6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Dietary Inflammatory Index, Dietary Non-Enzymatic Antioxidant Capacity, and Colorectal and Breast Cancer Risk (MCC-Spain Study)

      research-article
      1 , 2 , 3 , 4 , 5 , 6 , * , 3 , 4 , 7 , 3 , 8 , 9 , 10 , 11 , 12 , 10 , 11 , 12 , 3 , 13 , 3 , 4 , 7 , 14 , 1 , 2 , 3 , 15 , 1 , 2 , 3 , 3 , 16 , 17 , 18 , 17 , 18 , 3 , 19 , 20 , 19 , 3 , 21 , 22 , 23 , 3 , 22 , 23 , 22 , 23 , 3 , 24 , 25 , 24 , 25 , 26 , 3 , 27 , 3 , 28 , 3 , 27 , 29 ,   3 , 30 , 3 , 31 , 3 , 31 , 32 , 3 , 27 , 28 , 3 , 4 , 7 , 14 , 1 , 2 , 3 , 15 , 3 , 17 , 18
      Nutrients
      MDPI
      colorectal cancer, breast cancer, diet, dietary inflammatory index, antioxidants, NEAC, case-control study, MCC-Spain

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Inflammation and antioxidant capacity have been associated with colorectal and breast cancer. We computed the dietary inflammatory index (DII ®), and the total dietary non-enzymatic antioxidant capacity (NEAC) and associated them with colorectal and breast cancer risk in the population-based multi case-control study in Spain (MCC-Spain). We included 1852 colorectal cancer and 1567 breast cancer cases, and 3447 and 1486 population controls, respectively. DII score and NEAC were derived using data from a semi-quantitative validated food frequency questionnaire. Unconditional logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (95%CI) for energy-adjusted DII (E-DII), and a score combining E-DII and NEAC. E-DII was associated with colorectal cancer risk (OR = 1.93, highest quartile versus lowest, 95%CI:1.60–2.32; p-trend: <0.001); this increase was observed for both colon and rectal cancer. Less pronounced increased risks were observed for breast cancer (OR = 1.22, highest quartile versus lowest, 95%CI:0.99–1.52, p-trend: >0.10). The combined score of high E-DII scores and low antioxidant values were associated with colorectal cancer risk (OR = 1.48, highest quartile versus lowest, 95%CI: 1.26–1.74; p-trend: <0.001), but not breast cancer. This study provides evidence that a pro-inflammatory diet is associated with increased colorectal cancer risk while findings for breast cancer were less consistent.

          Related collections

          Most cited references47

          • Record: found
          • Abstract: found
          • Article: not found

          Oxidative stress and cancer: an overview.

          Reactive species, which mainly include reactive oxygen species (ROS), are products generated as a consequence of metabolic reactions in the mitochondria of eukaryotic cells. In normal cells, low-level concentrations of these compounds are required for signal transduction before their elimination. However, cancer cells, which exhibit an accelerated metabolism, demand high ROS concentrations to maintain their high proliferation rate. Different ways of developing ROS resistance include the execution of alternative pathways, which can avoid large amounts of ROS accumulation without compromising the energy demand required by cancer cells. Examples of these processes include the guidance of the glycolytic pathway into the pentose phosphate pathway (PPP) and/or the generation of lactate instead of employing aerobic respiration in the mitochondria. Importantly, ROS levels can be used as a thermostat to monitor the damage that cells can bear. The implications for ROS regulation are highly significant for cancer therapy because commonly used radio- and chemotherapeutic drugs influence tumor outcome through ROS modulation. Moreover, the discovery of novel biomarkers that are able to predict the clinical response to pro-oxidant therapies is a crucial challenge to overcome to allow for the personalization of cancer therapies. Copyright © 2012 Elsevier B.V. All rights reserved.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Anti-inflammatory effects of the Mediterranean diet: the experience of the PREDIMED study.

            Several epidemiological and clinical studies have evaluated the effects of a Mediterranean diet (Med-Diet) on total cardiovascular mortality, and all concluded that adherence to the traditional Med-Diet is associated with reduced cardiovascular risk. However, the molecular mechanisms involved are not fully understood. Since atherosclerosis is nowadays considered a low-grade inflammatory disease, recent studies have explored the anti-inflammatory effects of a Med-Diet intervention on serum and cellular biomarkers related to atherosclerosis. In a pilot study of the PREvencion con DIeta MEDiterranea (PREDIMED) trial, we analysed the short-term effects of two Med-Diet interventions, one supplemented with virgin olive oil and another with nuts, on vascular risk factors in 772 subjects at high risk for CVD, and in a second study we evaluated the effects of these interventions on cellular and serum inflammatory biomarkers in 106 high-risk subjects. Compared to a low-fat diet, the Med-Diet produced favourable changes in all risk factors. Thus, participants in both Med-Diet groups reduced blood pressure, improved lipid profile and diminished insulin resistance compared to those allocated a low-fat diet. In addition, the Med-Diet supplemented with virgin olive oil or nuts showed an anti-inflammatory effect reducing serum C-reactive protein, IL-6 and endothelial and monocytary adhesion molecules and chemokines, whereas these parameters increased after the low-fat diet intervention. In conclusion, Med-Diets down-regulate cellular and circulating inflammatory biomarkers related to atherogenesis in subjects at high cardiovascular risk. These results support the recommendation of the Med-Diet as a useful tool against CVD.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Chronic inflammation and oxidative stress in the genesis and perpetuation of cancer: role of lipid peroxidation, DNA damage, and repair.

              Chronic inflammation, induced by biological, chemical, and physical factors, was associated with increased risk of human cancer at various sites. Chronic inflammatory processes induce oxidative/nitrosative stress and lipid peroxidation (LPO), thereby generating excess reactive oxygen species (ROS), reactive nitrogen species (RNS), and DNA-reactive aldehydes. Miscoding etheno- and propano-modified DNA bases are generated inter alia by reaction of DNA with these major LPO products. Steady-state levels of LPO-derived (etheno-) DNA adducts in organs affected by persistent inflammatory processes were investigated as potential lead markers for assessing progression of inflammatory cancer-prone diseases. Using ultrasensitive and specific detection methods for the analysis of human tissues, cells, and urine, etheno-DNA adduct levels were found to be significantly elevated in the affected organs of subjects with chronic pancreatitis, ulcerative colitis, and Crohn's disease. Patients with alcohol-related liver diseases showed excess hepatic DNA damage progressively increasing from hepatitis, fatty liver, to liver cirrhosis. Ethenodeoxyadenosine excreted after DNA repair in urine of hepatitis B virus-related chronic hepatitis and liver cirrhosis patients was increased up to 90-fold. Putative mechanisms that may control DNA damage in inflamed tissues including impaired or imbalanced DNA repair pathways are reviewed. Persistent oxidative/nitrosative stress and excess LPO are induced by inflammatory processes in a self-perpetuating process and cause progressive accumulation of DNA damage in target organs. Together with deregulation of cell homeostasis, the resulting genetic changes act as driving force in chronic inflammation-associated human disease pathogenesis. Thus steady-state levels of DNA damage caused by ROS, RNS, and LPO end products provide promising molecular signatures for risk prediction and potential targets and biomarkers for preventive measures.
                Bookmark

                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                21 June 2019
                June 2019
                : 11
                : 6
                : 1406
                Affiliations
                [1 ]Oncology Data Analytics Program (ODAP), Catalan Institute of Oncology (ICO), L’Hospitalet del Llobregat, 08908 Barcelona, Spain; mobon@ 123456idibell.cat (M.O.-S.), fmoratalla@ 123456iconcologia.net (F.M.), e.guino@ 123456iconcologia.net (E.G.); v.moreno@ 123456iconcologia.net (V.M.)
                [2 ]ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL), L’Hospitalet de Llobregat, 08908 Barcelona, Spain
                [3 ]Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP), 28029 Madrid, Spain; esther.gracia@ 123456isglobal.org (E.G.-L.); au-molinuevo@ 123456euskadi.eus (A.M.); atardon@ 123456uniovi.es (A.T.); gemma.castano@ 123456isglobal.org (G.C.-V.); rmarcos@ 123456iconcologia.net (R.M.-G.); rocioolmedo@ 123456ugr.es (R.O.-R.); juan.alguacil@ 123456dbasp.uhu.es (J.A.); vicente.martin@ 123456unileon.es (V.M.); maria.ederra.sanz@ 123456cfnavarra.es (M.E.); bperez@ 123456isciii.es (B.P.); nuria.aragones@ 123456salud.madrid.org (N.A.); acastello@ 123456isciii.es (A.C.); jmhuerta.carm@ 123456gmail.com (J.M.H.); trinidad.dierssen@ 123456unican.es (T.D.-S.); ines.gomez@ 123456unican.es (I.G.-A.); mpollan@ 123456isciii.es (M.P.); manolis.kogevinas@ 123456isglobal.org (M.K.); epicss-san@ 123456euskadi.eus (P.A.)
                [4 ]Instituto de Salud Global de Barcelona (ISGlobal), 08036 Barcelona, Spain
                [5 ]Instituto de Investigación Sanitaria Illes Balears (IdISBa), 07120 Palma de Mallorca, Spain
                [6 ]CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), 28029 Madrid, Spain
                [7 ]Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), 08002 Barcelona, Spain
                [8 ]Genetic and Molecular Epidemiology Group, Spanish National Cancer Research Center (CNIO), 28029 Madrid, Spain; memolina@ 123456cnio.es
                [9 ]Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), 28029 Madrid, Spain
                [10 ]Cancer Prevention and Control Program, University of South Carolina, Columbia, SC 29208, USA.; shivappa@ 123456email.sc.edu (N.S.); JHEBERT@ 123456mailbox.sc.edu (J.R.H.)
                [11 ]Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA
                [12 ]Department of Nutrition, Connecting Health Innovations LLC (CHI), Columbia, SC 29201, USA
                [13 ]Department of Medicine, University of Oviedo, 33006 Oviedo, Spain
                [14 ]IMIM (Hospital del Mar Medical Research Institute), 08003 Barcelona, Spain
                [15 ]Department of Clinical Sciences, Faculty of Medicine, University of Barcelona, 08007 Barcelona, Spain
                [16 ]Genetics and Cancer Prevention Group, Epidemiology Unit and Girona Cancer Registry, Descriptive Epidemiology, IdIbGi, Catalan Institute of Oncology, 17007 Girona, Spain
                [17 ]Public Health Division of Gipuzkoa, 20003 San Sebastian, Spain; koor-tolosa@ 123456euskadi.eus (M.A.); l-gil@ 123456euskadi.eus (L.G.)
                [18 ]Biodonostia Research Institute, 20014 San Sebastian, Spain
                [19 ]Department of Preventive Medicine and Public Health, School of Medicine, University of Granada, 18016 Granada, Spain; macarenalozano@ 123456ugr.es
                [20 ]Instituto de Investigación Biosanitaria de Granada ibs.GRANADA, 18014 Granada, Spain
                [21 ]Centro de Investigación en Recursos Naturales, Salud y Medio Ambiente (RENSMA), Universidad de Huelva, 21071Huelva, Spain
                [22 ]The Research Group in Gene - Environment and Health Interactions (GIIGAS) / Institut of Biomedicine (IBIOMED), Universidad de León, 24071 León, Spain; tferv@ 123456unileon.es (T.F-V.); ajmolt@ 123456unileon.es (A J.M.)
                [23 ]Faculty of Health Sciences, Department of Biomedical Sciences, Area of Preventive Medicine and Public Health, Universidad de León, 24071 León, Spain
                [24 ]Navarra Public Health Institute, 31003 Pamplona, Spain; mc.moreno.iribas@ 123456cfnavarra.es
                [25 ]Navarra Institute for Health Research (IdiSNA), 31003 Pamplona, Spain
                [26 ]REDISSEC Red de Investigación en Servicios de Salud en Enfermedades Crónicas, 28029 Madrid, Spain
                [27 ]Cancer & Environmental Epidemiology Unit, Department of Epidemiology of Chronic Diseases, National Centre for Epidemiology, Carlos III Institute of Health, 28029 Madrid, Spain
                [28 ]Department of Health of Madrid, Cancer Epidemiology Section, Public Health Division, 28029 Madrid, Spain
                [29 ]Department of Surgery and Medical and Social Sciences. Alcalá de Henares University, 28801 Alcalá de Henares, Madrid, Spain
                [30 ]Department of Epidemiology, Murcia Regional Health Council, IMIB-Arrixaca, 30008 Murcia, Spain
                [31 ]Preventive Medicine, Universidad de Cantabria—IDIVAL, 39011 Santander, Spain
                [32 ]Cancer and Public Health Area, FISABIO—Public Health; 46020 Valencia, Spain; molina_anabar@ 123456gva.es
                Author notes
                [* ]Correspondence: mariaadoracion.romaguera@ 123456ssib.es ; Tel.: 871205000
                Author information
                https://orcid.org/0000-0003-4646-3513
                https://orcid.org/0000-0001-5150-1209
                https://orcid.org/0000-0003-4468-1816
                https://orcid.org/0000-0001-7858-5713
                https://orcid.org/0000-0001-9824-3657
                https://orcid.org/0000-0003-0054-6700
                https://orcid.org/0000-0002-4299-8214
                https://orcid.org/0000-0002-9637-3869
                https://orcid.org/0000-0001-5113-6475
                https://orcid.org/0000-0002-2818-5487
                Article
                nutrients-11-01406
                10.3390/nu11061406
                6628286
                31234427
                07117143-eafe-47aa-af87-de392a6ef7a2
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 02 May 2019
                : 19 June 2019
                Categories
                Article

                Nutrition & Dietetics
                colorectal cancer,breast cancer,diet,dietary inflammatory index,antioxidants,neac,case-control study,mcc-spain

                Comments

                Comment on this article