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1.
  • Albarqouni, Loai, et al. (författare)
  • Evaluation of evidence supporting NICE recommendations to change people's lifestyle in clinical practice: cross sectional survey
  • 2022
  • Ingår i: BMJ Medicine. - : BMJ. - 2754-0413. ; 1:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives To assess whether recommendations of individually oriented lifestyle interventions (IOLIs) in guidelines from the National Institute for Health and Care Excellence (NICE) were underpinned by evidence of benefit, and whether harms and opportunity costs were considered.Design Cross sectional survey.Setting UK.Data sources NICE guidelines and supporting evidence.Eligibility criteria All NICE pathways for IOLI recommendations (ie, non-drug interventions that healthcare professionals administer to adults to achieve a healthier lifestyle and improve health) were searched systematically on 26 August 2020. One author screened all retrieved pathways for candidate guidelines, while a second author verified these judgments. Two authors independently and in duplicate screened all retrieved guidelines and recommendations for eligibility, extracted data, and evaluated the evidence cited and the outcomes considered. Disagreements were noted and resolved by consensus.Results Within 57 guidelines, 379 NICE recommendations were found for IOLIs; almost all (n=374; 99%) recommended the lifestyle intervention and five (1%) recommended against the intervention. Of the 379 recommendations, 13 (3%) were supported by moderate or high certainty evidence of a beneficial effect on patient relevant outcomes (n=7; 2%) or surrogate outcomes (n=13; 3%). 19 (5%) interventions considered psychosocial harms, 32 (8%) considered physical harms, and one (<1%) considered the opportunity costs of implementation. No intervention considered the burden placed on individuals by these recommendations.Conclusion Few NICE recommendations of lifestyle interventions are supported by reliable evidence. While this finding does not contest the beneficial effects of healthy habits, guidelines recommending clinicians to try to change people’s lifestyle need to be reconsidered given the substantial uncertainty about the effectiveness, harms, and opportunity costs of such interventions.Data are available in a public, open access repository. All data is available in appendices, which are published in the Open Science Framework (osf.io/42juh).
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2.
  • Husby, A, et al. (författare)
  • Clinical outcomes of myocarditis after SARS-CoV-2 mRNA vaccination in four Nordic countries: population based cohort study
  • 2023
  • Ingår i: BMJ medicine. - : BMJ. - 2754-0413. ; 2:1, s. e000373-
  • Tidskriftsartikel (refereegranskat)abstract
    • To investigate the clinical outcomes of myocarditis associated with mRNA vaccines against the SARS-CoV-2 virus compared with other types of myocarditis.DesignPopulation based cohort study.SettingNationwide register data from four Nordic countries (Denmark, Finland, Norway, and Sweden), from 1 January 2018 to the latest date of follow-up in 2022.ParticipantsThe Nordic myocarditis cohort; 7292 individuals aged ≥12 years who had an incident diagnosis of myocarditis as a main or secondary diagnosis, in a population of 23 million individuals in Denmark, Finland, Norway, and Sweden.Main outcome measuresHeart failure, or death from any cause within 90 days of admission to hospital for new onset myocarditis, and hospital readmission within 90 days of discharge to hospital for new onset myocarditis. Clinical outcomes of myocarditis associated with SARS-CoV-2 mRNA vaccination, covid-19 disease, and conventional myocarditis were compared.ResultsIn 2018-22, 7292 patients were admitted to hospital with new onset myocarditis, with 530 (7.3%) categorised as having myocarditis associated with SARS-CoV-2 mRNA vaccination, 109 (1.5%) with myocarditis associated with covid-19 disease, and 6653 (91.2%) with conventional myocarditis. At the 90 day follow-up, 62, nine, and 988 patients had been readmitted to hospital in each group (vaccination, covid-19, and conventional myocarditis groups, respectively), corresponding to a relative risk of readmission of 0.79 (95% confidence interval 0.62 to 1.00) and 0.55 (0.30 to 1.04) for the vaccination type and covid-19 type myocarditis groups, respectively, compared with the conventional myocarditis group. At the 90 day follow-up, 27, 18, and 616 patients had a diagnosis of heart failure or died in the vaccination type, covid-19 type, and conventional myocarditis groups, respectively. The relative risk of heart failure within 90 days was 0.56 (95% confidence interval 0.37 to 0.85) and 1.48 (0.86 to 2.54) for myocarditis associated with vaccination and covid-19 disease, respectively, compared with conventional myocarditis; the relative risk of death was 0.48 (0.21 to 1.09) and 2.35 (1.06 to 5.19), respectively. Among patients aged 12-39 years with no predisposing comorbidities, the relative risk of heart failure or death was markedly higher for myocarditis associated with covid-19 disease than for myocarditis associated with vaccination (relative risk 5.78, 1.84 to 18.20).ConclusionsCompared with myocarditis associated with covid-19 disease and conventional myocarditis, myocarditis after vaccination with SARS-CoV-2 mRNA vaccines was associated with better clinical outcomes within 90 days of admission to hospital.
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3.
  • Larsson, Susanna C., et al. (författare)
  • Appraisal of the causal effect of plasma caffeine on adiposity, type 2 diabetes, and cardiovascular disease : two sample mendelian randomisation study
  • 2023
  • Ingår i: BMJ medicine. - : BMJ Publishing Group Ltd. - 2754-0413. ; 2:1
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To investigate the potential causal effects of long term plasma caffeine concentrations on adiposity, type 2 diabetes, and major cardiovascular diseases.DESIGN: Two sample mendelian randomisation study.SETTING: Genome-wide association study summary data for associations of two single nucleotide polymorphisms associated with plasma caffeine at the genome-wide significance threshold (rs2472297 near the CYP1A2 gene and rs4410790 near the AHR gene) and their association with the outcomes.PARTICIPANTS: Primarily individuals of European ancestry participating in cohorts contributing to genome-wide association study consortia.MAIN OUTCOME MEASURES: Outcomes studied were body mass index, whole body fat mass, whole body fat-free mass, type 2 diabetes, ischaemic heart disease, atrial fibrillation, heart failure, and stroke.RESULTS: Higher genetically predicted plasma caffeine concentrations were associated with lower body mass index (beta -0.08 standard deviation (SD) (95% confidence interval -0.10 to -0.06), where 1 SD equals about 4.8 kg/m2 in body mass index, for every standard deviation increase in plasma caffeine) and whole body fat mass (beta -0.06 SD (-0.08 to -0.04), 1 SD equals about 9.5 kg; P<0.001) but not fat-free mass (beta -0.01 SD (-0.02 to -0.00), 1 SD equals about 11.5 kg; P=0.17). Higher genetically predicted plasma caffeine concentrations were associated with a lower risk of type 2 diabetes in two consortia (FinnGen and DIAMANTE), with a combined odds ratio of 0.81 ((95% confidence interval 0.74 to 0.89); P<0.001). Approximately half (43%; 95% confidence interval 30% to 61%) of the effect of caffeine on type 2 diabetes was estimated to be mediated through body mass index reduction. No strong associations were reported between genetically predicted plasma caffeine concentrations and a risk of any of the studied cardiovascular diseases.CONCLUSIONS: Higher plasma caffeine concentrations might reduce adiposity and risk of type 2 diabetes. Further clinical study is warranted to investigate the translational potential of these findings towards reducing the burden of metabolic disease.
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4.
  • Yuan, Shuai, et al. (författare)
  • Effects of metabolic traits, lifestyle factors, and pharmacological interventions on liver fat : mendelian randomisation study
  • 2022
  • Ingår i: BMJ medicine. - : BMJ Publishing Group Ltd. - 2754-0413. ; 1
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To investigate the effects of metabolic traits, lifestyle factors, and drug interventions on liver fat using the mendelian randomisation paradigm.Design: Mendelian randomisation study.Setting: Publicly available summary level data from genome-wide association studies.Participants: Genome-wide association studies of 32 974 to 1 407 282 individuals who were predominantly of European descent.Exposures: Genetic variants predicting nine metabolic traits, six lifestyle factors, four lipid lowering drug targets, three antihypertensive drug targets, and genetic association estimates formagnetic resonance imaging measured liver fat.Main Outcome Measures: Mendelian randomisation analysis was used to investigate the effects of these exposures on liver fat, incorporating sensitivity analyses that relaxed the requisite modelling assumptions.Results: Genetically predicted liability to obesity, type 2 diabetes, elevated blood pressure, elevated triglyceride levels, cigarette smoking, and sedentary time watching television were associated with higher levels of liver fat. Genetically predicted lipid lowering drug effects were not associated with liver fat; however, β blocker and calcium channel blocker antihypertensive drug effects were associated with lower levels of liver fat.Conclusion: These analyses provide evidence of a causal effect of various metabolic traits, lifestyle factors, and drug targets on liver fat. The findings complement existing epidemiological associations, further provide mechanistic insight, and potentially supports a role for drug interventions in reducing the burden of hepatic steatosis and related disease. Further clinical study is now warranted to investigate the relevance of these genetic analyses for patient care.
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5.
  • Zöller, Bengt, et al. (författare)
  • Familial aggregation of multimorbidity in Sweden: national explorative family study
  • 2023
  • Ingår i: BMJ Medicine. - 2754-0413. ; 2:1, s. 1-13
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives To examine whether multimorbidity aggregates in families in Sweden.Design National explorative family study.Setting Swedish Multigeneration Register linked to the National Patient Register, 1997-2015. Multimorbidity was assessed with a modified counting method of 45 chronic non-communicable diseases according to ICD-10 (international classification of diseases, 10th revision) diagnoses.Participants 2 694 442 Swedish born individuals (48.73% women) who could be linked to their Swedish born first, second, and third degree relatives. Twins were defined as full siblings born on the same date.Main outcome measures Multimorbidity was defined as two or more non-communicable diseases. Familial associations for one, two, three, four, and five or more non-communicable diseases were assessed to examine risks depending on the number of non-communicable diseases. Familial adjusted odds ratios for multimorbidity were calculated for individuals with a diagnosis of multimorbidity compared with relatives of individuals unaffected by multimorbidity (reference). An initial principal component decomposition followed by a factor analysis with a principal factor method and an oblique promax rotation was used on the correlation matrix of tetrachoric correlations between 45 diagnoses in patients to identify disease clusters.Results The odds ratios for multimorbidity were 2.89 in twins (95% confidence interval 2.56 to 3.25), 1.81 in full siblings (1.78 to 1.84), 1.26 in half siblings (1.24 to 1.28), and 1.13 in cousins (1.12 to 1.14) of relatives with a diagnosis of multimorbidity. The odds ratios for multimorbidity increased with the number of diseases in relatives. For example, among twins, the odds ratios for multimorbidity were 1.73, 2.84, 4.09, 4.63, and 6.66 for an increasing number of diseases in relatives, from one to five or more, respectively. Odds ratios were highest at younger ages: in twins, the odds ratio was 3.22 for those aged ≤20 years, 3.14 for those aged 21-30 years, and 2.29 for those aged >30 years at the end of follow-up. Nine disease clusters (factor clusters 1-9) were identified, of which seven aggregated in families. The first three disease clusters in the principal component decomposition were cardiometabolic disease (factor 1), mental health disorders (factor 2), and disorders of the digestive system (factor 3). Odds ratios for multimorbidity in twins, siblings, half siblings, and cousins for the factor 1 cluster were 2.79 (95% confidence interval 0.97 to 8.06), 2.62 (2.39 to 2.88), 1.52 (1.34 to 1.73), and 1.31 (1.23 to 1.39), and for the factor 2 cluster, 5.79 (4.48 to 7.48) 3.24 (3.13 to 3.36), 1.51 (1.45 to 1.57), and 1.37 (1.341.40).Conclusions The results of this explorative family study indicated that multimorbidity aggregated in Swedish families. The findings suggest that map clusters of diseases should be used for the genetic study of common diseases to show new genetic patterns of non-communicable diseases.
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