Long-term Effects Of Alcohol Consumption Research Articles

Long-term effects of alcohol consumption on anxiety in adults: A systematic review

ObjectiveDespite the high prevalence and comorbidity of alcohol consumption and anxiety, it is unclear whether alcohol consumption influences long-term anxiety. This study aimed to systematically review the literature on the long-term longitudinal effects of alcohol consumption on anxiety in adults. MethodsEMBASE, PsychInfo, Medline, and Web of Science databases were systematically searched from inception to April 12th, 2024. Articles analysing the relationship between alcohol consumption and anxiety symptoms or anxiety disorder diagnosis at least three-months later in adults were eligible. Articles were screened and extracted by two independent reviewers with study quality assessed using the Mixed Methods Appraisal Tool. ResultsFrom 884 records, eight studies of mixed quality met inclusion criteria. One study using a sample representative of the USA population found low volume consumption was associated with lower long-term anxiety. All other studies used a convenience sample or a specific medical population sample. The significance and direction of the relationship between alcohol consumption and long-term anxiety in these studies varied, likely due to differences in alcohol consumption thresholds used and populations studied. ConclusionsA paucity of research on the longitudinal effects of alcohol consumption on anxiety was found, highlighting a significant gap in the research literature. Furthermore, existing research, primarily focussed on clinical subpopulations, has yielded mixed results. Further research is needed to explore the longitudinal dose dependent impact of alcohol consumption on anxiety using samples representative of national populations.

Adolescent alcohol exposure changes RNA modifications in adult brain by mass spectrometry-based comprehensive profiling analysis

Alcohol consumption is one of the leading causes of death worldwide. Adolescence is a critical period of structural and functional maturation of the brain. Adolescent alcohol use can alter epigenetic modifications. However, little is known on the long-term effects of alcohol consumption during adolescence on RNA epigenetic modifications in brain. Herein, we systematically explored the long-term effects of alcohol exposure during adolescence on small RNA modifications in adult rat brain tissues by comprehensive liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS) analysis. We totally detected 26 modifications in small RNA of brain tissues. Notably, we observed most of these modifications were decreased in brain tissues. These results suggest that alcohol exposure during adolescence may impose a long-lasting impact on RNA modifications in brain tissues. This is the first report that alcohol use during adolescence can alter RNA modifications in adult brain. Collectively, this study suggests a long-term adverse effects of alcohol consumption on brain from RNA epigenetics angle by comprehensive mass spectrometry analysis.

Long-term effects of alcohol consumption on cognitive function in seniors: a cohort study in China

BackgroundIn the context of increasing global aging, the long-term effects of alcohol consumption on cognitive function in older adults were analyzed in order to provide rationalized health recommendations to the elderly population.MethodsThe study used the Chinese Longitudinal Healthy Longevity Survey (CLHLS) dataset, from which 5354 Chinese seniors aged 65–112 years were selected as the subjects, spanning the years 1998–2018. Data on alcohol, diet, activity, and cognition were collected by questionnaire and cognitive levels were judged by the Mini-Mental State Examination scale (also referenced to the Functional Assessment Staging Test). Data cleaning and preprocessing was implemented by R software. The dynamic Cox model was applied for model construction and data analysis.ResultsThe results of the dynamic Cox model suggested that seniors who drank alcohol were at higher risk of cognitive decline compared to those who never drank (HR = 1.291, 95%CI: 1.175–1.419). The risk was similarly exacerbated by perennial drinking habits (i.e., longer drinking years, HR = 1.008, 95%CI: 1.004–1.013). Compared to non-alcoholic beverages, liquor (≥ 38°), liquor (< 38°), wine and rice wine all showed negative effects. Whereas, the risk of cognitive decline was relatively lower in seniors who consumed liquors (< 38°) and rice wine compared to the high-level liquor (HR: 0.672 (0.508, 0.887) and 0.732 (0.559, 0.957), respectively).ConclusionsAlcohol consumption has a negative and long-term effects on cognitive function in seniors. For the elderly, we suggested that alcohol intake should be avoided as much as possible.

Long-Term Exposure of Alcohol Induced Behavioral Impairments and Oxidative Stress in the Brain Mitochondria and Synaptosomes of Adult Zebrafish.

Alcoholism causes deleterious effects such as physiological and neuronal alterations leading to the cognitive and other behavioral impairments. Mitochondrial and synaptosomal deteriorations in the brain of alcoholic persons exhibited metabolic, biochemical changes and other related risk factors, which mainly affect the brain function. This study aimed to assess the effect of chronic alcohol-induced mitochondrial and synaptosomal oxidative damage along with behavioral impairment in adult zebrafish. Zebrafish of control group received the system water and normal diet ad libitum (group I); the other groups were treated with 0.20% alcohol (group II) and 0.40% alcohol (group III) directly in fish tank for 22 days. The result revealed significant increase in lipid peroxidation, protein carbonylation, superoxide dismutase, and glutathione, and significant decline in the activity of catalase and Na+/K+ ATPase compared to control. Furthermore, the alcohol-treated zebrafish also showed significant behavioral alterations. Collectively, this regulatory mechanism demonstrates the effect of long-term alcohol consumption in the zebrafish. Our results indicate that this recreational drug "alcohol" is harmful to brain mitochondria and synaptosomes, which are the main organelles, and play an important role in memory, learning, cognitive function, and ATP formation in the brain, which may represent a significant public health concern.

Blood-brain barrier integrity is the primary target of alcohol abuse

The effects of long-term alcohol consumptions on cognitive function remain elusive with contradictory results. Whilst it is widely accepted that long-term intoxication can cause cognitive impairment, moderate drinking can improve cognitive function. In reality, many older people and those with chronic medical conditions are long-term alcohol consumers in Asian countries. Our previous studies have suggested that long-term alcohol consumption can damage blood-brain barrier (BBB) integrity and aggravate cognitive deficit in APPswe/PS1De9 mice, but little is known about the underlying mechanisms, especially whether this consumption can cause cognitive decline via aggravating BBB damage in people who are exposed to the risk factors for cognitive disorders such as aging or inflammation. These questions were addressed in this study. The mouse models of cognitive deficit induced by d-galactose or lipopolysaccharide, the important risk conditions in human on cognitive function, were used to evaluate the effects of long-term alcohol consumption on the BBB integrity. After alcohol administration for 30 days in these models the BBB integrity was significantly destroyed with remarkably increased permeability and down-regulated protein expression of zonula occludens-1, VE-cadherin, occludin, low-density lipoprotein receptor-related protein-1, receptor for advanced glycation end products, major facilitator superfamily domain-containing protein-2a and aquaporin-4, which is the most closely related with the structure and function of BBB integrity. Meanwhile, the level of oxidative stress in d-galactose mice or inflammatory factors in cortex and serum in lipopolysaccharide mice, which might be involved in the cognitive dysfunctions, was significantly amplified. Furthermore, the impaired memory and hippocampal neuron damage induced by d-galactose and lipopolysaccharide were concurrently aggravated. Collectively, our study provided novel and compelling evidence that the structural and functional proteins for BBB integrity may be the primary targets for the detrimental effects of alcohol abuse that lead to cognitive dysfunction and neurological deficits in high risk populations.

Long-term effects of alcohol consumption on cognitive function: a systematic review and dose-response analysis of evidence published between 2007 and 2018

BackgroundUnderstanding the long-term health effects of low to moderate alcohol consumption is important for establishing thresholds for minimising the lifetime risk of harm. Recent research has elucidated the dose-response relationship between alcohol and cardiovascular outcomes, showing an increased risk of harm at levels of intake previously thought to be protective. The primary objective of this review was to examine (1) whether there is a dose-response relationship between levels of alcohol consumption and long-term cognitive effects, and (2) what the effects are of different levels of consumption.MethodsThe review was conducted according to a pre-specified protocol. Eligible studies were those published 2007 onwards that compared cognitive function among people with different levels of alcohol consumption (measured ≥ 6 months prior to first follow-up of cognition). Major cognitive impairment was excluded. Searches were limited to MEDLINE, Embase and PsycINFO (January 2007 to April 2018). Screening, data extraction, and risk of bias assessment (ROBINS-I) were piloted by three authors, then completed by a single author and checked by a second. Analyses were undertaken to identify and characterise dose-response relationships between levels of alcohol consumption and cognition. Certainty of evidence was assessed using GRADE.ResultsWe included 27 cohort studies (from 4786 citations). Eighteen studies examined the effects of alcohol consumption at different levels (risk of bias 16 serious, 2 critical). Ten studies provided data for dose-response analysis. The pooled dose-response relationship showed a maximum standardised mean difference (SMD) indicating slightly better cognition among women with moderate alcohol consumption compared to current non-drinkers (SMD 0.18, 95%CI 0.02 to 0.34, at 14.4 grams/day; 5 studies, very low certainty evidence), and a trivial difference for men (SMD 0.05, 95% CI 0.00 to 0.10, at 19.4 grams/day; 6 studies, very low certainty evidence).ConclusionsMajor limitations in the design and reporting of included studies made it impossible to discern if the effects of ‘lower’ levels of alcohol intake are due to bias. Further review of the evidence is unlikely to resolve this issue without meta-analysis of individual patient data from cohort studies that address biases in the selection of participants and classification of alcohol consumption.

Rasio AST/ALT pada Laki-Laki Pengkonsumsi Alkohol di Jalan Mendawai Kota Palangka Raya

Aspartate aminotransferase (AST) and Alanine aminotransferase (ALT) are enzymes predominantly found in hepatocytes, the increased activity in the serum shows liver damage. The AST / ALT ratio is used as a marker for alcoholic liver disease. This study aims to determine the effects of long-term alcohol consumption on the risk of alcoholic liver disease. This study was a descriptive study, involving 20 alcoholic drinkers aged 25-45 years, had consumed alcohol&gt; 5 years and consumed alcohol every day. Our results showed a significant increase (p &lt;0.05) in AST and ALT values based on age group, duration of consumption and dose. While the ratio of AST / ALT, a significant increase was found in the age group and period. In alcohol drinkers, the AST value is higher than ALT. The AST / ALT ratio for heavy drinkers is 1.64. Conclusion: Alcohol-consuming subjects in our study, especially heavy drinkers, were suspected of having a risk of alcoholic liver disease because most had an AST / ALT ratio &gt; 1,5.

Yawning elicited by intravenous ethanol in rhesus monkeys with experience self-administering cocaine and ethanol: Involvement of dopamine D3 receptors.

Characterization of the effects of long-term alcohol consumption on the brain would be aided by the development of behavioral assays that are relatively easy to implement in animal models of alcohol use disorders. Assessing unconditioned behaviors, such as drug-elicited yawning in models that permit long-term alcohol ingestion, may be a valuable complement to more invasive and costly procedures. The present studies investigated previous unexpected findings of ethanol-induced yawning in nonhuman primates. Subjects were adult male rhesus monkeys (n=8), all of which had experience self-administering intravenous cocaine for several years. Four monkeys also had experience consuming 2.0g/kg ethanol over 1h per day, 5 days per week, for 6.8-12.0 months. All monkeys received saline or ethanol (0.25-1.0g/kg) infused intravenously (i.v.) over 10min, and the number of yawns elicited during the infusion was counted. A second experiment in the ethanol-experienced monkeys examined whether ethanol-induced yawning could be blocked by PG01037 (1.0, 3.0mg/kg, i.v.), a selective antagonist at dopamine D3 receptors (D3R). Ethanol significantly and dose-dependently increased yawns in the ethanol-experienced animals, but not the ethanol-naïve animals. In the ethanol-experienced monkeys, this effect of ethanol was blocked by the D3R antagonist. The pharmacology of yawning is complex and a good deal of model development remains to be performed to characterize the potential involvement of other neurotransmitter systems. Nonetheless, drug-elicited yawning may be a useful unconditioned behavioral assay to assess the effects of long-term alcohol consumption in established nonhuman primate models.

The effect of alcohol consumption on periodontitis in older Danes.

To examine the association of alcohol consumption measured at different points in time and periodontitis at 20 years follow-up and to investigate whether long-term alcohol consumption is related to periodontitis in old age. Participants aged 65 years or older in 2003, from the longitudinal study Copenhagen City Heart Study (CCHS), were invited to participate in the Copenhagen Oral Health Senior Study. Clinical periodontal attachment loss was calculated to determine the progress of periodontitis. Alcohol consumption was measured at CCHS follow-ups in 1981-1983, 1991-1994 and 2001-2003, using a standard questionnaire. Alcohol consumption was defined as light, moderate and heavy drinking and used individually for each follow-up. The three follow-ups were summarized into long-term alcohol consumption. Logistic regression analysis was used to estimate the relation between alcohol consumption measured at different points in time and periodontitis and to assess the effect of long-term alcohol consumption on periodontitis. The results show that heavy drinkers in 1981-1983 had a higher odds ratio for having periodontitis compared to light drinkers (OR = 4.64 95% CI = [1.1; 19.42]). Early consumption of alcohol may increase the odds of having periodontitis 20 years later. There is a need for further studies including larger populations to investigate both alcohol consumption measured at different points in time, and long-term alcohol consumption and periodontitis progression over time.

ADH1B and ADH1C genotype, alcohol consumption and biomarkers of liver function: findings from a Mendelian randomization study in 58,313 European origin Danes.

BackgroundThe effect of alcohol consumption on liver function is difficult to determine because of reporting bias and potential residual confounding. Our aim was to determine this effect using genetic variants to proxy for the unbiased effect of alcohol.MethodsWe used variants in ADH1B and ADH1C genes as instrumental variables (IV) to estimate the causal effect of long-term alcohol consumption on alanine aminotransferase (ALT), γ-glutamyl-transferase (γ-GT), alkaline phosphatase (ALP), bilirubin and prothrombin action. Analyses were undertaken on 58,313 Danes (mean age 56).ResultsIn both confounder adjusted multivariable and genetic-IV analyses greater alcohol consumption, amongst those who drank any alcohol, was associated with higher ALT [mean difference per doubling of alcohol consumption: 3.4% (95% CI: 3.1, 3.7) from multivariable analyses and 3.7% (−4.5, 11.9) from genetic-IV analyses] and γ-GT [8.2% (7.8, 8.5) and 6.8% (−2.8, 16.5)]. The point estimates from the two methods were very similar and statistically the results from the two methods were consistent with each other for effects with ALT and γ-GT (both pdiff>0.3). Results from the multivariable analyses suggested a weak inverse association of alcohol with ALP [−1.5% (−1.7, −1.3)], which differed from the strong positive effect found in genetic-IV analyses [11.6% (6.8, 16.4)] (pdiff<0.0001). In both multivariable and genetic-IV analyses associations with bilirubin and protrombin action were weak and close to the null.ConclusionsOur results suggest that greater consumption of alcohol is related to poorer liver function as indicated by higher ALT, γ-GT and ALP, but not to clotting or bilirubin.

Hepatoprotective effect of Schisandra chinensis (Turcz.) Baill. lignans and its formula with Rubus idaeus on chronic alcohol-induced liver injury in mice.

This study aimed to investigate the liver protection effect of Schisandra chinensis (Turcz.) Baill. (SC) lignans and its combination with Rubus idaeus (RI) on chronic alcohol-induced mice. A low level of SC lignans (SL) was prepared from the clear juice of sarcocarp. Lignans were further extracted from the SC seeds and added to the SL to form high-level SC lignans (SH). Moreover, RI clear juice lyophilized powder was mixed with SL (SR), and the liver protection effects of SL, SH and SR were investigated. Male ICR mice were administered with the corresponding samples and gastrically infused with 50% alcohol (1 h later) once per day for 60 d. In the in vitro study, the characteristic lignans in the SC clear juice and the seed extract were analyzed by high performance liquid chromatography (HPLC). The total phenolic content (TPC) and antioxidant capability of SL, SH, and SR were determined. The results of the in vivo study showed that SC lignans exhibited a dose-dependent effect on the regulation of hepatic antioxidant status, serum transaminases levels, hyperlipidemia and hepatic fat deposition in mice. However, hepatic lesions were observed in the SH mice, which indicated a potential side effect caused by long-term consumption of SH under chronic alcohol administration. By contrast, SR exhibited a similar hepatoprotective effect as SH without any abnormality found in the histological analysis. After analysis with HPLC, Schizandrol A and Schizandrol B were identified in the SC clear juice, and two more kinds of lignans, Schisandrin A and Schisandrin B, were identified in the seed extracts. The SR sample had the highest TPC and exhibited the best antioxidant capability. In conclusion, RI strengthened the liver protection effect of SC lignans effectively and safely, which was probably achieved by enhancing the antioxidant status and the positive effect of their combination was possibly attributed to both lignans and polyphenols. This study demonstrated that the combination of low-level SC lignans and RI might be used as a potential safe formula for beverage development to alleviate the adverse effects of long-term alcohol consumption.

Exploring causal associations between alcohol and coronary heart disease risk factors: findings from a Mendelian randomization study in the Copenhagen General Population Study

To explore the causal effect of long-term alcohol consumption on coronary heart disease risk factors. We used variants in ADH1B and ADH1C genes as instrumental variables (IV) to estimate the causal effect of long-term alcohol consumption on body mass index (BMI), blood pressure (BP), lipids, fibrinogen, and glucose. Analyses were undertaken in 54 604 Danes (mean age 56 years). Both confounder-adjusted multivariable and IV analyses suggested that a greater alcohol consumption among those who drank any alcohol resulted in a higher BP [mean difference in SBP per doubling of alcohol consumption among drinkers: 0.76 mmHg (95% CI: 0.63, 0.90) from multivariable analyses and 0.94 mmHg (-3.03, 4.69) from IV analyses; P-value for difference in these results = 0.95]. The positive association of alcohol with HDLc in the multivariable analyses [4.9% (4.7, 5.1)] appeared stronger than in the IV analyses [1.5% (-4.5, 7.4)], and the weak inverse association with fibrinogen in the multivariable analysis [-2.0% (-2.1, -1.8)] was not present in the IV analyses [0.6% (-3.8, 5.0)], but statistically the results for both of these could not be reliably distinguished from each other (P-values 0.21 and 0.32, respectively). The weak inverse association of alcohol with BMI [-0.13 kg/m(2) (-0.16, -0.10)] and with triglycerides [-0.4% (-0.7, 0.4)] in multivariable analyses were in contrast to the strong positive association of alcohol with BMI [1.37 kg/m(2) (0.59, 2.15)] and the strong inverse association with triglycerides [-14.9% (-25.6, -4.3)] in IV analyses; P = 0.006 and 0.01, respectively, for difference between the two. Alcohol was not associated with non-HDLc or glucose. Our results show adverse effects of long-term alcohol consumption on BP and BMI. We also found novel evidence for a potentially beneficial effect on triglyceride levels, which needs further replication.

Differential Phosphorylation of GluN1-MAPKs in Rat Brain Reward Circuits following Long-Term Alcohol Exposure

The effects of long-term alcohol consumption on the mitogen-activated protein kinases (MAPKs) pathway and N-methyl-D-aspartate-type glutamate receptor 1 (GluN1) subunits in the mesocorticolimbic system remain unclear. In the present study, rats were allowed to consume 6% (v/v) alcohol solution for 28 consecutive days. Locomotor activity and behavioral signs of withdrawal were observed. Phosphorylation and expression of extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), p38 protein kinase and GluN1 in the nucleus accumbens, caudate putamen, amygdala, hippocampus and prefrontal cortex of these rats were also measured. Phosphorylation of ERK, but not JNK or p38, was decreased in all five brain regions studied in alcohol-drinking rats. The ratio of phospho/total-GluN1 subunit was reduced in all five brain regions studied. Those results suggest that the long-term alcohol consumption can inhibits GluN1 and ERK phosphorylation, but not JNK or p38 in the mesocorticolimbic system, and these changes may be relevant to alcohol dependence. To differentiate alcohol-induced changes in ERK and GluN1 between acute and chronic alcohol exposure, we have determined levels of phospho-ERK, phospho-GluN1 and total levels of GluN1 after acute alcohol exposure. Our data show that 30 min following a 2.5 g/kg dose of alcohol (administered intragastrically), levels of phospho-ERK are decreased while those of phospho-GluN1 are elevated with no change in total GluN1 levels. At 24 h following the single alcohol dose, levels of phospho-ERK are elevated in several brain regions while there are no differences between controls and alcohol treated animals in phospho-GluN1 or total GluN1. Those results suggest that alcohol may differentially regulate GluN1 function and ERK activation depending on alcohol dose and exposure time in the central nervous system.

The Great Recession, somatic symptomatology and alcohol use and abuse

While most research has examined the long-term effects of alcohol consumption on health, the current study examines how health status impacts on drinking behavior. Using data from a national study conducted between 2010 and 2011 to assess the impact of the recession on drinking behavior, this study examines how economic hardships linked to the recent economic recession affect physical health, and how physical health may in turn affect alcohol use. Structural equation models were used to test the predicted associations. The data demonstrate that many of the economic stressors linked to the recession are associated with increased somatic symptoms. Somatic symptoms are also associated with increased drinking for men, but not for women. These findings suggest that men may use alcohol to self medicate somatic symptomatology. The current findings are consistent with gender role-based explanations that account for gender disparities in the utilization of medical care.

Effect of alcohol consumption in prenatal life, childhood, and adolescence on child development

The effects of alcohol consumption in adults are well described in the literature, while knowledge about the effects of alcohol consumption in children is more limited and less systematic. The present review shows how alcohol consumption may negatively influence the neurobiological and neurobehavioral development of humans. Three different periods of life have been considered: the prenatal term, childhood, and adolescence. For each period, evidence of the short-term and long-term effects of alcohol consumption, including neurodevelopmental effects and associations with subsequent alcohol abuse or dependence, is presented.

Chronic alcohol feeding induces biochemical, histological, and functional alterations in rat retina

Ethanol consumption originates a wide spectrum of disorders, including alteration of visual function. Oxidative stress is included among the mechanisms by which alcohol predisposes nervous tissue to injury. Retina, which is the neurosensorial eye tissue, is particularly sensitive to oxidative stress. In this study we analyze the effect of long-term alcohol consumption on oxidative stress parameters of the rat retina, and its correlation to retinal function, as well as to the expression of the antiapoptotic protein Bcl-2. We also study the protective effect of ebselen, a synthetic selenoorganic antioxidant. Herein we show that ethanol has a toxic effect on rat retina associated with oxidative stress. Decreases in retina glutathione concentration and increases in malondialdehyde content in whole eye homogenate significantly correlate with ERG b-wave decrease and Bcl-2 overexpression. We also show how ebselen is able to prevent all the alterations observed. Chronic ethanol consumption induces oxidative stress in rat retina associated with an impairment of ERG and Bcl-2 overexpression, suggesting a role for glial cells. All these alterations in the rat allow the proposal of an alcoholic retinopathy in this species.

Long-term Effects of Alcohol Consumption in Male and Female Rats

Discrepancies exist regarding potential sex differences in the effects of ethanol on the myocardium. Therefore, the aims of this study were to determine if long-term ethanol consumption was associated with the development of a dilated cardiomyopathy (CM) in female rats and, second, to determine if the absence of ovarian hormones modulated this effect. Adult male and female (n=6-8/group) sham-operated and ovariectomized (OVX) Sprague-Dawley rats received the Lieber DeCarli ethanol-containing (8% vol/vol) or control liquid diet for 8 months. All ethanol groups showed echocardiographic evidence of a cardiomyopathy; however, more significant ethanol-elicited differences were found in the male ethanol group than in either the female or female OVX groups. In addition, the male ethanol group had significant reductions in in vivo measures of contractility, such as the maximum derivative of change in systolic pressure and preload recruitable stroke work. Sex differences were also apparent in the pattern and degree of posterior and septal wall thickness changes, in that the male ethanol group had more posterior and septal wall thinning. In conclusion, similar to male rats long-term ethanol consumption in gonad-intact and OVX female rats is associated with the development of a dilated cardiomyopathy.

Binge Drinking in Midlife and Dementia Risk

Studies examining the long-term effects of alcohol consumption on cognitive functioning have produced conflicting results. Our goal was to determine whether a long follow-up period combined with information about drinking patterns, in addition to total alcohol consumption, would provide new insights about the relationship of alcohol use with dementia risk. A population-based cohort of 554 Finnish twins, who had provided data on alcohol consumption in questionnaires in 1975 and 1981, was followed for 25 years. Subjects were age 65 years or older at the time of dementia assessment in 1999-2001. Dementia risk was analyzed with respect to varying patterns of alcohol use by log-linear modeling, adjusted for age, sex, and education. By the end of follow-up, 103 participants had developed dementia. Binge drinking (ie, alcohol exceeding the amount of 5 bottles of beer or a bottle of wine on 1 occasion at least monthly), as reported in 1975, was associated with a relative risk of 3.2 (95% confidence interval=1.2-8.6) for dementia. Passing out at least twice as a result of excessive alcohol use during the previous year, as reported in 1981, was associated with a relative risk of 10.5 (2.4-46) for dementia in drinkers. Binge drinking in midlife is associated with an increased risk of dementia.

Perspectives on alcohol consumption: liver polyunsaturated fatty acids and essential fatty acid metabolism

In this article, subjects diagnosed with alcoholic liver disease are shown to have lower concentrations of several polyunsaturated fatty acids (PUFAs), including 18:2n6, 18:3n6, 20:3n6, 18:3n3, 22:5n3, and 22:6n3, but not 20:4n6 and 22:4n6, nor 22:5n6, in the total lipid extracts of their livers compared with findings for specimens obtained from patients diagnosed with primary biliary cirrhosis and from control subjects. Findings of studies in animals have demonstrated that prolonged alcohol consumption reduces liver polyunsaturate content. However, the effect of ethanol on the elongation/desaturation of essential fatty acids is complex, as in vitro study results indicate that the direction of the effect of alcohol may be related to the dose of alcohol. Findings of studies in hepatocyte cell culture indicate that ethanol increased delta-5 and delta-6 desaturase activities throughout a broad concentration range. In contrast, lower liver desaturase activity has been reported in animals consuming high concentrations of alcohol (36%–40% energy) over a period of several months. Findings from in vivo isotope tracers studies in nonhuman primates and felines indicate that prolonged periods of moderate (mean consumption 2.6 g kg −1 d −1 and 1.2 g kg −1 d −1, respectively) alcohol consumption had no effect on the uptake of either linoleic (18:2n6) or alpha-linolenic (18:3n3) acids into the plasma and lead to an increased incorporation of these deuterated precursors into 20:4n6 and 22:6n3. Thus, this likely reflects a stimulated, rather than an inhibited, production of long-chain PUFAs. In numerous studies in various species, investigators have documented that alcohol consumption can increase the level of lipid peroxidation in tissues, and sustained periods of ethanol-induced peroxidation can deplete tissues of PUFAs. A hypothesis to rationalize the long-term effects of alcohol consumption on liver PUFA concentration that takes into consideration the effect of ethanol on essential fatty acid metabolism is presented.

Effect of alcohol consumption on diabetes mellitus: a systematic review.

Both diabetes mellitus and alcohol consumption are prevalent in the United States, yet physicians are poorly informed about how alcohol use affects risk for or management of diabetes. To conduct a systematic review assessing the effect of alcohol use on the incidence, management, and complications of diabetes mellitus in adults. English-language studies in persons 19 years of age or older that were identified by searching the MEDLINE database from 1966 to the third week of August 2003 and the reference lists of key articles. Two independent assessors reviewed 974 retrieved citations to identify all experimental, cohort, or case-control studies that assessed the effect of alcohol use on diabetes risk, control, self-management, adverse drug events, or complications. Two independent reviewers extracted data and evaluated study quality on the basis of established criteria. Thirty-two studies that met inclusion criteria were reviewed. Compared with no alcohol use, moderate consumption (one to 3 drinks/d) is associated with a 33% to 56% lower incidence of diabetes and a 34% to 55% lower incidence of diabetes-related coronary heart disease. Compared with moderate consumption, heavy consumption (>3 drinks/d) may be associated with up to a 43% increased incidence of diabetes. Moderate alcohol consumption does not acutely impair glycemic control in persons with diabetes. Moderate alcohol consumption is associated with a decreased incidence of diabetes mellitus and a decreased incidence of heart disease in persons with diabetes. Further studies are needed to assess the long-term effects of alcohol consumption on glycemic control and noncardiac complications in persons with diabetes.