Effects Of Alcohol Research Articles

Dyadic cannabis use, alcohol use and relationship satisfaction: A daily diary study

ObjectiveIntimate relationships are important contexts for understanding individuals’ substance use patterns and trajectories. Using a dyadic daily diary design reporting over 14 consecutive days, the present study examined the association between cannabis use, alcohol use, and momentary relationship satisfaction among adult couples MethodEligible individuals on Prolific were invited to participate. We identified 33 couples where both partners participated. Participants completed a baseline survey and a 14-day daily diary study assessing their daily cannabis use, alcohol use, and relationship satisfaction. Multilevel modeling was used, within an Actor-Partner Interdependence Model (APIM), to evaluate the individual and interactive effects of one’s own use and their partner’s use on relationship satisfaction ResultsSignificant actor and partner effects of alcohol and cannabis use were found using both baseline and daily report data. For individuals who use cannabis more heavily among sampled couples, cannabis and alcohol co-use was associated with reduction in their own next-day relationship satisfaction while alcohol-only use was significantly associated with increased next-day satisfaction. There were no significant effects of one’s own or their partner’s effects for individuals who use cannabis more lightly. ConclusionsFindings replicate and extend prior research by demonstrating the dynamic nature of dyadic substance use and highlighting the unique impact of alcohol and cannabis co-use on daily relationship functioning.

Decreasing brain activity caused by acute administration of ketamine and alcohol - A randomized, controlled, observer-blinded experimental study.

Substance abuse is a major public health problem. In recent years, ketamine, which is a parenteral anesthetic, has been consumed increasingly as an illicit drug together with alcohol, although little is known of how this association alters brain activity. The present study investigated the influence of progressive doses of ketamine, associated with alcohol, on electrophysiological activity. For this, 72 late-adolescent (8-10-week-old) male Wistar rats received either ketamine only, at low (10mg/kg), intermediate (20mg/kg) or high (30mg/kg) doses via intraperitoneal injection, or alcohol (2mL/100g) via oral gavage followed by ketamine (at low, intermediate, and high doses). Electroencephalograms (EEG) and electromyographic recordings were obtained 5min after the final application of the drug. When administered alone, ketamine resulted in an increase in delta, theta, beta, and gamma brainwaves, with a more pronounced effect being detected at the highest dose (30mg/kg) in the case of the delta, beta, and gamma waves. The amplitude of the alpha brainwaves was reduced at all doses of ketamine, but less intensively at the highest dose. When administered alone, alcohol reduced all the brainwaves, with the reduction in the alpha waves being exacerbated by ketamine at all doses, and that of the theta and beta waves being boosted at the lowest dose. The intermediate dose of ketamine (20mg/kg) reverted the alcohol-induced reduction in the theta and gamma waves, whereas the high dose increased delta, theta, beta, and gamma bandpower. Overall, then, while ketamine enhances the depressant effects of alcohol on the alpha brainwave at all doses, a low dose intensified this effect on the theta and beta 175 waves, whereas a high dose produces neuronal hyperexcitability in the theta and 176 gamma bandpower.

Examining the causal genetic effects of substance use on aging.

Substance use shortens lifespan, impedes health, and accelerates the biological aging process. We found widespread genetic correlations between alcohol, tobacco, cannabis, and opioid use and use disorders with indices of aging across the lifespan. There was evidence of tobacco and alcohol use and use disorders causally impacting physical, cognitive, and biological aging, with the effects of alcohol being more dependent on quantity of consumption; evidence of reverse causality was scant.

Rapid preparation of anti-retrogradation starch by choline chloride based deep eutectic solvents: A comparative study

Legumes are a widespread and cheap source of starch. However, legume starches are prone to retrogradation in applications. Therefore, enhancing the resistance to retrogradation is important to ensure the quality of starch products. In this study, the effects of amines, alcohols, and carboxylic acids deep eutectic solvents (DESs) on the retrogradation properties of pea starch (PS) were investigated. The results showed that the starches treated with carboxylic acid DESs for only 30 min exhibited low paste viscosity, high paste clarity and anti-retrogradation. The carboxylic acid DESs treatment resulted in holes or cracks appearing on the starch surface, a decrease in molecular ordering, relative crystallinity, and amylose content. The thermal enthalpy of starch as well as the pasting viscosity were substantially reduced after the treatment. The paste clarity and the resistance to retrogradation were significantly improved. Conversely, the structure, pasting and retrogradation properties of starch treated with amine and alcohol DESs exhibited only slight differences compared to PS. The carboxylic acid DESs took a short time for the starch modification, and the modified starch paste with low viscosity, high clarity, and resistance to retrogradation. The study could provide an environmentally-friendly and cost-effective method for the preparation of starch with well anti-retrogradation properties.

Relationship between friction reduction effect and solubility in base oil of organic friction modifiers

This study explored the relationship between the solubility of additives in base oils and their friction-reduction efficacy using cetyl alcohol as a model additive. Atomic force microscope friction tests demonstrated that the friction-reduction effect of cetyl alcohol varied significantly across the base oils. The solvation free energy was computed to evaluate the solubility of cetyl alcohol. A direct proportional relationship between friction-reduction and solvation free energy was observed, indicating additives with lower solubility have better friction-reduction performance. Neutron reflectometry experiments and molecular dynamics simulations revealed that lower solubility correlates with stronger adsorption. This study quantitatively clarified the relationship between solubility, adsorption, and friction reduction, providing insights into optimizing lubricant formulations and contributing to a deeper understanding of boundary lubrication mechanisms.

The Safety of Alcohol Pharmacotherapies in Pregnancy: A Scoping Review of Human and Animal Research.

Alcohol pharmacotherapies pose unknown teratogenic risks in pregnancy and are therefore recommended to be avoided. This limits treatment options for pregnant individuals with alcohol use disorders (AUD). The information on the safety of these medications during pregnancy is uncertain, prompting a scoping review. The objective of this review was to investigate available information on the safety of alcohol pharmacotherapies in pregnancy. Studies published between January 1990 and July 2023 were identified through searches in BIOSIS, Embase, PsycINFO and MEDLINE databases, using terms related to pregnancy and alcohol pharmacotherapies. The alcohol pharmacotherapies investigated were naltrexone, acamprosate, disulfiram, nalmefene, baclofen, gabapentin and topiramate. Studies were screened by two independent reviewers. Covidence software facilitated the management, screening and extraction of studies. A total of 105 studies were included in the review (naltrexone: 21, acamprosate: 4, disulfiram: 3, baclofen: 3, nalmefene: 0, topiramate: 55, gabapentin: 32) with some studies investigating multiple medications. Studies investigating naltrexone's safety in pregnancy focussed on opioid use disorders, with limited evidence regarding its safety in the context of AUD. Despite concerns about higher rates of some pregnancy complications, studies generally indicate naltrexone as a safer option compared with opioid agonists or alcohol during pregnancy. Acamprosate was not clearly associated with adverse effects of exposure in pregnancy, with two pre-clinical studies suggesting potential neuroprotective properties. Disulfiram has a high risk of congenital anomalies when used in pregnancy, believed to be due to its mechanism of action. Prenatal topiramate has also been associated with an increased risk of congenital anomalies, particularly oral clefts. There were mixed results concerning the safety of prenatal gabapentin and little to no literature investigating the safety of baclofen or nalmefene during pregnancy. There is insufficient research on the safety of alcohol pharmacotherapies in pregnancy. Despite this, given alcohol's teratogenic effects, naltrexone could be considered to help maintain abstinence in pregnant individuals with AUD, particularly when psychosocial treatments have failed.

Bidirectional associations between sleep and cannabis and alcohol (co-)use in daily life.

Poor sleep is common in the context of cannabis use, but experimental and daily-life studies provide mixed evidence for whether cannabis use helps or disturbs same-night sleep. Despite a high prevalence of co-use of alcohol and cannabis, most studies of cannabis use and sleep do not consider alcohol use. We sought to add to this literature by examining associations between cannabis and sleep in the context of alcohol co-use and to examine these associations bidirectionally using ecological momentary assessment. Participants were 88 adults reporting cannabis use at least 3×/week and simultaneous alcohol and cannabis use at least 2×/week. For 14 days, participants completed morning surveys assessing hours slept and perceived sleep quality from the night before. In morning surveys, random surveys, and substance-specific surveys, participants also reported on alcohol and cannabis craving, use, and amounts. Primary results from multilevel models demonstrated that cannabis use was not independently associated with sleep (duration or quality). However, cannabis use attenuated alcohol's negative effects on sleep quality. Results question the utility of cannabis use to improve sleep but highlight the attenuated negative effects of alcohol as a potential reinforcer of alcohol-cannabis co-use. Future work should continue to consider polysubstance use and integrate additional self-report and objective measures of sleep health to further clarify how cannabis use affects sleep.

Neutrophil extracellular traps activate hepatic stellate cells and monocytes via NLRP3 sensing in alcohol-induced acceleration of MASH fibrosis

ObjectiveAlcohol use in metabolic dysfunction-associated steatohepatitis (MASH) is associated with an increased risk of fibrosis and liver-related death. Here, we aimed to identify a mechanism through which repeated alcohol binges...

Effect of Allyl and Propargyl Alcohols on the Equilibrium Conditions of Methane Hydrate Formation

Effect of Allyl and Propargyl Alcohols on the Equilibrium Conditions of Methane Hydrate Formation

LEAP2, a ghrelin receptor inverse agonist, and its effect on alcohol-related responses in rodents

The underlying neurobiology of alcohol use disorder (AUD) is complex and needs further unraveling, with one of the key mechanisms being the gut-brain peptide ghrelin and its receptor (GHSR). However, additional substrates of the ghrelin pathway, such as liver-expressed antimicrobial peptide 2 (LEAP2), an endogenous GHSR inverse agonist, may contribute to this neurobiological framework. While LEAP2 modulates feeding and reward through central mechanisms, its effects on alcohol responses are unknown. The aim of the present study was therefore to identify the impact of central LEAP2 on the ability of alcohol to activate the mesolimbic dopamine system and to define its ability to control alcohol intake. These experiments revealed that central LEAP2 (i.e. into the third ventricle) prevented the ability of alcohol to cause locomotor stimulation in male mice, suppressed the memory of alcohol reward and attenuated the dopamine release in the nucleus accumbens caused by alcohol. Moreover, central LEAP2 reduced alcohol consumption in both male and female rats exposed to alcohol for 6 weeks before treatment. However, the serum levels of LEAP2 were similar between high- and low- alcohol-consuming (male) rats. Furthermore, central LEAP2 lowered the food intake in the alcohol-consuming male rats and reduced the body weight in the females. Collectively, the present study revealed that central LEAP2 mitigates alcohol-related responses in rodents, contributing to our understanding of the ghrelin pathway’s role in alcohol effects.

The TMEM132B-GABAA receptor complex controls alcohol actions in the brain.

Alcohol is the most consumed and abused psychoactive drug globally, but the molecular mechanisms driving alcohol action and its associated behaviors in the brain remain enigmatic. Here, we have discovered a transmembrane protein TMEM132B that is a GABAA receptor (GABAAR) auxiliary subunit. Functionally, TMEM132B promotes GABAAR expression at the cell surface, slows receptor deactivation, and enhances the allosteric effects of alcohol on the receptor. In TMEM132B knockout (KO) mice or TMEM132B I499A knockin (KI) mice in which the TMEM132B-GABAAR interaction is specifically abolished, GABAergic transmission is decreased and alcohol-induced potentiation of GABAAR-mediated currents is diminished in hippocampal neurons. Behaviorally, the anxiolytic and sedative/hypnotic effects of alcohol are markedly reduced, and compulsive, binge-like alcohol consumption is significantly increased. Taken together, these data reveal a GABAAR auxiliary subunit, identify the TMEM132B-GABAAR complex as a major alcohol target in the brain, and provide mechanistic insights into alcohol-related behaviors.

The effect of alcohol consumption on clinical outcomes and structural damage in patients with axial spondyloarthritis: A systematic literature review and meta-analysis

ObjectiveTo systematically review the effects of alcohol consumption (AC) on disease-specific outcomes in axial spondyloarthritis (axSpA). MethodsA systematic review of observational studies on axSpA and AC was conducted. Multiple electronic databases were searched for keywords. Two investigators reviewed articles to assess for inclusion eligibility. The Joanna Briggs Institute Critical Appraisal checklist was employed to evaluate the risk of bias. Standardized mean differences (SMD) were used to synthesize the data and I2 was used to ascertain heterogeneity. Spinal pain, disease activity as measured by Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Ankylosing Spondylitis Disease Activity Score (ASDAS), and spinal radiographic progression based on the modified Stokes Ankylosing Spondylitis Spinal Score (mSASSS) were examined as outcomes. ResultsSearch strategy identified 703 records; 13 articles were assessed for eligibility. Five studies (n=3858) were included. Compared to non-consumers, axSpA patients who consumed alcohol had lower BASDAI (SMD: −0.19, 95% CI: −0.37 to −0.02, I2=72.5%) and lower spinal pain (SMD: −0.17, 95% CI: −0.24 to −0.09, I2=0%). No significant difference was found for ASDAS (SMD: −0.19, 95% CI: −0.39 to 0.00, I2=36%). One cohort study on the spinal radiographic progression indicated greater radiographic progression among consumers (SMD: 0.35, 95% CI: 0.08 to 0.62). ConclusionAC appears to be associated with lower disease activity and spinal pain. However, these findings may reflect confounding by sex and smoking. Further longitudinal cohort studies with standardized measures for AC are warranted to assess the direction of alcohol's effect on structural damage progression.

Temporal differential effects of post-injury alcohol consumption in a mouse model of blast-induced traumatic brain injury

Traumatic brain injury is a prevalent condition that affects millions worldwide with no clear understanding or effective therapeutic management available. Military soldiers have a high risk of exposure to blast-induced traumatic brain injury (bTBI). Furthermore, alcohol drinking is common in this population, and studies have shown that post-TBI alcohol exposure can result in memory loss. Hence, it is possible that alcohol could contribute to the overall pathological outcome of brain trauma. However, such a possibility has not been explored in detail. Here, we combined a mild bTBI (mbTBI) model with the drinking-in-the-dark (DID) paradigm to investigate the pathological synergy between mbTBI and alcohol consumption by examining brain oxidative stress levels and behavioral alterations in mice. The results revealed the anxiolytic and short-term memory improvement effects of post-trauma alcohol drinking examined at an early timepoint post mbTBI. However, extended alcohol drinking for up to three weeks post mbTBI impaired long-term memory and was accompanied by intensified oxidative stress in brain regions associated with memory and anxiety. These findings, as well as those from previous in vitro TBI/alcohol studies, suggest a pathological synergy of physical force and post-impact alcohol exposure. This knowledge could potentially aid in establishing guidelines for TBI victims to avoid further injury to their brains as well as to help maximize their recovery following TBI.

The effects of moderate alcohol and THC co-use during male and female rat adolescence on AKT-GSK3ß signaling in adulthood

Alcohol and cannabis are often taken in combination, and extensive co-use has been linked to enduring changes in cognitive and metabolic functioning. The underlying mechanisms for these effects are unclear, but we recently demonstrated that co-administration of ethanol and delta-9-tetrahydrocannbinol (THC) to adolescent rats caused lasting adaptations in GABA and glycogen synthase kinase 3ß (GSK3ß) signaling in the medial prefrontal cortex (mPFC). As a ubiquitous protein kinase, GSK3ß is downstream to the protein kinase B (also known as AKT) pathway that is activated by insulin receptor signaling in a main control center for metabolism and energy homeostasis, the mediobasal hypothalamus (MBH). Our goal here was to investigate if volitional co-use of low to moderate levels of ethanol and THC would impact the total and phosphorylated levels (p) of AKT and GSK3ß in the mPFC and MBH. Peri-adolescent Long Evans rats [postnatal day (P) 30–47] consumed 10 % ethanol, cookies laced with THC (3–10 mg/kg/day), both drugs, or vehicle controls. On P114, we modeled re-exposure to a behaviorally relevant dose of THC by challenging rats (i.p.) with 5 mg/kg THC (or vehicle) and sacrificed them 30 min later. Western blot analysis revealed that THC challenge increased pAKT and pGSK3ß compared to control similarly across all treatment groups, sexes, and brain regions; no effects on total levels of AKT or GSK3ß were found. Previously reported behavioral results from these rats showed no differences in working memory assessed in adulthood. Although future studies will be necessary to determine the role of exposure dose on drug-induced adaptations in AKT and GSK3ß signaling, the current findings suggest that moderate volitional co-use of alcohol and THC may not produce long-term deficits that persist into adulthood.

The glucagon-like peptide-1 and other endocrine responses to alcohol ingestion in women with versus without metabolic surgery.

Glucagon-like peptide-1 (GLP-1)-based therapies, effective in treating obesity and type 2 diabetes, hold potential for reducing alcohol-seeking behaviour. However, the understanding of how alcohol consumption affects endogenous GLP-1 responses-important for understanding GLP-1-based therapies' potential in addressing alcohol misuse-is limited, given the absence of placebo-controlled studies examining these effects. This study aimed to determine the acute effects of alcohol ingestion on GLP-1 and other peptides and evaluate whether metabolic surgery, which increases GLP-1 responses, blood alcohol concentrations (BAC) and alcohol misuse risk, influences this effect. Additionally, we assessed the acute effects of alcohol on plasma glucose and insulin concentrations. Using a placebo-controlled crossover study, we examined hormonal and glucose responses after oral alcohol consumption (0.5g/kg of fat-free mass) versus placebo drinks in 18 women who underwent metabolic surgery <5years ago and in 14 non-operated controls (equivalent in age, body mass index [BMI], race and alcohol consumption patterns). Women had a mean (SD) age of 41 (10) years and a BMI of 33 (5) kg/m2. Compared with the control group, the surgery group exhibited a higher peak BAC (0.99 [0.20] g/L vs. 0.75 [0.16] g/L; P < 0.005). Alcohol decreased GLP-1 by 34% (95% CI, 16%-52%) in both groups and decreased ghrelin more in the control (27%) than in the surgery group (13%). Alcohol modestly decreased plasma glucose and transiently increased insulin secretion in both groups (P < 0.05). However, alcohol lowered blood glucose concentrations to the hypoglycaemic range in 28% of the women in the surgery group versus none in the control group. These findings provide compelling evidence that acute alcohol consumption decreases GLP-1, a satiation signal, elucidating alcohol's 'apéritif' effect. This study also highlights the potential increase in alcohol-related hypoglycaemic effects after metabolic surgery.

Receptor and metabolic insights on the ability of caffeine to prevent alcohol-induced stimulation of mesolimbic dopamine transmission

The consumption of alcohol and caffeine affects the lives of billions of individuals worldwide. Although recent evidence indicates that caffeine impairs the reinforcing properties of alcohol, a characterization of its effects on alcohol-stimulated mesolimbic dopamine (DA) function was lacking. Acting as the pro-drug of salsolinol, alcohol excites DA neurons in the posterior ventral tegmental area (pVTA) and increases DA release in the nucleus accumbens shell (AcbSh). Here we show that caffeine, via antagonistic activity on A2A adenosine receptors (A2AR), prevents alcohol-dependent activation of mesolimbic DA function as assessed, in-vivo, by brain microdialysis of AcbSh DA and, in-vitro, by electrophysiological recordings of pVTA DA neuronal firing. Accordingly, while the A1R antagonist DPCPX fails to prevent the effects of alcohol on DA function, both caffeine and the A2AR antagonist SCH 58261 prevent alcohol-dependent pVTA generation of salsolinol and increase in AcbSh DA in-vivo, as well as alcohol-dependent excitation of pVTA DA neurons in-vitro. However, caffeine also prevents direct salsolinol- and morphine-stimulated DA function, suggesting that it can exert these inhibitory effects also independently from affecting alcohol-induced salsolinol formation or bioavailability. Finally, untargeted metabolomics of the pVTA showcases that caffeine antagonizes alcohol-mediated effects on molecules (e.g. phosphatidylcholines, fatty amides, carnitines) involved in lipid signaling and energy metabolism, which could represent an additional salsolinol-independent mechanism of caffeine in impairing alcohol-mediated stimulation of mesolimbic DA transmission. In conclusion, the outcomes of this study strengthen the potential of caffeine, as well as of A2AR antagonists, for future development of preventive/therapeutic strategies for alcohol use disorder.

The effect of alcohol on brain structures involved in the formation of addiction

Annotation. The process of forming alcohol addiction leads to the occurrence of irreversible changes in the human body, which can be fatal. Neurons of the brain are among the most sensitive structures to the effects of ethanol. Brain neurons are one of the most sensitive structures to the action of ethanol. Understanding the mechanism of formation of alcohol dependence can help in the treatment of patients with this disorder. Therefore, goal is a detailed study of the areas of the brain that are responsible for the formation of this disorder. For this, was analyzed the PubMed database. Articles were selected that discussed the areas of the brain involved in the formation of this disorder, changes in dopaminergic and GABAergic neurons, increased or decreased expression of proteins that regulate neuroplasticity of these areas during chronic ethanol consumption. For the convenience of searching, articles are grouped by publication years: 2000-2010, 2011-2018, and 2019-2023. According to the results of this study, we believe that the hippocampus, prefrontal cortex (PFC), nucleus accumbens, the amygdala and the ventral tegmental area (VTA) are key brain structures involved in the formation of addiction; these areas are part of the mesocorticolimbic reward pathway; the hippocampus is responsible for the formation of pleasant memories, it can decrease under the influence of ethanol, which leads to the loss of episodic memory; the PFC has an influence on decision-making that is based on experience, alcohol suppresses PFC activity; the adjacent nucleus stimulates a person through dopamine connections to relapse, because plasticity changes under the influence of ethanol; the amygdala - is the center of formation of positive and negative emotions, and alcohol withdrawal reduces the activity of this structure and causes stress, while chronic use of ethanol, on the contrary, activates the amygdala; The VTA has connections with all structures of the mesocorticolimbic pathway, it can both facilitate alcohol use and stimulate aversion to it. Conclusion: in our opinion, these structures are the most important in the process of forming addiction. The perspective of the research, in our opinion, is the study of the molecular mechanisms of addiction.

Domestic violence: alcoholism as a cause and a contributing factor

The article examines the influence of alcoholism as one of the main factors contributing to domestic violence. It was established that alcoholism is a problem that significantly increases the psychological causes of violence, is a significant factor that affects the spread of domestic violence, as it significantly changes a person’s behavior and psycho-emotional state. Under the influence of alcohol, people can lose self-control, become more aggressive and prone to violent actions, which is especially dangerous in the home environment, where interaction takes place against the background of close relationships and emotional dependence. It is motivated that people under the influence of alcohol can exaggerate the importance of minor misunderstandings or react to them with disproportionate aggression, which leads to the escalation of conflicts that could be resolved without violence under normal circumstances. It is indicated that an important aspect is that alcoholism affects the psychological state of all family members. Victims of violence, especially domestic violence, often feel isolated and vulnerable, which can lead to social tension and conflict in communities. Victims of domestic violence may experience constant fear and stress due to the unpredictability of their partner’s behavior, which creates a state of chronic tension that can lead to mental disorders. It is highlighted how the use of alcohol changes a person’s behavior, reducing his ability to self-control and increasing the risk of aggressive actions. Particular attention is paid to how alcoholism creates economic instability and psychological stress for victims, making it difficult to get out of violent relationships. The social aspect of the problem was also investigated, in particular the influence of the cultural legitimization of alcohol on the perception of violence. In some societies, alcohol is part of a cultural practice that can contribute to the normalization of aggressive behavior and reduce the perceived seriousness of violence. To effectively combat domestic violence, it is necessary to change social norms and raise awareness of the negative consequences of alcoholism, while providing adequate support to victims.

The Dark Side of Alcohol: Implications for Muscle Growth, mTOR Pathway, and Athletic Recovery

Introduction and Objective: Alcohol is a prevalent substance in many cultures, often associated with socializing, relaxation, and even post-exercise rituals. Despite its widespread use, the effects of alcohol on muscle recovery and hypertrophy are not well understood by the general public. Emerging research suggests that alcohol may have negative health effects on these factors. Understanding the interaction between alcohol consumption and resistance training is crucial for athletes and individuals aiming to optimize their fitness outcomes. The main aim of this article is to show clinicians, patients and, above all, athletes, the negative effects of alcohol on training and leading a healthy lifestyle. Review and Methods: Review and summary of studies and meta-analysis of studies available in open-source format on Google Scholar, Web of Science and PubMed. Abbreviated Description of the State of Knowledge: Resistance training is a proven method for increasing muscle mass and strength through the process of hypertrophy, where muscle protein synthesis (MPS) exceeds muscle protein breakdown (MPB). The mechanistic/mammalian target of rapamycin (mTOR) signaling pathway plays a key role in regulating MPS and hypertrophy. Summary: Alcohol has been shown to impair muscle protein synthesis, primarily through its negative effects on the mTOR signaling pathway, which is crucial for muscle growth. Additionally, alcohol disrupts sleep quality, further hindering recovery and performance.

Combined effects of alcohol and lead on cerebrospinal fluid production

Currently, due to the development of industry, a high incidence of heavy metal salt poisoning is observed, especially in people with alcohol dependence. The study aims to investigate the combined effects of these pathogens on the central nervous system. The study demonstrates changes in intracranial pressure and cerebrospinal fluid production in isolated and combined poisoning of lead and ethanol based on experimental models on 10 and 40 days of exposure, 3 main groups were formed – the group of lead salts, ethanol, combined intoxication, after which the main indicators were measured. The effect of separate and combined action of alcohol and lead on cerebrospinal fluid production and haemodynamic indices in experimental animals was studied. It was found at 40-day intoxication indices remained above normal, systemic arterial pressure was 131.8 mmHg, and the rate of cerebrospinal fluid production was 0.073±0.002 ml/min. Combined 10-day combined action of alcohol and lead enhances their excitatory effect, which is characterised by an increase in systemic arterial pressure (to the level of 135.6 mmHg) and general psycho-somatic agitation, the rate of cerebrospinal fluid production was 0.077±0.008 ml/min. The 40-day co-exposure manifested mainly toxic effects of lead, as shown by a decrease in cerebrospinal fluid production of 0.049±0.001 ml/min, and a decrease in blood pressure to a level of 93.6 mmHg. The results of this study will make it possible to develop treatment protocols for patients with ethanol and heavy metal salt poisoning, especially in the field of anti-oedema therapy