Maternal knowledge of effective breastfeeding and its benefits, as potential determinant of attitudes to infant feeding: A survey in Calabar, Nigeria

Appropriate breastfeeding is a cost-effective child survival strategy. This study assessed relationship between knowledge of breastfeeding and attitude towards infant feeding among pregnant women in Calabar, Nigeria. By convenience sampling, consenting antenatal clinic attendees were recruited from secondary health centers in Calabar. Pre-tested questionnaire was used to assess knowledge of different aspects of breastfeeding, while the Iowa Infant Feeding Attitude Scale (IIFAS) was used to assess attitude towards infant feeding. Data was analyzed using SPSS version 21.0, with p-value of less than 0.05 considered statistically significant. Two hundred and fifty (250) pregnant women were surveyed with mean age of 29.7 ± 6.1 years. One hundred and eight respondents (43.2%) had unsatisfactory levels of knowledge. Common areas of misconception were oral thrush effect of breastfeeding (47.2%), frequency of breast milk expression (47.6%), and effects of inverted nipples (45.6%). Most respondents (92.0%) had neutral attitude to infant feeding, and there was no significant relationship between overall knowledge of breastfeeding and infant feeding attitude (p>0.05). Of all the knowledge areas assessed, only benefits to mothers (r=0.11, p=0.08) and effective breastfeeding (r=0.17, p=0.01), had knowledge scores that correlated positively with infant feeding attitude scores. These findings contribute to existing literature required for improvement in policies and strategies, for breastfeeding education and child survival, especially in resource-poor settings. There is need for further research towards improving priority content of maternal health education during the time-constrained ANC visits. Keywords: Knowledge, breastfeeding, infant feeding attitude, pregnant women, Calabar, Nigeria   L'allaitement maternel approprié est une stratégie rentable de survie de l'enfant. Cette étude a évalué la relation entre la connaissance de l'allaitement maternel et l'attitude envers l'alimentation du nourrisson chez les femmes enceintes à Calabar, au Nigéria. Par échantillonnage de convenance, les participants consentants des cliniques prénatales ont été recrutés dans les centres de santé secondaires de Calabar. Un questionnaire pré-testé a été utilisé pour évaluer les connaissances sur les différents aspects de l'allaitement maternel, tandis que l'Iowa Infant Feeding Attitude Scale (IIFAS) a été utilisé pour évaluer l'attitude envers l'alimentation du nourrisson. Les données ont été analysées à l'aide de la version 21.0 de SPSS, avec une valeur p inférieure à 0,05 considérée comme statistiquement significative. Deux cent cinquante (250) femmes enceintes ont été interrogées avec un âge moyen de 29,7 ± 6,1 ans. Cent huit répondants (43,2%) avaient des niveaux de connaissances insatisfaisants. Les points communs d'idées fausses étaient l'effet du muguet buccal de l'allaitement (47,2%), la fréquence d'expression du lait maternel (47,6%) et les effets des mamelons inversés (45,6%). La plupart des répondants (92,0%) avaient une attitude neutre à l'égard de l'alimentation du nourrisson, et il n'y avait pas de relation significative entre la connaissance globale de l'allaitement et l'attitude en matière d'alimentation du nourrisson (p> 0,05). Parmi tous les domaines de connaissances évalués, seuls les avantages pour les mères (r = 0,11, p = 0,08) et l'allaitement maternel efficace (r = 0,17, p = 0,01) présentaient des scores de connaissance qui étaient en corrélation positive avec les scores d'attitude en matière d'alimentation du nourrisson. Ces résultats contribuent à la littérature existante nécessaire pour améliorer les politiques et stratégies, pour l'éducation à l'allaitement maternel et la survie de l'enfant, en particulier dans les milieux pauvres en ressources. Des recherches supplémentaires sont nécessaires pour améliorer le contenu prioritaire de l'éducation à la santé maternelle pendant les visites prénatales limitées dans le temps. Mots-clés: Connaissances, allaitement, attitude en matière d'alimentation du nourrisson, femmes enceintes, Calabar, Nigéri

Shared genetic risk between eating disorder- and substance-use-related phenotypes:Evidence from genome-wide association studies

First published: 16 February 202

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

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

Reducing the environmental impact of surgery on a global scale: systematic review and co-prioritization with healthcare workers in 132 countries

Abstract Background Healthcare cannot achieve net-zero carbon without addressing operating theatres. The aim of this study was to prioritize feasible interventions to reduce the environmental impact of operating theatres. Methods This study adopted a four-phase Delphi consensus co-prioritization methodology. In phase 1, a systematic review of published interventions and global consultation of perioperative healthcare professionals were used to longlist interventions. In phase 2, iterative thematic analysis consolidated comparable interventions into a shortlist. In phase 3, the shortlist was co-prioritized based on patient and clinician views on acceptability, feasibility, and safety. In phase 4, ranked lists of interventions were presented by their relevance to high-income countries and low–middle-income countries. Results In phase 1, 43 interventions were identified, which had low uptake in practice according to 3042 professionals globally. In phase 2, a shortlist of 15 intervention domains was generated. In phase 3, interventions were deemed acceptable for more than 90 per cent of patients except for reducing general anaesthesia (84 per cent) and re-sterilization of ‘single-use’ consumables (86 per cent). In phase 4, the top three shortlisted interventions for high-income countries were: introducing recycling; reducing use of anaesthetic gases; and appropriate clinical waste processing. In phase 4, the top three shortlisted interventions for low–middle-income countries were: introducing reusable surgical devices; reducing use of consumables; and reducing the use of general anaesthesia. Conclusion This is a step toward environmentally sustainable operating environments with actionable interventions applicable to both high– and low–middle–income countries

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3,4,5,6,7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease