The natural history of atherosclerosis: an ecologic perspective.

Virologic findings reported in recent atherosclerosis literature may have profound implications. To assess them, we have viewed atherosclerosis in a broad biologic context and against a background of environmental, behavioral, and social change. Reasonable grounds exist, we believe, for regarding atherosclerosis as a chronic, low-grade infectious macroangiopathy which is aggravated by hypercholesterolemia and other recognized risk factors. There are probably multiple infective pathogens and transmission routes. The putative agents that initiate atherosclerosis might include ubiquitous viruses that produce clinically unapparent infections in many animal species. Pathways for their transmission to humans may include the food chain and contaminated water. Food-chain transmission may have been largely responsible for the parallel increases of meat consumption and mortality from coronary heart disease in the United States during the middle third of the century. It provides a hypothetical basis for considering thermal intervention as a heretofore unrecognized factor that may actually best account for the surprising reversal of climbing heart disease mortality rates. Improved sanitation and food hygiene as well as improvements in diet, lifestyle, and medical care may have shaped the downward mortality curve. The virus hypothesis may reconcile apparent epidemiologic conflicts and elucidate the natural history of atherosclerosis.

Perspectives on the etiology of Alzheimer's disease.

There is a lack of consensus among investigators concerning the etiology of Alzheimer's disease. Clues are not lacking, however, and we have assessed them in a broad biologic context. This inquiry has led us to regard Alzheimer's disease as a multifactorial disorder in which a putative infective agent is an essential element. Despite seeming competition among current hypotheses, there is overall unity. The concept that Down's syndrome is a congenital form of Alzheimer's disease and that both conditions are the result of a ubiquitous infective pathogen that affects genetically susceptible individuals offers the broadest unification. In both conditions slow infection develops against the background of aging. Indirect evidence involving immunologic and other biologic phenomena supports the postulated infectious origin. Overlapping pathologic and clinical features of Alzheimer's disease and the known transmissible encephalopathies suggest a similar pathogenesis.

Human cancer and the food chain: an alternative etiologic perspective.

Oncogenic viruses are among the known or presumed initiating agents of human cancer. Although evidence suggests that DNA and RNA oncoviruses may be acquired through multiple routes, our attention focuses chiefly on the ingestion pathway. We have two reasons for this. One is the possibility that viral as well as nonviral oncogenic amino acid sequences might be acquired at the top of the food chain. The other is that the food chain-infection hypothesis may reconcile several biological, ecological, and epidemiological phenomena. Transfection experiments suggest that the concept of infection may have to be broadened to embrace the cellular precursors of oncogenic viruses. Accumulating circumstantial evidence from viral oncology and molecular biology provides a basis for the belief that oncogenic viruses and their cellular precursors might be transmitted from animals to humans through the ingestion pathway. The possibility that such transmission may give rise to some human cancers must now be considered. The ingestion and genomic integration of food-associated DNA sequences may directly account for the increased risk of human cancer associated with an elevated intake of animal fat and protein. This paper addresses the role of infective oncogenic agents as the initiators, rather than the promoters, of cancer.

Reducing tobacco consumption in California. Development of a statewide anti-tobacco use campaign.

Cigarette smoking continues to be the leading preventable cause of death in California and the United States. Although substantial progress has been made over the past 25 years, there is growing recognition of the need for large-scale efforts to reduce tobacco use. Given their central roles in implementing public health programs and their ability to reach many of the groups most at risk of tobacco use uptake and tobacco-related disease, state health agencies have an important challenge before them. This article describes the development and operation of a statewide, publicly funded anti-tobacco use campaign currently undertaken by the California Department of Health Services under the auspices of the state's Tobacco Tax and Health Promotion Act of 1988 (Proposition 99), which increased excise taxes on cigarettes by 25 cents per pack sold in the state. A discussion of problems in implementation and operation being incurred may be relevant to the planning of similar campaigns elsewhere.