Alcohols and bowel cancer

Metabolism of ethanol causes the generation of acetaldehyde (AA) and free radicals. Acetaldehyde is
carcinogenic and mutagenic, binds to DNA and proteins, destroys folate and causes secondary
hyperproliferation. Acetaldehyde can also be produced by oral and fecal bacteria. Smoking, which alters
oral bacteria flora, and poor oral hygiene also increase acetaldehyde. In addition, smoking and some
alcoholic drinks such as calvados contain acetaldehyde. Other mechanisms that cause alcohol to
stimulate carcinogenesis include cytochrome P-4502E1 induction, which is associated with increased
free radical production and increased activation of various procarcinogens present in alcoholic
beverages; associated with tobacco smoke and food, metabolic changes and distribution of carcinogens;
Changes in cell cycle behavior such as the duration of cell cycle that causes hyperproliferation;
malnutrition, such as methyl deficiency, vitamin E, folate, pyridoxal phosphate, zinc- and selenium and
immune system changes eventually lead to susceptibility to certain viral infections such as hepatitis B
virus and hepatitis C virus. In addition, local mechanisms may be extremely important. Such mechanisms
cause tissue injuries such as liver cirrhosis, a major prerequisite for hepatocellular carcinoma (G. Pöschl,
H. K. Seitz, 2006)

Reference: G. Pöschl, H. K. Seitz. 2006. Alcohol and Cancer. Alcohol and Alcoholism, Volume 39, Issue 3,
1 May 2004, Pages 155–165, https://doi.org/10.1093/alcalc/agh057

The indirectly induced radical effects explain that the radiation exposing the individual body affects the
water component present in the so-called substance called free radicals. Free radicals that formed can
trigger cell death or cause mutations in DNA, so that new cell clones can be a malignancy. One of these
free radicals is derived from H2O commonly found in cigarettes. In the body H2O can react to be HOH
and then become OH. OH is part of reactive oxygen species (ROS) known as free radicals or hydroxyl
radicals (I Ketut Sudiana, 2008)

Reference: I Ketut Sudiana. 2008. Patobiologi Molekuler Kanker. Slamenda Medika. Jakarta. Indonesia