Alcohol consumption and the risk of cancer of non-Hodgkin lymphoma (NHL)
Two meta-analysis were identified evaluating the association between NHL and alcohol consumption (13,14). The first study found a 15% reduction of NHL risk in current alcohol drinkers compared with non-drinkers (relative risk RR 0,85, 95% CI 0,79-0,91), regardless of the amount of consumption [light: (RR 0,88, 95% CI 0,81-0,96); moderate: (RR 0,87, 95% CI 0,79-0,95); heavy: RR 0,84, 95% CI 0,70-1,00)], without finding significant differences across strata of sex, type of controls and the two main subtypes of NHL (i.e. T-cells versus B-cell lymphoma) (13). The second metanalysis reported a favourable role of alcohol drinking on NHL risk, both on ever and current drinkers (RR 0,89 95% CI 0,83-0,95). Interestingly, it was found a significant difference on the type of alcoholic beverage and on sex gender; only ever/current consumption of beer was associated with a reduced risk of NHL (RR 0,88 95% CI 0,81-0,95) compared to wine and liquor (respectively RR 0,96 95% CI 0,9-1,12; RR 0,9 95% CI 0,79-1,02), whereas the protective effect of alcohol drinking was demonstrated only in male subjects (RR 0,88 95% CI 0,78-0,98) (14). Finally, regarding the histological subtype of NHL, an inverse correlation between alcohol intake and NHL was proved in diffuse large B-cell lymphoma and follicular lymphoma (13,14).
Alcohol consumption and the risk of cancer of oesophageal cancer (OSCC)
Islamini and colleagues conducted a meta-analysis of 40 case-control studies and 12 cohort studies, showing a link between light, moderate and high alcohol drinking and the risk of OSCC (RR: 1.31 CI 95% 1.10-1.57; RR: 2.27 CI 95% 1.89-2.72; RR: 4.89 CI 95% 3.84-6.23); however, the increased risk in light alcohol drinkers was limited to the Asian population (RR, 1.63; 95% CI, 1.20-2.22) (15). These associations were also evidenced among never-smokers (RR, 0.74 95% CI 0.47-1.16 for light, 1.54; 95% CI, 1.09-2.17 for moderate, and RR, 3.09; 95% CI,1.75-5.46 for high intakes) (15). A second meta-analysis including 24 studies in 2012 reported no significant correlation between both oesophageal and gastric cardia adenocarcinoma risk and light (0.86; 95% CI 0.75–0.99), moderate (0.90 95% CI 0.73–1.10) and heavy (1.16; 95% CI 0.92–1.46) alcohol consumption (16).
|
Alcohol consumption and the risk of gastric cancer
A first meta-analysis showed no association between alcohol ingestion and gastric cancer for light and moderate alcohol assumption (RR: 0.95; 95% CI: 0.88–1.02; RR: 1.05; 95% CI: 0.98–1.13, respectively).Nevertheless,a significant increase in relative risk of development of gastric cancer in case of heavy consumption, was reported (RR: 1.13; 95% CI: 1.06–1.21).Interestingly, a lower risk of gastric cancer in women consuming low doses of alcohol, was found (RR: 0.74; 95% CI: 0.57–0.98. (17). A second meta-analysis by Rota and colleagues, reported an increase in the risk of developing gastric cancer in case of consumption of 4 to 6 drinks/day (RR: 1.26 95% CI, 1.08–1.48) and >6 drinks/day (RR: 1.48 95% CI 1.29–1.70), especially in never smoking subjects (RR 1.87, 95% CI 1.35–2.58). There was no significant correlation under that threshold (≤1 drink/day: RR 1.00 95% CI 0.86–1.16)(18).
Alcohol consumption and the risk of pancreatic cancer
Two studies were selected evaluating the role of alcohol intakes in the onset of pancreatic cancer (19,20). The first meta-analysis conducted by Wang and colleagues, concluded that only high level of consumption determined an increased risk of developing pancreatic cancer (RR, 1.15; 95 % CI: 1.06–1.25). The risk was higher in male gender (RR 1.18; 95 % CI: 1.00–1.39) and in case of liquor consumption (RR, 1.66; 95 % CI: 1.24–2.23) (19). A second study by Tramacere and colleagues, collecting 21 case control and 11 cohort studies, reported a 20% increase in the risk of pancreatic cancer among heavy alcohol drinkers (defined as 3 or more drinks/day), compared with non‐or occasional drinkers, with a relative risk of 1.22 (95% CI, 1.12–1.34). Furthermore, no significant increase in cancer risk in case of drinking less than 3 drinks/day was found (RR:0.92 95% CI, 0.86–0.97) (20).
Alcohol consumption and the risk of colon cancer
We selected four meta-analysis assessing the link between alcohol intakes and the overall risk of colorectal cancer (21-24). The first study, including 4687 cases of colorectal cancer, suggested an increased risk limited to alcohol intake of 30-45 g/day (RR: 1.21 CI 95% 1.04–1.42), and >45 g/day (RR: 1.51 CI 95% 1.25–1.83), but no significant correlation for consumption <30 g/day, and no significant differences among sex gender, type of alcohol beverage and tumor site (21). Fedirko and colleagues showed that drinkers of 12.6–49.9 g/day and more than ≥50 g/day of alcohol had respectively a 21% and 52% increased risk for colorectal cancer (RR: 1.21 95% CI 1.13–1.28 and 1.52 95% CI 1.27–1.81), whereas light alcohol consumption (≤12.5 g/day of ethanol) was not associated with an increased risk (RR: 1.00 95% CI 0.95–1.05). However, they found a slightly statistically significant 7% increase in the incidence of colorectal cancer risk for 10 g/day of alcohol intake at the dose-risk analysis; authors also highlighted an increase of overall risk in male moderate drinkers (RR = 1.24, 95% CI 1.13–1.37) and in Asiatic heavy drinkers (RR = 1.81, 95% CI 1.33–2.46) (22).
Another meta-analysis published by Mizoue and colleagues evidenced a strong correlation linking alcohol intakes and colon cancer in case of consumption of more than 23 g/day, while finding no correlation <23 g/day in men (RR: 1.22 CI 95% 0.92, 1.61), neither in women (RR: 0.93 CI 95% 0.70, 1.23) (23). Finally, the meta-analysis by Wang and colleagues, including 22 case-control and only 2 cohort studies, described a dose-response and a positive correlation in case of any amount of alcohol drinking, even in case of less than 12,5 g/day of ethanol (overall pooled RR: 1.07 95% CI, 1.02-1.13); however, by stratifying the results by study types, the increased risk was found only in case-control studies (RR= 1.08, CI 95% 1.02-1.14) and not in cohort studies (RR= 1.02, CI 95% 0.85-1.21)(24).
Alcohol consumption and the risk of brain tumours
One meta-analysis, including 13 case-control and 6 cohort studies, evidenced no association between alcohol and brain tumours (26). However, the authors reported a 20% increase in risk for spirit consumption (RR 1.20 95% CI 1.01-1.42; P 0.584).
Alcohol consumption and the risk of cutaneous melanoma (CM)
A first meta-analysis including 16 studies (14 case control and 2 cohort investigations), evidenced alcohol drinking as a risk factor for CM; the overall pooled RR was 1.20 (95% CI 1.06-1.37; P=0.006), similar between case-control (RR 1.20, 95%CI 1.01-1.44; Po.041) and cohort studies (RR1.26, 95% CI 1.19-1.35; P<0.001) (26).
The pooled RR estimates for the correlation between light alcohol drinking and CM were 1.10 (95% CI 0.90-1.26) overall, 1.06 (95% CI 0.90-1-25) among case-control studies and 1.25 (95% CI 1.15-1.35) among cohort studies. For moderate-heavy alcohol drinking vs no drinking, the pooled RR were 1.18 (95%CI 1.01-1.40) overall, 1.13 (95% CI 0.9-141) among case-control studies and 1.29 (95%CI 1.17-1.43) among cohort studies. However, no significant association was found in the pooled RR from 10 studies adjusted for sun exposure (RR1.12, CI 95% 0.86-1.45). Another meta-analysis found a moderate association with melanoma risk (27). The summary relative risk (SRR) was 1.29 (95% CI 1.14-1.45 I2=13%) for those in the highest vs. lowest category of current alcohol intake and 1.96 (95% CI 1.02-3.76, I2=0) for cumulative intake. Moreover, in the dose response analysis, the increase in risk associated with a 10 g increment in daily alcohol intake was 1.07 (95%CI 1.03-1.11, I2=50%).
Alcohol consumption and the risk of lung cancer
A study by Bagnardi and colleagues showed no association between lung cancer and alcohol drinking in never smokers (RR 1.21 95% CI: 0.95-1.55) (28). Moreover, at the dose–response analysis, RR for an increase in alcohol intake of 10 g/day was 1.01 (95% CI: 0.92-1.10) (28).
A second meta-analysis based on 10 studies, demonstrated a decrease in risk of lung cancer for light alcohol drinking (RR 0.91 95%CI: 0.90-0.94 I2=0) (29).
Alcohol consumption and the risk of laryngeal cancer
Regarding the correlation between alcohol consumption and the risk of laryngeal cancer, Islamini and colleagues showed a 2-fold increase in risk of laryngeal cancer for drinkers vs non-drinkers (RR 1.90 95% CI: 1.59-2.28 p <0.001) (30). While light alcohol drinking was not linked with the risk of developing laryngeal cancer (RR0.88 95% CI: 0.71-1.08), moderate alcohol drinking (RR 1.47, 95% CI: 1.25-1.72) and heavy alcohol drinking (RR 2.62, 95% CI: 2.13-3.23) determined respectively a 1.5 and 2.5-fold increase compared to non-/occasional drinking (30).
Alcohol consumption and the risk of oral and pharyngeal cancer
A meta-analysis of Bagnardi and colleagues showed an increased risk of developing oral and pharyngeal cancer with a RR of 1.13 (95% CI, 1.00-1.26) for light, RR 1.83 (95% CI, 1.62-2.07) for moderate and RR 5.13 (95% CI, 4.31-6.10) for heavy alcohol drinking (12). However, for light alcohol consumption, no increase in tumorigenic risk was found in cohort studies (RR 0.86 95% CI, 0.60-1.23). Moreover, light alcohol intake determined an increase in the risk only in the Asian population (RR 1.33 95% CI, 1.06-1.68), in contrast with European (RR 0.95, 95% CI 0.80-1.12) and North American population (RR 1.09 95%CI, 0.92-1.29).
Alcohol consumption and the risk of breast cancer
A first meta-analysis evidenced a higher risk of breast cancer with increasing consumption of alcoholic beverages; in comparison with non-drinkers, women that assume 12 g/day of alcohol had a relative risk of 1.10 (95% CI: 1.06-1.14).Moreover, no significant difference was found regarding the state of menopause or the type of drink consumed (31). Suzuki et colleagues evidenced a positive relationship between alcohol drinking and development of breast cancer. Authors reported that consumption of more than 10g of ethanol per day determined a 12% increase in the occurrence of oestrogen receptor positive breast cancer and 7% increase for oestrogen receptor negative tumours (32).
Alcohol consumption and the risk of ovarian cancer
A first meta-analysis by Kelemen and colleagues, evidenced that alcohol intake was not associated with risk of ovarian carcinoma (consumption of >3 drinks per day compared to none: OR=0.92, 95% CI=0.76-1.10, P trend=0.27) (33).
Another meta-analysis showed no effects of alcohol consumption on the incidence of ovarian cancer in drinkers vs non-drinkers (RR 1.03 95% CI 0.96-1.10). Furthermore, low (RR 1.02 95% CI 0.94-1.11), moderate (RR 1.08, 95% CI 0.92-1.27) and heavy alcohol consumption (RR 0.99, 95% CI 0.88-1.12) showed no significant effects on the risk of this neoplasm. Finally, authors also noticed a protective effect of low doses of alcohol on ovarian cancer incidence when the participants were from outside US (34).
Alcohol consumption and the risk of prostatic cancer
A recent meta-analysis by Rota and colleagues reported an association between alcohol consumption and prostate cancer (35). Interestingly, the authors noticed an overall RR of 1.06 (95% CI, 1.01–1.10) for any alcohol drinking compared with non/occasional drinking. Furthermore, the dose–risk analysis showed borderline statistically significant RRs of 1.05 (95% CI, 1.02–1.09) for light alcohol drinking (</= 1 drink/ day) and 1.06 (95% CI, 1.01–1.11) for moderate drinking (>1 to <4 drinks/day). Finally, they found a non-significant association at high levels of alcohol drinking (>/=4 drinks/day), with a pooled RR of 1.08 (95% CI, 0.97–1.20) (35).
Another meta-analysis reported a statistically significant dose-response relationship between alcohol consumption and risk of prostate cancer starting with<25 g ethanol / day (RR 1.08, 95% CI 1.04-1.11) (36). Medium (25-<45 g/day), high (45- <65 g / day) and higher volume drinkers (65+ g / day) had a significantly enhanced risk [RR1.07 (95% CI 1.02-1.12), 1.14 (95% CI 1.08-1.22) and 1.18 (95% CI 1.10-1.27) respectively]. The increase in incidence observed for low-volume drinkers was relatively small in the aggregate analysis (8%), but was 23% in studies without erroneous classification errors (for example, the common practice of considering drinkers like abstainers).
Alcohol consumption and the risk of bladder cancer
A large meta-analysis by Mao and colleagues, including 19 studies (both case-control studies and cohort studies) reported no significant association between alcohol drinking and bladder cancer (OR = 1.00, 95% CI 0.89–1.10) (37). The authors also found a negative relation between beer and wine consumption and the probability of bladder cancer.
Another more recent meta-analysis confirmed the findings from meta-analysis of Mao and colleagues (38).The pooled RRs for <3 drinks per day, were 1.00 (95% CI 0.92–1.09), specifically 1.07 (95% CI 0.85–1.36) among cohort and 0.99 (95% CI 0.89–1.09) among case–control studies. All the data on heavy drinkers were from case–control studies (RR = 1.02, 95% CI 0.78–1.33). Results were consistent in several subgroup analyses, including those of studies adjusted for smoking (38).
Alcohol intake and risk of renal cell carcinoma (RCC)
A first meta-analysis observed an inverse association between alcohol intake and risk of RCC, when comparing the highest versus the lowest alcohol consumption categories, with a statistically significant 30% reduction in incidence of RCC (RR 0.70, 95% CI 0.60-0.81) (39).
Remarkably, alcohol consumption of 12 g ethanol per day was correlated with a 5% reduction in the risk of RCC (OR 0,67, 95% CI 0,62-0,73).
Another meta-analysis confirmed an inverse relationship between alcohol intake and risk of RCC (RR 0.73, 95% CI 0.67-0.79) (40). Interestingly, the inverse association was stronger for cohort studies (RR 0.71, 05% CI 0.63-0.78) than for case-control studies (RR 0.76, 95% CI 0.68-0.85) (40). However, the authors highlighted that consumption up to 15 g per day of ethanol, could lead to a decrease in the risk of RCC, but additional consumption does not confer further benefits in the prevention of RCC.
Finally, a third meta-analysis, reported a negative link between alcohol consumption and risk of RCC, significant for both light (<12, 49 g/day) and moderate (12.5-49.9 g/day), but not for heavy drinking (≥50 g/day) [RR: 0.90 (95% CI: 0.84–0.97), 0.79 (95% CI:0.71–0.88) and 0.98 (95% CI 0.58-1.39), respectively) (41).