A review on alcohol: from the central action mechanism to chemical dependency

In contrast, prior studies had shown that ethanol-induced blockage of the NMDA receptor could increase neurotoxicity by decreasing the expression of brain-derived neurotrophic factor (BDNF) during chronic alcohol administration [62]. Therefore, more studies are needed to establish the role of the NMDA receptor in the mechanism of neurodegeneration or neuro-regeneration in patients with AUD. Although the risks of using central nervous system depressant (CNS-D) medications https://sober-house.org/cbt-and-dbt-in-alcohol-addiction-treatment/ with alcohol are well-documented, little is known about trends in prescribed use of these medications among individuals who regularly consume alcohol (i.e., trends in “concurrent use”). We examined changes in the prevalence of prescribed CNS-D medications among individuals who drank alcohol on 52 or more occasions in the past year (“regular drinking”). CNS-D medications included sedative-hypnotics (subclassified as anxiolytics or sleep medications) and opioids.

1. Thus, even with sobriety, recovering alcoholics are at a heightened risk of falling.
2. The study found that genotypic frequencies of STin2 VNTR polymorphism did not differ significantly across the three groups.
3. In a study conducted by,[65] which looked at the data collected from a large number of multiplex, alcoholic families under the COGA, no association was found between the GABRA1 and GABRA6 markers and AD.
4. If a person takes depressants for a long time, they may develop physical dependence and substance use disorder.

Sleep medications

The combination of fast absorption and taking in the drug through the lungs results in an immediate rush and noticeable effects. Metabolism and excretion vary depending on the chemical in question, but half-lives tend to be very short. https://sober-house.net/alcohol-withdrawal-symptoms-treatment-and-alcohol/ Nitrous oxide, for instance, is exhaled almost entirely through the lungs unchanged, resulting in a half-life of about 5 minutes. GHB found its main use as a club drug or party drug because of its euphoric effects at low doses.

Is there any way to prevent CNS depression?

Long-acting barbiturates such as phenobarbital have low lipid solubility and are slowly absorbed. In exchange for a delayed onset (about 1 hour), effects can last for up to 12 hours. This makes them useful as anticonvulsants since fewer doses are required to maintain the level of drug in the body. Barbiturates are derived from barbituric acid, https://sober-home.org/mesclun-vs-mesculin-everything-you-need-to-know/ first synthesized in 1864 by the Bayer Company. No use was found for it until 1903 when German chemists discovered the sedative-hypnotic effects of its derived compounds. The first barbiturate, barbital, was marketed by Bayer under the name Veronal® that year, and barbiturate use steadily increased in the first half of the 20th century.

Research Funded by NIMH

The gene encoding GABRA1 is located on chromosome 5 at 5q34-35 while the gene encoding GABRA6 is located on the same chromosome at 5q34. According to a study by,[62] a significant correlation was found with the GABRA1 genotype and Collaborative Study of the Genetics of Alcoholism (COGA) AD, history of blackouts, age at first drunkenness as well as the level of response to alcohol. The study concludes by stating that the efforts to characterize genetic contributions to AD may benefit by examining alcohol-related behaviors in addition to clinical AD. Despite its positive correlation, some studies have produced contradictory results. A study conducted by[39] to assess the association of Taq1A polymorphism and AD in south Indian population yielded negative results.[40,41] also did not find any association with Taq1A polymorphism and AD amongst Mexican-Americans. The Taq1A allele frequency of non-assessed controls was more than that of non-assessed alcoholics.

Alcohol’s impact on the functioning of the brain ranges from mild and anxiolytic disinhibitory effects, motor incoordination, sedation, emesis, amnesia, hypnosis and ultimately unconsciousness [4]. The synaptic transmission is heavily disturbed and altered by ethanol, and the intrinsic excitability in various areas of the brain is also compromised. The effects of ethanol may be pre-synaptic, post-synaptic, and at times, non-synaptic too. Alcohol being a psychotropic depressant of the CNS exerts a deeply profound impact on the neurons, which alters the biological and behavioural well-being of the one who consumes it by the promotion of interference in various neuronal pathways [5]. The treatments of many disorders of the CNS are shown to be affected by the consumption of alcohol, and thus, it is generally advised to keep oneself away from alcohol if one is undergoing treatment for any CNS manifestations, like anxiety or mood disorders [6].

NMDA receptor-mediated neurotoxicity

According to earlier studies, alcohol withdrawal seizures commonly occur due to an imbalance between glutamatergic and GABAergic neurotransmission which can be detected by MRS of the human brain [107]. Alcohol is the most commonly used recreational beverage and drug of abuse among the adult population, alcohol-related death is the third leading preventable cause of death in the United States which accounts for more than 3.3 million global deaths annually [1],[2]. According to the 2018-National Survey on Drug Use and Health (NSDUH), 14.4 million people suffered from alcohol use disorder (AUD) in the US, and over 100,000 deaths were attributable to alcohol [3]. The World Health Organization reported that more than 200 health conditions including cancer, liver cirrhosis, and neurocognitive impairment were also attributed to alcohol consumption [2].

For the last chapter in this unit, we will take a detailed look at alcohol, the most infamous depressant of all. Much of the terminology used to describe alcohol’s effects will have already been introduced in this chapter, so make sure you are comfortable with this chapter’s material before moving on. A common mode of nitrous oxide recreational use is inhalation or collection of the gas from cooking sprays and whipped cream canisters that use nitrous oxide as the propellant.

Similarly, another study conducted by[66] found no association between the genes encoding GABRA1 and GABRA6 with alcoholism. Likewise, in the study carried out by[59] which aimed at understanding the role of 5’-HTTLPR polymorphism with risky alcohol use in adolescence, there was no correlation with drinking to cope motives and the 5’-HTTLPR polymorphism. The study however found a positive correlation with drinking to cope motives and the Taq1A polymorphism of the DRD2 gene. Alcohol seldom leaves any system untouched as far as leaving its impression is concerned, spanning from single tissue involvement to complex organ system manifestations.

Once your CNS is back on track, you’ll need to address the source of the problem. If you have a condition that requires medication, you’ll need to follow your doctor’s instructions for care. If you’ve become addicted to alcohol or drugs, you’ll need to safely withdrawal from the chemicals and commit to long-term treatment for addiction. In small doses, these drugs slow brain function, producing a calm or sleepy feeling.

However, it is not clear that sleep medications are any less risky, given that they are pharmacologically related to benzodiazepines and still place individuals at high risk for several types of injuries and adverse effects (Chung et al., 2013; Bush, 2013). Apart from the dopamine pathways, the addiction to alcohol has also been suggested through the serotonin pathways. Serotonin is another neurotransmitter that is affected by many of the drugs of abuse, including cocaine, amphetamines, LSD and alcohol. Raphe nuclei neurons extend processes to and dump serotonin onto almost the entire brain, as well as the spinal cord. Serotonin plays a role in many brain processes, including regulation of body temperature, sleep, mood, appetite and pain.

2The nonunitary concept of memory posits that different types of memory exist (e.g., short term versus long term; episodic versus implicit) that represent either different mnemonic systems or different component processes of a system. Each system and component requires different brain regions for processing, and disruption of local brain regions or systems are the foundation of different types of memory impairment or amnesia. Caricatures depict “drunkards” as stumbling and uncoordinated, yet these motor signs are, for the most part, quelled with sobriety.

Signal transmission and cell interaction are accomplished by the formation and maintenance of the myelin sheath which is usually disrupted by alcohol metabolites. Alcohol interferes with the neuronal homeostasis process including the ability to form colonies, integrate, differentiate, and mainly proliferate [11]. The United States has undergone sharp increases in morbidity and mortality stemming from separate and combined use of alcohol and prescription drugs. Although the prevalence of current alcohol use and binge drinking has been increasing, changes in drinking patterns are modest in comparison to alcohol-related morbidity and mortality trends. Meta-analyses of data from six national surveys suggest that from 2000 to 2016, the prevalence of any past-year alcohol use increased by 0.3% per year and past-year binge drinking increased by about 0.7% per year among U.S. adults (18+) (Grucza et al., 2018). Notably, though, these increases have been highest among individuals age 50-64, with increases of 0.6% and 2.7% per year for any alcohol use and binge drinking respectively (Grucza et al., 2018).