Heavy Alcohol Drinking Research Articles

Sleep and circadian differences between light and heavy adult alcohol drinkers.

BackgroundNumerous studies have reported that eveningness is associated with increased alcohol consumption. However, biological markers of circadian timing, such as dim light melatonin onset (DLMO) and circadian photoreceptor responsivity (post‐illumination pupil response, PIPR), have rarely been assessed in the context of habitual alcohol consumption. This study aimed to examine sleep, circadian timing, and photoreceptor responsivity in adult alcohol drinkers.MethodsParticipants (21 to 45 years) included 28 light and 50 heavy drinkers. The 8‐day study consisted of a week of ad lib sleep monitored with wrist actigraphy, followed by a 9‐h laboratory session with a photoreceptor responsivity and circadian phase assessment.ResultsThe heavy drinkers obtained on average 28 more minutes of sleep (p = 0.002) and reported more eveningness than the light drinkers (p = 0.029). There was a trend for a shorter DLMO‐midsleep interval (p = 0.059) in the heavy drinkers, reflecting a tendency for them to sleep at an earlier circadian phase. The PIPR in the heavy drinkers was significantly smaller than in the light drinkers (p = 0.032), suggesting reduced circadian photoreceptor responsivity in the heavy drinkers. A larger PIPR was significantly associated with a later DLMO in the light drinkers (r = 0.44, p = 0.019), but this relationship was absent in the heavy drinkers (r = −0.01, p = 0.94).ConclusionsThese results are consistent with earlier reports of more eveningness and a shorter DLMO‐midsleep interval being associated with heavier alcohol drinking. The novel finding of reduced circadian photoreceptor responsivity in heavy drinkers is consistent with prior rodent studies. Future studies should explore the impact of habitual alcohol consumption on other measures of circadian photoreceptor responsivity.

Descriptive, analytical and molecular epidemiology of pancreatic cancer

The purpose of the study was to present current data on the role of lifestyle and heredity factors in the etiology of pancreatic cancer (PC). Material and Methods. A systemic literature search was conducted using Medline and Elibrary databases. Results. Pancreatic cancer is the 9th leading cause of cancer-related deaths worldwide. PC has an extremely poor prognosis. The 5-year survival rate of patients with PC does not exceed 9 %. The highest incidence and mortality rates from PC are found in Eastern Europe, including Russia. The incidence of PC in 2019 was 9.3 per 100,000 males and 5.7 per 100,000 females. In Russia, PC incidence and mortality rates in both males and females show a steady increase. Risk factors associated with PC include smoking, heavy alcohol drinking, overweight and obesity, diabetes and chronic pancreatitis. The microbiome of the oral cavity and colon infuence the risk of PС. Approximately 10 % of PC is estimated to have familial inheritance. The risk of PC in patients with inherited syndromes ranges from 2 (hereditary breast and ovarian cancer syndrome) to 132 (Peutz-Jeghers syndrome). Regions of the genome containing variants of single nucleotide polymorphism (SNPs), which are more common in patients with PC than in healthy people, were identifed. The most common somatic mutations include mutations in the driver genes of prostate cancer, which include the KRAS oncogene and tumor suppressor genes TP53, CDKN2A, and SMAD4.The less common mutations of genes include AIB1/NCOA, ERBB2/HER2/EGFR2, AKT2, BRAF, CCND1, RB1, etc. They are identifed as “passenger” mutations although the combined effect of polymorphism of these genes can be signifcant and comparable to the infuence of the driver gene. Conclusion. A signifcant disadvantage of our understanding of the process of carcinogenesis is the lack of information about carcinogenic factors that cause specifc mutations, i.e. the formation of mutational signatures. To solve this problem, in 2017, the international scientifc project GRAND CHALLENGE “Mutograph” was launched. The scientists of the Department of Cancer Epidemiology of N. N. Blokhin National Medical Research Center of Oncology are members of the international team working on this project.

Association of alcohol drinking with incident type 2 diabetes and pre-diabetes: The Guangzhou Biobank Cohort Study.

We examined associations of baseline alcohol drinking with incident type 2 diabetes (T2D) or impaired fasting glucose (IFG), and explore whether the associations were modified by genetic polymorphisms of aldehyde dehydrogenase-2 (ALDH2) and alcohol dehydrogenase-1B (ADH1B). All participants were aged 50+ (mean=60.45; standard deviation=6.88) years. Information of alcohol consumption was collected at baseline from 2003 to 2008. Incident T2D was defined as fasting glucose ≥7.0mmol/L or post-load glucose ≥11.1mmol/L at follow-up examination (2008-2012), self-reported T2D and/or initiation of hypoglycaemia medication or insulin during follow-up. Impaired fasting glucose was defined as fasting glucose ≥5.6mmol/L and <7mmol/L. Of 15,716 participants without diabetes and 11,232 participants without diabetes and IFG at baseline, 1624 (10.33%) developed incident T2D and 1004 (8.94%) developed incident IFG during an average 4years of follow-up. After multivariable adjustments, compared with never drinking, occasional or moderate alcohol drinking was not associated with risk of incident hyperglycaemia (T2D+IFG) (odds ratio (OR)=1.10, 95% confidence interval (CI) 0.95-1.27, and 0.90 (0.69-1.18), respectively), whereas heavy alcohol drinking was associated with a higher risk of incident hyperglycaemia (T2D+IFG) (OR=1.82, 95% CI 1.24-2.68). No interactions of sex, overweight/obesity and genetic polymorphisms of ADH1B/ALDH2 genes with alcohol drinking on incident T2D and/or IFG were found (P for interaction from 0.12 to 0.85). Our results support a detrimental effect of heavy alcohol use on IFG and T2D. No protective effect was found for those carrying lower risk alleles for ADH1B/ALDH2 genes.

0212 Habitual Heavy Alcohol Drinking in Healthy Adults is Associated With Reduced Circadian Photoreceptor Responsivity to Light

Abstract Introduction Habitual alcohol consumption and circadian timing are interconnected. Numerous studies have reported that heavy alcohol use is associated with eveningness. Only two studies have assessed the dim light melatonin onset (DLMO) in the context of habitual alcohol use, and both reported a shorter DLMO-midsleep interval was associated with heavier alcohol consumption. A gap in this research is the potential impact of alcohol use on the primary circadian photoreceptor, the intrinsically photosensitive retinal ganglion cells (ipRGCs), which influence circadian timing. This study aimed to compare sleep, circadian timing, and photoreceptor responsivity between light and heavy alcohol drinkers. Methods Participants were healthy (average age 27 years) and included 28 light (average 2.6 drinks/week) and 50 heavy (average 17.9 drinks/week) drinkers. They participated in an 8-day study protocol: 1 week of adlib sleep monitored with wrist actigraphy, followed by a 9-hour laboratory session with a photoreceptor responsivity (post-illumination pupil response, PIPR) and circadian phase assessment. Participants passed a breathalyzer test at the start of the laboratory session. Results Both drinking groups were good sleepers with minimal mood disturbance. Consistent with earlier studies, the heavy drinkers had more eveningness (p=0.029), and a trend for a shorter DLMO-midsleep interval (p=0.059) as compared to the light drinkers. The PIPR in the heavy drinkers was significantly smaller than in the light drinkers (p=0.006), suggesting reduced circadian photoreceptor responsivity in the heavy drinkers. In the light drinkers, a larger PIPR in the evening, reflecting greater sensitivity to phase-delaying light, was significantly associated with a later DLMO (r=0.42, p=0.028). However, this relationship was absent in the heavy drinkers (r=-0.07, p=0.68). Conclusion The findings replicate previous work examining the relationship between chronotype, DLMO, and habitual alcohol consumption. For the first time, circadian photoreceptor responsivity was examined, and found to be significantly reduced in heavy alcohol drinkers as compared to light alcohol drinkers. This finding is consistent with prior rodent studies that found reduced phase shifts to light with acute or chronic alcohol consumption, and suggests that habitual heavy alcohol use may impair the circadian response to light in humans. Support (If Any) Grant awarded from NIAAA R01 AA023839.

Chronic and Binge Alcohol Ingestion Increases Truncated Oxidized Phosphatidylcholines in Mice Lungs Due to Increased Oxidative Stress.

Heavy alcohol drinking has negative health effects in multiple organs. It predisposes lungs to inflammatory conditions associated with acute lung injury and increased incidence of pneumonia and sepsis, which may lead to death due to acute respiratory distress syndrome in some individuals with alcohol use disorder (AUD). In general, rodent models of alcohol exposure either do not recapitulate multiple organ injuries as seen in humans or require longer duration to establish tissue injury and inflammation. The recently introduced NIAAA model of alcohol-induced liver injury, characterized by a marked increase in steatosis and liver damage with 10 days of a liquid diet containing 5% ethanol followed by a single ethanol binge (5 g/kg). Therefore, we employed this model to explore the status of surfactant phospholipids, oxidative stress, tissue injury markers and inflammatory cytokines in lungs. In lungs of C57BL/6J mice, the alcohol feeding significantly increased levels of the surfactant phospholipid dipalmitoyl phosphatidylcholine (DPPC) as well as the truncated oxidized phosphatidylcholines palmitoyl oxovaleryl phosphatidyl-choline (POVPC), palmitoyl glutaryl phosphatidyl-choline (PGPC), palmitoyl oxo-nonanoyl phosphatidyl-choline (ALDO-PC), and palmitoyl azelaoyl phosphatidyl-choline (PAzePC) at 9 h post-binge. Additionally, gene expression of the enzymes catalyzing lipid oxidation, such as arachidonate 15-lipoxygenase (Alox15), prostaglandin synthase 2 (Ptgs2), Cytochrome P450 2E1 (Cyp2E1) and NADPH oxidase 1 (Nox1) were significantly increased. Furthermore, ethanol increased levels of the inflammatory cytokine Interleukin-17 in bronchoalveolar lavage fluid. In conclusion, the NIAAA alcohol feeding model might be suitable to study alcohol-induced lung injury and inflammation.

Prenatal Alcohol Exposure and the Risk of Depression in Offspring: a Meta-Analysis.

Background Prenatal alcohol exposure (PAE) has been related to poor consequences of mental health in offspring. However, it remains unknown whether maternal alcohol drinking during pregnancy is associated with depression in the offspring. Methods A meta-analysis was performed accordingly. Relevant observational studies were identified from Medline, Embase, and Web of Science databases. A fixed-effect or a random-effect model was selected dependending on the between-study heterogeneity. Results Eight cohort studies were included. The heterogeneity was not significant (I2 = 14%). A meta-analysis with a fixed-effect model showed that PAE was associated with a higher risk of depression in offspring (odds ratio (OR): 2.28, 95% confidence interval (CI): 1.61 to 3.25, p < 0.001). Subgroup analysis showed that moderate (OR: 1.74, 95% CI: 1.22 to 2.49, p=0.002, I2 = 0%) or heavy (OR: 2.41, 95% CI: 1.55 to 3.73, p < 0.001, I2 = 0%) maternal alcohol drinking in pregnancy was associated with depression in offspring, but not for those with low maternal alcohol drinking (OR: 1.18, 95% CI: 0.97 to 1.44, p=0.10, I2 = 0%). Further subgroup analyses according to study design, timing of PAE evaluation, age at depression diagnosis, and quality scores showed consistent results. Univariate metaregression showed a dose-response association between PAE and offspring depression (coefficient: 0.073, 95% CI: 0.019 to 0.127, p=0.014). Conclusions Current evidence suggests that PAE may be a risk factor of depression in offspring.

The Magnitude of NCD Risk Factors in Ethiopia: Meta-Analysis and Systematic Review of Evidence.

Background: Non-communicable Diseases (NCDs) and their risk factors are the leading contributors to morbidity and mortality globally, particularly in low- and middle-income countries including Ethiopia. To date, there has been no synthesis of the literature on the relative prevalence of NCD risk factors in Ethiopia. Methodology: We conducted a systematic review and meta-analysis of primary studies reporting on the prevalence of NCD risk factors in Ethiopia published in English from 2012 to July 2020. Pre-tested NCD search terms were applied to Medline, Embase, Scopus, CINAHL, and Global Health. Three reviewers screened and appraised the quality of the identified papers. Data extraction was conducted using a pilot tested proforma. Meta-analysis was conducted using Stata 16 and pooled prevalence estimated with associated 95% confidence intervals. Clinically heterogeneous studies that did not fulfil the eligibility criteria for meta-analysis were narratively synthesised. I2 was used to assess statistical heterogeneity. Results: 47 studies fulfilled the inclusion criteria and contributed 68 NCD risk factor prevalence estimates. Hypertension was the most frequently examined NCD risk factor, with a pooled prevalence of 21% (n = 27 studies). The pooled prevalence percentages for overweight and obesity were 19.2% and 10.3%, respectively (n = 7 studies each), with a combined prevalence of 26.8% (n = 1 study). It was not possible to pool the prevalence of alcohol consumption, smoking, metabolic disorders, or fruit consumption because of heterogeneity across studies. The prevalence of alcohol use, as reported from the included individual studies, ranged from 12.4% to 13.5% (n = 7 studies). More than 90% of participants met the WHO-recommended level of physical activity (n = 5 studies). The prevalence of smoking was highly variable, ranging between 0.8% and 38.6%, as was the prevalence of heavy alcohol drinking (12.4% to 21.1%, n = 6 studies) and metabolic syndrome (4.8% to 9.6%, n = 5 studies). Fruit consumption ranged from 1.5% up to the recommended level, but varied across geographic areas (n = 3 studies). Conclusion and recommendations: The prevalence of NCD risk factors in Ethiopia is relatively high. National NCD risk factor surveillance is required to inform the prioritisation of policies and interventions to reduce the NCD burden in Ethiopia.

Vascular Endothelial Growth Factor as a Potential Biomarker of Neuroinflammation and Frontal Cognitive Impairment in Patients with Alcohol Use Disorder.

(1) Background: Alcohol Use Disorder (AUD) is associated with functional disruption of several brain structures that may trigger cognitive dysfunction. One of the mechanisms of alcohol-associated cognitive impairment has been proposed to arise from its direct impact on the immune system, which culminates in the release of cytokines and chemokines which can eventually reach the brain. Alcohol can also disrupt the blood–brain barrier, facilitating the penetration of pro-inflammatory molecules throughout vascular endothelial growth factor A (VEGFA). Thus, alcohol-induced alterations in chemokines and VEGFA might contribute to the neuroinflammation and cognitive impairment associated with AUD. (2) Methods: The present cross-sectional study investigates whether patients with AUD (n = 86) present cognitive disability associated to alterations in plasma concentration of SDF-1, fractalkine, eotaxin, MCP-1, MIP-1α and VEGFA when compared to control subjects (n = 51). (3) Results: The analysis indicated that SDF-1 and MCP-1 concentrations were higher in AUD patients than in controls. Concentrations of VEGFA were higher in AUD patients with severe frontal deficits, and the score of frontal lobe functions was negatively correlated with VEGFA and fractalkine. Acute alcohol effects on VEGFA plasma levels in healthy volunteers demonstrated the induction of VEGFA release by heavy alcohol drinking. VEGFA was positively correlated with pro-inflammatory chemokines in AUD patients with frontal cognitive impairment. (4) Conclusions: we propose VEGFA/chemokine monitoring as biomarkers of potential cognitive impairment in AUD patients.

Association between changes in facial flushing and hypertension across drinking behavior patterns in South Korean adults.

Heavy alcohol drinking has been reported to be associated with hypertension. Moreover, when drinking alcohol, individuals may experience symptoms such as facial flushing. Therefore, this study aimed to examine the association between changes in facial flushing and hypertension across different drinking behavior patterns in South Korean adults.Data from the Korea Community Health Survey conducted in 2019 were used, and 118 129 (51 047 men and 67 082 women) participants were included. The participants were divided into five groups based on the change in facial flushing (non‐drinking, non‐flushing to non‐flushing, flushing to flushing, non‐flushing to flushing, flushing to non‐flushing). The risk of hypertension in each facial flushing group was analyzed by multiple logistic regression.Men in the non‐flushing to flushing group had a significantly higher association with hypertension than other groups (men: odds ratio (OR) 1.42, confidence interval (CI) 1.14–1.76). According to the level of alcohol use disorder, the non‐flushing to flushing group showed a significantly increased odds of hypertension compared to all levels of drinking (men: mild drinking: OR 1.95, CI 1.40–2.71; moderate drinking: OR 2.02, CI 1.41–2.90; women: moderate drinking: OR 1.71, CI 1.16–2.52; heavy drinking: OR 1.90, CI 1.19–3.04).This study found a significant association between changes in facial flushing and hypertension among adults in South Korea. In particular, individuals who changed from non‐flushing to flushing reactions had an increased association with hypertension than the other groups. Compared to people at the same drinking level, people with non‐flushing to flushing reactions were highly associated with hypertension at moderate drinking level.

Tobacco, alcohol and pancreatic disease: key findings from global consortia

(RR) were 1.74 (95% confidence interval, CI, 1.39-2.13) for current and 1.32 (95% CI 1.03-1.71) for former smokers [2, 3]. Chronic pancreatitis is associated to heavy alcohol drinking, though the risk estimates remain open to discussion. Epidemiological data are limited, but consistent with clinical ones to indicate that (heavy) drinking is related to chronic pancreatitis [2]. There is consistent evidence that tobacco is also a major factor for chronic pancreatitis. With reference to tobacco, the RRs from a meta-analysis were 2.8 (95% CI 1.7-4.8) for current and 1.4 (95% CI 1.1-1.9) for former smokers and these associations were not totally accounted for by heavy alcohol drinking [4]. Tobacco is responsible for 10 to 20% of all chronic pancreatitis. In non-alcoholic idiopathic chronic pancreatitis, smoking is associated with disease progression [5]. Cigarette smoking is the major risk factor for pancreatic cancer. In the Pancreatic Cancer Consortium (PanScan; 1481 cases, 1539 controls) the pooled RR was 1.77 (95% CI 1.38-2.26) for current and 1.09 (95% CI 0.91-1.30) for former smokers [6]. In the International Pancreatic Cancer Case-Control Consortium (PanC4; 6507 cases, 12,890 controls), the RR was 2.20 (95% CI 1.71-2.83) for current smokers and rose to 3.39 (95% CI 2.36-1.86) for heavy smokers; the RR was 1.17 (95% CI 1.02-2.83) for former smokers [7]. Cigar smoking was also associated with pancreatic cancer (RR 1.62, 95% CI 1.15-2.29), whereas no consistent association was found for smokeless tobacco, nor for pipe smoking [8]. A meta-analysis of 21 case-control and 11 cohort studies provided conclusive evidence that moderate drinking was unrelated to pancreatic cancer, but heavy drinking (3 or more drinks/day) gave a RR of 1.22 (95% CI 1.12-1.34) [9]. In the PanScan collaborative re-analysis of cohort studies (1530 cases, 1520 controls), there was no overall association with total alcohol intake, but the RR was 1.38 (95% CI 0.9-2.3) for drinking ≥60g day and rose to 2.23 (95% CI 1.0-4.9) for male heavy liquors drinkers [10]. In a pooled analysis of 14 cohort studies (2187 cases) the RR for >30g day was 1.22 (95% CI 1.031.45) [11]. In the PanC4 study (5585 cases, 11,822 controls), the RR was 1.46 (95% CI 1.16-1.83) for ≥6 drinks day; no association was observed with moderate drinking [12]. Possible mechanisms of action of alcohol include acetaldehyde, fatty acid ethyl esters, free radicals, DNA damage and inflammation [12]. Possible mechanisms of action of smoking include tobacco specific nitrosamines (NKK), polycyclic aromatic hydrocarbons (PAH) and other smoking-associated chemicals, and smoking as an inflammatory agent and a progressor in carcinogenesis [7].

The impact of heavy alcohol consumption on cognitive impairment in young old and middle old persons

BackgroundDementia indicates a significant disease burden worldwide with increased population aging. This study aimed to investigate the impact of alcohol consumption on the risk of cognitive impairment in older adults.MethodsParticipants ≥ 60 years were administered the Digit Symbol Substitution Test (DSST) to evaluate cognitive function in National Health and Nutrition Examination Survey (NHANES) cycles from 1999 to 2002 and 2011 to 2014 for enrollment in the present study. Participants were categorized into non-drinker, drinker, and heavy drinker groups. Logistic regression analyses were performed to explore associations between cognitive impairment and alcohol consumption.ResultsMultivariate analysis showed that older adults, men, people from minority races, persons with lower education or income levels, social difficulties, hypertension, or chronic kidney disease were significantly associated with a higher risk of cognitive impairment (all p < 0.05). In the young old (60–69 years), heavy amount of alcohol drinking was significantly associated with lower risk of cognitive impairment compared with drinkers [adjusted odds ratio (aOR): 0.280, 95% Confidence interval (CI) 0.095–0.826]. But in the middle old persons (≥ 70 years), heavy alcohol drinking was associated with higher risk of cognitive impairment (aOR: 2.929, 95% CI 0.624–13.74).ConclusionsOur study demonstrated that light to heavy drinking was associated with lower risk of cognitive impairment in participants aged between 60 and 69 years, but caution is needed in the middle old people with heavy alcohol drinking.

Barriers and Breakthroughs in Targeting the Oxytocin System to Treat Alcohol Use Disorder.

Development of better treatments for alcohol use disorder (AUD) is urgently needed. One promising opportunity for this development is the potential of targeting the oxytocin peptide system. Preclinical studies showed that administration of exogenous oxytocin or, more recently, stimulation of neurons expressing endogenous oxytocin lead to a decreased alcohol consumption across several rodent models. Initial clinical studies also showed that administration of oxytocin decreased craving for alcohol and heavy alcohol drinking. However, several more recent clinical studies were not able to replicate these effects. Thus, although targeting the oxytocin system holds promise for the treatment of AUD, more nuanced approaches toward development and application of these treatments are needed. In this mini-review we discuss potential caveats resulting in differential success of attempts to use oxytocin for modulating alcohol use disorder-related behaviors in clinical studies and evaluate three directions in which targeting the oxytocin system could be improved: (1) increasing potency of exogenously administered oxytocin, (2) developing oxytocin receptor agonists, and (3) stimulating components of the endogenous oxytocin system. Both advances and potential pitfalls of these directions are discussed.

The serotonin 2A receptor agonist TCB-2 attenuates heavy alcohol drinking and alcohol-induced midbrain inhibitory plasticity.

Disruption of neuronal chloride ion (Cl- ) homeostasis has been linked to several pathological conditions, including substance use disorder, yet targeted pharmacotherapies are lacking. In this study, we explored the potential of serotonin 2A receptor (5-HT2A R) agonism to reduce alcohol consumption in male wild-type C57Bl/6J mice and to ameliorate alcohol-induced inhibitory plasticity in the midbrain. We found that administration of the putative 5-HT2A R agonist TCB-2 attenuated alcohol consumption and preference but did not alter water or saccharin consumption. We hypothesized that the selective behavioural effects of TCB-2 on alcohol drinking were due, at least in part, to effects of the agonist on ventral tegmental area (VTA) neurocircuitry. Alcohol consumption impairs Cl- transport in VTA GABA neurons, which acts as a molecular adaptation leading to increased alcohol self-administration. Using ex vivo electrophysiological recordings, we found that exposure to either intermittent volitional alcohol drinking or an acute alcohol injection diminished homeostatic Cl- transport in VTA GABA neurons. Critically, in vivo TCB-2 administration normalized Cl- transport in the VTA after alcohol exposure. Thus, we show a potent effect of alcohol consumption on VTA inhibitory circuitry, in the form of dysregulated Cl- homeostasis that is reversible with agonism of 5-HT2A Rs. Our results provide insight into the potential therapeutic action of 5-HT2A R agonists for alcohol abuse.

Association Between Korean-Style Balanced Diet and Risk of Abdominal Obesity in Korean Adults: An Analysis Using KNHANES-VI (2013-2016).

Abdominal obesity is a critical factor for metabolic diseases, and specific eating patterns such as the Mediterranean diet help prevent metabolic diseases. This study aimed to investigate the association between the modified Korean health eating index (MKHEI), including a Korean-balanced diet, and abdominal obesity risk according to genders in adults aged 20–64 years (4,886 males and 7,431 females), using the Korea National Health and Nutrition Examination Survey VI (2013–2016). Adjusted means and 95% confidence intervals of MKHEI scores and nutrient intake estimated using the 24-h recall method were calculated according to abdominal obesity (waist circumference ≥90 cm for men and ≥85 cm for women) after adjusting for age, residence area, region, education, income, drinking status, smoking status, marital status, and exercise. Adjusted odds ratios (ORs) for abdominal obesity were measured according to MKHEI tertiles using logistic regression analysis while controlling for covariates. Individuals aged >50 years, married, below high school, lower-income, heavy alcohol drinkers, past and current smokers, and males living in the southern areas had a higher risk of abdominal obesity. In both genders, the scores of all MKHEI components were lower in the abdominal obesity group (n = 2,895) than in the control group (n = 9,422). Further, the scores of fruits with and without fruit juice and those of beans, including fermented beans, were lower in the abdominal obesity group only in females but not in males. Further, the scores of fast foods were higher in the abdominal obesity group than in the control group only in females. After adjusting for covariates, the adjusted OR for abdominal obesity was inversely associated with Korean balanced diet (KBD) related to KHEI scores. Unlike KBD, MKHEI of Western-style diet was not associated with abdominal obesity in either gender. In conclusion, KBD can lower the risk of abdominal obesity in females and should thus be recommended to prevent abdominal obesity.

Association Between Serum Midkine Level and Gastric Precancerous Lesion in Patients with Gastritis.

Gastric cancer is the fifth most common malignancy and the third highest cancer-related mortality worldwide after lung and colorectal cancers. The gastric carcinogenesis is started with precancerous lesion. Prompt diagnosis and management of gastric precancerous lesion may prevent disease progression. Midkine is a growth factor associated with various cancers and proposed as a marker for detecting gastric precancerous lesion. The aim of the study is to determine the association between serum midkine level and gastric precancerous lesion in patients with gastritis. A cross sectional study was conducted at Haji Adam Malik general hospital. Subjects were obtained by consecutive sampling. Inclusion criteria were patients aged 18 years or older, diagnosed with gastritis from gastroscopy and histopathology results, and willing to cooperate in the study. Each subjects underwent interview and endoscopic examination. Serum midkine level was determined using enzyme-linked immunosorbent assay (ELISA) method. Chi square, receiver operating characteristic (ROC) curve, and logistic regression tests were applied. A total of 160 subjects were enrolled with 29.4% had gastric precancerous lesion. Serum midkine level was associated with gastric premalignant lesion. Cut off point for serum midkine level was 252 pg/mL with area under the curve of 0.816 (p<0.001). It's sensitivity, specificity, and accuracy in diagnosing gastric precancerous lesion were 74.5%, 71.7%, and 72.5%, respectively. Helicobacter pylori infection, high serum midkine level, heavy alcohol drinker, and family history of gastric cancer were risk factors for gastric precancerous lesion. Serum midkine level is associated with gastric premalignant lesion in patients with gastritis and has good diagnostic values.

Abstract PR-01: Association of Affordable Care Act Medicaid expansions with healthcare access and utilization among people who smoke

Abstract Background: People who smoke have a higher risk of developing cancer and disproportionately lower incomes which worsens healthcare access and health outcomes. The Affordable Care Act expanded Medicaid eligibility to adults with income up to 138% of the federal poverty line. It is unknown if and how Medicaid expansions changed healthcare access, preventive service use, and health behaviors. Also, it is unknown whether expansions impacted income or racial/ethnic disparities in these measures, given historically lower healthcare access and utilization in lower income people and people of color. Methods: Data were from the nationally representative Behavioral Risk Factor Surveillance System surveys between 2011-2019 of adults ages 18-64 years who currently smoked cigarettes and former smokers who had quit in the past year (n=580,858). Generalized difference-in-differences (DID) analyses using logistic regression models examined the association of Medicaid expansions (staggered time-varying exposure, 34 states expanded as of December 2019) with healthcare access (insurance coverage, care affordability, usual source of care), preventive service use (routine checkup, flu shot, HIV test, breast and colorectal cancer screening, cholesterol check, dentist visit), and health/risk behaviors (heavy alcohol drinking, obesity), including cessation behaviors (past-year quit attempt, successful cessation for &amp;gt;3 months). Income and race/ethnicity differences were also tested. Results: Among people who smoke, Medicaid expansions were associated with healthcare access and preventive care utilization improvements, but not health behaviors, including cessation. Expansions resulted in narrowing of disparities in several measures across income levels and Black vs. White people in expansion states. For example, expansion associated gains in insurance coverage were significantly larger in low-income (expansion: 74.6% vs. nonexpansion: 60.8%; DID: 13.8% 95% CI: 12.8, 14.8%) than high-income (insurance: 87.5% vs. 93.7%, DID: -6.2% points 95% CI: -7.2, -5.2%); and in Black people (82.6% vs. 74.6%, DID: 7.9% points 95% CI: 6.3, 9.5%) than White people (79.5% vs. 75.7%; DID: 3.8%, 95% CI: 3, 4.6%). Medicaid expansions gains were also larger among lower than higher income people for all in preventive care utilization measures studied; and uptake of flu shots, mammograms, and HIV tests were larger in Black than White people. Significant gains in multiple measures were also observed for Hispanic and American Indian/Alaska Native people who smoke, but changes were generally no different than White people. Conclusions: Among people who smoke, Medicaid expansions improved healthcare access and preventive services use. Expansions were also associated with a reduction, but not elimination, of income and Black-White disparities in healthcare access and utilization. Despite insurance and preventive service gains, expansions were not associated with cessation behaviors, signaling the need for improving comprehensive cessation treatments in Medicaid expansion programs. Citation Format: Priti Bandi, Samuel Asare, J. Lee Westmaas, Nigar Nargis, Robin Yabroff, Ahmedin Jemal, Xuesong Han, Stacey Fedewa. Association of Affordable Care Act Medicaid expansions with healthcare access and utilization among people who smoke [abstract]. In: Proceedings of the AACR Virtual Conference: 14th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2021 Oct 6-8. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr PR-01.

Lifestyle risk factors and all-cause and cause-specific mortality: assessing the influence of reverse causation in a prospective cohort of 457,021 US adults.

Lifestyle risk factors have been associated with increased all-cause and cause-specific mortality, but the influence of reverse causation has been underappreciated as a limitation in epidemiological studies. Prospective cohort study including 457,021 US adults from the National Health Interview Survey 1997-2013 linked to the National Death Index records through December 31, 2015. Multivariable Cox models were performed to examine the association of lifestyle risk factors with all-cause and cause-specific mortality. Participants with prevalent diseases and thefirst 2, 5, 10, and 15years of follow-up were excluded to account for reverse causation. During 4,441,609 person-years, we identified 60,323 total deaths. Heavy alcohol drinking (HR 1.12; 95% CI 1.08 to 1.16), smoking (HR 1.78; 95% CI 1.74 to 1.83) and lack of physical activity (HR 1.51; 95% CI 1.47 to 1.54) were associated with increased all-cause mortality. Overweight was associated with lower all-causemortality (HR 0.88; 95% CI 0.86 to 0.90). After exclusion of participants with diseases and first 10years of follow-up, associations changed to: heavyalcoholdrinking (HR 1.31; 95% CI 1.20 to 1.43), smoking (HR 1.99; 95% CI 1.87 to 2.11), lack of physical activity (HR 1.21; 95% CI 1.15 to 1.27), and overweight (HR 1.05; 95% CI 1.00 to 1.10). Methods to account for reverse causation suggest different effects of reverse causation on the associations between lifestyle risk factors and mortality. Exclusion of participants with diseases at baseline, and exclusion of 5-10years of follow-up may be necessary to mitigate reverse causation.

Socio-demographic and substance use characteristics of unintentional injuries among Nunavik youth

ABSTRACT This study described the distribution of unintentional injuries among Inuit youth in Nunavik, Quebec, Canada, and examined the relationship between socio-demographic factors, substance use and unintentional injuries. A cross-sectional study design was used on data collected for the Nunavik Child Development Study (2013–2015) among eligible youth aged 16 to 21 years old. Unintentional injury occurrence and causes (last 12 months) were assessed through individual interviews. A multivariate logistic regression model tested the relationship between socio-demographic, substance use variables and unintentional injury occurrence. Among the 199 youth who participated (94% response rate), thirty youth reported being unintentionally injured in the past 12 months , of which 50% were female. All-terrain vehicle collisions were the most frequent injuries reported (23%). The odds of being injured decreased by 62% for youth who were currently employed compared to those who were unemployed, adjusting for other socio-demographic variables (p-value = 0.04). Heavy alcohol drinking in the past 12 months was not significantly associated with unintentional injury. This study highlights the burden of unintentional injuries among Nunavik youth and the need for future work to explore additional and diverse variables that may prevent or contribute to injuries in order to inform culturally and developmentally-appropriate injury prevention strategies.

Addressing methodological issues in a study of impulsivity and vulnerability for transition to alcohol use disorder

Heightened behavioral impulsivity has been advocated as a preexisting risk factor for the development of alcohol use disorder (AUD). Nonetheless, studies investigating impulsivity in adolescent/young adult at-risk drinkers-who are at increased risk of developing AUD-report mixed findings. This may be due to methodological limitations related to definitions of at-risk drinking, the retrospective assessment of alcohol intake, and/or the relatively modest sample size of some studies. Healthy individuals (N=814, Mage =22.50) completed online surveys and a measure of choice impulsivity. Of these, a number of participants also undertook an online measure of response inhibition (n=627, Mage =22.66), and a further subgroup submitted real-time alcohol consumption information for a period of 21days using an app (n=543, Mage =22.96). Differences in behavioral impulsivity were assessed as a function of various at-risk alcohol intake categories. Hierarchical multiple regression was employed to determine whether impulsivity predicted alcohol use in the form of a continuous index comprising variables related to intake and consequences of use. Significantly greater impulsivity was not evident in heavy, standard binge, high binge, harmful, or hazardous alcohol drinkers as compared to controls, regardless of the criteria employed to categorize these at-risk drinkers. Neither choice impulsivity nor reduced response inhibition significantly predicted the alcohol use index. While results could be attributed to the online nature of this research, it is possible that more sensitive measures of behavioral impulsivity are required when assessing nondependent drinkers.

Retraction: Alcohol drinking alters stress response to predator odor via BNST kappa opioid receptor signaling in male mice.

Maladaptive responses to stress are a hallmark of alcohol use disorder, but the mechanisms that underlie this are not well characterized. Here, we show that kappa opioid receptor signaling in the bed nucleus of the stria terminalis (BNST) is a critical molecular substrate underlying abnormal stress responses to predator odor following heavy alcohol drinking. Exposure to predator odor during protracted withdrawal from intermittent alcohol drinking resulted in enhanced prefrontal cortex (PFC)-driven excitation of prodynorphin-containing neurons in the BNST. Furthermore, deletion of prodynorphin in the BNST and chemogenetic inhibition of the PFC-BNST pathway restored abnormal responses to predator odor in alcohol-exposed mice. These findings suggest that increased corticolimbic drive may promote abnormal stress behavioral responses to predator odor during protracted withdrawal. Various nodes of this PFC-BNST dynorphin-related circuit may serve as potential targets for potential therapeutic mediation as well as biomarkers of negative responses to stress following heavy alcohol drinking.