Process of Aging: Part V-Arteriosclerosis

What are the relationships between aging, arteriosclerosis and its clinical manifestations, namely coronary heart disease (CHD) and cerebrovascular disease? CHD and cerebrovascular disease are responsible for about half the deaths that occur each year. In individuals over 65 years of age, they are responsible for 70 to 80% of the deaths. Knowledge about the process of arteriosclerosis would go a long way in helping develop methods to prevent this disease.

While aging may be one of the factors precipitating the arterosclerosis process, it is also well known that there are multiple factors that can cause the disease. The major risk factors for arterosclerosis are serum lipid concentrations, smoking, and hypertension. Another factor appears to be gender. Men are approximately twice as likely to develop atherosclerosis as equivalent aged women. Yet when all these factors are taken into account only about half of the variability of incidence of arteriosclerosis and coronary heart disease can be accounted for. Genetics may be a factor but conditions related to aging may also play a not so subtle role in developing the disease.

Start with the fact that as people age, there are changes in blood dynamics that can adversely affect vascular functioning and speed up the process of cardiovascular disease. It would appear that as an individual ages, his/her systolic blood pressure as well as pulse pressure rises. At the same time, elevated blood pressure coexists with other conditions that may increase cardiovascular disease such as obesity, diabetes mellitus and increased low-density lipid cholesterol. The Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure in its 5th report appearing in the Archives of Internal Medicine 1993; 153:154-183 indicated that effective control of hypertension decreases both stroke and coronary heart disease in the elderly.

Not only does blood pressure increase with age, but also plasma cholesterol and LDL-cholesterol, as well as triglycerides. Interestingly, plasma cholesterol and triglycerides show a pattern of increasing in men for the first 50 to 60 years of life, then plateau and finally begin to decline. For women, the same pattern exists, but appears to occur 10 years later than men. High density lipid cholesterol do not show the same pattern, but women tend to have higher HDL cholesterol concentrations at least in the premenopausal years which may account for lower incidence of CHD in premenopausal women.

It has been documented that arteriosclerosis begins in early childhood in the form of fatty streaks. Fatty streaks are slightly raised areas of fat-filled cells (called foam cells) found within the inner wall of blood vessels and would appear to arise from macrophages and contain a lot of cholesterol esters. One study showed that about 65% of the children have substantial accumulations of these cells. As individuals age, the fatty streaks increase into the second and third decades of life and then decrease, being replaced by lesions called atheromas at about the fourth decade. These lesions replace the normal cellular architecture and also fibrous plaques develop. The fibrous plaques cause complication in the lesions as well as ulceration, thrombosis, hemorrhage and mineralization with resultant myocardial infarctions and strokes due to occlusion of an artery.

If this is a normal process of aging, how come whole populations do not get CHD? Here researchers have suggested that a process called remodeling occur in the individuals who do not develop CHD. This involves a compensatory enlargement of the coronary arteries as part of the structural and functional changes occurring in all levels of arteries. This enlargement of the diameter of the artery is also accompanied by thickening of the artery wall and plaque formation.

The story doesn’t stop there. Other changes associated with aging including a progressive decline in glucose tolerance and the compensatory development of hyperinsulinemia to deal with the intolerance. The latter is a major risk factor for the development of CHD. The high plasma insulin levels affect foam cells which then have a cascading effect on the capacity of blood to circulate (atherosclerosis) resulting in CHD. Insular resistance involves peripheral tissue resistance to insulin action. Thus, it may be that hyperinsulinemia secondary to an acquired or genetic insular resistance enhances the arteriosclerotic process. This leads to the theory that if you could reduce the insulin levels, you may reduce the risk of arteriosclerosis and its clinical manifestation, CHD.

This leads to another level of this complicated and still not fully understood process. With aging, there is an increase in the total body fat usually seen as an elevated waist to hip ratio. Insulin resistance may play a role in this increased body fat and may be associated with abdominal obesity accompanying aging, rather than the aging process per se. Waist circumference involves two types of fat, depending on their location: subcutaneous fat, below skin level and visceral fat, within the abdominal cavity. It would appear that visceral fat accumulation is more closely associated with insulin resistance. One study showed that visceral fat was present in almost 90% of obese patients with ischemic heart disease, and in 40% of non-obese subjects with cardiovascular disease.

Thus if visceral fat accumulation could be controlled, society may have another way to reduce medical expenses and enhance the wellness to the aging individual. Determinants of this fat have been suggested to be physical inactivity, excessive sucrose (refined sugar) intake, sex hormone concentrations and aging. In this series of articles on aging, we wrote of the research in reducing caloric intake as a way of dealing with disease conditions of aging as well as moderate exercise and dietary changes as necessary concomitants of healthy living. While science struggles to figure out the processes of aging and disease, the individual is empowered to increase the odds of living a full and complete life via adopting a personal life style in tune with physiological changes going on as we all age. The strategy is to implement dietary changes to control disease risk while one is healthy. It is never too early to prevent disease.


Written by Harold Rubin, M.S., ABD, CRC, Guest Lecturer

Go to Part I of Aging Articles Mortality risk factors
Go to Part II of Aging Articles Gender differentiation
Go to Part III of Aging Articles Cellular senescence
Go to Part IV of Aging Articles Biological aging/health strategies
The Aging Process-Part VI-Aging in Males
The Aging Process-Part VII-Aging in Women
The Aging Process-Part VIII-Infectious Disease
Process of Aging-Part IX-DHEA
The Aging Process-Part X-Skin, Skeleton and Brain
The Aging Process:-Part XI-Apotosis and the Elderly
The Aging Process-Part XII-Biomarkers for Aging
The Aging Process- Part XIII- Body Odors

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