It follows from the previous sections that psychosocial factors, such as a physical threat, may induce an allostatic response and thus have profound effects on the integrity of the body and add to the wear and tear on tissues and organs. Excessive weight gain, for example, is a physical threat that, in turn, may be the outcome of a complex interaction between an adverse life style caused by psychosocial factors in the setting of a genetic predisposition to metabolic inflexibility  and complex cross-talk between the brain and the gut. In this section, the effect of psychosocial factors on the cardiovascular system and some new insight on the relationship between psychosocial factors and food intake are addressed.
Semiacute psychosocial stress is associated with increased cardiovascular morbidity and mortality. The incidence of sudden death increases directly after a major disaster . Also, reversible cardiac failure caused by sudden emotional distress has been reported . A major role in the pathogenesis of these complications has been ascribed to activation of the HPA axis. Evidence of neurohumoral arousal and elevation of arterial blood pressure has been noted in situations associated with acute and subacute stress [56,57]. Exaggerated physiologic responses to acute stressors also have been shown in depressed, hostile, and low-SES subjects [37,58,59]. Chronic stress and hostility have been linked to increased reactivity of the fibrinogen system and of platelets, both of which increase the risk of myocardial infarction [60,61]. Also, tension and anxiety over a more prolonged period of time have been observed to be independent risk factors of incident coronary heart disease, atrial fibrillation, and mortality . This notion is corroborated by animal studies among Cynomolgus monkeys that have reported an association between social isolation and hypercortisolemia and reversible increases in resting heart rates, suggesting that social factors promote atherogenesis through activation of the HPA axis and the autonomic nervous system [63,64].
Recently, the increased mortality of elderly people in the year following the hospital admittance of a spouse has been demonstrated . Notably, the hospitalization of a spouse was associated with a risk of death for the partner within the first 30 days that was almost as great as the risk associated with the death of a spouse. Although factors related to harmful behavior by the partner who has been left behind cannot be ruled out in the latter study, the time frame is such that a direct stress-mediated effect is suggested.
Other studies have linked sympathetic hyperresponsivity to the induction of myocardial ischemia during exercise and mental stress and to predictions of the future development of hypertension and progression of atherosclerosis [66-72]. Increased systemic vascular resistance during mental stress testing is the most significant hemodynamic factor associated with mental stress-induced myocardial ischemia and most likely is the result of peripheral endothelial dysfunction . Inhibition of cortisol production has been shown to prevent mental stress-induced endothelial dysfunction and baroreflex impairment, again pointing to a significant role of the HPA axis . Interestingly, endothelial dysfunction after mental stress has been shown in hypertensive subjects but not in patients who have hypercholesterolemia . This finding is noteworthy because both hypertension and hypercholesterolemia are risk factors for atherosclerosis and cardiovascular disease, and endothelial dysfunction is a distinct feature of both diseases. These findings suggest different underlying mechanisms for endothelial dysfunction to account for the observed difference. When a similar stressor exerts a distinct response in subjects that, depending on the disease, that makes them more susceptible to atherosclerosis, the question is raised whether different stressors might likewise evoke different pathophysiologic mechanisms and, possibly, different atherosclerotic manifestations. The latter possibility is supported by animal data. Exposure of Watanabe heritable hyperlipi-demic rabbits to two different chronic stressors (ie, an unstable social environment or social isolation) resulted in more atherosclerosis than seen in a control group, but the two stressed groups exhibited different metabolic consequences and patterns of accrued atherosclerosis . Animals that were socially isolated were relatively sedentary, gained more body weight, and developed more profound hyperinsulinemia than the socially unstable group. They exhibited no stressful behaviors, such as cowering, vocalizations, or sleep or feeding disturbances, and had low corticosterone levels compared with the socially unstable group. At the same time they had higher resting heart rates and more pronounced abdominal aortic atherosclerosis.
The extent to which psychosocial factors affect the cardiovascular system through its interaction with the immune system has not been widely investigated thus far, but its potential significance is suggested by studies that have documented increased severity of the common cold related to psychologic stress and lack of social support [77,78]. As in depression, insufficient dampening of the inflammatory response related to diminished glucocorti-coid sensitivity might be of importance . Whether facilitation of sustained expression of inflammatory mediators under the influence of psychosocial factors might foster cardiovascular complications remains speculative.
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