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  • 1.
    Adamsson, Viola
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Reumark, Anna
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Biochemial structure and function.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Role of a prudent breakfast in improving cardiometabolic risk factors in subjects with hypercholesterolemia: A randomized controlled trial2015In: Clinical Nutrition, ISSN 0261-5614, E-ISSN 1532-1983, Vol. 34, no 1, p. 20-26Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS:

    It is unclear whether advising a prudent breakfast alone is sufficient to improve blood lipids and cardiometabolic risk factors in overweight hypercholesterolemic subjects. The aim of this study was to investigate whether a prudent low-fat breakfast (PB) rich in dietary fiber lowers low-density lipoprotein cholesterol (LDL-C) and other cardiometabolic risk factors in subjects with elevated LDL-cholesterol levels.

    METHODS:

    In a parallel, controlled, 12-week study, 79 healthy overweight subjects (all regular breakfast eaters) were randomly allocated to a group that received a PB based on Nordic foods provided ad libitum or a control group that consumed their usual breakfast. The primary outcome was plasma LDL-C. Secondary outcomes were other blood lipids, body weight, sagittal abdominal diameter (SAD), glucose tolerance, insulin sensitivity and inflammation markers (C-reactive protein [CRP] and tumor necrosis factor receptor-2 [TNF-R2]), and blood pressure. The PB was in accordance with national and Nordic nutrition recommendations and included oat bran porridge with low-fat milk or yogurt, bilberry or lingonberry jam, whole grain bread, low-fat spread, poultry or fatty fish, and fruit.

    RESULTS:

    No differences were found in LDL-C, other blood lipids, body weight, or glucose metabolism, but SAD, plasma CRP, and TNF-R2 decreased more during PB compared with controls (p < 0.05). In the overall diet, PB increased dietary fiber and β-glucan compared with controls (p < 0.05).

    CONCLUSIONS:

    Advising a prudent breakfast for 3 months did not influence blood lipids, body weight, or glucose metabolism but reduced markers of visceral fat and inflammation. The trial was registered in the Current Controlled Trials database (http://www.controlled-trials.com); International Standard Randomized Controlled Trial Number (ISRCTN): 84550872.

  • 2.
    Alsharari, Zayed
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Hellenius, Mai-Lis
    Karolinska Inst, Inst Environm Med, Cardiovasc Epidemiol Unit, S-10401 Stockholm, Sweden..
    Laguzzi, Federica
    Karolinska Inst, Inst Environm Med, Cardiovasc Epidemiol Unit, S-10401 Stockholm, Sweden..
    Gigante, Bruna
    Karolinska Inst, Inst Environm Med, Cardiovasc Epidemiol Unit, S-10401 Stockholm, Sweden..
    Leander, Karen
    Karolinska Inst, Inst Environm Med, Cardiovasc Epidemiol Unit, S-10401 Stockholm, Sweden..
    Sjögren, Per
    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.
    de Faire, Ulf
    Karolinska Inst, Inst Environm Med, Cardiovasc Epidemiol Unit, S-10401 Stockholm, Sweden..
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Serum Biomarkers of Dietary Fatty Acids are Associated with Abdominal Obesity Measures in a Large Population-based Cohort of Men and Women2015In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 29, no 1 SupplementArticle in journal (Other academic)
  • 3.
    Alsharari, Zayed
    et al.
    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.
    Leander, Karin
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden..
    Sjögren, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Carlsson, Axel C.
    Karolinska Inst, Div Family Med, Dept Neurobiol Care Sci & Soc, Stockholm, Sweden..
    Vikstrom, Max
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden..
    Laguzzi, Federica
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden..
    Gigante, Bruna
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden.;Karolinska Inst, Danderyds Hosp, Div Cardiovasc Med, Dept Clin Sci, Stockholm, Sweden..
    Cederholm, Tommy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    De Faire, Ulf
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden.;Karolinska Univ Hosp, Karolinska Inst, Dept Med, Cardiol Unit, Stockholm, Sweden..
    Hellenius, Mai-Lis
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Cardiol Unit, Stockholm, Sweden..
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Serum Fatty Acids, Desaturase Activities and Abdominal Obesity - A Population-Based Study of 60-Year Old Men and Women2017In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, no 1, article id e0170684Article in journal (Refereed)
    Abstract [en]

    Abdominal obesity is a key contributor of metabolic disease. Recent trials suggest that dietary fat quality affects abdominal fat content, where palmitic acid and linoleic acid influence abdominal obesity differently, while effects of n-3 polyunsaturated fatty acids are less studied. Also, fatty acid desaturation may be altered in abdominal obesity. We aimed to investigate cross-sectional associations of serum fatty acids and desaturases with abdominal obesity prevalence in a population-based cohort study. Serum cholesteryl ester fatty acids composition was measured by gas chromatography in 60-year old men (n = 1883) and women (n = 2015). Cross-sectional associations of fatty acids with abdominal obesity prevalence and anthropometric measures (e.g., sagittal abdominal diameter) were evaluated in multivariable-adjusted logistic and linear regression models, respectively. Similar models were employed to investigate relations between desaturase activities (estimated by fatty acid ratios) and abdominal obesity. In logistic regression analyses, palmitic acid, stearoyl-CoA- desaturase and Delta 6-desaturase indices were associated with abdominal obesity; multivariable-adjusted odds ratios (95% confidence intervals) for highest versus lowest quartiles were 1.45 (1.19-1.76), 4.06 (3.27-5.05), and 3.07 (2.51-3.75), respectively. Linoleic acid, alpha-linolenic acid, docohexaenoic acid, and Delta 5-desaturase were inversely associated with abdominal obesity; multivariable-adjusted odds ratios (95% confidence intervals): 0.39 (0.32-0.48), 0.74 (0.61-0.89), 0.76 (0.62-0.93), and 0.40 (0.33-0.49), respectively. Eicosapentaenoic acid was not associated with abdominal obesity. Similar results were obtained from linear regression models evaluating associations with different anthropometric measures. Sex-specific and linear associations were mainly observed for n3-polyunsaturated fatty acids, while associations of the other exposures were generally non-linear and similar across sexes. In accordance with findings from short-term trials, abdominal obesity was more common among individuals with relatively high proportions of palmitic acid, whilst the contrary was true for linoleic acid. Further trials should examine the potential role of linoleic acid and its main dietary source, vegetable oils, in abdominal obesity prevention.

  • 4.
    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)
  • 5.
    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.

  • 6.
    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)
  • 7.
    Fretts, Amanda M.
    et al.
    Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA;Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
    Imamura, Fumiaki
    Univ Cambridge, MRC Epidemiol Unit, Cambridge, England.
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Micha, Renata
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
    Wu, Jason H. Y.
    Univ New South Wales, George Inst Global Hlth, Fac Med, Sydney, NSW, Australia.
    Murphy, Rachel A.
    Univ British Columbia, Sch Populat & Publ Hlth, Vancouver, BC, Canada.
    Chien, Kuo-Liong
    Natl Taiwan Univ, Inst Epidemiol & Prevent Med, Coll Publ Hlth, Taipei, Taiwan;Natl Taiwan Univ Hosp, Dept Internal Med, Taipei, Taiwan.
    McKnight, Barbara
    Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA;Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
    Tintle, Nathan
    Dordt Coll, Dept Stat, Sioux Ctr, IA USA.
    Forouhi, Nita G.
    Univ Cambridge, MRC Epidemiol Unit, Cambridge, England.
    Qureshi, Waqas T.
    Wake Forest Univ, Bowman Gray Sch Med, Div Cardiovasc Med, Winston Salem, NC USA;Wake Forest Univ, Bowman Gray Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
    Virtanen, Jyrki K.
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    Wong, Kerry
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia.
    Wood, Alexis C.
    Baylor Coll Med, USDA, ARS, Childrens Nutr Res Ctr, Houston, TX 77030 USA.
    Lankinen, Maria
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    Rajaobelina, Kalina
    Univ Bordeaux, Bordeaux Populat Hlth Res Ctr, INSERM, Bordeaux, France.
    Harris, Tamara B.
    NIA, NIH, Bethesda, MD 20892 USA.
    Djousse, Luc
    Brigham & Womens Hosp, Dept Med, Div Aging, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA 02115 USA.
    Harris, Bill
    OmegaQuant Analyt, Sioux Falls, SD USA;Univ South Dakota, Dept Internal Med, Sanford Sch Med, Vermillion, SD USA.
    Wareham, Nick J.
    Univ Cambridge, MRC Epidemiol Unit, Cambridge, England.
    Steffen, Lyn M.
    Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
    Laakso, Markku
    Univ Eastern Finland, Inst Clin Med, Internal Med, Kuopio, Finland.
    Veenstra, Jenna
    Dordt Coll, Dept Biol, Sioux Ctr, IA USA.
    Samieri, Cecilia
    Univ Bordeaux, Bordeaux Populat Hlth Res Ctr, INSERM, Bordeaux, France.
    Brouwer, Ingeborg A.
    Vrije Univ Amsterdam, Dept Hlth Sci, Fac Sci, Amsterdam, Netherlands.
    Yu, Chaoyu Ian
    Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
    Koulman, Albert
    Univ Cambridge, MRC Epidemiol Unit, Cambridge, England;Univ Cambridge, Natl Inst Hlth Res Biomed Res Ctr Core Nutr Bioma, Addenbrookes Hosp, Cambridge, England;Univ Cambridge, Natl Inst Hlth Res Biomed Res Ctr Core Metab & Li, Addenbrookes Hosp, Cambridge, England;Med Res Council ElsieWiddowson Lab, Cambridge, England.
    Steffen, Brian T.
    Univ Minnesota, Lab Med & Pathol, Minneapolis, MN USA.
    Helmer, Catherine
    Univ Bordeaux, Bordeaux Populat Hlth Res Ctr, INSERM, Bordeaux, France.
    Sotoodehnia, Nona
    Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA;Univ Washington, Dept Med, Seattle, WA USA.
    Siscovick, David
    New York Acad Med, New York, NY USA.
    Gudnason, Vilmundur
    Iceland Heart Assoc, Kopavogur, Iceland;Univ Iceland, Fac Med, Reyjavik, Iceland.
    Consortium, InterAct
    Univ Cambridge, MRC Epidemiol Unit, Cambridge, England.
    Wagenknecht, Lynne
    Wake Forest Univ, Bowman Gray Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
    Voutilainen, Sari
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    Tsai, Michael Y.
    Univ Minnesota, Lab Med & Pathol, Minneapolis, MN USA.
    Uusitupa, Matti
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    Kalsbeek, Anya
    Dordt Coll, Dept Biol, Sioux Ctr, IA USA.
    Berr, Claudine
    Univ Montpellier, Inserm, Neuropsychiat Epidemiol & Clin Res, Montpellier, France;Montpellier Univ Hosp, Memory Res & Resources Ctr, Dept Neurol, Montpellier, France.
    Mozaffarian, Dariush
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
    Lemaitre, Rozenn N.
    Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA;Univ Washington, Dept Med, Seattle, WA USA.
    Associations of circulating very-long-chain saturated fatty acids and incident type 2 diabetes: a pooled analysis of prospective cohort studies2019In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 109, no 4, p. 1216-1223Article in journal (Refereed)
    Abstract [en]

    Background: Saturated fatty acids (SFAs) of different chain lengths have unique metabolic and biological effects, and a small number of recent studies suggest that higher circulating concentrations of the very-long-chain SFAs (VLSFAs) arachidic acid (20:0), behenic acid (22:0), and lignoceric acid (24:0) are associated with a lower risk of diabetes. Confirmation of these findings in a large and diverse population is needed.

    Objective: We investigated the associations of circulating VLSFAs 20:0, 22:0, and 24:0 with incident type 2 diabetes in prospective studies.

    Methods: Twelve studies that are part of the Fatty Acids and Outcomes Research Consortium participated in the analysis. Using Cox or logistic regression within studies and an inverse-variance-weighted meta-analysis across studies, we examined the associations of VLSFAs 20:0, 22:0, and 24:0 with incident diabetes among 51,431 participants.

    Results: There were 14,276 cases of incident diabetes across participating studies. Higher circulating concentrations of 20:0, 22:0, and 24:0 were each associated with a lower risk of incident diabetes. Pooling across cohorts, the RR (95% CI) for incident diabetes comparing the 90th percentile to the 10th percentile was 0.78 (0.70, 0.87) for 20:0, 0.84 (0.77, 0.91) for 22:0, and 0.75 (0.69, 0.83) for 24:0 after adjustment for demographic, lifestyle, adiposity, and other health factors. Results were fully attenuated in exploratory models that adjusted for circulating 16:0 and triglycerides.

    Conclusions: Results from this pooled analysis indicate that higher concentrations of circulating VLSFAs 20:0, 22:0, and 24:0 are each associated with a lower risk of diabetes.

  • 8.
    Hanhineva, Kati
    et al.
    Department of Clinical Nutrition, Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
    Brunius, Carl
    Department of Food Science, Uppsala BioCenter, Swedish University of Argicultural Science, Uppsala, Sweden.
    Andersson, Agneta
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Food, Nutrition and Dietetics.
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Juvonen, Risto
    School of Pharmacy, University of Eastern Finland, Kuopio, Finland.
    Keski-Rahkonen, Pekka
    School of Pharmacy, University of Eastern Finland, Kuopio, Finland.
    Auriola, Seppo
    School of Pharmacy, University of Eastern Finland, Kuopio, Finland.
    Landberg, Rikard
    Department of Food Science, Uppsala BioCenter, Swedish University of Argicultural Science, Uppsala, Sweden.
    Discovery of urinary biomarkers of whole grain rye intake in free-living subjects using non-targeted LC-MS metabolite profiling2015In: Molecular Nutrition & Food Research, ISSN 1613-4125, E-ISSN 1613-4133, Vol. 59, no 11, p. 2315-2325Article in journal (Refereed)
    Abstract [en]

    SCOPE: Whole grain (WG) intake is associated with decreased risk of developing colorectal cancer, type 2 diabetes and cardiovascular disease and its comorbidities. However, the role of specific grains is unclear. Moreover, intake of specific WG is challenging to measure accurately with traditional dietary assessment methods. Our aim was to use non-targeted metabolite profiling to discover specific urinary biomarkers for WG rye to objectively reflect intake under free-living conditions.

    METHODS AND RESULTS: WG rye intake was estimated by weighed food records, and 24 h urine collections were analyzed by LC-MS. Multivariate modelling was undertaken by repeated double cross-validated partial least squares regression against reported WG rye intake, which correlated well with multivariate prediction estimates (r = 0.67-0.80, p<0.001), but not with intakes of WG wheat or oats. Hydroxyhydroxyphenyl acetamide (HHPA) sulfate, 3,5-dihydroxyphenylpropionic acid (DHPPA) sulfate, caffeic acid sulfate and hydroxyphenyl acetamide (HPAA) sulfate were among the 20 features which had the greatest potential as intake biomarkers of WG. In addition, three compounds exhibited MS/MS fragmentation of carnitine structures.

    CONCLUSION: With this non-targeted approach, we confirmed the specificity of alkylresorcinol metabolites as biomarkers for WG rye intake, but also discovered other compounds that should be evaluated as putative biomarkers in future studies.

  • 9.
    Imamura, Fumiaki
    et al.
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge, England.
    Fretts, Amanda
    Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Korat, Andres V. Ardisson
    Harvard TH Chan Sch Publ Hlth, Dept Nutr & Epidemiol, Boston, MA USA.
    Yang, Wei-Sin
    Natl Taiwan Univ, Coll Publ Hlth, Inst Epidemiol & Prevent Med, Taipei, Taiwan.
    Lankinen, Maria
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    Qureshi, Waqas
    Wake Forest Univ, Bowman Gray Sch Med, Dept Internal Med, Bowman Gray Ctr,Sect Cardiovasc Med, Winston Salem, NC 27103 USA.
    Helmer, Catherine
    Univ Bordeaux, Bordeaux Populat Hlth Res Ctr, INSERM, UMR 1219, Bordeaux, France.
    Chen, Tzu-An
    USDA ARS, Baylor Coll Med, Dept Pediat, Childrens Nutr Res Ctr, Houston, TX USA.
    Wong, Kerry
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia.
    Bassett, Julie K.
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia.
    Murphy, Rachel
    Univ British Columbia, Fac Med, Sch Populat & Publ Hlth, Ctr Excellence Canc Prevent, Vancouver, BC, Canada.
    Tintle, Nathan
    Dordt Coll, Dept Math & Stat, Sioux Ctr, IA USA.
    Yu, Chaoyu Ian
    Univ Washington, Sch Publ Hlth, Dept Biostat, Seattle, WA 98195 USA.
    Brouwer, Ingeborg A.
    Vrije Univ Amsterdam, Amsterdam Publ Hlth Res Inst, Fac Earth & Life Sci, Dept Hlth Sci, Amsterdam, Netherlands.
    Chien, Kuo-Liong
    Natl Taiwan Univ, Coll Publ Hlth, Inst Epidemiol & Prevent Med, Taipei, Taiwan.
    Frazier-Wood, Alexis C.
    USDA ARS, Baylor Coll Med, Dept Pediat, Childrens Nutr Res Ctr, Houston, TX USA.
    del Gobbo, Liana C.
    Stanford Univ, Sch Med, Dept Med, Div Cardiovasc Med, Stanford, CA USA.
    Djousse, Luc
    Brigham & Womens Hosp, Dept Med, Div Aging, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA USA.
    Geleijnse, Johanna M.
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands.
    Giles, Graham G.
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia;Univ Melbourne, Ctr Epidemiol & Biostat, Parkville, Vic, Australia.
    de Goede, Janette
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands.
    Gudnason, Vilmundur
    Iceland Heart Assoc Res Inst, Kopavogur, Iceland.
    Harris, William S.
    Univ South Dakota, Sanford Sch Med, Dept Internal Med, Sioux Falls, SD USA;OmegaQuant Analyt LLC, Sioux Falls, SD USA.
    Hodge, Allison
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia;Univ Melbourne, Ctr Epidemiol & Biostat, Parkville, Vic, Australia.
    Hu, Frank
    Harvard TH Chan Sch Publ Hlth, Dept Nutr & Epidemiol, Boston, MA USA.
    Koulman, Albert
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge, England;Univ Cambridge, Addenbrookes Hosp, Natl Inst Hlth Res Biomed Res Ctr Core Nutr Bioma, Cambridge, England;Univ Cambridge, Addenbrookes Hosp, Natl Inst Hlth Res Biomed Res Ctr Core Metabol &, Cambridge, England;MRC, Elsie Widdowson Lab, Cambridge, England;Univ Eastern Finland, Inst Clin Med, Internal Med, Kuopio, Finland.
    Laakso, Markku
    Kuopio Univ Hosp, Dept Med, Kuopio, Finland.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Lin, Hung-Ju
    Natl Taiwan Univ Hosp, Dept Internal Med, Taipei, Taiwan.
    McKnight, Barbara
    Univ Washington, Sch Publ Hlth, Dept Biostat, Seattle, WA 98195 USA.
    Rajaobelina, Kalina
    Univ Bordeaux, Bordeaux Populat Hlth Res Ctr, INSERM, UMR 1219, Bordeaux, France.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism. Uppsala Univ, Dept Publ Hlth & Caring Sci, Clin Nutr & Metab, Uppsala, Sweden.
    Robinson, Jennifer G.
    Univ Iowa, Dept Epidemiol, Coll Publ Hlth, Iowa City, IA USA;Univ Iowa, Dept Med, Coll Publ Hlth, Iowa City, IA 52242 USA.
    Samieri, Cecilia
    Univ Bordeaux, Bordeaux Populat Hlth Res Ctr, INSERM, UMR 1219, Bordeaux, France.
    Siscovick, David S.
    New York Acad Med, New York, NY USA.
    Soedamah-Muthu, Sabita S.
    Tilburg Univ, Ctr Res Psychol Somat Dis, Dept Med & Clin Psychol, Tilburg, Netherlands.
    Sotoodehnia, Nona
    Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
    Sun, Qi
    Harvard TH Chan Sch Publ Hlth, Dept Nutr & Epidemiol, Boston, MA USA.
    Tsai, Michael Y.
    Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
    Uusitupa, Matti
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    Wagenknecht, Lynne E.
    Wake Forest Sch Med, Publ Hlth Sci, Winston Salem, NC USA.
    Wareham, Nick J.
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge, England.
    Wu, Jason H. Y.
    Univ New South Wales, George Inst Global Hlth, Sydney, NSW, Australia;Univ New South Wales, Fac Med, Sydney, NSW, Australia.
    Micha, Renata
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
    Forouhi, Nita G.
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge, England.
    Lemaitre, Rozenn N.
    Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
    Mozaffarian, Dariush
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
    Fatty acid biomarkers of dairy fat consumption and incidence of type 2 diabetes: A pooled analysis of prospective cohort studies2018In: PLoS Medicine, ISSN 1549-1277, E-ISSN 1549-1676, Vol. 15, no 10, article id e1002670Article in journal (Refereed)
    Abstract [en]

    Background We aimed to investigate prospective associations of circulating or adipose tissue odd-chain fatty acids 15: 0 and 17: 0 and trans-palmitoleic acid, t16:1n-7, as potential biomarkers of dairy fat intake, with incident type 2 diabetes (T2D). Methods and findings Sixteen prospective cohorts from 12 countries (7 from the United States, 7 from Europe, 1 from Australia, 1 from Taiwan) performed new harmonised individual-level analysis for the prospective associations according to a standardised plan. In total, 63,682 participants with a broad range of baseline ages and BMIs and 15,180 incident cases of T2D over the average of 9 years of follow-up were evaluated. Study-specific results were pooled using inverse-variance-weighted meta-analysis. Prespecified interactions by age, sex, BMI, and race/ethnicity were explored in each cohort and were meta-analysed. Potential heterogeneity by cohort-specific characteristics (regions, lipid compartments used for fatty acid assays) was assessed with metaregression. After adjustment for potential confounders, including measures of adiposity (BMI, waist circumference) and lipogenesis (levels of palmitate, tri-glycerides), higher levels of 15:0, 17:0, and t16:1n-7 were associated with lower incidence of T2D. In the most adjusted model, the hazard ratio (95% CI) for incident T2D per cohort-specific 10th to 90th percentile range of 15:0 was 0.80 (0.73-0.87); of 17:0, 0.65 (0.59-0.72); of t16:1n7, 0.82 (0.70-0.96); and of their sum, 0.71 (0.63-0.79). In exploratory analyses, similar associations for 15:0, 17:0, and the sum of all three fatty acids were present in both genders but stronger in women than in men ((pinteraction) < 0.001). Whereas studying associations with biomarkers has several advantages, as limitations, the biomarkers do not distinguish between different food sources of dairy fat (e.g., cheese, yogurt, milk), and residual confounding by unmeasured or imprecisely measured confounders may exist. Conclusions In a large meta-analysis that pooled the findings from 16 prospective cohort studies, higher levels of 15:0, 17:0, and t16:1n-7 were associated with a lower risk of T2D.

  • 10.
    Laguzzi, F.
    et al.
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Nobels Vag 13,Box 210, S-17177 Stockholm, Sweden.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Vikström, M.
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Nobels Vag 13,Box 210, S-17177 Stockholm, Sweden.
    Sjögren, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Gigante, B.
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Nobels Vag 13,Box 210, S-17177 Stockholm, Sweden;Danderyd Hosp Univ, Karolinska Inst, Dept Clin Sci, Div Cardiovasc Med, S-18288 Stockholm, Sweden.
    Alsharari, Zayed
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Hellenius, M. -L
    Cederholm, Tommy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Frumento, P.
    Karolinska Inst, Unit Biostat, Inst Environm Med, Nobels Vag 13,Box 210, S-17177 Stockholm, Sweden.
    de Faire, U.
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Nobels Vag 13,Box 210, S-17177 Stockholm, Sweden;Karolinska Inst, Dept Med, Cardiol Unit, S-17176 Stockholm, Sweden.
    Leander, K.
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Nobels Vag 13,Box 210, S-17177 Stockholm, Sweden.
    Circulating fatty acids in relation to alcohol consumption: Cross-sectional results from a cohort of 60-year-old men and women2018In: Clinical Nutrition, ISSN 0261-5614, E-ISSN 1532-1983, Vol. 37, no 6, Part A, p. 2001-2010Article in journal (Refereed)
    Abstract [en]

    Background & aims: Alcohol consumption is considered to affect circulating fatty acids (FAs) but knowledge about specific associations is limited. We aimed to assess the relation between alcohol consumption and serum FAs in 60-year-old Swedish men and women.

    Methods: In a random sample of 1917 men and 2058 women residing in Stockholm county, cross-sectional associations between different categories of alcohol consumption and FAs were assessed using linear regression; beta(1) coefficients with 95% confidence interval (Cl) were calculated. Self-reported alcohol consumption was categorized as none, low (<= 9.9 g/day) (reference), moderate (10-29.9 g/day) and high (>= 30 g/day). Moderate alcohol consumption was further subdivided into consumption of beer, wine, liquor and their combinations. Thirteen serum cholesterol ester FM were measured by gas chromatography and individual FM were expressed as percentage of total FAs.

    Results: Increasing alcohol consumption was associated to linear increase of saturated myristic acid, monounsaturated FAs and n-6 polyunsaturated (PUFA) arachidonic acid, whereas linear decrease was noted for saturated pentadecanoic acid and for n-6 PUFA linoleic acid. With non-linear associations, increasing alcohol consumption also associated to decreased saturated stearic acid, n-6 PUFA dihomogamma-linolenic acid, and n-3 PUFA docosahexaenoic acid and increased saturated palmitic acid, n-6 PUFA gamma-linolenic acid and n-3 PUFA eicosapentaenoic acid. Among types of beverages, wine consumption was associated with n-6 PUFA arachidonic acid (beta(1) 0.59; 95% CI: 030;0.88) and the n-3 PUFAs eicosapentaenoic acid (beta(1) 0.54; 95% CI: 0.30;0.78), and docosahexaenoic acid (beta(1) 0.06; 95% CI: 0.00;0.12).

    Conclusions: These findings may give important basis for further investigations to better understand biological mechanisms behind the dose-dependent associations between alcohol consumption and health outcomes observed in many previous studies.

  • 11. Landberg, Rikard
    et al.
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Kamal-Eldin, Afaf
    Aman, Per
    An update on alkylresorcinols - Occurrence, bioavailability, bioactivity and utility as biomarkers2014In: Journal of Functional Foods, ISSN 1756-4646, Vol. 7, p. 77-89Article, review/survey (Refereed)
    Abstract [en]

    Alkylresorcinols (AR) with alkyl chains in the range of C15 to C25 are phenolic lipids particularly abundant in the outer parts of wheat and rye kernels and in food products containing these parts. The content in whole grain and bran products is high (200-4000 mu g/g), whereas only trace-levels are detected in refined products. Alkylresorcinols are absorbed in humans in proportion to intake and have therefore been suggested and evaluated as biomarkers for whole grain wheat and rye intake. In humans, plasma AR concentrations reach micromolar concentrations immediately after whole grain wheat and rye product consumption and nano-molar levels at fasting conditions. Results from different model studies have indicated that AR may have some bioactivities including enzyme inhibition, suppression of adipocyte lipolysis and inhibition of colon cancer tumor growth but it is currently unknown whether AR bioactive in vivo or not. This chapter details the recent research findings on alkylresorcinols with emphasis on their occurrence, bioavailability, bioactivity and utility as biomarkers.

  • 12.
    Lankinen, Maria
    et al.
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland..
    Schwab, Ursula
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.;Kuopio Univ Hosp, Inst Clin Med, Internal Med, SF-70210 Kuopio, Finland..
    Kolehmainen, Marjukka
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland..
    Paananen, Jussi
    Univ Eastern Finland, Inst Biomed, Kuopio, Finland..
    Nygren, Heli
    VTT Tech Res Ctr Finland, Espoo, Finland..
    Seppanen-Laakso, Tuulikki
    VTT Tech Res Ctr Finland, Espoo, Finland..
    Poutanen, Kaisa
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.;VTT Tech Res Ctr Finland, Espoo, Finland..
    Hyötylainen, Tuulia
    VTT Tech Res Ctr Finland, Espoo, Finland.;Steno Diabet Ctr, DK-2820 Gentofte, Denmark..
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Savolainen, Markku J.
    Univ Oulu, Res Ctr Internal Med & Bioctr Oulu, Oulu, Finland.;Oulu Univ Hosp, Dept Internal Med, Oulu, Finland.;Oulu Univ Hosp, Med Res Ctr Oulu, Oulu, Finland.;Univ Oulu, Oulu, Finland..
    Hukkanen, Janne
    Univ Oulu, Res Ctr Internal Med & Bioctr Oulu, Oulu, Finland.;Oulu Univ Hosp, Dept Internal Med, Oulu, Finland.;Oulu Univ Hosp, Med Res Ctr Oulu, Oulu, Finland.;Univ Oulu, Oulu, Finland..
    Brader, Lea
    Aarhus Univ Hosp, Dept Endocrinol & Internal Med, DK-8000 Aarhus, 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.
    Rosqvist, Fredrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Hermansen, Kjeld
    Aarhus Univ Hosp, Dept Endocrinol & Internal Med, DK-8000 Aarhus, Denmark..
    Cloetens, Lieselotte
    Lund Univ, Biomed Nutr Pure & Appl Biochem, Lund, Sweden..
    Önning, Gunilla
    Lund Univ, Biomed Nutr Pure & Appl Biochem, Lund, Sweden..
    Thorsdottir, Inga
    Univ Iceland, Sch Hlth Sci, Fac Food Sci & Nutr, Unit Nutr Res, Reykjavik, Iceland.;Landspitali Univ Hosp, Reykjavik, Iceland..
    Gunnarsdottir, Ingibjorg
    Univ Iceland, Sch Hlth Sci, Fac Food Sci & Nutr, Unit Nutr Res, Reykjavik, Iceland.;Landspitali Univ Hosp, Reykjavik, Iceland..
    Åkesson, Bjorn
    Lund Univ, Biomed Nutr Pure & Appl Biochem, Lund, Sweden.;Skane Univ Hosp, Dept Clin Nutr, Lund, Sweden..
    Dragsted, Lars Ove
    Univ Copenhagen, Fac Sci, Dept Nutr Exercise & Sports, Frederiksberg, Denmark..
    Uusitupa, Matti
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.;Kuopio Univ Hosp, Res Unit, SF-70210 Kuopio, Finland..
    Oresic, Matej
    VTT Tech Res Ctr Finland, Espoo, Finland.;Steno Diabet Ctr, DK-2820 Gentofte, Denmark..
    A Healthy Nordic Diet Alters the Plasma Lipidomic Profile in Adults with Features of Metabolic Syndrome in a Multicenter Randomized Dietary Intervention2016In: Journal of Nutrition, ISSN 0022-3166, E-ISSN 1541-6100, Vol. 146, no 4, p. 662-672Article in journal (Refereed)
    Abstract [en]

    Background: A healthy Nordic diet is associated with improvements in cardiometabolic risk factors, but the effect on lipidomic profile is not known.

    Objective: The aim was to investigate how a healthy Nordic diet affects the fasting plasma lipidomic profile in subjects with metabolic syndrome.

    Methods: Men and women (n = 200) with features of metabolic syndrome [mean age: 55 y; body mass index (in kg/m(2)): 31.6] were randomly assigned to either a healthy Nordic (n = 104) or a control (n = 96) diet for 18 or 24 wk at 6 centers. Of the participants, 156 completed the study with plasma lipidomic measurements. The healthy Nordic diet consisted of whole grains, fruits, vegetables, berries, vegetable oils and margarines, fish, low-fat milk products, and low-fat meat. An average Nordic diet served as the control diet and included low-fiber cereal products, dairy fat-based spreads, regular-fatmilk products, and a limited amount of fruits, vegetables, and berries. Lipidomic profiles were measured at baseline, week 12, and the end of the intervention (18 or 24wk) by using ultraperformance liquid chromatography mass spectrometry. The effects of the diets on the lipid variables were analyzed with linear mixed-effects models. Data from centers with 18- or 24-wk duration were also analyzed separately.

    Results: Changes in 21 plasma lipids differed significantly between the groups at week 12 (false discovery rate P < 0.05), including increases in plasmalogens and decreases in ceramides in the healthy Nordic diet group compared with the control group. At the end of the study, changes in lipidomic profiles did not differ between the groups. However, when the intervention lasted 24 wk, changes in 8 plasma lipids that had been identified at 12 wk, including plasmalogens, were sustained. There were no differences in changes in plasma lipids between groups with an intervention of 18 wk. By the dietary biomarker score, adherence to diet did not explain the difference in the results related to the duration of the study.

    Conclusions: A healthy Nordic diet transiently modified the plasma lipidomic profile, specifically by increasing the concentrations of antioxidative plasmalogens and decreasing insulin resistance-inducing ceramides.

  • 13.
    Marklund, Matti
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Leander, Karin
    Vikstrom, Max
    Laguzzi, Federica
    Gigante, Bruna
    Sjögren, Per
    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.
    de Faire, Ulf
    Hellenius, Mai-Lis
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Polyunsaturated Fat Intake Estimated by Circulating Biomarkers and Risk of Cardiovascular Disease and All-Cause Mortality in a Population-Based Cohort of 60-Year-Old Men and Women2015In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 132, no 7, p. 586-594Article in journal (Refereed)
    Abstract [en]

    Background High intake of polyunsaturated fatty acids (PUFAs) may reduce the risk of cardiovascular disease (CVD) and mortality. Large, prospective studies including both sexes and circulating PUFAs as dietary biomarkers are needed. We investigated sex-specific associations of the major dietary PUFAs, eicosapentaenoic acid, docohexaenoic acid, linoleic acid, and -linolenic acid, with incident CVD and all-cause mortality in a population-based cohort. Methods and Results PUFAs in serum cholesterol esters were measured at baseline in 60-year-old Swedish women (n=2193) and men (n=2039). With the use of national registers, 484 incident CVD events (294 men and 190 women) and 456 all-cause deaths (265 men and 191 women) were identified during follow-up (median, 14.5 years) in individuals without prior CVD at baseline. Associations of PUFAs with CVD and mortality were evaluated with Cox proportional hazard models. In multivariable-adjusted models, 1-SD increases in eicosapentaenoic acid and docohexaenoic acid were associated with lower risk of incident CVD among women (hazard ratio [HR], 0.79 [95% confidence interval (CI), 0.64-0.97] and 0.74 [95% CI, 0.61-0.89], respectively). -Linolenic acid was associated with moderately increased CVD risk in women (HR, 1.16; 95% CI, 1.02-1.32). Inverse associations with all-cause mortality were observed for eicosapentaenoic acid and docohexaenoic acid among all participants (HR, 0.81 [95% CI, 0.72-0.91] and 0.80 [95% CI, 0.72-0.89], respectively) and for linoleic acid in men (HR, 0.73; 95% CI, 0.64-0.83). Conclusions Serum linoleic acid and very-long-chain n-3 PUFAs, partly reflecting vegetable oil and fish intake, respectively, were inversely associated with all-cause mortality. Inverse associations of eicosapentaenoic acid and docohexaenoic acid with incident CVD were observed only in women.

  • 14.
    Marklund, Matti
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Leander, Karin
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden..
    Vikstrom, Max
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden..
    Laguzzi, Federica
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden..
    Gigante, Bruna
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden.;Danderyd Hosp, Karolinska Inst, Dept Clin Sci, Div Cardiovasc Med, Danderyds, Sweden..
    Sjögren, Per
    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.
    de Faire, Ulf
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden.;Karolinska Univ Hosp, Karolinska Inst, Dept Med, Cardiol Unit, Solna, Sweden..
    Hellenius, Mai-Lis
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Cardiol Unit, Solna, Sweden..
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Serum Pentadecanoic Acid, A Biomarker Of Dairy Fat Intake, Is Associated With Lower Risk Of Incident Cardiovascular Disease And All-Cause Mortality In Swedish Men And Women2017In: Annals of Nutrition and Metabolism, ISSN 0250-6807, E-ISSN 1421-9697, Vol. 71, p. 322-323Article in journal (Other academic)
  • 15.
    Marklund, Matti
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Magnusdottir, Ola K
    Rosqvist, Fredrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Cloetens, Lieselotte
    Landberg, Rikard
    Kolehmainen, Marjukka
    Brader, Lea
    Hermansen, Kjeld
    Poutanen, Kaisa S
    Herzig, Karl-Heinz
    Hukkanen, Janne
    Savolainen, Markku J
    Dragsted, Lars O
    Schwab, Ursula
    Paananen, Jussi
    Uusitupa, Matti
    Åkesson, Björn
    Thorsdottir, Inga
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    A dietary biomarker approach captures compliance and cardiometabolic effects of a healthy Nordic diet in individuals with metabolic syndrome2014In: Journal of Nutrition, ISSN 0022-3166, E-ISSN 1541-6100, Vol. 144, no 10, p. 1642-1649Article in journal (Refereed)
    Abstract [en]

    Assessment of compliance with dietary interventions is necessary to understand the observed magnitude of the health effects of the diet per se. To avoid reporting bias, different dietary biomarkers (DBs) could be used instead of self-reported data. However, few studies investigated a combination of DBs to assess compliance and its influence on cardiometabolic risk factors. The objectives of this study were to use a combination of DBs to assess compliance and to investigate how a healthy Nordic diet (ND) influences cardiometabolic risk factors in participants with high apparent compliance compared with the whole study population. From a recently conducted isocaloric randomized trial, SYSDIET (Systems Biology in Controlled Dietary Interventions and Cohort Studies), in 166 individuals with metabolic syndrome, several DBs were assessed to reflect different key components of the ND: canola oil (serum phospholipid α-linolenic acid), fatty fish [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)], vegetables (plasma β-carotene), and whole grains (plasma alkylresorcinols). High-fat dairy intake (expectedly low in the ND) was reflected by serum pentadecanoic acid. All participants with biomarker data (n = 154) were included in the analyses. Biomarkers were combined by using a biomarker rank score (DB score) and principal component analysis (PCA). The DB score was then used to assess compliance. During the intervention, median concentrations of alkylresorcinols, α-linolenic acid, EPA, and DHA were >25% higher in the ND individuals than in the controls (P < 0.05), whereas median concentrations of pentadecanoic acid were 14% higher in controls (P < 0.05). Median DB score was 57% higher in the ND than in controls (P < 0.001) during the intervention, and participants were ranked similarly by DB score and PCA score. Overall, estimates of group difference in cardiometabolic effects generally appeared to be greater among compliant participants than in the whole study population (e.g., estimates of treatment effects on blood pressure and lipoproteins were ∼1.5- to 2-fold greater in the most compliant participants), suggesting that poor compliance attenuated the dietary effects. With adequate consideration of their limitations, DB combinations (e.g., DB score) could be useful for assessing compliance in intervention studies investigating cardiometabolic effects of healthy dietary patterns.

  • 16. Marklund, Matti
    et al.
    McKeown, Nicola M
    Blumberg, Jeffrey B
    Chen, C-Y Oliver
    Hepatic biotransformation of alkylresorcinols is mediated via cytochrome P450 and β-oxidation: a proof of concept study.2013In: Food Chemistry, ISSN 0308-8146, E-ISSN 1873-7072, Vol. 139, no 1-4, p. 925-30Article in journal (Refereed)
    Abstract [en]

    Alkylresorcinols (AR) are phenolic lipids present in the bran of some cereals. AR may serve as a biomarker for whole grain wheat and rye intake. While AR pharmacokinetics and two major metabolites have been reported, the metabolic pathways contributing to their relatively rapid elimination from the circulation remain to be speculative. In this study, we investigated if ω- and β-oxidation mediate catabolism of the AR homologue C19:0 to form 3,5-dihydroxybenzoic acid and 3-(3,5-dihydroxyphenyl)-1-propanoic acid (DHPPA), using 3 in vitro platforms, human cytochrome P450 4F2 (CYP4F2), human liver S9, and HepG2 cells. One hydroxylated C19:0 metabolite was formed by CYP4F2 and one hydroxylated and one carboxylated C19:0 were tentatively identified after incubation of AR with S9. The formation of DHPPA was quantifiable when HepG2 cells were treated with C19:0 for 48 h. Our results are consistent with a metabolic pathway by which AR are degraded to phenolic acids via CYP4F2-mediated ω-oxidation and subsequent β-oxidation.

  • 17.
    Marklund, Matti
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism. Univ New South Wales, George Inst Global Hlth, Sydney, NSW 2042, Australia.
    Morris, Andrew P.
    Univ Liverpool, Dept Biostat, Liverpool L69 3GL, Merseyside, England.
    Mahajan, Anubha
    Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England.
    Ingelsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Stanford Univ, Dept Med, Div Cardiovasc Med, Sch Med, Stanford, CA 94305 USA;Stanford Univ, Stanford Cardiovasc Inst, Stanford, CA 94305 USA;Stanford Univ, Stanford Diabet Res Ctr, Stanford, CA 94305 USA.
    Lindgren, Cecilia M.
    Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England;Univ Oxford, Big Data Inst, Ka Shing Ctr Hlth Informat & Discovery, Oxford OX3 7LF, England.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Epidemiology.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Genome-Wide Association Studies of Estimated Fatty Acid Desaturase Activity in Serum and Adipose Tissue in Elderly Individuals: Associations with Insulin Sensitivity2018In: Nutrients, ISSN 2072-6643, E-ISSN 2072-6643, Vol. 10, no 11, article id 1791Article in journal (Refereed)
    Abstract [en]

    Fatty acid desaturases (FADS) catalyze the formation of unsaturated fatty acids and have been related to insulin sensitivity (IS). FADS activities differ between tissues and are influenced by genetic factors that may impact the link to IS. Genome-wide association studies of delta-5-desaturase (D5D), delta-6-desaturase (D6D) and stearoyl-CoA desaturase-1 (SCD) activities (estimated by product-to-precursor ratios of fatty acids analyzed by gas chromatography) in serum cholesterol esters (n = 1453) and adipose tissue (n = 783, all men) were performed in two Swedish population-based cohorts. Genome-wide significant associated loci were evaluated for associations with IS measured with a hyperinsulinemic euglycemic clamp (n = 554). Variants at the FADS1 were strongly associated with D5D in both cholesterol esters (p = 1.9 x 10(-70)) and adipose tissue (p = 1.1 x 10(-27)). Variants in three further loci were associated with D6D in cholesterol esters (FADS2, p = 3.0 x 10(-67); PDXDCI, p = 4.8 x 10(-8); and near MC4R, p = 3.7 x 10(-8)) but no associations with D6D in adipose tissue attained genome-wide significance. One locus was associated with SCD in adipose tissue (PKDL1, p = 2.2 x 10(-19)). Genetic variants near MC4R were associated with IS (p = 3.8 x 10(-3)). The FADS cluster was the main genetic determinant of estimated FADS activity. However, fatty acid (FA) ratios in adipose tissue and cholesterol esters represent FADS activities in separate tissues and are thus influenced by different genetic factors with potential varying effects on IS.

  • 18.
    Marklund, Matti
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Pingel, Ronnie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Rosqvist, Fredrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Lindroos, Anna Karin
    Natl Food Agency, Uppsala, Sweden;Univ Gothenburg, Dept Internal Med & Clin Nutr, Gothenburg, Sweden.
    Eriksson, Jan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical diabetology and metabolism.
    Vessby, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Oscarsson, Jan
    AstraZeneca Gothenburg, Molndal, Sweden.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Interrelationships Between Fatty Acid Composition in Plasma Cholesterol Esters and Phospholipids in Men and Women: A Pooled Analysis2017In: Annals of Nutrition and Metabolism, ISSN 0250-6807, E-ISSN 1421-9697, Vol. 71, p. 372-372Article in journal (Other academic)
  • 19.
    Marklund, Matti
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Pingel, Ronnie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Rosqvist, Fredrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Lindroos, Anna Karin
    Natl Food Agcy, Uppsala, Sweden.;Univ Gothenburg, Dept Internal Med & Clin Nutr, Gothenburg, Sweden..
    Eriksson, Jan W.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical diabetology and metabolism. en..
    Vessby, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Oscarsson, Jan
    AstraZeneca R&D, Gothenburg, Sweden..
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Fatty Acid Proportions in Plasma Cholesterol Esters and Phospholipids Are Positively Correlated in Various Swedish Populations2017In: Journal of Nutrition, ISSN 0022-3166, E-ISSN 1541-6100, Vol. 147, no 11, p. 2118-2125Article in journal (Refereed)
    Abstract [en]

    Background: Fatty acid (FA) proportions in cholesterol esters (CEs) and plasma phospholipids are widely used as dietary biomarkers. Information on how proportions in these fractions correlate could have implications for interpretation and use of FA biomarkers in observational and interventional studies. Objective: We investigated correlations between FA proportions in CEs and phospholipids in free-living individuals and assessed how diet-induced alterations of FA proportions correlate between fractions. Methods: Spearman's rank correlation coefficients (rs) between FA proportions (percentage of total FAs) in circulating CEs and phospholipids were calculated separately in 8 individual study populations including Swedish females and males (N = 2052; age range: 11-84 y), and pooled by inverse-variance weighted meta-analysis. In addition, study populations were stratified by age, sex, body mass index (BMI; in kg/m(2)), and diabetes status, and strata-specific rs were pooled by meta-analysis. In 2 randomized trials (N = 79) in which dietary saturated FAs were isocalorically replaced with unsaturated FAs, treatment-wise calculations of rs were conducted between FA changes in CEs and phospholipids. Results: Overall, FA proportions in CEs and phospholipids correlated well and especially strongly for polyunsaturated FAs (PUFAs), with pooled rs (95% CIs) ranging from 0.74 (0.72, 0.76) for a-linolenic acid to 0.92 (0.91, 0.93) for eicosapentaenoic acid. Weak correlations (pooled rs <0.4) were observed only for palmitic acid and stearic acid, with pooled rs (95% CIs): 0.29 (0.24, 0.33) and 0.30 (0.25, 0.34), respectively. Overall, correlations were not affected by age, sex, BMI, or diabetes status. Strong correlations (r(s) >= 0.6) between diet-induced FA changes in CEs and phospholipids were observed for most PUFAs. Conclusions: Proportions of most FAs in CEs and phospholipids ranked individuals similarly, suggesting that FA proportions in these fractions can be used interchangeably in populations of diverse age, sex, body composition, and diabetes status. Caution is advised, however, when comparing results from studies assessing palmitic acid or stearic acid in different lipid fractions.

  • 20.
    Marklund, Matti
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Strömberg, Eric A
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Hooker, Andrew C
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Hammarlund-Udenaes, Margareta
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Åman, Per
    Landberg, Rikard
    Kamal-Eldin, Afaf
    Chain length of dietary alkylresorcinols affects their in vivo elimination kinetics in rats2013In: Journal of Nutrition, ISSN 0022-3166, E-ISSN 1541-6100, Vol. 143, no 10, p. 1573-1578Article in journal (Refereed)
    Abstract [en]

    Two phenolic acids, 3,5-dihydroxybenzoic acid (DHBA) and 3-(3,5-dihydroxyphenyl)- propanoic acid (DHPPA), are the major metabolites of cereal alkylresorcinols (ARs). Like their precursors, AR metabolites have been suggested as biomarkers for intake of whole-grain wheat and rye and as such could aid the understanding of diet-disease associations. This study estimated and compared pharmacokinetic parameters of ARs and their metabolites in rats and investigated differences in metabolite formation after ingestion of different AR homologs. Rats were i.v. infused for 30 min with 2, 12, or 23 μmol/kg DHBA or DHPPA or orally given the same amounts of the AR homologs, C17:0 and C25:0. Repeated plasma samples, obtained from rats for 6 h (i.v.) or 36 h (oral), were simultaneously analyzed for ARs and their metabolites by GC-mass spectrometry. Pharmacokinetic parameters were estimated by population-based compartmental modeling and noncompartmental calculation. A 1-compartment model best described C25:0 pharmacokinetics, whereas C17:0 and AR metabolites best fitted 2-compartment models. Combined models for simultaneous prediction of AR and metabolite concentration were more complex, with less reliable estimates of pharmacokinetic parameters. Although the AUC of C17:0 was lower than that of C25:0 (P < 0.05), the total amount and composition of AR metabolites did not differ between rats given C17:0 or C25:0. The elimination half-life of ARs and their metabolites increased with length of the side chain (P-trend < 0.001) and ranged from 1.2 h (DHBA) to 8.8 h (C25:0). The formation of AR metabolites was slower than their elimination, indicating that the rate of AR metabolism and not excretion of DHBA and DHPPA determines their plasma concentrations in rats.

  • 21.
    Marklund, Matti
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Strömberg, Eric A
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Lærke, Helle N
    Knudsen, Knud E Bach
    Kamal-Eldin, Afaf
    Hooker, Andrew C.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Landberg, Rikard
    Simultaneous pharmacokinetic modeling of alkylresorcinols and their main metabolites indicates dual absorption mechanisms and enterohepatic elimination in humans2014In: Journal of Nutrition, ISSN 0022-3166, E-ISSN 1541-6100, Vol. 144, no 11, p. 1674-1680Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Alkylresorcinols have proven to be useful biomarkers of whole-grain wheat and rye intake in many nutritional studies. To improve their utility, more knowledge regarding the fate of alkylresorcinols and their metabolites after consumption is needed.

    OBJECTIVE: The objective of this study was to develop a combined pharmacokinetic model for plasma concentrations of alkylresorcinols and their 2 major metabolites, 3,5-dihydroxybenzoic acid (DHBA) and 3-(3,5-dihydroxyphenyl)-propanoic acid (DHPPA).

    METHODS: The model was established by using plasma samples collected from 3 women and 2 men after a single dose (120 g) of rye bran and validated against fasting plasma concentrations from 8 women and 7 men with controlled rye bran intake (23, 45, or 90 g/d). Alkylresorcinols in the lymph and plasma of a pig fed a single alkylresorcinol dose (1.3 mmol) were quantified to assess absorption. Human ileostomal effluent and pig bile after high and low alkylresorcinol doses were analyzed to evaluate biliary alkylresorcinol metabolite excretion.

    RESULTS: The model contained 2 absorption compartments: 1 that transferred alkylresorcinols directly to the systematic circulation and 1 in which a proportion of absorbed alkylresorcinols was metabolized before reaching the systemic circulation. Plasma concentrations of alkylresorcinols and their metabolites depended on absorption and formation, respectively, and the mean ± SEM terminal elimination half-life of alkylresorcinols (1.9 ± 0.59 h), DHPPA (1.5 ± 0.26 h), and DHBA (1.3 ± 0.22 h) did not differ. The model accurately predicted alkylresorcinol and DHBA concentrations after repeated alkylresorcinol intake but DHPPA concentration was overpredicted, possibly because of poorly modeled enterohepatic circulation. During the 8 h following administration, <2% of the alkylresorcinol dose was recovered in the lymph. DHPPA was identified in both human ileostomal effluent and pig bile, indicating availability of DHPPA for absorption and enterohepatic circulation.

    CONCLUSION: Intact alkylresorcinols have advantages over DHBA and DHPPA as plasma biomarkers for whole-grain wheat and rye intake because of lower susceptibility to factors other than alkylresorcinol intake.

  • 22.
    Marklund, Matti
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism. Univ New South Wales, George Inst Global Hlth, Sydney, NSW, Australia;Univ New South Wales, Fac Med, Sydney, NSW, Australia.
    Wu, Jason H. Y.
    Univ New South Wales, George Inst Global Hlth, Sydney, NSW, Australia;Univ New South Wales, Fac Med, Sydney, NSW, Australia.
    Imamura, Fumiaki
    Univ Cambridge, MRC, Epidemiol Unit, Cambridge, England.
    Del Gobbo, Liana C.
    Stanford Univ, Dept Med, Div Cardiovasc Med, Sch Med, Stanford, CA 94305 USA.
    Fretts, Amanda
    Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
    de Goede, Janette
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands.
    Shi, Peilin
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
    Tintle, Nathan
    Dordt Coll, Dept Math & Stat, Sioux Ctr, IA USA.
    Wennberg, Maria
    Umea Univ, Dept Publ Hlth & Clin Med, Nutr Res, Umea, Sweden.
    Aslibekyan, Stella
    Univ Alabama Birmingham, Dept Epidemiol, Birmingham, AL USA.
    Chen, Tzu-An
    Baylor Coll Med, USDA ARS, Childrens Nutr Res Ctr, Houston, TX 77030 USA.
    Otto, Marcia C. de Oliveira
    Univ Texas Houston, Hlth Sci Ctr, Sch Publ Hlth, Div Epidemiol Human Genet & Environm Sci, Houston, TX USA.
    Hirakawa, Yoichiro
    Kyushu Univ, Grad Sch Med Sci, Dept Med & Clin Sci, Fukuoka, Fukuoka, Japan.
    Eriksen, Helle Hojmark
    Aalborg Univ Hosp, Unit Epidemiol & Biostat, Aalborg, Denmark.
    Kroeger, Janine
    German Inst Human Nutr Potsdam Rehbrucke, Dept Mol Epidemiol, Nuthetal, Germany.
    Laguzzi, Federica
    Karolinska Inst, Unit Cardiovasc Epidemiol, Inst Environm Med, Stockholm, Sweden.
    Lankinen, Maria
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    Murphy, Rachel A.
    Univ British Columbia, Vancouver, BC, Canada.
    Prem, Kiesha
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore.
    Samieri, Cecilia
    Univ Bordeaux, INSERM, Bordeaux Populat Hlth Res Ctr, TUMR 1219, Bordeaux, France.
    Virtanen, Jyrki
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    Wood, Alexis C.
    Baylor Coll Med, USDA ARS, Childrens Nutr Res Ctr, Houston, TX 77030 USA.
    Wong, Kerry
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia.
    Yang, Wei-Sin
    Natl Taiwan Univ, Coll Publ Hlth, Inst Epidemiol & Prevent Med, Taipei, Taiwan.
    Zhou, Xia
    Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
    Baylin, Ana
    Univ Michigan, Sch Publ Hlth, Dept Nutr Sci, Ann Arbor, MI 48109 USA;Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
    Boer, Jolanda M. A.
    Natl Inst Publ Hlth & Environm, Ctr Nutr Prevent & Hlth Serv, Bilthoven, Netherlands.
    Brouwer, Ingeborg A.
    Vrije Univ, Hlth Sci, Amsterdam, Netherlands.
    Campos, Hannia
    Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
    Chaves, Paulo H. M.
    Florida Int Univ, Herbert Wertheim Coll Med, Benjamin Leon Geriatr Res & Educ, Miami, FL 33199 USA.
    Chien, Kuo-Liong
    Natl Taiwan Univ, Coll Publ Hlth, Inst Epidemiol & Prevent Med, Taipei, Taiwan;Natl Taiwan Univ Hosp, Dept Internal Med, Taipei, Taiwan.
    de Faire, Ulf
    Karolinska Inst, Unit Cardiovasc Epidemiol, Inst Environm Med, Stockholm, Sweden.
    Djousse, Luc
    Brigham & Womens Hosp, Boston Vet Affairs Healthcare Syst, Boston, MA 02115 USA.
    Eiriksdottir, Gudny
    Iceland Heart Assoc, Kopavogur, Iceland.
    El-Abbadi, Naglaa
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA;USDA, Jean Mayer Human Nutr Res Ctr, Boston, MA USA.
    Forouhi, Nita G.
    Univ Cambridge, MRC, Epidemiol Unit, Cambridge, England.
    Gaziano, J. Michael
    Brigham & Womens Hosp, Boston Vet Affairs Healthcare Syst, Boston, MA 02115 USA.
    Geleijnse, Johanna M.
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands.
    Gigante, Bruna
    Karolinska Inst, Unit Cardiovasc Epidemiol, Inst Environm Med, Stockholm, Sweden.
    Giles, Graham
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia.
    Guallar, Eliseo
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Div Environm Epidemiol, Baltimore, MD USA.
    Gudnason, Vilmundur
    Iceland Heart Assoc, Kopavogur, Iceland.
    Harris, Tamara
    NIA, Bethesda, MD 20892 USA.
    Harris, William S.
    Univ South Dakota, Dept Internal Med, Sanford Sch Med, Sioux Falls, SD USA;OmegaQuant Analyt LLC, Sioux Falls, SD USA.
    Helmer, Catherine
    Univ Bordeaux, INSERM, Bordeaux Populat Hlth Res Ctr, TUMR 1219, Bordeaux, France.
    Hellenius, Mai-Lis
    Karolinska Univ Hosp, Karolinska Inst, Cardiol Unit, Dept Med, Stockholm, Sweden.
    Hodge, Allison
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia.
    Hu, Frank B.
    Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Div Network Med, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA 02115 USA.
    Jacques, Paul F.
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA;USDA, Jean Mayer Human Nutr Res Ctr, Boston, MA USA.
    Jansson, Jan-Hakan
    Umea Univ, Dept Publ Hlth & Clin Med, Res Unit Skelleftea, Umea, Sweden.
    Kalsbeek, Anya
    Dordt Coll, Dept Math & Stat, Sioux Ctr, IA USA.
    Khaw, Kay-Tee
    Univ Cambridge, Dept Publ Hlth & Primary Care, Sch Clin Med, Cambridge, England.
    Koh, Woon-Puay
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore;Duke NUS Med Sch, Singapore, Singapore.
    Laakso, Markku
    Univ Eastern Finland, Inst Clin Med, Internal Med, Kuopio, Finland.
    Leander, Karin
    Karolinska Inst, Unit Cardiovasc Epidemiol, Inst Environm Med, Stockholm, Sweden.
    Lin, Hung-Ju
    Natl Taiwan Univ Hosp, Dept Internal Med, Taipei, Taiwan.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Epidemiology.
    Luben, Robert
    Univ Cambridge, Dept Publ Hlth & Primary Care, Sch Clin Med, Cambridge, England.
    Luo, Juhua
    Indiana Univ, Dept Epidemiol & Biostat, Bloomington, IN USA.
    McKnight, Barbara
    Univ Washington, Dept Biostat, Sch Publ Hlth, Seattle, WA 98195 USA.
    Mursu, Jaakko
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    Ninomiya, Toshiharu
    Kyushu Univ, Grad Sch Med Sci, Dept Epidemiol & Publ Hlth, Fukuoka, Fukuoka, Japan.
    Overvad, Kim
    Aarhus Univ, Dept Publ Hlth, Sect Epidemiol, Aarhus, Denmark;Aalborg Univ Hosp, Dept Cardiol, Aalborg, Denmark.
    Psaty, Bruce M.
    Univ Washington, Dept Med, Cardiovasc Hlth Study, Seattle, WA USA;Univ Washington, Dept Epidemiol, Cardiovasc Hlth Study, Seattle, WA 98195 USA;Univ Washington, Dept Hlth Serv, Cardiovasc Hlth Study, Seattle, WA 98195 USA;Kaiser Permanente Washington Hlth Res Inst, Seattle, WA USA.
    Rimm, Eric
    Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Div Network Med, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA 02115 USA.
    Schulze, Matthias B.
    German Inst Human Nutr Potsdam Rehbrucke, Dept Mol Epidemiol, Nuthetal, Germany.
    Siscovick, David
    New York Acad Med, New York, NY USA.
    Nielsen, Michael Skjelbo
    Aalborg Univ Hosp, Dept Cardiol, Aalborg, Denmark.
    Smith, Albert, V
    Iceland Heart Assoc, Kopavogur, Iceland.
    Steffen, Brian T.
    Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
    Steffen, Lyn
    Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
    Sun, Qi
    Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Div Network Med, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA 02115 USA.
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Epidemiology.
    Tsai, Michael Y.
    Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
    Tunstall-Pedoe, Hugh
    Univ Dundee, Cardiovasc Epidemiol Unit, Inst Cardiovasc Res, Dundee, Scotland.
    Uusitupa, Matti I. J.
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
    van Dam, Rob M.
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore.
    Veenstra, Jenna
    Dordt Coll, Dept Math & Stat, Sioux Ctr, IA USA.
    Verschuren, W. M. Monique
    Natl Inst Publ Hlth & Environm, Ctr Nutr Prevent & Hlth Serv, Bilthoven, Netherlands;Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
    Wareham, Nick
    Univ Cambridge, MRC, Epidemiol Unit, Cambridge, England.
    Willett, Walter
    Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Div Network Med, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA 02115 USA.
    Woodward, Mark
    Univ New South Wales, George Inst Global Hlth, Sydney, NSW, Australia;Univ New South Wales, Fac Med, Sydney, NSW, Australia;Univ Dundee, Cardiovasc Epidemiol Unit, Inst Cardiovasc Res, Dundee, Scotland;Univ Oxford, George Inst Global Hlth, Oxford, England.
    Yuan, Jian-Min
    Univ Pittsburgh, Div Canc Control & Populat Sci, UPMC Hillman Canc, Pittsburgh, PA 15260 USA;Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15260 USA.
    Micha, Renata
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
    Lemaitre, Rozenn N.
    Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
    Mozaffarian, Dariush
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality: An Individual-Level Pooled Analysis of 30 Cohort Studies2019In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 139, no 21, p. 2422-2436Article in journal (Refereed)
    Abstract [en]

    Background:

    Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies.

    Methods:

    We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease, ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytic plan. Levels of LA and AA, measured as the percentage of total fatty acids, were evaluated linearly according to their interquintile range (ie, the range between the midpoint of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance-weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes mellitus, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available).

    Results:

    In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15198 incident cardiovascular events occurred among 68659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI, 0.88-0.99), 0.78 (0.70-0.85), and 0.88 (0.79-0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88-1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; in a comparison of extreme quintiles, higher levels were associated with lower risk of total CVD (0.92; 0.86-0.99). No consistent heterogeneity by population subgroups was identified in the observed relationships.

    Conclusions:

    In pooled global analyses, higher in vivo circulating and tissue levels of LA and possibly AA were associated with lower risk of major cardiovascular events. These results support a favorable role for LA in CVD prevention.

  • 23.
    McKeown, Nicola M.
    et al.
    Tufts Univ, Jean Mayer US Dept Agr USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA.;Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA..
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Ma, Jiantao
    Tufts Univ, Jean Mayer US Dept Agr USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA..
    Ross, Alastair B.
    Chalmers, Dept Life Sci Engn, Food & Nutr Sci, S-41296 Gothenburg, Sweden..
    Lichtenstein, Alice H.
    Tufts Univ, Jean Mayer US Dept Agr USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA.;Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA..
    Livingston, Kara A.
    Tufts Univ, Jean Mayer US Dept Agr USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA..
    Jacques, Paul F.
    Tufts Univ, Jean Mayer US Dept Agr USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA.;Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA..
    Rasmussen, Helen M.
    Tufts Univ, Jean Mayer US Dept Agr USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA.;Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA..
    Blumberg, Jeffrey B.
    Tufts Univ, Jean Mayer US Dept Agr USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA.;Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA..
    Chen, C-Y. Oliver
    Tufts Univ, Jean Mayer US Dept Agr USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA.;Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA..
    Comparison of plasma alkylresorcinols (AR) and urinary AR metabolites as biomarkers of compliance in a short-term, whole-grain intervention study2016In: European Journal of Nutrition, ISSN 1436-6207, E-ISSN 1436-6215, Vol. 55, no 3, p. 1235-1244Article in journal (Refereed)
    Abstract [en]

    Alkylresorcinols (AR) are phenolic lipids present in the bran of wheat and rye. Plasma AR and their urinary metabolites may be suitable biomarkers of whole-grain (WG) wheat and rye consumption. The objective of this study was to examine plasma AR and urinary AR metabolites in response to WG wheat consumption. In a randomized crossover study, 19 subjects (10 males, 9 females; BMI 22.0 kg/m(2); age 26 years) incorporated either 3 servings (48 g) or 6 servings (96 g) of WG wheat daily into their regular diet for 1 week. Subjects completed a 2-week washout period, abstaining from all WG consumption, before each intervention. Fasting blood and 24-h urine were collected before and after each intervention. Plasma AR homologues (C19:0, C21:0, C23:0) were quantified by GC-MS after diethyl ether and solid phase extraction and derivatization. Urinary AR metabolites [3,5-dihydroxybenzoic acid and 3-(3,5-dihydroxyphenyl)-propanoic acid] were determined using HPLC with electrochemical detection after enzymatic deconjugation and ethyl acetate extraction. Urinary total AR metabolites were significantly higher after 6 compared with 3 servings of WG wheat (56 vs. 32 mu mol/day, P < 0.001). This dose-response relationship was independent of age, sex, energy intake, and baseline urinary AR metabolite concentration. Plasma total AR tended to be higher after 6 compared with 3 servings of WG wheat (103.0 vs. 86.9 nmol/L), but this difference was not significant (P = 0.42). The results suggest that urinary AR metabolites from 24-h urine collections may be useful as biomarkers of compliance in intervention studies of WG wheat.

  • 24.
    Risérus, Ulf
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Milk fat biomarkers and cardiometabolic disease2017In: Current Opinion in Lipidology, ISSN 0957-9672, E-ISSN 1473-6535, Vol. 28, no 1, p. 46-51Article, review/survey (Refereed)
    Abstract [en]

    Purpose of review Dairy is a major food group with potential impact on cardiometabolic health. Self-reported dairy intake has limitations that can partly be avoided by using biomarkers. This review aims to summarize the evidence of odd-chain saturated fatty acids (OCFAs), that is, pentadecanoic acid (C15 : 0) and heptadecanoic acid (17 : 0), as biomarkers of dairy fat intake. In addition, the associations of OCFA biomarkers with cardiometabolic disease will be overviewed. Recent findings Adipose tissue 15 : 0 is the preferred biomarker but also circulating 15 : 0, and to a weaker extent 17 : 0, reflects both habitual and changes in dairy intake. Whereas results from studies assessing cardiovascular outcomes are inconsistent, OCFA biomarkers are overall associated with lower diabetes risk. Residual confounding should however be considered until interventional data and mechanisms are available. Although OCFA biomarkers mainly reflect dairy fat intake, recently proposed endogenous synthesis and metabolism do motivate further research. Summary Taking into account the study population diet and limitations of OCFA biomarkers, both adipose and circulating levels of 15 : 0, in particular, are useful for estimating total dairy fat intake. OCFA biomarkers are overall not linked to cardiovascular disease risk, but a possible beneficial role of dairy foods in diabetes prevention warrant further study.

  • 25.
    Wu, Jason H. Y.
    et al.
    Univ New South Wales, George Inst Global Hlth, Fac Med, Sydney, NSW 2050, Australia..
    Marklund, Matti
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Imamura, Fumiaki
    Univ Cambridge, MRC, Epidemiol Unit, Cambridge, England..
    Tintle, Nathan
    Dordt Coll, Dept Math & Stat, Sioux Ctr, IA USA..
    Korat, Andres V. Ardisson
    Harvard TH Chan Sch Publ Hlth, Dept Nutr & Epidemiol, Boston, MA USA..
    de Goede, Janette
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands..
    Zhou, Xia
    Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA..
    Yang, Wei-Sin
    Natl Taiwan Univ, Inst Epidemiol & Prevent Med, Coll Publ Hlth, Taipei, Taiwan..
    Otto, Marcia C. de Oliveira
    Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Div Epidemiol Human Genet & Environm Sci, Houston, TX USA..
    Kroger, Janine
    German Inst Human Nutr, Potsdam, Germany..
    Qureshi, Waqas
    Wake Forest Univ, Winston Salem, NC 27109 USA..
    Virtanen, Jyrki K.
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland..
    Bassett, Julie K.
    Canc Council Victoria, Melbourne, Vic, Australia..
    Frazier-Wood, Alexis C.
    ARS, USDA, Childrens Nutr Res Ctr, Houston, TX USA..
    Lankinen, Maria
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland..
    Murphy, Rachel A.
    Univ British Columbia, Vancouver, BC, Canada..
    Rajaobelina, Kalina
    Univ Bordeaux, INSERM, Bordeaux Populat Hlth Res Ctr, UMR 1219, Bordeaux, France..
    Del Gobbo, Liana C.
    Stanford Univ, Dept Med, Div Cardiovasc Med, Sch Med, Stanford, CA 94305 USA..
    Forouhi, Nita G.
    Univ Cambridge, MRC, Epidemiol Unit, Cambridge, England..
    Luben, Robert
    Univ Cambridge, Dept Publ Hlth & Primary Care, Sch Clin Med, Cambridge, England..
    Khaw, Kay-Tee
    Univ Cambridge, Dept Publ Hlth & Primary Care, Sch Clin Med, Cambridge, England.;Dordt Coll, Dept Math & Stat, Sioux Ctr, IA USA..
    Wareham, Nick
    Univ Cambridge, MRC, Epidemiol Unit, Cambridge, England..
    Kalsbeek, Anya
    Dordt Coll, Dept Math & Stat, Sioux Ctr, IA USA.;Dordt Coll, Dept Biol, Sioux Ctr, IA USA..
    Veenstra, Jenna
    Dordt Coll, Dept Math & Stat, Sioux Ctr, IA USA.;Dordt Coll, Dept Biol, Sioux Ctr, IA USA..
    Luo, Juhua
    Indiana Univ, Dept Epidemiol & Biostat, Bloomington, IN USA..
    Hu, Frank B.
    Harvard TH Chan Sch Publ Hlth, Dept Nutr & Epidemiol, Boston, MA USA..
    Lin, Hung-Ju
    Natl Taiwan Univ Hosp, Dept Internal Med, Taipei, Taiwan..
    Siscovick, David S.
    New York Acad Med, New York, NY USA..
    Boeing, Heiner
    German Inst Human Nutr, Potsdam, Germany..
    Chen, Tzu-An
    ARS, USDA, Childrens Nutr Res Ctr, Houston, TX USA..
    Steffen, Brian
    Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA..
    Steffen, Lyn M.
    Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA..
    Hodge, Allison
    Canc Council Victoria, Melbourne, Vic, Australia..
    Eriksdottir, Gudny
    Iceland Heart Inst, Kopavogur, Iceland..
    Smith, Albert V.
    Iceland Heart Inst, Kopavogur, Iceland..
    Gudnason, Vilmunder
    Iceland Heart Inst, Kopavogur, Iceland..
    Harris, Tamara B.
    NIA, Bethesda, MD 20892 USA..
    Brouwer, Ingeborg A.
    Vrije Univ Amsterdam, Hlth Sci, Amsterdam, Netherlands..
    Berr, Claudine
    Montpellier Univ, INSERM, U1061, Neuropsychiat Epidemiol & Clin Res, Montpellier, France.;Montpellier Univ, Montpellier Univ Hosp, Montpellier, France..
    Helmer, Catherine
    Univ Bordeaux, INSERM, Bordeaux Populat Hlth Res Ctr, UMR 1219, Bordeaux, France..
    Samieri, Cecilia
    Univ Bordeaux, INSERM, Bordeaux Populat Hlth Res Ctr, UMR 1219, Bordeaux, France..
    Laakso, Markku
    Univ Eastern Finland, Inst Clin Med, Kuopio, Finland..
    Tsai, Michael Y.
    Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA..
    Giles, Graham G.
    Canc Council Victoria, Melbourne, Vic, Australia..
    Nurmi, Tarja
    Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland..
    Wagenknecht, Lynne
    Wake Forest Univ, Winston Salem, NC 27109 USA..
    Schulze, Matthias B.
    German Inst Human Nutr, Potsdam, Germany..
    Lemaitre, Rozenn N.
    Univ Washington, Cardiovasc Hlth Res Unit, Dept Med, Seattle, WA 98195 USA..
    Chien, Kuo-Liong
    Natl Taiwan Univ, Inst Epidemiol & Prevent Med, Coll Publ Hlth, Taipei, Taiwan.;Natl Taiwan Univ Hosp, Dept Internal Med, Taipei, Taiwan..
    Soedamah-Muthu, Sabita S.
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands..
    Geleijnse, Johanna M.
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands..
    Sun, Qi
    Harvard TH Chan Sch Publ Hlth, Dept Nutr & Epidemiol, Boston, MA USA..
    Harris, William S.
    Univ South Dakota, Sanford Sch Med, Dept Internal Med, Sioux Falls, SD USA.;OmegaQuant Analyt, Sioux Falls, SD USA..
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Arnlov, Johan
    Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Family Med, Stockholm, Sweden.;Dalarna Univ, Sch Hlth & Social Studies, Falun, Sweden..
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Micha, Renata
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA..
    Mozaffarian, Dariush
    Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA..
    Omega-6 fatty acid biomarkers and incident type 2 diabetes: pooled analysis of individual-level data for 39 740 adults from 20 prospective cohort studies2017In: The Lancet Diabetes and Endocrinology, ISSN 2213-8587, E-ISSN 2213-8595, Vol. 5, no 12, p. 965-974Article in journal (Refereed)
    Abstract [en]

    Background The metabolic effects of omega-6 polyunsaturated fatty acids (PUFAs) remain contentious, and little evidence is available regarding their potential role in primary prevention of type 2 diabetes. We aimed to assess the associations of linoleic acid and arachidonic acid biomarkers with incident type 2 diabetes. Methods We did a pooled analysis of new, harmonised, individual-level analyses for the biomarkers linoleic acid and its metabolite arachidonic acid and incident type 2 diabetes. We analysed data from 20 prospective cohort studies from ten countries (Iceland, the Netherlands, the USA, Taiwan, the UK, Germany, Finland, Australia, Sweden, and France), with biomarkers sampled between 1970 and 2010. Participants included in the analyses were aged 18 years or older and had data available for linoleic acid and arachidonic acid biomarkers at baseline. We excluded participants with type 2 diabetes at baseline. The main outcome was the association between omega-6 PUFA biomarkers and incident type 2 diabetes. We assessed the relative risk of type 2 diabetes prospectively for each cohort and lipid compartment separately using a prespecified analytic plan for exposures, covariates, effect modifiers, and analysis, and the findings were then pooled using inverse-variance weighted meta-analysis. Findings Participants were 39 740 adults, aged (range of cohort means) 49-76 years with a BMI (range of cohort means) of 23.3-28.4 kg/m(2), who did not have type 2 diabetes at baseline. During a follow-up of 366 073 person-years, we identified 4347 cases of incident type 2 diabetes. In multivariable-adjusted pooled analyses, higher proportions of linoleic acid biomarkers as percentages of total fatty acid were associated with a lower risk of type 2 diabetes overall (risk ratio [RR] per interquintile range 0.65, 95% CI 0.60-0.72, p<0.0001; I-2=53.9%, p(heterogeneity) = 0.002). The associations between linoleic acid biomarkers and type 2 diabetes were generally similar in different lipid compartments, including phospholipids, plasma, cholesterol esters, and adipose tissue. Levels of arachidonic acid biomarker were not significantly associated with type 2 diabetes risk overall (RR per interquintile range 0.96, 95% CI 0.88-1.05; p=0.38; I-2 = 63.0%, p(heterogeneity) < 0.0001). The associations between linoleic acid and arachidonic acid biomarkers and the risk of type 2 diabetes were not significantly modified by any prespecified potential sources of heterogeneity (ie, age, BMI, sex, race, aspirin use, omega-3 PUFA levels, or variants of the FADS gene; all p(heterogeneity) >= 0-13). Interpretation Findings suggest that linoleic acid has long-term benefits for the prevention of type 2 diabetes and that arachidonic acid is not harmful.

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