| Type of cancer . | Comments . |
|---|---|
| Upper aerodigestive tract (UADT)a: oral cavity, pharynx, larynx, esophagus | • A positive linear dose–response relationship has been reported, with a pooled RR of 2.83 (95% CI: 1.73–4.62). • Alcohol use also increases UADT mortality by 2-fold and favors the appearance of second primary cancers in patients with UADT cancer. • Conversely, drinking cessation may decrease the risk of developing both laryngeal and pharyngeal cancer, with an annual risk reduction of 2%. |
| Gastrica | • Alcohol use has been shown to increase gastric cancer risk by 7–39%. • Furthermore, every 10 g/d increment in alcohol consumption appears to increase its risk by 7%. • This relationship may be caused by the damage of alcohol on gastric mucosa, as well as its capacity to increase the carcinogenicity of N-nitroso compounds. |
| HCCa | • The risk of developing HCC appears to increase by 4% per each 10 g of alcohol use in a day. |
| Pancreasa | • Low-to-moderate alcohol use is not significantly associated with its appearance. • The risk increases with the consumption of ≥3 drinks/day, with an RR of 1.22 (95% CI: 1.12–1.34). |
| Colorectal (CRC)a | • There is a J-shaped association, with a significantly increased risk with consumptions of ≥3 drinks/day (OR: 1.25, 95% CI: 1.11–1.40, P < 0.001). • Intakes of ≥45 g/day increase the risk by 41% (RR = 1.41, 95% CI: 1.16–1.72). • Its use may also worsen the prognosis of CRC by promoting metastasis through a CCL5-induced and AMPK-pathway-mediated activation of autophagy. |
| Bladder (BCa)a | • Alcohol use does not appear to increase the risk of BCa in the general population. • However, heavy alcohol use may increase the risk in both spirit-drinking males (by 42%) and Japanese population (by 31%). • These findings may be explained by the damage exerted on DNA by its metabolite acetaldehyde, as well as its carcinogenic properties when excreted through the urinary tract. |
| Prostatea | • Any alcohol use increases the risk by 6% overall. • There is also a dose–response relationship, beginning at low levels of intake (>1.3, <24 g per day). • Low alcohol use appears to increase the risk by 8%, whereas the use of >65 g/day raises the risk by 18%. • This association may be explained by several mechanisms like acetaldehyde toxicity, dysfunction in DNA repair, oxidative stress and induction of CYP2E1. |
| Breast | • There is a positive dose–response association, without an identified lower threshold. • Alcohol use of ≤12.5 g per day has been shown to increase the risk by 4–5%, compared to non-drinkers. • Each additional 10 g/day of alcohol increases the risk by 10.5% (RR = 1.10, 95% CI: 1.08–1.13). |
| Skin: cutaneous melanoma and non-melanoma skin cancer (NMSC) | • Any alcohol drinking increases the risk of CM by 20% (RR = 1.20, 95% CI: 1.06–1.37). • It also may increase the risk of NMSC (both basal cell carcinoma and cutaneous squamous cell carcinoma) in a dose-dependent manner. |
| Hematological malignancies | • Multiple meta-analyses have linked alcohol use to a supposed decreased risk of leukemia, myeloma and both Hodgkin and non-Hodgkin lymphoma. • These findings may be partially explained by ethanol’s immunomodulatory properties, its capacity to reduce the activation of mTOR complex and the improvement of insulin sensitivity associated with its intake. • Nonetheless, these results should be interpreted carefully, as the inverse relationships tend to predominate on case–control rather than cohort studies’ data. |
| Type of cancer . | Comments . |
|---|---|
| Upper aerodigestive tract (UADT)a: oral cavity, pharynx, larynx, esophagus | • A positive linear dose–response relationship has been reported, with a pooled RR of 2.83 (95% CI: 1.73–4.62). • Alcohol use also increases UADT mortality by 2-fold and favors the appearance of second primary cancers in patients with UADT cancer. • Conversely, drinking cessation may decrease the risk of developing both laryngeal and pharyngeal cancer, with an annual risk reduction of 2%. |
| Gastrica | • Alcohol use has been shown to increase gastric cancer risk by 7–39%. • Furthermore, every 10 g/d increment in alcohol consumption appears to increase its risk by 7%. • This relationship may be caused by the damage of alcohol on gastric mucosa, as well as its capacity to increase the carcinogenicity of N-nitroso compounds. |
| HCCa | • The risk of developing HCC appears to increase by 4% per each 10 g of alcohol use in a day. |
| Pancreasa | • Low-to-moderate alcohol use is not significantly associated with its appearance. • The risk increases with the consumption of ≥3 drinks/day, with an RR of 1.22 (95% CI: 1.12–1.34). |
| Colorectal (CRC)a | • There is a J-shaped association, with a significantly increased risk with consumptions of ≥3 drinks/day (OR: 1.25, 95% CI: 1.11–1.40, P < 0.001). • Intakes of ≥45 g/day increase the risk by 41% (RR = 1.41, 95% CI: 1.16–1.72). • Its use may also worsen the prognosis of CRC by promoting metastasis through a CCL5-induced and AMPK-pathway-mediated activation of autophagy. |
| Bladder (BCa)a | • Alcohol use does not appear to increase the risk of BCa in the general population. • However, heavy alcohol use may increase the risk in both spirit-drinking males (by 42%) and Japanese population (by 31%). • These findings may be explained by the damage exerted on DNA by its metabolite acetaldehyde, as well as its carcinogenic properties when excreted through the urinary tract. |
| Prostatea | • Any alcohol use increases the risk by 6% overall. • There is also a dose–response relationship, beginning at low levels of intake (>1.3, <24 g per day). • Low alcohol use appears to increase the risk by 8%, whereas the use of >65 g/day raises the risk by 18%. • This association may be explained by several mechanisms like acetaldehyde toxicity, dysfunction in DNA repair, oxidative stress and induction of CYP2E1. |
| Breast | • There is a positive dose–response association, without an identified lower threshold. • Alcohol use of ≤12.5 g per day has been shown to increase the risk by 4–5%, compared to non-drinkers. • Each additional 10 g/day of alcohol increases the risk by 10.5% (RR = 1.10, 95% CI: 1.08–1.13). |
| Skin: cutaneous melanoma and non-melanoma skin cancer (NMSC) | • Any alcohol drinking increases the risk of CM by 20% (RR = 1.20, 95% CI: 1.06–1.37). • It also may increase the risk of NMSC (both basal cell carcinoma and cutaneous squamous cell carcinoma) in a dose-dependent manner. |
| Hematological malignancies | • Multiple meta-analyses have linked alcohol use to a supposed decreased risk of leukemia, myeloma and both Hodgkin and non-Hodgkin lymphoma. • These findings may be partially explained by ethanol’s immunomodulatory properties, its capacity to reduce the activation of mTOR complex and the improvement of insulin sensitivity associated with its intake. • Nonetheless, these results should be interpreted carefully, as the inverse relationships tend to predominate on case–control rather than cohort studies’ data. |
Abbreviations: CCL5, C-C motif ligand 5; AMPK, 5′ adenosine monophosphate-activated protein kinase; DNA, deoxyribonucleic acid; CYP2E1, cytochrome P450 2E1; mTOR, mammalian target of rapamycin.
aTobacco smoking may act as a synergistic risk factor.
| Type of cancer . | Comments . |
|---|---|
| Upper aerodigestive tract (UADT)a: oral cavity, pharynx, larynx, esophagus | • A positive linear dose–response relationship has been reported, with a pooled RR of 2.83 (95% CI: 1.73–4.62). • Alcohol use also increases UADT mortality by 2-fold and favors the appearance of second primary cancers in patients with UADT cancer. • Conversely, drinking cessation may decrease the risk of developing both laryngeal and pharyngeal cancer, with an annual risk reduction of 2%. |
| Gastrica | • Alcohol use has been shown to increase gastric cancer risk by 7–39%. • Furthermore, every 10 g/d increment in alcohol consumption appears to increase its risk by 7%. • This relationship may be caused by the damage of alcohol on gastric mucosa, as well as its capacity to increase the carcinogenicity of N-nitroso compounds. |
| HCCa | • The risk of developing HCC appears to increase by 4% per each 10 g of alcohol use in a day. |
| Pancreasa | • Low-to-moderate alcohol use is not significantly associated with its appearance. • The risk increases with the consumption of ≥3 drinks/day, with an RR of 1.22 (95% CI: 1.12–1.34). |
| Colorectal (CRC)a | • There is a J-shaped association, with a significantly increased risk with consumptions of ≥3 drinks/day (OR: 1.25, 95% CI: 1.11–1.40, P < 0.001). • Intakes of ≥45 g/day increase the risk by 41% (RR = 1.41, 95% CI: 1.16–1.72). • Its use may also worsen the prognosis of CRC by promoting metastasis through a CCL5-induced and AMPK-pathway-mediated activation of autophagy. |
| Bladder (BCa)a | • Alcohol use does not appear to increase the risk of BCa in the general population. • However, heavy alcohol use may increase the risk in both spirit-drinking males (by 42%) and Japanese population (by 31%). • These findings may be explained by the damage exerted on DNA by its metabolite acetaldehyde, as well as its carcinogenic properties when excreted through the urinary tract. |
| Prostatea | • Any alcohol use increases the risk by 6% overall. • There is also a dose–response relationship, beginning at low levels of intake (>1.3, <24 g per day). • Low alcohol use appears to increase the risk by 8%, whereas the use of >65 g/day raises the risk by 18%. • This association may be explained by several mechanisms like acetaldehyde toxicity, dysfunction in DNA repair, oxidative stress and induction of CYP2E1. |
| Breast | • There is a positive dose–response association, without an identified lower threshold. • Alcohol use of ≤12.5 g per day has been shown to increase the risk by 4–5%, compared to non-drinkers. • Each additional 10 g/day of alcohol increases the risk by 10.5% (RR = 1.10, 95% CI: 1.08–1.13). |
| Skin: cutaneous melanoma and non-melanoma skin cancer (NMSC) | • Any alcohol drinking increases the risk of CM by 20% (RR = 1.20, 95% CI: 1.06–1.37). • It also may increase the risk of NMSC (both basal cell carcinoma and cutaneous squamous cell carcinoma) in a dose-dependent manner. |
| Hematological malignancies | • Multiple meta-analyses have linked alcohol use to a supposed decreased risk of leukemia, myeloma and both Hodgkin and non-Hodgkin lymphoma. • These findings may be partially explained by ethanol’s immunomodulatory properties, its capacity to reduce the activation of mTOR complex and the improvement of insulin sensitivity associated with its intake. • Nonetheless, these results should be interpreted carefully, as the inverse relationships tend to predominate on case–control rather than cohort studies’ data. |
| Type of cancer . | Comments . |
|---|---|
| Upper aerodigestive tract (UADT)a: oral cavity, pharynx, larynx, esophagus | • A positive linear dose–response relationship has been reported, with a pooled RR of 2.83 (95% CI: 1.73–4.62). • Alcohol use also increases UADT mortality by 2-fold and favors the appearance of second primary cancers in patients with UADT cancer. • Conversely, drinking cessation may decrease the risk of developing both laryngeal and pharyngeal cancer, with an annual risk reduction of 2%. |
| Gastrica | • Alcohol use has been shown to increase gastric cancer risk by 7–39%. • Furthermore, every 10 g/d increment in alcohol consumption appears to increase its risk by 7%. • This relationship may be caused by the damage of alcohol on gastric mucosa, as well as its capacity to increase the carcinogenicity of N-nitroso compounds. |
| HCCa | • The risk of developing HCC appears to increase by 4% per each 10 g of alcohol use in a day. |
| Pancreasa | • Low-to-moderate alcohol use is not significantly associated with its appearance. • The risk increases with the consumption of ≥3 drinks/day, with an RR of 1.22 (95% CI: 1.12–1.34). |
| Colorectal (CRC)a | • There is a J-shaped association, with a significantly increased risk with consumptions of ≥3 drinks/day (OR: 1.25, 95% CI: 1.11–1.40, P < 0.001). • Intakes of ≥45 g/day increase the risk by 41% (RR = 1.41, 95% CI: 1.16–1.72). • Its use may also worsen the prognosis of CRC by promoting metastasis through a CCL5-induced and AMPK-pathway-mediated activation of autophagy. |
| Bladder (BCa)a | • Alcohol use does not appear to increase the risk of BCa in the general population. • However, heavy alcohol use may increase the risk in both spirit-drinking males (by 42%) and Japanese population (by 31%). • These findings may be explained by the damage exerted on DNA by its metabolite acetaldehyde, as well as its carcinogenic properties when excreted through the urinary tract. |
| Prostatea | • Any alcohol use increases the risk by 6% overall. • There is also a dose–response relationship, beginning at low levels of intake (>1.3, <24 g per day). • Low alcohol use appears to increase the risk by 8%, whereas the use of >65 g/day raises the risk by 18%. • This association may be explained by several mechanisms like acetaldehyde toxicity, dysfunction in DNA repair, oxidative stress and induction of CYP2E1. |
| Breast | • There is a positive dose–response association, without an identified lower threshold. • Alcohol use of ≤12.5 g per day has been shown to increase the risk by 4–5%, compared to non-drinkers. • Each additional 10 g/day of alcohol increases the risk by 10.5% (RR = 1.10, 95% CI: 1.08–1.13). |
| Skin: cutaneous melanoma and non-melanoma skin cancer (NMSC) | • Any alcohol drinking increases the risk of CM by 20% (RR = 1.20, 95% CI: 1.06–1.37). • It also may increase the risk of NMSC (both basal cell carcinoma and cutaneous squamous cell carcinoma) in a dose-dependent manner. |
| Hematological malignancies | • Multiple meta-analyses have linked alcohol use to a supposed decreased risk of leukemia, myeloma and both Hodgkin and non-Hodgkin lymphoma. • These findings may be partially explained by ethanol’s immunomodulatory properties, its capacity to reduce the activation of mTOR complex and the improvement of insulin sensitivity associated with its intake. • Nonetheless, these results should be interpreted carefully, as the inverse relationships tend to predominate on case–control rather than cohort studies’ data. |
Abbreviations: CCL5, C-C motif ligand 5; AMPK, 5′ adenosine monophosphate-activated protein kinase; DNA, deoxyribonucleic acid; CYP2E1, cytochrome P450 2E1; mTOR, mammalian target of rapamycin.
aTobacco smoking may act as a synergistic risk factor.
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