NUTRICASUS NUTRICASUS

Le Journal de la Mdecine Nutritionnelle et Fonctionnelle Pratique

N 15, Dcembre 2009

Editorial Editorial
Au Au moment moment de de cette cette priode priode privilgie privilgie des des ftes ftes de de fin fin danne, danne, le le laboratoire laboratoire Roman Roman Pais Pais est est heureux heureux et et fier fier de de vous vous annoncer annoncer larrive larrive dun dun nouveau nouveau venu venu dans dans la la famille famille des des NutriBilans NutriBilans :: l lOncoScreen OncoScreen.. Attendu Attendu par par de de trop trop nombreux nombreux mdecins, mdecins, soucieux soucieux de de prendre prendre en en charge de manire judicieuse et efficace le risque de leurs patients de dvelopper un cancer charge de manire judicieuse et efficace le risque de leurs patients de dvelopper un cancer ou, ou, pour pour ceux ceux dj dj atteints, atteints, de de rcidiver, rcidiver, l lOncoScreen OncoScreen reprsente reprsente une une avance avance significative significative dans la mise en place de stratgies de prvention personnalises efficaces. L OncoScreen dans la mise en place de stratgies de prvention personnalises efficaces. LOncoScreen est est une une rponse rponse adapte adapte et et ncessaire ncessaire au au constat, constat, avalis avalis par par lOrganisation lOrganisation Mondiale Mondiale de de la la Sant Sant (OMS), (OMS), selon selon lequel lequel lalimentation lalimentation est est responsable responsable de de plus plus dun dun tiers tiers des des cancers. cancers. Plus Plus que le tabac ! Depuis plusieurs annes, limpact de lalimentation sur le dveloppement que le tabac ! Depuis plusieurs annes, limpact de lalimentation sur le dveloppement de de tumeurs tumeurs malignes malignes est est le le sujet sujet de de dbats dbats srieux, srieux, aliments aliments par par des des tudes tudes aux aux rsultats rsultats souvent souvent opposs. opposs. Ainsi, Ainsi, certaines certaines tudes tudes tablissent tablissent un un lien lien clair clair et et causal causal entre entre le le stress stress oxydant oxydant et et lapparition lapparition de de lsions lsions noplasiques, noplasiques, alors alors que que dautres dautres clament clament que que lutilisation lutilisation danti-oxydants danti-oxydants augmente augmente le le risque risque de de dvelopper dvelopper ces ces maladies. maladies. In In medio medio stat stat veritas veritas !! En En effet, ce sont aussi bien les carences que les excs dun mme nutriment qui contribuent au effet, ce sont aussi bien les carences que les excs dun mme nutriment qui contribuent au dveloppement dveloppement des des cancers. cancers. L LOncoScreen OncoScreen value value un un rpertoire rpertoire de de paramtres paramtres nutritionnels nutritionnels et micronutritionnels qui sont indiscutablement impliqus dans le risque oncologique et micronutritionnels qui sont indiscutablement impliqus dans le risque oncologique lorsquils lorsquils sont sont perturbs perturbs :: profil profil en en acides acides gras, gras, homocystine, homocystine, stress stress oxydant, oxydant, taux taux sriques sriques de de vitamine vitamine D, D, des des carotnodes, carotnodes, du du slnium, slnium, du du cuivre cuivre et et du du zinc. zinc. Ainsi, Ainsi, l lOncoScreen OncoScreen se se rvle rvle tre tre un un outil outil bientt bientt incontournable incontournable puisquil puisquil va va contribuer contribuer rduire rduire denviron denviron 35% 35% le le risque risque de de vos vos patients patients (et (et du du vtre vtre dailleurs) dailleurs) de de dvelopper dvelopper un un cancer cancer !! Avec Avec cette cette nouvelle nouvelle qui, nous en sommes srs, vous rjouira, nous vous souhaitons un Joyeux Nol, qui, nous en sommes srs, vous rjouira, nous vous souhaitons un Joyeux Nol, une une excellente excellente fin fin danne danne 2009 2009 et et vous vous prsentons prsentons dj dj nos nos meilleurs meilleurs vux vux de de bonheur, bonheur, sant sant et et paix paix pour pour 2010. 2010. Nutritionnellement Nutritionnellement vtre, vtre, Ellipsys Ellipsys S.A. S.A.

Le Le Cancer Cancer est est une une maladie maladie vitable vitable qui qui requiert requiert des des modifications modifications importantes importantes du du mode mode de de vie vie !! Entre Entre 5 5 et et 10 10 % % seulement seulement de de tous tous les les cancers cancers sont sont attribuables attribuables des des facteurs facteurs gntiques (A et B). Cela veut dire que gntiques (A et B). Cela veut dire que 90 90 95% des cancers sont lis 95% des cancers sont lis lenvironnement. lenvironnement. Parmi Parmi les les facteurs facteurs environnementaux, environnementaux, lalimentation reprsente lalimentation reprsente la la cause cause la la plus plus importante importante de de cancers cancers suivie suivie par par le le tabagisme tabagisme et et les les infections infections (C). (C). Lorsque Lorsque lon lon prend prend en en compte compte les les cancers cancers les les plus plus frquents frquents de de notre notre population, population, lalimentation est considre lalimentation est considre comme comme responsable responsable de de 75% 75% des des cancers cancers de de la la prostate, 70% des cancers du colon et 50% prostate, 70% des cancers du colon et 50% des des cancers cancers du du sein, sein, du du pancras pancras et et de de lendomtre. lendomtre.

Anand P et al. Pharm Res. 2008 Sep;25(9):2097-116.

NUTRICASUS
Le Journal de la Mdecine Nutritionnelle et Fonctionnelle Pratique

OncoScreen
LOncoScreen LOncoScreen value value les les paramtres paramtres lis lis lalimentation lalimentation pour pour lesquels lesquels des des altrations altrations (excs (excs et et dficiences) dficiences) ont ont t t associes associes au au dveloppement dveloppement de de cancers cancers et et dont dont la la correction correction rduit rduit significativement significativement le le risque risque de de cancer. cancer.

NUTRICASUS
Le Journal de la Mdecine Nutritionnelle et Fonctionnelle Pratique

OnconScreen : Bas sur lEvidence et le Bon Sens

Overview of genes, diet and cancer. Mathers JC., Genes Nutr. 2007 Oct;2(1):67-70. Quantitative epidemiological analysis suggests that about one third of the variation in cancer risk can be attributed to variation in dietary exposure but it has proved difficult, using conventional epidemiological approaches, to identify which dietary components, in what amounts and over what time-scales are protective or potentially hazardous. Work in this area has been hampered by the lack of robust surrogate endpoints. However, the rapidly accumulating knowledge of the biological basis of cancer and the application of post-genomic technologies are helping the development of novel biomarkers of cancer risk. Genomic damage resulting in aberrant gene expression is the fundamental cause of all cancers. Such damage includes mutations, aberrant epigenetic marking, chromosomal damage and telomere shortening. Since both external agents and normal cell functions, such as mitosis, subject the genome to frequent and diverse insults, the human cell has evolved a battery of defence mechanisms which (a) attempt to minimize such damage (including inhibition of oxidative reactions by free radical scavenging and the detoxification of potential mutagens), (b) repair the damage or (c) remove severely damaged cells by shunting them into apoptosis. When such defences fail and a tumour becomes established, further genomic damage and further alterations in gene expression enable the tumour to grow, to cope with anoxia, to develop a novel blood supply (angiogenesis), to escape from the confines of its initiation site and to establish colonies elsewhere in the body (metastasis). All of these processes are potentially modifiable by food components and by nutritional status. In addition, interactions between dietary (and other environmental and lifestyle) factors and genetic make-up [seen principally in the assembly of single nucleotide polymorphisms (SNPs) which is unique to each individual] contributes to interindividual differences in cancer risk. Dietary intakes of omega-6 and omega-3 polyunsaturated fatty acids and the risk of breast cancer. Thibaut AC, Chajs V, Gerber M, Boutron-Ruault MC, Joulin V, Lenoir G, Berrino F, Riboli E, Bnichou J, Clavel-Chapelon F. Int J Cancer. 2009 Feb 15;124(4):924-31. Experimental studies suggest detrimental effects of omega-6 polyunsaturated fatty acids (PUFA), and beneficial effects of omega-3 PUFAs on mammary carcinogenesis, possibly in interaction with antioxidants. However, PUFA food sources are diverse in human diets and few epidemiologic studies have examined whether associations between dietary PUFAs and breast cancer risk vary according to food sources or antioxidant intakes. The relationship between individual PUFA intakes estimated from diet history questionnaires and breast cancer risk was examined among 56,007 French women. During 8 years of follow-up, 1,650 women developed invasive breast cancer. Breast cancer risk was not related to any dietary PUFA overall; however, opposite associations were seen according to food sources, suggesting other potential effects than PUFA per se. Breast cancer risk was inversely associated with alpha-linolenic acid (ALA) intake from fruit and vegetables [highest vs. lowest quintile, hazard ratio (HR) 0.74; 95% confidence interval (CI) 0.63, 0.88; p trend < 0.0001], and from vegetable oils (HR 0.83; 95% CI 0.71, 0.97; p trend 0.017). Conversely, breast cancer risk was positively related to ALA intake from nut mixes (p trend 0.004) and processed foods (p trend 0.068), as was total ALA intake among women in the highest quintile of dietary vitamin E (p trend 0.036). A significant interaction was also found between omega-6 and long-chain omega-3 PUFAs, with breast cancer risk inversely related to long-chain omega-3 PUFAs in women belonging to the highest quintile of omega-6 PUFAs (p interaction 0.042). These results emphasize the need to consider food sources, as well as interactions between fatty acids and with antioxidants, when evaluating associations between PUFA intakes and breast cancer risk. 8-hydroxy-2' -deoxyguanosine (8-OHdG): A critical biomarker of oxidative stress and carcinogenesis. Valavanidis A, Vlachogianni T, Fiotakis C. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2009 Apr;27(2):120-39. There is extensive experimental evidence that oxidative damage permanently occurs to lipids of cellular membranes, proteins, and DNA. In nuclear and mitochondrial DNA, 8-hydroxy-2' -deoxyguanosine (8-OHdG) or 8-oxo-7,8-dihydro-2' -deoxyguanosine (8-oxodG) is one of the predominant forms of free radical-induced oxidative lesions, and has therefore been widely used as a biomarker for oxidative stress and carcinogenesis. Studies showed that urinary 8-OHdG is a good biomarker for risk assessment of various cancers and degenerative diseases. The most widely used method of quantitative analysis is high-performance liquid chromatography (HPLC) with electrochemical detection (EC), gas chromatography-mass spectrometry (GC-MS), and HPLC tandem mass spectrometry. In order to resolve the methodological problems encountered in measuring quantitatively 8-OHdG, the European Standards Committee for Oxidative DNA Damage was set up in 1997 to resolve the artifactual oxidation problems during the procedures of isolation and purification of oxidative DNA products. The biomarker 8-OHdG or 8-oxodG has been a pivotal marker for measuring the effect of endogenous oxidative damage to DNA and as a factor of initiation and promotion of carcinogenesis. The biomarker has been used to estimate the DNA damage in humans after exposure to cancer-causing agents, such as tobacco smoke, asbestos fibers, heavy metals, and polycyclic aromatic hydrocarbons. In recent years, 8-OHdG has been used widely in many studies not only as a biomarker for the measurement of endogenous oxidative DNA damage but also as a risk factor for many diseases including cancer. Decreased incidence of prostate cancer with selenium supplementation: results of a double-blind cancer prevention trial. Clark LC, Dalkin B, Krongrad A, Combs GF Jr, Turnbull BW, Slate EH, Witherington R, Herlong JH, Janosko E, Carpenter D, Borosso C, Falk S, Rounder J Br J Urol 1998 May;81(5):730-4 OBJECTIVE: To test if supplemental dietary selenium is associated with changes in the incidence of prostate cancer. PATIENTS AND METHOD: A total of 974 men with a history of either a basal cell or squamous cell carcinoma were randomized to either a daily supplement of 200 microg of selenium or a placebo. Patients were treated for a mean of 4.5 years and followed for a mean of 6.5 years. RESULTS: Selenium treatment was associated with a significant (63%) reduction in the secondary endpoint of prostate cancer incidence during 1983-93. There were 13 prostate cancer cases in the selenium-treated group and 35 cases in the placebo group (relative risk, RR=0.37, P=0.002). Restricting the analysis to the 843 patients with initially normal levels of prostate-specific antigen (< or = 4 ng/mL),only four cases were diagnosed in the selenium-treated group and 16 cases were diagnosed in the placebo group after a 2 year treatment lag, (RR=0.26 P=0.009). There were significant health benefits also for the other secondary endpoints of total cancer mortality, and the incidence of total, lung and colorectal cancer. There was no significant change in incidence for the primary endpoints of basal and squamous cell carcinoma of the skin. In light of these results, the 'blinded' phase of this trial was stopped early. CONCLUSIONS: Although selenium shows no protective effects against the primary endpoint of squamous and basal cell carcinomas of the skin, the seleniumtreated group had substantial reductions in the incidence of prostate cancer, and total cancer incidence and mortality that demand further evaluation in well-controlled prevention trials. Vitamin D for cancer prevention: global perspective. Garland CF, Gorham ED, Mohr SB, Garland FC. Ann Epidemiol. 2009 Jul;19(7):468-83. PURPOSE: Higher serum levels of the main circulating form of vitamin D, 25-hydroxyvitamin D (25(OH)D), are associated with substantially lower incidence rates of colon, breast, ovarian, renal, pancreatic, aggressive prostate and other cancers. METHODS: Epidemiological findings combined with newly discovered mechanisms suggest a new model of cancer etiology that accounts for these actions of 25(OH)D and calcium. Its seven phases are disjunction, initiation, natural selection, overgrowth, metastasis, involution, and transition (abbreviated DINOMIT). Vitamin D metabolites prevent disjunction of cells and are beneficial in other phases. RESULTS/CONCLUSIONS: It is projected that raising the minimum year-around serum 25(OH)D level to 40 to 60 ng/mL (100-150 nmol/L) would prevent approximately 58,000 new cases of breast cancer and 49,000 new cases of colorectal cancer each year, and three fourths of deaths from these diseases in the United States and Canada, based on observational studies combined with a randomized trial. Such intakes also are expected to reduce case-fatality rates of patients who have breast, colorectal, or prostate cancer by half. There are no unreasonable risks from intake of 2000 IU per day of vitamin D(3), or from a population serum 25(OH)D level of 40 to 60 ng/mL. The time has arrived for nationally coordinated action to substantially increase intake of vitamin D and calcium.

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NUTRICASUS NUTRICASUS
Le Journal de la Mdecine Nutritionnelle et Fonctionnelle Pratique
Formations en Mdecine Nutritionnelle et Fonctionnelle : Vous souhaitez acqurir une formation de base solide en mdecine nutritionnelle et fonctionnelle ou vous voulez vous perfectionnez ? Plusieurs formations de niveau acadmique sont disponibles : Universit dEt de base : Fondements biochimiques et physiologiques de la mdecine nutritionnelle et fonctionnelle. Quand ? Du lundi 16 au vendredi 20 Aot 2010. O ? A Paris. Universit dEt Spcialise : Nutrition et Cerveau. Quand ? Du Dimanche 22 au Dimanche 29 Aot 2010. O ? Au ClubMed la Palmyre. Formations modulaires de Weekends : Module 4 : Nutrition et mtabolisme du glucose (obsit, syndrome mtabolique, diabte) Quand ? Le Weekend du 16 & 17 janvier 2010. O ? A Paris. Module 5 : Dtoxication. Quand ? Le Weekend du 20 & 21 mars 2010. O ? A Paris.

Pour plus dinformations, merci de contacter Annick Leflot a.leflot@rplab.be

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Editeur Editeurresponsable responsable Ellipsys EllipsysS.A. S.A.--Green GreenAlley AlleyOffice OfficePark Park--70 70Rue Ruedu duPanier PanierVert Vert B-1400 Nivelles Belgique B-1400 Nivelles - Belgique
info@rplab.be info@rplab.be Nutricasus Nutricasusest estrdig rdigpar pardes desexperts expertsdans dansle ledomaine domainede dela lanutrition nutrition sous la supervision du comit scientifique du laboratoire Roman sous la supervision du comit scientifique du laboratoire RomanPas. Pas.