Can mother-infant interaction produce vulnerability to schizophrenia?

Schizophrenia is regarded as a final common behavioral syndrome which may be arrived at though a variety of routes. Even with a probably genotype, environmental influence seems necessary for the phenotype to appear. The problem concerns the likelihood of an early experience-induced sequence of events within the person of infant and later adult vs. a continuing pathogenic environment. Either may or may not interact with a continuing genic factor(s) as a source of vulnerability. Vulnerability is here, then, viewed as epigenetically evolving via individual-environment transactions throughout life (although with major impacts from conception through adolescence). At any point, therapeutic intervention may preclude or minimize the actualization of the pathogenic potential. It may begin during pregnancy, with attention to such factors as diet, drugs, physical stress, and illness, influencing fetal development and obstetrical manipulations and the birth process. All influence earliest mother-infant interaction from the point of view both of the infant's evocation of maternal behavior and maternal responsivity. Therapeutic interventions also include attention to the multigenerational context of earliest interaction, with special reference to a woman's relationships with her own mother. At every point, nonspecific protective or pathogenic factors such as social support or stressful precipitating events may become important. Socioeconomic status appears to have a powerful nonspecific influence as the core of a cluster of factors which exert an enduring influence from infancy to adulthood. A continuing specific factor may reside in distorted communicative reciprocity between parent an child rooted in the preverbal period of infant development. Context-mediated cerebral deficits may influence learning capacity, hedonic capacity, behavioral rigidity, and many other factors leading ultimately to impaired social competence and increased vulnerability.