The primary hormonal mediators of the stress response, glucocorticoids and
catecholamines, have both protective and damaging effects art the body. III
the short run, they are essential for adaptation, maintenance of homeostas
is, and survival (allostasis). Yet, over longer time intervals, they exact
a cost (allostatic fond) that can accelerate disease processes. The concept
s of allostasis and allostatic fond center around the brain ns interpreter
and responder to environmental challenges and ns a target of those challeng
es. in anxiety disorders, depressive illness, hostile and aggressive states
/substance abuse, and post-traumatic stress disorder (PTSD), allostatic len
d takes the form of chemical imbalances ns well ns perturbations in the diu
rnal rhythm, and, in some cases, atrophy of brain structures. IIE addition,
growing evidence indicates that depressive illness and hostility are both
associated with cardiovascular disease (CVD) and other systemic disorders.
A major risk factor far these conditions is early childhood experiences of
abuse and neglect that increase allostatic lend later in life and lead indi
viduals into social isolation, hostility, depression, and conditions like e
xtreme obesity and CVD. Animal models support the notion of lifelong influe
nces of early experience on stress hormone reactivity. Whereas, depression
and childhood abuse and neglect tend to he more prevalent in individuals nt
the lower end of the socioeconomic ladder, cardiovascular and other diseas
es follow a gradient across the full range of socioeconomic status (SES): A
I I SES gradient is also evident for measures of allostatic load. Wide-rang
ing SES gradient have also beer? described for substance abuse and affectiv
e anxiety disorders as a function of education. These aspects are discussed
ns important, emerging public health issues where the brain plays cr key r
ole. (C) 1999 American College of Neuropsychopharmacology. Published hy Els
evier Science Inc.