Pathways to STI Diagnosis: A Test and Replication of Competing and Integrated Models

Introduction: In the U.S., sexually transmitted infection (STIs) rank among the top ten most commonly reported diseases and present a considerable public health concern. The current study examines individual and environmental antecedents of sexually transmitted infection in two longitudinal studies. Specifically, we tested four hypothesized pathways to STI diagnosis: a) a sexual risk behavior pathway; b) a general risk behavior pathway; c) an environmental risk pathway; and finally d) an integrated pathway.

Method: The current work is draws on data from two longitudinal studies of youth and adult development: the Seattle Social Development Project (SSDP) and the Raising Healthy Children (RHC) study. Lifetime STI diagnosis was measured by age 24. Early predictors included early puberty, behavioral disinhibition, family management, school bonding, and antisocial peers and were measured between the ages of 10 and 14. Early sexual debut and delinquency and substance use were assessed in adolescence. Lifetime number of sexual partners and engagement in sex under the influence of drugs or alcohol were assessed between the ages of 21 and 24. Hypothesized models (a) through (d) were developed in SSDP dataset using Structural Equation Modeling (SEM). A replication of the final model (d) was then tested in the RHC dataset.

Results: Support was evident for all three hypothesized component pathways: a) a sexual risk behavior pathway that included puberty onset, early sexual debut, and lifetime number of sexual partners; b) a general risk behavior pathway that focused on behavioral disinhibition, early sexual and non-sexual risk behavior, and adult sexual risk; and c) an early environmental risk pathway (including family, peer, school and neighborhood risk factors). An integrated model, in which STI diagnosis in adulthood resulted from the joint influence of all three pathways was supported in SSDP, and replicated in the RHC sample.

Conclusions:  A particular strength of this study is the effective test and replicate strategy that maximizes utility of developmental datasets. In addition to testing support for the hypothesized mechanisms, we were able to replicate the findings in another sample and increase the credibility of the analyses and the conclusions. Understanding the mechanisms of STI infection improve our understanding of the etiology of HIV/sexual risk behavior and introduce important early prevention targets. Results from this study suggest that HIV sexual risk prevention approaches would benefit by integrating general early environmental intervention approaches in conjunction with approaches targeting sexual risk behavior specifically.