Lifetime Alcohol Intake Research Articles

Abuse and neglect as indicators of unhealthy behaviours among 15-year-old schoolchildren in Albania

ObjectiveWe assessed the independent associations of lifetime child abuse and neglect indices with behavioural characteristics of children. Study designA cross-sectional study was conducted in Albania in 2022. MethodsParticipants consisted of a nationwide representative sample of 1877 schoolchildren aged 15 years (55 % girls; response: 96 %). Data on lifetime child abuse and neglect were collected, along with behavioural factors and sociodemographic characteristics. Binary logistic regression was used to assess the independent associations of child abuse and neglect with behavioural factors of schoolchildren. ResultsIrrespective of sociodemographic characteristics, lifetime physical abuse was positively related to lifetime smoking (OR = 1.8, 95%CI = 1.4–2.3), lifetime alcohol consumption (OR = 2.4, 95%CI = 1.9–2.9), and breakfast skipping (OR = 1.3, 95%CI = 1.0–1.6). Furthermore, positive independent factors associated with emotional abuse included lifetime alcohol intake (OR = 1.7, 95%CI = 1.3–2.1) and breakfast skipping (OR = 1.4, 95%CI = 1.0–1.8). Additionally, positive factors associated with lifetime emotional neglect consisted of lifetime smoking (OR = 2.2, 95%CI = 1.6–3.0) and alcohol intake (OR = 2.0, 95%CI = 1.5–2.6), and a lower fruit consumption (OR = 1.7, 95%CI = 1.3–2.3). Positive factors associated with lifetime sexual abuse included lifetime alcohol consumption (OR = 2.4, 95%CI = 1.4–4.1) and especially smoking (OR = 4.3, 95%CI = 2.6–7.3). Also, lifetime witnessing of family violence was positively related to lifetime smoking (OR = 2.7, 95%CI = 1.8–4.1) and alcohol intake (OR = 1.7, 95%CI = 1.2–2.6). ConclusionsWe evidenced strong and consistent links between child maltreatment indices and unhealthy behavioural practices among 15-year-old children in Albania. These findings underscore the potential impact of early trauma on developmental trajectories. The association between child abuse and the adoption of detrimental behaviours highlights the urgent need for comprehensive support and intervention strategies to break the cycle of harm.

Major Depressive Disorder Impacts Peripheral Artery Disease Risk Through Intermediary Risk Factors.

Major depressive disorder (MDD) has been identified as a causal risk factor for multiple forms of cardiovascular disease. Although observational evidence has linked MDD to peripheral artery disease (PAD), causal evidence of this relationship is lacking. Inverse variance weighted 2-sample Mendelian randomization was used to test the association the between genetic liability for MDD and genetic liability for PAD. Genetic liability for MDD was associated with increased genetic liability for PAD (odds ratio [OR], 1.17 [95% CI, 1.06-1.29]; P=2.6×10-3). Genetic liability for MDD was also associated with increased genetically determined lifetime smoking (β=0.11 [95% CI, 0.078-0.14]; P=1.2×10-12), decreased alcohol intake (β=-0.078 [95% CI, -0.15 to 0]; P=0.043), and increased body mass index (β=0.10 [95% CI, 0.02-0.19]; P=1.8×10-2), which in turn were associated with genetic liability for PAD (smoking: OR, 2.81 [95% CI, 2.28-3.47], P=9.8×10-22; alcohol: OR, 0.77 [95% CI, 0.66-0.88]; P=1.8×10-4; body mass index: OR, 1.61 [95% CI, 1.52-1.7]; P=1.3×10-57). Controlling for lifetime smoking index, alcohol intake, and body mass index with multivariable Mendelian randomization completely attenuated the association between genetic liability for MDD with genetic liability for PAD. This work provides evidence for a possible causal association between MDD and PAD that is dependent on intermediate risk factors, adding to the growing body of evidence suggesting that effective management and treatment of cardiovascular diseases may require a composite of physical and mental health interventions.

Alcohol intake is associated with a decreased risk of developing primary biliary cholangitis.

BACKGROUNDPrimary biliary cholangitis (PBC) is a chronic progressive liver disease of unknown aetiology characterised by immune-mediated destruction of small and medium-sized intrahepatic bile ducts. There are few well-established risk factors and epidemiological studies are needed to further evaluate the pathogenesis of the disease. AIMTo evaluate the relationship between alcohol intake, smoking and marijuana use with PBC development. METHODSWe conducted a prevalent case control study of 200 cases and 200 age (within a five year age band) and sex-matched controls, identified from the Victorian PBC prevalence study. We assessed lifetime alcohol intake and smoking behaviour (both tobacco and marijuana) prior to PBC onset and used conditional logistic regression for analyses. RESULTSAlcohol intake consistently showed a dose-dependent inverse association with case status, and this was most substantial for 21-30 years and 31-40 years (Ptrend < 0.001). Smoking was associated with PBC, with a stronger association with a longer duration of smoking [e.g., adjusted OR 2.27 (95%CI: 1.12- 4.62) for those who had smoked for 20-35 years]. There was no association between marijuana use and PBC. CONCLUSIONAlcohol appears to have an inverse relationship with PBC. Smoking has been confirmed as an environmental risk factor for PBC. There was no association between marijuana use and PBC.

Baseline and lifetime alcohol consumption and risk of skin cancer in the European Prospective Investigation into Cancer and Nutrition cohort (EPIC).

Experimental evidence suggests that alcohol induces cutaneous carcinogenesis, yet epidemiological studies on the link between alcohol intake and skin cancer have been inconsistent. The European Prospective Investigation into Cancer and Nutrition (EPIC) is a prospective cohort initiated in 1992 in 10 European countries. Alcohol intake at baseline and average lifetime alcohol intake were assessed using validated country-specific dietary and lifestyle questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated in Cox models. A total of 14 037 skin cancer cases (melanoma: n=2457; basal-cell carcinoma (BCC): n=8711; squamous-cell carcinoma (SCC): n=1928; unknown: n=941) were identified among 450 112 participants (average follow-up: 15 years). Baseline alcohol intake was positively associated with SCC (>15 vs 0.1-4.9 g/day: HR=1.44, 95% CI=1.17-1.77; Ptrend =.001), BCC (HR=1.12, 95% CI=1.01-1.23; Ptrend =.04), and melanoma risks in men (HR=1.17, 95% CI=0.95-1.44; Ptrend =.17), while associations were more modest in women (SCC: HR=1.09, 95% CI=0.90-1.30; Ptrend =.13; BCC: HR=1.08, 95% CI=1.00-1.17, Ptrend =.03; melanoma: HR=0.93, 95% CI=0.80-1.08, Ptrend =.13). Associations were similar for lifetime alcohol intake, with an attenuated linear trend. Lifetime liquor/spirit intake was positively associated with melanoma (fourth vs first quartile: HR=1.47, 95% CI=1.08-1.99; Ptrend =.0009) and BCC risks in men (HR=1.17, 95% CI=1.04-1.31; Ptrend =.14). Baseline and lifetime intakes of wine were associated with BCC risk (HR=1.25 in men; HR=1.11-1.12; in women). No statistically significant associations were found between beverage types and SCC risk. Intake of beer was not associated with skin cancer risk. Our study suggests positive relationships between alcohol intake and skin cancer risk, which may have important implications for the primary prevention of skin cancer.

Alcohol consumption patterns and unhealthy aging among older lifetime drinkers from Spain

BackgroundThe protective health effects of light alcohol consumption are debated due to potential selection biases, reverse causation and confounding. We examined cross-sectional and prospective associations of alcohol consumption patterns with unhealthy aging among older drinkers addressing these methodological issues. Methods2081 lifetime drinkers aged 65 + years from the Seniors-ENRICA-2 cohort followed-up for 2.4 years were classified as occasional (average lifetime alcohol intake [g/day] ≤1.43), low-risk (men: >1.43–20; women: >1.43–10), moderate-risk (men: >20–40; women: >10–20) and high-risk drinkers (men: >40; women: >20; or binge drinkers). A Mediterranean drinking pattern (MDP) was defined as occasional/low-risk drinking, wine preference and drinking only with meals. Unhealthy aging was measured with a 52-item health deficit accumulation index (DAI), with higher values indicating more health deficits. ResultsA 10-g/day increment in lifetime average alcohol intake was cross-sectionally associated with a higher DAI among all drinkers (mean difference [95% confidence interval] = 0.35 [0.16, 0.53]) and moderate-/high-risk drinkers (0.41 [0.17, 0.65]), but not among occasional/low-risk drinkers. Also, the DAI was 1.35 (0.06, 2.65) points higher in high-risk versus low-risk drinkers and 2.07 (0.59, 3.60) points higher in non-adherers versus adherers to the MDP. Most associations strengthened when restricting analyses to individuals with lower disease burden and did not generally remain after 2.4 years. ConclusionsWe found no evidence of a beneficial association between low-risk alcohol consumption and unhealthy aging, but a detrimental one for high-risk drinking, which strengthened when accounting for reverse causation, although attenuated over the follow-up likely due to selective attrition of those less resilient to the harmful effects of alcohol.

Alcohol consumption patterns and growth differentiation factor 15 among life-time drinkers aged 65+ years in Spain: a cross-sectional study.

To examine the association of alcohol consumption patterns with growth differentiation factor 15 (GDF-15) in older drinkers, separately among individuals with cardiovascular disease (CVD)/diabetes and those without them, as GDF-15 is a strong biomarker of chronic disease burden. Cross-sectional study. Population-based study in Madrid (Spain). A total of 2051 life-time drinkers aged 65+ years included in the Seniors-ENRICA-2 study in 2015-17. Participants' mean age was 71.4years and 55.4% were men. According to their average life-time alcohol intake, participants were classified as occasional (≤ 1.43 g/day), low-risk (men: > 1.43-20 g/day; women: > 1.43-10g/day), moderate-risk (men: > 20-40 g/day; women: > 10-20 g/day) and high-risk drinkers (men: > 40 g/day; women: > 20 g/day; or binge drinkers). We also ascertained wine preference (> 80% of alcohol derived from wine), drinking with meals and adherence to a Mediterranean drinking pattern (MDP) defined as low-risk drinking, wine preference and one of the following: drinking only with meals; higher adherence to the Mediterranean diet; or any of these. In participants without CVD/diabetes, GDF-15 increased by 0.27% [95% confidence interval (CI) = 0.06%, 0.48%] per 1g/day increment in alcohol among high-risk drinkers, but there was no clear evidence of association in those with lower intakes or in the overall group, or across categories of alcohol consumption status. Conversely, among those with CVD/diabetes, GDF-15 rose by 0.19% (95% CI = 0.05%, 0.33%) per 1g/day increment in the overall group and GDF-15 was 26.89% (95% CI = 12.93%, 42.58%) higher in high-risk versus low-risk drinkers. Drinking with meals did not appear to be related to GDF-15, but among those without CVD/diabetes, wine preference and adherence to the MDP were associated with lower GDF-15, especially when combined with high adherence to the Mediterranean diet. Among older life-time drinkers in Madrid, Spain, high-risk drinking was positively associated with growth differentiation factor 15 (a biomarker of chronic disease burden). There was inconclusive evidence of a beneficial association for low-risk consumption.

Prediagnosis alcohol intake and metachronous cancer risk in cancer survivors: A prospective cohort study.

Alcohol consumption is a known cause of cancer, but its role in the etiology of second primary (metachronous) cancer is uncertain. Associations between alcohol intake up until study enrollment (prediagnosis) and risk of metachronous cancer were estimated using 9435 participants in the Melbourne Collaborative Cohort Study who were diagnosed with their first invasive cancer after enrollment (1990-1994). Follow-up was from date of first invasive cancer until diagnosis of metachronous cancer, death or censor date (February 2018), whichever came first. Alcohol intake for 10-year periods from age 20 until decade encompassing baseline using recalled beverage-specific frequency and quantity was used to calculate baseline and lifetime intakes, and group-based intake trajectories. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs), adjusted for potential confounders. After a mean follow-up of 7 years, 1512 metachronous cancers were identified. A 10 g/d increment in prediagnosis lifetime alcohol intake (HR = 1.03, 95% CI = 1.00-1.06; Pvalue = .02) and an intake of ≥60 g/d (HR = 1.32, 95% CI = 1.01-1.73) were associated with increased metachronous cancer risk. We observed positive associations (per 10 g/d increment) for metachronous colorectal (HR = 1.07, 95% CI = 1.00-1.14), upper aero-digestive tract (UADT) (HR = 1.16, 95% CI = 1.00-1.34) and kidney cancer (HR = 1.24, 95% CI = 1.10-1.39). Although these findings were partly explained by effects of smoking, the association for kidney cancer remained unchanged when current smokers or obese individuals were excluded. Alcohol intake trajectories over the life course confirmed associations with metachronous cancer risk. Prediagnosis long-term alcohol intake, and particularly heavy drinking, may increase the risk of metachronous cancer, particularly of the colorectum, UADT and kidney.

Lifetime alcohol intake, drinking patterns over time and risk of stomach cancer: A pooled analysis of data from two prospective cohort studies.

Alcohol consumption is causally linked to several cancers but the evidence for stomach cancer is inconclusive. In our study, the association between long‐term alcohol intake and risk of stomach cancer and its subtypes was evaluated. We performed a pooled analysis of data collected at baseline from 491 714 participants in the European Prospective Investigation into Cancer and Nutrition and the Melbourne Collaborative Cohort Study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for incident stomach cancer in relation to lifetime alcohol intake and group‐based life course intake trajectories, adjusted for potential confounders including Helicobacter pylori infection. In all, 1225 incident stomach cancers (78% noncardia) were diagnosed over 7 094 637 person‐years; 984 in 382 957 study participants with lifetime alcohol intake data (5 455 507 person‐years). Although lifetime alcohol intake was not associated with overall stomach cancer risk, we observed a weak positive association with noncardia cancer (HR = 1.03, 95% CI: 1.00‐1.06 per 10 g/d increment), with a HR of 1.50 (95% CI: 1.08‐2.09) for ≥60 g/d compared to 0.1 to 4.9 g/d. A weak inverse association with cardia cancer (HR = 0.93, 95% CI: 0.87‐1.00) was also observed. HRs of 1.48 (95% CI: 1.10‐1.99) for noncardia and 0.51 (95% CI: 0.26‐1.03) for cardia cancer were observed for a life course trajectory characterized by heavy decreasing intake compared to light stable intake (P homogeneity = .02). These associations did not differ appreciably by smoking or H pylori infection status. Limiting alcohol use during lifetime, particularly avoiding heavy use during early adulthood, might help prevent noncardia stomach cancer. Heterogeneous associations observed for cardia and noncardia cancers may indicate etiologic differences.

Obesity, Diabetes, Coffee, Tea, and Cannabis Use Alter Risk for Alcohol-Related Cirrhosis in 2 Large Cohorts of High-Risk Drinkers.

Sustained high alcohol intake is necessary but not sufficient to produce alcohol-related cirrhosis. Identification of risk factors, apart from lifetime alcohol exposure, would assist in discovery of mechanisms and prediction of risk. We conducted a multicenter case-control study (GenomALC) comparing 1,293 cases (with alcohol-related cirrhosis, 75.6% male) and 754 controls (with equivalent alcohol exposure but no evidence of liver disease, 73.6% male). Information confirming or excluding cirrhosis, and on alcohol intake and other potential risk factors, was obtained from clinical records and by interview. Case-control differences in risk factors discovered in the GenomALC participants were validated using similar data from 407 cases and 6,573 controls from UK Biobank. The GenomALC case and control groups reported similar lifetime alcohol intake (1,374 vs 1,412 kg). Cases had a higher prevalence of diabetes (20.5% (262/1,288) vs 6.5% (48/734), P = 2.27 × 10-18) and higher premorbid body mass index (26.37 ± 0.16 kg/m2) than controls (24.44 ± 0.18 kg/m2, P = 5.77 × 10-15). Controls were significantly more likely to have been wine drinkers, coffee drinkers, smokers, and cannabis users than cases. Cases reported a higher proportion of parents who died of liver disease than controls (odds ratio 2.25 95% confidence interval 1.55-3.26). Data from UK Biobank confirmed these findings for diabetes, body mass index, proportion of alcohol as wine, and coffee consumption. If these relationships are causal, measures such as weight loss, intensive treatment of diabetes or prediabetic states, and coffee consumption should reduce the risk of alcohol-related cirrhosis.

Association of moderate alcohol intake with in vivo amyloid-beta deposition in human brain: A cross-sectional study.

BackgroundAn emerging body of literature has indicated that moderate alcohol intake may be protective against Alzheimer disease (AD) dementia. However, little information is available regarding whether moderate alcohol intake is related to reductions in amyloid-beta (Aβ) deposition, or is protective via amyloid-independent mechanisms in the living human brain. Here we examined the associations of moderate alcohol intake with in vivo AD pathologies, including cerebral Aβ deposition, neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMHs) in the living human brain.Methods and findingsThe present study was part of the Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer’s Disease (KBASE), an ongoing prospective cohort study that started in 2014. As of November 2016, 414 community-dwelling individuals with neither dementia nor alcohol-related disorders (280 cognitively normal [CN] individuals and 134 individuals with mild cognitive impairment [MCI]) between 56 and 90 years of age (mean age 70.9 years ± standard deviation 7.8; male, n [%] = 180 [43.5]) were recruited from 4 sites (i.e., 2 university hospitals and 2 public centers for dementia prevention and management) around Seoul, South Korea. All the participants underwent comprehensive clinical assessments comprising lifetime and current histories of alcohol intake and multimodal brain imaging, including [11C] Pittsburgh compound B positron emission tomography (PET), [18F] fluorodeoxyglucose (FDG) PET, and magnetic resonance imaging (MRI) scans. Lifetime and current alcohol intake were categorized as follows: no drinking, <1 standard drink (SD)/week, 1–13 SDs/week, and 14+ SDs/week. A moderate lifetime alcohol intake (1–13 SDs/week) was significantly associated with a lower Aβ positivity rate compared to the no drinking group, even after controlling for potential confounders (odds ratio 0.341, 95% confidence interval 0.163–0.714, p = 0.004). In contrast, current alcohol intake was not associated with amyloid deposition. Additionally, alcohol intake was not related to neurodegeneration of AD-signature regions or cerebral WMH volume. The present study had some limitations in that it had a cross-sectional design and depended on retrospective recall for alcohol drinking history.ConclusionsIn this study, we observed in middle- and old-aged individuals with neither dementia nor alcohol-related disorders that moderate lifetime alcohol intake was associated with lower cerebral Aβ deposition compared to a lifetime history of not drinking. Moderate lifetime alcohol intake may have a beneficial influence on AD by reducing pathological amyloid deposition rather than amyloid-independent neurodegeneration or cerebrovascular injury.

Volumetric Prefrontal Cortex Alterations in Patients With Alcohol Dependence and the Involvement of Self-Control.

Background:Aspects of self-control such as sensation seeking and impaired impulse control have been implicated in alcohol dependence (ALC). Conversely, sensation seeking has been ascribed a possible protective role in stress-related psychopathologies. We therefore examined gray matter (GM) morphology in individuals with ALC, focusing on differences in prefrontal regions that have been associated with self-control. Additionally, we accounted for differences in lifetime alcohol intake regarding self-control measures and cortical structures in ALC patients.Methods:With voxel-based morphometry (VBM) focusing on prefrontal a priori defined regions of interest, we assessed a group of 62 detoxified ALC patients and 62 healthy controls (HC). ALC patients were subsequently divided into high (n = 9) and low consumers (n = 53). Self-control was assessed by use of the Barratt Impulsiveness Scale and the Sensation Seeking Scale.Results:Compared to HC, ALC had significantly less GM volume in bilateral middle frontal gyrus (MFG) and right medial prefrontal cortex as well as in the right anterior cingulate. High-consuming ALC showed smaller GM in right orbitofrontal cortex as well as lower sensation seeking scores than low consumers. In low-consuming ALC, right MFG-GM was positively associated with magnitude of sensation seeking; particularly, larger MFG-GM correlated with greater thrill and adventure seeking.Conclusion:Thus, our findings (i) indicate deficient GM volume in prefrontal areas related to self-control and (ii) might accentuate the phenotypic divergence of ALC patients and emphasize the importance of the development of individual treatment options.

Addiction resistance to alcohol: What about heavy drinkers who avoid alcohol problems?

BackgroundSome individuals are resistant to alcohol use disorders despite high levels of intake. Addiction Resistance (AR) measures the disparity between alcohol consumption and alcohol use disorder (AUD) symptoms, such that some persons exhibit few (AUD) symptoms despite higher intake. The validity of the concept and the factors contributing to AR are not well understood. The aim of this study was to predict AR based on variables related to risk for addiction that are measured in the Family Health Patterns Project. MethodParticipants were healthy young adults (n = 1122) with and without a family history of alcohol and other substance use disorders who were given measures of mood stability and risk-taking tendencies, and were interviewed to determine alcohol intake, AUD symptoms, and other substance use disorders (SUD). AR was calculated using maximal lifetime alcohol intake and number of AUD symptoms. ResultsA principal components analysis was run with varimax rotation, which yielded three components: Component 1 indexed behavioral and mood regulation, Component 2 encompassed family and environmental factors, and Component 3 included cognitive factors. A multiple regression analysis revealed that Component 1 and Component 2 were predictive of AR whereas Component 3 was not. DiscussionIndividuals who reported greater emotional stability, norm adherence, risk avoidance, and fewer family members with substance use disorders were more resistant to AUD despite higher alcohol intake. These findings suggest that AUD risk and resistance may represent different points of the same continuum.

Lifetime prevalence and correlates of smoking behavior in Iranian adults\u2019 population; a cross-sectional study

AbstactBackgroundThere are few if any reports concerning the joint use of waterpipe, cigarette and exposure to second-hand smoking in Tehran, Iran. Here, we simultaneously investigated the prevalence and predictors of smoking habits in Iranian adults.MethodsIn this population-based cross-sectional study, we recruited 1057 Iranian adults between August 2013 and February 2015, in Tehran, a multi-ethnic city. Participants were selected using random digit dialing. Three separate logistic regression models were applied to estimate the adjusted odds ratios (95% CI).ResultsExposure to second-hand smoking was the most prevalent smoking type (37, 95% CI: 35–41%) followed by cigarette (23.9% (95% CI: 21–27%)) and water-pipe smoking (20.25% (95% CI: 18–23%)) in adults in Tehran. Almost 3.3 and 4.5% of adults reported three and two types of lifetime smoking behaviors, respectively. Age, sex, history of depression along with lifetime alcohol intake was the important predictors of all three types of smoking. Lifetime alcohol consumption was associated with increased prevalence of all three types of smoking (p for trend < 0.009). Lifetime drug abuse was also associated with increased prevalence of cigarette smoking (OR = 2.04, 95% CI: 1.61–2.59, p < 0.001).ConclusionsLifetime prevalence of waterpipe, cigarette and exposure to second-hand smoking is moderately high. Dual smoking behaviors are increasing in Iranian adults. An apparent age-related difference in pattern of waterpipe and cigarette smoking was observed. These findings highlight the need for further educational and preventive programs especially for dual smoking in Iranian young adults. This could provide practical information for evaluating and reforming the tobacco control programs and policies in Iran.

Lifetime alcohol intake and pancreatic cancer incidence and survival: findings from the Melbourne Collaborative Cohort Study.

Pancreatic cancer has one of the worst prognoses with 5-year survival below 10%. There is some evidence that alcohol consumption might increase the risk of pancreatic cancer. We examined associations of pre-diagnostic alcohol intake with (i) incidence of pancreatic cancer, and (ii) overall survival following pancreatic cancer. Usual alcohol intake was estimated at recruitment in 1990-1994 for 38,472 participants in the Melbourne Collaborative Cohort Study using recalled frequency and quantity of beverage-specific intake for 10-year periods from age 20. Pancreatic cancer incidence (C25 according to International Classification of Diseases for Oncology) and vital status were ascertained through to 30 September 2015. Cox regression was performed to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for associations with lifetime, age 20-29, and baseline alcohol intakes. By the end of follow-up (average 20.2years), 239 incident cases of pancreatic cancer were diagnosed, of which 228 had died. No evidence of an association was observed between alcohol intake and risk of pancreatic cancer. Higher lifetime alcohol intake was associated with lower overall survival following a diagnosis of pancreatic cancer (mortality HR 1.09 per 10g/day increment, 95% CI 1.00-1.19; p value = 0.04). A similar finding was observed for age 20-29 intake (HR 1.09 per 10g/day increment, 95% CI 1.02-1.18; p value = 0.01) but not with baseline intake. We observed an association between lower alcohol use from an early age and improved survival following pancreatic cancer, but this finding needs to be confirmed by other studies.

Early-Life Alcohol Intake and High-Grade Prostate Cancer: Results from an Equal-Access, Racially Diverse Biopsy Cohort.

Epidemiologic evidence for an association between alcohol and prostate cancer is mixed. Moreover, there is a lack of research investigating early-life alcohol intake as a risk factor for either overall or high-grade prostate cancer. We examined lifetime alcohol intake in association with prostate cancer diagnosis in an equal-access, racially diverse prostate biopsy cohort. Men undergoing prostate biopsy at the Durham Veterans Affairs Medical Center from 2007 to 2018 completed a survey indicating average number of alcoholic beverages consumed per week [categorized as none (ref), 1-6, ≥7] during each decade of life. Multivariable logistic regression was used to test the association between alcohol intake across decades and diagnosis of overall, low-grade [grade group (GG) 1-2] and high-grade prostate cancer (GG 3-5). Of 650 men ages 49-89 who underwent biopsy, 325 were diagnosed with prostate cancer, 238 with low-grade and 88 with high-grade disease. Relative to nondrinkers, men who consumed ≥7 drinks/week at ages 15 to 19 had increased odds of high-grade prostate cancer diagnosis (OR = 3.21, P trend = 0.020), with similar findings for ages 20 to 29, 30 to 39, and 40 to 49. Consistent with these results, men in the upper tertile of cumulative lifetime intake had increased odds of high-grade prostate cancer diagnosis (OR = 3.20, P trend = 0.003). In contrast, current alcohol intake was not associated with prostate cancer. In conclusion, among men undergoing prostate biopsy, heavier alcohol intake earlier in life and higher cumulative lifetime intake were positively associated with high-grade prostate cancer diagnosis, while current intake was unrelated to prostate cancer. Our findings suggest that earlier-life alcohol intake should be explored as a potential risk factor for high-grade prostate cancer. Cancer Prev Res; 11(10); 621-8. ©2018 AACR.

Alcohol consumption and all-cause mortality in older adults in Spain: an analysis accounting for the main methodological issues.

Observational evidence that light-to-moderate alcohol consumption lowers mortality is questioned because of potential selection biases and residual confounding. We assess the association between alcohol intake and all-cause death in older adults after accounting for those methodological issues. Data came from 3045 individuals representative of the non-institutionalized population aged ≥60years in Spain. Participants were recruited in 2008-10, when they reported current and life-time alcohol intake; drinkers were classified as occasional (<1.43g/day), light (≥ 1.43 but <20g/day for men and ≥ 1.43 but<10g/day for women), moderate (≥ 20 but<40g/day for men and ≥ 10but<20g/day for women) or heavy (≥40g/day for men and≥24g/day for women)/binge. Participants were followed-up to 2017 to assess vital status. In analyses, ex-drinkers were removed from the abstainer group and were classified according to their life-time intake to address the 'abstainer bias'. Moreover, analyses were replicated in individuals without functional limitations, and excluded deaths in the first year of follow-up, to address reverse causation. Also, occasional drinkers were used as reference in some analyses to reduce the 'healthy drinker/survivor' bias. Results were adjusted for many covariates to minimize residual confounding. Compared with never-drinkers, the hazard ratio (95% confidence interval) of mortality for light drinkers was 1.05 (0.71-1.56) and 1.20 (0.72-2.02) in those without functional limitations. Corresponding values for moderate drinkers were 1.28 (0.81-2.02) and 1.55 (0.87-2.75) and for heavy/binge drinkers 1.85 (1.07-3.23) and 2.15 (1.09-4.22). Results were consistent when occasional drinkers were used as reference. Among drinkers without functional limitations, the hazard ratio (95% confidence interval) of mortality per 10g/day of alcohol was 1.12 (1.02-1.23). After accounting for potential biases, light-to-moderate drinking among people 60+ years of age appears to have no statistically significant benefit on mortality compared with abstention from alcohol. By contrast, heavy/binge drinking shows a higher death risk compared with abstention from alcohol. Alcohol intake appears to have a positive dose-response with mortality among drinkers.

Lifetime alcohol intake and pattern of alcohol consumption in patients with alcohol-induced pancreatitis in comparison with patients with alcohol use disorder

Objective: To examine lifetime drinking patterns in men and women with alcohol-induced pancreatitis (AIP) in comparison with patients with alcoholic use disorder (AUD) without pancreatic disease.Methods: Alcohol consumption patterns were assessed using a validated questionnaire, the Lifetime Drinking History (LDH), during an outpatient visit. Patients diagnosed with AIP were matched for gender and age (+/− 5 years) with patients with AUD in addiction treatment.Results: A total of 45 patients with AIP (35 males, 10 females) and 45 AUD patients were included. Alcohol consumption patterns were not significantly different between males and females with AIP and those with history of acute AIP and chronic pancreatitis (CP). Alcohol consumption patterns of AIP and AUD patients were similar in terms of onset age and duration of alcohol consumption, lifetime alcohol intake and drinks per drinking day. A higher proportion of binge drinking was found among patients with AUD than those with AIP (median 1.00 vs. 0.94, p = .01). Males with AUD had lower onset age (15 vs. 16 years, p = .03), higher total amount of spirits (35520 vs. 10450 drinks, p = .04) and higher proportion of binge drinking (1.00 vs. 0.97, p = .01) than males with AIP, whereas females with AIP and AUD had similar drinking patterns.Conclusions: Alcohol drinking patterns and lifetime drinking history was similar in patients with AIP and patients with AUD. Males with AIP had lower total amount of spirits and lower proportion of binge drinking than those with AUD, suggesting the idiosyncratic etiology of AIP.

Lifetime alcohol intake and risk of non-Hodgkin lymphoma: Findings from the Melbourne Collaborative Cohort Study.

Cohort studies have reported inconsistent evidence regarding alcohol intake and risk of non-Hodgkin lymphoma (NHL), mostly based on alcohol intake assessed close to study enrolment. We examined this association using alcohol intake measured from age 20 onwards. We calculated usual alcohol intake for 10-year periods from age 20 using recalled frequency and quantity of beverage-specific consumption for 37,990 participants aged 40-69 years from the Melbourne Collaborative Cohort Study. Cox regression was performed to derive hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between alcohol intake (g/day) and NHL risk. After a mean follow-up of 19.3 years, 538 NHL cases were diagnosed. Approximately 80% of participants were either lifetime abstainers or consumed below 20 g of ethanol/day. All categories of lifetime alcohol intake were associated with about 20% lower incidence of NHL compared with lifetime abstention, but there was no evidence of a trend by amount consumed (HR = 0.97 per 10 g/day increment in intake, 95% CI: 0.92-1.03; p value = 0.3). HRs for beer, wine and spirits were 0.91 (95% CI: 0.83-1.00; p value = 0.05), 1.03 (95% CI: 0.94-1.12; p value = 0.6), and 1.06 (95% CI: 0.83-1.37; p value = 0.6), respectively, per 10 g/day increment in lifetime intake. There were no significant differences in associations between NHL subtypes. In this low-drinking cohort, we did not detect a dose-dependent association between lifetime alcohol intake and NHL risk.

Lifetime Alcohol Intake, Binge Drinking Behaviors, and Breast Cancer Risk.

The prevalence of binge drinking in the United States is rising. While alcohol is a risk factor for breast cancer, less is known about the impact of episodic heavy drinking. In 2003-2009, women aged 35-74 years who were free of breast cancer were enrolled in the Sister Study (n=50,884). Residents of the United States or Puerto Rico who had a sister with breast cancer were eligible. Multivariable Cox regression was used to estimate adjusted hazard ratios and 95% confidence intervals for breast cancer. During follow-up (mean=6.4 years), 1,843 invasive breast cancers were diagnosed. Increased breast cancer risk was observed for higher lifetime alcohol intake (for ≥230 drinks/year vs. <60 drinks/year, hazard ratio (HR)=1.35, 95% confidence interval (CI): 1.15, 1.58). Relative to low-level drinkers (<60 drinks/year), hazard ratios were increased for ever binge drinking (HR=1.29, 95% CI: 1.15, 1.45) or blacking out (HR=1.39, 95% CI: 1.17, 1.64). Compared with low-level drinkers who never binged, moderate drinkers (60-229 drinks/year) who binged had a higher risk (HR=1.25, 95% CI: 1.08, 1.44). There was evidence of effect modification between moderate lifetime drinking and binging (relative excess risk due to interaction=0.33, 95% CI: 0.10, 0.57). Our findings support the established association between lifetime alcohol intake and breast cancer and provide evidence for an increased risk associated with heavy episodic drinking, especially among moderate lifetime drinkers.

Age-Specific Indicators of a Healthy Lifestyle and Postmenopausal Breast Cancer.

Modifiable lifestyle factors have been consistently associated with breast cancer, and risk may vary by menopausal status. However, whether these associations vary according to age among postmenopausal women remains unresolved. Using postmenopausal women from a population-based case-control study (990 cases and 1006 frequency-matched controls), we conducted multivariable-adjusted unconditional logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for lifestyle factors (lifetime alcohol intake, body mass index [BMI] in the year before diagnosis, lifetime recreational physical activity [RPA], and nonsteroidal anti-inflammatory drug use) in association with breast cancer stratified by age (<65 vs. 65+). We examined estrogen-related subgroups by (1) further stratifying by hormone replacement therapy (HRT) use and (2) restricting cases to estrogen receptor (ER)+/progesterone receptor (PR)+ cancers. Postmenopausal breast cancer incidence in women 65 years and older was positively associated with alcohol intake (OR = 1.79 for 15-30 g/day vs. nondrinkers, 95% CI: 1.03-3.12) and BMI (OR = 1.83 for BMI ≥30 vs. <25, 95% CI: 1.29-2.60), and inversely with RPA (OR = 0.69 for fourth quartile vs. inactive, 95% CI: 0.47-1.03). For postmenopausal women younger than 65, ORs were closer to the null. Tests for heterogeneity by age were significant at the p < 0.10 level for BMI and RPA, but not alcohol. Among older women, associations were stronger among never users of HRT and for those with ER+/PR+ cancers. The inverse associations with aspirin use did not differ by age. Interventions targeting modifiable lifestyle factors may reduce the burden of postmenopausal breast cancer among older women.