uncommon for those who have experienced the consequences of untreated ADD to "burn out" and have resultant significant major depression.

    It is not uncommon for many people with untreated adult ADD to have experienced significant trauma in family relationships as they were growing up, since ADD is powerfully genetic and a parent or other relative with significant untreated ADD can be pretty difficult to live with or be raised by -- low frustration tolerance, quick tempers, impulse control problems, substance abuse, unpredictable, disorganized, and non-empathic, among other things.

    In my professional and scientific opinion, I would classify many of the uses of the term "co-morbidity" with respect to "co-existing with ADD" as an inaccurate characterization which can all too easily be interpreted as a "cover" for mistakes made with respect to correctly making the primary diagnosis of ADD. Most of these so-called "co-existing" disorders are often significant ADD symptoms which may either disappear completely or be significantly reduced when the ADD is treated properly.

    There are a number of very significant historical antecedents and political influences that have shaped the last 40 years of underdiagnosis and misdiagnosis related to ADD in the United States. That discussion is beyond the scope of this short article.

    However, for those of you who wish to begin understanding that there are powerful unscientific, emotionally-laden, and politically-motivated undercurrents that have significantly restricted access to the proper diagnosis and treatment of ADD over the past 40 years, I recommend taking a look at the "hysteria" that produced the 1971 U.S. Congressional action that resulted in an "order" to the Drug Enforcement Administration. I quote from Dr. Young's 2009 article, Why Now? Factors That Delay ADHD Diagnosis in Adults:

      "Another key reason why ADHD was not identified in childhood among many of today's adults with ADHD was that some very prominent popular publications warned of the pernicious effects of psychiatric medication; for example, Mayes and colleagues identified an influential Washington Post article in 1970 that estimated that 5%-10% of Omaha school children were dosed with behavior-controlling medications, with or without parental permission. In actuality, the medicated students were children with special needs and they were not forced into treatment.

      Nevertheless, people at that time often believed that what they had read must be true, and thus, parents were daunted. But they were not the only ones who believed the scary drug stories. The media hype also generated enormous concern in Washington over possible drug misuse and abuse. National conferences and congressional hearings were organized. In 1971, Congress ordered the Drug Enforcement Administration to categorize amphetamines and methylphenidate as Schedule II drugs. This action limited access to stimulants and placed them out of reach of children without resources or motivated parents. As a result, today's adult came of age in a climate that was indifferent and sometimes actively hostile to the legitimacy of ADHD."

    Below are a few links for further information about Attention Deficit Hyperactivity Disorder.

More Articles and Information Will be Posted Soon.

    Dr. Sterling is in the process of writing more articles for this page such as "ADD and IQ," "The Genetics of ADD," "Clinical Depression and ADD," and "Fibromyalgia and ADD." Please come back and visit soon.

Does Dr. Sterling Evaluate and Provide Treatment for ADD?

    Dr. Sterling is very experienced in the treatment of ADD with all the techniques that are available, including coaching, relationship counseling, psychotherapy, and medication. Please visit his office website at BellevuePsychiatry.com to read more about Dr. Sterling's practice or give him a call at 206-784-7842 to set up an appointment. You will often reach him directly during the week.

Thank You for Stopping By!

            -- Best wishes, Dr. Sterling


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