Association between socio-demographic factors, lifestyle, eating habits and hypertension risk among middle-aged and older rural Chinese adults.

BACKGROUND AND AIMS: Hypertension is a global health issue with increasing prevalence. This study aimed to understand the epidemiological characteristics and influencing factors of hypertension in rural Chinese populations and help develop effective prevention and control strategies. METHODS AND RESULTS: This cross-sectional study used database from the Early Diagnosis and Early Treatment Project of Esophageal Cancer conducted in a rural population from September 2012 to December 2017. A total of 10,111 subjects aged 35-75 years residing in Huai'an District, Huai'an City, Jiangsu Province for at least three years were included. Unconditional univariate and multivariate logistic regression models were performed to evaluate the association between socio-demographic information, lifestyle habits, dietary characteristics and the risk of hypertension. The prevalence of hypertension was 34.32 % in this rural population. Men and older individuals are more likely to have hypertension when compared with women and young individuals, respectively. Factors associated with an increased risk of hypertension included: fast eating speed, a high-salt diet (both currently and ten years ago), a high-spicy diet ten years ago, high BMI, poor educational attainment, preference for fatty meats, hot diet, green tea drinking, intake of pickled potherb mustard and corn flour, family smoking and alcohol consumption. Light smoking in males, consumption of fruits, adzuki bean, and pork liver were associated with reduced risk of hypertension. CONCLUSIONS: The study identified some factors, including eat habits and lifestyle, associated with hypertension risk, and highlighted the need for targeted policies and interventions in rural China to address potential risk factors for hypertension.

May Measurement Month 2021: an analysis of blood pressure screening results from Republic of the Congo, in the context of COVID-19 pandemic.

To determine the proportion of hypertension among opportunistic screenees in the Republic of the Congo, and the relationships between, blood pressure (BP), alcohol intake, and history of coronavirus disease 2019 (COVID-19). Screening was carried out in July and August 2021 in Brazzaville, Pointe-Noire, and Pokola, after ethical clearance had been obtained. The campaign followed the guidelines outlined in the MMM21 protocol, collecting ideally three BP readings for each participant. The screening was carried out during the partial confinement of the population, due to the COVID-19 pandemic. Social distancing measures and protection against the transmission of COVID-19 were adhered to. A total of 2135 subjects were screened of which 1138 (53.3%) were male. The mean age was 29.9 ± 9.9 years (range: 18-69 years), and 2110 participants (98.8%) were of black ethnic origin. A previous COVID-19 positive test was reported in 217 (10.2%) and vaccination in 93 (4.4%). Diabetes was reported in 113 (5.3%), 16 (0.7%) were current smokers, 171 (8.0%) reported using alcohol intake at least once per month, and 539 (25.3%) reported meeting the WHO guidelines on physical activity. The proportion of participants with hypertension (≥140/90 mmHg or taking BP-lowering medication) was 34.1%, of whom 24.5% were aware, 11.9% were on medication, and only 4.0% were controlled (<140/90 mmHg). Rates of hypertension are high in the Republic of Congo, with low rates of awareness and treatment, and national authorities should address the contributing factors highlighted in this report to improve health care for the population.

ß-Carotene Supplementation Improves Pancreas Function during Moderate Ethanol Consumption: Initial Characterization from a Morphological Overview.

Alcohol is believed to harm acinar cells, pancreatic ductal epithelium, and pancreatic stellate cells. After giving ethanol and/or ß-carotene to C57BL/6 mice, our goal was to evaluate their biochemistry, histology, and morpho-quantitative features. There were six groups of C57BL/6 mice: 1. Group C (control), 2. Group LA (low-dose alcohol), 3. Group MA (moderate-dose alcohol), 4. Group B (ß-carotene), 5. Group LA + B (low-dose alcohol combined with ß-carotene), and 6. Group MA + B (moderate-dose alcohol combined with ß-carotene). After the animals were euthanized on day 28, each specimen's pancreatic tissue was taken. Lipase, uric acid, and amylase were assessed using biochemical assessment. Furthermore, the examination of the pancreatic structure was conducted using Ammann's fibrosis scoring system. Finally, the morpho-quantitative characteristics of the pancreatic islets and acinar cells were determined. In the serum of the MA + B group, there were higher amounts of total amylase (825.953 ± 193.412 U/L) and lower amounts of lipase (47.139 ± 6.099 U/L) (p < 0.05). Furthermore, Ammann's fibrosis punctuation in the pancreas revealed significant variations between the groups (p < 0.001). Finally, the stereological analysis of pancreatic islets showed that the groups were different (p < 0.001). These findings suggest that antioxidant treatments might help decrease the negative effects of ethanol exposure in animal models.

Inhibition of the Sodium-Calcium Exchanger Reverse Mode Activity Reduces Alcohol Consumption in Rats.

Excessive and uncontrolled consumption of alcohol can cause alcohol use disorder (AUD), but its pharmacological mechanisms are not fully understood. Inhibiting the reverse mode activity of the sodium-calcium exchanger (NCX) can reduce the risk of alcohol withdrawal seizures, suggesting that NCX could play a role in controlling alcohol consumption. Here, we investigated how two potent inhibitors of NCX reverse mode activity, SN-6 (NCX1) and KB-R7943 (NCX3), affect voluntary alcohol consumption in adult male and female rats using the intermittent alcohol access two-bottle choice paradigm. Initially, animals were trained to drink 7.5% ethanol and water for four weeks before administering SN-6 and KB-R7934. Afterward, their alcohol intake, preference, and water intake were recorded 2 and 24 h after exposure to water and 7.5% ethanol. SN-6 significantly reduced alcohol consumption by 48% in male and 36% in female rats without affecting their water intake. Additionally, SN-6 significantly reduced alcohol preference in females by 27%. However, KB-R7943 reduced alcohol consumption by 42% in female rats and did not affect alcohol preference or water intake. These findings suggest that alcohol exposure increased NCX reverse activity, and targeting NCX1 could be an effective strategy for reducing alcohol consumption in subjects susceptible to withdrawal seizures.

Food security and diet quality in a racially diverse cohort of postpartum women in the USA.

Food insecurity has been associated with poor diet, but few studies focused on the postpartum period - an important time for women's health. We examined associations between food security and diet quality in postpartum women and assessed whether participation in federal food assistance programmes modified this potential relation. Using longitudinal data, we analysed the association between food security at 3 months postpartum and a modified Alternate Healthy Eating Index-2010 (AHEI) at 6 months postpartum (excluding alcohol). We conducted multivariable linear regressions examining associations between food security and AHEI. We assessed two food assistance programmes as potential effect modifiers. The sample included 363 postpartum women from the Nurture study, located in the Southeastern USA (2013-2017). Among women, 64·4 % were Black and 45·7 % had a high school diploma or less. We found no evidence of an interaction between food security and two federal food assistance programmes. In adjusted models, marginal, low and very low food security were not associated with AHEI. However, low (ß: -0·64; 95 % CI -1·15, -0·13; P = 0·01) and very low (ß: -0·57; 95 % CI -1·02, -0·13; P = 0·01) food security were associated with greater trans fat intake. Food security status was not associated with overall diet quality but was associated with higher trans fat (low and very low) and more moderate alcohol (marginal) intake. Future studies should assess the consistency and generalisability of these findings.

Plasma lipids, alcohol intake frequency and risk of Osteoarthritis: a Mendelian randomization study.

BACKGROUD: Plasma lipids and alcohol intake frequency have been reported to be associated with the risk of osteoarthritis (OA). However, it remains inconclusive whether plasma lipids and alcohol intake frequency play a role in the development of OA. METHODS: The study employed a comprehensive genome-wide association database to identify independent genetic loci strongly linked to plasma lipids and alcohol intake frequency, which were used as instrumental variables. The causal association between plasma lipids, alcohol intake frequency, and the risk of OA was then analyzed using two-sample Mendelian randomization methods such as inverse variance weighted (IVW), MR-Egger regression, and weighted median estimator (WME), with odds ratios (ORs) as the evaluation criteria. RESULTS: A total of 392 SNPs were included as instrumental variables in this study, including 32 for total cholesterol (TC), 39 for triglycerides (TG), 170 for high-density lipoproteins (HDL), 60 for low-density lipoproteins (LDL), and 91 for alcohol intake frequency. Using the above two-sample Mendelian Randomization method to derive the causal association between exposure and outcome, with the IVW method as the primary analysis method and other MR analysis methods complementing IVW. The results of this study showed that four exposure factors were causally associated with the risk of OA. TC obtained a statistically significant result for IVW (OR = 1.207, 95% CI: 1.018-1.431, P = 0.031); TG obtained a statistically significant result for Simple mode (OR = 1.855, 95% CI: 1.107-3.109, P = 0.024); LDL obtained three statistically significant results for IVW, WME and Weighted mode (IVW: OR = 1.363, 95% CI: 1.043-1.781, P = 0.023; WME: OR = 1.583, 95% CI: 1.088-2.303, P = 0.016; Weighted mode: OR = 1.521, 95% CI: 1.062-2.178, P = 0.026). Three statistically significant results were obtained for alcohol intake frequency with IVW, WME and Weighted mode (IVW: OR = 1.326, 95% CI: 1.047-1.678, P = 0.019; WME: OR = 1.477, 95% CI: 1.059-2.061, P = 0.022; Weighted mode: OR = 1.641, 95% CI: 1.060-2.541, P = 0.029). TC, TG, LDL, and alcohol intake frequency were all considered as risk factors for OA. The Cochran Q test for the IVW and MR-Egger methods indicated intergenic heterogeneity in the SNPs contained in TG, HDL, LDL, and alcohol intake frequency, and the test for pleiotropy indicated a weak likelihood of pleiotropy in all causal analyses. CONCLUSIONS: The results of two-sample Mendelian randomization analysis showed that TC, TG, LDL, and alcohol intake frequency were risk factors for OA, and the risk of OA increased with their rise.

Sexual Violence and Alcohol Intake: A Population-Based Explorative Study in a Northwestern Italian Area.

Background and Objectives: Sexual violence (SV) is a major global public health concern. While socioeconomic factors and familial relationships have been widely reported to contribute to SV, the role of alcohol consumption should not be ignored. Indeed, alcohol can impair cognition, distort reality, increase aggression, and ease drug-facilitated sexual assault. This retrospective study aims to explore the relationship between alcohol consumption and SV by examining the prevalence, characteristics, and consequences of violence episodes. Materials and Methods: A total of 1481 women accessed the Rape Centre "Centro Soccorso Violenza Sessuale" in Turin, Italy between 2008 and 2019, with 223 reporting alcohol consumption before the assault. Results: The alcohol group had a younger age profile, predominantly within the 18-25-year-old category. SV incidents involving alcohol consumers were more likely to occur in public places or in someone else's home, while the non-alcohol-consuming group experienced more violence in their own homes. Acquaintances and unknown individuals were primarily responsible, whereas partners were the most common perpetrators of violence against non-alcohol-consuming women. Alcohol consumers sought medical attention sooner after the assault and exhibited more symptoms and injuries, particularly of neurological origin. Concurrent use of recreational drugs was higher among alcohol consumers. The logistic regression analysis revealed higher odds of injury for Italian women and those in the 18-35 age groups after consuming alcohol. Conclusions: This study contributes to the understanding of the relationship between alcohol consumption and SV. The prevalence of alcohol-related sexual aggression is lower compared to that shown in previous studies. Nationality, age, and assailant identity influence SV dynamics. These findings can guide well-targeted interventions and prevention strategies to address SV and inform communities facing similar challenges.

Alcohol intake trajectories during the life course and risk of alcohol-related cancer: A prospective cohort study.

We examined associations between sex-specific alcohol intake trajectories and alcohol-related cancer risk using data from 22 756 women and 15 701 men aged 40 to 69 years at baseline in the Melbourne Collaborative Cohort Study. Alcohol intake for 10-year periods from age 20 until the decade encompassing recruitment, calculated using recalled beverage-specific frequency and quantity, was used to estimate group-based sex-specific intake trajectories. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated for primary invasive alcohol-related cancer (upper aerodigestive tract, breast, liver and colorectum). Three distinct alcohol intake trajectories for women (lifetime abstention, stable light, increasing moderate) and six for men (lifetime abstention, stable light, stable moderate, increasing heavy, early decreasing heavy, late decreasing heavy) were identified. 2303 incident alcohol-related cancers were diagnosed during 485 525 person-years in women and 789 during 303 218 person-years in men. For men, compared with lifetime abstention, heavy intake (mean ≥ 60 g/day) at age 20 to 39 followed by either an early (from age 40 to 49) (early decreasing heavy; HR = 1.75, 95% CI: 1.25-2.44) or late decrease (from age 60 to 69) (late decreasing heavy; HR = 1.94, 95% CI: 1.28-2.93), and moderate intake (mean <60 g/day) at age 20 to 39 increasing to heavy intake in middle-age (increasing heavy; HR = 1.45, 95% CI: 1.06-1.97) were associated with increased risk of alcohol-related cancer. For women, compared with lifetime abstention, increasing intake from age 20 (increasing moderate) was associated with increased alcohol-related cancer risk (HR = 1.25, 95% CI: 1.06-1.48). Similar associations were observed for colorectal (men) and breast cancer. Heavy drinking during early adulthood might increase cancer risk later in life.

Alcohol intake and stomach cancer risk in Japan: A pooled analysis of six cohort studies.

The association between alcohol intake and stomach cancer risk remains controversial. We undertook a pooled analysis of data from six large-scale Japanese cohort studies with 256 478 participants on this topic. Alcohol intake as ethanol was estimated using a validated questionnaire. The participants were followed for incidence of stomach cancer. We calculated study-specific hazard ratios (HRs) and 95% confidence intervals (CIs) for stomach cancer according to alcohol intake using a Cox regression model. Summary HRs were estimated by pooling the study-specific HRs using a random-effects model. During 4 265 551 person-years of follow-up, 8586 stomach cancer cases were identified. In men, the multivariate-adjusted HRs (95% CIs) of stomach cancer were 1.00 (0.87-1.15) for occasional drinkers, and 1.00 (0.91-1.11) for <23 g/d, 1.09 (1.01-1.18) for 23 to <46 g/d, 1.18 (1.09-1.29) for 46 to <69 g/d, 1.21 (1.05-1.39) for 69 to <92 g/d, and 1.29 (1.11-1.51) for ≥92 g/d ethanol in regular drinkers compared with nondrinkers. In women, the multivariate-adjusted HRs were 0.93 (0.80-1.08) for occasional drinkers, and 0.85 (0.74-0.99) for <23 g/d, and 1.22 (0.98-1.53) for ≥23 g/d in regular drinkers compared with nondrinkers. The HRs for proximal and distal cancer in drinkers vs nondrinkers were 1.69 (1.15-2.47) and 1.24 (0.99-1.55) for ≥92 g/d in men, and 1.60 (0.76-3.37) and 1.18 (0.88-1.57) for ≥23 g/d in women, respectively. Alcohol intake increased stomach cancer risk in men, and heavy drinkers showed a greater point estimate of risk for proximal cancer than for distal cancer.

Alcohol consumption and hepatocellular carcinoma: novel insights from a prospective cohort study and nonlinear Mendelian randomization analysis.

BACKGROUND: Heavy drinking was well associated with an increased risk of hepatocellular carcinoma (HCC), whereas the effect of low-to-moderate drinking on HCC remains under debate. METHODS: Participants from the UK Biobank with detailed information on alcohol use and free of common diseases were included. Daily pure alcohol intake (g/day) was calculated, and the predominant alcoholic beverage type was assigned for each participant. Additive Cox regression model and nonlinear Mendelian randomization (NLMR) analyses were performed to evaluate the association of alcohol intake with HCC. RESULTS: Of 329,164 participants (52.3% females, mean [SD] age = 56.7 [8.0] years), 201 incident HCC cases were recorded during the median follow-up of 12.6 years. The best-fitted Cox regression model suggested a J-shaped relationship between daily alcohol intake level and HCC risk. However, NLMR analysis did not detect a nonlinear correlation between alcohol use and HCC (nonlinearity P-value: 0.386). The J-shaped correlation pattern was detected only in subjects who mainly drank wine but not in those who mainly drank beer, spirits, or fortified wine. Moderate wine drinking showed a significant alanine transaminase (ALT)- and aspartate aminotransferase-lowering effect compared to that of the nondrinkers. In low-risk populations of HCC including women, people aged < 60 years, subjects with normal ALT levels, and those carrying non-risk genotypes of PNPLA3 rs738409 and TM6SF2 rs58542926, we observed a J-shaped correlation between alcohol use and HCC; however, a positive dose-response correlation was found in their respective counterparts, even in those predominantly drinking wine. CONCLUSIONS: Low-to-moderate drinking may be inversely associated with the risk of HCC in low-risk populations, which may be largely driven by wine drinking. However, those in high-risk populations of HCC, such as men and older people, and those with abnormal ALT levels and carry genetic risk variants, should abstain from drinking alcohol. Given the small HCC case number, further validations with larger case numbers are warranted in future works.

Inhibition of Phosphodiesterase 2 Ameliorates Post-Traumatic Stress-Induced Alcohol Intake Disorder by Regulating cAMP/cGMP Signaling.

BACKGROUND: Post-traumatic stress disorder (PTSD) is the prevalent psychiatric disorder that induces alcohol use disorders (AUD) such as abnormal alcohol intake and anxiety. However, little is known about whether phosphodiesterase 2 (PDE2)-cAMP/cGMP signaling is involved in PTSD-induced AUD. METHODS: The present study used single-prolonged stress (SPS) to mimic PTSD that induced increases in ethanol intake and preference (2-bottle choice test) and anxiety-like behavior (elevated-plus maze test and novelty suppressed feeding test). PDE2 inhibitor Bay 60-7550 (Bay) was administered to the mice and protein kinase A (PKA) inhibitor H89 and PKG inhibitor KT5823 were micro-injected into dorsolateral striatum (DLS) and central amygdala (CA) of mice to determine whether the effects of Bay on anxiety-like behavior in SPS mice are brain region dependent. RESULTS: PDE2 inhibitor Bay rescued SPS-induced decreases in open arm entries and open arm time exposure in elevated-plus maze test and reversed increased latency to feed in the novelty suppressed feeding test. Moreover, SPS-induced ethanol use disorder was reversed by Bay as evidenced by decreased ethanol intake and preference without changing total fluid intake in the SPS mice after treatment with Bay. However, Bay did not change the ethanol metabolism or sucrose or quinine intake and preference. The locomotor activity was not affected after treatment with Bay. Interestingly, microinjection of PKA or PKG inhibitor H89 or KT5823 into DLS prevented the effects of Bay on alcohol intake and preference and cAMP-response element binding proteins phosphorylation and brain derived neurotrophic factor expression in DLS but not on the anxiety-like behavior in SPS mice. Microinjection of these inhibitors into CA prevented Bay-induced anxiolytic-like effects and cAMP-response element binding proteins phosphorylation and brain derived neurotrophic factor levels in CA but did not affect ethanol intake in SPS mice, indicating that the effects of Bay on different behaviors are brain region dependent. CONCLUSIONS: These findings support the hypothesis that PDE2-cAMP/cGMP signaling may differentially mediate PTSD-induced AUD and anxiety-like behavior.

Assessing the influence of cannabis and alcohol use on different visual functions: A comparative study.

This study aimed to assess and compare the influence of alcohol intake and cannabis smoking on different visual functions. A total of 64 young and healthy volunteers took part in the study. All undertook several randomised experimental sessions in which different visual functions, namely distance stereopsis, retinal straylight, visual discrimination capacity, and contrast sensitivity, were tested. Cannabis smokers (N = 30) took a baseline session and a session after smoking a cannabis cigarette, whereas alcohol users (N = 34) underwent a baseline session, a session after a low alcohol intake (Alcohol 1), and a session after a moderate to high alcohol intake (Alcohol 2). All visual functions were impaired by cannabis and alcohol use, particularly for the Cannabis and Alcohol 2 groups. The deterioration of all visual variables was higher for the Alcohol 2 than for the Alcohol 1 and Cannabis groups, except for retinal straylight, the deterioration of which was equal for the Cannabis group, and distant stereopsis, which was more impaired for the Cannabis group. The Alcohol 2 group experienced the most impairing conditions, although very similar to the cannabis group, and that factors other than the experimental conditions, such as sex and age, also influenced these visual changes. Alcohol and cannabis use clearly impair vision. The deterioration caused by cannabis is similar to, but slightly lower than, that produced by a moderate to high alcohol intake, with the experimental conditions, sex and age all having an impact on the variability of visual deterioration.

Alcohol intake and the risk of glioma: a systematic review and updated meta-analysis of observational study.

The association between alcohol intake and the risk of glioma has been widely studied, but these results have yielded conflicting findings. Therefore, we conducted this systematic review and updated meta-analysis to systematically evaluate the association between alcohol intake and the risk of glioma. A systematic literature search of relevant articles published in PubMed, Web of Science, CNKI and Wan fang databases up to December 2021 was conducted. Pooled estimated of relative risk (RR) and 95 % CI were calculated using fixed-effects models. A total of eight articles with three case-control studies involving 2706 glioma cases and 2 189 927 participants were included in this meta-analysis. A reduced risk of glioma was shown for the low-moderate alcohol drinking v. non-drinking (RR = 0·87; 95 % CI (0·78, 0·97); P = 0·014). In addition, there was no evidence of an increased risk of glioma in the heavy alcohol drinking compared with non-drinking (RR = 0·89; 95 % CI (0·67, 1·18); P = 0·404). The findings suggest an inverse association between low-moderate alcohol drinking and the risk of glioma, in the absence, however, of a dose-response relationship. More prospective studies are needed to provide further insight into the association between alcohol drinking and glioma risk.

A longitudinal evaluation of alcohol intake throughout adulthood and colorectal cancer risk.

BACKGROUND: Alcohol intake is an established risk factor for colorectal cancer (CRC); however, there is limited knowledge on whether changing alcohol drinking habits during adulthood modifies CRC risk. OBJECTIVE: Leveraging longitudinal exposure assessments on alcohol intake at different ages, we examined the relationship between change in alcohol intake and subsequent CRC risk. METHODS: Within the European Prospective Investigation into Cancer and Nutrition, changes in alcohol intake comparing follow-up with baseline assessments were investigated in relation to CRC risk. The analysis included 191,180, participants and 1530 incident CRC cases, with exclusion of the first three years of follow-up to minimize reverse causation. Trajectory profiles of alcohol intake, assessed at ages 20, 30, 40, 50 years, at baseline and during follow-up, were estimated using latent class mixed models and related to CRC risk, including 407,605 participants and 5,008 incident CRC cases. RESULTS: Mean age at baseline was 50.2 years and the follow-up assessment occurred on average 7.1 years later. Compared to stable intake, a 12 g/day increase in alcohol intake during follow-up was positively associated with CRC risk (HR = 1.15, 95%CI 1.04, 1.25), while a 12 g/day reduction was inversely associated with CRC risk (HR = 0.86, 95%CI 0.78, 0.95). Trajectory analysis showed that compared to low alcohol intake, men who increased their alcohol intake from early- to mid- and late-adulthood by up to 30 g/day on average had significantly increased CRC risk (HR = 1.24; 95%CI 1.08, 1.42), while no associations were observed in women. Results were consistent by anatomical subsite. CONCLUSIONS: Increasing alcohol intake during mid-to-late adulthood raised CRC risk, while reduction lowered risk.

Excessive alcohol intake and liver fibrosis are associated with skeletal muscle mass reduction in elderly men: the Wakayama study.

BACKGROUND: Excessive alcohol intake complicated by liver dysfunction has been presumed to affect skeletal muscles. This study aimed to examine the association between excessive alcohol intake, liver fibrosis, and loss of skeletal muscle mass in elderly men. METHODS: The study participants comprised 799 community-dwelling elderly men (age, 71 ± 3 years) with no history of treatment for liver disease. Bioelectrical impedance analysis was performed to estimate the appendicular skeletal muscle mass (ASM) of each participant. The ASM values were also normalized for height (ASM index). Liver fibrosis was evaluated using the Fib4 index, which was calculated using participant age, AST level, ALT level, and platelet count. Usual alcohol intake was estimated based on the type of alcohol, frequency of drinking, and amount of alcohol consumed per day. RESULTS: Among the excess drinkers (≥ 20 g/day), the ASM index of the subgroup with liver fibrosis (Fib4 index ≥ 2.67) was significantly lower than that of the subgroup with no liver fibrosis (Fib4 index < 2.67). However, no significant difference between the subgroups was found in the non-drinkers and moderate drinkers (< 20 g/day). In multiple regression analysis, the Fib4 index was significantly associated with the ASM index, independent of potential confounding factors. The association between the Fib4 index and ASM index was more pronounced in excess drinkers than in non-drinkers and moderate drinkers. CONCLUSION: These results suggest that liver fibrosis is associated with loss of skeletal muscle mass in elderly men, and excessive alcohol intake combined with liver fibrosis may lead to greater muscle mass reduction than each individual condition.

Relationship between Alcohol Intake and Stroke Severity in Japanese Patients: a Sex- and Subtype-Stratified Analysis.

OBJECTIVES: This study aims to clarify the association between alcohol intake and stroke severity at admission and discharge according to sex and stroke subtype in Japanese patients with acute stroke. MATERIALS AND METHODS: We analyzed the data of 199,599 patients registered in the Japan Stroke Data Bank from 1999 to 2018, including sex, age, stroke subtypes (cardioembolic ischemic, noncardioembolic ischemic, hypertensive hemorrhagic, nonhypertensive hemorrhagic, and subarachnoid hemorrhagic), dates of onset and admission, National Institutes of Health Stroke Scale score at admission, modified Rankin Scale score at discharge, and alcohol intake. Multivariable logistic regression analysis adjusted for stroke-related factors was performed to estimate the odds ratios of alcohol intake for stroke severity. RESULTS: In cardioembolic ischemic stroke, a significant protective effect of moderate intake on severity at admission was observed in both sexes. In noncardioembolic ischemic stroke, a significant protective effect on stroke severity at admission was found for each sex. At discharge, the results also showed a significant protective effect for each sex with moderate intake. For both subtypes of ischemic stroke, a J-shaped relationship between alcohol intake and stroke severity at admission and discharge was observed in women and men. In hypertensive hemorrhagic stroke, a significant protective effect was found in men at both admission and discharge. In women, heavy drinking had a significant harmful effect on stroke severity at admission. CONCLUSIONS: Habitual alcohol intake is associated with stroke severity at admission and discharge regardless of sex.

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 (Phomogeneity = .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.

Evaluating the role of alcohol consumption in breast and ovarian cancer susceptibility using population-based cohort studies and two-sample Mendelian randomization analyses.

Alcohol consumption is correlated positively with risk for breast cancer in observational studies, but observational studies are subject to reverse causation and confounding. The association with epithelial ovarian cancer (EOC) is unclear. We performed both observational Cox regression and two-sample Mendelian randomization (MR) analyses using data from various European cohort studies (observational) and publicly available cancer consortia (MR). These estimates were compared to World Cancer Research Fund (WCRF) findings. In our observational analyses, the multivariable-adjusted hazard ratios (HR) for a one standard drink/day increase was 1.06 (95% confidence interval [CI]; 1.04, 1.08) for breast cancer and 1.00 (0.92, 1.08) for EOC, both of which were consistent with previous WCRF findings. MR ORs per genetically predicted one standard drink/day increase estimated via 34 SNPs using MR-PRESSO were 1.00 (0.93, 1.08) for breast cancer and 0.95 (0.85, 1.06) for EOC. Stratification by EOC subtype or estrogen receptor status in breast cancers made no meaningful difference to the results. For breast cancer, the CIs for the genetically derived estimates include the point-estimate from observational studies so are not inconsistent with a small increase in risk. Our data provide additional evidence that alcohol intake is unlikely to have anything other than a very small effect on risk of EOC.

A genome-wide association study on confection consumption in a Japanese population: the Japan Multi-Institutional Collaborative Cohort Study.

Differences in individual eating habits may be influenced by genetic factors, in addition to cultural, social or environmental factors. Previous studies suggested that genetic variants within sweet taste receptor genes family were associated with sweet taste perception and the intake of sweet foods. The aim of this study was to conduct a genome-wide association study (GWAS) to find genetic variations that affect confection consumption in a Japanese population. We analysed GWAS data on confection consumption using 14 073 participants from the Japan Multi-Institutional Collaborative Cohort study. We used a semi-quantitative FFQ to estimate food intake that was validated previously. Association of the imputed variants with confection consumption was performed by linear regression analysis with adjustments for age, sex, total energy intake and principal component analysis components 1-3. Furthermore, the analysis was repeated adjusting for alcohol intake (g/d) in addition to the above-described variables. We found 418 SNP located in 12q24 that were associated with confection consumption. SNP with the ten lowest P-values were located on nine genes including at the BRAP, ACAD10 and aldehyde dehydrogenase 2 regions on 12q24.12-13. After adjustment for alcohol intake, no variant was associated with confections intake with genome-wide significance. In conclusion, we found a significant number of SNP located on 12q24 genes that were associated with confections intake before adjustment for alcohol intake. However, all of them lost statistical significance after adjustment for alcohol intake.