CHAPTER 35 



The role of endocrines, stress, and 

 heredity on atherosclerosis 1 



L. N. KATZ 

 R. PICK 2 



Cardiovascular Institute, Michael Reese Hospital and Medical Center, Chicago, Illir, 



CHAPTER CONTENTS 



Hormones 

 Thyroid 



Pancreatic Hormones 

 Chronic pancreatitis 

 Diabetes mellitus 

 Adrenal and Pituitary Hormones 



Adrenal cortical hormones and ACTH 

 Adrenal medullary hormones 

 Anterior pituitary hormones 

 Conclusion 

 Sex Hormones 

 Heredity 

 Stress 



Physical Activity 

 Emotional Stress 

 Summary 



atherosclerosis, manifested in the lipid-containing 

 intimal lesions of small and large arteries, is the most 

 common pathological form of vascular disease and 

 the most detrimental in its effect on the blood and 

 oxygen supply to any given organ. It is one form of 

 arteriosclerosis, the most important one, leading to 

 widespread morbidity and mortality in man in our 

 Western civilization. 



Several investigative approaches have led to the 



1 Work of the institute mentioned in this communication 

 has been supported by grants from the National Institutes of 

 Health, National Heart Institute USPHS (H-2276, ^3031), the 

 Chicago Heart Association, the Albert and Mary Lasker 

 Foundation, and the Michael Reese Research Foundation. 



2 Established Investigator of the American Heart Association. 



conclusion, held by most but not by all workers in the 

 field, that it is a disease primarily due to disturbance 

 of the metabolism of lipid, lipoprotein, or cholesterol, 

 or all three (72). Whether atherosclerosis develops 

 into a major health problem within a population 

 depends to a large extent on the life-span pattern of 

 its diet. As early as 1934, Rosenthal (133) established 

 that in no population with a high intake of fat and 

 protein from animal sources is atherosclerosis absent, 

 while populations subsisting on a diet low in animal 

 fat and protein are uniformly free from the disease 

 anatomically and, therefore, from the sequelae which 

 produce morbidity and mortality. These findings 

 have been amply confirmed in recent years by world- 

 wide epidemiological studies (42, 74, 79, 107, 157). 

 A tangible concomitant of the ingestion of a diet 

 rich in saturated fats and cholesterol is a hypercholes- 

 terolemic tendency in a population. Thus, while 

 the mean serum cholesterol level of the atherosclero- 

 sis-free populations is 150 to 180 mg per cent, the 

 level for clinically healthy men of comparable age in 

 the United States is 220 mg per cent (74). It is also a 

 well-accepted fact today that serum cholesterol level 

 is the most closely related single factor determining 

 an individual's risk of developing clinical athero- 

 sclerotic coronary disease, i.e., the higher the serum 

 cholesterol, the greater is the risk (30). 



According to our present knowledge, the mode of 

 action by which a diet rich in fats, particularly satu- 

 rated fats and cholesterol, acts to influence lipid 

 metabolism and to produce atherosclerosis can be 

 summarized as follows: cholesterol synthesis in the 



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