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Objective: This study aimed to investigate associations between financial strain and emotional well-being, health, and physiological responses to acute mental stress., Methods: Participants were 542 healthy men and women aged 53 to 76 years from the Whitehall II study divided into those who reported no (n = 316), some (n = 135), or moderate/severe (n = 91) financial strain. Emotional well-being and self-reported health were assessed at baseline and 3 years later. Laboratory mental stress testing involved assessment of blood pressure (BP), heart rate, and lipid reactivity and recovery, and plasma interleukin 6 responses to challenging behavioral tasks. Analyses adjusted for objective financial status, age, sex, socioeconomic status (SES), and marital status., Results: Financial strain was positively associated with more depressive symptoms; lower positive affect; greater loneliness; lower optimism, self-esteem, and sense of control; and poorer self-reported physical health, mental health, and sleep (all, p < .001). Longitudinally, financial strain predicted poorer outcomes 3 years later, but associations were attenuated after baseline levels were taken into account. Financial strain was associated with reduced systolic and diastolic BP reactivity to acute stress (mean systolic BP increase = 32.34 [15.2], 28.95 [13.1], and 27.26 [15.2] mm Hg in the none, some, and moderate/severe financial strain groups), but not with heart rate, interleukin 6, or lipid responses., Conclusions: Financial strain was correlated with a range of emotional and health-related outcomes independently of objective financial status. The diminished BP reactions to acute mental stress suggest that financial strain may contribute to dynamic chronic allostatic load.

Human responses to brief psychological stressors are characterized by changes and large individual differences in autonomic, neuroendocrine, and immune function. The authors examined the effects of brief psychological stressors on cardiovascular, neuroendocrine, and cellular immune response in 22 older women to investigate the common effects of stress across systems. They also used interindividual variation in heart rate reactivity, cardiac sympathetic reactivity (as indexed by preejection period reactivity in their reactivity paradigm), and cardiac vagal reactivity (as indexed by respiratory sinus arrhythmia reactivity) to explore the heterogeneity in human responses to brief psychological stressors. The results revealed that brief psychological stressors heightened cardiac activation, elevated plasma catecholamine concentrations, and affected the cellular immune response. It was also found that individuals characterized by high, relative to low, cardiac sympathetic reactivity showed higher stress-related changes in adrenocorticotropic hormone and cortisol plasma levels but comparable changes in epinephrine and norepinephrine concentrations. These data suggest that the effects of psychological stressors on cardiovascular and cellular immune response are governed by coordinated regulatory mechanism(s) and that going beyond the simple notion of heart rate reactivity to examine neural substrates may shed light on the interrelationships among and the regulatory mechanisms for the autonomic, endocrine, and immune responses to stressors.

High and low reactors were preselected on the basis of their heart rate reactivity to a speech stressor in a prescreening session. In the main study, subjects were exposed to a mental arithmetic plus noise stressor. Cardiovascular activity was recorded during baseline and stressor, and blood was drawn prior to and following the stressor for endocrine and immune assays. Results revealed that the stressor decreased the blastogenic response to concanavalin A and increased natural killer cell numbers and cytotoxicity, absolute numbers of CD8+ T-lymphocytes, norepinephrine and epinephrine levels, heart rate, and blood pressure responses. In addition, cortisol and natural killer cell cytotoxicity responses to the stressor differentiated individuals high versus low in heart rate reactivity. These results suggest that the interactions among the autonomic nervous system, endocrine system, and immune system are not only amenable to psychophysiological analysis but that such analyses may play an important role in illuminating underlying mechanisms.