N15-Oncoscreen

7/27/2019 N15-Oncoscreen

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NUTRICASUS

Editorial

Au moment de cette priode privilgie des ftes de fin danne, le laboratoire Roman Paisest heureux et fier de vous annoncer larrive dun nouveau venu dans la famille des

NutriBilans : lOncoScreen . Attendu par de trop nombreux mdecins, soucieux de prendre en

charge de manire judicieuse et efficace le risque de leurs patients de dvelopper un cancer

ou, pour ceux dj atteints, de rcidiver, lOncoScreen reprsente une avance significative

dans la mise en place de stratgies de prvention personnalises efficaces. LOncoScreen

est une rponse adapte et ncessaire au constat, avalis par lOrganisation Mondiale de la

Sant (OMS), selon lequel lalimentation est responsable de plus dun tiers des cancers. Plus

que le tabac ! Depuis plusieurs annes, limpact de lalimentation sur le dveloppement de

tumeurs malignes est le sujet de dbats srieux, aliments par des tudes aux rsultats

souvent opposs. Ainsi, certaines tudes tablissent un lien clair et causal entre le stressoxydant et lapparition de lsions noplasiques, alors que dautres clament que lutilisation

danti-oxydants augmente le risque de dvelopper ces maladies. In medio stat veritas ! En

effet, ce sont aussi bien les carences que les excs dun mme nutriment qui contribuent au

dveloppement des cancers. LOncoScreen value un rpertoire de paramtres nutritionnels

et micronutritionnels qui sont indiscutablement impliqus dans le risque oncologique lorsquils

sont perturbs : profil en acides gras, homocystine, stress oxydant, taux sriques de

vitamine D, des carotnodes, du slnium, du cuivre et du zinc. Ainsi, lOncoScreen se

rvle tre un outil bientt incontournable puisquil va contribuer rduire denviron 35% le

risque de vos patients (et du vtre dailleurs) de dvelopper un cancer ! Avec cette nouvelle

qui, nous en sommes srs, vous rjouira, nous vous souhaitons un Joyeux Nol, une

excellente fin danne 2009 et vous prsentons dj nos meilleurs vux de bonheur, sant et

paix pour 2010.

Nutritionnellement vtre,

Ellipsys S.A.

Editorial

Au moment de cette priode privilgie des ftes de fin danne, le laboratoire Roman Paisest heureux et fier de vous annoncer larrive dun nouveau venu dans la famille des

NutriBilans : lOncoScreen . Attendu par de trop nombreux mdecins, soucieux de prendre en

charge de manire judicieuse et efficace le risque de leurs patients de dvelopper un cancer

ou, pour ceux dj atteints, de rcidiver, lOncoScreen reprsente une avance significative

dans la mise en place de stratgies de prvention personnalises efficaces. LOncoScreen

est une rponse adapte et ncessaire au constat, avalis par lOrganisation Mondiale de la

Sant (OMS), selon lequel lalimentation est responsable de plus dun tiers des cancers. Plus

que le tabac ! Depuis plusieurs annes, limpact de lalimentation sur le dveloppement de

tumeurs malignes est le sujet de dbats srieux, aliments par des tudes aux rsultats

souvent opposs. Ainsi, certaines tudes tablissent un lien clair et causal entre le stressoxydant et lapparition de lsions noplasiques, alors que dautres clament que lutilisation

danti-oxydants augmente le risque de dvelopper ces maladies. In medio stat veritas ! En

effet, ce sont aussi bien les carences que les excs dun mme nutriment qui contribuent au

dveloppement des cancers. LOncoScreen value un rpertoire de paramtres nutritionnels

et micronutritionnels qui sont indiscutablement impliqus dans le risque oncologique lorsquils

sont perturbs : profil en acides gras, homocystine, stress oxydant, taux sriques de

vitamine D, des carotnodes, du slnium, du cuivre et du zinc. Ainsi, lOncoScreen se

rvle tre un outil bientt incontournable puisquil va contribuer rduire denviron 35% le

risque de vos patients (et du vtre dailleurs) de dvelopper un cancer ! Avec cette nouvelle

qui, nous en sommes srs, vous rjouira, nous vous souhaitons un Joyeux Nol, une

excellente fin danne 2009 et vous prsentons dj nos meilleurs vux de bonheur, sant etpaix pour 2010.

Nutritionnellement vtre,

Ellipsys S.A.

NUTRICASUSLe Journal de la Mdecine Nutritionnelle et Fonctionnelle Pratique

N 15, Dcembre 2009

Entre 5 et 10 % seulement de tous lescancers sont attribuables des facteurs

gntiques (A et B). Cela veut dire que 90

95% des cancers sont lis

lenvironnement.

Parmi les facteurs environnementaux,

lalimentation reprsente la cause la plus

importante de cancers suivie par le

tabagisme et les infections (C).

Lorsque lon prend en compte les cancersles plus frquents de notre population,

lalimentation est considre comme

responsable de 75% des cancers de la

prostate, 70% des cancers du colon et 50%

des cancers du sein, du pancras et de

lendomtre.

Entre 5 et 10 % seulement de tous lescancers sont attribuables des facteurs

gntiques (A et B). Cela veut dire que 90

95% des cancers sont lis

lenvironnement.

Parmi les facteurs environnementaux,

lalimentation reprsente la cause la plus

importante de cancers suivie par le

tabagisme et les infections (C).

Lorsque lon prend en compte les cancersles plus frquents de notre population,

lalimentation est considre comme

responsable de 75% des cancers de la

prostate, 70% des cancers du colon et 50%

des cancers du sein, du pancras et de

lendomtre.

Anand P et al.

Pharm Res. 2008 Sep;25(9):2097-116.

Le Cancer est une maladie vitable qui requiert des modifications importantes du

mode de vie !

Le Cancer est une maladie vitable qui requiert des modifications importantes du

mode de vie !


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NUTRICASUSNUTRICASUS

Le Journal de la Mdecine Nutritionnelle et Fonctionnelle Pratique

OncoScreenLOncoScreen value les paramtres lis lalimentation pour lesquels des altrations (excs et dficiences) ont t

associes au dveloppement de cancers et dont la correction rduit significativement le risque de cancer.

LOncoScreen value les paramtres lis lalimentation pour lesquels des altrations (excs et dficiences) ont t

associes au dveloppement de cancers et dont la correction rduit significativement le risque de cancer.


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NUTRICASUSNUTRICASUS

Le Journal de la Mdecine Nutritionnelle et Fonctionnelle Pratique

OnconScreen : Bas sur lEvidence et le Bon Sens

Overview of g enes, 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 dietaryexposure but it has proved difficult, using conventional epidemiological approaches, to identify which dietary components, in whatamounts 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-genomictechnologies 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 andtelomere 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 severelydamaged cells by shunting them into apoptosis. When such defences fail and a tumour becomes established, further genomic damageand 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 theseprocesses 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.

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 ofthe 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 degenerativediseases. 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 themethodological problems encountered in measuring quantitatively 8-OHdG, the European Standards Committee for Oxidative DNADamage 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 damageto 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 aromatichydrocarbons. 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.

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-3PUFAs on mammary carcinogenesis, possibly in interaction with antioxidants. However, PUFA food sources are diverse in human dietsand 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) intakefrom 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 intakefrom nut mixes (p trend 0.004) and processed foods (p trend 0.068), as was total ALA intake among women in the highest quintile ofdietary 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 interaction0.042). 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.

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, andtransition (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 threefourths 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. Thetime has arrived for nationally coordinated action to substantially increase intake of vitamin D and calcium.

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 JBr 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 dailysupplement 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 yeartreatment 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 andsquamous 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 selenium-treated 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.

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NUTRICASUS

Editeur responsable

Ellipsys S.A. - Green Alley Office Park - 70 Rue du Panier Vert

B-1400 Nivelles - Belgique

[email protected] Nutricasus est rdig par des experts dans le domaine de la nutrition

sous la supervision du comit scientifique du laboratoire Roman Pas.

Editeur responsable

Ellipsys S.A. - Green Alley Office Park - 70 Rue du Panier Vert

B-1400 Nivelles - Belgique

[email protected] Nutricasus est rdig par des experts dans le domaine de la nutrition

sous la supervision du comit scientifique du laboratoire Roman Pas.

NUTRICASUSLe Journal de la Mdecine Nutritionnelle et Fonctionnelle Pratique

NUTRINFOS

KITS ONCOSCREEN : kits contenant le matriel ncessaire et les modalits de prlvement

- Ils peuvent tre obtenus sur simple demande - par tlphone au 067/645 200

- par fax au 067/21 70 68

- par mail [email protected]

- LOncoScreen peut tre prescrit sur les feuilles de demande habituelles.

- Modalits de prlvement : - 3 tubes rouges (srum) dont 1 emball dans de laluminium

- 1 tube gris

- 1 tube mauve.

Renseignements :

Toute information technique ou administrative peut tre obtenue auprs de Ellipsys par tlphone ou par mail.

Vous serez mis en contact avec le responsable comptent pour rpondre votre requte. Les mails seront

transfrs la personne concerne.

Voir feuille annexe

FORMATION- SEMINAIRES

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 bioch imiques et phys iologiques de la mdecine nutrit ionnelle 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 [email protected]

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N15-Oncoscreen