Umeå universitets logga

umu.sePublikationer
Ändra sökning
Avgränsa sökresultatet
1 - 15 av 15
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Träffar per sida
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sortering
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
Markera
Maxantalet träffar du kan exportera från sökgränssnittet är 250. Vid större uttag använd dig av utsökningar.
  • 1. Christakoudi, Sofia
    et al.
    Pagoni, Panagiota
    Ferrari, Pietro
    Cross, Amanda J.
    Tzoulaki, Ioanna
    Muller, David C.
    Weiderpass, Elisabete
    Freisling, Heinz
    Murphy, Neil
    Dossus, Laure
    Turzanski Fortner, Renee
    Agudo, Antonio
    Overvad, Kim
    Perez-Cornago, Aurora
    Key, Timothy J.
    Brennan, Paul
    Johansson, Mattias
    Tjønneland, Anne
    Halkjær, Jytte
    Boutron-Ruault, Marie-Christine
    Artaud, Fanny
    Severi, Gianluca
    Kaaks, Rudolf
    Schulze, Matthias B.
    Bergmann, Manuela M.
    Masala, Giovanna
    Grioni, Sara
    Simeon, Vittorio
    Tumino, Rosario
    Sacerdote, Carlotta
    Skeie, Guri
    Rylander, Charlotta
    Borch, Kristin Benjaminsen
    Quirós, J. Ramón
    Rodriguez-Barranco, Miguel
    Chirlaque, Maria-Dolores
    Ardanaz, Eva
    Amiano, Pilar
    Drake, Isabel
    Stocks, Tanja
    Häggström, Christel
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning. Department of Surgical Science, Uppsala University, Uppsala, Sweden.
    Harlid, Sophia
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Ellingjord-Dale, Merete
    Riboli, Elio
    Tsilidis, Konstantinos K.
    Weight change in middle adulthood and risk of cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort2021Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 148, nr 7, s. 1637-1651Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Obesity is a risk factor for several major cancers. Associations of weight change in middle adulthood with cancer risk, however, are less clear. We examined the association of change in weight and body mass index (BMI) category during middle adulthood with 42 cancers, using multivariable Cox proportional hazards models in the European Prospective Investigation into Cancer and Nutrition cohort. Of 241 323 participants (31% men), 20% lost and 32% gained weight (>0.4 to 5.0 kg/year) during 6.9 years (average). During 8.0 years of follow-up after the second weight assessment, 20 960 incident cancers were ascertained. Independent of baseline BMI, weight gain (per one kg/year increment) was positively associated with cancer of the corpus uteri (hazard ratio [HR] = 1.14; 95% confidence interval: 1.05-1.23). Compared to stable weight (+/- 0.4 kg/year), weight gain (>0.4 to 5.0 kg/year) was positively associated with cancers of the gallbladder and bile ducts (HR = 1.41; 1.01-1.96), postmenopausal breast (HR = 1.08; 1.00-1.16) and thyroid (HR = 1.40; 1.04-1.90). Compared to maintaining normal weight, maintaining overweight or obese BMI (World Health Organisation categories) was positively associated with most obesity-related cancers. Compared to maintaining the baseline BMI category, weight gain to a higher BMI category was positively associated with cancers of the postmenopausal breast (HR = 1.19; 1.06-1.33), ovary (HR = 1.40; 1.04-1.91), corpus uteri (HR = 1.42; 1.06-1.91), kidney (HR = 1.80; 1.20-2.68) and pancreas in men (HR = 1.81; 1.11-2.95). Losing weight to a lower BMI category, however, was inversely associated with cancers of the corpus uteri (HR = 0.40; 0.23-0.69) and colon (HR = 0.69; 0.52-0.92). Our findings support avoiding weight gain and encouraging weight loss in middle adulthood.

    Ladda ner fulltext (pdf)
    fulltext
  • 2. Christakoudi, Sofia
    et al.
    Tsilidis, Konstantinos K.
    Muller, David C.
    Freisling, Heinz
    Weiderpass, Elisabete
    Overvad, Kim
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Häggström, Christel
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning. Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
    Pischon, Tobias
    Dahm, Christina C.
    Zhang, Jie
    Tjonneland, Anne
    Halkjaer, Jytte
    MacDonald, Conor
    Boutron-Ruault, Marie-Christine
    Mancini, Francesca Romana
    Kuehn, Tilman
    Kaaks, Rudolf
    Schulze, Matthias B.
    Trichopoulou, Antonia
    Karakatsani, Anna
    Peppa, Eleni
    Masala, Giovanna
    Pala, Valeria
    Panico, Salvatore
    Tumino, Rosario
    Sacerdote, Carlotta
    Quiros, J. Ramon
    Agudo, Antonio
    Sanchez, Maria-Jose
    Cirera, Lluis
    Barricarte-Gurrea, Aurelio
    Amiano, Pilar
    Memarian, Ensieh
    Sonestedt, Emily
    Bueno-de-Mesquita, Bas
    May, Anne M.
    Khaw, Kay-Tee
    Wareham, Nicholas J.
    Tong, Tammy Y. N.
    Huybrechts, Inge
    Noh, Hwayoung
    Aglago, Elom K.
    Ellingjord-Dale, Merete
    Ward, Heather A.
    Aune, Dagfinn
    Riboli, Elio
    A Body Shape Index (ABSI) achieves better mortality risk stratification than alternative indices of abdominal obesity: results from a large European cohort2020Ingår i: Scientific Reports, E-ISSN 2045-2322, Vol. 10, nr 1, artikel-id 14541Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Abdominal and general adiposity are independently associated with mortality, but there is no consensus on how best to assess abdominal adiposity. We compared the ability of alternative waist indices to complement body mass index (BMI) when assessing all-cause mortality. We used data from 352,985 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) and Cox proportional hazards models adjusted for other risk factors. During a mean follow-up of 16.1 years, 38,178 participants died. Combining in one model BMI and a strongly correlated waist index altered the association patterns with mortality, to a predominantly negative association for BMI and a stronger positive association for the waist index, while combining BMI with the uncorrelated A Body Shape Index (ABSI) preserved the association patterns. Sex-specific cohort-wide quartiles of waist indices correlated with BMI could not separate high-risk from low-risk individuals within underweight (BMI<18.5 kg/m(2)) or obese (BMI<greater than or equal to>30 kg/m(2)) categories, while the highest quartile of ABSI separated 18-39% of the individuals within each BMI category, which had 22-55% higher risk of death. In conclusion, only a waist index independent of BMI by design, such as ABSI, complements BMI and enables efficient risk stratification, which could facilitate personalisation of screening, treatment and monitoring.

    Ladda ner fulltext (pdf)
    fulltext
  • 3. Deschasaux, Melanie
    et al.
    Huybrechts, Inge
    Julia, Chantal
    Hercberg, Serge
    Egnell, Manon
    Srour, Bernard
    Kesse-Guyot, Emmanuelle
    Latino-Martel, Paule
    Biessy, Carine
    Casagrande, Corinne
    Murphy, Neil
    Jenab, Mazda
    Ward, Heather A.
    Weiderpass, Elisabete
    Overvad, Kim
    Tjonneland, Anne
    Rostgaard-Hansen, Agnetha Linn
    Boutron-Ruault, Marie-Christine
    Mancini, Francesca Romana
    Mahamat-Saleh, Yahya
    Kuehn, Tilman
    Katzke, Verena
    Bergmann, Manuela M.
    Schulze, Matthias B.
    Trichopoulou, Antonia
    Karakatsani, Anna
    Peppa, Eleni
    Masala, Giovanna
    Agnoli, Claudia
    De Magistris, Maria Santucci
    Tumino, Rosario
    Sacerdote, Carlotta
    Boer, Jolanda M. A.
    Verschuren, W. M. Monique
    van der Schouw, Yvonne T.
    Skeie, Guri
    Braaten, Tonje
    Luisa Redondo, M.
    Agudo, Antonio
    Petrova, Dafina
    Colorado-Yohar, Sandra M.
    Barricarte, Aurelio
    Amiano, Pilar
    Sonestedt, Emily
    Ericson, Ulrika
    Otten, Julia
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Sundström, Björn
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Wareham, Nicholas J.
    Forouhi, Nita G.
    Vineis, Paolo
    Tsilidis, Konstantinos K.
    Knuppel, Anika
    Papier, Keren
    Ferrari, Pietro
    Riboli, Elio
    Gunter, Marc J.
    Touvier, Mathilde
    Association between nutritional profiles of foods underlying Nutri-Score front-of-pack labels and mortality: EPIC cohort study in 10 European countries2020Ingår i: The BMJ, E-ISSN 1756-1833, Vol. 370, artikel-id m3173Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE To determine if the Food Standards Agency nutrient profiling system (FSAm-NPS), which grades the nutritional quality of food products and is used to derive the Nutri-Score front-of-packet label to guide consumers towards healthier food choices, is associated with mortality. DESIGN Population based cohort study. SETTING European Prospective Investigation into Cancer and Nutrition (EPIC) cohort from 23 centres in 10 European countries. PARTICIPANTS 521 324 adults; at recruitment, country specific and validated dietary questionnaires were used to assess their usual dietary intakes. A FSAm-NPS score was calculated for each food item per 100 g content of energy, sugars, saturated fatty acids, sodium, fibre, and protein, and of fruit, vegetables, legumes, and nuts. The FSAm-NPS dietary index was calculated for each participant as an energy weighted mean of the FSAm-NPS score of all foods consumed. The higher the score the lower the overall nutritional quality of the diet. MAIN OUTCOME MEASURE Associations between the FSAm-NPS dietary index score and mortality, assessed using multivariable adjusted Cox proportional hazards regression models. RESULTS After exclusions, 501 594 adults (median follow-up 17.2 years, 8 162 730 person years) were included in the analyses. Those with a higher FSAm-NPS dietary index score (highest versus lowest fifth) showed an increased risk of all cause mortality (n=53 112 events from non-external causes; hazard ratio 1.07, 95% confidence interval 1.03 to 1.10, P(0.001 for trend) and mortality from cancer (1.08, 1.03 to 1.13, P(0.001 for trend) and diseases of the circulatory (1.04, 0.98 to 1.11, P=0.06 for trend), respiratory (1.39, 1.22 to 1.59, P(0.001), and digestive (1.22, 1.02 to 1.45, P=0.03 for trend) systems. The age standardised absolute rates for all cause mortality per 10 000 persons over 10 years were 760 (men=1237; women=563) for those in the highest fifth of the FSAm-NPS dietary index score and 661 (men=1008; women=518) for those in the lowest fifth. CONCLUSIONS In this large multinational European cohort, consuming foods with a higher FSAm-NPS score (lower nutritional quality) was associated with a higher mortality for all causes and for cancer and diseases of the circulatory, respiratory, and digestive systems, supporting the relevance of FSAm-NPS to characterise healthier food choices in the context of public health policies (eg, the Nutri-Score) for European populations. This is important considering ongoing discussions about the potential implementation of a unique nutrition labelling system at the European Union level.

    Ladda ner fulltext (pdf)
    fulltext
  • 4. Ibsen, Daniel B.
    et al.
    Steur, Marinka
    Imamura, Fumiaki
    Overvad, Kim
    Schulze, Matthias B.
    Bendinelli, Benedetta
    Guevara, Marcela
    Agudo, Antonio
    Amiano, Pilar
    Aune, Dagfinn
    Barricarte, Aurelio
    Ericson, Ulrika
    Fagherazzi, Guy
    Franks, Paul W.
    Freisling, Heinz
    Quiros, Jose R.
    Grioni, Sara
    Heath, Alicia K.
    Huybrechts, Inge
    Katze, Verena
    Laouali, Nasser
    Mancini, Francesca
    Masala, Giovanna
    Olsen, Anja
    Papier, Keren
    Ramne, Stina
    Rolandsson, Olov
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Allmänmedicin.
    Sacerdote, Carlotta
    Sánchez, Maria-José
    Santiuste, Carmen
    Simeon, Vittorio
    Spijkerman, Annemieke M. W.
    Srour, Bernard
    Tjønneland, Anne
    Tong, Tammy Y. N.
    Tumino, Rosario
    van der Schouw, Yvonne T.
    Weiderpass, Elisabete
    Wittenbecher, Clemens
    Sharp, Stephen J.
    Riboli, Elio
    Forouhi, Nita G.
    Wareham, Nick J.
    Replacement of Red and Processed Meat With Other Food Sources of Protein and the Risk of Type 2 Diabetes in European Populations: The EPIC-InterAct Study2020Ingår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 43, nr 11, s. 2660-2667Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: There is sparse evidence for the association of suitable food substitutions for red and processed meat on the risk of type 2 diabetes. We modeled the association between replacing red and processed meat with other protein sources and the risk of type 2 diabetes and estimated its population impact.

    RESEARCH DESIGN AND METHODS: The European Prospective Investigation into Cancer (EPIC)-InterAct case cohort included 11,741 individuals with type 2 diabetes and a subcohort of 15,450 participants in eight countries. We modeled the replacement of self-reported red and processed meat with poultry, fish, eggs, legumes, cheese, cereals, yogurt, milk, and nuts. Country-specific hazard ratios (HRs) for incident type 2 diabetes were estimated by Prentice-weighted Cox regression and pooled using random-effects meta-analysis.

    RESULTS: There was a lower hazard for type 2 diabetes for the modeled replacement of red and processed meat (50 g/day) with cheese (HR 0.90, 95% CI 0.83-0.97) (30 g/day), yogurt (0.90, 0.86-0.95) (70 g/day), nuts (0.90, 0.84-0.96) (10 g/day), or cereals (0.92, 0.88-0.96) (30 g/day) but not for replacements with poultry, fish, eggs, legumes, or milk. If a causal association is assumed, replacing red and processed meat with cheese, yogurt, or nuts could prevent 8.8%, 8.3%, or 7.5%, respectively, of new cases of type 2 diabetes.

    CONCLUSIONS: Replacement of red and processed meat with cheese, yogurt, nuts, or cereals was associated with a lower rate of type 2 diabetes. Substituting red and processed meat by other protein sources may contribute to the prevention of incident type 2 diabetes in European populations.

  • 5. Kliemann, Nathalie
    et al.
    Murphy, Neil
    Viallon, Vivian
    Freisling, Heinz
    Tsilidis, Konstantinos K.
    Rinaldi, Sabina
    Mancini, Francesca R.
    Fagherazzi, Guy
    Boutron-Ruault, Marie-Christine
    Boeing, Heiner
    Schulze, Matthias B.
    Masala, Giovanna
    Krogh, Vittorio
    Sacerdote, Carlotta
    de Magistris, Maria S.
    Bueno-de-Mesquita, Bas
    Weiderpass, Elisabete
    Kuehn, Tilman
    Kaaks, Rudolf
    Jakszyn, Paula
    Redondo-Sanchez, Daniel
    Amiano, Pilar
    Chirlaque, Maria-Dolores
    Gurrea, Aurelio B.
    Ericson, Ulrica
    Drake, Isabel
    Nost, Therese H.
    Aune, Dagfinn
    May, Anne M.
    Tjonneland, Anne
    Dahm, Christina C.
    Overvad, Kim
    Tumino, Rosario
    Quiros, Jose R.
    Trichopoulou, Antonia
    Karakatsani, Anna
    La Vecchia, Carlo
    Nilsson, Lena M.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Riboli, Elio
    Huybrechts, Inge
    Gunter, Marc J.
    Predicted basal metabolic rate and cancer risk in the European Prospective Investigation into Cancer and Nutrition2020Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 147, nr 3, s. 648-661Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Emerging evidence suggests that a metabolic profile associated with obesity may be a more relevant risk factor for some cancers than adiposity per se. Basal metabolic rate (BMR) is an indicator of overall body metabolism and may be a proxy for the impact of a specific metabolic profile on cancer risk. Therefore, we investigated the association of predicted BMR with incidence of 13 obesity-related cancers in the European Prospective Investigation into Cancer and Nutrition (EPIC). BMR at baseline was calculated using the WHO/FAO/UNU equations and the relationships between BMR and cancer risk were investigated using multivariable Cox proportional hazards regression models. A total of 141,295 men and 317,613 women, with a mean follow-up of 14 years were included in the analysis. Overall, higher BMR was associated with a greater risk for most cancers that have been linked with obesity. However, among normal weight participants, higher BMR was associated with elevated risks of esophageal adenocarcinoma (hazard ratio per 1-standard deviation change in BMR [HR1-SD]: 2.46; 95% CI 1.20; 5.03) and distal colon cancer (HR1-SD: 1.33; 95% CI 1.001; 1.77) among men and with proximal colon (HR1-SD: 1.16; 95% CI 1.01; 1.35), pancreatic (HR1-SD: 1.37; 95% CI 1.13; 1.66), thyroid (HR1-SD: 1.65; 95% CI 1.33; 2.05), postmenopausal breast (HR1-SD: 1.17; 95% CI 1.11; 1.22) and endometrial (HR1-SD: 1.20; 95% CI 1.03; 1.40) cancers in women. These results indicate that higher BMR may be an indicator of a metabolic phenotype associated with risk of certain cancer types, and may be a useful predictor of cancer risk independent of body fatness.

  • 6. Meidtner, Karina
    et al.
    Podmore, Clara
    Kroger, Janine
    van der Schouw, Yvonne T.
    Bendinelli, Benedetta
    Agnoli, Claudia
    Arriola, Larraitz
    Barricarte, Aurelio
    Boeing, Heiner
    Cross, Amanda J.
    Dow, Courtney
    Ekblom, Kim
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Klinisk kemi.
    Fagherazzi, Guy
    Franks, Paul W.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin. Department of Clinical Sciences, Lund University, Malmö, Sweden.
    Gunter, Marc J.
    Huerta, Jose Maria
    Jakszyn, Paula
    Jenab, Mazda
    Katzke, Verena A.
    Key, Timothy J.
    Khaw, Kay Tee
    Kuhn, Tilman
    Kyro, Cecilie
    Mancini, Francesca Romana
    Melander, Olle
    Nilsson, Peter M.
    Overvad, Kim
    Palli, Domenico
    Panico, Salvatore
    Quiros, J. Ramon
    Rodriguez-Barranco, Miguel
    Sacerdote, Carlotta
    Sluijs, Ivonne
    Stepien, Magdalena
    Tjonneland, Anne
    Tumino, Rosario
    Forouhi, Nita G.
    Sharp, Stephen J.
    Langenberg, Claudia
    Schulze, Matthias B.
    Riboli, Elio
    Wareham, Nicholas J.
    Interaction of Dietary and Genetic Factors Influencing Body Iron Status and Risk of Type 2 Diabetes Within the EPIC-InterAct Study2018Ingår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 41, nr 2, s. 277-285Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: Meat intake has been consistently shown to be positively associated with incident type 2 diabetes. Part of that association may be mediated by body iron status, which is influenced by genetic factors. We aimed to test for interactions of genetic and dietary factors influencing body iron status in relation to the risk of incident type 2 diabetes.

    RESEARCH DESIGN AND METHODS: The case-cohort comprised 9,347 case subjects and 12,301 subcohort participants from eight European countries. Single nucleotide polymorphisms (SNPs) were selected from genome-wide association studies on iron status biomarkers and candidate gene studies. A ferritin-related gene score was constructed. Multiplicative and additive interactions of heme iron and SNPs as well as the gene score were evaluated using Cox proportional hazards regression.

    RESULTS: Higher heme iron intake (per 1 SD) was associated with higher ferritin levels (β = 0.113 [95% CI 0.082; 0.144]), but not with transferrin (−0.019 [−0.043; 0.006]) or transferrin saturation (0.016 [−0.006; 0.037]). Five SNPs located in four genes (rs1799945 [HFE H63D], rs1800562 [HFE C282Y], rs236918 [PCK7], rs744653 [SLC40A1], and rs855791 [TMPRSS6V736A]) were associated with ferritin. We did not detect an interaction of heme iron and the gene score on the risk of diabetes in the overall study population (Padd = 0.16, Pmult = 0.21) but did detect a trend toward a negative interaction in men (Padd = 0.04, Pmult = 0.03).

    CONCLUSIONS: We found no convincing evidence that the interplay of dietary and genetic factors related to body iron status associates with type 2 diabetes risk above the level expected from the sum or product of the two individual exposures.

  • 7. Naudin, Sabine
    et al.
    Viallon, Vivian
    Hashim, Dana
    Freisling, Heinz
    Jenab, Mazda
    Weiderpass, Elisabete
    Perrier, Flavie
    McKenzie, Fiona
    Bueno-de-Mesquita, H. Bas
    Olsen, Anja
    Tjonneland, Anne
    Dahm, Christina C.
    Overvad, Kim
    Mancini, Francesca R.
    Rebours, Vinciane
    Boutron-Ruault, Marie-Christine
    Katzke, Verena
    Kaaks, Rudolf
    Bergmann, Manuela
    Boeing, Heiner
    Peppa, Eleni
    Karakatsani, Anna
    Trichopoulou, Antonia
    Pala, Valeria
    Masala, Giovana
    Panico, Salvatore
    Tumino, Rosario
    Sacerdote, Carlotta
    May, Anne M.
    van Gils, Carla H.
    Rylander, Charlotta
    Borch, Kristin Benjaminsen
    Chirlaque Lopez, Maria Dolores
    Sanchez, Maria-Jose
    Ardanaz, Eva
    Quiros, Jose Ramon
    Amiano Exezarreta, Pilar
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Drake, Isabel
    Regner, Sara
    Travis, Ruth C.
    Wareham, Nick
    Aune, Dagfinn
    Riboli, Elio
    Gunter, Marc J.
    Duell, Eric J.
    Brennan, Paul
    Ferrari, Pietro
    Healthy lifestyle and the risk of pancreatic cancer in the EPIC study2020Ingår i: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 35, nr 10, s. 975-986Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Pancreatic cancer (PC) is a highly fatal cancer with currently limited opportunities for early detection and effective treatment. Modifiable factors may offer pathways for primary prevention. In this study, the association between the Healthy Lifestyle Index (HLI) and PC risk was examined. Within the European Prospective Investigation into Cancer and Nutrition cohort, 1113 incident PC (57% women) were diagnosed from 400,577 participants followed-up for 15 years (median). HLI scores combined smoking, alcohol intake, dietary exposure, physical activity and, in turn, overall and central adiposity using BMI (HLIBMI) and waist-to-hip ratio (WHR, HLIWHR), respectively. High values of HLI indicate adherence to healthy behaviors. Cox proportional hazard models with age as primary time variable were used to estimate PC hazard ratios (HR) and 95% confidence intervals (CI). Sensitivity analyses were performed by excluding, in turn, each factor from the HLI score. Population attributable fractions (PAF) were estimated assuming participants’ shift to healthier lifestyles. The HRs for a one-standard deviation increment of HLIBMI and HLIWHR were 0.84 (95% CI: 0.79, 0.89; ptrend = 4.3e−09) and 0.77 (0.72, 0.82; ptrend = 1.7e−15), respectively. Exclusions of smoking from HLIWHR resulted in HRs of 0.88 (0.82, 0.94; ptrend = 4.9e−04). The overall PAF estimate was 19% (95% CI: 11%, 26%), and 14% (6%, 21%) when smoking was removed from the score. Adherence to a healthy lifestyle was inversely associated with PC risk, beyond the beneficial role of smoking avoidance. Public health measures targeting compliance with healthy lifestyles may have an impact on PC incidence.

  • 8. Papadimitriou, Nikos
    et al.
    Dimou, Niki
    Tsilidis, Konstantinos K.
    Banbury, Barbara
    Martin, Richard M.
    Lewis, Sarah J.
    Kazmi, Nabila
    Robinson, Timothy M.
    Albanes, Demetrius
    Aleksandrova, Krasimira
    Berndt, Sonja I.
    Bishop, D. Timothy
    Brenner, Hermann
    Buchanan, Daniel D.
    Bueno-de-Mesquita, Bas
    Campbell, Peter T.
    Castellvi-Bel, Sergi
    Chan, Andrew T.
    Chang-Claude, Jenny
    Ellingjord-Dale, Merete
    Figueiredo, Jane C.
    Gallinger, Steven J.
    Giles, Graham G.
    Giovannucci, Edward
    Gruber, Stephen B.
    Gsur, Andrea
    Hampe, Jochen
    Hampel, Heather
    Harlid, Sophia
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Harrison, Tabitha A.
    Hoffmeister, Michael
    Hopper, John L.
    Hsu, Li
    Maria Huerta, Jose
    Huyghe, Jeroen R.
    Jenkins, Mark A.
    Keku, Temitope O.
    Kuehn, Tilman
    La Vecchia, Carlo
    Le Marchand, Loic
    Li, Christopher I.
    Li, Li
    Lindblom, Annika
    Lindor, Noralane M.
    Lynch, Brigid
    Markowitz, Sanford D.
    Masala, Giovanna
    May, Anne M.
    Milne, Roger
    Monninkhof, Evelyn
    Moreno, Lorena
    Moreno, Victor
    Newcomb, Polly A.
    Offit, Kenneth
    Perduca, Vittorio
    Pharoah, Paul D. P.
    Platz, Elizabeth A.
    Potter, John D.
    Rennert, Gad
    Riboli, Elio
    Sanchez, Maria-Jose
    Schmit, Stephanie L.
    Schoen, Robert E.
    Severi, Gianluca
    Sieri, Sabina
    Slattery, Martha L.
    Song, Mingyang
    Tangen, Catherine M.
    Thibodeau, Stephen N.
    Travis, Ruth C.
    Trichopoulou, Antonia
    Ulrich, Cornelia M.
    van Duijnhoven, Franzel J. B.
    van Guelpen, Bethany
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi. Umeå universitet, Medicinska fakulteten, Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM).
    Vodicka, Pavel
    White, Emily
    Wolk, Alicja
    Woods, Michael O.
    Wu, Anna H.
    Peters, Ulrike
    Gunter, Marc J.
    Murphy, Neil
    Physical activity and risks of breast and colorectal cancer: a Mendelian randomisation analysis2020Ingår i: Nature Communications, E-ISSN 2041-1723, Vol. 11, nr 1Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Physical activity has been associated with lower risks of breast and colorectal cancer in epidemiological studies; however, it is unknown if these associations are causal or confounded. In two-sample Mendelian randomisation analyses, using summary genetic data from the UK Biobank and GWA consortia, we found that a one standard deviation increment in average acceleration was associated with lower risks of breast cancer (odds ratio [OR]: 0.51, 95% confidence interval [CI]: 0.27 to 0.98, P-value=0.04) and colorectal cancer (OR: 0.66, 95% CI: 0.48 to 0.90, P-value=0.01). We found similar magnitude inverse associations for estrogen positive (ER+ve) breast cancer and for colon cancer. Our results support a potentially causal relationship between higher physical activity levels and lower risks of breast cancer and colorectal cancer. Based on these data, the promotion of physical activity is probably an effective strategy in the primary prevention of these commonly diagnosed cancers. Physical activity has been linked to lower risks of colorectal and breast cancer. Here, the authors present a Mendelian randomisation analysis supporting a potentially causal relationship between higher physical activity levels and lower risks of breast cancer and colorectal cancer.

    Ladda ner fulltext (pdf)
    fulltext
  • 9. Schoemaker, Minouk J.
    et al.
    Nichols, Hazel B.
    Wright, Lauren B.
    Brook, Mark N.
    Jones, Michael E.
    O'Brien, Katie M.
    Adami, Hans-Olov
    Baglietto, Laura
    Bernstein, Leslie
    Bertrand, Kimberly A.
    Boutron-Ruault, Marie-Christine
    Chen, Yu
    Connor, Avonne E.
    Dossus, Laure
    Eliassen, A. Heather
    Giles, Graham G.
    Gram, Inger T.
    Hankinson, Susan E.
    Kaaks, Rudolf
    Key, Timothy J.
    Kirsh, Victoria A.
    Kitahara, Cari M.
    Larsson, Susanna C.
    Linet, Martha
    Ma, Huiyan
    Milne, Roger L.
    Ozasa, Kotaro
    Palmer, Julie R.
    Riboli, Elio
    Rohan, Thomas E.
    Sacerdote, Carlotta
    Sadakane, Atsuko
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Tamimi, Rulla M.
    Trichopoulou, Antonia
    Ursin, Giske
    Visvanathan, Kala
    Weiderpass, Elisabete
    Willett, Walter C.
    Wolk, Alicja
    Zeleniuch-Jacquotte, Anne
    Sandler, Dale P.
    Swerdlow, Anthony J.
    Adult weight change and premenopausal breast cancer risk: A prospective pooled analysis of data from 628,463 women2020Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 147, nr 5, s. 1306-1314Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Early-adulthood body size is strongly inversely associated with risk of premenopausal breast cancer. It is unclear whether subsequent changes in weight affect risk. We pooled individual-level data from 17 prospective studies to investigate the association of weight change with premenopausal breast cancer risk, considering strata of initial weight, timing of weight change, other breast cancer risk factors and breast cancer subtype. Hazard ratios (HR) and 95% confidence intervals (CI) were obtained using Cox regression. Among 628,463 women, 10,886 were diagnosed with breast cancer before menopause. Models adjusted for initial weight at ages 18-24 years and other breast cancer risk factors showed that weight gain from ages 18-24 to 35-44 or to 45-54 years was inversely associated with breast cancer overall (e.g., HR per 5 kg to ages 45-54: 0.96, 95% CI: 0.95-0.98) and with oestrogen-receptor(ER)-positive breast cancer (HR per 5 kg to ages 45-54: 0.96, 95% CI: 0.94-0.98). Weight gain from ages 25-34 was inversely associated with ER-positive breast cancer only and weight gain from ages 35-44 was not associated with risk. None of these weight gains were associated with ER-negative breast cancer. Weight loss was not consistently associated with overall or ER-specific risk after adjusting for initial weight. Weight increase from early-adulthood to ages 45-54 years is associated with a reduced premenopausal breast cancer risk independently of early-adulthood weight. Biological explanations are needed to account for these two separate factors.

    Ladda ner fulltext (pdf)
    fulltext
  • 10. Sieri, Sabina
    et al.
    Agnoli, Claudia
    Grioni, Sara
    Weiderpass, Elisabete
    Mattiello, Amalia
    Sluijs, Ivonne
    Sanchez, Maria Jose
    Jakobsen, Marianne Uhre
    Sweeting, Michael
    van der Schouw, Yvonne T.
    Nilsson, Lena Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Wennberg, Patrik
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Allmänmedicin.
    Katzke, Verena A.
    Kuhn, Tilman
    Overvad, Kim
    Tong, Tammy Y. N.
    Conchi, Moreno-Iribas
    Ramon Quiros, Jose
    Manuel Garcia-Torrecillas, Juan
    Mokoroa, Olatz
    Gomez, Jesus-Humberto
    Tjonneland, Anne
    Sonestedt, Emiliy
    Trichopoulou, Antonia
    Karakatsani, Anna
    Valanou, Elissavet
    Boer, Jolanda M. A.
    Verschuren, W. M. Monique
    Boutron-Ruault, Marie-Christine
    Fagherazzi, Guy
    Madika, Anne-Laure
    Bergmann, Manuela M.
    Schulze, Matthias B.
    Ferrari, Pietro
    Freisling, Heinz
    Lennon, Hannah
    Sacerdote, Carlotta
    Masala, Giovanna
    Tumino, Rosario
    Riboli, Elio
    Wareham, Nicholas J.
    Danesh, John
    Forouhi, Nita G.
    Butterworth, Adam S.
    Krogh, Vittorio
    Glycemic index, glycemic load, and risk of coronary heart disease: a pan-European cohort study2020Ingår i: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 112, nr 3, s. 631-643Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: High carbohydrate intake raises blood triglycerides, glucose, and insulin; reduces HDLs; and may increase risk of coronary heart disease (CHD). Epidemiological studies indicate that high dietary glycemic index (GI) and glycemic load (GL) are associated with increased CHD risk. Objectives: The aim of this study was to determine whether dietary GI, GL, and available carbohydrates are associated with CHD risk in both sexes. Methods: This large prospective study-the European Prospective Investigation into Cancer and Nutrition-consisted of 338,325 participants who completed a dietary questionnaire. HRs with 95% CIs for a CHD event, in relation to intake of GI, GL, and carbohydrates, were estimated using covariate-adjusted Cox proportional hazard models. Results: After 12.8 y (median), 6378 participants had experienced a CHD event. High GL was associated with greater CHD risk [HR 1.16 (95% CI: 1.02, 1.31) highest vs. lowest quintile, p-trend 0.035; HR 1.18 (95% CI: 1.07, 1.29) per 50 g/day of GL intake]. The association between GL and CHD risk was evident in subjects with BMI (in kg/m(2)) >= 25 [HR: 1.22 (95% CI: 1.11, 1.35) per 50 g/d] but not in those with BMI <25 [HR: 1.09 (95% CI: 0.98, 1.22) per 50 g/d) (P-interaction = 0.022). The GL-CHD association did not differ between men [HR: 1.19 (95% CI: 1.08, 1.30) per 50 g/d] and women [HR: 1.22 (95% CI: 1.07, 1.40) per 50 g/d] (test for interaction not significant). GI was associated with CHD risk only in the continuous model [HR: 1.04 (95% CI: 1.00, 1.08) per 5 units/d]. High available carbohydrate was associated with greater CHD risk [HR: 1.11 (95% CI: 1.03, 1.18) per 50 g/d]. High sugar intake was associated with greater CHD risk [HR: 1.09 (95% CI: 1.02, 1.17) per 50 g/d]. Conclusions: This large pan-European study provides robust additional support for the hypothesis that a diet that induces a high glucose response is associated with greater CHD risk.

  • 11. Stepien, Magdalena
    et al.
    Keski-Rahkonen, Pekka
    Kiss, Agneta
    Robinot, Nivonirina
    Duarte-Salles, Talita
    Murphy, Neil
    Perlemuter, Gabriel
    Viallon, Vivian
    Tjønneland, Anne
    Rostgaard-Hansen, Agnetha Linn
    Dahm, Christina C.
    Overvad, Kim
    Boutron-Ruault, Marie-Christine
    Mancini, Francesca Romana
    Mahannat-Saleh, Yahya
    Aleksandrova, Krasimira
    Kaaks, Rudolf
    Kühn, Tilman
    Trichopoulou, Antonia
    Karakatsani, Anna
    Panico, Salvatore
    Tumino, Rosario
    Palli, Domenico
    Tagliabue, Giovanna
    Naccarati, Alessio
    Vermeulen, Roel C. H.
    Bueno-de-Mesquita, Hendrik Bastiaan
    Weiderpass, Elisabete
    Skeie, Guri
    Ramón Quirós, Jose
    Ardanaz, Eva
    Mokoroa, Olatz
    Sala, Núria
    Sánchez, Maria-Jose
    María Huerta, José
    Winkvist, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa. The Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden.
    Harlid, Sophia
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Ohlsson, Bodil
    Sjöberg, Klas
    Schmidt, Julie A.
    Wareham, Nick
    Khaw, Kay-Tee
    Ferrari, Pietro
    Rothwell, Joseph A.
    Gunter, Marc
    Riboli, Elio
    Scalbert, Augustin
    Jenab, Mazda
    Metabolic perturbations prior to hepatocellular carcinoma diagnosis: findings from a prospective observational cohort study2021Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 148, nr 3, s. 609-625Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Hepatocellular carcinoma (HCC) development entails changes in liver metabolism. Current knowledge on metabolic perturbations in HCC is derived mostly from case-control designs, with sparse information from prospective cohorts. Our objective was to apply comprehensive metabolite profiling to detect metabolites whose serum concentrations are associated with HCC development, using biological samples from within the prospective European Prospective Investigation into Cancer and Nutrition (EPIC) cohort (>520 000 participants), where we identified 129 HCC cases matched 1:1 to controls. We conducted high-resolution untargeted liquid chromatography-mass spectrometry-based metabolomics on serum samples collected at recruitment prior to cancer diagnosis. Multivariable conditional logistic regression was applied controlling for dietary habits, alcohol consumption, smoking, body size, hepatitis infection and liver dysfunction. Corrections for multiple comparisons were applied. Of 9206 molecular features detected, 220 discriminated HCC cases from controls. Detailed feature annotation revealed 92 metabolites associated with HCC risk, of which 14 were unambiguously identified using pure reference standards. Positive HCC-risk associations were observed forN1-acetylspermidine, isatin,p-hydroxyphenyllactic acid, tyrosine, sphingosine,l,l-cyclo(leucylprolyl), glycochenodeoxycholic acid, glycocholic acid and 7-methylguanine. Inverse risk associations were observed for retinol, dehydroepiandrosterone sulfate, glycerophosphocholine, gamma-carboxyethyl hydroxychroman and creatine. Discernible differences for these metabolites were observed between cases and controls up to 10 years prior to diagnosis. Our observations highlight the diversity of metabolic perturbations involved in HCC development and replicate previous observations (metabolism of bile acids, amino acids and phospholipids) made in Asian and Scandinavian populations. These findings emphasize the role of metabolic pathways associated with steroid metabolism and immunity and specific dietary and environmental exposures in HCC development.

  • 12. Tong, Tammy Y. N.
    et al.
    Appleby, Paul N.
    Key, Timothy J.
    Dahm, Christina C.
    Overvad, Kim
    Olsen, Anja
    Tjonneland, Anne
    Katzke, Verena
    Kuhn, Tilman
    Boeing, Heiner
    Karakatsani, Anna
    Peppa, Eleni
    Trichopoulou, Antonia
    Weiderpass, Elisabete
    Masala, Giovanna
    Grioni, Sara
    Panico, Salvatore
    Tumino, Rosario
    Boer, Jolanda M. A.
    Verschuren, W. M. Monique
    Quiros, J. Ramon
    Agudo, Antonio
    Rodriguez-Barranco, Miguel
    Imaz, Liher
    Chirlaque, Maria-Dolores
    Moreno-Iribas, Conchi
    Engstrom, Gunnar
    Sonestedt, Emily
    Lind, Marcus
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Otten, Julia
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Khaw, Kay-Tee
    Aune, Dagfinn
    Riboli, Elio
    Wareham, Nicholas J.
    Imamura, Fumiaki
    Forouhi, Nita G.
    di Angelantonio, Emanuele
    Wood, Angela M.
    Butterworth, Adam S.
    Perez-Cornago, Aurora
    The associations of major foods and fibre with risks of ischaemic and haemorrhagic stroke: a prospective study of 418 329 participants in the EPIC cohort across nine European countries2020Ingår i: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 41, nr 28, s. 2632-2640Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Aim: To investigate the associations between major foods and dietary fibre with subtypes of stroke in a large prospective cohort.

    Methods and results: We analysed data on 418 329 men and women from nine European countries, with an average of 12.7 years of follow-up. Diet was assessed using validated country-specific questionnaires which asked about habitual intake over the past year, calibrated using 24-h recalls. Multivariable-adjusted Cox regressions were used to estimate hazard ratios (HRs) for ischaemic and haemorrhagic stroke associated with consumption of red and processed meat, poultry, fish, dairy foods, eggs, cereals, fruit and vegetables, legumes, nuts and seeds, and dietary fibre. For ischaemic stroke (4281 cases), lower risks were observed with higher consumption of fruit and vegetables combined (HR; 95% CI per 200 g/day higher intake, 0.87; 0.82–0.93, P-trend < 0.001), dietary fibre (per 10 g/day, 0.77; 0.69–0.86, P-trend < 0.001), milk (per 200 g/day, 0.95; 0.91–0.99, P-trend = 0.02), yogurt (per 100 g/day, 0.91; 0.85–0.97, P-trend = 0.004), and cheese (per 30 g/day, 0.88; 0.81–0.97, P-trend = 0.008), while higher risk was observed with higher red meat consumption which attenuated when adjusted for the other statistically significant foods (per 50 g/day, 1.07; 0.96–1.20, P-trend = 0.20). For haemorrhagic stroke (1430 cases), higher risk was associated with higher egg consumption (per 20 g/day, 1.25; 1.09–1.43, P-trend = 0.002).

    Conclusion: Risk of ischaemic stroke was inversely associated with consumption of fruit and vegetables, dietary fibre, and dairy foods, while risk of haemorrhagic stroke was positively associated with egg consumption. The apparent differences in the associations highlight the importance of examining ischaemic and haemorrhagic stroke subtypes separately.

    Ladda ner fulltext (pdf)
    fulltext
  • 13. Trabert, Britton
    et al.
    Tworoger, Shelley S.
    O'Brien, Katie M.
    Townsend, Mary K.
    Fortner, Renee T.
    Iversen, Edwin S.
    Hartge, Patricia
    White, Emily
    Amiano, Pilar
    Arslan, Alan A.
    Bernstein, Leslie
    Brinton, Louise A.
    Buring, Julie E.
    Dossus, Laure
    Fraser, Gary E.
    Gaudet, Mia M.
    Giles, Graham G.
    Gram, Inger T.
    Harris, Holly R.
    Bolton, Judith Hoffman
    Idahl, Annika
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Obstetrik och gynekologi.
    Jones, Michael E.
    Kaaks, Rudolf
    Kirsh, Victoria A.
    Knutsen, Synnove F.
    Kvaskoff, Marina
    Lacey, James, V
    Lee, I-Min
    Milne, Roger L.
    Onland-Moret, N. Charlotte
    Overvad, Kim
    Patel, Alpa, V
    Peters, Ulrike
    Poynter, Jenny N.
    Riboli, Elio
    Robien, Kim
    Rohan, Thomas E.
    Sandler, Dale P.
    Schairer, Catherine
    Schouten, Leo J.
    Setiawan, Veronica W.
    Swerdlow, Anthony J.
    Travis, Ruth C.
    Trichopoulou, Antonia
    van den Brandt, Piet A.
    Visvanathan, Kala
    Wilkens, Lynne R.
    Wolk, Alicja
    Zeleniuch-Jacquotte, Anne
    Wentzensen, Nicolas
    The Risk of Ovarian Cancer Increases with an Increase in the Lifetime Number of Ovulatory Cycles: An Analysis from the Ovarian Cancer Cohort Consortium (OC3)2020Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 80, nr 5, s. 1210-1218Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Repeated exposure to the acute proinflammatory environment that follows ovulation at the ovarian surface and distal fallopian tube over a woman's reproductive years may increase ovarian cancer risk. To address this, analyses included individual-level data from 558,709 naturally menopausal women across 20 prospective cohorts, among whom 3,246 developed invasive epithelial ovarian cancer (2,045 serous, 319 endometrioid, 184 mucinous, 121 clear cell, 577 other/unknown). Cox models were used to estimate multivariable-adjusted HRs between lifetime ovulatory cycles (LOC) and its components and ovarian cancer risk overall and by histotype. Women in the 90th percentile of LOC (>514 cycles) were almost twice as likely to be diagnosed with ovarian cancer than women in the 10th percentile (<294) [HR (95% confidence interval): 1.92 (1.60–2.30)]. Risk increased 14% per 5-year increase in LOC (60 cycles) [(1.10–1.17)]; this association remained after adjustment for LOC components: number of pregnancies and oral contraceptive use [1.08 (1.04–1.12)]. The association varied by histotype, with increased risk of serous [1.13 (1.09–1.17)], endometrioid [1.20 (1.10–1.32)], and clear cell [1.37 (1.18–1.58)], but not mucinous [0.99 (0.88–1.10), P-heterogeneity = 0.01] tumors. Heterogeneity across histotypes was reduced [P-heterogeneity = 0.15] with adjustment for LOC components [1.08 serous, 1.11 endometrioid, 1.26 clear cell, 0.94 mucinous]. Although the 10-year absolute risk of ovarian cancer is small, it roughly doubles as the number of LOC rises from approximately 300 to 500. The consistency and linearity of effects strongly support the hypothesis that each ovulation leads to small increases in the risk of most ovarian cancers, a risk that cumulates through life, suggesting this as an important area for identifying intervention strategies.

    Significance: Although ovarian cancer is rare, risk of most ovarian cancers doubles as the number of lifetime ovulatory cycles increases from approximately 300 to 500. Thus, identifying an important area for cancer prevention research.

  • 14. Ward, Heather A.
    et al.
    Gayle, Alicia
    Jakszyn, Paula
    Merritt, Melissa
    Melin, Beatrice
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Freisling, Heinz
    Weiderpass, Elisabete
    Tjonneland, Anne
    Olsen, Anja
    Dahm, Christina C.
    Overvad, Kim
    Katzke, Verena
    Kuehn, Tilman
    Boeing, Heiner
    Trichopoulou, Antonia
    Lagiou, Pagona
    Kyrozis, Andreas
    Palli, Domenico
    Krogh, Vittorio
    Tumino, Rosario
    Ricceri, Fulvio
    Mattiello, Amalia
    Bueno-de-Mesquita, Bas
    Peeters, Petra H.
    Quiros, Jose Ramon
    Agudo, Antonio
    Rodriguez-Barranco, Miguel
    Larranaga, Nerea
    Huerta, Jose M.
    Barricarte, Aurelio
    Sonestedt, Emily
    Drake, Isabel
    Sandström, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Travis, Ruth C.
    Ferrari, Pietro
    Riboli, Elio
    Cross, Amanda J.
    Meat and haem iron intake in relation to glioma in the European Prospective Investigation into Cancer and Nutrition study2018Ingår i: European Journal of Cancer Prevention, ISSN 0959-8278, E-ISSN 1473-5709, Vol. 27, nr 4, s. 379-383Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Diets high in red or processed meat have been associated positively with some cancers, and several possible underlying mechanisms have been proposed, including iron-related pathways. However, the role of meat intake in adult glioma risk has yielded conflicting findings because of small sample sizes and heterogeneous tumour classifications. The aim of this study was to examine red meat, processed meat and iron intake in relation to glioma risk in the European Prospective Investigation into Cancer and Nutrition study. In this prospective cohort study, 408751 individuals from nine European countries completed demographic and dietary questionnaires at recruitment. Multivariable Cox proportional hazards models were used to examine intake of red meat, processed meat, total dietary iron and haem iron in relation to incident glioma. During an average follow-up of 14.1 years, 688 incident glioma cases were diagnosed. There was no evidence that any of the meat variables (red, processed meat or subtypes of meat) or iron (total or haem) were associated with glioma; results were unchanged when the first 2 years of follow-up were excluded. This study suggests that there is no association between meat or iron intake and adult glioma. This is the largest prospective analysis of meat and iron in relation to glioma and as such provides a substantial contribution to a limited and inconsistent literature.

  • 15. Zheng, Ju-Sheng
    et al.
    Luan, Jian'an
    Sofianopoulou, Eleni
    Sharp, Stephen J.
    Day, Felix R.
    Imamura, Fumiaki
    Gundersen, Thomas E.
    Lotta, Luca A.
    Sluijs, Ivonne
    Stewart, Isobel D.
    Shah, Rupal L.
    van der Schouw, Yvonne T.
    Wheeler, Eleanor
    Ardanaz, Eva
    Boeing, Heiner
    Dorronsoro, Miren
    Dahm, Christina C.
    Dimou, Niki
    El-Fatouhi, Douae
    Franks, Paul W.
    Fagherazzi, Guy
    Grioni, Sara
    Huerta, Jose Maria
    Heath, Alicia K.
    Hansen, Louise
    Jenab, Mazda
    Jakszyn, Paula
    Kaaks, Rudolf
    Kuehn, Tilman
    Khaw, Kay-Tee
    Laouali, Nasser
    Masala, Giovanna
    Nilsson, Peter M.
    Overvad, Kim
    Olsen, Anja
    Panico, Salvatore
    Quiros, J. Ramon
    Rolandsson, Olov
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Allmänmedicin.
    Rodriguez-Barranco, Miguel
    Sacerdote, Carlotta
    Spijkerman, Annemieke M. W.
    Tong, Tammy Y. N.
    Tumino, Rosario
    Tsilidis, Konstantinos K.
    Danesh, John
    Riboli, Elio
    Butterworth, Adam S.
    Langenberg, Claudia
    Forouhi, Nita G.
    Wareham, Nicholas J.
    The association between circulating 25-hydroxyvitamin D metabolites and type 2 diabetes in European populations: A meta-analysis and Mendelian randomisation analysis2020Ingår i: PLoS Medicine, ISSN 1549-1277, E-ISSN 1549-1676, Vol. 17, nr 10, artikel-id e1003394Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Prior research suggested a differential association of 25-hydroxyvitamin D (25(OH)D) metabolites with type 2 diabetes (T2D), with total 25(OH)D and 25(OH)D3 inversely associated with T2D, but the epimeric form (C3-epi-25(OH)D3) positively associated with T2D. Whether or not these observational associations are causal remains uncertain. We aimed to examine the potential causality of these associations using Mendelian randomisation (MR) analysis.

    Methods and findings: We performed a meta-analysis of genome-wide association studies for total 25(OH)D (N = 120,618), 25(OH)D3 (N = 40,562), and C3-epi-25(OH)D3 (N = 40,562) in participants of European descent (European Prospective Investigation into Cancer and Nutrition [EPIC]–InterAct study, EPIC-Norfolk study, EPIC-CVD study, Ely study, and the SUNLIGHT consortium). We identified genetic variants for MR analysis to investigate the causal association of the 25(OH)D metabolites with T2D (including 80,983 T2D cases and 842,909 non-cases). We also estimated the observational association of 25(OH)D metabolites with T2D by performing random effects meta-analysis of results from previous studies and results from the EPIC-InterAct study. We identified 10 genetic loci associated with total 25(OH)D, 7 loci associated with 25(OH)D3 and 3 loci associated with C3-epi-25(OH)D3. Based on the meta-analysis of observational studies, each 1–standard deviation (SD) higher level of 25(OH)D was associated with a 20% lower risk of T2D (relative risk [RR]: 0.80; 95% CI 0.77, 0.84; p < 0.001), but a genetically predicted 1-SD increase in 25(OH)D was not significantly associated with T2D (odds ratio [OR]: 0.96; 95% CI 0.89, 1.03; p = 0.23); this result was consistent across sensitivity analyses. In EPIC-InterAct, 25(OH)D3 (per 1-SD) was associated with a lower risk of T2D (RR: 0.81; 95% CI 0.77, 0.86; p < 0.001), while C3-epi-25(OH)D3 (above versus below lower limit of quantification) was positively associated with T2D (RR: 1.12; 95% CI 1.03, 1.22; p = 0.006), but neither 25(OH)D3 (OR: 0.97; 95% CI 0.93, 1.01; p = 0.14) nor C3-epi-25(OH)D3 (OR: 0.98; 95% CI 0.93, 1.04; p = 0.53) was causally associated with T2D risk in the MR analysis. Main limitations include the lack of a non-linear MR analysis and of the generalisability of the current findings from European populations to other populations of different ethnicities.

    Conclusions: Our study found discordant associations of biochemically measured and genetically predicted differences in blood 25(OH)D with T2D risk. The findings based on MR analysis in a large sample of European ancestry do not support a causal association of total 25(OH)D or 25(OH)D metabolites with T2D and argue against the use of vitamin D supplementation for the prevention of T2D.

    Ladda ner fulltext (pdf)
    fulltext
1 - 15 av 15
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf