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A recent study in the Journal of Wine Economics presented forecasts of future alcohol consumption derived using the ARIMA (Box–Jenkins) method. Alcohol consumption forecasts can be developed using many different methodologies. In this Note we highlight the value of using multiple methods to develop alcohol consumption forecasts, and demonstrate the capability of the R software platform as a general forecasting tool. (JEL Classifications: D12, C53)
The National Institute for Health and Care Excellence referral guidelines prompting urgent two-week referrals were updated in 2015. Additional symptoms with a lower threshold of 3 per cent positive predictive values were integrated. This study aimed to examine whether current pan-London urgent referral guidelines for suspected head and neck cancer lead to efficient and accurate referrals by assessing frequency of presenting symptoms and risk factors, and examining their correlation with positive cancer diagnoses.
The risk factors and symptoms of 984 consecutive patients (over a six-month period in 2016) were collected retrospectively from urgent referral letters to University College London Hospital for suspected head and neck cancer.
Only 37 referrals (3.76 per cent) resulted in a head and neck cancer diagnosis. Four of the 23 recommended symptoms demonstrated statistically significant results. Nine of the 23 symptoms had a positive predictive value of over 3 per cent.
The findings indicate that the current referral guidelines are not effective at detecting patients with cancer. Detection rates have decreased from 10–15 per cent to 3.76 per cent. A review of the current head and neck cancer referral guidelines is recommended, along with further data collection for comparison.
We investigate alcohol consumption as one of the main factors contributing to variation in the gender gap in life expectancy in the Russian regions. We consider the socioeconomic indicators and mortality coefficients that enable us to capture the causes of death related primarily to alcohol abuse and smoking. We assume that macroeconomic situation, coupled with alcohol consumption are substantial determinants of the gender gap in life expectancy in the Russian regions. A panel data analysis confirms that alcohol consumption has a significant influence on the gender gap in life expectancy and reduces the life expectancy of men first and foremost, as they are more inclined toward unhealthy behaviours. We have determined that employment and income support policies should be conducted in conjunction with the anti-alcohol policy. Social policy aimed at reducing alcohol consumption should be vigorously reinforced during an economic recovery.
Despite established clinical associations among major depression (MD), alcohol dependence (AD), and alcohol consumption (AC), the nature of the causal relationship between them is not completely understood. We leveraged genome-wide data from the Psychiatric Genomics Consortium (PGC) and UK Biobank to test for the presence of shared genetic mechanisms and causal relationships among MD, AD, and AC.
Linkage disequilibrium score regression and Mendelian randomization (MR) were performed using genome-wide data from the PGC (MD: 135 458 cases and 344 901 controls; AD: 10 206 cases and 28 480 controls) and UK Biobank (AC-frequency: 438 308 individuals; AC-quantity: 307 098 individuals).
Positive genetic correlation was observed between MD and AD (rgMD−AD = + 0.47, P = 6.6 × 10−10). AC-quantity showed positive genetic correlation with both AD (rgAD−AC quantity = + 0.75, P = 1.8 × 10−14) and MD (rgMD−AC quantity = + 0.14, P = 2.9 × 10−7), while there was negative correlation of AC-frequency with MD (rgMD−AC frequency = −0.17, P = 1.5 × 10−10) and a non-significant result with AD. MR analyses confirmed the presence of pleiotropy among these four traits. However, the MD-AD results reflect a mediated-pleiotropy mechanism (i.e. causal relationship) with an effect of MD on AD (beta = 0.28, P = 1.29 × 10−6). There was no evidence for reverse causation.
This study supports a causal role for genetic liability of MD on AD based on genetic datasets including thousands of individuals. Understanding mechanisms underlying MD-AD comorbidity addresses important public health concerns and has the potential to facilitate prevention and intervention efforts.
Background. Frequency and quantity of alcohol consumption are metrics commonly used to measure alcohol consumption behaviors. Epidemiological studies indicate that these alcohol consumption measures are differentially associated with (mental) health outcomes and socioeconomic status (SES). The current study aims to elucidate to what extent genetic risk factors are shared between frequency and quantity of alcohol consumption, and how these alcohol consumption measures are genetically associated with four broad phenotypic categories: (i) SES; (ii) substance use disorders; (iii) other psychiatric disorders; and (iv) psychological/personality traits.
Methods. Genome-Wide Association analyses were conducted to test genetic associations with alcohol consumption frequency (N = 438 308) and alcohol consumption quantity (N = 307 098 regular alcohol drinkers) within UK Biobank. For the other phenotypes, we used genome-wide association studies summary statistics. Genetic correlations (rg) between the alcohol measures and other phenotypes were estimated using LD score regression.
Results. We found a substantial genetic correlation between the frequency and quantity of alcohol consumption (rg = 0.52). Nevertheless, both measures consistently showed opposite genetic correlations with SES traits, and many substance use, psychiatric, and psychological/personality traits. High alcohol consumption frequency was genetically associated with high SES and low risk of substance use disorders and other psychiatric disorders, whereas the opposite applies for high alcohol consumption quantity.
Conclusions. Although the frequency and quantity of alcohol consumption show substantial genetic overlap, they consistently show opposite patterns of genetic associations with SES-related phenotypes. Future studies should carefully consider the potential influence of SES on the shared genetic etiology between alcohol and adverse (mental) health outcomes.
The relationship between alcohol consumption and body weight is complex and inconclusive being potentially mediated by alcohol type, habitual consumption levels and sex differences. Heavy and regular alcohol consumption has been positively correlated with increasing body weight, although it is unclear whether this is due to alcohol consumption per se or to additional energy intake from food. This review explores the effects of alcohol consumption on food energy intake in healthy adults. CINAHL Plus, EMBASE, Medline and PsycINFO were searched through February 2018 for crossover and randomised controlled trials where an alcohol dose was compared with a non-alcohol condition. Study quality was assessed using the Effective Public Health Practice Project tool. A total of twenty-two studies involving 701 participants were included from the 18 427 papers retrieved. Studies consistently demonstrated no compensation for alcoholic beverage energy intake, with dietary energy intake not decreasing due to alcoholic beverage ingestion. Meta-analyses using the random-effects model were conducted on twelve studies and demonstrated that alcoholic beverage consumption significantly increased food energy intake and total energy intake compared with a non-alcoholic comparator by weighted mean differences of 343 (95 % CI 161, 525) and 1072 (95 % CI 820, 1323) kJ, respectively. Generalisability is limited to younger adults (18–37 years), and meta-analyses for some outcomes had substantial statistical heterogeneity or evidence of small-study effects. This review suggests that adults do not compensate appropriately for alcohol energy by eating less, and a relatively modest alcohol dose may lead to an increase in food consumption.
We provide a qualitative analysis of a system of nonlinear differential equations that model the spread of alcoholism through a population. Alcoholism is viewed as an infectious disease and the model treats it within a sir framework. The model exhibits two generic types of steady-state diagram. The first of these is qualitatively the same as the steady-state diagram in the standard sir model. The second exhibits a backwards transcritical bifurcation. As a consequence of this, there is a region of bistability in which a population of problem drinkers can be sustained, even when the reproduction number is less than one. We obtain a succinct formula for this scenario when the transition between these two cases occurs.
Excessive alcohol use is associated with brain damage but less is known about brain effects from moderate alcohol use. Previous findings indicate that patients with severe mental illness, particularly schizophrenia, are vulnerable to alcohol-related brain damage. We investigated the association between levels of alcohol consumption and cortical and subcortical brain structures in schizophrenia and bipolar disorder patients and healthy controls, and investigated for group differences for this association.
1.5 T structural magnetic resonance images were acquired of 609 alcohol-using participants (165 schizophrenia patients, 172 bipolar disorder patients, 272 healthy controls), mean (s.d.) age 34.2 (9.9) years, 52% men. Past year alcohol use was assessed with the Alcohol Use Disorder Identification Test – Consumption part (AUDIT-C). General linear models were used to investigate associations between AUDIT-C score and cortical thickness, surface area, and total brain and subcortical volumes.
Increasing AUDIT-C score was linearly associated with thinner cortex in medial and dorsolateral frontal and parieto-occipital regions, and with larger left lateral ventricle volume. There was no significant interaction between AUDIT-C score and diagnostic group. The findings remained significant after controlling for substance use disorders, antipsychotic medication and illness severity.
The results show a dose-dependent relationship between alcohol use and thinner cortex and ventricular expansion. The findings are present also at lower levels of alcohol consumption and do not differ between schizophrenia or bipolar disorder patients compared to healthy controls. Our results do not support previous findings of increased vulnerability for alcohol-related brain damage in severe mental illness.
High alcohol consumption is an important risk factor for chronic disease and liver degeneration. Paraoxonase (PON1) and arylesterase (AE) are functions of the enzyme paraoxonase, which is synthesised by the liver. Paraoxonase circulates in plasma bound to HDL and hydrolyses lipid peroxides, protecting lipoproteins against oxidative modification. It has been shown that excessive alcohol consumption leads to a reduction of serum PON1 and AE activities; however, studies investigating the association with low and moderate alcohol consumption are scarce. We investigated the cross-sectional association between alcohol consumption and serum activities of PON1 and AE using data from the population-based Bavarian Food Consumption Survey II survey. PON1 and AE activities were quantified in serum samples of 566 male and female study participants (aged 18–80 years), and dietary intake including alcohol consumption was estimated from three 24-h dietary recalls. The association between alcohol consumption and PON1 and AE activities was analysed using linear regression, adjusted for age, sex and socio-economic status. There was no strong association between alcohol consumption and enzymatic activities of PON1 and AE in the Bavarian population. PON1 activity was seen to be lowest in non-drinkers (0 g/d) and highest in people who consumed 15·1–30 g of alcohol/d. AE activity increased across alcohol consumption categories, with a mean maximum difference of 14 U/ml (Pfor linear trend 0·04). These associations were attenuated after adjustment for blood concentrations of HDL. The results of this study do not support the hypothesis that alcohol consumption is related to important alterations in PON1 and AE activities.
Older people consume less alcohol than any other adult age group. However, in recent years survey data on alcohol consumption in the United Kingdom have shown that while younger age groups have experienced a decline in alcohol consumption, drinking behaviours among the elderly have not reduced in the same way. This paper uses data from the English Longitudinal Study of Ageing to analyse both the frequency and quantity of older adult's alcohol consumption using a lifecourse approach over a ten-year period. Overall drinking declined over time and the analysis examined how socio-economic characteristics, partnership, employment and health statuses were associated with differences in drinking behaviours and how these changed over time. Higher wealth and level of education were associated with drinking more and drinking more frequently for men and women. Poorer self-rated health was associated with less frequent consumption and older people with poor and deteriorating health reported a steeper decline in the frequency of alcohol consumption over time. Men who were not in a partnership drank more than other men. For women, loss of a partner was associated with a steeper decline in drinking behaviours. These findings have implications for programmes to promote responsible drinking among older adults as they suggest that, for the most part, characteristics associated with sustaining wellbeing in later life are also linked to consuming more alcohol.
Drinking motives may change as adults age, yet few studies in the United States of America have examined older adults' perspectives about their own drinking habits. The current study explored beliefs and attitudes of alcohol use of retired adults residing in a congregate care setting in the Baltimore/Washington DC metro area. Individual interviews were conducted with a sub-sample of 11 individuals who participated in a daily diary study on alcohol use among older adults. All participants in the study were identified as regular drinkers, meaning they had an alcoholic beverage on at least six of the eight days prior to screening. The participants' mean age was 81.5 years with a majority being women (54.5%). Older adults reported alcohol use as a long-term habit or routine. Participants also recognised that their alcohol use was influenced by peer drinking and by the availability of alcohol at the congregate care setting. Participants normalised their drinking as a form of routine socialisation carried from earlier life stages. Participants did not report reactive drinking, suggesting that older drinkers do not see their alcohol use as driven by specific reactions to life stresses or losses associated with ageing. The study also indicates that drinking may provide older adults in congregate care with a sense of continuity from before retirement and preserve their identity and autonomy.
The present study investigated the rate and pattern of neuropsychological recovery in heavy episodic drinking teens during the initial days to weeks of abstinence from alcohol. Adolescents (ages, 16–18 years) with histories of heavy episodic drinking (HED; N = 39) and socio-demographically similar control teens (CON; N = 26) were recruited from San Diego area schools. HED and CON were comparable on 5th grade standardized math and language arts test performance to ensure similar functioning before onset of substance use. Participants were administered three neuropsychological test batteries with 2-week intervals during a 4-week monitored abstinence period. HED teens performed worse overall than CON on tests of prospective memory (p = .005), cognitive switching (p = .039), inhibition task accuracy (p = .001), verbal memory (p's < .045), visuospatial construction (p's < .043), and language and achievement (p's < .008). The statistically significant group × time interaction for block design demonstrated normalization within the 4 weeks of abstinence for the HED (p = .009). This study identified cognitive performance deficits associated with heavy episodic drinking in adolescence during early abstinence and with sustained 4-week abstention. These findings suggest alcohol-related influences on several underlying brain systems that may predate the onset of alcohol abuse or dependence or take longer than 4 weeks to recover. (JINS, 2014, 20, 218–229)
Considerable evidence now links childhood adversity to a variety of adult health problems. Unfortunately, almost all of these studies have relied upon retrospective assessment of childhood events, creating a vulnerability to bias. In this study, we sought to examine three associations using data sources that allowed for both prospective and retrospective assessment of childhood events.
Methods. A 1994 national survey of children between the ages of 0 and 11 collected data from a ‘person most knowledgeable’ (usually the mother) about a child. It was possible to link data for n = 1977 of these respondents to data collected from the same people in a subsequent adult study. The latter survey included retrospective reports of childhood adversity. We examined three adult health outcomes in relation to prospectively and retrospectively assessed childhood adversity: major depressive episodes, excessive alcohol consumption and painful conditions.
Results. A strong association between childhood adversities (as assessed by both retrospective and prospective methods) and major depression was identified although the association with retrospective assessment was stronger. Weaker associations were found for painful conditions, but these did not depend on the method of assessment. Associations were not found for excessive alcohol consumption irrespective of the method of assessment.
These findings help to allay concerns that associations between childhood adversities and health outcomes during adulthood are merely artefacts of recall bias. In this study, retrospective and prospective assessment strategies produced similar results.
This study investigated gender differences in the relationship between alcohol consumption and cognitive impairment among older adults in South Korea.
Using data from the Korean Longitudinal Study of Ageing, 2,471 females and 1,657 males were analyzed separately. Cognitive impairment was measured based on the Korean version of the Mini-Mental State Exam score. Logistic regression was conducted to examine the relationship between alcohol consumption and cognitive impairment among Korean older adults.
Multivariate analysis showed that compared to moderate drinkers, past drinkers were more likely to be cognitively impaired for women, while heavy drinkers were more likely to be cognitively impaired for men.
Findings suggest that the relationship between alcohol consumption and cognition varies with gender. Clinicians and service providers should consider gender differences when developing strategies for the prevention and treatment of alcohol-related cognitive decline among older adults.
Alcohol consumption is influenced by genetic factors. Previous studies have examined the heritability of alcohol consumption, or related phenotypes, from adolescence into adulthood, frequently finding that total heritability changes over time. However, it remains unclear whether the same genes underlie liability to alcohol consumption across development versus whether novel risk genes become important over time.
A population-based study of adult male twins (n=1790) born in Virginia, USA, retrospectively reported on their average monthly alcohol consumption from early adolescence through adulthood. We used twin modeling methods to explore genetic and environmental influences on alcohol consumption over time.
One latent genetic factor accounted for the majority of the heritability in alcohol consumption during mid- to late adolescence, but its influence declined thereafter; from young adulthood forward, heritability was largely attributable to a second genetic factor. The total heritability of alcohol consumption increased from 0 at ages 12–14 years to 0.40 by ages 18–21 years. Shared environmental factors declined in influence over time.
The heritability of alcohol consumption over time is dynamic both quantitatively and qualitatively. These results have important implications for gene identification endeavors. Furthermore, these findings could inform efforts to elucidate developmentally dynamic behaviors, such as antisocial behavior.
Cette étude compare la consommation d’alcool des Canadiens âgés de 55 ans et plus entre les années 1990 et 2000 et vérifie si les différences persistent lorsque la composition sociodémographique des échantillons est prise en compte. Les analyses incluent des sous-échantillons de répondants âgés de 55 à 74 ans provenant des enquêtes CADS de 1994 (1 071 hommes/1 446 femmes) et GENACIS de 2004 (1 494 hommes/2 176 femmes). Des ANOVA univariées font ressortir des taux de buveurs et de consommation excessive significativement plus élevés en 2004, mais aucune différence dans les profils de consommation. Des régressions montrent que la composition sociodémographique n’annule pas les différences observées. Le contexte social/environnemental plus favorable à l’alcool en 2004 expliquerait potentiellement les taux de buveurs plus élevés. Davantage de recherche sera nécessaire afin de préciser les effets de l’âge, de la cohorte et de la période sur la consommation d’alcool des Canadiens âgés.
The current discussion regarding ‘place effects on health’ is increasingly focusing on the characteristics of a specific physical environment. Our study investigated whether socially deprived residential areas are more likely than affluent neighbourhoods to provide access to addictive substances and fast food.
In this ecological study the total number of tobacco, alcohol and fast-food outlets was recorded and visualized using a geographic information system. Area affluence was measured through the percentage of parents with children of kindergarten or school age with joint annual taxable income <€12 272.
Eighteen social areas in Cologne, Germany.
All social areas in four districts in Cologne, Germany, with a total of 92 000 inhabitants, were analysed.
In the investigation area, 339 tobacco, 353 alcohol and sixty-seven fast-food outlets were identified. As area affluence declined the availability of the following potentially health damaging sources increased: cigarettes (Kendall's tau = 0·433; P = 0·012), alcohol (Kendall's tau = 0·341, P = 0·049) and fast food (Kendall's tau = 0·473; P = 0·009).
The availability of addictive substances and fast food can be seen to have a contextual influence on an individual's lifestyle and can, in the form of physical exposure to obesogenic and addictive environments, contribute to a culmination of health risks.
Objective: A case–control study was performed in Belgrade in order to investigate the association between Parkinson's disease (PD) and smoking, coffee and alcohol consumption.
Methods: During the period 2001–2005, 110 new PD cases and 220 hospital controls were interviewed. Cases and controls were matched by sex, age and place of residence (urban/rural). For the analysis of data conditional univariate and multivariate logistic regression methods were used.
Results: With PD were associated, independently from each other, current smoking [odds ratio (OR) = 0.44; 95% confidence interval (CI) = 0.23–0.82], alcohol consumption (OR = 4.78; 95% CI = 2.67–8.55) and coffee consumption (OR = 2.54; 95% CI = 1.36–4.75). In ever smokers the risk for PD significantly decreased with the increasing number of cigarettes smoked and with increasing duration of smoking. The risk for PD significantly increased with the increasing quantity of alcohol consumption. PD risk was significantly higher in subjects whose average daily consumption of coffee was 1 and 2–3 cups, and it was lower (but not significantly) in those whose daily coffee consumption was 4+ cups. Cases and controls did not differ in duration of alcohol and coffee consumption. The results of multivariate analyses did not substantially change after adjustment on family history positive on PD.
Conclusion: The findings of this study support the hypotheses of inverse association of smoking with PD, but an inverse association with coffee was not confirmed. PD was found to be positively associated with coffee and alcohol consumption.
Studies have suggested that moderate alcohol consumption is associated with a reduced risk of CVD and premature mortality in individuals with diabetes mellitus. However, history of alcohol consumption has hardly been taken into account. We investigated the association between current alcohol consumption and mortality in men and women with diabetes mellitus accounting for past alcohol consumption. Within the European Prospective Investigation into Cancer and Nutrition (EPIC), a cohort was defined of 4797 participants with a confirmed diagnosis of diabetes mellitus. Men and women were assigned to categories of baseline and past alcohol consumption. Hazard ratios (HR) and 95 % CI for total mortality were estimated with multivariable Cox regression models, using light alcohol consumption (>0–6 g/d) as the reference category. Compared with light alcohol consumption, no relationship was observed between consumption of 6 g/d or more and total mortality. HR for >6–12 g/d was 0·89 (95 % CI 0·61, 1·30) in men and 0·86 (95 % CI 0·46, 1·60) in women. Adjustment for past alcohol consumption did not change the estimates substantially. In individuals who at baseline reported abstaining from alcohol, mortality rates were increased relative to light consumers: HR was 1·52 (95 % CI 0·99, 2·35) in men and 1·81 (95 % CI 1·04, 3·17) in women. The present study in diabetic individuals showed no association between current alcohol consumption >6 g/d and mortality risk compared with light consumption. The increased mortality risk among non-consumers appeared to be affected by their past alcohol consumption rather than their current abstinence.
Moderate alcohol consumption has various effects on immune and inflammatory processes, which could accumulatively modulate chronic disease risk. So far, no comprehensive, integrative profiling has been performed to investigate the effects of longer-term alcohol consumption. Therefore, we studied the effects of alcohol consumption on gene expression patterns using large-scale profiling of whole-genome transcriptomics in blood cells and on a number of proteins in blood. In a randomised, open-label, cross-over trial, twenty-four young, normal-weight men consumed 100 ml vodka (30 g alcohol) with 200 ml orange juice or only orange juice daily during dinner for 4 weeks. After each period, blood was sampled for measuring gene expression and selected proteins. Pathway analysis of 345 down-regulated and 455 up-regulated genes revealed effects of alcohol consumption on various signalling responses, immune processes and lipid metabolism. Among the signalling processes, the most prominently changed was glucocorticoid receptor signalling. A network on immune response showed a down-regulated NF-κB gene expression together with increased plasma adiponectin and decreased pro-inflammatory IL-1 receptor antagonist and IL-18, and acute-phase proteins ferritin and α1-antitrypsin concentrations (all P < 0·05) after alcohol consumption. Furthermore, a network of gene expression changes related to lipid metabolism was observed, with a central role for PPARα which was supported by increased HDL-cholesterol and several apo concentrations (all P < 0·05) after alcohol consumption. In conclusion, an integrated approach of profiling both genes and proteins in blood showed that 4 weeks of moderate alcohol consumption altered immune responses and lipid metabolism.