cated a biopsychosocial model as a way to “broaden the approach to disease to include the psychosocial without sacrificing the enormous advantages of the biomedical approach” (p. 131). The biopsychosocial model maintains that health and illness are a function of multiple processes—biological, psychological, and social—and these processes must be considered simultaneously. In particular, the emergence of multifactorial approaches to the pathogenesis of disease enabled linkage between the behavioral and biomedical sciences (Weiss, 1987). Also important were systems theory perspectives and models of how biological and psychosocial processes act together in human development across the life span (Bronfenbrenner, 1977, 1979). A systems theory perspective focuses on the accommodations that occur through the life span between the developing organism and the changing environment.
The biopsychosocial model focuses on multiple factors in the etiology and progression of disease. Three primary mechanisms of effect have emerged: health behaviors, psychosocial processes, and genetics. Health behaviors include exercise, nutrition, smoking, and adherence to medical regimes. Psychosocial processes include a range of interpersonal and social processes that affect interpretation of environmental experiences and responses to stress. Risk-resiliency models are also prevalent and seek to identify factors and processes that enhance or decrease vulnerability to disease processes. A particular area of focus has been neuroendocrine and immune responses to stress. One mechanism of effect is through the impact of how individuals interpret and respond to the environment which influences the degree of stress experienced which in turn influences health behaviors and neuroendocrine and immune responses that in turn affect the etiology and progression of disease. Genetic mechanisms of effect involve the identification of internal and external factors that trigger the switching on or off of genes that modulate physiological processes.
The primary interest prompting this paper is enhanced understanding of the interaction of social, behavioral, and genetic factors on health. Sickle cell disease was selected as a good model for this investigation because it is a monogenetic event but the phenotype is multigenetic resulting in considerable individual differences in severity of the disease. More specifically, this paper addresses the following questions:
What do we know about the influence of social and behavioral factors and the effects of other genes?
What data do we have?
What data do we need?
What important questions remain to be answered about the influences of social and behavioral factors, including mechanisms, on sickle cell disease?