Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.

Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy.

http://apsychoserver.psych.arizona.edu/JJBAReprints/PSYC501A/Readings/PorgesBioPsychology_2007.pdf

The polyvagal perspective

Biological rhythms and the behavior of populations of coupled oscillators

Dogs which had 1st learned to panel press in a harness in order to escape shock subsequently showed normal acquisition of escape/ avoidance behavior in a shuttle box. In contrast, yoked, inescapable shock in the harness produced profound interference with subsequent escape responding in the shuttle box. Initial experience with escape in the shuttle box led to enhanced panel pressing during inescapable shock in the harness and prevented interference with later responding in the shuttle box. Inescapable shock in the harness and failure to escape in the shuttle box produced interference with escape responding after a 7-day rest. These results were interpreted as supporting a learned "helplessness" explanation of interference with escape responding: Ss failed to escape shock in the shuttle box following inescapable shock in the harness because they had learned that shock termination was independent of responding. Overmier and Seligman (1967) have shown that the prior exposure of dogs to inescapable shock in a Pavlovian harness reliably results in interference with subsequent escape/avoidance

/pdf/failure-to-escape-traumatic-shock-nnwn6t036k.pdf

Failure to Escape Traumatic Shock

We approach disgust as a food-related emotion and define it as revulsion at the prospect of oral incorporation of offensive objects. These objects have contamination properties; if they even briefly contact an otherwise acceptable food, they tend to render it inedible. Drawing on sources from many cultures, we explore the implications of this perspective on disgust. Some of the issues we consider are the nature of the objects of disgust and why they are virtually all of animal origin, the meaning of oral incorporation, the "belief" that people take on the properties of the foods they eat. and the nature of the contamination response and its relation to the laws of sympathetic magic (similarity and contagion). We consider the ontogeny of disgust, which we believe develops during the first 8 years of life. We explore the idea that feces, the universal disgust object, is also the first, and we examine the mechanisms for the acquisition of disgust. We recommend disgust as an easily studiable emotion, a model for cognitive-affective linkages, and a model for the acquisition of values and culture.

A perspective on disgust.

Adrenalectomized rats are known to have a defmitely increased salt need, inasmuch as the administration of large quantities of salt either greatly reduces or eliminates the symptoms of insufficiency, and actually increases the survival incidence But is this need accompanied by an increased salt appetite, and will the adrenalectomized rat, if given free access to salt take sufficient quantity to keep itself alive and free from symptoms of insufficiency. 3 In an effort to answer these questions the following experiments were undertaken. METHODS. It was necessary for this purpose to devise a method by which salt could be given freely, under circumstances which made possible measurement of the actual amount ingested, It would have been simplest , of course, to present granular salt in a separate container. However , the small amount ingested daily and the comparatively large amount spilled or carried away on the paws definitely ruled out a quantitative measure by this method. For this reason salt was offered in solution in the drinking water. At the outset a 1 per cent salt solution was used because Rubin and Krick obtained their successful results from a solution of approximately this strength; but since, with only the salt solution available, the rat's intake would depend partly on the salt need and partly on the thirst for water, access was given at the same time to tap water presented in a second container. In this way the rat could satisfy its thirst and its salt appetite independently. In the first series of experiments with the 1 per cent salt solution and water, the animals also received the usual amount of salt in the McCallum diet (approximately 0.145 gm. per day). Inasmuch as the normal rats did not distinguish between the salt solution and the water, a second series of experiments was started with the strength of the salt solution increased to 3 per cent and no salt given in the food. It was found then that the normal animals did differentiate very definitely between the 3 per cent salt solution and the water. The rats were kept in individual cages containing a food cup, and two inverted graduated bottles, one with salt solution, the other with tap 155

Increased salt appetite in adrenalectomized rats.

A behavioristic study of the activity of the rat

SummaryA phenomenon of sudden death has been described that occurs in man, rats, and many other animals apparently as a result of hopelessness; this seems to involve overactivity primarily of the parasympathetic system. In this instance as in many others, the ideas of Walter Cannon opened up a new a

Curt P. Richter

Papers

Increased salt appetite in adrenalectomized rats.

A behavioristic study of the activity of the rat

On the phenomenon of sudden death in animals and man.

Biological clocks in medicine and psychiatry

Alcohol Taste Thresholds and Concentrations of Solution Preferred by Rats