Alkol ve Kanser
Özet
Dünya geneli verileri düşünüldüğünde tüm kanser vakalarının %4 ü alkol tüketimi ile ilişkilendirilmiştir. 2020 yılı verilerine göre alkolün 100.000’den fazla yeni kanser vakasına neden olduğu düşünülmektedir. Vaka sayısı olarak bakıldığından özefagus, karaciğer ve meme kanserleri, alkol tüketimi ile ilişkili en fazla vaka sayısına sahip kanser türleri olarak ön plana çıksa da literatürde alkolün pek çok kanser türü için risk oluşturduğu gösterilmiştir. Karsinogenez açısından değerlendirildiğinde alkol tüketiminin miktarı ve süresi farklı kanser türlerine göre farklılık göstermektedir. Bununla beraber günlük hafif ve orta düzeye (10 gram ve altı) eşdeğer alkol tüketimi bile kanser riskini artırabilir. Genel olarak tüm kanser tiplerinde alkol tüketim miktarı ve sıklığı arttıkça kanser gelişimi riski artmaktadır. Ayrıca literatürde farklı alkol türleri arasında kanser gelişim riski açısından ispatlanmış bir farklılık yoktur. Alkol tüketimi ile kanser arasında doğrudan bir nedensel bağlantı olsa da, alkol tek başına bir kanserojen değildir. Ancak alkolün metaboliti olan asetaldehit, sitotoksik bir madde ve Grup 1 kanserojen olarak tanımlanmıştır. Asetaldehit aldehit dehidrogenaz enzimi tarafından toksik olmayan metabolitlerine ayrıştırılarak atılmaktadır. Doğu Asya toplumlarında sık görülen Aldehit dehidrogenaz (ALDH2*2) missense mutasyonu, üst gis kanserleri için ek bir genetik bir risk faktörü oluşturmaktadır. Coğrafik açıdan bakıldığında bu durum alkol kullanımının farklı toplumlarda kanser gelişimi üzerine farklı etkileri olduğunu göstermektedir. Literatürde alkolün bırakılmasının veya kullanılan miktarın azaltılmasının sürekli kullanıma göre kanser gelişme riskini genel olarak azalttığı gösterilmiştir.
Considering worldwide data, 4% of all cancer cases are associated with alcohol consumption. According to 2020 data, alcohol is thought to cause more than 100,000 new cancer cases. Although oesophageal, liver and breast cancers stand out as the cancer types with the highest number of cases associated with alcohol consumption, it has been shown in the literature that alcohol poses a risk for many cancer types. In terms of carcinogenesis, the amount and duration of alcohol consumption differ according to different cancer types. However, even daily consumption of alcohol equivalent to light and moderate levels (10 grams or less) may increase the risk of cancer. In general, the risk of cancer development increases as the amount and frequency of alcohol consumption increases in all cancer types. In addition, there is no proven difference between different types of alcohol in terms of cancer development risk in the literature. Although there is a direct causal link between alcohol consumption and cancer, alcohol alone is not a carcinogen. However, acetaldehyde, a metabolite of alcohol, has been identified as a cytotoxic substance and a Group 1 carcinogen. Acetaldehyde is broken down into non-toxic metabolites by the enzyme aldehyde dehydrogenase and excreted. Aldehyde dehydrogenase (ALDH2*2) missense mutation, which is common in East Asian populations, constitutes an additional genetic risk factor for upper GI cancers. From a geographical point of view, this situation shows that alcohol consumption has different effects on cancer development in different populations. In the literature, it has been shown that alcohol cessation or reduction in the amount of alcohol used generally reduces the risk of cancer development compared to continuous use.
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