94 research outputs found

    Successful scaling of Edible City Solutions to promote food citizenship and sustainability in food system transitions

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    Sustainable, productive and biodiversity-friendly urban landscapes are a strategic step in transitioning to future-proof, liveable and healthy cities Edible nature-based solutions, otherwise known as “Edible City Solutions”, comprise a wide range of different forms of sustainable urban food production, distribution and consumption which use innovative principles of ecological design combined with closed material and energy flows. Edible City Solutions contribute to a local green economy, reduce cities' overall ecological footprint, enhance social cohesion, human health and wellbeing and contribute to bridging the gap between “farm and fork”. These benefits have been tested and monitored in Living Labs where a wide portfolio of different solutions have been implemented and scaled in order to accelerate their uptake and use in urban landscapes. The study documents and analyses different scaling practices and activities of the co-created Living Labs – together with local actors within the “scaling community” in Andernach, Berlin, Havanna, Oslo and Rotterdam. We follow a mixed method approach and analyse data by applying the different scaling pathways of scaling up, scaling deep, scaling wide, scaling across and scaling soft previously identified through a systematic literature review. Results are presented as ongoing scaling stories, experiences and challenges in the Living Labs. The study also highlights examples of scaling practices beyond the Living Labs and suggests strategic plans for future scaling. Scaling processes, strategies and approaches are critically reviewed and discussed. Observations are condensed into eleven recommendations for scaling edible nature-based solutions.Peer Reviewe

    Health problems account for a small part of the association between socioeconomic status and disability pension award. Results from the Hordaland Health Study

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    <p>Abstract</p> <p>Background</p> <p>Low socioeconomic status is a known risk factor for disability pension, and is also associated with health problems. To what degree health problems can explain the increased risk of disability pension award associated with low socioeconomic status is not known.</p> <p>Methods</p> <p>Information on 15,067 participants in the Hordaland Health Study was linked to a comprehensive national registry on disability pension awards. Level of education was used as a proxy for socioeconomic status. Logistic regression analyses were employed to examine the association between socioeconomic status and rates of disability pension award, before and after adjusting for a wide range of somatic and mental health factors. The proportion of the difference in disability pension between socioeconomic groups explained by health was then calculated.</p> <p>Results</p> <p>Unadjusted odds ratios for disability pension was 4.60 (95% CI: 3.34-6.33) for the group with elementary school only (9 years of education) and 2.03 (95% CI 1.49-2.77) for the group with high school (12 years of education) when compared to the group with higher education (more than 12 years). When adjusting for somatic and mental health, odds ratios were reduced to 3.87 (2.73-5.47) and 1.81 (1.31-2.52). This corresponds to health explaining only a marginal proportion of the increased level of disability pension in the groups with lower socioeconomic status.</p> <p>Conclusion</p> <p>There is a socioeconomic gradient in disability pension similar to the well known socioeconomic gradient in health. However, health accounts for little of the socioeconomic gradient in disability pension. Future studies of socioeconomic gradients in disability pension should focus on explanatory factors beyond health.</p

    Risk of attention-deficit hyperactivity disorder in offspring of mothers with infections during pregnancy

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    Background Maternal infections during pregnancy are common events that have been suggested to be risk factors for Attention-deficit hyperactivity disorder (ADHD) in offspring. Only a few studies have been conducted to date and results are conflicting. The current study investigates the associations between specific groups of prenatal maternal infections and offspring ADHD, considering timing of exposure and the role of fever. Methods We used data from the prospective Norwegian Mother, Father and Child Cohort Study (MoBa), including more than 112,000 pregnancies, linked with data from the Medical Birth Registry of Norway and the Norwegian Patient Registry to estimate odds ratios for the likelihood that children develop ADHD after being exposed to maternal infections during gestation. Results Children exposed to any maternal infection during pregnancy showed increased risk of receiving an ADHD diagnosis (OR = 1.15, CI = 1.03–1.27). Specifically, increased ADHD risk was observed after exposure to genitourinary infections in second (OR = 1.42, CI = 1.06–1.90) or third trimester (OR = 2.04, CI = 1.19–3.49), and to respiratory infections in second trimester (OR = 1.31, CI = 1.12–1.54), provided these infections were accompanied by episodes of fever. Increased ADHD risk was also observed after exposure to diarrhea without fever in the third trimester (OR = 1.25, CI = 1.07–1.46). Conclusions Overall, our results suggest that prenatal exposure to maternal infections, particularly with co-occurring episodes of fever, are risk factors for ADHD. Fever (or severity of the infection) appears to be more important in mid-pregnancy associations. Our results indicate that type of infection and timing of exposure might influence the associations, but small effect sizes require careful interpretations. The association between infection and ADHD should be estimated using discordant siblings or other negative control designs that give better adjustment for unmeasured familial confounding.publishedVersio

    Educational attainment and mortality in schizophrenia

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    Background Individuals suffering from schizophrenia have a reduced life expectancy with cardiovascular disease (CVD) as a major contributor. Low educational attainment is associated with schizophrenia, as well as with all-cause and CVD mortality. However, it is unknown to what extent low educational attainment can explain the increased mortality in individuals with schizophrenia. Aim Here, we quantify associations between educational attainment and all-cause and CVD mortality in individuals with schizophrenia, and compare them with the corresponding associations in the general population. Method All Norwegian citizens born between January 1, 1925, and December 31, 1959, were followed up from January 1, 1990, to December 31, 2014. The total sample included 1,852,113 individuals, of which 6548 were registered with schizophrenia. We estimated hazard ratios (HR) for all-cause and CVD mortality with Cox models, in addition to life years lost. Educational attainment for index persons and their parents were included in the models. Results In the general population individuals with low educational attainment had higher risk of all-cause (HR: 1.48 [95% CI: 1.47–1.49]) and CVD (HR: 1.59 [95% CI: 1.57–1.61]) mortality. In individuals with schizophrenia these estimates were substantially lower (all-cause: HR: 1.13 [95% CI: 1.05–1.21] and CVD: HR: 1.12 [95% CI: 0.98–1.27]). Low educational attainment accounted for 3.28 (3.21–3.35) life years lost in males and 2.48 (2.42–2.55) years in females in the general population, but was not significantly associated with life years lost in individuals with schizophrenia. Results were similar for parental educational attainment. Conclusions Our results indicate that while individuals with schizophrenia in general have lower educational attainment and higher mortality rates compared with the general population, the association between educational attainment and mortality is smaller in schizophrenia subjects than in the general population.publishedVersio

    Smoking in pregnancy and child ADHD

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    BACKGROUND AND OBJECTIVE: There is a well-documented association between maternal smoking during pregnancy and offspring attention-deficit/hyperactivity disorder (ADHD). The degree to which this reflects causal intrauterine effects or is due to unmeasured confounding is not clear. We sought to compare the association between maternal smoking during pregnancy and offspring ADHD with the associations with paternal smoking, grandmother’s smoking when pregnant with mother, and maternal smoking in previous pregnancies. Each of these exposures is expected to be influenced by much of the same confounding factors as maternal smoking during pregnancy, but cannot have direct intrauterine effects. A sibling control design was also used. METHODS: The current study used data from the Norwegian Mother and Child Cohort Study (n > 100 000 children). Mothers and fathers reported on smoking during pregnancy, and mothers reported on smoking in previous pregnancies and their mother’s smoking when pregnant with them. Mothers reported on child ADHD symptoms at 5 years of age. Information about child ADHD diagnosis was obtained from the Norwegian Patient Registry. RESULTS: Maternal smoking during pregnancy was not more strongly associated with offspring ADHD diagnosis than was paternal smoking, grandmother’s smoking when pregnant with mother, or maternal smoking in previous pregnancies. Sibling control analyses showed no association between maternal smoking in pregnancy and child ADHD symptoms among siblings discordant for maternal smoking. CONCLUSIONS: These results suggest that the association between maternal smoking during pregnancy and offspring ADHD is not due to causal intrauterine effects, but reflects unmeasured confounding

    Prenatal Exposure to Acetaminophen and Risk of ADHD

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    OBJECTIVES: To estimate the association between maternal use of acetaminophen during pregnancy and of paternal use before pregnancy with attention-deficit/hyperactivity disorder (ADHD) in offspring while adjusting for familial risk for ADHD and indications of acetaminophen use. METHODS: Diagnoses were obtained from the Norwegian Patient Registry for 112 973 offspring from the Norwegian Mother and Child Cohort Study, including 2246 with ADHD. We estimated hazard ratios (HRs) for an ADHD diagnosis by using Cox proportional hazard models. RESULTS: After adjusting for maternal use of acetaminophen before pregnancy, familial risk for ADHD, and indications of acetaminophen use, we observed a modest association between any prenatal maternal use of acetaminophen in 1 (HR = 1.07; 95% confidence interval [CI] 0.96–1.19), 2 (HR = 1.22; 95% CI 1.07–1.38), and 3 trimesters (HR = 1.27; 95% CI 0.99–1.63). The HR for more than 29 days of maternal acetaminophen use was 2.20 (95% CI 1.50–3.24). Use for &amp;lt;8 days was negatively associated with ADHD (HR = 0.90; 95% CI 0.81–1.00). Acetaminophen use for fever and infections for 22 to 28 days was associated with ADHD (HR = 6.15; 95% CI 1.71–22.05). Paternal and maternal use of acetaminophen were similarly associated with ADHD. CONCLUSIONS: Short-term maternal use of acetaminophen during pregnancy was negatively associated with ADHD in offspring. Long-term maternal use of acetaminophen during pregnancy was substantially associated with ADHD even after adjusting for indications of use, familial risk of ADHD, and other potential confounders. </jats:sec

    Prenatal Exposure to Organophosphorus Pesticides and Preschool ADHD in the Norwegian Mother, Father and Child Cohort Study

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    Prenatal organophosphorus pesticide (OPP) exposure has been associated with child attention-deficit/hyperactivity disorder (ADHD) in agricultural communities and those that are exposed to residentially applied insecticides. To examine this association in populations that are exposed primarily through diet, we estimate the associations between prenatal OPP exposure and preschool ADHD in the Norwegian Mother, Father and Child Cohort Study (MoBa), and describe modification by paraoxonase 1 (PON1) gene variants. We used participants from the MoBa Preschool ADHD Sub-study (n = 259 cases) and a random sample of MoBa sub-cohort participants (n = 547) with birth years from 2004 to 2008. Prenatal urinary dialkylphosphate (DAP) metabolites (total diethylphosphate [∑DEP] and total dimethylphosphate [∑DMP]) were measured by an ultra-performance liquid chromatography-time-of-flight system and summed by molar concentration. Maternal DNA was genotyped for coding variants of PON1 (Q192R and L55M). We used a multivariable logistic regression to calculate the odds ratios (OR) and 95% confidence intervals, adjusted for maternal education, parity, income dependency, age, marital status, ADHD-like symptoms, pesticide use, produce consumption, and season. We found no associations between DAP metabolite concentrations and preschool ADHD. The adjusted ORs for exposure quartiles 2–4 relative to 1 were slightly inverse. No monotonic trends were observed, and the estimates lacked precision, likely due to the small sample size and variation in the population. We found no evidence of modification by PON1 SNP variation or child sex. Maternal urinary DAP concentrations were not associated with preschool ADHD

    Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

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    Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

    Performance audit and the importance of the public debate

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    The purpose of this article is to explore the impact of performance audit on public policy. The article investigates performance audit reports and the debates they initiate in the public realm. The case of Norway is analysed using mixed methods including a questionnaire, mapping and categorizing of reports, document studies and interviews. The results show that the Norwegian Supreme Audit Institution (SAI) is primarily preoccupied with managerial issues. It is nevertheless open to interpretation whether the preoccupation with managerial issues primarily implies an efficiency and effectiveness focus or an assessment of compliance to managerial standards. Most reports get moderate attention in the media and in the parliamentary control committee. Therefore the direct dialogue with the ministries becomes important for the performance audits’ influence. In the public debate the SAI, the ministries and the members of parliament base their argumentation in different institutional logics. These logics can lead to different interpretations of the control system, laws and regulations and hamper the State Audit Institution’s influence
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