growth factor of the neurotrophin family supporting the function and survival of many neurons (Neeper et al., 1995). Exposure of adult mice to enriched environments also increases neurogenesis in the dentate gyrus (van Praag et al., 1999). This increased cell proliferation, however, involved voluntary running, not maze running or yoked swimming, thereby underscoring the fine-tuned nature of positive biobehavioral linkages.
We urge that the scope of a positive health program at NIH be broad and integrative, running from molecular and cellular levels of analysis through neurophysiological systems to behavioral, environmental, and psychosocial levels of analysis. This is a call for increased support for multidisciplinary investigations that are centrally concerned with bridging between biomedical and social behavioral research. These have frequently been studied as separate realms or, when put together, have typically focused on adverse health consequences of maladaptive behaviors or on psychosocial stress and dysfunction. Comprehensive biopsychosocial understanding of how illness and disease are prevented (or delayed), as well as how positive health is promoted, is an overdue and much-needed priority, and we strongly encourage NIH to launch a new trans-institute initiative under the broad umbrella of positive health.
Across NIH, there is pervasive concern for risk factors (genetic, behavioral, environmental) that predict the onset of particular disease outcomes. Scientific attention has focused disproportionately on individuals who ultimately suffer adverse health outcomes and on the etiological routes through which such effects occur. While the importance of such programs goes undisputed, we stress the concomitant need for studies of people with known risk factors who do not develop the disorder or disease in question. This resistance is usefully illustrated with samples pertaining to genetic risk.
Among females with the BRCA1 gene, about 29 percent develop ovarian cancer by age 50 and 50 percent by age 85 (Ford et al., 1995). More than half do not develop the disease, despite having genetic risk. Similarly, among those with the DYT1 gene for idiopathic torsion dystonia, only about 30 percent develop the disease (Risch et al., 1995). The gene for familial dysautonomia (localized to chromosome 9Q31) is carried by 30 percent of Ashkenazi Jews, but the development of this hereditary sensory dysfunction is so sensitive to diverse environmental triggers (e.g., cumulative stress, persistent infections) that no single summary penetrance number is meaningful (Blumenfeld et al., 1993). Of those with genetic risk of primary pulmonary hypertension (25-27 region on chromosome 2q31-32), the frequency of developing the disease at some point in a lifetime is only