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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



It is apparent that there is room for further studies 

 of this important aspect of atherosclerosis. 



Emotional Stress 



A number of investigators have shown that emo- 

 tionally stressful life situations transiently elevate 

 serum cholesterol levels and shorten the blood- 

 clotting time. This has been noted in medical students 

 at the time of examination (36, 162), and Friedman 

 et al. (48) observed it in accountants when they were 

 under professional peak loads. Several other workers 

 have published data linking the acute episode of 

 coronary occlusion to immediately preceding stressful 

 life situations (37, 136, 169). The proponents of the 

 hypothesis that emotional stress influences athero- 

 genesis and may precipitate clinical episodes of 

 occlusion implicate the stresses of our modern 

 mechanized civilization in particular. Emotional 

 stress also produces elevation of blood pressure, and 

 this in turn may have a deleterious effect on the 

 vascular wall. In this and other ways hypertension 

 favors atheroma formation. 



The study of emotional factors in relation to 

 cardiovascular disease is in its infancy. The main 

 reason for the difficulties in the evaluation of this 

 factor is the lack of an effective measure of emotional 

 stress and of the various personality profiles (75). The 

 mechanism by which psychological stress influences 

 body homeostasis is also difficult to assess. It may 

 operate: a) by disturbing endocrine balance, e.g., via 

 pituitary-adrenal stimulation and catecholamine 

 release (50, 95, 132, 140, 162), thereby influencing 

 blood pressure, cholesterol metabolism, coagulation, 

 and fibrinolytic activity; or b) by other, as yet un- 

 known, mechanisms including an action via the 

 nervous system. Numerous acute psychological 

 episodes of this type over the life span may lead to the 

 establishment of chronic changes, such as those which 

 may operate in hypertension. 



Experience from the animal laboratory is equally 

 fragmentary. Cold stress was shown to produce 

 coronary artery changes in rats (141). Friedman & 

 Uhley (49) have shown that rats kept tense in antic- 

 ipation of electric shocks showed significantly 

 shortened blood-clotting time. They found no 

 difference in coronary atherosclerosis between aggres- 

 sive and passive chicks on an atherogenic diet. Other 

 results confirm this observation. Recent studies in 

 our laboratorv indicate that isolation of chicks in a 

 quiet, undisturbed room increases the atherogenic 

 response to a high-fat, high-cholesterol diet (124). 



Also, isolation during the healing phase of athero- 

 sclerosis prevents regression of lesions. Such isolated 

 cockerels, in addition, showed retarded sexual growth 

 as evidenced by decreased testis weight and comb 

 size, as well as a decreased food efficiency expressed by 

 smaller weight gain on a food intake similar to that of 

 the controls. 



It cannot yet be determined from these results 

 whether the observed effects of isolation of the birds 

 constituted a response to a severe stress, specifically 

 the unnatural isolation, or were, on the contrary, the 

 result of the lack of normal stresses. However, all 

 these data indicate that certain environmental 

 influences, mediated via the central nervous system 

 and involving the nervous and hormonal regulation 

 of body functions, including that of the vessels them- 

 selves, can influence the vascular response to a 

 potentially atherogenic diet. These findings may have 

 far reaching implications, particularly should "lack 

 of normal stress" be the underlying cause. 



The evidence relating emotional or psychological 

 stress to atherosclerosis, clinical or experimental, is 

 at best fragmentary. It is much too early to extrap- 

 olate the findings and to make any major generaliza- 

 tion. Many further well-controlled and systematic 

 studies are required to help our understanding of the 

 complicated mechanisms which operate in this elusive 

 area. 



SUMMARY 



From the data presented in this chapter the 

 following conclusions can be drawn: 



Whether or not atherosclerosis emerges as a major 

 health problem in a population is largely and mainly 

 determined by the life-span pattern of the diet. In 

 the case of any individual member of a population 

 group which is habitually ingesting a potentially 

 atherogenic diet, several other factors will determine 

 the degree and extent of atherosclerosis and clinical 

 atherosclerotic disease — this is not always mirrored 

 by the blood cholesterol or other lipid levels. There is 

 a complex interplay between diet and these other 

 factors which operate to accelerate or retard athero- 

 genesis. The most important of these accessory factors 

 determining the individual's fate with regard to 

 atherosclerosis are hormones, heredity, and stress. 



It is hopefully felt that by taking all these factors 

 into account it will become possible to single out 

 persons particularly prone to develop atherosclerotic 

 disease at a relatively early age and to suggest dietary 



