Study protocol for CELLAR (COVID-related Eating Limitations and Latent dietary effects in the Atlantic Region): population-based observational study to monitor dietary intakes and purchasing during COVID-19 in four Atlantic Canadian provinces.

INTRODUCTION: Poor diet is a leading preventable risk for the global burden of non-communicable disease. Robust measurement is needed to determine the effect of COVID-19 on dietary intakes and consumer purchasing, given the widespread changes to consumer food environments and economic precarity. The research objectives are as follows: (1) describe dietary intakes of foods, beverages and nutrients of concern during the COVID-19 pandemic; (2) quantify change in diet during COVID-19 as compared with prepandemic, previously captured in the provincial samples of the population-representative 2015 Canadian Community Health Survey-Nutrition and (3) examine how household purchasing practices predict dietary intakes during COVID-19. METHODS AND ANALYSES: Observational study of diet, using a population-based stratified probability sampling strategy allocated via dual-frame (landline and cellphone) calls to random-digit dialled numbers, followed by age-sex group quotas. The base population comprises the four provinces of the Atlantic region of Canada, jurisdictions with an excess burden of pre-existing dietary risk, compared with the rest of Canada. Our aim is n=1000 to obtain reliable estimates at a regional level to describe intakes and compare with prepandemic baseline. Data collection entails 12 weeks participation: (1) enrolment with sociodemographics (key dietary risk predictors such as age, sex, gender, pre-COVID-19 income, employment, household composition, receipt of economic relief, rural residence); (2) two 24hour diet recalls using the online ASA-24 Canada 2018 tool; and (3) online uploads of household food purchase receipts over the 12 weeks enrolled. Participation incentives will be offered. ETHICS AND DISSEMINATION: This research protocol received funding from the Canadian Institutes of Health Research (FRN VR5 172691) and ethics review approval from the Dalhousie University Research Ethics Board. Study protocol and instruments and a de-identified dataset will be made publicly available. We will submit the findings to peer-reviewed journals, as well as conferences geared towards scientific and decision-maker audiences.

A scoping review on the relations between urban form and health: a focus on Canadian quantitative evidence. / Examen de la portée sur les associations entre aménagement urbain et santé : les données quantitatives canadiennes.

INTRODUCTION: Despite the accumulating Canadian evidence regarding the relations between urban form and health behaviours, less is known about the associations between urban form and health conditions. Our study aim was to undertake a scoping review to synthesize evidence from quantitative studies that have investigated the relationship between built environment and chronic health conditions, self-reported health and quality of life, and injuries in the Canadian adult population. METHODS: From January to March 2017, we searched 13 databases to identify peer-reviewed quantitative studies from all years that estimated associations between the objectively-measured built environment and health conditions in Canadian adults. Studies under-taken within urban settings only were included. Relevant studies were catalogued and synthesized in relation to their reported study and sample design, and health outcome and built environment features. RESULTS: Fifty-five articles met the inclusion criteria, 52 of which were published after 2008. Most single province studies were undertaken in Ontario (n = 22), Quebec (n = 12), and Alberta (n = 7). Associations between the built environment features and 11 broad health outcomes emerged from the review, including injury (n = 19), weight status (n = 19), cardiovascular disease (n = 5), depression/anxiety (n = 5), diabetes (n = 5), mortality (n = 4), self-rated health (n = 2), chronic conditions (n = 2), metabolic condi-tions (n = 2), quality of life (n = 1), and cancer (n = 1). Consistent evidence for associations between aggregate built environment indicators (e.g., walkability) and diabetes and weight and between connectivity and route features (e.g., transportation route, trails, pathways, sidewalks, street pattern, intersections, route characteristics) and injury were found. Evidence for greenspace, parks and recreation features impacting multiple health outcomes was also found. CONCLUSION: Within the Canadian context, the built environment is associated with a range of chronic health conditions and injury in adults, but the evidence to date has limitations. More research on the built environment and health incorporating rigorous study designs are needed to provide stronger causal evidence to inform policy and practice.

Breathing manoeuvre-dependent changes in myocardial oxygenation in healthy humans.

AIMS: CO2 is an intrinsic vasodilator for cerebral and myocardial blood vessels. Myocardial vasodilation without a parallel increase of the oxygen demand leads to changes in myocardial oxygenation. Because apnoea and hyperventilation modify blood CO2, we hypothesized that voluntary breathing manoeuvres induce changes in myocardial oxygenation that can be measured by oxygenation-sensitive cardiovascular magnetic resonance (CMR). METHODS AND RESULTS: Fourteen healthy volunteers were studied. Eight performed free long breath-hold as well as a 1- and 2-min hyperventilation, whereas six aquatic athletes were studied during a 60-s breath-hold and a free long breath-hold. Signal intensity (SI) changes in T2*-weighted, steady-state free precession, gradient echo images at 1.5 T were monitored during breathing manoeuvres and compared with changes in capillary blood gases. Breath-holds lasted for 35, 58 and 117 s, and hyperventilation for 60 and 120 s. As expected, capillary pCO2 decreased significantly during hyperventilation. Capillary pO2 decreased significantly during the 117-s breath-hold. The breath-holds led to a SI decrease (deoxygenation) in the left ventricular blood pool, while the SI of the myocardium increased by 8.2% (P = 0.04), consistent with an increase in myocardial oxygenation. In contrast, hyperventilation for 120 s, however, resulted in a significant 7.5% decrease in myocardial SI/oxygenation (P = 0.02). Change in capillary pCO2 was the only independently correlated variable predicting myocardial oxygenation changes during breathing manoeuvres (r = 0.58, P < 0.01). CONCLUSION: In healthy individuals, breathing manoeuvres lead to changes in myocardial oxygenation, which appear to be mediated by CO2. These changes can be monitored in vivo by oxygenation-sensitive CMR and thus, may have value as a diagnostic tool.