Monitoring chronic diseases in Canada: the Chronic Disease Indicator Framework.

INTRODUCTION: The Public Health Agency of Canada developed the Chronic Disease Indicator Framework (the Framework) with the goal of systematizing and enhancing chronic disease surveillance in Canada by providing the basis for consistent and reliable information on chronic diseases and their determinants. METHODS: Available national and international health indicators, frameworks and national health databases were reviewed to identify potential indicators. To make sure that a comprehensive and balanced set of indicators relevant to chronic disease prevention was included, a conceptual model with "core domains" for grouping eligible indicators was developed. Specific selection criteria were applied to identify key measures. Extensive consultations with a broad range of government partners, non-governmental organizations and public health practitioners were conducted to reach consensus and refine and validate the Framework. RESULTS: The Framework contains 41 indicators organized in a model comprised of 6 core domains: social and environmental determinants, early life / childhood risk and protective factors, behavioural risk and protective factors, risk conditions, disease prevention practices, and health outcomes/status. Also planned is an annual release of updated data on the proposed set of indicators, including national estimates, breakdowns by demographic and socioeconomic variables, and time trends. CONCLUSIONS: Understanding the evidence related to chronic diseases and theirdeterminants is key to interpreting trends and crucial to the development of public health interventions. The Framework and its related products have the potential of becoming an indispensable tool for evidence-informed decision making in Canada.

TITRE: Surveillance des maladies chroniques au Canada : Cadre conceptuel d'indicateurs des maladies chroniques. INTRODUCTION: L'Agence de la santé publique du Canada a conçu le Cadre conceptuel d'indicateurs des maladies chroniques (le Cadre) dans le but de systématiser et d'améliorer la surveillance des maladies chroniques au Canada en instaurant les fondements d'une information uniforme et fiable sur les maladies chroniques et leurs déterminants. MÉTHODOLOGIE: Des indicateurs de santé nationaux et internationaux, des cadres conceptuels ainsi que des bases de données sur la santé nationale ont été examinés pour identifier les indicateurs potentiels. Pour s'assurer d'obtenir un ensemble complet et équilibré d'indicateurs pertinents en matière de prévention des maladies chroniques, nous avons élaboré un modèle conceptuel comprenant des « champs de référence ¼ pour le regroupement des indicateurs. Plusieurs critères de sélection ont été appliqués pour le choix des mesures clés. Des consultations approfondies avec un large éventail de partenaires du gouvernement, d'organismes non gouvernementaux et de professionnels de la santé publique ont été réalisées pour en arriver à un consensus et pour perfectionner et valider le Cadre. RÉSULTATS: Le Cadre comprend 41 indicateurs structurés autour de 6 champs de référence : les déterminants sociaux et environnementaux, les facteurs de risque et de protection en bas âge, les facteurs de risque et de protection comportementaux, les conditions à risque, les pratiques de prévention des maladies, l'état de santé global et les impacts sur la santé. Nous avons aussi prévu une mise à jour annuelle des données touchant l'ensemble des indicateurs proposés, que ce soit les estimations nationales, les ventilations par variables démographiques et socioéconomiques ou les tendances temporelles. CONCLUSION: Comprendre les données probantes liées aux maladies chroniques et leurs déterminants est nécessaire pour interpréter les tendances et crucial pour élaborer des interventions efficaces en matière de santé publique. Le Cadre et ses produits connexes sont susceptibles de devenir un outil indispensable d'aide à la décision axée sur des données probantes au Canada.

Dietary niacin deficiency lowers tissue poly(ADP-ribose) and NAD+ concentrations in Fischer-344 rats.

Poly(ADP-ribose) is synthesized in response to DNA strand breaks, using NAD+ as substrate, and has been implicated in the process of DNA repair. Because NAD+ can be synthesized from niacin or tryptophan, both of these components must be manipulated to alter niacin status. Six dietary treatments were used, including niacin-deficient (ND) diets and niacin-replete (NR) diets consumed ad libitum and the NR diets pair-fed (PF) to the ND intake. The ND, NR and PF diets contained either 80 g casein + 50 g gelatin/kg diet (8-5 diets) or 70 g casein + 60 g gelatin/kg diet (7-6 diets) to control tryptophan content. The 8-5ND and 7-6ND diets induced mild and severe symptoms of niacin deficiency, respectively, over a 3-wk period in male weanling Fischer-344 rats. Food intake and weight gain were suppressed in both of the ND groups compared with their respective NR controls. Weight gain was not different between ND animals and their PF counterparts. At 3 wk, blood, liver, kidney, heart and lung NAD+ concentrations for both 8-5ND and 7-6ND animals were all significantly lower than those for their respective PF groups. In the groups fed the 8-5 diets, liver poly(ADP-ribose) was lower in the ND group (64% of PF), with no difference between the NR and PF groups. In rats fed the 7-6 diets, poly(ADP-ribose) levels were further decreased in the ND group (43% of PF), but food restriction also exerted an independent effect (PF levels were 46% of NR levels).(ABSTRACT TRUNCATED AT 250 WORDS)

Diethylnitrosamine administration in vivo increases hepatic poly(ADP-ribose) levels in rats: results of a modified technique for poly(ADP-ribose) measurement.

Poly(ADP-ribose) (polymer) is enzymatically synthesized on nuclear proteins in response to DNA strand breaks. NAD+ is the substrate for this reaction, which is catalyzed by poly(ADP-ribose)polymerase. This post-translational modification occurs in response to DNA strand breaks and is thought to play an important role in DNA repair. Polymer synthesis resulting from DNA damage has been described in cultured cells, but measurement is more difficult in animal tissues. In this study, modifications were made to an earlier method to measure carcinogen-induced increases in polymer levels in vivo. RNase I was added to the enzyme mixture used to digest polymer to ribosyladenosine (RAdo). This prevented the inhibition of snake venom phosphodiesterase by RNA. The HPLC analysis was improved, allowing elimination of the second boronate affinity chromatography step traditionally used to purify epsilon RAdo. Using this technique, we have studied the effect of i.p. diethylnitrosamine (DEN) injection on hepatic NAD+ and poly(ADP-ribose) levels in Fischer-344 rats. Hepatic polymer levels rose 8-fold from 26 to 218 pmol/g liver wet weight, 10 h following 200 mg DEN/kg body weight (n = 4-5). Liver NAD+ decreased concurrently, to 61% of basal levels at 16 h post-treatment (n = 4-5). Erythrocyte NAD+ concentrations remained unchanged, despite carcinogen administration. The DEN-induced effects on tissue polymer and NAD+ levels were dose dependent from 0 to 200 mg DEN/kg body weight (n = 4).

Zinc deficiency in the rat alters the lipid composition of the erythrocyte membrane Triton shell.

The effect of dietary zinc deficiency on the lipid composition of the erythrocyte membrane Triton shell was determined. Weanling male Wistar rats were fed an egg white-based diet containing < 1.0 mg Zn/kg diet ad libitum. Control rats were either pair-fed or ad libitum-fed the basal diet supplemented with 100 mg Zn/kg diet. A Zn refed group was fed the -Zn diet until day 18 and then pair-fed the +Zn diet until day 21. Dietary Zn deficiency caused an increased cholesterol/phospholipid ratio in Triton shells compared to those from pair-fed controls. Zn deficiency caused a decreased double bond index of fatty acids in phosphatidylinositol (PI) and phosphatidylcholine (PC); there was a decreased proportion of 18:2n-6 and 22:4n-6 in PC and 20:4n-6 in PI as compared to that found in pair-fed controls. All glycerophospholipids that were retained in the shell had a lower double bond index and increased content of 16:0 and/or 18:0 relative to the phospholipid in the intact membrane.

The effect of dietary zinc deficiency on the lipid composition of the rat erythrocyte membrane.

The effect of dietary zinc deficiency in the rat on the lipid composition of the erythrocyte membrane was determined. Weanling male Wistar rats were fed an egg white-based diet containing less than 1.0 mg Zn/kg diet ad libitum. Control rats were either pair-fed or ad libitum-fed the basal diet supplemented with 100 mg Zn/kg diet. A zinc refed group was fed the -Zn diet until day 18 and then pair-fed the +Zn diet until day 21. The voluntary feed restriction associated with dietary zinc deficiency resulted in erythrocyte membranes that had depressed phospholipid/protein and elevated cholesterol/phospholipid ratios. Similarly, all feed restricted groups had elevated 22-carbon n-3 polyunsaturated fatty acids (PUFA) and depressed 22-carbon n-6 PUFA concentrations in alkenyl-acyl and diacyl glycerophosphoethanolamine, phosphatidylserine and phosphatidylcholine; they also had depressed 24:2n-6 levels in sphingomyelin. The relative concentrations of phospholipids in the membrane was similar between -Zn and +Zn (ad libitum) groups; however, the -Zn group had significantly less phosphatidyl-serine relative to +Zn (pair-fed) controls.

Effect of cellular growth state on indices of n - 6 polyunsaturated fatty acid status in human fibroblasts.

A 2 x 2 design was employed to examine the effect of cellular growth state and medium serum concentration on potential indices of n - 6 polyunsaturated fatty acid (PUFA) status in human skin fibroblasts. The cells were cultured either as nonmultiplying cell monolayers or as medium-density, log-phase multiplying cells. An interaction of cellular growth state and medium serum concentration influenced the accumulation of 20:3(n - 9), but not 22:3(n - 9), in the cellular phospholipids. The 20:3(n - 9)/20:4(n - 6) ratio was the most sensitive index of n - 6 PUFA status; however, the ratio was significantly affected by cellular growth state. The 22:3(n - 9)/22:4(n - 6) ratio appears to be an index of n - 6 PUFA status in fibroblasts that is not significantly affected by the growth state of cells.