There are several mechanisms by which alcohol consumption may exert its
carcinogenic effect. Acetaldehyde production, polymorphisms in ethanol
metabolizing genes, hormonal imbalances leading to breast cancer, dysregulation
of immune system, dysregulation of folate metabolism, and damages to the epithelium resulting in increased absorption of carcinogens are some of the mechanisms
that promote carcinogenesis (Boffetta and Hashibe 2006; Yu et al. 2010; Singletary
and Gapstur 2001; Watson et al. 1994; Hamid et al. 2009; Doll et al. 1999). It has
been found that methylation of p15-gene is accelerated by tobacco and alcohol
promoting the development of head and neck cancer (Chang et al. 2004) as alcohol
and tobacco are likely to be synergistic in causing head and neck cancer (Murata
et al. 1996). In studies where alcohol is co-administered with other cancer-causing
agents, it has been found to exert a synergistic effect in promoting carcinogenesis
(Hsu et al. 1991). This is true for the association between alcohol, smoking and head
and neck cancer risk though a study by Schlecht et al. (1999) found the joint effects
of alcohol and moderate smoking to be more than multiplicative in pharyngeal
cancers. The study pointed out that alcohol has both synergistic and independent
effects in promoting carcinogenesis of head and neck region. The synergistic action
could be by acting as a solvent for other carcinogens or promoting inflammation and
generation of reactive oxygen species. Studies have reported an association between
alcohol consumption and pancreatic and prostate cancer. With regard to pancreatic
cancer, heavy consumption of alcohol was associated with an increased risk by 19%
compared with non-drinkers or occasional drinkers while two studies reported a
significant positive association between alcohol consumption and prostate cancer.
Alcohol consumption is also associated with colorectal cancer, though gender
specific differences do exist as a meta-analysis did not find any significant association between alcohol and colorectal cancer mortality in women (Cai et al. 2014).
The association of alcohol consumption has also been studied with an increased
risk of melanoma. The possible mechanisms of alcohol-induced melanoma could be
enhanced cellular damage in the presence of UV radiation and subsequently formation of skin cancers (Saladi et al. 2010) and increased immunodeficiency and
immunosuppression (Watson et al. 1994), the conditions that facilitate melanoma
formation (Mukherji 2013). A meta-analysis conducted by Bagnardi et al. (2015)
found that heavy drinkers had a significant 15% increase of lung cancer risk as
compared with non-drinkers or occasional drinkers. However, in another metaanalysis published by the same group, alcohol consumption was not associated
with lung cancer risk in never smokers. Similarly, an association between alcohol
consumption and stomach cancer was also observed. These positive associations
must be interpreted with caution as the confounding effect of smoking cannot be
ruled out given the fact that alcohol users are most commonly smokers too. Another
important consideration is the influence of diet as heavy alcohol consumption leads
to compromised nutrition and, thus, confounding by poor diet (Klatsky 2001) could
not be ruled out. Inconsistent and inconclusive reports for the association between
alcohol consumption and cancers of endometrium, ovary, cervix, thyroid, and brain
have been reported though there are also studies which reported no association with
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M. Ruwali and R. Shukla
carcinogenic effect. Acetaldehyde production, polymorphisms in ethanol
metabolizing genes, hormonal imbalances leading to breast cancer, dysregulation
of immune system, dysregulation of folate metabolism, and damages to the epithelium resulting in increased absorption of carcinogens are some of the mechanisms
that promote carcinogenesis (Boffetta and Hashibe 2006; Yu et al. 2010; Singletary
and Gapstur 2001; Watson et al. 1994; Hamid et al. 2009; Doll et al. 1999). It has
been found that methylation of p15-gene is accelerated by tobacco and alcohol
promoting the development of head and neck cancer (Chang et al. 2004) as alcohol
and tobacco are likely to be synergistic in causing head and neck cancer (Murata
et al. 1996). In studies where alcohol is co-administered with other cancer-causing
agents, it has been found to exert a synergistic effect in promoting carcinogenesis
(Hsu et al. 1991). This is true for the association between alcohol, smoking and head
and neck cancer risk though a study by Schlecht et al. (1999) found the joint effects
of alcohol and moderate smoking to be more than multiplicative in pharyngeal
cancers. The study pointed out that alcohol has both synergistic and independent
effects in promoting carcinogenesis of head and neck region. The synergistic action
could be by acting as a solvent for other carcinogens or promoting inflammation and
generation of reactive oxygen species. Studies have reported an association between
alcohol consumption and pancreatic and prostate cancer. With regard to pancreatic
cancer, heavy consumption of alcohol was associated with an increased risk by 19%
compared with non-drinkers or occasional drinkers while two studies reported a
significant positive association between alcohol consumption and prostate cancer.
Alcohol consumption is also associated with colorectal cancer, though gender
specific differences do exist as a meta-analysis did not find any significant association between alcohol and colorectal cancer mortality in women (Cai et al. 2014).
The association of alcohol consumption has also been studied with an increased
risk of melanoma. The possible mechanisms of alcohol-induced melanoma could be
enhanced cellular damage in the presence of UV radiation and subsequently formation of skin cancers (Saladi et al. 2010) and increased immunodeficiency and
immunosuppression (Watson et al. 1994), the conditions that facilitate melanoma
formation (Mukherji 2013). A meta-analysis conducted by Bagnardi et al. (2015)
found that heavy drinkers had a significant 15% increase of lung cancer risk as
compared with non-drinkers or occasional drinkers. However, in another metaanalysis published by the same group, alcohol consumption was not associated
with lung cancer risk in never smokers. Similarly, an association between alcohol
consumption and stomach cancer was also observed. These positive associations
must be interpreted with caution as the confounding effect of smoking cannot be
ruled out given the fact that alcohol users are most commonly smokers too. Another
important consideration is the influence of diet as heavy alcohol consumption leads
to compromised nutrition and, thus, confounding by poor diet (Klatsky 2001) could
not be ruled out. Inconsistent and inconclusive reports for the association between
alcohol consumption and cancers of endometrium, ovary, cervix, thyroid, and brain
have been reported though there are also studies which reported no association with
216
M. Ruwali and R. Shukla