Death makes news: the social impact of disease on newspaper coverage.

UNLABELLED: This paper is an integrated analysis of newspaper coverage, epidemiological rates, and recent social history of six prominent diseases. HYPOTHESES: Newspaper coverage of a disease has three developmental stages (emergence, maturation, and decline & death). Trends in newspaper coverage of a disease reflect trends in its mortality, prevalence, and incidence. Magnitudes of newspaper coverage of diseases reflect their differential mortality rates. DATA: Using the LEXIS-NEXIS news archive for major U.S. newspapers, we retrieve articles about cancer, heart disease, AIDS, diabetes, Alzheimer disease, and arthritis for the period 1977-1997. We also obtain mortality, prevalence, and incidence trends for the six diseases. RESULTS: During the two decades, newspaper coverage emerges for AIDS and Alzheimer disease and is in the mature stage for the other diseases; declines begin for heart disease and AIDS. Trends in news coverage closely parallel mortality trends, and less consistently prevalence and incidence trends. Sharp downturns and upturns in mortality are mirrored in news volume. High-mortality diseases prompt both the most news coverage and the largest proportions of articles with death topics. CONCLUSION: Newspaper coverage of diseases is responsive to their mortality levels and trends.

The Alzheimerization of aging: a brief update.

This article extends the previously published opinion that the NIA disproportionately supports research related to Alzheimer's Disease at the expense of a more comprehensive research agenda. Letters to the editor, as well as newspaper interviews of partisans from the research community, both affirm and reject the opinion. The broader basic science community must overcome its traditional political apathy to pursue a more balanced research agenda at the NIA.

The Alzheimerization of aging.

The NIA invests a disproportionately large share of its resources in research on Alzheimer's Disease at the expense of other interests of the broader scientific community in gerontology. Complex social forces that continue to shape this outcome embrace discipline-specific traditions of science advocacy, as well as science-driven intellectual growth.

Aging enhances inhibitory action of somatostatin in rat pancreas.

This study examines the effects of donor age on exogenous somatostatin inhibition of insulin secretion stimulated by 10 mM D-glyceraldehyde and by 20 mM beta-D-glucose in isolated perfused rat pancreas. Both 6 and 30 nM synthetic somatostatin-14 affect both glyceraldehyde- and glucose-stimulated insulin secretion to a greater degree in pancreases from old animals (24-27 months) than in those from young (2-5 months). We conclude that an increased sensitivity to inhibitory actions of somatostatin during aging, observed in pituitary tissues in vitro, occurs in pancreatic tissues as well and may constitute a general phenomenon in tissues subject to somatostatin inhibition.

Regulation of insulin secretion by glucose during aging.

The purpose of this study was to investigate the sensitivity of insulin secretion to glucose and its possible relationship to changes in islet glucose utilization during aging. Pancreatic islets of Langerhans were isolated from male Sprague-Dawley rats aged 2- to 24-months and perifused in vitro with glucose. Insulin concentration was determined by radioimmunoassay. Glucose utilization was assessed by measuring the rate of conversion of 3H-5-D-glucose to 3H-H20. The sensitivity of isolated, perifused islets to glucose was reduced during aging. Less glucose metabolism, however, may be required to elicit comparable release of insulin by islets from old than from young rats.

The capability for regulation of insulin secretion by somatostatin in purified pancreatic islet B cells during aging.

Pancreatic islet B cells from Sprague-Dawley and Fisher 344 rats aged 3-27 months were separated from A and D cells by centrifugation over a linear percoll density gradient, and incubated in vitro with various concentrations of glucose and somatostatin. Elevation of glucose concentration in the incubation medium from 2.6 to 16.7 mM provokes an insulin secretory response that is independent of rat donor age. Inhibition of the insulin secretory response by somatostatin is independent of rat donor age beyond 12 months. These data indicate that the impaired regulation of insulin secretion during aging observed previously in vivo and in vitro in intact islets may not be intrinsic to the B cells, but instead reflect changes in islet paracrine regulatory mechanisms that relate to the quality and/or quantity of endogenous somatostatin and/or glucagon.

A role for somatostatin in the impaired insulin secretory response to glucose by islets from aging rats.

The purpose of this study was to investigate a possible contribution by somatostatin to the impairment in glucose-stimulated secretion of insulin during aging. Pancreatic islets of Langerhans were isolated from male Sprague-Dawley rats aged 2- to 24-months and challenged in vitro with effectors of insulin secretion. Concentrations of insulin, glucagon, and somatostatin were determined by radioimmunoassay. The impairment of glucose-stimulated secretion of insulin which characterizes islets isolated from aged rats may be overcome by treatment of islets with antibodies to somatostatin. Enhanced availability and/or effectiveness of endogenous pancreatic somatostatin during aging may be responsible for the modified pattern of glucose-stimulated secretion of insulin.

The role of hormones in changing adaptive mechanisms during aging.

A generalized characteristic of all aging populations is the progressively impaired ability to adapt to an altered environment. The increased latent period for the response of hepatic glucokinase activity to glucose in aging rats is one specific example of this phenomenon. The disturbed regulation of hepatic glucokinase activity probably is the consequence of altered control of the secretion of key hormones rather than effects of aging on hepatic function. Such changes in the regulation of hormone secretion already are documented or suspected at least for insulin, glucagon, adrenal glucocorticoids, and thyroid hormones. The regulation of insulin secretion by glucose is altered during aging within the predominant population of islets of Langerhans, perhaps by differences in cell-to-cell communication within these islets. Once the nature of limiting biochemical modifications is established within a specific cell population, it may be possible to identify the origin of at least a distinct set of gerontological phenomena.

Loss of adaptive mechanisms during aging.

Factors contributing to modifications in the capability for enzyme adaptation as an expression of aging are reviewed. Specific examples of altered enzyme adaptations during aging include the responses of hepatic glucokinase activity to glucose and hepatic tyrosine aminotransferase activity to starvation in Sprague-Dawley rats. These impaired enzyme adaptations apparently are not the consequence of alterations in hepatic function during aging. Instead, they reflect disturbances in extrahepatic hormonal regulatory mechanisms. Specific examples include modifications in the control of circulating levels of insulin glucagon, corticosteroids, and thyroid hormones. Age-dependent changes in the regulation of circulating levels of insulin probably originate within the impaired ability of pancreatic islets of Langerhans to secrete the hormone in response to glucose. The rationale for exploiting this experimental approach as a means to understand biological aging is discussed.