星空无限传媒

Consequences

Title: 

 

Citation: O'Connell CP, Berndt SI, Chudy-Onwugaje K, Kunzmann A, Huang WY, Barry KH, Loftfield E. Association of alcohol intake over the lifetime with colorectal adenoma and colorectal cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Cancer. 2026 Feb 1;132(3):e70201. doi: 10.1002/cncr.70201. Erratum in: Cancer. 2026 Feb 15;132(4):e70324. doi: 10.1002/cncr.70324. PMID: 41582658; PMCID: PMC12833583.

Study Objective: The objective of the current study was to estimate the association of lifetime alcohol drinking with incident colorectal adenoma and cancer.

Methods: US adults enrolled in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial reported alcohol intake during four age periods. Average lifetime alcohol intake was calculated as average drinks per week from age 18 years until study baseline; N= 12,327

Results: Current drinkers with an average lifetime alcohol intake of 14 or more drinks per week, compared with one drink or less per week, had:
1. A higher risk of CRC (Hazard Ratio – HR, 1.25; 95% CI, 1.01-1.53), especially rectal cancer (HR, 1.95; 95% CI, 1.17-3.28).
2. Consistent heavy drinking versus light drinking was positively associated with CRC risk (HR, 1.91; 95% CI, 1.17-3.12).
3. Compared with current drinkers averaging less than one drink per week, former drinkers had lower odds of non-advanced adenoma (OR, 0.58; 95% CI, 0.39-0.84).
4. Current drinkers averaging from seven to less than 14 drinks compared with less than one drink per week had a lower risk of CRC (HR, 0.79; 95% CI, 0.64-0.97), especially distal colon cancer (HR, 0.64; 95% CI, 0.42-1.00).

Conclusions: Consistent heavy alcohol intake and higher average lifetime alcohol drinking may increase CRC risk, whereas cessation may lower adenoma risk. Associations may differ by tumor site.

Notes from Duane McBride –
1. These data show that two drinks a day about double your risk of rectal cancer.
2. The good news is that stopping alcohol use reduced ones odds of by almost half for non-advanced adenoma when compared to very light drinkers (one drink per week).
3. These data further illustrate there is no safe level of alcohol use. There was a time when two drinks a day was considered healthy.

 

Title: 

Citation: Morford KL, Tetrault JM, O’Connor PG. Alcohol and Cancer Risk. JAMA. 2025;334(10):908–909. doi:10.1001/jama.2025.11229

Summary of Key Points:
1.  Any daily alcohol consumption is associated with certain cancers, and the risk of cancer increases with higher alcohol intake
2. In 2020, an estimated 740鈥�000 cancer cases globally (4.1%) were attributable to alcohol consumption, with most occurring in men (76.7%).2
3. In the US, alcohol was identified as the third-leading modifiable cancer risk factor after cigarette smoking and excess weight, contributing to 5.4% of cases and 4.1% of deaths   among adults 30 years or older in 2019.3

 

Title: 

Citation: Topiwala A, Levey DF, Zhou H, et alAlcohol use and risk of dementia in diverse populations: evidence from cohort, case–control and Mendelian randomisation approachesBMJ Evidence-Based Medicine Published Online First: 23 September 2025. doi: 10.1136/bmjebm-2025-113913

Abstract
Objectives: To investigate the relationship between alcohol consumption and dementia.

Design: Prospective cohort and case–control analyses combined with linear and non-linear Mendelian randomization.

Setting:  Two large-scale population-based cohorts: the US Million Veteran Programme and the UK Biobank. Genetic analyses used summary statistics from genome-wide association studies (GWAS).

Participants: 559 559 adults aged 56–72 years at baseline were included in observational analyses (mean follow-up: 4 years in the US cohort; 12 years in the UK cohort). Genetic analyses used summary data from multiple large GWAS consortia (2.4 million participants).

Main outcome measures: Incident all-cause dementia, determined through health record linkage, and genetic proxies.

Results:
1. During follow-up, 14 540 participants developed dementia and 48 034 died.                   
2.   Alcohol intake increased dementia,
3. Individuals who developed dementia also experienced a decline in alcohol intake over time, suggesting reverse causation—where early cognitive decline leads to reduced alcohol consumption—underlies the supposed protective alcohol effects in observational studies.
 
Conclusions: These findings provide evidence for a relationship between all types of alcohol use and increased dementia risk. While correlational observational data suggested a protective effect of light drinking, this could be in part attributable to reduced drinking seen in early dementia; genetic analyses did not support any protective effect, suggesting that any level of alcohol consumption may contribute to dementia risk. Public health strategies that reduce the prevalence of alcohol use disorder could potentially lower the incidence of dementia by up to 16%.
 

Title: 

Citation: Di Federico S, Filippini T, Whelton PK, Cecchini M, Iamandii I, Boriani G, Vinceti M. Alcohol Intake and Blood Pressure Levels: A Dose-Response Meta-Analysis of Nonexperimental Cohort Studies. Hypertension. 2023 Oct;80(10):1961-1969. doi: 10.1161/HYPERTENSIONAHA.123.21224. Epub 2023 Jul 31. PMID: 37522179; PMCID: PMC10510850.

Abstract
Background: Alcohol consumption may increase blood pressure but the details of the relationship are incomplete, particularly for the association at low levels of alcohol consumption, and no meta-analyses are available for nonexperimental cohort studies.

Methods: We performed a systematic search of longitudinal studies in healthy adults that reported on the association between alcohol intake and blood pressure.

Results:
1. Seven studies, with 19,548 participants and a median follow-up of 5.3 years (range, 4-12 years), were included in the analysis.
2. We observed a substantially linear positive association between baseline alcohol intake and changes over time in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure DBP), with no suggestion of an exposure-effect threshold.
3. Overall, average SBP was 1.25 and 4.90 mm Hg higher for 12 or 48 grams of daily alcohol consumption, compared with no consumption. The corresponding differences for DBP were 1.14 and 3.10 mm Hg.
4. Subgroup analyses by sex showed an almost linear association between baseline alcohol intake and SBP changes in both men and women, and for DBP in men while in women we identified an inverted U-shaped association. Alcohol consumption was positively associated with blood pressure changes in both Asians and North Americans, apart from DBP in the latter group.

Conclusions: Our results suggest the association between alcohol consumption and SBP is direct and linear with no evidence of a threshold for the association (i.e., no safe level), while for DBP the association is modified by sex and geographic location.

 

Title: 

Citation: Morford KL, Tetrault JM, O’Connor PG. Alcohol and Cancer Risk. JAMA. 2025;334(10):908–909. doi:10.1001/jama.2025.11229

Summary of Key Points:
1.  Any daily alcohol consumption is associated with certain cancers, and the risk of cancer increases with higher alcohol intake
2. In 2020, an estimated 740鈥�000 cancer cases globally (4.1%) were attributable to alcohol consumption, with most occurring in men (76.7%).2
3. In the US, alcohol was identified as the third-leading modifiable cancer risk factor after cigarette smoking and excess weight, contributing to 5.4% of cases and 4.1% of deaths among adults 30 years or older in 2019.3
 

Title: 


Citation: Topiwala A, Levey DF, Zhou H, et alAlcohol use and risk of dementia in diverse populations: evidence from cohort, case–control and Mendelian randomisation approachesBMJ Evidence-Based Medicine Published Online First: 23 September 2025. doi: 10.1136/bmjebm-2025-113913

Abstract
Objectives: To investigate the relationship between alcohol consumption and dementia.

Design: Prospective cohort and case–control analyses combined with linear and non-linear Mendelian randomization.

Setting:  Two large-scale population-based cohorts: the US Million Veteran Programme and the UK Biobank. Genetic analyses used summary statistics from genome-wide association studies (GWAS).

Participants: 559 559 adults aged 56–72 years at baseline were included in observational analyses (mean follow-up: 4 years in the US cohort; 12 years in the UK cohort). Genetic analyses used summary data from multiple large GWAS consortia (2.4 million participants).

Main outcome measures: Incident all-cause dementia, determined through health record linkage, and genetic proxies.

Results:
1. During follow-up, 14 540 participants developed dementia and 48 034 died.                   
2.  Alcohol intake increased dementia,
3. Individuals who developed dementia also experienced a decline in alcohol intake over time, suggesting reverse causation—where early cognitive       decline leads to reduced   alcohol consumption—underlies the supposed protective alcohol effects in observational   studies.
 

Conclusions: These findings provide evidence for a relationship between all types of alcohol use and increased dementia risk. While correlational observational data suggested a protective effect of light drinking, this could be in part attributable to reduced drinking seen in early dementia; genetic analyses did not support any protective effect, suggesting that any level of alcohol consumption may contribute to dementia risk. Public health strategies that reduce the prevalence of alcohol use disorder could potentially lower the incidence of dementia by up to 16%.
 

Title: 

Citation: Di Federico S, Filippini T, Whelton PK, Cecchini M, Iamandii I, Boriani G, Vinceti M. Alcohol Intake and Blood Pressure Levels: A Dose-Response Meta-Analysis of Nonexperimental Cohort Studies. Hypertension. 2023 Oct;80(10):1961-1969. doi: 10.1161/HYPERTENSIONAHA.123.21224. Epub 2023 Jul 31. PMID: 37522179; PMCID: PMC10510850.

Abstract
Background: Alcohol consumption may increase blood pressure but the details of the relationship are incomplete, particularly for the association at low levels of alcohol consumption, and no meta-analyses are available for nonexperimental cohort studies.

Methods: We performed a systematic search of longitudinal studies in healthy adults that reported on the association between alcohol intake and blood pressure.

Results:
1. Seven studies, with 19,548 participants and a median follow-up of 5.3 years (range, 4-12 years), were included in the analysis.
2. We observed a substantially linear positive association between baseline alcohol intake and changes over time in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP), with no suggestion of an exposure-effect threshold.
3. Overall, average SBP was 1.25 and 4.90 mm Hg higher for 12 or 48 grams of daily alcohol consumption, compared with no consumption. The corresponding differences for DBP were 1.14 and 3.10 mm Hg.
4. Subgroup analyses by sex showed an almost linear association between baseline alcohol intake and SBP changes in both men and women, and for DBP in men while in women we identified an inverted U-shaped association. Alcohol consumption was positively associated with blood pressure changes in both Asians and North Americans, apart from DBP in the latter group.

Conclusions: Our results suggest the association between alcohol consumption and SBP is direct and linear with no evidence of a threshold for the association (i.e., no safe level), while for DBP the association is modified by sex and geographic location.

 

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