Digitala Vetenskapliga Arkivet

Change search
Refine search result
123456 1 - 50 of 274
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 1.
    af Geijerstam, Peder
    et al.
    Linköping University, Department of Health, Medicine and Caring Sciences, Division of Prevention, Rehabilitation and Community Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Primary Care Center, Primary Health Care Center Cityhälsan Centrum.
    Joelsson, Annelie
    Region Östergötland, Primary Care Center, Primary Health Care Center Cityhälsan Centrum.
    Rådholm, Karin
    Linköping University, Department of Health, Medicine and Caring Sciences, Division of Prevention, Rehabilitation and Community Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Primary Care Center, Primary Health Care Center Kärna. The George Institute for Global Health, University of New South Wales, Sydney, Australia.
    Nyström, Fredrik H
    Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Primary Care Center, Primary Health Care Center Cityhälsan Centrum. Linköping University, Department of Health, Medicine and Caring Sciences, Division of Diagnostics and Specialist Medicine.
    A low dose of daily licorice intake affects renin, aldosterone, and home blood pressure in a randomized crossover trial2024In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 119, no 3, p. 682-691Article in journal (Refereed)
    Abstract [en]

    Background

    Licorice, through the effects of glycyrrhizic acid (GA), raises blood pressure (BP). The World Health Organization has suggested that 100 mg GA/d would be unlikely to cause adverse effects, but of 13 previously published studies none have been randomized and controlled and independently quantified the GA content.

    Objective

    Our aim was to analyze the effects on home BP of a daily licorice intake containing 100 mg GA.

    Methods

    Healthy volunteers were randomly assigned to start with either licorice or a control product in a nonblinded, 2 × 2 crossover study. Home BP was measured daily, and blood samples were collected at the end of each 2-wk period.

    Results

    There were 28 participants and no dropouts. The median age was 24.0 y (interquartile range 22.8–27.0 y). During the licorice compared with control intake period, the systolic home BP increased [mean difference: 3.1 mm Hg (95% confidence interval [CI]: 0.8, 5.4 mm Hg) compared with −0.3 mm Hg (95% CI: −1.8, 1.3 mm Hg); P = 0.018] and renin and aldosterone were suppressed [mean change: −30.0% (95% CI: −56.7%, −3.3%) compared with 15.8% (95% CI: −12.8%, 44.4%); P = 0.003; and −45.1% (95% CI: −61.5%, −28.7%) compared with 8.2% (95% CI: −14.7%, 31.1%); P <0.001, respectively]. In the quartile of participants with the most pronounced suppression of renin and aldosterone, N-terminal prohormone of brain natriuretic peptide concentration increased during the licorice compared with control period [mean change: 204.1% (95% CI: −11.6%, 419.7%) compared with 72.4% (95% CI: −52.2%, 197.1%); P = 0.016].

    Conclusions

    We found licorice to be more potent than previously known, with significant increases in BP, after a daily intake of only 100 mg GA. Thus, the safe limit of intake of this substance might need to be reconsidered.

  • 2. Agudo, Antonio
    et al.
    Cayssials, Valerie
    Bonet, Catalina
    Tjønneland, Anne
    Overvad, Kim
    Boutron-Ruault, Marie-Christine
    Affret, Aurélie
    Fagherazzi, Guy
    Katzke, Verena
    Schübel, Ruth
    Trichopoulou, Antonia
    Karakatsani, Anna
    La Vecchia, Carlo
    Palli, Domenico
    Grioni, Sara
    Tumino, Rosario
    Ricceri, Fulvio
    Panico, Salvatore
    Bueno-de-Mesquita, Bas
    Peeters, Petra H.
    Weiderpass, Elisabete
    Skeie, Guri
    Nøst, Theresa H.
    Lasheras, Cristina
    Rodríguez-Barranco, Miguel
    Amiano, Pilar
    Chirlaque, María-Dolores
    Ardanaz, Eva
    Ohlsson, Bodil
    Dias, Joana A.
    Nilsson, Lena M.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Myte, Robin
    Khaw, Kay-Tee
    Perez-Cornago, Aurora
    Gunter, Marc
    Huybrechts, Inge
    Cross, Amanda J.
    Tsilidis, Kostas
    Riboli, Elio
    Jakszyn, Paula
    Inflammatory potential of the diet and risk of gastric cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) study2018In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 107, no 4, p. 607-616Article in journal (Refereed)
    Abstract [en]

    Chronic inflammation plays a critical role in the pathogenesis of the 2 major types of gastric cancer. Several foods, nutrients, and nonnutrient food components seem to be involved in the regulation of chronic inflammation. We assessed the association between the inflammatory potential of the diet and the risk of gastric carcinoma, overall and for the 2 major subsites: cardia cancers and noncardia cancers. A total of 476,160 subjects (30% men, 70% women) from the European Investigation into Cancer and Nutrition (EPIC) study were followed for 14 y, during which 913 incident cases of gastric carcinoma were identified, including 236 located in the cardia, 341 in the distal part of the stomach (noncardia), and 336 with overlapping or unknown tumor site. The dietary inflammatory potential was assessed by means of an inflammatory score of the diet (ISD), calculated with the use of 28 dietary components and their corresponding inflammatory scores. The association between the ISD and gastric cancer risk was estimated by HRs and 95% CIs calculated by multivariate Cox regression models adjusted for confounders. The inflammatory potential of the diet was associated with an increased risk of gastric cancer. The HR (95% CI) for each increase in 1 SD of the ISD were 1.25 (1.12, 1.39) for all gastric cancers, 1.30 (1.06, 1.59) for cardia cancers, and 1.07 (0.89, 1.28) for noncardia cancers. The corresponding values for the highest compared with the lowest quartiles of the ISD were 1.66 (1.26, 2.20), 1.94 (1.14, 3.30), and 1.07 (0.70, 1.70), respectively. Our results suggest that low-grade chronic inflammation induced by the diet may be associated with gastric cancer risk. This pattern seems to be more consistent for gastric carcinomas located in the cardia than for those located in the distal stomach. This study is listed on the ISRCTN registry as ISRCTN12136108.

  • 3.
    Akner, Gunnar
    et al.
    Örebro University, School of Health and Medical Sciences.
    Cederholm, T.
    Treatment of protein-energy malnutrition in chronic nonmalignant disorders2001In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 74, no 1, p. 6-24Article, review/survey (Refereed)
    Abstract [en]

    Protein-energy malnutrition (PEM) is common in connection with chronic disease and is associated with increased morbidity and mortality. Because the risk of PEM is related to the degree of illness, the causal connections between malnutrition and a poorer prognosis are complex. It cannot automatically be inferred that nutritional support will improve the clinical course of patients with wasting disorders. We reviewed studies of the treatment of PEM in cases of chronic obstructive pulmonary disease, chronic heart failure, stroke, dementia, rehabilitation after hip fracture, chronic renal failure, rheumatoid arthritis, and multiple disorders in the elderly. Several methodologic problems are associated with nutrition treatment studies in chronically ill patients. These problems include no generally accepted definition of PEM, uncertain patient compliance with supplementation, and a wide range of outcome variables. Avail-able treatment studies indicate that dietary supplements, either alone or in combination with hormonal treatment, may have positive effects when given to patients with manifest PEM or to patients at risk of developing PEM. In chronic obstructive pulmonary disease, nutritional treatment may improve respiratory function. Nutritional therapy of elderly women after hip fractures may speed up the rehabilitation process. When administered to elderly patients with multiple disorders, diet therapy may improve functional capacity. The data regarding nutritional treatment of the conditions mentioned above is still inconclusive. There is still a great need for randomized controlled long-term studies of the effects of defined nutritional intervention programs in chronically ill and frail elderly with a focus on determining clinically relevant outcomes.

  • 4.
    Akpan, Edifofon
    et al.
    Univ Melbourne, Ctr Hlth Policy, Melbourne Sch Populat & Global Hlth, Parkville, Vic, Australia..
    Hossain, Sheikh Jamal
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Child Health and Nutrition. Bangladesh Icddr B, Maternal & Child Hlth Div, Int Ctr Diarrhoeal Dis Res, Dhaka, Bangladesh.;Uppsala Univ, Dept Womens & Childrens Hlth, Uppsala, Sweden..
    Devine, Angela
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Parkville, Vic, Australia.;Charles Darwin Univ, Menzies Sch Hlth Res, Div Global & Trop Hlth, Darwin, NT, Australia..
    Braat, Sabine
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Parkville, Vic, Australia.;Walter & Eliza Hall Inst Med Res, Populat Hlth & Immun Div, Parkville, Vic, Australia.;Univ Melbourne, Dept Med Peter Doherty Inst, Parkville, Vic, Australia..
    Hasan, Mohammed, I
    Bangladesh Icddr B, Maternal & Child Hlth Div, Int Ctr Diarrhoeal Dis Res, Dhaka, Bangladesh..
    Tipu, S. M. Mulk Uddin
    Bangladesh Icddr B, Maternal & Child Hlth Div, Int Ctr Diarrhoeal Dis Res, Dhaka, Bangladesh..
    Bhuiyan, Mohammad Saiful Alam
    Bangladesh Icddr B, Maternal & Child Hlth Div, Int Ctr Diarrhoeal Dis Res, Dhaka, Bangladesh..
    Hamadani, Jena D.
    Bangladesh Icddr B, Maternal & Child Hlth Div, Int Ctr Diarrhoeal Dis Res, Dhaka, Bangladesh..
    Biggs, Beverley-Ann
    Univ Melbourne, Dept Med Peter Doherty Inst, Parkville, Vic, Australia..
    Pasricha, Sant-Rayn
    Walter & Eliza Hall Inst Med Res, Populat Hlth & Immun Div, Parkville, Vic, Australia.;Royal Melbourne Hosp, Diagnost Hematol, Parkville, Vic, Australia.;Peter MacCallum Canc Ctr, Clin Hematol, Parkville, Vic, Australia.;Royal Melbourne Hosp, Parkville, Vic, Australia.;Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia..
    Carvalho, Natalie
    Univ Melbourne, Ctr Hlth Policy, Melbourne Sch Populat & Global Hlth, Parkville, Vic, Australia..
    Cost-effectiveness of universal iron supplementation and iron-containing micronutrient powders for anemia among young children in rural Bangladesh: analysis of a randomized, placebo-controlled trial2022In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 116, no 5, p. 1303-1313Article in journal (Refereed)
    Abstract [en]

    Background: Universal provision of iron supplements or iron-containing multiple micronutrient powders (MNPs) is widely used to prevent anemia in young children in low- and middle-income countries. The BRISC (Benefits and Risks of Iron Interventions in Children) trial compared iron supplements and MNPs with placebo in children <2 y old in rural Bangladesh. Objectives: We aimed to assess the cost-effectiveness of iron supplements or iron-containing MNPs among young children in rural Bangladesh. Methods: We did a cost-effectiveness analysis of MNPs and iron supplements using the BRISC trial outcomes and resource use data, and programmatic data from the literature. Health care costs were assessed from a health system perspective. We calculated incremental cost-effectiveness ratios (ICERs) in terms of US$ per disability-adjusted life-year (DALY) averted. To explore uncertainty, we constructed cost-effectiveness acceptability curves using bootstrapped data over a range of cost-effectiveness thresholds. One- and 2-way sensitivity analyses tested the impact of varying key parameter values on our results. Results: Provision of MNPs was estimated to avert 0.0031 (95% CI: 0.0022, 0.0041) DALYs/child, whereas iron supplements averted 0.0039 (95% CI: 0.0030, 0.0048) DALYs/child, over 1 y compared with no intervention. Incremental mean costs were $0.75 (95% CI: 0.73, 0.77) for MNPs compared with no intervention and $0.64 ($0.62, $0.67) for iron supplements compared with no intervention. Iron supplementation dominated MNPs because it was cheaper and averted more DALYs. Iron supplementation had an ICER of $1645 ($1333, $2153) per DALY averted compared with no intervention, and had a 0% probability of being the optimal strategy at cost-effectiveness thresholds of $200 (reflecting health opportunity costs in Bangladesh) and $985 [half of gross domestic product (GDP) per capita] per DALY averted. Scenario and sensitivity analyses supported the base case findings. Conclusions: These findings do not support universal iron supplementation or micronutrient powders as a cost-effective intervention for young children in rural Bangladesh.

  • 5. Aleksandrova, Krasimira
    et al.
    Bamia, Christina
    Drogan, Dagmar
    Lagiou, Pagona
    Trichopoulou, Antonia
    Jenab, Mazda
    Fedirko, Veronika
    Romieu, Isabelle
    Bueno-de-Mesquita, H. Bas
    Pischon, Tobias
    Tsilidis, Kostas
    Overvad, Kim
    Tjønneland, Anne
    Bouton-Ruault, Marie-Christine
    Dossus, Laure
    Racine, Antoine
    Kaaks, Rudolf
    Kuehn, Tilman
    Tsironis, Christos
    Papatesta, Eleni-Maria
    Saitakis, George
    Palli, Domenico
    Panico, Salvatore
    Grioni, Sara
    Tumino, Rosario
    Vineis, Paolo
    Peeters, Petra H.
    Weiderpass, Elisabete
    Lukic, Marko
    Braaten, Tonje
    Ramon Quiros, J.
    Lujan-Barroso, Leila
    Sanchez, Mara-Jose
    Chilarque, Maria-Dolores
    Ardanas, Eva
    Dorronsoro, Miren
    Nilsson, Lena Maria
    Umeå University, Arctic Research Centre at Umeå University.
    Sund, Malin
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Wallström, Peter
    Ohlsson, Bodil
    Bradbury, Kathryn E.
    Khaw, Kay-Tee
    Wareham, Nick
    Stepien, Magdalena
    Duarte-Salles, Talita
    Assi, Nada
    Murphy, Neil
    Gunter, Marc J.
    Riboli, Elio
    Boeing, Heiner
    Trichopoulos, Dimitrios
    The association of coffee intake with liver cancer risk is mediated by biomarkers of inflammation and hepatocellular injury: data from the European Prospective Investigation into Cancer and Nutrition2015In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 102, no 6, p. 1498-1508Article in journal (Refereed)
    Abstract [en]

    Background: Higher coffee intake has been purportedly related to a lower risk of liver cancer. However, it remains unclear whether this association may be accounted for by specific biological mechanisms. Objective: We aimed to evaluate the potential mediating roles of inflammatory, metabolic, liver injury, and iron metabolism biomarkers on the association between coffee intake and the primary form of liver cancer-hepatocellular carcinoma (HCC). Design: We conducted a prospective nested case-control study within the European Prospective Investigation into Cancer and Nutrition among 125 incident HCC cases matched to 250 controls using an incidence-density sampling procedure. The association of coffee intake with HCC risk was evaluated by using multivariable-adjusted conditional logistic regression that accounted for smoking, alcohol consumption, hepatitis infection, and other established liver cancer risk factors. The mediating effects of 21 biomarkers were evaluated on the basis of percentage changes and associated 95% CIs in the estimated regression coefficients of models with and without adjustment for biomarkers individually and in combination. Results: The multivariable-adjusted RR of having >= 4 cups (600mL) coffee/d compared with <2 cups (300 mL)/d was 0.25 (95% CI: 0.11, 0.62; P-trend = 0.006). A statistically significant attenuation of the association between coffee intake and HCC risk and thereby suspected mediation was confirmed for the inflammatory biomarker IL-6 and for the biomarkers of hepatocellular injury glutamate dehydrogenase, alanine aminotransferase, aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), and total bilirubin, which-in combination-attenuated the regression coefficients by 72% (95% CI: 7%, 239%). Of the investigated biomarkers, IL-6, AST, and GGT produced the highest change in the regression coefficients: 40%, 56%, and 60%, respectively. Conclusion: These data suggest that the inverse association of coffee intake with HCC risk was partly accounted for by biomarkers of inflammation and hepatocellular injury.

    Download full text (pdf)
    fulltext
  • 6.
    Andersson, Agneta
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Nälsén, Cecilia
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Tengblad, Siv
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Vessby, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Fatty acid composition of skeletal muscle reflects dietary fat compositionin humans2002In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 76, no 6, p. 1222-1229Article in journal (Refereed)
    Abstract [en]

    Background: It is still unknown whether the fatty acid composition of human skeletal muscle lipids is directly influenced by the fat composition of the diet.

    Objective: We investigated whether the fatty acid composition of the diet is reflected in the fatty acid profile of skeletal muscle phospholipids and triacylglycerols.

    Design: Thirty-two healthy adults (25 men and 7 women) included in a larger controlled, multicenter dietary study were randomly assigned to diets containing a high proportion of either saturated fatty acids (SFAs) [total fat, 36% of energy; SFAs, 18% of energy; monounsaturated fatty acids (MUFAs), 10% of energy] or MUFAs (total fat, 35% of energy; SFAs, 9% of energy; MUFAs, 19% of energy) for 3 mo. Within each diet group, there was a second random assignment to supplementation with fish oil capsules [containing 3.6 g n−3 fatty acids/d; 2.4 g eicosapentaenoic acid (20:5n−3) and docosahexaenoic acid (22:6n−3)] or placebo. A muscle biopsy sample was taken from the vastus lateralis muscle after the diet period. Parallel analyses of diet and supplementation effects were performed.

    Results: The proportions of myristic (14:0), pentadecanoic (15:0), heptadecanoic (17:0), and palmitoleic (16:1n−7) acids in the skeletal muscle phospholipids were higher and the proportion of oleic acid (18:1n−9) was lower in the SFA group than in the MUFA group. The proportion of total n−3 fatty acids in the muscle phospholipids was ≈2.5 times higher, with a 5 times higher proportion of eicosapentaenoic acid (20:5n−3), in subjects supplemented with n−3 fatty acids than in those given placebo. Similar differences were observed in the skeletal muscle triacylglycerols.

    Conclusion: The fatty acid composition of skeletal muscle lipids reflects the fatty acid composition of the diet in healthy men and women.

  • 7. Assi, Nada
    et al.
    Gunter, Marc J.
    Thomas, Duncan C.
    Leitzmann, Michael
    Stepien, Magdalena
    Chajès, Véronique
    Philip, Thierry
    Vineis, Paolo
    Bamia, Christina
    Boutron-Ruault, Marie-Christine
    Sandanger, Torkjel M.
    Molinuevo, Amaia
    Boshuizen, Hendriek
    Sundkvist, Anneli
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Kühn, Tilman
    Travis, Ruth
    Overvad, Kim
    Riboli, Elio
    Scalbert, Augustin
    Jenab, Mazda
    Viallon, Vivian
    Ferrari, Pietro
    Metabolic signature of healthy lifestyle and its relation with risk of hepatocellular carcinoma in a large European cohort2018In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 108, no 1, p. 117-126Article in journal (Refereed)
    Abstract [en]

    Background: Studies using metabolomic data have identified metabolites from several compound classes that are associated with disease-related lifestyle factors.

    Objective: In this study, we identified metabolic signatures reflecting lifestyle patterns and related them to the risk of hepatocellular carcinoma (HCC) in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.

    Design: Within a nested case-control study of 147 incident HCC cases and 147 matched controls, partial least squares (PLS) analysis related 7 modified healthy lifestyle index (HLI) variables (diet, BMI, physical activity, lifetime alcohol, smoking, diabetes, and hepatitis) to 132 targeted serum-measured metabolites and a liver function score. The association between the resulting PLS scores and HCC risk was examined in multivariable conditional logistic regression models, where ORs and 95% CIs were computed.

    Results: The lifestyle component's PLS score was negatively associated with lifetime alcohol, BMI, smoking, and diabetes, and positively associated with physical activity. Its metabolic counterpart was positively related to the metabolites sphingomyelin (SM) (OH) C14:1, C16:1, and C22:2, and negatively related to glutamate, hexoses, and the diacyl-phosphatidylcholine PC aaC32:1. The lifestyle and metabolomics components were inversely associated with HCC risk, with the ORs for a 1-SD increase in scores equal to 0.53 (95% CI: 0.38, 0.74) and 0.28 (0.18, 0.43), and the associated AUCs equal to 0.64 (0.57, 0.70) and 0.74 (0.69, 0.80), respectively.

    Conclusions: This study identified a metabolic signature reflecting a healthy lifestyle pattern which was inversely associated with HCC risk. The metabolic profile displayed a stronger association with HCC than did the modified HLI derived from questionnaire data. Measuring a specific panel of metabolites may identify strata of the population at higher risk for HCC and can add substantial discrimination compared with questionnaire data. This trial was registered at clinicaltrials.gov as NCT03356535.

  • 8. Astrup, Arne
    et al.
    Dyerberg, Jorn
    Elwood, Peter
    Hermansen, Kjeld
    Hu, Frank B.
    Jakobsen, Marianne Uhre
    Kok, Frans J.
    Krauss, Ronald M.
    Lecerf, Jean Michel
    LeGrand, Philippe
    Nestel, Paul
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Sanders, Tom
    Sinclair, Andrew
    Stender, Steen
    Tholstrup, Tine
    Willett, Walter C.
    The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?2011In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 93, no 4, p. 684-688Article in journal (Refereed)
    Abstract [en]

    Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of >= 2-3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical end-points could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.

  • 9. Azadbakht, Leila
    et al.
    Kimiagar, Masoud
    Mehrabi, Yadollah
    Esmaillzadeh, Ahmad
    Padyab, Mojgan
    School of Public Health, Shaheed Beheshti University of Medical Sciences, Tehran.
    Hu, Frank B
    Willett, Walter C
    Soy inclusion in the diet improves features of the metabolicsyndrome: a randomized crossover study in postmenopausal women2007In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 85, no 3, p. 735-741Article in journal (Refereed)
    Abstract [en]

    Background: Little evidence exists regarding the effects of soyconsumption on the metabolic syndrome in humans.Objective: We aimed to determine the effects of soy consumptionon components of the metabolic syndrome, plasma lipids, lipoproteins,insulin resistance, and glycemic control in postmenopausalwomen with the metabolic syndrome.Design: This randomized crossover clinical trial was undertaken in42 postmenopausal women with the metabolic syndrome. Participantswere randomly assigned to consume a control diet (DietaryApproaches to Stop Hypertension, DASH), a soy-protein diet, or asoy-nut diet, each for 8 wk. Red meat in the DASH period wasreplaced by soy-protein in the soy-protein period and by soy-nut inthe soy-nut period.Results: The soy-nut regimen decreased the homeostasis model ofassessment-insulin resistance score significantly compared with thesoy-protein (difference in percentage change:7.40.8; P0.01)or control (12.9 0.9; P 0.01) diets. Consumption of soy-nutalso reduced fasting plasma glucose more significantly than did thesoy-protein (5.30.5%; P0.01) or control (5.10.6%; P0.01) diet. The soy-nut regimen decreased LDL cholesterol morethan did the soy-protein period (5.0 0.6%; P 0.01) and thecontrol (9.5 0.6%; P 0.01) diet. Soy-nut consumptionsignificantly reduced serum C-peptide concentrations comparedwith control diet (8.0 2.1; P 0.01), but consumption ofsoy-protein did not.Conclusion: Short-term soy-nut consumption improved glycemiccontrol and lipid profiles in postmenopausal women with the metabolicsyndrome.

  • 10. Bakker, Marije F.
    et al.
    Peeters, Petra H. M.
    Klaasen, Veronique M.
    Bueno-de-Mesquita, H. Bas
    Jansen, Eugene H. J. M.
    Ros, Martine M.
    Travier, Noemie
    Olsen, Anja
    Tjønneland, Anne
    Overvad, Kim
    Rinaldi, Sabina
    Romieu, Isabelle
    Brennan, Paul
    Boutron-Ruault, Marie-Christine
    Perquier, Florence
    Cadeau, Claire
    Boeing, Heiner
    Aleksandrova, Krasimira
    Kaaks, Rudolf
    Kühn, Tilman
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Vineis, Paolo
    Krogh, Vittorio
    Panico, Salvatore
    Masala, Giovanna
    Tumino, Rosario
    Weiderpass, Elisabete
    Skeie, Guri
    Lund, Eiliv
    Ramon Quirós, J.
    Ardanaz, Eva
    Navarro, Carmen
    Amiano, Pilar
    Sánchez, María-José
    Buckland, Genevieve
    Ericson, Ulrika
    Sonestedt, Emily
    Johansson, Matthias
    Umeå University, Faculty of Medicine, Department of Biobank Research. International Agency for Research on Cancer, Lyon, France.
    Sund, Malin
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Travis, Ruth C.
    Key, Timothy J.
    Khaw, Kay-Tee
    Wareham, Nick
    Riboli, Elio
    van Gils, Carla H.
    Plasma carotenoids, vitamin C, tocopherols, and retinol and the risk of breast cancer in the European Prospective Investigation into Cancer and Nutrition cohort2016In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 103, no 2, p. 454-464Article in journal (Refereed)
    Abstract [en]

    Background: Carotenoids and vitamin C are thought to be associated with reduced cancer risk because of their antioxidative capacity.

    Objective: This study evaluated the associations of plasma carotenoid, retinol, tocopherol, and vitamin C concentrations and risk of breast cancer.

    Design: In a nested case-control study within the European Prospective Investigation into Cancer and Nutrition cohort, 1502 female incident breast cancer cases were included, with an oversampling of premenopausal (n = 582) and estrogen receptor-negative (ER-) cases (n = 462). Controls (n = 1502) were individually matched to cases by using incidence density sampling. Prediagnostic samples were analyzed for alpha-carotene, beta-carotene, lycopene, lutein, zeaxanthin, beta-cryptoxanthin, retinol, alpha-tocopherol, gamma-tocopherol, and 454 vitamin C. Breast cancer risk was computed according to hormone receptor status and age at diagnosis (proxy for menopausal status) by using conditional logistic regression and was further stratified by smoking status, alcohol consumption, and body mass index (BMI). All statistical tests were 2-sided.

    Results: In quintile 5 compared with quintile 1, alpha-carotene (OR: 0.61; 95% CI: 0.39, 0.98) and beta-carotene (OR: 0.41; 95% CI: 0.26, 0.65) were inversely associated with risk of ER- breast tumors. The other analytes were not statistically associated with ER- breast cancer. For estrogen receptor-positive (ER+) tumors, no statistically significant associations were found. The test for heterogeneity between ER- and ER+ tumors was statistically significant only for beta-carotene (P-heterogeneity = 0.03). A higher risk of breast cancer was found for retinol in relation to ER-/progesterone receptor-negative tumors (OR: 2.37; 95% CI: 1.20, 4.67; P-heterogeneity with ER+/progesterone receptor positive = 0.06). We observed no statistically significant interaction between smoking, alcohol, or BMI and all investigated plasma analytes (based on tertile distribution).

    Conclusion: Our results indicate that higher concentrations of plasma beta-carotene and alpha-carotene are associated with lower breast cancer risk of ER tumors.

  • 11.
    Bellavia, Andrea
    et al.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, S-17177 Stockholm, Sweden.;Karolinska Inst, Inst Environm Med, Biostat Unit, S-17177 Stockholm, Sweden..
    Larsson, Susanna C.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, S-17177 Stockholm, Sweden..
    Bottai, Matteo
    Karolinska Inst, Inst Environm Med, Biostat Unit, S-17177 Stockholm, Sweden..
    Wolk, Alicja
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, S-17177 Stockholm, Sweden..
    Orsini, Nicola
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, S-17177 Stockholm, Sweden.;Karolinska Inst, Inst Environm Med, Biostat Unit, S-17177 Stockholm, Sweden..
    Differences in survival associated with processed and with nonprocessed red meat consumption2014In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 100, no 3, p. 924-929Article in journal (Refereed)
    Abstract [en]

    Background: High red meat consumption is associated with an increased mortality risk. This association is partly explained by the negative effect of processed meat consumption, which is widely established. The role of nonprocessed meat is unclear. Objective: The objective was to examine the combined association of processed and nonprocessed meat consumption with survival in a Swedish large prospective cohort. Design: In a population-based cohort of 74,645 Swedish men (40,089) and women (34,556), red meat consumption was assessed through a self-administered questionnaire. We estimated differences in survival [15th percentile differences (PDs), differences in the time by which the first 15% of the cohort died] according to levels of total red meat and combined levels of processed and nonprocessed red meat consumption. Results: During 15 y of follow-up (January 1998 to December 2012), we documented 16,683 deaths (6948 women; 9735 men). Compared with no consumption, consumption of red meat >100 g/d was progressively associated with shorter survival-up to 2 y for participants consuming an average of 300 g/d (15th PD: -21 mo; 95% CI: -31, -10). Compared with no consumption, high consumption of processed red meat (100 g/d) was associated with shorter survival (15th PD: -9 mo; 95% CI: -16, -2). High and moderate intakes of nonprocessed red meat were associated with shorter survival only when accompanied by a high intake of processed red meat. Conclusions: We found that high total red meat consumption was associated with progressively shorter survival, largely because of the consumption of processed red meat. Consumption of nonprocessed red meat alone was not associated with shorter survival. The Swedish Mammography Cohort and the Cohort of Swedish Men were registered at clinicaltrials.gov as NCT01127698 and NCT01127711, respectively.

  • 12. Bellavia, Andrea
    et al.
    Larsson, Susanna C
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Bottai, Matteo
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Orsini, Nicola
    Fruit and vegetable consumption and all-cause mortality: a dose-response analysis.2013In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 98, no 2, p. 454-459Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The association between fruit and vegetable (FV) consumption and overall mortality has seldom been investigated in large cohort studies. Findings from the few available studies are inconsistent.

    OBJECTIVE: The objective was to examine the dose-response relation between FV consumption and mortality, in terms of both time and rate, in a large prospective cohort of Swedish men and women.

    DESIGN: FV consumption was assessed through a self-administrated questionnaire in a population-based cohort of 71,706 participants (38,221 men and 33,485 women) aged 45-83 y. We performed a dose-response analysis to evaluate 10th survival percentile differences (PDs) by using Laplace regression and estimated HRs by using Cox regression.

    RESULTS: During 13 y of follow-up, 11,439 deaths (6803 men and 4636 women) occurred in the cohort. In comparison with 5 servings FV/d, a lower consumption was progressively associated with shorter survival and higher mortality rates. Those who never consumed FV lived 3 y shorter (PD: -37 mo; 95% CI: -58, -16 mo) and had a 53% higher mortality rate (HR: 1.53; 95% CI: 1.19, 1.99) than did those who consumed 5 servings FV/d. Consideration of fruit and vegetables separately showed that those who never consumed fruit lived 19 mo shorter (PD: -19 mo; 95% CI: -29, -10 mo) than did those who ate 1 fruit/d. Participants who consumed 3 vegetables/d lived 32 mo longer than did those who never consumed vegetables (PD: 32 mo; 96% CI: 13, 51 mo).

    CONCLUSION: FV consumption <5 servings/d is associated with progressively shorter survival and higher mortality rates. The Swedish Mammography Cohort and the Cohort of Swedish Men were registered at clinicaltrials.gov as NCT01127698 and NCT01127711, respectively.

  • 13.
    Bellavia, Andrea
    et al.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden..
    Stilling, Frej
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden..
    Wolk, Alicja
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden..
    High red meat intake and all-cause cardiovascular and cancer mortality: is the risk modified by fruit and vegetable intake?2016In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 104, no 4, p. 1137-1143Article in journal (Refereed)
    Abstract [en]

    Background: High red meat consumption is associated with a shorter survival and higher risk of cardiovascular disease (CVD), cancer, and all-cause mortality. Fruit and vegetable (FV) consumption is associated with a longer survival and lower mortality risk. Whether high FV consumption can counterbalance the negative impact of high red meat consumption is unknown. Objective: We evaluated 2 large prospective cohorts of Swedish men and women (the Swedish Mammography Cohort and the Cohort of Swedish Men) to determine whether the association between red meat consumption and the risk of all-cause, CVD, and cancer specific mortality differs across amounts of FV intake. Design: The study population included 74,645 Swedish men and women. Red meat and FV consumption were assessed through a self-administered questionnaire. We estimated HRs of all-cause, CVD, and cancer mortality according to quintiles of total red meat consumption. We next investigated possible interactions between red meat and FV consumption and evaluated the dose-response associations at low, medium, and high FV intake. Results: Compared with participants in the lowest quintile of total red meat consumption, those in the highest quintile had a 21% increased risk of all-cause mortality (HR: 1.21; 95% CI: 1.13, 1.29), a 29% increased risk of CVD mortality (BR: 1.29; 95% CI: 1.14, 1.46), and no increase in the risk of cancer mortality (HR: 1.00; 95% CI: 0.88, 1.43). Results were remarkably similar across amounts of FV consumption, and no interaction between red meat and FV consumption was detected. Conclusion: High intakes of red meat were associated with a higher risk of all-cause and CVD mortality. The increased risks were consistently observed in participants with low, medium, and high FV consumption. The Swedish Mammography Cohort and the Cohort of Swedish Men were registered at clinicaltrials.gov as NCT01127698 and NCT01127711, respectively.

  • 14.
    Benedict, Christian
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
    Hallschmid, Manfred
    Lassen, Arne
    Mahnke, Christin
    Schultes, Bernd
    Schiöth, Helgi Birgir
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
    Born, Jan
    Lange, Tanja
    Acute sleep deprivation reduces energy expenditure in healthy men2011In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 93, no 6, p. 1229-1236Article in journal (Refereed)
    Abstract [en]

    Background

    Epidemiologic evidence indicates that chronic sleep curtailment increases risk of developing obesity, but the mechanisms behind this relation are largely unknown.

    Objective

    We examined the influence of a single night of total sleep deprivation on morning energy expenditures and food intakes in healthy humans.

    Design

    According to a balanced crossover design, we examined 14 normal-weight male subjects on 2 occasions during a regular 24-h sleep-wake cycle (including 8 h of nocturnal sleep) and a 24-h period of continuous wakefulness. On the morning after regular sleep and total sleep deprivation, resting and postprandial energy expenditures were assessed by indirect calorimetry, and the free-choice food intake from an opulent buffet was tested in the late afternoon at the end of the experiment. Circulating concentrations of ghrelin, leptin, norepinephrine, cortisol, thyreotropin, glucose, and insulin were repeatedly measured over the entire 24-h session.

    Results

    In comparison with normal sleep, resting and postprandial energy expenditures assessed on the subsequent morning were significantly reduced after sleep deprivation by approximate to 5% and 20%, respectively (P < 0.05 and P < 0.0001). Nocturnal wakefulness increased morning plasma ghrelin concentrations (P < 0.02) and nocturnal and daytime circulating concentrations of thyreotropin, cortisol, and norepinephrine (P < 0.05) as well as morning postprandial plasma glucose concentrations (P < 0.05). Changes in food intakes were variable, and no differences between wake and sleep conditions were detected.

    Conclusion

    Our findings show that one night of sleep deprivation acutely reduces energy expenditure in healthy men, which suggests that sleep contributes to the acute regulation of daytime energy expenditure in humans.

  • 15.
    Berglund, Staffan
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Lönnerdal, Bo
    The Department of Nutrition, University of California, Davis, CA, USA.
    Westrup, Björn
    The Department of Women and Child Health, Division of Neonatology, Karolinska Institute, Stockholm, Sweden.
    Domellöf, Magnus
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Effects of iron supplementation on serum hepcidin and serum erythropoietin in low-birth-weight infants2011In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 94, no 6, p. 1553-1561Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The iron-regulatory hormone hepcidin has not been studied in infants, who experience large physiologic changes in iron status. OBJECTIVE: The objective was to study hepcidin and erythropoietin and their correlation with iron status in iron-replete and iron-deficient low-birth-weight (LBW) infants-a group at particular risk of iron deficiency (ID). DESIGN: We randomly assigned 285 otherwise healthy LBW infants to receive, from 6 wk to 6 mo of age, 3 doses of iron supplements: 0 (placebo), 1, or 2 mg/kg daily. Hepcidin, erythropoietin, hemoglobin, and variables of iron status were analyzed. RESULTS: Serum hepcidin did not change over time in the placebo group, despite a rapid decrease in serum ferritin. In iron-supplemented infants, hepcidin increased significantly, reaching a mean (±SD) concentration of 19.2 ± 2.5 ng/mL in the 2-mg/kg group compared with 13.0 ± 2.6 ng/mL in the placebo group at age 6 mo (P < 0.001). The difference was even larger between iron-deficient and iron-replete infants. Hepcidin was independently positively correlated with ferritin at all ages and was negatively correlated with the transferrin receptor concentration at age 6 wk and with transferrin at age 6 mo. Erythropoietin was initially similar between groups but decreased significantly in iron-supplemented infants. In addition to being negatively correlated with hemoglobin, it was also independently negatively correlated with indicators of iron status. CONCLUSIONS: Hepcidin is closely associated with iron status and may be a useful indicator of iron stores and ID in infants. Erythropoietin is negatively correlated with iron status, which suggests a feedback mechanism that needs further study. This trial is registered at clinicaltrials.gov as NCT00558454.

  • 16.
    Biskup, Izabela
    et al.
    Swedish Univ Agr Sci, Dept Food Sci, Bioctr, Uppsala, Sweden..
    Kyro, Cecilie
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Olsen, Anja
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    van Dam, Rob M.
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore..
    Tjonneland, Anne
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    Lindahl, Beret
    Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden..
    Johansson, Ingegerd
    Umea Univ, Dept Odontol & Cariol, Umea, Sweden..
    Landberg, Rikard
    Swedish Univ Agr Sci, Dept Food Sci, Bioctr, Uppsala, Sweden..
    The role of nutritional biomarkers in prediction and understanding the etiology of type 2 diabetes Reply2016In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 104, no 6, p. 1725-1726Article in journal (Refereed)
  • 17.
    Biskup, Izabela
    et al.
    Swedish Univ Agr Sci, BioCtr, Dept Food Sci, Uppsala, Sweden.;Wroclaw Med Univ, Dept Pharmacognosy, Wroclaw, Poland..
    Kyro, Cecilie
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Olsen, Anja
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    van Dam, Rob M.
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore.;Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Med, Singapore, Singapore.;Natl Univ Hlth Syst, Singapore, Singapore.;Harvard Univ, Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA..
    Tjonneland, Anne
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    Overvad, Kim
    Aarhus Univ, Dept Publ Hlth, Epidemiol Sect, Aarhus, Denmark..
    Lindahl, Bernt
    Umea Univ, Dept Publ Hlth, Umea, Sweden.;Umea Univ, Dept Clin Med, Umea, Sweden..
    Johansson, Ingegerd
    Umea Univ, Dept Odontol & Cariol, Umea, Sweden..
    Landberg, Rikard
    Swedish Univ Agr Sci, BioCtr, Dept Food Sci, Uppsala, Sweden.;Karolinska Inst, Inst Environm Med, Nutr Epidemiol Unit, Stockholm, Sweden..
    Plasma alkylresorcinols, biomarkers of whole-grain wheat and rye intake, and risk of type 2 diabetes in Scandinavian men and women2016In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 104, no 1, p. 88-96Article in journal (Refereed)
    Abstract [en]

    Background: Studies that use dietary biomarkers to investigate the association between whole-grain intake and the risk of developing type 2 diabetes (T2D) are lacking. Objective: We examined the association between plasma total alkylresorcinols and the alkylresorcinol C17:0-to-C21:0 ratio, biomarkers of whole-grain wheat and rye intake and relative whole grain rye over whole-grain wheat intake, respectively, and the risk of T2D among Scandinavian men and women. Design: A nested case-control study was established within the Northern Sweden Health and Disease Study and the Danish Diet, Cancer and Health cohort. Alkylresorcinol concentrations and the ratios of C17:0 to C21:0 were determined in plasma samples from 931 case-control pairs. ORs for T2D were calculated for plasma total alkylresorcinol concentration or C17:0-to-C21:0 ratio in quartiles with the use of conditional logistic regression that was adjusted for potential confounders. Additional analyses with whole-grain wheat and rye intake estimated from food-frequency questionnaires (FFQs) as exposures were also performed. Results: The plasma total alkylresorcinol concentration was not associated with T2D risk (OR: 1.34; 95% CI: 0.95, 1.88) for the highest compared with the lowest quartiles in multivariable adjusted models. However, the C17:0-to-C21:0 ratio was associated with a lower diabetes risk (OR: 0.54; 95% CI: 0.37, 0.78). Analyses with whole-grain intake estimated from FFQs yielded similar results. Conclusions: Total whole-grain wheat and rye intake, reflected by alkylresorcinols in plasma, was not associated with a lower risk of T2D in a population with high whole-grain intake. In contrast, the proportion of whole-grain rye to whole-grain wheat intake, indicated by the plasma C17:0-to-C21:0 ratio, was inversely associated with T2D. This suggests that whole-grain intake dominated by rye may be favorable for T2D prevention.

  • 18.
    Biskup, Izabela
    et al.
    Swedish Univ Agr Sci, Bioctr, Dept Food Sci, Uppsala, Sweden.;Wroclaw Med Univ, Dept Pharmacognosy, Wroclaw, Poland..
    Kyro, Cecilie
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Olsen, Anja
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    van Dam, Rob M.
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore.;Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Med, Singapore, Singapore.;Natl Univ Hlth Syst, Singapore, Singapore.;Harvard Univ, Dept Nutr, Harvard TH Chan Sch Publ Hlth, Boston, MA 02115 USA..
    Tjonneland, Anne
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    Overvad, Kim
    Aarhus Univ, Epidemiol Sect, Dept Publ Hlth, Aarhus, Denmark..
    Lindahl, Bernt
    Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden..
    Johansson, Ingegerd
    Umea Univ, Dept Odontol & Cariol, Umea, Sweden..
    Landberg, Rikard
    Swedish Univ Agr Sci, Bioctr, Dept Food Sci, Uppsala, Sweden.;Karolinska Insitutet, Inst Environm Med, Nutr Epidemiol Unit, Stockholm, Sweden.;Chalmers, Dept Biol & Biol Engn, Gothenburg, Sweden..
    Whole-grain intake and risk of type 2 diabetes Reply2016In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 104, no 6, p. 1723-1724Article in journal (Refereed)
  • 19. Biskup, Izabela
    et al.
    Kyrø, Cecilie
    Marklund, Matti
    Olsen, Anja
    van Dam, Rob M.
    Tjonneland, Anne
    Overvad, Kim
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Landberg, Rikard
    Plasma alkylresorcinols, biomarkers of whole-grain wheat and rye intake, and risk of type 2 diabetes in Scandinavian men and women2016In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 104, no 1, p. 88-96Article in journal (Refereed)
    Abstract [en]

    Background: Studies that use dietary biomarkers to investigate the association between whole-grain intake and the risk of developing type 2 diabetes (T2D) are lacking. Objective: We examined the association between plasma total alkylresorcinols and the alkylresorcinol C17:0-to-C21:0 ratio, biomarkers of whole-grain wheat and rye intake and relative whole grain rye over whole-grain wheat intake, respectively, and the risk of T2D among Scandinavian men and women. Design: A nested case-control study was established within the Northern Sweden Health and Disease Study and the Danish Diet, Cancer and Health cohort. Alkylresorcinol concentrations and the ratios of C17:0 to C21:0 were determined in plasma samples from 931 case-control pairs. ORs for T2D were calculated for plasma total alkylresorcinol concentration or C17:0-to-C21:0 ratio in quartiles with the use of conditional logistic regression that was adjusted for potential confounders. Additional analyses with whole-grain wheat and rye intake estimated from food-frequency questionnaires (FFQs) as exposures were also performed. Results: The plasma total alkylresorcinol concentration was not associated with T2D risk (OR: 1.34; 95% CI: 0.95, 1.88) for the highest compared with the lowest quartiles in multivariable adjusted models. However, the C17:0-to-C21:0 ratio was associated with a lower diabetes risk (OR: 0.54; 95% CI: 0.37, 0.78). Analyses with whole-grain intake estimated from FFQs yielded similar results. Conclusions: Total whole-grain wheat and rye intake, reflected by alkylresorcinols in plasma, was not associated with a lower risk of T2D in a population with high whole-grain intake. In contrast, the proportion of whole-grain rye to whole-grain wheat intake, indicated by the plasma C17:0-to-C21:0 ratio, was inversely associated with T2D. This suggests that whole-grain intake dominated by rye may be favorable for T2D prevention.

  • 20. Biskup, Izabela
    et al.
    Kyrø, Cecilie
    Marklund, Matti
    Olsen, Anja
    van Dam, Rob M.
    Tjønneland, Anne
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Landberg, Rikard
    Reply to A Abbasi2016In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 104, no 6, p. 1725-1726Article in journal (Refereed)
  • 21. Biskup, Izabela
    et al.
    Kyrø, Cecilie
    Marklund, Matti
    Olsen, Anja
    van Dam, Rob M.
    Tjønneland, Anne
    Overvad, Kim
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Landberg, Rikard
    Reply to J-B Qin et al2016In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 104, no 6, p. 1723-1724Article in journal (Refereed)
  • 22. Bisschop, Charlotte N. Steins
    et al.
    van Gils, Carla H.
    Emaus, Marleen J.
    Bueno-de-Mesquita, H. Bas
    Monninkhof, Evelyn M.
    Boeing, Heiner
    Aleksandrova, Krasmira
    Jenab, Mazda
    Norat, Teresa
    Riboli, Elio
    Boutron-Rualt, Marie-Christine
    Fagherazzi, Guy
    Racine, Antoine
    Palli, Domenico
    Krogh, Vittorio
    Tumino, Rosario
    Naccarati, Alessio
    Mattiello, Amalia
    Vicente Argueeles, Marcial
    Jose Sanchez, Maria
    Jose Tormo, Maria
    Ardanaz, Eva
    Dorronsoro, Miren
    Bonet, Catalina
    Khaw, Kay-Tee
    Key, Tim
    Trichopoulou, Antonia
    Orfanos, Philippos
    Naska, Androniki
    Kaaks, Rudolph R.
    Lukanova, Annekatrin
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Pischon, Tobias
    Ljuslinder, Ingrid
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Jirstrom, Karin
    Ohlsson, Bodil
    Overvad, Kim
    Berentzen, Tina Landsvig
    Halkjaer, Jytte
    Tjonneland, Anne
    Weiderpass, Elisabete
    Skeie, Guri
    Braaten, Tonje
    Siersema, Peter D.
    Freisling, Heinz
    Ferrari, Pietro
    Peeters, Petra H. M.
    May, Anne M.
    Weight change later in life and colon and rectal cancer risk in participants in the EPIC-PANACEA study2014In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 99, no 1, p. 139-147Article in journal (Refereed)
    Abstract [en]

    Background: A moderate association exists between body mass index (BMI) and colorectal cancer. Less is known about the effect of weight change. Objective: We investigated the relation between BMI and weight change and subsequent colon and rectal cancer risk. Design: This was studied among 328,781 participants in the prospective European Prospective Investigation into Cancer Physical Activity, Nutrition, Alcohol, Cessation of Smoking, Eating study (mean age: 50 y). Body weight was assessed at recruitment and on average 5 y later. Self-reported weight change (kg/y) was categorized in sex-specific quintiles, with quintiles 2 and 3 combined as the reference category (men: -0.6 to 0.3 kg/y; women: -0.4 to 0.4 kg/y). In the subsequent years, participants were followed for the occurrence of colon and rectal cancer (median period: 6.8 y). Multivariable Cox proportional hazards regression analyses were used to study the association. Results: A total of 1261 incident colon cancer and 747 rectal cancer cases were identified. ME at recruitment was statistically significantly associated with colon cancer risk in men (HR: 1.04; 95% CI: 1.02, 1.07). Moderate weight gain (quintile 4) in men increased risk further (HR: 1.32; 95% CI: 1.04, 1.68), but this relation did not show a clear trend. In women, BMI or weight gain was not related to subsequent risk of colon cancer. No statistically significant associations for weight loss and colon cancer or for BMI and weight changes and rectal cancer were found. Conclusions: BMI attained at adulthood was associated with colon cancer risk. Subsequent weight gain or loss was not related to colon or rectal cancer risk in men or women.

  • 23.
    Bjermo, Helena
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Iggman, David
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Center for Clinical Research Dalarna.
    Kullberg, Joel
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Radiology.
    Dahlman, Ingrid
    Johansson, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Radiology.
    Persson, Lena
    Berglund, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Radiology.
    Pulkki, Kari
    Basu, Samar
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Oxidative Stress and Inflammation.
    Uusitupa, Matti
    Rudling, Mats
    Arner, Peter
    Cederholm, Tommy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Ahlström, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Radiology.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Effects of n-6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial2012In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 95, no 5, p. 1003-1012Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Replacing SFAs with vegetable PUFAs has cardiometabolic benefits, but the effects on liver fat are unknown. Increased dietary n-6 PUFAs have, however, also been proposed to promote inflammation-a yet unproven theory.

    OBJECTIVE:

    We investigated the effects of PUFAs on liver fat, systemic inflammation, and metabolic disorders.

    DESIGN:

    We randomly assigned 67 abdominally obese subjects (15% had type 2 diabetes) to a 10-wk isocaloric diet high in vegetable n-6 PUFA (PUFA diet) or SFA mainly from butter (SFA diet), without altering the macronutrient intake. Liver fat was assessed by MRI and magnetic resonance proton (1H) spectroscopy (MRS). Proprotein convertase subtilisin/kexin type-9 (PCSK9, a hepatic LDL-receptor regulator), inflammation, and adipose tissue expression of inflammatory and lipogenic genes were determined.

    RESULTS:

    A total of 61 subjects completed the study. Body weight modestly increased but was not different between groups. Liver fat was lower during the PUFA diet than during the SFA diet [between-group difference in relative change from baseline; 16% (MRI; P < 0.001), 34% (MRS; P = 0.02)]. PCSK9 (P = 0.001), TNF receptor-2 (P < 0.01), and IL-1 receptor antagonist (P = 0.02) concentrations were lower during the PUFA diet, whereas insulin (P = 0.06) tended to be higher during the SFA diet. In compliant subjects (defined as change in serum linoleic acid), insulin, total/HDL-cholesterol ratio, LDL cholesterol, and triglycerides were lower during the PUFA diet than during the SFA diet (P < 0.05). Adipose tissue gene expression was unchanged.

    CONCLUSIONS:

    Compared with SFA intake, n-6 PUFAs reduce liver fat and modestly improve metabolic status, without weight loss. A high n-6 PUFA intake does not cause any signs of inflammation or oxidative stress. Downregulation of PCSK9 could be a novel mechanism behind the cholesterol-lowering effects of PUFAs.

  • 24.
    Bjermo, Helena
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Iggman, David
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Should dietary SFA be exchanged for linoleic acid?: Reply2012In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 96, no 4, p. 945-946Article in journal (Refereed)
  • 25.
    Bouras, Emmanouil
    et al.
    Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece.
    Kim, Andre E.
    Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, CA, Los Angeles, United States.
    Lin, Yi
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States.
    Morrison, John
    Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, CA, Los Angeles, United States.
    Du, Mengmeng
    Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, NY, New York, United States.
    Albanes, Demetrius
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, MD, Bethesda, United States.
    Barry, Elizabeth L.
    Department of Epidemiology, Geisel School of Medicine at Dartmouth, NH, Hanover, United States.
    Baurley, James W.
    Bioinformatics and Data Science Research Center, Bina Nusantara University, Jakarta, Indonesia; BioRealm LLC, CA, Walnut, United States.
    Berndt, Sonja I.
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, MD, Bethesda, United States.
    Bien, Stephanie A.
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States.
    Bishop, Timothy D.
    Leeds Institute of Cancer and Pathology, University of Leeds, Leeds, United Kingdom.
    Brenner, Hermann
    Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany; Division of Preventive Oncology, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT), Heidelberg, Germany; German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
    Budiarto, Arif
    Bioinformatics and Data Science Research Center, Bina Nusantara University, Jakarta, Indonesia; Computer Science Department, School of Computer Science, Bina Nusantara University, Jakarta, Indonesia.
    Burnett-Hartman, Andrea
    Institute for Health Research, Kaiser Permanente Colorado, CO, Denver, United States.
    Campbell, Peter T.
    Department of Epidemiology and Population Health, Albert Einstein College of Medicine, NY, Bronx, United States.
    Carreras-Torres, Robert
    Unit of Biomarkers and Suceptibility (UBS), Oncology Data Analytics Program (ODAP), Catalan Institute of Oncology (ICO), L'Hospitalet del Llobregat, Barcelona, Spain; ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain; Digestive Diseases and Microbiota Group, Girona Biomedical Research Institute (IDIBGI), Salt, Girona, Spain.
    Casey, Graham
    Center for Public Health Genomics, University of Virginia, VA, Charlottesville, United States.
    Cenggoro, Tjeng Wawan
    Bioinformatics and Data Science Research Center, Bina Nusantara University, Jakarta, Indonesia; Computer Science Department, School of Computer Science, Bina Nusantara University, Jakarta, Indonesia.
    Chan, Andrew T.
    Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, MA, Boston, United States; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, MA, Boston, United States; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, MA, Boston, United States; Broad Institute of Harvard and MIT, MA, Cambridge, United States; Department of Epidemiology, Harvard TH Chan School of Public Health, Harvard University, MA, Boston, United States; Department of Immunology and Infectious Diseases, Harvard TH Chan School of Public Health, Harvard University, MA, Boston, United States.
    Chang-Claude, Jenny
    Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany; University Medical Centre Hamburg-Eppendorf, University Cancer Centre Hamburg (UCCH), Hamburg, Germany.
    Conti, David V.
    Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, CA, Los Angeles, United States.
    Cotterchio, Michelle
    Ontario Health (Cancer Care Ontario), ON, Toronto, Canada.
    Devall, Matthew
    Center for Public Health Genomics, Department of Public Health Sciences, University of Virginia, VA, Charlottesville, United States; Department of Public Health Sciences, Center for Public Health Genomics, VA, Charlottesville, United States.
    Diez-Obrero, Virginia
    Unit of Biomarkers and Suceptibility (UBS), Oncology Data Analytics Program (ODAP), Catalan Institute of Oncology (ICO), L'Hospitalet del Llobregat, Barcelona, Spain; ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain.
    Dimou, Niki
    Nutrition and Metabolism Branch, International Agency for Research on Cancer, Lyon, France.
    Drew, David A.
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, MA, Boston, United States.
    Figueiredo, Jane C.
    Department of Medicine, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, CA, Los Angeles, United States.
    Giles, Graham G.
    Cancer Epidemiology Division, Cancer Council Victoria, VIC, Melbourne, Australia; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, VIC, Melbourne, Australia; Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, VIC, Clayton, Australia.
    Gruber, Stephen B.
    Department of Medical Oncology & Therapeutics Research, City of Hope National Medical Center, CA, Duarte, United States.
    Gunter, Marc J.
    Nutrition and Metabolism Branch, International Agency for Research on Cancer, Lyon, France.
    Harrison, Tabitha A.
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States.
    Hidaka, Akihisa
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States.
    Hoffmeister, Michael
    Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
    Huyghe, Jeroen R.
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States.
    Joshi, Amit D.
    Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, MA, Boston, United States; Department of Epidemiology, Harvard TH Chan School of Public Health, Harvard University, MA, Boston, United States.
    Kawaguchi, Eric S.
    Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, CA, Los Angeles, United States; Department of Biostatistics, Fielding School of Public Health, University of California, Los Angeles, CA, Los Angeles, United States.
    Keku, Temitope O.
    Center for Gastrointestinal Biology and Disease, University of North Carolina, NC, Chapel Hill, United States.
    Kundaje, Anshul
    Department of Genetics, Stanford University, CA, Stanford, United States; Department of Computer Science, Stanford University, CA, Stanford, United States.
    Le Marchand, Loic
    University of Hawaii Cancer Center, HI, Honolulu, United States.
    Lewinger, Juan Pablo
    Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, CA, Los Angeles, United States.
    Li, Li
    Department of Family Medicine, University of Virginia, VA, Charlottesville, United States.
    Lynch, Brigid M.
    Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, VIC, Melbourne, Australia; Cancer Epidemiology Division, Cancer Council Victoria, VIC, Melbourne, Australia.
    Mahesworo, Bharuno
    Bioinformatics and Data Science Research Center, Bina Nusantara University, Jakarta, Indonesia.
    Männistö, Satu
    Department of Public Health Solutions, National Institute for Health and Welfare, Helsinki, Finland.
    Moreno, Victor
    Unit of Biomarkers and Suceptibility (UBS), Oncology Data Analytics Program (ODAP), Catalan Institute of Oncology (ICO), L'Hospitalet del Llobregat, Barcelona, Spain; ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain; Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP), Madrid, Spain; Department of Clinical Sciences, Faculty of Medicine and health Sciences and Universitat de Barcelona Institute of Complex Systems (UBICS), University of Barcelona (UB), L'Hospitalet de Llobregat, Barcelona, Spain.
    Murphy, Neil
    Nutrition and Metabolism Branch, International Agency for Research on Cancer, Lyon, France.
    Newcomb, Polly A.
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States; School of Public Health, University of Washington, WA, Seattle, United States.
    Obón-Santacana, Mireia
    Unit of Biomarkers and Suceptibility (UBS), Oncology Data Analytics Program (ODAP), Catalan Institute of Oncology (ICO), L'Hospitalet del Llobregat, Barcelona, Spain; ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain; Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP), Madrid, Spain.
    Ose, Jennifer
    Huntsman Cancer Institute, University of Utah, Utah, Salt Lake City, United States; Department of Population Health Sciences, University of Utah, UT, Salt Lake City, United States.
    Palmer, Julie R.
    Slone Epidemiology Center at Boston University, MA, Boston, United States.
    Papadimitriou, Nikos
    Nutrition and Metabolism Branch, International Agency for Research on Cancer, Lyon, France.
    Pardamean, Bens
    Bioinformatics and Data Science Research Center, Bina Nusantara University, Jakarta, Indonesia.
    Pellatt, Andrew J.
    Department of Cancer Medicine, MD Anderson Cancer Center, TX, Houston, United States.
    Peoples, Anita R.
    Huntsman Cancer Institute, University of Utah, Utah, Salt Lake City, United States; Department of Population Health Sciences, University of Utah, UT, Salt Lake City, United States.
    Platz, Elizabeth A.
    Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, MD, Baltimore, United States.
    Potter, John D.
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States; Research Centre for Hauora and Health, Massey University, Wellington, New Zealand.
    Qi, Lihong
    Department of Public Health Sciences, University of California Davis, CA, Davis, United States.
    Qu, Conghui
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States.
    Rennert, Gad
    Department of Community Medicine and Epidemiology, Lady Davis Carmel Medical Center, Haifa, Israel; Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel; Clalit National Cancer Control Center, Haifa, Israel.
    Ruiz-Narvaez, Edward
    Department of Nutritional Sciences, University of Michigan School of Public Health, MI, Ann Arbor, United States.
    Sakoda, Lori C.
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States; Division of Research, Kaiser Permanente Northern California, CA, Oakland, United States.
    Schmit, Stephanie L.
    Genomic Medicine Institute, Cleveland Clinic, OH, Cleveland, United States; Population and Cancer Prevention Program, Case Comprehensive Cancer Center, OH, Cleveland, United States.
    Shcherbina, Anna
    Department of Genetics, Stanford University, CA, Stanford, United States; Department of Computer Science, Stanford University, CA, Stanford, United States.
    Stern, Mariana C.
    Department of Population and Public Health Sciences and Norris Comprehensive Cancer Center, Preventive Medicine, Keck School of Medicine, University of Southern California, CA, Los Angeles, United States.
    Su, Yu-Ru
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States.
    Tangen, Catherine M.
    SWOG Statistical Center, Fred Hutchinson Cancer Research Center, WA, Seattle, United States.
    Thomas, Duncan C.
    Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, CA, Los Angeles, United States.
    Tian, Yu
    Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany; School of Public Health, Capital Medical University, Beijing, China.
    Um, Caroline Y.
    Department of Population Science, American Cancer Society, GA, Atlanta, United States.
    van Duijnhoven, Franzel JB.
    Division of Human Nutrition and Health, Wageningen University & Research, Wageningen, Netherlands.
    van Guelpen, Bethany
    Umeå University, Faculty of Medicine, Wallenberg Centre for Molecular Medicine at Umeå University (WCMM). Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Visvanathan, Kala
    Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, MD, Baltimore, United States.
    Wang, Jun
    Department of Population and Public Health Sciences and Norris Comprehensive Cancer Center, Preventive Medicine, Keck School of Medicine, University of Southern California, CA, Los Angeles, United States.
    White, Emily
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States; Department of Epidemiology, University of Washington School of Public Health, WA, Seattle, United States.
    Wolk, Alicja
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Woods, Michael O.
    Memorial University of Newfoundland, Discipline of Genetics, St John's, Canada.
    Ulrich, Cornelia M.
    Huntsman Cancer Institute, University of Utah, Utah, Salt Lake City, United States; Department of Population Health Sciences, University of Utah, UT, Salt Lake City, United States.
    Hsu, Li
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States; Department of Biostatistics, University of Washington, WA, Seattle, United States.
    Gauderman, W James
    Division of Biostatistics, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, CA, Los Angeles, United States.
    Peters, Ulrike
    Public Health Sciences Division, Fred Hutchinson Cancer Center, WA, Seattle, United States; Department of Epidemiology, University of Washington, WA, Seattle, United States.
    Tsilidis, Konstantinos K.
    Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece; Department of Epidemiology and Biostatistics, Imperial College London, School of Public Health, London, United Kingdom.
    Genome-wide interaction analysis of folate for colorectal cancer risk2023In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 118, no 5, p. 881-891Article in journal (Refereed)
    Abstract [en]

    Background: Epidemiological and experimental evidence suggests that higher folate intake is associated with decreased colorectal cancer (CRC) risk; however, the mechanisms underlying this relationship are not fully understood. Genetic variation that may have a direct or indirect impact on folate metabolism can provide insights into folate's role in CRC.

    Objectives: Our aim was to perform a genome-wide interaction analysis to identify genetic variants that may modify the association of folate on CRC risk.

    Methods: We applied traditional case-control logistic regression, joint 3-degree of freedom, and a 2-step weighted hypothesis approach to test the interactions of common variants (allele frequency >1%) across the genome and dietary folate, folic acid supplement use, and total folate in relation to risk of CRC in 30,550 cases and 42,336 controls from 51 studies from 3 genetic consortia (CCFR, CORECT, GECCO).

    Results: Inverse associations of dietary, total folate, and folic acid supplement with CRC were found (odds ratio [OR]: 0.93; 95% confidence interval [CI]: 0.90, 0.96; and 0.91; 95% CI: 0.89, 0.94 per quartile higher intake, and 0.82 (95% CI: 0.78, 0.88) for users compared with nonusers, respectively). Interactions (P-interaction < 5×10-8) of folic acid supplement and variants in the 3p25.2 locus (in the region of Synapsin II [SYN2]/tissue inhibitor of metalloproteinase 4 [TIMP4]) were found using traditional interaction analysis, with variant rs150924902 (located upstream to SYN2) showing the strongest interaction. In stratified analyses by rs150924902 genotypes, folate supplementation was associated with decreased CRC risk among those carrying the TT genotype (OR: 0.82; 95% CI: 0.79, 0.86) but increased CRC risk among those carrying the TA genotype (OR: 1.63; 95% CI: 1.29, 2.05), suggesting a qualitative interaction (P-interaction = 1.4×10-8). No interactions were observed for dietary and total folate.

    Conclusions: Variation in 3p25.2 locus may modify the association of folate supplement with CRC risk. Experimental studies and studies incorporating other relevant omics data are warranted to validate this finding.

    Download full text (pdf)
    fulltext
  • 26. Braem, Marieke G. M.
    et al.
    Onland-Moret, N. Charlotte
    Schouten, Leo J.
    Tjonneland, Anne
    Hansen, Louise
    Dahm, Christina C.
    Overvad, Kim
    Lukanova, Annekatrin
    Dossus, Laure
    Floegel, Anna
    Boeing, Heiner
    Clavel-Chapelon, Francoise
    Chabbert-Buffet, Nathalie
    Fagherazzi, Guy
    Trichopoulou, Antonia
    Benetou, Vassiliki
    Goufa, Ioulia
    Pala, Valeria
    Galasso, Rocco
    Mattiello, Amalia
    Sacerdote, Carlotta
    Palli, Domenico
    Tumino, Rosario
    Gram, Inger T.
    Lund, Eiliv
    Gavrilyuk, Oxana
    Sanchez, Maria-Jose
    Quiros, Ramon
    Gonzales, Carlos A.
    Dorronsoro, Miren
    Huerta Castano, Jose M.
    Barricarte Gurrea, Aurelio
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynaecology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Ohlson, Nina
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Jirstrom, Karin
    Witfalt, Elisabet
    Allen, Naomi E.
    Tsilidis, Konstantinos K.
    Kaw, Kay-Tee
    Bueno-de-Mesquita, H. Bas
    Dik, Vincent K.
    Rinaldi, Sabina
    Fedirko, Veronika
    Norat, Teresa
    Riboli, Elio
    Kaaks, Rudolf
    Peeters, Petra H. M.
    Coffee and tea consumption and the risk of ovarian cancer: a prospective cohort study and updated meta-analysis2012In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 95, no 5, p. 1172-1181Article in journal (Refereed)
    Abstract [en]

    Background: In 2007 the World Cancer Research Fund Report concluded that there was limited and inconsistent evidence for an effect of coffee and tea consumption on the risk of epithelial ovarian cancer (EOC). Objective: In the European Prospective Investigation into Cancer and Nutrition (EPIC), we aimed to investigate whether coffee intakes, tea intakes, or both are associated with the risk of EOC. Design: All women participating in the EPIC (n = 330,849) were included in this study. Data on coffee and tea consumption were collected through validated food-frequency questionnaires at baseline. HRs and 95% CIs were estimated by using Cox proportional hazards models. Furthermore, we performed an updated meta-analysis of all previous prospective studies until April 2011 by comparing the highest and lowest coffee- and tea-consumption categories as well as by using dose-response random-effects meta-regression analyses. Results: During a median follow-up of 11.7 y, 1244 women developed EOC. No association was observed between the risk of EOC and coffee consumption [HR: 1.05 (95% CI: 0.75, 1.46) for the top quintile compared with no intake] or tea consumption [HR: 1.07 (95% Cl: 0.78, 1.45) for the top quintile compared with no intake]. This lack of association between coffee and tea intake and EOC risk was confirmed by the results of our meta-analysis. Conclusion: Epidemiologic studies do not provide sufficient evidence to support an association between coffee and tea consumption and risk of ovarian cancer. Am J Clin Nutr 2012;95:1172-81.

  • 27. Bratteby, L E
    et al.
    Sandhagen, B
    Fan, H
    Enghardt, H
    Samuelson, Gösta
    Total energy expenditure and physical activity as assessed by the doubly labeled water method in Swedish adolescents in whom energy intake was underestimated by 7-d diet records.1998In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 67, no 5, p. 905-11Article in journal (Refereed)
    Abstract [en]

    Swedish children and adolescents may be adopting a sedentary lifestyle with low energy expenditures and intakes, but no quantitative data are available. The purpose of the present study in 50 adolescents aged 15 y was to investigate whether assessment of total energy expenditure (TEE) and physical activity level (PAL) by the doubly labeled water method and indirect calorimetry and estimation of energy intake by a 7-d diet record would indicate physical inactivity. The boys' (n = 25) mean weight was 112% and the girls' (n = 25) was 109% of Swedish reference values from 1976; the mean height of both boys and girls was 102% of those reference values. Mean TEE in the boys and girls, 13.82 +/- 1.90 and 10.70 +/- 1.59 MJ/d, and mean PAL (TEE/basal metabolic rate), 1.89 +/- 0.16 and 1.79 +/- 0.22, respectively, were nonsignificantly higher than corresponding figures from other published studies. Mean energy intake as a percentage of TEE was 81.9 +/- 17.9% in the boys and 78.3 +/- 16.4% in the girls. Significant negative correlations were found both between energy intake as a percentage of TEE and percentage body fat and between energy intake as a percentage of TEE and body mass index. These results add to the evidence that 7-d diet records underestimate energy intake in adolescents, particularly those with a tendency for overweight and increased body fat. The results support indications of a trend of increasing body weight and height in Swedish adolescents, but conflict with the presumptions of low physical activity, low energy expenditure, and low energy intake. These results support the view that current recommendations for energy intake during adolescence are too low.

  • 28. Brigelius-Flohé, R
    et al.
    Kelly, FJ
    Salonen, JT
    Neuzil, Jiri
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology.
    Zing, JM
    Azzi, A
    The European perspective on vitamin E: Current knowledge and future research2002In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 76, no 4, p. 703-716Article in journal (Refereed)
    Abstract [en]

    Vitamin E is indispensible for reproduction in female rats. In humans, vitamin E deficiency primarily causes neurologic dysfunctions, but the underlying molecular mechanisms are unclear. Because of its antioxidative properties, vitamin E is believed to help prevent diseases associated with oxidative stress, such as cardiovascular disease, cancer, chronic inflammation, and neurologic disorders. However, recent clinical trials undertaken to prove this hypothesis failed to verify a consistent benefit. Given these findings, a group of European scientists met to analyze the most recent knowledge of vitamin E function and metabolism. An overview of their discussions is presented in this article, which includes considerations of the mechanisms of absorption, distribution, and metabolism of different forms of vitamin E, including the a-tocopherol transfer protein and a-tocopherol-associated proteins, the mechanism of tocopherol side-chain degradation and its putative interaction with drug metabolism, the usefulness of tocopherol metabolites as biomarkers, and the novel mechanisms of the antiatherosclerotic and anticarcinogenic properties of vitamin E, which involve modulation of cellular signaling, transcriptional regulation, and induction of apoptosis. Clinical trials were analyzed on the basis of the selection of subjects, the stage of disease, and the mode of intake, dosage, and chemical form of vitamin E. In addition, the scarce knowledge on the role of vitamin E in reproduction was summarized. In conclusion, the scientists agreed that the functions of vitamin E were underestimated if one considered only its antioxidative properties. Future research on this essential vitamin should focus on what makes it essential for humans, why the body apparently utilizes a-tocopherol preferentially, and what functions other forms of vitamin E have.

  • 29. Brunkwall, Louise
    et al.
    Chen, Yan
    Hindy, George
    Rukh, Gull
    Ericson, Ulrika
    Barroso, Ines
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden; Department of Nutrition, Harvard School of Public Health, Boston, MA.
    Orho-Melander, Marju
    Renström, Frida
    Umeå University, Faculty of Medicine, Department of Biobank Research. Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
    Sugar-sweetened beverage consumption and genetic predisposition to obesity in 2 Swedish cohorts2016In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 104, no 3, p. 809-815Article in journal (Refereed)
    Abstract [en]

    Background: The consumption of sugar-sweetened beverages (SSBs), which has increased substantially during the last decades, has been associated with obesity and weight gain.

    Objective: Common genetic susceptibility to obesity has been shown to modify the association between SSB intake and obesity risk in 3 prospective cohorts from the United States. We aimed to replicate these findings in 2 large Swedish cohorts.

    Design: Data were available for 21,824 healthy participants from the Malmö Diet and Cancer study and 4902 healthy participants from the Gene-Lifestyle Interactions and Complex Traits Involved in Elevated Disease Risk Study. Self-reported SSB intake was categorized into 4 levels (seldom, low, medium, and high). Unweighted and weighted genetic risk scores (GRSs) were constructed based on 30 body mass index [(BMI) in kg/m2]-associated loci, and effect modification was assessed in linear regression equations by modeling the product and marginal effects of the GRS and SSB intake adjusted for age-, sex-, and cohort-specific covariates, with BMI as the outcome. In a secondary analysis, models were additionally adjusted for putative confounders (total energy intake, alcohol consumption, smoking status, and physical activity).

    Results: In an inverse variance-weighted fixed-effects meta-analysis, each SSB intake category increment was associated with a 0.18 higher BMI (SE = 0.02; P = 1.7 × 10−20n = 26,726). In the fully adjusted model, a nominal significant interaction between SSB intake category and the unweighted GRS was observed (P-interaction = 0.03). Comparing the participants within the top and bottom quartiles of the GRS to each increment in SSB intake was associated with 0.24 (SE = 0.04; P = 2.9 × 10−8n = 6766) and 0.15 (SE = 0.04; P = 1.3 × 10−4n = 6835) higher BMIs, respectively.

    Conclusions: The interaction observed in the Swedish cohorts is similar in magnitude to the previous analysis in US cohorts and indicates that the relation of SSB intake and BMI is stronger in people genetically predisposed to obesity.

    Download full text (pdf)
    fulltext
  • 30. Buckland, Genevieve
    et al.
    Agudo, Antonio
    Luján, Leila
    Jakszyn, Paula
    Bueno-de-Mesquita, H Bas
    Palli, Domenico
    Boeing, Heiner
    Carneiro, Fátima
    Krogh, Vittorio
    Sacerdote, Carlotta
    Tumino, Rosario
    Panico, Salvatore
    Nesi, Gabriella
    Manjer, Jonas
    Regnér, Sara
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Stenling, Roger
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Sanchez, María-José
    Dorronsoro, Miren
    Barricarte, Aurelio
    Navarro, Carmen
    Quirós, J Ramón
    Allen, Naomi E
    Key, Timothy J
    Bingham, Sheila
    Kaaks, Rudolf
    Overvad, Kim
    Jensen, Majken
    Olsen, Anja
    Tjønneland, Anne
    Peeters, Petra H M
    Numans, Mattijs E
    Ocké, Marga C
    Clavel-Chapelon, Françoise
    Morois, Sophie
    Boutron-Ruault, Marie-Christine
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Lund, Eiliv
    Couto, Elisabeth
    Boffeta, Paolo
    Jenab, Mazda
    Riboli, Elio
    Romaguera, Dora
    Mouw, Traci
    González, Carlos A
    Adherence to a Mediterranean diet and risk of gastric adenocarcinoma within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort study2010In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 91, no 2, p. 381-390Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The Mediterranean dietary pattern is believed to protect against cancer, although evidence from cohort studies that have examined particular cancer sites is limited.

    OBJECTIVE: We aimed to explore the association between adherence to a relative Mediterranean diet (rMED) and incident gastric adenocarcinoma (GC) within the European Prospective Investigation into Cancer and Nutrition study.

    DESIGN: The study included 485,044 subjects (144,577 men) aged 35-70 y from 10 European countries. At recruitment, dietary and lifestyle information was collected. An 18-unit rMED score, incorporating 9 key components of the Mediterranean diet, was used to estimate rMED adherence. The association between rMED and GC with respect to anatomic location (cardia and noncardia) and histologic types (diffuse and intestinal) was investigated. A calibration study in a subsample was used to control for dietary measurement error.

    RESULTS: After a mean follow-up of 8.9 y, 449 validated incident GC cases were identified and used in the analysis. After stratification by center and age and adjustment for recognized cancer risk factors, high compared with low rMED adherence was associated with a significant reduction in GC risk (hazard ratio: 0.67; 95% CI: 0.47, 0.94). A 1-unit increase in the rMED score was associated with a decreased risk of GC of 5% (95% CI: 0.91, 0.99). There was no evidence of heterogeneity between different anatomic locations or histologic types. The calibrated results showed similar trends (overall hazard ratio for GC: 0.93; 95% CI: 0.89, 0.99).

    CONCLUSION: Greater adherence to an rMED is associated with a significant reduction in the risk of incident GC.

  • 31. Burgaz, Ann
    et al.
    Åkesson, Agneta
    Öster, Annette
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Wolk, Alicja
    Associations of diet, supplement use, and ultraviolet B radiation exposure with vitamin D status in Swedish women during winter2007In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 86, no 5, p. 1399-1404Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Vitamin D is produced endogenously after sun exposure but can also be obtained from natural food sources, food fortification, and dietary supplements. OBJECTIVE: We aimed to determine the vitamin D status of women (61-86 y old) living in central Sweden (latitude 60 degrees ) during winter and its relation with vitamin D intake and exposure to ultraviolet B radiation. DESIGN: In a cross-sectional study, we assessed the vitamin D status (serum 25-hydroxyvitamin D [25(OH)D]) of 116 women by using an enzyme immunoassay. The women completed questionnaires covering food habits, use of dietary supplements, and sun-related behavior. RESULTS: In a multiple linear regression model, the main determinants of serum 25(OH)D concentrations (x +/- SD: 69 +/- 23 mmol/L) were dietary vitamin D (6.0 +/- 1.8 mug/d), travel to a sunny location during winter within the previous 6 mo (26%), and the use of dietary supplements (16%). There was no association between serum 25(OH)D status during the winter and age, time spent outdoors, the use of sunscreen, or skin type. Serum 25(OH)D concentrations increased by 25.5 nmol/L with 2-3 servings (130 g/wk) fatty fish/wk, by 6.2 nmol/L with the daily intake of 300 g vitamin D-fortified reduced-fat dairy products, by 11.0 nmol/L with regular use of vitamin D supplements, and by 14.5 nmol/L with a sun vacation during winter. Among nonsupplement users without a wintertime sun vacation, 2-3 servings fatty fish/wk increased serum vitamin D concentrations by 45%. CONCLUSION: Fatty fish, vitamin D-fortified reduced-fat dairy products, regular supplement use, and taking a sun vacation are important predictors for serum concentrations of 25(OH)D during winter at a latitude of 60 degrees .

  • 32.
    Byberg, Liisa
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Kilander, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Warensjö Lemming, Eva
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Vessby, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Cancer death is related to high palmitoleic acid in serum and to polymorphisms in the SCD-1 gene in healthy Swedish men2014In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 99, no 3, p. 551-558Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    A high proportion of monounsaturated fatty acids (MUFAs) or a high ratio of MUFAs to saturated fatty acids in plasma, reflecting a high activity of the lipogenic enzyme stearoyl-CoA desaturase-1 (SCD-1), has been shown to be related to cancer death and incidence in some studies.

    OBJECTIVES:

    The objective was to study whether the serum cholesteryl ester proportion of palmitoleic acid [16:1n-7 (16:1ω-3)] and the ratio of palmitoleic to palmitic acid (16:1n-7/16:0), as an estimation of the activity of SCD-1, are related to cancer death and to investigate whether polymorphisms in the SCD-1 gene are related to cancer mortality.

    DESIGN:

    A community-based cohort of 50-y-old men was followed for a maximum of >40 y. Survival analysis was used to relate fatty acid composition in serum, analyzed at baseline by gas-liquid chromatography (n = 1981), and single nucleotide polymorphisms in the SCD-1 gene (n = 986) to cancer death. A 7-d dietary record was completed at age 70 y (n = 880).

    RESULTS:

    The proportions of 16:1n-7 and the ratio of 16:1n-7 to 16:0 were associated with cancer mortality during follow-up in a comparison of the highest with the lowest quartile of 16:1n-7 (adjusted HR: 1.37; 95% CI: 1.04, 1.82). Inherited variance of the SCD-1 gene seemed to be related to cancer death, especially among men with a low proportion of PUFA in the diet in a comparison of the highest with the lowest weighted genetic risk score (HR: 2.14; 95% CI: 1.13, 4.04).

    CONCLUSION:

    The findings are compatible with the hypothesis that there is an association between endogenously synthesized MUFAs and cancer death.

  • 33.
    Byberg, Liisa
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Olsson, Erika
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Karlström, Brita
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Cederholm, Tommy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Melhus, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical pharmacogenomics and osteoporosis.
    Sjögren, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Kilander, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Reply to WB Grant2017In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 106, no 2, p. 700-701Article in journal (Other academic)
  • 34.
    Byberg, Liisa
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Olsson, Erika
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Karlström, Brita
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Cederholm, Tommy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Melhus, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical pharmacogenomics and osteoporosis.
    Sjögren, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Kilander, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Reply to Y Mao and H Yu.2017In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 106, no 2, p. 698-699Article in journal (Other academic)
  • 35.
    Bälter, Katarina
    Mälardalen University, School of Health, Care and Social Welfare, Health and Welfare. Karolinska Institutet, Stockholm, Sweden.
    The importance of considering both nutrient quality and climate impact to support sustainable development2021In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 114, no 2, p. 412-413Article in journal (Refereed)
  • 36.
    Callahan, Emily A.
    et al.
    EAC Health and Nutrition, LLC, VA, United States.
    Chatila, Talal
    Boston Children's Hospital, MA, United States; Harvard Medical School, MA, United States.
    Deckelbaum, Richard J.
    Institute of Human Nutrition and Department of Pediatrics, Columbia University Irving Medical Center, NY, United States.
    Field, Catherine J.
    Department of Agricultural, Food & Nutritional Science, University of Alberta, AB, Canada.
    Greer, Frank R.
    Department of Pediatrics (Emeritus), University of Wisconsin, WI, United States.
    Hernell, Olle
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Järvinen, Kirsi M.
    Department of Pediatrics, University of Rochester Medical Center, NY, United States.
    Kleinman, Ronald E.
    Harvard Medical School, MA, United States; MassGeneral Hospital for Children, MA, United States; Massachusetts General Hospital, MA, United States.
    Milner, Joshua
    Department of Pediatrics, Columbia University Irving Medical Center, NY, United States.
    Neu, Josef
    Department of Pediatrics, University of Florida, FL, United States.
    Smolen, Kinga K.
    Boston Children's Hospital, MA, United States; Harvard Medical School, MA, United States.
    Wallingford, John C.
    LLC, WA, United States.
    Assessing the safety of bioactive ingredients in infant formula that affect the immune system: recommendations from an expert panel2022In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 115, no 2, p. 570-587Article in journal (Refereed)
    Abstract [en]

    Bioactive ingredients for infant formula have been sought to reduce disparities in health outcomes between breastfed and formula-fed infants. Traditional food safety methodologies have limited ability to assess some bioactive ingredients. It is difficult to assess the effects of nutrition on the infant immune system because of coincident developmental adaptations to birth, establishment of the microbiome and introduction to solid foods, and perinatal environmental factors. An expert panel was convened to review information on immune system development published since the 2004 Institute of Medicine report on evaluating the safety of new infant formula ingredients and to recommend measurements that demonstrate the safety of bioactive ingredients intended for that use. Panel members participated in a 2-d virtual symposium in November 2020 and in follow-up discussions throughout early 2021. Key topics included identification of immune system endpoints from nutritional intervention studies, effects of human milk feeding and human milk substances on infant health outcomes, ontologic development of the infant immune system, and microbial influences on tolerance. The panel explored how "nonnormal" conditions such as preterm birth, allergy, and genetic disorders could help define developmental immune markers for healthy term infants. With consideration of breastfed infants as a reference, ensuring proper control groups, and attention to numerous potential confounders, the panel recommended a set of standard clinical endpoints including growth, response to vaccination, infection and other adverse effects related to inflammation, and allergy and atopic diseases. It compiled a set of candidate markers to characterize stereotypical patterns of immune system development during infancy, but absence of reference ranges, variability in methods and populations, and unreliability of individual markers to predict disease prevented the panel from including many markers as safety endpoints. The panel's findings and recommendations are applicable for industry, regulatory, and academic settings, and will inform safety assessments for immunomodulatory ingredients in foods besides infant formula.

  • 37.
    Carlsson-Kanyama, Annika
    et al.
    KTH, School of Industrial Engineering and Management (ITM), Industrial Ecology.
    Gonzalez, A. D.
    Potential contributions of food consumption patterns to climate change2009In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 89, no 5, p. S1704-S1709Article in journal (Refereed)
    Abstract [en]

    Anthropogenic warming is caused mainly by emissions of greenhouse gases (GHGs), such as carbon dioxide, methane, and nitrous oxide, with agriculture as a main contributor for the latter 2 gases. Other parts of the food system contribute carbon dioxide emissions that emanate from the use of fossil fuels in transportation, processing, retailing, storage, and preparation. Food items differ substantially when GHG emissions are calculated from farm to table. A recent study of approximate to 20 items sold in Sweden showed a span of 0.4 to 30 kg CO2 equivalents/kg edible product. For protein-rich food, such as legumes, meat, fish, cheese, and eggs, the difference is a factor of 30 with the lowest emissions per kilogram for legumes, poultry, and eggs and the highest for beef, cheese, and pork. Large emissions for ruminants are explained mainly by methane emissions from enteric fermentation. For vegetables and fruits, emissions usually are <= 2.5 kg CO2 equivalents/kg product, even if there is a high degree of processing and substantial transportation. Products transported by plane are an exception because emissions may be as large as for certain meats. Emissions from foods rich in carbohydrates, such as potatoes, pasta, and wheat, are <1.1 kg/kg edible food. We suggest that changes in the diet toward more plant-based foods, toward meat from animals with little enteric fermentation, and toward foods processed in an energy-efficient manner offer an interesting and little explored area for mitigating climate change.

  • 38.
    Cedernaes, Jonathan
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
    Benedict, Christian
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
    Sleep duration and energy intake: timing matters2014In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 100, no 5, p. 1402-1403Article in journal (Other academic)
  • 39.
    Chapman, Colin Daniel
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
    Benedict, Christian
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
    Brooks, Samantha Jane
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
    Schiöth, Helgi Birgir
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
    Lifestyle determinants of the drive to eat: a meta-analysis2012In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 96, no 3, p. 492-497Article in journal (Refereed)
    Abstract [en]

    Background: Obesity is emerging as the most significant health concern of the 21st century. Although this is attributable in part to changes in our environment-including the increased prevalence of energy-dense food-it also appears that several lifestyle factors may increase our vulnerability to this calorie-rich landscape. Epidemiologic studies have begun to show links between adiposity and behaviors such as television watching, alcohol intake, and sleep deprivation. However, these studies leave unclear the direction of this association. In addition, studies that investigated the acute impact of these factors on food intake have reported a wide variety of effect sizes, from highly positive to slightly negative.

    Objective: The purpose of this article was to provide a meta-analysis of the relation between lifestyle choices and increases in acute food intake.

    Design: An initial search was performed on PubMed to collect articles relating television watching, sleep deprivation, and alcohol consumption to food intake. Only articles published before February 2012 were considered. Studies that took place in a controlled, laboratory setting with healthy individuals were included. Studies were analyzed by using 3 meta-analyses with random-effects models. In addition, a 1-factor ANOVA was run to discover any main effect of lifestyle.

    Results: The 3 most prominent lifestyle factors-television watching, alcohol intake, and sleep deprivation-had significant short-term effects on food intake, with alcohol being more significant (Cohen's d = 1.03) than sleep deprivation (Cohen's d = 0.49) and television watching (Cohen's d = 0.2).

    Conclusions: Our results suggest that television watching, alcohol intake, and sleep deprivation are not merely correlated with obesity but likely contribute to it by encouraging excessive eating. Because these behaviors are all known to affect cognitive functions involved in reward saliency and inhibitory control, it may be that they represent common mechanisms through which this eating is facilitated.

  • 40. Chuang, Shu-Chun
    et al.
    Norat, Teresa
    Murphy, Neil
    Olsen, Anja
    Tjonneland, Anne
    Overvad, Kim
    Boutron-Ruault, Marie Christine
    Perquier, Florence
    Dartois, Laureen
    Kaaks, Rudolf
    Teucher, Birgit
    Bergmann, Manuela M.
    Boeing, Heiner
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Grioni, Sara
    Sacerdote, Carlotta
    Panico, Salvatore
    Palli, Domenico
    Tumino, Rosario
    Peeters, Petra H. M.
    Bueno-de-Mesquita, Bas
    Ros, Martine M.
    Brustad, Magritt
    Asli, Lene Angell
    Skeie, Guri
    Quiros, J. Ramon
    Gonzalez, Carlos A.
    Sanchez, Maria-Jose
    Navarro, Carmen
    Aicua, Eva Ardanaz
    Dorronsoro, Miren
    Drake, Isabel
    Sonestedt, Emily
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology, Cariology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Key, Timothy
    Crowe, Francesca
    Khaw, Kay-Tee
    Wareham, Nicholas
    Ferrari, Pietro
    Slimani, Nadia
    Romieu, Isabelle
    Gallo, Valentina
    Riboli, Elio
    Vineis, Paolo
    Fiber intake and total and cause-specific mortality in the European Prospective Investigation into Cancer and Nutrition cohort2012In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 96, no 1, p. 164-174Article in journal (Refereed)
    Abstract [en]

    Background: Previous studies have shown that high fiber intake is associated with lower mortality. However, little is known about the association of dietary fiber with specific causes of death other than cardiovascular disease (CVD). Objective: The aim of this study was to assess the relation between fiber intake, mortality, and cause-specific mortality in a large European prospective study of 452,7 I 7 men and women. Design: HRs and 95% CIs were estimated by using Cox proportional hazards models, stratified by age, sex, and center and adjusted for education, smoking, alcohol consumption, BMI, physical activity, total energy intake, and, in women, ever use of menopausal hormone therapy. Results: During a mean follow-up of 12.7 y, a total of 23,582 deaths were recorded. Fiber intake was inversely associated with total mortality (HRper (10-g/d) (increase): 0.90; 95% Cl: 0.88, 0.92); with mortality from circulatory (HRper (10-g/d increase): 0.90 and 0.88 for men and women, respectively), digestive (HR: 0.61 and 0.64), respiratory (HR: 0.77 and 0.62), and non-CVD noncancer inflammatory (HR: 0.85 and 0.80) diseases; and with smoking-related cancers (HR: 0.86 and 0.89) but not with non-smoking-related cancers (HR: 1.05 and 0.97). The associations were more evident for fiber from cereals and vegetables than from fruit. The associations were similar across BMI and physical activity categories but were stronger in smokers and participants who consumed >18 g alcohol/d. Conclusions: Higher fiber intake is associated with lower mortality, particularly from circulatory, digestive, and non-CVD noncancer inflammatory diseases. Our results support current recommendations of high dietary fiber intake for health maintenance. Am J Clin Nutr 2012;96:164-74.

  • 41. Clasen, Joanna L.
    et al.
    Heath, Alicia K.
    Van Puyvelde, Heleen
    Huybrechts, Inge
    Park, Jin Young
    Ferrari, Pietro
    Johansson, Mattias
    Scelo, Ghislaine
    Ulvik, Arve
    Midttun, Øivind
    Ueland, Per Magne
    Dahm, Christina C.
    Halkjær, Jytte
    Olsen, Anja
    Johnson, Theron
    Katzke, Verena
    Schulze, Matthias B.
    Masala, Giovanna
    Segrado, Francesco
    de Magistris, Maria Santucci
    Sacerdote, Carlotta
    Ocké, Marga C.
    Luján-Barroso, Leila
    Ching-López, Ana
    Huerta, José María
    Ardanaz, Eva
    Amiano, Pilar
    Ericson, Ulrika
    Manjer, Jonas
    Gylling, Björn
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Schmidt, Julie
    Weiderpass, Elisabete
    Riboli, Elio
    Cross, Amanda J.
    Muller, David C.
    A comparison of complementary measures of vitamin B6 status, function, and metabolism in the European Prospective Investigation into Cancer and Nutrition (EPIC) study2021In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 114, no 1, p. 338-347Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Vitamin B6 insufficiency has been linked to increased risk of cancer and other chronic diseases. The circulating concentration of pyridoxal 5'-phosphate (PLP) is a commonly used measure of vitamin B6 status. Ratios of substrates indicating PLP coenzymatic function and metabolism may be useful complementary measures to further explore the role of vitamin B6 in health.

    OBJECTIVES: We explored the sensitivity of 5 outcomes, namely PLP concentration, homocysteine:cysteine (Hcy:Cys), cystathionine:cysteine (Cysta:Cys), the 3´-hydroxykynurenine ratio (HKr), and the 4-pyridoxic acid ratio (PAr) to vitamin B6 intake as well as personal and lifestyle characteristics.

    MEDTHODS: Dietary intake and biomarker data were collected from participants from 3 nested case-control studies within the European Prospective Investigation into Cancer and Nutrition (EPIC). Bayesian regression models assessed the associations of the 5 biomarker outcomes with vitamin B6 intake and personal and lifestyle covariates. Analogous models examined the relations of Hcy:Cys, Cysta:Cys, and HKr with PLP.

    RESULTS: In total, 4608 participants were included in the analyses. Vitamin B6 intake was most strongly associated with PLP, moderately associated with Hcy:Cys, Cysta:Cys, and HKr, and not associated with PAr (fold change in marker given a doubling of vitamin B6 intake: PLP 1.60 [95% credible interval (CrI): 1.50, 1.71]; Hcy:Cys 0.87 [95% CrI: 0.84, 0.90]; Cysta:Cys 0.89 [95% CrI: 0.84, 0.94]; HKr 0.88 [95% CrI: 0.85, 0.91]; PAr 1.00 [95% CrI: 0.95, 1.05]). PAr was most sensitive to age, and HKr was least sensitive to BMI and alcohol intake. Sex and menopause status were strongly associated with all 5 markers.

    CONCLUSIONS: We found that 5 different markers, capturing different aspects of vitamin B6-related biological processes, varied in their associations with vitamin B6 intake and personal and lifestyle predictors.

    Download full text (pdf)
    fulltext
  • 42. Dahm, Christina C.
    et al.
    Gorst-Rasmussen, Anders
    Crowe, Francesca L.
    Roswall, Nina
    Tjonneland, Anne
    Drogan, Dagmar
    Boeing, Heiner
    Teucher, Birgit
    Kaaks, Rudolf
    Adarakis, George
    Zylis, Dimosthenes
    Trichopoulou, Antonia
    Fedirko, Veronika
    Chajes, Veronique
    Jenab, Mazda
    Palli, Domenico
    Pala, Valeria
    Tumino, Rosario
    Ricceri, Fulvio
    van Kranen, Henk
    Bueno-de-Mesquita, H. Bas
    Quiros, Jose R.
    Sanchez, Maria-Jose
    Lujan-Barroso, Leila
    Larranaga, Nerea
    Chirlaque, Maria-Dolores
    Ardanaz, Eva
    Johansson, Mattias
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. The Nutrition and Metabolism Section, International Agency for Research on Cancer, Lyon, France.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Khaw, Kay-Tee
    Wareham, Nick
    Wark, Petra A.
    Norat, Teresa
    Riboli, Elio
    Key, Tim J.
    Overvad, Kim
    Fatty acid patterns and risk of prostate cancer in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition2012In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 96, no 6, p. 1354-1361Article in journal (Refereed)
    Abstract [en]

    Background: Fatty acids in blood may be related to the risk of prostate cancer, but epidemiologic evidence is inconsistent. Blood fatty acids are correlated through shared food sources and common endogenous desaturation and elongation pathways. Studies of individual fatty acids cannot take this into account, but pattern analysis can. Treelet transform (TT) is a novel method that uses data correlation structures to derive sparse factors that explain variation. Objective: The objective was to gain further insight in the association between plasma fatty acids and risk of prostate cancer by applying TT to take data correlations into account. Design: We reanalyzed previously published data from a case-control study of prostate cancer nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. TT was used to derive factors explaining the variation in 26 plasma phospholipid fatty acids of 962 incident prostate cancer cases matched to 1061 controls. Multiple imputation was used to deal with missing data in covariates. ORs of prostate cancer according to factor scores were determined by using multivariable conditional logistic regression. Results: Four simple factors explained 38% of the variation in plasma fatty acids. A high score on a factor reflecting a long-chain n-3 PUFA pattern was associated with greater risk of prostate cancer (OR for highest compared with lowest quintile: 1.36; 95% CI: 0.99, 1.86; P-trend = 0.041). Conclusion: Pattern analyses using TT groupings of correlated fatty acids indicate that intake or metabolism of long-chain n-3 PUFAs may be relevant to prostate cancer etiology. Am J Clin Nutr 2012;96:1354-61.

  • 43.
    Dai, Lu
    et al.
    Stockholm University, Faculty of Social Sciences, Aging Research Center (ARC), (together with KI).
    Massy, Ziad A.
    Stenvinkel, Peter
    Chesnaye, Nicholas C.
    Larabi, Islam Amine
    Alvarez, Jean Claude
    Caskey, Fergus J.
    Torino, Claudia
    Porto, Gaetana
    Szymczak, Maciej
    Krajewska, Magdalena
    Drechsler, Christiane
    Wanner, Christoph
    Jager, Kitty J.
    Dekker, Friedo W.
    Evenepoel, Pieter
    Evans, Marie
    The association between TMAO, CMPF, and clinical outcomes in advanced chronic kidney disease: results from the European QUALity (EQUAL) Study2022In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 116, no 6, p. 1842-1851Article in journal (Refereed)
    Abstract [en]

    Background: Trimethylamine N-oxide (TMAO), a metabolite from red meat and fish consumption, plays a role in promoting cardiovascular events. However, data regarding TMAO and its impact on clinical outcomes are inconclusive, possibly due to its undetermined dietary source.

    Objectives: We hypothesized that circulating TMAO derived from fish intake might cause less harm compared with red meat sources by examining the concomitant level of 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF), a known biomarker of fish intake, and investigated the association between TMAO, CMPF, and outcomes.

    Methods: Patients were recruited from the European QUALity (EQUAL) Study on treatment in advanced chronic kidney disease among individuals aged ≥65 y whose estimated glomerular filtration rate (eGFR) had dropped for the first time to ≤20 mL/min per 1.73 m2 during the last 6 mo. The association between TMAO, CMPF, and outcomes including all-cause mortality and kidney replacement therapy (KRT) was assessed among 737 patients. Patients were further stratified by median cutoffs of TMAO and CMPF, suggesting high/low red meat and fish intake.

    Results: During a median of 39 mo of follow-up, 232 patients died. Higher TMAO was independently associated with an increased risk of all-cause mortality (multivariable HR: 1.46; 95% CI: 1.17, 1.83). Higher CMPF was associated with a reduced risk of both all-cause mortality (HR: 0.79; 95% CI: 0.71, 0.89) and KRT (HR: 0.80; 95% CI: 0.71, 0.90), independently of TMAO and other clinically relevant confounders. In comparison to patients with low TMAO and CMPF, patients with low TMAO and high CMPF had reduced risk of all-cause mortality (adjusted HR: 0.49; 95% CI: 0.31, 0.73), whereas those with high TMAO and high CMPF showed no association across adjusted models.

    Conclusions: High CMPF conferred an independent role in health benefits and might even counteract the unfavorable association between TMAO and outcomes. Whether higher circulating CMPF concentrations are due to fish consumption, and/or if CMPF is a protective factor, remains to be verified.

  • 44.
    Delisle Nyström, Christine
    et al.
    Karolinska Institute, Sweden.
    Sandin, Sven
    Karolinska Institute, Sweden; Icahn School Medical Mt Sinai, NY 10029 USA; Icahn School Medical Mt Sinai, NY 10029 USA.
    Henriksson, Pontus
    University of Granada, Spain.
    Henriksson, Hanna
    University of Granada, Spain.
    Trolle-Lagerros, Ylva
    Karolinska Institute, Sweden; Karolinska University Hospital, Sweden.
    Larsson, Christel
    University of Gothenburg, Sweden.
    Maddison, Ralph
    Deakin University, Australia.
    Ortega, Francisco B.
    University of Granada, Spain.
    Pomeroy, Jeremy
    Marshfield Clin Research Fdn, WI USA.
    Ruiz, Jonatan R.
    University of Granada, Spain.
    Silfvernagel, Kristin
    Linköping University, Department of Behavioural Sciences and Learning, Psychology. Linköping University, Faculty of Arts and Sciences.
    Timpka, Toomas
    Linköping University, Department of Medical and Health Sciences, Division of Community Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Business support and Development, Department of Health and Care Development.
    Löf, Marie
    Karolinska Institute, Sweden.
    Mobile-based intervention intended to stop obesity in preschool-aged children: the MINISTOP randomized controlled trial2017In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 105, no 6, p. 1327-1335Article in journal (Refereed)
    Abstract [en]

    Background: Traditional obesity prevention programs are time-and cost-intensive. Mobile phone technology has been successful in changing behaviors and managing weight; however, to our knowledge, its potential in young children has yet to be examined. Objective: We assessed the effectiveness of a mobile health (mHealth) obesity prevention program on body fat, dietary habits, and physical activity in healthy Swedish children aged 4.5 y. Design: From 2014 to 2015, 315 children were randomly assigned to an intervention or control group. Parents in the intervention group received a 6-mo mHealth program. The primary outcome was fat mass index (FMI), whereas the secondary outcomes were intakes of fruits, vegetables, candy, and sweetened beverages and time spent sedentary and in moderate-to-vigorous physical activity. Composite scores for the primary and secondary outcomes were computed. Results: No statistically significant intervention effect was observed for FMI between the intervention and control group (mean +/- SD: -0.23 +/- 0.56 compared with -0.20 +/- 0.49 kg/m(2)). However, the intervention group increased their mean composite score from baseline to follow-up, whereas the control group did not (+ 0.36 +/- 1.47 compared with -0.06 +/- 1.33 units; P = 0.021). This improvement was more pronounced among the children with an FMI above the median (4.11 kg/m(2)) (P = 0.019). The odds of increasing the composite score for the 6 dietary and physical activity behaviors were 99% higher for the intervention group than the control group (P = 0.008). Conclusions: This mHealth obesity prevention study in preschool-aged children found no difference between the intervention and control group for FMI. However, the intervention group showed a considerably higher postintervention composite score (a secondary outcome) than the control group, especially in children with a higher FMI. Further studies targeting specific obesity classes within preschool-aged children are warranted.

  • 45.
    den Hoed, Marcel
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology.
    Brage, Soren
    Zhao, Jing Hua
    Westgate, Kate
    Nessa, Ayrun
    Ekelund, Ulf
    Spector, Tim D.
    Wareham, Nicholas J.
    Loos, Ruth J. F.
    Heritability of objectively assessed daily physical activity and sedentary behavior2013In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 98, no 5, p. 1317-1325Article in journal (Refereed)
    Abstract [en]

    Background: Twin and family studies that estimated the heritability of daily physical activity have been limited by poor measurement quality and a small sample size. Objective: We examined the heritability of daily physical activity and sedentary behavior assessed objectively by using combined heart rate and movement sensing in a large twin study. Design: Physical activity traits were assessed in daily life for a mean (+/- SD) 6.7 +/- 1.1 d in 1654 twins from 420 monozygotic and 352 dizygotic same-sex twin pairs aged 56.3 +/- 10.4 y with body mass index (in kg/m(2)) of 26.1 +/- 4.8. We estimated the average daily movement, physical activity energy expenditure, and time spent in moderate-to-vigorous intensity physical activity and sedentary behavior from heart rate and acceleration data. We used structural equation modeling to examine the contribution of additive genetic, shared environmental, and unique environmental factors to between-individual variation in traits. Results: Additive genetic factors (le, heritability) explained 47% of the variance in physical activity energy expenditure (95% CI: 23%, 53%) and time spent in moderate-to-vigorous intensity physical activity (95% CI: 29%, 54%), 35% of the variance in acceleration of the trunk (95% CI: 0%, 44%), and 31% of the variance in the time spent in sedentary behavior (95% CI: 9%, 51%). The remaining variance was predominantly explained by unique environmental factors and random error, whereas shared environmental factors played only a marginal role for all traits with a range of 0-15%. Conclusions: The between-individual variation in daily physical activity and sedentary behavior is mainly a result of environmental influences. Nevertheless, genetic factors explain up to one-half of the variance, suggesting that innate biological processes may be driving some of our daily physical activity.

  • 46. den Hoed, Marcel
    et al.
    Westerterp-Plantenga, Margriet S
    Bouwman, Freek G
    Mariman, Edwin C M
    Westerterp, Klaas R
    Postprandial responses in hunger and satiety are associated with the rs9939609 single nucleotide polymorphism in FTO.2009In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 90, no 5Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The common rs9939609 single nucleotide polymorphism (SNP) in the fat mass and obesity-associated (FTO) gene is associated with adiposity, possibly by affecting satiety responsiveness.

    OBJECTIVE: The objective was to determine whether postprandial responses in hunger and satiety are associated with rs9939609, taking interactions with other relevant candidate genes into account.

    DESIGN: Sixty-two women and 41 men [age: 31 +/- 14 y; body mass index (in kg/m(2)): 25.0 +/- 3.1] were genotyped for 5 SNPs in FTO, DNMT1, DNMT3B, LEP, and LEPR. Individuals received fixed meals provided in energy balance. Hunger and satiety were determined pre- and postprandially by using visual analog scales.

    RESULTS: A general association test showed a significant association between postprandial responses in hunger and satiety with rs9939609 (P = 0.036 and P = 0.050, respectively). Individuals with low postprandial responses in hunger and satiety were overrepresented among TA/AA carriers in rs9939609 (FTO) compared with TT carriers (dominant and additive model: P = 0.013 and P = 0.020, respectively). Moreover, multifactor dimensionality reduction showed significant epistatic interactions for the postprandial decrease in hunger involving rs9939609 (FTO), rs992472 (DNMT3B), and rs1137101 (LEPR). Individuals with a low postprandial decrease in hunger were overrepresented among TA/AA (dominant), CC/CA (recessive), and AG/GG (dominant) carriers in rs9939609 (FTO), rs992472 (DNMT3B), and rs1137101 (LEPR), respectively (n = 39), compared with TT, AA, and/or AA carriers in these SNPs, respectively (P = 0.00001). Each SNP had an additional effect.

    CONCLUSIONS: Our results confirm a role for FTO in responsiveness to hunger and satiety cues in adults in an experimental setting. The epistatic interaction suggests that DNA methylation, an epigenetic process, affects appetite.

  • 47. Dixon, L Beth
    et al.
    Balder, Helena F
    Virtanen, Mikko J
    Rashidkhani, Bahram
    Männistö, Satu
    Krogh, Vittorio
    van Den Brandt, Piet A
    Hartman, Anne M
    Pietinen, Pirjo
    Tan, Frans
    Virtamo, Jarmo
    Wolk, Alicja
    Goldbohm, R Alexandra
    Dietary patterns associated with colon and rectal cancer: results from the Dietary Patterns and Cancer (DIETSCAN) Project2004In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 80, no 4, p. 1003-11Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: An analysis of dietary patterns or combinations of foods may provide insight regarding the influence of diet on the risk of colon and rectal cancer.

    OBJECTIVE: A primary aim of the Dietary Patterns and Cancer (DIETSCAN) Project was to develop and apply a common methodologic approach to study dietary patterns and cancer in 4 European cohorts: the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study (Finland-ATBC), the Netherlands Cohort Study (NLCS) on Diet and Cancer, the Swedish Mammography Cohort (SMC), and the Ormoni e Dieta nella Eziologia dei Tumori (Italy-ORDET). Three cohorts (ATBC, NLCS, and SMC) provided data on colon and rectal cancer for the present study.

    DESIGN: The cohorts were established between 1985 and 1992; follow-up data were obtained from national cancer registries. The participants completed validated semiquantitative food-frequency questionnaires at baseline.

    RESULTS: Exploratory factor analysis, conducted within each cohort, identified 3-5 stable dietary patterns. Two dietary patterns-Vegetables and Pork, Processed Meats, Potatoes (PPP)-were common across all cohorts. After adjustment for potential confounders, PPP was associated with an increased risk of colon cancer in the SMC women (quintile 4(multivariate) relative risk: 1.62; 95% CI: 1.12, 2.34; P for trend = 0.01). PPP was also associated with an increased risk of rectal cancer in the ATBC men (quintile 4(multivariate) relative risk: 2.21; 95% CI: 1.07, 4.57; P for trend = 0.05). Neither pattern was associated with the risk of colon or rectal cancer in the NLCS women and men.

    CONCLUSION: Although certain dietary patterns may be consistent across European countries, associations between these dietary patterns and the risk of colon and rectal cancer are not conclusive.

  • 48.
    Domellöf, Magnus
    et al.
    Umeå University, Faculty of Medicine, Clinical Sciences, Paediatrics.
    Hernell, Olle
    Umeå University, Faculty of Medicine, Clinical Sciences, Paediatrics.
    Abrams, Steven A
    Chen, Zhensheng
    Lönnerdal, Bo
    Iron supplementation does not affect copper and zinc absorption in breastfed infants.2009In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 89, no 1, p. 185-190Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Iron supplements are commonly recommended for infants but were suggested to inhibit zinc and copper absorption. OBJECTIVE: The objective of this study was to investigate potential effects of iron supplementation, infant age, and mineral status on zinc and copper absorption in infants at 6 and 9 mo of age. DESIGN: Twenty-five healthy breastfed term infants were recruited from a larger randomized iron supplementation trial. Six of these infants received iron supplements (1 mg . kg(-1) . d(-1)) from 4 to 9 mo, 8 were supplemented from 6 to 9 mo, and 11 received placebo only. Zinc and copper absorption was measured at 6 and 9 mo of age, using orally administered (70)Zn and (65)Cu and fecal monitoring of recovered stable isotopes. RESULTS: Mean (+/-SD) zinc absorption was 51.9 +/- 17.9%, and mean copper absorption was 79.0 +/- 13.5%. No significant difference was observed in zinc or copper absorption between 6 and 9 mo of age. When combining all measurements, no significant effect of prior iron supplementation was observed on zinc or copper absorption. No significant correlation was observed between plasma zinc and zinc absorption or between plasma copper and copper absorption. No significant correlation was observed between erythrocyte copper-zinc-dependent superoxide dismutase activity and copper absorption. CONCLUSIONS: The study does not support the contention that iron supplements inhibit the absorption of zinc or copper in healthy breastfed infants at 6-9 mo of age. In addition, we did not find any age-related changes in zinc or copper absorption between 6 and 9 mo of age.

  • 49.
    Domellöf, Magnus
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Lönnerdal, Bo
    Abrams, Steven A
    Hernell, Olle
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Iron absorption in breast-fed infants: effects of age, iron status, iron supplements, and complementary foods.2002In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 76, no 1, p. 198-204Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Iron supplements are often recommended for older breast-fed infants, but little is known about factors affecting iron absorption from human milk or supplements. OBJECTIVE: We investigated the effects of age, iron status, and iron intake on iron absorption in healthy, term, breast-fed infants. DESIGN: Twenty-five infants were randomly assigned to receive either 1) iron supplements (1 mg x kg(-1) x d(-1)) from 4 to 9 mo of age, 2) placebo from 4 to 6 mo and iron supplements from 6 to 9 mo, or 3) placebo from 4 to 9 mo. Infants were exclusively breast-fed to 6 mo and partially breast-fed to 9 mo of age. Iron absorption was assessed by giving (58)Fe with mother's milk at 6 and 9 mo. Blood samples were obtained at 4, 6, and 9 mo, and complementary food intake was recorded at 9 mo. RESULTS: At 6 mo, mean (+/-SD) fractional iron absorption from human milk was relatively low (16.4 +/- 11.4%), with no significant difference between iron-supplemented and unsupplemented infants. At 9 mo, iron absorption from human milk remained low in iron-supplemented infants (16.9 +/- 9.3%) but was higher (P = 0.01) in unsupplemented infants (36.7 +/- 18.9%). Unexpectedly, iron absorption at 9 mo was not correlated with iron status but was significantly correlated with intake of dietary iron, including supplemental iron. CONCLUSIONS: Changes in the regulation of iron absorption between 6 and 9 mo enhance the infant's ability to adapt to a low-iron diet and provide a mechanism by which some, but not all, infants avoid iron deficiency despite low iron intakes in late infancy.

  • 50. Duell, Eric J
    et al.
    Travier, Noémie
    Lujan-Barroso, Leila
    Clavel-Chapelon, Françoise
    Boutron-Ruault, Marie-Christine
    Morois, Sophie
    Palli, Domenico
    Krogh, Vittorio
    Panico, Salvatore
    Tumino, Rosario
    Sacerdote, Carlotta
    Quirós, J Ramón
    Sánchez-Cantalejo, Emilio
    Navarro, Carmen
    Gurrea, Aurelio Barricarte
    Dorronsoro, Miren
    Khaw, Kay-Tee
    Allen, Naomi E
    Key, Timothy J
    Bueno-de-Mesquita, H Bas
    Ros, Martine M
    Numans, Mattijs E
    Peeters, Petra Hm
    Trichopoulou, Antonia
    Naska, Androniki
    Dilis, Vardis
    Teucher, Birgit
    Kaaks, Rudolf
    Boeing, Heiner
    Schütze, Madlen
    Regner, Sara
    Lindkvist, Björn
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Overvad, Kim
    Umeå University, Faculty of Medicine, Department of Medical Biosciences.
    Egeberg, Rikke
    Tjønneland, Anne
    Lund, Eiliv
    Weiderpass, Elisabete
    Braaten, Tonje
    Romieu, Isabelle
    Ferrari, Pietro
    Jenab, Mazda
    Stenling, Roger
    Umeå University, Faculty of Medicine, Department of Medical Biosciences.
    Aune, Dagfinn
    Norat, Teresa
    Riboli, Elio
    González, Carlos A
    Alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.2011In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 94, no 5, p. 1266-75Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Gastric cancer (GC) is the second leading cause of cancer death worldwide. The association between alcohol consumption and GC has been investigated in numerous epidemiologic studies with inconsistent results.

    OBJECTIVE: We evaluated the association between alcohol consumption and GC risk.

    DESIGN: We conducted a prospective analysis in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, which included 444 cases of first primary gastric adenocarcinoma. HRs and 95% CIs for GC were estimated by using multivariable Cox proportional hazards regression for consumption of pure ethanol in grams per day, with stratification by smoking status, anatomic subsite (cardia, noncardia), and histologic subtype (diffuse, intestinal). In a subset of participants, results were further adjusted for baseline Helicobacter pylori serostatus.

    RESULTS: Heavy (compared with very light) alcohol consumption (≥60 compared with 0.1-4.9 g/d) at baseline was positively associated with GC risk (HR: 1.65; 95% CI: 1.06, 2.58), whereas lower consumption amounts (<60 g/d) were not. When we analyzed GC risk by type of alcoholic beverage, there was a positive association for beer (≥30 g/d; HR: 1.75; 95% CI: 1.13, 2.73) but not for wine or liquor. Associations were primarily observed at the highest amounts of drinking in men and limited to noncardia subsite and intestinal histology; no statistically significant linear dose-response trends with GC risk were observed.

    CONCLUSION: Heavy (but not light or moderate) consumption of alcohol at baseline (mainly from beer) is associated with intestinal-type noncardia GC risk in men from the EPIC cohort.

123456 1 - 50 of 274
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf