The concept of any disease arising from a single cause is obsolete and misleading. Much evidence now suggests that most of the lethalness of a high fat diet in Western society may actually be dependent on the “catalytic” influence of stressful living. Indeed, while habitual diet and psychic stress both appear implicated in the pathogenesis of clinical coronary disease, there is mounting evidence to suggest that each of these factors is dependent upon the other for pathologic significance . Observations in the animal kingdom, in the experimental laboratory, and in epidemiologic surveys all attest to the validity of this pathogenetic interrelationship. Like “stressed” animals in the laboratory, “stressed” humans have manifested no increased susceptibility to atherosclerosis unless the composition of the diet had been high in animal fat. Contrariwise, numerous examples are now at hand to indicate the low atherogenicity of a high fat diet when there is relative freedom from serious psychologic stress. Despite the profound effect of “stress” on homeostatic mechanisms this factor has been largely ignored by most authorities in the field of coronary artery disease. Major emphasis has been placed on hypercholesterolemia, overweight, high blood pressure, lack of exercise, cigarette smoking and diabetes. Nevertheless, nervous strain is known to elevate blood pressure, to increase the tendency to obesity, to contribute to excessive smoking and lack of exercise, to participate in hypercholesterolemia, and to aggravate diabetes, through psychic influence and alteration of the functional characteristics of the mode of life. Consequently, even such indirect effects of emotional stress, barring all others, must elevate this factor to a position of considerable significance in the etiologic picture of coronary heart disease.