Human behavior, pathology and self-regulation

Abstract

EDITORIALAt some point along the bell curve human behavior crosses a threshold of pathology and falls within the boundaries of clinical psychiatry. Yet psychiatric pathology is not a black and white phenomenon. Conditions of the DSM and ICD are not discrete entities. Many symptoms of psychiatric conditions represent qualities of human behavior distributed along a normal bell curve. Individuals at the lower tail of the curve are so different from others and experience such a severe level of adversity and impairment as to warrant diagnosis and intervention. In fact, it is increasingly apparent the bell curve phenomenon is reflective of many of the most common psychiatric conditions. As efforts are underway to create DSM-V, it is also increasingly apparent that a symptom count system is necessary but not sufficient to provide valid and reliable diagnostic categories. In facts, recent editions of the DSM and ICD have focused increasingly on age of onset, situational presentation and most importantly, levels of impairment. Relative to impairment, equal presentation of symptoms is not the equivalent of suggesting equal presentation of impairment (Gordon et al., 2006). In the condition currently defined in the DSM as attention deficit hyperactivity disorder, these researchers demonstrated that symptom presentation and severity predicts only a part of the variance in explaining overall level of impairment in every day life.It is also increasingly recognized that weaknesses in certain neuropsychological processes such as self-regulation, executive functioning or planning contribute to psychiatric symptom presentation and impairment. These therefore represent the foundational explanations for certain psychiatric conditions. ADHD is one such condition in which symptoms and, to some extent, impairment are driven by weak abilities. Weaknesses in executive functions related to planning, working memory and impulse control compromise an individual's ability to meet daily expectations leading to symptoms and impairments crossing clinical, diagnostic thresholds (Boonstra et al., 2005).Rates of ADHD among relatives of each subtype group of ADHD have been found to be greater than among relatives of controls (Faraone et al., 2000). The genetic contribution to ADHD has been postulated by a number of authors (Hechtman, 1993; Swanson et al., 2000). The underlying genetic mechanism has been suggested to be associated with multiple genes principally involving polymorphisms in the dopamine system. The heritability of ADHD has also repeatedly been found to be high. As Levy et al. (1997) note ADHD has an exceptionally high heritability compared with other behavioral disorders. These authors reported that 82% of monozygotic twins and 38% of dizygotic twins made an eight symptom ADHD cut-off for proband concordances.