Cellular and Mitochondrial Effects of Alcohol Consumption PMC

As a normal phenotype, microglia (guardian cells) in the CNS play an essential role in performing phagocytic activity. Microglia are the main drivers of neuroinflammation and mediate the onset and progression of AUD. These cells act as first responders to protect the brain from neuroinflammation [86,87]. Microglia sense the changes in the CNS and then immediately switch their phenotype to either proinflammatory M1 or anti-inflammatory M2, or mixed phenotypes [88,89]. The phenotypic switch of microglia in response to inflammatory responses is implicated in various neurological disorders, including AUD.

Structural and Volumetric Changes

Furthermore, association studies have undoubtedly affirmed the presence of fluctuating levels of inflammatory markers in alcoholic heart disease. For example, IL-6,−8,−12, TNF-α and its receptors-TNF-R were high in patients with alcoholic cardiomyopathy; the higher the severity of the cardiomyopathy the higher the level of these markers (Panchenko et al., 2015). Moiseev and colleagues found the same results in patients with congestive heart failure who had a previous history of alcohol-induced cardiac damage compared to patients who have ischemic cardiomyopathy (Moiseev et al., 2013). There is strong evidence supporting the fact that alcohol exposure during developmental stages results in devastating selective neuronal damage resulting in profound central nervous system (CNS) deficits. The severity of this damage depends on the duration, and frequency of exposure to ethanol during gestation.

• Alcohol use, especially excessive alcohol consumption, can harm your physical and mental health.
• Mayo Clinic Health System Fountain Centers is a chemical dependency treatment program that helps patients safely address substance-use problems and the life circumstances surrounding them.

Long-Term Effects of Alcohol on the Brain, Kidneys and Liver

Chronic alcohol use raises your risk for health problems, including heart disease, liver disease, cancer, and mental health disorders. The liver metabolizes most of the alcohol you consume, breaking it down into acetaldehyde. Acetaldehyde is a toxin that can damage the body’s organs and tissues before it is further broken down into acetate. Years of moderate to heavy drinking can cause liver scarring (fibrosis), increasing the risk of liver diseases like how does alcohol affect the kidneys cirrhosis, alcoholic hepatitis, fatty liver disease, and liver cancer. Neuropsychological performance correlated with a reduction in GM and WM in different regions of the brain, signifying a significant GM and WM tissue loss that can have long-term effects due to alcohol consumption (Hommer, 2003). Both GM and WM losses were observed in the anterior superior vermis, while the cerebellar hemisphere only displayed a GM reduction (Sullivan et al., 2000).

2. Contribution of Enteric Glial Cells in Alcohol-Induced Gut Inflammation

Another study with dogs (Beard et al. 1965) disclosed that the effects of chronic alcohol consumption endured even longer. The investigators noted increased plasma and extracellular fluid volume 1 week after chronic alcohol ingestion, and these volume expansions persisted for the remaining 7 weeks of the study. Similar alterations have been found in body fluid volumes among chronic alcoholic patients. One way in which alcohol directly affects the kidneys is by altering the form and structure of this pair of organs, as demonstrated by various animal studies. For example, in an early study on dogs (Chaikoff et al. 1948), investigators observed several striking alterations after chronic alcohol administration. The basement membrane of the glomerulus (see sidebar figure) became abnormally thickened and was characterized by cell proliferation.

• An important role of cytokines pertaining to their pro-inflammatory effect is their ability to upregulate cell adhesion molecules leading to alteration of the BBB integrity.
• Alcohol exposure resulted in increased DNA binding of the inflammatory factor nuclear factor κB (NF-κB) and decreased binding of the pro-survival factor cAMP responsive element-binding protein (CREB) (Crews and Nixon, 2009).
• Someone who is already feeling sleepy probably will feel sleepier after drinking alcohol.
• In fact, a strain of 5-HT1B receptor knockout mice exhibited less intoxication in response to alcohol compared with the normal mice, suggesting the role of 5-HT1B receptor in producing some of alcohol’s intoxication symptoms (Crabbe et al., 1996).

The effect on the body and sleep

Particularly, the relationship between inflammation and inflammatory markers with alcoholic heart disease has gained much attention lately. This review summarizes the recent progress on the deleterious effects of alcohol abuse on a person’s general health with special focus on the heart and brain (Figure ​(Figure1).1). These organs consist of permanent cells, where the mechanisms underlying ethanol mediated damage is still not clear. Understanding the nature of the deleterious effects of alcohol on these organs may provide new insights on how to manage and/or combat effectors of alcohol-induced cell injury. Alcohol affects differentially on the CNS, depending on the different areas of the brain.

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