34 results on '"Bjørngaard, Johan H"'
Search Results
2. Psychosocial factors and risk of chronic widespread pain: An 11-year follow-up study—The HUNT study
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Mundal, Ingunn, Gråwe, Rolf W., Bjørngaard, Johan H., Linaker, Olav M., and Fors, Egil A.
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- 2014
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3. Heavier smoking increases coffee consumption: findings from a Mendelian randomization analysis
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Bjørngaard, Johan H, Nordestgaard, Ask Tybjærg, Taylor, Amy E, Treur, Jorien L, Gabrielsen, Maiken E, Munafò, Marcus R, Nordestgaard, Børge Grønne, Åsvold, Bjørn Olav, Romundstad, Pål, and Davey Smith, George
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- 2017
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4. Health and unemployment: 14 years of follow-up on job loss in the Norwegian HUNT Study
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Kaspersen, Silje L., Pape, Kristine, Vie, Gunnhild Å., Ose, Solveig O., Krokstad, Steinar, Gunnell, David, and Bjørngaard, Johan H.
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- 2016
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5. Intergenerational polygenic obesity risk throughout adolescence in a cross‐sectional study design: The HUNT study, Norway
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Næss, Marit, primary, Sund, Erik R., additional, Vie, Gunnhild Å., additional, Bjørngaard, Johan H., additional, Åsvold, Bjørn Olav, additional, Holmen, Turid Lingaas, additional, and Kvaløy, Kirsti, additional
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- 2021
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6. Causal associations of tobacco smoking with cardiovascular risk factors: a Mendelian randomization analysis of the HUNT Study in Norway
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Åsvold, Bjørn O, Bjørngaard, Johan H, Carslake, David, Gabrielsen, Maiken E, Skorpen, Frank, Davey Smith, George, and Romundstad, Pål R
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- 2014
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7. Body mass index and all cause mortality in HUNT and UK Biobank studies: linear and non-linear mendelian randomisation analyses
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Sun, Yi-Qian, Burgess, Stephen, Staley, James R, Wood, Angela M, Bell, Steven, Kaptoge, Stephen K, Guo, Qi, Bolton, Thomas R, Mason, Amy M, Butterworth, Adam S, Di Angelantonio, Emanuele, Vie, Gunnhild Å, Bjørngaard, Johan H, Kinge, Jonas Minet, Chen, Yue, and Mai, Xiao-Mei
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Adult ,Male ,Norway ,Research ,nutritional and metabolic diseases ,Mendelian Randomization Analysis ,Middle Aged ,United Kingdom ,Body Mass Index ,Thinness ,Cardiovascular Diseases ,Risk Factors ,Cause of Death ,Neoplasms ,Humans ,Female ,Obesity ,Sex Distribution ,Aged - Abstract
Objective To investigate the shape of the causal relation between body mass index (BMI) and mortality. Design Linear and non-linear mendelian randomisation analyses. Setting Nord-Trøndelag Health (HUNT) Study (Norway) and UK Biobank (United Kingdom). Participants Middle to early late aged participants of European descent: 56 150 from the HUNT Study and 366 385 from UK Biobank. Main outcome measures All cause and cause specific (cardiovascular, cancer, and non-cardiovascular non-cancer) mortality. Results 12 015 and 10 344 participants died during a median of 18.5 and 7.0 years of follow-up in the HUNT Study and UK Biobank, respectively. Linear mendelian randomisation analyses indicated an overall positive association between genetically predicted BMI and the risk of all cause mortality. An increase of 1 unit in genetically predicted BMI led to a 5% (95% confidence interval 1% to 8%) higher risk of mortality in overweight participants (BMI 25.0-29.9) and a 9% (4% to 14%) higher risk of mortality in obese participants (BMI ≥30.0) but a 34% (16% to 48%) lower risk in underweight (BMI
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- 2019
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8. Unemployment and disability pension-an 18-year follow-up study of a 40-year-old population in a Norwegian county
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Støver Morten, Pape Kristine, Johnsen Roar, Fleten Nils, Sund Erik R, Claussen Bjørgulf, and Bjørngaard Johan H
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Disability benefit ,Disability pension ,Unemployment ,Work disability ,Multilevel modelling ,Public aspects of medicine ,RA1-1270 - Abstract
Abstract Background This study explored the association of unemployment and an increased risk of receiving disability pension, and the possibility that this risk is attributed to municipality-specific characteristics. Methods A cohort of 7,985 40-42 year olds was followed for 18 years in national registers, identifying new episodes of unemployment and cases of disability pension. The association between an unemployment period and disability pension in the subsequent year was estimated using discrete time multilevel logistic regressions and clustering individuals by municipality. The association between unemployment and disability pension was adjusted for age in the follow up-period, sex, baseline health status, health behaviour and education level. A conditional intra-class correlation coefficient (ICC) was estimated as a measure of inter-municipality variance. Results In the follow-up period, 2784 (35%) of the participants were granted disability pension. The crude odds ratio for receiving disability pension after unemployment (adjusted for age in follow-up period and sex only) was 1.42 (95% CI 1.1-1.8). Adjusting for baseline health indicators reduced the odds ratio of unemployment to 1.33 (CI 1.1-1.7). A fully adjusted model, including education level, further reduced the odds ratio of unemployment to 1.25 (CI 1.00-1.6). The ICC of the municipality level was approximately 2%. Conclusions Becoming unemployed increased the risk of receiving subsequent disability pension. However, adjusting for baseline health status, health behaviour and education attenuated this impact considerably. The multilevel analysis indicated that a minor, yet statistically significant, proportion of the risk of disability pension can be attributed to the municipality of residence.
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- 2012
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9. Changes in General Practitioners’ consultation frequency over time for patients with hypertension or anxiety/depression symptoms: a 10-year follow-up of the Norwegian HUNT study
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Skarshaug, Lena J, primary, Kaspersen, Silje L, additional, Bjørngaard, Johan H, additional, and Pape, Kristine, additional
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- 2019
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10. Contact with primary health care physicians before an acute hospitalisation
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Skarshaug, Lena J., primary, Svedahl, Ellen R., additional, Bjørngaard, Johan H., additional, Steinsbekk, Aslak, additional, and Pape, Kristine, additional
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- 2019
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11. Body mass index and all cause mortality in HUNT and UK Biobank studies: linear and non-linear mendelian randomisation analyses
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Sun, Yi-Qian, primary, Burgess, Stephen, additional, Staley, James R, additional, Wood, Angela M, additional, Bell, Steven, additional, Kaptoge, Stephen K, additional, Guo, Qi, additional, Bolton, Thomas R, additional, Mason, Amy M, additional, Butterworth, Adam S, additional, Di Angelantonio, Emanuele, additional, Vie, Gunnhild Å, additional, Bjørngaard, Johan H, additional, Kinge, Jonas Minet, additional, Chen, Yue, additional, and Mai, Xiao-Mei, additional
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- 2019
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12. Reading and writing difficulties in adolescence and later risk of welfare dependence. A ten year follow-up, the HUNT Study, Norway
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Holmen Turid L, Westin Steinar, Bjørngaard Johan H, Pape Kristine, and Krokstad Steinar
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Public aspects of medicine ,RA1-1270 - Abstract
Abstract Background Welfare dependence and low work participation among young people have raised concern in many European countries. Reading and writing difficulties (RWD) might make young people vulnerable to work integration problems and welfare dependence through negative influences on education and health. Our main objective of this study was to examine if RWD in adolescence affected the risk of welfare dependence in young adulthood. Methods Baseline information on self-reported RWD, health and family was obtained for 8950 school-attending adolescents in Nord-Trøndelag County, Norway, participating in the Young-HUNT1 survey, 1995-97. All individuals were linked to biological parents to identify siblings and parental education from national registers. Welfare dependence was assessed by the reception of social benefits (medical and economic) from the national social insurance database (1998-2007). Only long-term benefits (> 180 days) were included. Results The adolescents who reported RWD at baseline were more likely to receive medical or social benefits during follow-up compared with those who did not report RWD. In girls with RWD, the adjusted 5-year risk (at age 24 to 28) for receiving medical benefits was 0.20 (95% confidence interval 0.14-0.26), compared with 0.11 (0.09-0.12) in girls without RWD. In boys the corresponding risks were 0.13 (0.09-0.17) and 0.08 (0.07-0.09). Conclusions The associations between RWD in adolescence and welfare dependence later in life suggest that increased attention should be paid to these problems when discussing the public health aspects of work integration, since there might be a potential for prevention.
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- 2011
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13. Changes in General Practitioners' consultation frequency over time for patients with hypertension or anxiety/depression symptoms: a 10-year follow-up of the Norwegian HUNT study.
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Skarshaug, Lena J, Kaspersen, Silje L, Bjørngaard, Johan H, and Pape, Kristine
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GENERAL practitioners ,MULTILEVEL models ,HYPERTENSION ,ANXIETY ,CONTINUUM of care - Abstract
Background: General Practitioners' (GPs') workload has been suggested to increase in many countries; how does this impact patient follow-up?Objective: To investigate trends in GP consultation patterns for adults according to baseline hypertension and anxiety/depression symptoms and attribution of the GP to trend differences.Methods: Prospective cohort study, linking survey data and clinical measurements from the Norwegian HUNT3 study (2006-08) with national administrative data on GP list assignment and consultations with GP services. We grouped participants aged 40-59 years according to sex and their baseline status regarding hypertension and anxiety/depression symptoms. We registered GP consultations in 2007-16 and used general estimation equation models to estimate the level of GP consultations per month per year during follow-up. We used multilevel models with participants nested in their assigned regular GP to calculate GP-level intra-class correlation coefficients, reflecting to what extent patients' consultation patterns could be attributed to the individual GP.Results: In total, 47 550 HUNT3 participants were registered with 102 different GPs in Nord-Trøndelag County, Norway, in 2007. Adjusted for age, we observed an overall increase in GP consultations in 2007-16, particularly in those with a better health status at baseline. About 2% of the variance of patient consultations could be attributed to differences between GPs and 10% to the use of lengthy consultations. Out-of-hours consultations did not change much in the study period 2007-16.Conclusion: Increased use of GP consultations, mainly among the healthiest participants, encourage further research into whether these patients displace patients with heavier and more complex needs. [ABSTRACT FROM AUTHOR]- Published
- 2020
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14. Heavier smoking increases coffee consumption:findings from a Mendelian randomization analysis
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Bjørngaard, Johan H, Nordestgaard, Ask Tybjærg, Taylor, Amy E, Treur, Jorien L, Gabrielsen, Maiken E, Munafò, Marcus R, Nordestgaard, Børge Grønne, Åsvold, Bjørn Olav, Romundstad, Pål, Davey Smith, George, Bjørngaard, Johan H, Nordestgaard, Ask Tybjærg, Taylor, Amy E, Treur, Jorien L, Gabrielsen, Maiken E, Munafò, Marcus R, Nordestgaard, Børge Grønne, Åsvold, Bjørn Olav, Romundstad, Pål, and Davey Smith, George
- Abstract
Background: There is evidence for a positive relationship between cigarette and coffee consumption in smokers. Cigarette smoke increases metabolism of caffeine, so this may represent a causal effect of smoking on caffeine intake.Methods: We performed Mendelian randomization analyses in the UK Biobank ( N = 114 029), the Norwegian HUNT study ( N = 56 664) and the Copenhagen General Population Study (CGPS) ( N = 78 650). We used the rs16969968 genetic variant as a proxy for smoking heaviness in all studies and rs4410790 and rs2472297 as proxies for coffee consumption in UK Biobank and CGPS. Analyses were conducted using linear regression and meta-analysed across studies.Results: Each additional cigarette per day consumed by current smokers was associated with higher coffee consumption (0.10 cups per day, 95% CI: 0.03, 0.17). There was weak evidence for an increase in tea consumption per additional cigarette smoked per day (0.04 cups per day, 95% CI: -0.002, 0.07). There was strong evidence that each additional copy of the minor allele of rs16969968 (which increases daily cigarette consumption) in current smokers was associated with higher coffee consumption (0.16 cups per day, 95% CI: 0.11, 0.20), but only weak evidence for an association with tea consumption (0.04 cups per day, 95% CI: -0.01, 0.09). There was no clear evidence that rs16969968 was associated with coffee or tea consumption in never or former smokers or that the coffee-related variants were associated with cigarette consumption.Conclusions: Higher cigarette consumption causally increases coffee intake. This is consistent with faster metabolism of caffeine by smokers, but could also reflect a behavioural effect of smoking on coffee drinking.
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- 2017
15. Investigating the causal effect of smoking on hay fever and asthma:a Mendelian randomization meta-analysis in the CARTA consortium
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Skaaby, Tea, Taylor, Amy E, Jacobsen, Rikke K, Paternoster, Lavinia, Thuesen, Betina H, Ahluwalia, Tarunveer S, Larsen, Sofus C, Zhou, Ang, Wong, Andrew, Gabrielsen, Maiken E, Bjørngaard, Johan H, Flexeder, Claudia, Männistö, Satu, Hardy, Rebecca, Kuh, Diana, Barry, Sarah J, Tang Møllehave, Line, Cerqueira, Charlotte, Friedrich, Nele, Bonten, Tobias N, Noordam, Raymond, Mook-Kanamori, Dennis O, Taube, Christian, Jessen, Leon E, McConnachie, Alex, Sattar, Naveed, Upton, Mark N, McSharry, Charles, Bønnelykke, Klaus, Bisgaard, Hans, Schulz, Holger, Strauch, Konstantin, Meitinger, Thomas, Peters, Annette, Grallert, Harald, Nohr, Ellen A, Kivimaki, Mika, Kumari, Meena, Völker, Uwe, Nauck, Matthias, Völzke, Henry, Power, Chris, Hyppönen, Elina, Hansen, Torben, Jørgensen, Torben, Pedersen, Oluf, Salomaa, Veikko, Grarup, Niels, Langhammer, Arnulf, Romundstad, Pål R, Skorpen, Frank, Kaprio, Jaakko, R Munafò, Marcus, Linneberg, Allan, Skaaby, Tea, Taylor, Amy E, Jacobsen, Rikke K, Paternoster, Lavinia, Thuesen, Betina H, Ahluwalia, Tarunveer S, Larsen, Sofus C, Zhou, Ang, Wong, Andrew, Gabrielsen, Maiken E, Bjørngaard, Johan H, Flexeder, Claudia, Männistö, Satu, Hardy, Rebecca, Kuh, Diana, Barry, Sarah J, Tang Møllehave, Line, Cerqueira, Charlotte, Friedrich, Nele, Bonten, Tobias N, Noordam, Raymond, Mook-Kanamori, Dennis O, Taube, Christian, Jessen, Leon E, McConnachie, Alex, Sattar, Naveed, Upton, Mark N, McSharry, Charles, Bønnelykke, Klaus, Bisgaard, Hans, Schulz, Holger, Strauch, Konstantin, Meitinger, Thomas, Peters, Annette, Grallert, Harald, Nohr, Ellen A, Kivimaki, Mika, Kumari, Meena, Völker, Uwe, Nauck, Matthias, Völzke, Henry, Power, Chris, Hyppönen, Elina, Hansen, Torben, Jørgensen, Torben, Pedersen, Oluf, Salomaa, Veikko, Grarup, Niels, Langhammer, Arnulf, Romundstad, Pål R, Skorpen, Frank, Kaprio, Jaakko, R Munafò, Marcus, and Linneberg, Allan
- Abstract
Observational studies on smoking and risk of hay fever and asthma have shown inconsistent results. However, observational studies may be biased by confounding and reverse causation. Mendelian randomization uses genetic variants as markers of exposures to examine causal effects. We examined the causal effect of smoking on hay fever and asthma by using the smoking-associated single nucleotide polymorphism (SNP) rs16969968/rs1051730. We included 231,020 participants from 22 population-based studies. Observational analyses showed that current vs never smokers had lower risk of hay fever (odds ratio (OR) = 0·68, 95% confidence interval (CI): 0·61, 0·76; P < 0·001) and allergic sensitization (OR = 0·74, 95% CI: 0·64, 0·86; P < 0·001), but similar asthma risk (OR = 1·00, 95% CI: 0·91, 1·09; P = 0·967). Mendelian randomization analyses in current smokers showed a slightly lower risk of hay fever (OR = 0·958, 95% CI: 0·920, 0·998; P = 0·041), a lower risk of allergic sensitization (OR = 0·92, 95% CI: 0·84, 1·02; P = 0·117), but higher risk of asthma (OR = 1·06, 95% CI: 1·01, 1·11; P = 0·020) per smoking-increasing allele. Our results suggest that smoking may be causally related to a higher risk of asthma and a slightly lower risk of hay fever. However, the adverse events associated with smoking limit its clinical significance.
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- 2017
16. Maternal Smoking in Pregnancy and Offspring Depression: a cross cohort and negative control study
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Taylor, Amy E., primary, Carslake, David, additional, de Mola, Christian Loret, additional, Rydell, Mina, additional, Nilsen, Tom I. L., additional, Bjørngaard, Johan H., additional, Horta, Bernardo Lessa, additional, Pearson, Rebecca, additional, Rai, Dheeraj, additional, Galanti, Maria Rosaria, additional, Barros, Fernando C., additional, Romundstad, Pål R., additional, Davey Smith, George, additional, and Munafò, Marcus R., additional
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- 2017
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17. Investigating the causal effect of smoking on hay fever and asthma: a Mendelian randomization meta-analysis in the CARTA consortium
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Skaaby, Tea, primary, Taylor, Amy E., additional, Jacobsen, Rikke K., additional, Paternoster, Lavinia, additional, Thuesen, Betina H., additional, Ahluwalia, Tarunveer S., additional, Larsen, Sofus C., additional, Zhou, Ang, additional, Wong, Andrew, additional, Gabrielsen, Maiken E., additional, Bjørngaard, Johan H., additional, Flexeder, Claudia, additional, Männistö, Satu, additional, Hardy, Rebecca, additional, Kuh, Diana, additional, Barry, Sarah J., additional, Tang Møllehave, Line, additional, Cerqueira, Charlotte, additional, Friedrich, Nele, additional, Bonten, Tobias N., additional, Noordam, Raymond, additional, Mook-Kanamori, Dennis O., additional, Taube, Christian, additional, Jessen, Leon E., additional, McConnachie, Alex, additional, Sattar, Naveed, additional, Upton, Mark N., additional, McSharry, Charles, additional, Bønnelykke, Klaus, additional, Bisgaard, Hans, additional, Schulz, Holger, additional, Strauch, Konstantin, additional, Meitinger, Thomas, additional, Peters, Annette, additional, Grallert, Harald, additional, Nohr, Ellen A., additional, Kivimaki, Mika, additional, Kumari, Meena, additional, Völker, Uwe, additional, Nauck, Matthias, additional, Völzke, Henry, additional, Power, Chris, additional, Hyppönen, Elina, additional, Hansen, Torben, additional, Jørgensen, Torben, additional, Pedersen, Oluf, additional, Salomaa, Veikko, additional, Grarup, Niels, additional, Langhammer, Arnulf, additional, Romundstad, Pål R., additional, Skorpen, Frank, additional, Kaprio, Jaakko, additional, R Munafò, Marcus, additional, and Linneberg, Allan, additional
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- 2017
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18. Cigarette smoking increases coffee consumption: findings from a Mendelian randomisation analysis
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Bjørngaard, Johan H, primary, Nordestgaard, Ask Tybjærg, additional, Taylor, Amy E, additional, Treur, Jorien L, additional, Gabrielsen, Maiken E., additional, Munafò, Marcus R, additional, Nordestgaard, Børge Grønne, additional, Åsvold, Bjørn Olav, additional, Romundstad, Pål, additional, and Smith, George Davey, additional
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- 2017
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19. Body mass index and all cause mortality in HUNT and UK Biobank studies: linear and non-linear mendelian randomisation analyses.
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Yi-Qian Sun, Burgess, Stephen, Staley, James R., Wood, Angela M., Bell, Steven, Kaptoge, Stephen K., Qi Guo, Bolton, Thomas R., Mason, Amy M., Butterworth, Adam S., Di Angelantonio, Emanuele, Vie, Gunnhild Å, Bjørngaard, Johan H., Kinge, Jonas Minet, Yue Chen, and Mai, Xiao-Mei
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- 2019
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20. Premature Adult Death in Individuals Born Preterm: A Sibling Comparison in a Prospective Nationwide Follow-Up Study
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Risnes, Kari R., primary, Pape, Kristine, additional, Bjørngaard, Johan H., additional, Moster, Dag, additional, Bracken, Michael B., additional, and Romundstad, Pal R., additional
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- 2016
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21. Heavier smoking may lead to a relative increase in waist circumference:evidence for a causal relationship from a Mendelian randomisation meta-analysis. The CARTA consortium
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Morris, Richard W, Taylor, Amy E, Fluharty, Meg E, Bjørngaard, Johan H, Åsvold, Bjørn Olav, Elvestad Gabrielsen, Maiken, Campbell, Archie, Marioni, Riccardo, Kumari, Meena, Korhonen, Tellervo, Männistö, Satu, Marques-Vidal, Pedro, Kaakinen, Marika, Cavadino, Alana, Postmus, Iris, Husemoen, Lise Lotte N, Skaaby, Tea, Ahluwalia, Tarun Veer Singh, Treur, Jorien L, Willemsen, Gonneke, Dale, Caroline, Wannamethee, S Goya, Lahti, Jari, Palotie, Aarno, Räikkönen, Katri, McConnachie, Alex, Padmanabhan, Sandosh, Wong, Andrew, Dalgård, Christine, Paternoster, Lavinia, Ben-Shlomo, Yoav, Tyrrell, Jessica, Horwood, John, Fergusson, David M, Kennedy, Martin A, Nohr, Ellen A, Christiansen, Lene, Kyvik, Kirsten Ohm, Kuh, Diana, Watt, Graham, Eriksson, Johan G, Whincup, Peter H, Vink, Jacqueline M, Boomsma, Dorret I, Davey Smith, George, Lawlor, Debbie, Linneberg, Allan, Ford, Ian, Jukema, J Wouter, Power, Chris, Hyppönen, Elina, Jarvelin, Marjo-Riitta, Preisig, Martin, Borodulin, Katja, Kaprio, Jaakko, Kivimaki, Mika, Smith, Blair H, Hayward, Caroline, Romundstad, Pål R, Sørensen, Thorkild I A, Munafò, Marcus R, Sattar, Naveed, Morris, Richard W, Taylor, Amy E, Fluharty, Meg E, Bjørngaard, Johan H, Åsvold, Bjørn Olav, Elvestad Gabrielsen, Maiken, Campbell, Archie, Marioni, Riccardo, Kumari, Meena, Korhonen, Tellervo, Männistö, Satu, Marques-Vidal, Pedro, Kaakinen, Marika, Cavadino, Alana, Postmus, Iris, Husemoen, Lise Lotte N, Skaaby, Tea, Ahluwalia, Tarun Veer Singh, Treur, Jorien L, Willemsen, Gonneke, Dale, Caroline, Wannamethee, S Goya, Lahti, Jari, Palotie, Aarno, Räikkönen, Katri, McConnachie, Alex, Padmanabhan, Sandosh, Wong, Andrew, Dalgård, Christine, Paternoster, Lavinia, Ben-Shlomo, Yoav, Tyrrell, Jessica, Horwood, John, Fergusson, David M, Kennedy, Martin A, Nohr, Ellen A, Christiansen, Lene, Kyvik, Kirsten Ohm, Kuh, Diana, Watt, Graham, Eriksson, Johan G, Whincup, Peter H, Vink, Jacqueline M, Boomsma, Dorret I, Davey Smith, George, Lawlor, Debbie, Linneberg, Allan, Ford, Ian, Jukema, J Wouter, Power, Chris, Hyppönen, Elina, Jarvelin, Marjo-Riitta, Preisig, Martin, Borodulin, Katja, Kaprio, Jaakko, Kivimaki, Mika, Smith, Blair H, Hayward, Caroline, Romundstad, Pål R, Sørensen, Thorkild I A, Munafò, Marcus R, and Sattar, Naveed
- Abstract
OBJECTIVES: To investigate, using a Mendelian randomisation approach, whether heavier smoking is associated with a range of regional adiposity phenotypes, in particular those related to abdominal adiposity.DESIGN: Mendelian randomisation meta-analyses using a genetic variant (rs16969968/rs1051730 in the CHRNA5-CHRNA3-CHRNB4 gene region) as a proxy for smoking heaviness, of the associations of smoking heaviness with a range of adiposity phenotypes.PARTICIPANTS: 148,731 current, former and never-smokers of European ancestry aged ≥ 16 years from 29 studies in the consortium for Causal Analysis Research in Tobacco and Alcohol (CARTA).PRIMARY OUTCOME MEASURES: Waist and hip circumferences, and waist-hip ratio.RESULTS: The data included up to 66,809 never-smokers, 43,009 former smokers and 38,913 current daily cigarette smokers. Among current smokers, for each extra minor allele, the geometric mean was lower for waist circumference by -0.40% (95% CI -0.57% to -0.22%), with effects on hip circumference, waist-hip ratio and body mass index (BMI) being -0.31% (95% CI -0.42% to -0.19), -0.08% (-0.19% to 0.03%) and -0.74% (-0.96% to -0.51%), respectively. In contrast, among never-smokers, these effects were higher by 0.23% (0.09% to 0.36%), 0.17% (0.08% to 0.26%), 0.07% (-0.01% to 0.15%) and 0.35% (0.18% to 0.52%), respectively. When adjusting the three central adiposity measures for BMI, the effects among current smokers changed direction and were higher by 0.14% (0.05% to 0.22%) for waist circumference, 0.02% (-0.05% to 0.08%) for hip circumference and 0.10% (0.02% to 0.19%) for waist-hip ratio, for each extra minor allele.CONCLUSIONS: For a given BMI, a gene variant associated with increased cigarette consumption was associated with increased waist circumference. Smoking in an effort to control weight may lead to accumulation of central adiposity.
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- 2015
22. Effect of Smoking on Blood Pressure and Resting Heart Rate:A Mendelian Randomisation Meta-Analysis in the CARTA Consortium
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Linneberg, Allan, Jacobsen, Rikke K, Skaaby, Tea, Taylor, Amy E, Fluharty, Meg E, Jeppesen, Jørgen L, Bjørngaard, Johan H, Åsvold, Bjørn O, Gabrielsen, Maiken E, Campbell, Archie, Marioni, Riccardo E, Kumari, Meena, Marques-Vidal, Pedro, Kaakinen, Marika, Cavadino, Alana, Postmus, Iris, Ahluwalia, Tarun Veer Singh, Wannamethee, S Goya, Lahti, Jari, Räikkönen, Katri, Palotie, Aarno, Wong, Andrew, Dalgård, Christine, Ford, Ian, Ben-Shlomo, Yoav, Christiansen, Lene, Kyvik, Kirsten O, Kuh, Diana, Eriksson, Johan G, Whincup, Peter H, Mbarek, Hamdi, de Geus, Eco J C, Vink, Jacqueline M, Boomsma, Dorret I, Davey Smith, George, Lawlor, Debbie A, Kisialiou, Aliaksei, McConnachie, Alex, Padmanabhan, Sandosh, Jukema, J Wouter, Power, Chris, Hyppönen, Elina, Preisig, Martin, Waeber, Gerard, Vollenweider, Peter, Korhonen, Tellervo, Laatikainen, Tiina, Salomaa, Veikko, Kaprio, Jaakko, Kivimäki, Mika, Smith, Blair H, Hayward, Caroline, Sørensen, Thorkild I A, Thuesen, Betina H, Sattar, Naveed, Morris, Richard W, Romundstad, Pål R, Munafò, Marcus R, Jarvelin, Marjo-Riitta, Husemoen, Lise Lotte N, Linneberg, Allan, Jacobsen, Rikke K, Skaaby, Tea, Taylor, Amy E, Fluharty, Meg E, Jeppesen, Jørgen L, Bjørngaard, Johan H, Åsvold, Bjørn O, Gabrielsen, Maiken E, Campbell, Archie, Marioni, Riccardo E, Kumari, Meena, Marques-Vidal, Pedro, Kaakinen, Marika, Cavadino, Alana, Postmus, Iris, Ahluwalia, Tarun Veer Singh, Wannamethee, S Goya, Lahti, Jari, Räikkönen, Katri, Palotie, Aarno, Wong, Andrew, Dalgård, Christine, Ford, Ian, Ben-Shlomo, Yoav, Christiansen, Lene, Kyvik, Kirsten O, Kuh, Diana, Eriksson, Johan G, Whincup, Peter H, Mbarek, Hamdi, de Geus, Eco J C, Vink, Jacqueline M, Boomsma, Dorret I, Davey Smith, George, Lawlor, Debbie A, Kisialiou, Aliaksei, McConnachie, Alex, Padmanabhan, Sandosh, Jukema, J Wouter, Power, Chris, Hyppönen, Elina, Preisig, Martin, Waeber, Gerard, Vollenweider, Peter, Korhonen, Tellervo, Laatikainen, Tiina, Salomaa, Veikko, Kaprio, Jaakko, Kivimäki, Mika, Smith, Blair H, Hayward, Caroline, Sørensen, Thorkild I A, Thuesen, Betina H, Sattar, Naveed, Morris, Richard W, Romundstad, Pål R, Munafò, Marcus R, Jarvelin, Marjo-Riitta, and Husemoen, Lise Lotte N
- Abstract
BACKGROUND: -Smoking is an important cardiovascular disease risk factor, but the mechanisms linking smoking to blood pressure are poorly understood.METHODS AND RESULTS: -Data on 141,317 participants (62,666 never, 40,669 former, 37,982 current smokers) from 23 population-based studies were included in observational and Mendelian randomisation (MR) meta-analyses of the associations of smoking status and smoking heaviness with systolic and diastolic blood pressure (SBP, DBP), hypertension, and resting heart rate. For the MR analyses, a genetic variant rs16969968/rs1051730 was used as a proxy for smoking heaviness in current smokers. In observational analyses, current as compared with never smoking was associated with lower SBP, DBP, and lower hypertension risk, but with higher resting heart rate. In observational analyses amongst current smokers, one cigarette/day higher level of smoking heaviness was associated with higher (0.21 beats/minute; 95% CI 0.19; 0.24) resting heart rate, and slightly higher DBP (0.05 mmHg; 95% CI 0.02; 0.08) and SBP (0.08 mmHg; 95% CI 0.03; 0.13). However, in MR analyses amongst current smokers, while each smoking increasing allele of rs16969968/rs1051730 was associated with higher resting heart rate (0.36 beats/minute/allele; 95% CI 0.18; 0.54), there was no strong association with DBP, SBP, or hypertension. This would suggest a 7 beats/minute higher heart rate in those who smoke 20 cigarettes/day.CONCLUSIONS: -This MR meta-analysis supports a causal association of smoking heaviness with higher level of resting heart rate, but not with blood pressure. These findings suggest that part of the cardiovascular risk of smoking may operate through increasing resting heart rate.
- Published
- 2015
23. Health and unemployment: 14 years of follow-up on job loss in the Norwegian HUNT Study
- Author
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Kaspersen, Silje L., primary, Pape, Kristine, additional, Vie, Gunnhild Å., additional, Ose, Solveig O., additional, Krokstad, Steinar, additional, Gunnell, David, additional, and Bjørngaard, Johan H., additional
- Published
- 2015
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24. Heavier smoking may lead to a relative increase in waist circumference: evidence for a causal relationship from a Mendelian randomisation meta-analysis. The CARTA consortium: Table 1
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Morris, Richard W, primary, Taylor, Amy E, additional, Fluharty, Meg E, additional, Bjørngaard, Johan H, additional, Åsvold, Bjørn Olav, additional, Elvestad Gabrielsen, Maiken, additional, Campbell, Archie, additional, Marioni, Riccardo, additional, Kumari, Meena, additional, Korhonen, Tellervo, additional, Männistö, Satu, additional, Marques-Vidal, Pedro, additional, Kaakinen, Marika, additional, Cavadino, Alana, additional, Postmus, Iris, additional, Husemoen, Lise Lotte N, additional, Skaaby, Tea, additional, Ahluwalia, Tarun Veer Singh, additional, Treur, Jorien L, additional, Willemsen, Gonneke, additional, Dale, Caroline, additional, Wannamethee, S Goya, additional, Lahti, Jari, additional, Palotie, Aarno, additional, Räikkönen, Katri, additional, McConnachie, Alex, additional, Padmanabhan, Sandosh, additional, Wong, Andrew, additional, Dalgård, Christine, additional, Paternoster, Lavinia, additional, Ben-Shlomo, Yoav, additional, Tyrrell, Jessica, additional, Horwood, John, additional, Fergusson, David M, additional, Kennedy, Martin A, additional, Nohr, Ellen A, additional, Christiansen, Lene, additional, Kyvik, Kirsten Ohm, additional, Kuh, Diana, additional, Watt, Graham, additional, Eriksson, Johan G, additional, Whincup, Peter H, additional, Vink, Jacqueline M, additional, Boomsma, Dorret I, additional, Davey Smith, George, additional, Lawlor, Debbie, additional, Linneberg, Allan, additional, Ford, Ian, additional, Jukema, J Wouter, additional, Power, Chris, additional, Hyppönen, Elina, additional, Jarvelin, Marjo-Riitta, additional, Preisig, Martin, additional, Borodulin, Katja, additional, Kaprio, Jaakko, additional, Kivimaki, Mika, additional, Smith, Blair H, additional, Hayward, Caroline, additional, Romundstad, Pål R, additional, Sørensen, Thorkild I A, additional, Munafò, Marcus R, additional, and Sattar, Naveed, additional
- Published
- 2015
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25. Investigating the possible causal association of smoking with depression and anxiety using Mendelian randomisation meta-analysis:the CARTA consortium
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Taylor, Amy E, Fluharty, Meg E, Bjørngaard, Johan H, Gabrielsen, Maiken Elvestad, Skorpen, Frank, Marioni, Riccardo E, Campbell, Archie, Engmann, Jorgen, Mirza, Saira Saeed, Loukola, Anu, Laatikainen, Tiina, Partonen, Timo, Kaakinen, Marika, Ducci, Francesca, Cavadino, Alana, Husemoen, Lise Lotte N, Ahluwalia, Tarun Veer Singh, Jacobsen, Rikke Kart, Skaaby, Tea, Ebstrup, Jeanette Frost, Mortensen, Erik Lykke, Minica, Camelia C, Vink, Jacqueline M, Willemsen, Gonneke, Marques-Vidal, Pedro, Dale, Caroline E, Amuzu, Antoinette, Lennon, Lucy T, Lahti, Jari, Palotie, Aarno, Räikkönen, Katri, Wong, Andrew, Paternoster, Lavinia, Wong, Angelita Pui-Yee, Horwood, L John, Murphy, Michael, Johnstone, Elaine C, Kennedy, Martin A, Pausova, Zdenka, Paus, Tomáš, Ben-Shlomo, Yoav, Nohr, Ellen A, Kuh, Diana, Kivimaki, Mika, Eriksson, Johan G, Morris, Richard W, Casas, Juan P, Preisig, Martin, Boomsma, Dorret I, Linneberg, Allan, Power, Chris, Hyppönen, Elina, Veijola, Juha, Jarvelin, Marjo-Riitta, Korhonen, Tellervo, Tiemeier, Henning, Kumari, Meena, Porteous, David J, Hayward, Caroline, Romundstad, Pål R, Smith, George Davey, Munafò, Marcus R, Taylor, Amy E, Fluharty, Meg E, Bjørngaard, Johan H, Gabrielsen, Maiken Elvestad, Skorpen, Frank, Marioni, Riccardo E, Campbell, Archie, Engmann, Jorgen, Mirza, Saira Saeed, Loukola, Anu, Laatikainen, Tiina, Partonen, Timo, Kaakinen, Marika, Ducci, Francesca, Cavadino, Alana, Husemoen, Lise Lotte N, Ahluwalia, Tarun Veer Singh, Jacobsen, Rikke Kart, Skaaby, Tea, Ebstrup, Jeanette Frost, Mortensen, Erik Lykke, Minica, Camelia C, Vink, Jacqueline M, Willemsen, Gonneke, Marques-Vidal, Pedro, Dale, Caroline E, Amuzu, Antoinette, Lennon, Lucy T, Lahti, Jari, Palotie, Aarno, Räikkönen, Katri, Wong, Andrew, Paternoster, Lavinia, Wong, Angelita Pui-Yee, Horwood, L John, Murphy, Michael, Johnstone, Elaine C, Kennedy, Martin A, Pausova, Zdenka, Paus, Tomáš, Ben-Shlomo, Yoav, Nohr, Ellen A, Kuh, Diana, Kivimaki, Mika, Eriksson, Johan G, Morris, Richard W, Casas, Juan P, Preisig, Martin, Boomsma, Dorret I, Linneberg, Allan, Power, Chris, Hyppönen, Elina, Veijola, Juha, Jarvelin, Marjo-Riitta, Korhonen, Tellervo, Tiemeier, Henning, Kumari, Meena, Porteous, David J, Hayward, Caroline, Romundstad, Pål R, Smith, George Davey, and Munafò, Marcus R
- Abstract
OBJECTIVES: To investigate whether associations of smoking with depression and anxiety are likely to be causal, using a Mendelian randomisation approach.DESIGN: Mendelian randomisation meta-analyses using a genetic variant (rs16969968/rs1051730) as a proxy for smoking heaviness, and observational meta-analyses of the associations of smoking status and smoking heaviness with depression, anxiety and psychological distress.PARTICIPANTS: Current, former and never smokers of European ancestry aged ≥16 years from 25 studies in the Consortium for Causal Analysis Research in Tobacco and Alcohol (CARTA).PRIMARY OUTCOME MEASURES: Binary definitions of depression, anxiety and psychological distress assessed by clinical interview, symptom scales or self-reported recall of clinician diagnosis.RESULTS: The analytic sample included up to 58 176 never smokers, 37 428 former smokers and 32 028 current smokers (total N=127 632). In observational analyses, current smokers had 1.85 times greater odds of depression (95% CI 1.65 to 2.07), 1.71 times greater odds of anxiety (95% CI 1.54 to 1.90) and 1.69 times greater odds of psychological distress (95% CI 1.56 to 1.83) than never smokers. Former smokers also had greater odds of depression, anxiety and psychological distress than never smokers. There was evidence for positive associations of smoking heaviness with depression, anxiety and psychological distress (ORs per cigarette per day: 1.03 (95% CI 1.02 to 1.04), 1.03 (95% CI 1.02 to 1.04) and 1.02 (95% CI 1.02 to 1.03) respectively). In Mendelian randomisation analyses, there was no strong evidence that the minor allele of rs16969968/rs1051730 was associated with depression (OR=1.00, 95% CI 0.95 to 1.05), anxiety (OR=1.02, 95% CI 0.97 to 1.07) or psychological distress (OR=1.02, 95% CI 0.98 to 1.06) in current smokers. Results were similar for former smokers.CONCLUSIONS: Findings from Mendelian randomisation analyses do not support a causal role of
- Published
- 2014
26. Investigating the possible causal association of smoking with depression and anxiety using Mendelian randomisation meta-analysis: the CARTA consortium
- Author
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Taylor, Amy E, primary, Fluharty, Meg E, additional, Bjørngaard, Johan H, additional, Gabrielsen, Maiken Elvestad, additional, Skorpen, Frank, additional, Marioni, Riccardo E, additional, Campbell, Archie, additional, Engmann, Jorgen, additional, Mirza, Saira Saeed, additional, Loukola, Anu, additional, Laatikainen, Tiina, additional, Partonen, Timo, additional, Kaakinen, Marika, additional, Ducci, Francesca, additional, Cavadino, Alana, additional, Husemoen, Lise Lotte N, additional, Ahluwalia, Tarunveer Singh, additional, Jacobsen, Rikke Kart, additional, Skaaby, Tea, additional, Ebstrup, Jeanette Frost, additional, Mortensen, Erik Lykke, additional, Minica, Camelia C, additional, Vink, Jacqueline M, additional, Willemsen, Gonneke, additional, Marques-Vidal, Pedro, additional, Dale, Caroline E, additional, Amuzu, Antoinette, additional, Lennon, Lucy T, additional, Lahti, Jari, additional, Palotie, Aarno, additional, Räikkönen, Katri, additional, Wong, Andrew, additional, Paternoster, Lavinia, additional, Wong, Angelita Pui-Yee, additional, Horwood, L John, additional, Murphy, Michael, additional, Johnstone, Elaine C, additional, Kennedy, Martin A, additional, Pausova, Zdenka, additional, Paus, Tomáš, additional, Ben-Shlomo, Yoav, additional, Nohr, Ellen A, additional, Kuh, Diana, additional, Kivimaki, Mika, additional, Eriksson, Johan G, additional, Morris, Richard W, additional, Casas, Juan P, additional, Preisig, Martin, additional, Boomsma, Dorret I, additional, Linneberg, Allan, additional, Power, Chris, additional, Hyppönen, Elina, additional, Veijola, Juha, additional, Jarvelin, Marjo-Riitta, additional, Korhonen, Tellervo, additional, Tiemeier, Henning, additional, Kumari, Meena, additional, Porteous, David J, additional, Hayward, Caroline, additional, Romundstad, Pål R, additional, Smith, George Davey, additional, and Munafò, Marcus R, additional
- Published
- 2014
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27. Prevalence and long-term predictors of persistent chronic widespread pain in the general population in an 11-year prospective study: the HUNT study
- Author
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Mundal, Ingunn, primary, Gråwe, Rolf W, additional, Bjørngaard, Johan H, additional, Linaker, Olav M, additional, and Fors, Egil A, additional
- Published
- 2014
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28. Reading and writing difficulties in adolescence and later risk of welfare dependence. A ten year follow-up, the HUNT Study, Norway
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Pape, Kristine, primary, Bjørngaard, Johan H, additional, Westin, Steinar, additional, Holmen, Turid L, additional, and Krokstad, Steinar, additional
- Published
- 2011
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29. Body mass index and all cause mortality in HUNT and UK Biobank studies: linear and non-linear mendelian randomisation analyses
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Sun, Yi-Qian, Burgess, Stephen, Staley, James R, Wood, Angela, Bell, Steven, Kaptoge, Stephen, Guo, Qi, Bolton, Thomas, Mason, Amy, Butterworth, Adam, Di Angelantonio, Emanuele, Vie, Gunnhild Å, Bjørngaard, Johan H, Kinge, Jonas Minet, Chen, Yue, and Mai, Xiao-Mei
- Subjects
2. Zero hunger ,Adult ,Male ,Norway ,nutritional and metabolic diseases ,Middle Aged ,Mendelian Randomization Analysis ,United Kingdom ,3. Good health ,Body Mass Index ,Thinness ,Cardiovascular Diseases ,Risk Factors ,Neoplasms ,Cause of Death ,Humans ,Female ,Obesity ,Sex Distribution ,Aged - Abstract
Objective: To investigate the shape of the causal relationship between body mass index (BMI) and mortality. Design: Linear and non-linear Mendelian randomization analyses of two prospective population-based cohorts. Setting: Middle-aged to early late-aged individuals of European descent. Participants: 56,150 participants from the Nord-Trøndelag Health Study (HUNT) in Norway and 366,385 participants from UK Biobank recruited by postal invitation. Main outcome measures: All-cause and cause-specific (cardiovascular, cancer, and non-cardiovascular non-cancer) mortality. Results: In total 12,015 and 10,344 participants died during a median of 18.5 and 7.0 years’ follow-up in the HUNT and UK Biobank studies respectively. Linear Mendelian randomization analyses indicated an overall positive association between genetically-predicted BMI and all-cause mortality risk. A 1 kg/m2 increase in genetically-predicted BMI led to a 5% (95% confidence interval [CI]: 1%, 8%) higher mortality risk in overweight individuals (BMI 25.0-29.9), and a 9% (95% CI: 4%, 14%) higher mortality risk in obese individuals (BMI ≥ 30.0), but 34% (95% CI: 16%, 48%), lower risk in underweight (BMI < 18.5) and 14% (95% CI: -1%, 27%) lower risk in low normal weight individuals (BMI 18.5-19.9). Non-linear Mendelian randomization indicated a J-shaped relationship between genetically-predicted BMI and all-cause mortality risk, with the nadir of risk at BMI about 22-25 kg/m2 for the overall sample. Increased risk of all-cause mortality in overweight and obese individuals was more evident in women. However, subgroup analyses by smoking status suggested a monotone increasing relationship of BMI with mortality in never-smokers, but a non-monotone relationship in ever-smokers. Conclusion: The previously observed J-shaped relationship between BMI and mortality appears to have a causal basis, but subgroup analyses by smoking status revealed the BMI—mortality relationship is likely comprised of at least two distinct curves, rather than a single J-shaped relationship. Increased mortality risk for being underweight was only evident in ever-smokers., YQS and this work were supported by The Norwegian Cancer Society (project ID 5769155-2015) and The Research Council of Norway “Gaveforsterkning”. GÅV and JMK were supported by The Research Council of Norway (grant number 250335). S Burgess is supported by a Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society (Grant Number 204623/Z/16/Z). The funders had no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; and in the decision to submit the article for publication
30. Body mass index and all cause mortality in HUNT and UK Biobank studies : linear and non-linear mendelian randomisation analyses
- Author
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Sun, Yi-Qian, Burgess, Stephen, Staley, James R, Wood, Angela M, Bell, Steven, Kaptoge, Stephen K, Guo, Qi, Bolton, Thomas R, Mason, Amy M, Butterworth, Adam S, Di Angelantonio, Emanuele, Vie, Gunnhild Å, Bjørngaard, Johan H, Kinge, Jonas Minet, Chen, Yue, and Mai, Xiao-Mei
31. Contact with primary health care physicians prior to a severe emergency hospitalisation.
- Author
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Skarshaug, Lena J., Svedahl, Ellen R., Bjørngaard, Johan H., Steinsbekk, Aslak, and Pape, Kristine
- Subjects
- *
PRIMARY health care , *PHYSICIANS , *HOSPITAL care , *EMERGENCY medical services , *GENERALIZED estimating equations , *MYOCARDIAL infarction - Abstract
Introduction: There is scarce knowledge on the use of primary health care prior to emergency hospitalisation. Aims: To assess contacts with general practitioners (regular GP and municipal out-of-hours emergency services) during the year prior to hospitalisation for five common acute diagnoses (acute myocardial infarction; hip fracture; stroke; heart failure; and pneumonia) for patients aged 50 years and older. Methods: Longitudinal population-based design with linked data from Norwegian national- and municipal registers. Register-based information on all health care contacts and use of municipality services for the inhabitants aged 50 and older in four municipalities in central Norway collected for a two-year period from 2012 to 2013. In total, 66952 participants were included: 53% female, and mean age (in 2012) 65 years (11.1SD). We used generalized estimation equation models (GEE) to investigate the use of health care during 1) the year and 2) the month prior to hospitalisation for each of the six patient groups. We used the estimates to calculate the predicted level of health care use at different time points prior to hospitalisation. Results: Patients in the age group 50 years and older hospitalised for different severe conditions had a stable and frequent contact with general practitioners the year prior to the admission. Level and patterns of increase close to the time of hospital admission differed between the diagnose groups. The group hospitalised for heart failure stood out with a clear increasing share that visited their general practitioner and municipal out-of-hours emergency services the closer they got to the acute admission; OR 1.97 (CI 1.44-2.68) for seeing a GP the last month prior to hospitalisation compared to 6 months prior to hospitalisation. Nevertheless, 21% (heart failure) to 50% (hip fracture) of hospitalised patients were "non-users"; they visited neither their general practitioner nor municipal out-of-hours emergency services the last month prior to admission. Conclusion: General practitioners are in frequent contact with patients hospitalised for different severe emergency conditions. This underscores the general practitioners vital role in these patients' health care. [ABSTRACT FROM AUTHOR]
- Published
- 2018
32. Socioeconomic inequalities in multimorbidity and joint associations with mortality in a general population. The HUNT Study
- Author
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Vinjerui, Kristin Hestmann, Sund, Erik R, Douglas, Kirsty, Bjørngaard, Johan H, and Krokstad, Steinar
- Abstract
Background: Multimorbidity, the concurrence of multiple chronic conditions, is highly frequent. Varying definitions and measures of multimorbidity hamper comparability of research, which is exemplified with wide ranges of prevalence estimates but a steady association with mortality. The complexity in the treatment and burden of multimorbidity are associated with the combinations of conditions, presence of associated health concepts, such as frailty, personal factors, and social context, such as biology, lifestyle, and living conditions. Frailty is a dynamic measure of biological age, with impaired function (physical, psychological, or social) and increased risk of adverse events including death. Social health inequalities, in which the burden of poor health and premature death is higher with lower socioeconomic position, is well-known worldwide, and multimorbidity is no exception, in that it occurs at higher rates at younger ages, and with more complex combinations of conditions in socioeconomically deprived groups. There are few studies on complex measures of multimorbidity, suggested to detect those with increased care needs and severity and their association with socioeconomic position; there is also a research gap on the joint association of socioeconomic position and multimorbidity with mortality. Thus, the aims of this thesis are to describe the socioeconomic distribution of complex measures of multimorbidity (article I, article II, and supplemental analysis on writing this dissertation) and how socioeconomic position may modify the association of multimorbidity with mortality (article III) in an adult general population. Examining several multimorbidity measures in the same cohort makes possible a unique direct comparison of socioeconomic gradients in prevalence and joint associations with mortality. Methods: The total county health survey Trøndelag Health Study 2006-2008 (HUNT3) provided data on chronic conditions, impairments, and mortality (until February 1, 2019), as well as socioeconomic position. Several multimorbidity measures were explored based on individual and organ system group counts and the presence of frailty. Socioeconomic differences in prevalence were explored cross-sectionally, and joint association with mortality were explored prospectively. Results: The overall prevalence varied by the complex measure of multimorbidity from 18% to 63%. All multimorbidity measures were more prevalent in the lower socioeconomic groups, in women, and with increased age but were common across age groups in both sexes. Socioeconomic inequalities in prevalence varied by sex and age but persisted from young adulthood to old age. Mortality increased by the number of conditions with varying but intact socioeconomic gradients, and relative mortality risk increased with the presence of multimorbidity and lower socioeconomic position. Conclusions: Even complex measures of multimorbidity were common in the general population, with socioeconomic inequalities in prevalence throughout adulthood and socioeconomic inequalities in mortality across multimorbidity measures. The findings call for continuous public policy and public health to prevent socioeconomic inequalities in health. The magnitude of multimorbidity in all age groups suggest a demand for generalist and person-centered approaches that consider socioeconomic context in health care. In Norway, family doctors are in a unique position to offer continuous care, and this arrangement should be kept as a high priority. Future research on trajectories, associations with a variety of social determinants of health, health care utilization, and mortality would be relevant to enhance future prevention and management of multimorbidity.
- Published
- 2021
33. Associations between parental polygenic obesity risk and offspring's weight at birth, early and late adolescence-The HUNT Study, Norway.
- Author
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Næss, Marit, Sund, Erik R., Vie, Gunnhild Å., Bjørngaard, Johan H., Åsvold, Bjørn Olav, Holmen, Turid Lingaas, and Kvaløy, Kirsti
- Subjects
- *
OBESITY risk factors , *BIRTH weight , *BODY mass index , *ADOLESCENT physiology , *FOLLOW-up studies (Medicine) - Abstract
Introduction and Aims: Obesity develops in a complex interplay between genetic and environmental factors. We aimed to examine how genetic predisposition influences obesity development early in life, by estimating the association between polygenic obesity risk and weight at birth (ponderal index) and throughout adolescence (BMI). Methods: We included 8561 parent-offspring trios who participated in the HUNT/Young-HUNT surveys in 1995-97 or 2006-08 when the offspring were 13-19 years of age. Additional weight data were included from a follow-up study in 2000-01 and from birth for 1026 and 8370 offspring participants, respectively. A weighted parental genetic risk score (GRS) based on maternal and paternal genetic data was constructed from 96 SNPs that have been robustly associated with adult BMI previously. Linear mixed effect models were employed to study sex-specific associations between parental GRS and children's ponderal index at birth and BMI at adolescents (ranging from 13-19 years). Results: The parental GRS was positively associated with BMI in both boys and girls at all ages from 13 to 19 years. The estimates were of similar magnitude as associations between parents' own GRS and their BMI at age 42. No association was found between the parental GRS and ponderal index at birth, nor did parental education modify any associations. Conclusions: Genetic predisposition for adult obesity, expressed by a parental genetic risk score for BMI, had an adverse effect on adolescent BMI that was similar in boys and girls at all ages from 13 to 19 years, but was not associated with ponderal index at birth. [ABSTRACT FROM AUTHOR]
- Published
- 2018
34. Intergenerational polygenic obesity risk throughout adolescence in a cross-sectional study design: The HUNT study, Norway.
- Author
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Naess M, Sund ER, Vie GÅ, Bjørngaard JH, Åsvold BO, Holmen TL, and Kvaløy K
- Subjects
- Adolescent, Body Mass Index, Cross-Sectional Studies, Humans, Male, Norway epidemiology, Polymorphism, Single Nucleotide, Risk Factors, Young Adult, Multifactorial Inheritance, Obesity epidemiology, Obesity genetics, Parents
- Abstract
Objective: This study examined the relationship between parental obesity polygenic risk and children's BMI throughout adolescence. Additionally, from a smaller subsample, the objective was to assess whether parental polygenic risk score (PRS) may act as a proxy for offspring PRS in studies lacking offspring genetic data., Methods: A total of 8,561 parent-offspring (age 13-19 years) trios from the Trøndelag Health Study (the HUNT Study) were included, of which, 1,286 adolescents had available genetic data. Weighted parental PRSs from 900 single-nucleotide polymorphisms robustly associated with adult BMI were constructed and applied in linear mixed-effects models., Results: A positive association between parental PRS and offspring sex- and age-adjusted BMI (iso-BMI) throughout adolescence was identified. The estimated marginal effects per standard deviation increase in parental PRS were 0.26 (95% CI: 0.18-0.33), 0.36 (95% CI: 0.29-0.43), and 0.62 kg/m
2 (95% CI: 0.51-0.72) for maternal, paternal, and combined parental PRS, respectively. In subsample analyses, the magnitude of association of the parental PRS versus offspring PRS with iso-BMI in adolescents was similar., Conclusions: Parental PRS was consistently associated with offspring iso-BMI throughout adolescence. Results from subsample analyses support the use of parental PRS of obesity as a proxy for adolescent PRS in the absence of offspring genetic data., (© 2021 The Authors. Obesity published by Wiley Periodicals LLC on behalf of The Obesity Society (TOS).)- Published
- 2021
- Full Text
- View/download PDF
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