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DOI: 10.1055/s-2006-952096
Karl F. Haug Verlag in MVS Medizinverlage Stuttgart GmbH & Co. KG
Ernährungsfaktoren, Gen-Nährstoff-Interaktion und kolorektales Karzinom - eine Übersicht des aktuellen Kenntnisstandes
Publication History
Publication Date:
28 December 2006 (online)
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Zusammenfassung
Die Entstehung kolorektaler Karzinome wird maßgeblich durch die Ernährungsweise beeinflusst. Aktuelle Kohortenstudien und Metaanalysen erlauben eine Neubewertung der Risikomodifikation im Hinblick auf einzelne Lebensmittelgruppen sowie auf bestimmte Nährstoffe wie Ballaststoffe und Folsäure. Auf Basis der Evidenzkriterien der WHO/FAO zeigt sich, dass ein risikosenkender Effekt eines hohen Obstverzehrs als möglich, der eines hohen Gemüseverzehrs als wahrscheinlich einzustufen ist. Insbesondere in roher Form kommt Obst und Gemüse vermutlich ein antikanzerogenes Potenzial zu. Die Evidenz für einen risikosenkenden Effekt des Vollkornverzehrs im Hinblick auf Tumoren des Kolons und Rektums gilt als möglich, wohingegen die Evidenz für eine potenzielle Risikoerhöhung durch einen hohen Verzehr an Auszugsmehlprodukten und Süßwaren trotz einiger Hinweise (noch) als unzureichend zu bewerten ist. Bei Milch(produkten) wird die Evidenz für einen risikosenkenden Effekt als möglich bewertet. Demgegenüber spricht die Datenlage bei Eiern und rotem Fleisch für einen möglichen risikoerhöhenden Effekt. Deutlichere Hinweise auf einen risikosteigernden Effekt ergeben sich für Fleischwaren, so dass die Evidenz in Bezug auf das kolorektale Karzinom hier als wahrscheinlich eingestuft wird. Aufgrund widersprüchlicher Interpretationen der Datenlage wird die Evidenz für einen risikosenkenden Effekt von Ballaststoffen bei Dickdarmkrebs als möglich oder unzureichend eingestuft. Im Gegensatz zu früheren Bewertungen scheinen fettreiche Ernährungsformen nur indirekt das Krebsrisiko zu steigern, indem sie im Rahmen einer hyperkalorischen Kost zur Entwicklung von Übergewicht beitragen. So gilt die Evidenz, dass Übergewicht, insbesondere viszerale Adipositas, das Risiko für Dickdarmkarzinome erhöht, heute als überzeugend.
Beobachtungsstudien untermauern die Vermutung, dass eine unzureichende Folsäure-Versorgung die Entstehung kolorektaler Tumore begünstigt. Für einen derartigen Zusammenhang sprechen insbesondere die Ergebnisse prospektiver Studien, wenngleich die Datenlage z.T. uneinheitlich ist. Eine Ursache für die widersprüchlichen Studienergebnisse könnte in der genetischen Variabilität, insbesondere im Gen-Polymorphismus des Enzyms Methylentetrahydrofolat-Reduktase (MTHFR), zu suchen sein. Insbesondere Träger des MTHFR-677-TT-Genotyps sind bei schlechter Folatversorgung einem erhöhten Krankheitsrisiko ausgesetzt.
Im Rahmen der Primärprävention ist eine vorwiegend pflanzlich orientierte Kost, die einen hohen Anteil an Gemüse, Obst, Vollkornprodukten und Hülsenfrüchten aufweist zu empfehlen, ergänzt um Nüsse, fettarme Milchprodukte, Fischgerichte und Geflügel. Dagegen sollte der Konsum von energiereichen Süßwaren, Auszugsmehlprodukten und Fleischwaren eingeschränkt werden.
Summary
Diet plays an important role in the pathogenesis of colorectal cancer. Current cohort studies and meta analysis enable a reevaluation of how food or nutrients such as fiber and folic acid influence cancer risk. Based on the evidence criteria of the WHO/FAO, risk reduction by a high intake of fruit is assessed as possible, while a lowered risk by a high vegetable intake is probable. Especially raw vegetables and fruits seem to exert anticancer properties. The evidence of a risk reducing effect of whole grain relating to colorectal cancer is assessed as probable whereas the evidence of an increased risk by high consumption of refined white flour products and sweets is (still) insufficient despite some evidences. There is a probable risk reducing effect of milk and dairy products. The available data on eggs and red meat indicate a possible risk increasing influence. Stronger clues for a risk increasing effect have been shown for meat products leading to evidence assessed as probable. Owing to varied interpretations of the data on fiber, the evidence of a risk reducing effect relating to colorectal cancer is assessed as possible or insufficient. In contrast to former evaluations, diets rich in fat seem to increase colorectal cancer risk only indirectly as part of a hypercaloric diet by advancing the obesity risk. Thus, the evidence of obesity, especially visceral obesity, as a risk of colorectal cancer is judged as convincing today.
Epidemiological studies suggest that insufficient folic acid intake may elevate the risk of colorectal cancer. Although the data is partly controversial, especially results of prospective studies support this association. One reason for the contradictory results may be the genetic variability especially the MTHFR polymorphism. Individuals with the homozygote genotype for the MTHFR (677C → T) polymorphism are at higher risk when folic acid supply is low. As primary prevention, a diet rich in vegetables, fruits, whole grain products, and legumes added by nuts, low-fat dairy products, fish, and poultry can be recommended. In contrast the consumption of sweets, refined white flour products and meat products should be reduced.
“What are we to do when the irresistible force of the need to offer clinical advice meets with the immovable object of flawed evidence? All we can do is our best: give the advice, but alert the advisees to the flaws in the evidence on which it is based.” [22]
Schlüsselwörter
Ernährung - kolorektales Karzinom - Folsäure - MTHFR-Polymorphismus
Keywords
diet - nutrition - colorectal cancer - folic acid - MTHFR polymorphism
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Korrespondenzadresse
Dipl. oec. troph. Alexander Ströhle
Abteilung Ernährungsphysiologie und Humanernährung
Institut für Lebensmittelwissenschaft
Zentrum Angewandte Chemie
Universität Hannover
Wunstorfer Str. 14
30453 Hannover
Email: alexander.stroehle@lw.uni-hannover.de