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Currently available data on the effect of age in tissue protein synthesis and turnover are reviewed and experimental evidence is presented on age changes in amino acid incorporation by rat liver purified microsomes. It has been observed that the purification of ‘crude’ microsomal preparations from contaminating lysosomes by density gradient centrifugation is accompanied by an increase in amino acid incorporatmg activity of the microsomal preparations, no matter whether these are prepared from young or from old animals, and that the amino acid incorporating activity of rat liver purified microsomes prepared from old animals (19–25 months) is lower than that prepared from adult animals (7–11 months) which in turn is lower than that from young animals (2–3 months), no matter whether the activity is expressed per mg of microsomal protein or per mg of microsomal RNA. Also, experimental evidence is presented which is consistent with the presence in liver purified microsomes of heat-labile inhibitor(s) of amino acid incorporation, and with their accumulation (or increase in effect) in the microsomes with the age of the animal. Several major features of the decline with age in tissue protein synthesis are outlined and a number of possible factors or causes, beside the microsomal inhibitor(s), contributing to the decline with age in tissue protein synthesis, are discussed.

Since the period of great progress against epidemic and acute diseases, a host of major chronic diseases afflicting older adults have emerged as the key health problems of our time. Concomitantly there arises the need for deeper knowledge of the causes, dimensions and subtleties of age decline in the individual's reserve capacities and resistance to disease, and the need for better understanding of the relationship of chronic diseases to environmental factors as an integral part of our search for basic measures toward health maintenance and disease prevention in older adults. The age decline in reserve capacities and in resistance to disease can either be slowed down by preventive measures and even reversed to some extent by physical exercise, or it can be further aggravated by excessive demands beyond their declining limits. The relationship of chronic diseases to environmental factors is illustrated by the effects of nutrition on the life span, on atherosclerosis and on other diseases. The relationship of obesity, diabetes and coronary heart disease to one another, to the increased ingestion of fat or sugar, to gorging, and to long‐spaced, heavy meal‐eating habits is discussed. In view of the sum total of environmental influences, a lifetime application of basic measures for health maintenance and disease prevention is stressed. Unfortunately, much too often a compromise with health is becoming an accepted pattern, possibly because of an increasing willingness to consider health not as a pure and incontestable human good, but as a generally desirable element, in active competition with other human needs such as economic gain or just plain pleasurable living.

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