Author: John Carter

Effects of Alcohol Consumption on Various Systems of the Human Body: A Systematic Review PMC

cns depressant alcohol

If severe CNS depression is left untreated, it can be fatal for the person living with the condition. Naloxone is administered to people who are suffering from an opioid overdose. In certain cases, CNS depression could also be caused by a stroke, brain trauma, an aneurysm, or a tumor. Some research shows that even conditions that don’t directly affect the brain, like diabetes or kidney and heart disease, could cause CNS depression.

  1. People have also been known to overdose on these medications deliberately to end their lives.
  2. Thus, analyses utilized data from participants who participated in both the in-home interview and MEC portions of the NHANES.
  3. Some people also use opioids and opiates, such as heroin, as recreational drugs.
  4. Research has also shown that drinking alcohol increases the risk of developing cancer.

Evidence from animal models and cell culture reports further strengthens the idea that chronic excessive alcohol exposure downregulates the tight junction proteins (claudin, occludin, zonula occludens) which are responsible for maintaining BBB integrity [43]. Both acute and chronic alcohol exposure can increase the production of ROS and enhance peroxidation of lipids, protein, and phosphorylation of mitochondria resulting in decreased ATP production by disrupting phospholipid-containing cell membrane structure [44]. Astrocytes maintain the BBB integrity by forming paracrine interactions to coordinates the CNS blood flow and neural function between pericytes and CNS vasculature [45]. Alcohol-induced tight junction disassembly is usually mediated via activation of expression protein kinase C (PKC) which subsequently allows toxic substances to enter the brain which in turn affects CNS homeostasis. Loss of astrocytes function to maintain the neurovascular coupling is not recovered by the proliferation of adjacent astrocytes resulting in long-term effect in neurovascular damage.

All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus. Alcohol seldom leaves any system untouched as far as leaving its impression is concerned, spanning from single tissue involvement to complex organ system manifestations.

It can also cause other side effects, including a risk for dependence and addiction. Several substances can depress the CNS, ranging from anti-anxiety and sleep medications to so-called recreational drugs, such as heroin. Mild CNS depression is often the goal of taking some CNS depressants, especially sleep and anxiety disorders. It’s important to take the medication exactly as your doctor prescribes to avoid a more severe form of the condition.

Drugs & Supplements

Under the guidance of a medical professional, stimulants may be helpful for certain individuals. However, misuse of stimulants can have serious health consequences, including physical dependence and stimulant addiction, also known as stimulant use disorder. When alcohol enters the body, most of it is absorbed into the bloodstream through the intestines. Blood, and therefore alcohol, is quickly distributed throughout the body and the brain. Naltrexone may also be used to reduce drinking without quitting cold turkey. This approach, known as the Sinclair Method, aims to reduce drinking by having people take naltrexone when consuming alcohol.

These are strong pain-relieving drugs that come from opium, a substance made from the seeds of the poppy. People with any of these conditions should check with a doctor before using a CNS depressant. Combining different CNS depressants, such as painkillers and alcohol, can be life-threatening.

cns depressant alcohol

The liver is the predominant organ for ethanol metabolism which usually occurs via two oxidative pathways mediated by alcohol dehydrogenase (ADH) and cytochrome P450 2E1 (CYP2E1) [30] (Figure 1). In brief, after drinking alcohol, absorption Occurs in the gastrointestinal tract then the liver converts the alcohol to acetaldehyde through the first-pass metabolism in the liver, this oxidation reaction is catalyzed by the alcohol dehydrogenase enzyme [31],[32]. After the first-pass metabolism, alcohol metabolites are distributed throughout the body, it goes to the brain through the blood vessels then it enters into the endothelial cells from the blood and alters the expression of signaling molecules which adhere to the BMVEC [33]. The metabolism of EtOH in the brain is controversial than the metabolism of acetaldehyde due to undetectable evidence of homogenous ADH activity in the whole brain. Animal experimental studies demonstrate the presence of cytochrome p4502E1 in the smooth endoplasmic reticulum of brain cells that are capable of Ethanol metabolism in brain by catalyzing the H2O2 with catalase enzyme [34]. However, the oxidation of acetaldehyde in brain cell is established because of ALDH (aldehyde dehydrogenase) have been well known to be found in mitochondria of brain cells [35].

Impairment of glucose transport system leads to neurodegeneration

Depolarization and activation of the nerve action potential are maintained by the influx of different types of ions (Na+ and Ca2+) into the cell through the NMDA receptors [58]. It is believed that alcohol acts as an antagonist for the NMDA receptor, so in the case of AUD, it causes hypofunction of the NMDA receptor which may result in neuronal network impairment with loss of synaptic plasticity [60]. To maintain normal neuronal function and homeostasis, the physiological actions of the NMDA receptor are required.

Anti-inflammatory and neuroprotective agents can be one of the novel therapeutic options to treat or diminish the progression of neurodegenerative disease. Among these factors, glial cell line-derived neurotrophic factor (GDNF) and mesencephalic astrocyte-derived neurotrophic factor (MANF) play a key role as neuroprotective agents in neuro restoration and neurogenesis to protect the neuron from oxidative damage [119],[112]. This review provides insight into alcohol mediated brain damage and establishes evidence that changes in the pathophysiology and lifestyle modifications can be an option for recovery and cell restoration in alcohol-induced neurodegeneration.

cns depressant alcohol

Records involving sedative-hypnotics or opioids were extracted according to the classification terms described in Box 1. Certain drugs with low abuse potential were excluded, such as antihistamines and supplements. Sedative-hypnotics were sub-classified by indication as anxiolytics and sleep medications. Anxiolytics were primarily benzodiazepines, and sleep medicines were predominantly zolpidem, eszopiclone, zaleplon, and ramelteon. To exclude medications used short-term for acute medical problems, we extracted only records for which medications were prescribed for 30 days or more. Before discussing the effect of alcohol on BBB damage, we have to look through alcohol absorption and metabolism.

How CNS Depression Works?

Continued use of some CNS depressants can be harmful long-term, as the body becomes unable to flush out these substances. CNS depressants are medications and other substances that slow down the CNS. A person may benefit from taking the correct dose of a CNS depressant, such as an opioid pain relief medication. Recreational use can be illegal and dangerous, as people may not understand the risks of misuse. If you are on CNS depressants and suspect it’s making you more lethargic than you should be, don’t stop it until you speak to your doctor.

Sonata and Ambien are two types of sleeping medication that are CNS depressants. Although they have a lower risk of dependency than other CNS depressants, long-term use may cause the condition. Over 140,000 people in the U.S. die from overconsuming alcohol each year. Alcohol overuse also increases the risk of developing other conditions, including depression. While alcohol can have some stimulating effects (like increased heart rate and anxiety), these effects are brief. Alcohol is a depressant that slows down your central nervous system, leading to decreased blood pressure, drowsiness, poor coordination, and reduced alertness.

Data Source.

This would typically go away when you stop using the medication or when your body adjusts to the medication. You might experience mild CNS depression from the prescribed use of CNS depressants or severe CNS depression from the misuse of CNS depressants, traumatic brain injury, or certain other conditions. These medications are prescribed in the form of a pill, capsule, or liquid that you take orally. They work by increasing your brain’s production of a chemical called gamma-aminobutyric acid (GABA). People may develop an addiction to alcohol after using it to cope with stress or traumatic life events. Addressing emotional or mental health concerns can help people with AUD find ways to cope that do not involve alcohol.

Her expertise focuses primarily on mental wellness and women’s health topics. Opioids are strong pain relievers that are obtained from opiates like heroin and oxycodone. They have a high risk of becoming addictive, which is why they are often prescribed in small doses for only short periods.

It is a common finding that one could perceive that alcohol is most of the time in the list of risk factors for various diseases. Alcohol has been found to adversely affect our immune system and the matter of concern as far as this issue is concerned is that immune responses are influenced by even moderate amounts of alcohol intake [26]. Alcohol affects innate immunity and also interferes with almost all the various aspects of the adaptive immune response. Alcohol is a key player in impairing anti-inflammatory cytokines and also promotes proinflammatory immune responses. The gastrointestinal biome is severely manipulated by the use of alcohol over a long period of time, which in turn is found to have a link with the establishment of various complications [27]. Alcohol and its metabolites are found to promote inflammation in the intestines and they do so through varied pathways [28].