Journal of Clinical Oncology · 7 authors, 5 centres
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This large Korean cohort study found that moderate and heavy alcohol consumption increased the risk of early-onset colorectal cancer (CRC) by 9% and 20%, respectively, compared with light drinking. The association was strongest for left-sided (distal colon and rectal) cancers, with a dose-response relationship for both amount and frequency of drinking. These findings highlight the need for alcohol reduction interventions and tailored CRC screening in young adults.
**Background:** Colorectal cancer (CRC) is the third most common cancer worldwide, and early-onset CRC (diagnosed before age 50) accounts for about 10% of cases, with increasing incidence. Alcohol consumption is a known carcinogen, but large-scale studies on dose-response associations by tumor location and sex are limited. This study aimed to investigate the association between graded alcohol intake and early-onset CRC risk, focusing on tumor site and sex differences.
**Methods:** This retrospective cohort study used data from the Korean National Health Insurance Service (NHIS) database, including 5,666,576 individuals aged 20-49 years who underwent health checkups in 2009. Participants were followed until December 31, 2019, or until age 50. Alcohol consumption was calculated from self-reported frequency and amount, converted to grams of ethanol per day. Categories were: nondrinker (0 g/d), light (<10 g/d, reference), moderate (10 to <30 g/d for men, 10 to <20 g/d for women), and heavy (≥30 g/d for men, ≥20 g/d for women). Multivariable Cox proportional hazards models estimated adjusted hazard ratios (aHRs) with 95% CIs, adjusting for age, sex, smoking, exercise, income, and comorbidities (hypertension, diabetes, dyslipidemia). Subgroup analyses by tumor location (proximal colon, distal colon, rectum, unspecified colon) and sex were performed.
**Key Results:** During a median follow-up of 9.1 years, 8,314 incident early-onset CRC cases were identified. Compared with light drinkers, moderate and heavy drinkers had significantly increased risk (aHR 1.09 [95% CI, 1.02-1.16] and aHR 1.20 [95% CI, 1.11-1.29], respectively). Dose-response trends were significant for men (P<.0001) and women (P=.003), though women's moderate and heavy categories did not reach statistical significance individually. By tumor location, significant positive associations were found for distal colon (moderate: aHR 1.14 [95% CI, 1.00-1.30]; heavy: aHR 1.27 [95% CI, 1.09-1.48]; P trend=.006), rectum (heavy: aHR 1.15 [95% CI, 1.02-1.30]; P trend<.0001), and unspecified colon (heavy: aHR 1.27 [95% CI, 1.05-1.53]; P trend=.009), but not for proximal colon (P trend=.439). Nondrinkers had a 10% reduced risk of rectal cancer versus light drinkers (aHR 0.90 [95% CI, 0.82-0.98]). Drinking frequency also showed dose-response: 1-2, 3-4, and ≥5 days/week increased risk by 7%, 14%, and 27% versus nondrinkers (P trend<.0001), with strongest effects for distal colon and rectal cancers.
**Clinical Implications:** This study provides strong evidence that excessive alcohol consumption increases early-onset CRC risk in a dose-response manner, particularly for left-sided (distal colon and rectal) cancers. The findings support public health interventions to reduce alcohol intake among young adults and suggest that individuals with heavy alcohol consumption may benefit from CRC screening before age 50. The lack of association for proximal colon cancer suggests site-specific carcinogenic mechanisms. Limitations include self-reported alcohol data, potential confounding by unmeasured factors (e.g., family history, diet), and restriction to a Korean population, which may limit generalizability. Nonetheless, these results underscore alcohol as a modifiable risk factor for early-onset CRC.