Patrones de consumo de alcohol en estudiantes universitarios de Ciencias de la Salud / Alcohol consumption patterns of university students of health sciences

Objetivo: Describir los patrones de consumo de alcohol y de episodios de consumo intensivo (ECI) en una muestra de estudiantes de Ciencias de la Salud, así como identificar factores asociados. Método: Estudio descriptivo que mediante cuestionario autoadministrado recoge variables sociodemográficas y el diario consumo de alcohol, registrando el número de unidades de bebida estándar consumidas en varios momentos del día. Resultados: Participaron 286 estudiantes (66,1% mujeres) pertenecientes a la Universidad de Cádiz (193 Medicina y 93 Enfermería), con una edad media de 21,1 años (DE 2,8). El 44,8% vive en domicilio familiar. El 65,7% consumió alcohol en la última semana, siendo más frecuente en varones. El patrón de consumo semanal fue del 74,5% para consumo de riesgo bajo, 21% riesgo moderado y 4,5% riesgo elevado. Un 33,9% tuvo entre 1-2 ECI en la última semana, apareciendo estos independientemente del patrón de consumo semanal. De los alumnos que residen fuera del domicilio familiar, un 26,6% tuvieron un consumo de riesgo moderado, un 8,2% riesgo elevado y un 41,8% ECI. Se evidencian asociaciones estadísticamente significativas entre el consumo semanal de alcohol y las variables sexo, domicilio habitual y ECI. Conclusiones: Más de la mitad de los estudiantes consumió alcohol en la última semana, con un consumo mayoritariamente de fin de semana, destacando la alta prevalencia de ECI. Se propone incidir en la detección precoz y campañas en estos grupos

Aim: To describe the alcohol drinking patterns and binge drinking episodes (BDE) in a sample of Health Science students, as well as identify associated factors. Method: It is a descriptive study, in which sociodemographic variables and a weekly alcohol consumption diary recording the number of standard drinking units consumed at different times of the day are collected by means of a self-administered questionnaire. Results: 286 students (66.1% women) from Cadiz University (193 Medical students and 93 Nursing students), with a mean age of 21.1 (SD 2.8) years, took part in this study. Forty-four point 8 percent of the students live with their families. Sixty-five point 7 percent of the students drank alcohol in the previous week, this was more usual in the males. The weekly alcohol consumption pattern was 74.5% for low-risk alcohol consumption, 21% for moderate-risk and 4.5% for a high-risk consumption. Thirty-three point 9 percent had 1-2 BDE over the previous week apart from their weekly consumption pattern. Twenty-six point 6 percent of the students who were emancipated had moderate-risk consumption, 8.2% had a high-risk consumption and 41.8% had a binge drinking episode. There were statistically significant associations between the weekly consumption pattern regarding sex, habitual residence and BDE variables. Conclusions: More than half the students had taken alcohol the previous week, mainly at weekends. The high prevalence of BDE is highlighted. We propose enhancing early detection and prevention campaigns in this population

Effect of lacosamide on ethanol induced conditioned place preference and withdrawal associated behavior in mice: Possible contribution of hippocampal CRMP-2.

BACKGROUND: Excessive consumption of ethanol is known to activate the mTORC1 pathway and to enhance the Collapsin Response Mediator Protein-2 (CRMP-2) levels in the limbic region of brain. The latter helps in forming microtubule assembly that is linked to drug taking or addiction-like behavior in rodents. Therefore, in this study, we investigated the effect of lacosamide, an antiepileptic drug and a known CRMP-2 inhibitor, which binds to CRMP-2 and inhibits the formation of microtubule assembly, on ethanol-induced conditioned place preference (CPP) in mice. METHODS: The behavior of mice following ethanol addiction and withdrawal was assessed by performing different behavioral paradigms. Mice underwent ethanol-induced CPP training with alternate dose of ethanol (2 g/kg, po) and saline (10 ml/kg, po). The effect of lacosamide on the expression of ethanol-induced CPP and on ethanol withdrawal associated anxiety and depression-like behavior was evaluated. The effect of drug on locomotor activity was also assessed and hippocampal CRMP-2 levels were measured. RESULTS: Ethanol-induced CPP was associated with enhanced CRMP-2 levels in the hippocampus. Lacosamide significantly reduced the expression of ethanol-induced CPP and alleviated the levels of hippocampal CRMP-2 but aggravated withdrawal-associated anxiety and depression in mice. CONCLUSION: The present study demonstrated the beneficial effect of lacosamide in attenuation of expression of ethanol induced conditioned place preference via reduction of hippocampal CRMP-2 level. These findings suggest that lacosamide may be investigated further for ethanol addiction but not for managing withdrawal.

Intranasal mesenchymal stem cell secretome administration markedly inhibits alcohol and nicotine self-administration and blocks relapse-intake: mechanism and translational options.

BACKGROUND: Chronic consumption of most drugs of abuse leads to brain oxidative stress and neuroinflammation, which inhibit the glutamate transporter GLT-1, proposed to perpetuate drug intake. The present study aimed at inhibiting chronic ethanol and nicotine self-administration and relapse by the non-invasive intranasal administration of antioxidant and anti-inflammatory secretome generated by adipose tissue-derived activated mesenchymal stem cells. The anti-addiction mechanism of stem cell secretome is also addressed. METHODS: Rats bred for their alcohol preference ingested alcohol chronically or were trained to self-administer nicotine. Secretome of human adipose tissue-derived activated mesenchymal stem cells was administered intranasally to animals, both (i) chronically consuming alcohol or nicotine and (ii) during a protracted deprivation before a drug re-access leading to relapse intake. RESULTS: The intranasal administration of secretome derived from activated mesenchymal stem cells inhibited chronic self-administration of ethanol or nicotine by 85% and 75%, respectively. Secretome administration further inhibited by 85-90% the relapse "binge" intake that occurs after a protracted drug deprivation followed by a 60-min drug re-access. Secretome administration fully abolished the oxidative stress induced by chronic ethanol or nicotine self-administration, shown by the normalization of the hippocampal oxidized/reduced glutathione ratio, and the neuroinflammation determined by astrocyte and microglial immunofluorescence. Knockdown of the glutamate transporter GLT-1 by the intracerebral administration of an antisense oligonucleotide fully abolished the inhibitory effect of the secretome on ethanol and nicotine intake. CONCLUSIONS: The non-invasive intranasal administration of secretome generated by human adipose tissue-derived activated mesenchymal stem cells markedly inhibits alcohol and nicotine self-administration, an effect mediated by the glutamate GLT-1 transporter. Translational implications are envisioned.

PARP inhibition in vivo blocks alcohol-induced brain neurodegeneration and neuroinflammatory cytosolic phospholipase A2 elevations.

Chronic alcoholism promotes brain damage that impairs memory and cognition. High binge alcohol levels in adult rats also cause substantial neurodamage to memory-linked regions, notably, the hippocampus (HC) and entorhinal cortex (ECX). Concurrent with neurodegeneration, alcohol elevates poly (ADP-ribose) polymerase-1 (PARP-1) and cytosolic phospholipase A2 (cPLA2) levels. PARP-1 triggers necrosis when excessively activated, while cPLA2 liberates neuroinflammatory ω-6 arachidonic acid. Inhibitors of PARP exert in vitro neuroprotection while suppressing cPLA2 elevations in alcohol-treated HC-ECX slice cultures. Here, we examined in vivo neuroprotection and cPLA2 suppression by the PARP inhibitor, veliparib, in a recognized adult rat model of alcohol-binging. Adult male rats received Vanilla Ensure containing alcohol (ethanol, 7.1 ±â€¯0.3 g/kg/day), or control (dextrose) ±â€¯veliparib (25 mg/kg/day), by gavage 3x daily for 4 days. Rats were sacrificed on the morning after the final binge. HC and ECX neurodegeneration was assessed in fixed sections by Fluoro-Jade B (FJB) staining. Dorsal HC, ventral HC, and ECX cPLA2 levels were quantified by immunoblotting. Like other studies using this model, alcohol binges elevated FJB staining in the HC (dentate gyrus) and ECX, indicating neurodegeneration. Veliparib co-treatment significantly reduced dentate gyrus and ECX neurodegeneration by 79% and 66%, respectively. Alcohol binges increased cPLA2 in the ventral HC by 34% and ECX by 72%, which veliparib co-treatment largely prevented. Dorsal HC cPLA2 levels remained unaffected by alcohol binges, consistent with negligible FJB staining in this brain region. These in vivo results support an emerging key role for PARP in binge alcohol-induced neurodegeneration and cPLA2-related neuroinflammation.

Rosmarinic acid protects against chronic ethanol-induced learning and memory deficits in rats.

OBJECTIVES: Ethanol consumption induces neurological disorders including cognitive dysfunction. Oxidative damage is considered a likely cause of cognitive deficits. We aimed to investigate the effects of rosmarinic acid (RA) in different doses for 30 days on chronic ethanol-induced cognitive dysfunction using the passive avoidance learning (PAL) and memory task in comparison with donepezil, a reference drug. We also evaluated the levels of superoxide dismutase (SOD), catalase (CAT), and lipid peroxidation in hippocampus as possible mechanisms. METHODS: Memory impairment was induced by 15% w/v ethanol (2 g/kg, i.g.) administration for 30 days. RA (8, 16, and 32 mg/kg, i.g.) or donepezil (2 mg/kg, i.g.) was administered 30 minutes before ethanol. The acquisition trial was done 1 hour after the last administration of RA and donepezil. At the end, animals were weighed and hippocami were isolated for analyzing of oxidant/antioxidant markers. RESULTS: Ethanol caused cognition deficits in the PAL and memory task. While RA 16 and 32 mg/kg improved cognition in control rats, it prevented learning and memory deficits of alcoholic groups. RA 8 mg/kg did not influence cognitive function in both control and alcoholic rats. RA 32 mg/kg had comparable effects with donepezil in prevention of acquisition and retention memory impairment. The higher doses of RA not only prevented increased lipid peroxidation and nitrite content but also decreased SOD, CAT, GSH, and FRAP levels in alcoholic groups and exerted antioxidant effects in non-alcoholic rats. DISCUSSION: We showed that RA administration dose-dependently prevented cognitive impairment induced by chronic ethanol in PAL and memory and disturbed oxidant/antioxidant status as a possible mechanism. The antioxidant, anticholinesterase, and neuroprotective properties of RA may be involved in the observed effects. Therefore, RA represents a potential therapeutic option against chronic ethanol-induced amnesia which deserves consideration and further examination.

Why adolescents are at risk of misusing alcohol and gambling.

AIMS: The aim of the study was to explore the reasons for alcohol misuse and other risk-taking behaviours in adolescence. METHODS: Narrative review. RESULTS: Vulnerable adolescents make suboptimal addictive-related choices in the period of initiation of alcohol use and gambling, which is also a period of cognitive and brain development, and in health behaviours. Hyperactive response to rewards as well as possibly hypoactive responses to punishments combined with weaknesses in the abilities to regulate strong impulses results in greater risk of alcohol and gambling misuse. CONCLUSION: Abnormal patterns of alcohol consumption (e.g. binge drinking) could dramatically reinforce this disequilibrium by enhancing salience for alcohol and associated information and compromising self-regulatory processes. There are some preventive and therapeutic cognitive training strategies that can strengthen willpower in adolescents.

'Lead us not into temptation': adolescence and alcohol policy in Europe.

Although the World Health Organization and the European Community recognize harm to children and young people due to alcohol-whether their own or someone else's drinking-effective policies to reduce harm are not widely followed. The alcohol beverage industry's drive to use social networking systems blurs the line between user-generated and industry marketing materials, such that young people are more frequently and at a younger age, potentially exposed to the promotion of alcoholic drinks. This contravenes recommendations arising out of the emerging scientific literature that delaying the onset of drinking and reducing the prevalence of heavy session drinking are likely to promote a healthier next generation.

Adolescence and Alcohol: a review of the literature.

Up to two thirds of adolescents consume alcohol and about a quarter engage in abusive behavior at some point. Many users begin alcohol use at young ages, and binge drinking is a dominant pattern for a proportion of youth. Because neurogenesis is inhibited by ethanol, consequences of adolescent alcohol abuse include changes in brain development and impairment of neurocognitive performance. A variety of mental and psychosocial problems are also often witnessed in alcohol abusing youth. Apart from the influence exerted by genetic and psychosocial factors, the chance of developing problematic alcohol consumption is increased by consumption in a binge drinking manner and by first contact with alcohol at a young age. Discrimination of alcohol consumption within the frames of normal adolescent behavior from problematic use is still a challenging issue. Different prevention programs provide treatment either directly to the adolescent, in the context of the school, or within the frame of the adolescent's family. Although some of these efforts have been shown to be effective in reducing alcohol misuse in youth, hardly any intervention reveals satisfactory outcomes in a long-term prospect. Successful prevention strategies would need to comprise treatment of current neuropsychological impairment as well as of comorbid mental health problems and concurrent other substance misuse.

Stress and alcohol cues exert conjoint effects on go and stop signal responding in male problem drinkers.

Stress, cues, and pharmacological priming are linked with relapse to addictive behavior. Increased salience and decreased inhibitory control are thought to mediate the effects of relapse-related stimuli. However, the functional relationship between these two processes is unclear. To address this issue, a modified Stop Signal Task was employed, which used Alcohol, Neutral, and Non-Words as Go stimuli, and lexical decision as the Go response. Subjects were 38 male problem drinkers (mean Alcohol Dependence Scale (ADS) score: 18.0). Uncontrollable noise (∼ 10 min at 110 dB) was the stressor; nonalcoholic placebo beer (P-Beer) was the cue manipulation, and alcohol (0.7 g/kg), the pharmacological prime. Half the sample received alcohol, and half P-Beer. Stress and beverage (test drink vs soft drink) were manipulated within subjects on two sessions, with half the sample receiving active manipulations together and half receiving them separately. Go response time (RT) and Stop Signal RT (SSRT) were slower to Alcohol than Neutral words. Stress augmented this bias. Alcohol and P-Beer impaired overall SSRT. Stress impaired neither overall SSRT nor Go RT. SSRT to Neutral words and Non-Words correlated inversely with Go RT to Alcohol and Neutral words, and Non-Words. ADS correlated directly with SSRT to Alcohol words. A resource allocation account was proposed, whereby diversion of limited resources to salient cues effectively yoked otherwise independent Go and Stop processes. Disturbances of prefrontal norepinephrine and dopamine were cited as possibly accounting for these effects. Treatments that optimize prefrontal catecholamine transmission may deter relapse by reducing disinhibitory effects of salient eliciting stimuli.

Linear correlation between phenobarbital dose and concentration in alcohol withdrawal patients.

INTRODUCTION: Barbiturates are potent drugs for treatment of alcohol withdrawal symptoms, but they entail a risk of over-dosage and respiratory depression. The purpose of the present study was to investigate the correlation between phenobarbital dose and phenobarbital blood concentration in patients withdrawing from long-term alcohol intoxication. MATERIAL AND METHODS: A total of 497 patients who were hospitalized for treatment of alcohol withdrawal symptoms during an 18-month period were enrolled in the study. Phenobarbital 200 mg was administered orally every 30 or 60 minutes in response to the observed symptoms. Within the first 24 hours after admission, i.e. at 8 AM, blood was collected for determination of phenobarbital concentration, and the cumulated dose of phenobarbital at the time of the blood sampling was registered. RESULTS: The mean cumulated phenobarbital dose at the time of the blood sampling was 877 mg +/- 557 mg, while the mean plasma phenobarbital concentration was 104 micromol/l +/- 62 micromol/l. A statistically significant linear correlation between phenobarbital dose and concentration was found for both males and females as 83% and 84% of the variation in drug concentration, respectively, could be explained by the phenobarbital dose. We observed no serious complications of the phenobarbital treatment--including respiratory problems or severe sedation. DISCUSSION: The strong linear correlation between phenobarbital dose and concentration suggests that absorption of plasma phenobarbital from the gastrointestinal system is highly predictable.

Ethanol causes and lithium prevents neuroapoptosis and suppression of pERK in the infant mouse brain.

Transient exposure of immature animals during the brain growth spurt period to ethanol triggers neuroapoptosis in the developing brain. Here we report that lithium, when administered in a single, well-tolerated dose to infant mice, suppresses spontaneous neuroapoptosis that occurs naturally in the developing brain, and prevents ethanol from triggering neuroapoptosis. To explore lithium's mechanism of action, we focused on kinase signaling systems (ERK, Akt, JNK) that are believed to play a regulatory role in cell survival, and found that very rapidly after ethanol administration there is a suppression of ERK phosphorylation, and that lithium stimulates ERK phosphorylation and prevents ethanol from suppressing this phosphorylation process. Ethanol also suppressed pAKT, but lithium did not counteract this effect. We also found that ethanol activates the JNK system, but this cannot explain the neurotoxic action of ethanol, because JNK activation did not occur in the same neuronal populations that are killed by ethanol.

[Thiamine metabolism disorders in the rat brain in experimental alcoholism and a possibility of their correction by vitamin E].

The influence of the chronic consumption of alcohol on biochemical reactions of thiamine metabolism in the rat brain is investigated. It is shown that the content of thiamine diphosphate (ThDP) in the brain tissue does not change at these conditions, though there is an essential decrease in the thiamine-kinase activity. The ability of the isolated nerve terminals (synaptosomes) to absorb labelled thiamine also decreases under this condition. The specified disturbances are probably the reason for deceleration of exchange of free (uncombined with proteins) thiamine and its phosphates in nervous cells, that results in the observed reduction in activity of pyruvate dehydrogenase complex (PDC) due to inactivation by phosphorylation. Thiamine-binding and thiaminetriphosphatase activities of thiamine-binding protein (ThBP) in the structure of synaptic plasma membranes (SPM), isolated from the rat brain in various experimental groups, have been investigated. The increase, with respect to control, in the both enzymes activity in SPM, isolated from the brain of rats with chronic alcoholism has been shown. Kinetic researches testify to an increase of affinity of SPM (ThBP) for thiamine and thiaminetriphosphate in these conditions. When vitamin E was given to animals with a model of chronic alcoholism the normalization of PDC activity in nervous cells was observed, that can testify to the transient character of these changes. Inability of vitamin E to normalize biological activities of ThBP in PMS, that has been analyzed, can testify to more deep disturbances in the structure of SPM or thiamine binding protein in their structure.

Effects of maternal administration of vitamins C and E on ethanol neurobehavioral teratogenicity in the guinea pig.

Consumption of ethanol during human pregnancy can produce a wide spectrum of teratogenic effects, including neurobehavioral dysfunction. This study, in the guinea pig, tested the hypothesis that chronic maternal administration of antioxidant vitamins C plus E, together with ethanol, mitigates ethanol neurobehavioral teratogenicity. Pregnant guinea pigs received one of the following four chronic oral regimens: ethanol and vitamins C plus E; ethanol and vitamin vehicle; isocaloric-sucrose/pair-feeding and vitamins C plus E; or isocaloric-sucrose/pair-feeding and vehicle. Vitamins C (250 mg) plus E (100mg) or vehicle were given daily, and ethanol (4 g/kg maternal body weight/day) (E) or isocaloric-sucrose/pair-feeding was given for 5 consecutive days followed by 2 days of no treatment each week throughout gestation. One neonate from selected litters was studied on postnatal day (PD) 0. Neurobehavioral function was determined by measuring task acquisition and task retention using an 8-day moving-platform version of the Morris water-maze task, starting on PD 45. Thereafter, in vivo electrophysiologic assessment of changes in hippocampal synaptic plasticity was conducted. There was an ethanol-induced decrease in neonatal brain weight compared with sucrose. The vitamins C plus E regimen protected hippocampal weight relative to brain weight in ethanol offspring, and mitigated the ethanol-induced deficit in the task-retention component of the water-maze task. However, in the sucrose group, this Vit regimen produced deficits in both task acquisition and task retention. The vitamins C plus E regimen did not mitigate the ethanol-induced impairment of hippocampal long-term potentiation. These results indicate that maternal administration of this high-dose vitamins C plus E regimen throughout gestation has limited efficacy and potential adverse effects as a therapeutic intervention for E neurobehavioral teratogenicity.

The neurotoxicity of alcohol.

Patterns of drinking are changing throughout the world and in many countries this will be detrimental to the health and welfare of the local population. Even uncomplicated alcoholics who have no specific neurological or hepatic problems show signs of regional brain damage and cognitive dysfunction. Many of these changes are exaggerated and other brain regions damaged in patients who have additional vitamin B1 (thiamine) deficiency (Wernicke-Korsakoff syndrome). Quantitative neuropathology techniques and improvements in neuroimaging have contributed significantly to the documentation of these changes but mechanisms underlying the damage are not understood. A human brain bank targeting alcohol cases has been established in Sydney, Australia and provides fresh and frozen tissue for alcohol researchers. The tissues can be used to test hypotheses developed from structural neuropathological studies or from animal models and in vitro studies. Identification of reversible pathological changes and preventative medical approaches in alcoholism should enhance rehabilitation and treatment efforts, thereby mitigating debilitating morbidities and reducing mortality associated with this universal public health problem.

Grape seed flavanols, but not Port wine, prevent ethanol-induced neuronal lipofuscin formation.

Lipofuscin is an end-product of lipid peroxidation which dramatically increases following ethanol consumption, as we have shown in hippocampal and cerebellar neurons. In this work, we corroborated observations indicating that supplementation of ethanol with 200 mg/l of grape seed flavanols prevents increased lipofuscin formation, an action that has been ascribed to the antioxidant properties of the flavanols. Because wine is an alcoholic beverage naturally rich in flavanols, we decided to study the effect of chronic ingestion of Port wine (PW), which also contains 20% ethanol and approximately 200 mg/l of flavanol oligomers, upon lipofuscin accumulation in the hippocampal CA1 and CA3 pyramidal neurons and in the cerebellar Purkinje cells. Six months old rats were fed with PW and results were compared with those obtained in ethanol-treated groups and pair-fed controls. After 6 months of treatment, the volume of lipofuscin per neuron was estimated using unbiased stereological methods. Treatment with PW resulted in an increase of lipofuscin in all neuronal populations studied when compared to controls and to rats treated with ethanol supplemented with flavanols. No differences were observed when comparisons were made with ethanol drinking rats. We conclude that PW, despite containing 20% ethanol and flavanols, does not prevent ethanol-induced lipofuscin formation as previously found in animals drinking ethanol plus flavanols. The reduced antioxidant capacity of PW might depend on the type and amount of flavanols present and on its content in sugars.

Anticonvulsive effects of kappa-opioid receptor modulation in an animal model of ethanol withdrawal.

Although the neurochemical mechanisms contributing to alcohol withdrawal seizures are poorly understood, withdrawal seizures probably reflect neuronal hyperexcitability resulting from adaptation to chronic alcohol. Altered kappa-Opioid receptor (KOP-R) signaling has been observed in multiple seizure types; however, a role for this system in ethanol withdrawal seizures has not been systematically characterized. We hypothesized that pharmacological manipulations of the KOP-R would alter withdrawal in mice selectively bred for differences in ethanol withdrawal severity. Withdrawal Seizure-Prone (WSP) and Withdrawal Seizure-Resistant (WSR) mice were made physically dependent using chronic ethanol vapor inhalation, and the effects of the KOP-R antagonist nor-binaltorphimine or agonist U-50,488H on withdrawal severity were examined. Pretreatment with nor-binaltorphimine significantly increased handling-induced convulsion (HIC) severity in withdrawing WSR mice, with no observable effects in withdrawing WSP mice. In contrast, U-50,488H significantly decreased HIC severity in WSP mice, with no effects in WSR mice. During extended withdrawal (i.e. hours 12+), a rebound hyperexcitability was observed in WSP mice given agonist. Thus, administration of a KOP-R antagonist increased withdrawal severity in mice normally resistant to withdrawal seizures, while a KOP-R agonist reduced convulsion severity in animals susceptible to withdrawal seizures. These observations are consistent with differences in the KOP-R system observed in these lines at the molecular level, and suggest the KOP-R system may be a promising therapeutic target for management of ethanol withdrawal seizures. Finally, these findings underscore the importance of determining the potential for rebound increases in withdrawal severity during later withdrawal episodes.