A large US trial shows that the cumulative burden of alcohol over decades matters for colorectal cancer risk, with heavy lifelong drinking increasing danger and stopping alcohol linked to fewer early precancerous polyps.
Study: Association of alcohol intake over the lifetime with colorectal adenoma and colorectal cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Image Credit: crystal light / Shutterstock
In a recent study published in the journal Cancer, researchers used data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial to examine the association between lifetime alcohol intake and the risk of developing colorectal adenomas (precancerous polyps) and invasive cancer.
Study findings revealed that higher lifetime alcohol intake was associated with an increased risk of colorectal cancer (CRC), particularly rectal cancer, among current drinkers. Conversely, the data suggested that alcohol cessation was associated with lower odds of developing nonadvanced adenomas detected at screening, a very early precursor lesion.
These findings highlight the importance of viewing alcohol consumption as a cumulative exposure and suggest that reducing intake may influence early carcinogenic processes, although causal effects cannot be inferred.
Background: Alcohol as a Modifiable Colorectal Cancer Risk Factor
CRC remains a leading cause of cancer mortality, currently ranked third in incidence across the United States (US). While overall incidence rates have declined, diagnoses among adults under 55 are rising, prompting urgent calls to identify and address modifiable risk factors.
The International Agency for Research on Cancer (IARC) has long classified alcoholic beverages as carcinogenic to humans, specifically linking them to CRC.
Most prior epidemiological studies have relied on snapshots of participants’ lives, often measuring alcohol consumption only within the 12 months before the study. This approach fails to account for the fact that cancer development is a slow process often spanning decades.
Furthermore, the relationship between alcohol and colorectal adenomas, the precursor lesions that may progress to cancer, remains poorly understood.
Study Rationale: Capturing Lifetime Drinking Exposure
The present study aimed to address this knowledge gap by reconstructing participants’ drinking histories from age 18 onward. Understanding this relationship is vital, as preventing an adenoma may effectively prevent cancer incidence.
The study leveraged data from the PLCO Cancer Screening Trial, a large-scale randomized controlled trial of US adults aged 55 to 74.
Study data examined two distinct groups: an incident adenoma cohort of 12,327 participants who underwent flexible sigmoidoscopy screening and a larger CRC cohort of 88,092 participants followed prospectively for clinically diagnosed cancer.
Assessment of Alcohol Intake and Participant Classification
The study data comprised participants’ long-term sociodemographic and medical histories. Participants also completed a Dietary History Questionnaire (DHQ) that asked about beer, wine, and liquor consumption across four age groups: 18–24, 25–39, 40–54, and 55 years and older.
These data were collated and analysed to calculate a weighted average of lifetime alcohol intake.
Participants were categorized based on lifetime average alcohol consumption among current drinkers, with those consuming less than one drink per week serving as the reference group, as follows: less than one drink per week, 1 to <7 drinks per week, 7 to <14 drinks per week, and 14 or more drinks per week.
Former drinkers were analysed separately to reduce potential bias related to lifetime abstention.
The study further investigated drinking patterns, identifying participants who were consistent heavy drinkers versus those who changed their habits over time, using sex-specific thresholds aligned with US dietary guidelines.
Statistical models included logistic regression for adenomas and Cox proportional hazards regression for cancer, adjusting for confounders such as smoking, body mass index (BMI), and family history.
Key Findings: Alcohol Intake and Colorectal Cancer Risk
The study revealed a robust association between heavy, long-term alcohol consumption and increased cancer risk. Among current drinkers, those with a lifetime average of 14 or more drinks per week demonstrated a 25% higher risk of developing CRC compared with those consuming less than one drink per week (hazard ratio, 1.25; 95% CI, 1.01–1.53; p = 0.003).
Associations were strongest for rectal cancer, where heavy lifetime drinkers faced nearly double the risk of those in the lowest intake group (hazard ratio, 1.95; 95% CI, 1.17–3.28).
Participants identified as consistent heavy drinkers throughout adulthood demonstrated a 91% higher risk of CRC compared with consistent light drinkers (hazard ratio, 1.91; 95% CI, 1.17–3.12).
Nonlinear Associations and Moderate Drinking
Study analyses identified a nonlinear association for moderate drinking. Participants averaging 7 to <14 drinks per week showed a lower risk of CRC (hazard ratio, 0.79) compared with those consuming less than one drink per week, particularly for distal colon cancer.
The authors cautioned that this apparent inverse association may reflect residual confounding, differences in health behaviours, or reference group effects and does not indicate a protective effect of alcohol consumption.
Alcohol Cessation and Colorectal Adenomas
Former drinkers had significantly lower odds of developing nonadvanced adenomas than current very light drinkers (odds ratio, 0.58; 95% CI, 0.39–0.84), suggesting that cessation may be associated with reduced risk at the earliest detectable stages of colorectal neoplasia.
Associations for advanced adenomas and overall adenoma risk were less consistent.
Conclusions: Cumulative Alcohol Exposure and Cancer Prevention
The present study provides evidence that cumulative lifetime alcohol exposure is associated with CRC risk. Study data indicate that consistent heavy drinking is a robust risk factor for CRC, especially rectal cancer.
Findings related to adenomas suggest that alcohol cessation is associated with lower odds of nonadvanced precursor lesions detected at screening, reinforcing the potential value of lifestyle modification even later in adulthood. However, the observational nature of the study precludes causal conclusions, and the findings of adenomas should be interpreted cautiously.
Limitations include reliance on self-reported alcohol intake and a predominantly white, educated cohort. The study underscores that public health messaging may need to emphasize that reducing alcohol intake is not only about immediate health outcomes but also about reducing long-term cumulative cancer risk.
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