Numerous epidemiological studies of various kinds of stress and preterm del
ivery have produced either negative or weakly positive results. Those incon
clusive findings could be either because of the absence of an association o
r because of recognised methodological problems that may have masked an ass
ociation. The biological plausibility of the stress hypothesis provides one
rationale for continuing stress research, using better study designs. To f
urther this agenda, we propose an epidemiological model, based on the class
ic 'host, environment, agent' triangle of epidemiological causality. The ho
st is the individual woman, more or less susceptible to stressor-induced pa
thology. The environment includes the social and cultural conditions that a
re ongoing stressors as well as social and cultural modifiers of stress e.g
. those factors that may influence how a particular stressor is experienced
or what the physical response to it may be. The agent is the immediate emo
tional or physical stressor requiring her response. We draw from recent lit
erature, published principally since 1990, to illustrate this model.
This epidemiological model posits that whether the individual is overwhelme
d by stressors depends not only on the strength of the agents but also upon
host susceptibility to stress, as well as the background level of acute, e
nvironmental and contextual stressors, and the moderating influence of host
, environmental and contextual resources for handling stress. Future resear
ch needs to be based on stress hypotheses that include all sides of the tri
angle, data collection instruments that adequately capture relevant stresso
rs and stress responses, and analytical techniques capable of handling comp
lex, multilevel relationships.