19 september 2010

Cayenne genezende kracht voor hart-kanker en de..

........ EFFECTIEVE SUPPLEMENTEN Q10 en VASOLASTICA BIJ HARTAANDOENINGEN........
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CAYENNE OF CHILIPEPER
Cayenne of chilipeper is een scherp kruid en is anti-bacterieel, anti-schimmel, anti-parasi-tair en anti-viraal, omdat het deze micro-organismes letterlijk wegbrand. Daarnaast is de stof capsaicine in cayennepeper kankerwerend en bloedzuiverend. Bloedproppen en on-zuiverheden worden dus ook letterlijk weggebrand. Te gebruiken in capsules en.... als thee.
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Onderzoek: Hete pepers (waaronder chili of cayenne) goed voor het hart en bloedvaten.

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Cayennepeper is ook bekend omdat het hartaanvallen binnen 30 seconden stopt en zou in iedere EHBO kit thuishoren. Cayenne werkt als een katalysator en is daarnaast rijk aan vita-minen A en C, heeft de volledige complexen vitamine B en zeer rijk aan organisch calcium-kalium, wat ook... één van de redenen is waarom het goed voor het hart is. Lees hier verder.
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Stof in cayenne of chilipeper kan leiden tot nieuwe pijnstiller...... Lees hier verder.
Cayenne en kanker-reuma (vertaling)....... http://www.encognitive.com/node/2489
Cayenne de genezende kracht (Nieuwe Dokters)........... http://tinyurl.com/yhn7pj7
Cayenne in capsules (Solgar)............................................. http://tinyurl.com/y99fezy
Cayenne doet ook bloeddruk dalen (4-8-2010)............... http://tinyurl.com/33kk6pt

Cayenne ook een gunstige invloed op kanker................. http://tinyurl.com/ybb7e3f

Onderzoek (Engels).......... http://www.longecity.org/forum/topic/43603-can-chili-peppers-cause-cancer/..

Naast de populariteit van cayennepeper voor zijn natuurlijke genezings capaciteiten is er gedocumenteerd bewijs bij de 'American Association of Cancer Research' dat aangeeft dat cayennepeper een afweermiddel is voor kanker. Ook studies uit Japan onderschrijven dit, bovendien is capsaicin, hoofdbestanddeel cayennepeper, werkzaam tegen prostaatkanker.
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In een Reuters artikel van 16 maart 2006 getiteld: “Hot Pepper Kills Prostate Cancer Cells in Study“, verklaard Dr. Soren Lehmann van het Sedar-Sinai Medical Centre dat capsaicin een diepgaand effect op menselijke prostaat kankercellen heeft. Bij testen op muizen wer-den 80% van de kankercellen gedood en werd de groei van tumoren aanmerkelijk geremd! Mogelijk is datzelfde effect ook van toepassing op meerdere en/of..... andere kankersoorten.
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De laatste jaren hebben ruim 1300 wetenschappelijke studies plaatsgevonden over cap-saicin, de meest actieve stof in cayenne. Lees verder bij..... Mike Donkers 'Super Smoothie'.
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We weten echter nog zoveel meer over de oorzaak van kanker, deze te voorkomen en op een natuurlijke manier te bestrijden. Het verliezen en winnen van de kanker 'oorlog'.
Hier een overzicht op de website van 'Star-People' voorheen 'Nieuw Bewust Nederland'.
Kun je de dokter nog wel vertrouwen en is chemotherapie de echte 'killer'? Lees verder.

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Q10... BIJZONDER SUPPLEMENT BIJ HARTAANDOENINGEN
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Q10 (co-enzym)  is een belangrijke stof die binnen de reguliere behandeling van hartfa-len helaas zelden wordt ingezet. Dat komt doordat de stof als supplement wordt ge-zien, en daarom 'verdacht' is. Ook speelt een rol dat er geen patentering mogelijk is en het dus niet onder de aandacht van artsen wordt gebracht door de..... farmaceuten!
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Q10 kan bij patiënten met hartfalen een significante bijdrage leveren en naast gewone medicatie gegeven worden. Uit studies is duidelijk geworden dat de bloeddruk zich zo-danig normaliseert dat sommige patiënten kunnen stoppen met drukverlagende pillen.
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MEER INFO EN/OF BESTELLEN
Co-enzym Q10 en kanker (vertaling)............................ http://www.encognitive.com/node/2494
Co-enzym Q10 energie voor het hart (bestellen)... http://www.hartvitaal.nl/Coenzym_Q10.asp
Co-enzym Q10 energie voor het hart (AOV-bestellen)......................... http://tinyurl.com/2vg9faq
Wat is Q10... http://mens-en-gezondheid.infonu.nl/diversen/57883-wat-is-q10-eigenlijk.html
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ONDERZOEK
De laatste decennia is er veel onderzoek gedaan naar de functie bij hartaandoeningen, vooral hartfalen. Men vond dat in het bloed en weefsels, zoals het hartspierweefsel, veel te lage concentraties Q10 aanwezig waren. Verder is gebleken dat de ernst van het hartfalen, waarbij de patient bijvoorbeeld niet meer kan traplopen zonder buiten adem te zijn, samen-hangt met ernst en tekort aan Q10. Dus..... hoe groter het tekort, hoe ernstiger het hartfalen.
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VASOLASTICA... EFFECTIEVE NATUURLIJKE AANPAK HART- EN VAATAANDOENINGEN

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Hart- en vaatziekten zijn op het ogenblik een van de meest voorkomende ziekten in onze samenleving. Ruim 800.000 mensen in Nederland hebben beginnende of ernstige klachten op dit gebied. Er zijn verschillende oorzaken voor deze klachten. Naast erfelijke factoren is het zeker dat onze voeding, onze leefwijze en de stressomstandigheden waarin velen van ons leven, een grote rol spelen in het ontstaan van hart- en vaatziekten. Intussen kunnen we deze ziekten gerust volksvijand nummer één noemen, andere volgen explosief!

Hart- en vaatziekten worden doorgaans als volgt behandeld:

• met chemische geneesmiddelen zoals vaatverwijdende middelen en bloedverdunners

• technische ingrepen zoals dotteren, stents, operatief ingrijpen door open hartoperaties, vaattransplantaties, kunstvaten en amputaties.

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Een andere oplossing
Er is echter ook een totaal andere en een meer natuurlijke oplossing voor dit probleem, na-melijk het toepassen van enzymtherapie met Vasolastica die men met andere therapieën en medicatie kan combineren. Organen worden beter doorbloed en werken daarom beter. 

Vasolastica is een natuurlijk enzympreparaat wat is vervaardigd uit niet genetisch gema-nipuleerde planten en tropische vruchten. Het heeft een sterk reinigend vermogen, waar-door vernauwingen verdwijnen en kan worden toegepast bij alle vaataandoeningen.. verder
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De onafhankelijke patiëntenvereniging ‘Enzymtherapie’ heeft een analyse gemaakt van de gezondheidszorg uit oprechte bezorgdheid over het lot van de patiënten, want uit onze 28 jaar ervaring weten we dat het anders en veel beter kan! Daarom geven wij adviezen en suggesties voor een andere en betere aanpak die ook nog.... grote besparingen opleveren.
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Medicijnen (90%) werken onvoldoende of niet!
Door huisartsen en specialisten voorgeschreven reguliere medicijnen zijn in 90% van de gevallen voor slechts een minderheid heilzaam. Voor 50 tot 70% van de patiënten heeft het innemen van medicijnen zelfs geen enkele heilzame werking..... lees verder.
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De vijf medische mythes betreffende hartaandoeningen en cholesterol....... lees verder!

................................Wij verkopen niets, dicteren niets, maar... informeren slechts!.............. ..............

Ton Claessen, lid van de landelijke Werkgroep Welzijn Kankerpatienten (W.W.K.): http://www.kankerwelzijn.nl en het boek: http://www.chemo-versus-hippocrates.nl/ en tevens webmaster van: http://www.natriumbicarbonaat.blogspot.com voor de verdere info.

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................................  ......LAATSTE UPDATE VAN DIT BERICHT: 31 maart 2012        ...............................

Geplaatst door Ton Claessen - WWK - op 19.9.10

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http://wapensindestrijdtegenkanker.blogspot.nl/2010/09/cayenne-chilipeper-genezende-kracht.html

 

 

Krachtige -alternatieve- wapens in de strijd tegen.... kanker!

Op dit weblog hebben wij fragmentarisch op internet verspreide informatie samengebracht dat kan bijdragen in de strijd... tegen kanker en/of andere aandoeningen en veelal niet door de reguliere media voor het voetlicht wordt gebracht, maar.. van levensbelang kan zijn!

Jaarlijks overlijden wereldwijd bijna 10 miljoen mensen aan kanker en meer dan 12 miljoen krijgen de diagnose en de tendens is alleen maar toename!

Behandelen van kanker is in 40 jaar met slechts 5 % verbeterd en onderzoekers-oncologen falen volledig met de huidige aanpak van kanker is een hoofdarti-kel in de 'New York Times' waarin de vloer wordt aangeveegt met deze aanpak! Ons motto: 'zorg dat uw gezondheid in de beste handen is.. uw eigen handen'!

Er worden dus al decennia lang miljarden aan onderzoek uitgegeven om vast te stellen wat de oorzaak is en hoe te genezen. Tot nu toe met...... een beperkt en niet consisten resultaat. De vraag is dan ook of het ingeslagen pad (jaar of 90 geleden) het enige juiste is en of die miljarden niet gewoon verkwist danwel weggegooid geld zijn?!! Wij willen daarom informatie verschaffen over verschillende vormen van kankertherapieen, waarvan de resultaten een nieuw inzicht in kanker en de behandeling van kanker moeten geven, met als uiteindelijk doel het genezen van deze verschrikkelijke ziekte, want... er zijn andere moge-lijkheden zoals ook de subtitel luidt van het boek 'Chemo? Of kan ik zelf kiezen'? van mede initiatiefnemer WWK-werkgroep Drs. H.J. (Henk) Trentelman!
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16 augustus 2010

Kurkuma Longa -curcumine- doodt..... kankercellen!

OORZAAK EN GENEZEN VAN KANKER AL DECENNIA LANG BEKEND!  INFO... KLIK HIER 

Kanker = georganiseerde genocide! Chemokuren en gepatenteerde medicijnen maken de burgers almaar zieker en zwakker. Lees verder.... ‘Das ist ein Befehl’!
Betere, kankergenezende methodes dan vergiftigen-verbranden-verminken bestaan wél! Lees hier en hier!

.     .In tegenstelling tot (veel) andere therapieën is kurkuma direct inzetbaar en betaalbaar!.     ...

HEKSENJACHT ONTKETEND OP WAT NATUURLIJK EN/OF GEZOND IS! INFO.. KLIK HIER
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TER INLEIDING
Kurkuma ookwel Curcuma is helend voor lever, gal, darmen, longen en het bloed en heeft krachtige kankerwerende en ontstekingsremmende eigenschappen. Het is anti-bacterieel, anti-schimmel, anti-parasitair en ook anti-viraal. Kurkuma is een van de krachtigste en meest veelzijdige natuurlijke geneesmiddelen en een van de belangrijkste medicijnen uit de Indische en Chinese geneeskundige traditie.  In de Ayurveda geneeskunde is het medi-cijn nummer een! Kurkuma een super gezondheidskruid en.. het doodt zelfs kankercellen!!
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WETENSCHAPPELIJK ONDERZOEK

Kurkuma, ook wel de Indiase geelwortel genoemd, wordt geassocieerd met een grote variëteit aan gezondheidseffecten. Dat meldt de BBC. Studies hebben aangetoond dat kurkuma kan worden gebruikt om in laboratorium gekweekte kankercellen te vernieti-gen. Ook zijn positieve effecten vastgesteld bij patiënten die zijn getroffen door een be-roerte of die lijden aan dementie. Wetenschappers gaan nu onderzoeken of een vast bestanddeel darmkanker kan helpen genezen. Lees hier verder (Niburu, 07 mei 2012).
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Kurkuma wordt in India traditioneel gebruikt voor de behandeling van wonden en schrammen. In Azië wordt het gebruikt als medicijn tegen trombose en hersenaandoe-ningen waaronder de ziekte van Alzheimer en Parkinson. Onderzoek door de Rhodes-universiteit in Zuid-Afrika heeft de werking van curcumine bevestigd in de binding van zware metalen. Bij ratten bleek dat de stof het brein beschermt tegen beschadiging door cyanide, lood en cadmium. De studie concludeerde dat door veelvuldige gebruik van curcumine in de Indiase gerechten.. de ziekte van Alzheimer nauwelijks voorkomt.
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BRITSE VROUW BESTRIJDT BORSTKANKER MET SUPERVOEDSEL (KURKUMA)
Ze was bezorgd over de bijwerkingen van het (reguliere) medicijn dat ze kreeg voorge-schreven voor de behandeling van haar aandoening. Ze keerde zich tot supervoedsel, waaronder kurkuma. Volgens haar zorgt het specerij ervoor dat ‘kankercellen zelf-moord plegen’. Vier jaar later en geheel kankervrij is ze het middelpunt van een onderzoeksproject waarbij wordt gekeken hoe levensstijl kan worden toegepast om andere slachtoffers van de ziekte te helpen. Lees hier gehele artikel (25 juni 2012).

De Britse studie gaat kijken hoe levensstijl de terugkeer van borstkanker na de operatie kan helpen voorkomen. Het betreft de grootste studie naar borstkanker ter wereld. Er doen 56 ziekenhuizen in heel Groot-Brittannië en 3400 patiënten aan mee.
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Curcumine veilig-effectief bij reuma en werkt beter dan ontstekingsremmer diclofenac.

Kurkuma werkt beter tegen dementie dan... een antipsychoticum (ondermeer Haldol).

OVERIGE PUBLICATIES
Stichting Iocob... van keuken naar kliniek. Nationaal Fonds Kanker... krachtig kruid tegen kanker. Henk Mutsaers... super geneeskrachtige werking. Ode-magazine... levenskrachtige kruiden.  Ron Fonteine.... ruim overzicht. Wetenschappelijk onderzoek..... overzicht (Engels). De eigenschappen en toepassingen die men toeschrijft aan curcuma bij Paradijsvogel.

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PUBMED PUBLICATIES
Ook op Pubmed, wereldwijde wetenschappelijke databank, zijn vele honderden onder-zoeken omtrent kurkuma (werkzame stof curcumine) te vinden, die nagenoeg allemaal positief tot zeer positief zijn. Ron Fonteine met leefbewust heeft  een verzameling  (248). Ook bij Google  zijn na invoering van trefwoorden.... vele duizenden vermeldingen te vinden!
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NOG MEER KURKUMA
Kurkuma helpt ook bij bijpassoperatie............................................................... Lees hier verder
Pancreaskanker........ http://www.abcgezondheid.nl/nl/news/kurkuma_bij_pancreaskanker/
Kurkuma - Gember en nog veel meer info bij........ http://www.ergogenics.org/index08b.html

Kurkuma-verslag op webste 'Bovendien'........................................... http://tinyurl.com/3gxzy9m
Kurkuma en kanker (vertaling)........................ http://www.encognitive.com/node/2504
Kurkuma met BCM95® extract................... http://www.ergomax.nl/Curcumine_Ergomax.html

Kurkuma report.. http://www.lef.org/magazine/mag2002/jul2002_report_curcumin_01.html

Kurkuma verhoogt opname glucose spiercel................. http://www.ergogenics.org/305.html
Kurkuma bij Kanker Actueel............... http://www.kanker-actueel.nl/on-vokurkuma-5752.html

Kurkuma wondermiddel.... http://www.faqt.nl/wetenschap/specerij-kurkuma-wondermiddel/

Kurkuma op seniorennet................. http://www.seniorennet.nl/Dossier/Vitaliteit/curcuma.php
Kurkuma en het krachtigste uit de natuur............................ http://www.vitanzahq.eu/nl/duolife/

Kurkuma en overige (smoothie).... http://kruiden.hetbewustepad.nl/index.php?pag_id=54
Kurkuma en reuma....... http://www.dhanvantari.nl/attachments/File/Ayurveda_en_reuma.pdf
Kurkuma en borstkanker: http://vita-info.nl/2010/08/curcumin-en-broccoli-tegen-borstkanker/
Kurkuma natuurlijk alternatief............ www.warenwelenwee.nl/supplementen_combipil.html

Kurkuma en bloedvaten........... http://vita-info.nl/2010/01/curcumin-goed-voor-de-bloedvaten/
Kurkuma en darmaandoeningen............ http://vita-info.nl/2009/02/curcumin-colitis-poliepen/
Kurkuma vernietigd kankercellen binnen 24 uur................................... http://tinyurl.com/yjkb6cx
Kurkuma breekt kankercellen slokdarm af............................................ http://tinyurl.com/ydlkeaq

Kurkuma en Alzheimer (dementie)........................................................... http://tinyurl.com/ydhv3fy
Prof. Dr. Patrick McGeer over kurkuma.................................................. http://tinyurl.com/yb79nr3
Prof. Dr. David Servan-Schreiber.................... http://vita-info.nl/2009/12/kurkuma-gezondheid/
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OVERZICHT INZETBAARHEID
Kurkuma Longa of geelwortel-turmeric (werkzame stof curcumine) is breed inzetbaar bij gezondheidsklachten. Zie overzicht op de.. website van Vitamor.
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Overzicht Kurkuma Longa nieuws (inclusief het AMC onderzoek) bij.... 'Kanker Actueel'.
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RECENT ONDERZOEK

Ongelooflijk, baanbrekend nieuw onderzoek net gepubliceerd (10 oktober 2012) in het blad van de Medical Association van Thailand heeft aangetoond dat de primaire poly-fenol in kurkuma - curcumine in staat is gebleken om het leverweefsel te herstellen en te regenereren bij diabetische ratten. De curcumine was in staat om een significante omkering van de aandoening te bewerkstelligen. Lees verder NaturalNews (Engels).

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VLEESBOMEN (EN CURCUMINE)

Er zijn een aantal natuurlijke middelen en supplementen die veelbelovend zijn voor de behandeling van vleesbomen. Bepaalde dieetadviezen zijn daarbij belangrijk. Lees verder.

 

Gezondheidsmagazine ‘Goed Gevoel’  (Belgie) en hun grote... dossier kanker..

........... KURKUMA LONGA ONDERZOEK AMC AMSTERDAM ( DR. MICHAL HEGER) ...........

AMC KURKUMA ONDERZOEK
Het is bijna onvoorstelbaar dat een middel, waarvan inmiddels in meer dan 1000 wetenschappelijke studies is aangetoond dat het tegen kanker werkt, voor een paar euro in de schappen ligt van de supermarkt.  Daarom  financiert ‘Stichting Nationaal Fonds te-gen Kanker’ onderzoek naar de werkingsmechanismen van curcumine alswel de toe-dieningsvormen van de actieve stof. Om dit onderzoek door te zetten zijn subsidies no-dig, welke afhangen van uw donaties. Klik hier voor online donaties en hier actiepagina.
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Stichting Nationaal Fonds tegen Kanker sponsort op dit moment twee onderzoeken in het AMC (Academisch Medische Centrum van de Universiteit van Amsterdam) naar kurkuma. Wij steunen deze onderzoeken, omdat de resultaten kunnen bijdragen aan een grotere kans op overleving van kankerpatiënten en een betere kwaliteit van leven. Kurkuma heeft immers.... geen bijwerkingen, in tegenstelling tot de meeste andere kankerbehandelingen.
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LAATSTE NIEUWS KURKUMA (juli 2012)
Nieuw initiatief: Stichting Curcuma Promotions Nederland… Curcuma Roots for Moods, ondersteund het internationaal onderzoek naar kurkuma als medicijn voor kankerpatiënten. Meer informatie bij ‘Stichting Nationaal Fonds tegen Kanker’.
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..........................................................KLIK HIER VOOR NIEUWSBRIEF..........................................................


KANKERSPECIALIST WAARSCHUWT VOOR CHEMO EN BESTRALING!

Dr. Max Wicha, kankerspecialist, waarschuwt voor chemotherapie en bestraling -  Curcumine-Piperine veelbelovende alternatieven! 

De Pittsburgh Post-Gazette pakte op 24 februari 2010 uit met het opmerkelijke nieuws dat standaard kankerbehandelingen alleen er niet in slagen kanker uit te roeien, maar dat ze het bovendien nog erger kunnen maken. Voor het Faché Instituut is dat niet echt verras-send nieuws. De beoefenaars en aanhangers van de orthomoleculaire geneeskunde pro-beren mensen daar al tientallen jaren van te overtuigen. Het verrassende nieuws is dat de uitspraak deze keer niet uit de ‘alternatieve’ hoek komt, maar van een...... kankerspecialist!

CURCUMA VERRASSEND VEELZIJDIG
Drs. Selma Timmer (geneeskunde) is medisch journalist met specialisatie voeding, sup-plementen en kruiden. Zie hier haar pdf-verslag (2007)...... ‘Curcuma verrassend veelzijdig’.
Interacties met curcumine en meer info....... http://www.naturafoundation.nl/?objectID=450
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Achtergrond en werking van Kurkuma (curcumine) dat bij nagenoeg alle kankersoorten en naast chemo en bestraling een bewezen therapeutisch effect heeft! Update per 16-11-2010.
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Wordt het geen tijd om aspirine te verruilen voor kurkuma, ook wel aspirine van Azië ge-noemd? Lees verder 'Ode-magazine'.... levenskrachtige kruiden. Update..... 21 juni 2011.
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Curcumine heeft op dit moment de meest evidence-based ondersteunende literatuur m.b.t. het gebruik ervan bij kanker dan welke andere voedingsstof ook. Lees verder bij het indrukwekkende overzicht (Engels) van Dr. Mercola, gepubliceerd op...... 13 juni 2011.

NADERE UITLEG
De werkzame stof van kurkuma is curcumine, waarvan de poedervorm bestaat uit 5% en de capsulevorm maar liefst 95% (extract) bevat. Het is pas echt effectief in het lichaam als het wordt gebruikt in combinatie met zwarte peper (werkzaam piperine) en olijf/lijnzaadolie, of andere vetachtige substantie. Het ligt dus voor de hand om de capsulevorm te gebruiken.

Zwarte peper werkt als een katalysator en kan de werkzaamheid van curcumine meer dan 1000x versterken! Olijf-lijnzaadolie (biologisch) of een andere vetachtige substantie dient als transporteur (dus ook naar kankercellen) omdat curcumine... niet in water oplosbaar is!
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Bioperine is ook een uitzonderlijk pure en veilige vorm van piperine, de belangrijkste alka-loide in zwarte peper. Omdat Bioperine een extract is bevat het 95% werkbare stof en is het vele malen sterker dan gewone zwarte peper dat slechts 3 tot 5% van de werbare stof bevat.
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AANSCHAF CAPSULEVORM
De capsulevorm is met en zonder toevoeging zwarte peper verkrijgbaar. Het moge duidelijk zijn dat de combinatie met zwarte peper de absolute voorkeur geniet. Het is verkrijgbaar bij natuur of reformwinkels in uw omgeving of te bestellen middels internet. Kies altijd voor natuurlijke en/of biologische supplementen, dus zonder (schadelijke) toevoegingen! AOV is een gerenomeerd-betrouwbaar merk en ondermeer hier te bestellen. Kurkuma is er ook in poedervorm, maar heeft natuurlijk weinig zin gezien het lage percentage... (5 %) curcumine.
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De Roode Roos, initiatief Moermanvereniging, is leverancier van een breed assortiment supplementen, waaronder kurkuma-zwarte peper. Onder voorwaarden met..... 25 % korting.
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SUPER CURCUMINE EN BIOLOGISCHE BESCHIKBAARHEID (update 26-02-2011)

.Curcumine, het extract van geelwortel met de vele geneeskrachtige eigenschappen, heeft een betere biologische beschikbaarheid door de Meriva-samenstelling. Ook Ergomax de leverancier van BioCurcumine BCM95 beschrijft een 5-7 maal effectievere werking. Gebruik in combinatie met Bioperine lijkt zeker aanbevelingswaardig... nog betere werkzaamheid.  

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OOK FARMACEUTISCHE INDUSTRIE INMIDDELS OVERTUIGD!
Het belangrijkste bewijs dat curcumin over krachtige eigenschappen beschikt is het feit dat de farmaceutische industrie (veel te dure) synthetische varianten probeert te ontwikkelen die als geneesmiddelen kunnen worden toegepast. Op het zuivere natuurproduct dat in reformwinkels en op websites te koop is kan immers geen patent worden verkregen en dus ook geen geld worden verdiend. Ook van toepassing op andere.. natuurlijke producten.
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DOSERING EN GEBRUIK 

Preventief wordt 2x daags een capsule (500-600 mg) curcuma-zwarte peper aanbevolen. Therapeutisch (bij kanker of andere aandoening) is het aan te bevelen  3x daags twee cap-sules te gebruiken. Vergeet daarbij niet om dit te doen in combinatie met een vettige sub-stantie (bijvoorbeeld in eten) of een scheut (biologische) olijf- of lijnzaadolie in een glas (Zonnatura) groentesap voor de broodnodige vitaminen, dat de...... beste keuze blijkt te zijn.
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SOLE OOK EEN ABSOLUTE AANRADER!
Voeg aan de groentesap zeker ook een theelepeltje 'Sole' toe, voor de onmisbare mine-ralen en spoorelementen. Sole-oplossing kun je zelf  maken van Keltisch zeezout en is hier te bestellen. Met dank aan Mike Donkers voor zijn waardevolle bijdrage en de vele ande-re columns en zeker niet te vergeten Henk Mutsaers met 'Uitdagingnet' en Ron Fonteine  met 'Leefbewust'. Genoemden zijn ook regelmatig te beluisteren bij..... 'Gezondheid Radio'
.
KRUIDEN HEBBEN FANTASTISCHE GENEZENDE KRACHTEN, MAAR....
Geneeskrachtige kruiden worden (waarschijnlijk) per 1 april 2011 verboden in de EU en zul-len daarna worden bestempeld als illegaal, want de farmaceutische industrie slaat grote slag! Kom in actie want er rest ons nog maar weinig tijd om deze krankzinnige en volsla-gen waanzin te stoppen!! Een en ander is onderdeel van de gevaarlijke Codex Alimentarius!
.
---------------------------------------------------------------------------------------------------------------------------
MAGNESIUM EN VITAMINE D3 OOK VAN CRUCIAAL BELANG!
Veel mensen hebben (vaak) onwetend een ernstig chronisch tekort aan vitamine d3 en het mineraal magnesium met alle daaruit voortkomende dramatische gevolgen voor de ge-zondheid, want ze zijn van cruciaal belang. De symptomen van deze tekorten zijn indrukwek-kend te noemen! Vaststelling van een (eventueel) tekort kan plaatsvinden via.... de huisarts.
.

Dr. Marianne Mousain-Bosc (magnesium) en Dr. Gert Schuitemaker (d3), zullen zeker de laatsten zijn om dit tegen te spreken. Zeer vele andere medici.... onderschrijven dit!

.

Zie eventueel ook... vitamine d3 tekort golft over de wereld en... in Nederland 7000 onno-dige kankerdoden per jaar van Dr. Gert Schuitemaker en... helft van de wereldbevolking heeft een tekort aan vitamine d3 en tot slot een Ortho overzicht... nieuw licht op vitamine d3, en/of de kracht van magnesium het wondermineraal, ook vonk van het leven genoemd.

.
TOT SLOT

In relatie tot kanker lijkt knoflook wel de grootste overwinning te behalen en zou, volgens verschillende medische tijdschriften, tumoren doen afnemen, zelfs kwaadaardige! Knof-look is er ook in capsules. Om een nog krachtiger en natuurlijk wapen tegen kanker te creëren ligt het dus erg voor de hand om curcuma longa en knoflook samen te combineren.

Allicine wordt beschouwd als het belangrijkste en krachtigste ingrediënt van knoflook. ALLIMAX® is het enige voedingssupplement met 100% (240 ppm) gestabiliseerde Allicine.

.

Geraadpleegde bronnen ondermeer 'Antikanker' het boek van Dr. David Servan-Schreiber (genezen kanker) en boek 'Eten tegen kanker' van.... Dr. Richard Beliveau en Dr. D.Gingras.
.
We weten echter nog zoveel meer over de oorzaak van kanker, deze te voorkomen en op een natuurlijke manier te bestrijden. Het verliezen en winnen van de kanker 'oorlog'.
Hier een overzicht op de website van 'Star-People' voorheen 'Nieuw Bewust Nederland'.
Kun je de dokter nog wel vertrouwen en is chemotherapie de echte 'killer'? Lees verder.
.

...............................Wij verkopen niets, dicteren niets, maar... informeren slechts!................................

.

Ton Claessen, lid van de landelijke Werkgroep Welzijn Kankerpatienten (W.W.K.): http://www.kankerwelzijn.nl en het boek: http://www.chemo-versus-hippocrates.nl/ en tevens webmaster van: http://www.natriumbicarbonaat.blogspot.com voor de verdere info.

.

[1]

 

http://wapensindestrijdtegenkanker.blogspot.nl/2010/08/curcuma-longa-een-super-supplement.html

 

Pancreatic Cancer

The pancreas lies behind the stomach and secretes enzymes that help digestion and insulin to help metabolize sugars. Pancreatic cancer often spreads rapidly and is usually undetectable early in the disease process. Signs do not often appear until the cancer has advanced to a point where surgery is no longer possible. Symptoms of pancreatic cancer often include upper abdominal pain that radiates to the back, yellowing of the skin and eyes known as jaundice, weight loss, depression, blood clots and loss of appetite. Treatment for pancreatic cancer often includes surgery, chemotherapy, radiation and targeted therapy.

How It May Help

The American Cancer Society says that researchers are exploring the use of turmeric to slow and prevent certain types of cancer, including cancers of the esophagus, mouth, stomach, skin and breast. One theory regarding how turmeric works purports that curcumin, the active chemical in turmeric, may interfere with the blood supply to cancerous tumors causing them to shrink or die. It may also help prevent certain cancers due to antioxidants in the turmeric that protect from cellular damage. According to the American Cancer Society, one research study showed that curcumin repressed the development in cancer-causing enzymes in rats. Researchers have many clinical trials testing turmeric for several forms of cancer. A handful of clinical trials are under way testing the use of turmeric specifically on pancreatic cancer. More research is needed before the scientific community can form any conclusive results. Always consult your oncologist before using turmeric to treat your pancreatic cancer.

Warnings

Turmeric does not have any reported side effects but may interact with some medications. Taking turmeric with anti-platelet or anti-coagulant medications, such as aspirin, clopidogrel and warfarin, may cause excessive bleeding or bruising. Using turmeric may interfere with medications that reduce stomach acid, such as omeprazole, lansoprazole, cimetidine, ranitidine and esomepraozole.

Sponsored Links


Read more: http://www.livestrong.com/article/353650-turmeric-curcumin-for-pancreatic-cancer/#ixzz2FyWidsPl
 

http://www.cancerresearchuk.org/cancer-help/type/pancreatic-cancer/about/pancreatic-cancer-risks-and-causes#quick

 

http://hsionlineorders.net/video/ACS_LP_pic_signup_OLP/?pco=PHSINC03&efo=HSIOP121129&xco=XHSINC03

 

If you go this route you MUST make sure your getting high levels of Potassium else you could die. Cesium is alkalising the cancer from the inside because it is one of the few things which can enter a tumour. I would suggest looking at Cayenne Pepper drinks, Vitamin C, high levels of Potassium balanced with Himalayan salts and plenty of water. Cayenne Pepper can sometimes supply the cancer with too much blood and also its very alkalising and will destroy the tumour from the outside in. Vitamin C (sodium ascorbate in this case) will enter the cancer and oxidise from the inside out. Potassium can enter a tumour and it alkalises like Cesium Chloride and alot safer. The Himalayan salts will make sure the large amounts of potassium don't deplete the need salt balance as well as providing seriously good health benefits.

I would suggest 3-5 Cayenne Pepper drinks a day (1 tsp in 250 ml warm water)
Sodium Ascorbate Vitamin C 30-100 grams a day
Himalayan Salt 1 tsp breakfast and 1 tsp before bed
Dr.Fereydoon Batmanghelidj's recommendations on WATER amounts.

I didn't mention Ascorbic Acid (Vitamin C) on purpose in this case because I was looking at this from an alkalising viewpoint. We don't want to acidify the body and have to buffer with alkalinity. If you want the full pelt from the above then Sodium Ascorbate is the one. Ascorbic is excellent but talking about Cesium etc it goes against what we are trying to achieve in this particular route.

You need to find a good source of bioavailable Potassium and Ionic is one of the best along with plant varieties. Find out the ratio's of Potassium to salts and work out whats needed. You don't need to go this route but if your interested in alkalising from the inside out then this, cesium etc are the way. Personally water, himalayan salt, Vitamin C, Cayenne Pepper will do just find on their own.

 

 

Caesium chloride

From Wikipedia, the free encyclopedia

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Caesium chloride

IUPAC name[hide]

Caesium chloride

Other names[hide]

Cesium chloride

Identifiers

CAS number

7647-17-8 Yes

ChemSpider

22713 Yes

UNII

GNR9HML8BA Yes

EC number

231-600-2

Jmol-3D images

Image 1

SMILES

[show]

InChI

[show]

Properties

Molecular formula

CsCl

Molar mass

168.36 g/mol

Appearance

white solid
hygroscopic

Density

3.99 g/cm3

Melting point

645 °C

Boiling point

1297 °C (vaporizes)

Solubility in water

1865 g/L[2]

Solubility

soluble in ethanol[3]

Band gap

8.35 eV (80 K)[1]

Refractive index (nD)

1.64[4]

Structure

Crystal structure

Caesium chloride (see text), Pm3m, space group No. 221, Pearson symbol cP2

Coordination
geometry

simple cubic (interpenetrating)

Related compounds

Other anions

Caesium fluoride
Caesium bromide
Caesium iodide
Caesium astatide

Other cations

Lithium chloride
Sodium chloride
Potassium chloride
Rubidium chloride

 Yes (verify) (what is: Yes/?)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)

Infobox references

Caesium chloride (cesium chloride in North America), is the inorganic compound with the formula CsCl. This colorless solid is an important source of caesium ions in a variety of applications. Its crystal structure forms a major structural type where each caesium ion is coordinated by 8 chlorine ions. Caesium chloride crystals are thermally stable, but easily dissolve in water and concentrated hydrochloric acid, and therefore gradually disintegrate in the ambient conditions due to moisture. Caesium chloride occurs naturally in mineral waters and as an impurity in carnallite (up to 0.002%), sylvite and kainite. Less than 20 tonnes of CsCl is produced annually worldwide, mostly from a caesium-bearing mineral pollucite.[5]

Caesium chloride is widely used in isopycnic centrifugation for separating various types of DNA. It is a reagent in analytical chemistry, where it is used to identify ions by the color and morphology of the precipitate. When enriched in radioisotopes, such as 137CsCl or 131CsCl, caesium chloride is used in nuclear medicine applications such as treatment of cancer and diagnosis of myocardial infarction. Another form of cancer treatment was studied using conventional non-radioactive CsCl. Whereas conventional caesium chloride has a rather low toxicity to humans and animals, the radioactive form easily contaminates the environment due to the high solubility of CsCl in water. Spread of 137CsCl powder from a 93-gram container in 1987 in Goiânia, Brazil, resulted in one of the worst-ever radiation spill accidents killing four and directly affecting more than 100,000 people.

Contents

Crystal structure

Main article: Cubic crystal system

Ball-and-stick model of the coordination of Cs and Cl in CsCl

The caesium chloride structure adopts a primitive cubic lattice with a two-atom basis, where both atoms have eightfold coordination. The chloride atoms lie upon the lattice points at the edges of the cube, while the caesium atoms lie in the holes in the center of the cubes. This structure is shared with CsBr and CsI and many binary metallic alloys. In contrast, the other alkaline halides have the sodium chloride (rocksalt) structure.[6] When both ions are similar in size (Cs+ ionic radius 174 pm for this coordination number, Cl 181 pm) the CsCl structure is adopted, when they are different (Na+ ionic radius 102 pm, Cl 181 pm) the sodium chloride structure is adopted. Upon heating to above 450 °C, the normal caesium chloride structure (α-CsCl) converts to the β-CsCl form with the rocksalt structure (space group Fm3m).[7][8]

Physical properties

Caesium chloride is colorless in the form of large crystals and white when powdered. It readily dissolves in water with the maximum solubility increasing from 1865 g/L at 20 °C to 2705 g/L at 100 °C.[9][10] The crystals are very hygroscopic and gradually disintegrate at ambient conditions.[11] Caesium chloride does not form hydrates.[12]

Solubility of CsCl in water[13]

Т (°C)

0

10

20

25

30

40

50

60

70

80

90

100

S (wt%)

61.83

63.48

64.96

65.64

66.29

67.50

68.60

69.61

70.54

71.40

72.21

72.96

In contrast to sodium chloride and potassium chloride, caesium chloride readily dissolves in concentrated hydrochloric acid.[14][15] Caesium chloride has also a relatively high solubility in formic acid (1077 g/L at 18 °C) and hydrazine; medium solubility in methanol (31.7 g/L at 25 °C) and low solubility in ethanol (7.6 g/L at 25 °C),[12][15][16] sulfur dioxide (2.95 g/L at 25 °C), ammonia (3.8 g/L at 0 °C),[17] acetone (0.004% at 18 °С), acetonitrile (0.083 g/L at 18 °С),[15] ethylacetates and other complex ethers, butanone, acetophenone, pyridine and chlorobenzene.[18]

Despite its wide band gap of about 8.35 eV at 80 K,[1] caesium chloride weakly conducts electricity, and the conductivity is not electronic but ionic. The conductivity has a value of the order 10−7 S/cm at 300 °C. It occurs through nearest-neighbor jumps of lattice vacancies, and the mobility is much higher for the Cl- than Cs+ vacancies. The conductivity increases with temperature up to about 450 °C, with an activation energy changing from 0.6 to 1.3 eV at about 260 °C. It then sharply drops by two orders of magnitude because of the phase transition from the α-CsCl to β-CsCl phase. The conductivity is also suppressed by application of pressure (about 10 times decrease at 0.4 GPa) which reduces the mobility of lattice vacancies.[8]

Properties of aqueous solutions of CsCl at 20 °C[19][20]

[show]Concentration,
wt%

Density,
kg/L

Concentration,
mol/L

refractive index
(at 589 nm)

Freezing point depression, °С relative to water

Viscosity,
10−3 Pa·s

Chemical properties

Caesium chloride completely dissociates upon dissolution in water, and the Cs+ cations are solvated in dilute solutions:

\mathsf{CsCl+6H_2O=[Cs(H_2O)_6]^++Cl^-}

In aqueous solutions it enters common substitution reactions, for example:

\mathsf{CsCl+AgNO_3=CsNO_3+AgCl\downarrow}

\mathsf{CsCl+NaClO_4=NaCl+CsClO_4\downarrow}

\mathsf{2CsCl+H_2[PtCl_6]=2HCl+Cs_2[PtCl_6]\downarrow}

\mathsf{2CsCl+H_2[CeCl_6]=2HCl+Cs_2[CeCl_6]\downarrow}

CsCl converts to caesium sulfate when boiled in concentrated sulfuric acid or heated with caesium hydrogen sulfate at 550–700 °С:[21]

2 CsCl + H2SO4 → Cs2SO4 + 2 HCl

CsCl + CsHSO4 → Cs2SO4 + HCl

Caesium chloride forms a variety of double salts with other chlorides. Examples include 2CsCl·BaCl2,[22] 2CsCl·CuCl2, CsCl·2CuCl and CsCl·LiCl,[23] and with interhalogen compounds:[24]

CsCl + ICl3 → Cs[ICl4]

In laboratory, CsCl can be obtained by treating caesium hydroxide, carbonate, caesium bicarbonate, or caesium sulfide with hydrochloric acid:

CsOH + HCl → CsCl + H2O

Cs2CO3 + 2 HCl → 2 CsCl + 2 H2O + CO2

Occurrence and production

Caesium chloride occurs naturally as an impurity in the halide minerals carnallite (KMgCl3·6H2O with up to 0.002% CsCl),[25] sylvite (KCl) and kainite (MgSO4·KCl·3H2O),[26] and in mineral waters. For example, the water of Bad Dürkheim spa, which was used in isolation of caesium, contained about 0.17 mg/L of CsCl.[27] None of these minerals are commercially important.

On industrial scale, CsCl is produced from the mineral pollucite, which is powdered and treated with hydrochloric acid at elevated temperature. The extract is treated with antimony chloride, iodine monochloride, or cerium(IV) chloride to give the poorly soluble double salt, e.g.:[28]

CsCl + SbCl3 → CsSbCl4

Treatment of the double with hydrogen sulfide gives CsCl:[28]

2 CsSbCl4 + 3 H2S → 2 CsCl + Sb2S3 + 8 HCl

High-purity CsCl is also produced from recrystallized Cs[ICl2] (and Cs[ICl4]) by thermal decomposition:[29]

Cs[ICl2] → 2 CsCl + ICl

Only about 20 tonnes of caesium compounds, with a major contribution from CsCl, were being produced annually around the 1970s[30] and 2000s worldwide.[31] Caesium chloride enriched with caesium-137 for radiation therapy applications is produced at a single facility Mayak in the Ural Region of Russia[32] and is sold internationally through a UK dealer. The salt is synthesized at 200 °C because of its hygroscopic nature and sealed in a thimble-shaped steel container which is then enclosed into another steel casing. The sealing is required to protect the salt from moisture.[33]

Uses

Precursor to Cs metal

Caesium chloride is the main precursor to caesium metal by high temperature reduction:[30]

2 CsCl + Mg → MgCl2 + Cs

An analogous reaction – heating CsCl with calcium in vacuum in presence of phosphorus was first reported in 1905 by the French chemist M. L. Hackspill[34] and is still used industrially.[30]

Caesium hydroxide is obtained by electrolysis of aqueous caesium chloride solution:[35]

2 CsCl + 2 H2O → 2 CsOH + Cl2 + H2

Solute for ultracentrifugation

Caesium chloride is widely used in centrifugation in a technique known as isopycnic centrifugation. Centripetal and diffusive forces establish a density gradient that allow separation of mixtures on the basis of their molecular density. This technique allows separation of DNA of different densities (e.g. DNA fragments with differing A-T or G-C content).[30] This application requires a solution with high density and yet relatively low viscosity, and CsCl suits it because of its high solubility in water, high density owing to the large mass of Cs, as well as low viscosity and high stability of CsCl solutions.[28]

Organic chemistry

Caesium chloride is rarely used in organic chemistry. It can act as a phase transfer catalyst reagent in selected reactions. One of these reactions is the synthesis of glutamic acid derivatives

\mathrm{CH_2\!\!=\!\!CHCOOCH_3+ArCH\!\!=\!\!N\!\!-\!\!CH(CH_3)\!\!-\!\!COOC(CH_3)_3\ \xrightarrow[CPME,\ 0^oC]{TBAB,\ CsCl,\ K_2CO_3}\ ArCH\!\!=\!\!N\!\!-\!\!C(C_2H_4COOCH_3)(CH_3)\!\!-\!\!COOC(CH_3)_3}

where TBAB is tetrabutylammonium bromide (interphase catalyst) and CPME is a cyclopentyl methyl ether (solvent).[36]

Another reaction is substitution of tetranitromethane[37]

\mathrm{C(NO_2)_4+CsCl\ \xrightarrow[]{DMF}\ C(NO_2)_3Cl+CsNO_2}

where DMF is dimethylformamide (solvent).

Analytical chemistry

Caesium chloride is a reagent in traditional analytical chemistry used for detecting inorganic ions via the color and morphology of the precipitates.[38] Quantitative concentration measurement of some of these ions, e.g. Mg2+, with inductively coupled plasma mass spectrometry, is used to evaluate the hardness of water.[39]

[show]Ion

Accompanying reagents

Residue

Morphology

Detection limit (µg)

It is also used for detection of the following ions:[40]

Ion

Accompanying reagents

Detection

Detection limit (µg/mL)

Al3+

K2SO4

Colorless crystals form in neutral media after evaporation

0.01

Ga3+

KHSO4

Colorless crystals form upon heating

0.5

Cr3+

KHSO4

Pale-violet crystals precipitate in slightly acidic media

0.06

Medicine

Medical properties of caesium chloride were studied back in 1888 by Ivan Pavlov and S. S. Botkin. They found that CsCl and RbCl induce long-term narrowing of the blood vessels (vasoconstriction) and the associated increase in the blood pressure (hypertension), stimulating the cardiovascular activity. These properties were then applied in the treatment of cardiovascular diseases.[41]

Later research indicated that CsCl alleviates cardiac dysrhythmia and that the life expectancy is higher in regions characterized by elevated levels of CsCl in water and food. Preliminary results indicate that CsCl can be used in the treatment of depressions.[42] The neurological action of CsCl is related to the protection of neurons from apoptosis and activation of caspase 3 caused by reduced potassium content.[43]

Several reports suggested that non-radioactive caesium chloride can be used in a complex treatment of some forms of cancer.[42][44][45] However, it has been linked to the deaths of over 50 patients, when it was used as part of a scientifically unvalidated cancer treatment.[46] The American Cancer Society considers caesium chloride therapy as requiring further study for benefits and side effects.[47]

Nuclear medicine and radiography

Caesium chloride composed of radioisotopes such as 137CsCl and 131CsCl,[48][49] is used in nuclear medicine, including treatment of cancer (brachytherapy) and diagnosis of myocardial infarction.[50][51] In the production of radioactive sources, it is normal to choose a chemical form of the radioisotope which would not be readily dispersed in the environment in the event of an accident. For instance, radiothermal generators (RTGs) often use strontium titanate, which is insoluble in water. For teletherapy sources, however, the radioactive density (Ci in a given volume) needs to be very high, which is not possible with known insoluble caesium compounds. A thimble-shaped container of radioactive caesium chloride provides the active source.

Miscellaneous applications

Caesium chloride is used in the preparation of electrically conducting glasses[49][52] and screens of cathode ray tubes.[30] It is a non-toxic provider of a halogen gas in exciplex lamps (exilamps) – a gas-discharge source of ultraviolet light which uses, for example, electrically excited XeCl molecules.[53] Other uses include activation of electrodes in welding;[54] manufacture of mineral water, beer[55] and drilling muds;[56] repellents[57] and high-temperature solders.[58] High-quality CsCl single crystals have a wide transparency range from UV to the infrared and therefore had been used for cuvettes, prisms and windows in optical spectrometers;[30] this use was discontinued with the development of less hygroscopic materials.

CsCl is a potent inhibitor of HCN channels which carry the h-current in excitable cells such as neurons.[59] It can therefore be useful as a tool in electrophyisiology experiments in neuroscience.

Toxicity

Caesium chloride has a low toxicity to human and animals.[60] Its median lethal dose (LD50) in mice is 2300 mg per kilogram of body weight for oral administration and 910 mg/kg for intravenous injection.[61] The toxicity of CsCl is related to its ability to lower the concentration of potassium in the body and partly substitute it in biochemical processes.[62] Caesium chloride powder can irritate the mucous membranes and cause asthma.[56]

Because of its high solubility in water, caesium chloride is highly mobile and can even diffuse through concrete. This is a drawback for its radioactive form which urges a search for more stable radioisotope materials. Commercial sources of radioactive caesium chloride are well sealed in a double steel enclosure.[33] However, in the Goiânia accident in Brazil, such a source containing about 93 gram of 137CsCl, was stolen from an abandoned hospital and forced open by two scavengers. The blue glow emitted in the dark by the radioactive caesium chloride attracted the thieves and their relatives who were unaware of the associated dangers and spread the powder. This resulted in one of the worst radiation spill accidents in which 4 people died within a month from the exposure, 20 showed signs of radiation sickness, 249 people were contaminated with radioactive caesium chloride, and about a thousand received a dose exceeding a yearly amount of background radiation. More than 110,000 people overwhelmed the local hospitals, and several city blocks had to be demolished in the cleanup operations. In the first days of the contamination, stomach disorders and nausea due to radiation sickness were experienced by several people, but only after several days one person associated the symptoms with the powder and brought a sample to the authorities.[63][64]

References

1.                              ^ a b Lushchik, A; Feldbach, E; Frorip, A; Ibragimov, K; Kuusmann, I; Lushchik, C (1994). Journal of Physics: Condensed Matter 6 (12): 2357–2366. doi:10.1088/0953-8984/6/12/009.

2.                              ^ Lide

3.                              ^ Lide, pp. 4–67, 4–1363

4.                              ^ Lide, p. 10-227

5.                              ^ Greenwood, Norman N.; Earnshaw, Alan (1997). Chemistry of the Elements (2nd ed.). Butterworth–Heinemann. ISBN 0080379419.

6.                              ^ Wells A.F. (1984) Structural Inorganic Chemistry 5th edition Oxford Science Publications ISBN 0-19-855370-6

7.                              ^ Plyushev, p. 96

8.                              ^ a b Henry Ehrenreich (1984). Solid state physics: advances in research and applications. Academic Press. pp. 29–31. ISBN 978-0-12-607738-4. Retrieved 4 June 2011.

9.                              ^ Lidin, p. 620

10.                          ^ Alikbaeva LA, ed. (2005). "Таблица неорганических и координационных соединений" (in Russian). Новый справочник химика и технолога. 1. Основные свойства неорганических, органических и элементоорганических соединений. St. Petersburg. ISBN 5-98371-025-7.

11.                          ^ "ЭСБЕ/Цезий". Brockhaus and Efron Encyclopedic Dictionary. 1890–1907. Retrieved 2011-04-15.

12.                          ^ a b Knunyants, I. L, ed. (1998). "Цезия галогениды". Химическая энциклопедия (Chemical encyclopedia). 5. Moscow: Soviet Encyclopedia. p. 657. ISBN 5-85270-310-9.

13.                          ^ Lide, p. 8-112

14.                          ^ Turova, N. Ya. (1997). = Неорганическая химия в таблицах. Moscow. p. 85.

15.                          ^ a b c Plyushev, V.E. and Stepin, B. D (1975). Аналитическая химия рубидия и цезия. Moscow: Nauka. pp. 22–26.

16.                          ^ Plyushev, p. 97

17.                          ^ Alikbaeva LA, ed. (2005). "Растворимость неорганических соединений в смешанных и неводных растворителях" (in Russian). Новый справочник химика и технолога. Химическое равновесие. Свойства растворов. St. Petersburg. ISBN 5-98371-025-7.

18.                          ^ Plyushev, V.E. et al. (1976). Bolshakov, K. A.. ed. Химия и технология редких и рассеянных элементов. 1 (2 ed.). Moscow: Vysshaya Shkola. pp. 101–103.

19.                          ^ Lide, pp. 8–61,62

20.                          ^ Lidin, p. 645

21.                          ^ Lidin, R. A; Molochko V. and Andreeva, L. L. A. (2000). Химические свойства неорганических веществ (3 ed.). Moscow: Khimiya. p. 49. ISBN 5-7245-1163-0.

22.                          ^ Knunyants, I. L, ed. (1988). "Бария хлорид". Химическая энциклопедия. 1. Moscow: Soviet Encyclopedia. p. 463.

23.                          ^ National Research Council (U.S.). Office of Critical Tables, ed. (1962). Consolidated Index of Selected Property Values: Physical Chemistry and Thermodynamics (Publication 976 ed.). Washington, D.C.: National Academy of Science. p. 271.

24.                          ^ Knunyants, I. L, ed. (1992). "Полигалогениды". Химическая энциклопедия. 3. Moscow: Soviet encyclopedia. pp. 1237–1238. ISBN 5-85270-039-8.

25.                          ^ Knunyants, I. L, ed. (1998). "Цезий". Химическая энциклопедия (Chemical encyclopedia). 5. Moscow: Soviet Encyclopedia. pp. 654–656. ISBN 5-85270-310-9.

26.                          ^ Plyushev, pp. 210–211

27.                          ^ Plyushev, p. 206

28.                          ^ a b c "Cesium and Cesium Compounds". Kirk-Othmer Encyclopedia of Chemical Technology. 5 (4-th ed.). New York: John Wiley & Sons. 1994. pp. 375–376.

29.                          ^ Plsyushev, pp. 357–358

30.                          ^ a b c d e f Manfred Bick and Horst Prinz "Cesium and Cesium Compounds” in Ullmann’s Encyclopedia of Industrial Chemistry, 2002, Wiley-VCH, Weinheim.doi:10.1002/14356007.a06_153 Vol. A6, pp. 153–156 .

31.                          ^ Halka M., Nordstrom B. (2010). Alkali and Alkaline Earth Metals. Infobase Publishing. p. 52. ISBN 978-0-8160-7369-6.

32.                          ^ Enrique Lima "Cesium: Radionuclide" in Encyclopedia of Inorganic Chemistry, 2006, Wiley-VCH, Weinheim. doi:10.1002/0470862106.ia712

33.                          ^ a b National Research Council (U.S.). Committee on Radiation Source Use and Replacement; National Research Council (U.S.). Nuclear and Radiation Studies Board (January 2008). Radiation source use and replacement: abbreviated version. National Academies Press. pp. 28–. ISBN 978-0-309-11014-3. Retrieved 4 June 2011.

34.                          ^ Hackspill M. L. (1905). "Sur une nouvelle prepapratíon du rubidium et du cæsium" (in French). Comptes rendus hebdomadaires des séances de l'Académie des sciences 141: 106.

35.                          ^ Plyushev, p. 90

36.                          ^ Kano T., Kumano T., Maruoka K. (2009). "Rate Enhancement of Phase Transfer Catalyzed Conjugate Additions by CsCl". Organic Letters 11 (9): 2023–2025. doi:10.1021/ol900476e. PMID 19348469.

37.                          ^ Katritzky A. R., Meth-Cohn O., Rees Ch. W. (1995). Volume editor: Gilchrist T. L.. ed. Comprehensive Organic Functional Group Transformations. 6: Synthesis: Carbon with Three or Four Attached Heteroatoms (First ed.). New York: Elsevier. p. 283. ISBN 978-0-08-040604-6.

38.                          ^ Alikbaeva LA, ed. (2005) (in Russian). Новый справочник химика и технолога. Аналитическая химия (часть II). Микрокристаллоскопия. St. Petersburg. ISBN 5-98371-025-7.

39.                          ^ ГОСТ 52407-2005. Вода питьевая. Методы определения жесткости. Moscow: Стандартинформ. 2006.

40.                          ^ Alikbaeva LA, ed. (2005) (in Russian). Новый справочник химика и технолога. Аналитическая химия (часть II). Химические методы обнаружения ионов.(Качественный химический метод анализа). St. Petersburg. ISBN 5-98371-025-7.

41.                          ^ Цезий, (in Russian)

42.                          ^ a b Brewer, AK (1984). "The High pH Therapy for Cancer, Tests on Mice and Humans". Pharmacology, Biochemistry, and Behavior 21 Suppl 1: 1–5. PMID 6522424.

43.                          ^ Zhong, J; Yao, W; Lee, W (2007). "Cesium chloride protects cerebellar granule neurons from apoptosis induced by low potassium". International Journal of Developmental Neuroscience 25 (6): 359–365. doi:10.1016/j.ijdevneu.2007.07.003. PMID 17804190.

44.                          ^ Sartori, HE (1984). "Cesium therapy in cancer patients". Pharmacology, Biochemistry, and Behavior 21 (Suppl 1): 11–3. doi:10.1016/0091-3057(84)90154-0. PMID 6522427.

45.                          ^ Low, JC; Wasan, KM; Fazli, L; Eberding, A; Adomat, H; Guns, ES (2007). "Assessing the therapeutic and toxicological effects of cesium chloride following administration to nude mice bearing PC-3 or LNCaP prostate cancer xenografts". Cancer chemotherapy and pharmacology 60 (6): 821–9. doi:10.1007/s00280-007-0429-4. PMID 17294190.

46.                          ^ Wood, Leonie. "'Cured' cancer patients died, court told". The Sydney Morning Herald. 20 November 2010.

47.                          ^ "Cesium Chloride". Complementary and Alternative Medicine: Herbs, Vitamins, and Minerals. American Cancer Society. 30 November 2008. Retrieved 2011-05-13.

48.                          ^ Alikbaeva LA, ed. (2005). "11.1. Источники радиоактивных загрязнений" (in Russian). Новый справочник химика и технолога. 11. Радиоактивные вещества. Вредные вещества. Гигиенические нормативы.. St. Petersburg. ISBN 5-98371-025-7.

49.                          ^ a b Cesium. Mineral Commodity Summaries January 2010. U.S. Geological Survey

50.                          ^ Carrea, JR; Gleason, G; Shaw, J; Krontz, B (1964). "The direct diagnosis of myocardial infarction by photoscanning after administration of cesium-131". American heart journal 68: 627–36. PMID 14222401.

51.                          ^ Cesium 131 Photoscan: Aid in the Diagnosis of Myocardial Infarction. doi:10.1001/jama.1968.03140200025006.

52.                          ^ Tver'yanovich Y. S. et al. (1998). Glass Phys. Chem. 24: 446.

53.                          ^ Кленовский М. С., Кельман В. А., Жменяк Ю. В., Шпеник Ю. О. (2010). "Электроразрядный источник УФ-излучения на основе парогазовой смеси Xe-CsCl". Журнал технической физики 80 (5): 117–122.

54.                          ^ "Тугоплавкие и химически активные металлы". Migatronic. Retrieved 2011-02-24.

55.                          ^ Morris Ch. G., ed. (1992). "Cesium chloride". Academic Press Dictionary of Science and Technology. San Diego: Academic Press. p. 395. ISBN 0-12-200400-0.

56.                          ^ a b "Cesium Chloride MSDS" (pdf). Cesium Fine Chemicals. Cabot Corporation. Retrieved 2011-04-11.

57.                          ^ Qureshi J. A., Buschman L. L., Throne J. E., Whaley P. M., Ramaswamy S. B. (2004). "Rubidium Chloride and Cesium Chloride Sprayed on Maize Plants and Evaluated for Marking Diatraea grandiosella (Lepidoptera: Crambidae) in Mark–Recapture Dispersal Studies". Environmental Entomology 33 (4): 930–940. doi:10.1603/0046-225X-33.4.930.

58.                          ^ Kogel J. E., Trivedi N. C., Barker J. M, ed. (2006). Industrial Minerals & Rocks: Commodities, Markets, and Uses (7th ed.). Littleton: Society for Mining, Metallurgy, and Exploration. p. 1430. ISBN 978-0-87335-233-8.

59.                          ^ Biel, Martin; Christian Wahl-Schott, Stylianos Michalakis, and Xiangang Zong (2009). "Hyperpolarization-Activated Cation Channels: From Genes to Function". Physiological Reviews.

60.                          ^ "Chemical Safety Data: Caesium chloride". Hands-on Science (H-Sci) Project: Chemical Safety Database. Physical and Theoretical Chemistry Laboratory, Oxford University. Retrieved 2011-04-08.

61.                          ^ "Safety data for caesium chloride". Chemical and Other Safety Information. The Physical and Theoretical Chemistry Laboratory Oxford University. Retrieved 2011-04-08.

62.                          ^ Lazarev NV and И. Д. Gadaskina, ID, ed. (1977) (in Russian). Вредные вещества в промышленности. Справочник для химиков, инженеров и врачей. 3 (7 ed.). St. Petersburg: Khimiya. pp. 328–329.

63.                          ^ The Radiological Accident in Goiânia. Vienna: IAEA. 1988. ISBN 92-0-129088-8.. See pp. 1–6 for summary and p. 22 for the source description

64.                          ^ The Worst Nuclear Disasters, Time Magazine

Bibliography

http://curezone.com/FORUMS/am.asp?i=335555

 

Kombu

Stof die erin zit:

kukoidon

Makes cancercells die in 72 hours

Graveoli

 

http://en.wikipedia.org/wiki/Caesium_chloride

Pancreatitis


The pancreas is a large gland behind the stomach which secretes digestive enzymes into the small intestines. Under normal conditions these enzymes remain inactive until they reach the small intestine. But sometimes the enzymes become active in the pancreas and can actually digest the pancreas itself.

The pancreas can become inflamed – a condition known as pancreatitis. In severe cases, pancreatitis can cause bleeding, tissue damage, and a release of enzymes into the blood. When this occurs other organs can be damaged.

Pancreatitis is one of the more potentially serious statin side effects. And all statins can cause pancreatitis.

However – according to Sonal Singh, M.D. – the occurrence of pancreatitis caused by statin use is rather rare. It is estimated that only one out of every 300,000 patients who use statins for at least a year will experience this side effect.

Despite the rather low incidence of severe pancreatitis associated with statin therapy you should be aware that it still does happen. If you are on statins and are experiencing any of the following symptoms…

... it is worth checking with your doctor. He or she is aware that pancreatitis is one of the potential statin side effects. Left untreated it could become very serious.

 

http://www.optimal-heart-health.com/statinsideeffects.html

Chronic pancreatitis

Chronic pancreatitis is a long-term inflammation of the pancreas. This condition is linked with an increased risk of pancreatic cancer, but most patients with pancreatitis never develop pancreatic cancer. The link between chronic pancreatitis and pancreatic cancer is strongest in smokers.

A small number of cases of chronic pancreatitis appear to be due to an inherited gene mutation (see "Family history"). People with this inherited form of chronic pancreatitis seem to have a high lifetime risk for developing pancreatic cancer (about 40% to 75%).

http://www.cancer.org/cancer/pancreaticcancer/detailedguide/pancreatic-cancer-risk-factors

nother nail in the coffin for statin drugs - New research finds statins increase artery calcification

8/31/2012 - In yet another blow to the claimed benefits of statin drugs, newly published research has found that statin drug use leads to accelerated coronary artery and aortic artery calcification, both of which greatly contribute to cardiovascular disease and mortality. The new study comes on top of findings...

 

Big pharma 'research' suggests all people over 50 should take statins every day for life

5/20/2012 - Big pharma propaganda has reached a new height in the UK this week, with the release of a new study that appears to show the benefits of taking statins. The report goes on to claim that everyone over 50 years of age should be taking the drug on a daily basis, for the rest of their lives. According...

 

Prominent heart doctor exposes the myths about cholesterol, statins and low fat diets

4/10/2012 - Renowned heart surgeon Dr. Dwight Lundell recently stepped forward to expose how embracing the high cholesterol myth has been wrong and the harm that has resulted, stating that the recommendations to lower cholesterol and severely restrict fat intake "are no longer scientifically or morally defensible." Dr....

 

Statins can cause muscle damage without necessarily exhibiting pain symptoms

3/14/2012 - If you take statin drugs to lower your cholesterol levels, these medications could be damaging your muscles without you even knowing it. Several studies not typically mentioned by the pro-statin drug lobby reveal that HMG-CoA reductase inhibitors can cause skeletal muscle damage that may not always...

 

FDA mandates new safety warnings for statin drugs due to risks of memory loss, diabetes and muscle pain

3/3/2012 - On February 28, federal health officials added new safety alerts to the prescribing information for statin drugs, citing increased risks of memory loss, diabetes and muscle pain. It is the first time the United States Food and Drug Administration (FDA) has officially linked statins to cognitive problems...

 

Statins increase diabetes in postmenopausal women by seventy percent

2/1/2012 - The result of a study published in the Archives of Internal Medicine finds that statin use in postmenopausal women significantly increases the risk of developing diabetes. In spite of this damning evidence, researchers do not recommend that the American Diabetes Association guidelines for primary and...

 

Study - statin drugs linked to higher diabetes risk

1/12/2012 - A new study confirms a dangerous statin drug side effect: diabetes. Researchers at Harvard Medical School report women over the age of 45 are much more likely to develop diabetes if they're taking a statin drug. The study followed more than 153,000 postmenopausal women who enrolled in the Women's...

 

Study: Statins cause memory loss, depression

4/19/2011 - The growing list of serious negative side effects caused by statin drugs now includes memory loss and depression, according to a new study published in the Cochrane Library. Researchers discovered that the vast majority of drug trials allegedly showing statins to be safe have been conducted by drug...

 

 

Statins prove useless, ineffective in children with lupus

11/13/2010 - The push to expand the market for statin drugs has hit a major roadblock. A recent study presented at the annual meeting of the American College of Rheumatology has revealed that the "preventive" administration of statin drugs does nothing to prevent children with lupus from developing atherosclerosis,...

 

 

Statins Cause Serious Structural Muscle Damage

8/27/2009 - If there is a super star in Big Pharma's list of money making drugs, it may well be the group of medications known as statins. The New York Times reported last year that statins are, in fact, the biggest selling drugs in the world. Their names, like Lipitor and Crestor, are familiar from countless television...

 

 

Statins Given to Prevent Pneumonia in Elderly Actually Increase Pneumonia Risk by 61 Percent

7/14/2009 - Published reports say that between 11 million to 30 million Americans are taking the supposedly wonder drugs called statins. These cholesterol lowering medications brought in over $34 billion in sales last year and have raked in a quarter of a trillion dollars since they were introduced two decades...

 

 

Statins Cause Heart Attacks in Some Users

3/30/2009 - Over 38 million people in the U.S. are currently taking statin drugs to lower high cholesterol levels. However, German scientists at the Martin Luther-University in Halle-Wittenberg have just published research in the Journal of Lipid Research that shows, for some people, taking statins actually increases...

 

 

Another Blow to Magic Bullet Drugs: Statins Impair Brains

2/24/2009 - Statin drugs can reduce soaring cholesterol levels, according to countless ads touting these supposed "wonder" drugs, that means they are brimming with health benefits because they lower the risk of cardiovascular disease. The problem is a host of side effects from eye problems and muscle pain to heart...

 

 

Researchers Detail Statin Drug Dangers

2/9/2009 - With familiar and widely-advertised names like Levacor, Zocor, Pravachol, Lipitor, and Crestor, statin drugs have become some of the most widely prescribed drugs in the world. In fact, the medications (technically a class of drugs called HMG-CoA reductase inhibitors) have been so hyped as a pill-popping...

 

 

Statins Raise Prostate Cancer Risk of Obese Men

1/3/2009 - A study conducted earlier this year at the Fred Hutchinson Cancer Research in Seattle found that the use of cholesterol-lowering statin drugs, especially when used long-term, seems to raise the risk of prostate cancer among obese men. Background Statin drugs inhibits the enzyme which controls...

 

Despite the Hype, Statin Drugs Found Medically Useless in Preventing Alzheimer's

9/8/2008 - Cholesterol-lowering statin drugs do not provide any protection against Alzheimer's disease, according to a study conducted by researchers from the Rush University Medical Center in Chicago and published in Neurology, the journal of the American Academy of Neurology. "This study adds to the growing...

 

The Statin Scam Marches On

12/12/2007 - Considering that tens of millions of Americans now take statins to lower cholesterol, the following headline was conspicuously absent from the major media this month: "Statins Found To Turn On Gene That Causes Muscle Damage." It's now a fact of science; a new study shows that taking statins destroys...

 

Public Comment Date Announced for Sale of Behind the Counter Drugs

10/18/2007 - FDA announces public comment date for Behind the Counter (BTC) sales of prescription medications   On October 3, 2007 the FDA posted FDA Docket number 2007N-0356 announcing that it is open to public comment on November 14, 2007. According to the FDA this docket "regards the behind-the-counter (BTC)...

 

Statin drugs expose patients to dangerous, debilitating side effects

1/8/2007 - Millions of Americans take statin drugs to help lower their cholesterol, making it one of the most popular classes of prescription drugs on the market today, but like most prescription medications, these drugs are often unnecessary, as most Americans could lower their LDL (bad) cholesterol levels simply...

 

 

High Doses of Statins Carry Dangers, Swedish Report Says (press release)

7/14/2006 - A Swedish warning on the potential risks of using statins in high doses has triggered strong criticism from some of the top U.S. cardiologists. The timing of the debate is apt: Recently revised recommendations in the United States call for lowering cholesterol more than ever before as a way of reducing...

 

Despite the claims of the mainstream media, Lesco and other statins are not magic bullets for cholesterol

6/20/2006 - We all want a "quick fix" for disorders like high cholesterol, it seems. We want to be able to eat all the pizza and cheeseburgers we want and then take a magic pill so all the LDL cholesterol running through our bloodstream just disappears. No matter what the statin drug commercials tell you, there...

 

 

Corruption exposed: drug companies gave grants, consulting fees to panelists who issued new cholesterol guidelines that are driving demand for statins

7/15/2004 - The new cholesterol lowering guidelines are proving to be a windfall for statin drug manufacturers like Pfizer and Merck: most news articles and medical advice concerning the new guidelines recommend drugs -- and drugs only -- to reduce cholesterol level. As a result, the guidelines are perhaps better...

 

 

Statin drug side effects list

7/15/2004 - Here's a quick list of known side effects caused by taking statin drugs. People who take statins have suffered ravaging health consequences, including permanent damage to their liver, muscles and nervous system. Statins frequently cause people to lose their memories or feel confused. Here's the full...

 

 

If prescription drugs are so good, where are all the healthy drug takers?

7/15/2004 - When observing the state of modern medicine and the unprecedented influence of pharmaceuticals, an interesting paradox arises. The drug companies claim that pharmaceuticals can do wonders for people: lower their cholesterol, end clinical depression, reverse osteoporosis, eliminate allergies, calm your...

 

 

Health officials launch the great statin marketing con by announcing that tens of millions of people suddenly need lower cholesterol

7/12/2004 - It's the pharmaceutical industry's marketing hype machine in full action: a new announcement that all of a sudden everybody should pursue drastically lower cholesterol levels. Previously, the recommended level was 130. Now it's suddenly 100, and can you guess what people are being urged to do in order...

 

 

Medical fraud alert: cholesterol lowering statin drugs save zero lives, says comprehensive research published in JAMA

7/6/2004 - The hype about statin drugs is relentless these days. Physicians are urging patients to take statins even when they don't have high cholesterol. The American Diabetes Association, for its part, ridiculously suggests that all diabetic patients should be on statins just in case scientists one day discover...

 

 

Mass media hypes up statins, calling them wonder drugs while ignoring their dangerous side effects

7/1/2004 - The mass media hype about statins has reached stratospheric proportions. USA Today, in this article, calls statins a "wonder drug" and poses the ridiculous question, "Should statins be in every medicine cabinet?" Statins are extremely potent prescription drugs with dangerous side effects that include...


Learn more: http://www.naturalnews.com/statins.html#ixzz2G5kUbqqr
 

http://www.naturalnews.com/statins.html

our results suggest that there is no association between statin use and pancreatic cancer risk, when statins are taken at daily doses for cardiovascular event prevention.

http://www.docguide.com/statin-use-and-risk-pancreatic-cancer-meta-analysis?tsid=5

How to Prevent Pancreas CancerPhoto Credit adn ? image by G.g1 from Fotolia.com

Risk factors for cancer of the pancreas can be controlled but may not prevent the disease. The pancreas helps control metabolism in the body. Pancreas cancer occurs when genes mutate and form tumors that can spread to other organs. Once the disease spreads it is incurable, according to the National Cancer Institute. Researchers are still studying factors that increase the chances of developing the disease.

Step 1

Avoid smoking. Johns Hopkins Medicine warns that smoking can alter genes, increasing the risk of pancreatic cancer. The risk increases two to three times in college students who smoke. Stopping smoking reduces the chances of the disease. Active smokers should discuss strategies for smoking cessation with a health care provider.

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Step 2

Maintain a healthy weight. Engage in regular physical activity and consume a diet rich in fruits and vegetables and low in saturated fats. Obesity is linked to pancreatic cancer at a younger age compared to patients with the disease whose weight is normal. Obesity is also associated with shorter survival time for overweight patients, according to the Journal of the American Medical Association's editorial "Overweight, Obesity, and Pancreatic Cancer" published June 24, 2009.

Step 3

Speak with your doctor about taking statins. There could be some benefits for preventing cancer of the pancreas from taking drugs used to treat cholesterol, known as statins, especially for individuals with a family history of pancreas cancer. The March 2007 study published by the National Institutes of Health, "Statins reduce the risk of pancreatic cancer in humans: a case-control study of half a million veterans", showed a 67 percent risk reduction of the disease among participants taking statins for more than six months, including diabetics, across various ethnic groups, despite smoking and regardless of alcohol use.


Read more: http://www.livestrong.com/article/224644-how-to-prevent-pancreas-cancer/#ixzz2G5n3SML1
 

http://www.livestrong.com/article/224644-how-to-prevent-pancreas-cancer/

 

Cheryl Rounds · Works at Self employed

My Mom died of pancreatic cancer 7 years after starting on statins. I have always blamed the statins and had warned her not to take the drugs.
Another mechanism that I believe may cause cancer is the side effect of lowering Q10 in the body. Q10 is almost always low in people with cancer.

http://thepeopleschemist.com/popular-wonder-drugs-may-cause-cancer/

he risk of cancer. 2 Specifically, the increased risk of cancer has been significantly correlated with the lowering of LDL cholesterol- an unforeseen negative outcome. With statin use, the increase in cancer deaths counteracts the supposed lower cardiac mortality associated with lower cholesterol, resulting in a neutral effect or increased overall mortality. Translation: with statin use, even if you don't die of a heart attack, you will likely die of cancer.

 

However, statins are now being shown to not prevent or reduce heart disease. The inability of statins to have a positive impact on heart disease was predicted in a Journal of the American Medical Association (JAMA) article over ten years ago, which concluded that low cholesterol, by itself, did not significantly prevent heart disease:

 

Also, the Journal of American College of Cardiology (2007;50[18]:1735-1741) published "Beyond Low-Density Lipoprotein Cholesterol-Defining the Role of Low-Density Lipoprotein Heterogeneity in Coronary Artery Disease," stating more discouraging conclusions:

This recent finding and its implications will be the key to explaining the statin/cancer connection.

Cholesterol-Lowering Drugs Were Known to Cause Cancer a Decade Ago

A dire warning about statin use was published by two physicians, Thomas B. Newman and Stephen B. Hulley, at the University of California in San Francisco in 1996.5 This same warning was published in the cancer journals over a decade ago. One example appeared in Cancer Research:6

"Several trials of cholesterol lowering with drugs to prevent cardiovascular disease events have demonstrated an increase in cancer incidents in the subjects treated with lipid-altering drugs. The trials were randomized, double-blinded, and lasted an average of five years ... A statistically significant excess of malignancy was seen in elderly subjects and women randomized to the drug groups."

None of these studies or their conclusions has ever been refuted, yet we continue to prescribe more and more cholesterol-lowering drugs. Are physicians missing something? Yes. Take the following,for example.

Arterial Plaques-It's Not the Saturated Fat

For decades, saturated fat was blamed for the buildup of arterial plaque, the material that can significantly narrow the diameter of arteries. However, a landmark article published in the Lancet in 1994 shattered that myth.7 The investigators analyzed plaque and found it contained more than ten different compounds, none of which consisted of saturated fat. There are also other independent analyses confirming the lack of saturated fat in any arterial plaque.8,9

Arterial Plaque-Normally a Harmless Natural Repair Mechanism

As the vasculature ages, it is constantly repaired with new collagen. A number of other repair mechanisms are concurrently working, with cholesterol and Lp(a) lipoprotein acting as "sticky patches" to seal cracks when injury or damage to an arterial wall occurs.

"Remember the best and most secure place to invest your money is in your health. You always have solid returns and you never lose your principal!"

-Sherri Tenpenny, D.O., May 10, 2009 issue of OsteoMed II News; www.osteomed2.com

Statins, previously reported to have relatively few serious side effects, can significantly increase the risk of cancer

In healthy individuals, arterial plaques form as a result of these patching activities, but without serious consequences. However, in many individuals, the plaques do not disappear, but build up over time. To explain these perplexing observations, we need to explore cholesterol's makeup.

Importance of Cholesterol-"Good" or "Bad" Terms Are Misleading

Cholesterol itself can't be "bad," because it is critical in the production of the hormones estrogen, progesterone, and testosterone,10 keeping our skin water and chemical resistant, manufacturing bile salts for digestion of fats, forming our bones, and delivering parent essential oils (PEOs) to all of our 100 trillion cells. Without plenty of cholesterol, we would all be dead.11

While free cholesterol does exist in the body, 80-90% is esterified, meaning it is chemically bound to a fatty acid, with a strong preference given to parent omega-6 (linoleic acid, or LA).

The Structure of Cholesterol Itself Never Changes

That's right; the structure of cholesterol itself never changes; the esterified component does. It is only the hydrocarbon (alkyl) portion of the ester group that changes. If you term something as "bad," presumably you want to get rid of it or at least get it as low as possible. This is what the pharmaceutical industry is saying.

However, if you got rid of all the LDL-C, you would be wiping out valuable fatty acids as well as a mechanism for removing oxidized fatty acids that should be removed from the body. It would be like stopping "garbage pick-up."

These cholesteryl esters are transported throughout the body in lipoprotein particles that are classified according to the ratio of protein to fat, or more simply, the density of the particle, in the following increasing order: chylomicrons, very low-density lipoprotein, intermediate-density lipoprotein, low-density lipoprotein, and high-density lipoprotein.12 LDL particles contain the highest percentage of cholesteryl esters (mainly parent omega-6, with a small portion of approximately three percent parent omega-3).

Importance of Esterified Cholesterol

Esterified cholesterol comprises the majority of LDL. LDL is much more than just "cholesterol," although few people, including nutritionists and physicians, understand this. It is essential to understand the term cholesterol "esters" if you hope to understand the vital role of LDL in your body. Medical journals confirm this important fact: "LDL contains up to 80% lipid, including polyunsaturated fatty acids and cholesterol, mainly esters.

Linoleic acid [is] one of the most abundant fatty acids in LDL ..."13

Furthermore, H. M. Sinclair, a top EFA researcher and famous English nutritional biochemist (bio available at: http://www.britathsoc.org/bas_hugh_sinclair.html), made clear in 1984 that about 20% of the free fatty acids of the phospholipids in both LDL and HDL are composed of parent omega-6, too.14 America's top cardiology publication, the Journal of American College of Cardiology (2007;50[18]:1735-1741), published information stating that it is the esterified cholesterol that is the problem in heart disease, but didn't address the reasons why the problem occurs or offer ideas on how to solve it.

Esterification of LA with cholesterol was known as early as 194115 and is one of the keys to understanding the statin/cancer connection. However, due to widespread inaccurate terminology, we first need to discuss PEOs, essential fatty acids (EFAs), and EFA derivatives..

Statins are now being shown to not prevent or reduce heart disease

Parent Essential Oils: An Essential Difference

The term "essential fatty acids" is so frequently misused that I was compelled to coin a new phrase, "parent essential oils" (PEOs). "PEOs" refer to the only two true essential fatty acids: parent omega-6 (LA) and parent omega-3 (alpha-linolenic acid, or ALA). The term "parent" is used because these are the whole, unadulterated forms of the only two essential fats your body demands, as they occur in nature. Once PEOs are consumed, your body changes only five to ten percent of them to "derivatives."16-18 That means 90-95% stay in the parent form in the cell and mitochondrial membranes.19,20 There are a host of omega-6 and omega-3 derivative-based oils being marketed to physicians as EFAs that are, in fact, non-essential derivatives such as eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and gamma-linolenic acid (GLA). Fish oils are made up almost exclusively of omega-3 derivatives. Scientifically and biochemically, calling these derivatives "EFAs" is incorrect. Derivatives are not EFAs because they are not essential-your body has the ability to make them as needed from the PEOs. Taking fish oil and other health-food-store "EFAs" often leads to pharmacological overdoses, which can be very harmful.

Food Processing Adulterates Most Parent Omega-6

In the last several decades, processed foods-in particular, frozen foods and restaurant cooking oils-have increasingly contained trans fats (hydrogenated) and other unhealthy fats and oils, resulting in less parent omega-6 (LA) for incorporation into cell membranes and conversion into arachidonic acid, which is a source of many prostanoids and leukotrienes used in inflammatory, immune, and signaling functions.21,22

Membrane fluidity increases when more PEOs (in particular, parent omega-6) are available to incorporate in the membrane lipid bi-layer. When natural PEOs are replaced by trans fats (hydrogenated), the fluidity changes, and that can cause significant reduction in critical cellular O2 transfer.

A category of synthetic fat that is increasingly used as a substitute for trans fats is interesterified fats, termed IE fat. Consequently, IE has its own set of health problems such as abnormally raised resting blood glucose levels.24,25

It is important to understand that cooking oil manufacturers avoid omega-3 oils because they are much more unstable than the parent omega-6 series oils. Therefore, most omega-3 in the diet is unadulterated and of no concern in our analysis of adulterated PEOs. Many seeds, nuts, grains, eggs, etc., contain omega-3 and omega-6 unsaturated fatty acids, but typically the amount of omega-6 far outweighs the amount of omega-3; flax seeds are an exception.

Even when margarine and other hydrogenated products contain relatively few trans fats-as little as one to two percent-this translates to an enormous number of defective trans fat molecules. In absolute numbers, there are 1x1021 molecules in each tablespoon of oil. Therefore, the potential to cause great damage, either integrally in the cellular structure or in biochemical reactions, is highly significant, since many of us consume much more than a single tablespoon of processed oil each day. Add to this number of defective oil molecules the huge number of defective fat molecules from other processed sources, and you should be terrified at what you, your family, and your patients have been consuming for decades.

Avoiding Fat Isn't a CAD Solution-PEOs Are

As the New England Journal of Medicine makes clear, "Diets high in polyunsaturated fat (PEOs) have been more effective than low-fat, high-carbohydrate diets in lowering cholesterol as well as the incidence of heart disease."26 The key is making sure the PEOs are unadulterated.

Otto Warburg, M.D., Ph.D.: "Lowered CellularOxygen Equals Cancer!"

Oxygen deprivation is cancer's prime cause, and the high ratio of fermentation to respiration is cancer's prime characteristic

Just as oxygen deprivation causes heart disease, sustained oxygen deprivation causes cancer, too. Over 70 years ago, the Nobel prize-winning physician and master chemist Otto Warburg, M.D., Ph.D., demonstrated that a sustained reduction of 35% in the level of cellular oxygen causes cancer, and does so each and every time the deficiency occurs for an extended period. Oxygen deprivation is cancer's prime cause, and the high ratio of fermentation to respiration is cancer's prime characteristic.27,28 Cancer's prime cause, cellular hypo-oxygenation (hypoxia), was directly proven by American research scientists in the 1950s.29,30 Back then, they didn't know how to increase cellular oxygenation, whereas today we do, and this is the key in answering why the "statin/increased cancer" connection occurs and how to prevent its tragic consequences:

  1. Warburg proved depressed cellular respiration and phosphorylation are the cancer-causing effects of decreased cellular oxygen.31
  2. Physico-chemical experiments (Campbell et al.) show that parent omega-6 (LA) can bind twice as much oxygen and disassociates (releases its oxygen) at a much higher pressure (physiologically useful), much closer to hemoglobin, than non-essential oleic acid does.32 Therefore, the 35% cancer-causing hypo-oxygenation (deprivation) threshold is breached with insufficient or adulterated parent omega-6.
  3. Oxygen disassociation curves for oleic acid compared with LA prove a 50% reduction in oxygen transfer is possible.
  4. Decreased cellular oxygenation can therefore systemically occur in any membrane; any tissue in the body can become a potential cancer site.32 Campbell et al.'s seminal experiment conclusively showed a 50% reduction in oxygenation when a PEO deficiency occurred.32 Now, imagine this effect coupled with already lowered parent omega-6 esterified cholesterol from statins.

The chain of events is as follows:

Lowered Cholesterol = Fewer PEOs = Less Cellular O2 = Cancer

The body has no cholesterol sensor because the absolute cholesterol number is irrelevant.

We have already explained in detail that the common link between LDL cholesterol and decreased oxygenation occurs because cholesterol is esterified with large amounts of parent omega-6 before it is combined with lipoprotein as LDL particles for transportation within the body.15,33 Even though statins increase the uptake of LDL cholesterol from the blood, they decrease overall cellular LA because absolute levels of cholesterol are decreased. This affects oxygen transmission across the cell membranes, since the structure of the phospholipids that form a major portion of the cell membrane is a reflection of the composition of unsaturated fatty acids and bioavailability in the blood.23 It is known that the fatty acid component of cell membrane phospholipids reflects diet.28

Defective LDL Cholesterol Becomes a "Defective Delivery System"

With the consumption of organic, unprocessed PEOs from natural sources such as walnuts, almonds, Brazil nuts, sunflower seeds, or their (unprocessed) cooking oils-rather than adulterated oils and trans fats-LDL cholesterol should be made up of significant amounts of properly functioning LA. However, since LDL cholesterol is the transport vehicle for PEO delivery into your cells, it does not care about the state of the essential fatty acids it is carrying.

LDL cholesterol will transport adulterated essential fats already damaged by food processors into the cell. It is primarily the adulterated (defective) parent omega-6 that causes plaque, not saturated fat. So, while statins reduce LDL cholesterol by reducing the amount of defective parent omega-6 from processed food, and therefore decreasing plaque, the statins are simultaneously reducing the transport of vital oxygenating unadulterated PEOs into the cells.

This is the reason why patient cholesterol numbers steadily decrease, yet patient heart attacks continue to increase. The popular belief, even among physicians, is that evidence, such as the 2007 METEOR trial, shows there is a decrease in heart attacks in patients taking statins.42

The facts are that cholesterol was lowered and the progression of atherosclerosis halted in the placebo group, in which no patient suffered a serious cardiovascular event; whereas in the treatment group (taking rosuvastatin), there were eight serious cardiovascular events, including heart attack and angina, a bad outcome. In addition, this randomized controlled trial had a number of serious flaws that were pointed out in an editorial in JAMA, which accompanied the article.43

Another negative, unexplainable, and baffling result of statins was published by Reuters, December 3, 2007 (available at: http://www.reuters.com/article/healthNews/idUSN2922862020071129). It included the following:

For the first time, this baffling outcome is now both predictable and explained. Any drug that artificially lowers cholesterol also lowers transport of cancer-fighting, oxygenating PEOs!

Parent Essential Oils Decrease Arterial Plaque

Stop Blaming Cholesterol

LDL cholesterol continues to be improperly blamed for a myriad of health problems, while the real culprit is defective PEOs. LDL cholesterol has no alternative but to transport these killers throughout our bodies, since, due to food processors' requirement for extended shelf life in the oils they sell, we have insufficient properly functioning LA in our diets. The nutritionists never make this critical connection and incorrectly identify the "problem" as LDL cholesterol. To repeat: the reason for the ineffectiveness of statins to stop heart disease is they simply can't eliminate enough of the defective PEOs being transported in LDL esterified cholesterol. In addition, they simultaneously remove correctly functioning PEOs, because they reduce its cholesterol carrier-a doubly bad effect. You now understand why the absolute LDL number is irrelevant if the diet contains sufficient unadulterated PEOs.

Statins don't discriminate between eliminating functional, unadulterated PEOs and nonfunctional, adulterated PEOs.

LDL cholesterol continues to be improperly blamed for a myriad of health problems, while the real culprit is defective PEOs

Reducing LDL Cholesterol Increases Blood Clots and Facilitates Metastasis of Cancer

Defective parent omega-6 is also the root cause of thrombosis/blood clots forming in the arteries and then being unable to dissolve away naturally, as they do with external cuts. As referenced earlier, blood clots are a tremendous problem with cancer cases, responsible for over 80% of the cancer mortality rate, because they facilitate cancer transport throughout the body when it would not have spread otherwise. This fact was known in 1958.34,35

Experiments from Florida Hospital Institute of Translational Research show that blood clots are often caused by biochemical factors contained in small cancerous tumors, like tissue factor (TF), which otherwise is found only in normal tissue-not in the blood-and normally causes clotting only from vascular injury. When a cancer cell carrying TF enters the blood, small clots are formed on the cancer cell's surfaces. The blood platelets, which are small cells that stick to injured blood vessels to help prevent blood loss, then stick to the clot-covered cancer cell. This sticky "sandwich" of cancer cell, blood clot, and platelets is able to stick to the inside of the blood vessel wall. A clot provides a "safe haven" for the cancer cell, giving it the time it needs to squeeze between the cells that line the blood vessel and escape into the tissues, where it can multiply into a secondary tumor.

Arachidonic Acid Is Important to Counteract Cancerous Clotting and CAD

Humans obtain arachidonic acid (AA) either ready-made in food or from the parent omega-6, if it is unadulterated. AA is not harmful: it is the precursor to prostacyclin-the most potent anti-aggretory agent (natural "blood thinner") and inhibitor of platelet adhesion.36 Lowering esterified LA through the lowering of LDL cholesterol automatically decreases the body's natural anti-aggretory AA.36 In view of the above, this is a very bad effect, as it will directly lead to increased risk of a blood clot and ultimately contracting cancer (and CAD).

Atherogenesis, Adulterated PUFAs, and LDL Cholesterol: More Connections

The eminent researcher H. M. Sinclair published his finding that PEO deficiency causes an enormous permeability increase in skin along with increased capillary fragility.37 We will use this information and connect it to the vascular system in an unexpected way.

Intima Is 100% Parent Omega-6

We need to know the innermost arterial layer, the intima, is epithelial tissue that is 100% parent omega-6 (LA); there is no omega-3 in skin.38,39 The delicate intima requires unadulterated parent omega-6 and doesn't get enough because of surplus adulterated fats or because statins decrease LDL cholesterol, which transports the parent omega-6 and lowers the associated LA to hypooxygenating, cancer-causing levels.

The authors of a 1982 British Medical Journal (BMJ) article understood the parent essential oil connection in 1982, but few of us heard the news reported in that article that LA and most polyunsaturated fatty acids, including AA and EPA, were found to be lower (depleted) in heart attack victims. Their conclusion was that the fatty acid patterns of the phospholipids [PEOs] constitute an independent risk factor for heart disease.40

This BMJ article "hits the nail on the head." Deficiency of PEOs is associated with increased heart attack risk. Don't think that the solution is to minimize parent omega-6 (along with parent omega-3) because of "oxidation" concerns. It is true that, in part, fats and oils oxidize for energy. Normal oxidation of fatty acids (for energy production) proceeds in the mitochondria via beta oxidation after activation by acyl-CoA synthetase.

Physicians utilizing the Peskin Protocol report significant improvements in patient outcomes across a broad spectrum of disease conditions. Following is a description of the results when one of America's top cancer consultants and researchers incorporated the protocol:

Peskin's The Hidden Story of Cancer has provided a great breakthrough in the treatment of our cancer patients.

The addition of 11,000 mg Peskin Protocol EFA capsules t.i.d., along with our protocol, has brought a dramatic difference; unbelievable and rapid improvement:

We believe Peskin Protocol EFAs are the "missing link" in cancer therapy. The cost of treating our patients has dropped from $20,000 (US) per month to $1,500 (US) per month by completely eliminating hospitalization. We saw no side effects. Within two weeks, patients typically see a great physical and mental improvement.
-Bernardo C. Majalca, N.D.
Stage 4 Cancer Researcher
Chula Vista (San Diego), California
619-591-7094

Adulterated parent omega-6 deposits in cell membranes lead to abnormal oxidation-oxidation from adulterated oils at the site of vascular injury causing injurious inflammation. Abnormal oxidation involves formation of hydroperoxides from the double bonds of the PEOs. This harmful partial oxidation involves no energy (ATP) production. All cells oxidize fuels for energy, and this is a normal process. However, food processing oxidizes PEOs, which prematurely become nonfunctional foods, causing vascular injury and destroying the body's inherent repair mechanism.

Medical Journals Often Unknowingly Mislead

Medical journals and some of the pharmaceutical manufacturers continue with the discredited theory that somehow your body's own cholesterol "causes" heart disease, so researchers continue to "discover" different types and sizes of cholesterol particles. Think about this conclusion: The body has no cholesterol sensor because the absolute cholesterol number is irrelevant.

The Solution

1. Ensure that the patient's diet contains generous amounts of unadulterated PEOs with a ratio of LA:ALA greater than 1:1 and less than 2.5:1 by advising them to eat unadulterated, unprocessed foods. To make this simpler and easier with noncompliant patients, patients should consider supplements.41

2. Have patients minimize foods containing significant amounts of trans fats (hydrogenated), interesterified fats, and other adulterated hypo-oxygenating fats. My research strongly supports the (prophylactic) use of an unprocessed organic supplement with a ratio of parent omega-6 to parent omega- 3 between 1:1 and 2.5:1. With this ratio, suggested use is 725 mg. per 40 lb. of body weight (e.g., 3 grams for a 160-lb. person on a daily basis). I call this the "Peskin Protocol." Cancer patients require significantly more. (For an in-depth analysis of how this specific ratio is determined, see "The Scientific Calculation of the Optimum Omega-6/3 Ratio" at www.CambridgeMedScience.org ["Optimum PEO Ratio"] or www.BrianPeskin.com ["EFA Report"].)

Clinical Results: PEOs Combat Cancer

Food processing oxidizes PEOs, which prematurely become nonfunctional foods, causing vascular injury

This article was written by Brian Peskin with Amid Habib, M.D., available from Pinnacle Press, P.O. Box 56507, Houston, Texas 77256 or by phoning 713-979-0065, internationally. More at www.BrianPeskin.com.

Special thanks to cardiologist David Sim, M.D., and endocrinologist Amid Habib, M.D., Debra Peskin, Pharm.D., Marissa Carter, Ph.D., and Daveda Lamont for their assistance in this article.

Brian Scott Peskin, B.S., electrical engineering (MIT), founded the field of Life-Systems Engineering Science in 1995. He was adjunct professor at Texas Southern University in the Department of Pharmacy and Health Science from 1998-1999. He is chief research scientist at Cambridge International Institute for Medical Science (www.CambridgeMedScience.org). This article is based on information in The Hidden Story of Cancer, 44 September/October 2009 www.wellbeingjournal.com Well Being Journal

One of my patients, a 68-year-old male, smoker, I have followed on a yearly basis beginning in 2005.... In spite of all routine conventional treatment, which included blood pressure medication, a "statin" drug, high-dose niacin, co-enzyme Q-10, and a daily aspirin, his coronary plaque volume continued to progress ... [However,] from 2007 to 2008, the volume of plaque decreased ...22% ... I have never seen a decrease of coronary artery plaque volume by more than 5% in one year. I called the patient to inquire about what else he was doing ... He told me the only thing different about his regimen was the "oxygen pills" that he was taking for the past 8 months.... [The] "oxygen pills" [were] the parent essential oils (PEOs) advocated by professor Brian Peskin.... Needless to say, personally, I have stopped taking my "statin" drug (Lipitor), and I have now implemented professor Peskin's PEOs into my therapeutic regimen.
-Robert Kagan, M.D.

From a letter to Jonathan Collin, M.D., 6-18-2008. (Kagan is medical director, MRI Scan and Imaging Centers.)

Courtesy of Townsend Letter for Doctors and Patients,
911 Tyler Street, Pt. Townsend, WA 98368,
http:// www.tldp.com.

References

1. Guyton A, Hall J. Textbook of Medical Physiology. 9th ed. Philadelphia, PA: W.B. Saunders; 1996:873.

2. Alsheikh-Ali A, Maddukuri PV, Han H, Karas RH. Effect of the magnitude of lipid lowering on risk of elevated enzymes, rhabdomyolysis, and cancer. J Am Coll Cardiol. 2007;50:409-418.

3. Krumholz HM, Seeman TE, Merrill SS, et al. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. JAMA. 1994;272:1335-1340.

4. Colpo A. LDL Cholesterol: "Bad' cholesterol or bad science. J Am Phys Surg. 2005;10:83-89.

5. Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. JAMA. 1996; 275:55-60.

6. Goldstein MR. Lipid-altering drugs: Decreasing cardiovascular disease at the expense of increasing colon cancer? Cancer Res. 2004;64:6831-6832.

7. Felton CV, Crook D, Davies MJ, Oliver MF. Dietary polyunsaturated fatty acids and composition of human aortic plaques. Lancet. 1994;344:1195-1196.

8. Waddington E, Sienuarine K, Puddey I, Croft K. Identification and quantification of unique fatty acid and oxidative products in human atherosclerotic plaque using high-performance lipid chromatography. Anal Biochem. 2001;292:234-244.

9. Kuhn H, Belkner J, Wiesner R, Schewe T, Lankin VZ, Tikhaze AK. Structure elucidation of oxygenated lipids in human atherosclerotic lesions. Eicosanoids. 1992;5:17-22.

10. Guyton A, Hall J. Textbook of Medical Physiology. 9th ed. Philadelphia, PA: W.B. Saunders; 1996:873,958,1010.

11. Alberts B, Bray D, Lewis J, Raff M, Roberts K, Watson JD. Molecular Biology of the Cell. 3rd ed. New York: Garland; 1994:481.

12. Voet D, Voet JG. Biochemistry Vol. 1: Biomolecules, Mechanisms of Enzyme Action, and Metabolism. 3rd ed. Wiley, NY; 2003:439.

13. Bowen PE, Borthakur G. Postprandial lipid oxidation and cardiovascular disease risk. Curr Atheroscler Rep. 2004;6:477-484.

14. Sinclair HM. Essential fatty acids in perspective. Hum Nutrit. 1984;38C:245-260.

15. Kelsey FE, Longenecker HE. J. Biol. Chem. 1941;139:727.

16. Salem N, Lin Y, Brenna JT, Pawlosky RJ. Alpha-linolenic acid conversion revisited. PUFA Newsletter, December 2003.

17. Pawlosky RJ, Hibbeln JR, Novotny JA, Salem N Jr. Physiological compartmental analysis of alpha-linolenic acid metabolism in adult humans. J Lipid Res. 2001;42:1257-1265.

18. Goyens PLL, Spilker ME, Zock PL, Katan MB, Mensink RP. Conversion of alpha-linolenic acid in humans is influenced by the absolute amounts of alpha-linolenic acid and linoleic acid in the diet and not by their ratio. Am J Clin Nutr. 2006;84:44-53.

19. Murray RK, Granner DK, Mayes PA, Rodwell VW. Harper's Illustrated Biochemistry. 26th ed. New York: McGraw Hill; 2003:191-192.

20. Meisenberg G, Simmons WH. Principles of Biomedical Chemistry. 1st edition. St.

Louis, MO: Mosby; 1998:226.

21. Vidgren HM, Louheranta AM, Agreb JJ, Scwab US, Uusitupa MI. Divergent incorporation of dietary trans fatty acids in different serum lipid fractions. Lipids. 1998;33:955-962.

22. Ibrahim A, Natrajan S, Ghafoorunissa R. Dietary trans-fatty acids alter adipocyte plasma membrane fatty acid composition and insulin sensitivity in rats. Metabolism. 2005;54:240-246.

23. Berlin E, Bhathena SJ, McClure D, Peters RC. Dietary menhaden and corn oils and the red blood cell membrane lipid composition and fluidity in hyper- and normocholesterolemic miniature swine. J Nutr. 1998;128:14211428.

24. Sundram K, Karupaiah T, Hayes KC. Stearic acid–rich interesterified fat and transrich fat raise the LDL/HDL ratio and plasma glucose relative to palm olein in humans. Nutr Metab. (Lond) 2007;4:3.

25. Prades J, Funari S, Escribá PV, Barceló F. Effects of unsaturated fatty acids and triacylglyerols on phosphatidylethanolamine membrane structure. J Lipid Res. 2003;44:1720-1727.

26. Hu FB, Stampfer MJ, Manson JE, et al. Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med. 1997;337:1491-1499.

27. Warburg, O. The metabolism of carcinoma cells. J Cancer Res. 1925;9:148-163.

28. Warburg, O. On the origin of cancer cells. Science. 1956;123:309-314.

29. Goldblatt H, Cameron G. Induced malignancy in cells from rat myocardium subjected to intermittent anaerobiosis during long propagation in vitro. J Exp Med. 1953;97:525-552.

30. Malmgren, RA, Flanigan CC. Localization of the vegetative form of Clostridium tetani in mouse tumors following intravenous spore administration. Cancer Res. 1955;15:473-478.

31. Warburg, O. The Metabolism of Tumours: Investigations from the Kaiser Wilhelm Institute for Biology, tr. Frank Dickens. Constable & Co Ltd: 1930 (out of print).

32. Campbell IM, Crozier DN, Caton RB. Abnormal fatty acid composition and impaired oxygen supply in cystic fibrosis patients. Pediatrics. 57, 480-486, 1976.

33. Guyton AC, Hall JE. Textbook of Medical Physiology. 10th ed. Philadelphia: W.B. Saunders Co.; 2000:874.

34. Weinberg RA. One Renegade Cell: How Cancer Begins. New York: Basic Books; 1998: 146.

35. Wood S Jr. Pathogenesis of metastasis formation observed in vivo in the rabbit ear chamber. AMA Arch Pathol. 1958;66:550-568.

36. Bunting S, Moncada S, Vane JR. The prostacyclin-thromboxane A2 balance: Pathophysiological and therapeutic implications. BMJ. 1983;39:271-276.

37. Sinclair HM. Deficiency of essential fatty acids and atherosclerosis, et cetera. Lancet. 1956;270:381-383.

38. Chapkin RS, Ziboh VA, Marcelo CL, Voorhees JJ. Metabolism of essential fatty acids by human epidermal enzyme preparations: evidence of chain elongation. J Lipid Res. 1986;27:945-954.

39. Andersson A, Sjödin A, Hedman A, Olsson R, Vessby B. Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men. Am J Physiol Endocrinol Metab 2000;279:E744–751.

40. Miettinen TA, Naukkarinen V, Huttunen JK, Mattila S, Kumlin T. Fatty acid composition of serum lipids predicts myocardial infarction. BMJ. 1982; 285:993-996.

41. Peskin BS. Scientific calculation of the optimum PEO ratio. Parent essential oils: omega-6/3 defined. Cambridge International Institute for Medical Science; 2006.

42. Crouse III, J, et al. Effect of rosuvastatin on progression of carotid intima-media thickness in low-risk individuals with subclinical atherosclerosis: the METEOR trial. JAMA. 2007;297:1344-1353.

43. Lauer MS. JAMA. 2007;297:1376-8

http://www.life-enthusiast.com/index/Concerns/Cancer/Cancer_Cholesterol_Statins

Peskin Protocol

Patient 4: Female. Stage IV pancreatic cancer. Told it was hopeless. Eight weeks later, tumor reduced 75%.

http://www.life-enthusiast.com/index/Concerns/Cancer/Cancer_Cholesterol_Statins

The following 3 supplements comprise the Peskin Protocol daily supplementation program. These supplements are based on Science - NOT opinion! Taking this supplementation program has independently been shown to produce phenomenal results.

1) PEO's™ or Parent Essential Oils. Our bodies can not make PEOs; they must come from food. Unfortunately, food processing, modern farming methods, and even "fresh" food preparation, destroys PEOs™ and the results can be disastrous to your health. Supplementing with this patent pending all organic PEO formulation ensures we get these in the proper form and ratio. This is vital in getting these nutrients back into your diet the way Nature intended.

Each bottle contains 120 - geletin caps. The PEOS are scientificallpeosy formulated to achieve optimum results allowing one capsule for each 40lbs of body weight. In otherwords, this is a one-month supply for those weighing approximately 160 lbs or less at 4-caps per day. If you weigh more or have other medical conditions you should use more to acchieve quicker, faster results. You can not take to many. Read more by clicking on the title or the bottle.

The first bottle ordered is $49.95. Order a second additional bottle per month for quicker, faster, results and each bottle is only $39.95.

 

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There are 60 - capsules in each bottle or a month's supply. Simply take 2-capsule once per day when eating any type of animal based protein.

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Groene thee

Informatie voor een gezonder en fitter leven


Introductie

Voor mijn site fonteine.com stuitte ik zo vaak op de voordelen van groene thee
dat ik even een aparte site wil maken om deze thee extra aandacht te geven.
Wel wil ik even toevoegen dat het onderzoek naar witte thee (de thee voor de
vroegere Chinese keizers) nog in de kinderschoenen staat maar dat in de toekomst
heel goed kan blijken dat groene thee gezond is maar dat witte thee nog een
stukje gezonder is. Dit zie je ook bij algen waar de chlorella soort net weer meer
voordelen biedt dan bijvoorbeeld spirulina. Wat ik wil bereiken met mijn sites is
dat mensen meer gaan nadenken over hun dagelijkse voeding omdat veel recente
informatie mbt onderzoeken gewoon via internet beschikbaar is. Als spruitjes en
brocolli bijvoorbeeld een belangrijke rol spelen bij preventie dan kun je bijvoorbeeld
dat soort groenten meer eten. Wil je deze extra moeite doen dan zul je sterker
staan tegenover de vele ziektes die ons teisteren. Je kan ook gewoon doorleven
en wel zien waar het schip strandt maar dat is je eigen keuze. Ik zal ieder geval
mijn best doen om zoveel mogelijk info voor je te verzamelen zodat je betere
keuzes kunt maken.

Ron Fonteine

De voordelen van groene thee

De gewoonte om groene thee te drinken in Japan stamt al van heel lang geleden. De thee staat vanouds bekend om zijn gezondheidsbevorderende en levens verlengende eigenschappen. Hoewel de gezondheidsbevorderende eigenschappen van de groene thee door de eeuwen heen proefondervindelijk zijn bewezen, neemt de wetenschapper van tegenwoordig daar geen genoegen meer mee en vindt dat de werkzaamheid in het laboratorium bewezen moet zijn. Recente studies over de groene thee hebben het geloof en de voordelen van het drinken van groene thee dan ook gerechtvaardigd. Sebastiaan Kneipp had ook al de stelling: 'laat je voeding je medicijn zijn en je medicijn je voeding.'

Omdat groene thee niet wordt gefermenteerd (gistingsproces), blijven alle natuurlijke stoffen behouden. Dit heeft tot gevolg dat de groene thee nog vol zit met waardevolle stoffen. Hieronder zal ik ze op een rijtje zetten, alhoewel er nog aanzienlijk veel meer stoffen zijn gevonden in de theestruik:

·        provitamine A

·        vitamine A

·        vitamine B1

·        vitamine B2

·        vitamine B12

·        vitamine C

·        vitamine E

·        vitamine D

·        caroteen

·        calcium

·        chroom

·        ijzer

·        kalium

·        kobalt

·        koper

·        mangaan

·        magnesium

·        molybdeen

·        natrium

·        nikkel

·        fosfor

·        tannine

·        theobromine

·        theofylline

·        selenium

·        strontium

·        zink

Verder treft men nog vele verschillende aminozuren (eiwitten) in groene thee aan en catechinen, waarover later meer. Zoals u in bovenstaande lijst kunt zien vindt men bijvoorbeeld ook selenium in groene thee. Al naar gelang de bodem waar de thee op groeide, zal het wat meer of minder zijn, maar uit onderzoek is gebleken dat de thee een rijke bron van selenium is. Sommige studies tonen aan dat het sterftecijfer wat betreft kanker, lager ligt bij mensen met een hogere seleniumspiegel in het bloed. Ook veel van de andere stoffen in deze thee zijn van belang voor het algemeen welbevinden. Door de afzonderlijke stoffen op internet te zoeken, bijvoorbeeld als zoekwoord: selenium en kanker kan men hierover weer een heleboel te weten komen. Mensen met een gestoorde suikerstofwisseling hebben behoefte aan chroom, en mangaan is belangrijk voor de eiwitstofwisseling én de bloedsuikerspiegel. Ook zink is van belang voor een goed werkend immuunsysteem.

Het sterftecijfer door kanker is zeer laag bij mannen en vrouwen in Japan. In de regio van Shizuoka waar 87 % van de Japanse groene thee wordt verwerkt en waar men zo'n vijf à zes kopjes groene thee per dag drinkt, blijken de cijfers die de sterfte aangeven van maagkanker behoorlijk te zijn afgenomen door het dagelijks drinken van groene thee. Wetenschappelijke studies die zijn gedaan door het Nationale Kanker Instituut in Tokyo tonen aan dat de primaire inhoudstoffen van groene thee, tannine en catechine die in voldoende mate aanwezig zijn, het percentage van mensen met kanker kan verminderen. Een studie van professor Shu-Jun Cheng van het Kanker Instituut in Beijing heeft met cijfers aangetoond dat een extract van groene thee het aantal gevallen van kanker met 50 % heeft doen verminderen.

Nu even iets in het kort over catechinen. Catechinen hebben zeer sterke antioxidatieve eigenschappen ten opzichte van de zogenaamde vrije radicalen.

-Antioxidanten beschermen het menselijk lichaam tegen de schadelijke invloed van vrije radicalen, ze gaan de beschadiging van celwanden tegen.
-Vrije radicalen zijn elektrisch geladen deeltjes. Ze kunnen celwanden en celkernen beschadigen en versnellen zo de veroudering. Vrije radicalen zijn ook agressieve stoffen, die bijvoorbeeld kunnen ontstaan door stress.

[Bron: paradijsvogel.nl]


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Groene Thee heeft aanzienlijk minder caffeïne dan koffie. Daar waar koffie een directe stoot van hyperactiviteit, trillende handen, incontinentie en irritatie veroorzaakt, wordt de caffeïne in de Groene Thee langzamer opgenomen, wat een gelijkmatige, voedende energie geeft in plaats van de beruchte 'pieken en dalen' van de koffie. Veel van het onderzoek naar de gezondheidsvoordelen is gedaan op basis van het gemiddelde gebruik in Aziatische landen, ca. 3 koppen per dag, hetgeen overeenkomt met 240 tot 320mg polyphenolen per dag. 5 gram Groene theebladeren in 250ml water is een standaard recept. Tabletten en capsules met Groene thee bevatten gestandaardiseerd extract, met name EGCG.

Drink tips:
- Laat thee 3 tot 5 min trekken (dan worden alle werkzame stoffen opgenomen)
- Drink je thee zo vers mogelijk, thee uit automaten of uit flesjes bevat minder flavonoïde dan verse.
- Drink ongeveer drie keer per dag een bak thee
- Thee kan de opname van ijzer uit fruit en groenten verhinderen. Het toevoegen van citroen of melk of het drinken van thee tussen maaltijden in kan dit effect tegengaan.

Onderzoekers van de universiteit van Toledo in Ohio in Amerika ontdekten dat groene thee een stof bevat die de werking van een belangrijk enzym van celwoekeringen blokkeert. Onderzoek door de Japanse overheid heeft uitgewezen dat er veel minder sterfte voorkomt in gebieden, steden en dorpen waar veel groene thee wordt gedronken.

Groene thee is rijk aan looizuur en vitamine C en bevat 10 keer meer epigallocatechine gallate, een sterk antioxidant, dan zwarte thee en 2,5 keer meer dan Oolong thee.

Zuid-Koreaanse onderzoekers deden een interessante ontdekking in verband met het drinken van thee bij rokers. Nicotine bevordert de plaquevorming en induceert arteriosclerose als gevolg van een verhoogde oxidatieve stress. Dit zijn negatieve aspecten die gedeeltelijk onder controle kunnen gehouden worden door het drinken van groene thee. In de bedoelde studie dronken 20 rokers 600 ml (vier kopjes) groene thee per dag en dit gedurende zes maanden. Uit de vergelijking van de bloedwaarden voor en na het experiment bleek dat het geoxideerd LDL significant was gedaald. Dit gold ook voor het oplosbaar P-selectine, een endotheliaal eiwit dat een belangrijke rol speelt bij het ontstaan van een ontsteking. Hiermee kunnen wellicht enkele cardiovasculaire beschadigingen als gevolg van het roken beperkt worden, al blijft uiteraard de beste remedie te stoppen met roken.
Bron:Lee W et al, Clin Biochem 2005 ;38(1) :84-7

vitamine C supplement


Groene thee laat vetcellen krimpen

Poeder van gedroogde groene thee remt de groei van de vetlagen. Dat ontdekten Japanse onderzoekers. Volgens hun proeven komt de vetverbrandende werking van het preparaat op het conto van de bijna weer vergeten anti-oxidantwerking van groene thee.

De Japanse onderzoeksgroep bestudeert de werking van groene thee al enkele jaren. In de jaren negentig ontdekte de groep dat groene theepoeder de opslag van vetzuren in vetcellen afremt. In reageerbuizen, tenminste. Maar werkt thee ook in organismen? Om daar achter te komen gaven onderzoekers de extracten tien dagen lang aan mannelijke ratten. Elke rat kreeg dagelijks 130 milligram extract, opgelost in water, toegediend via een slangetje in de mond dat doorliep tot in de maag.

De dieren kregen een dieet dat voor vijftig procent uit suiker bestond, en voor 15 procent uit boter. Zo hoopten de onderzoekers de dieren vet te mesten. Dat lukte prima. De ratten werden snel zwaarder. Maar zoals je in de onderstaande figuur kunt zien remde het extract de gewichtstoename af. PGT staat trouwens voor powdered green tea.

De verminderde groei betekende ook minder vetmassa, bleek toen de Japanners de epidymale, perirenale en mesenterische vetmassa's uit de dieren haalden en wogen. Ook de lever was minder zwaar.

Uit reageerbuisproeven wisten de Japanners al dat groene thee-extract de hoeveelheid triglyceriden in vetcellen vermindert. De resultaten hieronder zijn verkregen door vetcellen bloot te stellen aan een concentratie van 0.1 milligram per milliliter. Dat is hoog.

In de vetcellen was de aanmaak van het enzym SOD - voluit: superoxide dismutase - verhoogd, ontdekten de onderzoekers. SOD is een anti-oxidant die agressieve verbindingen uitschakelt. Als vetcellen insuline waarnemen gebruiken ze zulke agressieve stoffen om het insulinesignaal aan de rest van de cel door te geven, waardoor de cel vetten gaat opslaan. Groene thee blokkeert dat proces, vermoeden de Japanners.

Eerder ontdekten de Japanners al dat vitamine C dat het afslankeffect van groen thee versterkt. In reageerbuizen legden vetcellen, in een omgeving met groene thee-extract, minder triglyceriden vast naarmate de onderzoekers er meer vitamine C aan hadden toegevoegd. (VC-L staat voor een concentratie van 0.18 microgram vitamine per milliliter, VC-H voor 0.35 microgram per milliliter.)

Bronnen

1. Hasegawa N, Yamda N, Mori M. Powdered green tea has antilipogenic effect on Zucker rats fed a high-fat diet. Phytother Res. 2003 May; 17(5): 477-80. [PubMed]
2. Mori M, Hasegawa N. Superoxide dismutase activity enhanced by green tea inhibits lipid accumulation in 3T3-L1 cells. Phytother Res. 2003 May; 17(5): 566-7. [PubMed]
3. Hasegawa N, Niimi N, Odani F. Vitamin C is one of the lipolytic substances in green tea. Phytother Res. 2002 Mar; 16 Suppl 1: S91-2. [PubMed]
4. Ergogenics.org

 


Groene thee tegen huidkanker

Huidkanker blijft steeds toenemen. De schadelijke invloed van UV licht staat vast. Hoewel de non-melanoom huidkankers meestal zeer goed te behandelen zijn als ze tijdig worden ontdekt , zorgen ze toch voor heel wat ongemak. Lelijke littekens, werkverlet, angst en frequente recidieven als ze laat worden opgespoord. Ook deze non-melanoomkankers hebben meestal een dodelijk verloop als men ze helemaal niet behandelt.

Deze huidtumoren kunnen goed voorkomen worden door een correct UV-gedrag maar er is ook de mogelijkheid van chemopreventie. Onderzoekers uit de Cleveland University (Ohio-USA) vonden dat het innemen en/of toedienen van sterke antioxidantia het ontstaan van huidkanker kan afremmen. Een van de sterkste antioxidantia in de natuur zijn de polyfenolen die we terugvinden in groene thee. Het dagelijks drinken van of smeren van cosmetica op basis van groene thee kunnen het ontstaan van huidtumoren afremmen. Ze vervangen uiteraard de zonbescherming niet, maar zijn complementair en aan te raden.

Bron: Gezondheid.be


Afvallen met groene thee

Een onderzoek van het Duitse Instituut voor Voedingsonderzoek in Potsdam heeft uitgewezen dat groene thee kan helpen bij het afvallen.

EGCG
De verhalen deden al de ronde: groene thee helpt het metabolisme versnellen en zou daarom goed werken in de strijd tegen overtollige kilo’s. Onderzoekers hebben nu vast kunnen stellen dat een bepaalde stof die in het drankje voorkomt de toename van lichaamsvet bij muizen vermindert. Het bestanddeel zorgt niet dat je minder trek krijgt, maar remt de opname van voedsel in de darmen en bevordert de verbranding van vet. De test met muizen hield in dat ze een vetrijk dieet kregen aangevuld met groene thee. Na 29 dagen waren ze minder zwaar dan hun soortgenoten die het zonder de thee moesten doen. Ook het vetpercentage was drastisch afgenomen. De wetenschappers gebruikten voor de test een extract van de thee, dat voor 94 procent bestond uit de werkzame stof EGCG. Het is nog maar de vraag of EGCG kan worden gebruikt als afslankmiddel.

Gezond
Bij eerdere onderzoeken is al gebleken dat groene thee grote hoeveelheden polyphenolen bevat die het cholesterolgehalte verlagen en het verbranden van vetten verbeteren. EGCG behoort tot deze stoffen. Tevens bezit de warme drank kankerremmende en antibacteriële eigenschappen. Daarbij zou thee een kalmerende werking hebben op de zenuwen. De drank zit boordevol antioxidanten, die de weerstand versterken, en vitamines en mineralen, zoals calcium, magnesium, fluoride en ijzer.Met al deze goede eigenschappen ligt het voor de hand dat groene thee de gevolgen van het ouder worden vertraagt.

Momenteel staat groene thee vanwege de preventieve werking tegen kanker en hartziekten, enorm in de belangstelling. Men doet daar op dit moment allerlei onderzoeken naar. Toch is ook matigheid geboden. In groene thee zit, overigens minder dan in koffie, namelijk ook cafeïne. En wie te veel cafeïne binnenkrijgt, kan last krijgen van rusteloosheid, beven, duizeligheid, suizende oren en hartkloppingen.

Bronnen: DlfE, ANP, Achmea Health


Groene thee - preventie middel tegen kanker

Hirota Fujiki, Saitama Cancer Centre Research Institute, Japan.

Deze onderzoeker rapporteerde over de resultaten van een aantal dierproeven. Hieruit bleek dat groene thee een remmend effect heeft op de groei van kankercellen. Het betreft hier een breed werkingsgebied, onder andere het maagdarmkanaal, de lever, longen, pancreas, nieren en hersenen. Ook met betrekking tot borst en baarmoeder is er sprake van een preventieve werking.

Bij reeds aanwezige kanker is ten gevolge van groene thee een remming van de groei en metastasering waargenomen. Wat de werkingsmechanismen betreft, liet groene thee onder andere een afname zien van urokinase, telomerase en lipide peroxidase. Hirota Fujiki: "Op grond van onderzoeksresultaten adviseer ik om dagelijks 10 kopjes groene thee te drinken". Op grond van deze en andere onderzoekingen adviseerde hij om dagelijks tien kopjes groene thee te drinken. Indien dit op praktische bezwaren stuit, kan men deze thee in de vorm van tabletten of capsules innemen.


Groene thee supplementen

Groene thee, hoe lekker ook, heeft meer effect op onze gezondheid wanneer we het capsules innemen dan als drankje. Onderzoek aan de Universiteit van Californië wijst namelijk uit dat polyfenolen (anti-oxidanten) uit groene thee beter door ons lichaam worden opgenomen wanneer ze als extract (of capsulevorm) worden ingenomen dan wanneer de groene thee als drank wordt bereid. Dit onderzoek onderbouwt de sterk toenemende activiteiten rondom en belangstelling voor voedingssuppelmenten met groene thee. Groene thee, een traditionele drank in Azië, is onderwerp van verschillende onderzoeken omdat de sterke anti-oxidanten in de thee in verband wordeb gebracht met bescherming tegen kanker, bacteriën eb het risico van hart-en vaatziekten.

Bron: Marketing Results, maart 2005


AOV Groene thee extract
Groene thee-extract 250 mg bevat een hoge concentratie polyfenolen, waarvan bekend is dat ze een bijdrage kunnen leveren aan de goede conditie van de bloedvaten en de lever en dat ze krachtige eigenschappen bezitten ter bescherming tegen vrije radicalen. Het polyfenolencomplex in groene thee-extract bevat voornamelijk flavonoïden. Andere in groene thee aanwezige substanties zijn koffiezuur, galzuur, syringinezuur en een relatief kleine hoeveelheid cafeïne. Groene thee is bovendien een goede bron van vitamine K. In diverse studies is een verband geconstateerd tussen een hoge consumptie van groene thee en het behoud van een goede celdeling en van gezonde cellen en weefsels. Naast het feit dat groene thee een zeer krachtige vrije radicalen-vanger is en daardoor gezonde cellen en weefsels beschermt, heeft deze stof een sterk remmend effect op de vorming van gevaarlijke nitroso-verbindingen uit nitraat en nitriet. Ook bij zware rokers die veel groene thee dronken werd een gunstige effect op het terugdringen van de vrije radicaal-belasting waargenomen. De hoeveelheid lipide peroxidatie nam af tot het niveau van niet-rokers. Groene thee blijkt tevens een gunstig effect te hebben op het hart en de bloedvaten, onder meer doordat het helpt bij de verlaging van het cholesterolgehalte. Zo werd in een Japans onderzoek vastgesteld dat het drinken van veel groene thee gepaard ging met beduidend lagere gehaltes aan triglyceriden en totaal-cholesterol in het bloed. Bij een hoge consumptie van groene thee waren ook het schadelijke VLDL- en LDL-cholesterol verlaagd, terwijl het gunstige HDL-cholesterol juist was verhoogd. In dit verband is tevens belangrijk dat groene thee-extract een gunstige invloed heeft op de bloedsomloop en de doorbloeding bevordert. Een hoge consumptie van groene thee helpt ook diverse aspecten van de leverstofwisseling te optimaliseren. Daarbij moet er echter wel rekening mee worden gehouden dat men door het drinken van grote hoeveelheden groene thee ook veel looizuur naar binnen krijgt, waardoor de opname van essentiële mineralen uit het spijsverteringskanaal kan worden belemmerd en op den duur zelfs nierbeschadigingen kunnen optreden. Daarom is het belangrijk dat AOV's Groene thee-extract 250 mg géén looizuur bevat. Meer info hier


Groene thee - goed voor je geheugen

Wie vergeetachtig van aard is, zou misschien wat meer thee kunnen drinken. Uit Brits onderzoek blijkt namelijk dat thee het geheugen flink stimuleert. Ook Alzheimerpatiënten zijn er mogelijk bij gebaat. De Britten staan mede bekend om hun gewoonte om veel thee te drinken. Volgens Britse onderzoekers van de Universiteit van Newcastle is dat niet alleen gezellig, maar ook goed voor de geheugencellen. Groene en zwarte thee remt de ontwikkeling van de enzymen in de hersenen die geheugenverlies veroorzaken, zo ontdekten de onderzoekers. Uit diverse laboratorium-tests is naar voren gekomen dat door het drinken van groene of zwarte thee de productie van het acetylcholinesterase-enzym (AChE) wordt afgeremd. Dit enzym breekt de stof acetylcholine, die een rol speelt in het geheugen, af. De onderzoekers hopen dat de resultaten uit hun studie zullen leiden tot de ontwikkeling van een nieuwe behandeling voor patiënten met Alzheimer. Deze aandoening is niet te genezen, maar de thee zou een nieuwe manier kunnen zijn om de ziekte af te remmen. De werking van groene en zwarte thee is vergelijkbaar met die van speciale geneesmiddelen die momenteel tegen Alzheimer worden ingezet. Een tekort aan acetylcholine in de hersenen wordt in verband gebracht met Alzheimer. Ook speelt hierbij mee dat de beide theesoorten eveneens de werking van het enzym butyrylcholinesterase, dat is aangetroffen in de hersenen van Alzheimer-patiënten, zouden verhinderen. Overigens zijn er wel belangrijke verschillen tussen het drinken van groene en zwarte thee. Groene thee blijft volgens de wetenschappers namelijk een week werkzaam, zwarte thee een dag. Groene thee gaat bovendien een stap verder, doordat het de productie van beta-secretase, een stof die ook met Alzheimer in verband wordt gebracht, sterk vermindert.

Bronnen: BBC, University of Newcastle, Phytotherapy Research


Groene thee soorten

Groene thee  is ‘echte’ thee (dat wil zeggen, gemaakt van de bladeren van de Camellia sinensis) die minimale fermentering heeft ondergaan tijdens de productie. Groene thee is popular in China en Japan, en is recentelijk populairder in het Westen geworden, waar traditioneel zwarte thee (een ‘echte’ thee gemaakt van zwaarder gefermenteerde bladeren dan witte, groene, en oolong variëteiten) wordt gedronken.

Chinese groene thee
Soorten chinese thee (luchá) zijn:

Longjing ( lóngjing, "dragon well"; ook wel lung ching) is een beroemde thee uit Longjing, bij Hangzhou (Zhejiang). Longjing wordt verder onderverdeeld in 7 klassen: Superior (qiqiang), Special (queshe) en dan van 1 naar beneden tot 5.
De thee kenmerkt zich door lange vlakgedrukte helgroene bladeren.
Longjing heeft een helder geel stralende doorkijk met een kruidig aromatische smaak. Groene thee word van dezelfde plant gewonnen als de zwarte thee. De verschillende bewerking maakt onderscheid tussen groene Oolong of zwarte thee.

Mao feng ("Mao Peak") is een beroemde thee uit Huangshan.

Gunpowder is een groene thee uit China's Anhui Provincie. Deze thee ontleent zijn naam van de grijs-groen balletjes van operold blad. In het Chinees wordt het  (zhuchá, "pearl thee" / "bead thee," genoemd, niet te verwarren met Boba thee). Deze thee wordt geëxporteerd naar de Maghreb en gebruikt bij de bereiding van de traditionele Noord-Afrikaanse muntthee.

Zhenmei (zhenméi chá, "precious eyebrow thee", ook chun mee), het gewoonst type in China, wordt zo genoemd naar de vorm van de theebladeren.

Jasmijn thee
Hyson is een vroeggeoogste thee waarvan de balderen in een lange, dunne manier worden gerold.

Japanse groene thee
Groene thee (ryokucha) is zo alomtegenwoordig in Japan dat het gewoonlijk "thee" wordt genoemd (ocha) of zelfs "Japanese thee" (nihoncha). Types van deze thee worden gewoonlijk geklasseerd afhankelijk van de kwaliteit en de gebruikte delen van de plant.

Gyokuro ("jewel dew") Gyokuro thee is in het algemeen zoet en delicaat in smaak. Geselecteerd uit een klasse groene thee die tencha (??) genoemd wordt, wordt Gyokuro beschouwd als de hoogste klasse thee die in Japan gemaakt wordt. Gyokuro's naam verwijst naar de bleke groene kleur van thet aftreksel.
Matcha ("rubbed tea") wordt voornamelijk in de theeceremonie gebruikt. Matcha komt van gyokurobladeren die gestoomd en gedroogd zijn.
Sencha ("broiled tea")
Shincha ("new tea")
Bancha ("number tea")
Genmaicha ("brown rice tea")
Hojicha ("roasted tea")
Kukicha ("stem tea")
Kabusecha

[Bron: Wikipedia]


Groene thee leveranciers

Green balance - Yogitea

Green Balance heeft zijn naam te danken aan de gebalanceerde hoeveelheid Groene Thee met Kombucha, Chinese kruiden en andere unieke ingrediënten die dienen als catalysator, het verbeteren van de circulatie en stofwisseling door het hele lichaam.

Green energy - Yogitea

Al eeuwen lang schrijven de Zuid-Amerikaanse Indianen aan Guarana energie gevende krachten toe. De Brazilianen zijn zo overtuigd van haar kracht dat ze samen gemiddeld zo’n twee miljoen koppen Guarana thee per dag drinken.

Green guardian - Yogitea

Deze melange heeft als extra vlierbes toegevoegd aan de Groene Thee en Kombucha formule. Vlierbes werd van oudsher gebruikt om het spijsverterings-systeem te helpen en om het immuun-systeem optimaal te houden, speciaal gedurende de seisoenswisselingen.

Green jasmine - Yogitea

De weldadige geur van Jasmijn bloemen wordt als sinds de vijfde eeuw gemengd
met Groene Thee. Ons unieke recept accentueert de voordelen van Groene
Thee en de delicate geur van Jasmijn met de verwarmende en stimulerende kwaliteiten van gember.

Morrocan Mint Green Tea - Dilmah
Een milde, stimulerende en aromatische combinatie. Een pure groene Ceylon-thee "Young Hyson" met als toevoeging de blaadjes van de pepermuntplant. Een levendige natuurlijke combinatie van de fijnste groene thee, met het zoetige van pepermunt. De olijfgroene, sterk gedraaide blaadjes, ontvouwen zich na het opschenken volledig en geven de thee van gemiddelde sterkte een amberkleur. De delicate smaak van de pepermunt overheerst hierbij niet, maar geeft de thee een bijzonder mooie frisse smaak. Een thee voor na het eten, als neutraliserende smaak in de mond. De thee is een typische Marokkaanse drank, die al honderden jaren als welkomstdrank wordt geserveerd.

Green Tea with Jasmine Flowers - Dilmah
Mooi groene thee, met een gelige theedrank, natuurlijk gearomatiseerd met Jasmijnbloesems. Al in de tijd van de Zuidelijke Song-Dynastie (960 - 1279) geldt deze thee als lievelingsdrank van de Chinezen. De zoet ruikende jasmijnbloesems worden met de groene thee gemengd, waardoor er een theedrank ontstaat met een fluweelzacht aroma. De bloem van de bladverliezende klimplant Jasmijn, bestrijdt nervositeit en brengt de actieve geest tot rust.

Sencha Green Tea - Dilmah
De Sencha is een groene thee, die extra wordt behandeld met stoom. Het is de lievelingsthee van de Japanner. Zij kunnen de zachte aroma, de milde licht zoete smaak, zeer waarderen. Van deze thee kan je de hele dag genieten. Prima geschikt voor na het eten; hij verfrist uw gehele mondholte.

Ming Mei - Famous Plum - Green Tea - Dilmah
De bekendste "Eyebrow"-thee, zo genoemd vanwege zijn wenkbrauw vorm. De Ming Mei, die in de Shangmeizhou-regio verbouwd wordt, is ook bekend om zijn pruimenthee. Het verkrijgen van een Ming Mei thee, vergt bijzondere vaardigheden. De bladeren - jadegroene van kleur - geven na het begieten een doorzichtige, geelachtige drank met die karakteristieke pruimachtige ondertoon. Tijdens het opgieten, gaat het blad van de thee open, om de met de hand geplukte knoppen te laten zien. Een heldere, lichte en verfrissende thee van buitengewone kwaliteit.

Ceylon Whole Leaf Green Tea - Dilmah
Mooie groene Ceylon-thee, verbouwd op 420m hoogte, in het Gampola gebied. Zijn elegante, lange, gerolde bladeren, gaan na het opgieten geheel open. en geven een aangename milde theedrank met een diep gele kleur en een licht zoete bijsmaak. Aangenaam prikkelt deze thee het gehemelte, dat maakt hem ook ideaal geschikt voor na het eten. Een thee met een ronde kruidensmaak, met een kleine fruitachtige tint.


Groene thee truc

De actieve stoffen in groene thee zijn 'catechinen'.

De verschillende vormen worden afgekort als EGC, EGCG, ECG en EC. Ze dienen
als antioxidanten en helpen je lichaam reinigen.

EGCG verhoogt ook het metabolisme, oftewel je stofwisseling, oftewel je dagelijks
calorieverbruik. Drink je veel groene thee, dan kan EGCG je dus ook helpen om
slank te blijven of om af te vallen.

Helaas breken deze catechinen snel af wanneer ze vloeibaar zijn. Binnen 12 minuten
ben je al 86% EGCG kwijt in water. Na 6 uur is 't allerlaatste weg. Zo snel breekt
dit goedje af.

Dit wil zeggen dat je dus niets hebt aan groene thee uit een fles of tetrapak die weken
of maanden geleden al gemengd is.

Er is wel een trucje om de actieve stoffen in groene thee in ieder geval voor
een uurtje goed te houden. Dat doe je door het een beetje zuur te
maken. In een zure omgeving is EGCG wat stabieler en gek genoeg wordt het
daardoor beter opgenomen in de dunne darm.

Dat kan heel makkelijk met een goede dosis citroensap, eventueel met wat
rietsuiker of honing erbij. Met dit kleine trucje houd je 95% van de actieve stoffen uit
groene thee langer actief wanneer vloeibaar. Voor een uurtje dan, niet meer.

Koop je een ijsthee gemaakt van groene thee-extract, zorg dan dat het een droog
poeder mengproduct is en dat er een beetje citroensap in de formule zit.

Bron: vitamins.nl


Groene thee in bier

iKi Refreshment Beer is een bovengistend bier. De smaak is fris en de bitterheid is lager dan die van de gangbare bieren. Hierdoor is iKi goed doordrinkbaar en dorstlessend. De basis van iKi wordt gevormd door water, gerstemout, hop en gist. Maar iKi bevat bijzondere ingrediënten: sencha en de Japanse vruchten nashi en yuzu. Sencha is een Japanse groene theesoort. Omdat de theebladeren meteen na de pluk gestoomd worden, wordt het fermentatieproces onderdrukt en blijven de gezonde elementen behouden.

Yuzu is een citrusvrucht die veel in de Japanse keuken wordt gebruikt. De vrucht heeft een oneffen oppervlak. De schil is zoet en licht bitter. De smaak van het sap komt overeen met het sap van de grapefruit/mandarijn/citroen. Yuzu geeft iKi een verfrissende en lichtzure smaak. De Japanse bruingele nashi-vrucht heeft het uiterlijk van een appel en de textuur van een peer. Het vruchtvlees is wit en sappig en de vruchtsuikers spelen belangrijke rol bij de nagisting van iKi.

Omdat iKi ongefilterd is en nagist op fles is het licht troebel. Bij langere rijping, meer dan vier weken, neemt de troebelheid af. Het stamwortgehalte van 11.5 graden plato is vergelijkbaar met reguliere bieren. Het alcohol percentage is 4.1%. Dat is één procentpunt lager dan andere bieren. Door de brouwmethode en de toevoeging van groene thee behoudt het bier zijn volle smaak.

Internationaal

Green Tea as Cancer Preventive
Continuing research on the beneficial properties of green tea to human health has produced several new findings. Most notable is a study by Japanese scientists of the Saitama Cancer Research Institute relating the delay of cancer onset with the consumption of green tea. The study shows that early stage breast cancer spreads less rapidly in women with a history of drinking five or more cups of green tea a day. As a result, there is a lower recurrence rate and a longer disease-free period. With the evidence that green tea and EGCG, a catechin found only in green tea, are a natural and readily available inhibitor of TNF-, a gene expression which promotes the growth in cancer cells and in their surrounding tissue, it is possible for researchers to extend this idea to other various human diseases. Since EGCG has also been proven to kill cultured cancer cells without causing harm to surrounding healthy cells, green tea could be beneficial not only for cancer prevention but also in the therapy and prevention of other diseases.

Drinking Green Tea Reduces the Effects of Cigarete Smoking
In two different studies, one by scientists at the Academy of Preventive Medicine in Beijing, China and the other by James Klaunig at the Indiana University School of Medicine in Indianapolis, the effects of green tea on oxidative stress, brought on by the toxins of cigarette smoke, were investigated. Oxidative stress, an imbalance in the pro-oxidant/antioxidant status of a cell, appears to cause or participate in the development of certain diseases-notably cancer. Researches found that when cigarette users drank an equivalent of six cups of green tea a day, their bodies suffered 40% to 50% less oxidative damage. This potentially lowers their risk of cancer, emphysema, heart disease and other illnesses. Oxidative damage was reduced to that of levels found in nonsmokers prior to drinking green tea. However, it is important to note that those who drink green tea and continue to smoke are still raising their risk of experiencing oxidative damage. Nonsmokers who were studied exhibited significant decreases in oxidative damage as well.

Green Tea May Prevent Rheumatoid Arthritis
Medical researchers at Case Western Reserve University in Cleveland, published a study in April, 1999 reporting that drinking four or more cups of green tea a day may prevent rheumatoid arthritis and reduce the severity of it in those who are currently battling the disease. The study was conducted on mice with collagen induced arthritis, which is similar to that of rheumatoid arthritis in humans. The mice that received green tea were less likely to develop arthritis than the mice who received plain drinking water. However, the mice that received green tea and yet still developed arthritis had less severe forms of arthritis. It was concluded that the antioxidants present in green tea possess not only cancer-preventeing properties but also anti-inflammatory properties. Rheumatoid arthritis is an inflammatory disease that causes pain, swelling, stiffness, and loss of function in the joints. The antioxidants in green tea may prevent or reduce the severity of these symptoms.

Green Tea May Prevent Oral Cancer
At a symposium in Washington DC, 1998, a team of Chinese scientists, Ning Li from the Institute of Nutrition and Food Hygiene, Zheng Sun from the Chinese Academy of Preventive Medicine and Junshi Chen from the Beijing Dental Hospital, revealed that drinking green tea improves pre-cancerous conditions of oral leukoplakia in patients and suggests it may have certain preventive effects in oral cancer. The study involved 32 patients, 20 males and 12 females, 23-28 years of age with oral mucosa leukoplakia, a pre-cancerous lesion of oral cancer. During a six month period, patients drank three cups of green tea a day and applied a mixture of green tea and glycerin directly to the lesion. As a result, 38% of the patients experienced a reduction in the size of a single lesion or in the total size of multiple lesion by 30% or more. 59% saw no changes at all. At the same time, the frequency and rate of formation of cancerous cells decreased significantly.  

New Insight Into Green Tea's Action on Bladder Cancer
Green tea extract is able to target cancer cells while leaving healthy cells alone, researchers have found for the first time, adding further support to its potential as a cancer prevention agent. The UCLA team has also uncovered more about how Green tea extract counteracts the development of cancer. This could allow researchers to work out which people could benefit from the extract. About 500 metric tons of green tea extract were sold in Europe during 2003, mostly for use in beverages and cosmetics. But the extracts are set to be increasingly used in supplements as evidence of their benefits gain weight. Numerous epidemiological and animal studies have suggested that green tea extract provides strong anti-cancer effects in several human cancers, including bladder cancer. In 2003, U.S. researchers found that the active ingredient in green tea, epigallocatechin-3-gallate (EGCG), blocked the growth of bladder tumors in rats. Green tea extract has been shown to induce death in cancer cells, as well as inhibiting the development of an independent blood supply that cancers develop so they can grow and spread. In the new study on bladder cancer cell lines, scientists demonstrated that the plant extract interrupts a process that is crucial in allowing bladder cancer to become invasive and spread to other areas of the body. The findings, published in the 15 February issue of Clinical Cancer Research, “add a new dimension in understanding the mechanisms of green tea extract," said senior author JianYu Rao.
Bron: Nutraingredients

Green tea may fight leukaemia
The active component in green tea, epigallocatechin-3-gallate (EGCG), already shown to fight several types of cancer, also appears to kill cells of the most common form of leukaemia, reports a US team. The researchers found that EGCG interrupts the communication signals needed by cancer cells to survive, prompting them to die in eight of 10 patient samples tested in the laboratory. The cells came from patients with B-cell chronic lymphocytic leukaemia (CLL), most often diagnosed in patients in their mid-to-late 60s and currently without cure. While chemotherapy is administered in the most severe cases, doctors have tended to stall use of this treatment in early stage patients, some of whom may live with it for decades and not require treatment. Green tea could however offer a less harmful, but effective alternative for this category of patients. "We're continuing to look for therapeutic agents that are nontoxic to the patient but kill cancer cells, and this finding with EGCG is an excellent start,” said Neil Kay from the Mayo Clinic. “Understanding this mechanism and getting these positive early results gives us a lot to work with in terms of offering patients with this disease more effective, easily tolerated therapies earlier." Since the 1970s, epidemiological studies of cancer have shown that in parts of the world where green tea is consumed, the incidence of solid tumour cancers such as breast, lung and gastrointestinal cancers is lower. Mouse-model testing of green tea's cancer-prevention properties and lab tests on EGCG have confirmed that they protect against solid tumours and induce death in cancer cells from solid tumours.

Recent findings of green tea extract AR25 (Exolise) and its activity for the treatment of obesity
These results suggest the green tea extract AR25 to be a natural product for the treatment of obesity, which exerts its activity by several ways: inhibition of lipases and stimulation of thermogenesis.

Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans
Green tea has thermogenic properties and promotes fat oxidation beyond that explained by its caffeine content per se. The green tea extract may play a role in the control of body composition via sympathetic activation of thermogenesis, fat oxidation, or both.

Green tea shown to prevent prostate cancer
First clinical study shows 90 percent efficacy in men with pre-malignant lesions Anaheim, Calif. – After a year's oral administration of green tea catechins (GTCs), only one man in a group of 32 at high risk for prostate cancer developed the disease, compared to nine out of 30 in a control, according to a team of Italian researchers from the University of Parma and University of Modena and Reggio Emilia led by Saverio Bettuzzi, Ph.D. Their results were reported at the 96th Annual Meeting of the American Association for Cancer Research. "Numerous earlier studies, including ours, have demonstrated that green tea catechins, or pure EGCG (a major component of GTCs), inhibited cancer cell growth in laboratory models," Bettuzzi explained. "We wanted to conduct a clinical trial to find out whether catechins could prevent cancer in men. The answer clearly is yes." Earlier research demonstrated primarily that green tea catechins were safe for use in humans. Bettuzzi and his colleagues had found that EGCG targets prostate cancer cells specifically for death, without damaging the benign controls. They identified Clusterin, the most important gene involved in apoptosis, or programmed cell death in the prostate, as a possible mediator of catechins action. "EGCG induced death in cancer cells, not normal cells, inducing Clusterin expression" said Bettuzzi. The interest in green tea catechins and other polyphenols – antioxidants found in many plants that give some flowers, fruits and vegetables their coloring – derives from traditional Chinese medicine, and the observation of lower cancer rates among Asian populations. Bettuzzi observed that the Mediterranean diet is rich in vegetables, and lower rates of prostate cancer are found in that region, as well.
Bron: American Association for Cancer Research 

The power of green tea
Twenty years ago, if you had told Lester Mitscher that he would be best known as an expert on green tea and other natural medicines, he probably would have laughed in your face. "Those would have been fighting words," says Mitscher, KU distinguished professor of medicinal chemistry. Despite a prolific career that spans more than four decades and includes 14 U.S. patents, six books on drug chemistry and numerous awards, Mitscher is perhaps most widely recognized for his research on the benefits of green tea. In 1997, Mitscher found that green tea contained high levels of the disease-fighting antioxidant epigallocatechin gallate, or EGCg. His research concluded that the EGCg in green tea was up to 100 times more effective than vitamin C and up to 75 times more effective than vitamin E at protecting the body against free radicals - renegade oxygen-filled molecules that can cause damage to cells and DNA strands, making them more susceptible to diseases such as diabetes, some forms of cancer and arthritis, Alzheimer's disease and many others. Since Mitscher delivered those findings, the popularity of green tea has skyrocketed, and with it Mitscher has been in high demand as an expert on the benefits of drinking the age-old Chinese beverage - something this modest and dedicated scientist could never have imagined. His most recent book, The Green Tea Book: China's Fountain of Youth, already has exceeded his wildest expectations. Bron: University of Kansas

Epigallocatechin gallate attenuates diet-induced obesity in mice by decreasing energy absorption and increasing fat oxidation
Dietary EGCG attenuated diet-induced body fat accretion in mice. EGCG apparently promoted fat oxidation, but its fat-reducing effect could be entirely explained by its effect in reducing diet digestibility.

Green tea polyphenol epigallocatechin gallate inhibits adipogenesis and induces apoptosis in 3T3-L1 adipocytes
These results demonstrate that EGCG can act directly to inhibit differentiation of preadipocytes and to induce apoptosis of mature adipocytes and, thus, could be an important adjunct in the treatment of obesity.

Modulation of obesity by a green tea catechin
The effects of long-term daily oral consumption of 2–4 cups (500–1000 mL) of green tea or EGCG-containing green tea extracts may mimic some of the acute effects of EGCG. Studies have shown that oral consumption of green tea, EGCG, or EGCG-containing green tea extract can lower serum and LDL cholesterol, increase HDL cholesterol, and lower serum glucose (1, 3, 8). On the basis of the in vivo effects of EGCG on body weight loss, body fat, serum lipid nutrients, thermogenesis, and fat oxidation (1–4, 8) and of the in vitro effects of EGCG on fat cell functions (4, 7), long-term consumption of green tea may decrease the incidence of obesity and, perhaps, green tea components such as EGCG may be useful for treating obesity.

Effect of green tea supplementation on insulin sensitivity in Sprague-Dawley rats
Results demonstrated that green tea increases insulin sensitivity in Sprague-Dawley rats and that green tea polyphenol is one of the active components

Green tea boosts exercise endurance
A new study tested the effect of regularly taking green tea extract (GTE) and found that over 10 weeks, endurance exercise performance was boosted up to 24% with 0.5% GTE supplementation, and 8% with 0.2% by-weight addition to food. Reporting in the online edition of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology researchers at the Biological Sciences Laboratories of Kao Corp., Tochigi, Japan, said the 8-24% increase in swimming time-to-exhaustion was "accompanied by lower respiratory quotients and higher rates of fat oxidation." The results "indicate that GTE is beneficial for improving endurance capacity and support the hypothesis that the stimulation of fatty acid utilization is a promising strategy for improving endurance capacity," according to the study entitled, "Green tea extract improves endurance capacity and increases muscle lipid oxidation in mice." Research was conducted by Takatoshi Murase, Satoshi Haramizu, Akira Shimotoyodome, Azumi Nagasawa and Ichiro Tokimitsu, working at Kao Corp., a Japanese maker of healthcare products, including green tea beverages. Bron: Medical Study News

 

Links:

http://www.adagio.com/info/health_benefits.html


Ander nuttige links

Chlorella Alg
Deze alg uit Japan en Korea helpt u snel uw gezondheid drastische te verbeteren. De alg zorgt voor een flinke groei van uw darmflora waardoor u meer energie krijgt en de voeding beter verteerd wordt. Verder bevat de alg een zeer hoge dosis chlorophyl (bladgroen) die het lichaam helpt bij het afvoeren van metalen zoals kwik, cadnium, lood etc die veel schade aan de hersenen kunnen veroorzaken. Daarnaast bevat de alg een hoge kwaliteit plantaardig eiwit, aminozuren, mineralen en hoge dosis ijzer en betacaroteen (provitamine A)

Supervoeding.com
Een overzicht van de geneeskrachtige werking van groente en fruit en informatie over minder bekende produkten zoals witte thee, zeegroenten, kiemen, acerola, stevia etc

Wat de dokter u niet vertelt - fonteine.com
Een kritische kijk op onze gezondheidszorg en haar kortzichtigheid. Kritische artikelen over zuivel, brood, verhit eten maar ook veel nuttige tips voor mensen
die langer en gezonder willen leven. Uitleg over: wat is kefir ? wat is olieslurpen ?
hoe voorkom ik onstekingen in de darmen ? welke rol speelt voeding bij autisme en schizofrenie ? Is er meel zonder gluten ? Is zuivel gezond ? Welk gevaar
schuilt er in verzuring van het lichaam ? Hoe gezond is groene thee ?

 

Succes met je gezondheid !

Ron Fonteine

Verder wil ik Luc bedanken voor zijn hulp met deze site.

 

http://www.groenethee.com/



[1]

antikanker dieet en voeding  
 


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Anti-kanker dieet

Af en toe vind ik kleine juweeltjes op het net. Het onderstaande artikel is helaas in het Engels maar misschien dat iemand wil helpen dit artikel voor andere lezers te vertalen. Ik ben te druk met het zoeken naar nuttige info dus alle hulp is welkom.

In de korte versie (abstract) staat eigenlijk alles samengevat en wordt wederom de rol van lijnzaadolie genoemd (flaxseed), deze olie komt ook terug in het antikanker dieet van Anna Budwig uit de jaren vijftig (Budwig papje). Ook worden de broccoli kiemen (liggen nu ook hier in de supermarkt) en rol van selenium, b12, vitamine d, folium zuur, lycopeen (tomaten puree), vitamine C en chlorophyl (groene groentes, algen) genoemd.

Een echte aanrader!

Ron

Korte samenvatting Mike Donkers:

Naar schatting 30 tot 40 % van de bestaande kankers kunnen voorkomen worden door alleen al maatregelen te nemen op het gebied van dieet en levensstijl.

Voedingsarme stoffen zoals geconcentreerde suikers en verfijnde meelprodukten, die mede veroorzakers zijn van een slecht functionerende glucose stofwisseling (dat op zijn beurt weer leid tot diabetes) lage vezelinname, consumptie van rood vlees en een slechte balans van Omega 3 en 6 vetzuren dragen allen bij aan het bestaan van een overmatig risico op de ontwikkeling van kankers.

De inname van vlaszaad en met name het lijnzaad gedeelte evenals overvloedige hoeveelheden groente en fruit zullen het risico op het ontwikkelen van kanker verlagen.

Vooral Allium en kruisbloemige groenten zijn heilzaam waarbij broccoli relatief gezien het meeste Sulforophane bevat.

Beschermende elementen in een dieet ter preventie van kanker zijn onder andere selenium, foliumzuur, vitamine B-12, vitamine D, chlorofyl en anti-oxidanten zoals de carotenen (A-caroteen, B-caroteen, lycopene, luteine, cryptoxanthine).

Ascorbinezuur heeft weinig effect als het oraal ingenomen wordt maar zou intravenously (geinjecteerd?) wel behulpzaam kunnen zijn.
Aanvullende orale inname van digestieve enzymen en probiotics heeft ook nut als dieet onderdeel tegen de ontwikkeling van kanker.

Een dieet samengesteld volgens deze richtlijnen leid waarschijnlijk tot een afname van minimaal 60 tot 70% op het ontwikkelen van borst, darm en prostaatkankers en zelfs tot een 40 tot 50% afname op het ontwikkelen van longkanker, dit tezamen met gelijkwaardige afnames van kansen voor het ontwikkelen van kanker op andere plekken in het lichaam.

Een dergelijk dieet zou kankers kunnen voorkomen en zou het herstel na een kanker kunnen bevorderen.

Recensie achtergrond

Het veld van onderzoek over de rol van voeding in het kanker proces is heel breed. Naarmate het onderzoek vordert wordt ook steeds duidelijker dat voeding bij de ontwikkeling van kankers een grote rol speelt.

Door het Amerikaans Instituut voor Kankeronderzoek en het Wereld Kanker Onderzoeksfonds wordt geschat dat 30 a 40 % van alle kankers door toepasselijke dieten, fysieke beweging en het behoud van van normaal lichaamsgewicht voorkomen kunnen worden. Waarschijnlijk is dit percentage nog hoger bij enkele individuele kankers.

Tot op heden is het onderzoek naar kanker geïsoleerd van aard geweest.
Er is dan bijvoorbeeld één type voedsel of voedingstof bestudeerd op zijn invloed op de groei of afname van een tumor of een ander eindpunt van een kanker maar slechts in een bepaald deel van het lichaam.
Voor het bekijken van details van de ziekte mechanismen zijn dit zeer hulpzame studies, ze slagen er echter niet in om inzicht te verkrijgen in hoe een kanker nou door middel van dieetmaatregelen te voorkomen is.

Ze laten ook weinig los over wat men moet eten wanneer kanker geconstateerd is en wanneer men een dieet wil volgen wat gunstig is voor het herstel van de ziekte. Deze ¨nieuwe kijk op de situatie¨ zal zich richten op die onderdelen van het dieet waarvan aangetoond is dat ze een groei van het kanker risico veroorzaken.

Daarna zal de focus gelegd worden op de dieetmaatregelen die het kanker risico verkleinen. Ter afsluiting zullen er een aantal studies betreffende het gehele dieet aangehaald worden zodat er een beter beeld ontstaat hoe met behulp van deze afzonderlijke onderdelen tezamen het kanker risico verkleind kan gaan worden.

Overconsumptie van energie (calorieen)

Een van de hoofdrisico factoren voor de ontwikkeling van kanker is de consumptie van te veel voedsel. En wel vanwege (1) het bijkomende risico op het krijgen van ziektes door zwaarlijvigheid en (2) het feit dat het consumeren van weinig voedsel een beschermend effect heeft.

Zwaarlijvigheid heeft in Amerika epidemische vormen aangenomen.
64% van de volwassen bevolking heeft overgewicht of is zwaarlijvig (2) en één op de vijftig inwoners is momenteel ernstig zwaarlijvig (BMI >40kg/m2) (3) Mokdat et al (4) vond uit dat de combinatie van een slecht eetpatroon en te weinig beweging de op één na belangrijkste doodsoorzaak is (400.000 doden per jaar in de VS) en dat deze combinatie waarschijnlijk tabak gaat aflossen als doodsoorzaak nummer één.


Nutrition and cancer: A review of the evidence for an anti-cancer diet


Abstract

It has been estimated that 30–40 percent of all cancers can be prevented by lifestyle and dietary measures alone. Obesity, nutrient sparse foods such as concentrated sugars and refined flour products that contribute to impaired glucose metabolism (which leads to diabetes), low fiber intake, consumption of red meat, and imbalance of omega 3 and omega 6 fats all contribute to excess cancer risk. Intake of flax seed, especially its lignan fraction, and abundant portions of fruits and vegetables will lower cancer risk. Allium and cruciferous vegetables are especially beneficial, with broccoli sprouts being the densest source of sulforophane. Protective elements in a cancer prevention diet include selenium, folic acid, vitamin B-12, vitamin D, chlorophyll, and antioxidants such as the carotenoids (a-carotene, ß-carotene, lycopene, lutein, cryptoxanthin). Ascorbic acid has limited benefits orally, but could be very beneficial intravenously. Supplementary use of oral digestive enzymes and probiotics also has merit as anticancer dietary measures. When a diet is compiled according to the guidelines here it is likely that there would be at least a 60–70 percent decrease in breast, colorectal, and prostate cancers, and even a 40–50 percent decrease in lung cancer, along with similar reductions in cancers at other sites. Such a diet would be conducive to preventing cancer and would favor recovery from cancer as well.

Review

Background

The field of investigation of the role of nutrition in the cancer process is very broad. It is becoming clearer as research continues that nutrition plays a major role in cancer. It has been estimated by the American Institute for Cancer Research and the World Cancer Research Fund that 30–40 percent of all cancers can be prevented by appropriate diets, physical activity, and maintenance of appropriate body weight [1]. It is likely to be higher than this for some individual cancers.

Most of the research on nutrition and cancer has been reductionist; that is, a particular food or a nutrient has been studied in relation to its impact on tumor formation/regression or some other end point of cancer at a particular site in the body. These studies are very helpful in seeing the details of the mechanisms of disease. However, they do not help give an overall picture of how to prevent cancer on a dietary level. Even less, they tell little of how to eat when a person already has a cancer and would like to eat a diet that is favorable to their recovery.

This review will focus on those dietary factors which has been shown to be contribute to increased risk of cancer and then on those additional protective dietary factors which reduce cancer risk. Finally, some whole-diet studies will be mentioned which give a more complete picture of how these individual factors work together to reduce cancer risk.

Over Consumption of Energy (Calories)

Eating too much food is one of the main risk factors for cancer. This can be shown two ways: (1) by the additional risks of malignancies caused by obesity, and (2) by the protective effect of eating less food.

Obesity has reached epidemic proportions in the United States. Sixty-four percent of the adult population is overweight or obese [2]. About 1 in 50 are now severely obese (BMI > 40 kg/m2) [3]. Mokdad et al [4] found that poor diet and physical inactivity was the second leading cause of death (400,000 per year in the USA), and would likely overtake tobacco as the leading cause of death.

It was estimated in a recent study, from a prospective cancer prevention cohort, that overweight and obesity accounted for 14 percent of all cancer deaths in men and 20 percent of those in women [5]. Significant positive associations were found between obesity and higher death rates for the following cancers: esophagus, colon and rectum, liver, gallbladder, pancreas, kidney, stomach (in men), prostate, breast, uterus, cervix, and ovary [5]. The authors estimated that over 90,000 cancer deaths per year could be avoided if the adult population all maintained a normal weight (BMI < 25.0) [5]. Clearly, obesity is a major risk factor for cancer.

On the other side, careful menu planning brings about an approach entitled CRON-Calorie Restriction with Optimal Nutrition. The basic idea is to eat a reduced amount of food (about 70–80 percent of the amount required to maintain "normal" body weight) while still consuming all of the necessary amounts of vitamins, minerals, and other necessary nutrients. The only restriction is the total amount of energy (calories) that is consumed. While being difficult to practice, this approach has a lot of scientific merit for being able to extend average life spans of many species of animals including rats, mice, fish, and possibly primates (currently being tested). Along with this life span extension is a reduction in chronic diseases that are common to mankind, reviewed in Hursting et al [6]. A recent meta-analysis of 14 experimental studies found that energy restriction resulted in a 55% reduction in spontaneous tumors in laboratory mice [7]. Calorie restriction inhibited induced mammary tumors in mice [8] and suppressed implanted tumor growth and prolonged survival in energy restricted mice [9]. Among Swedish women who had been hospitalized for anorexia nervosa (definitely lower caloric intake, but not adequate nutrition) prior to age 40, there was a 23% lower incidence of breast cancer for nulliparous women and a 76% lower incidence for parous women [10]. So, too many calories is definitely counter-productive, and slightly less than normal is very advantageous.

Glucose Metabolism

Refined sugar is a high energy, low nutrient food – junk food. "Unrefined" sugar (honey, evaporated cane juice, etc) is also very concentrated and is likely to contribute to the same problems as refined sugar. Refined wheat flour products are lacking the wheat germ and bran, so they have 78 percent less fiber, an average of 74 percent less of the B vitamins and vitamin E, and 69 percent less of the minerals (USDA Food database, data not shown). Concentrated sugars and refined flour products make up a large portion of the carbohydrate intake in the average American diet. One way to measure the impact of these foods on the body is through the glycemic index.

The glycemic index is an indication of the blood sugar response of the body to a standardized amount of carbohydrate in a food. The glycemic load takes into account the amount of food eaten. An international table of the glycemic index and glycemic load of a wide variety of foods has been published [11].

Case-control studies and prospective population studies have tested the hypothesis that there is an association between a diet with a high glycemic load and cancer. The case control studies have found consistent increased risk of a high glycemic load with gastric [12], upper aero digestive tract [13], endometrial [14], ovarian [15], colon or colorectal cancers [16,17]. The prospective studies' results have been mixed. Some studies showed increased risk of cancer in the whole cohort with high glycemic load [18-20]; some studies found only increased risk among subgroups such as sedentary, overweight subjects [21-24]; other studies concluded that there was no increased risk for any of their cohort [25-28]. Even though there were no associations between glycemic load and colorectal, breast, or pancreatic cancer in the Nurses' Health Study there was still a strong link between diabetes and colorectal cancer [29].

Perhaps the dietary glycemic load is not consistently related to glucose disposal and insulin metabolism due to individual's different responses to the same glycemic load. Glycated hemoglobin (HbA1c) is a time-integrated measurement of glucose control, and indirectly, of insulin levels. Increased risk in colorectal cancer was seen in the EPIC-Norfolk study with increasing HbA1c; subjects with known diabetes had a three-fold increased risk of colorectal cancer [30]. In a study of a cohort in Washington county, Maryland, increased risk of colorectal cancer was seen in subjects with elevated HbA1c, BMI > 30 kg/m2, or who used medications to control diabetes [31]. However, glycated hemoglobin was not found to be associated with increased risk of colorectal cancer in a small nested case-control study within the Nurses' Health Study [32]. Elevated fasting glucose, fasting insulin, 2 hour levels of glucose and insulin after an oral glucose challenge, and larger waist circumference were associated with a higher risk of colorectal cancer [33]. In multiple studies diabetes has been linked with increased risk of colorectal cancer [34-37], endometrial cancer [38], and pancreatic cancer [35,39]. It is clear that severe dysregulation of glucose metabolism is a risk factor for cancer. Foods which contribute to hyperinsulinemia, such as refined sugar, foods containing refined sugar, and refined flour products should be avoided and eliminated from a cancer protective diet.

Low Fiber

Unrefined plant foods typically have an abundance of fiber. Dairy products, eggs, and meat all have this in common – they contain no fiber. Refined grain products also have most of the dietary fiber removed from them. So, a diet high in animal products and refined grains (a typical diet in the USA) is low in fiber. In prospective health studies low fiber was not found to be a risk for breast cancer [25]. It is possible that fiber measurements are just a surrogate measure for unrefined plant food intake. Slattery et al [40] found an inverse correlation between vegetable, fruit and whole grain intake plant food intake and rectal cancer, while refined grains were associated with increased risk of rectal cancer. A threshold of about 5 daily servings of vegetables was needed to reduce cancer risk and the effect was stronger among older subjects [40]. Many other nutrients are co-variants with fiber, including folic acid, which is covered in detail below.

Red Meat

Red meat has been implicated in colon and rectal cancer. A Medline search in February 2003 uncovered 26 reports of human studies investigating the link between diet and colon or colorectal cancer. Of the 26 reports, 21 of them reported a significant positive relationship between red meat and colon or colorectal cancer [17,41-64]. A recent meta-analysis also found red meat, and processed meat, to be significantly associated with colorectal cancer [65]. Meat, and the heterocyclic amines formed in cooking, have been correlated to breast cancer in a case-control study in Uruguay as well [66].

Omega 3:6 Ratio Imbalance

Omega 3 fats (alpha-linolenic acid, EPA, DHA) have been shown in animal studies to be protect from cancer, while omega 6 fats (linoleic acid, arachidonic acid) have been found to be cancer promoting fats. Now there have been several studies that have tested this hypothesis in relation to breast cancer, summarized in Table 1. Except for the study by London et al [67], all of these studies found an association between a higher ratio of N-3 to N-6 fats and reduced risk of breast cancer. Long chain N-3 and N-6 fats have a different effect on the breast tumor suppressor genes BRCA1 and BRCA2. Treatment of breast cell cultures with N-3 fats (EPA or DHA) results in increased expression of these genes while arachadonic acid had no effect [68]. Flax seed oil and DHA (from an algae source) both can be used to increase the intake of N-3 fat, with DHA being a more efficient, sure source.

Flax seed

Flax seed provides all of the nutrients from this small brown or golden hard-coated seed. It is an excellent source of dietary fiber, omega 3 fat (as alpha-linolenic acid), and lignans. The lignans in flax seed are metabolized in the digestive tract to enterodiol and enterolactone, which have estrogenic activity. In fact, flax seed is a more potent source of phytoestrogens than soy products, as flax seed intake caused a bigger change in the excretion of 2-hydroxyestrone compared to soy protein [69].

Ground flax seeds have been studied for its effect on cancer, including several excellent studies by Lilian Thompson's research group at the University of Toronto. In one study the flax seed, its lignan fraction, or the oil were added to the diet of mice who had previously been administered a chemical carcinogen to induce cancer. All three treatments reduced the established tumor load; the lignan fraction containing secoisolariciresinol diglycoside (SDG) and the flax seed also reduced metastasis [70]. In another study the flax lignan SDG was fed to mice starting 1 week after treatment with the carcinogen dimethylbenzanthracene. The number of tumors per rat was reduced by 46% compared to the control in this study [71]. Flax or its lignan (SDG) were tested to see if they would prevent melanoma metastasis. The flax or lignan fraction were fed to mice two weeks before and after injection of melanoma cells. The flax treatment (at 2.5, 5, or 10% of diet intake) resulted in a 32, 54, and 63 percent reduction in the number of tumors, compared to the control [72]. The SDG, fed at amounts equivalent to the amount in 2.5, 5, or 10% flax seed, also reduced the tumor number, from a median number of 62 in the control group to 38, 36, and 29 tumors per mouse in the SDG groups, respectively [73].

More recently Thompson's research group studied mice that were injected with human breast cancer cells. After the injection the mice were fed a basal diet (lab mouse chow) for 8 weeks while the tumors grew. Then one group continued the basal diet and another was fed a 10% flax seed diet. The flax seed reduced the tumor growth rate and reduced metastasis by 45% [74].

Flax seed has been shown to enhance mammary gland morphogenesis or differentiation in mice. Nursing dams were fed the 10% flax seed diet (or an equivalent amount of SDG). After weaning the offspring mice were fed a regular mouse chow diet. Researchers then examined the female offspring and found an increased number of terminal end buds and terminal ducts in their mammary glands with more epithelial cell proliferation, all demonstrating that mammary gland differentiation was enhanced [75]. When these female offspring were challenged with a carcinogen to induce mammary gland tumors there were significantly lower incidence of tumors (31% and 42% lower in the flax seed and SDG groups, respectively), significantly lower tumor load (51% and 62% lower in the flax seed and SDG groups, respectively), significantly lower mean tumor size (44% and 68% lower in the flax seed and SDG groups, respectively), and significantly lower tumor number (47% and 45% lower in the flax seed and SDG groups, respectively) [76]. So, flax seed and its lignan were able to reduce tumor growth (both in number and size of tumors), prevent metastasis, and even cause increased differentiation of mouse mammary tissue in suckling mice, making the offspring less susceptible to carcinogenesis even when not consuming any flax products.

Other researchers have tested flax seed and prostate cancer. In an animal model using mice, Lin et al [77] found that a diet supplemented with 5% flax inhibited the growth and development of prostate cancer in their experimental mouse model. A pilot study of 25 men who were scheduled for prostatectomy surgery were instructed to eat a low-fat diet (20% or less of energy intake) and to supplement with 30 g of ground flaxseed per day. During the follow-up of an average of 34 days there were significant changes in serum cholesterol, total testosterone, and the free androgen index [78]. The mean proliferation index of the experimental group was significantly lower and apoptotic indexes higher compared to historical matched controls. Ground flax seed may be a very beneficial food for men battling prostate cancer. However, a meta-analysis of nine cohort and case-control studies revealed an association between flax seed oil intake or high blood levels of alpha-linolenic acid and prostate cancer risk [79]. It is quite likely that the lignans in flax seed are a major component of flax's anti-cancer effects so that flax oil without the lignans is not very beneficial. Some brands of flax seed oil retain some of the seed particulate because of the beneficial properties of the lignans.

Fruits and Vegetables

One of the most important messages of modern nutrition research is that a diet rich in fruits and vegetables protects against cancer. (The greatest message is that this same diet protects against almost all other diseases, too, including cardiovascular disease and diabetes.) There are many mechanisms by which fruits and vegetables are protective, and an enormous body of research supports the recommendation for people to eat more fruits and vegetables.

Block et al [80] reviewed about 200 studies of cancer and fruit and vegetable intake. A statistically significant protective effect of fruits and vegetables was found in 128 of 156 studies that gave relative risks. For most cancers, people in the lower quartile (1/4 of the population) who ate the least amount of fruits and vegetables had about twice the risk of cancer compared to those who in the upper quartile who ate the most fruits and vegetables. Even in lung cancer, after accounting for smoking, increasing fruits and vegetables reduces lung cancer; an additional 20 to 33 percent reduction in lung cancers is estimated [1].

Steinmetz and Potter reviewed the relationship between fruits, vegetables, and cancer in 206 human epidemiologic studies and 22 animal studies [81]. They found "the evidence for a protective effect of greater vegetable and fruit consumption is consistent for cancers of the stomach, esophagus, lung, oral cavity and pharynx, endometrium, pancreas, and colon." Vegetables, and particularly raw vegetables, were found to be protective; 85% of the studies that queried raw vegetable consumption found a protective effect. Allium vegetables, carrots, green vegetables, cruciferous vegetables, and tomatoes also had a fairly consistent protective effect [81]. Allium vegetables (garlic, onion, leeks, and scallions) are particularly potent and have separately been found to be protective for stomach and colorectal cancers [82,83] and prostate cancer [84].

There are many substances that are protective in fruits and vegetables, so that the entire effect is not very likely to be due to any single nutrient or phytochemical. Steinmetz and Potter list possible protective elements: dithiolthiones, isothiocyanates, indole-32-carbinol, allium compounds, isoflavones, protease inhibitors, saponins, phytosterols, inositol hexaphosphate, vitamin C, D-limonene, lutein, folic acid, beta carotene (and other carotenoids), lycopene, selenium, vitamin E, flavonoids, and dietary fiber [81].

A joint report by the World Cancer Research Fund and the American Institute for Cancer Research found convincing evidence that a high fruit and vegetable diet would reduce cancers of the mouth and pharynx, esophagus, lung, stomach, and colon and rectum; evidence of probable risk reduction was found for cancers of the larynx, pancreas, breast, and bladder [1].

Many of the recent reports from prospective population-based studies of diet and cancer have not found the same protective effects of fruits and vegetables that were reported earlier in the epidemiological and case-control studies [reviewed in [85]]. One explanation is that people's memory of what they ate in a case-cohort study may have been tainted by their disease state. Another problem might be that the food frequency questionnaires (FFQ) used to measure food intake might not be accurate enough to detect differences. Such a problem was noted in the EPIC study at the Norfolk, UK site. Using a food diary the researchers found a significant correlation between saturated fat intake and breast cancer, but using a FFQ there was no significant correlation [86]. So, inaccurate measurement of fruit and vegetable intake might be part of the explanation as well.

It must be noted that upper intakes of fruits and vegetables in these studies are usually within the range of what people on an American omnivorous diet normally eat. In the Nurses Health Study the upper quintiles of fruit and vegetable intake were 4.5 and 6.2 servings/day, respectively [87]. Similarly, the upper quintiles of fruit and vegetable intake in the Health Professionals Follow-up Study were 4.3 and 5.4 serving/day for fruits and vegetables, respectively [87]. Intakes of fruits and vegetables on the Hallelujah Diet are much higher, with median reported intakes of six servings of fruits (646 g/day) and eleven servings of vegetables per day (971 g/day) [88] in addition to a green powder from the juice of barley leaves and alfalfa that is equivalent to approximately another 100 g/day of fresh dark greens. So, it is very possible that the range of intakes in the prospective population based studies do not have a wide enough intake on the upper end to detect the true possible impact of a very high intake of fruits and vegetables on cancer risk.

Cruciferous Vegetables

Cruciferous vegetables (broccoli, cauliflower, cabbage, Brussels sprouts) contain sulforophane, which has anti-cancer properties. A case-control study in China found that intake of cruciferous vegetables, measured by urinary secretion of isothiocyanates, was inversely related to the risk of breast cancer; the quartile with the highest intake only had 50% of the risk of the lowest intake group [89]. In the Nurses' Health Study a high intake of cruciferous vegetables (5 or more servings/week vs less than two servings/week) was associated with a 33% lower risk of non-Hodgkin's lymphoma [90]. In the Health Professionals Follow-up Study bladder cancer was only weakly associated with low intake of fruits and vegetables, but high intake (5 or more servings/week vs 1 or less servings/wk) of cruciferous vegetables was associated with a statistically significant 51% decrease in bladder cancer [91]. Also, prostate cancer risk was found to be reduced by cruciferous vegetable consumption in a population-based case-control study carried out in western Washington state. Three or more servings per week, compared to less than one serving of cruciferous vegetables per week resulted in a statistically significant 41% decrease in prostate cancer risk [92]. Similar protective effects of cruciferous vegetables were seen in a multi-ethnic case-control study [93]. A prospective study in Shanghai, China found that men with detectable amounts of isothiocyanates in their urine (metabolic products that come from cruciferous vegetables) had a 35% decreased risk of lung cancer. Among men that had one or two genetic polymorphisms that caused them to eliminate these isothiocyanates slower there was a 64% or 72% decreased risk of lung cancer, respectively [94].

Broccoli sprouts have a very high concentration of sulforophane since this compound originates in the seed and is not made in the plant as it grows [95,96]. One sprout contains all of the sulforophane that is present in a full-grown broccoli plant. So, if sulforophane is especially cancer-protective, it would seem reasonable to include some broccoli sprouts in an anti-cancer diet.

Selenium

Selenium is a mineral with anti-cancer properties. Many studies in the last several years have shown that selenium is a potent protective nutrient for some forms of cancer. The Arizona Cancer Center posted a selenium fact sheet listing the major functions of selenium in the body [97]. These functions are as follows:

1. Selenium is present in the active site of many enzymes, including thioredoxin reductase, which catalyze oxidation-reduction reactions. These reactions may encourage cancerous cells to under apoptosis.

2. Selenium is a component of the antioxidant enzyme glutathione peroxidase.

3. Selenium improved the immune systems' ability to respond to infections.

4. Selenium causes the formation of natural killer cells.

5. P450 enzymes in the liver may be induced by selenium, leading to detoxification of some carcinogenic molecules.

6. Selenium inhibits prostaglandins that cause inflammation.

7. Selenium enhances male fertility by increased sperm motility.

8. Selenium can decrease the rate of tumor growth.

A serendipitous randomized, double-blind, controlled trial of a 200 µg/day selenium supplement in the southeastern region of the USA (where soil selenium levels are low) found that the primary endpoints of skin cancer were not improved by the selenium supplement, but that other cancer incidence rates were decreased by selenium [98,99]. There was a significant reduction in total cancer incidence (105 vs 137 cases, P = 0.03), prostate cancer (22 vs 42 cases, P = 0.005), a marginally significant reduction in colorectal cancer incidence (9 vs 19 cases, P = 0.057), and a reduction in cancer mortality, all cancer sites (40 vs 66 deaths, P = 0.008) (selenium versus control group cases reported, respectively) [98]. The selenium supplement was most effective in ex-smokers and for those who began the study with the lowest levels of serum selenium. Several prospective studies have also examined the role of selenium in cancer prevention, particularly for prostate cancer, summarized in Table 2.

Overall, it appears that poor selenium levels, especially for men, are a cancer risk. If a person has low selenium levels and other antioxidant defenses are also low the cancer risk is increased even further. Women do not appear to be as sensitive to selenium, as breast cancer has not been found to be influenced by selenium status in several studies [100-104], although both men and women were found to be protected by higher levels of selenium from colon cancer [100] and lung cancer [105,106]. Good vegetarian sources of selenium are whole grains and legumes grown in selenium-rich soil in the western United States, brazil nuts (by far the most dense source of selenium), nutritional yeast, brewers yeast, and sunflower seeds.

Chlorophyll

All green plants also contain chlorophyll, the light-collecting molecule. Chlorophyll and its derivatives are very effective at binding polycyclic aromatic hydrocarbons (carcinogens largely from incomplete combustion of fuels), heterocyclic amines (generated when grilling foods), aflatoxin (a toxin from molds in foods which causes liver cancer), and other hydrophobic molecules. The chlorophyll-carcinogen complex is much harder for the body to absorb, so most of it is swept out with the feces. The chemoprotective effect of chlorophyll and its derivatives has been tested in laboratory cell cultures and animals [107,108]. There is so much compelling evidence for anti-carcinogenic effects of chlorophyll that a prospective randomized controlled trial is being conducted in Qidong, China to see if chlorophyllin can reduce the amount of liver cancer cases, which arise from aflatoxin exposure in their foods (corn, peanuts, soy sauce, and fermented soy beans). A 55% reduction in aflatoxin-DNA adducts were found in the group that took 100 mg of chlorophyllin three times a day [109]. It was supposed that the chlorophyllin bound up aflatoxins, but there were chlorophyllin derivatives also detected in the sera (which had a green tint to it) of the volunteers who took the supplement, indicating a possible role in the body besides binding carcinogens in the gut [110].

Protective Vitamins

Vitamin B-12

Vitamin B-12 has not been proven to be an anti-cancer agent, but there is some evidence indicating that it could be beneficial. The form of administered vitamin B-12 may be important.

Some experimental cancer studies have been carried out with various forms of vitamin B-12. Methylcobalamin inhibited tumor growth of SC-3 injected into mice [111], and caused SC-3 mouse mammary tumor cells to undergo apoptosis, even when stimulated to grow by the presence of growth-inducing androgen [112]. Methylcobalamin, but not cyanocobalamin, increased the survival time of mice bearing implanted leukemia tumor cells [113]. 5'-deoxyadenosylcobalamin and methylcobalamin, but not cyanocobalamin, were shown to be effective cytotoxic agents [114]. Methylcobalamin also was able to increase survival time and reduce tumor growth in laboratory mice [115].

Laboratory mechanistic evidence for the effects of vitamin B12 were seen in a laboratory study with vitamin B-12 deficient rats. Choi et al [116] found that the colonic DNA of the B-12 deficient rats had a 35% decrease in genomic methylation and a 105% increase in uracil incorporation, both changes that could increase risk of carcinogenesis. In two prospective studies (one in Washington Country, Maryland and the Nurses' Health Study) a relation between lower vitamin B12 status (but not deficiency) and statistically significant higher risk of breast cancer was found [117,118]. So, there is evidence from laboratory studies, prospective cohort studies, and mechanistic studies showing that vitamin B-12 is an important nutrient for genetic stability, DNA repair, carcinogenesis, and cancer therapy.

Folic Acid

Folic acid is the dark green leafy vegetable vitamin. It has an integral role in DNA methylation and DNA synthesis. Folic acid works in conjunction with vitamin B-6 and vitamin B-12 in the single carbon methyl cycle. If insufficient folic acid is not available uracil is substituted for thymidine in DNA, which leads to DNA strand breakage. About 10% of the US population (and higher percentages among the poor) has low enough intakes of folic acid to make this a common problem [119]. As shown in Tables 3 and 4, many studies have found a significant reduction in colon, rectal, and breast cancer with higher intakes of folic acid and their related nutrients (vitamin B-6 and B-12). Alcohol is an antagonist of folate, so that drinking alcoholic beverages greatly magnifies the cancer risk of a low-folate diet. Genetic polymorphisms (common single DNA base mutations resulting in a different amino acid encoded into a protein) in the methylenetetrahydrofolate reductase and the methionine synthase genes which increase the relative amount of folate available for DNA synthesis and repair also reduces the risk of colon cancer [120-123]. Cravo et al [124] used 5 mg of folic acid a day (a supraphysiological dose) in a prospective, controlled, cross-over study of 20 patients with colonic adenoma polyps. They found that the folic acid could reverse DNA hypomethylation in 7 of 12 patients who had only one polyp.

Folate may be more important for rapidly dividing tissue, like the colonic mucosa. Therefore, the cancer risk associated with low folate intake is probably higher for colon cancer than for breast cancer. Most of the breast cancer studies only found a protective effect of folate among women who consumed alcohol (see Table 4). However, among women residents of Shanghai who consumed no alcohol, no vitamin supplements and ate unprocessed, unfortified foods there was a 29% decreased risk of breast cancer among those with the highest intake of folate [125]. So, there may be a true protective effect that is masked in the western populations by so many other risk factors. Two studies showed that the risk of cancer due to family history can be modified by high folate intake, so a prudent anti-cancer diet would be high in dark green leafy vegetables. The mean intake of folic acid on the Hallelujah Diet was 594 µg/day for men and 487 µg/day for women [88].

Vitamin D

Vitamin D is produced primarily from the exposure of the skin to sunshine. Even casual exposure of the face, hands, and arms in the summer generates a large amount of vitamin D. In fact, simulated sunshine, equivalent to standing on a sunny beach until a slight pinkness of the skin was detected, was equivalent to a 20,000 IU oral dose of vitamin D2 [126]. (Note that the RDA is 400 IU for most adults.) It has been estimated that 1,000 IU per day is the minimal amount needed to maintain adequate levels of vitamin D in the absence of sunshine [126], and that up to 4,000 IU per day can be safely used with additional benefit [127].

The concentration of the active hormonal form of vitamin D is tightly regulated in the blood by the kidneys. This active hormonal form of vitamin D has the potent anti-cancer properties. It has been discovered that various types of normal and cancerous tissues, including prostate cells [128], colon tissue [129], breast, ovarian and cervical tissue [130], pancreatic tissue [131] and a lung cancer cell line [132] all have the ability to convert the major circulating form of vitamin D, 25(OH)D, into the active hormonal form, 1,25(OH)2D. So, there is a local mechanism in many tissues of the body for converting the form of vitamin D in the body that is elevated by sunshine exposure into a hormone that has anticancer activity.

Indeed, 25(OH)D has been shown to inhibit growth of colonic epithelial cells [133], primary prostatic epithelial cells [134], and pancreatic cells [131]. So, the laboratory work is confirming what had been seen some time ago in ecological studies of populations and sunshine exposure.

The mortality rates for colon, breast, and ovary cancer in the USA show a marked north-south gradient [135]. In ecological studies of populations and sunlight exposure (no individual data) sunlight has been found to have a protective effect for prostate cancer [136], ovarian cancer [137], and breast cancer [138]. Recently Grant found that sunlight was also protective for bladder, endometrial, renal cancer, multiple myeloma, and Non-Hodgkins lymphoma in Europe [139] and bladder, esophageal, kidney, lung, pancreatic, rectal, stomach, and corpus uteri cancer in the USA [140]. Several prospective studies of vitamin D and cancer have also shown a protective effect of vitamin D (see Table 5). It could be that sunshine and vitamin D are protective factors for cancers of many organs that can convert 25(OH)D into 1,25(OH)D2.

Antioxidants

a- and ß-Carotene and other Carotenoids

Carotenoids have been studied vigorously to see if these colorful compounds can decrease cancer risk. In ecological studies and early case-control studies it appeared that ß-carotene was a cancer-protective agent. Randomized controlled trials of ß-carotene found that the isolated nutrient was either neutral [141] or actually increased risk of lung cancer in smokers [142,143]. Beta-carotene may be a marker for intake of fruits and vegetables, but it does not have a powerful protective effect in isolated pharmacological doses.

However, there is a large body of literature that indicates that dietary carotenoids are cancer preventative (See Table 6). Alpha-carotene has been found to be a stronger protective agent than its well-known isomer ß-carotene. Studies tend to agree that overall intake of carotenoids is more protective than a high intake of a single carotenoid. So, a variety of fruits and vegetables is still a better anti-cancer strategy than just using a single vegetable high in a specific carotenoid.

The richest source of a-carotene is carrots and carrot juice, with pumpkins and winter squash as a second most-dense source. There is approximately one µg of a-carotene for every two µg of ß-carotene in carrots. The most common sources of ß-cryptoxanthin are citrus fruits and red sweet peppers.

Lycopene

Of the various carotenoids lycopene has been found to be very protective, particularly for prostate cancer. The major dietary source of lycopene is tomatoes, with the lycopene in cooked tomatoes being more bioavailable than that in raw tomatoes. Several prospective cohort studies have found associations between high intake of lycopene and reduced incidence of prostate cancer, though not all studies have produced consistent results [144,145]. Some studies suffer from a lack of good correlation between lycopene intake assessed by questionnaire and actual serum levels, and other studies measured intakes among a population that consumed very few tomato products. The studies with positive results will be reviewed here.

In the Health Professionals Follow-up Study there was a 21% decrease in prostate cancer risk, comparing the highest quintile of lycopene intake with the lowest quintile. Combined intake of tomatoes, tomato sauce, tomato juice, and pizza (which accounted for 82% of the lycopene intake) were associated with a 35% lower risk of prostate cancer. Furthermore, lycopene was even more protective for advanced stages of prostate cancer, with a 53% decrease in risk [146]. A more recent follow-up report on this same cohort of men confirmed these original findings that lycopene or frequent tomato intake is associated with about a 30–40% decrease in risk of prostate cancer, especially advanced prostate cancer [147].

In addition to the two reports above a nested case control study from the Health Professional Follow-up Study with 450 cases and controls found an inverse relation between plasma lycopene and prostate cancer risk (OR 0.48) among older subjects (>65 years of age) without a family history of prostate cancer [148]. Among younger men high plasma ß-carotene was associated with a statistically significant 64% decrease in prostate cancer risk. So, the results for lycopene have been found for dietary intakes as well as plasma levels.

In a nested case-control study from the Physicians' Health Study cohort, a placebo-controlled study of aspirin and ß-carotene, there was a 60% reduction in advanced prostate cancer risk (P-trend = 0.006) for those subjects in the placebo group with the highest plasma lycopene levels, compared to the lowest quintile. The ß-carotene also had a protective effect, especially for those men with low lycopene levels [149].

In addition to these observational studies, two clinical trials have been conducted to supplement lycopene for a short period before radical prostatectomy. In one study 30 mg/day of lycopene were given to 15 men in the intervention group while the 11 men were in the control group were instructed to follow the National Cancer Institute's recommendations to consume at least 5 servings of fruits and vegetables daily. Results showed that the lycopene slowed the growth of prostate cancer. Prostate tissue lycopene concentration was 47% higher in the intervention group. Subjects that took the lycopene for 3 weeks had smaller tumors, less involvement of the surgical margins, and less diffuse involvement of the prostate by pre-cancerous high-grade prostatic intraepithelial neoplasia [150]. In another study before radical prostatectomy surgery 32 men were given a tomato sauce-based pasta dish every day, which supplied 30 mg of lycopene per day. After 3 weeks serum and prostate lycopene levels increaed 2-fold and 2.9-fold, respectively. PSA levels decreased 17%, as seen also by Kucuk et al [150]. Oxidative DNA damage was 21% lower in subjects' leukocytes and 28% lower in prostate tissue, compared to non-study controls. The apoptotic index was 3-fold higher in the resected prostate tissue, compared to biopsy tissue [151]. These intervention studies raise the question of what could have been done in this intervention was longer and combined synergistically with other effective intervention methods, such as flax seed, increased selenium and possibly vitamin E, in the context of a diet high in fruits and vegetable?

Vitamin C

Vitamin C, or ascorbic acid, has been studied in relation to health and is the most common supplement taken in the USA. Low blood levels of ascorbic acid are detrimental to health (for a recent article see Fletcher et al [152]) and vitamin C is correlated with overall good health and cancer prevention [153]. Use of vitamin C for cancer therapy was popularized by Linus Pauling. At high concentrations ascorbate is preferentially toxic to cancer cells. There is some evidence that large doses of vitamin C, either in multiple divided oral doses or intravenously, have beneficial effects in cancer therapy [154-156]. Oral doses, even in multiple divided doses, are not as effective as intravenous administration. Vitamin C at a dose of 1.25 g administered orally produced mean peak plasma concentrations of 135 ± 21 µmol/L compared with 885 ± 201 µmol/L for intravenous administration [154].

While vitamin C is quite possibly an effective substance, the amounts required for these therapeutic effects are obviously beyond dietary intakes. However, intravenous ascorbate may be a very beneficial adjuvant therapy for cancer with no negative side effects when administered properly.

Other Antioxidants

There are many more substances that will have some benefit for cancer therapy. Most of these substances are found in foods, but their effective doses for therapy are much higher than the normal concentration in the food. For example, grape seed extract contains proanthocyanidin, which shows anticarcinogenic properties (reviewed by Cos et al \ [157]. Also, green tea contains a flavanol, epigallocatechin-3-gallate (EGCG), which can inhibit metalloproteinases, among several possible other mechanisms [158]. And there are claims for various other herbal substances and extracts that might be of benefit, which are beyond the scope of this review.

Probiotics

The bacteria that reside in the intestinal tract generally have a symbiotic relationship with their host. Beneficial bacteria produce natural antibiotics to keep pathogenic bugs in check (preventing diarrhea and infections) and produce some B vitamins in the small intestine where they can be utilized. Beneficial bacteria help with food digestion by providing extra enzymes, such as lactase, in the small intestine. Beneficial bacteria help strengthen the immune system right in the gut where much of the interaction between the outside world and the body goes on. Beneficial bacteria can help prevent food allergies. They can help prevent cancer at various stages of development. These good bacteria can improve mineral absorption, maximizing food utilization.

However, the balance of beneficial and potentially pathogenic bacteria in the gut is dependent on the diet. Vegetable fiber encourages the growth of beneficial bacteria. A group of Adventist vegetarians was found to have a higher amount of beneficial bacteria and lower amount of potentially pathogenic bacteria compared to non-vegetarians on a conventional American diet [159]. Differences in bacterial populations were seen between patients who recently had a colon polyp removed, Japanese-Hawaiians, North American Caucasians, native rural Japanese, and rural native Africans. Lactobacillus species and Eubacterium aerofaciens, both producers of lactic acid, were associated with the populations with the lower risk of colon cancer, while Bacteroides and Bifidobacterium species were associated with higher risk of colon cancer [160]

There is a solid theoretical basis for why probiotics should help prevent cancer, especially colon cancer, and even reverse cancer. Probiotics produce short chain fatty acids in the colon, which acidify the environment. Lower colon pH is associated with lower incidence of colon cancer. Probiotic bacteria reduce the level of procarcinogenic enzymes such as beta-glucuronidase, nitroreductase, and azoreductase [161].

L. casei was used in two trials of patients with superficial bladder cancer. In the first trial, the probiotic group had a 50% disease free time of 350 days, compared to 195 days for the control group [162]. The second trial also showed that the probiotics worked better than the placebo, except for multiple recurring tumors [163].

Except for the two studies noted above, most of the research of probiotics and cancer has been done in animals. Studies have looked at markers of tumor growth or at animals with chemically induced tumors.

Studies in rats have shown that probiotics can inhibit the formation of aberrant crypt foci, thought to be a pre-cancerous lesion in the colon. Some of the best results were obtained with a probiotic strain consumed with inulin, a type of fructooligosaccharide. Total aberrant crypt foci, chemically induced, were reduced 74% by the treatment of rats with inulin and B. longum, but only 29 and 21% by B. longum and inulin alone, respectively [164]. There was a synergistic effect in using both products together. Similar synergy was seen in rats with azoxymethane-induced colon cancer in another study. Rats fed Raftilose, a mixture of inulin and oligofructose, or Raftilose with Lactobacilli rhamnosus (LGG) and Bifidobacterium lactis (Bb12) had a significantly lower number of tumors compared to the control group [165]. A probiotic mixture, without any prebiotic, given to rats fed azoxymethane reduced colon tumors compared to the control (50% vs 90%), and also reduced the number of tumors per tumor-bearing rat [166].

In lab mice bred to be susceptible to colitis and colon cancer, a probiotic supplement, Lactobacillus salivarium ssp. Salivarius UCC118, reduced fecal coliform levels, the number of potentially pathogenic Clostridium perfringens, and reduced intestinal inflammation. In this small study two mice died of fulminant colitis and 5 mice developed adenocarcinoma in the control group of 10 mice, while there was no colitis and only 1 mouse with adenocarcinoma in the probiotic test group [167].

The research on probiotics and disease is still an emerging field. There is a high degree of variation of health benefits between different strains of bacteria. As new methods for selecting and screening probiotics become available, the field will be able to advance more rapidly.

Oral Enzymes

Many people diagnosed with cancer have digestion or intestinal tract disorders as well. Impaired digestion will greatly hinder a nutritional approach to treating cancer. If the nutrients cannot be released from the food and taken up by the body, then the excellent food provided by the Hallelujah Diet will go to waste. Digestive enzyme supplements are used to ensure proper and adequate digestion of food. Even raw foods, which contain many digestive enzymes to assist in their digestion, will be more thoroughly digested with less of the body's own resources with the use of digestive enzymes. So, the enzymes taken with meals do not have a direct effect upon a tumor, but assist the body in getting all of the nutrition out of the food for healing and restoring the body to normal function. Recently, an in vitro system was used to test the use of supplemental digestive enzymes. The digestive enzymes improved the digestibility and bioaccessibility of proteins and carbohydrates in the lumen of the small intestine, not only under impaired digestive conditions, but also in healthy human digestion [168].

There is evidence that indicates the presence of an enteropancreatic circulation of digestive enzymes [169]. Digestive enzymes appear to be preferentially absorbed into the bloodstream and then reaccumulated by the pancreas for use again. There appears to be a mechanism by which digestive enzymes can reach systemic circulation.

Enzymes, especially proteases, if they reach systemic circulation, can have direct anti-tumor activity. Wald et al [170] reported on the anti-metastatic effect of enzyme supplements. Mice inoculated with the Lewis lung carcinoma were treated with a proteolytic enzyme supplement, given rectally (to avoid digestion). The primary tumor was cut out, so that the metastatic spread of the cancer could be measured. After surgical removal of the primary tumor (day 0), 90% of the control mice died by day 18 due to metastasized tumors. In the first group, which received the rectal enzyme supplement from the time of the tumor-removal surgery, 30% of the mice had died from metastasized cancer by day 25. In the second group, which received the enzymes from 6 days prior to removal of the primary tumor, only 10% of the animals showed the metastatic process by day 15. In the third group, which received the enzyme treatment since the initial inoculation of the Lewis lung carcinoma, no metastatic spread of the tumor was discernible. One hundred day-survival rates for the control, first, second, and third groups were 0, 60%, 90%, and 100%.

In a similar experiment, an enzyme mixture of papain, trypsin, and chymotrypsin, as used in the preparation Wobe-Mugos E, was rectally given to mice that were inoculated with melanoma cells. Survival time was prolonged in the test group (38 days in the enzyme group compared to 24 days in the control mice) and 3 of the 10 enzyme-supplemented mice were cured. Again, a strong anti-metastatic effect of the proteolytic enzymes was seen [171].

Further evidence of the efficacy of oral enzyme supplementation is available from clinical trials in Europe. Two different studies have demonstrated that two different oral proteolytic enzyme supplements were able to reduce high levels of transforming growth factor-ß, which may be a factor in some cancers [172,173]. In the Slovak Republic an oral enzyme supplement was tested in a placebo-controlled trial of multiple myeloma. For stage III multiple myeloma, control group survival was 47 months, compared to 83 months (a 3 year gain) for patients who took the oral enzymes for more than 6 months [174].

Enzyme supplements have also been shown to reduce side effects of cancer therapy. Enzyme supplementation resulted in fewer side effects for women undergoing radiation therapy for carcinomas of the uterine cervix [175], for patients undergoing radiation therapy for head and neck cancers [176], and for colorectal cancer patients undergoing conventional cancer treatments [177]. In a large multi-site study in Germany women undergoing conventional cancer therapy were put into a control group or a group that received an oral enzyme supplement. Disease and therapy related symptoms were all reduced, except tumor pain, by the enzyme supplement. Also, survival was longer with less recurrence and less metastases in the enzyme group [178]. In all of these studies the oral enzyme supplements were well tolerated, with only a small amount of mild to moderate gastrointestinal symptoms.

Even though these few studies don't give a lot of evidence of the effectiveness of oral enzyme supplementation, it is clear that there are some circumstances that will be helped by enzyme supplementation, with very little danger of negative side effects. At the least, enzymes will improve digestion and lessen the digestive burden on the body, leaving more reserves for disease eradication. However, as the research indicates, the effect may be much greater than that, with the potential for direct anti-tumor activity.

Whole Diet Studies

A diet-based cancer therapy, the Gerson Therapy, was used to treat melanoma cancer. The five-year survival rates from their therapy compared very favorably to conventional therapy reported in the medical literature, especially for more advanced stages of melanoma [179] (see Table 7).

An Italian cohort of 8,984 women was followed for an average of 9.5 years, with 207 incident cases of breast cancer during that time. Their diets were analyzed by patterns – salad vegetables (raw vegetables and olive oil), western (potatoes, red meat, eggs and butter), canteen (pasta and tomato sauce), and prudent (cooked vegetables, pulses, and fish). Only the salad vegetable diet pattern was associated with a significantly lower risk of breast cancer, about 35% lower. For women of normal weight (BMI <25) the salad vegetable pattern was even more protective, about a 61% decreased risk of breast cancer [180]. The overall dietary pattern does make a very significant difference.

In US-based studies the "prudent" diet has been shown to be protective for colon cancer, while the "western" diet has been shown to be detrimental. The "western" dietary pattern, with its higher intakes of red meat and processed meats, sweets and desserts, French fries, and refined grains, was associated with a 46% increase relative risk of colon cancer in the Nurses' Health Study [45]. Slattery et al [17] found a two-fold increase in relative risk of colon cancer associated with a "western" dietary pattern, and a 35–40% decrease in relative risk associated with the "prudent" pattern, especially among those diagnosed at an earlier age (<67 years old). The "salad vegetable" pattern is still more likely to be protective compared to the prudent dietary pattern, but this pattern did not exist in this study population.

In an analysis of the colon cancer data from the Health Professionals Follow-up Study, Platz et al [56] found that there was a 71% decrease in colon cancer risk when men with none of six established risk factors were compared to men with at least one of these risk factors (obesity, physical inactivity, alcohol consumption, early adulthood cigarette smoking, red meat consumption, and low intake of folic acid from supplements). So, if all men had the same health profile as these healthier 3% of the study population, colon cancer rates would have been only 29% of what they measured.

A plant-based dietary pattern in being currently tested in the Women's healthy Eating and Living (WHEL) Study. About 3,000 women who were treated for an early stage of breast cancer have been randomized into two groups. The dietary goals for the test group of the study are 5 servings of vegetables, 16 oz of vegetable juice, 3 servings of fruit, 30 g of fiber, and <20% of energy from fat. No guidelines were given for animal product intake, and initial results seem to confirm, since there were no changes in body weight, total cholesterol, or LDL cholesterol [181], which would be affected by animal protein intake. However, over the first year of follow-up vegetable intake did increase to seven servings/day, fruit intake increased to 3.9 servings/day, energy from fat decreased from 28% to 23%. Also, plasma carotenoid concentrations increased significantly in the intervention group, but not in the control group. a-Carotene increased 223%, ß-carotene increased 87%, lutein increase 29%, and lycopene increased 17% [182], indicating that a substantial dietary change had been made by these women. It will be very interesting to follow the results of this study.


Conclusions

What is the result when all of these things are put together? What if all of these factors reviewed here were taken into account and put into practice? This anticancer diet would have:

• adequate, but not excessive calories,

• 10 or more servings of vegetables a day, including cruciferous and allium vegetables; vegetable juice could meet part of this goal,

• 4 or more servings of fruits a day,

• high in fiber,

• no refined sugar,

• no refined flour,

• low in total fat, but containing necessary essential fatty acids,

• no red meat,

• a balanced ratio of omega 3 and omega 6 fats and would include DHA,

• flax seed as a source of phytoestrogens,

• supplemented with ~200 µg/day selenium,

• supplemented with 1,000 µg/day methylcobalamin (B-12),

• very rich in folic acid (from dark green vegetables),

• adequate sunshine to get vitamin D, or use 1,000 IU/day supplement,

• very rich in antioxidants and phytochemicals from fruits and vegetables, including a-carotene, ß-carotene, ß-cryptoxanthin, vitamin C (from foods), vitamin E (from foods),

• very rich in chlorophyll,

• supplemented with beneficial probiotics,

• supplemented with oral enzymes

As reviewed above, reductions of 60 percent in breast cancer rates have already been seen in human diet studies, and a 71 percent reduction in colon cancer for men without the known modifiable risk factors. These reductions are without taking into account many of the other factors considered in this review, such as markedly increased fruit and vegetable intake, balanced omega 3 and 6 fats, vitamin D, reduced sugar intake, probiotics, and enzymes – factors which all are likely to have an impact on cancer. Certainly cancer prevention would be possible, and cancer reversal in some cases is quite likely.


Competing Interests

Michael Donaldson is a research scientist at the Hallelujah Acres Foundation, a foundation for investigations pertaining to the Hallelujah Diet. Funding for this review was provided by the Hallelujah Acres Foundation.

Author

Michael S Donaldson - Director of Research, Hallelujah Acres Foundation, 13553 Vantage Hwy, Ellensburg, WA 98926, USA

Nutrition Journal 2004, 3:19     doi:10.1186/1475-2891-3-19

© 2004 Donaldson; licensee BioMed Central Ltd.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

References

 
1.   WCRF/AICR: Food, nutrition and the prevention of cancer: a global perspective:.
World Cancer Research Fund / American Institute for Cancer Research 1997. OpenURL
    Return to citation in text: [1] [2] [3]
 
2.   Vastag B: Obesity Is Now on Everyone's Plate.
Jama 2004, 291:1186-1188. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
3.   Sturm R: Increases in clinically severe obesity in the United States, 1986–2000.
Arch Intern Med 2003, 163:2146-2148. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
4.   Mokdad AH, Marks JS, Stroup DF, Gerberding JL: Actual causes of death in the United States, 2000.
Jama 2004, 291:1238-1245. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
5.   Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ: Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults.
N Engl J Med 2003, 348:1625-1638. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2] [3]
 
6.   Hursting SD, Lavigne JA, Berrigan D, Perkins SN, Barrett JC: Calorie restriction, aging, and cancer prevention: mechanisms of action and applicability to humans.
Annu Rev Med 2003, 54:131-152. [PubMed Abstract] OpenURL
    Epub 2001 Dec 2003.
Return to citation in text: [1]
 
7.   Dirx MJ, Zeegers MP, Dagnelie PC, van den Bogaard T, van den Brandt PA: Energy restriction and the risk of spontaneous mammary tumors in mice: a meta-analysis.
Int J Cancer 2003, 106:766-770. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
8.   Harvell DM, Strecker TE, Xie B, Pennington KL, McComb RD, Shull JD: Dietary energy restriction inhibits estrogen-induced mammary, but not pituitary, tumorigenesis in the ACI rat.
Carcinogenesis 2002, 23:161-169. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
9.   Matsuzaki J, Yamaji R, Kiyomiya K, Kurebe M, Inui H, Nakano Y: Implanted tumor growth is suppressed and survival is prolonged in sixty percent of food-restricted mice.
J Nutr 2000, 130:111-115. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
10.   Michels KB, Ekbom A: Caloric restriction and incidence of breast cancer.
Jama 2004, 291:1226-1230. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
11.   Foster-Powell K, Holt SH, Brand-Miller JC: International table of glycemic index and glycemic load values: 2002.
Am J Clin Nutr 2002, 76:5-56. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
12.   Augustin LS, Gallus S, Negri E, La Vecchia C: Glycemic index, glycemic load and risk of gastric cancer.
Ann Oncol 2004, 15:581-584. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
13.   Augustin LS, Gallus S, Franceschi S, Negri E, Jenkins DJ, Kendall CW, Dal Maso L, Talamini R, La Vecchia C: Glycemic index and load and risk of upper aero-digestive tract neoplasms (Italy).
Cancer Causes Control 2003, 14:657-662. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
14.   Augustin LS, Gallus S, Bosetti C, Levi F, Negri E, Franceschi S, Dal Maso L, Jenkins DJ, Kendall CW, La Vecchia C: Glycemic index and glycemic load in endometrial cancer.
Int J Cancer 2003, 105:404-407. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
15.   Augustin LS, Polesel J, Bosetti C, Kendall CW, La Vecchia C, Parpinel M, Conti E, Montella M, Franceschi S, Jenkins DJ, Dal Maso L: Dietary glycemic index, glycemic load and ovarian cancer risk: a case-control study in Italy.
Ann Oncol 2003, 14:78-84. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
16.   Franceschi S, Dal Maso L, Augustin L, Negri E, Parpinel M, Boyle P, Jenkins DJ, La Vecchia C: Dietary glycemic load and colorectal cancer risk.
Ann Oncol 2001, 12:173-178. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
17.   Slattery ML, Boucher KM, Caan BJ, Potter JD, Ma KN: Eating patterns and risk of colon cancer.
Am J Epidemiol 1998, 148:4-16. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2] [3]
 
18.   Bostick RM, Potter JD, Kushi LH, Sellers TA, Steinmetz KA, McKenzie DR, Gapstur SM, Folsom AR: Sugar, meat, and fat intake, and non-dietary risk factors for colon cancer incidence in Iowa women (United States).
Cancer Causes Control 1994, 5:38-52. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
19.   Frazier AL, Li L, Cho E, Willett WC, Colditz GA: Adolescent diet and risk of breast cancer.
Cancer Causes Control 2004, 15:73-82. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
20.   Higginbotham S, Zhang ZF, Lee IM, Cook NR, Giovannucci E, Buring JE, Liu S: Dietary glycemic load and risk of colorectal cancer in the Women's Health Study.
J Natl Cancer Inst 2004, 96:229-233. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
21.   Cho E, Spiegelman D, Hunter DJ, Chen WY, Colditz GA, Willett WC: Premenopausal dietary carbohydrate, glycemic index, glycemic load, and fiber in relation to risk of breast cancer.
Cancer Epidemiol Biomarkers Prev 2003, 12:1153-1158. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
22.   Folsom AR, Demissie Z, Harnack L: Glycemic index, glycemic load, and incidence of endometrial cancer: the Iowa women's health study.
Nutr Cancer 2003, 46:119-124. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
23.   Higginbotham S, Zhang ZF, Lee IM, Cook NR, Buring JE, Liu S: Dietary glycemic load and breast cancer risk in the Women's Health Study.
Cancer Epidemiol Biomarkers Prev 2004, 13:65-70. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
24.   Michaud DS, Liu S, Giovannucci E, Willett WC, Colditz GA, Fuchs CS: Dietary sugar, glycemic load, and pancreatic cancer risk in a prospective study.
J Natl Cancer Inst 2002, 94:1293-1300. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
25.   Holmes MD, Liu S, Hankinson SE, Colditz GA, Hunter DJ, Willett WC: Dietary carbohydrates, fiber, and breast cancer risk.
Am J Epidemiol 2004, 159:732-739. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
26.   Jonas CR, McCullough ML, Teras LR, Walker-Thurmond KA, Thun MJ, Calle EE: Dietary glycemic index, glycemic load, and risk of incident breast cancer in postmenopausal women.
Cancer Epidemiol Biomarkers Prev 2003, 12:573-577. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
27.   Oh K, Willett WC, Fuchs CS, Giovannucci EL: Glycemic index, glycemic load, and carbohydrate intake in relation to risk of distal colorectal adenoma in women.
Cancer Epidemiol Biomarkers Prev 2004, 13:1192-1198. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
28.   Terry PD, Jain M, Miller AB, Howe GR, Rohan TE: Glycemic load, carbohydrate intake, and risk of colorectal cancer in women: a prospective cohort study.
J Natl Cancer Inst 2003, 95:914-916. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
29.   Hu FB, Manson JE, Liu S, Hunter D, Colditz GA, Michels KB, Speizer FE, Giovannucci E: Prospective study of adult onset diabetes mellitus (type 2) and risk of colorectal cancer in women.
J Natl Cancer Inst 1999, 91:542-547. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
30.   Khaw KT, Wareham N, Bingham S, Luben R, Welch A, Day N: Preliminary communication: glycated hemoglobin, diabetes, and incident colorectal cancer in men and women: a prospective analysis from the European prospective investigation into cancer-Norfolk study.
Cancer Epidemiol Biomarkers Prev 2004, 13:915-919. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
31.   Saydah SH, Platz EA, Rifai N, Pollak MN, Brancati FL, Helzlsouer KJ: Association of markers of insulin and glucose control with subsequent colorectal cancer risk.
Cancer Epidemiol Biomarkers Prev 2003, 12:412-418. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
32.   Platz EA, Hankinson SE, Rifai N, Colditz GA, Speizer FE, Giovannucci E: Glycosylated hemoglobin and risk of colorectal cancer and adenoma (United States).
Cancer Causes Control 1999, 10:379-386. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
33.   Schoen RE, Tangen CM, Kuller LH, Burke GL, Cushman M, Tracy RP, Dobs A, Savage PJ: Increased blood glucose and insulin, body size, and incident colorectal cancer.
J Natl Cancer Inst 1999, 91:1147-1154. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
34.   Colangelo LA, Gapstur SM, Gann PH, Dyer AR, Liu K: Colorectal cancer mortality and factors related to the insulin resistance syndrome.
Cancer Epidemiol Biomarkers Prev 2002, 11:385-391. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
35.   Coughlin SS, Calle EE, Teras LR, Petrelli J, Thun MJ: Diabetes mellitus as a predictor of cancer mortality in a large cohort of US adults.
Am J Epidemiol 2004, 159:1160-1167. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
36.   La Vecchia C, Negri E, Decarli A, Franceschi S: Diabetes mellitus and colorectal cancer risk.
Cancer Epidemiol Biomarkers Prev 1997, 6:1007-1010. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
37.   Sandhu MS, Luben R, Khaw KT: Self reported non-insulin dependent diabetes, family history, and risk of prevalent colorectal cancer: population based, cross sectional study.
J Epidemiol Community Health 2001, 55:804-805. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
38.   Anderson KE, Anderson E, Mink PJ, Hong CP, Kushi LH, Sellers TA, Lazovich D, Folsom AR: Diabetes and endometrial cancer in the Iowa women's health study.
Cancer Epidemiol Biomarkers Prev 2001, 10:611-616. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
39.   Calle EE, Murphy TK, Rodriguez C, Thun MJ, Heath CW Jr: Diabetes mellitus and pancreatic cancer mortality in a prospective cohort of United States adults.
Cancer Causes Control 1998, 9:403-410. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
40.   Slattery ML, Curtin KP, Edwards SL, Schaffer DM: Plant foods, fiber, and rectal cancer.
Am J Clin Nutr 2004, 79:274-281. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
41.   Bingham SA, Hughes R, Cross AJ: Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response.
J Nutr 2002, 132:3522S-3525S. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
42.   Chen J, Stampfer MJ, Hough HL, Garcia-Closas M, Willett WC, Hennekens CH, Kelsey KT, Hunter DJ: A prospective study of N-acetyltransferase genotype, red meat intake, and risk of colorectal cancer.
Cancer Res 1998, 58:3307-3311. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
43.   Fernandez E, La Vecchia C, D'Avanzo B, Negri E, Franceschi S: Risk factors for colorectal cancer in subjects with family history of the disease.
Br J Cancer 1997, 75:1381-1384. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
44.   Franceschi S, Favero A, La Vecchia C, Negri E, Conti E, Montella M, Giacosa A, Nanni O, Decarli A: Food groups and risk of colorectal cancer in Italy.
Int J Cancer 1997, 72:56-61. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
45.   Fung T, Hu FB, Fuchs C, Giovannucci E, Hunter DJ, Stampfer MJ, Colditz GA, Willett WC: Major dietary patterns and the risk of colorectal cancer in women.
Arch Intern Med 2003, 163:309-314. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
46.   Giovannucci E, Stampfer MJ, Colditz G, Rimm EB, Willett WC: Relationship of diet to risk of colorectal adenoma in men.
J Natl Cancer Inst 1992, 84:91-98. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
47.   Giovannucci E, Rimm EB, Stampfer MJ, Colditz GA, Ascherio A, Willett WC: Intake of fat, meat, and fiber in relation to risk of colon cancer in men.
Cancer Res 1994, 54:2390-2397. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
48.   Hsing AW, McLaughlin JK, Chow WH, Schuman LM, Co Chien HT, Gridley G, Bjelke E, Wacholder S, Blot WJ: Risk factors for colorectal cancer in a prospective study among U.S. white men.
Int J Cancer 1998, 77:549-553. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
49.   Hughes R, Pollock JR, Bingham S: Effect of vegetables, tea, and soy on endogenous N-nitrosation, fecal ammonia, and fecal water genotoxicity during a high red meat diet in humans.
Nutr Cancer 2002, 42:70-77. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
50.   Kampman E, Verhoeven D, Sloots L, van 't Veer P: Vegetable and animal products as determinants of colon cancer risk in Dutch men and women.
Cancer Causes Control 1995, 6:225-234. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
51.   Kampman E, Slattery ML, Bigler J, Leppert M, Samowitz W, Caan BJ, Potter JD: Meat consumption, genetic susceptibility, and colon cancer risk: a United States multicenter case-control study.
Cancer Epidemiol Biomarkers Prev 1999, 8:15-24. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
52.   Kato I, Akhmedkhanov A, Koenig K, Toniolo PG, Shore RE, Riboli E: Prospective study of diet and female colorectal cancer: the New York University Women's Health Study.
Nutr Cancer 1997, 28:276-281. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
53.   La Vecchia C, Chatenoud L, Altieri A, Tavani A: Nutrition and health: epidemiology of diet, cancer and cardiovascular disease in Italy.
Nutr Metab Cardiovasc Dis 2001, 11:10-15. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
54.   Le Marchand L, Donlon T, Seifried A, Wilkens LR: Red meat intake, CYP2E1 genetic polymorphisms, and colorectal cancer risk.
Cancer Epidemiol Biomarkers Prev 2002, 11:1019-1024. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
55.   Levi F, Pasche C, La Vecchia C, Lucchini F, Franceschi S: Food groups and colorectal cancer risk.
Br J Cancer 1999, 79:1283-1287. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
56.   Platz EA, Willett WC, Colditz GA, Rimm EB, Spiegelman D, Giovannucci E: Proportion of colon cancer risk that might be preventable in a cohort of middle-aged US men.
Cancer Causes Control 2000, 11:579-588. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
57.   Seow A, Quah SR, Nyam D, Straughan PT, Chua T, Aw TC: Food groups and the risk of colorectal carcinoma in an Asian population.
Cancer 2002, 95:2390-2396. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
58.   Silvester KR, Bingham SA, Pollock JR, Cummings JH, O'Neill IK: Effect of meat and resistant starch on fecal excretion of apparent N-nitroso compounds and ammonia from the human large bowel.
Nutr Cancer 1997, 29:13-23. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
59.   Singh PN, Fraser GE: Dietary risk factors for colon cancer in a low-risk population.
Am J Epidemiol 1998, 148:761-774. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
60.   Sinha R, Chow WH, Kulldorff M, Denobile J, Butler J, Garcia-Closas M, Weil R, Hoover RN, Rothman N: Well-done, grilled red meat increases the risk of colorectal adenomas.
Cancer Res 1999, 59:4320-4324. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
61.   Slattery ML, Curtin K, Ma K, Edwards S, Schaffer D, Anderson K, Samowitz W: Diet activity, and lifestyle associations with p53 mutations in colon tumors.
Cancer Epidemiol Biomarkers Prev 2002, 11:541-548. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
62.   Thun MJ, Calle EE, Namboodiri MM, Flanders WD, Coates RJ, Byers T, Boffetta P, Garfinkel L, Heath CW Jr: Risk factors for fatal colon cancer in a large prospective study.
J Natl Cancer Inst 1992, 84:1491-1500. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
63.   Tiemersma EW, Kampman E, Bueno de Mesquita HB, Bunschoten A, van Schothorst EM, Kok FJ, Kromhout D: Meat consumption, cigarette smoking, and genetic susceptibility in the etiology of colorectal cancer: results from a Dutch prospective study.
Cancer Causes Control 2002, 13:383-393. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
64.   Willett WC, Stampfer MJ, Colditz GA, Rosner BA, Speizer FE: Relation of meat, fat, and fiber intake to the risk of colon cancer in a prospective study among women.
N Engl J Med 1990, 323:1664-1672. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
65.   Norat T, Lukanova A, Ferrari P, Riboli E: Meat consumption and colorectal cancer risk: dose-response meta-analysis of epidemiological studies.
Int J Cancer 2002, 98:241-256. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
66.   De Stefani E, Ronco A, Mendilaharsu M, Guidobono M, Deneo-Pellegrini H: Meat intake, heterocyclic amines, and risk of breast cancer: a case-control study in Uruguay.
Cancer Epidemiol Biomarkers Prev 1997, 6:573-581. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
67.   London SJ, Sacks FM, Stampfer MJ, Henderson IC, Maclure M, Tomita A, Wood WC, Remine S, Robert NJ, Dmochowski JR: Fatty acid composition of the subcutaneous adipose tissue and risk of proliferative benign breast disease and breast cancer.
J Natl Cancer Inst 1993, 85:785-793. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
68.   Bernard-Gallon DJ, Vissac-Sabatier C, Antoine-Vincent D, Rio PG, Maurizis JC, Fustier P, Bignon YJ: Differential effects of n-3 and n-6 polyunsaturated fatty acids on BRCA1 and BRCA2 gene expression in breast cell lines.
Br J Nutr 2002, 87:281-289. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
69.   Brooks JD, Ward WE, Lewis JE, Hilditch J, Nickell L, Wong E, Thompson LU: Supplementation with flaxseed alters estrogen metabolism in postmenopausal women to a greater extent than does supplementation with an equal amount of soy.
Am J Clin Nutr 2004, 79:318-325. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
70.   Thompson LU, Rickard SE, Orcheson LJ, Seidl MM: Flaxseed and its lignan and oil components reduce mammary tumor growth at a late stage of carcinogenesis.
Carcinogenesis 1996, 17:1373-1376. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
71.   Thompson LU, Seidl MM, Rickard SE, Orcheson LJ, Fong HH: Antitumorigenic effect of a mammalian lignan precursor from flaxseed.
Nutr Cancer 1996, 26:159-165. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
72.   Yan L, Yee JA, Li D, McGuire MH, Thompson LU: Dietary flaxseed supplementation and experimental metastasis of melanoma cells in mice.
Cancer Lett 1998, 124:181-186. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
73.   Li D, Yee JA, Thompson LU, Yan L: Dietary supplementation with secoisolariciresinol diglycoside (SDG) reduces experimental metastasis of melanoma cells in mice.
Cancer Lett 1999, 142:91-96. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
74.   Chen J, Stavro PM, Thompson LU: Dietary flaxseed inhibits human breast cancer growth and metastasis and downregulates expression of insulin-like growth factor and epidermal growth factor receptor.
Nutr Cancer 2002, 43:187-192. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
75.   Tan KP, Chen J, Ward WE, Thompson LU: Mammary gland morphogenesis is enhanced by exposure to flaxseed or its major lignan during suckling in rats.
Exp Biol Med (Maywood) 2004, 229:147-157. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
76.   Chen J, Tan KP, Ward WE, Thompson LU: Exposure to flaxseed or its purified lignan during suckling inhibits chemically induced rat mammary tumorigenesis.
Exp Biol Med (Maywood) 2003, 228:951-958. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
77.   Lin X, Gingrich JR, Bao W, Li J, Haroon ZA, Demark-Wahnefried W: Effect of flaxseed supplementation on prostatic carcinoma in transgenic mice.
Urology 2002, 60:919-924. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
78.   Demark-Wahnefried W, Price DT, Polascik TJ, Robertson CN, Anderson EE, Paulson DF, Walther PJ, Gannon M, Vollmer RT: Pilot study of dietary fat restriction and flaxseed supplementation in men with prostate cancer before surgery: exploring the effects on hormonal levels, prostate-specific antigen, and histopathologic features.
Urology 2001, 58:47-52. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
79.   Brouwer IA, Katan MB, Zock PL: Dietary alpha-linolenic acid is associated with reduced risk of fatal coronary heart disease, but increased prostate cancer risk: a meta-analysis.
J Nutr 2004, 134:919-922. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
80.   Block G, Patterson B, Subar A: Fruit, vegetables, and cancer prevention: a review of the epidemiological evidence.
Nutr Cancer 1992, 18:1-29. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
81.   Steinmetz KA, Potter JD: Vegetables, fruit, and cancer prevention: a review.
J Am Diet Assoc 1996, 96:1027-1039. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2] [3]
 
82.   Fleischauer AT, Poole C, Arab L: Garlic consumption and cancer prevention: meta-analyses of colorectal and stomach cancers.
Am J Clin Nutr 2000, 72:1047-1052. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
83.   Fleischauer AT, Arab L: Garlic and cancer: a critical review of the epidemiologic literature.
J Nutr 2001, 131:1032S-1040S. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
84.   Hsing AW, Chokkalingam AP, Gao YT, Madigan MP, Deng J, Gridley G, Fraumeni JF Jr: Allium vegetables and risk of prostate cancer: a population-based study.
J Natl Cancer Inst 2002, 94:1648-1651. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
85.   Riboli E, Norat T: Epidemiologic evidence of the protective effect of fruit and vegetables on cancer risk.
Am J Clin Nutr 2003, 78:559S-569S. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
86.   Bingham SA, Luben R, Welch A, Wareham N, Khaw KT, Day N: Are imprecise methods obscuring a relation between fat and breast cancer?
Lancet 2003, 362:212-214. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
87.   Joshipura KJ, Ascherio A, Manson JE, Stampfer MJ, Rimm EB, Speizer FE, Hennekens CH, Spiegelman D, Willett WC: Fruit and vegetable intake in relation to risk of ischemic stroke.
Jama 1999, 282:1233-1239. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
88.   Donaldson MS: Food and nutrient intake of Hallelujah vegetarians.
Nutrition & Food Science 2001, 31:293-303. OpenURL
    Return to citation in text: [1] [2]
 
89.   Fowke JH, Chung FL, Jin F, Qi D, Cai Q, Conaway C, Cheng JR, Shu XO, Gao YT, Zheng W: Urinary isothiocyanate levels, brassica, and human breast cancer.
Cancer Res 2003, 63:3980-3986. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
90.   Zhang SM, Hunter DJ, Rosner BA, Giovannucci EL, Colditz GA, Speizer FE, Willett WC: Intakes of fruits, vegetables, and related nutrients and the risk of non-Hodgkin's lymphoma among women.
Cancer Epidemiol Biomarkers Prev 2000, 9:477-485. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
91.   Michaud DS, Spiegelman D, Clinton SK, Rimm EB, Willett WC, Giovannucci EL: Fruit and vegetable intake and incidence of bladder cancer in a male prospective cohort.
J Natl Cancer Inst 1999, 91:605-613. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
92.   Cohen JH, Kristal AR, Stanford JL: Fruit and vegetable intakes and prostate cancer risk.
J Natl Cancer Inst 2000, 92:61-68. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
93.   Kolonel LN, Hankin JH, Whittemore AS, Wu AH, Gallagher RP, Wilkens LR, John EM, Howe GR, Dreon DM, West DW, Paffenbarger RS Jr: Vegetables, fruits, legumes and prostate cancer: a multiethnic case-control study.
Cancer Epidemiol Biomarkers Prev 2000, 9:795-804. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
94.   London SJ, Yuan JM, Chung FL, Gao YT, Coetzee GA, Ross RK, Yu MC: Isothiocyanates, glutathione S-transferase M1 and T1 polymorphisms, and lung-cancer risk: a prospective study of men in Shanghai, China.
Lancet 2000, 356:724-729. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
95.   Fahey JW, Zhang Y, Talalay P: Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens.
Proc Natl Acad Sci U S A 1997, 94:10367-10372. [PubMed Abstract][PubMed Central Full Text] OpenURL
    Return to citation in text: [1]
 
96.   Shapiro TA, Fahey JW, Wade KL, Stephenson KK, Talalay P: Chemoprotective glucosinolates and isothiocyanates of broccoli sprouts: metabolism and excretion in humans.
Cancer Epidemiol Biomarkers Prev 2001, 10:501-508. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
97.   Selenium Information Sheet
[http://www.selenium.arizona.edu/INFOse.htm] OpenURL
    Return to citation in text: [1]
 
98.   Duffield-Lillico AJ, Reid ME, Turnbull BW, Combs GF Jr, Slate EH, Fischbach LA, Marshall JR, Clark LC: Baseline characteristics and the effect of selenium supplementation on cancer incidence in a randomized clinical trial: a summary report of the Nutritional Prevention of Cancer Trial.
Cancer Epidemiol Biomarkers Prev 2002, 11:630-639. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
99.   Clark LC, Combs GF Jr, Turnbull BW, Slate EH, Chalker DK, Chow J, Davis LS, Glover RA, Graham GF, Gross EG, Krongrad A, Lesher JL Jr, Park HK, Sanders BB Jr, Smith CL, Taylor JR: Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. Nutritional Prevention of Cancer Study Group.
Jama 1996, 276:1957-1963. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
100.   Ghadirian P, Maisonneuve P, Perret C, Kennedy G, Boyle P, Krewski D, Lacroix A: A case-control study of toenail selenium and cancer of the breast, colon, and prostate.
Cancer Detect Prev 2000, 24:305-313. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
101.   van den Brandt PA, Goldbohm RA, van't Veer P, Bode P, Dorant E, Hermus RJ, Sturmans F: Toenail selenium levels and the risk of breast cancer.
Am J Epidemiol 1994, 140:20-26. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
102.   Hunter DJ, Morris JS, Stampfer MJ, Colditz GA, Speizer FE, Willett WC: A prospective study of selenium status and breast cancer risk.
Jama 1990, 264:1128-1131. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
103.   van 't Veer P, van der Wielen RP, Kok FJ, Hermus RJ, Sturmans F: Selenium in diet, blood, and toenails in relation to breast cancer: a case-control study.
Am J Epidemiol 1990, 131:987-994. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
104.   van Noord PA, Collette HJ, Maas MJ, de Waard F: Selenium levels in nails of premenopausal breast cancer patients assessed prediagnostically in a cohort-nested case-referent study among women screened in the DOM project.
Int J Epidemiol 1987, 16:318-322. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
105.   Reid ME, Duffield-Lillico AJ, Garland L, Turnbull BW, Clark LC, Marshall JR: Selenium supplementation and lung cancer incidence: an update of the nutritional prevention of cancer trial.
Cancer Epidemiol Biomarkers Prev 2002, 11:1285-1291. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
106.   van den Brandt PA, Goldbohm RA, van 't Veer P, Bode P, Dorant E, Hermus RJ, Sturmans F: A prospective cohort study on selenium status and the risk of lung cancer.
Cancer Res 1993, 53:4860-4865. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
107.   Chernomorsky S, Segelman A, Poretz RD: Effect of dietary chlorophyll derivatives on mutagenesis and tumor cell growth.
Teratog Carcinog Mutagen 1999, 19:313-322. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
108.   Sarkar D, Sharma A, Talukder G: Chlorophyll and chlorophyllin as modifiers of genotoxic effects.
Mutat Res 1994, 318:239-247. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
109.   Egner PA, Wang JB, Zhu YR, Zhang BC, Wu Y, Zhang QN, Qian GS, Kuang SY, Gange SJ, Jacobson LP, Helzlsouer KJ, Bailey GS, Groopman JD, Kensler TW: Chlorophyllin intervention reduces aflatoxin-DNA adducts in individuals at high risk for liver cancer.
Proc Natl Acad Sci U S A 2001, 98:14601-14606. [PubMed Abstract][PubMed Central Full Text] OpenURL
    Return to citation in text: [1]
 
110.   Egner PA, Stansbury KH, Snyder EP, Rogers ME, Hintz PA, Kensler TW: Identification and characterization of chlorin e(4) ethyl ester in sera of individuals participating in the chlorophyllin chemoprevention trial.
Chem Res Toxicol 2000, 13:900-906. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
111.   Nishizawa Y, Yamamoto T, Terada N, Fushiki S, Matsumoto K: Effects of methylcobalamin on the proliferation of androgen-sensitive or estrogen-sensitive malignant cells in culture and in vivo.
Int J Vitam Nutr Res 1997, 67:164-170. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
112.   Nishizawa Y, Goto HG, Tanigaki Y, Fushiki S: Induction of apoptosis in an androgen-dependent mouse mammary carcinoma cell line by methylcobalamin.
Anticancer Res 2001, 21:1107-1110. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
113.   Tsao CS, Myashita K: Influence of cobalamin on the survival of mice bearing ascites tumor.
Pathobiology 1993, 61:104-108. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
114.   Tsao CS, Miyashita K, Young M: Cytotoxic activity of cobalamin in cultured malignant and nonmalignant cells.
Pathobiology 1990, 58:292-296. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
115.   Shimizu N, Hamazoe R, Kanayama H, Maeta M, Koga S: Experimental study of antitumor effect of methyl-B12.
Oncology 1987, 44:169-173. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
116.   Choi SW, Friso S, Ghandour H, Bagley PJ, Selhub J, Mason JB: Vitamin B-12 deficiency induces anomalies of base substitution and methylation in the DNA of rat colonic epithelium.
J Nutr 2004, 134:750-755. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
117.   Wu K, Helzlsouer KJ, Comstock GW, Hoffman SC, Nadeau MR, Selhub J: A prospective study on folate, B12, and pyridoxal 5'-phosphate (B6) and breast cancer.
Cancer Epidemiol Biomarkers Prev 1999, 8:209-217. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
118.   Zhang SM, Willett WC, Selhub J, Hunter DJ, Giovannucci EL, Holmes MD, Colditz GA, Hankinson SE: Plasma folate, vitamin B6, vitamin B12, homocysteine, and risk of breast cancer.
J Natl Cancer Inst 2003, 95:373-380. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
119.   Blount BC, Mack MM, Wehr CM, MacGregor JT, Hiatt RA, Wang G, Wickramasinghe SN, Everson RB, Ames BN: Folate deficiency causes uracil misincorporation into human DNA and chromosome breakage: implications for cancer and neuronal damage.
Proc Natl Acad Sci U S A 1997, 94:3290-3295. [PubMed Abstract][PubMed Central Full Text] OpenURL
    Return to citation in text: [1]
 
120.   Ma J, Stampfer MJ, Giovannucci E, Artigas C, Hunter DJ, Fuchs C, Willett WC, Selhub J, Hennekens CH, Rozen R: Methylenetetrahydrofolate reductase polymorphism, dietary interactions, and risk of colorectal cancer.
Cancer Res 1997, 57:1098-1102. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
121.   Ma J, Stampfer MJ, Christensen B, Giovannucci E, Hunter DJ, Chen J, Willett WC, Selhub J, Hennekens CH, Gravel R, Rozen R: A polymorphism of the methionine synthase gene: association with plasma folate, vitamin B12, homocyst(e)ine, and colorectal cancer risk.
Cancer Epidemiol Biomarkers Prev 1999, 8:825-829. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
122.   Giovannucci E, Chen J, Smith-Warner SA, Rimm EB, Fuchs CS, Palomeque C, Willett WC, Hunter DJ: Methylenetetrahydrofolate reductase, alcohol dehydrogenase, diet, and risk of colorectal adenomas.
Cancer Epidemiol Biomarkers Prev 2003, 12:970-979. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
123.   Le Marchand L, Donlon T, Hankin JH, Kolonel LN, Wilkens LR, Seifried A: B-vitamin intake, metabolic genes, and colorectal cancer risk (United States).
Cancer Causes Control 2002, 13:239-248. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
124.   Cravo ML, Pinto AG, Chaves P, Cruz JA, Lage P, Nobre Leitao C, Costa Mira F: Effect of folate supplementation on DNA methylation of rectal mucosa in patients with colonic adenomas: correlation with nutrient intake.
Clin Nutr 1998, 17:45-49. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
125.   Shrubsole MJ, Jin F, Dai Q, Shu XO, Potter JD, Hebert JR, Gao YT, Zheng W: Dietary folate intake and breast cancer risk: results from the Shanghai Breast Cancer Study.
Cancer Res 2001, 61:7136-7141. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
126.   Holick MF: Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis.
Am J Clin Nutr 2004, 79:362-371. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
127.   Vieth R, Kimball S, Hu A, Walfish PG: Randomized comparison of the effects of the vitamin D3 adequate intake versus 100 mcg (4000 IU) per day on biochemical responses and the wellbeing of patients.
Nutr J 2004, 3:8. [PubMed Abstract][PubMed Central Full Text] OpenURL
    Return to citation in text: [1]
 
128.   Schwartz GG, Whitlatch LW, Chen TC, Lokeshwar BL, Holick MF: Human prostate cells synthesize 1,25-dihydroxyvitamin D3 from 25-hydroxyvitamin D3.
Cancer Epidemiol Biomarkers Prev 1998, 7:391-395. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
129.   Tangpricha V, Flanagan JN, Whitlatch LW, Tseng CC, Chen TC, Holt PR, Lipkin MS, Holick MF: 25-hydroxyvitamin D-1alpha-hydroxylase in normal and malignant colon tissue.
Lancet 2001, 357:1673-1674. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
130.   Friedrich M, Rafi L, Mitschele T, Tilgen W, Schmidt W, Reichrath J: Analysis of the vitamin D system in cervical carcinomas, breast cancer and ovarian cancer.
Recent Results Cancer Res 2003, 164:239-246. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
131.   Schwartz GG, Eads D, Rao A, Cramer SD, Willingham MC, Chen TC, Jamieson DP, Wang L, Burnstein KL, Holick MF, Koumenis C: Pancreatic cancer cells express 25-hydroxyvitamin D-1alpha-hydroxylase and their proliferation is inhibited by the prohormone 25-hydroxyvitamin D3.
Carcinogenesis 2004, 25:1015-1026. [PubMed Abstract] OpenURL
    Epub 2004 Jan 1023.
Return to citation in text: [1] [2]
 
132.   Mawer EB, Hayes ME, Heys SE, Davies M, White A, Stewart MF, Smith GN: Constitutive synthesis of 1,25-dihydroxyvitamin D3 by a human small cell lung cancer cell line.
J Clin Endocrinol Metab 1994, 79:554-560. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
133.   Holt PR, Arber N, Halmos B, Forde K, Kissileff H, McGlynn KA, Moss SF, Kurihara N, Fan K, Yang K, Lipkin M: Colonic epithelial cell proliferation decreases with increasing levels of serum 25-hydroxy vitamin D.
Cancer Epidemiol Biomarkers Prev 2002, 11:113-119. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
134.   Barreto AM, Schwartz GG, Woodruff R, Cramer SD: 25-Hydroxyvitamin D3, the prohormone of 1,25-dihydroxyvitamin D3, inhibits the proliferation of primary prostatic epithelial cells.
Cancer Epidemiol Biomarkers Prev 2000, 9:265-270. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
135.   Sunlight, Nutrition And Health Research Center
[http://www.sunarc.org] OpenURL
    Return to citation in text: [1]
 
136.   Hanchette CL, Schwartz GG: Geographic patterns of prostate cancer mortality. Evidence for a protective effect of ultraviolet radiation.
Cancer 1992, 70:2861-2869. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
137.   Lefkowitz ES, Garland CF: Sunlight, vitamin D, and ovarian cancer mortality rates in US women.
Int J Epidemiol 1994, 23:1133-1136. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
138.   Gorham ED, Garland FC, Garland CF: Sunlight and breast cancer incidence in the USSR.
Int J Epidemiol 1990, 19:820-824. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
139.   Grant WB: Ecologic studies of solar UV-B radiation and cancer mortality rates.
Recent Results Cancer Res 2003, 164:371-377. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
140.   Grant WB: An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation.
Cancer 2002, 94:1867-1875. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
141.   Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, Belanger C, LaMotte F, Gaziano JM, Ridker PM, Willett W, Peto R: Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease.
N Engl J Med 1996, 334:1145-1149. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
142.   Omenn GS, Goodman GE, Thornquist MD, Balmes J, Cullen MR, Glass A, Keogh JP, Meyskens FL, Valanis B, Williams JH, Barnhart S, Hammar S: Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease.
N Engl J Med 1996, 334:1150-1155. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
143.   The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group
N Engl J Med 1994, 330:1029-1035. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
144.   Schuurman AG, Goldbohm RA, Brants HA, van den Brandt PA: A prospective cohort study on intake of retinol, vitamins C and E, and carotenoids and prostate cancer risk (Netherlands).
Cancer Causes Control 2002, 13:573-582. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
145.   Hsing AW, Comstock GW, Abbey H, Polk BF: Serologic precursors of cancer. Retinol, carotenoids, and tocopherol and risk of prostate cancer.
J Natl Cancer Inst 1990, 82:941-946. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
146.   Giovannucci E, Ascherio A, Rimm EB, Stampfer MJ, Colditz GA, Willett WC: Intake of carotenoids and retinol in relation to risk of prostate cancer.
J Natl Cancer Inst 1995, 87:1767-1776. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
147.   Giovannucci E, Rimm EB, Liu Y, Stampfer MJ, Willett WC: A prospective study of tomato products, lycopene, and prostate cancer risk.
J Natl Cancer Inst 2002, 94:391-398. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
148.   Wu K, Erdman JW Jr, Schwartz SJ, Platz EA, Leitzmann M, Clinton SK, DeGroff V, Willett WC, Giovannucci E: Plasma and dietary carotenoids, and the risk of prostate cancer: a nested case-control study.
Cancer Epidemiol Biomarkers Prev 2004, 13:260-269. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
149.   Gann PH, Ma J, Giovannucci E, Willett W, Sacks FM, Hennekens CH, Stampfer MJ: Lower prostate cancer risk in men with elevated plasma lycopene levels: results of a prospective analysis.
Cancer Res 1999, 59:1225-1230. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
150.   Kucuk O, Sarkar FH, Sakr W, Djuric Z, Pollak MN, Khachik F, Li YW, Banerjee M, Grignon D, Bertram JS, Crissman JD, Pontes EJ, Wood DP Jr: Phase II randomized clinical trial of lycopene supplementation before radical prostatectomy.
Cancer Epidemiol Biomarkers Prev 2001, 10:861-868. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
151.   Bowen P, Chen L, Stacewicz-Sapuntzakis M, Duncan C, Sharifi R, Ghosh L, Kim HS, Christov-Tzelkov K, van Breemen R: Tomato sauce supplementation and prostate cancer: lycopene accumulation and modulation of biomarkers of carcinogenesis.
Exp Biol Med (Maywood) 2002, 227:886-893. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
152.   Fletcher AE, Breeze E, Shetty PS: Antioxidant vitamins and mortality in older persons: findings from the nutrition add-on study to the Medical Research Council Trial of Assessment and Management of Older People in the Community.
Am J Clin Nutr 2003, 78:999-1010. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
153.   Lee KW, Lee HJ, Surh YJ, Lee CY: Vitamin C and cancer chemoprevention: reappraisal.
Am J Clin Nutr 2003, 78:1074-1078. [PubMed Abstract] OpenURL
    Return to citation in text: [1]
 
154.   Padayatty SJ, Sun H, Wang Y, Riordan HD, Hewitt SM, Katz A, Wesley RA, Levine M: Vitamin C pharmacokinetics: implications for oral and intravenous use.
Ann Intern Med 2004, 140:533-537. [PubMed Abstract] OpenURL
    Return to citation in text: [1] [2]
 
155.   Riordan HD, Hunninghake RB, Riordan NH, Jackson JJ, Meng X, Taylor P, Casciari JJ, Gonzalez MJ, Miranda-Massari JR, Mora EM, Rosario N, Rivera A: Intravenous ascorbic acid: protocol for its application and use.
P R Health Sci J 2003, 22:287-290. [PubMed Abstract] OpenURL
   

http://www.fonteine.com/antikanker_dieet.html

Ginseng for Pancreatitis

Pancreatitis is characterized by inflammation of pancreas. Diet regulation and increase in fluid intake to rejuvenate pancreas should cure mild cases of pancreatitis. But if the ailment turns worse, it may lead to formation of gallstones, impairing normal functioning of the pancreas.

Pancreas is responsible for insulin and glycogen secretions that regulate the blood sugar level in the body. It also secretes certain digestive enzymes that are essential for digestion. Improper functioning of the pancreas may lead to pancreatic diseases like pancreatitis and improper production of pancreatic enzymes which can adversely affect functioning of the body in several ways. Regular cleansing of the body to rejuvenate pancreas can avoid pancreatitis and can stimulate insulin secretion by the pancreas.

The Chinese herb ginseng, especially the Korean variety is a natural rejuvenator of pancreas. Regular intake of Korean Ginseng can gradually lessen the damage to the pancreas caused by pancreatitis.

Testimonials

I was released from the hospital with the diagnosis of pancreatitis/pseudocyst. The pseudocyst was five centimeters at the time I was discharged. The doctors gave me pain medication and enzymes to help digest the food I ate.
I wanted to learn more about pancreatitis. I went to ILHWA & Co. to see what I could do to help myself. After I explained my illness, you then told me what I needed to do. I started on ginseng tea, Aloe Vera, DC-1, and the Internal Cleansing Program's diet for the first week as you indicated.
Within a couple of days the pain started lessening. After the first week I began the whole Internal Cleansing Program. I also incorporated some of my own herbal products.
When I was in my fifth week of cleansing, I had another CAT scan done. The results were negative, the five centimeter pseudocyst was entirely gone. I am now in the sixth week of cleansing and feel that I am still making progress.
Thanks to ILHWA and its staff, I am well on the road to recovery.
Yours truly,
Mark E. Hughes


In May I had surgery to repair a bile duct obstruction. It was during that surgery that a cancerous growth was discovered on my pancreas. Pancreatic cancer is one of the worse kinds of cancer. The oncologist told me that I have 3 months to live without chemo and 9 months if I have chemo. Needless to say, for me and my wife this was terrible news.
The day after I was released from the hospital I walked into your store. You happened to be there and explained to me your Internal Cleansing Program. I began Level 1 immediately. I also began chemo therapy two weeks later. Here's what happened. Last month the oncologist told me that my blood work looked so good that he felt that chemo could be stopped. I just got this month's blood work result. Here's what the doctor said: "As good as last month was, this month looks even better!" He added, saying: "Whatever you are doing, keep doing it."
In more than one way, ILHWA I can say that I am feeling just great!
Thank you very much for all of your guidance.
Sincerely,
Philip Longbrake
Columbus, Ohio

http://www.ilhwakoreanginseng.com/ginseng_for_pancreatitis.html

Bij gebruik van veel natuurlijke vitamines kun je kanker voorkomen.
In veel gevallen kun je kanker natuurlijk blokkeren, met de juiste natuurlijke middelen.

Voedingsstoffen en borstkanker: 32 vrouwen in de leeftijd van 32 tot 81 jaar met borstkanker kregen, naast de gebruikelijke therapie van o.a. operaties, de volgende dosering vitaminetabletten per dag te slikken: 2850mg vitamine C, 2500ie vitamine E, 32mg bèta caroteen, 387µg selenium, 90mg coënzyme Q10 plus nog een multivitaminetablet en een behoorlijke doses teunisbloem- en EPA visolie. De vooruitzichten voor deze vrouwen waren niet al te best aangezien er uitzaaiingen waren in de lymfklieren. Na 18 maanden bleek

dat niemand was overleden (het verwachte aantal was vier)
dat bij geen van de patiënten de kanker zich verder had uitgezaaid
de kwaliteit van het leven was verbeterd (geen gewichtsverlies en minder gebruik van pijnstillers)
bij zes patiënten er gedeeltelijke remissie was opgetreden waaronder de enige twee die nog 300mg extra coënzyme Q10 per dag hadden genomen..
Deze Deense, niet 'dubbelblinde', studie is enkele jaren oud maar we hebben er nu pas een gedetailleerde beschrijving van gevonden in (Encyclopedia of Nutritional Supplements-M.T. Murray, 1996)

Selenium en prostaatkanker: De bewijzen dat een tekort aan het mineraal selenium de belangrijkste risicofactor voor het krijgen van prostaatkanker is stapelen zich op. In een Amerikaans onderzoek werd het seleniumgehalte van de teennagel van 181 mannen met gevorderde prostaatkanker vergeleken met 181 soortgelijke mensen zonder deze ziekte. De mensen werden voor wat betreft het seleniumgehalte in 5 groepen verdeeld. Gecorrigeerd naar andere bekende risicofactoren zoals het vóórkomen in de familie, bleek dat de groep met de hoogste seleniuminname (geschat circa 160µg per dag) 65% minder risico hadden gelopen op het krijgen van gevorderde prostaatkanker dan mensen met de laagste inname (circa 86µg per dag). (The Lancet, 1998)

Dit percentage is bijna hetzelfde als het percentage minder gevallen van deze ziekte bij inname van 200µg selenium extra bij het onderzoek beschreven op pagina 16 van de catalogus. Overigens werd de gemiddelde inname van selenium in Nederland ooit geschat op 53µg per dag.

Koreaanse Ginseng en kanker: Aan 4634 Koreanen werd het ginsenggebruik opgeschreven. Na vijf jaar werd gekeken of er een verband was met het aantal kankergevallen. Onder de ginsenggebruikers kwam 60% minder kanker voor dan onder de niet-gebruikers. Vooral maagkanker (67%) en longkanker (70%) kwam minder voor. Onderverdeeld naar de verschillende soorten Koreaanse Ginseng (verse, witte (ook in onze tabletten) en rode) vond men geen belangrijke verschillen. Wel was de hoeveelheid van belang. Gezien de aard van het onderzoek - de korte duur en het ontbreken van nadere informatie omtrent andere gewoonten en het vóórkomen van kanker in Korea - kunnen er geen al te grote conclusies uit dit onderzoek getrokken worden. (Ortho, 1998)

Vitaminen en blaaskanker: De helft van zestig blaaskankerpatiënten kreeg na behandeling 40000i.e. vitamine A, 100mg vitamine B6, 2000mg vitamine C en 400i.e. vitamine E per dag te slikken. De andere dertig kregen maar 5000i.e. vitamine A, 2mg vitamine B6, 60mg vitamine C en 30i.e. vitamine E per dag extra. Na vijf jaar bleek 43% van de hooggedoseerde vitaminegroep opnieuw een kankergezwel te hebben gekregen. In de laaggedoseerde groep was dit percentage echter 80%. De opzet van dit onderzoek bewijst dat positieve effecten van vitaminen bij kanker niet veroorzaakt worden door het wegwerken van eventuele ernstige tekorten maar dat hoge doses nodig zijn. Overigens zullen veel deskundigen van mening zijn dat de gegeven doses nog veel te laag was. (Orthomoleculair Jaarboek, 1996)

Vitamine C en maagkanker: Diverse studies wijzen op een bescherming van vitamine C tegen maagkanker. In de zeven landen studie, waarbij van 12000 personen uit zeven landen de voedingsgewoonten werden geanalyseerd, vond men een verband tussen een lage vitamine C inname en een grotere kans op het krijgen van deze ziekte.

We hebben al eerder gezien dat extra vitamine C schade aan het DNA kon verminderen bij mensen met gastritis en dat mensen geïnfecteerd met de bacterie Helicobacter Pylori (veroorzaakt maagzweer) zeer lage gehaltes van deze vitamine in de maag hebben. Dit is ook het geval bij andere maagaandoeningen. Mensen die lijden aan deze kwalen hebben een grotere kans op het krijgen van maagkanker. (Orthomoleculair Jaarboek, 1996 en 1997; Nieuwsoverzicht 3)

Bescherming tegen blaaskanker: U weet al dat hoge doses vitamine A, B6, C en E de vooruitzichten voor blaaskankerpatiënten aanmerkelijk kan verbeteren.

De laatste tijd zijn enkele studies verschenen die licht werpen op de vraag welke factoren de kans op het krijgen van deze ziekte kunnen vergroten of verkleinen. Het binnenkrijgen van zogenaamde aromatische amines blijkt een belangrijke oorzaak van blaaskanker te zijn Deze stoffen worden gevormd bij verbranding. De belangrijkste bronnen zijn sigarettenrook, gefrituurd voedsel en hard gebakken vlees.

Het veel eten van groene groente en van fruit en het slikken van multivitaminen, vitamine A, C, E en selenium blijken het risico op het krijgen van blaaskanker te verkleinen. Hiervan zijn voor het slikken van minstens 500mg vitamine C per dag gedurende tien jaar de sterkste bewijzen. Dit zou volgens een Amerikaans onderzoek de kans op het krijgen van de ziekte met een percentage dat moet liggen tussen 24 en 79% verkleinen. Verder lijkt het veel drinken van water - vooral bij vrouwen - ook bescherming te bieden. (Orthomoleculaire Koerier, 1997; Orthomoleculair Jaarboek, 1997)


Visolie en vermagering bij kanker: Uit verschillende onderzoeken blijkt dat visolie het gewichtsverlies bij kanker tegengaat. In Nederland is een onderzoek gestart om o.m. vast te stellen wat de gewenste dosering is. In een Amerikaans onderzoek met alvleesklierkanker patiënten bleek circa 7 capsules een stabiliserend effect te hebben. Overigens blijkt uit eerdere studies dat het eten van vis of visoliecapsules enige bescherming biedt tegen het ontstaan van kanker. (Haagsche Courant, 1997; Journal of Nutrition 1999)

Vitamine E en kanker: Epidemiologische studies wijzen op een bescherming van vitamine E tegen kanker, met name van het spijsverteringskanaal. We hebben hier al eerder over bericht. Toch nog even de laatste studie: 444 dikke darmkankerpatiënten werden vergeleken met 427 anderen. Degenen die gedurende 10 jaar 200ie vitamine E per dag hadden ingenomen hadden 57% minder risico gelopen op het krijgen van deze ziekte. Voor multivitaminegebruikers was dit percentage 50%. De resultaten waren gecorrigeerd voor gewicht, lichaamsbeweging en alcohol-, vezel-, en vitaminegehalte van de voeding. (The Lancet, 1997)

http://www.kankerpatient.net/viewtopic.php?f=7&t=1041&start=165

chemotherapie - gezonde voeding - het geheim om af te vallen en een betere weerstand te krijgen
 


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Chemotherapie, risico's  en voeding


Na de diagnose kanker is stap 2 vaak chemotherapie. Een echt paardenmiddel waarbij ook de gezonde cellen flink er van langs gaan krijgen is het raadzaam uw lichaam gezond te houden door gezonde voeding zodat u de schade misschien voor een deel kan beperken. Verdiep u goed in de risico's en voordelen van chemotherapie. Sylvia Millecam weigerde een reguliere behandeling en moest dit met de dood bekopen. Wat het verhaal nog treuriger maakt is dat haar artsen worden gemangeld terwijl het toch echt haar eigen keuze was.

Als een patiënt overlijdt terwijl die wel een chemo heeft gevolgd dan is dit een doodnormale zaak zonder gevolgen voor de behandelaars. Maar goed, we zitten in een land waar de reguliere artsen lijnrecht staan tegen alternatieve artsen en we zullen ons dus zelf moeten verdiepen in de behandelmethodes en risico's daarvan en dan een keuze maken. Ik weet dat veel patiënten die regulier behandelt worden daarnaast ook alternatieve wegen volgen en dit niet aan hun arts durven te vertellen omdat deze niet openstaat voor andere visies en mogelijkheden.

En als je nog geen kanker heeft lees dan alles over voeding die een rol kan spelen bij de preventie van kanker, er zijn genoeg boeken, websites, forums etc waar u informatie uit kunt halen. Laat het niet zover komen. Roken, alcohol, teveel rood vlees, zware metalen, chemische stoffen in voeding, overschot aan omega 6 etc kunnen allemaal de reden zijn dat ook u aan de beurt komt. Eet gevarieerd, vermijdt industrie voer, eet zo vers mogelijk, zorg voor voldoende omega 3 zuren, vermijdt verbrande plantaardige olie en vlees en blijf uit de buurt van rokers, meeroken kan ook dodelijk zijn. Alleen in Engeland overlijden al 16000 mensen per jaar aan het meeroken.

Ron


Chemotherapy can do more harm than good, study suggests

A study of more than 600 cancer patients who died within 30 days of receiving treatment, chemotherapy probably caused or hastened death in 27 per cent of cases, the inquiry found.

Link


Support for adjunctive vitamin C treatment in cancer

Serious flaws in a recent study, which concluded that high doses of vitamin C reduce the effectiveness of chemotherapeutic drugs in the treatment of cancer, are revealed in the current issue of Alternative and Complementary Therapies, a journal published by Mary Ann Liebert, Inc. (www.liebertpub.com). This report is available free online at www.liebertpub.com/act

In the Medical Journal Watch column of the latest issue, Jack Challem, a personal nutrition coach and nutrition author from Tucson, Arizona, and a regular contributor to the Journal, challenges the findings of a study published in Cancer Research (2008;68:8031-8038), in which the authors conclude that vitamin C given to mice or cultured cells treated with common anti-cancer drugs reduces the antitumor effects of the chemotherapeutic agents.

Challem points out two main problems with the study: the oxidized form of vitamin C (dehydroascorbic acid) and not actual vitamin C (ascorbic acid) was used; and in the mouse experiments, the animals were given toxic doses of dehydroascorbic acid, a compound that is not used as a dietary supplement in humans. "This study and the subsequent headlines [it generated] were a grievous disservice to physicians and patients with cancer," says Challem. He adds that "considerable positive research…has shown striking benefits from high-dose vitamin C (ascorbic acid) in cancer cells and animals—and in actual human beings."

High-dose intravenous vitamin C is a common form of alternative and complementary therapy for patients receiving chemotherapeutic drugs and is believed to help bring about tumor cell death. In addition, it may promote postsurgical healing by enhancing collagen formation, and increase tissue resistance to tumor spread. Challem suggests that, "The ideal therapeutic approach would be to tailor individual treatment, including IV vitamin C, from a menu of options."


Lorraine Day's strijd tegen kanker mbv natuurlijke middelen

Beste Ron

Ik ben een trouwe lezer van je website, en met veel plezier lees ik de interessante zaken die je aan de orde stelt.  Je vroeg om nieuwe artikelen en links over kanker, en deze wil ik je sturen. Het gaat om een Amerikaanse arts, Lorraine Day, die helemaal hersteld is van borstkanker door natuurlijke middelen. Zij weet als geen ander (omdat zij zelf arts is) hoe belastend en desastreus de "normale" medicijnen zoals chemotherapie en bestraling zijn. Zij wilde deze dus niet gebruiken. Hoe zij genezen is vertelt zij in deze film! Ik vond de film een eye-opener.

Veel leesplezier!

Bekijk de site

Tip: Titia van der Kloet


De schade aan de hersenen en zenuwgestel veroorzaakt door chemo in kaart gebracht

Researchers Detail Chemotherapy's Damage to the Brain

A commonly used chemotherapy drug causes healthy brain cells to die off long after treatment has ended and may be one of the underlying biological causes of the cognitive side effects – or “chemo brain” – that many cancer patients experience. That is the conclusion of a study published today in the Journal of Biology.

A team of researchers at the University of Rochester Medical Center (URMC) and Harvard Medical School have linked the widely used chemotherapy drug 5-fluorouracil (5-FU) to a progressing collapse of populations of stem cells and their progeny in the central nervous system.

“This study is the first model of a delayed degeneration syndrome that involves a global disruption of the myelin-forming cells that are essential for normal neuronal function,” said Mark Noble, Ph.D., director of the University of Rochester Stem Cell and Regenerative Medicine Institute and senior author of the study. “Because of our growing knowledge of stem cells and their biology, we can now begin to understand and define the molecular mechanisms behind the cognitive difficulties that linger and worsen in a significant number of cancer patients.”

Cancer patients have long complained of neurological side effects such as short-term memory loss and, in extreme cases, seizures, vision loss, and even dementia. Until very recently, these cognitive side effects were often dismissed as the byproduct of fatigue, depression, and anxiety related to cancer diagnosis and treatment. Now a growing body of evidence has documented the scope of these conditions, collectively referred to as chemo brain. And while it is increasingly acknowledged by the scientific community that many chemotherapy agents may have a negative impact on brain function in a subset of cancer patients, the precise mechanisms that underlie this dysfunction have not been identified.

Virtually all cancer survivors experience short-term memory loss and difficulty concentrating during and shortly after treatment. A study two years ago by researchers with the James P. Wilmot Cancer Center at the University of Rochester showed that upwards of 82 percent of breast cancer patients reported that they suffer from some form of cognitive impairment.

While these effects tend to wear off over time, a subset of patients, particularly those who have been administered high doses of chemotherapy, begin to experience these cognitive side effects months or longer after treatment has ceased and the drugs have long since departed their systems. For example, a recent study estimates that somewhere between 15 percent and 20 percent of the nation's 2.4 million female breast cancer survivors have lingering cognitive problems years after treatment. Another study showed that 50 percent of women had not recovered their previous level of cognitive function one year after treatment.

Two years ago, Noble and his team showed that three common chemotherapy drugs used to treat a wide range of cancers were more toxic to healthy brain cells than the cancer cells they were intended to treat. While these experiments were among the first to establish a biological basis for the acute onset of chemo brain, they did not explain the lingering impact that many patients experience.

The scientists conducted a similar series of experiments in which they exposed both individual cell populations and mice to doses of 5-fluorouracil (5-FU) in amounts comparable to those used in cancer patients. 5-FU is among a class of drugs called antimetabolites that block cell division and has been used in cancer treatment for more than 40 years. The drug, which is often administered in a “cocktail” with other chemotherapy drugs, is currently used to treat breast, ovarian, stomach, colon, pancreatic and other forms of cancer.

The researchers discovered that months after exposure, specific populations of cells in the central nervous – oligodendrocytes and dividing precursor cells from which they are generated – underwent such extensive damage that, after six months, these cells had all but disappeared in the mice.

Oligodendrocytes play an important role in the central nervous system and are responsible for producing myelin, the fatty substance that, like insulation on electrical wires, coats nerve cells and enables signals between cells to be transmitted rapidly and efficiently. The myelin membranes are constantly being turned over, and without a healthy population of oligodendrocytes, the membranes cannot be renewed and eventually break down, resulting in a disruption of normal impulse transmission between nerve cells.

These findings parallel observations in studies of cancer survivors with cognitive difficulties. MRI scans of these patients’ brains revealed a condition similar to leukoencephalopathy. This demyelination – or the loss of white matter – can be associated with multiple neurological problems.

“It is clear that, in some patients, chemotherapy appears to trigger a degenerative condition in the central nervous system,” said Noble. “Because these treatments will clearly remain the standard of care for many years to come, it is critical that we understand their precise impact on the central nervous system, and then use this knowledge as the basis for discovering means of preventing such side effects.”

Noble points out that not all cancer patients experience these cognitive difficulties and determining why some patients are more vulnerable may be an important step in developing new ways to prevent these side effects. Because of this study, researchers now have a model which, for the first time, allows scientists to begin to examine this condition in a systematic manner.

Other investigators participating in the study include Ruolan Han, Ph.D., Yin M. Yang, M.D., Anne Luebke, Ph.D., Margot Mayer-Proschel, Ph.D., all with URMC, and Joerg Dietrich, M.D., Ph.D., formerly with URMC and now with Harvard Medical School. The study was funded by the National Institutes of Neurological Disorders and Stroke, the Komen Foundation for the Cure, and the Wilmot Cancer Center.


Chemotherapy Kills 27% of Sick Patients; Doctors Urged to Stop Killing People with Chemo

A UK report is warning doctors about the consequences of using chemotherapy on sick cancer patients, citing new data that reveals chemotherapy kills 27% of those patients. I never thought I'd see the day that researchers from the world of conventional medicine actually admit the truth about chemotherapy: It's a toxic, poisonous therapy better suited for barbaric torture than anything resembling the healing arts. The cancer industry is a grand fraud, and it kills millions of people with chemotherapy, radiation and surgical procedures that do nothing to address the root causes of cancer.

Lees verder

Marjan


Chemotherapy Doesn't Work, So Blame Vitamin C

When Memorial Sloan-Kettering Cancer Center announces that vitamin C may interfere with chemotherapy, the news media trumpet it far and wide. But before cancer patients throw away their vitamin C supplements, they need to know rest of the story.

Lees artikel

Leendert


DO en DON'T DO during chemotherapy

Chemotherapie en bestraling zijn zware aanslagen op het lichaam.Een aantal voedingssoorten, supplementen en je levensstijl kunnen de therapie beter laten werken, je weerstand verbeteren en meer energie geven. Een groot aantal voedingsmiddelen zijn wetenschappelijk onderzocht en hebben eigenschappen die celdood van kankercellen veroorzaken of en resistentie van kankercellen tegen cytostatica, target medicijnen en bestraling aanzienlijk verlagen.

http://www.chemotherapy-support.com/

Tip: Elmer Pennewaard   


Het falen van de chemotherapie

Dr. Giuseppe Nacci

Elke vorm van chemotherapie veroorzaakt onherstelbare schade aan de fysieke gesteldheid van wie zich blootstelt aan de werking van deze vergiften die ‘cytotoxische geneesmiddelen’ worden genoemd. De eed van Hippocrates omvat het verbod om de patiënt ‘gif’ toe te dienen, ook indien de zieke hier zelf om vraagt (zie eed van Hippocrates). Deze vergiften (‘cytotoxische geneesmiddelen’) komen in de bloedbaan door middel van een injectie en/of een intraveneus druppelinfuus, of door middel van indirecte opname via de maag of het darmslijmvlies. Dit type behandeling wijkt af van chirurgie of bestraling, die hun werking richten op specifieke punten of gebieden van het menselijke lichaam (‘gerichte’ behandelingen).

In ziekenhuizen wordt gebruik gemaakt van chemotherapie wanneer de kans bestaat dat de tumorcellen aanwezig zijn in andere delen van het organisme en niet alleen op de plaats van de primaire tumor.
Maar slechts zelden garandeert chemotherapie een overlevingsperiode van ten minste vijf jaar, die onjuist wordt aangeduid als ‘behandelingsperiode’. Chemotherapie remt de abnormale celgroei tijdelijk af, of kan de pijn enige tijd verlichten of de overlevingstijd iets verlengen. Slechts zelden kan er worden gesproken van ‘remissie’: bibliografische gegevens spreken van slagingspercentages van minder dan 1% in het geval van alvleesklierkanker, van 3% in het geval van leverkanker en van 7% in het geval van darmkanker…..In de hele wereld zijn er ongeveer 60-70 cytotoxische geneesmiddelen in de
handel.

Voor Italië zijn de handelsnamen opgenomen in tabel 2a (gedeeltelijke lijst). Enkele van deze vergiften veroorzaken minder problemen dan andere, zoals slapeloosheid, verzwakking, diarree, haaruitval, stomatitis, leukopenie, trombocytopenie, bloedarmoede, misselijkheid, overgeven enz. Dit zijn de directe bijwerkingen die bekend zijn, omdat ze zichtbaar zijn. Waar zelden over wordt gesproken, zijn de ernstigere en langdurigere bijwerkingen met gevolgen die het leven van de patiënt en het verloop van zijn of haar ziekte sterk verslechteren, waardoor zelfs behandelingen op basis van de immunostimulering van de Natural Killer-lymfocyten en van de apoptotische en ontgiftende activiteit van medische plantenextracten zinloos worden.

Deze grote en onherstelbare schade, waarover zelden wordt gesproken, bestaat uit:

1) ernstige, aanhoudende en duurzame reductie van het aantal van bepaalde typen en subtypen witte bloedlichaampjes die onmisbaar zijn voor de specifieke immuunreactie tegen de tumor.
2) celmutaties van het somatische type waarbij andere secundaire tumoren en/of metastasen verdwijnen
3) celmutaties van het germinale type (testikels of eierstokken) met verschijnselen van onvruchtbaarheid, miskramen of misvormde kinderen bij een ouder die chemotherapie en kanker heeft overleefd.
4) versnelde groei van de tumor, in plaats van reductie daarvan, met verschijnselen van kruisresistentie van de tumor tegen andere vergiften (membraan glycoproteïnepomp).

Chemotherapie wordt dus absoluut afgeraden bij elke vorm van combinatiemet immunotherapie.

Lees verder op:
http://www.curenaturalicancro.nl/pdf/falen-chemotherapie.pdf


De big pharma censuur op wikipedia

Goed voorbeeld van iemand die kritisch kijkt naar de kankerindustrie maar die wordt geblocked op wikipedia, de zogenaamde onpartijdige encyclopedie. Je ziet in Nederland dezelfde censuur bij big pharma clubs als de KWF die elke alternatieve visie op kanker en genezing van kanker afdoen als kwakzalverij. Hierbij gesteund door de antikwakjes. Steun je de KWF dan steun je dus de propaganda machine en zullen veel mensen onnodig sterven doordat ze geen keuze hebben naast chemotherapie of bestraling. We hebben recht op de andere kant van het verhaal en artsen/specialisten die de waarheid durven te vertellen. Een ziek lijf nog zieker maken is geen genezen maar echte kwakzalverij....de focus moet zijn het sterker maken van de eigen afweer en aanpak van toxines die worden gestapeld en DNA schade veroorzaken. Of gelooft u dat alles in de laatste 50 jaar een erfelijke oorzaak heeft?
Onmogelijk in zo'n korte periode, er is veel meer aan de hand en de grootste ziekmaker is dezelfde industrie die kankermiddelen maakt. Zo verdien je dus aan twee kanten.....

Kijk hieronder maar eens hoe ver het establishment gaat om de massa dom te houden, we zouden toch eens andere keuzes gaan maken !

Ron

The cancer industry, described in books by Ralph Moss and Samuel Epstein, now seeks to exercise the same censorship and suppression on the Internet. Wikipedia represents a media outlet that could get outside the cancer industry’s control and embarrass the medical profession. Very strong influences will be therefore be brought to bear to ensure that this doesn’t happen. Jfdwolff and others who seek to suppress this information, unwittingly represents those interests. I represent those who believe there should be an ongoing debate about one of the world’s greatest killers: what it is and how it should be treated. I believe that this debate should be based on scientific principles so that vested interests cannot be assumed to have a monopoly on the truth.

My credentials: As a scientist I have published two papers: One in 1993 questioning the efficacy of cancer surgery; and one in 1996 questioning the claim that mammograms reduce overall mortality. The conclusion from my 1996 paper in Medical Hypotheses was confirmed in 2001 by the Nordic Cochrane Group that specialises in evidence based medicine. For the past 25 years I have been Convenor of a Sydney-based charity called the Cancer Information & Support Society that provides people with cancer with objective information about the benefits and harm from cancer therapies and emotional support to those who choose to use them. We evaluate the efficacy of both orthodox and alternative cancer therapies.

The medical skeptics Leading medical scientists and researchers who question the current paradigm to some degree or other, and whom I quote in my articles, include the following:

Ulrich Abel, epidemiologist and biostatistician at the Heidelberg Tumor Centre, Germany. Author of “Chemotherapy of Advanced Epithelial Cancer: a critical review”.

John Bailar, former US presidential adviser on cancer, former chair of the Department of Health Studies, University of Chicago, former editor of the Journal of the National Cancer Institute (JNCI), former professor of epidemiology and biostatistics at McGill University in Montreal, Chair of the Department of Health Studies at the University of Chicago. Author of “Cancer Undefeated” in the New England Journal of Medicine.

Michael Baum, Emeritus Professor of Surgery at University College, London, former pioneer and advocate of mammography screening in the UK. Author of “False premises, false promises and false positives--the case against mammographic screening for breast cancer” in the International Journal of Epidemiology.

William Black, Department of Radiology, Dartmouth–Hitchcock Medical Center, Lebanon, NH, and Center for the Evaluative Clinical Sciences, Department of Community and Family Medicine, Dartmouth Medical School, Hanover, NH. Author of “Overdiagnosis: An Underrecognized Cause of Confusion and Harm in Cancer Screening” in JNCI.

Barry W. Brown, Chief, Section of Computer Science, University of California at Berkeley; Larry and Pat McNeil Professor of Biomathematics, specialising in the mathematical modeling of cancer processes. Author of “Non-cancer deaths in White Adult Cancer Patients” in JNCI.

David M. Eddy, Senior Advisor for Health Policy and Management, Kaiser Permanente Medical Care Program, Pasadena, California. Former Professor at Stanford University, former J. Alexander McMahon Professor of health policy and management at Duke University. Author of “The Use of Evidence and Cost Effectiveness by the Courts: How Can It Help Improve Health Care?”

Ralph Moss, author of “The Cancer Industry”, “Cancer Therapy” and Questioning Chemotherapy”.

Candace Pert, microbiologist, discoverer of receptors on the brain for endorphins. Author of “Molecules of Emotion”.

Gilbert Welch, Professor of Medicine and Community and Family Medicine, Dartmouth Medical School; Co-Director of the VA Outcomes Group. Author of “Should I Be Tested for Cancer?” and “Dangers in Early Detection".

http://en.wikipedia.org/wiki/Wikipedia:Mediation_Cabal/Cases/2006-01-29_Cancer_evidence


75% van de artsen weigert zelf chemotherapie

Uit onderzoeken en enquêtes onder Amerikaanse oncologen komt naar voren dat drie van de vier artsen (75%) elke vorm van chemotherapie zou weigeren vanwege de ondoeltreffendheid en de vernietigende effecten die deze behandeling heeft op het menselijke organisme. Dit zeggen de artsen en onderzoekers erover:

“Het grootste deel van de kankerpatiënten in dit land overlijdt ten gevolge van chemotherapie, die tumoren in de borst, in het colon of in de longen niet wegneemt. Dit aspect is al ruim een decennium lang bekend en toch gebruiken artsen chemotherapie nog steeds ter bestrijding van deze tumoren.”

Allen Levin, MD (UCSF ‘The healing of Cancer, Marcus Books 1990)

 

Most cancer patients in this country die of chemotherapy. Chemotherapy does not eliminate breast, colon or lung cancers. The fact has been documented for over a decade.... Women with breast cancer are likely to die faster with chemotherapy than without it.” (Dr. Alan Levin, Professor of Immunology, University of California Medical School, 1987)

Dr. John Cairns says that chemotherapy at most prevents “perhaps 2% or 3%” of the cancer deaths each year. If 19 you have been diagnosed with cancer, find out if your type will be hurt or helped by chemotherapy. (See Resources)

Ulrich Abel, Ph.D., of West Germany, did a comprehensive study on chemotherapy. In 1990 he wrote, “There is no evidence for the vast majority of cancers that treatment with these drugs exerts any positive influence on survival or quality of life in patients with advanced disease.” He stated that although chemotherapy does shrink tumors initially in many patients, unfortunately this did not prolong survival because the cancer usually returned, often more aggressively than at first. In Abel’s poll of hundreds of cancer doctors worldwide, he discovered that many oncologists would not take chemotherapy themselves if they had cancer. Publicity about Abel’s research was completely suppressed in the U.S. (So much for freedom of speech in the media.)

The great lack of trust is evident even amongst doctors. Polls and questionnaires show that three doctors out of four (75 per cent) would refuse any chemotherapy because of its ineffectiveness against the disease and its devastating effects on the entire human organism. This is what many doctors and scientists have to say about chemotherapy:“The majority of the cancer patients in this country die because of chemotherapy, which does not cure breast, colon or lung cancer. This has been documented for over a decade and nevertheless doctors still utilize chemotherapy to fight these tumors.” (Allen Levin, MD, UCSF, “The Healing of Cancer”, Marcus Books, 1990).

“If I were to contract cancer, I would never turn to a certain standard for the therapy of this disease. Cancer patients who stay away from these centers have some chance to make it.” (Prof. Gorge Mathe, “Scientific Medicine Stymied”, Medicines Nouvelles, Paris, 1989)

“Dr. Hardin Jones, lecturer at the University of California, after having analyzed for many decades statistics on cancer survival, has come to this conclusion: ‘… when not treated, the patients do not get worse or they even get better’. The unsettling conclusions of Dr. Jones have never been refuted”. (Walter Last, “The Ecologist”, Vol. 28, no. 2, March-April 1998)

“Many oncologists recommend chemotherapy for almost any type of cancer, with a faith that is unshaken by the almost constant failures”.(Albert Braverman, MD, “Medical Oncology in the 90s”, Lancet, 1991, Vol. 337, p. 901)

“Our most efficacious regimens are loaded with risks, side effects and practical problems; and after all the patients we have treated have paid the toll, only a miniscule percentage of them is paid off with an ephemeral period of tumoral regression and generally a partial one” (Edward G. Griffin “World Without Cancer”, American Media Publications, 1996)

“After all, and for the overwhelming majority of the cases, there is no proof whatsoever that chemotherapy prolongs survival expectations. And this is the great lie about this therapy, that there is a correlation between the reduction of cancer and the extension of the life of the patient”. (Philip Day, “Cancer: Why we’re still dying to know the truth”, Credence Publications, 2000)

“Several full-time scientists at the McGill Cancer Center sent to 118 doctors, all experts on lung cancer, a questionnaire to determine the level of trust they had in the therapies they were applying; they were asked to imagine that they themselves had contracted the disease and which of the six current experimental therapies they would choose. 79 doctors answered, 64 of them said that they would not consent to undergo any treatment containing cis-platinum – one of the common chemotherapy drugs they used – while 58 out of 79 believed that all the experimental therapies above were not accepted because of the ineffectiveness and the elevated level of toxicity of chemotherapy.” (Philip Day, “Cancer: Why we’re still dying to know the truth”, Credence Publications, 2000)


Oncologists Must be Stopped from Using Children for Experimentation

For example, the so-called "state-of-the-art" chemo protocol that the oncologists had administered to our son had proven its ineffectiveness in pediatric brain tumors many years before. In fact, in 1994, the exact same chemo drugs Alexander received in 1998 had been administered to children the same age with the same brain tumor (medulloblastoma) as Alexander. This experiment proved so unsuccessful that tumors spread within five months and the oncologists terminated the protocol. It was incredible to us to discover that chemotherapy that had already proven so ineffective that it required termination was being presented to parents as "state of the art" years later. We were never informed about the failure of this therapy. We also discovered that we weren't the only parents being purposefully misinformed. Today, parents are still being misled and children with brain cancer are still getting these same toxic drugs that have proven their ineffectiveness in the past. But even if you are informed that orthodox therapy does not work you still may not have a choice. When we hesitated to bring Alexander in for chemo the oncologists were already gearing up to take him from us by court order.

http://www.ouralexander.org/


Chemotherapy linked to lasting brain change

The baseline level of brain activity (indicated by yellow and orange) in the frontal cortex is higher in patients who have not undergone chemotherapy (Image: Dan Silverman, UCLA)  The side effects of chemotherapy linger in the brain for at least a decade following treatment – it may explain why many patients complain of cognitive difficulties years later, new research suggests. The study on breast cancer patients pinpoints changes in brain metabolism that might account for patients’ memory problems and difficulty in doing more than one thing at a time.

Chemotherapy involves powerful chemical compounds which prevent cancer from spreading or slows its process. But a quarter of patients complain of “chemo brain” – a condition that describes a sense of reduced mental capacities, or lack of focus. One recent study suggests as many as 82% of patients are affected. The effects are relatively subtle, says Daniel Silverman at the David Geffen School of Medicine at the University of California, Los Angeles, US. “People are not going from an IQ of 120 to 80.” But the changes are real, he adds: “Typically you’ll see a patient who says ‘I can’t multitask like I used to’.”

Memory tests

Silverman and colleagues recruited 21 women who had undergone surgery to remove breast cancer, 16 of whom had received chemotherapy for the disease five to 10 years before the study.  Subjects completed tasks that tested their short-term memory as a machine recorded blood flow to regions of their brain, using a scanning technique known as positron emission tomography (PET scanning). Greater blood flow to a region indicates a higher rate of metabolism – more activity – in those brain cells. Researchers compared the brain activity of these participants to that of 13 healthy controls. Patients who had received chemotherapy had reduced rates of metabolism in specific regions of the frontal cortex – an area involved in memory recall – compared to the controls.

Toxic effects

The women whose scans revealed more abnormalities in brain metabolism, were the ones that preformed worst in the short-term memory test, the researchers found. The toxic effects of the cancer treatment – either directly or indirectly – damages brain cells and reduces their function, Silverman says. He suggests that closer monitoring of patiwents’ brain response to chemotherapy could allow doctors to adjust treatment to avoid causing “chemo brain”.


Boek - Questioning Chemotherapy - Ralph W. Moss

Equinox Press
ISBN 188102525X

I started as a believer in chemotherapy. As a science writer at Memorial Sloan-Kettering Cancer Center in New York, I wrote articles praising the latest advances in chemotherapy. I was impressed by the then-emerging cures for Hodgkin's disease, acute lymphocytic leukemia and some other relatively rare cancers. At the same time, I began to learn how skeptical many good scientists were about chemotherapy's future.

The major objection to "chemo" was that these drugs did not discriminate between normal and cancerous cells, but attacked all rapidly dividing cells . One scientist described this method as "trying to melt a patient's left ear , while leaving the right one alone." It seemed particularly inappropriate in the treatment of solid tumors of adults, which are often slow-growing.

Because chemotherapy drugs were general cellular poisons, they could be terribly toxic. They were also very expensive for patients and for society as a whole. When I learned about the links between the pharmaceutical industry and the cancer establishment (later detailed in my book, The Cance r Industry) I understood the commercial reason that such an inadequate modality was so heavily promoted.

In 1989, a German biostatistician named Ulrich Abel, Ph.D. published a groundbreaking monograph called "Chemotherapy of Advanced Epithelial Cancer. It made few waves in the U.S. and soon went out of print. In this excellent work, however, Dr. Abel rigorously demonstrated that chemotherapy had never been scientifically proven to extend life through randomized clinical trials (RCTs) in the vast majority of "epithelial cancers." These are the common types of carcinoma that affect most cancer patients in the Western world.

Some years later, in response to many requests, I decided to write a critical book about chemotherapy (a sort of companion piece to Cancer Therapy). I took Abel's out-of-print work as my starting point, but also consulted the work of many other students of chemotherapy. In this book, I update statistics and speak about all cancers and not just carcinomas. I go into depth on the politics and economics of the chemotherapy industry, on the biases, fallacies and frauds that occur, and on ways of warding off the sometimes catastrophic side effects that accompany this treatment.

The essential point of the book is that one must question the measure of success in chemotherapy. Oncologists have tended to equate an increasing percentage of "responses" with progress. However, responses are generally measurements of tumor shrinkage, for as little as one month's duration. One cannot automatically assume that a response--even a complete response--will lead to increased survival. One must look for increased survival. Yet the number of cancers for which life prolongation through chemotherapy has been proven through randomized clinical trials is very small. (I do bend over backwards to point these out, when they occur.)

So when a doctor says her regimen yields a 40 percent response rate, "what exactly is she promising? A short-term shrinkage of tumors--or actual life-prolongation? What effect is this treatment likely to have on the patient's quality of life? And what is the cost?" It is only by obtaining information such as this that patients are able to make rational treatment choices. Questioning Chemotherapy is intended to help patients by providing them with a critical perspective on this now dominant modality.

http://www.ralphmoss.com/


How much harm does chemotherapy do?

There are three main areas of harm:

· Weakening the body's natural defences

· increasing mortality

· decreasing the quality of life

Weakening the immune system

Chemotherapy has been found to reduce the activity of natural killer cells by 96%8. So if there are tumours growing elsewhere in the body and the immune system helps to control tumour growth, then chemotherapy could make things worse by allowing more rapid growth of other tumours present. However there is little hard evidence from orthodox immunotherapy that the immune system is a major controlling factor. In fact a recent editorial reporting on an immunotherapy conference in Canberra in September 1998 suggests it might be a major factor only in cancers of viral origin9. On the other hand Immuno-Augmentative Therapy as practised at the IAT Clinic in the Bahamas appears to produce between 15 and 18% 5-year survival with late stage cancer patients10. Similarly the Issels Wholebody Therapy produced 16.6% 5-year survival among late-stage cancer patients11. (Expected 5-year survival for late-stage cancer patients using orthodox therapies is less than 2%.) As these two therapies are based on boosting the immune system using natural methods, it appears that that orthodox immunotherapy and alternative immune-boosting techniques must be completely different.

Increasing mortality

By analysing non-cancer deaths among cancer patients it is clear that orthodox therapies often do more harm than good, a phenomenon that helps explain certain claims of apparently effective treatments. (For example cancer treatment can damage the heart and cause deaths from heart failure. This means fewer deaths from cancer.) As there is little evidence that surgery actually causes harm other than temporarily suppressing the immune system8, it would appear that most of the harm is done by radiotherapy and chemotherapy. Analysis of the results of records of 1.2 million cancer cases in the US SEER (Surveillance Evaluation & End Results) database showed that non-cancer deaths accounted for 21% of all deaths. These deaths were in excess of the rate expected for such patients. This excess was observed in all types of cancer with an overall figure of 37%. The excess ranged from 9% for breast cancer to 173% for lung cancer12. During the year following diagnosis this excess was about 5 times higher, so it ranged from about 50% for breast cancer to about 800% for lung cancer. The authors attributed this effect to the damage caused by cancer treatment (presumably mainly radiotherapy and chemotherapy).

Decreasing the quality of life

There is no shortage of evidence that chemotherapy usually causes a serious reduction in the quality of life. The only question is whether or not the worsening in the quality of life is justified in view of the very limited claimed increased survival.

http://www.ciss.org.au/documents/chemo2.html

REFERENCES

Moss, RW. Questioning Chemotherapy. Equinox Press, New York 1995.
Lilleyman, JS. Childhood leukemia, The facts. OUP, Oxford, 1994.
Enstrom, JE & Austin, DF. Interpreting cancer survival rates. Science 1977; 195: 847-851.
Peto, J & Easton, D. Cancer treatment trials – past failures, current progress and future prospects. Cancer Surv 1989; 8: 513-533.
Benjamin, DJ. The efficacy of surgical treatment of cancer. Medical Hypotheses 1993; 40 (2): 129-138.
Abel, U. Chemotherapy of advanced epithelial cancer: a critical review. Biomedicine & Pharmacotherapy 1992; 46: 439-452.
Bross, ID. NEJM 1994; 331: 809.
Beitsch, P et al. Natural immunity in breast cancer patients during neoadjuvant chemotherapy and after surgery. Surgical Oncology 1994; 3 (4): 211-219.
Goodnow, CC. Editorial. MJA 1998; 169: 570.
Walters, R. Options, The Alternative Cancer Therapy Book, Avery Publishing, New York, 1993.
Issels, J. Immunotherapy in Progressive Metastatic Cancer - A Fifteen-Year Follow-up. Clinical Trials Journal, August 1970: 357-365 with editorial on pp 355-356.
Brown, Barry W et al. Non-cancer deaths in White Adult Cancer Patients. JNCI 1993; 85 (12): 979-987.
Chemotherapy Report, Do we need a new approach to cancer? Burzynski Research Institute Home Page, http://www.cancermed.com/chemo.htm.
McKillop, WJ, et al. The use of expert surrogates to evaluate clinical trials in non-small cell lung cancer. Br J Cancer 1986; 54: 661-667.
Hansen, HH. Advanced non-small-cell lung cancer: To treat or not to treat? J Clin Oncol 1987; 5: 1711-12.
Anonym. Ein gnadenloses Zuviel an Therapie. Teil I. Zweifel an den chemischen Waffen. Der Spiegel, 1987; 26, 128-47.
Moore, MJ, Tannock, IF. How expert physicians would wish to be treated if they developed genito-urinary cancer. Abstract No. 455. Proc. Amer. Soc. Clin. Oncol. 1988; 7: 118.
Holli, K, Hakama, M. Treatment of the terminal stages of breast cancer. BMJ. (Jan 7) 1989); 298(6665):13-14.
Bailar JC & Gornik HL. Cancer Undefeated. NEJM 1997; 336 (22): 1569-1574.


German magazine Der Spiegel blasts chemotherapy

While I was in Germany last October an article on chemotherapy appeared in Der Spiegel, which is Germany's - in fact Europe's - highest-circulating news magazine. On average, over one million copies are sold every week, making it the German equivalent of Time or Newsweek. The article, highly critical of chemotherapy, created quite a stir. Der Spiegel, which has a history of being iconoclastic, has criticized the cancer establishment before. In the early 1990s it gave ample coverage to a critical report from Heidelberg epidemiologist Ulrich Abel, PhD, showing that chemotherapy was ineffective in the treatment of advanced carcinomas. (It was Abel's book that first inspired me to write Questioning Chemotherapy.) The latest article shows that for patients in the advanced stages of the major forms of cancer, chemotherapy has no appreciable effect on survival. This will come as no surprise to long-time readers of this newsletter. But the Spiegel article comes at a time when the pharmaceutical industry is already reeling from revelations of price gouging and the suppression of research data that indicated life-threatening side effects from some of its best-selling drugs. It follows a similarly hard-hitting exposé last spring in the American news magazine, Fortune. Perhaps such widely circulated articles will lead to a public outcry or at least to a changed perception of the value of chemotherapy—a treatment method that normally goes unquestioned in the mainstream media.

http://www.cancerdecisions.com/011605_page.html


Chemo veroorzaakt vertraagde zware schade aan het centrale zenuwgestel

Cancer treatment with chemotherapeutic agents is often associated with delayed adverse neurological consequences - an occurrence often referred to as “chemobrain” - that may compromise the quality of life of a proportion of cancer survivors. Now, research published in the open access Journal of Biology demonstrates that treatment with a single chemotherapeutic agent, 5-fluorouracil (5-FU), by itself is sufficient to cause a syndrome of delayed degeneration in the central nervous system (CNS). 5-FU is a widely used chemotherapeutic agent that is employed, alone or in combination with other agents, in the treatment of cancers of the colon, rectum, breast, stomach, pancreas, ovaries and bladder. Little is known about the side-effects of chemotherapy on the CNS, despite their obvious clinical importance. Until now researchers have not fully understood the underlying biology, including whether these effects require: exposure to multiple chemotherapeutic agents; chemotherapeutic agents plus the body’s own response to cancer; blood-brain barrier damage; or inflammation. Clinicians have also lacked animal models to study this important problem.

Professor Mark Noble and colleagues of the University of Rochester Stem Cell and Regenerative Medicine Institute and the Harvard Medical School, Boston discovered that short-term systemic administration of 5-FU to mice caused both acute CNS damage and a syndrome of progressively worsening delayed damage. This damage was not self-repairing, and instead became worse over time. In addition, Noble and colleagues also demonstrated that treatment with chemotherapy also had delayed effects on the speed with which information is transferred from the ear to the brain. Myelin sheaths are necessary for normal neuronal function. One key finding of the study was that clinically relevant concentrations of 5-FU were toxic not only for dividing cells of the CNS but also for the cells that produce the insulating myelin sheaths (non-dividing oligodendrocytes). The delayed damage the researchers measured was to the myelinated tracts of the CNS and associated with extensive myelin pathology. The findings regarding the speed of ear-to-brain information transfer may offer a non-invasive means of analyzing myelin damage associated with cancer treatment.

“Multiple clinical reports have identified neurotoxicity as a complication of treatment regimens in which chemotherapeutic agents such as 5-fluorouracil are components,” says Noble. “As treatments with chemotherapeutic agents will clearly remain the standard of care for cancer patients for many years to come, the need to better understand such damage is great.” Professor Noble continues “These studies extend the field of stem cell medicine beyond the use of cell transplantation for tissue repair. It is our knowledge of stem cell biology that allows us to begin to understand some of the causes of this syndrome, as well as providing the means of preventing or repairing this damage.” This research provides the first demonstration that delayed CNS damage can be induced by a single chemotherapeutic agent and also generates the first animal model of such damage. These studies further demonstrate that this syndrome differs from that caused by irradiation and thus may represent a new class of delayed CNS degenerative damage.

http://jbiol.com/press/noble.pdf
http://www.urmc.rochester.edu/pr/news/story.cfm?id=1963


Bij borstkanker minder chemo nodig

Duizenden borstkankerpatiënten krijgen chemo terwijl ze dat bespaard zou kunnen blijven. Dit blijkt uit Amerikaans onderzoek.

http://www.nu.nl/news/1355708/151/rss/Bij_borstkanker_minder_chemo_nodig.html


Gezondheidsrisico's van beroepsmatige blootstelling aan chemotherapie

Bij de huidige blootstellingsniveaus heeft ongeveer 50% van de populatie oncologieverpleegkundigen een verhoogd risico op een verlengde tijd tot zwangerschap vergeleken met niet-blootgestelde verpleegkundigen en ongeveer 10% heeft een verhoogd risico op een vroeggeboorte of het krijgen van een kind met een te laag geboortegewicht.

http://www.abc.uu.nl/newsagenda/news/october/
promotiesoct/43275main.html


Bijwerkingen bestraling genetisch bepaald

Sommige kankerpatiënten lijken op basis van hun erfelijke kenmerken extra gevoelig voor de bijwerkingen van de therapeutische bestraling. Dat blijkt uit een publicatie van onderzoekers uit het Leids Universitair Medisch Centrum (LUMC), het Academisch ziekenhuis in Uppsala (Zweden) en het Academisch Medisch Centrum (AMC) in Amsterdam. De onderzoekers kunnen een relatie leggen tussen de activiteit van groepen genen, en de kans dat een patiënt na bestraling ernstige, chronische bijwerkingen ondervindt.

http://www.amc.nl/index.cfm?sid=221&contentitemid=125&itemid=95


Chemotherapie verandert de werking van de hersenen

Volgens Dr. Daniel Silverman van de David Geffen School of Medicine (UCLA) verandert de werking en doorbloeding van de hersenen tot wel 10 jaar na de chemo behandeling. Dit verklaart ook de problemen van veel kankerpatiënten die na de bestraling geheugenproblemen hebben, niet kunnen focussen of niet meer meerdere dingen tegelijk kunnen doen.

http://healthsciences.ucla.edu/news/


Foute voeding in ziekenhuizen

Eén op de vier mensen in Europa overlijdt aan kanker. Veel soorten kanker zijn mede ontstaan door een ongezonde manier van leven ("lifestyle-choices)". Gewoonten als roken, alcohol drinken, ongezonde voeding, onverstandig zonnen, veel stress en blootstelling aan toxische stoffen (diesel, lood, kwik, cadmium) kunnen allen bijdragen aan een verhoogde kans op kanker. Als een bepaalde levensstijl kanker kan bevorderen zou je verwachten dat patiënten bij de behandeling ook adviezen krijgen in het kiezen van een gezondere manier van leven en dat er meer aandacht aan preventie wordt gegeven. Helaas is er nog nauwelijks effect van preventieve maatregelen te merken. Er wordt zeer ongezond gegeten, veel mensen hebben tekorten aan vitaminen en mineralen en het aantal vrouwen dat rookt is de laatste jaren alleen maar toegenomen. Bovendien blijft de commercie ons bestoken met reclames om aan te tonen hoe fijn het is om vlees te eten en hoe goed je je voelt door snoep, chips of cola te nuttigen. Zelfs kankerpatiënten krijgen in ziekenhuizen vaak extra vlees, suikerdrankjes en toetjes om aan te sterken voor de komende chemotherapie. En dat terwijl bekend is dat deze middelen ook de groei van tumorcellen stimuleren en dat ze het immuunsysteem onderdrukken.

Meer info hier:

http://www.natuurarts.nl/achemo.htm


Vrouw (40) dood na dubbele bestralingdosis

Ernstige berekeningsfouten bij de bestraling van een kankergezwel, blijken begin vorige maand het leven te hebben gekost van een 40-jarige vrouw uit Hoek van Holland.

http://www.telegraaf.nl/binnenland/53704071/Vrouw_(40)_
dood_na_br___dubbele_bestralingdosis.html?p=5,1

 

Lieve Astrid
wat heb je een pijn gehad. Maar die pijn is nu voorbij. Wat heb je geknokt. Maar je heb het gevecht verloren. De kanker was weg, maar de arstsen hebben je verziekt. Laat dit een les zijn voor de Daniel de Hoed kliniek.

Voor jou ging het sterven niet ineens Je hebt er moedig voor gestreden.
Niemand kan weten wat jij heb gevoelt. 
En ook niet wat je hebt geleden.
Waarom zijn er zoveel vragen.
Waarom is er zoveel pijn
Waarom zijn er zoveel dingen
Die niet te begrijpen zijn

http://joycedekorte.web-log.nl/joycedekorte/2006/10/dag_lieve_as_ru.html
http://joycedekorte.web-log.nl/joycedekorte/2006/11/vandaag_in_de_t.html


Chemotherapie heeft nadelig effect op botgroei en –sterkte

Steeds meer kinderen genezen van kanker, maar het is nog onduidelijk wat op latere leeftijd de gevolgen zijn van de behandeling. Barbara van Leeuwen onderzocht bij proefdieren wat het effect is op de groei van het skelet van drie bij kinderen veelgebruikte chemotherapeutische middelen. Ze ontdekte dat de botten zwakker zijn en sneller breken, en dat het gehele skelet kleiner blijft. Van Leeuwen promoveerde op 14 mei 2003 in de medische wetenschappen.

Onderzoekers hebben de afgelopen jaren met name onderzocht wat de nadelige effecten van bestraling zijn voor kinderen. Dit kan leiden tot cognitieve problemen en een verstoring van de hormoonbalans. Ook van bepaalde chemotherapeutica werd bekend dat er op de lange duur ongewenste bijwerkingen zijn, onder andere voor het hart en de nieren.

Drie tegenwoordig bij kinderen veelgebruikte chemotherapeutische middelen zijn doxorubicine, methotrexaat en cisplatinum. Van Leeuwen testte deze drie bij ratten in de groei en onderzocht de gevolgen voor het skelet. Chemotherapeutica remmen de celdeling. Dat is gewenst voor tumorcellen, maar ook de cellen in gezonde weefsels reageren op deze middelen. Vooral voor kinderen is dit nadelig omdat ze nog in de groei zijn. Bij een behandeling krijgen kankerpatiënten vaak een combinatie van verschillende middelen. Om duidelijk te krijgen welk middel welke nadelen heeft, testte Van Leeuwen de chemotherapeutica afzonderlijk. Methotrexaat en vooral doxorubicine blijken de lengtegroei te remmen; cisplatinum heeft hierop geen effect. Ook de met de behandeling gepaard gaande verminderde eetlust en de ondervoeding die daar het gevolg van is, blijkt bij te dragen aan een groeiachterstand. Vervolgens stelt de promovendus vast dat een afname van de botsterkte door alle drie de middelen wordt veroorzaakt. De buigweerstand blijkt te verminderen, waardoor de botten sneller breken. Tot slot onderzocht Van Leeuwen welke verandering er optreedt in het breukpatroon van de groeischijf. /ImK

Barbara van Leeuwen (Capelle a/d IJssel, 1971) studeerde geneeskunde in Rotterdam. Ze verrichtte haar promotieonderzoek bij de basiseenheid Chirurgische oncologie van de RUG. Het onderzoek is gefinancierd door Stichting Kinderoncologie Groningen (SKOG). Momenteel is Van Leeuwen assistent geneeskunde in opleiding bij de afdeling Heelkunde van het Academisch Ziekenhuis Groningen.

Bron: Universiteit Groningen


Beperken van bijwerkingen chemotherapie dikkedarmkanker

Bij chemotherapie is het belangrijk om de, vaak ernstige, nadelige effecten van de medicatie te voorkomen, beperken en behandelen. Frank Jansman onderzocht hoe de behandeling van dikkedarmkanker met chemotherapie optimaler kan zijn en stelt dat de ziekenhuisapotheker hierin een grotere rol kan spelen. Op basis van Jansmans onderzoek kan de ziekenhuisapotheker betere individuele doseerschema's en medicatiedoses bepalen.

De promovendus pleit er onder meer voor om de dosis niet alleen te berekenen op basis van het lichaamsoppervlak van de patiënt, maar meer individuele factoren in overweging te nemen. Van verschillende soorten medicijnen bracht hij in kaart welke factoren de bijwerkingen kunnnen beïnvloeden. Dit gaat om vele factoren zoals leeftijd, geslacht en conditie of lage aantallen witte bloedcellen en nierfunctiestoornissen. Verder maakte de promovendus een overzicht van maatregelen ter preventie of verlichting van bijwerkingen waarmee de ziekenhuisapotheker een bijdrage aan de behandelrichtlijn kan leveren.

Interacties tussen chemotherapeutica en andere geneesmiddelen kunnen bijwerkingen veroorzaken en de effectiviteit hinderen, maar toch wordt in de praktijk nauwelijks rekening gehouden met interacties. Jansman inventariseerde daarom geneesmiddelen-interacties met drie soorten chemotherapie (5-fluorouracil, irinotecan en oxaliplatin), waarmee in de praktijk ten onrechte geen rekening wordt gehouden. Tot slot bepaalde hij dat een nieuw, oraal te gebruiken middel (capecitabine) kostenbesparend is ten opzichte van het het intraveneus toegediende 5-fluorouracil.

Frank Jansman (Zwolle, 1966) studeerde farmacie in Groningen. Hij verrichtte zijn hoofdonderzoek in de Isala klinieken te Zwolle (en bepaalde aspecten ook in de ziekenhuizen van Leeuwarden, Enschede, Arnhem en Nijmegen) met wetenschappelijke begeleiding van de onderzoekschool GUIDE en de Basiseenheid Farmacotherapie en Farmaceutische Patiëntenzorg van de Rijksuniversiteit Groningen. Het onderzoek is deels gefinancierd door de Isala klinieken (zorgvernieuwingsproject) en de Koninklijke Nederlandse Maatschappij ter bevordering der Pharmacie (KNMP). Jansman is verbonden als ziekenhuisapotheker aan de Isala klinieken te Zwolle. Hij volgt daar nog de opleiding voor klinisch farmacoloog.

Bron: Universiteit Groningen


Waarom is het risico op hart- en vaatziekten verhoogd na zaadbalkanker?

Testiskanker is een goed te genezen vorm van kanker. De behandeling van uitgezaaide testiskanker bestaat uit het verwijderen van het aangedane testikel en chemotherapie. De bijwerkingen worden soms pas jaren later zichtbaar. Zo heeft deze groep mannen na tien jaar een grotere kans op de ontwikkeling van hart- en vaatziekten dan mannen in de rest van de bevolking.

Janine Nuver deed onderzoek naar de ontwikkeling van deze complicaties en zocht naar de oorzaken. Ze stelt vast dat deze patiënten vaker biochemische stoornissen in hun bloed hebben. Mogelijk verhogen deze stoornissen het risico op slagaderverkalking. Daarnaast blijkt het verwijderen van één testikel en chemotherapie schadelijk te zijn voor de testosteronproductie. Ook dat zou een rol kunnen spelen bij de ontwikkeling van hart- en vaatziekten. De testosteronspiegel van patiënten met verschillende risicofactoren voor hart- en vaatziekten blijkt namelijk lager te zijn dan die van patiënten zonder deze risicofactoren. Tenslotte brengt chemotherapie mogelijk ook direct schade toe aan de bloedvaten.

De promovendus beveelt daarom aan om patiënten na de behandeling periodiek te screenen op risicofactoren voor hart- en vaatziekten.

Janine Nuver (Bedum, 1976) studeerde geneeskunde in Groningen . Ze verrichte haar onderzoek bij de afdeling Medische Oncologie van het Universitair Medisch Centrum Groningen. Het onderzoek is gefinancierd door het Koningin Wilhelmina Fonds / de Nederlandse Kankerbestrijding. Momenteel is Nuver assistent-geneeskundige in opleiding tot internist in het Medisch Centrum Leeuwarden.

Bron: Universiteit Groningen


Overbodige operatie en chemokuur bij slokdarmkanker voorkomen

Patiënten met slokdarmkanker worden soms ten onrechte geopereerd. En niet elke patiënt heeft baat bij chemotherapie. Michiel Heeren ontdekte dat de PET-scan enige uitkomst kan bieden bij het vaststellen van de juiste behandeling.

Een operatie is alleen zinvol als de slokdarmtumor nog niet uitgezaaid is. De gebruikelijke CT-scan weet deze uitzaaiingen echter niet altijd op te sporen. De meer geavanceerde onderzoekstechniek Positron Emissie Tomografie (PET) blijkt in sommige aspecten nauwkeuriger te zijn, constateert Heeren. Toch weet ook de PET-scan in een aantal gevallen geen onderscheid te maken tussen uitzaaiingen, ontstekingen of infecties. Bij een positieve uitslag is aanvullend onderzoek dus aan te bevelen.

Chemotherapie voorafgaand aan een slokdarm-operatie slaat soms niet aan. De kuur vermindert dan de kwaliteit van leven, voegt niets toe aan de levensverwachting en vertraagt een mogelijk zinvolle operatie. Een beoordeling vooraf - op basis van de bepaling van bepaalde tumormarkers - blijft echter lastig, ontdekte Heeren. Door operatief verwijderd tumorweefsel te testen op bepaalde eiwitten, kan wel iets gezegd worden over de prognose na aanvullende chemotherapie.

Heeren onderzocht tevens de voorspellende waarde van het eiwit COX-2, dat betrokken zou zijn bij de vorming van slokdarmtumoren. De aanmaak van dit eiwit blijkt geremd te kunnen worden door bepaalde ontstekingswerende stoffen, zogeheten COX-2 remmers.

Michiel Heeren (Vlissingen, 1967) studeerde medische wetenschappen aan de Vrije Universiteit van Brussel. Hij verrichtte zijn promotieonderzoek bij de afdeling Oncologische Chirurgie van het Universitair Medisch Centrum Groningen. Het onderzoek is deels gefinancierd door de Jan Cornelis de Cock stichting. Momenteel is Heeren werkzaam in het Maaslandziekenhuis te Sittard als oncologisch chirurg.

Bron: Universiteit Groningen


Chemotherapie op maat op basis van je genen

Wetenschappers van de Duke University's Institute for Genome Sciences hebben een serie genen tests ontwikkeld dat de unieke samenstelling van een kankertumor kan analyseren en zodoende kan bepalen welk chemotherapie de sterkste aanval op de kanker kan bieden. De nu gedane tests waren in 80% van de gevallen juist in het voorspellen van de juiste therapie.

http://www.dukemednews.duke.edu/news/article.php?id=9916


Dr. Ulrich Abel analyzed thousands of scientific articles

In 1990, the highly respected German epidemiologist, Dr. Ulrich Abel from the Tumor Clinic of the University of Heidelberg, conducted the most comprehensive investigation of every major clinical study on chemotherapy drugs ever done. Abel contacted 350 medical centers and asked them to send him anything they had ever published on chemotherapy. He also reviewed and analyzed thousands of scientific articles published in the most prestigious medical journals. It took Abel several years to collect and evaluate the data. Abel's epidemiological study, which was published on August 10, 1991 in The Lancet, should have alerted every doctor and cancer patient about the risks of one of the most common treatments used for cancer and other diseases. In his paper, Abel came to the conclusion that the overall success rate of chemotherapy was "appalling." According to this report, there was no scientific evidence available in any existing study to show that chemotherapy can "extend in any appreciable way the lives of patients suffering from the most common organic cancers." Abel points out that chemotherapy rarely improves the quality of life. He describes chemotherapy as "a scientific wasteland" and states that even though there is no scientific evidence that chemotherapy works, neither doctor nor patient is willing to give up on it. The mainstream media has never reported on this hugely important study, which is hardly surprising, given the enormous vested interests of the groups that sponsor the media, that is, the pharmaceutical companies. A recent search turned up exactly zero reviews of Abel's work in American journals, even though it was published in 1990. I believe this is not because his work was unimportant -- but because it is irrefutable.

http://houston.craigslist.org/pol/768479395.html


Linus Pauling - Everyone should know that the “war on cancer” is largely a fraud

Despite the public’s support and growing interest in nontoxic, noninvasive alternative approaches, the medical establishment has waged a fierce campaign against such therapies, labeling them quackery.... Official medicine pours billions of dollars into narrow research supporting chemotherapy, radiation and surgery as the major weapons in ‘the war on cancer.’ That war has been a total failure in slowing the death rate... “‘Everyone should know that the “war on cancer” is largely a fraud,’ wrote Dr. Linus Pauling, two-time Nobel Prize Winner.


ACS (American Cancer Society)

"The field of U.S. cancer care is organized around a medical monopoly that ensures a continuous flow of money to the pharmaceutical companies, medical technology firms, research institutes, and government agencies such as the Food and Drug Administration (FDA) and the National Cancer Institute (NCI) and quasi-public organizations such as the American Cancer Society (ACS)." Dr John Diamond, M.D., & Dr Lee Cowden, M.D.

http://www.encognitive.com/organizations/acs-american-cancer-society-2008-apr-12.html


Are we treating cancer, but killing the patient?

Dr. George J Georgiou, Ph.D.,ND.,D.Sc (AM)

Don't we live in a crazy toxic world! It's unbelievable some of the things that intelligent human beings get up to, destroying their own kind in the name of "medicine!" Read the following paragraph to understand what I mean:

The consultant oncologist picks up the phone angrily and calls his oncologist colleague who has been treating the patient sitting in front of him, “stop all chemotherapy immediately,” he says, “you have completely destroyed her liver which is pretty much irrecoverable!” This is exactly how this patient, who I was seeing for support using natural medicine, told me the story. She has received over 20 courses of chemotherapy and radiation treatment, plus countless surgeries, for a breast cancer that metastized to the bones. Only God knows what her destiny will be!

Download pdf


Massive gene screening points way to more effective chemotherapy

Using a technology that can quickly screen all 20,000-plus human genes for biological activity, scientists have isolated 87 genes that seem to affect how sensitive human cancer cells are to certain chemotherapy drugs.

http://www.utsouthwestern.edu/utsw/cda/dept353744/files/355758.html


Herbs may help beat chemo pain

The agony of side-effects caused by breast cancer drugs could be overcome with Chinese herbal remedies, experts believe. They say medicinal herbs may protect immune systems from the effects of chemotherapy. About 60 per cent of women having chemotherapy for the disease experience side-effects ranging from nausea, vomiting and fatigue to inflammation of the gut lining, a lower blood cell count and a weaker immune system.

http://www.metro.co.uk/news/article.html?in_article_id=45679&in_page_id=34


Researchers find the mechanism by which cells resist chemotherapy

team of researchers from the UAB's Mutagenesis Group, led by Dr Jordi Surrallés, has identified one of the mechanisms used by cancer cells to resist chemotherapy.

In his paper, to be published in The EMBO Jorunal, Dr Surrallés describes how proteins of the Fanconi/BRCA pathway recognise the presence of genetic mutations in order to repair them. The researchers also found that alteration of this mechanism makes tumour cells much more sensitive to certain drugs. This discovery will make it possible to develop strategies to make tumours more vulnerable to chemotherapy.

One of the main mechanisms responsible for repairing mutations in humans is the cancer-suppressing Fanconi anaemia/BRCA pathway. This mechanism makes it possible for the cells to identify genetic mutations in order to correct them.

If this mechanism does not function correctly, it leads to Fanconi anaemia, a rare genetic disorder characterised by progressive bone-marrow failure, various congenital malformations and a very high risk of cancer.

http://www.uab.es/servlet/Satellite?cid=1096476786473&pagename=UAB%2FPage%2
FTemplatePlanaNoticiasDetall&c=Page¬iciaid=1096483204993


Radiation for breast cancer ups heart disease risk

As a treatment for breast cancer, radiation, even modern regimens, appears to increase the risk of cardiovascular disease, according to a report in the Journal of the National Cancer Institute for March 7.Earlier reports have indicated that radiotherapy regimens used in the 1970s elevate heart disease risk, but it has been less clear if more recent regimens also increase the risk.

http://today.reuters.com/news/articlenews.aspx?type=healthNews&storyID=2007-03-07
T030921Z_01_TON711346_RTRUKOC_0_US-RADIATION-BREAST-CANCER.xml&page
Number=0&imageid=&cap=&sz=13&WTModLoc=NewsArt-C1-ArticlePage2


Major discovery raises prospect of better patient care by improving platelet life span

The research team led by Drs Benjamin Kile and David Huang has discovered that platelet life span is controlled by two key molecules. The discovery raises the prospect of developing a new drug to prolong the life span of platelets stored in blood banks, effectively increasing the availability of this life-saving blood product.

An undesirable side effect of cancer chemotherapy is extensive bruising and potentially life-threatening bleeding. This is caused by the unintended depletion of platelets, tiny circulating blood cells that are essential for blood clotting and wound healing. Consequently, the well being of some patients depends upon platelet transfusions, particularly during the vulnerable periods that follow anti-cancer treatment. The significant demand for high quality platelets, coupled with their short shelf life of only five days, presents major logistical challenges in clinical practice.

The scientific team has found that two specialised molecules act in opposition to each other to control platelet life span by regulating the process known as "apoptosis." This term refers to the normal and healthy self destruction of old, damaged and surplus cells. One protein (known as Bcl-xL) acts to preserve the life of the platelet, while the other protein (Bak) prepares the cell to self-destruct after its usual life span within the body - about a week.

WEHI's Dr David Huang said, "Apoptosis is an essential process, common in other cells, but the central role it plays in controlling the life span of the highly specialised platelet has not been previously appreciated. With this new knowledge, we are in a much stronger position to devise better therapies for the management of platelet-related diseases."

Dr Kile added, "For fifty years doctors have speculated about what controls platelet life span. We now know the identity of the precise molecular switch responsible. The team is now actively pursuing a drug development program aimed at manipulating this switch in order to prolong the life span of blood bank platelets, increasing their availability to patients receiving cancer treatment and others in danger of serious bleeding".

At the opposite end of the scale, shortening platelet life span may be useful in the treatment of other diseases. For instance, too many platelets can trigger dangerous blood clots leading to strokes or heart attacks. Reducing platelet life span may therefore prove valuable in the prevention and management of these life-threatening conditions.

http://www.eurekalert.org/pub_releases/2007-03/ra-mdr032007.php


A faster way to recover from chemotherapy and marrow transplant

Researchers at Children's Hospital Boston report finding a practical way to increase stem cells in blood, suggesting a possible treatment to help patients recover from chemotherapy or bone marrow transplant for cancer, regaining immune function more quickly. The discovery, reported in the June 21 Nature and made possible through high-volume drug screening in fish, marks the first time stem-cell production has been induced by a small-molecule drug.

http://www.eurekalert.org/pub_releases/2007-06/chb-afw061407.php


Chemo/radiation therapy may fuel cancer spread

Treating cancer with surgery, chemotherapy or radiation may sometimes cause tumors to spread, researchers say. Tests in mice show that using the chemotherapy drug doxorubicin or radiation both raised levels of TGF-beta, which in turn helped breast cancer tumors spread to the lung. But using an antibody to block TGF-beta stopped the process, Dr. Carlos Arteaga and colleagues at Vanderbilt University in Tennessee have reported. "We'll be looking to see in what proportion of patients the serum and tumor TGF-beta goes up, and whether the increase correlates with the inability of the therapy to eliminate the cancer in the breast," Arteaga said. Higher levels of TGF-beta after treatment may be a way to predict which patients are likely to have their cancer come back after treatment, Arteaga added. TGF-beta, however, is not the only element that is having this effect. Many other compounds, including some immune system signaling chemicals, are also associated with tumor spread and growth. Researchers are also testing drugs that interfere with TGF-beta to see if they improve chances of survival. [Frank]

http://www.presstv.ir/detail.aspx?id=5148§ionid=3510210


Chemotherapy Fog Is No Longer Ignored as Illusion

On an Internet chat room popular with breast cancer survivors, one thread — called “Where’s My Remote?” — turns the mental fog known as chemo brain into a stand-up comedy act. When she can’t remember where she parked her car, Lu Ann Hudson uses a key fob that sets off a beep in it. One woman reported finding five unopened gallons of milk in her refrigerator and having no memory of buying the first four. A second had to ask her husband which toothbrush belonged to her. At a family celebration, one woman filled the water glasses with turkey gravy. Another could not remember how to carry over numbers when balancing the checkbook. [Ben Licher]

http://www.nytimes.com/2007/04/29/health/29chemo.html?ex=1335499200
&en=052308156473c531&ei=5088&partner=rssnyt&emc=rss


Temporary Brain Shrinkage May Explain 'Chemobrain'

The thought-fogging phenomenon known as "chemobrain" appears to be related to a reversible shrinking of brain structures induced by chemotherapy, researchers here have found.

http://www.medpagetoday.com/HematologyOncology/
Chemotherapy/tb/4590


Study says chemotherapy kills healthy brain cells

New research by the University of Rochester Medical Center has found that chemotherapy drugs may be harmful to healthy brain cells. The results, which also indicate that chemotherapy may cause long-term brain damage, represent the closest that scientists have come to pinpointing the underlying cause of "chemo brain," a common side effect of cancer treatment.

http://www.pharmaceutical-business-review.com/article_news.
asp?guid=FC697238-2328-4631-9B81-CE175880C390


Common Cancer Treatments Toxic to Healthy Brain Cells

Common drugs used to treat cancer may be more harmful to healthy brain cells than the cancer cells that they are intended to destroy. That is the conclusion of a study conducted by researchers at the University of Rochester Medical Center and published today in the Journal of Biology. The results, which also indicate that chemotherapy may cause long-term brain damage, represent the closest that scientists have come to pinpointing the underlying physiological cause of “chemo brain,” a common side effect of cancer treatment that scientists are only now beginning to comprehend.

http://www.urmc.rochester.edu/pr/news/story.cfm?id=1312


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Zelfs het kanker instituut is kritisch tegenover chemotherapie. Veel thee drinken om de afvalstoffen te verwijderen wordt hier aangeraden:

http://www.tegenkanker.nl/images/stories/brochures/chemotherapieweb.pdf

You Tube film over kanker en winstbejag

https://www.youtube.com/watch?v=7QD72iiJ8rU&feature=youtu.be

Essiac

From Wikipedia, the free encyclopedia
Jump to: navigation, search

Essiac, marketed as Flor Essence, is an herbal tea promoted as an herbal alternative treatment for cancer and other illnesses.[1] As with many alternative remedies, the exact composition of essiac is unclear, but it reportedly contains burdock, Indian rhubarb, sheep sorrel, and slippery elm bark. Some formulations may also contain watercress, blessed thistle, red clover, and kelp.[2] From the 1920s through the 1970s, essiac was promoted as a cancer treatment by Rene Caisse, a Canadian nurse, who claimed that it had been given to her by a patient and that the recipe derived from an Ontario Ojibwa medicine man.[2] The name is Caisse's surname spelled backwards.

http://en.wikipedia.org/wiki/Essiac

https://www.youtube.com/watch?v=7QD72iiJ8rU&feature=youtu.be

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Gember, h.walnoten, i. zonnebloempitten, j. bosbessen, k.zeewier, l.wortelsap, m.ginkgobiloba,n. guldenroede, o.peu dárco, p. driekleurig | Bijlage 37 a. Aloe Vera | Bijlage 38 The Problem with Wheat | Bijlage 39 Himalaya Zout vs De rotzooi die voor zout doorgaat | Bijlage 40 Benefits of Goats milk over Cows milk | Bijlage 41 The problem with most vegetable oils and margarine | bijlage 42 for healthy bones calcium, vitamin D, vitamine k2, magnesium, trace elements | Bijlage 43 The dangers of acrylamide (carbohydrates baked above 210 degrees Celcius) | Bijlage 44 Gevaren van plastic, aluminium en andere verpakkingsmaterialen | bijlage 45 Dangers of Fishoil and better sources for omega 3 | bijlage 46 fruit tegen kanker (aardbeien, cranberries etc) | bijlage 47 Hoog tijd voor een nieuwe schijf van 5 | bijlage 48 Uitleg hoe inentingen autisme veroorzaken door glutamaat productie in de hersenen te stimuleren wat schadelijk is voor de hersenen en voor de hersen ontwikkeling | bijlage 49 Korte Geschiedenis van Monsanto, pagina van Dr Mercola± In Amerika vechten ze voor wat hier heel gewoon is±etiketten waar op staat wat er in voedsel zit. | Bijlage 50 Nep ADHD diagnoses | Bijlage 51 Vrouw vertelt over uitgelekt NASA document over oorlog tegen de mensheid | bijlage 52 Bij medicijn dat zogenaamd cholesterol verlaagd juist 52$ hogere kans op plak in de aderen rondom het hart/ 52@ higher chance of heart plaque when tajking certain cholesterol lowering medicines. | Bijlage 53 Welke oliën zijn veilig om te verhitten? | Bijlage 54 Dr Mercola over Genetisch Gemanipuleerd voedsel"de tekenen dat de hegemonie van Monsanto begint te tanen | bijlage 55 Dr Mercola: genetisch gemanipuleerd voedsel: ontworpen om insecten te doden, maar het maakt ook onze cellen kapot. | Bijlage 56 Dr Mercola Alzeheimer detectie methode, en g4dv ook preventief voor Alzheimer | Bijlage 57 Het einde van het antibiotisch tijdperk aangebroken door toenemend aantal antibiotica resistente bacteriën, Ook hierop is de g4dv een antwoord. | Bijlage 58 Vaccinaties gaan om geld, niet om ziektebestrijding | Bijlage 59 Artikel Dr. Mercola over kankerverwekkende zaken in persoonlijke verzorgings- en huishoud producten | Bijlage 60 Dr. Mercola: Pesticiden kunnen neurologische schade aanrichten, gebruik liever etherische olie voor huisdieren en plant liever goudsbloem in de tuin | Bijlage 61 5 miljoen chronisch zieken in Nederland, zorg VS ook waardeloos | Bijlage 62 Gevaar vaccinaties | Bijlage 63: Gevaren antibiotica in vlees (artikel va Dr. Mercola) | Bijlage 64: Gevaren Testosteron behandeling | Bijlage 65 transvetten zijn de boosdoeners, verzadigde vetten zijn juist goed! 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De meeste helpen ons. Zullen we hun ook helpen? | Bijlage 85 Belang van licht en slaap | Bijlage 86 Artikel Dr Mercola over vergissingen in voeding die tot voedings tekorten leiden. | Bijlage 87 In Amerika beïnvloedt Junkfoodindustrie diëtistenopleidingen | bijlage 88 Dr Coldwell: Elke kanker kan in 2 tot 16 weken genezen worden | Bijlage 89: Want to Know over Tetanus | Bijlage 90: Dr. Russel Blaylock | Bijlage 91 Wat zijn opvliegers? | Bijlage 92, Dr Mercola: One in 25 Patients End Up with Hospital-Acquired Infections, CDC Warns | Bijlage 93 Dr Mercola Toxic Combo of Roundup and Fertilizers Blamed for Tens of Thousands of Deaths | Bijlqge 94 New Studies Show Optimizing Vitamin D Levels May Double Chances of Surviving Breast Cancer, Lower LDL Cholesterol, and Helps Prevent Autism | Bijlage 95, Dr.Mercola: How Vitamin D Performance Testing Can Help Optimize Your Health | Bijlage 96: Be Wary About This Food - It Can Wreck Your Ability to Walk, Talk, and Think | Bijlage 97 Gevaren van Vaccinaties (Mercola) | Bijlage 98: Ouders moeten geïnformeerd worden over de gevaren van vaccineren om een goede keus te kunnen maken | Bijlag 99: Zonnebrandmiddelen gevaarlijker dan zon als het gaat om huidkanker | Bijlage 100 Ignoring This Inflammatory Early Warning Signal Could Cost Your Life | Bijlage 101 Mijd Giffen, Niet Voedingsmiddelen! | Bijlage 102 Mentale rust | Bijlage 103: Voordelen van Kurkuma | Bijlage 104: Dr Mercola article Kruid tegen kanker | No Words | Bijlage 105: Dr Mercola: Sun , vitamin D and vitamin B3 crucial for longevity | Bijlage 106 Cowspiracy film en kritiek | Bijlage 107 Artemesia een effectief anti-malaria kruid | Bijlage 108, Chemotherapie is gevaarlijk | Bijlage 109 Canola oil, what is it, and is it good or bad for people? | Bijlage 110 Are peanuts good or bad for you? | Bijlage 111 Halloween recipes | Bijlage 112 Vaccinatieschade | Bijlage 113 Immigrants seek herbal remedies | Bijlage 114 more_doctors_confessing_to_intentionally_diagnosing_healthy_people_with_cancer | Bijlage 115 Dangers of vaccinating pregnant women | Bijlage 116 Omega 3-6-9 mengsel | Bijlage 117 Waarom er geen koolzaadolie zit in het omega 3-6-9- mengsel van de g4dv | Bijlage 118 Vaccinaties | Bijlage 119 Judy Wilyman, PhD on amti vaccination | Bijlage 120 Wetenschappelijke argumenten die de Keshe scam blootleggen | Bijlage 121 ECEH bacterie | Bijlage 122 grains | Bijlage 123 Make your own chocolate | Bijlage 124 Vaccine Violence | Bijlage 125 Italian court rules mercury and aluminum in vaccines cause autism: US media continues total blackout of medical truth | Bijlage 126 Dr Mercola: Vaccines and Neurological Damage | Bijlage 127 Why many doctors do not vaccinate their own children | Bijlage 128 These graphs show why many doctors don't vaccinate their own children | Bijlage 129 Leaflet Infanrix | Bijlage 130 Vaccine Madness | Bijlage 131 Japanse slachtoffers vaccin baarmoederhalskanker slepen overheid en farmareuzen voor de rechter | Bijlage 132 Pregnancy, labour, delivery and child care | Appendix 133 healing diet for our canine friends | Bijlage 134 Flowchart edible or non-edible | Bijlage 135 Keeping children healthy naturally | Bijlage 136 Vaccines and the Amygdala | Bijlage 137 Revolving door between politics and big pharma explained | Bijlage 138 Ingrediënten Vaccins | Bijlage 139: Medisch scheikundige geeft drie redenen waarom hij zijn kinderen niet laat vaccineren | Bijlage 140 Ryan's story | Bijlage 141 NVKP lezingen dr Hans Moolenburgh | Bijlage 142 HPV vaccine | Bijlage 143 Dr. Hans Moolenburgh over fluoride | Bijlage 144 Baby dies three days after getting six vaccines | Bijlage 145 Interview Trouw met Dr Hans Moolenburgh | Bijlage 146 Jacob van Lennep | Bijlage 147 Flow chart "to believe or not to believe medical or nutritional advice" | Appendix 148 The case experts make against vaccines | Apendix 149 Dr Mercola article: Experts admit Zika threat fraud | Appendix 150 Sudden deaths among health advocates | Appendix 151 Thimerosal | appendix 152 Herd immunity? | Appendix 153 Formaldehyde in vaccines | Appendix 154 Why doctor's say "Do not take the flu shot!" | Bijlage 155 Vaccineren? Natuurlijk niet! En wel hierom: | Appendix 156 Vaccine makers bypass WHO regulations | Bijlage 157 Het probleem van overbehandeling bij borstkanker | Bijlage 158 Chemotherapie vermoordt u | Bijlage 159 Borstbesparende operatie beter dan amputatie voor overlevingskansen bij borstkanker | Appendix 160 Vaccine induced bone fractures | Bijlage 161 hulpstoffen in Vaccins toegegeven door CDC | Appendix 162 meningitis: symptoms, how to prevent, how to treat | Appendix 163 Training of nutrtionists often shady | Appendix 164 Molecular Biochemist Dr.Lucija Tomljenovic, PhD, explains why vaccines not only don't work, but are extremely harmful and can be lethal as well | Appendix 165 CDC knew about MMR vaccine autism link as early as 1999, but covered it up | Appendix 166 Scientists at the vaccine safety debate January 2011 | Appendix 167 Vaccinated children 5 times more likely to contract auto immune diseases | Appendix 168 Before and after vaccine: this is what mass brain destruction looks like | Appendix 169 Hepatitis B | Appendix 170 Countries where vaccines are not mandatory and the nazi roots of vaccines and drugcompanies | Appendix 171 The dangers of soybean oil | Appendix 172 Vaccines do not protect against Measles | Appendix 173 HPV vaccine | Appendix 174 Hoogleraar Peter Gøtzsche over corruptie in de farmaceutische industrie | Appendix 175 Dr Arlan Cage | Appendix 176 How vaccines damage your immune system | Appendix 177 Vaccines are not tested properly | Appendix 178 Documentaries exposing pharma fraud | Appendix 179 Dr Suzanne Humphries | Appendix 180 Dr Russel Blaylock: Vaccinations can kill you or ruin your life | Appendix 181 Doctors who clearly explain why vaccines are neither safe nor effective | Appendix 182 Dr Sherri Tenpenny | Appendix 183 Alan Phillips attorney Vaccine Rights | Appendix 184 Dr Rebecca Carley | Appendix 185 Vaccines bargain basement of the medical industry, says Maurice Hilleman (who developed 36 vaccins) admits AIDS and Cancer causing virusses were added to vaccines | Appendix 186 Many independent studies show vaccine dangers, Damages paid by pharmaceutical companies for vaccine damahge | Appendix 187 The truth behind Vaccinations | Appendix 188: Guess what happened to Nazi war criminals responsible for the genoside of millions: After aquittal or a short prison sentence they went back to being CEO's for big Pharma! | Appendix 189: Mercola: What?s the Right Dose of Exercise for a Longer Life? | Appendix 190 What happened to Dr Mercola? | Bijlage 191: hoofd RIVM zegt Kindervaccinaties veroorzaken hersenvliesontsteking

Laatste wijziging op: 10-03-2013 14:28