What prompts me to write this dissertation is that several nights ago I attended a lecture given by a National Institutes of Health physician who spouted his research on Bipolar Disease in children. I asked the question whether he was aware of individuals performing studies on the role of nutrition as one of the potential influencing causes and as possible method of treatment of bipolar disease. After listening to his lecture for over one and a quarter hours, I was not surprised when he answered that, although he was aware that perhaps others were involved in these pursuits, his research involved another approach.

During his talk he described some differences between bipolar disease and other manifestations of childhood aberrant behavior, such as hyperactivity and attention deficit disorder (ADD) which is now being referred to as Attention Deficit-Hyperactivity Disorder (ADHD). It seems that with the passage of time physicians keep changing the names of these diseases to accommodate both changes in reclassification and to be more politically correct. Evidence for the latter is when the term @minimal brain dysfunction@ (MBD) was being used. When individuals decided that no one wanted to be labeled as Aminimally brain dysfunctioned,@ we quickly changed the name to a less emotionally charge term.

Also during his talk, this NIH researcher stated that one of the symptoms which separate the bipolar child from the ADD child was that the bipolar child exhibited mood changes. To me this was a typical way of fitting the definition to a set of criteria. By definition, the bipolar child exhibits mood changes because the researcher says it does.

Over the years, I have observed children who were labeled Hyperactive, ADD (now ADHD), Autistic, and Bipolar. Years ago I believed that each one of these so-defined conditions were external manifestations of impaired brain chemistry (for-want-of-a-better-term). What, perhaps, distinguished the different outward clinical manifestations were: 1) what particular part or region of the brain was affected, 2) the exact chemical nature (either some brain chemical deficiency or some toxic element) of the process, and 3) the degree of involvement, either more than one part or region involved simultaneously or more than one chemical deficiency or toxic element).

One child might exhibit dyslexia because the particular region of the brain involved in spatially relating letters in a word or sentence is impaired. Another child may exhibit antisocial behavior in school because that particular region of the brain modulating such activity is impaired. What really complicates the entire interpretation is the situation of dyslexia may in itself cause the child to question his abilities, he may feel inadequate, and this entire situation may be a causative factor in his getting upset and lash out as antisocial behavior, regardless of any impaired brain chemistry which may or not exist.

Stated differently, any behavior results from a combination of activities from the brain (as a physical organ) and from the mind (as a functioning non-physical thinking entity). Impaired brain chemistry can cause the physical computer brain not to function normally. Additionally, the non-physical mind B the programmed and programming software B gets into the act. Do we call Dell who manufactured the computer box or call Microsoft who provided the software?

When viewed in this way, it becomes imperative to fix the brain problem early before more bad programming situations become increasingly difficult to correct. For unlike a Microsoft software problem, the human mind is self reprogramming, the software is constantly changing and updating.

nicola michael c. Tauraso, M.D.

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Frederick , Maryland 21702

www.drtauraso.com