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Investigating the Association between Alcohol and Risk of Head and Neck Cancer in Taiwan
Cheng-Chih Huang1, Jenn-Ren Hsiao1, Wei-Ting Lee1
1Department of Otolaryngology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 Sheng Li Road, Tainan, 70456, Taiwan.
Scientific Reports
|August 31, 2017
Summary
Alcohol consumption significantly increases head and neck cancer (HNC) risk, especially for individuals with slow ethanol metabolism. Reducing alcohol intake can lower HNC incidence.
Area of Science:
- Oncology
- Genetics
- Epidemiology
Background:
- Alcohol is a known risk factor for head and neck cancer (HNC).
- Existing literature has limitations in detailing alcohol's role in HNC development.
- Genetic factors influencing alcohol metabolism may modify HNC risk.
Purpose of the Study:
- To investigate the association between detailed alcohol consumption patterns and HNC risk.
- To examine HNC risk by specific cancer sites and by ADH1B and ALDH2 genotypes.
- To quantify the proportion of HNCs attributable to alcohol consumption.
Main Methods:
- Analysis of detailed alcohol consumption data (amount, beverage type) from 811 HNC patients and 940 controls.
- Stratification of HNC risk by cancer sub-site (hypopharynx, oropharynx, larynx).
- Evaluation of risk based on ADH1B and ALDH2 genotypes, particularly slow metabolizer variants.
Main Results:
- A dose-response relationship was observed between alcohol intake and increased HNC risk.
- Liquor consumption showed a stronger association with HNC than beer or wine.
- Individuals with slow ADH1B and slow/non-functional ALDH2 genotypes exhibited the highest HNC risk.
- Alcohol was attributable to a significant proportion of HNCs, particularly hypopharyngeal and oropharyngeal cancers.
- Alcohol-attributable HNC risk decreased significantly after 10+ years of cessation.
Conclusions:
- Alcohol consumption is a significant risk factor for head and neck cancer, with varying risk by cancer site and beverage type.
- Genetic variations in alcohol-metabolizing enzymes (ADH1B, ALDH2) strongly influence individual HNC risk.
- Alcohol cessation can mitigate HNC risk, especially for genetically susceptible individuals.
- Public health strategies focusing on alcohol reduction and cessation are crucial for lowering HNC incidence.
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