ABSTRACT
The practice of public health has been criticized as being too involved with a narrow, managerial agenda focused on health care rather than the wider horizons of public good. Public accountability is central to the practice of public health, but is not mentioned in current definitions. We offer a new definition that recognizes the centrality of the public, and which should help public health professionals interpret their own role: 'Use of theory, experience and evidence derived through the population sciences to improve the health of the population, in a way that best meets the implicit and explicit needs of the community (the public)'.
Subject(s)
Public Health/classification , Health Planning , Health Priorities , Humans , Organizational ObjectivesABSTRACT
The practice of public health involves the application of evidence to improving population health, and should be accountable to the public. Accountability to the public can be considered either at the individual doctor-patient interface or through population-level policy making. The public, at both patient and population levels, should join the professionals at each stage of the 'population health evidence cycle'-in asking for, collecting, understanding and using evidence. A greater appreciation of the non-professional, public perspective would represent a substantial commitment to transforming our understanding and needs for different kinds of evidence required to improve the health of the population.
Subject(s)
Evidence-Based Medicine , Public Health Practice/standards , Community Participation , Decision Making , Health Policy , Humans , Physician-Patient RelationsABSTRACT
Previous studies have demonstrated that the specific activities of several proximal small intestinal mucosal enzymes fall in the aging rat. This reduction was due to a delay in the full expression of activity of these enzymes during epithelial cell transit from the crypt onto the intestinal villus. We now show in the ad libitum fed Fischer 344 rat that jejunal sucrase, maltase, and alkaline phosphatase specific activities do not fall gradually throughout the life span, but are reduced during senescence. Caloric restriction to 60% of ad libitum intake (DR) abolishes or delays this fall in enzyme activity. Jejunal mucosal immunoprecipitable sucrase-isomaltase (S-I) content also falls with age, but sucrase specific activity per molecule of S-I is less in the older ad libitum fed (approximately 45) than in the DR rats (approximately 60). Jejunal lactase activity falls gradually throughout the life span of ad libitum and DR rats, but lactase activity consistently was higher in DR animals. These observations indicate that DR alters the age-related changes in the activity of several enzymes in the rapidly replicating gut mucosa.
Subject(s)
Aging/metabolism , Energy Intake , Intestine, Small/metabolism , Alkaline Phosphatase/metabolism , Animals , DNA/metabolism , Ileum/enzymology , Ileum/metabolism , Intestinal Mucosa/enzymology , Intestinal Mucosa/metabolism , Intestine, Small/enzymology , Jejunum/enzymology , Jejunum/metabolism , Lactase , Proteins/metabolism , Rats , Rats, Inbred F344 , Sucrase/metabolism , alpha-Glucosidases/metabolism , beta-Galactosidase/metabolismABSTRACT
Previous studies have reported that small and large intestinal crypt hyperplasia and hyperproliferation occur in senescent rats about 27 mo of age. We have studied duodenal and ileal architecture in ad libitum chow-fed rats and have demonstrated that the increase in duodenal crypt depth and crypt hyperplasia do not develop throughout the life span, but become apparent at 21 and 27 mo of age. These crypt hyperplastic features occur without a change in duodenal villus cell number. Ileal villus cellularity increased throughout the life span, suggesting exposure to a gradually increasing luminal nutrient load. Diet restriction to 60% of the ad libitum feeding rate prolonged the life span of animals from 27 to greater than 33 mo and prevented both the duodenal hyperplasia and the increase in ileal villus cell numbers to the age of 27 mo. Thirty-three-month diet-restricted rats did show evidence of duodenal crypt hyperplasia. We conclude that proximal intestinal hyperplasia is a phenomenon that develops in advanced age, but that ileal villus cellularity increases throughout the ad libitum-fed rodent life span. Diet restriction dramatically retards these intestinal changes that are seen with ad libitum feeding and provides an experimental model for the study of age-related cellular changes of the rodent gastrointestinal tract.