Household-level financial uncertainty could be the primary driver of the global obesity epidemic.

Evidence has accumulated in support of the notion that changes in household-level financial uncertainty (or "economic insecurity") may be an important fundamental cause of the global obesity epidemic. The timing and spatial/demographic incidence of the obesity epidemic suggest that economic policies aimed at expanding economic freedom may have inadvertently shifted risk to households, thereby generating a costly public health problem.

Smart food policies for obesity prevention.

Prevention of obesity requires policies that work. In this Series paper, we propose a new way to understand how food policies could be made to work more effectively for obesity prevention. Our approach draws on evidence from a range of disciplines (psychology, economics, and public health nutrition) to develop a theory of change to understand how food policies work. We focus on one of the key determinants of obesity: diet. The evidence we review suggests that the interaction between human food preferences and the environment in which those preferences are learned, expressed, and reassessed has a central role. We identify four mechanisms through which food policies can affect diet: providing an enabling environment for learning of healthy preferences, overcoming barriers to the expression of healthy preferences, encouraging people to reassess existing unhealthy preferences at the point-of-purchase, and stimulating a food-systems response. We explore how actions in three specific policy areas (school settings, economic instruments, and nutrition labelling) work through these mechanisms, and draw implications for more effective policy design. We find that effective food-policy actions are those that lead to positive changes to food, social, and information environments and the systems that underpin them. Effective food-policy actions are tailored to the preference, behavioural, socioeconomic, and demographic characteristics of the people they seek to support, are designed to work through the mechanisms through which they have greatest effect, and are implemented as part of a combination of mutually reinforcing actions. Moving forward, priorities should include comprehensive policy actions that create an enabling environment for infants and children to learn healthy food preferences and targeted actions that enable disadvantaged populations to overcome barriers to meeting healthy preferences. Policy assessments should be carefully designed on the basis of a theory of change, using indicators of progress along the various pathways towards the long-term goal of reducing obesity rates.

Incidence and survival of primary central nervous system tumors diagnosed in 4 Canadian provinces from 2010 to 2015.

Background: The Brain Tumor Registry of Canada was established in 2016 to enhance infrastructure for surveillance and clinical research on Central Nervous System (CNS) tumors. We present information on primary CNS tumors diagnosed among residents of Canada from 2010 to 2015. Methods: Data from 4 provincial cancer registries were analyzed representing approximately 67% of the Canadian population. Age-standardized incidence rates (ASIR) and 95% confidence intervals (CI) were calculated using the 2011 Canadian population age distribution. Net survival was estimated using the Pohar-Perme method. Results: A total of 31 644 primary tumors were identified for an ASIR of 22.8 per 100 000 person-years. Nonmalignant tumors made up 47.1% of all classified tumors, with mixed behaviors present in over half of histology groupings. Unclassified were 19.5% of all tumors. The most common histological subtypes are meningiomas (ASIR = 5.5 per 100 000 person-years); followed by glioblastomas (ASIR 4.0 per 100 000 person-years). The overall 5-year net survival rate for CNS tumors was 65.5%; females 70.2% and males 60.4%. GBMs continue to be the most lethal CNS tumors for all sex and age groups. Conclusions: The low annual frequency of most CNS tumor subtypes emphasizes the value of population-based data on all primary CNS tumors diagnosed among Canadians. The large number of histological categories including mixed behaviors and the proportion of unclassified tumors emphasizes the need for complete reporting. Variation in incidence and survival across histological groups by sex and age highlights the need for comprehensive and histology-specific reporting. These data can be used to better inform research and health system planning.

Distribution of HPV genotypes among women with abnormal cytology results in Alberta, Canada.

Background: Persistent infection with a subset of human papillomavirus (HPV) genotypes can cause abnormal cytology and invasive cervical cancer. This study examines the circulating HPV genotype strains in a local population of the province of Alberta (a largely unvaccinated population) to establish baseline frequency of vaccine and non-vaccine genotypes causing abnormal cervical cytology. Method: Remnant liquid-based cytology specimens from the Alberta Cervical Cancer Screening Program (March 2014-January 2016) were examined. Only specimens from women who had a cytology grading of atypical squamous cells of undetermined significance or higher were included. HPV genotype was determined for all samples, and results were stratified by demographics and cytology results. Results: Forty-four unique HPV genotypes were identified from 4,794 samples. Of the 4,241 samples with a genotype identified, the most common genotypes were HPV 16, 18, 31, and 51, with 1,599 (37.7%), 441 (12.2%), 329 (7.8%), and 354 (8.4%), respectively. HPV9 vaccine genotypes made up 73.2% of these genotyped samples. Compared with specimens in which HPV9 vaccine genotypes were not detected, those with a genotype covered by the HPV9 vaccine were from younger women (33 [interquartile range {IQR] 28 to 42] y versus 40 [IQR 32 to 51] y; p < 0.00001). Conclusions: The baseline distribution of HPV genotypes in this largely unvaccinated population indicates that the HPV9 vaccine provides good protection from high-risk HPV infections. Determining the frequency of genotypes causing abnormal cytology in this population post-vaccine implementation will be important to assess efficacy of vaccination and monitor for any potential genotype replacement.

Historique: L'infection persistante par un sous-groupe de génotypes du virus du papillome humain (VPH) peut être responsable d'une cytologie anormale et d'un cancer invasif du col de l'utérus. La présente étude porte sur les souches du génotype du VPH en circulation dans une population locale de la province de l'Alberta (largement non vaccinée) pour établir la fréquence de base des génotypes vaccinaux et non vaccinaux responsables de cytologies du col de l'utérus anormales. Méthodologie: Les chercheurs ont examiné les résidus de prélèvement de cytologie en milieu liquide du programme albertain de dépistage du cancer du col de l'utérus (de mars 2014 à janvier 2016). Seuls les prélèvements de femmes dont la cytologie était classée d'après la présence de cellules squameuses (ou malpighiennes) atypiques à caractère non déterminé ou plus graves ont été retenus. Les chercheurs ont déterminé le génotype du VPH de tous les prélèvements et stratifié les résultats selon les résultats démographiques et cytologiques. Résultats: Les chercheurs ont retenu 44 génotypes uniques du VPH à partir de 4 794 prélèvements. Les VPH 16, 18, 31 et 51 étaient les principaux génotypes observés, correspondant à 1 599 (37,7 %), 441 (12,2 %), 329 (7,8 %) et 354 (8,4 %) cas, respectivement. Les génotypes du vaccin contre le VPH9 représentaient 73,2 % des prélèvements. Par rapport aux prélèvements dans lesquels les génotypes du vaccin contre le VPH9 n'avaient pas été décelés, ceux dont le génotype était couvert par le vaccin contre le VPH9 provenaient de femmes plus jeunes (33 ans [plage interquartile {PIQ} de 28 à 42] par rapport à 40 ans chez les autres [PIQ de 32 à 51]; p < 0,00001). Conclusion: Selon la distribution de référence des génotypes du VPH dans cette population largement non vaccinée, le vaccin contre le VPH9 assure une bonne protection contre les infections à VPH à haut risque. Il sera important de déterminer la fréquence des génotypes responsables d'une cytologie anormale dans cette population après l'adoption du vaccin pour en évaluer l'efficacité et surveiller le remplacement potentiel des génotypes.

The Importance of Cancer Registry Linkage for Studying Rare Cancers in Prospective Cohorts.

Large prospective cohort studies may offer an opportunity to study the etiology and natural history of rare cancers. Cancer diagnoses in observational cohort studies are often self-reported. Little information exists on the validity of self-reported cancer diagnosis, especially rare cancers, in Canada. This study evaluated the validity of self-reported cancer diagnosis in Alberta's Tomorrow Project (ATP), a provincial cohort in Canada. ATP data were linked to the Alberta Cancer Registry (ACR). The first instance of self-reported cancer in a follow-up survey was compared to the first cancer diagnosis in the ACR after enrollment. The sensitivity and positive predictive value (PPV) were estimated for the reporting of cancer status, reporting of common or rare cancer, and reporting of site-specific cancer. Logistic regression analysis explored factors associated with false positive, false negative, and incorrect cancer site reporting. In the 30,843 ATP participants who consented to registry linkage, there were 810 primary cancer diagnoses in the ACR and 959 self-reports of first cancer post-enrollment, for a cancer status sensitivity of 92.1% (95% CI: 90.0-93.9) and PPV of 77.8% (95% CI: 75.0-80.4). Compared to common cancers, rare cancers had a lower sensitivity (62.8% vs. 89.6%) and PPV (35.8% vs. 84.5%). Participants with a rare cancer were more likely to report an incorrect site than those with a common cancer. Rare cancers were less likely to be captured by active follow-up than common cancers. While rare cancer research may be feasible in large cohort studies, registry linkage is necessary to capture rare cancer diagnoses completely and accurately.

Examination of a Canadian provincial prenatal HIV screening program: 2010 to 2014.

OBJECTIVES: Universal prenatal screening in the Canadian province of Alberta employs an 'opt-out' HIV screening strategy. We examined all women giving birth in the province and determined the frequency and characteristics of women having and not having HIV screening. METHODS: All livebirths in Alberta from January 1, 2010 to December 31, 2014 were compiled from the Vital Statistics database and linked to HIV screening data to determine maternal demographic and prenatal care characteristics. Correlates associated with prenatal HIV screening, opting out of HIV screening, and not having any prenatal communicable disease screening were determined by multivariable statistics. RESULTS: Of the 256,280 live births, 94.2% had prenatal HIV screening, 1.9% declined prenatal HIV screening, and 3.9% had no record of any prenatal communicable disease testing. Compared with those who had HIV screening, those who opted out of prenatal HIV screening were more likely to be over 40 years of age (adjusted odds ratio (AOR), 2.83 [2.12-3.78]) and less likely to be single (AOR, 0.67 [0.62-0.73]) and First Nations (AOR, 0.67 [0.56-0.82]). Those who received no prenatal communicable disease screening were less likely to be over 40 years of age (AOR, 0.81 [0.69-0.95]) and more likely to be single (AOR, 1.27 [1.21-1.33]) and have received no prenatal care (AOR, 6.78 [6.40-7.19]). Both the HIV decliners and prenatal non-testers were more likely to have used a midwife (AOR, 4.52 [3.83-5.35] and AOR, 2.44 [2.03-2.92], respectively). CONCLUSION: Demographic and prenatal care characteristics differ by a pregnant woman's prenatal screening status. Policies to improve HIV screening coverage should take these variations into account.

Evaluating the individuality of animal-habitat relationships.

Examining the ways in which animals use habitat and select resources to satisfy their life history requirements has important implications for ecology, evolution, and conservation. The advent of radio-tracking in the mid-20th century greatly expanded the scope of animal-habitat modeling. Thereafter, it became common practice to aggregate telemetry data collected on a number of tagged individuals and fit one model describing resource selection at the population level. This convention, however, runs the risk of masking important individuality in the nature of associations between animals and their environment. Here, we investigated the importance of individual variation in animal-habitat relationships via the study of a highly gregarious species. We modeled elk (Cervus elaphus) location data, collected from Global Positioning System (GPS) collars, using Bayesian discrete choice resource selection function (RSF) models. Using a high-performance computing cluster, we batch-processed these models at the level of each individual elk (n = 88) and evaluated the output with respect to: (a) the composition of parameters in the most supported models, (b) the estimates of the parameters featured in the global models, and (c) spatial maps of the predicted relative probabilities of use. We detected considerable individual variation across all three metrics. For instance, the most supported models varied with respect to parameter composition with a range of seven to 17 and an average of 14.4 parameters per individual elk. The estimates of the parameters featured in the global models also varied greatly across individual elk with little conformity detected across age or sex classes. Finally, spatial mapping illustrated stark differences in the predicted relative probabilities of use across individual elk. Our analysis identifies that animal-habitat relationships, even among the most gregarious of species, can be highly variable. We discuss the implications of our results for ecology and present some guiding principles for the development of RSF models at the individual-animal level.

Effects of household composition and income security on body weight in working-age men.

OBJECTIVE: Many recent studies have provided evidence suggesting that increases in body weight may spread via social networks. The mechanism(s) by which this might occur have become the subject of much speculation, but to date little direct evidence has been available. Building on evidence from economics, anthropology, and behavioral biology, within-household peers might influence body weight via implicit provision of income security was hypothesized. DESIGN AND METHODS: Using a sample of 2,541 working-age men from the National Longitudinal Survey of Youth (1979), the effect of cohabitation on weight gain over a 6-year period was estimated. The potential confound caused by the joint determination of economic insecurity and cohabitation status with instrumental variables that exploit variation in local and state-level macroeconomic conditions and the presence of children in the home was addressed. RESULTS: The marginal effect of cohabitation with adults on body weight is negative. Moreover, the magnitude of the effect is more than six times greater when the cohabitant is engaged in paid employment. CONCLUSIONS: Income insecurity may play an important role in peer-to-peer transmission of weight gain.

Ectopic DICER-LIKE1 expression in P1/HC-Pro Arabidopsis rescues phenotypic anomalies but not defects in microRNA and silencing pathways.

Expression of the viral silencing suppressor P1/HC-Pro in plants causes severe developmental anomalies accompanied by defects in both short interfering RNA (siRNA) and microRNA (miRNA) pathways. P1/HC-Pro transgenic lines fail to accumulate the siRNAs that mediate RNA silencing and are impaired in both miRNA processing and function, accumulating abnormally high levels of miRNA/miRNA* processing intermediates as well as miRNA target messages. Both miRNA and RNA silencing pathways require participation of DICER-LIKE (DCL) ribonuclease III-like enzymes. Here, we investigate the effects of overexpressing DCL1, one of four Dicers in Arabidopsis thaliana, on P1/HC-Pro-induced defects in development and small RNA metabolism. Expression of a DCL1 cDNA transgene (35S:DCL1) produced a mild gain-of-function phenotype and largely rescued dcl1 mutant phenotypes. The 35S:DCL1 plants were competent for virus-induced RNA silencing but were impaired in transgene-induced RNA silencing and in the accumulation of some miRNAs. Ectopic DCL1 largely alleviated developmental anomalies in P1/HC-Pro plants but did not correct the P1/HC-Pro-associated defects in small RNA pathways. The ability of P1/HC-Pro plants to suppress RNA silencing and the levels of miRNAs, miRNA*s, and miRNA target messages in these plants were essentially unaffected by ectopic DCL1. These data suggest that P1/HC-Pro defects in development do not result from general impairments in small RNA pathways and raise the possibility that DCL1 participates in processes in addition to miRNA biogenesis.