Monday, November 24, 2008
Monday, November 17, 2008
- First of all. there is the problem that the very definition of what constitutes executive functions varies from one authority to another; there is no standard or accepted definition.
- When parents or teachers fill out checklists or ratings of executive functions, there appears to be agreement with standard definitions of ADHD (e.g. with DSM-IV clinical symptom definitions), but there is no relationship to executive functions as measured by actual cognitive functions measured in performance tests. (For instance, tests of working memory do not agree with ratings of memory performance.
- Impairment of executive functions is common in many disorders other than ADHD, for example anxiety, depression, psychosis, etc. In fact, executive dysfunction cuts across almost all mental disorders and cognitive impairments. It would thus appear to be more a consequence of disorders than a specific cause of disorders.
- Finally, a number of investigations fail to find the executive dysfunctions postulated for ADHD.
For these reasons I believe that while it is useful to assess executive functions in ADHD, particularly since these functions may be trainable and coachable, a full assessment of ADHD requires a much broader range of symptoms and diagnostic criteria.
Tuesday, October 14, 2008
Wednesday, October 8, 2008
Recently the National Comorbidity Survey of the World Health Organization (WHO) under Harvard scholar, Ron Kessler, has placed the figure at 4 to 5 percent whereas the estimates for childhood ADHD average around 2 to 4 percent. What gives? Can there be more adult ADHD than child ADHD?
First, there are now dozens of studies throughout the world that consistently place childhood ADHD as high as 10 percent of the population, and averaging round 4 to 6 percent. Are there really 10 kids out of a hundred with ADHD (3 or 4 in every average classroom)? Well how does one KNOW? Remember that these studies usually involve hundreds or thousands of children, so that defining a case cannot usually involve individual clinical interviews. Instead, they may involve telephone surveys, checklists of symptoms, or surveys of parents.
Remember too, that according to the standard psychiatric definition (the Diagnostic and Statistical Manual of the American Psychiatric Association, now in its 4th revision, called DSM-4), there are 5 criteria that must be met. The most important of those criteria is the one that requires that the symptoms not be better explained by some other illness; that is, a "differential diagnosis" must be made. If it's autism, or depression, or anxiety, etc., then the 18 ADHD symptoms could be caused by one of these other illnesses.
But wait! Doesn't that mean you have to do a COMPLETE psychiatric examination? If you don't then the presumed "case" of ADHD could be something else, and the total count of ADHD cases would include all the other possible diagnostic contenders. Now examining all of the epidemiological studies of ADHD, the only one that I know of that actually used a complete diagnostic interview on enough children to form a reliable prevalence estimate was a study by Adrian Angold and Jane Costello in the Western counties of North Carolina. Their prevalence rate for ADHD: less than 2 percent. Incidentally, they found that a great many children who did NOT meet ADHD criteria were being treated for it, and a great many who DID meet criteria were not being treated for it. Obviously a correct diagnosis is necessary to avoid both kinds of mistakes. Wow! ADHD IS BOTH UNDERESTIMATED AND OVERESTIMATED at the same time, and they are being unter-treated and over-treated at the same time.
Now what about the adults? The big problem here is that there are no agreed-upon criteria for adult ADHD, though there is much work being done to alter the criteria to account for developmental changes in symptomatology, age of onset, and types of impairment associated with the condition. DSM-V will undoubtedly give us the basis for a real epidemiologic survey. However, the afore-mentioned WHO study started with a subsample of the very large survey carried out around the world, and by using statistical methods (e.g. imputing the actual numbers for the whole sample from a smaller subsample), they used 6 symptoms that were included in the original survey, to arrive at a prevalence estimate for adult ADHD, based on followup telephone interviews of the smaller subsample. The result: 4 to 6 percent prevalence of adult ADHD.
Here again, there really is no full psychiatric interview, so that in my mind these high figures must remain suspect. Incidentally, I am not reassured by the fact that this "WHO Study", which I participated in, was sponsored in part by a drug company, and that shortly after the first findings the drug company was using the 6 symptoms as a diagnostic guide for recommending adults to see their physician for possible treatment. So here we have another possible explanation of the explosive growth of adult ADHD: it is a boon for pharmaceutical companies who are now virtually all scrambling to get FDA approval for ADHD drugs in children to be approved for adults as well.
Don't get me wrong; adult ADHD is a real problem, and one that can be successfully treated by medication and other methods, and is a condition that has serious consequences for the patient and their families. But if ADHD, as we and most scientists agree, is a developmental problem starting early in life, then it seems unlikely that the true prevalence for adults can be more than the prevalence for children. Adults will pass through the age of risk for many other psychiatric and emotional conditions than is the case for children, so that they will have more comorbidities and more impact on their adult lives than they did as children. On the whole they could be sicker, though many compensate or adjust to their illness, especially those well-treated as children. But it is precisely these other conditions which might better explain their illness and dysfunctions, so they may be mis-diagnosed as ADHD when they are not ADHD cases at all, just as many children have likewise been mis-diagnosed because their symtoms could be due to other disorders that were not screened for. The bottom line: SYMPTOMS ALONE CANNOT MAKE A TRUE DIAGNOSIS. It is a mistake to make the diagnosis without carefully ruling out other explanations. To do this requires a sound clinical interview by a trained mental health professional.
Wednesday, September 24, 2008
Tuesday, September 16, 2008
Monday, September 15, 2008
- Ben Feingold was an honest scientist and allergist with a sincere belief that Food Additives caused hyperactivity; a white-haired, persuasive charismatic figure who convinced thousands of his theory.
- Just as he alleged, it was possible to "turn the hyperactivity on and off by giving or removing food additives." An effect we replicated in an ABAB design;
- But all of the effect could be accounted for by placebo once a proper control group was added.
- The only exception appeared to be for pre-school children where there was a slight indication that food additives increased hyperactivity (replicated by the Wisconsin group of nutritionists).
The power of placebo was strikingly illustrated by the very first child in our double-blind trial where food additve-loaded chocolate cookies were compared with additive-free chocolate cookies. On the first day of the trial the parent of the 6 yr old boy called, angrily threatening to sue us: "I don't know what you guys put in those cookies, but Kevin grabbed a knife and tore up our couch; he then took a hammer next door and destroyed the neighbor's motorcycle." Oh, oh...a looming court suit with big dollars flashed before me, but as fate would have it, you guessed it, he was on the placebo cookies. (Incidentally, this confirms Denny Cantwell's dictum that any red-haired boy named Kevin will grow up to be hyperactive.)
As Martin Orne once showed, the first thing a subject learns in an experiment is to obey what they think the experimenter wants to find.
Now back to feeding the brain. While at G. Washington and Children's Hospital in Washington DC, I carried out a number of experiments based on the Wurtman-Fernstrom hypothesis. They had demonstrated that a carbohydrate challenge elicits an insulin reaction which causes an efflux of large neutral amino acids (LNAA) from the blood, with the exception of tryptophan, which is lightly bound to albumin. Since LNAA cross the blood-brain barrier by competitive transport, tryptophan is given preferential input to the brain. Since tryptophan is a precursor for serotonin, the result is an increase in serotonin output, which is not regulated by positive feedback, so a burst of it can produce a sedative effect or other effects on the neurotransmitter systems.
We carried out several experiments in which we pre-fed normal and ADHD children with either a high protein breakfast, a carbohydrate breakfast, or a fasting condition, and tested them following a high level of carbohydrate beverage or aspartame placebo. An indwelling catheter was used to monitor hormonal responses, and tests of attention (CPT), cardiac response to warned reaction time (RT), and event-related potentials (ERP), monitored throughout the day. There were several results compatible with the Wurtman-Fernstrom hypothesis:
- Baseline levels of carbohydrate were significantly higher in the ADHD than normals. (Judy Rapaport at the NIMH had reported no differences in serum carbohydrate levels, but the breakfast the children ate beforehand was not monitored, thus invalidating the results).
- Attentional performance on the CPT (continuous performance task) and evoked cardiac response was impaired in the ADHD, but only when they had a carbohydrate breakfast, not a protein or fasting breakfast. The effect aoppeared to be in the early processing phase.
- ERPs showed marked lowering of amplitude and slowed latency in the carb condition but only for the ADHD children.
- Two hormones important in regulating carb levels (cortisol and growth hormone), were under-reactive in response to the carb challenge compared with controls.
I don't think we can conclude that high carbohydrate levels and increased serotonin cause ADHD. Instead, we propose that the recognized deficits in dopamine production or dopamine receptor function may be responsible for the hormonal effects, which in turn lead to a dysregulation of carb levels and the tryptophan/serotonin effect. This hypothesis has not to my knowledge been tested, and remains in my mind as an important future research problem.
Now, back to the fish oil issue. There is a small number of studies on the role of essential fatty acids (EFA), particularly omega-3, and ADHD, and some related areas like bipolar disorder and depression. In my next posting I will review this evidence. As a preview I can say that unlike neurofeedback and megavitamins, it is not the dictum of "Let the buyer beware" that applies, but the Scottish one, "Not proven."
Sunday, September 14, 2008
- Do foods, fish oil, additives, supplements, vitamins, etc. affect or cause ADHD?
- Are there really as many ADHD children out there as are being reported in the media?
- What are the important issues in the use of pharmacologic treatment of ADHD?
- Is ADHD an evolutionary advantage of some kind? Is it truly increasing in the world?
- What are the advantages and disadvantages of using rating scales in the diagnostic process?
- What should we think about the big pharmaceutical companies in the world of ADHD?
- Is there any role for sedatives, hypnotics, and tranquilizers in therapy of ADHD?
- What ar some the myths about ADHD?
- ADHD in schools: should we be concerned about how they are labeled and treated there?
In the meanwhile, I welcome any and all queries and comments from my colleagues, physicians and psychologists alike; as well as concerns and comments from parents or patients. I cannot of course give medical advice, but only my opinions based first on good science, and second on my own educated guesses acquired over my lifetime in the trenches of ADHD World. Join me!